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Triglycerides and Cardiovascular Disease: A Scientific Statement From the American Heart Association
Abstract
For the purpose of this statement, CVD is inclusive of coronary heart disease and coronary artery disease.
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339 Not checked yet · 48 No basis given · 44 Own interpretation · 2 Sources not found
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In the paper
“However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites NHANES 1988-1994
- Not checked yetcites NHANES 1999-2008
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.
None of the sources cited for this claim have been checked yet.
In the paper
“Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites NHANES 1988-1994
- Not checked yetcites NHANES 1999-2008
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.
In the paper
“The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites NHANES 1999-2008
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.
None of the sources cited for this claim have been checked yet.
In the paper
“Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites [6] 6. Carroll MD, Lacher DA, Sorlie PD, Cleeman JI, Gordon DJ, Wolz M, Grundy SM, Johnson CL. Trends in serum lipids and lipoproteins of adults, 1960 -2002. JAMA. 2005;294:1773-1781.
- Not checked yetcites [4] 4. Consensus Conference: treatment of hypertriglyceridemia. JAMA. 1984; 251:1196 -1200.
- Not checked yetcites [10] 10. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001;285:2486 -2497. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites NHANES 1999-2008
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.
In the paper
“High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites NHANES 1999-2008
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.
In the paper
“Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites NHANES 1999-2008
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.
None of the sources cited for this claim have been checked yet.
In the paper
“In many of these studies, subjects with elevated triglyceride levels exhibited improvement in CVD risk, irrespective of drug class or targeted lipid fraction, 38 -40 primarily because elevated triglyceride level at baseline was commonly accompanied by high LDL-C and low HDL-C, and this combination (ie, the atherogenic dyslipidemic triad) was associated with the highest CVD risk.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.4. Insights From Clinical Trials
What the sources say
- Not checked yetcites [38] 38. Carlson LA, Rosenhamer G. Reduction of mortality in the Stockholm Ischaemic Heart Disease Secondary Prevention Study by combined treatment with clofibrate and nicotinic acid. Acta Med Scand. 1988;223: 405-418.
- Not checked yetcites [39] 39. Manninen V, Tenkanen L, Koskinen P, Huttunen JK, Ma ¨ntta ¨ri M, Heinonen OP, Frick MH. Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study: implications for treatment. Circulation. 1992;85:37-45.
- Not checked yetcites [40] 40. Ballantyne CM, Olsson AG, Cook TJ, Mercuri MF, Pedersen TR, Kjekshus J. Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S. Circulation. 2001;104:3046 -3051. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In another case-control study, case subjects were 3-fold more likely to exhibit small, dense low-density lipoprotein (LDL) particles, referred to as the “pattern B” phenotype.35”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.2. Case-Control Studies, Including Angiographic Studies
What the sources say
- Not checked yetcites [35] 35. Austin MA, Breslow JL, Hennekens CH, Buring JE, Willett WC, Krauss RM. Low-density lipoprotein subclass patterns and risk of myocardial infarction. JAMA. 1988;260:1917-1921. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
What the sources say
- Not checked yetcites [13] 13. Criqui MH, Heiss G, Cohn R, Cowan LD, Suchindran CM, Bangdiwala S, Kritchevsky S, Jacobs DR Jr, O'Grady HK, Davis CE. Plasma triglyceride level and mortality from coronary heart disease. N Engl J Med. 1993;328:1220 -1225.
- Not checked yetcites [20] 20. Jeppesen J, Hein HO, Suadicani P, Gyntelberg F. Triglyceride concen- tration and ischemic heart disease: an eight-year follow-up in the Copenhagen Male Study [published correction appears in Circulation. 1998;97:1995]. Circulation. 1998;97:1029 -1036.
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In the paper
“Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
What the sources say
- Not checked yetcites [21] 21. Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007;298:299 -308. source
- Not checked yetcites [22] 22. Bansal S, Buring JE, Rifai N, Mora S, Sacks FM, Ridker PM. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA. 2007;298:309 -316. source
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In the paper
“In univariate analysis, the relative risk per 1 mmol/L (88.5 mg/dL) of triglyceride for CVD in men was 1.32 (95% confidence interval 1.26 to 1.39) and 1.14 (95% confidence interval 1.05 to 1.28) after adjustment for HDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies
What the sources say
- Not checked yetcites [36] 36. Hokanson JE, Austin MA. Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein choles- terol level: a meta-analysis of population-based prospective studies. J Cardiovasc Risk. 1996;3:213-219. source
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“In univariate analysis, the relative risk per 1 mmol/L (88.5 mg/dL) of triglyceride for CVD in men was 1.32 (95% confidence interval 1.26 to 1.39) and 1.14 (95% confidence interval 1.05 to 1.28) after adjustment for HDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies
What the sources say
- Not checked yetcites [36] 36. Hokanson JE, Austin MA. Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein choles- terol level: a meta-analysis of population-based prospective studies. J Cardiovasc Risk. 1996;3:213-219. source
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In the paper
“In many of these studies, subjects with elevated triglyceride levels exhibited improvement in CVD risk, irrespective of drug class or targeted lipid fraction, 38 -40 primarily because elevated triglyceride level at baseline was commonly accompanied by high LDL-C and low HDL-C, and this combination (ie, the atherogenic dyslipidemic triad) was associated with the highest CVD risk.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.4. Insights From Clinical Trials
What the sources say
- Not checked yetcites [38] 38. Carlson LA, Rosenhamer G. Reduction of mortality in the Stockholm Ischaemic Heart Disease Secondary Prevention Study by combined treatment with clofibrate and nicotinic acid. Acta Med Scand. 1988;223: 405-418.
- Not checked yetcites [39] 39. Manninen V, Tenkanen L, Koskinen P, Huttunen JK, Ma ¨ntta ¨ri M, Heinonen OP, Frick MH. Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study: implications for treatment. Circulation. 1992;85:37-45.
- Not checked yetcites [40] 40. Ballantyne CM, Olsson AG, Cook TJ, Mercuri MF, Pedersen TR, Kjekshus J. Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S. Circulation. 2001;104:3046 -3051. source
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In the paper
“Experimental studies suggest that hypertriglyceridemic HDL may be dysfunctional, 55,56 that small, dense LDL particles may be more susceptible to oxidative modification, 57,58 and that an increased number of atherogenic particles may adversely influence CVD risk 59 ; however, no clinical outcome trials to date have determined whether normalization of particle composition or reduction of particle”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.4. Metabolic Consequences of Hypertriglyceridemia
What the sources say
- Not checked yetcites [57] 57. Chait A, Brazg RL, Tribble DL, Krauss RM. Susceptibility of small, dense, low-density lipoproteins to oxidative modification in subjects with the atherogenic lipoprotein phenotype, pattern B. Am J Med. 1993; 94:350 -356.
- Not checked yetcites [58] 58. Kwiterovich PO Jr. Clinical relevance of the biochemical, metabolic, and genetic factors that influence low-density lipoprotein heterogeneity. Am J Cardiol. 2002;90:30i-47i.
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In the paper
“However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
What the sources say
- Not checked yetcites [19] 19. Ninomiya JK, L'Italien G, Criqui MH, Whyte JL, Gamst A, Chen RS. Association of the metabolic syndrome with history of myocardial infarction and stroke in the Third National Health and Nutrition Exam- ination Survey. Circulation. 2004;109:42-46.
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In the paper
“Although many early cohort studies found a univariate association of triglycerides with CVD, this association often became nonsignificant after adjustment for either TC or LDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“At baseline, triglyceride levels in the top quintile were associated with a 4-fold increased risk of CVD compared with the lowest triglyceride quintile, even after adjustment for other risk factors, including HDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies
What the sources say
- Not checked yetcites [37] 37. Tirosh A, Rudich A, Shochat T, Tekes-Manova D, Israeli E, Henkin Y, Kochba I, Shai I. Changes in triglyceride levels and risk for coronary heart disease in young men. Ann Intern Med. 2007;147:377-385. source
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In the paper
“With adjustment for age and sex, triglycerides showed a strong, stepwise association with both CVD and ischemic stroke; however, after adjustment for standard risk factors and for HDL-C and non-HDL-C, the associations for both CVD and stroke were no longer significant.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies
What the sources say
- Not checked yetcites [17] 17. Di Angelantonio E, Sarwar N, Perry P, Kaptoge S, Ray KK, Thompson A, Wood AM, Lewington S, Sattar N, Packard CJ, Collins R, Thompson SG, Danesh J; Emerging Risk Factors Collaboration. Major lipids, apolipoproteins, and risk of vascular disease. JAMA. 2009;302: 1993-2000. source
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In the paper
“In 13 953 men 26 to 45 years old who were followed up for 10.5 years, there were significant correlations between adoption of a favorable lifestyle (eg, weight loss, physical activity) and a decrease in triglyceride levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies
What the sources say
- Not checked yetcites [37] 37. Tirosh A, Rudich A, Shochat T, Tekes-Manova D, Israeli E, Henkin Y, Kochba I, Shai I. Changes in triglyceride levels and risk for coronary heart disease in young men. Ann Intern Med. 2007;147:377-385. source
plaincorrelationaln = 13,953- Asserted: passes — The authors put it forward as true.
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In the paper
“Experimental studies suggest that hypertriglyceridemic HDL may be dysfunctional, 55,56 that small, dense LDL particles may be more susceptible to oxidative modification, 57,58 and that an increased number of atherogenic particles may adversely influence CVD risk 59 ; however, no clinical outcome trials to date have determined whether normalization of particle composition or reduction of particle”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.4. Metabolic Consequences of Hypertriglyceridemia
What the sources say
- Not checked yetcites [55] 55. Greene DJ, Skeggs JW, Morton RE. Elevated triglyceride content diminishes the capacity of high density lipoprotein to deliver cholesteryl esters via the scavenger receptor class B type I (SR-BI). J Biol Chem. 2001;276:4804 -4811. source
- Not checked yetcites [56] 56. Skeggs JW, Morton RE. LDL and HDL enriched in triglyceride promote abnormal cholesterol transport. J Lipid Res. 2002;43:1264 -1274. source
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In the paper
“Evaluation of the change in triglyceride levels over the first 5 years and incident CVD in the next 5 years found a direct correlation between increases in triglyceride levels and CVD risk.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies
What the sources say
- Not checked yetcites [37] 37. Tirosh A, Rudich A, Shochat T, Tekes-Manova D, Israeli E, Henkin Y, Kochba I, Shai I. Changes in triglyceride levels and risk for coronary heart disease in young men. Ann Intern Med. 2007;147:377-385. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In many of these studies, subjects with elevated triglyceride levels exhibited improvement in CVD risk, irrespective of drug class or targeted lipid fraction, 38 -40 primarily because elevated triglyceride level at baseline was commonly accompanied by high LDL-C and low HDL-C, and this combination (ie, the atherogenic dyslipidemic triad) was associated with the highest CVD risk.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.4. Insights From Clinical Trials
What the sources say
- Not checked yetcites [38] 38. Carlson LA, Rosenhamer G. Reduction of mortality in the Stockholm Ischaemic Heart Disease Secondary Prevention Study by combined treatment with clofibrate and nicotinic acid. Acta Med Scand. 1988;223: 405-418.
- Not checked yetcites [39] 39. Manninen V, Tenkanen L, Koskinen P, Huttunen JK, Ma ¨ntta ¨ri M, Heinonen OP, Frick MH. Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study: implications for treatment. Circulation. 1992;85:37-45.
- Not checked yetcites [40] 40. Ballantyne CM, Olsson AG, Cook TJ, Mercuri MF, Pedersen TR, Kjekshus J. Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S. Circulation. 2001;104:3046 -3051. source
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In the paper
“TRL may also act to suppress the atheroprotective and antiinflammatory effects of HDL.70 -72”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.1. Remnant Lipoprotein Particles A number of experimental systems have demonstrated that TRLs can produce proatherogenic responses in isolated endothelial cells.RLPs are a by-product of TRL that can be isolated from the postprandial plasma of hypertriglyceridemic subjects; they are intestinal (ie, CMRs) or liver-derived (eg, VLDL remnants) TRLs that have undergone partial hydrolysis by LPL.Liu et al 64 have shown that these particles can accelerate senescence and interfere with the function of endothelial progenitor cells; these cells play an important role in the organismal reparative response to in vivo vessel wall injury.Postprandial TRL (ppTG) has also been shown to increase the expression of proinflammatory genes (eg, interleukin-6, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1), 65 induce apoptosis, 66 and accentuate the inflammatory response of cultured endothelial cells to tumor necrosis factor-␣.67 After a high-fat meal, ppTG may increase the level of circulating endothelial cell microparticles, a measure of endothelial cell dysfunction in vivo.68 That is, a high-fat diet increases the level of these particles more effectively than a low-fat diet and is correlated with ppTG levels.Moreover, Rutledge and colleagues have shown that fatty acids released by lipolysis of TRL elicit proinflammatory responses in endothelial cells.69 TRL may also act to suppress the atheroprotective and antiinflammatory effects of HDL.70 -72 Finally, fatty acid-binding proteins play a role in the intracellular transport of long-chain fatty acids.Recent data support a role for adipocyte-and macrophage-derived fatty acid-binding proteins in systemic inflammatory responses 73 that are likely amplified by high triglyceride loads provided by RLPs to the arterial macrophages.
What the sources say
- Not checked yetcites [70] 70. Palmer AM, Murphy N, Graham A. Triglyceride-rich lipoproteins inhibit cholesterol efflux to apolipoprotein (apo) A1 from human mac- rophage foam cells. Atherosclerosis. 2004;173:27-38.
- Not checked yetcites [71] 71. Patel S, Puranik R, Nakhla S, Lundman P, Stocker R, Wang XS, Lambert G, Rye KA, Barter PJ, Nicholls SJ, Celermajer DS. Acute hypertriglyceridaemia in humans increases the triglyceride content and decreases the anti-inflammatory capacity of high density lipoproteins. Atherosclerosis. 2009;204:424 -428.
- Not checked yetcites [72] 72. Linsel-Nitschke P, Jansen H, Aherrarhou Z, Belz S, Mayer B, Lieb W, Huber F, Kremer W, Kalbitzer HR, Erdmann J, Schunkert H. Macro- phage cholesterol efflux correlates with lipoprotein subclass distribution and risk of obstructive coronary artery disease in patients undergoing coronary angiography. Lipids Health Dis. 2009;8:14.
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“After a high-fat meal, ppTG may increase the level of circulating endothelial cell microparticles, a measure of endothelial cell dysfunction in vivo.68”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.1. Remnant Lipoprotein Particles A number of experimental systems have demonstrated that TRLs can produce proatherogenic responses in isolated endothelial cells.RLPs are a by-product of TRL that can be isolated from the postprandial plasma of hypertriglyceridemic subjects; they are intestinal (ie, CMRs) or liver-derived (eg, VLDL remnants) TRLs that have undergone partial hydrolysis by LPL.Liu et al 64 have shown that these particles can accelerate senescence and interfere with the function of endothelial progenitor cells; these cells play an important role in the organismal reparative response to in vivo vessel wall injury.Postprandial TRL (ppTG) has also been shown to increase the expression of proinflammatory genes (eg, interleukin-6, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1), 65 induce apoptosis, 66 and accentuate the inflammatory response of cultured endothelial cells to tumor necrosis factor-␣.67 After a high-fat meal, ppTG may increase the level of circulating endothelial cell microparticles, a measure of endothelial cell dysfunction in vivo.68 That is, a high-fat diet increases the level of these particles more effectively than a low-fat diet and is correlated with ppTG levels.Moreover, Rutledge and colleagues have shown that fatty acids released by lipolysis of TRL elicit proinflammatory responses in endothelial cells.69 TRL may also act to suppress the atheroprotective and antiinflammatory effects of HDL.70 -72 Finally, fatty acid-binding proteins play a role in the intracellular transport of long-chain fatty acids.Recent data support a role for adipocyte-and macrophage-derived fatty acid-binding proteins in systemic inflammatory responses 73 that are likely amplified by high triglyceride loads provided by RLPs to the arterial macrophages.
What the sources say
- Not checked yetcites [68] 68. Ferreira AC, Peter AA, Mendez AJ, Jimenez JJ, Mauro LM, Chirinos JA, Ghany R, Virani S, Garcia S, Horstman LL, Purow J, Jy W, Ahn YS, de Marchena E. Postprandial hypertriglyceridemia increases circulating levels of endothelial cell microparticles. Circulation. 2004;110: 3599 -3603.
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In the paper
“Emerging evidence from a number of in vitro studies has shown that apo CIII, alone or as an integral component of TRL, can produce proatherogenic responses in cultured endothelial and monocytic cells.74,76”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.2. Apo CIII
What the sources say
- Not checked yetcites [74] 74. Ooi EM, Barrett PH, Chan DC, Watts GF. Apolipoprotein C-III: under- standing an emerging cardiovascular risk factor. Clin Sci (Lond). 2008; 114:611-624. source
- Not checked yetcites [76] 76. Caron S, Staels B. Apolipoprotein CIII: a link between hypertriglycer- idemia and vascular dysfunction? Circ Res. 2008;103:1348 -1350.
plaindirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Experimental studies suggest that hypertriglyceridemic HDL may be dysfunctional, 55,56 that small, dense LDL particles may be more susceptible to oxidative modification, 57,58 and that an increased number of atherogenic particles may adversely influence CVD risk 59 ; however, no clinical outcome trials to date have determined whether normalization of particle composition or reduction of particle”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.4. Metabolic Consequences of Hypertriglyceridemia
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Experimental studies suggest that hypertriglyceridemic HDL may be dysfunctional, 55,56 that small, dense LDL particles may be more susceptible to oxidative modification, 57,58 and that an increased number of atherogenic particles may adversely influence CVD risk 59 ; however, no clinical outcome trials to date have determined whether normalization of particle composition or reduction of particle”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.4. Metabolic Consequences of Hypertriglyceridemia
What the sources say
- Not checked yetcites [59] 59. Ip S, Lichtenstein AH, Chung M, Lau J, Balk EM. Systematic review: association of low-density lipoprotein subfractions with cardiovascular outcomes. Ann Intern Med. 2009;150:474 -484. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Recent data support a role for adipocyte-and macrophage-derived fatty acid-binding proteins in systemic inflammatory responses 73 that are likely amplified by high triglyceride loads provided by RLPs to the arterial macrophages.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.1. Remnant Lipoprotein Particles A number of experimental systems have demonstrated that TRLs can produce proatherogenic responses in isolated endothelial cells.RLPs are a by-product of TRL that can be isolated from the postprandial plasma of hypertriglyceridemic subjects; they are intestinal (ie, CMRs) or liver-derived (eg, VLDL remnants) TRLs that have undergone partial hydrolysis by LPL.Liu et al 64 have shown that these particles can accelerate senescence and interfere with the function of endothelial progenitor cells; these cells play an important role in the organismal reparative response to in vivo vessel wall injury.Postprandial TRL (ppTG) has also been shown to increase the expression of proinflammatory genes (eg, interleukin-6, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1), 65 induce apoptosis, 66 and accentuate the inflammatory response of cultured endothelial cells to tumor necrosis factor-␣.67 After a high-fat meal, ppTG may increase the level of circulating endothelial cell microparticles, a measure of endothelial cell dysfunction in vivo.68 That is, a high-fat diet increases the level of these particles more effectively than a low-fat diet and is correlated with ppTG levels.Moreover, Rutledge and colleagues have shown that fatty acids released by lipolysis of TRL elicit proinflammatory responses in endothelial cells.69 TRL may also act to suppress the atheroprotective and antiinflammatory effects of HDL.70 -72 Finally, fatty acid-binding proteins play a role in the intracellular transport of long-chain fatty acids.Recent data support a role for adipocyte-and macrophage-derived fatty acid-binding proteins in systemic inflammatory responses 73 that are likely amplified by high triglyceride loads provided by RLPs to the arterial macrophages.
What the sources say
- Not checked yetcites [73] 73. Furuhashi M, Fucho R, Go ¨rgu ¨n CZ, Tuncman G, Cao H, Hotamisligil GS. Adipocyte/macrophage fatty acid-binding proteins contribute to metabolic deterioration through actions in both macrophages and adi- pocytes in mice. J Clin Invest. 2008;118:2640 -2650.
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“Moreover, Rutledge and colleagues have shown that fatty acids released by lipolysis of TRL elicit proinflammatory responses in endothelial cells.69”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.1. Remnant Lipoprotein Particles A number of experimental systems have demonstrated that TRLs can produce proatherogenic responses in isolated endothelial cells.RLPs are a by-product of TRL that can be isolated from the postprandial plasma of hypertriglyceridemic subjects; they are intestinal (ie, CMRs) or liver-derived (eg, VLDL remnants) TRLs that have undergone partial hydrolysis by LPL.Liu et al 64 have shown that these particles can accelerate senescence and interfere with the function of endothelial progenitor cells; these cells play an important role in the organismal reparative response to in vivo vessel wall injury.Postprandial TRL (ppTG) has also been shown to increase the expression of proinflammatory genes (eg, interleukin-6, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1), 65 induce apoptosis, 66 and accentuate the inflammatory response of cultured endothelial cells to tumor necrosis factor-␣.67 After a high-fat meal, ppTG may increase the level of circulating endothelial cell microparticles, a measure of endothelial cell dysfunction in vivo.68 That is, a high-fat diet increases the level of these particles more effectively than a low-fat diet and is correlated with ppTG levels.Moreover, Rutledge and colleagues have shown that fatty acids released by lipolysis of TRL elicit proinflammatory responses in endothelial cells.69 TRL may also act to suppress the atheroprotective and antiinflammatory effects of HDL.70 -72 Finally, fatty acid-binding proteins play a role in the intracellular transport of long-chain fatty acids.Recent data support a role for adipocyte-and macrophage-derived fatty acid-binding proteins in systemic inflammatory responses 73 that are likely amplified by high triglyceride loads provided by RLPs to the arterial macrophages.
What the sources say
- Not checked yetcites [69] 69. Wang L, Gill R, Pedersen TL, Higgins LJ, Newman JW, Rutledge JC. Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation. J Lipid Res. 2009;50: 204 -213. source
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“Lipolytic products of TRL have also been shown to produce cytotoxicity and apoptosis in isolated macrophages.85”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.3. Macrophage LPL Macrophages are a rich source of LPL in the vessel wall, 81 and expression of LPL by macrophages could play a role in accelerating atherogenesis by a mechanism that depends on interaction with circulating TRL.82 For example, direct incubation of mouse peritoneal macrophages with TRL increases macrophage cell triglyceride and fatty acid content; more importantly, this incubation increases expression of macrophage inflammatory proteins, including tumor necrosis factor-␣, interleukin-1, monocyte chemotactic protein-1, intercellular adhesion molecule-1, and matrix metalloproteinase-3. 83,84 Lipolytic products of TRL have also been shown to produce cytotoxicity and apoptosis in isolated macrophages.85 Macrophage apoptosis is considered an important event that impacts the in vivo atherogenic process.86 In summary, in vitro experimental models examining the response of isolated endothelial cells or monocytes and macrophages to TRL have produced results consistent with atherogenicity of this class of particles.These particles, or their lipolytic degradation products, can increase the expression of inflammatory proteins, adhesion molecules, and coagulation factors in endothelial cells or monocytes and macrophages.TRLs may interfere with the ability of HDL to suppress inflammatory responses in cultured endothelial cells and the capacity of apo AI or HDL to promote sterol efflux from monocytes or macrophages.TRLs also impair endothelial cell-dependent vasodilation, enhance the recruitment and attachment of monocytes to endothelium, may be directly cytotoxic, and produce apoptosis in isolated vessel wall cells.However, although the results from in vitro studies provide important pathophysiological context and proof of concept, final conclusions about atherogenicity and clinical significance of lowering triglyceride levels as a surrogate of TRL particles must be based on in vivo studies that use appropriate models of human dyslipidemia in randomized controlled trials (RCTs), as will be elaborated on in Section 15.
What the sources say
- Not checked yetcites [85] 85. Wehinger A, Tancevski I, Schgoer W, Eller P, Hochegger K, Morak M, Hermetter A, Ritsch A, Patsch JR, Foeger B. Phospholipid transfer protein augments apoptosis in THP-1-derived macrophages induced by lipolyzed hypertriglyceridemic plasma. Arterioscler Thromb Vasc Biol. 2007;27:908 -915.
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In the paper
“Apo CIII contained in TRLs has also been shown to promote proatherogenic responses in macrophages and endothelial cells.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5. Atherogenicity of TRLs
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In the paper
“A number of experimental systems have demonstrated that TRLs can produce proatherogenic responses in isolated endothelial cells.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.1. Remnant Lipoprotein Particles A number of experimental systems have demonstrated that TRLs can produce proatherogenic responses in isolated endothelial cells.RLPs are a by-product of TRL that can be isolated from the postprandial plasma of hypertriglyceridemic subjects; they are intestinal (ie, CMRs) or liver-derived (eg, VLDL remnants) TRLs that have undergone partial hydrolysis by LPL.Liu et al 64 have shown that these particles can accelerate senescence and interfere with the function of endothelial progenitor cells; these cells play an important role in the organismal reparative response to in vivo vessel wall injury.Postprandial TRL (ppTG) has also been shown to increase the expression of proinflammatory genes (eg, interleukin-6, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1), 65 induce apoptosis, 66 and accentuate the inflammatory response of cultured endothelial cells to tumor necrosis factor-␣.67 After a high-fat meal, ppTG may increase the level of circulating endothelial cell microparticles, a measure of endothelial cell dysfunction in vivo.68 That is, a high-fat diet increases the level of these particles more effectively than a low-fat diet and is correlated with ppTG levels.Moreover, Rutledge and colleagues have shown that fatty acids released by lipolysis of TRL elicit proinflammatory responses in endothelial cells.69 TRL may also act to suppress the atheroprotective and antiinflammatory effects of HDL.70 -72 Finally, fatty acid-binding proteins play a role in the intracellular transport of long-chain fatty acids.Recent data support a role for adipocyte-and macrophage-derived fatty acid-binding proteins in systemic inflammatory responses 73 that are likely amplified by high triglyceride loads provided by RLPs to the arterial macrophages.
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In the paper
“the effect size has typically been modest compared with standard CVD risk factors, including other lipid and lipoprotein parameters.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Ͻ250 Ͻ200 Ͻ150
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In the paper
“A long-standing association exists between elevated triglyceride levels and cardiovascular disease* (CVD).1,2”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 1. Introduction A long-standing association exists between elevated triglyceride levels and cardiovascular disease* (CVD).1,2 However, the extent to which triglycerides directly promote CVD or represent a biomarker of risk has been debated for 3 decades.3 To this end, 2 National Institutes of Health consensus conferences evaluated the evidentiary role of triglycerides in cardiovascular risk assessment and provided therapeutic recommendations for hypertriglyceridemic states.4,5 Since 1993, additional insights have been made vis-a `-vis the atherogenicity of triglyceride-rich lipoproteins (TRLs; ie, chylomicrons and very low-density lipoproteins), genetic and metabolic regulators of triglyceride metabolism, and classification and treatment of hypertriglyceridemia.It is especially disconcerting that in the United States, mean triglyceride levels have risen since 1976, in concert with the growing epidemic of obesity, insulin resistance (IR), and type 2 diabetes mellitus (T2DM).6,7 In contrast, mean low-density lipoprotein cholesterol (LDL-C) levels have receded.7 Therefore, the purpose of this scientific statement is to update clinicians on the increasingly crucial role of triglycerides in the evaluation and management of CVD risk and highlight approaches aimed at minimizing the adverse public health-related consequences associated with hypertriglyceridemic states.This statement will complement recent American Heart Association scientific statements on childhood and adolescent obesity 8 and dietary sugar intake 9 by emphasizing effective lifestyle strategies designed to lower triglyceride levels and improve overall cardiometabolic health.It is not intended to serve as a specific guideline but will be of value to the Adult Treatment Panel IV (ATP IV) of the National Cholesterol Education Program, from which evidence-based guidelines will ensue.Topics to be addressed include epidemiology and CVD risk, ethnic and racial differences, metabolic determinants, genetic and family determinants, risk factor correlates, and effects related to nutrition, physical activity, and lipid medications.
What the sources say
- Not checked yetcites [1] 1. Austin MA, Hokanson JE, Edwards KL. Hypertriglyceridemia as a cardiovascular risk factor. Am J Cardiol. 1998;81:7B-12B. source
- Not checked yetcites [2] 2. Sarwar N, Danesh J, Eiriksdottir G, Sigurdsson G, Wareham N, Bingham S, Boekholdt SM, Khaw KT, Gudnason V. Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies. Circulation. 2007;115: 450 -458. source
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In the paper
“It is especially disconcerting that in the United States, mean triglyceride levels have risen since 1976, in concert with the growing epidemic of obesity, insulin resistance (IR), and type 2 diabetes mellitus (T2DM).6,7”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 1. Introduction A long-standing association exists between elevated triglyceride levels and cardiovascular disease* (CVD).1,2 However, the extent to which triglycerides directly promote CVD or represent a biomarker of risk has been debated for 3 decades.3 To this end, 2 National Institutes of Health consensus conferences evaluated the evidentiary role of triglycerides in cardiovascular risk assessment and provided therapeutic recommendations for hypertriglyceridemic states.4,5 Since 1993, additional insights have been made vis-a `-vis the atherogenicity of triglyceride-rich lipoproteins (TRLs; ie, chylomicrons and very low-density lipoproteins), genetic and metabolic regulators of triglyceride metabolism, and classification and treatment of hypertriglyceridemia.It is especially disconcerting that in the United States, mean triglyceride levels have risen since 1976, in concert with the growing epidemic of obesity, insulin resistance (IR), and type 2 diabetes mellitus (T2DM).6,7 In contrast, mean low-density lipoprotein cholesterol (LDL-C) levels have receded.7 Therefore, the purpose of this scientific statement is to update clinicians on the increasingly crucial role of triglycerides in the evaluation and management of CVD risk and highlight approaches aimed at minimizing the adverse public health-related consequences associated with hypertriglyceridemic states.This statement will complement recent American Heart Association scientific statements on childhood and adolescent obesity 8 and dietary sugar intake 9 by emphasizing effective lifestyle strategies designed to lower triglyceride levels and improve overall cardiometabolic health.It is not intended to serve as a specific guideline but will be of value to the Adult Treatment Panel IV (ATP IV) of the National Cholesterol Education Program, from which evidence-based guidelines will ensue.Topics to be addressed include epidemiology and CVD risk, ethnic and racial differences, metabolic determinants, genetic and family determinants, risk factor correlates, and effects related to nutrition, physical activity, and lipid medications.
What the sources say
- Not checked yetcites [6] 6. Carroll MD, Lacher DA, Sorlie PD, Cleeman JI, Gordon DJ, Wolz M, Grundy SM, Johnson CL. Trends in serum lipids and lipoproteins of adults, 1960 -2002. JAMA. 2005;294:1773-1781.
- Not checked yetcites [7] 7. Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in obesity among US adults, 1999 -2000. JAMA. 2002;288:1723-1727. source
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In the paper
“In contrast, mean low-density lipoprotein cholesterol (LDL-C) levels have receded.7”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 1. Introduction A long-standing association exists between elevated triglyceride levels and cardiovascular disease* (CVD).1,2 However, the extent to which triglycerides directly promote CVD or represent a biomarker of risk has been debated for 3 decades.3 To this end, 2 National Institutes of Health consensus conferences evaluated the evidentiary role of triglycerides in cardiovascular risk assessment and provided therapeutic recommendations for hypertriglyceridemic states.4,5 Since 1993, additional insights have been made vis-a `-vis the atherogenicity of triglyceride-rich lipoproteins (TRLs; ie, chylomicrons and very low-density lipoproteins), genetic and metabolic regulators of triglyceride metabolism, and classification and treatment of hypertriglyceridemia.It is especially disconcerting that in the United States, mean triglyceride levels have risen since 1976, in concert with the growing epidemic of obesity, insulin resistance (IR), and type 2 diabetes mellitus (T2DM).6,7 In contrast, mean low-density lipoprotein cholesterol (LDL-C) levels have receded.7 Therefore, the purpose of this scientific statement is to update clinicians on the increasingly crucial role of triglycerides in the evaluation and management of CVD risk and highlight approaches aimed at minimizing the adverse public health-related consequences associated with hypertriglyceridemic states.This statement will complement recent American Heart Association scientific statements on childhood and adolescent obesity 8 and dietary sugar intake 9 by emphasizing effective lifestyle strategies designed to lower triglyceride levels and improve overall cardiometabolic health.It is not intended to serve as a specific guideline but will be of value to the Adult Treatment Panel IV (ATP IV) of the National Cholesterol Education Program, from which evidence-based guidelines will ensue.Topics to be addressed include epidemiology and CVD risk, ethnic and racial differences, metabolic determinants, genetic and family determinants, risk factor correlates, and effects related to nutrition, physical activity, and lipid medications.
What the sources say
- Not checked yetcites [7] 7. Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in obesity among US adults, 1999 -2000. JAMA. 2002;288:1723-1727. source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites [11] 11. Cohen JD, Cziraky MJ, Cai Q, Wallace A, Wasser T, Crouse JR, Jacobson TA. 30-Year trends in serum lipids among United States adults: results from the National Health and Nutrition Examination Surveys II, III, and 1999 -2006 [published correction appears in Am J Cardiol. 2010;106:1826]. Am J Cardiol. 2010;106:969 -975.
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In the paper
“Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
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In the paper
“Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, the independence of triglyceride level as a causal factor in promoting CVD remains debatable.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.4. Insights From Clinical Trials
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
What the sources say
- Not checked yetcites [21] 21. Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007;298:299 -308. source
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“Hypertriglyceridemia that results from either increased production or decreased catabolism of TRL directly influences LDL and HDL composition and metabolism.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.4. Metabolic Consequences of Hypertriglyceridemia
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“For example, the hypertriglyceridemia of IR is a consequence of adipocyte lipolysis that results in FFA flux to the liver and increased VLDL secretion.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.4. Metabolic Consequences of Hypertriglyceridemia
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In the paper
“The triglyceride content within these particles is hydrolyzed by HTGL, which results in small, dense LDL and HDL particles.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.4. Metabolic Consequences of Hypertriglyceridemia
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In the paper
“Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
What the sources say
- Not checked yetcites [17] 17. Di Angelantonio E, Sarwar N, Perry P, Kaptoge S, Ray KK, Thompson A, Wood AM, Lewington S, Sattar N, Packard CJ, Collins R, Thompson SG, Danesh J; Emerging Risk Factors Collaboration. Major lipids, apolipoproteins, and risk of vascular disease. JAMA. 2009;302: 1993-2000. source
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In the paper
“Triglyceride has routinely been identified as a “risk factor” in case-control and angiographic studies, even after adjustment for total cholesterol (TC) or LDL-C [23][24][25][26][27][28][29][30][31][32][33][34] and HDL-C.24,[27][28][29]33,34”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.2. Case-Control Studies, Including Angiographic Studies
What the sources say
- Not checked yetcites [23] 23. Brunner D, Altman S, Loebl K, Schwartz S, Levin S. Serum cholesterol and triglycerides in patients suffering from ischemic heart disease and in healthy subjects. Atherosclerosis. 1977;28:197-204.
- Not checked yetcites [24] 24. Castelli WP, Doyle JT, Gordon T, Hames CG, Hjortland MC, Hulley SB, Kagan A, Zukel WJ. HDL cholesterol and other lipids in coronary heart disease: the Cooperative Lipoprotein Phenotyping Study. Circulation. 1977; 55:767-772. source
- Not checked yetcites [25] 25. Wilhelmsen L, Bengtsson C, Elmfeldt D, Vedin A, Wilhelmsson C, Tibblin G, Lindqvist O, Wedel H. Multiple risk prediction of myocardial infarction in women as compared with men. Br Heart J. 1977;39: 1179 -1185.
- Not checked yetcites [26] 26. Scott DW, Gotto AM, Cole JS, Gorry GA. Plasma lipids as collateral risk factors in coronary artery disease: a study of 371 males with chest pain. J Chronic Dis. 1978;31:337-345.
- Not checked yetcites [27] 27. Fager G, Wiklund O, Olofsson SO, Wilhelmsen L, Bondjers G. Multi- variate analyses of serum apolipoproteins and risk factors in relation to acute myocardial infarction. Arteriosclerosis. 1981;1:273-279.
- Not checked yetcites [28] 28. Kukita H, Imamura Y, Hamada M, Joh T, Kokubu T. Plasma lipids and lipoproteins in Japanese male patients with coronary artery disease and in their relatives. Atherosclerosis. 1982;42:21-29.
- Not checked yetcites [29] 29. Hamsten A, Walldius G, Dahle ´n G, Johansson B, De Faire U. Serum lipoproteins and apolipoproteins in young male survivors of myocardial infarction. Atherosclerosis. 1986;59:223-235.
- Not checked yetcites [30] 30. Gotto AM, Gorry GA, Thompson JR, Cole JS, Trost R, Yeshurun D, DeBakey ME. Relationship between plasma lipid concentrations and coronary artery disease in 496 patients. Circulation. 1977;56:875-883.
- Not checked yetcites [31] 31. Anderson AJ, Barboriak JJ, Rimm AA. Risk factors and angio- graphically determined coronary occlusion. Am J Epidemiol. 1978; 107:8 -14.
- Not checked yetcites [32] 32. Cabin HS, Roberts WC. Relation of serum total cholesterol and triglyc- eride levels to the amount and extent of coronary arterial narrowing by atherosclerotic plaque in coronary heart disease: quantitative analysis of 2,037 five mm segments of 160 major epicardial coronary arteries in 40 necropsy patients. Am J Med. 1982;73:227-234.
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In the paper
“Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
What the sources say
- Not checked yetcites [18] 18. American Diabetes Association. Economic costs of diabetes in the U.S. in 2007 [published correction appears in Diabetes Care. 2008;31:1271]. Diabetes Care. 2008;31:596 -615. source
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“Rather, triglyceride levels appear to provide unique information as a biomarker of risk, especially when combined with low HDL-C and elevated LDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.4. Insights From Clinical Trials
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In the paper
“Overall, data from case-control studies have supported triglyceride level as an independent CVD risk factor.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.2. Case-Control Studies, Including Angiographic Studies
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“TRLs also possess unique constituents that may contribute to atherogenicity.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5. Atherogenicity of TRLs
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In the paper
“In addition, TRLs share a number of constituents with classic atherogenic LDL particles.They include the presence of apo B and CE.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5. Atherogenicity of TRLs
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In the paper
“To understand these disorders, one must focus on LPL regulation, because LPL is needed for the hydrolysis of plasma triglyceride to FFA. 96”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [96] 96. Goldberg IJ. Hypertriglyceridemia: impact and treatment. Endocrinol Metab Clin North Am. 2009;38:137-149.
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In the paper
“Familial syndromes with triglyceride levels above the 95th percentile by age and sex may be associated with an increased risk of premature CVD, as in familial combined hyperlipidemia (FCHL).[87][88][89][90]”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [87] 87. Goldstein JL, Schrott HG, Hazzard WR, Bierman EL, Motulsky AG. Hyperlipidemia in coronary heart disease, II: genetic analysis of lipid levels in 176 families and delineation of a new inherited disorder, combined hyperlipidemia. J Clin Invest. 1973;52:1544 -1568.
- Not checked yetcites [88] 88. Brunzell JD, Schrott HG, Motulsky AG, Bierman EL. Myocardial infarction in the familial forms of hypertriglyceridemia. Metabolism. 1976;25:313-320.
- Not checked yetcites [89] 89. Genest JJ Jr, Martin-Munley SS, McNamara JR, Ordovas JM, Jenner J, Myers RH, Silberman SR, Wilson PW, Salem DN, Schaefer EJ. Familial lipoprotein disorders in patients with premature coronary artery disease. Circulation. 1992;85:2025-2033.
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“However, the by-product of TRLs (ie, RLPs) may lead to foam cell formation 63 in a manner analogous to modified LDL.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5. Atherogenicity of TRLs
What the sources say
- Not checked yetcites [63] 63. Botham KM, Moore EH, De Pascale C, Bejta F. The induction of macrophage foam cell formation by chylomicron remnants. Biochem Soc Trans. 2007;35:454 -458.
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In the paper
“In human observational studies, TRLs have been associated with measures of coronary atherosclerosis.62”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5. Atherogenicity of TRLs
What the sources say
- Not checked yetcites [62] 62. Colhoun HM, Otvos JD, Rubens MB, Taskinen MR, Underwood SR, Fuller JH. Lipoprotein subclasses and particle sizes and their rela- tionship with coronary artery calcification in men and women with and without type 1 diabetes. Diabetes. 2002;51:1949 -1956.
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In the paper
“Alternatively, when triglyceride elevation is very severe (ie, Ͼ1000 mg/dL), fasting chylomicronemia may be the consequence of rare but recognizable single gene mutations.[91][92][93]”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [91] 91. Brunzell JD. Familial lipoprotein lipase deficiency and other causes of chylomicronemia syndrome. In: Scriver CR, Beaudet AL, Sly WS, Valle D, eds. The Metabolic and Molecular Base of Inherited Disease. New York, NY: McGraw-Hill; 1995:1913-1932.
- Not checked yetcites [92] 92. Priore Oliva C, Pisciotta L, Li Volti G, Sambataro MP, Cantafora A, Bellocchio A, Catapano A, Tarugi P, Bertolini S, Calandra S. Inherited apolipoprotein A-V deficiency in severe hypertriglyceridemia. Arte- rioscler Thromb Vasc Biol. 2005;25:411-417.
- Not checked yetcites [93] 93. Hegele RA. Monogenic dyslipidemias: window on determinants of plasma lipoprotein metabolism. Am J Hum Genet. 2001;69:1161-1177.
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In the paper
“Factors that reduce VLDL clearance can raise triglyceride concentrations in those with high baseline levels (eg, usually Ͼ500 mg/dL, because of the competition of VLDL and chylomicrons for a common saturable removal mechanism).97”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [97] 97. Brunzell JD, Hazzard WR, Porte D Jr, Bierman EL. Evidence for a common, saturable, triglyceride removal mechanism for chylomicrons and very low density lipoproteins in man. J Clin Invest. 1973;52: 1578 -1585. source
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“For example, the action of LPL on the triglycerides contained in these particles releases fatty acid, which in microcapillary beds could be associated with pathophysiological responses in macrophages and endothelial cells.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5. Atherogenicity of TRLs
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In the paper
“In summary, in vitro experimental models examining the response of isolated endothelial cells or monocytes and macrophages to TRL have produced results consistent with atherogenicity of this class of particles.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.3. Macrophage LPL Macrophages are a rich source of LPL in the vessel wall, 81 and expression of LPL by macrophages could play a role in accelerating atherogenesis by a mechanism that depends on interaction with circulating TRL.82 For example, direct incubation of mouse peritoneal macrophages with TRL increases macrophage cell triglyceride and fatty acid content; more importantly, this incubation increases expression of macrophage inflammatory proteins, including tumor necrosis factor-␣, interleukin-1, monocyte chemotactic protein-1, intercellular adhesion molecule-1, and matrix metalloproteinase-3. 83,84 Lipolytic products of TRL have also been shown to produce cytotoxicity and apoptosis in isolated macrophages.85 Macrophage apoptosis is considered an important event that impacts the in vivo atherogenic process.86 In summary, in vitro experimental models examining the response of isolated endothelial cells or monocytes and macrophages to TRL have produced results consistent with atherogenicity of this class of particles.These particles, or their lipolytic degradation products, can increase the expression of inflammatory proteins, adhesion molecules, and coagulation factors in endothelial cells or monocytes and macrophages.TRLs may interfere with the ability of HDL to suppress inflammatory responses in cultured endothelial cells and the capacity of apo AI or HDL to promote sterol efflux from monocytes or macrophages.TRLs also impair endothelial cell-dependent vasodilation, enhance the recruitment and attachment of monocytes to endothelium, may be directly cytotoxic, and produce apoptosis in isolated vessel wall cells.However, although the results from in vitro studies provide important pathophysiological context and proof of concept, final conclusions about atherogenicity and clinical significance of lowering triglyceride levels as a surrogate of TRL particles must be based on in vivo studies that use appropriate models of human dyslipidemia in randomized controlled trials (RCTs), as will be elaborated on in Section 15.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“These particles, or their lipolytic degradation products, can increase the expression of inflammatory proteins, adhesion molecules, and coagulation factors in endothelial cells or monocytes and macrophages.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.3. Macrophage LPL Macrophages are a rich source of LPL in the vessel wall, 81 and expression of LPL by macrophages could play a role in accelerating atherogenesis by a mechanism that depends on interaction with circulating TRL.82 For example, direct incubation of mouse peritoneal macrophages with TRL increases macrophage cell triglyceride and fatty acid content; more importantly, this incubation increases expression of macrophage inflammatory proteins, including tumor necrosis factor-␣, interleukin-1, monocyte chemotactic protein-1, intercellular adhesion molecule-1, and matrix metalloproteinase-3. 83,84 Lipolytic products of TRL have also been shown to produce cytotoxicity and apoptosis in isolated macrophages.85 Macrophage apoptosis is considered an important event that impacts the in vivo atherogenic process.86 In summary, in vitro experimental models examining the response of isolated endothelial cells or monocytes and macrophages to TRL have produced results consistent with atherogenicity of this class of particles.These particles, or their lipolytic degradation products, can increase the expression of inflammatory proteins, adhesion molecules, and coagulation factors in endothelial cells or monocytes and macrophages.TRLs may interfere with the ability of HDL to suppress inflammatory responses in cultured endothelial cells and the capacity of apo AI or HDL to promote sterol efflux from monocytes or macrophages.TRLs also impair endothelial cell-dependent vasodilation, enhance the recruitment and attachment of monocytes to endothelium, may be directly cytotoxic, and produce apoptosis in isolated vessel wall cells.However, although the results from in vitro studies provide important pathophysiological context and proof of concept, final conclusions about atherogenicity and clinical significance of lowering triglyceride levels as a surrogate of TRL particles must be based on in vivo studies that use appropriate models of human dyslipidemia in randomized controlled trials (RCTs), as will be elaborated on in Section 15.
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In the paper
“When one evaluates the usefulness of these systems, it is important to recognize that triglyceride overload is not a classic pathological feature of human atherosclerotic lesions, because the end product, FFA, serves as an active energy source for myocytes or as an inactive fuel reserve in adipocytes.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5. Atherogenicity of TRLs
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“That is, a high concentration of circulating atherogenic particles is not reliably assessed simply by measurement of TC and/or LDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.4. Metabolic Consequences of Hypertriglyceridemia
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In the paper
“Macrophage apoptosis is considered an important event that impacts the in vivo atherogenic process.86”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.3. Macrophage LPL Macrophages are a rich source of LPL in the vessel wall, 81 and expression of LPL by macrophages could play a role in accelerating atherogenesis by a mechanism that depends on interaction with circulating TRL.82 For example, direct incubation of mouse peritoneal macrophages with TRL increases macrophage cell triglyceride and fatty acid content; more importantly, this incubation increases expression of macrophage inflammatory proteins, including tumor necrosis factor-␣, interleukin-1, monocyte chemotactic protein-1, intercellular adhesion molecule-1, and matrix metalloproteinase-3. 83,84 Lipolytic products of TRL have also been shown to produce cytotoxicity and apoptosis in isolated macrophages.85 Macrophage apoptosis is considered an important event that impacts the in vivo atherogenic process.86 In summary, in vitro experimental models examining the response of isolated endothelial cells or monocytes and macrophages to TRL have produced results consistent with atherogenicity of this class of particles.These particles, or their lipolytic degradation products, can increase the expression of inflammatory proteins, adhesion molecules, and coagulation factors in endothelial cells or monocytes and macrophages.TRLs may interfere with the ability of HDL to suppress inflammatory responses in cultured endothelial cells and the capacity of apo AI or HDL to promote sterol efflux from monocytes or macrophages.TRLs also impair endothelial cell-dependent vasodilation, enhance the recruitment and attachment of monocytes to endothelium, may be directly cytotoxic, and produce apoptosis in isolated vessel wall cells.However, although the results from in vitro studies provide important pathophysiological context and proof of concept, final conclusions about atherogenicity and clinical significance of lowering triglyceride levels as a surrogate of TRL particles must be based on in vivo studies that use appropriate models of human dyslipidemia in randomized controlled trials (RCTs), as will be elaborated on in Section 15.
What the sources say
- Not checked yetcites [86] 86. Seimon T, Tabas I. Mechanisms and consequences of macrophage apoptosis in atherosclerosis. J Lipid Res. 2009;50(suppl):S382-S387.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Thus, the increasing prevalence of both obesity and MetS appears to increase the frequency, onset of expression, and severity of genetic triglyceride syndromes.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > FCHL or FHTG.
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153 Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154 In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).For visceral adipose tissue, the multivariable-adjusted residual effect was approximately twice that for subcutaneous abdominal adipose tissue for both women and men (PϽ0.0001 for both).Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156 Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158 A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.
boosteddirectn = 5,610- Asserted: passes — The authors put it forward as true.
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In the paper
“In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153 Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154 In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).For visceral adipose tissue, the multivariable-adjusted residual effect was approximately twice that for subcutaneous abdominal adipose tissue for both women and men (PϽ0.0001 for both).Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156 Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158 A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.
What the sources say
- Not checked yetcites [155] 155. Fox CS, Massaro JM, Hoffmann U, Pou KM, Maurovich-Horvat P, Liu CY, Vasan RS, Murabito JM, Meigs JB, Cupples LA, D'Agostino RB Sr, O'Donnell CJ. Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the Fra- mingham Heart Study. Circulation. 2007;116:39 -48. source
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In the paper
“The rare but monogenic disorders that cause a marked impairment of LPL activity have clinical expression in childhood.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The increased prevalence of the MetS alone could account for the elevated CVD risk associated with both FCHL and FHTG.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > FCHL or FHTG.
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In the paper
“When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153 Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154 In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).For visceral adipose tissue, the multivariable-adjusted residual effect was approximately twice that for subcutaneous abdominal adipose tissue for both women and men (PϽ0.0001 for both).Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156 Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158 A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.
What the sources say
- Not checked yetcites [153] 153. Ford ES, Li C, Zhao G, Pearson WS, Mokdad AH. Hypertriglyceridemia and its pharmacologic treatment among US adults. Arch Intern Med. 2009;169:572-578. source
plaincorrelationaln = 5,610- Asserted: passes — The authors put it forward as true.
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In the paper
“Genetic studies that used ultrasound findings and alanine aminotransferase as surrogates for fatty liver have shown that fatty liver is a hereditable aspect of FCHL.139”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [139] 139. Brouwers MC, Cantor RM, Kono N, Yoon JL, van der Kallen CJ, Bilderbeek-Beckers MA, van Greevenbroek MM, Lusis AJ, de Bruin TW. Heritability and genetic loci of fatty liver in familial combined hyperlipidemia. J Lipid Res. 2006;47:2799 -2807.
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In the paper
“Importantly, FCHL is strongly represented in studies of survivors of myocardial infarction, 87 especially those survivors Ͻ40 years of age.143”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [143] 143. Wiesbauer F, Blessberger H, Azar D, Goliasch G, Wagner O, Gerhold L, Huber K, Widhalm K, Abdolvahab F, Sodeck G, Maurer G, Schil- linger M. Familial-combined hyperlipidaemia in very young myocardial infarction survivors (Ͻ or ϭ40 years of age). Eur Heart J. 2009;30: 1073-1079.
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In the paper
“The molecular basis underlying FCHL is largely unknown; genetic variants in the APOA1/C3/A4/A5 cluster and the upstream stimulatory factor 1 (USF1) gene may play a role.140 -142”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [140] 140. Eichenbaum-Voline S, Olivier M, Jones EL, Naoumova RP, Jones B, Gau B, Patel HN, Seed M, Betteridge DJ, Galton DJ, Rubin EM, Scott J, Shoulders CC, Pennacchio LA. Linkage and association between distinct variants of the APOA1/C3/A4/A5 gene cluster and familial combined hyperlipidemia. Arterioscler Thromb Vasc Biol. 2004;24: 167-174. 141. 100. Pajukanta P, Lilja HE, Sinsheimer JS, Cantor RM, Lusis AJ, Gentile M, Duan XJ, Soro-Paavonen A, Naukkarinen J, Saarela J, Laakso M, Ehnholm C, Taskinen MR, Peltonen L. Familial combined hyperlipid- emia is associated with upstream transcription facto
- Not checked yetcites [141]
- Not checked yetcites [142] 142. Lee JC, Weissglas-Volkov D, Kytta ¨la ¨M, Sinsheimer JS, Jokiaho A, de Bruin TW, Lusis AJ, Brennan ML, van Greevenbroek MM, van der Kallen CJ, Hazen SL, Pajukanta P. USF1 contributes to high serum lipid levels in Dutch FCHL families and U.S. whites with coronary artery disease. Arterioscler Thromb Vasc Biol. 2007;27:2222-2227.
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- Rests on an assumption: The molecular basis underlying FCHL is largely unknown.
None of the sources cited for this claim have been checked yet.
In the paper
“High triglyceride levels that accompany either normal or impaired fasting glucose predict the development of T2DM, 166,167 and therefore, hypertriglyceridemic states should prompt surveillance to rule out T2DM.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6. Diabetes Mellitus
What the sources say
- Not checked yetcites [166] 166. Haffner SM, Stern MP, Hazuda HP, Mitchell BD, Patterson JK. Car- diovascular risk factors in confirmed prediabetic individuals: does the clock for coronary heart disease start ticking before the onset of clinical diabetes? JAMA. 1990;263:2893-2898. source
- Not checked yetcites [167] 167. D'Agostino RB Jr, Hamman RF, Karter AJ, Mykkanen L, Wagenknecht LE, Haffner SM; Insulin Resistance Atherosclerosis Study Investigators. Cardiovascular disease risk factors predict the development of type 2 diabetes: the Insulin Resistance Atherosclerosis Study. Diabetes Care. 2004;27:2234 -2240.
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In the paper
“In the absence of age-and sex-adjusted values for a population, it has been further suggested that FCHL may be present if hypertriglyceridemia (Ͼ133 mg/dL) and hyperapo B (Ͼ120 mg/dL) are present.58”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [58] 58. Kwiterovich PO Jr. Clinical relevance of the biochemical, metabolic, and genetic factors that influence low-density lipoprotein heterogeneity. Am J Cardiol. 2002;90:30i-47i.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153 Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154 In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).For visceral adipose tissue, the multivariable-adjusted residual effect was approximately twice that for subcutaneous abdominal adipose tissue for both women and men (PϽ0.0001 for both).Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156 Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158 A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“cholesterol, triglyceride, or apo B, at least 2 of the lipid abnormalities identified in the patient also segregate among the patient's first-degree relatives.137”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [137] 137. Cantor RM, de Bruin T, Kono N, Napier S, van Nas A, Allayee H, Lusis AJ. Quantitative trait loci for apolipoprotein B, cholesterol, and triglyc- erides in familial combined hyperlipidemia pedigrees. Arterioscler Thromb Vasc Biol. 2004;24:1935-1941.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Although the phenotypic expression of FCHL is delayed until young adulthood, as childhood obesity rates increase, the higher adipose tissue mass that drives apo B secretion accelerates the number of cases of FCHL diagnosed in the young adult population.145”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [145] 145. ter Avest E, Sniderman AD, Bredie SJ, Wiegman A, Stalenhoef AF, de Graaf J. Effect of aging and obesity on the expression of dyslipidaemia in children from families with familial combined hyperlipidaemia. Clin Sci (Lond). 2007;112:131-139.
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In the paper
“Affected individuals may be extraordinarily responsive to a low-carbohydrate (CHO) diet.149”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [149] 149. Retterstøl K, Hennig CB, Iversen PO. Improved plasma lipids and body weight in overweight/obese patients with type III hyperlipoproteinemia after 4 weeks on a low glycemic diet. Clin Nutr. 2009;28:213-215.
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In the paper
“Finally, genome-wide association studies have uncovered multiple loci associated with high levels of triglyceride.150”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > FCHL or FHTG.
What the sources say
- Not checked yetcites [150] 150. Kathiresan S, Willer CJ, Peloso GM, Demissie S, Musunuru K, Schadt EE, Kaplan L, Bennett D, Li Y, Tanaka T, Voight BF, Bonnycastle LL, Jackson AU, Crawford G, Surti A, Guiducci C, Burtt NP, Parish S, Clarke R, Zelenika D, Kubalanza KA, Morken MA, Scott LJ, Stringham HM, Galan P, Swift AJ, Kuusisto J, Bergman RN, Sundvall J, Laakso M, Ferrucci L, Scheet P, Sanna S, Uda M, Yang Q, Lunetta KL, Dupuis J, de Bakker PI, O'Donnell CJ, Chambers JC, Kooner JS, Hercberg S, Meneton P, Lakatta EG, Scuteri A, Schlessinger D, Tuomilehto J, Collins FS, Groop L, Altshuler D, Collins R, Lathrop GM, Meland source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153 Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154 In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).For visceral adipose tissue, the multivariable-adjusted residual effect was approximately twice that for subcutaneous abdominal adipose tissue for both women and men (PϽ0.0001 for both).Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156 Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158 A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.
What the sources say
- Not checked yetcites [153] 153. Ford ES, Li C, Zhao G, Pearson WS, Mokdad AH. Hypertriglyceridemia and its pharmacologic treatment among US adults. Arch Intern Med. 2009;169:572-578. source
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In the paper
“For those with less severe genetic disorders of triglyceride metabolism, complex interactions between genetic and environmental factors may lead to the type V phenotype (fasting chylomicronemia and increased VLDL).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
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In the paper
“Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153 Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154 In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).For visceral adipose tissue, the multivariable-adjusted residual effect was approximately twice that for subcutaneous abdominal adipose tissue for both women and men (PϽ0.0001 for both).Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156 Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158 A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.
What the sources say
- Not checked yetcites [153] 153. Ford ES, Li C, Zhao G, Pearson WS, Mokdad AH. Hypertriglyceridemia and its pharmacologic treatment among US adults. Arch Intern Med. 2009;169:572-578. source
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In the paper
“Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153 Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154 In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).For visceral adipose tissue, the multivariable-adjusted residual effect was approximately twice that for subcutaneous abdominal adipose tissue for both women and men (PϽ0.0001 for both).Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156 Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158 A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.
What the sources say
- Not checked yetcites [155] 155. Fox CS, Massaro JM, Hoffmann U, Pou KM, Maurovich-Horvat P, Liu CY, Vasan RS, Murabito JM, Meigs JB, Cupples LA, D'Agostino RB Sr, O'Donnell CJ. Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the Fra- mingham Heart Study. Circulation. 2007;116:39 -48. source
- Not checked yetcites [156] 156. Nicklas BJ, Penninx BW, Ryan AS, Berman DM, Lynch NA, Dennis KE. Visceral adipose tissue cutoffs associated with metabolic risk factors for coronary heart disease in women. Diabetes Care. 2003;26: 1413-1420.
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In the paper
“In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [204] 204. Rainwater DL, McMahan CA, Malcom GT, Scheer WD, Roheim PS, McGill HC Jr, Strong JP; PDAY Research Group. Lipid and apolipo- protein predictors of atherosclerosis in youth: apolipoprotein concen- trations do not materially improve prediction of arterial lesions in PDAY subjects. Arterioscler Thromb Vasc Biol. 1999;19:753-761.
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In the paper
“Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [219] 219. Gardner CD, Winkleby MA, Fortmann SP. Population frequency distri- bution of non-high-density lipoprotein cholesterol (Third National Health and Nutrition Examination Survey [NHANES III], 1988 -1994). Am J Cardiol. 2000;86:299 -304.
- Not checked yetcites [220] 220. Srinivasan SR, Frontini MG, Xu J, Berenson GS. Utility of childhood non-high-density lipoprotein cholesterol levels in predicting adult dys- lipidemia and other cardiovascular risks: the Bogalusa Heart Study. Pediatrics. 2006;118:201-206.
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In the paper
“The prevalence of triglyceride levels Ն150 mg/dL is nearly twice as high in subjects with MetS as in those without MetS.184,185”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 7.1. Prevalence of Elevated Triglyceride in MetS
What the sources say
- Not checked yetcites [184] 184. Schwartz GG, Olsson AG, Szarek M, Sasiela WJ. Relation of charac- teristics of metabolic syndrome to short-term prognosis and effects of intensive statin therapy after acute coronary syndrome: an analysis of the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) trial. Diabetes Care. 2005;28:2508 -2513. source
- Not checked yetcites [185] 185. Suzuki T, Katz R, Jenny NS, Zakai NA, LeWinter MM, Barzilay JI, Cushman M. Metabolic syndrome, inflammation, and incident heart failure in the elderly: the Cardiovascular Health Study. Circ Heart Fail. 2008;1:242-248.
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In the paper
“Overproduction of VLDL, with increased secretion of both triglycerides and apo B 100 , appears to be the central cause of increased plasma VLDL levels in patients with T2DM.176”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.2. VLDL Metabolism Overproduction of VLDL, with increased secretion of both triglycerides and apo B 100 , appears to be the central cause of increased plasma VLDL levels in patients with T2DM.176 Increased assembly and secretion of VLDL is probably a direct result of both IR (with loss of insulin's action to stimulate degradation of newly synthesized apo B) and increases in FFA flux to the liver and de novo hepatic lipogenesis (with increased triglyceride synthesis).LPL levels have been reported to be reduced 112 in T2DM, and this may contribute significantly to elevated triglyceride levels, particularly in severely hyperglycemic patients.Because obesity, IR, and concomitant familial forms of hyperlipidemia are common in T2DM, study of the pathophysiology is difficult.The interaction of these overlapping traits also makes therapy less effective.In contrast to T1DM, in which intensive insulin therapy normalizes (or even "supernormalizes") VLDL levels and metabolism, insulin or oral agents only partly correct VLDL abnormalities in the majority of individuals with T2DM.113 Therapies such as metformin and the thiazolidinediones can lower plasma triglyceride concentrations 10% to 15% and 15% to 25%, respectively.177 The thiazolidinediones appear to improve peripheral insulin sensitivity, and this leads to inhibition of lipolysis in adipose tissue.Plasma levels of FFAs fall Ϸ25% at the highest dose of both of the presently available thiazolidinediones, and such changes should lead to lower hepatic triglyceride synthesis and reduced VLDL secretion.However, pioglitazone lowers triglyceride levels by increasing LPL-mediated lipolysis, whereas VLDL secretion remains unchanged.178 Rosiglitazone does not affect triglyceride levels, although the basis for this difference is unclear.179
What the sources say
- Not checked yetcites [176] 176. Kissebah AH, Alfarsi S, Evans DJ, Adams PW. Integrated regulation of very low density lipoprotein triglyceride and apolipoprotein-B kinetics in non-insulin-dependent diabetes mellitus. Diabetes. 1982;31:217-225.
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In the paper
“A high prevalence of triglyceride levels Ն150 mg/dL (72%) was also observed in patients with MetS and CVD.187”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 7.1. Prevalence of Elevated Triglyceride in MetS
What the sources say
- Not checked yetcites [187] 187. Anderson JL, Horne BD, Jones HU, Reyna SP, Carlquist JF, Bair TL, Pearson RR, Lappe ´DL, Muhlestein JB; Intermountain Heart Collab- orative (IHC) Study. Which features of the metabolic syndrome predict the prevalence and clinical outcomes of angiographic coronary artery disease? Cardiology. 2004;101:185-193.
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In the paper
“Similarly, in T2DM, especially in the presence of increased secretion of apo B-containing lipoproteins and concomitant hyperlipidemia, CE transfer protein-mediated transfer of HDL CE to those lipoproteins results in lower levels of HDL-C (and increased HDL triglycerides).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.4. Reduced HDL-C
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In the paper
“Among individual components of MetS, high triglyceride level was the second most common (74%), after elevated blood pressure.186”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 7.1. Prevalence of Elevated Triglyceride in MetS
What the sources say
- Not checked yetcites [186] 186. Kasai T, Miyauchi K, Kurata T, Ohta H, Okazaki S, Miyazaki T, Kajimoto K, Kubota N, Daida H. Prognostic value of the metabolic syndrome for long-term outcomes in patients undergoing percutaneous coronary intervention. Circ J. 2006;70:1531-1537.
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In the paper
“Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [213] 213. Cui Y, Blumenthal RS, Flaws JA, Whiteman MK, Langenberg P, Bachorik PS, Bush TL. Non-high-density lipoprotein cholesterol level as a predictor of cardiovascular disease mortality. Arch Intern Med. 2001; 161:1413-1419.
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In the paper
“In addition, hypertriglyceridemia is associated with small, dense, and CE-depleted LDL particles.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.3. Small LDL Particles
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In the paper
“In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [214] 214. Zhang L, Qiao Q, Tuomilehto J, Hammar N, Ruotolo G, Stehouwer CD, Heine RJ, Eliasson M, Zethelius B; DECODE Study Group. The impact of dyslipidaemia on cardiovascular mortality in individuals without a prior history of diabetes in the DECODE Study. Atherosclerosis. 2009; 206:298 -302.
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In the paper
“Of 2 clinical outcome trials completed recently, neither demonstrated benefits of LDL-C and lowering triglyceride levels in hemodialysis patients.201,202”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 8. Chronic Kidney Disease
What the sources say
- Not checked yetcites [201] 201. Wanner C, Krane V, Ma ¨rz W, Olschewski M, Mann JF, Ruf G, Ritz E; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis [pub- lished correction appears in N Engl J Med. 2005;353:1640]. N Engl J Med. 2005;353:238 -248. source
- Not matchedcites [202] 202. Fellstro ¨m BC, Jardine AG, Schmieder RE, Holdaas H, Bannister K, Beutler J, Chae DW, Chevaile A, Cobbe SM, Gro ¨nhagen-Riska C, De Lima JJ, Lins R, Mayer G, McMahon AW, Parving HH, Remuzzi G, Samuelsson O, Sonkodi S, Sci D, Su ¨leymanlar G, Tsakiris D, Tesar V, Todorov V, Wiecek A, Wu ¨thrich RP, Gottlow M, Johnsson E, Zannad F; AURORA Study Group. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis [published correction appears in N Engl J Med. 2010;362:1450]. 103. N Engl J Med. 2009;360:1395-1407.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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In the paper
“Until then, the benefit of lowering triglyceride levels in CKD remains unproven.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 8. Chronic Kidney Disease
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In the paper
“Nonetheless, clinical outcome studies have failed to demonstrate the prognostic significance of triglyceride levels in MetS.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 7.2. Prognostic Significance of Triglyceride in MetS
What the sources say
- Not checked yetcites [184] 184. Schwartz GG, Olsson AG, Szarek M, Sasiela WJ. Relation of charac- teristics of metabolic syndrome to short-term prognosis and effects of intensive statin therapy after acute coronary syndrome: an analysis of the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) trial. Diabetes Care. 2005;28:2508 -2513. source
- Not checked yetcites [185] 185. Suzuki T, Katz R, Jenny NS, Zakai NA, LeWinter MM, Barzilay JI, Cushman M. Metabolic syndrome, inflammation, and incident heart failure in the elderly: the Cardiovascular Health Study. Circ Heart Fail. 2008;1:242-248.
- Not checked yetcites [186] 186. Kasai T, Miyauchi K, Kurata T, Ohta H, Okazaki S, Miyazaki T, Kajimoto K, Kubota N, Daida H. Prognostic value of the metabolic syndrome for long-term outcomes in patients undergoing percutaneous coronary intervention. Circ J. 2006;70:1531-1537.
- Not checked yetcites [187] 187. Anderson JL, Horne BD, Jones HU, Reyna SP, Carlquist JF, Bair TL, Pearson RR, Lappe ´DL, Muhlestein JB; Intermountain Heart Collab- orative (IHC) Study. Which features of the metabolic syndrome predict the prevalence and clinical outcomes of angiographic coronary artery disease? Cardiology. 2004;101:185-193.
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In the paper
“The basis for increased VLDL in subjects with poorly controlled but nonketotic T1DM is usually overproduction of these lipoproteins.113”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.1.2. VLDL Metabolism
What the sources say
- Not checked yetcites [113] 113. Dunn FL. Hyperlipidemia in diabetes mellitus. Diabetes Metab Rev. 1990;6:47-61.
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In the paper
“whereas non-HDL-C has only been more predictive in limited cases.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [231] 231. de Graaf J, Couture P, Sniderman A. A diagnostic algorithm for the atherogenic apolipoprotein B dyslipoproteinemias. Nat Clin Pract Endo- crinol Metab. 2008;4:608 -618.
- Not checked yetcites [143] 143. Wiesbauer F, Blessberger H, Azar D, Goliasch G, Wagner O, Gerhold L, Huber K, Widhalm K, Abdolvahab F, Sodeck G, Maurer G, Schil- linger M. Familial-combined hyperlipidaemia in very young myocardial infarction survivors (Ͻ or ϭ40 years of age). Eur Heart J. 2009;30: 1073-1079.
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In the paper
“A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [222] 222. Robinson JG, Wang S, Smith BJ, Jacobson TA. Meta-analysis of the relationship between non-high-density lipoprotein cholesterol reduction and coronary heart disease risk. J Am Coll Cardiol. 2009;53:316 -322.
boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [221] 221. National Cholesterol Education Program (U.S.). Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III): Final Report. Washington, DC: National Institutes of Health, National Heart, Lung, and Blood Institute; 2002. NIH publication No. 02-5215.
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In the paper
“in some cases, more closely linked to CVD outcomes than LDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [58] 58. Kwiterovich PO Jr. Clinical relevance of the biochemical, metabolic, and genetic factors that influence low-density lipoprotein heterogeneity. Am J Cardiol. 2002;90:30i-47i.
- Not checked yetcites [228] 228. Sniderman AD, Furberg CD, Keech A, Roeters van Lennep JE, Frohlich J, Jungner I, Walldius G. Apolipoproteins versus lipids as indices of coronary risk and as targets for statin treatment. Lancet. 2003;361: 777-780.
- Not checked yetcites [229] 229. Barter PJ, Ballantyne CM, Carmena R, Castro Cabezas M, Chapman MJ, Couture P, de Graaf J, Durrington PN, Faergeman O, Frohlich J, Furberg CD, Gagne C, Haffner SM, Humphries SE, Jungner I, Krauss RM, Kwiterovich P, Marcovina S, Packard CJ, Pearson TA, Reddy KS, Rosenson R, Sarrafzadegan N, Sniderman AD, Stalenhoef AF, Stein E, Talmud PJ, Tonkin AM, Walldius G, Williams KM. Apo B versus cholesterol in estimating cardiovascular risk and in guiding therapy: report of the thirty-person/ten-country panel. J Intern Med. 2006;259: 247-258.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“case-control and prospective studies have linked the ratio of triglycerides to HDL-C to CVD incidence, outcomes, and all-cause mortality”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.3. Ratio of Triglycerides to HDL-C
What the sources say
- Not checked yetcites [237] 237. Gaziano JM, Hennekens CH, O'Donnell CJ, Breslow JL, Buring JE. Fasting triglycerides, high-density lipoprotein, and risk of myocardial infarction. Circulation. 1997;96:2520 -2525. 238. 106. Drexel H, Aczel S, Marte T, Benzer W, Langer P, Moll W, Saely CH. Is atherosclerosis in diabetes and impaired fasting glucose driven by elevated LDL cholesterol or by decreased HDL cholesterol? Diabetes Care. 2005;28:101-107.
- Not checked yetcites [238]
- Not checked yetcites [239] 239. Bittner V, Johnson BD, Zineh I, Rogers WJ, Vido D, Marroquin OC, Bairey-Merz CN, Sopko G. The triglyceride/high-density lipoprotein cholesterol ratio predicts all-cause mortality in women with suspected myocardial ischemia: a report from the Women's Ischemia Syndrome Evaluation (WISE). Am Heart J. 2009;157:548 -555.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“apo B provides a direct measure of the number of atherogenic particles present in the circulation.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [58] 58. Kwiterovich PO Jr. Clinical relevance of the biochemical, metabolic, and genetic factors that influence low-density lipoprotein heterogeneity. Am J Cardiol. 2002;90:30i-47i.
- Not checked yetcites [226] 226. Kwiterovich PO Jr. Identification and treatment of heterozygous familial hypercholesterolemia in children and adolescents. Am J Cardiol. 1993; 72:30D-37D.
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“because each of these lipoprotein particles contains 1 apo B molecule”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [58] 58. Kwiterovich PO Jr. Clinical relevance of the biochemical, metabolic, and genetic factors that influence low-density lipoprotein heterogeneity. Am J Cardiol. 2002;90:30i-47i.
- Not checked yetcites [226] 226. Kwiterovich PO Jr. Identification and treatment of heterozygous familial hypercholesterolemia in children and adolescents. Am J Cardiol. 1993; 72:30D-37D.
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“with improved predictive power in some studies compared with LDL-C or non-HDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.3. Ratio of Triglycerides to HDL-C
What the sources say
- Not checked yetcites [238]
- Not checked yetcites [239] 239. Bittner V, Johnson BD, Zineh I, Rogers WJ, Vido D, Marroquin OC, Bairey-Merz CN, Sopko G. The triglyceride/high-density lipoprotein cholesterol ratio predicts all-cause mortality in women with suspected myocardial ischemia: a report from the Women's Ischemia Syndrome Evaluation (WISE). Am Heart J. 2009;157:548 -555.
- Not checked yetcites [242] 242. Barzi F, Patel A, Woodward M, Lawes CM, Ohkubo T, Gu D, Lam TH, Ueshima H; Asia Pacific Cohort Studies Collaboration. A comparison of lipid variables as predictors of cardiovascular disease in the Asia Pacific region. Ann Epidemiol. 2005;15:405-413.
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In the paper
“The link between IR and the ratio of triglycerides to HDL-C is already apparent in youth.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.3. Ratio of Triglycerides to HDL-C
What the sources say
- Not checked yetcites [236] 236. Hannon TS, Bacha F, Lee SJ, Janosky J, Arslanian SA. Use of markers of dyslipidemia to identify overweight youth with insulin resistance. Pediatr Diabetes. 2006;7:260 -266.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [231] 231. de Graaf J, Couture P, Sniderman A. A diagnostic algorithm for the atherogenic apolipoprotein B dyslipoproteinemias. Nat Clin Pract Endo- crinol Metab. 2008;4:608 -618.
- Not checked yetcites [143] 143. Wiesbauer F, Blessberger H, Azar D, Goliasch G, Wagner O, Gerhold L, Huber K, Widhalm K, Abdolvahab F, Sodeck G, Maurer G, Schil- linger M. Familial-combined hyperlipidaemia in very young myocardial infarction survivors (Ͻ or ϭ40 years of age). Eur Heart J. 2009;30: 1073-1079.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“post hoc analyses of clinical trials suggest that patients who have both adverse markers tend to benefit more from treatment than those who do not.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.3. Ratio of Triglycerides to HDL-C
What the sources say
- Not checked yetcites [39] 39. Manninen V, Tenkanen L, Koskinen P, Huttunen JK, Ma ¨ntta ¨ri M, Heinonen OP, Frick MH. Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study: implications for treatment. Circulation. 1992;85:37-45. source
- Not checked yetcites [40] 40. Ballantyne CM, Olsson AG, Cook TJ, Mercuri MF, Pedersen TR, Kjekshus J. Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S. Circulation. 2001;104:3046 -3051. source
- Not checked yetcites [232] 232. Assmann G, Schulte H. Relation of high-density lipoprotein cholesterol and triglycerides to incidence of atherosclerotic coronary artery disease (the PROCAM experience): Prospective Cardiovascular Mu ¨nster Study. Am J Cardiol. 1992;70:733-737. 233. 105. McLaughlin T, Reaven G, Abbasi F, Lamendola C, Saad M, Waters D, Simon J, Krauss RM. Is there a simple way to identify insulin-resistant individuals at increased risk of cardiovascular disease? Am J Cardiol. 2005;96:399 -404. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: The joint occurrence of high triglyceride level and low HDL-C characterizes the dyslipidemia of MetS.
In the paper
“Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [224] 224. Ghandehari H, Kamal-Bahl S, Wong ND. Prevalence and extent of dyslipidemia and recommended lipid levels in US adults with and without cardiovascular comorbidities: the National Health and Nutrition Examination Survey 2003-2004. Am Heart J. 2008;156:112-119.
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“the ATP III guidelines favored use of non-HDL-C rather than apo B”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [221] 221. National Cholesterol Education Program (U.S.). Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III): Final Report. Washington, DC: National Institutes of Health, National Heart, Lung, and Blood Institute; 2002. NIH publication No. 02-5215.
plain- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“It strongly predicts CVD in observational studies”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.3. Ratio of Triglycerides to HDL-C
What the sources say
- Not checked yetcites [39] 39. Manninen V, Tenkanen L, Koskinen P, Huttunen JK, Ma ¨ntta ¨ri M, Heinonen OP, Frick MH. Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study: implications for treatment. Circulation. 1992;85:37-45. source
- Not checked yetcites [40] 40. Ballantyne CM, Olsson AG, Cook TJ, Mercuri MF, Pedersen TR, Kjekshus J. Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S. Circulation. 2001;104:3046 -3051. source
- Not checked yetcites [232] 232. Assmann G, Schulte H. Relation of high-density lipoprotein cholesterol and triglycerides to incidence of atherosclerotic coronary artery disease (the PROCAM experience): Prospective Cardiovascular Mu ¨nster Study. Am J Cardiol. 1992;70:733-737. 233. 105. McLaughlin T, Reaven G, Abbasi F, Lamendola C, Saad M, Waters D, Simon J, Krauss RM. Is there a simple way to identify insulin-resistant individuals at increased risk of cardiovascular disease? Am J Cardiol. 2005;96:399 -404. source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: The joint occurrence of high triglyceride level and low HDL-C characterizes the dyslipidemia of MetS.
In the paper
“Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [231] 231. de Graaf J, Couture P, Sniderman A. A diagnostic algorithm for the atherogenic apolipoprotein B dyslipoproteinemias. Nat Clin Pract Endo- crinol Metab. 2008;4:608 -618.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [58] 58. Kwiterovich PO Jr. Clinical relevance of the biochemical, metabolic, and genetic factors that influence low-density lipoprotein heterogeneity. Am J Cardiol. 2002;90:30i-47i.
- Not checked yetcites [226] 226. Kwiterovich PO Jr. Identification and treatment of heterozygous familial hypercholesterolemia in children and adolescents. Am J Cardiol. 1993; 72:30D-37D.
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“Although apo B and non-HDL-C are highly correlated”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [148] 148. Sniderman AD, Hogue JC, Bergeron J, Gagne C, Couture P. Non-HDL cholesterol and apoB in dyslipidaemia. Clin Sci (Lond). 2008;114: 149 -155.
- Not checked yetcites [230] 230. Ballantyne CM, Raichlen JS, Cain VA. Statin therapy alters the rela- tionship between apolipoprotein B and low-density lipoprotein choles- terol and non-high-density lipoprotein cholesterol targets in high-risk patients: the MERCURY II (Measuring Effective Reductions in Cho- lesterol Using Rosuvastatin) trial. J Am Coll Cardiol. 2008;52:626 -632.
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“their interrelationship varies depending on the underlying lipid disorder and treatment status.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [148] 148. Sniderman AD, Hogue JC, Bergeron J, Gagne C, Couture P. Non-HDL cholesterol and apoB in dyslipidaemia. Clin Sci (Lond). 2008;114: 149 -155.
- Not checked yetcites [230] 230. Ballantyne CM, Raichlen JS, Cain VA. Statin therapy alters the rela- tionship between apolipoprotein B and low-density lipoprotein choles- terol and non-high-density lipoprotein cholesterol targets in high-risk patients: the MERCURY II (Measuring Effective Reductions in Cho- lesterol Using Rosuvastatin) trial. J Am Coll Cardiol. 2008;52:626 -632.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“numerous studies that supported apo B as being highly predictive of CVD”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [227] 227. Sedlis SP, Schechtman KB, Ludbrook PA, Sobel BE, Schonfeld G. Plasma apoproteins and the severity of coronary artery disease. Circulation. 1986; 73:978 -986.
- Not checked yetcites [58] 58. Kwiterovich PO Jr. Clinical relevance of the biochemical, metabolic, and genetic factors that influence low-density lipoprotein heterogeneity. Am J Cardiol. 2002;90:30i-47i.
- Not checked yetcites [228] 228. Sniderman AD, Furberg CD, Keech A, Roeters van Lennep JE, Frohlich J, Jungner I, Walldius G. Apolipoproteins versus lipids as indices of coronary risk and as targets for statin treatment. Lancet. 2003;361: 777-780.
- Not checked yetcites [229] 229. Barter PJ, Ballantyne CM, Carmena R, Castro Cabezas M, Chapman MJ, Couture P, de Graaf J, Durrington PN, Faergeman O, Frohlich J, Furberg CD, Gagne C, Haffner SM, Humphries SE, Jungner I, Krauss RM, Kwiterovich P, Marcovina S, Packard CJ, Pearson TA, Reddy KS, Rosenson R, Sarrafzadegan N, Sniderman AD, Stalenhoef AF, Stein E, Talmud PJ, Tonkin AM, Walldius G, Williams KM. Apo B versus cholesterol in estimating cardiovascular risk and in guiding therapy: report of the thirty-person/ten-country panel. J Intern Med. 2006;259: 247-258.
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [225] 225. Pambianco G, Lombardero M, Bittner V, Forker A, Kennedy F, Krish- naswami A, Mooradian AD, Pop-Busui R, Rana JS, Rodriguez A, Steffes M, Orchard TJ. Control of lipids at baseline in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trial. Prev Cardiol. 2009;12:9 -18. source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [223] 223. Davidson MH, Maki KC, Pearson TA, Pasternak RC, Deedwania PC, McKenney JM, Fonarow GC, Maron DJ, Ansell BJ, Clark LT, Bal- lantyne CM. Results of the National Cholesterol Education (NCEP) Program Evaluation ProjecT Utilizing Novel E-Technology (NEPTUNE) II survey and implications for treatment under the recent NCEP Writing Group recommendations. Am J Cardiol. 2005;96: 556 -563. source
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In the paper
“In normotriglyceridemic subjects (ie, fasting triglyceride levels Ͻ150 mg/dL), consumption of a low-fat breakfast (ie, Ͻ15 g) before blood sampling would not be expected to raise ppTG levels above 200 mg/dL.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.3. Fasting Versus Nonfasting Levels Although an overnight fast has been the traditional method for assessment of triglyceride levels, there are several lines of evidence that support a nonfasting measurement to screen for hypertriglyceridemia. First, the fasting state only represents a small proportion of time spent each day and therefore understates levels that are attained in the postprandial state.From a pathophysiological standpoint, a postprandial state enriched in dietary fat (eg, 70 to 100 g) may affect saturation parameters and impede hepatic removal of circulating CMRs, 248 thereby permitting their uptake and incorporation by macrophages.63,249,250 Supportive observational studies have recently identified nonfasting triglyceride levels to be a superior predictor of CVD risk compared with fasting levels.21,22 The relationship between fasting and ppTG levels and factors that influence the response to dietary fat in healthy normolipidemic subjects were reviewed in 39 studies approximating 1500 ppTG measurements.68, Although baseline dietary characteristics, fat content, and composition of test meals often varied between studies, a graded association existed between the amount of dietary fat in the test meal and the ppTG response.For example, a meal that contained up to 15 g of fat was associated with minimal (20%) increases in peak ppTG levels, 276 whereas high-fat meals (eg, 50 g), including those served in popular fast-food restaurants, increased triglyceride levels by at least 50% beyond fasting levels.68,273,275,279 Because median triglyceride levels in US adults range between 106 (women) and 122 (men) mg/dL, measurement of nonfasting triglyceride levels in the absence of a high-fat meal (eg, Ͻ15 g) would be expected to eliminate the requirement for a fasting lipid panel in a sizeable proportion of otherwise healthy adults. A practical algorithm for screening triglyceride measurements is suggested in Figure 5.In normotriglyceridemic subjects (ie, fasting triglyceride levels Ͻ150 mg/dL), consumption of a low-fat breakfast (ie, Ͻ15 g) before blood sampling would not be expected to raise ppTG levels above 200 mg/dL.In these cases, no further testing for hypertriglyceridemia is indicated, although further discussion of lifestyle measures may be advocated on the basis of that individual's level of risk.However, if nonfasting triglyceride levels equal or exceed 200 mg/dL, a fasting lipid panel is recommended within a reasonable (eg, 2 to 4 weeks) time frame.
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In the paper
“with more modest decreases when a person changes from standing to sitting (ie, 8% and 10%, respectively).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.1. Postural Effects
What the sources say
- Not checked yetcites [245] 245. Miller M, Bachorik PS, Cloey TA. Normal variation of plasma lipo- proteins: postural effects on plasma concentrations of lipids, lipo- proteins, and apolipoproteins. Clin Chem. 1992;38:569 -574.
- Not checked yetcites [246] 246. Hagan RD, Upton SJ, Avakian EV, Grundy S. Increases in serum lipid and lipoprotein levels with movement from the supine to standing position in adult men and women. Prev Med. 1986;15:18 -27.
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In the paper
“there are several lines of evidence that support a nonfasting measurement to screen for hypertriglyceridemia.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.3. Fasting Versus Nonfasting Levels Although an overnight fast has been the traditional method for assessment of triglyceride levels, there are several lines of evidence that support a nonfasting measurement to screen for hypertriglyceridemia. First, the fasting state only represents a small proportion of time spent each day and therefore understates levels that are attained in the postprandial state.From a pathophysiological standpoint, a postprandial state enriched in dietary fat (eg, 70 to 100 g) may affect saturation parameters and impede hepatic removal of circulating CMRs, 248 thereby permitting their uptake and incorporation by macrophages.63,249,250 Supportive observational studies have recently identified nonfasting triglyceride levels to be a superior predictor of CVD risk compared with fasting levels.21,22 The relationship between fasting and ppTG levels and factors that influence the response to dietary fat in healthy normolipidemic subjects were reviewed in 39 studies approximating 1500 ppTG measurements.68, Although baseline dietary characteristics, fat content, and composition of test meals often varied between studies, a graded association existed between the amount of dietary fat in the test meal and the ppTG response.For example, a meal that contained up to 15 g of fat was associated with minimal (20%) increases in peak ppTG levels, 276 whereas high-fat meals (eg, 50 g), including those served in popular fast-food restaurants, increased triglyceride levels by at least 50% beyond fasting levels.68,273,275,279 Because median triglyceride levels in US adults range between 106 (women) and 122 (men) mg/dL, measurement of nonfasting triglyceride levels in the absence of a high-fat meal (eg, Ͻ15 g) would be expected to eliminate the requirement for a fasting lipid panel in a sizeable proportion of otherwise healthy adults. A practical algorithm for screening triglyceride measurements is suggested in Figure 5.In normotriglyceridemic subjects (ie, fasting triglyceride levels Ͻ150 mg/dL), consumption of a low-fat breakfast (ie, Ͻ15 g) before blood sampling would not be expected to raise ppTG levels above 200 mg/dL.In these cases, no further testing for hypertriglyceridemia is indicated, although further discussion of lifestyle measures may be advocated on the basis of that individual's level of risk.However, if nonfasting triglyceride levels equal or exceed 200 mg/dL, a fasting lipid panel is recommended within a reasonable (eg, 2 to 4 weeks) time frame.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“a meal that contained up to 15 g of fat was associated with minimal (20%) increases in peak ppTG levels”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.3. Fasting Versus Nonfasting Levels Although an overnight fast has been the traditional method for assessment of triglyceride levels, there are several lines of evidence that support a nonfasting measurement to screen for hypertriglyceridemia. First, the fasting state only represents a small proportion of time spent each day and therefore understates levels that are attained in the postprandial state.From a pathophysiological standpoint, a postprandial state enriched in dietary fat (eg, 70 to 100 g) may affect saturation parameters and impede hepatic removal of circulating CMRs, 248 thereby permitting their uptake and incorporation by macrophages.63,249,250 Supportive observational studies have recently identified nonfasting triglyceride levels to be a superior predictor of CVD risk compared with fasting levels.21,22 The relationship between fasting and ppTG levels and factors that influence the response to dietary fat in healthy normolipidemic subjects were reviewed in 39 studies approximating 1500 ppTG measurements.68, Although baseline dietary characteristics, fat content, and composition of test meals often varied between studies, a graded association existed between the amount of dietary fat in the test meal and the ppTG response.For example, a meal that contained up to 15 g of fat was associated with minimal (20%) increases in peak ppTG levels, 276 whereas high-fat meals (eg, 50 g), including those served in popular fast-food restaurants, increased triglyceride levels by at least 50% beyond fasting levels.68,273,275,279 Because median triglyceride levels in US adults range between 106 (women) and 122 (men) mg/dL, measurement of nonfasting triglyceride levels in the absence of a high-fat meal (eg, Ͻ15 g) would be expected to eliminate the requirement for a fasting lipid panel in a sizeable proportion of otherwise healthy adults. A practical algorithm for screening triglyceride measurements is suggested in Figure 5.In normotriglyceridemic subjects (ie, fasting triglyceride levels Ͻ150 mg/dL), consumption of a low-fat breakfast (ie, Ͻ15 g) before blood sampling would not be expected to raise ppTG levels above 200 mg/dL.In these cases, no further testing for hypertriglyceridemia is indicated, although further discussion of lifestyle measures may be advocated on the basis of that individual's level of risk.However, if nonfasting triglyceride levels equal or exceed 200 mg/dL, a fasting lipid panel is recommended within a reasonable (eg, 2 to 4 weeks) time frame.
What the sources say
- Not checked yetcites [276] 276. Dubois C, Beaumier G, Juhel C, Armand M, Portugal H, Pauli AM, Borel P, Latge ´C, Lairon D. Effects of graded amounts (0 -50 g) of dietary fat on postprandial lipemia and lipoproteins in normolipidemic adults. Am J Clin Nutr. 1998;67:31-38.
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In the paper
“Triglyceride levels were independently associated with physical activity levels and sugar-sweetened beverage intake in the NHANES 1999 -2004 studies of adolescents (nϭ6967) 12 to 19 years of age.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1.3. IR and T2DM in Childhood Studies in children, including the Cardiovascular Risk in Young Finns Study 296 and a Pima Indian population study, 297 indicate that IR precedes the development of other risk factors, including obesity, hypertension, and hypertriglyceridemia.There are some impediments to the study of IR in youth, namely, lack of consensus for serum insulin norms and the well-documented physiological IR of puberty.Despite ongoing controversy in this area, 1 recent study identified IR (measured by fasting insulin) as being associated with failure to respond to therapeutic lifestyle change in obese adolescents.298 In fact, recent data from NHANES III found a 7% prevalence of impaired fasting glucose in US adolescents.However, Mexican Americans and overweight adolescents had the highest rates (13% and 17.8% respectively) of impaired fasting glucose, which was associated with significantly higher fasting insulin, dyslipidemia, and hypertension.299 Impaired glucose tolerance is also associated with an increased incidence of hypertriglyceridemia.For example, in the NHANES cohort of 1999 -2000, Williams et al 299 found that mean triglyceride levels were 28% higher in adolescents with impaired glucose tolerance than in those with normal fasting glucose concentrations.Triglyceride levels were independently associated with physical activity levels and sugar-sweetened beverage intake in the NHANES 1999 -2004 studies of adolescents (nϭ6967) 12 to 19 years of age.Each additional daily serving of sugar-sweetened beverages was associated with a 2.25-mg/dL increase in triglyceride levels, as well as increases in IR, LDL-C, and systolic blood pressure and a decrease in HDL-C.In boys but not in girls, the combination of a high level of physical activity coupled with low intake of sugar-sweetened beverages was significantly associated with lower triglyceride levels, higher HDL-C, and reduced IR.300
What the sources say
- Not checked yetcites [300] 300. Bremer AA, Auinger P, Byrd RS. Relationship between insulin resistance-associated metabolic parameters and anthropometric mea- surements with sugar-sweetened beverage intake and physical activity levels in US adolescents: findings from the 1999 -2004 National Health and Nutrition Examination Survey. Arch Pediatr Adolesc Med. 2009; 163:328 -335.
plaincorrelationaln = 6,967- Asserted: passes — The authors put it forward as true.
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In the paper
“recent data from NHANES III found a 7% prevalence of impaired fasting glucose in US adolescents.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1.3. IR and T2DM in Childhood Studies in children, including the Cardiovascular Risk in Young Finns Study 296 and a Pima Indian population study, 297 indicate that IR precedes the development of other risk factors, including obesity, hypertension, and hypertriglyceridemia.There are some impediments to the study of IR in youth, namely, lack of consensus for serum insulin norms and the well-documented physiological IR of puberty.Despite ongoing controversy in this area, 1 recent study identified IR (measured by fasting insulin) as being associated with failure to respond to therapeutic lifestyle change in obese adolescents.298 In fact, recent data from NHANES III found a 7% prevalence of impaired fasting glucose in US adolescents.However, Mexican Americans and overweight adolescents had the highest rates (13% and 17.8% respectively) of impaired fasting glucose, which was associated with significantly higher fasting insulin, dyslipidemia, and hypertension.299 Impaired glucose tolerance is also associated with an increased incidence of hypertriglyceridemia.For example, in the NHANES cohort of 1999 -2000, Williams et al 299 found that mean triglyceride levels were 28% higher in adolescents with impaired glucose tolerance than in those with normal fasting glucose concentrations.Triglyceride levels were independently associated with physical activity levels and sugar-sweetened beverage intake in the NHANES 1999 -2004 studies of adolescents (nϭ6967) 12 to 19 years of age.Each additional daily serving of sugar-sweetened beverages was associated with a 2.25-mg/dL increase in triglyceride levels, as well as increases in IR, LDL-C, and systolic blood pressure and a decrease in HDL-C.In boys but not in girls, the combination of a high level of physical activity coupled with low intake of sugar-sweetened beverages was significantly associated with lower triglyceride levels, higher HDL-C, and reduced IR.300
What the sources say
- Not checked yetcites [299] 299. Williams DE, Cadwell BL, Cheng YJ, Cowie CC, Gregg EW, Geiss LS, Engelgau MM, Narayan KM, Imperatore G. Prevalence of impaired fasting glucose and its relationship with cardiovascular disease risk factors in US adolescents, 1999 -2000. Pediatrics. 2005;116:1122-1126.
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In the paper
“Considerable biological and, to a lesser extent, analytic variability exists in the measurement of triglycerides, with a median variation of 23.5% compared with 4.9% for TC, 6.9% for HDL-C, and 6.5% for calculated LDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10. Factors That Influence Triglyceride Measurements
What the sources say
- Not checked yetcites [243] 243. National Cholesterol Education Program (U.S.). Working Group on Lipoprotein Measurement. Recommendations on Lipoprotein Mea- surement. Bethesda, Md.: National Institutes of Health, National Heart, Lung, and Blood Institute; 1995. NIH publication No. 95-3044.
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In the paper
“the degree to which these risk factors are present in childhood is predictive of their prevalence in adulthood.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1. Children and Adolescent Obesity
What the sources say
- Not checked yetcites [290] 290. Berenson GS, Srinivasan SR, Bao W, Newman WP 3rd, Tracy RE, Wattigney WA. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults: the Bogalusa Heart Study. N Engl J Med. 1998;338:1650 -1656. source
- Not checked yetcites [291] 291. Lauer RM, Clarke WR. Use of cholesterol measurements in childhood for the prediction of adult hypercholesterolemia: the Muscatine Study. JAMA. 1990;264:3034 -3038. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“a graded association existed between the amount of dietary fat in the test meal and the ppTG response.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.3. Fasting Versus Nonfasting Levels Although an overnight fast has been the traditional method for assessment of triglyceride levels, there are several lines of evidence that support a nonfasting measurement to screen for hypertriglyceridemia. First, the fasting state only represents a small proportion of time spent each day and therefore understates levels that are attained in the postprandial state.From a pathophysiological standpoint, a postprandial state enriched in dietary fat (eg, 70 to 100 g) may affect saturation parameters and impede hepatic removal of circulating CMRs, 248 thereby permitting their uptake and incorporation by macrophages.63,249,250 Supportive observational studies have recently identified nonfasting triglyceride levels to be a superior predictor of CVD risk compared with fasting levels.21,22 The relationship between fasting and ppTG levels and factors that influence the response to dietary fat in healthy normolipidemic subjects were reviewed in 39 studies approximating 1500 ppTG measurements.68, Although baseline dietary characteristics, fat content, and composition of test meals often varied between studies, a graded association existed between the amount of dietary fat in the test meal and the ppTG response.For example, a meal that contained up to 15 g of fat was associated with minimal (20%) increases in peak ppTG levels, 276 whereas high-fat meals (eg, 50 g), including those served in popular fast-food restaurants, increased triglyceride levels by at least 50% beyond fasting levels.68,273,275,279 Because median triglyceride levels in US adults range between 106 (women) and 122 (men) mg/dL, measurement of nonfasting triglyceride levels in the absence of a high-fat meal (eg, Ͻ15 g) would be expected to eliminate the requirement for a fasting lipid panel in a sizeable proportion of otherwise healthy adults. A practical algorithm for screening triglyceride measurements is suggested in Figure 5.In normotriglyceridemic subjects (ie, fasting triglyceride levels Ͻ150 mg/dL), consumption of a low-fat breakfast (ie, Ͻ15 g) before blood sampling would not be expected to raise ppTG levels above 200 mg/dL.In these cases, no further testing for hypertriglyceridemia is indicated, although further discussion of lifestyle measures may be advocated on the basis of that individual's level of risk.However, if nonfasting triglyceride levels equal or exceed 200 mg/dL, a fasting lipid panel is recommended within a reasonable (eg, 2 to 4 weeks) time frame.
What the sources say
- Not checked yetcites [68] 68. Ferreira AC, Peter AA, Mendez AJ, Jimenez JJ, Mauro LM, Chirinos JA, Ghany R, Virani S, Garcia S, Horstman LL, Purow J, Jy W, Ahn YS, de Marchena E. Postprandial hypertriglyceridemia increases circulating levels of endothelial cell microparticles. Circulation. 2004;110: 3599 -3603.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The same risk factors associated with disease severity and progression in adults are present in the pediatric population”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1. Children and Adolescent Obesity
What the sources say
- Not checked yetcites [290] 290. Berenson GS, Srinivasan SR, Bao W, Newman WP 3rd, Tracy RE, Wattigney WA. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults: the Bogalusa Heart Study. N Engl J Med. 1998;338:1650 -1656. source
- Not checked yetcites [291] 291. Lauer RM, Clarke WR. Use of cholesterol measurements in childhood for the prediction of adult hypercholesterolemia: the Muscatine Study. JAMA. 1990;264:3034 -3038. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Studies in children, including the Cardiovascular Risk in Young Finns Study 296 and a Pima Indian population study, 297 indicate that IR precedes the development of other risk factors, including obesity, hypertension, and hypertriglyceridemia.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1.3. IR and T2DM in Childhood Studies in children, including the Cardiovascular Risk in Young Finns Study 296 and a Pima Indian population study, 297 indicate that IR precedes the development of other risk factors, including obesity, hypertension, and hypertriglyceridemia.There are some impediments to the study of IR in youth, namely, lack of consensus for serum insulin norms and the well-documented physiological IR of puberty.Despite ongoing controversy in this area, 1 recent study identified IR (measured by fasting insulin) as being associated with failure to respond to therapeutic lifestyle change in obese adolescents.298 In fact, recent data from NHANES III found a 7% prevalence of impaired fasting glucose in US adolescents.However, Mexican Americans and overweight adolescents had the highest rates (13% and 17.8% respectively) of impaired fasting glucose, which was associated with significantly higher fasting insulin, dyslipidemia, and hypertension.299 Impaired glucose tolerance is also associated with an increased incidence of hypertriglyceridemia.For example, in the NHANES cohort of 1999 -2000, Williams et al 299 found that mean triglyceride levels were 28% higher in adolescents with impaired glucose tolerance than in those with normal fasting glucose concentrations.Triglyceride levels were independently associated with physical activity levels and sugar-sweetened beverage intake in the NHANES 1999 -2004 studies of adolescents (nϭ6967) 12 to 19 years of age.Each additional daily serving of sugar-sweetened beverages was associated with a 2.25-mg/dL increase in triglyceride levels, as well as increases in IR, LDL-C, and systolic blood pressure and a decrease in HDL-C.In boys but not in girls, the combination of a high level of physical activity coupled with low intake of sugar-sweetened beverages was significantly associated with lower triglyceride levels, higher HDL-C, and reduced IR.300
What the sources say
- Not checked yetcites [296] 296. Raitakari OT, Porkka KV, Ro ¨nnemaa T, Knip M, Uhari M, Akerblom HK, Viikari JS. The role of insulin in clustering of serum lipids and blood pressure in children and adolescents: the Cardiovascular Risk in Young Finns Study. Diabetologia. 1995;38:1042-1050.
- Not checked yetcites [297] 297. Odeleye OE, de Courten M, Pettitt DJ, Ravussin E. Fasting hyperinsu- linemia is a predictor of increased body weight gain and obesity in Pima Indian children. Diabetes. 1997;46:1341-1345.
hedgeddirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“measurement of nonfasting triglyceride levels in the absence of a high-fat meal (eg, Ͻ15 g) would be expected to eliminate the requirement for a fasting lipid panel in a sizeable proportion of otherwise healthy adults.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.3. Fasting Versus Nonfasting Levels Although an overnight fast has been the traditional method for assessment of triglyceride levels, there are several lines of evidence that support a nonfasting measurement to screen for hypertriglyceridemia. First, the fasting state only represents a small proportion of time spent each day and therefore understates levels that are attained in the postprandial state.From a pathophysiological standpoint, a postprandial state enriched in dietary fat (eg, 70 to 100 g) may affect saturation parameters and impede hepatic removal of circulating CMRs, 248 thereby permitting their uptake and incorporation by macrophages.63,249,250 Supportive observational studies have recently identified nonfasting triglyceride levels to be a superior predictor of CVD risk compared with fasting levels.21,22 The relationship between fasting and ppTG levels and factors that influence the response to dietary fat in healthy normolipidemic subjects were reviewed in 39 studies approximating 1500 ppTG measurements.68, Although baseline dietary characteristics, fat content, and composition of test meals often varied between studies, a graded association existed between the amount of dietary fat in the test meal and the ppTG response.For example, a meal that contained up to 15 g of fat was associated with minimal (20%) increases in peak ppTG levels, 276 whereas high-fat meals (eg, 50 g), including those served in popular fast-food restaurants, increased triglyceride levels by at least 50% beyond fasting levels.68,273,275,279 Because median triglyceride levels in US adults range between 106 (women) and 122 (men) mg/dL, measurement of nonfasting triglyceride levels in the absence of a high-fat meal (eg, Ͻ15 g) would be expected to eliminate the requirement for a fasting lipid panel in a sizeable proportion of otherwise healthy adults. A practical algorithm for screening triglyceride measurements is suggested in Figure 5.In normotriglyceridemic subjects (ie, fasting triglyceride levels Ͻ150 mg/dL), consumption of a low-fat breakfast (ie, Ͻ15 g) before blood sampling would not be expected to raise ppTG levels above 200 mg/dL.In these cases, no further testing for hypertriglyceridemia is indicated, although further discussion of lifestyle measures may be advocated on the basis of that individual's level of risk.However, if nonfasting triglyceride levels equal or exceed 200 mg/dL, a fasting lipid panel is recommended within a reasonable (eg, 2 to 4 weeks) time frame.
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“in the NHANES cohort of 1999 -2000, Williams et al 299 found that mean triglyceride levels were 28% higher in adolescents with impaired glucose tolerance than in those with normal fasting glucose concentrations.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1.3. IR and T2DM in Childhood Studies in children, including the Cardiovascular Risk in Young Finns Study 296 and a Pima Indian population study, 297 indicate that IR precedes the development of other risk factors, including obesity, hypertension, and hypertriglyceridemia.There are some impediments to the study of IR in youth, namely, lack of consensus for serum insulin norms and the well-documented physiological IR of puberty.Despite ongoing controversy in this area, 1 recent study identified IR (measured by fasting insulin) as being associated with failure to respond to therapeutic lifestyle change in obese adolescents.298 In fact, recent data from NHANES III found a 7% prevalence of impaired fasting glucose in US adolescents.However, Mexican Americans and overweight adolescents had the highest rates (13% and 17.8% respectively) of impaired fasting glucose, which was associated with significantly higher fasting insulin, dyslipidemia, and hypertension.299 Impaired glucose tolerance is also associated with an increased incidence of hypertriglyceridemia.For example, in the NHANES cohort of 1999 -2000, Williams et al 299 found that mean triglyceride levels were 28% higher in adolescents with impaired glucose tolerance than in those with normal fasting glucose concentrations.Triglyceride levels were independently associated with physical activity levels and sugar-sweetened beverage intake in the NHANES 1999 -2004 studies of adolescents (nϭ6967) 12 to 19 years of age.Each additional daily serving of sugar-sweetened beverages was associated with a 2.25-mg/dL increase in triglyceride levels, as well as increases in IR, LDL-C, and systolic blood pressure and a decrease in HDL-C.In boys but not in girls, the combination of a high level of physical activity coupled with low intake of sugar-sweetened beverages was significantly associated with lower triglyceride levels, higher HDL-C, and reduced IR.300
What the sources say
- Not checked yetcites [299] 299. Williams DE, Cadwell BL, Cheng YJ, Cowie CC, Gregg EW, Geiss LS, Engelgau MM, Narayan KM, Imperatore G. Prevalence of impaired fasting glucose and its relationship with cardiovascular disease risk factors in US adolescents, 1999 -2000. Pediatrics. 2005;116:1122-1126.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“a postprandial state enriched in dietary fat (eg, 70 to 100 g) may affect saturation parameters and impede hepatic removal of circulating CMRs, 248 thereby permitting their uptake and incorporation by macrophages.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.3. Fasting Versus Nonfasting Levels Although an overnight fast has been the traditional method for assessment of triglyceride levels, there are several lines of evidence that support a nonfasting measurement to screen for hypertriglyceridemia. First, the fasting state only represents a small proportion of time spent each day and therefore understates levels that are attained in the postprandial state.From a pathophysiological standpoint, a postprandial state enriched in dietary fat (eg, 70 to 100 g) may affect saturation parameters and impede hepatic removal of circulating CMRs, 248 thereby permitting their uptake and incorporation by macrophages.63,249,250 Supportive observational studies have recently identified nonfasting triglyceride levels to be a superior predictor of CVD risk compared with fasting levels.21,22 The relationship between fasting and ppTG levels and factors that influence the response to dietary fat in healthy normolipidemic subjects were reviewed in 39 studies approximating 1500 ppTG measurements.68, Although baseline dietary characteristics, fat content, and composition of test meals often varied between studies, a graded association existed between the amount of dietary fat in the test meal and the ppTG response.For example, a meal that contained up to 15 g of fat was associated with minimal (20%) increases in peak ppTG levels, 276 whereas high-fat meals (eg, 50 g), including those served in popular fast-food restaurants, increased triglyceride levels by at least 50% beyond fasting levels.68,273,275,279 Because median triglyceride levels in US adults range between 106 (women) and 122 (men) mg/dL, measurement of nonfasting triglyceride levels in the absence of a high-fat meal (eg, Ͻ15 g) would be expected to eliminate the requirement for a fasting lipid panel in a sizeable proportion of otherwise healthy adults. A practical algorithm for screening triglyceride measurements is suggested in Figure 5.In normotriglyceridemic subjects (ie, fasting triglyceride levels Ͻ150 mg/dL), consumption of a low-fat breakfast (ie, Ͻ15 g) before blood sampling would not be expected to raise ppTG levels above 200 mg/dL.In these cases, no further testing for hypertriglyceridemia is indicated, although further discussion of lifestyle measures may be advocated on the basis of that individual's level of risk.However, if nonfasting triglyceride levels equal or exceed 200 mg/dL, a fasting lipid panel is recommended within a reasonable (eg, 2 to 4 weeks) time frame.
What the sources say
- Not matchedcites [248] 248. Berr F. Characterization of chylomicron remnant clearance by retinyl palmitate label in normal humans. J Lipid Res. 1992;33:915-930.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites [63] 63. Botham KM, Moore EH, De Pascale C, Bejta F. The induction of macrophage foam cell formation by chylomicron remnants. Biochem Soc Trans. 2007;35:454 -458. source
- Not matchedcites [249] 249. Zilversmit DB. Atherogenesis: a postprandial phenomenon. Circulation. 1979;60:473-485.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [250] 250. Yu KC, Cooper AD. Postprandial lipoproteins and atherosclerosis. Front Biosci. 2001;6:D332-D354.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“women in the highest triglyceride quintile had a 2.5-fold greater risk of CVD mortality than women in the lowest quintile, even after adjustment for preexisting CVD, T2DM, obesity, and alcohol consumption.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2. Triglycerides as a Cardiovascular Risk Factor in Women
What the sources say
- Not checked yetcites [303] 303. Mazza A, Tikhonoff V, Schiavon L, Casiglia E. Triglyceridesϩhigh- density-lipoprotein-cholesterol dyslipidaemia, a coronary risk factor in elderly women: the CArdiovascular STudy in the ELderly. Intern Med J. 2005;35:604 -610. source
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In the paper
“In boys but not in girls, the combination of a high level of physical activity coupled with low intake of sugar-sweetened beverages was significantly associated with lower triglyceride levels, higher HDL-C, and reduced IR.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1.3. IR and T2DM in Childhood Studies in children, including the Cardiovascular Risk in Young Finns Study 296 and a Pima Indian population study, 297 indicate that IR precedes the development of other risk factors, including obesity, hypertension, and hypertriglyceridemia.There are some impediments to the study of IR in youth, namely, lack of consensus for serum insulin norms and the well-documented physiological IR of puberty.Despite ongoing controversy in this area, 1 recent study identified IR (measured by fasting insulin) as being associated with failure to respond to therapeutic lifestyle change in obese adolescents.298 In fact, recent data from NHANES III found a 7% prevalence of impaired fasting glucose in US adolescents.However, Mexican Americans and overweight adolescents had the highest rates (13% and 17.8% respectively) of impaired fasting glucose, which was associated with significantly higher fasting insulin, dyslipidemia, and hypertension.299 Impaired glucose tolerance is also associated with an increased incidence of hypertriglyceridemia.For example, in the NHANES cohort of 1999 -2000, Williams et al 299 found that mean triglyceride levels were 28% higher in adolescents with impaired glucose tolerance than in those with normal fasting glucose concentrations.Triglyceride levels were independently associated with physical activity levels and sugar-sweetened beverage intake in the NHANES 1999 -2004 studies of adolescents (nϭ6967) 12 to 19 years of age.Each additional daily serving of sugar-sweetened beverages was associated with a 2.25-mg/dL increase in triglyceride levels, as well as increases in IR, LDL-C, and systolic blood pressure and a decrease in HDL-C.In boys but not in girls, the combination of a high level of physical activity coupled with low intake of sugar-sweetened beverages was significantly associated with lower triglyceride levels, higher HDL-C, and reduced IR.300
What the sources say
- Not checked yetcites [300] 300. Bremer AA, Auinger P, Byrd RS. Relationship between insulin resistance-associated metabolic parameters and anthropometric mea- surements with sugar-sweetened beverage intake and physical activity levels in US adolescents: findings from the 1999 -2004 National Health and Nutrition Examination Survey. Arch Pediatr Adolesc Med. 2009; 163:328 -335.
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In the paper
“increases of as much as 10% to 15% in triglyceride levels have been reported with prolonged venous occlusion times”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.2. Phlebotomy-Related Issues
What the sources say
- Not checked yetcites [243] 243. National Cholesterol Education Program (U.S.). Working Group on Lipoprotein Measurement. Recommendations on Lipoprotein Mea- surement. Bethesda, Md.: National Institutes of Health, National Heart, Lung, and Blood Institute; 1995. NIH publication No. 95-3044.
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In the paper
“the Lipid Research Clinics Follow-Up Study found a triglyceride level Ͼ200 mg/dL to be strongly predictive of cardiovascular death.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2. Triglycerides as a Cardiovascular Risk Factor in Women
What the sources say
- Not checked yetcites [302] 302. Bass KM, Newschaffer CJ, Klag MJ, Bush TL. Plasma lipoprotein levels as predictors of cardiovascular death in women. Arch Intern Med. 1993;153:2209 -2216.
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In the paper
“Because TRLs do not readily diffuse between vascular and extravascular compartments”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.1. Postural Effects
What the sources say
- Not checked yetcites [244] 244. Dixon M, Paterson CR. Posture and the composition of plasma. Clin Chem. 1978;24:824 -826.
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“When low HDL-C was also present, risk increased 3.8-fold.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2. Triglycerides as a Cardiovascular Risk Factor in Women
What the sources say
- Not checked yetcites [303] 303. Mazza A, Tikhonoff V, Schiavon L, Casiglia E. Triglyceridesϩhigh- density-lipoprotein-cholesterol dyslipidaemia, a coronary risk factor in elderly women: the CArdiovascular STudy in the ELderly. Intern Med J. 2005;35:604 -610. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“1 recent study identified IR (measured by fasting insulin) as being associated with failure to respond to therapeutic lifestyle change in obese adolescents.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1.3. IR and T2DM in Childhood Studies in children, including the Cardiovascular Risk in Young Finns Study 296 and a Pima Indian population study, 297 indicate that IR precedes the development of other risk factors, including obesity, hypertension, and hypertriglyceridemia.There are some impediments to the study of IR in youth, namely, lack of consensus for serum insulin norms and the well-documented physiological IR of puberty.Despite ongoing controversy in this area, 1 recent study identified IR (measured by fasting insulin) as being associated with failure to respond to therapeutic lifestyle change in obese adolescents.298 In fact, recent data from NHANES III found a 7% prevalence of impaired fasting glucose in US adolescents.However, Mexican Americans and overweight adolescents had the highest rates (13% and 17.8% respectively) of impaired fasting glucose, which was associated with significantly higher fasting insulin, dyslipidemia, and hypertension.299 Impaired glucose tolerance is also associated with an increased incidence of hypertriglyceridemia.For example, in the NHANES cohort of 1999 -2000, Williams et al 299 found that mean triglyceride levels were 28% higher in adolescents with impaired glucose tolerance than in those with normal fasting glucose concentrations.Triglyceride levels were independently associated with physical activity levels and sugar-sweetened beverage intake in the NHANES 1999 -2004 studies of adolescents (nϭ6967) 12 to 19 years of age.Each additional daily serving of sugar-sweetened beverages was associated with a 2.25-mg/dL increase in triglyceride levels, as well as increases in IR, LDL-C, and systolic blood pressure and a decrease in HDL-C.In boys but not in girls, the combination of a high level of physical activity coupled with low intake of sugar-sweetened beverages was significantly associated with lower triglyceride levels, higher HDL-C, and reduced IR.300
What the sources say
- Not matchedcites [298] 298. Pinhas-Hamiel O, Lerner-Geva L, Copperman N, Jacobson MS. Insulin resistance and parental obesity as predictors to response to therapeutic life style change in obese children and adolescents 10 -18 years old. J Adolesc Health. 2008;43:437-443.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“the increase in plasma volume that accompanies movement from a standing to a supine position also results in a temporary decrease in triglyceride concentrations.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.1. Postural Effects
What the sources say
- Not checked yetcites [244] 244. Dixon M, Paterson CR. Posture and the composition of plasma. Clin Chem. 1978;24:824 -826.
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“high-fat meals (eg, 50 g), including those served in popular fast-food restaurants, increased triglyceride levels by at least 50% beyond fasting levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.3. Fasting Versus Nonfasting Levels Although an overnight fast has been the traditional method for assessment of triglyceride levels, there are several lines of evidence that support a nonfasting measurement to screen for hypertriglyceridemia. First, the fasting state only represents a small proportion of time spent each day and therefore understates levels that are attained in the postprandial state.From a pathophysiological standpoint, a postprandial state enriched in dietary fat (eg, 70 to 100 g) may affect saturation parameters and impede hepatic removal of circulating CMRs, 248 thereby permitting their uptake and incorporation by macrophages.63,249,250 Supportive observational studies have recently identified nonfasting triglyceride levels to be a superior predictor of CVD risk compared with fasting levels.21,22 The relationship between fasting and ppTG levels and factors that influence the response to dietary fat in healthy normolipidemic subjects were reviewed in 39 studies approximating 1500 ppTG measurements.68, Although baseline dietary characteristics, fat content, and composition of test meals often varied between studies, a graded association existed between the amount of dietary fat in the test meal and the ppTG response.For example, a meal that contained up to 15 g of fat was associated with minimal (20%) increases in peak ppTG levels, 276 whereas high-fat meals (eg, 50 g), including those served in popular fast-food restaurants, increased triglyceride levels by at least 50% beyond fasting levels.68,273,275,279 Because median triglyceride levels in US adults range between 106 (women) and 122 (men) mg/dL, measurement of nonfasting triglyceride levels in the absence of a high-fat meal (eg, Ͻ15 g) would be expected to eliminate the requirement for a fasting lipid panel in a sizeable proportion of otherwise healthy adults. A practical algorithm for screening triglyceride measurements is suggested in Figure 5.In normotriglyceridemic subjects (ie, fasting triglyceride levels Ͻ150 mg/dL), consumption of a low-fat breakfast (ie, Ͻ15 g) before blood sampling would not be expected to raise ppTG levels above 200 mg/dL.In these cases, no further testing for hypertriglyceridemia is indicated, although further discussion of lifestyle measures may be advocated on the basis of that individual's level of risk.However, if nonfasting triglyceride levels equal or exceed 200 mg/dL, a fasting lipid panel is recommended within a reasonable (eg, 2 to 4 weeks) time frame.
What the sources say
- Not checked yetcites [68] 68. Ferreira AC, Peter AA, Mendez AJ, Jimenez JJ, Mauro LM, Chirinos JA, Ghany R, Virani S, Garcia S, Horstman LL, Purow J, Jy W, Ahn YS, de Marchena E. Postprandial hypertriglyceridemia increases circulating levels of endothelial cell microparticles. Circulation. 2004;110: 3599 -3603.
- Not checked yetcites [273] 273. Vogel RA, Corretti MC, Plotnick GD. Effect of a single high-fat meal on endothelial function in healthy subjects. Am J Cardiol. 1997;79: 350 -354.
- Not checked yetcites [275] 275. Plotnick GD, Corretti MC, Vogel RA. Effect of antioxidant vitamins on the transient impairment of endothelium-dependent brachial artery vaso- activity following a single high-fat meal. JAMA. 1997;278:1682-1686.
- Not checked yetcites [279]
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Supportive observational studies have recently identified nonfasting triglyceride levels to be a superior predictor of CVD risk compared with fasting levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.3. Fasting Versus Nonfasting Levels Although an overnight fast has been the traditional method for assessment of triglyceride levels, there are several lines of evidence that support a nonfasting measurement to screen for hypertriglyceridemia. First, the fasting state only represents a small proportion of time spent each day and therefore understates levels that are attained in the postprandial state.From a pathophysiological standpoint, a postprandial state enriched in dietary fat (eg, 70 to 100 g) may affect saturation parameters and impede hepatic removal of circulating CMRs, 248 thereby permitting their uptake and incorporation by macrophages.63,249,250 Supportive observational studies have recently identified nonfasting triglyceride levels to be a superior predictor of CVD risk compared with fasting levels.21,22 The relationship between fasting and ppTG levels and factors that influence the response to dietary fat in healthy normolipidemic subjects were reviewed in 39 studies approximating 1500 ppTG measurements.68, Although baseline dietary characteristics, fat content, and composition of test meals often varied between studies, a graded association existed between the amount of dietary fat in the test meal and the ppTG response.For example, a meal that contained up to 15 g of fat was associated with minimal (20%) increases in peak ppTG levels, 276 whereas high-fat meals (eg, 50 g), including those served in popular fast-food restaurants, increased triglyceride levels by at least 50% beyond fasting levels.68,273,275,279 Because median triglyceride levels in US adults range between 106 (women) and 122 (men) mg/dL, measurement of nonfasting triglyceride levels in the absence of a high-fat meal (eg, Ͻ15 g) would be expected to eliminate the requirement for a fasting lipid panel in a sizeable proportion of otherwise healthy adults. A practical algorithm for screening triglyceride measurements is suggested in Figure 5.In normotriglyceridemic subjects (ie, fasting triglyceride levels Ͻ150 mg/dL), consumption of a low-fat breakfast (ie, Ͻ15 g) before blood sampling would not be expected to raise ppTG levels above 200 mg/dL.In these cases, no further testing for hypertriglyceridemia is indicated, although further discussion of lifestyle measures may be advocated on the basis of that individual's level of risk.However, if nonfasting triglyceride levels equal or exceed 200 mg/dL, a fasting lipid panel is recommended within a reasonable (eg, 2 to 4 weeks) time frame.
What the sources say
- Not checked yetcites [21] 21. Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007;298:299 -308. source
- Not checked yetcites [22] 22. Bansal S, Buring JE, Rifai N, Mora S, Sacks FM, Ridker PM. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA. 2007;298:309 -316. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The Framingham Heart Study was among the first observational studies to recognize elevated triglyceride level as a predictor of CVD in women”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2. Triglycerides as a Cardiovascular Risk Factor in Women
What the sources say
- Not matchedcites [301] 301. Castelli WP. The triglyceride issue: a view from Framingham. Am Heart J. 1986;112:432-437.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [329] 329. Saarelainen H, Laitinen T, Raitakari OT, Juonala M, Heiskanen N, Lyyra-Laitinen T, Viikari JS, Vanninen E, Heinonen S. Pregnancy- related hyperlipidemia and endothelial function in healthy women. Circ J. 2006;70:768 -772.
plain- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [315]
- Not checked yetcites [316] 316. Valkenburg O, Steegers-Theunissen RP, Smedts HP, Dallinga-Thie GM, Fauser BC, Westerveld EH, Laven JS. A more atherogenic serum lipo- protein profile is present in women with polycystic ovary syndrome: a case-control study. J Clin Endocrinol Metab. 2008;93:470 -476.
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In the paper
“whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [314] 314. Reed RG, Kris-Etherton P, Stewart PW, Pearson TA; DELTA (Dietary Effects on Lipoproteins and Thrombogenic Activity) Investigators. Variation of lipids and lipoproteins in premenopausal women compared with men and postmenopausal women. Metabolism. 2000;49: 1101-1105. 315. 110. Talbott E, Guzick D, Clerici A, Berga S, Detre K, Weimer K, Kuller L. Coronary heart disease risk factors in women with polycystic ovary syndrome. Arterioscler Thromb Vasc Biol. 1995;15:821-826.
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [320] 320. Connelly PW, Stachenko S, MacLean DR, Petrasovits A, Little JA; Canadian Heart Health Surveys Research Group. The prevalence of hyperlipidemia in women and its association with use of oral contra- ceptives, sex hormone replacement therapy and nonlipid coronary artery disease risk factors. Can J Cardiol. 1999;15:419 -427.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [317] 317. Greenlund KJ, Webber LS, Srinivasan S, Wattigney W, Johnson C, Berenson GS. Associations of oral contraceptive use with serum lipids and lipoproteins in young women: the Bogalusa Heart Study. Ann Epidemiol. 1997;7:561-567.
- Not checked yetcites [318] 318. Godsland IF, Crook D, Simpson R, Proudler T, Felton C, Lees B, Anyaoku V, Devenport M, Wynn V. The effects of different formu- lations of oral contraceptive agents on lipid and carbohydrate metabo- lism. N Engl J Med. 1990;323:1375-1381.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Triglyceride elevations are not usually observed with transdermally administered estrogens.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [337] 337. Godsland IF. Effects of postmenopausal hormone replacement therapy on lipid, lipoprotein, and apolipoprotein (a) concentrations: analysis of studies published from 1974 -2000. Fertil Steril. 2001;75:898 -915. source
- Not checked yetcites [341] 341. Seed M, Sands RH, McLaren M, Kirk G, Darko D. The effect of hormone replacement therapy and route of administration on selected cardiovascular risk factors in post-menopausal women. Fam Pract. 2000;17:497-507.
- Not checked yetcites [342] 342. Crook D, Cust MP, Gangar KF, Worthington M, Hillard TC, Stevenson JC, Whitehead MI, Wynn V. Comparison of transdermal and oral estrogen-progestin replacement therapy: effects on serum lipids and lipoproteins. Am J Obstet Gynecol. 1992;166:950 -955.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [322] 322. Koukkou E, Watts GF, Mazurkiewicz J, Lowy C. Ethnic differences in lipid and lipoprotein metabolism in pregnant women of African and Caucasian origin. J Clin Pathol. 1994;47:1105-1107.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [338] 338. Weintraub MS, Grosskopf I, Charach G, Eckstein N, Ringel Y, Maharshak N, Rotmensch HH, Rubinstein A. Fluctuations of lipid and lipoprotein levels in hyperlipidemic postmenopausal women receiving hormone replacement therapy. Arch Intern Med. 1998;158:1803-1806. 339. 111. Grady D, Applegate W, Bush T, Furberg C, Riggs B, Hulley SB. Heart and Estrogen/progestin Replacement Study (HERS): design, methods, and baseline characteristics. Control Clin Trials. 1998;19:314 -335.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [335] 335. Derby CA, Crawford SL, Pasternak RC, Sowers M, Sternfeld B, Matthews KA. Lipid changes during the menopause transition in relation to age and weight: the Study of Women's Health Across the Nation. Am J Epidemiol. 2009;169:1352-1361.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Triglyceride levels in the 1999 -2002 NHANES survey were higher than those documented in earlier NHANES surveys in 1976 -1980 and 1988 -1994.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.1. Triglyceride Levels During the Lifespan in Women
What the sources say
- Not checked yetcites [6] 6. Carroll MD, Lacher DA, Sorlie PD, Cleeman JI, Gordon DJ, Wolz M, Grundy SM, Johnson CL. Trends in serum lipids and lipoproteins of adults, 1960 -2002. JAMA. 2005;294:1773-1781.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [328] 328. Son GH, Kwon JY, Kim YH, Park YW. Maternal serum triglycerides as predictive factors for large-for-gestational age newborns in women with gestational diabetes mellitus. Acta Obstet Gynecol Scand. 2010;89: 700 -704.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Additional data from the Strong Heart Study have identified non-HDL-C as an important predictor of CVD in this subgroup.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities
What the sources say
- Not checked yetcites [208] 208. Lu W, Resnick HE, Jablonski KA, Jones KL, Jain AK, Howard WJ, Robbins DC, Howard BV. Non-HDL cholesterol as a predictor of cardiovascular disease in type 2 diabetes: the Strong Heart Study. Diabetes Care. 2003;26:16 -23.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines As described in Section 2: Scope of the Problem, triglyceride levels are classified as normal (Ͻ150 mg/dL), borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), or very high (Ն500 mg/dL) based on measurements after a 12-hour fast.The most clinically relevant complication of hypertriglyceridemia is acute pancreatitis, yet only 10% of cases are a direct consequence of triglyceride levels.Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL 105,353 ; however, because only 20% of subjects presenting with these extremely high levels develop pancreatitis, 354 it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.Table 5 lists genetic and secondary causes (disorders of metabolism, diet, drugs, and diseases that cause hypertriglyceridemia-induced pancreatitis [91][92][93][94][95]355,356 ).Even when a secondary cause is identified, family screening to uncover a genetic lipid disorder is also in order.357 In addition to pancreatitis, other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.Therefore, very high triglyceride levels often require both therapeutic lifestyle change and pharmacological therapy as outlined in ATP III. 10 Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.74 The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).156,157,360 It is important to recognize that individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment. A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.6 Consistent with a reduced likelihood of abnormal metabolic parameters (eg, IR) are observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load (Section 10.3., Fasting Versus Nonfasting Levels). An "optimal" triglyceride cut point is only intended to define one physiological parameter of cardiometabolic health.It does not represent a therapeutic target, because there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.Nevertheless, the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8 is of great concern.These developments have provided the impetus for intensification of efforts aimed at therapeutic lifestyle change to halt and potentially reverse an alarming trend that, if not proactively addressed, may eradicate the considerable progress in CVD risk reduction that has been achieved in recent years.381
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines As described in Section 2: Scope of the Problem, triglyceride levels are classified as normal (Ͻ150 mg/dL), borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), or very high (Ն500 mg/dL) based on measurements after a 12-hour fast.The most clinically relevant complication of hypertriglyceridemia is acute pancreatitis, yet only 10% of cases are a direct consequence of triglyceride levels.Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL 105,353 ; however, because only 20% of subjects presenting with these extremely high levels develop pancreatitis, 354 it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.Table 5 lists genetic and secondary causes (disorders of metabolism, diet, drugs, and diseases that cause hypertriglyceridemia-induced pancreatitis [91][92][93][94][95]355,356 ).Even when a secondary cause is identified, family screening to uncover a genetic lipid disorder is also in order.357 In addition to pancreatitis, other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.Therefore, very high triglyceride levels often require both therapeutic lifestyle change and pharmacological therapy as outlined in ATP III. 10 Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.74 The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).156,157,360 It is important to recognize that individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment. A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.6 Consistent with a reduced likelihood of abnormal metabolic parameters (eg, IR) are observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load (Section 10.3., Fasting Versus Nonfasting Levels). An "optimal" triglyceride cut point is only intended to define one physiological parameter of cardiometabolic health.It does not represent a therapeutic target, because there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.Nevertheless, the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8 is of great concern.These developments have provided the impetus for intensification of efforts aimed at therapeutic lifestyle change to halt and potentially reverse an alarming trend that, if not proactively addressed, may eradicate the considerable progress in CVD risk reduction that has been achieved in recent years.381
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The magnitude of decrease in triglycerides is directly related to the amount of weight loss.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.1.1. Weight Status, Body Fat Distribution, and Weight Loss
What the sources say
- Not checked yetcites [387] 387. Poobalan A, Aucott L, Smith WC, Avenell A, Jung R, Broom J, Grant AM. Effects of weight loss in overweight/obese individuals and long-term lipid outcomes: a systematic review. Obes Rev. 2004;5:43-50.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines As described in Section 2: Scope of the Problem, triglyceride levels are classified as normal (Ͻ150 mg/dL), borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), or very high (Ն500 mg/dL) based on measurements after a 12-hour fast.The most clinically relevant complication of hypertriglyceridemia is acute pancreatitis, yet only 10% of cases are a direct consequence of triglyceride levels.Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL 105,353 ; however, because only 20% of subjects presenting with these extremely high levels develop pancreatitis, 354 it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.Table 5 lists genetic and secondary causes (disorders of metabolism, diet, drugs, and diseases that cause hypertriglyceridemia-induced pancreatitis [91][92][93][94][95]355,356 ).Even when a secondary cause is identified, family screening to uncover a genetic lipid disorder is also in order.357 In addition to pancreatitis, other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.Therefore, very high triglyceride levels often require both therapeutic lifestyle change and pharmacological therapy as outlined in ATP III. 10 Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.74 The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).156,157,360 It is important to recognize that individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment. A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.6 Consistent with a reduced likelihood of abnormal metabolic parameters (eg, IR) are observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load (Section 10.3., Fasting Versus Nonfasting Levels). An "optimal" triglyceride cut point is only intended to define one physiological parameter of cardiometabolic health.It does not represent a therapeutic target, because there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.Nevertheless, the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8 is of great concern.These developments have provided the impetus for intensification of efforts aimed at therapeutic lifestyle change to halt and potentially reverse an alarming trend that, if not proactively addressed, may eradicate the considerable progress in CVD risk reduction that has been achieved in recent years.381
What the sources say
- Not checked yetcites [3] 3. Hulley SB, Rosenman RH, Bawol RD, Brand RJ. Epidemiology as a guide to clinical decisions: the association between triglyceride and coronary heart disease. N Engl J Med. 1980;302:1383-1389. source
- Not checked yetcites [232] 232. Assmann G, Schulte H. Relation of high-density lipoprotein cholesterol and triglycerides to incidence of atherosclerotic coronary artery disease (the PROCAM experience): Prospective Cardiovascular Mu ¨nster Study. Am J Cardiol. 1992;70:733-737. 233. 105. McLaughlin T, Reaven G, Abbasi F, Lamendola C, Saad M, Waters D, Simon J, Krauss RM. Is there a simple way to identify insulin-resistant individuals at increased risk of cardiovascular disease? Am J Cardiol. 2005;96:399 -404. source
- Not matchedcites [367] 367. He Y, Lam TH, Li LS, He SF, Liang BQ. Triglyceride and coronary heart disease mortality in a 24-year follow-up study in Xi'an, China. Ann Epidemiol. 2004;14:1-7.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [374] 374. Castelli WP. Cholesterol and lipids in the risk of coronary artery disease: the Framingham Heart Study. Can J Cardiol. 1988;(suppl A):5A-10A.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [375] 375. Menotti A, Scanga M, Morisi G. Serum triglycerides in the prediction of coronary artery disease (an Italian experience). Am J Cardiol. 1994;73: 29 -32.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [376] 376. Miller M, Seidler A, Moalemi A, Pearson TA. Normal triglyceride levels and coronary artery disease events: the Baltimore Coronary Observational Long-Term Study. J Am Coll Cardiol. 1998;31: 1252-1257.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites [377] 377. Stavenow L, Kjellstrom T. Influence of serum triglyceride levels on the risk for myocardial infarction in 12,510 middle aged males: interaction with serum cholesterol. Atherosclerosis. 1999;147:243-247. source
- Not matchedcites [378] 378. Miller M, Cannon CP, Murphy SA, Qin J, Ray KK, Braunwald E. Impact of triglyceride levels beyond low-density lipoprotein cholesterol after acute coronary syndrome in the PROVE IT-TIMI 22 trial. J Am Coll Cardiol. 2008;51:724 -730.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites [379] 379. Morrison JA, Glueck CJ, Horn PS, Yeramaneni S, Wang P. Pediatric triglycerides predict cardiovascular disease events in the fourth to fifth decade of life. Metabolism. 2009;58:1277-1284. source
- Not matchedcites [380] 380. Onat A, Sari I, Yazici M, Can G, Hergenc G, Avci GS. Plasma triglyc- erides, an independent predictor of cardiovascular disease in men: a prospective study based on a population with prevalent metabolic syndrome. Int J Cardiol. 2006;108:89 -95.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [121] 121. Carr MC, Knopp RH, Brunzell JD, Wheeler BS, Zhu X, Lakshmanan M, Rosen AS, Anderson PW. Effect of raloxifene on serum triglycerides in women with a history of hypertriglyceridemia while on oral estrogen therapy. Diabetes Care. 2005;28:1555-1561. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Weight loss has a beneficial effect on lipids and lipoproteins.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.1.1. Weight Status, Body Fat Distribution, and Weight Loss
What the sources say
- Not checked yetcites [385] 385. Pasanisi F, Contaldo F, de Simone G, Mancini M. Benefits of sustained moderate weight loss in obesity. Nutr Metab Cardiovasc Dis. 2001;11: 401-406. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“only 20% of subjects presenting with these extremely high levels develop pancreatitis”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines As described in Section 2: Scope of the Problem, triglyceride levels are classified as normal (Ͻ150 mg/dL), borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), or very high (Ն500 mg/dL) based on measurements after a 12-hour fast.The most clinically relevant complication of hypertriglyceridemia is acute pancreatitis, yet only 10% of cases are a direct consequence of triglyceride levels.Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL 105,353 ; however, because only 20% of subjects presenting with these extremely high levels develop pancreatitis, 354 it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.Table 5 lists genetic and secondary causes (disorders of metabolism, diet, drugs, and diseases that cause hypertriglyceridemia-induced pancreatitis [91][92][93][94][95]355,356 ).Even when a secondary cause is identified, family screening to uncover a genetic lipid disorder is also in order.357 In addition to pancreatitis, other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.Therefore, very high triglyceride levels often require both therapeutic lifestyle change and pharmacological therapy as outlined in ATP III. 10 Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.74 The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).156,157,360 It is important to recognize that individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment. A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.6 Consistent with a reduced likelihood of abnormal metabolic parameters (eg, IR) are observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load (Section 10.3., Fasting Versus Nonfasting Levels). An "optimal" triglyceride cut point is only intended to define one physiological parameter of cardiometabolic health.It does not represent a therapeutic target, because there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.Nevertheless, the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8 is of great concern.These developments have provided the impetus for intensification of efforts aimed at therapeutic lifestyle change to halt and potentially reverse an alarming trend that, if not proactively addressed, may eradicate the considerable progress in CVD risk reduction that has been achieved in recent years.381
What the sources say
- Not checked yetcites [354] 354. Lloret Linares C, Pelletier AL, Czernichow S, Vergnaud AC, Bonnefont-Rousselot D, Levy P, Ruszniewski P, Bruckert E. Acute pancreatitis in a cohort of 129 patients referred for severe hypertriglyc- eridemia. Pancreas. 2008;37:13-12.
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In the paper
“there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines As described in Section 2: Scope of the Problem, triglyceride levels are classified as normal (Ͻ150 mg/dL), borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), or very high (Ն500 mg/dL) based on measurements after a 12-hour fast.The most clinically relevant complication of hypertriglyceridemia is acute pancreatitis, yet only 10% of cases are a direct consequence of triglyceride levels.Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL 105,353 ; however, because only 20% of subjects presenting with these extremely high levels develop pancreatitis, 354 it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.Table 5 lists genetic and secondary causes (disorders of metabolism, diet, drugs, and diseases that cause hypertriglyceridemia-induced pancreatitis [91][92][93][94][95]355,356 ).Even when a secondary cause is identified, family screening to uncover a genetic lipid disorder is also in order.357 In addition to pancreatitis, other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.Therefore, very high triglyceride levels often require both therapeutic lifestyle change and pharmacological therapy as outlined in ATP III. 10 Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.74 The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).156,157,360 It is important to recognize that individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment. A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.6 Consistent with a reduced likelihood of abnormal metabolic parameters (eg, IR) are observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load (Section 10.3., Fasting Versus Nonfasting Levels). An "optimal" triglyceride cut point is only intended to define one physiological parameter of cardiometabolic health.It does not represent a therapeutic target, because there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.Nevertheless, the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8 is of great concern.These developments have provided the impetus for intensification of efforts aimed at therapeutic lifestyle change to halt and potentially reverse an alarming trend that, if not proactively addressed, may eradicate the considerable progress in CVD risk reduction that has been achieved in recent years.381
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“each 1% replacement of trans fatty acids for monounsaturated fat (MUFA) or polyunsaturated fat (PUFA) lowers triglyceride levels by Ϸ1%.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.1. Dietary and Weight-Losing Strategies
What the sources say
- Not checked yetcites [384] 384. Mozaffarian D, Clarke R. Quantitative effects on cardiovascular risk factors and coronary heart disease risk of replacing partially hydro- genated vegetable oils with other fats and oils. Eur J Clin Nutr. 2009; 63(suppl 2):S22-S33. source
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“In a subsequent meta-analysis of 30 controlled feeding studies in patients with or without T2DM (nϭ1213), a moderate-fat diet (32.5% to 50% of calories from fat) versus a lower-fat diet (18% to 30% of calories from fat) resulted in a decrease in triglyceride level of 9.4 mg/dL (range from Ϫ6.1 to Ϫ12.2 mg/dL, PϽ0.00001) in those without T2DM”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
What the sources say
- Not checked yetcites [391] 391. Cao YMD, Pelkman CL, Zhao G, Townsend SM, Kris-Etherton PM. Effects of moderate (MF) versus lower fat (LF) diets on lipids and lipoproteins: a meta-analysis of clinical trials in subjects with and without diabetes. J Clin Lipidol. 2009;3:19 -32. source
plaindirectn = 1,213 ·- Asserted: passes — The authors put it forward as true.
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In the paper
“the Lyon Diet Heart Study, 403 which found no significant change in triglyceride levels on a MUFA-enriched versus low-fat, high-n-6 PUFA diet”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.2. Mediterranean-Style Dietary Pattern Epidemiological and clinical trial evidence suggests that the Mediterranean-style dietary pattern 398,399 is associated with decreased triglyceride levels.In the Framingham Heart Study Offspring Cohort (nϭ2730), subjects in the highest quintile for Mediterranean-style dietary pattern score had the lowest triglyceride levels (103 versus 114 mg/dL, PϽ0.001) over a 7-year follow-up.398 Several clinical trials have reported beneficial effects of a Mediterranean-style diet on triglycerides compared with a lower-fat diet.Esposito et al 400 compared the effects of a Mediterranean-style diet with a control diet over a 2-year period on markers of CVD risk in patients (nϭ180) with MetS.The Mediterranean-style diet comprised more foods rich in MUFA, PUFA, and dietary fiber.Total fruit, vegetables, nuts, whole grains, and olive oil were higher in the intervention group.The intervention diet provided 28% of calories from total fat, with 8%, 12%, and 8% of calories from SFA, MUFA, and PUFA, respectively.The control diet provided 30% of calories from total fat, with 14%, 10%, and 7% of calories from SFA, MUFA, and PUFA, respectively.After 2 years, triglyceride levels decreased 12% in the intervention group (Pϭ0.001versus the control diet).In addition, subjects on the intervention diet decreased body weight by 6.2 lb or 2.8 kg (PϽ0.001) and waist circumference by 0.8 inches or 2 cm (Pϭ0.01)compared with the control group.Similarly, reduced triglyceride levels were reported in the Mediterranean Diet, Cardiovascular Risks and Gene Polymorphisms (Medi-RIVAGE) Study.401 Finally, the PREDIMED (Prevencio ´n con Dieta Mediterra ´nea) Study evaluated the effects of a Mediterranean diet plus virgin olive oil (1 L per week) and a Mediterranean diet plus mixed nuts (30 g/d; walnuts, hazelnuts, and almonds) versus a low-fat diet (control diet) in subjects (nϭ1224) at increased risk for CVD.402 Both Mediterranean-style diets provided higher energy intake from fat than the control diet (41% to 43% versus 38% of calories) and were higher in MUFA content (21% to 22% versus 19.4% of calories).After 1 year, hypertriglyceridemia was less prevalent in both Mediterranean-style diet groups (12.3% and 13.6%) than in those eating the control diet (21.3%).With few exceptions, such as the Lyon Diet Heart Study, 403 which found no significant change in triglyceride levels on a MUFA-enriched versus low-fat, high-n-6 PUFA diet, implementation of a Mediterranean-style diet versus a low-fat diet is more commonly associated with an approximately 10% to 15% lowering of triglycerides and a reduced prevalence of hypertriglyceridemia.
What the sources say
- Not checked yetcites [403] 403. de Lorgeril M, Salen P, Martin JL, Monjaud I, Delaye J, Mamelle N. Mediterranean diet, traditional risk factors, and the rate of cardiovascu- lar complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation. 1999;99:779 -785. source
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“In 7 studies (nϭ98) that compared moderate CHO and high fiber versus moderate CHO and low fiber, triglyceride levels decreased by 8% in the high-fiber groups.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.1. Dietary Fiber
What the sources say
- Not checked yetcites [406] 406. Anderson JW, Randles KM, Kendall CW, Jenkins DJ. Carbohydrate and fiber recommendations for individuals with diabetes: a quantitative assessment and meta-analysis of the evidence. J Am Coll Nutr. 2004; 23:5-17.
plaindirectn = 98- Asserted: passes — The authors put it forward as true.
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“The lowest triglyceride levels were observed when added sugar represented Ͻ10% of total energy.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.2. Added Sugars
What the sources say
- Not checked yetcites [408] 408. Welsh JA, Sharma A, Abramson JL, Vaccarino V, Gillespie C, Vos MB. Caloric sweetener consumption and dyslipidemia among US adults. JAMA. 2010;303:1490 -1497.
plaincorrelationaln = 6,113- Asserted: passes — The authors put it forward as true.
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In the paper
“In contrast, data exist related to fiber intake and triglycerides in individuals with or at increased risk for T2DM.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.1. Dietary Fiber
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“the Women's Health Initiative (WHI) Dietary Modification Trial of 48 835 postmenopausal women, found no differences in triglyceride levels (142 versus 145 mg/dL) between the low-fat dietary intervention and a higher-fat comparator group after 3 years of follow-up.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
What the sources say
- Not checked yetcites [397] 397. Howard BV, Van Horn L, Hsia J, Manson JE, Stefanick ML, Wassertheil-Smoller S, Kuller LH, LaCroix AZ, Langer RD, Lasser NL, Lewis CE, Limacher MC, Margolis KL, Mysiw WJ, Ockene JK, Parker LM, Perri MG, Phillips L, Prentice RL, Robbins J, Rossouw JE, Sarto GE, Schatz IJ, Snetselaar LG, Stevens VJ, Tinker LF, Trevisan M, Vitolins MZ, Anderson GL, Assaf AR, Bassford T, Beresford SA, Black HR, Brunner RL, Brzyski RG, Caan B, Chlebowski RT, Gass M, Granek I, Greenland P, Hays J, Heber D, Heiss G, Hendrix SL, Hubbell FA, Johnson KC, Kotchen JM. Low-fat dietary pattern and risk of cardio- vascul source
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“in a large meta-analysis of 60 controlled feeding studies, 392 replacement of any fatty acid class with a mixture of dietary CHOs increased fasting triglyceride levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
What the sources say
- Not checked yetcites [392] 392. Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 con- trolled trials. Am J Clin Nutr. 2003;77:1146 -1155. source
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“Conversely, higher triglyceride levels (5% to 10%) were observed when added sugar represented a greater proportion of energy intake.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.2. Added Sugars
What the sources say
- Not checked yetcites [408] 408. Welsh JA, Sharma A, Abramson JL, Vaccarino V, Gillespie C, Vos MB. Caloric sweetener consumption and dyslipidemia among US adults. JAMA. 2010;303:1490 -1497.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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“In the Framingham Heart Study Offspring Cohort (nϭ2730), subjects in the highest quintile for Mediterranean-style dietary pattern score had the lowest triglyceride levels (103 versus 114 mg/dL, PϽ0.001) over a 7-year follow-up.398”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.2. Mediterranean-Style Dietary Pattern Epidemiological and clinical trial evidence suggests that the Mediterranean-style dietary pattern 398,399 is associated with decreased triglyceride levels.In the Framingham Heart Study Offspring Cohort (nϭ2730), subjects in the highest quintile for Mediterranean-style dietary pattern score had the lowest triglyceride levels (103 versus 114 mg/dL, PϽ0.001) over a 7-year follow-up.398 Several clinical trials have reported beneficial effects of a Mediterranean-style diet on triglycerides compared with a lower-fat diet.Esposito et al 400 compared the effects of a Mediterranean-style diet with a control diet over a 2-year period on markers of CVD risk in patients (nϭ180) with MetS.The Mediterranean-style diet comprised more foods rich in MUFA, PUFA, and dietary fiber.Total fruit, vegetables, nuts, whole grains, and olive oil were higher in the intervention group.The intervention diet provided 28% of calories from total fat, with 8%, 12%, and 8% of calories from SFA, MUFA, and PUFA, respectively.The control diet provided 30% of calories from total fat, with 14%, 10%, and 7% of calories from SFA, MUFA, and PUFA, respectively.After 2 years, triglyceride levels decreased 12% in the intervention group (Pϭ0.001versus the control diet).In addition, subjects on the intervention diet decreased body weight by 6.2 lb or 2.8 kg (PϽ0.001) and waist circumference by 0.8 inches or 2 cm (Pϭ0.01)compared with the control group.Similarly, reduced triglyceride levels were reported in the Mediterranean Diet, Cardiovascular Risks and Gene Polymorphisms (Medi-RIVAGE) Study.401 Finally, the PREDIMED (Prevencio ´n con Dieta Mediterra ´nea) Study evaluated the effects of a Mediterranean diet plus virgin olive oil (1 L per week) and a Mediterranean diet plus mixed nuts (30 g/d; walnuts, hazelnuts, and almonds) versus a low-fat diet (control diet) in subjects (nϭ1224) at increased risk for CVD.402 Both Mediterranean-style diets provided higher energy intake from fat than the control diet (41% to 43% versus 38% of calories) and were higher in MUFA content (21% to 22% versus 19.4% of calories).After 1 year, hypertriglyceridemia was less prevalent in both Mediterranean-style diet groups (12.3% and 13.6%) than in those eating the control diet (21.3%).With few exceptions, such as the Lyon Diet Heart Study, 403 which found no significant change in triglyceride levels on a MUFA-enriched versus low-fat, high-n-6 PUFA diet, implementation of a Mediterranean-style diet versus a low-fat diet is more commonly associated with an approximately 10% to 15% lowering of triglycerides and a reduced prevalence of hypertriglyceridemia.
What the sources say
- Not checked yetcites [398] 398. Rumawas ME, Meigs JB, Dwyer JT, McKeown NM, Jacques PF. Mediterranean-style dietary pattern, reduced risk of metabolic syndrome traits, and incidence in the Framingham Offspring Cohort. Am J Clin Nutr. 2009;90:1608 -1614. source
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In the paper
“After 2 years, triglyceride levels decreased 12% in the intervention group (Pϭ0.001versus the control diet).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.2. Mediterranean-Style Dietary Pattern Epidemiological and clinical trial evidence suggests that the Mediterranean-style dietary pattern 398,399 is associated with decreased triglyceride levels.In the Framingham Heart Study Offspring Cohort (nϭ2730), subjects in the highest quintile for Mediterranean-style dietary pattern score had the lowest triglyceride levels (103 versus 114 mg/dL, PϽ0.001) over a 7-year follow-up.398 Several clinical trials have reported beneficial effects of a Mediterranean-style diet on triglycerides compared with a lower-fat diet.Esposito et al 400 compared the effects of a Mediterranean-style diet with a control diet over a 2-year period on markers of CVD risk in patients (nϭ180) with MetS.The Mediterranean-style diet comprised more foods rich in MUFA, PUFA, and dietary fiber.Total fruit, vegetables, nuts, whole grains, and olive oil were higher in the intervention group.The intervention diet provided 28% of calories from total fat, with 8%, 12%, and 8% of calories from SFA, MUFA, and PUFA, respectively.The control diet provided 30% of calories from total fat, with 14%, 10%, and 7% of calories from SFA, MUFA, and PUFA, respectively.After 2 years, triglyceride levels decreased 12% in the intervention group (Pϭ0.001versus the control diet).In addition, subjects on the intervention diet decreased body weight by 6.2 lb or 2.8 kg (PϽ0.001) and waist circumference by 0.8 inches or 2 cm (Pϭ0.01)compared with the control group.Similarly, reduced triglyceride levels were reported in the Mediterranean Diet, Cardiovascular Risks and Gene Polymorphisms (Medi-RIVAGE) Study.401 Finally, the PREDIMED (Prevencio ´n con Dieta Mediterra ´nea) Study evaluated the effects of a Mediterranean diet plus virgin olive oil (1 L per week) and a Mediterranean diet plus mixed nuts (30 g/d; walnuts, hazelnuts, and almonds) versus a low-fat diet (control diet) in subjects (nϭ1224) at increased risk for CVD.402 Both Mediterranean-style diets provided higher energy intake from fat than the control diet (41% to 43% versus 38% of calories) and were higher in MUFA content (21% to 22% versus 19.4% of calories).After 1 year, hypertriglyceridemia was less prevalent in both Mediterranean-style diet groups (12.3% and 13.6%) than in those eating the control diet (21.3%).With few exceptions, such as the Lyon Diet Heart Study, 403 which found no significant change in triglyceride levels on a MUFA-enriched versus low-fat, high-n-6 PUFA diet, implementation of a Mediterranean-style diet versus a low-fat diet is more commonly associated with an approximately 10% to 15% lowering of triglycerides and a reduced prevalence of hypertriglyceridemia.
What the sources say
- Not checked yetcites [400] 400. Esposito K, Marfella R, Ciotola M, Di Palo C, Giugliano F, Giugliano G, D'Armiento M, D'Andrea F, Giugliano D. Effect of a Mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. JAMA. 2004;292:1440 -1446. source
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“in those with T2DM, the moderate-fat diet resulted in greater triglyceride reduction (Ϫ24.8 mg/dL, PϽ0.05) than seen with the low-fat diet.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
What the sources say
- Not checked yetcites [391] 391. Cao YMD, Pelkman CL, Zhao G, Townsend SM, Kris-Etherton PM. Effects of moderate (MF) versus lower fat (LF) diets on lipids and lipoproteins: a meta-analysis of clinical trials in subjects with and without diabetes. J Clin Lipidol. 2009;3:19 -32. source
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In the paper
“The role of GI and GL in CVD risk assessment remains controversial.[411][412][413]”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load
What the sources say
- Not checked yetcites [411] 411. Dickinson S, Brand-Miller J. Glycemic index, postprandial glycemia and cardiovascular disease. Curr Opin Lipidol. 2005;16:69 -75. source
- Not checked yetcites [412] 412. Franz MJ. Is there a role for the glycemic index in coronary heart disease prevention or treatment? Curr Atheroscler Rep. 2008;10:497-502.
- Not checked yetcites [413] 413. Mente A, de Koning L, Shannon HS, Anand SS. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med. 2009;169:659 -669.
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“the evidence specifically for associations or effects on triglycerides is limited, especially in the absence of T2DM.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.1. Dietary Fiber
What the sources say
- Not checked yetcites [404] 404. Erkkila AT, Lichtenstein AH. Fiber and cardiovascular disease risk: how strong is the evidence? J Cardiovasc Nurs. 2006;21:3-8. source
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In the paper
“Since ATP III, several large clinical trials have reported no increase in triglycerides in response to a reduction in total fat and a concurrent increase in dietary CHOs.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
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“A positive correlation between GI/GL and triglyceride levels was also reported in a cohort of Japanese women.416”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load
What the sources say
- Not checked yetcites [416] source
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“The Botnia Dietary Study, a population study of 248 male and 304 female adult nondiabetic relatives of patients with T2DM from West Finland, reported an inverse association between serum triglycerides and total dietary fiber, water-insoluble fiber, and water-soluble fiber.405”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.1. Dietary Fiber
What the sources say
- Not checked yetcites [405] 405. Ylo ¨nen K, Saloranta C, Kronberg-Kippila ¨C, Groop L, Aro A, Virtanen SM; Botnia Dietary Study. Associations of dietary fiber with glucose metabolism in nondiabetic relatives of subjects with type 2 diabetes: the Botnia Dietary Study. Diabetes Care. 2003;26:1979 -1985.
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In the paper
“Similarly, reduced triglyceride levels were reported in the Mediterranean Diet, Cardiovascular Risks and Gene Polymorphisms (Medi-RIVAGE) Study.401”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.2. Mediterranean-Style Dietary Pattern Epidemiological and clinical trial evidence suggests that the Mediterranean-style dietary pattern 398,399 is associated with decreased triglyceride levels.In the Framingham Heart Study Offspring Cohort (nϭ2730), subjects in the highest quintile for Mediterranean-style dietary pattern score had the lowest triglyceride levels (103 versus 114 mg/dL, PϽ0.001) over a 7-year follow-up.398 Several clinical trials have reported beneficial effects of a Mediterranean-style diet on triglycerides compared with a lower-fat diet.Esposito et al 400 compared the effects of a Mediterranean-style diet with a control diet over a 2-year period on markers of CVD risk in patients (nϭ180) with MetS.The Mediterranean-style diet comprised more foods rich in MUFA, PUFA, and dietary fiber.Total fruit, vegetables, nuts, whole grains, and olive oil were higher in the intervention group.The intervention diet provided 28% of calories from total fat, with 8%, 12%, and 8% of calories from SFA, MUFA, and PUFA, respectively.The control diet provided 30% of calories from total fat, with 14%, 10%, and 7% of calories from SFA, MUFA, and PUFA, respectively.After 2 years, triglyceride levels decreased 12% in the intervention group (Pϭ0.001versus the control diet).In addition, subjects on the intervention diet decreased body weight by 6.2 lb or 2.8 kg (PϽ0.001) and waist circumference by 0.8 inches or 2 cm (Pϭ0.01)compared with the control group.Similarly, reduced triglyceride levels were reported in the Mediterranean Diet, Cardiovascular Risks and Gene Polymorphisms (Medi-RIVAGE) Study.401 Finally, the PREDIMED (Prevencio ´n con Dieta Mediterra ´nea) Study evaluated the effects of a Mediterranean diet plus virgin olive oil (1 L per week) and a Mediterranean diet plus mixed nuts (30 g/d; walnuts, hazelnuts, and almonds) versus a low-fat diet (control diet) in subjects (nϭ1224) at increased risk for CVD.402 Both Mediterranean-style diets provided higher energy intake from fat than the control diet (41% to 43% versus 38% of calories) and were higher in MUFA content (21% to 22% versus 19.4% of calories).After 1 year, hypertriglyceridemia was less prevalent in both Mediterranean-style diet groups (12.3% and 13.6%) than in those eating the control diet (21.3%).With few exceptions, such as the Lyon Diet Heart Study, 403 which found no significant change in triglyceride levels on a MUFA-enriched versus low-fat, high-n-6 PUFA diet, implementation of a Mediterranean-style diet versus a low-fat diet is more commonly associated with an approximately 10% to 15% lowering of triglycerides and a reduced prevalence of hypertriglyceridemia.
What the sources say
- Not checked yetcites [401] 401. Vincent-Baudry S, Defoort C, Gerber M, Bernard MC, Verger P, Helal O, Portugal H, Planells R, Grolier P, Amiot-Carlin MJ, Vague P, Lairon D. The Medi-RIVAGE study: reduction of cardiovascular disease risk factors after a 3-mo intervention with a Mediterranean-type diet or a low-fat diet. Am J Clin Nutr. 2005;82:964 -971. source
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In the paper
“After 1 year, hypertriglyceridemia was less prevalent in both Mediterranean-style diet groups (12.3% and 13.6%) than in those eating the control diet (21.3%).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.2. Mediterranean-Style Dietary Pattern Epidemiological and clinical trial evidence suggests that the Mediterranean-style dietary pattern 398,399 is associated with decreased triglyceride levels.In the Framingham Heart Study Offspring Cohort (nϭ2730), subjects in the highest quintile for Mediterranean-style dietary pattern score had the lowest triglyceride levels (103 versus 114 mg/dL, PϽ0.001) over a 7-year follow-up.398 Several clinical trials have reported beneficial effects of a Mediterranean-style diet on triglycerides compared with a lower-fat diet.Esposito et al 400 compared the effects of a Mediterranean-style diet with a control diet over a 2-year period on markers of CVD risk in patients (nϭ180) with MetS.The Mediterranean-style diet comprised more foods rich in MUFA, PUFA, and dietary fiber.Total fruit, vegetables, nuts, whole grains, and olive oil were higher in the intervention group.The intervention diet provided 28% of calories from total fat, with 8%, 12%, and 8% of calories from SFA, MUFA, and PUFA, respectively.The control diet provided 30% of calories from total fat, with 14%, 10%, and 7% of calories from SFA, MUFA, and PUFA, respectively.After 2 years, triglyceride levels decreased 12% in the intervention group (Pϭ0.001versus the control diet).In addition, subjects on the intervention diet decreased body weight by 6.2 lb or 2.8 kg (PϽ0.001) and waist circumference by 0.8 inches or 2 cm (Pϭ0.01)compared with the control group.Similarly, reduced triglyceride levels were reported in the Mediterranean Diet, Cardiovascular Risks and Gene Polymorphisms (Medi-RIVAGE) Study.401 Finally, the PREDIMED (Prevencio ´n con Dieta Mediterra ´nea) Study evaluated the effects of a Mediterranean diet plus virgin olive oil (1 L per week) and a Mediterranean diet plus mixed nuts (30 g/d; walnuts, hazelnuts, and almonds) versus a low-fat diet (control diet) in subjects (nϭ1224) at increased risk for CVD.402 Both Mediterranean-style diets provided higher energy intake from fat than the control diet (41% to 43% versus 38% of calories) and were higher in MUFA content (21% to 22% versus 19.4% of calories).After 1 year, hypertriglyceridemia was less prevalent in both Mediterranean-style diet groups (12.3% and 13.6%) than in those eating the control diet (21.3%).With few exceptions, such as the Lyon Diet Heart Study, 403 which found no significant change in triglyceride levels on a MUFA-enriched versus low-fat, high-n-6 PUFA diet, implementation of a Mediterranean-style diet versus a low-fat diet is more commonly associated with an approximately 10% to 15% lowering of triglycerides and a reduced prevalence of hypertriglyceridemia.
What the sources say
- Not checked yetcites [402] 402. Salas-Salvado ´J, Ferna ´ndez-Ballart J, Ros E, Martı ´nez-Gonza ´lez MA, Fito ´M, Estruch R, Corella D, Fiol M, Go ´mez-Gracia E, Aro ´s F, Flores G, Lapetra J, Lamuela-Ravento ´s R, Ruiz-Gutie ´rrez V, Bullo ´M, Basora J, Covas MI; PREDIMED Study Investigators. Effect of a Mediter- ranean diet supplemented with nuts on metabolic syndrome status: one-year results of the PREDIMED randomized trial. Arch Intern Med. 2008;168:2449 -2458.
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In the paper
“Epidemiological and clinical trial evidence suggests that the Mediterranean-style dietary pattern 398,399 is associated with decreased triglyceride levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.2. Mediterranean-Style Dietary Pattern Epidemiological and clinical trial evidence suggests that the Mediterranean-style dietary pattern 398,399 is associated with decreased triglyceride levels.In the Framingham Heart Study Offspring Cohort (nϭ2730), subjects in the highest quintile for Mediterranean-style dietary pattern score had the lowest triglyceride levels (103 versus 114 mg/dL, PϽ0.001) over a 7-year follow-up.398 Several clinical trials have reported beneficial effects of a Mediterranean-style diet on triglycerides compared with a lower-fat diet.Esposito et al 400 compared the effects of a Mediterranean-style diet with a control diet over a 2-year period on markers of CVD risk in patients (nϭ180) with MetS.The Mediterranean-style diet comprised more foods rich in MUFA, PUFA, and dietary fiber.Total fruit, vegetables, nuts, whole grains, and olive oil were higher in the intervention group.The intervention diet provided 28% of calories from total fat, with 8%, 12%, and 8% of calories from SFA, MUFA, and PUFA, respectively.The control diet provided 30% of calories from total fat, with 14%, 10%, and 7% of calories from SFA, MUFA, and PUFA, respectively.After 2 years, triglyceride levels decreased 12% in the intervention group (Pϭ0.001versus the control diet).In addition, subjects on the intervention diet decreased body weight by 6.2 lb or 2.8 kg (PϽ0.001) and waist circumference by 0.8 inches or 2 cm (Pϭ0.01)compared with the control group.Similarly, reduced triglyceride levels were reported in the Mediterranean Diet, Cardiovascular Risks and Gene Polymorphisms (Medi-RIVAGE) Study.401 Finally, the PREDIMED (Prevencio ´n con Dieta Mediterra ´nea) Study evaluated the effects of a Mediterranean diet plus virgin olive oil (1 L per week) and a Mediterranean diet plus mixed nuts (30 g/d; walnuts, hazelnuts, and almonds) versus a low-fat diet (control diet) in subjects (nϭ1224) at increased risk for CVD.402 Both Mediterranean-style diets provided higher energy intake from fat than the control diet (41% to 43% versus 38% of calories) and were higher in MUFA content (21% to 22% versus 19.4% of calories).After 1 year, hypertriglyceridemia was less prevalent in both Mediterranean-style diet groups (12.3% and 13.6%) than in those eating the control diet (21.3%).With few exceptions, such as the Lyon Diet Heart Study, 403 which found no significant change in triglyceride levels on a MUFA-enriched versus low-fat, high-n-6 PUFA diet, implementation of a Mediterranean-style diet versus a low-fat diet is more commonly associated with an approximately 10% to 15% lowering of triglycerides and a reduced prevalence of hypertriglyceridemia.
What the sources say
- Not checked yetcites [398] 398. Rumawas ME, Meigs JB, Dwyer JT, McKeown NM, Jacques PF. Mediterranean-style dietary pattern, reduced risk of metabolic syndrome traits, and incidence in the Framingham Offspring Cohort. Am J Clin Nutr. 2009;90:1608 -1614. source
- Not checked yetcites [399] 399. Rumawas ME, Dwyer JT, McKeown NM, Meigs JB, Rogers G, Jacques PF. The development of the Mediterranean-style dietary pattern score and its application to the American diet in the Framingham Offspring Cohort. J Nutr. 2009;139:1150 -1156. source
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In the paper
“Results also suggest that moderate intake of predominately unsaturated fat (30% to 35% of energy or more) and plant-based proteins (17% to 25% of energy) may produce a triglyceride-lowering effect.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
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In the paper
“Two epidemiological studies, the Nurses' Health Study and the Women's Health Study, reported a positive association between GL and/or GI and fasting triglyceride levels.414,415”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load
What the sources say
- Not checked yetcites [414] 414. Liu S, Manson JE, Stampfer MJ, Holmes MD, Hu FB, Hankinson SE, Willett WC. Dietary glycemic load assessed by food-frequency ques- tionnaire in relation to plasma high-density-lipoprotein cholesterol and fasting plasma triacylglycerols in postmenopausal women. Am J Clin Nutr. 2001;73:560 -566. source
- Not checked yetcites [415] 415. Levitan EB, Cook NR, Stampfer MJ, Ridker PM, Rexrode KM, Buring JE, Manson JE, Liu S. Dietary glycemic index, dietary glycemic load, blood lipids, and C-reactive protein. Metabolism. 2008;57:437-443. 416. 113. Amano Y, Kawakubo K, Lee JS, Tang AC, Sugiyama M, Mori K. Correlation between dietary glycemic index and cardiovascular disease risk factors among Japanese women. Eur J Clin Nutr. 2004;58: 1472-1478. source
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In the paper
“Therefore, these data support a triglyceride-lowering effect for dietary fiber in individuals with T2DM.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.1. Dietary Fiber
What the sources say
- Not checked yetcites [406] 406. Anderson JW, Randles KM, Kendall CW, Jenkins DJ. Carbohydrate and fiber recommendations for individuals with diabetes: a quantitative assessment and meta-analysis of the evidence. J Am Coll Nutr. 2004; 23:5-17.
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In the paper
“it has not been demonstrated convincingly that viscous fiber can fully negate the triglyceride-raising or HDLlowering actions of very high intakes of carbohydrates.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
What the sources say
- Not checked yetcites [221] 221. National Cholesterol Education Program (U.S.). Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III): Final Report. Washington, DC: National Institutes of Health, National Heart, Lung, and Blood Institute; 2002. NIH publication No. 02-5215.
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In the paper
“Several clinical trials have reported beneficial effects of a Mediterranean-style diet on triglycerides compared with a lower-fat diet.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.2. Mediterranean-Style Dietary Pattern Epidemiological and clinical trial evidence suggests that the Mediterranean-style dietary pattern 398,399 is associated with decreased triglyceride levels.In the Framingham Heart Study Offspring Cohort (nϭ2730), subjects in the highest quintile for Mediterranean-style dietary pattern score had the lowest triglyceride levels (103 versus 114 mg/dL, PϽ0.001) over a 7-year follow-up.398 Several clinical trials have reported beneficial effects of a Mediterranean-style diet on triglycerides compared with a lower-fat diet.Esposito et al 400 compared the effects of a Mediterranean-style diet with a control diet over a 2-year period on markers of CVD risk in patients (nϭ180) with MetS.The Mediterranean-style diet comprised more foods rich in MUFA, PUFA, and dietary fiber.Total fruit, vegetables, nuts, whole grains, and olive oil were higher in the intervention group.The intervention diet provided 28% of calories from total fat, with 8%, 12%, and 8% of calories from SFA, MUFA, and PUFA, respectively.The control diet provided 30% of calories from total fat, with 14%, 10%, and 7% of calories from SFA, MUFA, and PUFA, respectively.After 2 years, triglyceride levels decreased 12% in the intervention group (Pϭ0.001versus the control diet).In addition, subjects on the intervention diet decreased body weight by 6.2 lb or 2.8 kg (PϽ0.001) and waist circumference by 0.8 inches or 2 cm (Pϭ0.01)compared with the control group.Similarly, reduced triglyceride levels were reported in the Mediterranean Diet, Cardiovascular Risks and Gene Polymorphisms (Medi-RIVAGE) Study.401 Finally, the PREDIMED (Prevencio ´n con Dieta Mediterra ´nea) Study evaluated the effects of a Mediterranean diet plus virgin olive oil (1 L per week) and a Mediterranean diet plus mixed nuts (30 g/d; walnuts, hazelnuts, and almonds) versus a low-fat diet (control diet) in subjects (nϭ1224) at increased risk for CVD.402 Both Mediterranean-style diets provided higher energy intake from fat than the control diet (41% to 43% versus 38% of calories) and were higher in MUFA content (21% to 22% versus 19.4% of calories).After 1 year, hypertriglyceridemia was less prevalent in both Mediterranean-style diet groups (12.3% and 13.6%) than in those eating the control diet (21.3%).With few exceptions, such as the Lyon Diet Heart Study, 403 which found no significant change in triglyceride levels on a MUFA-enriched versus low-fat, high-n-6 PUFA diet, implementation of a Mediterranean-style diet versus a low-fat diet is more commonly associated with an approximately 10% to 15% lowering of triglycerides and a reduced prevalence of hypertriglyceridemia.
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In the paper
“for each 1% isoenergetic replacement of CHOs, decreases in triglyceride levels resulted with saturated fat (SFA; 1.9 mg/dL), MUFA (1.7 mg/dL), or PUFA (2.3 mg/dL) interchange (all PϽ0.001), which translated into an approximate 1% to 2% decrease in triglyceride levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
What the sources say
- Not checked yetcites [392] 392. Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 con- trolled trials. Am J Clin Nutr. 2003;77:1146 -1155. source
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In the paper
“Consumption of added sugars has increased markedly in the United States from 1977-1978, when it was 10.6% of calories, to the current intake of 15.8% of calories.407,408”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.2. Added Sugars
What the sources say
- Not checked yetcites [407] 407. Glinsmann WH, Irausquin H, Park YK. Evaluation of health aspects of sugars contained in carbohydrate sweeteners: report of Sugars Task Force, 1986. J Nutr. 1986;116(suppl):S1-S216. source
- Not checked yetcites [408] 408. Welsh JA, Sharma A, Abramson JL, Vaccarino V, Gillespie C, Vos MB. Caloric sweetener consumption and dyslipidemia among US adults. JAMA. 2010;303:1490 -1497.
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In the paper
“Similarly, in 9 studies (nϭ119) that compared high CHO and high fiber versus moderate CHO and low fiber, triglyceride levels decreased 13% in the high-fiber group.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.1. Dietary Fiber
What the sources say
- Not checked yetcites [406] 406. Anderson JW, Randles KM, Kendall CW, Jenkins DJ. Carbohydrate and fiber recommendations for individuals with diabetes: a quantitative assessment and meta-analysis of the evidence. J Am Coll Nutr. 2004; 23:5-17.
plaindirectn = 119- Asserted: passes — The authors put it forward as true.
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“Recent data suggest that dietary supplementation with fructose increases ppTG and CMRs compared with glucose.427”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose
What the sources say
- Not checked yetcites [427] 427. Stanhope KL, Havel PJ. Fructose consumption: recent results and their potential implications. Ann N Y Acad Sci. 2010;1190:15-24.
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In the paper
“An exaggerated rise in triglycerides occurs in the setting of excess alcohol intake combined with a meal high in saturated fat.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.5. Alcohol
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In the paper
“Prospective studies have demonstrated an inverse relationship between moderate alcohol consumption (ie, up to 1 oz daily) and CVD.442”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.5. Alcohol
What the sources say
- Not checked yetcites [442] 442. Goldberg IJ, Mosca L, Piano MR, Fisher EA; Nutrition Committee, Council on Epidemiology and Prevention, and Council on Cardio- vascular Nursing of the American Heart Association. AHA Science Advisory: wine and your heart: a science advisory for healthcare pro- fessionals from the Nutrition Committee, Council on Epidemiology and Prevention, and Council on Cardiovascular Nursing of the American Heart Association. Circulation. 2001;103:472-475. source
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In the paper
“Similarly, in the 12 studies that monitored ppTG, a dose-dependent increase was observed above the 50-g fructose dose.428”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose
What the sources say
- Not checked yetcites [428] 428. Livesey G, Taylor R. Fructose consumption and consequences for gly- cation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. Am J Clin Nutr. 2008; 88:1419 -1437.
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In the paper
“but another study finding no appreciable differences in triglyceride levels in 162 subjects with T2DM assigned to a low-or high-GI diet.424”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load
What the sources say
- Not checked yetcites [424] 424. Wolever TM, Gibbs AL, Mehling C, Chiasson JL, Connelly PW, Josse RG, Leiter LA, Maheux P, Rabasa-Lhoret R, Rodger NW, Ryan EA. The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y con- trolled trial of low-glycemic-index dietary carbohydrate in type 2 dia- betes: no effect on glycated hemoglobin but reduction in C-reactive protein. Am J Clin Nutr. 2008;87:114 -125.
plainn = 162- Asserted: passes — The authors put it forward as true.
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In the paper
“The lack of effect was demonstrated irrespective of whether fructose replaced starch, sucrose, or glucose.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose
What the sources say
- Not checked yetcites [428] 428. Livesey G, Taylor R. Fructose consumption and consequences for gly- cation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. Am J Clin Nutr. 2008; 88:1419 -1437.
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In the paper
“The relationship between GI/GL and triglycerides also remains unresolved in patients with T2DM”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load
What the sources say
- Not checked yetcites [406] 406. Anderson JW, Randles KM, Kendall CW, Jenkins DJ. Carbohydrate and fiber recommendations for individuals with diabetes: a quantitative assessment and meta-analysis of the evidence. J Am Coll Nutr. 2004; 23:5-17.
- Not checked yetcites [424] 424. Wolever TM, Gibbs AL, Mehling C, Chiasson JL, Connelly PW, Josse RG, Leiter LA, Maheux P, Rabasa-Lhoret R, Rodger NW, Ryan EA. The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y con- trolled trial of low-glycemic-index dietary carbohydrate in type 2 dia- betes: no effect on glycated hemoglobin but reduction in C-reactive protein. Am J Clin Nutr. 2008;87:114 -125.
plainn = 162- Asserted: passes — The authors put it forward as true.
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In the paper
“Irrespective of macronutrient composition, all diets decreased triglyceride levels similarly (12% to 17%).433”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet
What the sources say
- Not checked yetcites [433] 433. Sacks FM, Bray GA, Carey VJ, Smith SR, Ryan DH, Anton SD, McManus K, Champagne CM, Bishop LM, Laranjo N, Leboff MS, Rood JC, de Jonge L, Greenway FL, Loria CM, Obarzanek E, Wil- liamson DA. Comparison of weight-loss diets with different compo- sitions of fat, protein, and carbohydrates. N Engl J Med. 2009;360: 859 -873.
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In the paper
“with 1 meta-analysis having identified a 6% reduction in triglyceride level in low-versus high-GI diets 406”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load
What the sources say
- Not checked yetcites [406] 406. Anderson JW, Randles KM, Kendall CW, Jenkins DJ. Carbohydrate and fiber recommendations for individuals with diabetes: a quantitative assessment and meta-analysis of the evidence. J Am Coll Nutr. 2004; 23:5-17.
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In the paper
“Rimm et al 449 estimated that ingestion of 1 oz/d would correspond to a 5% to 10% higher triglyceride concentration than found in nondrinkers.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.5. Alcohol
What the sources say
- Not checked yetcites [449] 449. Rimm EB, Williams P, Fosher K, Criqui M, Stampfer MJ. Moderate alcohol intake and lower risk of coronary heart disease: meta-analysis of effects on lipids and haemostatic factors. BMJ. 1999;319:1523-1528.
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In the paper
“Recently, 2 additional transcription factors, X-box binding protein 1 (XBP1) and CHO response element-binding protein (ChREBP), have been identified as inducers of hepatic lipogenesis in response to ingested CHOs (eg, fructose and glucose) that is independent of insulin.431,432”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose
What the sources say
- Not checked yetcites [431] 431. Glimcher LH, Lee AH. From sugar to fat: how the transcription factor XBP1 regulates hepatic lipogenesis. Ann N Y Acad Sci. 2009;1173(suppl 1): E2-E9. source
- Not checked yetcites [432] 432. Uyeda K, Repa JJ. Carbohydrate response element binding protein, ChREBP, a transcription factor coupling hepatic glucose utilization and lipid synthesis. Cell Metab. 2006;4:107-110.
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In the paper
“In an extensive meta-analysis of 60 studies that evaluated the effects of fructose consumption on triglyceride levels, intakes Յ100 g/d had no significant effects on fasting plasma triglycerides.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose
What the sources say
- Not checked yetcites [428] 428. Livesey G, Taylor R. Fructose consumption and consequences for gly- cation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. Am J Clin Nutr. 2008; 88:1419 -1437.
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In the paper
“Another analysis of the Diabetes Prevention Program that evaluated subjects with MetS reported a downward shift in the prevalence of triglyceride levels Ն150 mg/dL from 73% to 60% in the intensive-lifestyle versus placebo group.437”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet
What the sources say
- Not checked yetcites [437] 437. Orchard TJ, Temprosa M, Goldberg R, Haffner S, Ratner R, Marcovina S, Fowler S; Diabetes Prevention Program Research Group. The effect of metformin and intensive lifestyle intervention on the metabolic syn- drome: the Diabetes Prevention Program randomized trial. Ann Intern Med. 2005;142:611-619. source
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In the paper
“Weight loss was similar after 12 months (4.8 to 7.3 kg) for all 4 diets.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet
What the sources say
- Not checked yetcites [440] 440. Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ. Com- parison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial. JAMA. 2005;293:43-53. source
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In the paper
“Thus, diets that produce significant and sustained weight loss offer the most favorable reductions in triglyceride levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet
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In the paper
“At higher intakes, triglyceride levels increase, 447,448”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.5. Alcohol
What the sources say
- Not checked yetcites [447] 447. Chrysohoou C, Panagiotakos DB, Pitsavos C, Skoumas J, Toutouza M, Papaioannou I, Toutouzas PK, Stefanadis C. Effects of chronic alcohol consumption on lipid levels, inflammatory and haemostatic factors in the general population: the "ATTICA" Study. Eur J Cardiovasc Prev Rehabil. 2003;10:355-361.
- Not checked yetcites [448] 448. Foerster M, Marques-Vidal P, Gmel G, Daeppen JB, Cornuz J, Hayoz D, Pe ´coud A, Mooser V, Waeber G, Vollenweider P, Paccaud F, Rodondi N. Alcohol drinking and cardiovascular risk in a population with high mean alcohol consumption. Am J Cardiol. 2009;103:361-368.
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In the paper
“A Cochrane review of 15 RCTs from 1982 to 2003 assessing the relationship between low-GI diets and lipids found no evidence that low-GI diets affected plasma triglycerides 421”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load
What the sources say
- Not checked yetcites [421] 421. Kelly S, Frost G, Whittaker V, Summerbell C. Low glycaemic index diets for coronary heart disease. Cochrane Database Syst Rev. 2004;(4): CD004467.
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In the paper
“In an elderly population, however, there was no association between GI and triglyceride levels.418”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load
What the sources say
- Not checked yetcites [418] 418. van Dam RM, Visscher AW, Feskens EJ, Verhoef P, Kromhout D. Dietary glycemic index in relation to metabolic risk factors and incidence of coronary heart disease: the Zutphen Elderly Study. Eur J Clin Nutr. 2000;54:726 -731.
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In the paper
“however, 2 subsequent studies reported lower triglyceride levels with low-GI diets.422,423”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load
What the sources say
- Not checked yetcites [422] 422. Ebbeling CB, Leidig MM, Sinclair KB, Seger-Shippee LG, Feldman HA, Ludwig DS. Effects of an ad libitum low-glycemic load diet on cardiovascular disease risk factors in obese young adults. Am J Clin Nutr. 2005;81:976 -982. source
- Not checked yetcites [423] 423. Sichieri R, Moura AS, Genelhu V, Hu F, Willett WC. An 18-mo randomized trial of a low-glycemic-index diet and weight change in Brazilian women. Am J Clin Nutr. 2007;86:707-713.
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In the paper
“some studies have shown no association, [443][444][445]”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.5. Alcohol
What the sources say
- Not checked yetcites [443] 443. Marques-Vidal P, Cambou JP, Nicaud V, Luc G, Evans A, Arveiler D, Bingham A, Cambien F. Cardiovascular risk factors and alcohol con- sumption in France and Northern Ireland. Atherosclerosis. 1995;115: 225-232.
- Not checked yetcites [444] 444. Nanchahal K, Ashton WD, Wood DA. Alcohol consumption, metabolic cardiovascular risk factors and hypertension in women. Int J Epidemiol. 2000;29:57-64.
- Not checked yetcites [445] 445. Burger M, Mensink G, Bro ¨nstrup A, Thierfelder W, Pietrzik K. Alcohol consumption and its relation to cardiovascular risk factors in Germany. Eur J Clin Nutr. 2004;58:605-614.
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In the paper
“A meta-analysis of RCTs that evaluated low-CHO versus low-fat (Ͻ30% of energy) diets found greater reductions in triglyceride levels on the low-CHO diet.435”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet
What the sources say
- Not checked yetcites [435] 435. Nordmann AJ, Nordmann A, Briel M, Keller U, Yancy WS Jr, Brehm BJ, Bucher HC. Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors: a meta-analysis of randomized controlled trials [published correction appears in Arch Intern Med. 2006;166:932]. Arch Intern Med. 2006;166:285-293.
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In the paper
“After 2.8 years, the intensively treated group lost weight (mean 5.6 kg) in association with a reduction in triglyceride levels (22 mg/ dL).436”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet
What the sources say
- Not checked yetcites [436] 436. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, Nathan DM; Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346:393-403. source
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In the paper
“Ethanolinduced lipemia may be due to inhibition of LPL-mediated hydrolysis of chylomicrons.126,451,452”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.5. Alcohol
What the sources say
- Not checked yetcites [126] 126. Pownall HJ, Ballantyne CM, Kimball KT, Simpson SL, Yeshurun D, Gotto AM Jr. Effect of moderate alcohol consumption on hypertriglyc- eridemia: a study in the fasting state. Arch Intern Med. 1999;159: 981-987.
- Not checked yetcites [451] 451. Pownall HJ. Dietary ethanol is associated with reduced lipolysis of intestinally derived lipoproteins. J Lipid Res. 1994;35:2105-2113.
- Not checked yetcites [452] 452. Erkelens DW, Brunzell JD. Effect of controlled alcohol feeding on triglycerides in patients with outpatient "alcohol hypertriglyceridemia." J Hum Nutr. 1980;34:370 -375.
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In the paper
“Similar results were reported in the Look AHEAD (Action for Health in Diabetes) Trial, 438 in which weight reduction also translated into appreciable triglyceride lowering.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet
What the sources say
- Not checked yetcites [438] 438. Wadden TA, West DS, Delahanty L, Jakicic J, Rejeski J, Williamson D, Berkowitz RI, Kelley DE, Tomchee C, Hill JO, Kumanyika S; Look AHEAD Research Group. The Look AHEAD study: a description of the lifestyle intervention and the evidence supporting it [published cor- rection appears in Obesity (Silver Spring). 2007;15:1339]. Obesity (Silver Spring). 2006;14:737-752. source
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In the paper
“In contrast, intakes of fructose that exceeded 100 g/d revealed a dose-related increase in plasma triglycerides.428”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose
What the sources say
- Not checked yetcites [428] 428. Livesey G, Taylor R. Fructose consumption and consequences for gly- cation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. Am J Clin Nutr. 2008; 88:1419 -1437.
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In the paper
“Mechanistically, decreased VLDL triglyceride secretion results from preferential shunting of omega-3 PUFA into phospholipid cellular synthesis, reduced expression of SREBP-1, and enhanced peroxisomal -oxidation.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.6. Marine-Derived Omega-3 PUFA
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In the paper
“A dose-response relationship exists between marine-derived omega-3 PUFA and triglyceride lowering, with an approximate 5% to 10% reduction in triglycerides for every 1 g of EPA/DHA consumed 455”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.6. Marine-Derived Omega-3 PUFA
What the sources say
- Not checked yetcites [455] source
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In the paper
“Overall, optimization of nutrition-related practices can result in a marked triglyceride-lowering effect that ranges between 20% and 50%.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.8. Dietary Summary
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In the paper
“This recommendation is based on a large body of evidence showing triglyceride-lowering effects of marine-derived omega-3 PUFA.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.6. Marine-Derived Omega-3 PUFA
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In the paper
“However, CVD event reductions were similar across categories of baseline triglycerides in the Long-Term Intervention with Pravastatin in Ischemic Disease (LIPID), 488 the Heart Protection Study, 489 and WOSCOPS, 490”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
What the sources say
- Not checked yetcites [488] 488. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med. 1998;339:1349 -1357. source
- Not checked yetcites [489] 489. Heart Protection Study Collaborative Group. MRC/BHF Heart Pro- tection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002;360:7-22. source
- Not checked yetcites [490] 490. Shepherd J, Cobbe SM, Ford I, Isles CG, Lorimer AR, MacFarlane PW, McKillop JH, Packard CJ; West of Scotland Coronary Prevention Study Group. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med. 1995;333:1301-1307. source
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In the paper
“However, a reduction in energy intake (300 kcal/d) resulted in a 23% reduction in fasting triglyceride levels during the 1-year trial.478”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 14. Physical Activity and Hypertriglyceridemia
What the sources say
- Not checked yetcites [478] 478. Fontana L, Villareal DT, Weiss EP, Racette SB, Steger-May K, Klein S, Holloszy JO; and the Washington University School of Medicine CALERIE Group. Calorie restriction or exercise: effects on coronary heart disease risk factors: a randomized, controlled trial. Am J Physiol Endocrinol Metab. 2007;293:E197-E202.
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In the paper
“Dietary marine-derived omega-3 PUFA intake is very low, at Ͻ0.2 g of the Ϸ1.4 g of total omega-3 PUFA consumed daily in the United States.464,465”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.7. Nonmarine Omega-3 PUFA
What the sources say
- Not checked yetcites [464] 464. Kris-Etherton PM, Harris WS, Appel LJ; Nutrition Committee. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease [published correction appears in Arterioscler Thromb Vasc Biol. 2003; 23:151-152]. Arterioscler Thromb Vasc Biol. 2003;23:e20 -e30. source
- Not checked yetcites [465] 465. Adkins Y, Kelley DS. Mechanisms underlying the cardioprotective effects of omega-3 polyunsaturated fatty acids. J Nutr Biochem. 2010; 21:781-792.
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In the paper
“this may reflect very low conversion rates of ␣-linolenic acid and its intermediary, stearidonic acid, 468 to the active triglyceride-lowering omega-3 compounds EPA and DHA.469”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.7. Nonmarine Omega-3 PUFA
What the sources say
- Not checked yetcites [468] 468. Whelan J. Dietary stearidonic acid is a long chain (n-3) polyunsaturated fatty acid with potential health benefits. J Nutr. 2009;139:5-10.
- Not checked yetcites [469] 469. Brenna JT, Salem N Jr, Sinclair AJ, Cunnane SC. alpha-Linolenic acid supplementation and conversion to n-3 long-chain polyunsaturated fatty acids in humans. Prostaglandins Leukot Essent Fatty Acids. 2009;80: 85-91.
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In the paper
“In fact, 60 minutes of aerobic exercise daily abolishes the CHO-induced increases in TRL.480”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 14. Physical Activity and Hypertriglyceridemia
What the sources say
- Not checked yetcites [480] 480. Koutsari C, Karpe F, Humphreys SM, Frayn KN, Hardman AE. Exercise prevents the accumulation of triglyceride-rich lipoproteins and their remnants seen when changing to a high-carbohydrate diet. Arterioscler Thromb Vasc Biol. 2001;21:1520 -1525. 480a.Jones PH. Fibrates. In: Ballantyne C, ed. Clinical Lipidology, A Com- panion to Braunwald's Heart Disease. Philadelphia, PA: Saunders; 2009: 315-325. 117. 480b.Harris WS, Jacobson TA. Omega-3 Fatty Acids. In: Ballantyne C, ed. Clinical Lipidology, A Companion to Braunwald's Heart Disease. Phil- adelphia, PA: Saunders; 2009:326 -338. 118. 480c.M
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In the paper
“As monotherapy, fibrates offer the most triglyceride reduction, followed by immediate-release niacin, omega-3 methyl esters, extended-release niacin, statins, and ezetimibe.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
What the sources say
- Not checked yetcites 504,480a-480d
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In the paper
“efficacy is greater in individuals with higher triglyceride levels before treatment.[455][456][457]”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.6. Marine-Derived Omega-3 PUFA
What the sources say
- Not checked yetcites [455] source
- Not checked yetcites [456] 456. Lungershausen YK, Abbey M, Nestel PJ, Howe PR. Reduction of blood pressure and plasma triglycerides by omega-3 fatty acids in treated hypertensives. J Hypertens. 1994;12:1041-1045.
- Not checked yetcites [457] 457. Jacobson TA. Role of n-3 fatty acids in the treatment of hypertriglyc- eridemia and cardiovascular disease. Am J Clin Nutr. 2008;87: 1981S-1990S.
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In the paper
“In addition, upregulation of LPL facilitates VLDL triglyceride clearance.459,460”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.6. Marine-Derived Omega-3 PUFA
What the sources say
- Not checked yetcites [459] 459. Harris WS, Miller M, Tighe AP, Davidson MH, Schaefer EJ. Omega-3 fatty acids and coronary heart disease risk: clinical and mechanistic perspectives. Atherosclerosis. 2008;197:12-24. source
- Not checked yetcites [460] 460. Sampath H, Ntambi JM. Polyunsaturated fatty acid regulation of gene expression. Nutr Rev. 2004;62:333-339. source
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In the paper
“In the Veterans Affairs HDL Intervention Trial (VA-HIT), 496,497 fibrate therapy reduced cardiovascular risk across all categories of baseline triglycerides.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
What the sources say
- Not checked yetcites [496] 496. Rubins HB, Robins SJ, Collins D, Fye CL, Anderson JW, Elam MB, Faas FH, Linares E, Schaefer EJ, Schectman G, Wilt TJ, Wittes J; Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial Study Group. Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipo- protein cholesterol. N Engl J Med. 1999;341:410 -418.
- Not checked yetcites [497] 497. Robins SJ, Collins D, Wittes JT, Papademetriou V, Deedwania PC, Schaefer EJ, McNamara JR, Kashyap ML, Hershman JM, Wexler LF, Rubins HB; for the VA-HIT Study Group. Relation of gemfibrozil treatment and lipid levels with major coronary events: VA-HIT: a randomized controlled trial. JAMA. 2001;285:1585-1591. source
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In the paper
“Skulas-Ray et al 458 reviewed studies that evaluated baseline triglyceride levels and the response to EPA plus DHA dose and found that the response was curvilinear, with individuals at lower baseline triglyceride levels having less of a triglyceride-lowering effect (Ϸ20% versus 30% for higher triglyceride levels).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.6. Marine-Derived Omega-3 PUFA
What the sources say
- Not checked yetcites [458] 458. Skulas-Ray AC, West SG, Davidson MH, Kris-Etherton PM. Omega-3 fatty acid concentrates in the treatment of moderate hypertriglyceride- mia. Expert Opin Pharmacother. 2008;9:1237-1248.
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In the paper
“However, other studies evaluating walking duration, frequency, and intensity (30 minutes daily at a maximum 65% to 75% of age-predicted heart rate) in the absence of weight loss did not demonstrate differences in postexercise triglyceride levels.477”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 14. Physical Activity and Hypertriglyceridemia
What the sources say
- Not checked yetcites [477] 477. Duncan GE, Anton SD, Sydeman SJ, Newton RL Jr, Corsica JA, Durning PE, Ketterson TU, Martin AD, Limacher MC, Perri MG. Prescribing exercise at varied levels of intensity and frequency: a ran- domized trial. Arch Intern Med. 2005;165:2362-2369. source
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In the paper
“In contrast, bile acid resins may raise triglyceride levels ( Table 5).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
What the sources say
- Not checked yetcites Table 5
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In the paper
“The effect of physical activity on triglyceride levels varies depending on baseline triglyceride, level of intensity, caloric expenditure, and duration of activity.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 14. Physical Activity and Hypertriglyceridemia
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In the paper
“and CVD event reduction was greater in patients without MetS in the Anglo-Scandinavian Cardiac Outcome Trial.491”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
What the sources say
- Not checked yetcites [491] 491. Sever PS, Dahlo ¨f B, Poulter NR, Wedel H, Beevers G, Caulfield M, Collins R, Kjeldsen SE, Kristinsson A, McInnes GT, Mehlsen J, Nieminen M, O'Brien E, Ostergren J; ASCOT Investigators. Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet. 2003; 361:1149 -1158. source
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In the paper
“Higher baseline triglyceride levels (mean 197 mg/dL) also translated into significant triglyceride reductions (26%) in a 6-month trial of overweight subjects who walked 12 miles weekly at 40% to 55% of peak oxygen consumption.476”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 14. Physical Activity and Hypertriglyceridemia
What the sources say
- Not checked yetcites [476] 476. Kraus WE, Houmard JA, Duscha BD, Knetzger KJ, Wharton MB, McCartney JS, Bales CW, Henes S, Samsa GP, Otvos JD, Kulkarni KR, Slentz CA. Effects of the amount and intensity of exercise on plasma lipoproteins. N Engl J Med. 2002;347:1483-1492.
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In the paper
“Yet non-marine-based PUFAs have not demonstrated consistent reductions in triglycerides 467”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.7. Nonmarine Omega-3 PUFA
What the sources say
- Not checked yetcites [467] 467. Prasad K. Flaxseed and cardiovascular health. J Cardiovasc Pharmacol. 2009;54:369 -377.
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Thus, in patients with hypertriglyceridemia, statin therapy may be beneficial in the setting of an LDL-C level that merits treatment.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: Reducing elevated triglyceride levels reduces cardiovascular risk.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Similarly, increasing energy expenditure through physical activity without changing energy intake did not result in lower triglyceride levels if baseline levels were relatively normal (ie, mean 110 mg/dL).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 14. Physical Activity and Hypertriglyceridemia
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, the aggregate data suggest that statin or fibrate monotherapy may be beneficial in patients with high triglyceride levels, low HDL-C, or both.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: Reducing elevated triglyceride levels reduces cardiovascular risk.
In the paper
“In contrast, aerobic activity enhances lipid oxidation, thereby facilitating the hydrolysis and utilization of triglycerides in skeletal muscle.473”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 14. Physical Activity and Hypertriglyceridemia
What the sources say
- Not checked yetcites [473] 473. Martin WH 3rd. Effects of acute and chronic exercise on fat metabolism. Exerc Sport Sci Rev. 1996;24:203-231.
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In the paper
“and to have greater CVD risk reduction with lipid therapy in 4S 482,483 and CARE.487”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
What the sources say
- Not checked yetcites [482] 482. Girman CJ, Rhodes T, Mercuri M, Pyo ¨ra ¨la ¨K, Kjekshus J, Pedersen TR, Beere PA, Gotto AM, Clearfield M; 4S Group and the AFCAPS/ TexCAPS Research Group. The metabolic syndrome and risk of major coronary events in the Scandinavian Simvastatin Survival Study (4S) and the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS). Am J Cardiol. 2004;93:136 -141.
- Not checked yetcites [483] 483. Pyo ¨ra ¨la ¨K, Pedersen TR, Kjekshus J, Faergeman O, Olsson AG, Thor- geirsson G. Cholesterol lowering with simvastatin improves prognosis of diabetic patients with coronary heart disease: a subgroup analysis of the Scandinavian Simvastatin Survival Study (4S) [published correction appears in Diabetes Care. 1997;20:1048]. Diabetes Care. 1997;20: 614 -620.
- Not checked yetcites [487] 487. Pfeffer MA, Sacks FM, Moye ´LA, East C, Goldman S, Nash DT, Rouleau JR, Rouleau JL, Sussex BA, Theroux P, Vanden Belt RJ, Braunwald E. Influence of baseline lipids on effectiveness of pravastatin in the CARE Trial: Cholesterol And Recurrent Events. J Am Coll Cardiol. 1999;33:125-130.
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In the paper
“For example, an optimal fasting triglyceride level (eg, Ͻ100 mg/dL) was associated with minimal (ie, Ͻ5%) reductions in postexercise triglyceride levels compared with greater (ie, 15% to 20%) reductions if baseline triglyceride levels exceeded 150 mg/dL.474”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 14. Physical Activity and Hypertriglyceridemia
What the sources say
- Not checked yetcites [474] 474. Couillard C, Despre ´s JP, Lamarche B, Bergeron J, Gagnon J, Leon AS, Rao DC, Skinner JS, Wilmore JH, Bouchard C. Effects of endurance exercise training on plasma HDL cholesterol levels depend on levels of triglycerides: evidence from men of the Health, Risk Factors, Exercise Training and Genetics (HERITAGE) Family Study. Arterioscler Thromb Vasc Biol. 2001;21:1226 -1232.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Unfortunately, there are limited data on the potential benefit of adding a second drug in high-risk patients treated with a statin who continue to have high triglyceride levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3. Do patients with elevated triglyceride levels while undergoing statin therapy receive additional cardiovascular risk reduction by the addition of a second drug that targets triglycerides or TRL? In the Japan EPA Lipid Intervention Study (JELIS), in which patients received a statin plus either EPA or a placebo, CVD risk reduction with combination therapy was not statistically significant in either baseline triglyceride subgroup (Ͻ151 or Ն151 mg/dL).502 However, subgroup analysis of primary prevention patients in JELIS (80% of the study population) indicated that patients with baseline triglyceride levels at or exceeding 150 mg/dL and HDL-C Ͻ40 mg/dL had significantly increased CVD risk.Moreover, combination therapy with statin plus EPA in this high-risk subgroup reduced CVD risk by 53% compared with statin monotherapy, 503 even though the dose of EPA (up to 1.8 g/d) translated into minimal triglyceride reduction (5% between groups).Consequently, the cardiovascular benefit in JELIS was not a primary triglyceride-mediated effect.Trials that used statin plus niacin (or in some cases bile acid resin) combination therapy have shown a reduction in coronary arteriographic progression and regression, as well as regression of carotid artery intima-media thickness.504,505 Reduction in CVD outcomes were observed in several of these studies, although event rates were low, a statin placebo group was not used, and the studies were neither powered nor prespecified to address CVD events as a primary outcome measure.Nevertheless, they set the stage for the statin-niacin outcome trials listed below. Unfortunately, there are limited data on the potential benefit of adding a second drug in high-risk patients treated with a statin who continue to have high triglyceride levels.As noted above, the ACCORD trial 498 did not find that fibrate therapy added to statin reduced cardiovascular events in DM patients (median triglyceride level of 162 mg/dL) except in the subgroup in the upper triglyceride tertile and lowest HDL-C tertile (Pϭ0.06).Although ongoing clinical trials are not specifically designed to examine this issue, secondary analyses of the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes (AIM-HIGH), 506
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“In the Japan EPA Lipid Intervention Study (JELIS), in which patients received a statin plus either EPA or a placebo, CVD risk reduction with combination therapy was not statistically significant in either baseline triglyceride subgroup (Ͻ151 or Ն151 mg/dL).502”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3. Do patients with elevated triglyceride levels while undergoing statin therapy receive additional cardiovascular risk reduction by the addition of a second drug that targets triglycerides or TRL? In the Japan EPA Lipid Intervention Study (JELIS), in which patients received a statin plus either EPA or a placebo, CVD risk reduction with combination therapy was not statistically significant in either baseline triglyceride subgroup (Ͻ151 or Ն151 mg/dL).502 However, subgroup analysis of primary prevention patients in JELIS (80% of the study population) indicated that patients with baseline triglyceride levels at or exceeding 150 mg/dL and HDL-C Ͻ40 mg/dL had significantly increased CVD risk.Moreover, combination therapy with statin plus EPA in this high-risk subgroup reduced CVD risk by 53% compared with statin monotherapy, 503 even though the dose of EPA (up to 1.8 g/d) translated into minimal triglyceride reduction (5% between groups).Consequently, the cardiovascular benefit in JELIS was not a primary triglyceride-mediated effect.Trials that used statin plus niacin (or in some cases bile acid resin) combination therapy have shown a reduction in coronary arteriographic progression and regression, as well as regression of carotid artery intima-media thickness.504,505 Reduction in CVD outcomes were observed in several of these studies, although event rates were low, a statin placebo group was not used, and the studies were neither powered nor prespecified to address CVD events as a primary outcome measure.Nevertheless, they set the stage for the statin-niacin outcome trials listed below. Unfortunately, there are limited data on the potential benefit of adding a second drug in high-risk patients treated with a statin who continue to have high triglyceride levels.As noted above, the ACCORD trial 498 did not find that fibrate therapy added to statin reduced cardiovascular events in DM patients (median triglyceride level of 162 mg/dL) except in the subgroup in the upper triglyceride tertile and lowest HDL-C tertile (Pϭ0.06).Although ongoing clinical trials are not specifically designed to examine this issue, secondary analyses of the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes (AIM-HIGH), 506
What the sources say
- Not checked yetcites [502] 502. Yokoyama M, Origasa H, Matsuzaki M, Matsuzawa Y, Saito Y, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Itakura H, Kita T, Kita- batake A, Nakaya N, Sakata T, Shimada K, Shirato K; Japan EPA Lipid Intervention Study (JELIS) Investigators. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis [published correction appears in Lancet. 2007;370:220]. Lancet. 2007;369: 1090 -1098.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Consequently, the cardiovascular benefit in JELIS was not a primary triglyceride-mediated effect.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3. Do patients with elevated triglyceride levels while undergoing statin therapy receive additional cardiovascular risk reduction by the addition of a second drug that targets triglycerides or TRL? In the Japan EPA Lipid Intervention Study (JELIS), in which patients received a statin plus either EPA or a placebo, CVD risk reduction with combination therapy was not statistically significant in either baseline triglyceride subgroup (Ͻ151 or Ն151 mg/dL).502 However, subgroup analysis of primary prevention patients in JELIS (80% of the study population) indicated that patients with baseline triglyceride levels at or exceeding 150 mg/dL and HDL-C Ͻ40 mg/dL had significantly increased CVD risk.Moreover, combination therapy with statin plus EPA in this high-risk subgroup reduced CVD risk by 53% compared with statin monotherapy, 503 even though the dose of EPA (up to 1.8 g/d) translated into minimal triglyceride reduction (5% between groups).Consequently, the cardiovascular benefit in JELIS was not a primary triglyceride-mediated effect.Trials that used statin plus niacin (or in some cases bile acid resin) combination therapy have shown a reduction in coronary arteriographic progression and regression, as well as regression of carotid artery intima-media thickness.504,505 Reduction in CVD outcomes were observed in several of these studies, although event rates were low, a statin placebo group was not used, and the studies were neither powered nor prespecified to address CVD events as a primary outcome measure.Nevertheless, they set the stage for the statin-niacin outcome trials listed below. Unfortunately, there are limited data on the potential benefit of adding a second drug in high-risk patients treated with a statin who continue to have high triglyceride levels.As noted above, the ACCORD trial 498 did not find that fibrate therapy added to statin reduced cardiovascular events in DM patients (median triglyceride level of 162 mg/dL) except in the subgroup in the upper triglyceride tertile and lowest HDL-C tertile (Pϭ0.06).Although ongoing clinical trials are not specifically designed to examine this issue, secondary analyses of the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes (AIM-HIGH), 506
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, subgroup analysis of primary prevention patients in JELIS (80% of the study population) indicated that patients with baseline triglyceride levels at or exceeding 150 mg/dL and HDL-C Ͻ40 mg/dL had significantly increased CVD risk.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3. Do patients with elevated triglyceride levels while undergoing statin therapy receive additional cardiovascular risk reduction by the addition of a second drug that targets triglycerides or TRL? In the Japan EPA Lipid Intervention Study (JELIS), in which patients received a statin plus either EPA or a placebo, CVD risk reduction with combination therapy was not statistically significant in either baseline triglyceride subgroup (Ͻ151 or Ն151 mg/dL).502 However, subgroup analysis of primary prevention patients in JELIS (80% of the study population) indicated that patients with baseline triglyceride levels at or exceeding 150 mg/dL and HDL-C Ͻ40 mg/dL had significantly increased CVD risk.Moreover, combination therapy with statin plus EPA in this high-risk subgroup reduced CVD risk by 53% compared with statin monotherapy, 503 even though the dose of EPA (up to 1.8 g/d) translated into minimal triglyceride reduction (5% between groups).Consequently, the cardiovascular benefit in JELIS was not a primary triglyceride-mediated effect.Trials that used statin plus niacin (or in some cases bile acid resin) combination therapy have shown a reduction in coronary arteriographic progression and regression, as well as regression of carotid artery intima-media thickness.504,505 Reduction in CVD outcomes were observed in several of these studies, although event rates were low, a statin placebo group was not used, and the studies were neither powered nor prespecified to address CVD events as a primary outcome measure.Nevertheless, they set the stage for the statin-niacin outcome trials listed below. Unfortunately, there are limited data on the potential benefit of adding a second drug in high-risk patients treated with a statin who continue to have high triglyceride levels.As noted above, the ACCORD trial 498 did not find that fibrate therapy added to statin reduced cardiovascular events in DM patients (median triglyceride level of 162 mg/dL) except in the subgroup in the upper triglyceride tertile and lowest HDL-C tertile (Pϭ0.06).Although ongoing clinical trials are not specifically designed to examine this issue, secondary analyses of the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes (AIM-HIGH), 506
What the sources say
- Not checked yetcites [502] 502. Yokoyama M, Origasa H, Matsuzaki M, Matsuzawa Y, Saito Y, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Itakura H, Kita T, Kita- batake A, Nakaya N, Sakata T, Shimada K, Shirato K; Japan EPA Lipid Intervention Study (JELIS) Investigators. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis [published correction appears in Lancet. 2007;370:220]. Lancet. 2007;369: 1090 -1098.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, reductions of 50% or more in triglyceride levels may be attained through intensive therapeutic lifestyle change.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 17. Statement Summary and Recommendations This scientific statement reviews the pivotal role of triglycerides in lipid metabolism and reaffirms that triglyceride is not directly atherogenic but represents an important biomarker of CVD risk because of its association with atherogenic remnant particles and apo CIII.Although some familial disorders of triglyceride metabolism are associated with increased risk for pancreatitis when fasting triglyceride level exceeds 1000 mg/dL, others are associated with increased atherosclerotic risk.Moreover, IR, obesity, and sedentary lifestyle can all lead to or aggravate metabolic syndrome risk factors, which should urgently prompt clinicians to focus first on improving the patient's lifestyle.Knowledge of the metabolic pathways of triglyceride-rich particles and the consequences of hypertriglyceridemia is crucial in understanding the characteristic lipid alterations in DM, lipodystrophic disorders including those seen with HIV, and chronic renal disease.Measurements of non-HDL-C, apo B, or both may be especially useful in those with prominent triglyceride/ HDL abnormalities in which LDL-C measurements may underestimate true atherosclerotic vascular risk.This statement suggests the following new designations: (1) Optimal fasting triglyceride levels, defined as Ͻ100 mg/dL, as a parameter of metabolic health, and (2) nonfasting triglyceride levels, to screen for those with high fasting triglyceride levels.A suggested practical algorithm for screening and management of elevated triglyceride levels is outlined in Figure 5.A nonfasting level of Ͻ200 mg/dL is commensurate with a normal (Ͻ150 mg/dL) or optimal (Ͻ100 mg/dL) fasting triglyceride level and requires no further testing.Fasting samples are used to designate borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), and very high (Ն500 mg/dL) triglyceride levels.Nonfasting triglyceride levels are not used in the definition of MetS and should not be used in the calculation of LDL-C by the Friedewald formula. Overall, the treatment of elevated triglyceride levels focuses on intensive therapeutic lifestyle change.For example, a 5% to 10% reduction in body weight anticipates a triglyceride-lowering response of 20%.Further offsets in CHO calories by reducing added sugars and fructose while increasing unsaturated fat intake may contribute an additional 10% to 20% reduction in triglyceride levels.Elimination of trans fats, restriction of SFA, 524 -527 and increasing consumption of marine-based omega-3 products, coupled with aerobic activity, will further optimize triglyceride-lowering efforts.Taken together, reductions of 50% or more in triglyceride levels may be attained through intensive therapeutic lifestyle change. In subjects with very high triglyceride levels or a history of triglyceride-induced pancreatitis, additional dietary considerations include complete abstinence from alcohol, the nutrition practices listed above, the possible use of MCTs 528 and pharmacological therapies (see also Tables 11 and 12).The subject of medication and triglycerides is still lacking crucial clinical trial evidence.Nonetheless, several points should be made.First, clinicians should rule out medications as a potential cause of an elevated triglyceride value.For example, hormone therapy (Table 5) can greatly influence triglyceride levels; in women of reproductive age who develop hypertriglyceridemia while taking oral contraceptive therapy, lower estrogen-containing preparations or other forms of contraception should be considered.For postmenopausal women with hypertriglyceridemia who require postmenopausal hormone preparations, switching to transdermal preparations may blunt the triglyceride increases observed with oral compounds.Second, utilizing triglyceride-lowering medications to prevent pancreatitis in those with triglyceride levels Ͼ500 mg/dL is reasonable in addition to intensive therapeutic lifestyle change.In those with a history of triglyceride-induced pancreatitis, it is especially important to keep triglyceride levels well controlled, and this will require both lifestyle and pharmacological approaches.What remains to be established is whether these modalities favorably influence CVD outcomes beyond proven therapies (eg, statins).Therefore, additional clinical outcome trials are necessary. None Abbott*; Merck/ Schering-Plough*; Sanofi*; Sanofi-Aventis* None None Abbott*; Genzyme-ISIS*; Merck*; Roche*; Sanofi-Aventis* None William James Howard Washington Hospital Center AstraZeneca*; Pfizer* None Abbott*; Merck †; Pfizer*; Sankyo*; Schering-Plough † None None None None Marc S. Jacobson Private practice Merck (formerly Schering-Plough) † None None None None None None Terry A. Lennie University of Kentucky None None None None None None None Moshe Levi University of Colorado Abbott*; Genzyme*; Intercept Pharmaceuticals* None None None None None None
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: A 5% to 10% reduction in body weight anticipates a triglyceride-lowering response of 20%.
- Rests on an assumption: Reducing added sugars and fructose while increasing unsaturated fat intake may contribute an additional 10% to 20% reduction in triglyceride levels.
None of the sources cited for this claim have been checked yet.
In the paper
“The rise in triglyceride levels coinciding with the current epidemic of juvenile obesity, IR, and DM 509 -511 has created new opportunities for establishing and disseminating CVD health promotion efforts aimed at maximizing primordial prevention.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > High Triglyceride Levels The rise in triglyceride levels coinciding with the current epidemic of juvenile obesity, IR, and DM 509 -511 has created new opportunities for establishing and disseminating CVD health promotion efforts aimed at maximizing primordial prevention.For example, resolutions have now been adopted in all 50 states targeting obesity, including the elimination of high caloric sugared sodas and trans fatty acid products from public school vending machines and increasing the number of walking and bicycle paths.512,513 Initiatives such as reducing access to low-nutrient, energy-dense foods in school cafeterias serve as other adjunctive measures for controlling high triglyceride and obesity rates.514 Among the most comprehensive national programs has been Healthy People 2010, the initiative established by the Centers for Disease Control and Prevention in 1998 for health promotion and disease prevention.515 The principal objectives are to improve the quality of healthy living and eliminate health disparities through interventions aimed at heart disease and stroke prevention.515,516 In addition to community-based outreach programs, nutrition education beginning in elementary school may yield considerable dividends toward reducing obesity rates, because dietary behaviors are often established in childhood.517 Prototypical pilot studies demonstrate a greater understanding of healthy food choices, which in turn may also improve academic performance.518,519 Strategies to attenuate hypertriglyceridemia and its associated metabolic complications include increasing physical activity during school and afterschool sessions, 520,521 incentivizing schools committed to fostering nutrition education, 522 and offering a variety of fresh fruits and vegetables daily to school cafeterias.523 Overall, identification of the most successful pilot programs for implementation on a national level will require coordinated efforts by clinicians, policymakers, and advocacy groups focused on reducing hypertriglyceridemia, obesity, and IR through a greater emphasis on and implementation of intensive lifestyle interventions.
What the sources say
- Not checked yetcites [509] 509. Ogden CL, Flegal KM, Carroll MD, Johnson CL. Prevalence and trends in overweight among US children and adolescents, 1999 -2000. JAMA. 2002;288:1728 -1732.
- Not checked yetcites [510] 510. Flegal KM, Carroll MD, Kuczmarski RJ, Johnson CL. Overweight and obesity in the United States: prevalence and trends, 1960 -1994. Int J Obes Relat Metab Disord. 1998;22:39 -47.
- Not checked yetcites [511] 511. Dietz WH. Health consequences of obesity in youth: childhood pre- dictors of adult disease. Pediatrics. 1998;101:518 -525.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“For example, hormone therapy (Table 5) can greatly influence triglyceride levels”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 17. Statement Summary and Recommendations This scientific statement reviews the pivotal role of triglycerides in lipid metabolism and reaffirms that triglyceride is not directly atherogenic but represents an important biomarker of CVD risk because of its association with atherogenic remnant particles and apo CIII.Although some familial disorders of triglyceride metabolism are associated with increased risk for pancreatitis when fasting triglyceride level exceeds 1000 mg/dL, others are associated with increased atherosclerotic risk.Moreover, IR, obesity, and sedentary lifestyle can all lead to or aggravate metabolic syndrome risk factors, which should urgently prompt clinicians to focus first on improving the patient's lifestyle.Knowledge of the metabolic pathways of triglyceride-rich particles and the consequences of hypertriglyceridemia is crucial in understanding the characteristic lipid alterations in DM, lipodystrophic disorders including those seen with HIV, and chronic renal disease.Measurements of non-HDL-C, apo B, or both may be especially useful in those with prominent triglyceride/ HDL abnormalities in which LDL-C measurements may underestimate true atherosclerotic vascular risk.This statement suggests the following new designations: (1) Optimal fasting triglyceride levels, defined as Ͻ100 mg/dL, as a parameter of metabolic health, and (2) nonfasting triglyceride levels, to screen for those with high fasting triglyceride levels.A suggested practical algorithm for screening and management of elevated triglyceride levels is outlined in Figure 5.A nonfasting level of Ͻ200 mg/dL is commensurate with a normal (Ͻ150 mg/dL) or optimal (Ͻ100 mg/dL) fasting triglyceride level and requires no further testing.Fasting samples are used to designate borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), and very high (Ն500 mg/dL) triglyceride levels.Nonfasting triglyceride levels are not used in the definition of MetS and should not be used in the calculation of LDL-C by the Friedewald formula. Overall, the treatment of elevated triglyceride levels focuses on intensive therapeutic lifestyle change.For example, a 5% to 10% reduction in body weight anticipates a triglyceride-lowering response of 20%.Further offsets in CHO calories by reducing added sugars and fructose while increasing unsaturated fat intake may contribute an additional 10% to 20% reduction in triglyceride levels.Elimination of trans fats, restriction of SFA, 524 -527 and increasing consumption of marine-based omega-3 products, coupled with aerobic activity, will further optimize triglyceride-lowering efforts.Taken together, reductions of 50% or more in triglyceride levels may be attained through intensive therapeutic lifestyle change. In subjects with very high triglyceride levels or a history of triglyceride-induced pancreatitis, additional dietary considerations include complete abstinence from alcohol, the nutrition practices listed above, the possible use of MCTs 528 and pharmacological therapies (see also Tables 11 and 12).The subject of medication and triglycerides is still lacking crucial clinical trial evidence.Nonetheless, several points should be made.First, clinicians should rule out medications as a potential cause of an elevated triglyceride value.For example, hormone therapy (Table 5) can greatly influence triglyceride levels; in women of reproductive age who develop hypertriglyceridemia while taking oral contraceptive therapy, lower estrogen-containing preparations or other forms of contraception should be considered.For postmenopausal women with hypertriglyceridemia who require postmenopausal hormone preparations, switching to transdermal preparations may blunt the triglyceride increases observed with oral compounds.Second, utilizing triglyceride-lowering medications to prevent pancreatitis in those with triglyceride levels Ͼ500 mg/dL is reasonable in addition to intensive therapeutic lifestyle change.In those with a history of triglyceride-induced pancreatitis, it is especially important to keep triglyceride levels well controlled, and this will require both lifestyle and pharmacological approaches.What remains to be established is whether these modalities favorably influence CVD outcomes beyond proven therapies (eg, statins).Therefore, additional clinical outcome trials are necessary. None Abbott*; Merck/ Schering-Plough*; Sanofi*; Sanofi-Aventis* None None Abbott*; Genzyme-ISIS*; Merck*; Roche*; Sanofi-Aventis* None William James Howard Washington Hospital Center AstraZeneca*; Pfizer* None Abbott*; Merck †; Pfizer*; Sankyo*; Schering-Plough † None None None None Marc S. Jacobson Private practice Merck (formerly Schering-Plough) † None None None None None None Terry A. Lennie University of Kentucky None None None None None None None Moshe Levi University of Colorado Abbott*; Genzyme*; Intercept Pharmaceuticals* None None None None None None
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 163
- Probably not a substantial claim. 34
In the paper
“High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites NHANES 1999-2008
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.
In the paper
“Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%),”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites NHANES 1999-2008
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.
None of the sources cited for this claim have been checked yet.
In the paper
“Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites NHANES 1988-1994
- Not checked yetcites NHANES 1999-2008
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.
None of the sources cited for this claim have been checked yet.
In the paper
“However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites NHANES 1999-2008
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.
In the paper
“Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 2. Scope of the Problem: Prevalence of Hypertriglyceridemia in the United States In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.Accordingly, increases in fasting serum triglyceride levels observed between surveys conducted in 1976 -1980 and 1999 -2002 6 coincided with adjustments in the classification of hypertriglyceridemia 4,10 (Table 1).Current designations are as follows: 150 to 199 mg/dL, borderline high; 200 to 499 mg/dL, high; and Ն500 mg/dL, very high.The prevalence of hypertriglyceridemia by ethnicity in NHANES 1988 -1994 and 1999 -2008 according to these cut points is shown in Figure 1.Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.Among ethnicities, Mexican Americans have the highest rates (34.9%),followed by non-Hispanic whites (33%) and blacks (15.6%) in NHANES 1999 -2008 (Table 2).High (Ն200 mg/dL) and very high (Ն500 mg/dL) fasting triglyceride levels were observed in 16.2% and 1.1% of adults, respectively, with Mexican Americans being overrepresented at both cut points (19.5% and 1.4%, respectively).Figure 2 illustrates the sex-and age-related prevalence of triglyceride levels Ն150 mg/dL in NHANES 1999 -2008.Within each group, the highest prevalence rates were observed in Mexican American men (50 to 59 years old, 58.8%) and Mexican American women (Ն70 years old, 50.5%), followed by non-Hispanic white men and women (60 to 69 years old, 43.6% and 42.2%, respectively) and non-Hispanic black men (40 to 49 years old, 30.4%) and women (60 to 69 years old, 25.3%).The prevalence of triglyceride levels Ն200 mg/dL was also highest in Mexican American men (Ն30 years old) and women (Ն40 years old; 21% to 36%), followed by non-Hispanic white men (30 to 69 years old, 20% to 25%).Although the prevalence of triglyceride levels Ն500 mg/dL was relatively low (1% to 2%), Mexican American men 50 to 59 years of age exhibited the highest rate (9%) in NHANES 1999 -2008. Serum triglyceride levels by selected percentiles and geometric means are shown in Table 3.Because triglyceride levels are not normally distributed in the population (Section 3.1), the geometric mean, as derived by log transformation, is favored over the arithmetic mean to reduce the potential impact of outliers that might otherwise overestimate triglyceride levels.11 Over the past 20 years, there were small increases in median triglyceride levels in both men (122 versus 119 mg/dL) and women (106 versus 101 mg/dL).However, the increases in triglycerides primarily were observed in younger age groups (20 to 49 years old), and overall, triglyceride levels continue to be higher than in less industrialized societies (Section 12.1).We now address the epidemiological and putative pathophysiological consequences of high triglyceride levels.
What the sources say
- Not checked yetcites NHANES 1999-2008
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.
In the paper
“With adjustment for age and sex, triglycerides showed a strong, stepwise association with both CVD and ischemic stroke; however, after adjustment for standard risk factors and for HDL-C and non-HDL-C, the associations for both CVD and stroke were no longer significant.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies
What the sources say
- Not checked yetcites [17] 17. Di Angelantonio E, Sarwar N, Perry P, Kaptoge S, Ray KK, Thompson A, Wood AM, Lewington S, Sattar N, Packard CJ, Collins R, Thompson SG, Danesh J; Emerging Risk Factors Collaboration. Major lipids, apolipoproteins, and risk of vascular disease. JAMA. 2009;302: 1993-2000. source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Most of these earlier studies did not measure HDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“In women, the association was more robust in both univariate analysis (relative risk 1.76 per mmol/L) and after adjustment for HDL-C (relative risk 1.37, 95% confidence interval 1.13 to 1.66).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies
What the sources say
- Not checked yetcites [36] 36. Hokanson JE, Austin MA. Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein choles- terol level: a meta-analysis of population-based prospective studies. J Cardiovasc Risk. 1996;3:213-219. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“However, the triglyceride level explained most of the risk of the pattern B phenotype and was a stronger covariate than LDL-C, intermediate-density lipoprotein (IDL) cholesterol, or HDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.2. Case-Control Studies, Including Angiographic Studies
What the sources say
- Not checked yetcites [35] 35. Austin MA, Breslow JL, Hennekens CH, Buring JE, Willett WC, Krauss RM. Low-density lipoprotein subclass patterns and risk of myocardial infarction. JAMA. 1988;260:1917-1921. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“For example, direct incubation of mouse peritoneal macrophages with TRL increases macrophage cell triglyceride and fatty acid content; more importantly, this incubation increases expression of macrophage inflammatory proteins, including tumor necrosis factor-␣, interleukin-1, monocyte chemotactic protein-1, intercellular adhesion molecule-1, and matrix metalloproteinase-3. 83,84”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.3. Macrophage LPL Macrophages are a rich source of LPL in the vessel wall, 81 and expression of LPL by macrophages could play a role in accelerating atherogenesis by a mechanism that depends on interaction with circulating TRL.82 For example, direct incubation of mouse peritoneal macrophages with TRL increases macrophage cell triglyceride and fatty acid content; more importantly, this incubation increases expression of macrophage inflammatory proteins, including tumor necrosis factor-␣, interleukin-1, monocyte chemotactic protein-1, intercellular adhesion molecule-1, and matrix metalloproteinase-3. 83,84 Lipolytic products of TRL have also been shown to produce cytotoxicity and apoptosis in isolated macrophages.85 Macrophage apoptosis is considered an important event that impacts the in vivo atherogenic process.86 In summary, in vitro experimental models examining the response of isolated endothelial cells or monocytes and macrophages to TRL have produced results consistent with atherogenicity of this class of particles.These particles, or their lipolytic degradation products, can increase the expression of inflammatory proteins, adhesion molecules, and coagulation factors in endothelial cells or monocytes and macrophages.TRLs may interfere with the ability of HDL to suppress inflammatory responses in cultured endothelial cells and the capacity of apo AI or HDL to promote sterol efflux from monocytes or macrophages.TRLs also impair endothelial cell-dependent vasodilation, enhance the recruitment and attachment of monocytes to endothelium, may be directly cytotoxic, and produce apoptosis in isolated vessel wall cells.However, although the results from in vitro studies provide important pathophysiological context and proof of concept, final conclusions about atherogenicity and clinical significance of lowering triglyceride levels as a surrogate of TRL particles must be based on in vivo studies that use appropriate models of human dyslipidemia in randomized controlled trials (RCTs), as will be elaborated on in Section 15.
What the sources say
- Not checked yetcites [83] 83. Van Eck M, Zimmermann R, Groot PH, Zechner R, Van Berkel TJ. Role of macrophage-derived lipoprotein lipase in lipoprotein metabolism and atherosclerosis. Arterioscler Thromb Vasc Biol. 2000;20:E53-E62.
- Not checked yetcites [84] 84. Saraswathi V, Hasty AH. The role of lipolysis in mediating the proin- flammatory effects of very low density lipoproteins in mouse peritoneal macrophages. J Lipid Res. 2006;47:1406 -1415. source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Recently, a mutation in APOC3 was identified in association with low triglyceride levels, reduced coronary artery calcification, and suggestion of familial longevity.75”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.2. Apo CIII
What the sources say
- Not checked yetcites [75] 75. Pollin TI, Damcott CM, Shen H, Ott SH, Shelton J, Horenstein RB, Post W, McLenithan JC, Bielak LF, Peyser PA, Mitchell BD, Miller M, O'Connell JR, Shuldiner AR. A null mutation in human APOC3 confers a favorable plasma lipid profile and apparent cardioprotection. Science. 2008;322:1702-1705. source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These include activation of adhesion and proinflammatory molecule expression and impairment of endothelial nitric oxide production and insulin signaling pathways.74,76 -80”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.2. Apo CIII
What the sources say
- Not checked yetcites [74] 74. Ooi EM, Barrett PH, Chan DC, Watts GF. Apolipoprotein C-III: under- standing an emerging cardiovascular risk factor. Clin Sci (Lond). 2008; 114:611-624. source
- Not checked yetcites [76] 76. Caron S, Staels B. Apolipoprotein CIII: a link between hypertriglycer- idemia and vascular dysfunction? Circ Res. 2008;103:1348 -1350.
- Not checked yetcites [77] 77. Kawakami A, Aikawa M, Alcaide P, Luscinskas FW, Libby P, Sacks FM. Apolipoprotein CIII induces expression of vascular cell adhesion molecule-1 in vascular endothelial cells and increases adhesion of monocytic cells. Circulation. 2006;114:681-687.
- Not checked yetcites [78] 78. Kawakami A, Aikawa M, Libby P, Alcaide P, Luscinskas FW, Sacks FM. Apolipoprotein CIII in apolipoprotein B lipoproteins enhances the adhesion of human monocytic cells to endothelial cells. Circulation. 2006;113:691-700.
- Not checked yetcites [79] 79. Kawakami A, Osaka M, Tani M, Azuma H, Sacks FM, Shimokado K, Yoshida M. Apolipoprotein CIII links hyperlipidemia with vascular endothelial cell dysfunction. Circulation. 2008;118:731-742.
- Not checked yetcites [80] 80. Kawakami A, Osaka M, Aikawa M, Uematsu S, Akira S, Libby P, Shimokado K, Sacks FM, Yoshida M. Toll-like receptor 2 mediates apolipoprotein CIII-induced monocyte activation. Circ Res. 2008;103: 1402-1409.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Postprandial TRL (ppTG) has also been shown to increase the expression of proinflammatory genes (eg, interleukin-6, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1), 65 induce apoptosis, 66 and accentuate the inflammatory response of cultured endothelial cells to tumor necrosis factor-␣.67”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.1. Remnant Lipoprotein Particles A number of experimental systems have demonstrated that TRLs can produce proatherogenic responses in isolated endothelial cells.RLPs are a by-product of TRL that can be isolated from the postprandial plasma of hypertriglyceridemic subjects; they are intestinal (ie, CMRs) or liver-derived (eg, VLDL remnants) TRLs that have undergone partial hydrolysis by LPL.Liu et al 64 have shown that these particles can accelerate senescence and interfere with the function of endothelial progenitor cells; these cells play an important role in the organismal reparative response to in vivo vessel wall injury.Postprandial TRL (ppTG) has also been shown to increase the expression of proinflammatory genes (eg, interleukin-6, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1), 65 induce apoptosis, 66 and accentuate the inflammatory response of cultured endothelial cells to tumor necrosis factor-␣.67 After a high-fat meal, ppTG may increase the level of circulating endothelial cell microparticles, a measure of endothelial cell dysfunction in vivo.68 That is, a high-fat diet increases the level of these particles more effectively than a low-fat diet and is correlated with ppTG levels.Moreover, Rutledge and colleagues have shown that fatty acids released by lipolysis of TRL elicit proinflammatory responses in endothelial cells.69 TRL may also act to suppress the atheroprotective and antiinflammatory effects of HDL.70 -72 Finally, fatty acid-binding proteins play a role in the intracellular transport of long-chain fatty acids.Recent data support a role for adipocyte-and macrophage-derived fatty acid-binding proteins in systemic inflammatory responses 73 that are likely amplified by high triglyceride loads provided by RLPs to the arterial macrophages.
What the sources say
- Not checked yetcites [65] 65. Norata GD, Grigore L, Raselli S, Redaelli L, Hamsten A, Maggi F, Eriksson P, Catapano AL. Post-prandial endothelial dysfunction in hy- pertriglyceridemic subjects: molecular mechanisms and gene expression studies. Atherosclerosis. 2007;193:321-327.
- Not checked yetcites [66] 66. Shin HK, Kim YK, Kim KY, Lee JH, Hong KW. Remnant lipoprotein particles induce apoptosis in endothelial cells by NAD(P)H oxidase- mediated production of superoxide and cytokines via lectin-like oxidized low-density lipoprotein receptor-1 activation: prevention by cilostazol. Circulation. 2004;109:1022-1028. source
- Not checked yetcites [67] 67. Ting HJ, Stice JP, Schaff UY, Hui DY, Rutledge JC, Knowlton AA, Passerini AG, Simon SI. Triglyceride-rich lipoproteins prime aortic endothelium for an enhanced inflammatory response to tumor necrosis factor-alpha. Circ Res. 2007;100:381-390. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Liu et al 64 have shown that these particles can accelerate senescence and interfere with the function of endothelial progenitor cells; these cells play an important role in the organismal reparative response to in vivo vessel wall injury.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.1. Remnant Lipoprotein Particles A number of experimental systems have demonstrated that TRLs can produce proatherogenic responses in isolated endothelial cells.RLPs are a by-product of TRL that can be isolated from the postprandial plasma of hypertriglyceridemic subjects; they are intestinal (ie, CMRs) or liver-derived (eg, VLDL remnants) TRLs that have undergone partial hydrolysis by LPL.Liu et al 64 have shown that these particles can accelerate senescence and interfere with the function of endothelial progenitor cells; these cells play an important role in the organismal reparative response to in vivo vessel wall injury.Postprandial TRL (ppTG) has also been shown to increase the expression of proinflammatory genes (eg, interleukin-6, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1), 65 induce apoptosis, 66 and accentuate the inflammatory response of cultured endothelial cells to tumor necrosis factor-␣.67 After a high-fat meal, ppTG may increase the level of circulating endothelial cell microparticles, a measure of endothelial cell dysfunction in vivo.68 That is, a high-fat diet increases the level of these particles more effectively than a low-fat diet and is correlated with ppTG levels.Moreover, Rutledge and colleagues have shown that fatty acids released by lipolysis of TRL elicit proinflammatory responses in endothelial cells.69 TRL may also act to suppress the atheroprotective and antiinflammatory effects of HDL.70 -72 Finally, fatty acid-binding proteins play a role in the intracellular transport of long-chain fatty acids.Recent data support a role for adipocyte-and macrophage-derived fatty acid-binding proteins in systemic inflammatory responses 73 that are likely amplified by high triglyceride loads provided by RLPs to the arterial macrophages.
What the sources say
- Not checked yetcites [64] 64. Liu L, Wen T, Zheng XY, Yang DG, Zhao SP, Xu DY, Lu GH. Remnant-like particles accelerate endothelial progenitor cells senescence and induce cellular dysfunction via an oxidative mechanism. Atherosclerosis. 2009;202:405-414.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“That is, a high-fat diet increases the level of these particles more effectively than a low-fat diet and is correlated with ppTG levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.1. Remnant Lipoprotein Particles A number of experimental systems have demonstrated that TRLs can produce proatherogenic responses in isolated endothelial cells.RLPs are a by-product of TRL that can be isolated from the postprandial plasma of hypertriglyceridemic subjects; they are intestinal (ie, CMRs) or liver-derived (eg, VLDL remnants) TRLs that have undergone partial hydrolysis by LPL.Liu et al 64 have shown that these particles can accelerate senescence and interfere with the function of endothelial progenitor cells; these cells play an important role in the organismal reparative response to in vivo vessel wall injury.Postprandial TRL (ppTG) has also been shown to increase the expression of proinflammatory genes (eg, interleukin-6, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1), 65 induce apoptosis, 66 and accentuate the inflammatory response of cultured endothelial cells to tumor necrosis factor-␣.67 After a high-fat meal, ppTG may increase the level of circulating endothelial cell microparticles, a measure of endothelial cell dysfunction in vivo.68 That is, a high-fat diet increases the level of these particles more effectively than a low-fat diet and is correlated with ppTG levels.Moreover, Rutledge and colleagues have shown that fatty acids released by lipolysis of TRL elicit proinflammatory responses in endothelial cells.69 TRL may also act to suppress the atheroprotective and antiinflammatory effects of HDL.70 -72 Finally, fatty acid-binding proteins play a role in the intracellular transport of long-chain fatty acids.Recent data support a role for adipocyte-and macrophage-derived fatty acid-binding proteins in systemic inflammatory responses 73 that are likely amplified by high triglyceride loads provided by RLPs to the arterial macrophages.
What the sources say
- Not checked yetcites [68] 68. Ferreira AC, Peter AA, Mendez AJ, Jimenez JJ, Mauro LM, Chirinos JA, Ghany R, Virani S, Garcia S, Horstman LL, Purow J, Jy W, Ahn YS, de Marchena E. Postprandial hypertriglyceridemia increases circulating levels of endothelial cell microparticles. Circulation. 2004;110: 3599 -3603.
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In the paper
“However, this was reexamined in the National Heart, Lung, and Blood Institute's Family Heart Study, which studied 5381 subjects from 1245 families.90 FCHL and FHTG were diagnosed in 10.2% and 12.3% of 334 random control families, respectively, and in 16.7% and 20.5% of 293 families with at least 1 case of premature CVD.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [90] 90. Hopkins PN, Heiss G, Ellison RC, Province MA, Pankow JS, Eckfeldt JH, Hunt SC. Coronary artery disease risk in familial combined hyper- lipidemia and familial hypertriglyceridemia: a case-control comparison from the National Heart, Lung, and Blood Institute Family Heart Study. Circulation. 2003;108:519 -523.
plaincorrelationaln = 293- Asserted: passes — The authors put it forward as true.
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In the paper
“Overall, alcohol abuse and gallstone disease account for at least 80% of all cases of acute pancreatitis, with hypertriglyceridemia contributing Ϸ10% of cases.105,134”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [105] 105. Ewald N, Hardt PD, Kloer HU. Severe hypertriglyceridemia and pan- creatitis: presentation and management. Curr Opin Lipidol. 2009;20: 497-504. source
- Not checked yetcites [134] 134. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic pancreatitis. Gastroenterol Hepatol (N Y). 2010;6(suppl 3): 1-16.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“In some populations, such as French Canadians, as many as 70% of cases can be traced to a single founder.104”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [104] 104. Ma Y, Henderson HE, Murthy V, Roederer G, Monsalve MV, Clarke LA, Normand T, Julien P, Gagne C, Lambert M, Davignon J, Lupien PJ, Brunzell J, Hayden MR. A mutation in the human lipoprotein lipase gene as the most common cause of familial chylomicronemia in French Canadians. N Engl J Med. 1991;324:1761-1766.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
What the sources say
- Not checked yetcites [13] 13. Criqui MH, Heiss G, Cohn R, Cowan LD, Suchindran CM, Bangdiwala S, Kritchevsky S, Jacobs DR Jr, O'Grady HK, Davis CE. Plasma triglyceride level and mortality from coronary heart disease. N Engl J Med. 1993;328:1220 -1225.
- Not checked yetcites [14] 14. Laakso M, Lehto S, Penttila ¨I, Pyo ¨ra ¨la ¨K. Lipids and lipoproteins predicting coronary heart disease mortality and morbidity in patients with non-insulin-dependent diabetes. Circulation. 1993;88:1421-1430.
- Not checked yetcites [15] 15. West KM, Ahuja MM, Bennett PH, Czyzyk A, De Acosta OM, Fuller JH, Grab B, Grabauskas V, Jarrett RJ, Kosaka K. The role of circulating glucose and triglyceride concentrations and their interactions with other "risk factors" as determinants of arterial disease in nine diabetic popu- lation samples from the WHO multinational study. Diabetes Care. 1983;6:361-369.
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Second, variability is high (Section 10) and increases with the level of triglyceride.12”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.1. Methodological Considerations and Effect Modification Triglyceride has long been the most problematic lipid measure in the evaluation of cardiovascular risk.First, the distribution is markedly skewed, which necessitates categorical definitions or log transformations.Second, variability is high (Section 10) and increases with the level of triglyceride.12 Third, the strong inverse association with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) AI, suggests an intricate biological relationship that may not be most suitably represented by the results of multivariate analysis.Finally, evidence from prospective studies of the triglyceride association supports a stronger link with CVD risk in people with lower levels of HDL-C 13,14 and LDL-C 13,14 and with T2DM.15,16 Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17 In addition to the inverse association with HDL-C, triglyceride levels are closely aligned with T2DM, even though T2DM is not always examined as a confounding factor, and when it is, the diagnosis is commonly based on history.Yet at least 25% of subjects with T2DM are undiagnosed, 18 and they are often concentrated within a hypertriglyceridemic population.Similarly, many subjects with high triglyceride levels and impaired fasting glucose who subsequently develop T2DM are not adjusted for in multivariate analysis.Hence, these limitations restrict conclusions that support triglyceride level as an independent CVD risk factor.Compounding the aforementioned problem is the argument that an elevated triglyceride level is simply an epiphenomenon (ie, a by-product) of IR or the metabolic syndrome (MetS).However, analysis of NHANES data evaluating the association of all 5 MetS components with cardiovascular risk found the strongest association with triglycerides.19 A pivotal consideration is how triglycerides may directly impact the atherosclerotic process in view of epidemiological studies that have failed to demonstrate a strong relationship between very high triglyceride levels and increased CVD death.13,20 As will be described in Section 4, hydrolysis of TRLs (eg, chylomicrons, very low-density lipoproteins [VLDL]) re- Table 2. Overall Prevalence (%) of Hypertriglyceridemia Based on 150, 200, and 500 mg/dL Cut Points by Age, Sex, and Ethnicity in US Adults, NHANES 1999 -2008 Triglyceride Cut Points, mg/dL Demographic Ն150 Ն200 Ն500 Overall (age Ն20 y) 31.0 16.2 1.1 Age, y 20-29 20.7 9.5 0.8 30-39 25.8 14.1 0.7 40-49 32.8 16.7 1.6 50-59 36.7 20.1 1.8 60-69 41.6 22.6 1.0 Ն70 34.5 17.2 0.5 Sex Men 35.4 19.8 1.8 Women* 26.8 12.7 0.5 Ethnicity Mexican American 34.9 19.5 1.4 Non-Hispanic, black 15.6 7.6 0.4 Non-Hispanic, white 33.0 17.6 1.1 NHANES indicates National Health and Nutrition Examination Survey.Data provided by the Epidemiology Branch, National Heart, Lung, and Blood Institute.*Excludes pregnant women.Source: NHANES 1999 -2008. sults in atherogenic cholesterol-enriched remnant lipoprotein particles (RLPs).Accordingly, recent evidence suggests that nonfasting triglyceride is strongly correlated with RLPs, 21 and in 2 recent studies, nonfasting triglyceride was a superior predictor of incident CVD compared with fasting levels.21,22
What the sources say
- Not checked yetcites [12] 12. Jacobs DR Jr, Barrett-Connor E. Retest reliability of plasma cholesterol and triglyceride: the Lipid Research Clinics Prevalence Study. Am J Epidemiol. 1982;116:878 -885.
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In the paper
“Higher VLDL triglyceride output activates cholesteryl ester transfer protein, which results in triglyceride enrichment of LDL and HDL (Figure 4).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.4. Metabolic Consequences of Hypertriglyceridemia
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“Apo CIII is a 79-amino acid glycoprotein that is a major component of circulating TRL and is correlated with triglyceride levels.74”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.2. Apo CIII
What the sources say
- Not checked yetcites [74] 74. Ooi EM, Barrett PH, Chan DC, Watts GF. Apolipoprotein C-III: under- standing an emerging cardiovascular risk factor. Clin Sci (Lond). 2008; 114:611-624. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The persistence of fasting chylomicronemia leads to a syndrome characterized by eruptive xanthomas, lipemia retinalis, and hepatosplenomegaly and is associated, although not invariably, with acute pancreatitis.94,95”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [94] 94. Leaf DA. Chylomicronemia and the chylomicronemia syndrome: a practical approach to management. Am J Med. 2008;121:10 -12.
- Not checked yetcites [95] 95. Chait A, Brunzell JD. Chylomicronemia syndrome. Adv Intern Med. 1992;37:249 -273.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Macrophages are a rich source of LPL in the vessel wall, 81 and expression of LPL by macrophages could play a role in accelerating atherogenesis by a mechanism that depends on interaction with circulating TRL.82”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.3. Macrophage LPL Macrophages are a rich source of LPL in the vessel wall, 81 and expression of LPL by macrophages could play a role in accelerating atherogenesis by a mechanism that depends on interaction with circulating TRL.82 For example, direct incubation of mouse peritoneal macrophages with TRL increases macrophage cell triglyceride and fatty acid content; more importantly, this incubation increases expression of macrophage inflammatory proteins, including tumor necrosis factor-␣, interleukin-1, monocyte chemotactic protein-1, intercellular adhesion molecule-1, and matrix metalloproteinase-3. 83,84 Lipolytic products of TRL have also been shown to produce cytotoxicity and apoptosis in isolated macrophages.85 Macrophage apoptosis is considered an important event that impacts the in vivo atherogenic process.86 In summary, in vitro experimental models examining the response of isolated endothelial cells or monocytes and macrophages to TRL have produced results consistent with atherogenicity of this class of particles.These particles, or their lipolytic degradation products, can increase the expression of inflammatory proteins, adhesion molecules, and coagulation factors in endothelial cells or monocytes and macrophages.TRLs may interfere with the ability of HDL to suppress inflammatory responses in cultured endothelial cells and the capacity of apo AI or HDL to promote sterol efflux from monocytes or macrophages.TRLs also impair endothelial cell-dependent vasodilation, enhance the recruitment and attachment of monocytes to endothelium, may be directly cytotoxic, and produce apoptosis in isolated vessel wall cells.However, although the results from in vitro studies provide important pathophysiological context and proof of concept, final conclusions about atherogenicity and clinical significance of lowering triglyceride levels as a surrogate of TRL particles must be based on in vivo studies that use appropriate models of human dyslipidemia in randomized controlled trials (RCTs), as will be elaborated on in Section 15.
What the sources say
- Not checked yetcites [81] 81. Babaev VR, Fazio S, Gleaves LA, Carter KJ, Semenkovich CF, Linton MF. Macrophage lipoprotein lipase promotes foam cell formation and atherosclerosis in vivo. J Clin Invest. 1999;103:1697-1705.
- Not checked yetcites [82] 82. Goldberg IJ. Lipoprotein lipase and lipolysis: central roles in lipoprotein metabolism and atherogenesis. J Lipid Res. 1996;37:693-707.
hedgedconditional- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“TRLs may interfere with the ability of HDL to suppress inflammatory responses in cultured endothelial cells and the capacity of apo AI or HDL to promote sterol efflux from monocytes or macrophages.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.3. Macrophage LPL Macrophages are a rich source of LPL in the vessel wall, 81 and expression of LPL by macrophages could play a role in accelerating atherogenesis by a mechanism that depends on interaction with circulating TRL.82 For example, direct incubation of mouse peritoneal macrophages with TRL increases macrophage cell triglyceride and fatty acid content; more importantly, this incubation increases expression of macrophage inflammatory proteins, including tumor necrosis factor-␣, interleukin-1, monocyte chemotactic protein-1, intercellular adhesion molecule-1, and matrix metalloproteinase-3. 83,84 Lipolytic products of TRL have also been shown to produce cytotoxicity and apoptosis in isolated macrophages.85 Macrophage apoptosis is considered an important event that impacts the in vivo atherogenic process.86 In summary, in vitro experimental models examining the response of isolated endothelial cells or monocytes and macrophages to TRL have produced results consistent with atherogenicity of this class of particles.These particles, or their lipolytic degradation products, can increase the expression of inflammatory proteins, adhesion molecules, and coagulation factors in endothelial cells or monocytes and macrophages.TRLs may interfere with the ability of HDL to suppress inflammatory responses in cultured endothelial cells and the capacity of apo AI or HDL to promote sterol efflux from monocytes or macrophages.TRLs also impair endothelial cell-dependent vasodilation, enhance the recruitment and attachment of monocytes to endothelium, may be directly cytotoxic, and produce apoptosis in isolated vessel wall cells.However, although the results from in vitro studies provide important pathophysiological context and proof of concept, final conclusions about atherogenicity and clinical significance of lowering triglyceride levels as a surrogate of TRL particles must be based on in vivo studies that use appropriate models of human dyslipidemia in randomized controlled trials (RCTs), as will be elaborated on in Section 15.
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In the paper
“TRLs also impair endothelial cell-dependent vasodilation, enhance the recruitment and attachment of monocytes to endothelium, may be directly cytotoxic, and produce apoptosis in isolated vessel wall cells.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.3. Macrophage LPL Macrophages are a rich source of LPL in the vessel wall, 81 and expression of LPL by macrophages could play a role in accelerating atherogenesis by a mechanism that depends on interaction with circulating TRL.82 For example, direct incubation of mouse peritoneal macrophages with TRL increases macrophage cell triglyceride and fatty acid content; more importantly, this incubation increases expression of macrophage inflammatory proteins, including tumor necrosis factor-␣, interleukin-1, monocyte chemotactic protein-1, intercellular adhesion molecule-1, and matrix metalloproteinase-3. 83,84 Lipolytic products of TRL have also been shown to produce cytotoxicity and apoptosis in isolated macrophages.85 Macrophage apoptosis is considered an important event that impacts the in vivo atherogenic process.86 In summary, in vitro experimental models examining the response of isolated endothelial cells or monocytes and macrophages to TRL have produced results consistent with atherogenicity of this class of particles.These particles, or their lipolytic degradation products, can increase the expression of inflammatory proteins, adhesion molecules, and coagulation factors in endothelial cells or monocytes and macrophages.TRLs may interfere with the ability of HDL to suppress inflammatory responses in cultured endothelial cells and the capacity of apo AI or HDL to promote sterol efflux from monocytes or macrophages.TRLs also impair endothelial cell-dependent vasodilation, enhance the recruitment and attachment of monocytes to endothelium, may be directly cytotoxic, and produce apoptosis in isolated vessel wall cells.However, although the results from in vitro studies provide important pathophysiological context and proof of concept, final conclusions about atherogenicity and clinical significance of lowering triglyceride levels as a surrogate of TRL particles must be based on in vivo studies that use appropriate models of human dyslipidemia in randomized controlled trials (RCTs), as will be elaborated on in Section 15.
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In the paper
“Although TRLs contain much less CE than LDL particles on a per particle basis, there are pathophysiological states (eg, poorly controlled diabetes mellitus [DM]) in which CEs can become enriched in this fraction.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5. Atherogenicity of TRLs
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In the paper
“The generation of FFA by LPL is regulated by cofactors such as insulin and thyroid hormone.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
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In the paper
“However, although the results from in vitro studies provide important pathophysiological context and proof of concept, final conclusions about atherogenicity and clinical significance of lowering triglyceride levels as a surrogate of TRL particles must be based on in vivo studies that use appropriate models of human dyslipidemia in randomized controlled trials (RCTs), as will be elaborated on in”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.3. Macrophage LPL Macrophages are a rich source of LPL in the vessel wall, 81 and expression of LPL by macrophages could play a role in accelerating atherogenesis by a mechanism that depends on interaction with circulating TRL.82 For example, direct incubation of mouse peritoneal macrophages with TRL increases macrophage cell triglyceride and fatty acid content; more importantly, this incubation increases expression of macrophage inflammatory proteins, including tumor necrosis factor-␣, interleukin-1, monocyte chemotactic protein-1, intercellular adhesion molecule-1, and matrix metalloproteinase-3. 83,84 Lipolytic products of TRL have also been shown to produce cytotoxicity and apoptosis in isolated macrophages.85 Macrophage apoptosis is considered an important event that impacts the in vivo atherogenic process.86 In summary, in vitro experimental models examining the response of isolated endothelial cells or monocytes and macrophages to TRL have produced results consistent with atherogenicity of this class of particles.These particles, or their lipolytic degradation products, can increase the expression of inflammatory proteins, adhesion molecules, and coagulation factors in endothelial cells or monocytes and macrophages.TRLs may interfere with the ability of HDL to suppress inflammatory responses in cultured endothelial cells and the capacity of apo AI or HDL to promote sterol efflux from monocytes or macrophages.TRLs also impair endothelial cell-dependent vasodilation, enhance the recruitment and attachment of monocytes to endothelium, may be directly cytotoxic, and produce apoptosis in isolated vessel wall cells.However, although the results from in vitro studies provide important pathophysiological context and proof of concept, final conclusions about atherogenicity and clinical significance of lowering triglyceride levels as a surrogate of TRL particles must be based on in vivo studies that use appropriate models of human dyslipidemia in randomized controlled trials (RCTs), as will be elaborated on in Section 15.
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“The severity of hypertriglyceridemia is related to the extent of the loss of fat, 161 and mechanisms include decreased storage capacity of fat, with delayed clearance of TRLs and increased hepatic lipid synthesis.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.3.1. Genetic Disorders Lipodystrophy can be inherited or acquired.The inherited lipodystrophies are rare disorders that are characterized by loss of adipose tissue.These disorders may be inherited in either autosomal recessive or dominant patterns.The loss of adipose tissue is selective and variable and may be partial or complete.Some forms manifest at birth, whereas others become evident later in life, with loss of fat beginning in childhood and puberty.160 Hypertriglyceridemia is seen in many lipodystrophic disorders, often in association with low HDL-C.The severity of hypertriglyceridemia is related to the extent of the loss of fat, 161 and mechanisms include decreased storage capacity of fat, with delayed clearance of TRLs and increased hepatic lipid synthesis.Fat accumulation in insulin target organs may cause lipotoxicity and IR.One of the most severe forms is congenital generalized lipodystrophy, a rare autosomal recessive disorder that presents at birth with a nearly complete absence of subcutaneous adipose tissue.Affected children may present with metabolic derangements, including severe hypertriglyceridemia, with eruptive xanthomas and pancreatitis.162 At least 3 molecular variants have been described that involve genes whose products are necessary for the formation and maturation of lipid droplets in adipocytes.160 Varieties of familial partial lipodystrophy, which are rare autosomal dominant disorders, involve fat loss from the extremities more than the trunk.Hypertriglyceridemia is most severe in the Dunnigan variety, which is caused by a defect in the gene for lamin A and tends to be more severe in women than in men.162,163
What the sources say
- Not checked yetcites [161] 161. Simha V, Garg A. Lipodystrophy: lessons in lipid and energy metabo- lism. Curr Opin Lipidol. 2006;17:162-169.
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In the paper
“Additional genetic syndromes in the differential diagnosis of hypertriglyceridemia include mixed or familial combined hyperlipidemia (FCHL), type III dysbetalipoproteinemia, and familial hypertriglyceridemia (FHTG).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
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In the paper
“These young patients present with the chylomicronemia syndrome and an increased risk for pancreatitis and may be homozygous for either LPL deficiency, apo CII deficiency, or the more recently described APOA5 and GPIHBP1 loss-of-function mutations.[91][92][93]102,103”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [91] 91. Brunzell JD. Familial lipoprotein lipase deficiency and other causes of chylomicronemia syndrome. In: Scriver CR, Beaudet AL, Sly WS, Valle D, eds. The Metabolic and Molecular Base of Inherited Disease. New York, NY: McGraw-Hill; 1995:1913-1932.
- Not checked yetcites [92] 92. Priore Oliva C, Pisciotta L, Li Volti G, Sambataro MP, Cantafora A, Bellocchio A, Catapano A, Tarugi P, Bertolini S, Calandra S. Inherited apolipoprotein A-V deficiency in severe hypertriglyceridemia. Arte- rioscler Thromb Vasc Biol. 2005;25:411-417.
- Not checked yetcites [93] 93. Hegele RA. Monogenic dyslipidemias: window on determinants of plasma lipoprotein metabolism. Am J Hum Genet. 2001;69:1161-1177.
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In the paper
“In these cases, triglyceride concentrations exceed 1000 mg/dL, and when exacerbated by weight gain, certain medications (Table 5) or metabolic perturbations can lead to the chylomicronemia syndrome and increased risk of pancreatitis.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
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In the paper
“Although there is no single threshold of triglyceride concentration above which pancreatitis may occur, increased risk is defined arbitrarily by levels exceeding 1000 mg/L.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
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In the paper
“Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153 Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154 In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).For visceral adipose tissue, the multivariable-adjusted residual effect was approximately twice that for subcutaneous abdominal adipose tissue for both women and men (PϽ0.0001 for both).Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156 Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158 A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.
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In the paper
“Patients with heterozygous LPL deficiency present with elevated triglyceride levels and low HDL-C, but in association with excess alcohol, steroids, estrogens, poorly controlled DM, hypothyroidism, renal disease, or the third trimester of pregnancy, triglyceride levels can rapidly exceed 2000 mg/dL and produce the clinical sequelae of the chylomicronemia syndrome.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Hypertriglyceridemia is seen in many lipodystrophic disorders, often in association with low HDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.3.1. Genetic Disorders Lipodystrophy can be inherited or acquired.The inherited lipodystrophies are rare disorders that are characterized by loss of adipose tissue.These disorders may be inherited in either autosomal recessive or dominant patterns.The loss of adipose tissue is selective and variable and may be partial or complete.Some forms manifest at birth, whereas others become evident later in life, with loss of fat beginning in childhood and puberty.160 Hypertriglyceridemia is seen in many lipodystrophic disorders, often in association with low HDL-C.The severity of hypertriglyceridemia is related to the extent of the loss of fat, 161 and mechanisms include decreased storage capacity of fat, with delayed clearance of TRLs and increased hepatic lipid synthesis.Fat accumulation in insulin target organs may cause lipotoxicity and IR.One of the most severe forms is congenital generalized lipodystrophy, a rare autosomal recessive disorder that presents at birth with a nearly complete absence of subcutaneous adipose tissue.Affected children may present with metabolic derangements, including severe hypertriglyceridemia, with eruptive xanthomas and pancreatitis.162 At least 3 molecular variants have been described that involve genes whose products are necessary for the formation and maturation of lipid droplets in adipocytes.160 Varieties of familial partial lipodystrophy, which are rare autosomal dominant disorders, involve fat loss from the extremities more than the trunk.Hypertriglyceridemia is most severe in the Dunnigan variety, which is caused by a defect in the gene for lamin A and tends to be more severe in women than in men.162,163
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In this disorder, apo B is not a useful marker of overall atherogenicity, as in FCHL; non-HDL-C would be a more appropriate target.148”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [148] 148. Sniderman AD, Hogue JC, Bergeron J, Gagne C, Couture P. Non-HDL cholesterol and apoB in dyslipidaemia. Clin Sci (Lond). 2008;114: 149 -155.
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In the paper
“It is genetically heterogeneous, and its expression is accentuated by the presence of a secondary factor such as obesity or IR.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153 Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154 In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).For visceral adipose tissue, the multivariable-adjusted residual effect was approximately twice that for subcutaneous abdominal adipose tissue for both women and men (PϽ0.0001 for both).Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156 Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158 A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.
What the sources say
- Not checked yetcites [153] 153. Ford ES, Li C, Zhao G, Pearson WS, Mokdad AH. Hypertriglyceridemia and its pharmacologic treatment among US adults. Arch Intern Med. 2009;169:572-578. source
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In the paper
“FHTG has a population prevalence of Ϸ5% to 10% and is defined by the familial occurrence of isolated high VLDL levels with triglyceride values most commonly in the 200 to 500 mg/dL range.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
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In the paper
“Specifically, common variants in APOA5, glucose kinase regulatory protein (GCKR), LPL, and APOB have been identified, thereby supporting a role for both common and rare variants responsible for hypertriglyceridemia. 151”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > FCHL or FHTG.
What the sources say
- Not checked yetcites [151] 151. Johansen CT, Wang J, Lanktree MB, Cao H, McIntyre AD, Ban MR, Martins RA, Kennedy BA, Hassell RG, Visser ME, Schwartz SM, Voight BF, Elosua R, Salomaa V, O'Donnell CJ, Dallinga-Thie GM, Anand SS, Yusuf S, Huff MW, Kathiresan S, Hegele RA. Excess of rare variants in genes identified by genome-wide association study of hyper- triglyceridemia. Nat Genet. 2010;42:684 -687. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153 Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154 In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).For visceral adipose tissue, the multivariable-adjusted residual effect was approximately twice that for subcutaneous abdominal adipose tissue for both women and men (PϽ0.0001 for both).Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156 Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158 A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.
What the sources say
- Not checked yetcites [157] 157. Despre ´s JP, Lemieux I, Bergeron J, Pibarot P, Mathieu P, Larose E, Rode ´s-Cabau J, Bertrand OF, Poirier P. Abdominal obesity and the metabolic syndrome: contribution to global cardiometabolic risk [pub- lished correction appears in Arterioscler Thromb Vasc Biol. 2008;28: e151]. Arterioscler Thromb Vasc Biol. 2008;28:1039 -1049. source
- Not checked yetcites [158] 158. Rosito GA, Massaro JM, Hoffmann U, Ruberg FL, Mahabadi AA, Vasan RS, O'Donnell CJ, Fox CS. Pericardial fat, visceral abdominal fat, cardiovascular disease risk factors, and vascular calcification in a community-based sample: the Framingham Heart Study. Circulation. 2008;117:605-613.
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In the paper
“In addition, Ϸ35% of T2DM adults have fasting triglyceride levels Ն200 mg/dL 168 associated with decreased HDL-C and small, dense LDL particles.41,53,112,113,169,170”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6. Diabetes Mellitus
What the sources say
- Not checked yetcites [168] 168. Resnick HE, Foster GL, Bardsley J, Ratner RE. Achievement of American Diabetes Association clinical practice recommendations among U.S. adults with diabetes, 1999 -2002: the National Health and Nutrition Examination Survey. Diabetes Care. 2006;29:531-537.
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In the paper
“Homozygosity for the rare apo E2 isoform, which displays defective binding to the LDL receptor compared with the most common apo E3 isoform, is necessary for the expression of type III, but it is not sufficient.Rather, additional factors (eg, obesity, T2DM, or hypothyroidism) are generally required for expression of the type III phenotype”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
plainconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Familial type III hyperlipoproteinemia or dysbetalipoproteinemia is due to the accumulation of cholesterol-rich VLDL, 146,147 which results in a higher ratio of core CE to triglyceride (Ͼ0.3) than in normal VLDL (0.2).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [146] 146. Breslow JL. Genetics of lipoprotein abnormalities associated with coronary artery disease susceptibility. Annu Rev Genet. 2000;34: 233-254.
- Not checked yetcites [147] 147. Mahley RW, Huang Y, Rall SC Jr. Pathogenesis of type III hyperlipo- proteinemia (dysbetalipoproteinemia): questions, quandaries, and par- adoxes. J Lipid Res. 1999;40:1933-1949. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153 Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154 In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).For visceral adipose tissue, the multivariable-adjusted residual effect was approximately twice that for subcutaneous abdominal adipose tissue for both women and men (PϽ0.0001 for both).Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156 Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158 A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.
What the sources say
- Not checked yetcites [154] 154. Centers for Disease Control and Prevention. Prevalence of abnormal lipid levels among youths: United States, 1999 -2006 [published cor- rection appears in MMWR Morb Mortal Wkly Rep. 2010;59:78]. MMWR Morb Mortal Wkly Rep. 2010;59:29 -33.
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In the paper
“Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle Evidence from epidemiological and controlled clinical trials has demonstrated that triglyceride levels are markedly affected by body weight status and body fat distribution.Data from 5610 participants Ն20 years of age from NHANES between 1999 and 2004 reported a relationship between body mass index (BMI) and triglyceride concentration.153 Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.When the triglyceride cut point was Ն200 mg/dL, Ϸ83% of participants were classified as overweight or obese (Table 6).Participants with a normal BMI (Ͻ25 kg/m 2 ) were more likely to have triglyceride levels Ͻ150 mg/dL (43%) and Ͻ200 mg/dL (39%).A similar trend was reported recently for youths in the NHANES Survey 1999 -2006 154 ; only 5.9% of participants in the normalweight category had high triglyceride levels (Ն150 mg/dL), whereas 13.8% and 24% of overweight or obese individuals had elevated triglyceride levels.154 In addition to the association between triglyceride levels and BMI, the Framingham Heart Study 155 reported strong associations of triglyceride levels with both subcutaneous abdominal adipose tissue and visceral adipose tissue in men and women (mean age 50 years).For visceral adipose tissue, the multivariable-adjusted residual effect was approximately twice that for subcutaneous abdominal adipose tissue for both women and men (PϽ0.0001 for both).Thus, although it is clear that excess adiposity is associated with elevated triglyceride levels, visceral adiposity is a greater contributor than subcutaneous adipose tissue.155,156 Excess visceral fat in patients with IR may further expose the liver to higher levels of FFAs via the portal circulation, and increased flux of FFAs to the liver contributes to increased secretion of VLDL.A consequence of excessive fat combined with impaired clearance or storage of triglycerides in subcutaneous fat is ectopic fat deposition in skeletal muscle, liver, and myocardium, which may result in IR, nonalcoholic fatty liver disease, and pericardial fat.157,158 A disproportionate amount of visceral versus subcutaneous adipose tissue may also reflect a lack of adipocyte storage capacity, with saturation of the normal sites of fat deposition.Subcutaneous fat may serve as a protective factor with regard to the metabolic consequences of obesity 159 ; a relative paucity (ie, lipodystrophy) is associated with hypertriglyceridemia.
What the sources say
- Not checked yetcites [159] 159. Porter SA, Massaro JM, Hoffmann U, Vasan RS, O'Donnel CJ, Fox CS. Abdominal subcutaneous adipose tissue: a protective fat depot? Diabetes Care. 2009;32:1068 -1075.
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In the paper
“FCHL is characterized by multiple lipoprotein abnormalities due to hepatic overproduction of apo B-containing VLDL, IDL, and LDL, whereby apo B levels exceed the 90th percentile.87,88”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
What the sources say
- Not checked yetcites [87] 87. Goldstein JL, Schrott HG, Hazzard WR, Bierman EL, Motulsky AG. Hyperlipidemia in coronary heart disease, II: genetic analysis of lipid levels in 176 families and delineation of a new inherited disorder, combined hyperlipidemia. J Clin Invest. 1973;52:1544 -1568.
- Not checked yetcites [88] 88. Brunzell JD, Schrott HG, Motulsky AG, Bierman EL. Myocardial infarction in the familial forms of hypertriglyceridemia. Metabolism. 1976;25:313-320.
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In the paper
“Rather, other factors (eg, low HDL-C, elevated glucose, or elevated blood pressure) independently predicted CVD and all-cause mortality in RCTs.184 -187”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 7.2. Prognostic Significance of Triglyceride in MetS
What the sources say
- Not checked yetcites [184] 184. Schwartz GG, Olsson AG, Szarek M, Sasiela WJ. Relation of charac- teristics of metabolic syndrome to short-term prognosis and effects of intensive statin therapy after acute coronary syndrome: an analysis of the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) trial. Diabetes Care. 2005;28:2508 -2513. source
- Not checked yetcites [185] 185. Suzuki T, Katz R, Jenny NS, Zakai NA, LeWinter MM, Barzilay JI, Cushman M. Metabolic syndrome, inflammation, and incident heart failure in the elderly: the Cardiovascular Health Study. Circ Heart Fail. 2008;1:242-248.
- Not checked yetcites [186] 186. Kasai T, Miyauchi K, Kurata T, Ohta H, Okazaki S, Miyazaki T, Kajimoto K, Kubota N, Daida H. Prognostic value of the metabolic syndrome for long-term outcomes in patients undergoing percutaneous coronary intervention. Circ J. 2006;70:1531-1537.
- Not checked yetcites [187] 187. Anderson JL, Horne BD, Jones HU, Reyna SP, Carlquist JF, Bair TL, Pearson RR, Lappe ´DL, Muhlestein JB; Intermountain Heart Collab- orative (IHC) Study. Which features of the metabolic syndrome predict the prevalence and clinical outcomes of angiographic coronary artery disease? Cardiology. 2004;101:185-193.
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In the paper
“In summary, T1DM may be associated with elevations of VLDL triglyceride and LDL-C if glycemic control is poor or if the patient is ketotic.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.5. Summary
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In the paper
“In T1DM, triglycerides correlate closely with glycemic control, and marked hyperlipidemia can be found in patients with DM and ketoacidosis.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.1.2. VLDL Metabolism
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In the paper
“A triglyceride level Ͼ200 mg/dL is present in Ϸ50% of those with CKD, often in association with low HDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 8. Chronic Kidney Disease
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In the paper
“As discussed previously in this statement, TRLs and RLPs in particular are atherogenic.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1. Non-HDL-C, Apo B, and Ratio of Triglycerides to HDL-C
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216]”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [61] 61. Frost PH, Havel RJ. Rationale for use of non-high-density lipoprotein cholesterol rather than low-density lipoprotein cholesterol as a tool for lipoprotein cholesterol screening and assessment of risk and therapy. Am J Cardiol. 1998;81:26B-31B. source
- Not checked yetcites [203] 203. Miller M, Ginsberg HN, Schaefer EJ. Relative atherogenicity and pre- dictive value of non-high-density lipoprotein cholesterol for coronary heart disease. Am J Cardiol. 2008;101:1003-1008. source
- Not checked yetcites [204] 204. Rainwater DL, McMahan CA, Malcom GT, Scheer WD, Roheim PS, McGill HC Jr, Strong JP; PDAY Research Group. Lipid and apolipo- protein predictors of atherosclerosis in youth: apolipoprotein concen- trations do not materially improve prediction of arterial lesions in PDAY subjects. Arterioscler Thromb Vasc Biol. 1999;19:753-761. source
- Not checked yetcites [205] 205. Martin SS, Qasim AN, Mehta NN, Wolfe M, Terembula K, Schwartz S, Iqbal N, Schutta M, Bagheri R, Reilly MP. Apolipoprotein B but not LDL cholesterol is associated with coronary artery calcification in type 2 diabetic whites. Diabetes. 2009;58:1887-1892. 206. 104. Orakzai SH, Nasir K, Blaha M, Blumenthal RS, Raggi P. Non-HDL cholesterol is strongly associated with coronary artery calcification in asymptomatic individuals. Atherosclerosis. 2009;202:289 -295. source
- Not matchedcites [206]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites [207] 207. Blankenhorn DH, Alaupovic P, Wickham E, Chin HP, Azen SP. Pre- diction of angiographic change in native human coronary arteries and aortocoronary bypass grafts: lipid and nonlipid factors. Circulation. 1990;81:470 -476. source
- Not checked yetcites [208] 208. Lu W, Resnick HE, Jablonski KA, Jones KL, Jain AK, Howard WJ, Robbins DC, Howard BV. Non-HDL cholesterol as a predictor of cardiovascular disease in type 2 diabetes: the Strong Heart Study. Diabetes Care. 2003;26:16 -23. source
- Not checked yetcites [209] 209. Liu J, Sempos CT, Donahue RP, Dorn J, Trevisan M, Grundy SM. Non-high-density lipoprotein and very-low-density lipoprotein choles- terol and their risk predictive values in coronary heart disease. Am J Cardiol. 2006;98:1363-1368. source
- Not checked yetcites [210] 210. Ridker PM, Rifai N, Cook NR, Bradwin G, Buring JE. Non-HDL cholesterol, apolipoproteins A-I and B100, standard lipid measures, lipid ratios, and CRP as risk factors for cardiovascular disease in women. JAMA. 2005;294:326 -333. source
- Not checked yetcites [211] 211. Bittner V, Hardison R, Kelsey SF, Weiner BH, Jacobs AK, Sopko G; Bypass Angioplasty Revascularization Investigation. Non-high-density lipoprotein cholesterol levels predict five-year outcome in the Bypass Angioplasty Revascularization Investigation (BARI). Circulation. 2002; 106:2537-2542. source
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In the paper
“However, pioglitazone lowers triglyceride levels by increasing LPL-mediated lipolysis, whereas VLDL secretion remains unchanged.178”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.2. VLDL Metabolism Overproduction of VLDL, with increased secretion of both triglycerides and apo B 100 , appears to be the central cause of increased plasma VLDL levels in patients with T2DM.176 Increased assembly and secretion of VLDL is probably a direct result of both IR (with loss of insulin's action to stimulate degradation of newly synthesized apo B) and increases in FFA flux to the liver and de novo hepatic lipogenesis (with increased triglyceride synthesis).LPL levels have been reported to be reduced 112 in T2DM, and this may contribute significantly to elevated triglyceride levels, particularly in severely hyperglycemic patients.Because obesity, IR, and concomitant familial forms of hyperlipidemia are common in T2DM, study of the pathophysiology is difficult.The interaction of these overlapping traits also makes therapy less effective.In contrast to T1DM, in which intensive insulin therapy normalizes (or even "supernormalizes") VLDL levels and metabolism, insulin or oral agents only partly correct VLDL abnormalities in the majority of individuals with T2DM.113 Therapies such as metformin and the thiazolidinediones can lower plasma triglyceride concentrations 10% to 15% and 15% to 25%, respectively.177 The thiazolidinediones appear to improve peripheral insulin sensitivity, and this leads to inhibition of lipolysis in adipose tissue.Plasma levels of FFAs fall Ϸ25% at the highest dose of both of the presently available thiazolidinediones, and such changes should lead to lower hepatic triglyceride synthesis and reduced VLDL secretion.However, pioglitazone lowers triglyceride levels by increasing LPL-mediated lipolysis, whereas VLDL secretion remains unchanged.178 Rosiglitazone does not affect triglyceride levels, although the basis for this difference is unclear.179
What the sources say
- Not checked yetcites [178] 178. Nagashima K, Lopez C, Donovan D, Ngai C, Fontanez N, Bensadoun A, Fruchart-Najib J, Holleran S, Cohn JS, Ramakrishnan R, Ginsberg HN. Effects of the PPARgamma agonist pioglitazone on lipoprotein metab- olism in patients with type 2 diabetes mellitus. J Clin Invest. 2005;115: 1323-1332. source
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In the paper
“Causes of hypertriglyceridemia in DM include increased hepatic VLDL production and defective removal of chylomicrons and CMRs, which often reflects poor glycemic control.171”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6. Diabetes Mellitus
What the sources say
- Not checked yetcites [171] 171. Kreisberg RA. Diabetic dyslipidemia. Am J Cardiol. 1998;82:67U-73U.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [205] 205. Martin SS, Qasim AN, Mehta NN, Wolfe M, Terembula K, Schwartz S, Iqbal N, Schutta M, Bagheri R, Reilly MP. Apolipoprotein B but not LDL cholesterol is associated with coronary artery calcification in type 2 diabetic whites. Diabetes. 2009;58:1887-1892. 206. 104. Orakzai SH, Nasir K, Blaha M, Blumenthal RS, Raggi P. Non-HDL cholesterol is strongly associated with coronary artery calcification in asymptomatic individuals. Atherosclerosis. 2009;202:289 -295.
- Not checked yetcites [206]
- Not checked yetcites [207] 207. Blankenhorn DH, Alaupovic P, Wickham E, Chin HP, Azen SP. Pre- diction of angiographic change in native human coronary arteries and aortocoronary bypass grafts: lipid and nonlipid factors. Circulation. 1990;81:470 -476.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Thus, individuals with T2DM and mild to moderate hypertriglyceridemia exhibit the pattern B profile of LDL (smaller, denser particles) described by Austin and Krauss 180 ; these particles may be more susceptible to oxidative modification and catabolism via macrophage scavenger receptors than pattern A LDL particles.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.3. Small LDL Particles
What the sources say
- Not checked yetcites [180] 180. Austin MA, Krauss RM. LDL density and atherosclerosis. JAMA. 1995; 273:115.
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In the paper
“In untreated or poorly controlled T1DM, LPL activity will be low, and ppTG levels will in turn be increased.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.1.1. Chylomicron Metabolism
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In contrast, T2DM is often accompanied by high triglyceride levels, reduced HDL-C, and the presence of smaller CE-depleted LDL particles.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.5. Summary
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [22] 22. Bansal S, Buring JE, Rifai N, Mora S, Sacks FM, Ridker PM. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA. 2007;298:309 -316. source
- Not checked yetcites [217] 217. Mora S, Rifai N, Buring JE, Ridker PM. Fasting compared with non- fasting lipids and apolipoproteins for predicting incident cardiovascular events. Circulation. 2008;118:993-1001.
- Not checked yetcites [61] 61. Frost PH, Havel RJ. Rationale for use of non-high-density lipoprotein cholesterol rather than low-density lipoprotein cholesterol as a tool for lipoprotein cholesterol screening and assessment of risk and therapy. Am J Cardiol. 1998;81:26B-31B.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Results from RCTs to date cannot be extrapolated to milder forms of CKD, and therefore, an RCT is warranted in this subgroup.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 8. Chronic Kidney Disease
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
In the paper
“Therapies such as metformin and the thiazolidinediones can lower plasma triglyceride concentrations 10% to 15% and 15% to 25%, respectively.177”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.2. VLDL Metabolism Overproduction of VLDL, with increased secretion of both triglycerides and apo B 100 , appears to be the central cause of increased plasma VLDL levels in patients with T2DM.176 Increased assembly and secretion of VLDL is probably a direct result of both IR (with loss of insulin's action to stimulate degradation of newly synthesized apo B) and increases in FFA flux to the liver and de novo hepatic lipogenesis (with increased triglyceride synthesis).LPL levels have been reported to be reduced 112 in T2DM, and this may contribute significantly to elevated triglyceride levels, particularly in severely hyperglycemic patients.Because obesity, IR, and concomitant familial forms of hyperlipidemia are common in T2DM, study of the pathophysiology is difficult.The interaction of these overlapping traits also makes therapy less effective.In contrast to T1DM, in which intensive insulin therapy normalizes (or even "supernormalizes") VLDL levels and metabolism, insulin or oral agents only partly correct VLDL abnormalities in the majority of individuals with T2DM.113 Therapies such as metformin and the thiazolidinediones can lower plasma triglyceride concentrations 10% to 15% and 15% to 25%, respectively.177 The thiazolidinediones appear to improve peripheral insulin sensitivity, and this leads to inhibition of lipolysis in adipose tissue.Plasma levels of FFAs fall Ϸ25% at the highest dose of both of the presently available thiazolidinediones, and such changes should lead to lower hepatic triglyceride synthesis and reduced VLDL secretion.However, pioglitazone lowers triglyceride levels by increasing LPL-mediated lipolysis, whereas VLDL secretion remains unchanged.178 Rosiglitazone does not affect triglyceride levels, although the basis for this difference is unclear.179
What the sources say
- Not checked yetcites [177] 177. van Wijk JP, de Koning EJ, Martens EP, Rabelink TJ. Thiazolidin- ediones and blood lipids in type 2 diabetes. Arterioscler Thromb Vasc Biol. 2003;23:1744 -1749.
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Rosiglitazone does not affect triglyceride levels, although the basis for this difference is unclear.179”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.2. VLDL Metabolism Overproduction of VLDL, with increased secretion of both triglycerides and apo B 100 , appears to be the central cause of increased plasma VLDL levels in patients with T2DM.176 Increased assembly and secretion of VLDL is probably a direct result of both IR (with loss of insulin's action to stimulate degradation of newly synthesized apo B) and increases in FFA flux to the liver and de novo hepatic lipogenesis (with increased triglyceride synthesis).LPL levels have been reported to be reduced 112 in T2DM, and this may contribute significantly to elevated triglyceride levels, particularly in severely hyperglycemic patients.Because obesity, IR, and concomitant familial forms of hyperlipidemia are common in T2DM, study of the pathophysiology is difficult.The interaction of these overlapping traits also makes therapy less effective.In contrast to T1DM, in which intensive insulin therapy normalizes (or even "supernormalizes") VLDL levels and metabolism, insulin or oral agents only partly correct VLDL abnormalities in the majority of individuals with T2DM.113 Therapies such as metformin and the thiazolidinediones can lower plasma triglyceride concentrations 10% to 15% and 15% to 25%, respectively.177 The thiazolidinediones appear to improve peripheral insulin sensitivity, and this leads to inhibition of lipolysis in adipose tissue.Plasma levels of FFAs fall Ϸ25% at the highest dose of both of the presently available thiazolidinediones, and such changes should lead to lower hepatic triglyceride synthesis and reduced VLDL secretion.However, pioglitazone lowers triglyceride levels by increasing LPL-mediated lipolysis, whereas VLDL secretion remains unchanged.178 Rosiglitazone does not affect triglyceride levels, although the basis for this difference is unclear.179
What the sources say
- Not checked yetcites [179] 179. Ginsberg H, Plutzky J, Sobel BE. A review of metabolic and cardio- vascular effects of oral antidiabetic agents: beyond glucose-level lowering. J Cardiovasc Risk. 1999;6:337-346.
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“The primary abnormality in CKD subjects is reduced catabolism of TRL, 131 which results in elevated levels of RLPs and prolonged ppTG that begins during the early stages of CKD.194”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 8. Chronic Kidney Disease
What the sources say
- Not checked yetcites [131] 131. Vaziri ND. Causes of dysregulation of lipid metabolism in chronic renal failure. Semin Dial. 2009;22:644 -651.
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, although elevated triglyceride is highly prevalent in subjects with MetS, it is less predictive of CVD outcomes than other MetS components, thus relegating triglyceride level as an important biomarker rather than a prognosticator of CVD.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 7.2. Prognostic Significance of Triglyceride in MetS
plaincorrelational- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Insulin therapy rapidly reverses this condition, which results in improved clearance of chylomicron triglyceride from plasma.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.1.1. Chylomicron Metabolism
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Treatment with hypoglycemic agents has a variable drug-dependent effect on plasma lipid levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.5. Summary
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Although apo AI levels are reduced consistently, correction of hypertriglyceridemia does not usually alter apo AI levels.53,181”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.4. Reduced HDL-C
What the sources say
- Not checked yetcites [53] 53. Ginsberg HN. Lipoprotein physiology in nondiabetic and diabetic states: relationship to atherogenesis. Diabetes Care. 1991;14:839 -855.
- Not checked yetcites [181] 181. Horowitz BS, Goldberg IJ, Merab J, Vanni TM, Ramakrishnan R, Ginsberg HN. Increased plasma and renal clearance of an exchangeable pool of apolipoprotein A-I in subjects with low levels of high density lipoprotein cholesterol. J Clin Invest. 1993;91:1743-1752.
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“It is linked to IR in whites 233,234 (but not in blacks)”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.3. Ratio of Triglycerides to HDL-C
What the sources say
- Not checked yetcites [233]
- Not checked yetcites [234] 234. Sumner AE, Finley KB, Genovese DJ, Criqui MH, Boston RC. Fasting triglyceride and the triglyceride-HDL cholesterol ratio are not markers of insulin resistance in African Americans. Arch Intern Med. 2005;165: 1395-1400.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“and to small, dense LDL particles and higher LDL particle numbers.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.3. Ratio of Triglycerides to HDL-C
What the sources say
- Not matchedcites [233]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites [235] 235. Hanak V, Munoz J, Teague J, Stanley A Jr, Bittner V. Accuracy of the triglyceride to high-density lipoprotein cholesterol ratio for prediction of the low-density lipoprotein phenotype B. Am J Cardiol. 2004;94: 219 -222. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Not matched
In the paper
“Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [219] 219. Gardner CD, Winkleby MA, Fortmann SP. Population frequency distri- bution of non-high-density lipoprotein cholesterol (Third National Health and Nutrition Examination Survey [NHANES III], 1988 -1994). Am J Cardiol. 2000;86:299 -304.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [209] 209. Liu J, Sempos CT, Donahue RP, Dorn J, Trevisan M, Grundy SM. Non-high-density lipoprotein and very-low-density lipoprotein choles- terol and their risk predictive values in coronary heart disease. Am J Cardiol. 2006;98:1363-1368.
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.2. Apo B Apo B is contained within all potentially atherogenic lipoproteins, including lipoprotein(a), LDL, IDL, VLDL, and TRL remnants.Moreover, because each of these lipoprotein particles contains 1 apo B molecule, apo B provides a direct measure of the number of atherogenic particles present in the circulation.58,226 A direct link between apo B and severity of CVD in patients undergoing diagnostic cardiac catheterization 227 was followed by numerous studies that supported apo B as being highly predictive of CVD and, in some cases, more closely linked to CVD outcomes than LDL-C.58,228,229 In contrast, findings of studies that compared apo B with non-HDL-C have been more heterogeneous.Although apo B and non-HDL-C are highly correlated, their interrelationship varies depending on the underlying lipid disorder and treatment status.148,230 As reviewed recently, 231 many epidemiological studies have compared the predictive value of apo B with non-HDL-C for CVD outcomes and have more commonly identified apo B to be either superior or equivalent to non-HDL-C, whereas non-HDL-C has only been more predictive in limited cases.143 Yet in studies that demonstrated statistically significant differences between apo B and non-HDL-C, the differences in point estimates were often quite small and therefore unlikely to have a major impact in day-to-day clinical practice.231 Consequently, the ATP III guidelines favored use of non-HDL-C rather than apo B; this was related in part to the limited availability of apo B assays in clinical laboratories, compounded by the relative lack of standardization of the apo B assay and higher cost than for non-HDL-C.221 Nevertheless, in view of additional data and in the presence of standardization that has accrued since ATP III was released in 2001, a panel of international experts has recommended a revision of this assessment.229
What the sources say
- Not checked yetcites [229] 229. Barter PJ, Ballantyne CM, Carmena R, Castro Cabezas M, Chapman MJ, Couture P, de Graaf J, Durrington PN, Faergeman O, Frohlich J, Furberg CD, Gagne C, Haffner SM, Humphries SE, Jungner I, Krauss RM, Kwiterovich P, Marcovina S, Packard CJ, Pearson TA, Reddy KS, Rosenson R, Sarrafzadegan N, Sniderman AD, Stalenhoef AF, Stein E, Talmud PJ, Tonkin AM, Walldius G, Williams KM. Apo B versus cholesterol in estimating cardiovascular risk and in guiding therapy: report of the thirty-person/ten-country panel. J Intern Med. 2006;259: 247-258.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“Among women, non-HDL-C levels were inversely related to education.219”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.1. Non-HDL-C The value of non-HDL-C in CVD risk assessment was first proposed by Frost and Havel in 1998, 61 and this relationship has now been confirmed in many studies. [203]3][204][205][206][207][208][209][210][211][212][213][214][215][216] In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study, an autopsy study of 15-to 34-year-old individuals who died of non-CVD causes, non-HDL-C was correlated with fatty streaks and raised lesions in the right coronary artery.204 In adults, non-HDL-C correlates with coronary calcification 205,206 and CVD progression.207 Although the relationship between non-HDL-C and CVD outcomes has been studied less extensively than the relationship between LDL-C, myocardial infarction, and cardiovascular death, there are prospective studies that have demonstrated strong relationships between non-HDL-C levels and CVD events in the ab-sence 208 -210 or presence 211,212 of preexisting CVD or acute coronary syndrome.Long-term data from the Lipid Research Clinics Follow-Up Study demonstrated that non-HDL-C levels were strongly predictive of CVD mortality after 19 years of follow-up.213 In the Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe (DECODE) study, non-HDL-C predicted 10-year CVD mortality only among those with impaired fasting glucose, not among those with normal fasting glucose.214 Non-HDL-C levels also predicted ischemic stroke, 215,216 and its predictive value has been further demonstrated in both men and women, across all age and ethnic groups, and with or without CVD or associated risk factors.Non-HDL-C can be assessed in the nonfasting state 22,217 and is more accurately determined because it does not depend on fasting triglyceride concentrations, as calculated LDL-C does.61 Data on the distribution of non-HDL-C in the US population are available for children (Bogalusa cohort 218 ) and adults (NHANES III 219 ), and non-HDL-C levels in childhood strongly predict such levels in adulthood.219,220 Among adults, age-adjusted non-HDL-C concentrations are lower among women than men, increase with age through age 65 years (to a greater degree in women than in men), and decline in individuals Ͼ65 years of age (more so in men than in women).209 Non-Hispanic black women and men have the lowest non-HDL-C levels, whites are intermediate, and Mexican Americans have the highest level.Among women, non-HDL-C levels were inversely related to education.219 The ATP III guidelines recommended that non-HDL-C serve as a secondary treatment target if elevated levels of triglyceride (Ն200 mg/dL) persisted after LDL-C target levels had been achieved.10,221 The non-HDL-C target was set 30 mg/dL higher than LDL-C, based on the fact that a triglyceride level of 150 mg/dL corresponds to a VLDL cholesterol level of 30 mg/dL.221 A meta-analysis of clinical trial data supports a 1:1 relationship between the percent of non-HDL-C lowering and the percent of cardiovascular reduction.222 Yet recent data indicate that non-HDL-C remains undertreated in the United States.For example, in the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology (NEPTUNE) II survey, the proportion of individuals with triglyceride levels Ն200 mg/dL who had achieved their non-HDL-C goal ranged from 64% with 0 to 1 risk factor to 52% with Ն2 risk factors and only 27% with CVD risk equivalents.223 Data from NHANES also showed that only a modest proportion (37%) of high-risk individuals were at their non-HDL-C goal.224 Finally, in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI-2D) study of men and women with CVD and DM, the mean non-HDL-C level (131Ϯ40 mg/dL) was above the recommended goal of Ͻ130 mg/dL.225
What the sources say
- Not checked yetcites [219] 219. Gardner CD, Winkleby MA, Fortmann SP. Population frequency distri- bution of non-high-density lipoprotein cholesterol (Third National Health and Nutrition Examination Survey [NHANES III], 1988 -1994). Am J Cardiol. 2000;86:299 -304.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Mexican Americans and overweight adolescents had the highest rates (13% and 17.8% respectively) of impaired fasting glucose, which was associated with significantly higher fasting insulin, dyslipidemia, and hypertension.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1.3. IR and T2DM in Childhood Studies in children, including the Cardiovascular Risk in Young Finns Study 296 and a Pima Indian population study, 297 indicate that IR precedes the development of other risk factors, including obesity, hypertension, and hypertriglyceridemia.There are some impediments to the study of IR in youth, namely, lack of consensus for serum insulin norms and the well-documented physiological IR of puberty.Despite ongoing controversy in this area, 1 recent study identified IR (measured by fasting insulin) as being associated with failure to respond to therapeutic lifestyle change in obese adolescents.298 In fact, recent data from NHANES III found a 7% prevalence of impaired fasting glucose in US adolescents.However, Mexican Americans and overweight adolescents had the highest rates (13% and 17.8% respectively) of impaired fasting glucose, which was associated with significantly higher fasting insulin, dyslipidemia, and hypertension.299 Impaired glucose tolerance is also associated with an increased incidence of hypertriglyceridemia.For example, in the NHANES cohort of 1999 -2000, Williams et al 299 found that mean triglyceride levels were 28% higher in adolescents with impaired glucose tolerance than in those with normal fasting glucose concentrations.Triglyceride levels were independently associated with physical activity levels and sugar-sweetened beverage intake in the NHANES 1999 -2004 studies of adolescents (nϭ6967) 12 to 19 years of age.Each additional daily serving of sugar-sweetened beverages was associated with a 2.25-mg/dL increase in triglyceride levels, as well as increases in IR, LDL-C, and systolic blood pressure and a decrease in HDL-C.In boys but not in girls, the combination of a high level of physical activity coupled with low intake of sugar-sweetened beverages was significantly associated with lower triglyceride levels, higher HDL-C, and reduced IR.300
What the sources say
- Not checked yetcites [299] 299. Williams DE, Cadwell BL, Cheng YJ, Cowie CC, Gregg EW, Geiss LS, Engelgau MM, Narayan KM, Imperatore G. Prevalence of impaired fasting glucose and its relationship with cardiovascular disease risk factors in US adolescents, 1999 -2000. Pediatrics. 2005;116:1122-1126.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“plasma tubes contain ethylenediaminetetraacetic acid and reduce triglyceride levels by 3% compared with serum because of the relative dilution of nondiffusible components in plasma.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.2. Phlebotomy-Related Issues
What the sources say
- Not checked yetcites [247] 247. Laboratory Methods Committee of the Lipid Research Clinics Program of the National Heart, Lung, and Blood Institute. Cholesterol and tri- glyceride concentrations in serum/plasma pairs. Clin Chem. 1977;23: 60 -63.
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“triglyceride levels are reduced by Ϸ12% after 20 to 30 minutes and by 15% to 20% by 40 minutes”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.1. Postural Effects
What the sources say
- Not checked yetcites [245] 245. Miller M, Bachorik PS, Cloey TA. Normal variation of plasma lipo- proteins: postural effects on plasma concentrations of lipids, lipo- proteins, and apolipoproteins. Clin Chem. 1992;38:569 -574.
- Not checked yetcites [246] 246. Hagan RD, Upton SJ, Avakian EV, Grundy S. Increases in serum lipid and lipoprotein levels with movement from the supine to standing position in adult men and women. Prev Med. 1986;15:18 -27.
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Approximately 1 in 5 children with a BMI above the 95th percentile are hypertriglyceridemic, a rate that is 7-fold higher than for nonobese children 6 to 10 years of age.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1.2. Obesity and High Triglyceride Levels in Childhood
What the sources say
- Not checked yetcites [294] 294. Freedman DS, Dietz WH, Srinivasan SR, Berenson GS. The relation of overweight to cardiovascular risk factors among children and ado- lescents: the Bogalusa Heart Study. Pediatrics. 1999;103:1175-1182. source
- Not checked yetcites [295] 295. Daniels SR, Jacobson MS, McCrindle BW, Eckel RH, Sanner BM. American Heart Association Childhood Obesity Research Summit: executive summary. Circulation. 2009;119:2114 -2123. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Each additional daily serving of sugar-sweetened beverages was associated with a 2.25-mg/dL increase in triglyceride levels, as well as increases in IR, LDL-C, and systolic blood pressure and a decrease in HDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1.3. IR and T2DM in Childhood Studies in children, including the Cardiovascular Risk in Young Finns Study 296 and a Pima Indian population study, 297 indicate that IR precedes the development of other risk factors, including obesity, hypertension, and hypertriglyceridemia.There are some impediments to the study of IR in youth, namely, lack of consensus for serum insulin norms and the well-documented physiological IR of puberty.Despite ongoing controversy in this area, 1 recent study identified IR (measured by fasting insulin) as being associated with failure to respond to therapeutic lifestyle change in obese adolescents.298 In fact, recent data from NHANES III found a 7% prevalence of impaired fasting glucose in US adolescents.However, Mexican Americans and overweight adolescents had the highest rates (13% and 17.8% respectively) of impaired fasting glucose, which was associated with significantly higher fasting insulin, dyslipidemia, and hypertension.299 Impaired glucose tolerance is also associated with an increased incidence of hypertriglyceridemia.For example, in the NHANES cohort of 1999 -2000, Williams et al 299 found that mean triglyceride levels were 28% higher in adolescents with impaired glucose tolerance than in those with normal fasting glucose concentrations.Triglyceride levels were independently associated with physical activity levels and sugar-sweetened beverage intake in the NHANES 1999 -2004 studies of adolescents (nϭ6967) 12 to 19 years of age.Each additional daily serving of sugar-sweetened beverages was associated with a 2.25-mg/dL increase in triglyceride levels, as well as increases in IR, LDL-C, and systolic blood pressure and a decrease in HDL-C.In boys but not in girls, the combination of a high level of physical activity coupled with low intake of sugar-sweetened beverages was significantly associated with lower triglyceride levels, higher HDL-C, and reduced IR.300
What the sources say
- Not checked yetcites [300] 300. Bremer AA, Auinger P, Byrd RS. Relationship between insulin resistance-associated metabolic parameters and anthropometric mea- surements with sugar-sweetened beverage intake and physical activity levels in US adolescents: findings from the 1999 -2004 National Health and Nutrition Examination Survey. Arch Pediatr Adolesc Med. 2009; 163:328 -335.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“More recent data from NHANES 1999 -2006 identified a triglyceride level Ն150 mg/dL in 11.4% of boys and 8.8% of girls 12 to 19 years of age, with the highest rate (16.4%) in the 18-to 19-year-old group.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1. Children and Adolescent Obesity
What the sources say
- Not checked yetcites [154] 154. Centers for Disease Control and Prevention. Prevalence of abnormal lipid levels among youths: United States, 1999 -2006 [published cor- rection appears in MMWR Morb Mortal Wkly Rep. 2010;59:78]. MMWR Morb Mortal Wkly Rep. 2010;59:29 -33.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the fasting state only represents a small proportion of time spent each day and therefore understates levels that are attained in the postprandial state.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.3. Fasting Versus Nonfasting Levels Although an overnight fast has been the traditional method for assessment of triglyceride levels, there are several lines of evidence that support a nonfasting measurement to screen for hypertriglyceridemia. First, the fasting state only represents a small proportion of time spent each day and therefore understates levels that are attained in the postprandial state.From a pathophysiological standpoint, a postprandial state enriched in dietary fat (eg, 70 to 100 g) may affect saturation parameters and impede hepatic removal of circulating CMRs, 248 thereby permitting their uptake and incorporation by macrophages.63,249,250 Supportive observational studies have recently identified nonfasting triglyceride levels to be a superior predictor of CVD risk compared with fasting levels.21,22 The relationship between fasting and ppTG levels and factors that influence the response to dietary fat in healthy normolipidemic subjects were reviewed in 39 studies approximating 1500 ppTG measurements.68, Although baseline dietary characteristics, fat content, and composition of test meals often varied between studies, a graded association existed between the amount of dietary fat in the test meal and the ppTG response.For example, a meal that contained up to 15 g of fat was associated with minimal (20%) increases in peak ppTG levels, 276 whereas high-fat meals (eg, 50 g), including those served in popular fast-food restaurants, increased triglyceride levels by at least 50% beyond fasting levels.68,273,275,279 Because median triglyceride levels in US adults range between 106 (women) and 122 (men) mg/dL, measurement of nonfasting triglyceride levels in the absence of a high-fat meal (eg, Ͻ15 g) would be expected to eliminate the requirement for a fasting lipid panel in a sizeable proportion of otherwise healthy adults. A practical algorithm for screening triglyceride measurements is suggested in Figure 5.In normotriglyceridemic subjects (ie, fasting triglyceride levels Ͻ150 mg/dL), consumption of a low-fat breakfast (ie, Ͻ15 g) before blood sampling would not be expected to raise ppTG levels above 200 mg/dL.In these cases, no further testing for hypertriglyceridemia is indicated, although further discussion of lifestyle measures may be advocated on the basis of that individual's level of risk.However, if nonfasting triglyceride levels equal or exceed 200 mg/dL, a fasting lipid panel is recommended within a reasonable (eg, 2 to 4 weeks) time frame.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“the early pathophysiological changes in arteries begin soon after birth and accelerate during adolescence.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1. Children and Adolescent Obesity
What the sources say
- Not checked yetcites [289] 289. McGill HC Jr, McMahan CA, Zieske AW, Sloop GD, Walcott JV, Troxclair DA, Malcom GT, Tracy RE, Oalmann MC, Strong JP; Patho- biological Determinants of Atherosclerosis in Youth (PDAY) Research Group. Associations of coronary heart disease risk factors with the intermediate lesion of atherosclerosis in youth. Arterioscler Thromb Vasc Biol. 2000;20:1998 -2004.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The prevalence of triglyceride levels Ն150 mg/dL has increased among US women Ն20 years of age from 24.6% in 1988 -1994 to 29.9% in 1999 -2000, 307 with stabilization at 26.8% (1999 -2008; Table 2).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.2. Prevalence of Hypertriglyceridemia in Women
What the sources say
- Not checked yetcites [307] 307. Ford ES, Giles WH, Mokdad AH. Increasing prevalence of the meta- bolic syndrome among U.S. adults. Diabetes Care. 2004;27:2444 -2449. 308. 108. McNeill AM, Rosamond WD, Girman CJ, Golden SH, Schmidt MI, East HE, Ballantyne CM, Heiss G. The metabolic syndrome and 11-year risk of incident cardiovascular disease in the atherosclerosis risk in commu- nities study. Diabetes Care. 2005;28:385-390.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [335] 335. Derby CA, Crawford SL, Pasternak RC, Sowers M, Sternfeld B, Matthews KA. Lipid changes during the menopause transition in relation to age and weight: the Study of Women's Health Across the Nation. Am J Epidemiol. 2009;169:1352-1361.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [336] 336. The Writing Group for the PEPI Trial. Effects of estrogen or estrogen/ progestin regimens on heart disease risk factors in postmenopausal women: the Postmenopausal Estrogen/Progestin Interventions (PEPI) Trial [published correction appears in JAMA. 1995;274:1676]. JAMA. 1995;273:199 -208.
- Not checked yetcites [337] 337. Godsland IF. Effects of postmenopausal hormone replacement therapy on lipid, lipoprotein, and apolipoprotein (a) concentrations: analysis of studies published from 1974 -2000. Fertil Steril. 2001;75:898 -915. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Although higher triglyceride levels among female newborns than among male newborns have been reported”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.1. Triglyceride Levels During the Lifespan in Women
What the sources say
- Not checked yetcites [305] 305. Bansal N, Cruickshank JK, McElduff P, Durrington PN. Cord blood lipoproteins and prenatal influences. Curr Opin Lipidol. 2005;16: 400 -408. source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“In pregnancy, women experience a “physiological hyperlipidemia” due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [109] 109. Herrera E, Amusquivar E, Lo ´pez-Soldado I, Ortega H. Maternal lipid metabolism and placental lipid transfer. Horm Res. 2006;65(suppl 3):59 -64.
- Not checked yetcites [110] 110. Mazurkiewicz JC, Watts GF, Warburton FG, Slavin BM, Lowy C, Koukkou E. Serum lipids, lipoproteins and apolipoproteins in pregnant non-diabetic patients. J Clin Pathol. 1994;47:728 -731.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [323] 323. Silliman K, Shore V, Forte TM. Hypertriglyceridemia during late pregnancy is associated with the formation of small dense low-density lipoproteins and the presence of large buoyant high-density lipoproteins. Metabolism. 1994;43:1035-1041.
- Not checked yetcites [324] 324. Hubel CA, Shakir Y, Gallaher MJ, McLaughlin MK, Roberts JM. Low-density lipoprotein particle size decreases during normal pregnancy in association with triglyceride increases. J Soc Gynecol Investig. 1998;5:244 -250.
- Not checked yetcites [325] 325. Winkler K, Wetzka B, Hoffmann MM, Friedrich I, Kinner M, Baumstark MW, Wieland H, Ma ¨rz W, Zahradnik HP. Low density lipoprotein (LDL) subfractions during pregnancy: accumulation of buoyant LDL with advancing gestation. J Clin Endocrinol Metab. 2000; 85:4543-4550.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [321] 321. Foulon T, Payen N, Laporte F, Bijaoui S, Dupont G, Roland F, Gros- lambert P. Effects of two low-dose oral contraceptives containing ethi- nylestradiol and either desogestrel or levonorgestrel on serum lipids and lipoproteins with particular regard to LDL size. Contraception. 2001; 64:11-16.
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“This increase occurred despite the fact that the use of lipid-lowering medications among adult women Ն20 years of age increased from 3.5% to 8% between the 1988 -1994 and the 1999 -2002 surveys.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.1. Triglyceride Levels During the Lifespan in Women
What the sources say
- Not checked yetcites [6] 6. Carroll MD, Lacher DA, Sorlie PD, Cleeman JI, Gordon DJ, Wolz M, Grundy SM, Johnson CL. Trends in serum lipids and lipoproteins of adults, 1960 -2002. JAMA. 2005;294:1773-1781.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [330] 330. Davis CE, Pajak A, Rywik S, Williams DH, Broda G, Pazucha T, Ephross S. Natural menopause and cardiovascular disease risk factors: the Poland and US Collaborative Study on Cardiovascular Disease Epidemiology. Ann Epidemiol. 1994;4:445-448.
- Not checked yetcites [331] 331. Lindquist O, Bengtsson C, Lapidus L. Relationships between the menopause and risk factors for ischaemic heart disease. Acta Obstet Gynecol Scand Suppl. 1985;130:43-47.
- Not checked yetcites [332] 332. Bonithon-Kopp C, Scarabin PY, Darne B, Malmejac A, Guize L. Menopause-related changes in lipoproteins and some other cardiovas- cular risk factors. Int J Epidemiol. 1990;19:42-48.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Population-based data in US adults indicate that compared with men triglyceride levels are lower in young and middle-aged females and among non-Hispanic whites, blacks, and Mexican Americans; in contrast, older women have higher levels than men in all ethnic groups.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.1. Triglyceride Levels During the Lifespan in Women
What the sources say
- Not checked yetcites [6] 6. Carroll MD, Lacher DA, Sorlie PD, Cleeman JI, Gordon DJ, Wolz M, Grundy SM, Johnson CL. Trends in serum lipids and lipoproteins of adults, 1960 -2002. JAMA. 2005;294:1773-1781.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [319] 319. Kim C, Siscovick DS, Sidney S, Lewis CE, Kiefe CI, Koepsell TD. Oral contraceptive use and association with glucose, insulin, and diabetes in young adult women: the CARDIA Study: Coronary Artery Risk Devel- opment in Young Adults. Diabetes Care. 2002;25:1027-1032. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“This difference is present in women as young as 18 to 24 years of age and persists thereafter.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [315]
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [326] 326. McIntyre HD, Chang AM, Callaway LK, Cowley DM, Dyer AR, Radaelli T, Farrell KA, Huston-Presley L, Amini SB, Kirwan JP, Catalano PM; Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study Cooperative Research Group. Hormonal and metabolic factors associated with variations in insulin sensitivity in human pregnancy. Diabetes Care. 2010;33:356 -360.
- Not checked yetcites [327] 327. Montelongo A, Lasuncio ´n MA, Pallardo LF, Herrera E. Longitudinal study of plasma lipoproteins and hormones during pregnancy in normal and diabetic women. Diabetes. 1992;41:1651-1659.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In adolescence, girls experience a decrease in triglycerides, whereas boys experience an increase, likely due to a greater degree of IR among males.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.1. Triglyceride Levels During the Lifespan in Women
What the sources say
- Not checked yetcites [306] 306. Moran A, Jacobs DR Jr, Steinberger J, Steffen LM, Pankow JS, Hong CP, Sinaiko AR. Changes in insulin resistance and cardiovascular risk during adolescence: establishment of differential risk in males and females. Circulation. 2008;117:2361-2368.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [312] 312. Magkos F, Patterson BW, Mittendorfer B. No effect of menstrual cycle phase on basal very-low-density lipoprotein triglyceride and apolipo- protein B-100 kinetics. Am J Physiol Endocrinol Metab. 2006;291: E1243-E1249. 313. 109. Barnett JB, Woods MN, Lamon-Fava S, Schaefer EJ, McNamara JR, Spiegelman D, Hertzmark E, Goldin B, Longcope C, Gorbach SL. Plasma lipid and lipoprotein levels during the follicular and luteal phases of the menstrual cycle. J Clin Endocrinol Metab. 2004;89:776 -782.
- Not checked yetcites [313]
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In the paper
“Prevalence is highest among Mexican American women, intermediate among non-Hispanic white women, and lowest among black women”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.2. Prevalence of Hypertriglyceridemia in Women
What the sources say
- Not checked yetcites [308] source
- Not checked yetcites [309] 309. Park YW, Zhu S, Palaniappan L, Heshka S, Carnethon MR, Heymsfield SB. The metabolic syndrome: prevalence and associated risk factor findings in the US population from the Third National Health and Nutrition Examination Survey, 1988 -1994. Arch Intern Med. 2003;163: 427-436.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Women who develop DM experience a greater rise in triglyceride levels and have an overall more adverse lipid profile than men who develop DM.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.2. Prevalence of Hypertriglyceridemia in Women
What the sources say
- Not checked yetcites [310] 310. Walden CE, Knopp RH, Wahl PW, Beach KW, Strandness E Jr. Sex differences in the effect of diabetes mellitus on lipoprotein triglyceride and cholesterol concentrations. N Engl J Med. 1984;311:953-959. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Current guidelines for CVD prevention in women encourage fasting triglyceride levels Ͻ150 mg/dL and non-HDL-C Ͻ130 mg/dL through TLC.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2. Triglycerides as a Cardiovascular Risk Factor in Women
What the sources say
- Not checked yetcites [304] 304. Mosca L, Benjamin EJ, Berra K, Bezanson JL, Dolor RJ, Lloyd-Jones DM, Newby LK, Pina IL, Roger VL, Shaw LJ, Zhao D, Beckie TM, Bushnell C, D'Armiento J, Kris-Etherton PM, Fang J, Ganiats TG, Gomes AS, Gracia CR, Haan CK, Jackson EA, Judelson DR, Kelepouris E, Lavie CJ, Moore A, Nussmeier NA, Ofili E, Oparil S, Ouyang P, Pinn VW, Sherif K, Smith SC, Jr, Sopko G, Chandra-Strobos N, Urbina EM, Vaccarino V, Wenger NK. Effectiveness-based guidelines for the pre- vention of cardiovascular disease in women-2011 update: a guideline from the American Heart Association. Circulation. 2011;123: 1243-
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Mexican American women have the highest triglyceride levels, whereas non-Hispanic white women have intermediate levels, and black women have the lowest levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.1. Triglyceride Levels During the Lifespan in Women
What the sources say
- Not checked yetcites [6] 6. Carroll MD, Lacher DA, Sorlie PD, Cleeman JI, Gordon DJ, Wolz M, Grundy SM, Johnson CL. Trends in serum lipids and lipoproteins of adults, 1960 -2002. JAMA. 2005;294:1773-1781.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“non-Hispanic blacks often possess lower levels of triglycerides; the mechanism for this inherent difference may be increased LPL activity.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities
What the sources say
- Not checked yetcites [350] 350. Sumner AE, Cowie CC. Ethnic differences in the ability of triglyceride levels to identify insulin resistance. Atherosclerosis. 2008;196:696 -703.
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“A weight loss of 5% to 10% results in a 20% decrease in triglycerides, approximately a 15% reduction in LDL-C, and an 8% to 10% increase in HDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.1.1. Weight Status, Body Fat Distribution, and Weight Loss
What the sources say
- Not checked yetcites [386] 386. Van Gaal LF, Mertens IL, Ballaux D. What is the relationship between risk factor reduction and degree of weight loss? Eur Heart J Suppl. 2005;7(suppl L):L21-L26.
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In the paper
“Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines As described in Section 2: Scope of the Problem, triglyceride levels are classified as normal (Ͻ150 mg/dL), borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), or very high (Ն500 mg/dL) based on measurements after a 12-hour fast.The most clinically relevant complication of hypertriglyceridemia is acute pancreatitis, yet only 10% of cases are a direct consequence of triglyceride levels.Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL 105,353 ; however, because only 20% of subjects presenting with these extremely high levels develop pancreatitis, 354 it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.Table 5 lists genetic and secondary causes (disorders of metabolism, diet, drugs, and diseases that cause hypertriglyceridemia-induced pancreatitis [91][92][93][94][95]355,356 ).Even when a secondary cause is identified, family screening to uncover a genetic lipid disorder is also in order.357 In addition to pancreatitis, other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.Therefore, very high triglyceride levels often require both therapeutic lifestyle change and pharmacological therapy as outlined in ATP III. 10 Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.74 The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).156,157,360 It is important to recognize that individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment. A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.6 Consistent with a reduced likelihood of abnormal metabolic parameters (eg, IR) are observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load (Section 10.3., Fasting Versus Nonfasting Levels). An "optimal" triglyceride cut point is only intended to define one physiological parameter of cardiometabolic health.It does not represent a therapeutic target, because there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.Nevertheless, the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8 is of great concern.These developments have provided the impetus for intensification of efforts aimed at therapeutic lifestyle change to halt and potentially reverse an alarming trend that, if not proactively addressed, may eradicate the considerable progress in CVD risk reduction that has been achieved in recent years.381
What the sources say
- Not checked yetcites [105] 105. Ewald N, Hardt PD, Kloer HU. Severe hypertriglyceridemia and pan- creatitis: presentation and management. Curr Opin Lipidol. 2009;20: 497-504. source
- Not checked yetcites [353] 353. Fortson MR, Freedman SN, Webster PD 3rd. Clinical assessment of hyperlipidemic pancreatitis. Am J Gastroenterol. 1995;90:2134 -2139.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines As described in Section 2: Scope of the Problem, triglyceride levels are classified as normal (Ͻ150 mg/dL), borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), or very high (Ն500 mg/dL) based on measurements after a 12-hour fast.The most clinically relevant complication of hypertriglyceridemia is acute pancreatitis, yet only 10% of cases are a direct consequence of triglyceride levels.Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL 105,353 ; however, because only 20% of subjects presenting with these extremely high levels develop pancreatitis, 354 it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.Table 5 lists genetic and secondary causes (disorders of metabolism, diet, drugs, and diseases that cause hypertriglyceridemia-induced pancreatitis [91][92][93][94][95]355,356 ).Even when a secondary cause is identified, family screening to uncover a genetic lipid disorder is also in order.357 In addition to pancreatitis, other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.Therefore, very high triglyceride levels often require both therapeutic lifestyle change and pharmacological therapy as outlined in ATP III. 10 Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.74 The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).156,157,360 It is important to recognize that individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment. A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.6 Consistent with a reduced likelihood of abnormal metabolic parameters (eg, IR) are observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load (Section 10.3., Fasting Versus Nonfasting Levels). An "optimal" triglyceride cut point is only intended to define one physiological parameter of cardiometabolic health.It does not represent a therapeutic target, because there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.Nevertheless, the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8 is of great concern.These developments have provided the impetus for intensification of efforts aimed at therapeutic lifestyle change to halt and potentially reverse an alarming trend that, if not proactively addressed, may eradicate the considerable progress in CVD risk reduction that has been achieved in recent years.381
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“One intervention is to eliminate dietary trans fatty acids, which increase triglycerides and atherogenic lipoproteins (ie, lipoprotein[a], LDL-C) 382 and are linked to increased cardiovascular risk.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.1. Dietary and Weight-Losing Strategies
What the sources say
- Not checked yetcites [382] 382. Kreisberg RA, Oberman A. Medical management of hyperlipidemia/ dyslipidemia. J Clin Endocrinol Metab. 2003;88:2445-2461. source
- Not checked yetcites [383] 383. Mozaffarian D, Stampfer MJ. Removing industrial trans fat from foods. BMJ. 2010;340:c1826.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines As described in Section 2: Scope of the Problem, triglyceride levels are classified as normal (Ͻ150 mg/dL), borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), or very high (Ն500 mg/dL) based on measurements after a 12-hour fast.The most clinically relevant complication of hypertriglyceridemia is acute pancreatitis, yet only 10% of cases are a direct consequence of triglyceride levels.Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL 105,353 ; however, because only 20% of subjects presenting with these extremely high levels develop pancreatitis, 354 it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.Table 5 lists genetic and secondary causes (disorders of metabolism, diet, drugs, and diseases that cause hypertriglyceridemia-induced pancreatitis [91][92][93][94][95]355,356 ).Even when a secondary cause is identified, family screening to uncover a genetic lipid disorder is also in order.357 In addition to pancreatitis, other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.Therefore, very high triglyceride levels often require both therapeutic lifestyle change and pharmacological therapy as outlined in ATP III. 10 Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.74 The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).156,157,360 It is important to recognize that individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment. A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.6 Consistent with a reduced likelihood of abnormal metabolic parameters (eg, IR) are observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load (Section 10.3., Fasting Versus Nonfasting Levels). An "optimal" triglyceride cut point is only intended to define one physiological parameter of cardiometabolic health.It does not represent a therapeutic target, because there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.Nevertheless, the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8 is of great concern.These developments have provided the impetus for intensification of efforts aimed at therapeutic lifestyle change to halt and potentially reverse an alarming trend that, if not proactively addressed, may eradicate the considerable progress in CVD risk reduction that has been achieved in recent years.381
What the sources say
- Not checked yetcites [6] 6. Carroll MD, Lacher DA, Sorlie PD, Cleeman JI, Gordon DJ, Wolz M, Grundy SM, Johnson CL. Trends in serum lipids and lipoproteins of adults, 1960 -2002. JAMA. 2005;294:1773-1781.
- Not checked yetcites [9] 9. Johnson RK, Appel LJ, Brands M, Howard BV, Lefevre M, Lustig RH, Sacks F, Steffen LM, Wylie-Rosett J; on behalf of American Heart Association Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism and the Council on Epidemiology and Pre- vention. Dietary sugars intake and cardiovascular health: a scientific statement from the American Heart Association. Circulation. 2009;120: 1011-1020.
- Not checked yetcites [8] 8. Daniels SR, Arnett DK, Eckel RH, Gidding SS, Hayman LL, Kumanyika S, Robinson TN, Scott BJ, St Jeor S, Williams CL. Over- weight in children and adolescents: pathophysiology, consequences, prevention, and treatment. Circulation. 2005;111:1999 -2012.
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In the paper
“This often occurs without a sufficient increase in waist circumference that meets the criteria of MetS as defined by ATP III, thereby resulting in a lower threshold for abnormal waist circumference for South Asians and several other ethnic groups; a BMI of 23 kg/m 2 in South Asians corresponds to a BMI of 25 kg/m 2 in whites.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities
What the sources say
- Not checked yetcites [347] 347. Misra A, Khurana L. The metabolic syndrome in South Asians: epide- miology, determinants, and prevention. Metab Syndr Relat Disord. 2009;7:497-514.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“A study of 185 blacks in whom IR was documented by the euglycemic-hyperinsulinemic clamp procedure demonstrated mean triglyceride levels (109 mg/dL) below the cut point for elevated triglyceride used in MetS, although they were higher than in the insulin-sensitive cohort (mean 77 mg/dL).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities
What the sources say
- Not checked yetcites [351] 351. Stein E, Kushner H, Gidding S, Falkner B. Plasma lipid concentrations in nondiabetic African American adults: associations with insulin resistance and the metabolic syndrome. Metabolism. 2007;56:954 -960.
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines As described in Section 2: Scope of the Problem, triglyceride levels are classified as normal (Ͻ150 mg/dL), borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), or very high (Ն500 mg/dL) based on measurements after a 12-hour fast.The most clinically relevant complication of hypertriglyceridemia is acute pancreatitis, yet only 10% of cases are a direct consequence of triglyceride levels.Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL 105,353 ; however, because only 20% of subjects presenting with these extremely high levels develop pancreatitis, 354 it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.Table 5 lists genetic and secondary causes (disorders of metabolism, diet, drugs, and diseases that cause hypertriglyceridemia-induced pancreatitis [91][92][93][94][95]355,356 ).Even when a secondary cause is identified, family screening to uncover a genetic lipid disorder is also in order.357 In addition to pancreatitis, other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.Therefore, very high triglyceride levels often require both therapeutic lifestyle change and pharmacological therapy as outlined in ATP III. 10 Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.74 The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).156,157,360 It is important to recognize that individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment. A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.6 Consistent with a reduced likelihood of abnormal metabolic parameters (eg, IR) are observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load (Section 10.3., Fasting Versus Nonfasting Levels). An "optimal" triglyceride cut point is only intended to define one physiological parameter of cardiometabolic health.It does not represent a therapeutic target, because there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.Nevertheless, the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8 is of great concern.These developments have provided the impetus for intensification of efforts aimed at therapeutic lifestyle change to halt and potentially reverse an alarming trend that, if not proactively addressed, may eradicate the considerable progress in CVD risk reduction that has been achieved in recent years.381
What the sources say
- Not checked yetcites [156] 156. Nicklas BJ, Penninx BW, Ryan AS, Berman DM, Lynch NA, Dennis KE. Visceral adipose tissue cutoffs associated with metabolic risk factors for coronary heart disease in women. Diabetes Care. 2003;26: 1413-1420.
- Not checked yetcites [157] 157. Despre ´s JP, Lemieux I, Bergeron J, Pibarot P, Mathieu P, Larose E, Rode ´s-Cabau J, Bertrand OF, Poirier P. Abdominal obesity and the metabolic syndrome: contribution to global cardiometabolic risk [pub- lished correction appears in Arterioscler Thromb Vasc Biol. 2008;28: e151]. Arterioscler Thromb Vasc Biol. 2008;28:1039 -1049. source
- Not checked yetcites [360] 360. Kashyap SR, Diab DL, Baker AR, Yerian L, Bajaj H, Gray-McGuire C, Schauer PR, Gupta M, Feldstein AE, Hazen SL, Stein CM. Triglyceride levels and not adipokine concentrations are closely related to severity of nonalcoholic fatty liver disease in an obesity surgery cohort. Obesity (Silver Spring). 2009;17:1696 -1701.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“the Strong Heart Study, a cross-sectional prospective observational study of 4600 American Indians, 348 found a moderate elevation in triglyceride levels and a significantly increased prevalence of T2DM to have contributed to incident CVD.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities
What the sources say
- Not checked yetcites [348] 348. Howard BV, Lee ET, Cowan LD, Fabsitz RR, Howard WJ, Oopik AJ, Robbins DC, Savage PJ, Yeh JL, Welty TK. Coronary heart disease prevalence and its relation to risk factors in American Indians: the Strong Heart Study. Am J Epidemiol. 1995;142:254 -268.
- Not checked yetcites [349] 349. Howard BV, Lee ET, Cowan LD, Devereux RB, Galloway JM, Go OT, Howard WJ, Rhoades ER, Robbins DC, Sievers ML, Welty TK. Rising tide of cardiovascular disease in American Indians: the Strong Heart Study. Circulation. 1999;99:2389 -2395.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines As described in Section 2: Scope of the Problem, triglyceride levels are classified as normal (Ͻ150 mg/dL), borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), or very high (Ն500 mg/dL) based on measurements after a 12-hour fast.The most clinically relevant complication of hypertriglyceridemia is acute pancreatitis, yet only 10% of cases are a direct consequence of triglyceride levels.Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL 105,353 ; however, because only 20% of subjects presenting with these extremely high levels develop pancreatitis, 354 it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.Table 5 lists genetic and secondary causes (disorders of metabolism, diet, drugs, and diseases that cause hypertriglyceridemia-induced pancreatitis [91][92][93][94][95]355,356 ).Even when a secondary cause is identified, family screening to uncover a genetic lipid disorder is also in order.357 In addition to pancreatitis, other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.Therefore, very high triglyceride levels often require both therapeutic lifestyle change and pharmacological therapy as outlined in ATP III. 10 Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.74 The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).156,157,360 It is important to recognize that individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment. A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.6 Consistent with a reduced likelihood of abnormal metabolic parameters (eg, IR) are observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load (Section 10.3., Fasting Versus Nonfasting Levels). An "optimal" triglyceride cut point is only intended to define one physiological parameter of cardiometabolic health.It does not represent a therapeutic target, because there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.Nevertheless, the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8 is of great concern.These developments have provided the impetus for intensification of efforts aimed at therapeutic lifestyle change to halt and potentially reverse an alarming trend that, if not proactively addressed, may eradicate the considerable progress in CVD risk reduction that has been achieved in recent years.381
What the sources say
- Not checked yetcites [358] 358. Nagra PK, Ho AC, Dugan JD Jr. Lipemia retinalis associated with branch retinal vein occlusion. Am J Ophthalmol. 2003;135:539 -542.
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In the paper
“Populations from South Asia, including India, Pakistan, Sri Lanka, Bangladesh, and Nepal, have an increased prevalence of MetS and T2DM compared with Europeans.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities
What the sources say
- Not checked yetcites [345] 345. Forouhi NG, Sattar N. CVD risk factors and ethnicity: a homogeneous relationship? Atheroscler Suppl. 2006;7:11-19.
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In the paper
“Thus, blacks with MetS or T2DM may not possess high triglyceride levels as commonly as observed in other ethnic groups, thereby attenuating the predictive value of triglycerides or triglycerides-to-HDL ratios in this subgroup to identify IR.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities
What the sources say
- Not checked yetcites [234] 234. Sumner AE, Finley KB, Genovese DJ, Criqui MH, Boston RC. Fasting triglyceride and the triglyceride-HDL cholesterol ratio are not markers of insulin resistance in African Americans. Arch Intern Med. 2005;165: 1395-1400.
- Not checked yetcites [350] 350. Sumner AE, Cowie CC. Ethnic differences in the ability of triglyceride levels to identify insulin resistance. Atherosclerosis. 2008;196:696 -703.
- Not checked yetcites [352] 352. Sharma MD, Pavlik VN. Dyslipidaemia in African Americans, His- panics and whites with type 2 diabetes mellitus and hypertension. Diabetes Obes Metab. 2001;3:41-45.
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines As described in Section 2: Scope of the Problem, triglyceride levels are classified as normal (Ͻ150 mg/dL), borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), or very high (Ն500 mg/dL) based on measurements after a 12-hour fast.The most clinically relevant complication of hypertriglyceridemia is acute pancreatitis, yet only 10% of cases are a direct consequence of triglyceride levels.Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL 105,353 ; however, because only 20% of subjects presenting with these extremely high levels develop pancreatitis, 354 it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.Table 5 lists genetic and secondary causes (disorders of metabolism, diet, drugs, and diseases that cause hypertriglyceridemia-induced pancreatitis [91][92][93][94][95]355,356 ).Even when a secondary cause is identified, family screening to uncover a genetic lipid disorder is also in order.357 In addition to pancreatitis, other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.Therefore, very high triglyceride levels often require both therapeutic lifestyle change and pharmacological therapy as outlined in ATP III. 10 Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.74 The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).156,157,360 It is important to recognize that individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment. A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.6 Consistent with a reduced likelihood of abnormal metabolic parameters (eg, IR) are observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load (Section 10.3., Fasting Versus Nonfasting Levels). An "optimal" triglyceride cut point is only intended to define one physiological parameter of cardiometabolic health.It does not represent a therapeutic target, because there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.Nevertheless, the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8 is of great concern.These developments have provided the impetus for intensification of efforts aimed at therapeutic lifestyle change to halt and potentially reverse an alarming trend that, if not proactively addressed, may eradicate the considerable progress in CVD risk reduction that has been achieved in recent years.381
What the sources say
- Not checked yetcites [74] 74. Ooi EM, Barrett PH, Chan DC, Watts GF. Apolipoprotein C-III: under- standing an emerging cardiovascular risk factor. Clin Sci (Lond). 2008; 114:611-624. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [343] 343. Reid IR, Eastell R, Fogelman I, Adachi JD, Rosen A, Netelenbos C, Watts NB, Seeman E, Ciaccia AV, Draper MW. A comparison of the effects of raloxifene and conjugated equine estrogen on bone and lipids in healthy postmenopausal women. Arch Intern Med. 2004;164: 871-879.
- Not checked yetcites [344] 344. Barrett-Connor E, Grady D, Sashegyi A, Anderson PW, Cox DA, Hoszowski K, Rautaharju P, Harper KD; MORE Investigators (Multiple Outcomes of Raloxifene Evaluation). Raloxifene and cardiovascular events in osteoporotic postmenopausal women: four-year results from the MORE (Multiple Outcomes of Raloxifene Evaluation) randomized trial. JAMA. 2002;287:847-857.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.3. Hormonal Influences Triglyceride levels in women are significantly impacted by the endogenous hormonal environment and by exogenously administered reproductive hormones.The impact of cyclic hormonal fluctuations on lipoprotein levels during the menstrual cycle in premenopausal women is controversial.311 Recent studies have reported no change in basal VLDL triglyceride and apo B 100 kinetics 312 and triglyceride levels, 313 whereas other studies have shown small changes in triglyceride levels during the cycle but with overall coefficients of variation similar to those of postmenopausal women and men.314 These findings suggest that screening and risk assessment in premenopausal women can be performed without standardization of lipoprotein measurements to the phase of the menstrual cycle.Women with polycystic ovarian syndrome have higher triglyceride levels than women with normal premenopausal physiology, even after correction for BMI.315,316 This difference is present in women as young as 18 to 24 years of age and persists thereafter.315 Lipid metabolic effects of oral contraceptives vary on the basis of their estrogen and progestin content.317,318 In the CARDIA study (Coronary Artery Risk Development in Young Adults), which did not distinguish between various formulations, oral contraceptive users had higher triglyceride levels than nonusers, despite their use being associated with lower fasting glucose levels and reduced odds of DM. 319 Higher triglyceride levels among oral contraceptive users were also found in a population-based survey in Canada.320 Although most studies suggest increases in the 20% to 30% range, triglyceride level increases of as much as 57% (and decreases in LDL particle size) have been reported in some populations.321 In pregnancy, women experience a "physiological hyperlipidemia" due to enhanced lipolytic activity in adipose tissue, with Ͼ2-fold increases in circulating triglyceride levels during the third trimester.109,110 As is the case in the nonpregnant state, non-Hispanic black women have lower triglyceride levels during pregnancy than their white counterparts.322 Although some studies find a hypertriglyceridemia-associated shift toward smaller, denser LDL particle size, 323,324 others have shown a shift toward larger, buoyant LDL particles in late pregnancy.325 Both IR 326 and hyperestrogenemia 327 represent causative factors for the development or amplification of hypertriglyceridemia during pregnancy and may present a therapeutic challenge, especially if pancreatitis develops. 105Maternal hypertriglyceridemia in gestational DM also predicts babies that are large for their gestational age.328 In contrast, endothelial function is not adversely affected as a result of pregnancy-induced hyperlipidemia.329 As women transition through menopause in middle age, triglyceride levels increase, but it is not clear how much of this increase is mediated by aging and accompanying lifestyle changes (eg, reduced physical activity) versus a consequence of menopausal hormonal transition.330 -334 In the Study of Women's Health Across the Nation (SWAN), the triglyceride increase peaked during late perimenopause/early postmenopause.The magnitude of change attributable to aging was similar to that associated with the menopausal transition; both were substantially greater than changes directly attributable to decreases in estradiol or increases in follicle stimulating hormone.335 Orally administered exogenous estrogens increase triglyceride levels, whereas exogenously administered progestins tend to ameliorate this estrogen-induced hypertriglyceridemia to varying degrees depending on dose and type of progestin.336,337 Triglyceride levels vary substantially over time in women who are receiving cyclic hormone regimens.338 It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia; therefore, hypertriglyceridemia has often been an exclusionary criteria in hormone-based RCTs.339,340 Triglyceride elevations are not usually observed with transdermally administered estrogens.337,341,342 Selective estrogen-receptor modulators have less impact on the lipid profile than oral hormone therapy in the absence of hypertriglyceridemia with estrogen therapy.121 Raloxifene, for example, increased triglyceride levels by 8% in a 3-year study among healthy women but only by 1.5% in the much larger Multiple Outcomes of Raloxifene Evaluation trial, which included women with and without CVD.343,344 Finally, tamoxifen has been reported to cause marked elevation in triglyceride levels, 124 with rare reports of pancreatitis (Table 5).
What the sources say
- Not checked yetcites [124] 124. Hozumi Y, Kawano M, Saito T, Miyata M. Effect of tamoxifen on serum lipid metabolism. J Clin Endocrinol Metab. 1998;83:1633-1635.
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Meta-analyses have reported that for every kilogram of weight loss, triglyceride levels decrease Ϸ1.9%, or 1.5 mg/dL.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.1.1. Weight Status, Body Fat Distribution, and Weight Loss
What the sources say
- Not checked yetcites [388] 388. Anderson JW, Konz EC. Obesity and disease management: effects of weight loss on comorbid conditions. Obes Res. 2001;9(suppl 4): 326S-334S. source
- Not checked yetcites [389] 389. Dattilo AM, Kris-Etherton PM. Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis. Am J Clin Nutr. 1992;56: 320 -328.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“South Asians have increased fat compared with muscle tissue, with a more central distribution of body fat, which has been attributed to the “adipose tissue overflow hypothesis.””
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities
What the sources say
- Not checked yetcites [346] 346. Bainey KR, Jugdutt BI. Increased burden of coronary artery disease in South-Asians living in North America: need for an aggressive man- agement algorithm. Atherosclerosis. 2009;204:1-10.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines As described in Section 2: Scope of the Problem, triglyceride levels are classified as normal (Ͻ150 mg/dL), borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), or very high (Ն500 mg/dL) based on measurements after a 12-hour fast.The most clinically relevant complication of hypertriglyceridemia is acute pancreatitis, yet only 10% of cases are a direct consequence of triglyceride levels.Because documentation for a specific threshold in triglyceride-induced pancreatitis is lacking, levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL 105,353 ; however, because only 20% of subjects presenting with these extremely high levels develop pancreatitis, 354 it is often difficult to identify a high-risk subject on the basis of triglyceride levels alone.Table 5 lists genetic and secondary causes (disorders of metabolism, diet, drugs, and diseases that cause hypertriglyceridemia-induced pancreatitis [91][92][93][94][95]355,356 ).Even when a secondary cause is identified, family screening to uncover a genetic lipid disorder is also in order.357 In addition to pancreatitis, other potentially adverse clinical manifestations of chylomicronemia include retinal thrombosis 358 and, in rare cases, blindness.Therefore, very high triglyceride levels often require both therapeutic lifestyle change and pharmacological therapy as outlined in ATP III. 10 Although borderline-high and high triglyceride levels (150 to 500 mg/dL) are not associated with pancreatitis, they are correlated with atherogenic RLPs and apo CIII-enriched particles.74 The elevations in triglyceride levels serve as a biomarker for visceral adiposity, IR, DM, and nonalcoholic hepatic steatosis (fatty liver).156,157,360 It is important to recognize that individuals with values in this range may remain at risk for pancreatitis, especially if they are placed on triglyceride-lowering treatment for very high levels (ie, Ն500 mg/dL) and experience an exacerbation due to secondary factors or interruption of treatment. A low fasting triglyceride level (ie, Ͻ100 mg/dL) is commonly found in underdeveloped societies and countries at low CVD risk (eg, Africa, China, Greece, and Japan), [361][362][363][364][365][366][367][368][369][370][371][372][373] as contrasted with the United States, where mean levels are Ϸ15% to 30% higher.6 Consistent with a reduced likelihood of abnormal metabolic parameters (eg, IR) are observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.Taken together, these data raise the possibility that an optimal fasting triglyceride level may be Ͻ100 mg/dL; similarly, an optimal nonfasting triglyceride level may be Ͻ150 mg/dL because of the Ͻ50% anticipated increase in ppTG levels after a fat load (Section 10.3., Fasting Versus Nonfasting Levels). An "optimal" triglyceride cut point is only intended to define one physiological parameter of cardiometabolic health.It does not represent a therapeutic target, because there is insufficient evidence that lowering triglyceride levels improves CVD risk prediction beyond LDL-C and non-HDL-C target goal recommendations.Nevertheless, the Ϸ25% rise in triglyceride levels in US adults during the past several decades 6 that has coincided with higher caloric intake 9 and higher rates of juvenile obesity and T2DM 8 is of great concern.These developments have provided the impetus for intensification of efforts aimed at therapeutic lifestyle change to halt and potentially reverse an alarming trend that, if not proactively addressed, may eradicate the considerable progress in CVD risk reduction that has been achieved in recent years.381
What the sources say
- Not checked yetcites [361] 361. Gebre-Yohannes A, Rahlenbeck SI. Coronary heart disease risk factors among blood donors in northwest Ethiopia. East Afr Med J. 1998;75: 495-500.
- Not checked yetcites [362] 362. Vorster HH, Kruger A, Venter CS, Margetts BM, Macintyre UE. Car- diovascular disease risk factors and socio-economic position of Africans in transition: the THUSA study. Cardiovasc J Afr. 2007;18:282-289.
- Not checked yetcites [363] 363. Murray MJ, Murray AB, Murray NJ, Murray MB. Serum cholesterol, triglycerides and heart disease of nomadic and sedentary tribesmen consuming isoenergetic diets of high and low fat content. Br J Nutr. 1978;39:159 -163.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Thus, although many studies of high-CHO diets have shown increases in triglyceride levels, others (eg, DASH, OmniHeart, and WHI) have shown no effect.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
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In the paper
“TC, LDL-C, HDL-C, and triglyceride levels did not change with the fruits and vegetables diet.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
What the sources say
- Not checked yetcites [394] 394. Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N; DASH Collaborative Research Group. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med. 1997;336: 1117-1124. source
- Not checked yetcites [395] 395. Obarzanek E, Sacks FM, Vollmer WM, Bray GA, Miller ER 3rd, Lin PH, Karanja NM, Most-Windhauser MM, Moore TJ, Swain JF, Bales CW, Proschan MA; DASH Research Group. Effects on blood lipids of a blood pressure-lowering diet: the Dietary Approaches to Stop Hyper- tension (DASH) Trial. Am J Clin Nutr. 2001;74:80 -89. source
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In the paper
“The association of added sugars with increased obesity, T2DM, dental carries, and decreased diet quality is evident, which is part of the evidence base for recommendations made by other organizations to limit added sugars.409,410”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.2. Added Sugars
What the sources say
- Not checked yetcites [409] 409. Dietary Guidelines for Americans. 2005; 6th ed. US Department of Health and Human Services Web site. http://www.healthierus.gov/ dietaryguidelines. Accessed September 13, 2010.
- Not checked yetcites [410] 410. Nishida C, Uauy R, Kumanyika S, Shetty P. The joint WHO/FAO expert consultation on diet, nutrition and the prevention of chronic diseases: process, product and policy implications. Public Health Nutr. 2004;7: 245-250.
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In the paper
“Compared with a Western diet, the DASH diet reduced TC (Ϫ9.5%),LDL-C (Ϫ9.1%), and HDL-C (Ϫ9.2%) but did not adversely affect triglycerides.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
What the sources say
- Not checked yetcites [394] 394. Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N; DASH Collaborative Research Group. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med. 1997;336: 1117-1124. source
- Not checked yetcites [395] 395. Obarzanek E, Sacks FM, Vollmer WM, Bray GA, Miller ER 3rd, Lin PH, Karanja NM, Most-Windhauser MM, Moore TJ, Swain JF, Bales CW, Proschan MA; DASH Research Group. Effects on blood lipids of a blood pressure-lowering diet: the Dietary Approaches to Stop Hyper- tension (DASH) Trial. Am J Clin Nutr. 2001;74:80 -89. source
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In the paper
“Compared with baseline levels, triglyceride levels decreased significantly after the highunsaturated-fat and high-protein diets (Ϫ9.3 and Ϫ16.4 mg/dL, respectively) but not after the high-CHO diet (increase of 0.1 mg/dL).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
What the sources say
- Not checked yetcites [396] 396. Appel LJ, Sacks FM, Carey VJ, Obarzanek E, Swain JF, Miller ER 3rd, Conlin PR, Erlinger TP, Rosner BA, Laranjo NM, Charleston J, McCarron P, Bishop LM; OmniHeart Collaborative Research Group. Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial. JAMA. 2005;294:2455-2464. source
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In the paper
“With few exceptions, such as the Lyon Diet Heart Study, 403 which found no significant change in triglyceride levels on a MUFA-enriched versus low-fat, high-n-6 PUFA diet, implementation of a Mediterranean-style diet versus a low-fat diet is more commonly associated with an approximately 10% to 15% lowering of triglycerides and a reduced prevalence of hypertriglyceridemia.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.2. Mediterranean-Style Dietary Pattern Epidemiological and clinical trial evidence suggests that the Mediterranean-style dietary pattern 398,399 is associated with decreased triglyceride levels.In the Framingham Heart Study Offspring Cohort (nϭ2730), subjects in the highest quintile for Mediterranean-style dietary pattern score had the lowest triglyceride levels (103 versus 114 mg/dL, PϽ0.001) over a 7-year follow-up.398 Several clinical trials have reported beneficial effects of a Mediterranean-style diet on triglycerides compared with a lower-fat diet.Esposito et al 400 compared the effects of a Mediterranean-style diet with a control diet over a 2-year period on markers of CVD risk in patients (nϭ180) with MetS.The Mediterranean-style diet comprised more foods rich in MUFA, PUFA, and dietary fiber.Total fruit, vegetables, nuts, whole grains, and olive oil were higher in the intervention group.The intervention diet provided 28% of calories from total fat, with 8%, 12%, and 8% of calories from SFA, MUFA, and PUFA, respectively.The control diet provided 30% of calories from total fat, with 14%, 10%, and 7% of calories from SFA, MUFA, and PUFA, respectively.After 2 years, triglyceride levels decreased 12% in the intervention group (Pϭ0.001versus the control diet).In addition, subjects on the intervention diet decreased body weight by 6.2 lb or 2.8 kg (PϽ0.001) and waist circumference by 0.8 inches or 2 cm (Pϭ0.01)compared with the control group.Similarly, reduced triglyceride levels were reported in the Mediterranean Diet, Cardiovascular Risks and Gene Polymorphisms (Medi-RIVAGE) Study.401 Finally, the PREDIMED (Prevencio ´n con Dieta Mediterra ´nea) Study evaluated the effects of a Mediterranean diet plus virgin olive oil (1 L per week) and a Mediterranean diet plus mixed nuts (30 g/d; walnuts, hazelnuts, and almonds) versus a low-fat diet (control diet) in subjects (nϭ1224) at increased risk for CVD.402 Both Mediterranean-style diets provided higher energy intake from fat than the control diet (41% to 43% versus 38% of calories) and were higher in MUFA content (21% to 22% versus 19.4% of calories).After 1 year, hypertriglyceridemia was less prevalent in both Mediterranean-style diet groups (12.3% and 13.6%) than in those eating the control diet (21.3%).With few exceptions, such as the Lyon Diet Heart Study, 403 which found no significant change in triglyceride levels on a MUFA-enriched versus low-fat, high-n-6 PUFA diet, implementation of a Mediterranean-style diet versus a low-fat diet is more commonly associated with an approximately 10% to 15% lowering of triglycerides and a reduced prevalence of hypertriglyceridemia.
What the sources say
- Not checked yetcites [403] 403. de Lorgeril M, Salen P, Martin JL, Monjaud I, Delaye J, Mamelle N. Mediterranean diet, traditional risk factors, and the rate of cardiovascu- lar complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation. 1999;99:779 -785. source
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In the paper
“In terms of race/ethnicity, GL was positively associated with triglyceride levels in whites but not in blacks or Hispanics.417”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load
What the sources say
- Not checked yetcites [417] 417. Shikany JM, Tinker LF, Neuhouser ML, Ma Y, Patterson RE, Phillips LS, Liu S, Redden DT. Association of glycemic load with cardiovascu- lar disease risk factors: the Women's Health Initiative Observational Study. Nutrition. 2010;26:641-647.
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In the paper
“This discrepancy may reflect higher fiber intake (Ϸ30 g/d; DASH, OmniHeart), higher protein intake (Ͼ15% of energy; DASH, OmniHeart, WHI), or a combined effect.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
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In the paper
“In addition, subjects on the intervention diet decreased body weight by 6.2 lb or 2.8 kg (PϽ0.001) and waist circumference by 0.8 inches or 2 cm (Pϭ0.01)compared with the control group.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.2. Mediterranean-Style Dietary Pattern Epidemiological and clinical trial evidence suggests that the Mediterranean-style dietary pattern 398,399 is associated with decreased triglyceride levels.In the Framingham Heart Study Offspring Cohort (nϭ2730), subjects in the highest quintile for Mediterranean-style dietary pattern score had the lowest triglyceride levels (103 versus 114 mg/dL, PϽ0.001) over a 7-year follow-up.398 Several clinical trials have reported beneficial effects of a Mediterranean-style diet on triglycerides compared with a lower-fat diet.Esposito et al 400 compared the effects of a Mediterranean-style diet with a control diet over a 2-year period on markers of CVD risk in patients (nϭ180) with MetS.The Mediterranean-style diet comprised more foods rich in MUFA, PUFA, and dietary fiber.Total fruit, vegetables, nuts, whole grains, and olive oil were higher in the intervention group.The intervention diet provided 28% of calories from total fat, with 8%, 12%, and 8% of calories from SFA, MUFA, and PUFA, respectively.The control diet provided 30% of calories from total fat, with 14%, 10%, and 7% of calories from SFA, MUFA, and PUFA, respectively.After 2 years, triglyceride levels decreased 12% in the intervention group (Pϭ0.001versus the control diet).In addition, subjects on the intervention diet decreased body weight by 6.2 lb or 2.8 kg (PϽ0.001) and waist circumference by 0.8 inches or 2 cm (Pϭ0.01)compared with the control group.Similarly, reduced triglyceride levels were reported in the Mediterranean Diet, Cardiovascular Risks and Gene Polymorphisms (Medi-RIVAGE) Study.401 Finally, the PREDIMED (Prevencio ´n con Dieta Mediterra ´nea) Study evaluated the effects of a Mediterranean diet plus virgin olive oil (1 L per week) and a Mediterranean diet plus mixed nuts (30 g/d; walnuts, hazelnuts, and almonds) versus a low-fat diet (control diet) in subjects (nϭ1224) at increased risk for CVD.402 Both Mediterranean-style diets provided higher energy intake from fat than the control diet (41% to 43% versus 38% of calories) and were higher in MUFA content (21% to 22% versus 19.4% of calories).After 1 year, hypertriglyceridemia was less prevalent in both Mediterranean-style diet groups (12.3% and 13.6%) than in those eating the control diet (21.3%).With few exceptions, such as the Lyon Diet Heart Study, 403 which found no significant change in triglyceride levels on a MUFA-enriched versus low-fat, high-n-6 PUFA diet, implementation of a Mediterranean-style diet versus a low-fat diet is more commonly associated with an approximately 10% to 15% lowering of triglycerides and a reduced prevalence of hypertriglyceridemia.
What the sources say
- Not checked yetcites [400] 400. Esposito K, Marfella R, Ciotola M, Di Palo C, Giugliano F, Giugliano G, D'Armiento M, D'Andrea F, Giugliano D. Effect of a Mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. JAMA. 2004;292:1440 -1446. source
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In the paper
“In this analysis comparing low-fat, high-CHO diets versus higher-fat diets, for every 5% decrease in total fat, triglyceride level was predicted to increase by 6% and HDL-C to decrease by 2.2%.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
What the sources say
- Not checked yetcites [390] 390. Panel on Macronutrients, Panel on the Definition of Dietary Fiber, Subcommittee on Upper References Levels of Nutrients, Subcommittee on Interpretation and Uses of Dietary Reference Intakes, and the Standing Committee on the Scientific Evaluation of Dietary Ref- erence Intakes, Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. Washington, DC: National Academies Press; 2005. source
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In the paper
“very high intakes of carbohydrate (Ͼ60 percent of total calories) are accompanied by a reduction in HDL cholesterol and a rise in triglyceride”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein
What the sources say
- Not checked yetcites [221] 221. National Cholesterol Education Program (U.S.). Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III): Final Report. Washington, DC: National Institutes of Health, National Heart, Lung, and Blood Institute; 2002. NIH publication No. 02-5215.
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In the paper
“After 6 months, triglyceride levels were reduced the most in the low-CHO group (22%), but after 12 months, similar reductions were observed in both the low-CHO and Mediterranean-style groups, with minimal change in the low-fat group.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet
What the sources say
- Not checked yetcites [439] 439. Shai I, Schwarzfuchs D, Henkin Y, Shahar DR, Witkow S, Greenberg I, Golan R, Fraser D, Bolotin A, Vardi H, Tangi-Rozental O, Zuk-Ramot R, Sarusi B, Brickner D, Schwartz Z, Sheiner E, Marko R, Katorza E, Thiery J, Fiedler GM, Bluher M, Stumvoll M, Stampfer MJ; Dietary Intervention Randomized Controlled Trial (DIRECT) Group. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet [published correction appears in N Engl J Med. 2009;361:2681]. N Engl J Med. 2008;359:229 -241.
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In the paper
“These data support limiting fructose in men and women with borderline or elevated triglyceride levels (Figure 5).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose
What the sources say
- Not checked yetcites [428] 428. Livesey G, Taylor R. Fructose consumption and consequences for gly- cation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. Am J Clin Nutr. 2008; 88:1419 -1437.
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In the paper
“whereas in the Whitehall II Study, GI but not GL correlated with triglyceride levels.420”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load
What the sources say
- Not checked yetcites [420] 420. Mosdøl A, Witte DR, Frost G, Marmot MG, Brunner EJ. Dietary glycemic index and glycemic load are associated with high-density- lipoprotein cholesterol at baseline but not with increased risk of diabetes in the Whitehall II study. Am J Clin Nutr. 2007;86:988 -994.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In contrast to glucose metabolism, which is regulated in part by phosphofructokinase, fructose metabolism is relatively unregulated.425”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose
What the sources say
- Not checked yetcites [425] 425. Stanhope KL, Havel PJ. Endocrine and metabolic effects of consuming beverages sweetened with fructose, glucose, sucrose, or high-fructose corn syrup. Am J Clin Nutr. 2008;88:1733S-1737S. 426. 114. Putnam JJ, Allshouse JE. Food Consumption, Prices, and Expenditures, 1970 -97. Washington, DC: Food and Rural Economics Division, Economic Research Service, US Department of Agriculture; 1999. Sta- tistical Bulletin No. 965. source
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In the paper
“the Insulin Resistance Atherosclerosis Study 419 found GL but not GI to be positively associated with triglycerides”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load
What the sources say
- Not checked yetcites [419] 419. Liese AD, Gilliard T, Schulz M, D'Agostino RB Jr, Wolever TM. Carbohydrate nutrition, glycaemic load, and plasma lipids: the Insulin Resistance Atherosclerosis Study. Eur Heart J. 2007;28:80 -87. source
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In the paper
“Mechanistically, high CHO intake triggers pancreatic insulin release in response to increased blood glucose.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose
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In the paper
“Insulin, in turn, activates sterol regulatory element-binding protein, (SREBP-1c), a transcription factor that regulates fatty acid and triglyceride synthesis.430”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose
What the sources say
- Not checked yetcites [430] 430. Horton JD, Goldstein JL, Brown MS. SREBPs: activators of the complete program of cholesterol and fatty acid synthesis in the liver. J Clin Invest. 2002;109:1125-1131.
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In the paper
“In contrast, alcohol abuse may be associated with hypertriglyceridemia; nearly 1 in 5 hospitalized alcoholics have triglyceride levels exceeding 250 mg/dL.450”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.5. Alcohol
What the sources say
- Not checked yetcites [450] 450. Feinman L, Lieber CS. Ethanol and lipid metabolism. Am J Clin Nutr. 1999;70:791-792. source
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In the paper
“In the study by Gardner et al, 441 which compared the Atkins, Zone, LEARN (Lifestyle, Exercise, Attitudes, Relationships, and Nutrition) and Ornish diets, weight loss was greatest on the Atkins diet (4.7 kg) followed by LEARN (2.6 kg), Ornish (2.2 kg), and Zone (1.6 kg), with corresponding reductions in triglyceride levels (3% to 23%).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet
What the sources say
- Not checked yetcites [441] 441. Gardner CD, Kiazand A, Alhassan S, Kim S, Stafford RS, Balise RR, Kraemer HC, King AC. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial. JAMA. 2007;297:969 -977. source
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In the paper
“Fructose enhances lipogenesis and triglyceride synthesis.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose
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In the paper
“After 2 years, weight loss was similar in participants assigned to low and high protein (15% versus 25%), low and high fat (20% versus 40%), or low and high CHO (65% versus 35%).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet
What the sources say
- Not checked yetcites [433] 433. Sacks FM, Bray GA, Carey VJ, Smith SR, Ryan DH, Anton SD, McManus K, Champagne CM, Bishop LM, Laranjo N, Leboff MS, Rood JC, de Jonge L, Greenway FL, Loria CM, Obarzanek E, Wil- liamson DA. Comparison of weight-loss diets with different compo- sitions of fat, protein, and carbohydrates. N Engl J Med. 2009;360: 859 -873.
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In the paper
“Bonow and Eckel 434 concluded that low-CHO diets produced a more robust triglyceride-lowering effect than low-fat diets despite a similar magnitude of weight loss after 1 year.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet
What the sources say
- Not checked yetcites [434] 434. Bonow RO, Eckel RH. Diet, obesity, and cardiovascular risk. N Engl J Med. 2003;348:2057-2058. source
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In the paper
“In contrast, unsaturated fatty acids reduce or inhibit SREBP-1c transcription, thereby reducing hepatic fatty acid synthesis 430 and plasma triglycerides.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose
What the sources say
- Not checked yetcites [430] 430. Horton JD, Goldstein JL, Brown MS. SREBPs: activators of the complete program of cholesterol and fatty acid synthesis in the liver. J Clin Invest. 2002;109:1125-1131.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Although significant reductions in triglycerides occurred after 2 months on the Atkins and Zone diets, these effects were no longer significant after 12 months.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet
What the sources say
- Not checked yetcites [440] 440. Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ. Com- parison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial. JAMA. 2005;293:43-53. source
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In the paper
“Overall, exercise is most effective in lowering triglycerides (eg, 20% to 30%) when baseline levels are elevated (ie, Ͼ150 mg/dL), activity is moderate to intensive, and total caloric intake is reduced.481”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 14. Physical Activity and Hypertriglyceridemia
What the sources say
- Not checked yetcites [481] 481. Durstine JL, Grandjean PW, Cox CA, Thompson PD. Lipids, lipo- proteins, and exercise. J Cardiopulm Rehabil. 2002;22:385-398.
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In the paper
“Additional benefits of exercise include reduction in the ppTG response and attenuation of the triglyceride elevations observed after consumption of a lowfat, high-CHO diet.479”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 14. Physical Activity and Hypertriglyceridemia
What the sources say
- Not checked yetcites [479] 479. Gill JM, Hardman AE. Exercise and postprandial lipid metabolism: an update on potential mechanisms and interactions with high-carbohydrate diets (review). J Nutr Biochem. 2003;14:122-132.
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In the paper
“Because the amount needed for significant triglyceride lowering (2 to 4 g) is difficult to attain through diet alone on a daily basis, supplementation with capsules may be needed.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.6. Marine-Derived Omega-3 PUFA
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In the paper
“Dietary practices or factors that are associated with elevated triglyceride levels include excess body weight, especially visceral adiposity; simple CHOs, including added sugars and fructose; a high glycemic load; and alcohol.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.8. Dietary Summary
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In the paper
“Although statins have consistently shown benefit in subgroups with or without high triglyceride levels, fibrates have more commonly been shown to provide greater benefit in subgroups with increased triglyceride levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
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In the paper
“However, in LIPID, although baseline triglyceride level was not significantly associated with CVD risk in patients given placebo, each 89-mg/dL decrease in on-treatment triglyceride level in patients given pravastatin significantly decreased CVD risk by 11%, as well as by 14% after adjustment for nonlipid risk factors.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
What the sources say
- Not checked yetcites [500] 500. Simes RJ, Marschner IC, Hunt D, Colquhoun D, Sullivan D, Stewart RA, Hague W, Keech A, Thompson P, White H, Shaw J, Tonkin A; LIPID Study Investigators. Relationship between lipid levels and clinical outcomes in the Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) Trial: to what extent is the reduction in coronary events with pravastatin explained by on-study lipid levels? Circulation. 2002;105:1162-1169. source
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In the paper
“In a comprehensive review of human studies, Harris 454 reported that Ϸ4 g of marine-derived omega-3 PUFA per day decreased serum triglyceride concentrations by 25% to 30%, with accompanying increases of 5% to 10% in LDL-C and 1% to 3% in HDL-C.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.6. Marine-Derived Omega-3 PUFA
What the sources say
- Not checked yetcites [454] 454. Harris WS. n-3 Fatty acids and serum lipoproteins: human studies. Am J Clin Nutr. 1997;65(suppl):1645S-1654S. 455. 115. Balk E, Chung M, Lichtenstein A, Chew P, Kupelnick B, Lawrence A, DeVine D, Lau J. Effects of Omega-3 Fatty Acids on Cardiovascular Risk Factors and Intermediate Markers of Cardiovascular Disease. Evidence Report/Technology Assessment No. 93 (prepared by Tufts-New England Medical Center Evidence-Based Practice Center under contract No. 290-02-0022). AHRQ publication No. 04-E010-2. 116. Rockville, MD: Agency for Healthcare Research and Quality; 2004. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“On-treatment triglyceride level was not associated with CVD risk in AFCAPS/TexCAPS 499 and was not predictive of CVD event rate or risk reduction in VA-HIT.497”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
What the sources say
- Not checked yetcites [499] 499. Gotto AM Jr, Whitney E, Stein EA, Shapiro DR, Clearfield M, Weis S, Jou JY, Langendo ¨rfer A, Beere PA, Watson DJ, Downs JR, de Cani JS. Relation between baseline and on-treatment lipid parameters and first acute major coronary events in the Air Force/Texas Coronary Athero- sclerosis Prevention Study (AFCAPS/TexCAPS). Circulation. 2000; 101:477-484. source
- Not checked yetcites [497] 497. Robins SJ, Collins D, Wittes JT, Papademetriou V, Deedwania PC, Schaefer EJ, McNamara JR, Kashyap ML, Hershman JM, Wexler LF, Rubins HB; for the VA-HIT Study Group. Relation of gemfibrozil treatment and lipid levels with major coronary events: VA-HIT: a randomized controlled trial. JAMA. 2001;285:1585-1591. source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“The recent Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, which did not show an overall benefit for fibrate therapy added to statin therapy in T2DM, did show benefit in the subgroup with elevated triglyceride levels (Ͼ204 mg/dL) and low HDL-C (Ͻ34 mg/dL).498”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
What the sources say
- Not checked yetcites [498] 498. Ginsberg HN, Elam MB, Lovato LC, Crouse JR 3rd, Leiter LA, Linz P, Friedewald WT, Buse JB, Gerstein HC, Probstfield J, Grimm RH, Ismail-Beigi F, Bigger JT, Goff DC Jr, Cushman WC, Simons-Morton DG, Byington RP; ACCORD Study Group. Effects of combination lipid therapy in type 2 diabetes mellitus [published correction appears in N Engl J Med. 2010;362:1748]. 121. N Engl J Med. 2010;362:1563-1574.
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Although marine-derived omega-3 PUFA capsules have been shown to be free of contaminants, their clinical efficacy at high doses (2 to 4 g/d) has yet to be established.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.6. Marine-Derived Omega-3 PUFA
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
In the paper
“Moreover, in a study of 2906 middleaged men, moderately intensive activity (ie, jogging 10 miles weekly) versus no activity was associated with a 20% lower fasting triglyceride level; the highest activity level (Ͼ20 miles weekly) was also accompanied by the lowest mean fasting triglyceride level (86 mg/dL).475”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 14. Physical Activity and Hypertriglyceridemia
What the sources say
- Not checked yetcites [475] 475. Kokkinos PF, Holland JC, Narayan P, Colleran JA, Dotson CO, Papa- demetriou V. Miles run per week and high-density lipoprotein choles- terol levels in healthy, middle-aged men: a dose-response relationship. Arch Intern Med. 1995;155:415-420.
plaincorrelationaln = 2,906- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Individually, EPA or DHA may reduce triglyceride, 461 ppTG, 462 or CMR 463 levels.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.6. Marine-Derived Omega-3 PUFA
What the sources say
- Not checked yetcites [461] 461. Grimsgaard S, Bonaa KH, Hansen JB, Nordøy A. Highly purified eicosapentaenoic acid and docosahexaenoic acid in humans have similar triacylglycerol-lowering effects but divergent effects on serum fatty acids. Am J Clin Nutr. 1997;66:649 -659.
- Not checked yetcites [462] 462. Hansen JB, Grimsgaard S, Nilsen H, Nordøy A, Bønaa KH. Effects of highly purified eicosapentaenoic acid and docosahexaenoic acid on fatty acid absorption, incorporation into serum phospholipids and post- prandial triglyceridemia. Lipids. 1998;33:131-138. source
- Not checked yetcites [463] 463. Kelley DS, Siegel D, Vemuri M, Mackey BE. Docosahexaenoic acid supplementation improves fasting and postprandial lipid profiles in hypertriglyceridemic men. Am J Clin Nutr. 2007;86:324 -333. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The content of EPA/DHA per capsule is highly variable and ranges from 300 mg to Ϸ850 mg.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.6. Marine-Derived Omega-3 PUFA
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This scientific statement reviews the pivotal role of triglycerides in lipid metabolism and reaffirms that triglyceride is not directly atherogenic but represents an important biomarker of CVD risk because of its association with atherogenic remnant particles and apo CIII.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 17. Statement Summary and Recommendations This scientific statement reviews the pivotal role of triglycerides in lipid metabolism and reaffirms that triglyceride is not directly atherogenic but represents an important biomarker of CVD risk because of its association with atherogenic remnant particles and apo CIII.Although some familial disorders of triglyceride metabolism are associated with increased risk for pancreatitis when fasting triglyceride level exceeds 1000 mg/dL, others are associated with increased atherosclerotic risk.Moreover, IR, obesity, and sedentary lifestyle can all lead to or aggravate metabolic syndrome risk factors, which should urgently prompt clinicians to focus first on improving the patient's lifestyle.Knowledge of the metabolic pathways of triglyceride-rich particles and the consequences of hypertriglyceridemia is crucial in understanding the characteristic lipid alterations in DM, lipodystrophic disorders including those seen with HIV, and chronic renal disease.Measurements of non-HDL-C, apo B, or both may be especially useful in those with prominent triglyceride/ HDL abnormalities in which LDL-C measurements may underestimate true atherosclerotic vascular risk.This statement suggests the following new designations: (1) Optimal fasting triglyceride levels, defined as Ͻ100 mg/dL, as a parameter of metabolic health, and (2) nonfasting triglyceride levels, to screen for those with high fasting triglyceride levels.A suggested practical algorithm for screening and management of elevated triglyceride levels is outlined in Figure 5.A nonfasting level of Ͻ200 mg/dL is commensurate with a normal (Ͻ150 mg/dL) or optimal (Ͻ100 mg/dL) fasting triglyceride level and requires no further testing.Fasting samples are used to designate borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), and very high (Ն500 mg/dL) triglyceride levels.Nonfasting triglyceride levels are not used in the definition of MetS and should not be used in the calculation of LDL-C by the Friedewald formula. Overall, the treatment of elevated triglyceride levels focuses on intensive therapeutic lifestyle change.For example, a 5% to 10% reduction in body weight anticipates a triglyceride-lowering response of 20%.Further offsets in CHO calories by reducing added sugars and fructose while increasing unsaturated fat intake may contribute an additional 10% to 20% reduction in triglyceride levels.Elimination of trans fats, restriction of SFA, 524 -527 and increasing consumption of marine-based omega-3 products, coupled with aerobic activity, will further optimize triglyceride-lowering efforts.Taken together, reductions of 50% or more in triglyceride levels may be attained through intensive therapeutic lifestyle change. In subjects with very high triglyceride levels or a history of triglyceride-induced pancreatitis, additional dietary considerations include complete abstinence from alcohol, the nutrition practices listed above, the possible use of MCTs 528 and pharmacological therapies (see also Tables 11 and 12).The subject of medication and triglycerides is still lacking crucial clinical trial evidence.Nonetheless, several points should be made.First, clinicians should rule out medications as a potential cause of an elevated triglyceride value.For example, hormone therapy (Table 5) can greatly influence triglyceride levels; in women of reproductive age who develop hypertriglyceridemia while taking oral contraceptive therapy, lower estrogen-containing preparations or other forms of contraception should be considered.For postmenopausal women with hypertriglyceridemia who require postmenopausal hormone preparations, switching to transdermal preparations may blunt the triglyceride increases observed with oral compounds.Second, utilizing triglyceride-lowering medications to prevent pancreatitis in those with triglyceride levels Ͼ500 mg/dL is reasonable in addition to intensive therapeutic lifestyle change.In those with a history of triglyceride-induced pancreatitis, it is especially important to keep triglyceride levels well controlled, and this will require both lifestyle and pharmacological approaches.What remains to be established is whether these modalities favorably influence CVD outcomes beyond proven therapies (eg, statins).Therefore, additional clinical outcome trials are necessary. None Abbott*; Merck/ Schering-Plough*; Sanofi*; Sanofi-Aventis* None None Abbott*; Genzyme-ISIS*; Merck*; Roche*; Sanofi-Aventis* None William James Howard Washington Hospital Center AstraZeneca*; Pfizer* None Abbott*; Merck †; Pfizer*; Sankyo*; Schering-Plough † None None None None Marc S. Jacobson Private practice Merck (formerly Schering-Plough) † None None None None None None Terry A. Lennie University of Kentucky None None None None None None None Moshe Levi University of Colorado Abbott*; Genzyme*; Intercept Pharmaceuticals* None None None None None None
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Elimination of trans fats, restriction of SFA, 524 -527 and increasing consumption of marine-based omega-3 products, coupled with aerobic activity, will further optimize triglyceride-lowering efforts.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 17. Statement Summary and Recommendations This scientific statement reviews the pivotal role of triglycerides in lipid metabolism and reaffirms that triglyceride is not directly atherogenic but represents an important biomarker of CVD risk because of its association with atherogenic remnant particles and apo CIII.Although some familial disorders of triglyceride metabolism are associated with increased risk for pancreatitis when fasting triglyceride level exceeds 1000 mg/dL, others are associated with increased atherosclerotic risk.Moreover, IR, obesity, and sedentary lifestyle can all lead to or aggravate metabolic syndrome risk factors, which should urgently prompt clinicians to focus first on improving the patient's lifestyle.Knowledge of the metabolic pathways of triglyceride-rich particles and the consequences of hypertriglyceridemia is crucial in understanding the characteristic lipid alterations in DM, lipodystrophic disorders including those seen with HIV, and chronic renal disease.Measurements of non-HDL-C, apo B, or both may be especially useful in those with prominent triglyceride/ HDL abnormalities in which LDL-C measurements may underestimate true atherosclerotic vascular risk.This statement suggests the following new designations: (1) Optimal fasting triglyceride levels, defined as Ͻ100 mg/dL, as a parameter of metabolic health, and (2) nonfasting triglyceride levels, to screen for those with high fasting triglyceride levels.A suggested practical algorithm for screening and management of elevated triglyceride levels is outlined in Figure 5.A nonfasting level of Ͻ200 mg/dL is commensurate with a normal (Ͻ150 mg/dL) or optimal (Ͻ100 mg/dL) fasting triglyceride level and requires no further testing.Fasting samples are used to designate borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), and very high (Ն500 mg/dL) triglyceride levels.Nonfasting triglyceride levels are not used in the definition of MetS and should not be used in the calculation of LDL-C by the Friedewald formula. Overall, the treatment of elevated triglyceride levels focuses on intensive therapeutic lifestyle change.For example, a 5% to 10% reduction in body weight anticipates a triglyceride-lowering response of 20%.Further offsets in CHO calories by reducing added sugars and fructose while increasing unsaturated fat intake may contribute an additional 10% to 20% reduction in triglyceride levels.Elimination of trans fats, restriction of SFA, 524 -527 and increasing consumption of marine-based omega-3 products, coupled with aerobic activity, will further optimize triglyceride-lowering efforts.Taken together, reductions of 50% or more in triglyceride levels may be attained through intensive therapeutic lifestyle change. In subjects with very high triglyceride levels or a history of triglyceride-induced pancreatitis, additional dietary considerations include complete abstinence from alcohol, the nutrition practices listed above, the possible use of MCTs 528 and pharmacological therapies (see also Tables 11 and 12).The subject of medication and triglycerides is still lacking crucial clinical trial evidence.Nonetheless, several points should be made.First, clinicians should rule out medications as a potential cause of an elevated triglyceride value.For example, hormone therapy (Table 5) can greatly influence triglyceride levels; in women of reproductive age who develop hypertriglyceridemia while taking oral contraceptive therapy, lower estrogen-containing preparations or other forms of contraception should be considered.For postmenopausal women with hypertriglyceridemia who require postmenopausal hormone preparations, switching to transdermal preparations may blunt the triglyceride increases observed with oral compounds.Second, utilizing triglyceride-lowering medications to prevent pancreatitis in those with triglyceride levels Ͼ500 mg/dL is reasonable in addition to intensive therapeutic lifestyle change.In those with a history of triglyceride-induced pancreatitis, it is especially important to keep triglyceride levels well controlled, and this will require both lifestyle and pharmacological approaches.What remains to be established is whether these modalities favorably influence CVD outcomes beyond proven therapies (eg, statins).Therefore, additional clinical outcome trials are necessary. None Abbott*; Merck/ Schering-Plough*; Sanofi*; Sanofi-Aventis* None None Abbott*; Genzyme-ISIS*; Merck*; Roche*; Sanofi-Aventis* None William James Howard Washington Hospital Center AstraZeneca*; Pfizer* None Abbott*; Merck †; Pfizer*; Sankyo*; Schering-Plough † None None None None Marc S. Jacobson Private practice Merck (formerly Schering-Plough) † None None None None None None Terry A. Lennie University of Kentucky None None None None None None None Moshe Levi University of Colorado Abbott*; Genzyme*; Intercept Pharmaceuticals* None None None None None None
What the sources say
- Not checked yetcites [524] 524. Watts GF, Lewis B, Brunt JN, Lewis ES, Coltart DJ, Smith LD, Mann JI, Swan AV. Effects on coronary artery disease of lipid-lowering diet, or diet plus cholestyramine, in the St Thomas' Atherosclerosis Regression Study (STARS). Lancet. 1992;339:563-569.
- Not checked yetcites [525] 525. Miller M. Hold the patty, not the lettuce: processing foods for over a quarter century in the Nurses' Health Study. Circulation. 2010;122: 859 -860. Letter.
- Not checked yetcites [526] 526. Bernstein AM SQ, Hu FB, Stampfer MJ, Manson JE, Willet WC. Major dietary protein sources and risk of coronary heart disease in women. Circulation. 2010;122:876 -883.
- Not checked yetcites [527] 527. Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010;7:e1000252. 528. 123. Hauenschild A, Bretzel RG, Schnell-Kretschmer H, Kloer HU, Hardt PD, Ewald N. Successful treatment of severe hypertriglyceridemia with a formula diet rich in omega-3 fatty acids and medium-chain triglycer- ides. Ann Nutr Metab. 2010;56:170 -175. 124. KEY WORDS: AHA Scientific Statements Ⅲ triglycerides Ⅲ atherosclerosis Ⅲ diabetes mellitus Ⅲ epidemiology
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
In the paper
“As noted above, the ACCORD trial 498 did not find that fibrate therapy added to statin reduced cardiovascular events in DM patients (median triglyceride level of 162 mg/dL) except in the subgroup in the upper triglyceride tertile and lowest HDL-C tertile (Pϭ0.06).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3. Do patients with elevated triglyceride levels while undergoing statin therapy receive additional cardiovascular risk reduction by the addition of a second drug that targets triglycerides or TRL? In the Japan EPA Lipid Intervention Study (JELIS), in which patients received a statin plus either EPA or a placebo, CVD risk reduction with combination therapy was not statistically significant in either baseline triglyceride subgroup (Ͻ151 or Ն151 mg/dL).502 However, subgroup analysis of primary prevention patients in JELIS (80% of the study population) indicated that patients with baseline triglyceride levels at or exceeding 150 mg/dL and HDL-C Ͻ40 mg/dL had significantly increased CVD risk.Moreover, combination therapy with statin plus EPA in this high-risk subgroup reduced CVD risk by 53% compared with statin monotherapy, 503 even though the dose of EPA (up to 1.8 g/d) translated into minimal triglyceride reduction (5% between groups).Consequently, the cardiovascular benefit in JELIS was not a primary triglyceride-mediated effect.Trials that used statin plus niacin (or in some cases bile acid resin) combination therapy have shown a reduction in coronary arteriographic progression and regression, as well as regression of carotid artery intima-media thickness.504,505 Reduction in CVD outcomes were observed in several of these studies, although event rates were low, a statin placebo group was not used, and the studies were neither powered nor prespecified to address CVD events as a primary outcome measure.Nevertheless, they set the stage for the statin-niacin outcome trials listed below. Unfortunately, there are limited data on the potential benefit of adding a second drug in high-risk patients treated with a statin who continue to have high triglyceride levels.As noted above, the ACCORD trial 498 did not find that fibrate therapy added to statin reduced cardiovascular events in DM patients (median triglyceride level of 162 mg/dL) except in the subgroup in the upper triglyceride tertile and lowest HDL-C tertile (Pϭ0.06).Although ongoing clinical trials are not specifically designed to examine this issue, secondary analyses of the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes (AIM-HIGH), 506
What the sources say
- Not checked yetcites [498] 498. Ginsberg HN, Elam MB, Lovato LC, Crouse JR 3rd, Leiter LA, Linz P, Friedewald WT, Buse JB, Gerstein HC, Probstfield J, Grimm RH, Ismail-Beigi F, Bigger JT, Goff DC Jr, Cushman WC, Simons-Morton DG, Byington RP; ACCORD Study Group. Effects of combination lipid therapy in type 2 diabetes mellitus [published correction appears in N Engl J Med. 2010;362:1748]. 121. N Engl J Med. 2010;362:1563-1574.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Prototypical pilot studies demonstrate a greater understanding of healthy food choices, which in turn may also improve academic performance.518,519”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > High Triglyceride Levels The rise in triglyceride levels coinciding with the current epidemic of juvenile obesity, IR, and DM 509 -511 has created new opportunities for establishing and disseminating CVD health promotion efforts aimed at maximizing primordial prevention.For example, resolutions have now been adopted in all 50 states targeting obesity, including the elimination of high caloric sugared sodas and trans fatty acid products from public school vending machines and increasing the number of walking and bicycle paths.512,513 Initiatives such as reducing access to low-nutrient, energy-dense foods in school cafeterias serve as other adjunctive measures for controlling high triglyceride and obesity rates.514 Among the most comprehensive national programs has been Healthy People 2010, the initiative established by the Centers for Disease Control and Prevention in 1998 for health promotion and disease prevention.515 The principal objectives are to improve the quality of healthy living and eliminate health disparities through interventions aimed at heart disease and stroke prevention.515,516 In addition to community-based outreach programs, nutrition education beginning in elementary school may yield considerable dividends toward reducing obesity rates, because dietary behaviors are often established in childhood.517 Prototypical pilot studies demonstrate a greater understanding of healthy food choices, which in turn may also improve academic performance.518,519 Strategies to attenuate hypertriglyceridemia and its associated metabolic complications include increasing physical activity during school and afterschool sessions, 520,521 incentivizing schools committed to fostering nutrition education, 522 and offering a variety of fresh fruits and vegetables daily to school cafeterias.523 Overall, identification of the most successful pilot programs for implementation on a national level will require coordinated efforts by clinicians, policymakers, and advocacy groups focused on reducing hypertriglyceridemia, obesity, and IR through a greater emphasis on and implementation of intensive lifestyle interventions.
What the sources say
- Not checked yetcites [518] 518. DeVault N, Kennedy T, Hermann J, Mwavita M, Rask P, Jaworsky A. It's all about kids: preventing overweight in elementary school children in Tulsa, OK. J Am Diet Assoc. 2009;109:680 -687.
- Not checked yetcites [519] 519. Shilts MK, Lamp C, Horowitz M, Townsend MS. Pilot study: EatFit impacts sixth graders' academic performance on achievement of math- ematics and English education standards. J Nutr Educ Behav. 2009;41: 127-131.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The principal objectives are to improve the quality of healthy living and eliminate health disparities through interventions aimed at heart disease and stroke prevention.515,516”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > High Triglyceride Levels The rise in triglyceride levels coinciding with the current epidemic of juvenile obesity, IR, and DM 509 -511 has created new opportunities for establishing and disseminating CVD health promotion efforts aimed at maximizing primordial prevention.For example, resolutions have now been adopted in all 50 states targeting obesity, including the elimination of high caloric sugared sodas and trans fatty acid products from public school vending machines and increasing the number of walking and bicycle paths.512,513 Initiatives such as reducing access to low-nutrient, energy-dense foods in school cafeterias serve as other adjunctive measures for controlling high triglyceride and obesity rates.514 Among the most comprehensive national programs has been Healthy People 2010, the initiative established by the Centers for Disease Control and Prevention in 1998 for health promotion and disease prevention.515 The principal objectives are to improve the quality of healthy living and eliminate health disparities through interventions aimed at heart disease and stroke prevention.515,516 In addition to community-based outreach programs, nutrition education beginning in elementary school may yield considerable dividends toward reducing obesity rates, because dietary behaviors are often established in childhood.517 Prototypical pilot studies demonstrate a greater understanding of healthy food choices, which in turn may also improve academic performance.518,519 Strategies to attenuate hypertriglyceridemia and its associated metabolic complications include increasing physical activity during school and afterschool sessions, 520,521 incentivizing schools committed to fostering nutrition education, 522 and offering a variety of fresh fruits and vegetables daily to school cafeterias.523 Overall, identification of the most successful pilot programs for implementation on a national level will require coordinated efforts by clinicians, policymakers, and advocacy groups focused on reducing hypertriglyceridemia, obesity, and IR through a greater emphasis on and implementation of intensive lifestyle interventions.
What the sources say
- Not checked yetcites [515] 515. Labarthe DR. Heart-healthy and stroke-free, 2008. Prev Chronic Dis. 2008;5:A32. source
- Not checked yetcites [516] 516. Veazie MA, Galloway JM, Matson-Koffman D, LaBarthe DR, Brownstein JN, Emr M, Bolton E, Freund E Jr, Fulwood R, Guyton- Krishnan J, Hong Y, Lebowitz M, Ochiai E, Schoeberl M, Robertson RM. Taking the initiative: implementing the American Heart Asso- ciation Guide for Improving Cardiovascular Health at the Community Level: Healthy People 2010 Heart Disease and Stroke Partnership Community Guideline Implementation and Best Practices Workgroup. Circulation. 2005;112:2538 -2554. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Among the most comprehensive national programs has been Healthy People 2010, the initiative established by the Centers for Disease Control and Prevention in 1998 for health promotion and disease prevention.515”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > High Triglyceride Levels The rise in triglyceride levels coinciding with the current epidemic of juvenile obesity, IR, and DM 509 -511 has created new opportunities for establishing and disseminating CVD health promotion efforts aimed at maximizing primordial prevention.For example, resolutions have now been adopted in all 50 states targeting obesity, including the elimination of high caloric sugared sodas and trans fatty acid products from public school vending machines and increasing the number of walking and bicycle paths.512,513 Initiatives such as reducing access to low-nutrient, energy-dense foods in school cafeterias serve as other adjunctive measures for controlling high triglyceride and obesity rates.514 Among the most comprehensive national programs has been Healthy People 2010, the initiative established by the Centers for Disease Control and Prevention in 1998 for health promotion and disease prevention.515 The principal objectives are to improve the quality of healthy living and eliminate health disparities through interventions aimed at heart disease and stroke prevention.515,516 In addition to community-based outreach programs, nutrition education beginning in elementary school may yield considerable dividends toward reducing obesity rates, because dietary behaviors are often established in childhood.517 Prototypical pilot studies demonstrate a greater understanding of healthy food choices, which in turn may also improve academic performance.518,519 Strategies to attenuate hypertriglyceridemia and its associated metabolic complications include increasing physical activity during school and afterschool sessions, 520,521 incentivizing schools committed to fostering nutrition education, 522 and offering a variety of fresh fruits and vegetables daily to school cafeterias.523 Overall, identification of the most successful pilot programs for implementation on a national level will require coordinated efforts by clinicians, policymakers, and advocacy groups focused on reducing hypertriglyceridemia, obesity, and IR through a greater emphasis on and implementation of intensive lifestyle interventions.
What the sources say
- Not checked yetcites [515] 515. Labarthe DR. Heart-healthy and stroke-free, 2008. Prev Chronic Dis. 2008;5:A32. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Trials that used statin plus niacin (or in some cases bile acid resin) combination therapy have shown a reduction in coronary arteriographic progression and regression, as well as regression of carotid artery intima-media thickness.504,505”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3. Do patients with elevated triglyceride levels while undergoing statin therapy receive additional cardiovascular risk reduction by the addition of a second drug that targets triglycerides or TRL? In the Japan EPA Lipid Intervention Study (JELIS), in which patients received a statin plus either EPA or a placebo, CVD risk reduction with combination therapy was not statistically significant in either baseline triglyceride subgroup (Ͻ151 or Ն151 mg/dL).502 However, subgroup analysis of primary prevention patients in JELIS (80% of the study population) indicated that patients with baseline triglyceride levels at or exceeding 150 mg/dL and HDL-C Ͻ40 mg/dL had significantly increased CVD risk.Moreover, combination therapy with statin plus EPA in this high-risk subgroup reduced CVD risk by 53% compared with statin monotherapy, 503 even though the dose of EPA (up to 1.8 g/d) translated into minimal triglyceride reduction (5% between groups).Consequently, the cardiovascular benefit in JELIS was not a primary triglyceride-mediated effect.Trials that used statin plus niacin (or in some cases bile acid resin) combination therapy have shown a reduction in coronary arteriographic progression and regression, as well as regression of carotid artery intima-media thickness.504,505 Reduction in CVD outcomes were observed in several of these studies, although event rates were low, a statin placebo group was not used, and the studies were neither powered nor prespecified to address CVD events as a primary outcome measure.Nevertheless, they set the stage for the statin-niacin outcome trials listed below. Unfortunately, there are limited data on the potential benefit of adding a second drug in high-risk patients treated with a statin who continue to have high triglyceride levels.As noted above, the ACCORD trial 498 did not find that fibrate therapy added to statin reduced cardiovascular events in DM patients (median triglyceride level of 162 mg/dL) except in the subgroup in the upper triglyceride tertile and lowest HDL-C tertile (Pϭ0.06).Although ongoing clinical trials are not specifically designed to examine this issue, secondary analyses of the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes (AIM-HIGH), 506
What the sources say
- Not checked yetcites [504] 504. Brown B, Canner PL, McGovern ME, Guyton JR, Carlson LA. Nicotinic acid. In: Ballantyne C, ed. Clinical Lipidology, A Companion to Braun- wald's Heart Disease. Philadelphia, PA: Saunders; 2009:298 -314.
- Not checked yetcites [505] 505. Taylor AJ, Villines TC, Stanek EJ, Devine PJ, Griffen L, Miller M, Weissman NJ, Turco M. Extended-release niacin or ezetimibe and carotid intima-media thickness. N Engl J Med. 2009;361:2113-2122.
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“However, the lipid-related parameters most strongly associated with CVD risk in LIPID were apo B, LDL-C, and the ratio of TC to HDL-C.500”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
What the sources say
- Not checked yetcites [500] 500. Simes RJ, Marschner IC, Hunt D, Colquhoun D, Sullivan D, Stewart RA, Hague W, Keech A, Thompson P, White H, Shaw J, Tonkin A; LIPID Study Investigators. Relationship between lipid levels and clinical outcomes in the Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) Trial: to what extent is the reduction in coronary events with pravastatin explained by on-study lipid levels? Circulation. 2002;105:1162-1169. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In addition to community-based outreach programs, nutrition education beginning in elementary school may yield considerable dividends toward reducing obesity rates, because dietary behaviors are often established in childhood.517”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > High Triglyceride Levels The rise in triglyceride levels coinciding with the current epidemic of juvenile obesity, IR, and DM 509 -511 has created new opportunities for establishing and disseminating CVD health promotion efforts aimed at maximizing primordial prevention.For example, resolutions have now been adopted in all 50 states targeting obesity, including the elimination of high caloric sugared sodas and trans fatty acid products from public school vending machines and increasing the number of walking and bicycle paths.512,513 Initiatives such as reducing access to low-nutrient, energy-dense foods in school cafeterias serve as other adjunctive measures for controlling high triglyceride and obesity rates.514 Among the most comprehensive national programs has been Healthy People 2010, the initiative established by the Centers for Disease Control and Prevention in 1998 for health promotion and disease prevention.515 The principal objectives are to improve the quality of healthy living and eliminate health disparities through interventions aimed at heart disease and stroke prevention.515,516 In addition to community-based outreach programs, nutrition education beginning in elementary school may yield considerable dividends toward reducing obesity rates, because dietary behaviors are often established in childhood.517 Prototypical pilot studies demonstrate a greater understanding of healthy food choices, which in turn may also improve academic performance.518,519 Strategies to attenuate hypertriglyceridemia and its associated metabolic complications include increasing physical activity during school and afterschool sessions, 520,521 incentivizing schools committed to fostering nutrition education, 522 and offering a variety of fresh fruits and vegetables daily to school cafeterias.523 Overall, identification of the most successful pilot programs for implementation on a national level will require coordinated efforts by clinicians, policymakers, and advocacy groups focused on reducing hypertriglyceridemia, obesity, and IR through a greater emphasis on and implementation of intensive lifestyle interventions.
What the sources say
- Not checked yetcites [517] 517. Strauss R. Childhood obesity. Curr Probl Pediatr. 1999;29:1-29.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Moreover, IR, obesity, and sedentary lifestyle can all lead to or aggravate metabolic syndrome risk factors”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 17. Statement Summary and Recommendations This scientific statement reviews the pivotal role of triglycerides in lipid metabolism and reaffirms that triglyceride is not directly atherogenic but represents an important biomarker of CVD risk because of its association with atherogenic remnant particles and apo CIII.Although some familial disorders of triglyceride metabolism are associated with increased risk for pancreatitis when fasting triglyceride level exceeds 1000 mg/dL, others are associated with increased atherosclerotic risk.Moreover, IR, obesity, and sedentary lifestyle can all lead to or aggravate metabolic syndrome risk factors, which should urgently prompt clinicians to focus first on improving the patient's lifestyle.Knowledge of the metabolic pathways of triglyceride-rich particles and the consequences of hypertriglyceridemia is crucial in understanding the characteristic lipid alterations in DM, lipodystrophic disorders including those seen with HIV, and chronic renal disease.Measurements of non-HDL-C, apo B, or both may be especially useful in those with prominent triglyceride/ HDL abnormalities in which LDL-C measurements may underestimate true atherosclerotic vascular risk.This statement suggests the following new designations: (1) Optimal fasting triglyceride levels, defined as Ͻ100 mg/dL, as a parameter of metabolic health, and (2) nonfasting triglyceride levels, to screen for those with high fasting triglyceride levels.A suggested practical algorithm for screening and management of elevated triglyceride levels is outlined in Figure 5.A nonfasting level of Ͻ200 mg/dL is commensurate with a normal (Ͻ150 mg/dL) or optimal (Ͻ100 mg/dL) fasting triglyceride level and requires no further testing.Fasting samples are used to designate borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), and very high (Ն500 mg/dL) triglyceride levels.Nonfasting triglyceride levels are not used in the definition of MetS and should not be used in the calculation of LDL-C by the Friedewald formula. Overall, the treatment of elevated triglyceride levels focuses on intensive therapeutic lifestyle change.For example, a 5% to 10% reduction in body weight anticipates a triglyceride-lowering response of 20%.Further offsets in CHO calories by reducing added sugars and fructose while increasing unsaturated fat intake may contribute an additional 10% to 20% reduction in triglyceride levels.Elimination of trans fats, restriction of SFA, 524 -527 and increasing consumption of marine-based omega-3 products, coupled with aerobic activity, will further optimize triglyceride-lowering efforts.Taken together, reductions of 50% or more in triglyceride levels may be attained through intensive therapeutic lifestyle change. In subjects with very high triglyceride levels or a history of triglyceride-induced pancreatitis, additional dietary considerations include complete abstinence from alcohol, the nutrition practices listed above, the possible use of MCTs 528 and pharmacological therapies (see also Tables 11 and 12).The subject of medication and triglycerides is still lacking crucial clinical trial evidence.Nonetheless, several points should be made.First, clinicians should rule out medications as a potential cause of an elevated triglyceride value.For example, hormone therapy (Table 5) can greatly influence triglyceride levels; in women of reproductive age who develop hypertriglyceridemia while taking oral contraceptive therapy, lower estrogen-containing preparations or other forms of contraception should be considered.For postmenopausal women with hypertriglyceridemia who require postmenopausal hormone preparations, switching to transdermal preparations may blunt the triglyceride increases observed with oral compounds.Second, utilizing triglyceride-lowering medications to prevent pancreatitis in those with triglyceride levels Ͼ500 mg/dL is reasonable in addition to intensive therapeutic lifestyle change.In those with a history of triglyceride-induced pancreatitis, it is especially important to keep triglyceride levels well controlled, and this will require both lifestyle and pharmacological approaches.What remains to be established is whether these modalities favorably influence CVD outcomes beyond proven therapies (eg, statins).Therefore, additional clinical outcome trials are necessary. None Abbott*; Merck/ Schering-Plough*; Sanofi*; Sanofi-Aventis* None None Abbott*; Genzyme-ISIS*; Merck*; Roche*; Sanofi-Aventis* None William James Howard Washington Hospital Center AstraZeneca*; Pfizer* None Abbott*; Merck †; Pfizer*; Sankyo*; Schering-Plough † None None None None Marc S. Jacobson Private practice Merck (formerly Schering-Plough) † None None None None None None Terry A. Lennie University of Kentucky None None None None None None None Moshe Levi University of Colorado Abbott*; Genzyme*; Intercept Pharmaceuticals* None None None None None None
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
In the paper
“However, additional adjustment for HDL-C and the ratio of apo B to apo AI decreased the predictive ability of on-treatment triglyceride levels, and further adjustment for baseline glucose, BMI, hypertension, T2DM, and smoking eliminated the association.501”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
What the sources say
- Not checked yetcites [501] 501. Faergeman O, Holme I, Fayyad R, Bhatia S, Grundy SM, Kastelein JJ, LaRosa JC, Larsen ML, Lindahl C, Olsson AG, Tikkanen MJ, Waters DD, Pedersen TR; Steering Committees of IDEAL and TNT Trials. Plasma triglycerides and cardiovascular events in the Treating to New Targets and Incremental Decrease in End-Points through Aggressive Lipid Lowering trials of statins in patients with coronary artery disease. Am J Cardiol. 2009;104:459 -463. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“For example, resolutions have now been adopted in all 50 states targeting obesity, including the elimination of high caloric sugared sodas and trans fatty acid products from public school vending machines and increasing the number of walking and bicycle paths.512,513”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > High Triglyceride Levels The rise in triglyceride levels coinciding with the current epidemic of juvenile obesity, IR, and DM 509 -511 has created new opportunities for establishing and disseminating CVD health promotion efforts aimed at maximizing primordial prevention.For example, resolutions have now been adopted in all 50 states targeting obesity, including the elimination of high caloric sugared sodas and trans fatty acid products from public school vending machines and increasing the number of walking and bicycle paths.512,513 Initiatives such as reducing access to low-nutrient, energy-dense foods in school cafeterias serve as other adjunctive measures for controlling high triglyceride and obesity rates.514 Among the most comprehensive national programs has been Healthy People 2010, the initiative established by the Centers for Disease Control and Prevention in 1998 for health promotion and disease prevention.515 The principal objectives are to improve the quality of healthy living and eliminate health disparities through interventions aimed at heart disease and stroke prevention.515,516 In addition to community-based outreach programs, nutrition education beginning in elementary school may yield considerable dividends toward reducing obesity rates, because dietary behaviors are often established in childhood.517 Prototypical pilot studies demonstrate a greater understanding of healthy food choices, which in turn may also improve academic performance.518,519 Strategies to attenuate hypertriglyceridemia and its associated metabolic complications include increasing physical activity during school and afterschool sessions, 520,521 incentivizing schools committed to fostering nutrition education, 522 and offering a variety of fresh fruits and vegetables daily to school cafeterias.523 Overall, identification of the most successful pilot programs for implementation on a national level will require coordinated efforts by clinicians, policymakers, and advocacy groups focused on reducing hypertriglyceridemia, obesity, and IR through a greater emphasis on and implementation of intensive lifestyle interventions.
What the sources say
- Not checked yetcites [512] 512. Boehmer TK, Brownson RC, Haire-Joshu D, Dreisinger ML. Patterns of childhood obesity prevention legislation in the United States. Prev Chronic Dis. 2007;4:A56.
- Not checked yetcites [513] 513. Greves HM, Rivara FP. Report card on school snack food policies among the United States' largest school districts in 2004 -2005: room for improvement. Int J Behav Nutr Phys Act. 2006;3:1. 514. 122. Fox MK, Dodd AH, Wilson A, Gleason PM. Association between school food environment and practices and body mass index of US public school children. J Am Diet Assoc. 2009;109(suppl):S108 -S117.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Initiatives such as reducing access to low-nutrient, energy-dense foods in school cafeterias serve as other adjunctive measures for controlling high triglyceride and obesity rates.514”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > High Triglyceride Levels The rise in triglyceride levels coinciding with the current epidemic of juvenile obesity, IR, and DM 509 -511 has created new opportunities for establishing and disseminating CVD health promotion efforts aimed at maximizing primordial prevention.For example, resolutions have now been adopted in all 50 states targeting obesity, including the elimination of high caloric sugared sodas and trans fatty acid products from public school vending machines and increasing the number of walking and bicycle paths.512,513 Initiatives such as reducing access to low-nutrient, energy-dense foods in school cafeterias serve as other adjunctive measures for controlling high triglyceride and obesity rates.514 Among the most comprehensive national programs has been Healthy People 2010, the initiative established by the Centers for Disease Control and Prevention in 1998 for health promotion and disease prevention.515 The principal objectives are to improve the quality of healthy living and eliminate health disparities through interventions aimed at heart disease and stroke prevention.515,516 In addition to community-based outreach programs, nutrition education beginning in elementary school may yield considerable dividends toward reducing obesity rates, because dietary behaviors are often established in childhood.517 Prototypical pilot studies demonstrate a greater understanding of healthy food choices, which in turn may also improve academic performance.518,519 Strategies to attenuate hypertriglyceridemia and its associated metabolic complications include increasing physical activity during school and afterschool sessions, 520,521 incentivizing schools committed to fostering nutrition education, 522 and offering a variety of fresh fruits and vegetables daily to school cafeterias.523 Overall, identification of the most successful pilot programs for implementation on a national level will require coordinated efforts by clinicians, policymakers, and advocacy groups focused on reducing hypertriglyceridemia, obesity, and IR through a greater emphasis on and implementation of intensive lifestyle interventions.
What the sources say
- Not checked yetcites [514] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Moreover, combination therapy with statin plus EPA in this high-risk subgroup reduced CVD risk by 53% compared with statin monotherapy, 503 even though the dose of EPA (up to 1.8 g/d) translated into minimal triglyceride reduction (5% between groups).”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3. Do patients with elevated triglyceride levels while undergoing statin therapy receive additional cardiovascular risk reduction by the addition of a second drug that targets triglycerides or TRL? In the Japan EPA Lipid Intervention Study (JELIS), in which patients received a statin plus either EPA or a placebo, CVD risk reduction with combination therapy was not statistically significant in either baseline triglyceride subgroup (Ͻ151 or Ն151 mg/dL).502 However, subgroup analysis of primary prevention patients in JELIS (80% of the study population) indicated that patients with baseline triglyceride levels at or exceeding 150 mg/dL and HDL-C Ͻ40 mg/dL had significantly increased CVD risk.Moreover, combination therapy with statin plus EPA in this high-risk subgroup reduced CVD risk by 53% compared with statin monotherapy, 503 even though the dose of EPA (up to 1.8 g/d) translated into minimal triglyceride reduction (5% between groups).Consequently, the cardiovascular benefit in JELIS was not a primary triglyceride-mediated effect.Trials that used statin plus niacin (or in some cases bile acid resin) combination therapy have shown a reduction in coronary arteriographic progression and regression, as well as regression of carotid artery intima-media thickness.504,505 Reduction in CVD outcomes were observed in several of these studies, although event rates were low, a statin placebo group was not used, and the studies were neither powered nor prespecified to address CVD events as a primary outcome measure.Nevertheless, they set the stage for the statin-niacin outcome trials listed below. Unfortunately, there are limited data on the potential benefit of adding a second drug in high-risk patients treated with a statin who continue to have high triglyceride levels.As noted above, the ACCORD trial 498 did not find that fibrate therapy added to statin reduced cardiovascular events in DM patients (median triglyceride level of 162 mg/dL) except in the subgroup in the upper triglyceride tertile and lowest HDL-C tertile (Pϭ0.06).Although ongoing clinical trials are not specifically designed to examine this issue, secondary analyses of the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes (AIM-HIGH), 506
What the sources say
- Not checked yetcites [503] 503. Saito Y, Yokoyama M, Origasa H, Matsuzaki M, Matsuzawa Y, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Itakura H, Kita T, Kita- batake A, Nakaya N, Sakata T, Shimada K, Shirato K; JELIS Investi- gators, Japan. Effects of EPA on coronary artery disease in hypercho- lesterolemic patients with multiple risk factors: sub-analysis of primary prevention cases from the Japan EPA Lipid Intervention Study (JELIS) [published correction appears in Atherosclerosis. 2009;204:233]. Atherosclerosis. 2008;200:135-140. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Although some familial disorders of triglyceride metabolism are associated with increased risk for pancreatitis when fasting triglyceride level exceeds 1000 mg/dL, others are associated with increased atherosclerotic risk.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 17. Statement Summary and Recommendations This scientific statement reviews the pivotal role of triglycerides in lipid metabolism and reaffirms that triglyceride is not directly atherogenic but represents an important biomarker of CVD risk because of its association with atherogenic remnant particles and apo CIII.Although some familial disorders of triglyceride metabolism are associated with increased risk for pancreatitis when fasting triglyceride level exceeds 1000 mg/dL, others are associated with increased atherosclerotic risk.Moreover, IR, obesity, and sedentary lifestyle can all lead to or aggravate metabolic syndrome risk factors, which should urgently prompt clinicians to focus first on improving the patient's lifestyle.Knowledge of the metabolic pathways of triglyceride-rich particles and the consequences of hypertriglyceridemia is crucial in understanding the characteristic lipid alterations in DM, lipodystrophic disorders including those seen with HIV, and chronic renal disease.Measurements of non-HDL-C, apo B, or both may be especially useful in those with prominent triglyceride/ HDL abnormalities in which LDL-C measurements may underestimate true atherosclerotic vascular risk.This statement suggests the following new designations: (1) Optimal fasting triglyceride levels, defined as Ͻ100 mg/dL, as a parameter of metabolic health, and (2) nonfasting triglyceride levels, to screen for those with high fasting triglyceride levels.A suggested practical algorithm for screening and management of elevated triglyceride levels is outlined in Figure 5.A nonfasting level of Ͻ200 mg/dL is commensurate with a normal (Ͻ150 mg/dL) or optimal (Ͻ100 mg/dL) fasting triglyceride level and requires no further testing.Fasting samples are used to designate borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), and very high (Ն500 mg/dL) triglyceride levels.Nonfasting triglyceride levels are not used in the definition of MetS and should not be used in the calculation of LDL-C by the Friedewald formula. Overall, the treatment of elevated triglyceride levels focuses on intensive therapeutic lifestyle change.For example, a 5% to 10% reduction in body weight anticipates a triglyceride-lowering response of 20%.Further offsets in CHO calories by reducing added sugars and fructose while increasing unsaturated fat intake may contribute an additional 10% to 20% reduction in triglyceride levels.Elimination of trans fats, restriction of SFA, 524 -527 and increasing consumption of marine-based omega-3 products, coupled with aerobic activity, will further optimize triglyceride-lowering efforts.Taken together, reductions of 50% or more in triglyceride levels may be attained through intensive therapeutic lifestyle change. In subjects with very high triglyceride levels or a history of triglyceride-induced pancreatitis, additional dietary considerations include complete abstinence from alcohol, the nutrition practices listed above, the possible use of MCTs 528 and pharmacological therapies (see also Tables 11 and 12).The subject of medication and triglycerides is still lacking crucial clinical trial evidence.Nonetheless, several points should be made.First, clinicians should rule out medications as a potential cause of an elevated triglyceride value.For example, hormone therapy (Table 5) can greatly influence triglyceride levels; in women of reproductive age who develop hypertriglyceridemia while taking oral contraceptive therapy, lower estrogen-containing preparations or other forms of contraception should be considered.For postmenopausal women with hypertriglyceridemia who require postmenopausal hormone preparations, switching to transdermal preparations may blunt the triglyceride increases observed with oral compounds.Second, utilizing triglyceride-lowering medications to prevent pancreatitis in those with triglyceride levels Ͼ500 mg/dL is reasonable in addition to intensive therapeutic lifestyle change.In those with a history of triglyceride-induced pancreatitis, it is especially important to keep triglyceride levels well controlled, and this will require both lifestyle and pharmacological approaches.What remains to be established is whether these modalities favorably influence CVD outcomes beyond proven therapies (eg, statins).Therefore, additional clinical outcome trials are necessary. None Abbott*; Merck/ Schering-Plough*; Sanofi*; Sanofi-Aventis* None None Abbott*; Genzyme-ISIS*; Merck*; Roche*; Sanofi-Aventis* None William James Howard Washington Hospital Center AstraZeneca*; Pfizer* None Abbott*; Merck †; Pfizer*; Sankyo*; Schering-Plough † None None None None Marc S. Jacobson Private practice Merck (formerly Schering-Plough) † None None None None None None Terry A. Lennie University of Kentucky None None None None None None None Moshe Levi University of Colorado Abbott*; Genzyme*; Intercept Pharmaceuticals* None None None None None None
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Strategies to attenuate hypertriglyceridemia and its associated metabolic complications include increasing physical activity during school and afterschool sessions, 520,521 incentivizing schools committed to fostering nutrition education, 522 and offering a variety of fresh fruits and vegetables daily to school cafeterias.523”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > High Triglyceride Levels The rise in triglyceride levels coinciding with the current epidemic of juvenile obesity, IR, and DM 509 -511 has created new opportunities for establishing and disseminating CVD health promotion efforts aimed at maximizing primordial prevention.For example, resolutions have now been adopted in all 50 states targeting obesity, including the elimination of high caloric sugared sodas and trans fatty acid products from public school vending machines and increasing the number of walking and bicycle paths.512,513 Initiatives such as reducing access to low-nutrient, energy-dense foods in school cafeterias serve as other adjunctive measures for controlling high triglyceride and obesity rates.514 Among the most comprehensive national programs has been Healthy People 2010, the initiative established by the Centers for Disease Control and Prevention in 1998 for health promotion and disease prevention.515 The principal objectives are to improve the quality of healthy living and eliminate health disparities through interventions aimed at heart disease and stroke prevention.515,516 In addition to community-based outreach programs, nutrition education beginning in elementary school may yield considerable dividends toward reducing obesity rates, because dietary behaviors are often established in childhood.517 Prototypical pilot studies demonstrate a greater understanding of healthy food choices, which in turn may also improve academic performance.518,519 Strategies to attenuate hypertriglyceridemia and its associated metabolic complications include increasing physical activity during school and afterschool sessions, 520,521 incentivizing schools committed to fostering nutrition education, 522 and offering a variety of fresh fruits and vegetables daily to school cafeterias.523 Overall, identification of the most successful pilot programs for implementation on a national level will require coordinated efforts by clinicians, policymakers, and advocacy groups focused on reducing hypertriglyceridemia, obesity, and IR through a greater emphasis on and implementation of intensive lifestyle interventions.
What the sources say
- Not checked yetcites [520] 520. Kelder SH, Springer AS, Barroso CS, Smith CL, Sanchez E, Ranjit N, Hoelscher DM. Implementation of Texas Senate Bill 19 to increase physical activity in elementary schools. J Public Health Policy. 2009; 30(suppl 1):S221-S247.
- Not checked yetcites [521] 521. Topp R, Jacks DE, Wedig RT, Newman JL, Tobe L, Hollingsworth A. Reducing risk factors for childhood obesity: the Tommie Smith Youth Athletic Initiative. West J Nurs Res. 2009;31:715-730.
- Not checked yetcites [522] 522. He M, Callaghan C, Evans A, Mandich G. Healthy eating champions award for elementary schools. Can J Diet Pract Res. 2009;70:101-104.
- Not checked yetcites [523] 523. Davis EM, Cullen KW, Watson KB, Konarik M, Radcliffe J. A Fresh Fruit and Vegetable Program improves high school students' con- sumption of fresh produce. J Am Diet Assoc. 2009;109:1227-1231.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Measurements of non-HDL-C, apo B, or both may be especially useful in those with prominent triglyceride/ HDL abnormalities in which LDL-C measurements may underestimate true atherosclerotic vascular risk.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 17. Statement Summary and Recommendations This scientific statement reviews the pivotal role of triglycerides in lipid metabolism and reaffirms that triglyceride is not directly atherogenic but represents an important biomarker of CVD risk because of its association with atherogenic remnant particles and apo CIII.Although some familial disorders of triglyceride metabolism are associated with increased risk for pancreatitis when fasting triglyceride level exceeds 1000 mg/dL, others are associated with increased atherosclerotic risk.Moreover, IR, obesity, and sedentary lifestyle can all lead to or aggravate metabolic syndrome risk factors, which should urgently prompt clinicians to focus first on improving the patient's lifestyle.Knowledge of the metabolic pathways of triglyceride-rich particles and the consequences of hypertriglyceridemia is crucial in understanding the characteristic lipid alterations in DM, lipodystrophic disorders including those seen with HIV, and chronic renal disease.Measurements of non-HDL-C, apo B, or both may be especially useful in those with prominent triglyceride/ HDL abnormalities in which LDL-C measurements may underestimate true atherosclerotic vascular risk.This statement suggests the following new designations: (1) Optimal fasting triglyceride levels, defined as Ͻ100 mg/dL, as a parameter of metabolic health, and (2) nonfasting triglyceride levels, to screen for those with high fasting triglyceride levels.A suggested practical algorithm for screening and management of elevated triglyceride levels is outlined in Figure 5.A nonfasting level of Ͻ200 mg/dL is commensurate with a normal (Ͻ150 mg/dL) or optimal (Ͻ100 mg/dL) fasting triglyceride level and requires no further testing.Fasting samples are used to designate borderline high (150 to 199 mg/dL), high (200 to 499 mg/dL), and very high (Ն500 mg/dL) triglyceride levels.Nonfasting triglyceride levels are not used in the definition of MetS and should not be used in the calculation of LDL-C by the Friedewald formula. Overall, the treatment of elevated triglyceride levels focuses on intensive therapeutic lifestyle change.For example, a 5% to 10% reduction in body weight anticipates a triglyceride-lowering response of 20%.Further offsets in CHO calories by reducing added sugars and fructose while increasing unsaturated fat intake may contribute an additional 10% to 20% reduction in triglyceride levels.Elimination of trans fats, restriction of SFA, 524 -527 and increasing consumption of marine-based omega-3 products, coupled with aerobic activity, will further optimize triglyceride-lowering efforts.Taken together, reductions of 50% or more in triglyceride levels may be attained through intensive therapeutic lifestyle change. In subjects with very high triglyceride levels or a history of triglyceride-induced pancreatitis, additional dietary considerations include complete abstinence from alcohol, the nutrition practices listed above, the possible use of MCTs 528 and pharmacological therapies (see also Tables 11 and 12).The subject of medication and triglycerides is still lacking crucial clinical trial evidence.Nonetheless, several points should be made.First, clinicians should rule out medications as a potential cause of an elevated triglyceride value.For example, hormone therapy (Table 5) can greatly influence triglyceride levels; in women of reproductive age who develop hypertriglyceridemia while taking oral contraceptive therapy, lower estrogen-containing preparations or other forms of contraception should be considered.For postmenopausal women with hypertriglyceridemia who require postmenopausal hormone preparations, switching to transdermal preparations may blunt the triglyceride increases observed with oral compounds.Second, utilizing triglyceride-lowering medications to prevent pancreatitis in those with triglyceride levels Ͼ500 mg/dL is reasonable in addition to intensive therapeutic lifestyle change.In those with a history of triglyceride-induced pancreatitis, it is especially important to keep triglyceride levels well controlled, and this will require both lifestyle and pharmacological approaches.What remains to be established is whether these modalities favorably influence CVD outcomes beyond proven therapies (eg, statins).Therefore, additional clinical outcome trials are necessary. None Abbott*; Merck/ Schering-Plough*; Sanofi*; Sanofi-Aventis* None None Abbott*; Genzyme-ISIS*; Merck*; Roche*; Sanofi-Aventis* None William James Howard Washington Hospital Center AstraZeneca*; Pfizer* None Abbott*; Merck †; Pfizer*; Sankyo*; Schering-Plough † None None None None Marc S. Jacobson Private practice Merck (formerly Schering-Plough) † None None None None None None Terry A. Lennie University of Kentucky None None None None None None None Moshe Levi University of Colorado Abbott*; Genzyme*; Intercept Pharmaceuticals* None None None None None None
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, high-risk statin-treated patients who continue to have elevated triglyceride levels display an increased risk for CVD, but these patients also have other metabolic abnormalities, and adjustment for measures of these associated abnormalities, such non-HDL-C and apo B, decreases the predictive effect of triglycerides.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > Elevated Triglyceride Levels
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
NHANES surveys provide representative estimates of the US adult population's triglyceride levels.
“In the United States, the National Health and Nutrition Examination Survey (NHANES) has monitored biomarkers of CVD risk for Ͼ3 decades.”
“Overall, 31% of the adult US population has a triglyceride level Ն150 mg/dL, with no appreciable change between NHANES 1988 -1994 and 1999 -2008.”
The paper relies on this without support.
The molecular basis underlying FCHL is largely unknown.
“The molecular basis underlying FCHL is largely unknown; genetic variants in the APOA1/C3/A4/A5 cluster and the upstream stimulatory factor 1 (USF1) gene may play a role.140 -142”
The paper relies on this without support.
The joint occurrence of high triglyceride level and low HDL-C characterizes the dyslipidemia of MetS.
“The joint occurrence of high triglyceride level and low HDL-C characterizes the dyslipidemia of MetS.”
The authors state this as an assumption.
The increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia.
“It is assumed, but not well documented, that the increase in triglyceride levels induced by oral estrogens is enhanced among women with preexisting hypertriglyceridemia”
The paper relies on this without support.
In South Asians and other minorities, MetS is uniformly accompanied by an increase in atherogenic TRLs, thereby contributing to increased CVD risk in these populations.
“In South Asians and other minorities (eg, Mexican Americans, Native Hawaiians, and American Indians), MetS is uniformly accompanied by an increase in atherogenic TRLs, thereby contributing to increased CVD risk in these populations.”
The paper relies on this without support.
Reducing elevated triglyceride levels reduces cardiovascular risk.
“The association of elevated triglycerides with increased CVD risk and clustered metabolic abnormalities (as discussed in other sections of this scientific statement) has led to research and clinical interest in the potential protective benefit of reducing high levels of triglycerides.”
“Although no published clinical trials have been designed specifically to examine the effect of triglyceride reduction on CVD event rate, secondary analyses from major trials of lipid-regulating therapy have assessed CVD risk in subgroups with high triglyceride levels.”
The paper relies on this without support.
A nonfasting triglyceride level below 200 mg/dL is commensurate with a normal (below 150 mg/dL) or optimal (below 100 mg/dL) fasting triglyceride level.
“A nonfasting level of Ͻ200 mg/dL is commensurate with a normal (Ͻ150 mg/dL) or optimal (Ͻ100 mg/dL) fasting triglyceride level and requires no further testing.”
The paper relies on this without support.
A 5% to 10% reduction in body weight anticipates a triglyceride-lowering response of 20%.
“For example, a 5% to 10% reduction in body weight anticipates a triglyceride-lowering response of 20%.”
The paper relies on this without support.
Reducing added sugars and fructose while increasing unsaturated fat intake may contribute an additional 10% to 20% reduction in triglyceride levels.
“Further offsets in CHO calories by reducing added sugars and fructose while increasing unsaturated fat intake may contribute an additional 10% to 20% reduction in triglyceride levels.”
The paper relies on this without support.
For postmenopausal women with hypertriglyceridemia who require postmenopausal hormone preparations, switching to transdermal preparations may blunt the triglyceride increases observed with oral compounds.
“For postmenopausal women with hypertriglyceridemia who require postmenopausal hormone preparations, switching to transdermal preparations may blunt the triglyceride increases observed with oral compounds.”
The paper relies on this without support.
The subject of medication and triglycerides is still lacking crucial clinical trial evidence.
“The subject of medication and triglycerides is still lacking crucial clinical trial evidence.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“As reviewed in the 2011 AHA statement on triglycerides and cardiovascular disease, 1 alcohol consumption just before testing may elevate fasting triglyceride measurements.118,119”
From Omega-3 Fatty Acids for the Management of Hypertriglyceridemia: A Science Advisory From the American Heart Association (2019) · cites this paper as [1]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This risk is accelerated in the presence of other ASCVD risk factors(18,19).”
From 2016 ACC Expert Consensus Decision Pathway on the Role of Non-Statin Therapies for LDL-Cholesterol Lowering in the Management of Atherosclerotic Cardiovascular Disease Risk (2016) · cites this paper as [18]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“IPE, a highly purified and prescription form of eicosapentaenoic acid (EPA), reduced TG, a prominent biomarker of CVD risk [13]”
From Icosapent ethyl reduces CVD risk in cardiovascular-kidney-metabolic syndrome: REDUCE-IT CKM (2026) · cites this paper as [13]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Although commonly recognized for their impact on LDL-C, statins also provide a 10% to 30% dose-dependent reduction in triglycerides in patients with elevated triglyceride levels (45).”
From 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia (2021) · cites this paper as [45]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The 2011 statement cited epidemiological evidence that a moderate elevation in triglycerides is often associated with increased atherosclerotic cardiovascular disease (ASCVD) risk.”
From Omega-3 Fatty Acids for the Management of Hypertriglyceridemia: A Science Advisory From the American Heart Association (2019) · cites this paper as [1]
The cited source says what the claim attributes to it.
In the citing paper
“Small lipid-depleted LDL subfractions contain less cholesterol than larger ones.”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [11]
The cited source says what the claim attributes to it.
In the citing paper
“They are typically predominant in patients with moderately elevated triglyceride (TG) concentrations or related conditions, such as diabetes and the metabolic syndrome, without necessarily having high LDLC concentration [11].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [11]
The cited source says what the claim attributes to it.
In the citing paper
“Diabetes and abdominal obesity, disorders that underlie the clinical expression of complex dyslipidemias without elevated LDLC, are attaining epidemic proportions [11].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [11]
The cited source says what the claim attributes to it.
In the citing paper
“The association between triglycerides and cardiovascular (CV) risk is well established from epidemiological studies,1-5 genome-wide analyses,6-8 and Mendelian randomization studies.9,10”
The cited source says what the claim attributes to it.
In the citing paper
“Optimization of a dietary intervention coupled with regular aerobic physical activity can result in 20% to 50% reductions in triglyceride levels; for this reason, this combination is the first line of treatment in individuals with hypertriglyceridemia (45).”
From 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia (2021) · cites this paper as [45]
In the citing paper
“The spectrum of apoB100- and apoB48-containing remnants varies with plasma TG levels (Figure 1). At optimal levels (<1.2 mmol/L or <100 mg/dL),4 efficient lipolysis results in limited accumulation of remnant particles, predominantly in the small VLDL and IDL size range.”
In the citing paper
“At fasting TG levels >1.7 mmol/L (>150 mg/dL), there is consensus that ASCVD risk becomes clinically relevant;4,20,38”
In the citing paper
“TRL and TRL remnants accumulate in the plasma at fasting TG levels >1.2 mmol/L (>100 mg/dL).”
In the citing paper
“Metabolic syndrome and insulin resistance may lead to further elevated TG levels, and should be prevented.35”
From Familial chylomicronemia syndrome: Bringing to life dietary recommendations throughout the life span (2018) · cites this paper as [35]
In the citing paper
“The AHA has indicated doses from 2 to 4 g/day of EPA/DHA to reduce TG levels by 25–30% [80].”
From Nutraceuticals in the Management of Dyslipidemia: Which, When, and for Whom? Could Nutraceuticals Help Low-Risk Individuals with Non-optimal Lipid Levels? (2021) · cites this paper as [80]
In the citing paper
“Patients with baseline elevation of LDL-C $190 mg/dL not due to secondary modifiable causes are at very high risk of first and recurrent ASCVD events because of their lifetime exposure to markedly elevated LDL-C levels.”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated major: it would touch a result — a value a result rests on, reported and recomputed p-values on opposite sides of the significance level, two passages that conflict with no sign which is right, or a cited work retracted before this paper was published.
In the paper
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.2. Obesity and Sedentary Lifestyle
“Approximately 80% of participants classified as overweight (BMI 25 to 30 kg/m 2 ) and obese (BMI Ն30 kg/m 2 ) had triglyceride levels Ն150 mg/dL.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.3.2. Acquired Disorders
“TG Concentration, mg/dL TG Concentration, mg/dL BMI, kg/m 2 Ն150 (nϭ1744) Ͻ150 (nϭ3250) Ն200 (nϭ937) Ͻ200 (nϭ4057) Ͻ25 20.1 42.7 17.5 39.0 25 to Ͻ30 39.9 31.6 39.6 33.3 Ն30 39.9 25.6 42.9 27.7”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels
“increased risk is defined arbitrarily by levels exceeding 1000 mg/L.”
§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 12.1. Defining Levels of Risk per the National Cholesterol Education Program ATP Guidelines
“levels associated with increased risk are arbitrarily defined as triglyceride levels Ն1000 mg/dL”
Citations
Cites
2 retracted
Apolipoprotein CIII Links Hyperlipidemia With Vascular Endothelial Cell Dysfunction
Kawakami, A., Osaka, M., Tani, M., Azuma, H., Sacks, F. M., Shimokado, K., & Yoshida, M. (2008) · Circulation · doi:10.1161/circulationaha.108.784785 · Cited by 92
RetractedToll-Like Receptor 2 Mediates Apolipoprotein CIII–Induced Monocyte Activation: Retracted
Kawakami, A., Osaka, M., Aikawa, M., Uematsu, S., Akira, S., Libby, P., Shimokado, K., Sacks, F. M., & Yoshida, M. (2008) · Circulation Research · doi:10.1161/circresaha.108.178426 · Cited by 76
RetractedFriedewald, W. T., Levy, R. I., & Fredrickson, D. S. (1972) · Clinical Chemistry · doi:10.1093/clinchem/18.6.499 · Cited by 32,423
Grundy, S. M., Bilheimer, D. W., Chait, A., Clark, L. T., Denke, M. A., Havel, R. J., Hazzard, W. R., Hulley, S. B., Hunninghake, D. B., Kreisberg, R. A., et al. (1993) · JAMA · doi:10.1001/jama.269.23.3015 · Cited by 27,944
Self-citationExpert Panel on Detection, E. (2001) · JAMA: The Journal of the American Medical Association · doi:10.1001/jama.285.19.2486 · Cited by 26,011
Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin
(2002) · New England Journal of Medicine · doi:10.1056/nejmoa012512 · Cited by 19,011
Alberti, K. G. M. M., Eckel, R. H., Grundy, S. M., Zimmet, P. Z., Cleeman, J. I., Donato, K. A., Fruchart, J.-C., James, W. P. T., Loria, C. M., & Smith, S. C. (2009) · Circulation · doi:10.1161/circulationaha.109.192644 · Cited by 14,860
Detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III)
Grundy, S. M., Becker, D. M., Clark, L. T., Cooper, R., Denke, M. A., Howard, J. L., Hunninghake, D. B., Illingworth, D. R., Luepker, R. V., McBride, P. E., et al. (2002) · Civil War Book Review · Cited by 12,198
Self-citationThe Metabolic and Molecular Bases of Inherited Disease
Scriver, R. C. (1995) · Medical Entomology and Zoology · Cited by 12,101
Research works printed but not linked: 5
- National Cholesterol Education Program (U.S.). Working Group on Lipoprotein Measurement. Recommendations on Lipoprotein Measurement. Bethesda, Md.: National Institutes of Health, National Heart, Lung, and Blood Institute; 1995. NIH publication No. 95-3044.
- Putnam JJ, Allshouse JE. Food Consumption, Prices, and Expenditures, 1970–97. Washington, DC: Food and Rural Economics Division, Economic Research Service, US Department of Agriculture; 1999. Statistical Bulletin No. 965.
- McKenney JM, Ganz P, Wiggins BS, Saseen JS. Statins. In: , Ballantyne C, ed. Clinical Lipidology, A Companion to Braunwald's Heart Disease. Philadelphia, PA: Saunders; 2009: 253–280.
- Norata GD, Catapano AL. In: , Ballantyne C, ed. Clinical Lipidology, A Companion to Braunwald's Heart Disease. Philadelphia, PA: Saunders; 2009: 288–297.
- Brown B, Canner PL, McGovern ME, Guyton JR, Carlson LA. Nicotinic acid. In: , Ballantyne C, ed. Clinical Lipidology, A Companion to Braunwald's Heart Disease. Philadelphia, PA: Saunders; 2009: 298–314.
Cited by
Sorted by citations
Stone, N. J., Robinson, J. G., Lichtenstein, A. H., Bairey Merz, C. N., Blum, C. B., Eckel, R. H., Goldberg, A. C., Gordon, D., Levy, D., Lloyd-Jones, D. M., et al. (2014) · Circulation · doi:10.1161/01.cir.0000437738.63853.7a · Cited by 7,081
Self-citationGrundy, S. M., Stone, N. J., Bailey, A. L., Beam, C., Birtcher, K. K., Blumenthal, R. S., Braun, L. T., de Ferranti, S., Faiella-Tommasino, J., Forman, D. E., et al. (2019) · Circulation · doi:10.1161/cir.0000000000000625 · Cited by 6,185
Self-citationStone, N. J., Robinson, J. G., Lichtenstein, A. H., Bairey Merz, C. N., Blum, C. B., Eckel, R. H., Goldberg, A. C., Gordon, D., Levy, D., Lloyd-Jones, D. M., et al. (2014) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2013.11.002 · Cited by 3,845
Self-citationGrundy, S. M., Stone, N. J., Bailey, A. L., Beam, C., Birtcher, K. K., Blumenthal, R. S., Braun, L. T., de Ferranti, S., Faiella-Tommasino, J., Forman, D. E., et al. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.11.003 · Cited by 2,691
Self-citationAuthors Task Force Members, Rydén, L., Grant, P. J., Anker, S. D., Berne, C., Cosentino, F., Danchin, N., Deaton, C., Escaned, J., Hammes, H., et al. (2013) · European Heart Journal · doi:10.1093/eurheartj/eht108 · Cited by 1,994
Metadata
- Authors
- Miller, M., Stone, N. J., Ballantyne, C., Bittner, V., Criqui, M. H., Ginsberg, H. N., Goldberg, A. C., Howard, W. J., Jacobson, M. S., Kris-Etherton, P. M., Lennie, T. A., Levi, M., Mazzone, T., & Pennathur, S.
- Affiliations
- University of Maryland, College Park (US)
- ORCID
- Venue
- Circulation
- Published
- 2011-05-24
- Volume
- 123
- Issue
- 20
- Pages
- 2292-2333
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2036747551
- Cited by
- 1,871
- References
- 557
- Citations by year
- 2026: 85 · 2025: 102 · 2024: 108 · 2023: 96 · 2022: 123 · 2021: 125 · 2020: 118 · 2019: 123 · 2018: 122 · 2017: 162 · 2016: 147 · 2015: 142 · 2014: 156 · 2013: 151 · 2012: 74
- FWCI
- 135.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- Northwestern Medical Faculty Foundation
- Bristol-Myers Squibb
- Pfizer
- AstraZeneca
- GlaxoSmithKline
- Sanofi
- General Mills
- Northwestern University
- Almond Board of California
- Archer Daniels Midland
- Amarin Corporation
- Canola Council of Canada
- Peanut Institute
- Kowa Company
- National Institutes of Health
- Centers for Disease Control and Prevention
- University of California, San Diego
- National Heart, Lung, and Blood Institute
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- triglycerides, cardiovascular disease, coronary artery disease, dyslipidemia
- MeSH terms
- American Heart Association, Cardiovascular Diseases, Humans, Risk Factors, Triglycerides, United States, Hypertriglyceridemia
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-11, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-11 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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