Triglycerides and Cardiovascular Disease: A Scientific Statement From the American Heart Association

§ 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.

It may state two separate claims as one.

• AssumptionRests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.

§ 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.

It may state two separate claims as one.

• AssumptionRests 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.

§ 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.

It may state two separate claims as one.

• AssumptionRests 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.

§ 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.

Probably not a substantial claim. The paper’s conclusions may not depend on it.

§ 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.

It may state two separate claims as one.

• AssumptionRests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.

§ 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.

It may state two separate claims as one.

• AssumptionRests on an assumption: NHANES surveys provide representative estimates of the US adult population's triglyceride levels.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies

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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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies

Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.3. Prospective Population-Based Cohort Studies

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 3.2. Case-Control Studies, Including Angiographic Studies

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§ 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.

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.2. Apo CIII

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§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.2. Apo CIII

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§ 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.

It may state two separate claims as one.

§ 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.

It may state two separate claims as one.

§ 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.

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

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§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

Probably not a substantial claim. The paper’s conclusions may not depend on it.

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.

§ 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

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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

It may state two separate claims as one.

§ 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

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.4. Metabolic Consequences of Hypertriglyceridemia

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5.2. Apo CIII

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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.

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.

§ 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.

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.

§ 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.

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 4.5. Atherogenicity of TRLs

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

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.

§ 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.

Probably not a substantial claim. It may be too vague to check against evidence.

§ 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

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

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.

§ 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.

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

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.

§ 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

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

It may state two separate claims as one.

§ 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.

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > FCHL or FHTG.

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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.

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6. Diabetes Mellitus

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

It may state two separate claims as one.

§ 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.

It may state two separate claims as one.

§ 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.

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 5.1. Familial Disorders With High Triglyceride Levels

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 7.2. Prognostic Significance of Triglyceride in MetS

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.5. Summary

Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no 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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.1.2. VLDL Metabolism

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 8. Chronic Kidney Disease

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.

§ 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

Probably not a substantial claim. The paper may give no reason why it holds.

None of the sources cited for this claim have been checked yet.

§ 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

It may state two separate claims as one.

§ 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

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6. Diabetes Mellitus

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.3. Small LDL Particles

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.1.1. Chylomicron Metabolism

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.5. Summary

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 8. Chronic Kidney Disease

Probably not a substantial claim. It may state two separate claims as one.

§ 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

It may state two separate claims as one.

§ 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

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 8. Chronic Kidney Disease

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 7.2. Prognostic Significance of Triglyceride in MetS

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.1.1. Chylomicron Metabolism

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.5. Summary

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 6.2.4. Reduced HDL-C

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.3. Ratio of Triglycerides to HDL-C

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 9.1.3. Ratio of Triglycerides to HDL-C

It may state two separate claims as one.

§ 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

It may state two separate claims as one.

§ 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

It may state two separate claims as one.

§ 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

Probably not a substantial claim.

§ 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

Probably not a substantial claim. The paper’s conclusions may not depend on it.

§ 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

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.2. Phlebotomy-Related Issues

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 10.1. Postural Effects

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1.2. Obesity and High Triglyceride Levels in Childhood

It may state two separate claims as one.

§ 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

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1. Children and Adolescent Obesity

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.

§ 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.

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.1. Children and Adolescent Obesity

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.2. Prevalence of Hypertriglyceridemia in Women

It may state two separate claims as one.

§ 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).

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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).

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.1. Triglyceride Levels During the Lifespan in Women

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.

§ 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).

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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).

It may state two separate claims as one.

§ 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).

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.1. Triglyceride Levels During the Lifespan in Women

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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).

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.1. Triglyceride Levels During the Lifespan in Women

It may state two separate claims as one.

§ 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).

It may state two separate claims as one.

§ 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).

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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).

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.1. Triglyceride Levels During the Lifespan in Women

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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).

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.2. Prevalence of Hypertriglyceridemia in Women

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.2. Prevalence of Hypertriglyceridemia in Women

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2. Triglycerides as a Cardiovascular Risk Factor in Women

Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.2.1. Triglyceride Levels During the Lifespan in Women

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.1.1. Weight Status, Body Fat Distribution, and Weight Loss

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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

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.

§ 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

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.1. Dietary and Weight-Losing Strategies

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities

It may state two separate claims as one.

§ 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

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities

It may state two separate claims as one.

§ 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

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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).

It may state two separate claims as one.

§ 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).

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.1.1. Weight Status, Body Fat Distribution, and Weight Loss

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 11.3. Triglycerides in Ethnic Minorities

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ 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

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.2. Added Sugars

It may state two separate claims as one.

None of the sources cited for this claim have been checked yet.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein

It may state two separate claims as one.

§ 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.

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein

It may state two separate claims as one.

§ 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.

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.2.1. Total Fat, CHO, and Protein

Probably not a substantial claim. It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose

Probably not a substantial claim.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.3. Glycemic Index/Load

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose

Probably not a substantial claim. The paper’s conclusions may not depend on it.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.5. Alcohol

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet

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.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.3.4. Fructose

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet

It may state two separate claims as one.

§ Triglycerides and Cardiovascular Disease A Scientific Statement From the American Heart Association > 13.4. Weight Loss and Macronutrient Profile of the Diet