Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?: New Insights From the Framingham Offspring Study
Open accessAbstract
Background—: Although the inverse association between high-density lipoprotein cholesterol (HDL-C) and risk of cardiovascular disease (CVD) has been long established, it remains unclear whether low HDL-C remains a CVD risk factor when levels of low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG) are not elevated. This is a timely issue because recent studies have questioned whether HDL-C is truly an independent predictor of CVD. Methods and Results—: 3590 men and women from the Framingham Heart Study offspring cohort without known CVD were followed between 1987 and 2011. Low HDL-C (<40 mg/dL in men and <50 mg/dL in women) was defined as isolated if TG and LDL-C were both low (<100 mg/dL). We also examined higher thresholds for TG (150 mg/dL) and LDL-C (130 mg/dL) and compared low versus high HDL-C phenotypes using logistic regression analysis to assess association with CVD. Compared with isolated low HDL-C, CVD risks were higher when low HDL-C was accompanied by LDL-C ≥100 mg/dL and TG <100 mg/dL (odds ratio 1.3 [1.0, 1.6]), TG ≥100 mg/dL and LDL-C <100 mg/dL (odds ratio 1.3 [1.1, 1.5]), or TG and LDL-C ≥100 mg/dL (odds ratio 1.6, [1.2, 2.2]), after adjustment for covariates. When low HDL-C was analyzed with higher thresholds for TG (≥150 mg/dL) and LDL-C (≥130 mg/dL), results were essentially the same. In contrast, compared with isolated low HDL-C, high HDL-C was associated with 20% to 40% lower CVD risk except when TG and LDL-C were elevated. Conclusions—: CVD risk as a function of HDL-C phenotypes is modulated by other components of the lipid panel.
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Written from the paper’s full text.
TL;DR
In the Framingham Offspring Study, isolated low HDL-C was uncommon and less predictive of incident CVD than low HDL-C accompanied by higher LDL-C, higher triglycerides, or both. HDL-C phenotypes were not uniformly predictive; TG and LDL-C modified CVD risk at both low and high HDL-C levels.
Key findings
- Among 3590 men and women without known CVD followed from 1987 to 2011, isolated low HDL-C (HDL-C <40 mg/dL in men or <50 mg/dL in women, with TG and LDL-C both <100 mg/dL) occurred in only 84 participants (2.3%).
- Compared with isolated low HDL-C, adjusted CVD odds ratios were higher when low HDL-C was accompanied by LDL-C ≥100 mg/dL and TG <100 mg/dL (OR 1.3 [1.0, 1.6]), TG ≥100 mg/dL and LDL-C <100 mg/dL (OR 1.3 [1.1, 1.5]), or both TG and LDL-C ≥100 mg/dL (OR 1.6 [1.2, 2.2]).
- Using higher thresholds for TG (≥150 mg/dL) and/or LDL-C (≥130 mg/dL) produced essentially the same results.
- Compared with isolated low HDL-C, isolated high HDL-C was associated with lower CVD risk (OR 0.6 [0.5, 0.7]); this persisted with higher LDL-C or higher TG alone, but was no longer significantly protective when both LDL-C and TG were ≥100 mg/dL.
Methods
- Prospective cohort analysis of Framingham Heart Study Offspring Cohort participants whose baseline evaluation was Examination cycle 4 (1987–1991), with incident CVD monitored through 2011.
- From 3925 initial samples, 188 were excluded for loss to follow-up, baseline CVD history, or TG >400 mg/dL; after excluding 147 lipid-lowering therapy users, the final sample was 3590.
- Logistic regression estimated odds ratios for incident CVD (fatal/nonfatal MI, stroke, or CVD death), adjusted for age, gender, diabetes, hypertension, and smoking status; isolated low HDL-C was the referent.
Limitations
- The paper states that the study lacked additional measures such as apoB or LDL particle concentration that may improve CVD risk prediction beyond conventional lipids and lipoproteins.
- The paper states there was a relative paucity of cases with isolated low HDL-C using the stringent <100 mg/dL thresholds for TG and LDL-C.
- Evident from the methods: blood samples were single measurements from Examination cycle 4, and the observational design leaves potential for residual confounding despite covariate adjustment.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
0 of 46 cited sources checked · 0 supported · 0 flagged
- Findingown data
Isolated low HDL-C using the lowest thresholds (<100 mg/dL for TG and LDL-C) was uncommon (n=84, 2.3% of the study cohort).
“Whereas isolated low HDL-C using the lowest thresholds to define low TG and LDL-C (i.e., < 100 mg/dL) was uncommon (n=84, 2.3% of the study cohort)”
Quote in the paperNot a substantial claim - Findingown data
When low HDL-C was analyzed with higher thresholds for TG (≥150 mg/dL) and/or LDL-C (≥130 mg/dL), results were essentially the same.
“When low HDL-C was analyzed with higher thresholds for TG (≥150 mg/dL) and/or LDL-C (≥130 mg/dL) results were essentially the same.”
- Also stated in: § Discussion · plain
“we observed similar trends with higher thresholds of the other risk factors that had larger cell sizes.”
Quote in the paperNot a substantial claim - Also stated in: § Discussion · plain
- Findingown data
Compared to isolated low HDL-C, isolated high HDL-C was associated with reduced CVD risk (OR = 0.6 [0.5, 0.7]).
“In contrast, compared to isolated low HDL-C, isolated high HDL-C (low levels of TG and LDL-C in the presence of high HDL-C) was consistently associated with reduced CVD risk (OR = 0.6, [0.5,0.7]).”
Quote in the paperSubstantial claim - Findingown data
Compared to isolated low HDL-C, CVD risk was higher when low HDL-C was accompanied by LDL-C ≥100 mg/dL and TG <100 mg/dL (OR 1.3 [1.0, 1.6]) after adjustment for covariates.
“Compared to isolated low HDL-C, CVD risks were higher when low HDL-C was accompanied by LDL-C ≥100 mg/dL and TG <100 mg/dL (OR 1.3 [1.0, 1.6])”
- Also stated in: § Results · plain
“Compared to isolated low HDL-C, CVD was higher when low HDL-C was accompanied by LDL-C ≥100 mg/dL (OR 1.3 [1.0, 1.6]”
Quote in the paperSubstantial claim - Also stated in: § Results · plain
- Findingown data
Compared to isolated low HDL-C, CVD risk was higher when low HDL-C was accompanied by TG ≥100 mg/dL and LDL-C <100 mg/dL (OR 1.3 [1.1, 1.5]) after adjustment.
“TG ≥100 mg/dL and LDL-C <100 mg/dL (OR 1.3 [1.1, 1.5])”
- Also stated in: § Results · plain
“TG ≥100 mg/dL (OR 1.3 [1.1, 1.5])”
Quote in the paperSubstantial claim - Also stated in: § Results · plain
- Findingown data
The presence of higher TG (>200 mg/dL) within the high HDL-C and LDL-C <100 subgroup was associated with increased CVD risk to the level shown by the subgroup with higher LDL-C and lower TG (<100 mg/dL).
“However, the presence of higher TG (> 200 mg/dL) within this subgroup was associated with increased CVD risk to the level shown by the subgroup with higher LDL-C and lower TG (<100 mg/dL).”
Quote in the paperSubstantial claim - Findingown data
The association between high HDL-C and reduced CVD risk was no longer significantly protective when both LDL-C and TG were ≥100 mg/dL.
“This association persisted even when high HDL-C was accompanied by higher LDL-C (≥ 100 and ≥ 130 mg/dL) or higher TG (≥ 100 and ≥ 150 mg/dL), but was no longer significantly protective when both LDL-C and TG equaled or exceeded 100 mg/dL.”
Quote in the paperSubstantial claim - Findingown data
The association between isolated high HDL-C and reduced CVD risk persisted when high HDL-C was accompanied by higher LDL-C (≥100 and ≥130 mg/dL) or higher TG (≥100 and ≥150 mg/dL).
“This association persisted even when high HDL-C was accompanied by higher LDL-C (≥ 100 and ≥ 130 mg/dL) or higher TG (≥ 100 and ≥ 150 mg/dL), but was no longer significantly protective when both LDL-C and TG equaled or exceeded 100 mg/dL.”
Quote in the paperSubstantial claim - Findingown data
A similar pattern of TG-associated risk emerged with low HDL-C.
“A similar pattern emerged with low HDL-C.”
Quote in the paperSubstantial claim - Findingown data
The prevalence of diabetes in Framingham Offspring subjects with low HDL-C, LDL-C<100 and TG<100 was approximately 50% lower compared to higher TG.
“Indeed, the prevalence of diabetes in Framingham Offspring subjects with low HDL- C, LDL-C<100 and TG < 100 mg/dL was approximately 50% lower compared to higher TG (Table 1)”
Quote in the paperSubstantial claim - Findingown data
Subgroups with LDL-C <100 mg/dL were generally at lower risk of CVD than comparable groups with LDL-C ≥100 mg/dL, regardless of HDL-C phenotype.
“As expected, the subgroups with LDL-C <100 mg/dL were generally at a lower risk of CVD than comparable groups with LDL-C ≥100 mg/dL, regardless of HDL-C phenotype.”
Quote in the paperSubstantial claim - Findingreasoning
Higher HDL-C is associated with lower CVD risk when other risk factors are constant.
“Within this context, higher HDL-C is associated with lower CVD risk, when other risk factors are constant.”
Quote in the paperSubstantial claim - Findingown data
At TG <100 mg/dL, CVD risk was low in the setting of high HDL-C and LDL-C <100 (or <130) mg/dL.
“For example, at TG <100 mg/dL, CVD risk was low in the setting of high HDL-C and LDL-C <100 (or <130) mg/dL.”
Quote in the paperSubstantial claim - Findingown data
Compared to isolated low HDL-C, CVD risk was higher when low HDL-C was accompanied by both TG and LDL-C ≥100 mg/dL (OR 1.6 [1.2, 2.2]) after adjustment.
“or TG and LDL-C ≥ 100 mg/dL (OR 1.6, [1.2, 2.2]), after adjustment for covariates.”
- Also stated in: § Results · plain
“or both (OR 1.6, [1.2, 2.2]).”
Quote in the paperSubstantial claim - Also stated in: § Results · plain
- Findingown data
Baseline characteristics of isolated high and low HDL-C groups were similar regardless of TG and LDL-C measures.
“Overall, the baseline characteristics of the isolated high and low HDL-C groups were similar regardless of TG and LDL-C measures (Supplementary Tables 1-3).”
Quote in the paperNot a substantial claim - Premisecitation
Outcome trials targeting HDL-C pharmacologically in patients with low HDL-C at baseline have not demonstrated reduced CVD risk despite appreciable increases in HDL-C.
“outcome trials that have targeted HDL-C pharmacologically and have included patients with low HDL-C at baseline, have not demonstrated reduced CVD risk despite appreciable increases in HDL-C.5-10”
Quote in the paperSubstantial claim0 of 6 sources checked- cites [5] Barter PJ Caulfield M Eriksson M Grundy SM Kastelein JJ Komajda M Lopez-Sendon J Mosca L Tardif JC Waters DD Shear CL Revkin JH Buhr KA Fisher MR Tall AR Brewer B ILLUMINATE Investigators. Effects of torcetrapib in patients at high risk for coronary events. N Engl J Med 2007 357 2109 22 17984165 source
Not checked in the free run.
- cites [6] Schwartz GG Olsson AG Abt M Ballantyne CM Barter PJ Brumm J Chaitman BR Holme IM Kallend D Leiter LA Leitersdorf E McMurray JJ Mundl H Nicholls SJ Shah PK Tardif JC Wright RS dal-OUTCOMES Investigators. Effects of dalcetrapib in patients with a recent acute coronary syndrome. N Engl J Med 2012 367 2089 99 23126252 source
Not checked in the free run.
- cites [7] AIM-HIGH Investigators Boden WE Probstfield JL Anderson T Chaitman BR Desvignes-Nickens P Koprowicz K McBride R Teo K Weintraub W Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med 2011 365 2255 67 22085343 source
Not checked in the free run.
- cites [8] HPS2-THRIVE Collaborative Group HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle and liver outcomes, and reasons for stopping study treatment. Eur Heart J 2013 34 1279 91 23444397 PMC3640201 source
Not checked in the free run.
- cites [9] HPS2-THRIVE Collaborative Group Landray MJ Haynes R Hopewell JC Parish S Aung T Tomson J Wallendszus K Craig M Jiang L Collins R Armitage J Effects of extended-release niacin with laropiprant in high-risk patients. N Engl J Med 2014 371 203 12 25014686 source
Not checked in the free run.
- cites [10] Keene D Price C Shun-Shin MJ Francis DP Effect on cardiovascular risk of high density lipoprotein targeted drug treatments niacin, fibrates, and CETP inhibitors: meta-analysis of randomised controlled trials including 117,411 patients. BMJ 2014 349 g4379 25038074 PMC4103514 source
Not checked in the free run.
- Premisecitation
The relationships between HDL-C, TG and LDL-C have complicated efforts toward establishing the extent to which low HDL-C independently increases CVD risk when other lipids are within normal ranges.
“However, the relationships between HDL-C, triglycerides (TG) and LDL-C have complicated efforts toward establishing the extent to which low HDL-C independently increases CVD risk when other lipids are within the normal ranges4.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [4] Castelli WP Doyle JT Gordon T Hames CG Hjortland MC Hulley SB Kagan A Zukel WJ HDL cholesterol and other lipids in coronary heart disease. The cooperative lipoprotein phenotyping study. Circulation 1977 55 767 72 191215 source
Not checked in the free run.
- Premisecitation
A Mendelian randomization study failed to identify polymorphisms associated with high HDL-C that correlate with reduced CVD risk.
“Similarly, a Mendelian randomization study failed to identify polymorphisms associated with high HDL-C that correlate with reduced CVD risk.11”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [11] Voight BF Peloso GM Orho-Melander M Frikke-Schmidt R Barbalic M Jensen MK Hindy G Hólm H Ding EL Johnson T Schunkert H Samani NJ Clarke R Hopewell JC Thompson JF Li M Thorleifsson G Newton-Cheh C Musunuru K Pirruccello JP Saleheen D Chen L Stewart A Schillert A Thorsteinsdottir U Thorgeirsson G Anand S Engert JC Morgan T Spertus J Stoll M Berger K Martinelli N Girelli D McKeown PP Patterson CC Epstein SE Devaney J Burnett MS Mooser V Ripatti S Surakka I Nieminen MS Sinisalo J Lokki ML Perola M Havulinna A de Faire U Gigante B Ingelsson E Zeller T Wild P de Bakker PI Klungel OH Maitland-van der source
Not checked in the free run.
- Premisecitation
Recent studies have failed to demonstrate that high HDL-C acquired naturally or pharmacologically is associated with reduced CVD risk.
“In contrast, recent studies have failed to demonstrate that high HDL-C acquired naturally or pharmacologically, is associated with reduced CVD risk.5-11,18”
Quote in the paperSubstantial claim0 of 8 sources checked- cites [5] Barter PJ Caulfield M Eriksson M Grundy SM Kastelein JJ Komajda M Lopez-Sendon J Mosca L Tardif JC Waters DD Shear CL Revkin JH Buhr KA Fisher MR Tall AR Brewer B ILLUMINATE Investigators. Effects of torcetrapib in patients at high risk for coronary events. N Engl J Med 2007 357 2109 22 17984165 source
Not checked in the free run.
- cites [6] Schwartz GG Olsson AG Abt M Ballantyne CM Barter PJ Brumm J Chaitman BR Holme IM Kallend D Leiter LA Leitersdorf E McMurray JJ Mundl H Nicholls SJ Shah PK Tardif JC Wright RS dal-OUTCOMES Investigators. Effects of dalcetrapib in patients with a recent acute coronary syndrome. N Engl J Med 2012 367 2089 99 23126252 source
Not checked in the free run.
- cites [7] AIM-HIGH Investigators Boden WE Probstfield JL Anderson T Chaitman BR Desvignes-Nickens P Koprowicz K McBride R Teo K Weintraub W Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med 2011 365 2255 67 22085343 source
Not checked in the free run.
- cites [8] HPS2-THRIVE Collaborative Group HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle and liver outcomes, and reasons for stopping study treatment. Eur Heart J 2013 34 1279 91 23444397 PMC3640201 source
Not checked in the free run.
- cites [9] HPS2-THRIVE Collaborative Group Landray MJ Haynes R Hopewell JC Parish S Aung T Tomson J Wallendszus K Craig M Jiang L Collins R Armitage J Effects of extended-release niacin with laropiprant in high-risk patients. N Engl J Med 2014 371 203 12 25014686 source
Not checked in the free run.
- cites [10] Keene D Price C Shun-Shin MJ Francis DP Effect on cardiovascular risk of high density lipoprotein targeted drug treatments niacin, fibrates, and CETP inhibitors: meta-analysis of randomised controlled trials including 117,411 patients. BMJ 2014 349 g4379 25038074 PMC4103514 source
Not checked in the free run.
- cites [11] Voight BF Peloso GM Orho-Melander M Frikke-Schmidt R Barbalic M Jensen MK Hindy G Hólm H Ding EL Johnson T Schunkert H Samani NJ Clarke R Hopewell JC Thompson JF Li M Thorleifsson G Newton-Cheh C Musunuru K Pirruccello JP Saleheen D Chen L Stewart A Schillert A Thorsteinsdottir U Thorgeirsson G Anand S Engert JC Morgan T Spertus J Stoll M Berger K Martinelli N Girelli D McKeown PP Patterson CC Epstein SE Devaney J Burnett MS Mooser V Ripatti S Surakka I Nieminen MS Sinisalo J Lokki ML Perola M Havulinna A de Faire U Gigante B Ingelsson E Zeller T Wild P de Bakker PI Klungel OH Maitland-van der source
Not checked in the free run.
- cites [18] Zanoni P Khetarpal SA Larach DB Hancock-Cerutti WF Millar JS Cuchel M DerOhannessian S Kontush A Surendran P Saleheen D Trompet S Jukema JW De Craen A Deloukas P Sattar N Ford I Packard C Majumder Aa Alam DS Di Angelantonio E Abecasis G Chowdhury R Erdmann J Nordestgaard BG Nielsen SF Tybjærg-Hansen A Schmidt RF Kuulasmaa K Liu DJ Perola M Blankenberg S Salomaa V Männistö S Amouyel P Arveiler D Ferrieres J Müller-Nurasyid M Ferrario M Kee F Willer CJ Samani N Schunkert H Butterworth AS Howson JM Peloso GM Stitziel NO Danesh J Kathiresan S Rader DJ CHD Exome+ Consortium; CARDIoGRAM Exome Consor source
Not checked in the free run.
- Interpretationnone given
The LDL-C and TG thresholds used in the prior study (160 and 200 mg/dL) may have been too high to evaluate the true risk of isolated HDL-C.
“but the LDL-C and TG thresholds used (160 and 200 mg/dL, respectively), may have been too high to evaluate the true risk of isolated HDL-C.”
Quote in the paperSubstantial claim - Premisecitation
Genetic defects controlling TG metabolism, including APOC3, ANGPTL3 and ANGPTL4, linked to reduced TG are associated with reduced coronary calcification or reduced CVD risk.
“defects in genes controlling TG metabolism, including APOC3, ANGPTL3 and ANGPTL4 that have been linked to reduced TG and are associated with reduced coronary calcification25 or reduced CVD risk.26-30”
Quote in the paperNot a substantial claim0 of 6 sources checked- cites [25] Pollin TI Damcott CM Shen H Ott SH Shelton J Horenstein RB Post W McLenithan JC Bielak LF Peyser PA Mitchell BD Miller M O'Connell JR Shuldiner AR A null mutation in human APOC3 confers a favorable plasma lipid profile and apparent cardioprotection. Science 2008 322 1702 5 19074352 PMC2673993 source
Not checked in the free run.
- cites [26] Jorgensen AB Frikke-Schmidt R Nordestgaard BG Tybjaerg-Hansen A Loss-of-function mutations in APOC3 and risk of ischemic vascular disease. N Engl J Med 2014 371 32 41 24941082 source
Not checked in the free run.
- cites [27] TG and HDL Working Group of the Exome Sequencing Project, National Heart, Lung, and Blood Institute Crosby J Peloso GM Auer PL Crosslin DR Stitziel NO Lange LA Lu Y Tang ZZ Zhang H Hindy G Masca N Stirrups K Kanoni S Do R Jun G Hu Y Kang HM Xue C Goel A Farrall M Duga S Merlini PA Asselta R Girelli D Olivieri O Martinelli N Yin W Reilly D Speliotes E Fox CS Hveem K Holmen OL Nikpay M Farlow DN Assimes TL Franceschini N Robinson J North KE Martin LW DePristo M Gupta N Escher SA Jansson JH Van Zuydam N Palmer CN Wareham N Koch W Meitinger T Peters A Lieb W Erbel R Konig IR Kruppa J Degenhardt F source
Not checked in the free run.
- cites [28] Musunuru K Pirruccello JP Do R Peloso GM Guiducci C Sougnez C Garimella KV Fisher S Abreu J Barry AJ Fennell T Banks E Ambrogio L Cibulskis K Kernytsky A Gonzalez E Rudzicz N Engert JC DePristo MA Daly MJ Cohen JC Hobbs HH Altshuler D Schonfeld G Gabriel SB Yue P Kathiresan S Exome sequencing ANGPTL3 mutations, and familial combined hypolipidemia. N Engl J Med 2010 363 2220 7 20942659 PMC3008575 source
Not checked in the free run.
- cites [29] Myocardial Infarction Genetics and CARDIoGRAM Exome Consortia Investigators Coding Variation in ANGPTL4, LPL, and SVEP1 and the Risk of Coronary Disease. N Engl J Med 2016 374 1134 44 24 26934567 PMC4850838 source
Not checked in the free run.
- cites [30] Dewey FE Gusarova V O'Dushlaine C Gottesman O Trejos J Hunt C Van Hout CV Habegger L Buckler D Lai KV Leader JB Murray MF Ritchie MD Kirchner HL Ledbetter DH Penn J Lopez A Borecki IB Overton JD Reid JG Carey DJ Murphy AJ Yancopoulos GD Baras A Gromada J Shuldiner AR Inactivating Variants in ANGPTL4 and Risk of Coronary Artery Disease. N Engl J Med 2016 374 1123 33 26933753 PMC4900689 source
Not checked in the free run.
- Interpretationown data
TG and LDL-C (other components of the lipid panel) modulate CVD risk across HDL-C phenotypes.
“TG and LDL-C represent important modifiers of incident CVD risk at both ends of the HDL-C spectrum.”
- Also stated in: § Conclusions · plain
“CVD risk as a function of HDL-C phenotypes is modulated by other components of the lipid panel.”
Quote in the paperSubstantial claim - Also stated in: § Conclusions · plain
- Premisecitation
Post-hoc analyses found TG to be more accurate than HDL-C in predicting recurrent CVD events after an acute coronary syndrome.
“and post-hoc analyses found TG to be more accurate than HDL-C in predicting recurrent CVD events after an acute coronary syndrome.19,31”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [19] Miller M Cannon CP Murphy SA Qin J Ray KK Braunwald E PROVE IT-TIMI 22 Investigators. Impact of triglyceride levels beyond low-density lipoprotein cholesterol after acute coronary syndrome in the PROVE IT-TIMI 22 trial. J Am Coll Cardiol 2008 51 724 30 18279736 source
Not checked in the free run.
- cites [31] Schwartz GG Abt M Bao W DeMicco D Kallend D Miller M Mundl H Olsson AG Fasting triglycerides predict recurrent ischemic events in patients with acute coronary syndrome treated with statins. J Am Coll Cardiol 2015 65 2267 75 26022813 source
Not checked in the free run.
- Interpretationown data
TG levels essentially reclassify risk of CVD irrespective of HDL-C.
“Therefore, TG levels essentially reclassify risk of CVD irrespective of HDL-C.”
Quote in the paperSubstantial claim - Premisecitation
Another study of CVD survivors with desirable total cholesterol found low HDL-C to be predictive of recurrent events.
“Another study of CVD survivors with desirable total cholesterol34 also found low HDL-C to be predictive of recurrent events”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [34] Miller M Seidler A Kwiterovich PO Pearson TA Long-term predictors of subsequent cardiovascular events with coronary artery disease and 'desirable' levels of plasma total cholesterol. Circulation 1992 86 1165 70 1394924 source
Not checked in the free run.
- Study design and conductown data
There was a relative paucity of cases with isolated low HDL-C using the stringent threshold (<100 mg/dL) for TG and LDL-C.
“As noted above, there was also a relative paucity of cases with isolated low HDL-C using the stringent threshold (< 100 mg/dL) for TG and LDL-C”
Quote in the paperNot a substantial claim - Interpretationown data
Low HDL-C in isolation is considerably less predictive of CVD risk in the presence of high TG, high LDL-C, or both.
“The most novel finding in this study is that low HDL-C in isolation is considerably less predictive of CVD risk in the presence of high TG, high LDL-C, or both.”
Quote in the paperSubstantial claim - Premisecitation
A recent genome-wide association study identified common polymorphisms associated with TG to strongly influence risk of coronary disease.
“Moreover, a recent genome-wide association study identified common polymorphisms associated with TG to strongly influence risk of coronary disease20”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [20] Do R Willer CJ Schmidt EM Sengupta S Gao C Peloso GM Gustafsson S Kanoni S Ganna A Chen J Buchkovich ML Mora S Beckmann JS Bragg-Gresham JL Chang HY Demirkan A Den Hertog HM Donnelly LA Ehret GB Esko T Feitosa MF Ferreira T Fischer K Fontanillas P Fraser RM Freitag DF Gurdasani D Heikkilä K Hyppönen E Isaacs A Jackson AU Johansson A Johnson T Kaakinen M Kettunen J Kleber ME Li X Luan J Lyytikäinen LP Magnusson PK Mangino M Mihailov E Montasser ME Müller-Nurasyid M Nolte IM O'Connell JR Palmer CD Perola M Petersen AK Sanna S Saxena R Service SK Shah S Shungin D Sidore C Song C Strawbridge RJ Su source
Not checked in the free run.
- Interpretationown data
Low and high HDL-C phenotypes are not uniformly predictive of CVD risk in the Framingham Offspring Study.
“In the Framingham Offspring Study, low and high HDL-C phenotypes are not uniformly predictive of CVD risk.”
Quote in the paperSubstantial claim - Study design and conductcitation
The study lacked additional measures (e.g., apoB or LDL particle concentration) that may provide incremental CVD risk prediction beyond conventional lipids and lipoproteins.
“Limitations of the current study include the lack of additional measures (e.g., apoB or LDL particle concentration) that may provide incremental CVD risk prediction beyond conventional lipids and lipoproteins.41”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [41] AACC Lipoproteins and Vascular Diseases Division Working Group on Best Practices Cole TG Contois JH Csako G McConnell JP Remaley AT Devaraj S Hoefner DM Mallory T Sethi AA Warnick GR Association of apolipoprotein B and nuclear magnetic resonance spectroscopy-derived LDL particle number with outcomes in 25 clinical studies: assessment by the AACC Lipoprotein and Vascular Diseases Division Working Group on Best Practices. Clin Chem 2013 59 752 70 23386699 source
Not checked in the free run.
- Interpretationown data
The increased risk of CVD associated with low HDL-C is most evident in the presence of higher levels of other lipids or lipoproteins.
“The increased risk of CVD associated with low HDL-C is most evident in the presence of higher levels of other lipids or lipoproteins.”
Quote in the paperSubstantial claim
- May combine two claims. 7
- Classified as probably not a substantial claim. 11
May combine two claims.
Findingown dataCompared to isolated low HDL-C, high HDL-C was associated with 20-40% lower CVD risk except when TG and LDL-C were elevated.
“In contrast, compared to isolated low HDL-C, high HDL-C was associated with 20-40% lower CVD risk except when TG and LDL-C were elevated.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataCVD risk was associated with low HDL-C but this relationship was influenced by LDL-C and/or TG.
“CVD risk was associated with low HDL-C but this relationship was influenced by LDL-C and/or TG (Table 2).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataIncreased TG and LDL-C appreciably raised CVD risk.
“We also found that increased TG and LDL-C appreciably raised CVD risk”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataThe isolated low HDL-C group had relatively normal mean BMI (26.1±6.3 kg/m2), SBP (118±20 mmHg), and low diabetes prevalence (6%).
“The group with isolated low HDL-C (mean: 35±4 mg/dL [men], 44±4 mg/dL [women]) was characterized by a relatively normal mean body mass index (BMI= 26.1±6.3 kg/m2), systolic blood pressure (SBP= 118±20 mmHg) and a low prevalence of diabetes (6%)”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationHDL particles drive reverse cholesterol transport and may exert a variety of anti-atherogenic effects.
“This is biologically plausible since HDL particles drive reverse cholesterol transport and may exert a variety of anti-atherogenic effects3.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [3] Toth PP Barter PJ Rosenson RS Boden WE Chapman MJ Cuchel M D'Agostino RB Sr Davidson MH Davidson WS Heinecke JW Karas RH Kontush A Krauss RM Miller M Rader DJ High-density lipoproteins: a consensus statement from the National Lipid Association. J Clin Lipidol 2013 7 484 525 24079290 source
Not checked in the free run.
Classified as probably not a substantial claim.
PremisecitationLow HDL-C has been documented as a critical risk factor for estimating 10-year risk of CVD.
“have been documented as a critical risk factor for estimating 10-year risk of CVD2.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [2] Sheridan S Pignone M Mulrow C Framingham-based tools to calculate the global risk of coronary heart disease: a systematic review of tools for clinicians. J Gen Intern Med 2003 18 1039 52 14687264 PMC1494957 source
Not checked in the free run.
Classified as probably not a substantial claim.
PremisecitationLow HDL-C has long been viewed as a robust and independent CVD risk factor.
“For many decades, a low level of HDL-C has been viewed as a robust and independent CVD risk factor1-4.”
- Also stated in: § Introduction · plain
“Low levels of high-density lipoprotein cholesterol (HDL-C) have long been associated with increased risk for cardiovascular disease (CVD)1”
Quote in the paperSubstantial claim0 of 4 sources checked- cites [1] Miller GJ Miller NE Plasma-high-density-lipoprotein concentration and development of ischaemic heart-disease. Lancet 1975 1 16 9 46338 source
Not checked in the free run.
- cites [2] Sheridan S Pignone M Mulrow C Framingham-based tools to calculate the global risk of coronary heart disease: a systematic review of tools for clinicians. J Gen Intern Med 2003 18 1039 52 14687264 PMC1494957 source
Not checked in the free run.
- cites [3] Toth PP Barter PJ Rosenson RS Boden WE Chapman MJ Cuchel M D'Agostino RB Sr Davidson MH Davidson WS Heinecke JW Karas RH Kontush A Krauss RM Miller M Rader DJ High-density lipoproteins: a consensus statement from the National Lipid Association. J Clin Lipidol 2013 7 484 525 24079290 source
Not checked in the free run.
- cites [4] Castelli WP Doyle JT Gordon T Hames CG Hjortland MC Hulley SB Kagan A Zukel WJ HDL cholesterol and other lipids in coronary heart disease. The cooperative lipoprotein phenotyping study. Circulation 1977 55 767 72 191215 source
Not checked in the free run.
- Also stated in: § Introduction · plain
Classified as probably not a substantial claim.
Study design and conductnone givenAnalyses were adjusted for age at initial lipid profiling, gender, diabetes, hypertension, and smoking status.
“Analyses were adjusted for age at initial lipid profiling, gender, diabetes, hypertension, and smoking status.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationTRLs have been implicated in pro-inflammatory signaling pathways, impairment of insulin sensitivity and upregulation of factors promoting thrombosis.
“Specifically, TRLs have been implicated in pro-inflammatory signaling pathways, impairment of insulin sensitivity and upregulation of factors promoting thrombosis.22,23”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [22] Welty FK How do elevated triglycerides and low HDL-cholesterol affect inflammation and atherothrombosis? Curr Cardiol Rep 2013 15 400 23881582 PMC4465984 source
Not checked in the free run.
- cites [23] Rosenson RS Davidson MH Hirsh BJ Kathiresan S Gaudet D Genetics and causality of triglyceride-rich lipoproteins in atherosclerotic cardiovascular disease. J Am Coll Cardiol 2014 64 2535 2540 25500239 source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationFunctionality rather than cholesterol content of HDL has been viewed as a better predictor of CVD risk based on anti-inflammatory, anti-oxidant and endothelial restorative properties of HDL.
“As such, functionality rather than the cholesterol content of HDL has been viewed as a better predictor of CVD risk based on the well-established anti-inflammatory, anti-oxidant and endothelial restorative properties of HDL.36”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [36] Lefer AM Prostacyclin, high density lipoproteins, and myocardial ischemia. Circulation 1990 81 2013 5 2111745 source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationHDL function may be more predictive of CVD risk compared with its cholesterol content (HDL-C levels).
“Indeed recent studies suggest that HDL function may be more predictive of CVD risk compared with its cholesterol content35, as reflected by HDL-C levels.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [35] Khera AV Cuchel M de la Llera-Moya M Rodrigues A Burke MF Jafri K French BC Phillips JA Mucksavage ML Wilensky RL Mohler ER Rothblat GH Rader DJ Cholesterol efflux capacity, high-density lipoprotein function, and atherosclerosis. N Engl J Med 2011 364 127 35 21226578 PMC3030449 source
Not checked in the free run.
May combine two claims.
PremisecitationElevated TG and insulin resistance may both impair HDL function and predate the development of diabetes.
“In this regard, elevated TG and insulin resistance may both impair HDL function37-39 and predate the development of diabetes.40”
Quote in the paperNot a substantial claim0 of 4 sources checked- cites [37] Skeggs JW Morton RE LDL and HDL enriched in triglyceride promote abnormal cholesterol transport. J Lipid Res 2002 43 1264 74 12177170 source
Not checked in the free run.
- cites [38] Greene DJ Skeggs JW Morton RE Elevated triglyceride content diminishes the capacity of high density lipoprotein to deliver cholesteryl esters via the scavenger receptor class B type I (SR-BI). J Biol Chem 2001 276 4804 11 11067853 source
Not checked in the free run.
- cites [39] Barylski M Toth PP Nikolic D Banach M Rizzo M Montalto G Emerging therapies for raising high-density lipoprotein cholesterol (HDL-C) and augmenting HDL particle functionality. Best Pract Res Clin Endocrinol Metab 2014 28 453 61 24840270 source
Not checked in the free run.
- cites [40] Haffner SM Stern MP Hazuda HP Mitchell BD Patterson JK Cardiovascular risk factors in confirmed prediabetic individuals. Does the clock for coronary heart disease start ticking before the onset of clinical diabetes? JAMA 1990 263 2893 8 2338751 source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThe Framingham Heart Study was the first large epidemiological study in the U.S. to demonstrate an inverse association between low HDL-C and coronary heart disease.
“The Framingham Heart Study was the first large epidemiological study in the U.S to demonstrate an inverse association between low HDL-C and coronary heart disease32”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [32] Gordon T Castelli WP Hjortland MC Kannel WB Dawber TR High density lipoprotein as a protective factor against coronary heart disease. The Framingham Study. Am J Med 1977 62 707 14 193398 source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationPrior studies demonstrate a 30-60% increase in CVD risk when LDL-C exceeded 130 mg/dL.
“consistent with prior studies demonstrating a 30-60% increase in CVD risk when LDL-C exceeded 130 mg/dL15”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [15] National Cholesterol Education Program Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation 2002 106 3143 421 12485966 source
Not checked in the free run.
Probably not a substantial claim: may not pass S1 (asserted), S3 (load-bearing).
PremisecitationTG-rich lipoproteins (TRLs) and their cholesterol-enriched remnants play a causative role in disease.
“some proposing that TG-rich lipoproteins (TRLs; e.g., very low density lipoprotein) and their cholesterol-enriched remnants play a causative role in disease.20,21”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [20] Do R Willer CJ Schmidt EM Sengupta S Gao C Peloso GM Gustafsson S Kanoni S Ganna A Chen J Buchkovich ML Mora S Beckmann JS Bragg-Gresham JL Chang HY Demirkan A Den Hertog HM Donnelly LA Ehret GB Esko T Feitosa MF Ferreira T Fischer K Fontanillas P Fraser RM Freitag DF Gurdasani D Heikkilä K Hyppönen E Isaacs A Jackson AU Johansson A Johnson T Kaakinen M Kettunen J Kleber ME Li X Luan J Lyytikäinen LP Magnusson PK Mangino M Mihailov E Montasser ME Müller-Nurasyid M Nolte IM O'Connell JR Palmer CD Perola M Petersen AK Sanna S Saxena R Service SK Shah S Shungin D Sidore C Song C Strawbridge RJ Su source
Not checked in the free run.
- cites [21] Varbo A Benn M Tybjaerg-Hansen A Nordestgaard BG Elevated remnant cholesterol causes both low-grade inflammation and ischemic heart disease, whereas elevated low-density lipoprotein cholesterol causes ischemic heart disease without inflammation. Circulation 2013 128 1298 309 23926208 source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationPrior studies demonstrate an approximate 10-20% increase in CVD risk when TG exceeded 150 mg/dL compared to <100 mg/dL.
“and an approximate 10-20% increase in CVD risk when TG exceeded 150 mg/dL compared to < 100 mg/dL.19”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [19] Miller M Cannon CP Murphy SA Qin J Ray KK Braunwald E PROVE IT-TIMI 22 Investigators. Impact of triglyceride levels beyond low-density lipoprotein cholesterol after acute coronary syndrome in the PROVE IT-TIMI 22 trial. J Am Coll Cardiol 2008 51 724 30 18279736 source
Not checked in the free run.
The paper relies on this without support.
Fasting TG levels were not routinely measured in the original Framingham cohort until approximately 2 decades ago.
“This issue could not have been addressed in the original Framingham cohort because fasting TG levels were not routinely measured until approximately 2 decades ago.”
The paper relies on this without support.
The Framingham offspring cohort provides a unique opportunity to systematically investigate the effects of low HDL-C, both in isolation and within the framework of elevated TG and LDL-C.
“Consequently, the Framingham offspring cohort provides a unique opportunity to systematically investigate the effects of low HDL-C, both in isolation and within the framework of elevated TG and LDL-C.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
When both triglycerides and LDL-C are at least 100 mg/dl, cardiovascular risk increases by 60% in the setting of low HDL-C.
“When both TG and LDL-C are ≥100 mg/dl, CV risk increases by 60% [6].”
From HDL cholesterol: reappraisal of its clinical relevance (2017) · cites this paper as [6]
Compared with low HDL-C in isolation, cardiovascular risk increases by 30% when low HDL-C occurs together with high LDL-C and/or high triglycerides.
“Cardiovascular (CV) risk increases by 30% for LDL-C ≥ 100 mg/dl and TG < 100 mg/dl or LDL-C < 100 mg/dl and TG ≥ 100 mg/dl.”
From HDL cholesterol: reappraisal of its clinical relevance (2017) · cites this paper as [6]
The predictive value of HDL-C is modified by LDL-C and triglycerides.
“A very recent analysis of the Framingham study reports that the predictive value of HDL-C is modified by LDL cholesterol (LDL-C) and triglycerides (TG):”
From HDL cholesterol: reappraisal of its clinical relevance (2017) · cites this paper as [6]
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- Authors
- Bartlett, J., Predazzi, I. M., Williams, S. M., Bush, W. S., Kim, Y., Havas, S., Toth, P. P., Fazio, S., & Miller, M.
- Affiliations
- Dartmouth College (US)
- Venue
- Circulation: Cardiovascular Quality and Outcomes
- Published
- 2016-05
- Volume
- 9
- Issue
- 3
- Pages
- 206-212
- ISSN
- 1941-7705 (ISSN-L)
- 1941-7713
- PMC
- PMC4871717
- OpenAlex
- W2365864671
- Semantic Scholar
- 6fffc5f3c405e13423824ec8f95b03c9fcae331d
- Cited by
- 96
- References
- 48
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 10 · 2023: 6 · 2022: 8 · 2021: 12 · 2020: 13 · 2019: 11 · 2018: 12 · 2017: 7 · 2016: 5 · 2014: 1
- FWCI
- 12.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation Cardiovascular Quality and Outcomes (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01CX000147)
- National Heart, Lung, and Blood Institute (R01HL057986, T32HL007751, R01HL106845, R21HL094980)
- National Institute of General Medical Sciences (P20GM103534)
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Keywords
- low HDL cholesterol, cardiovascular risk, triglycerides, LDL cholesterol, lipid profile, Framingham Offspring cohort
- MeSH terms
- Adult, Cardiovascular Diseases, Female, Humans, Cholesterol, HDL, Cholesterol, LDL, Male, Massachusetts, Middle Aged, Phenotype, Risk Factors, Time Factors, Triglycerides, Biomarkers, Down-Regulation, Incidence, Logistic Models, Odds Ratio, Dyslipidemias
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