The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk

In the paper

“However, the association was attenuated after adjustment for HDL-C”

What the sources say

• Partly supported

  The Results (Triglyceride; page not provided) report that the triglyceride–CHD association weakened after adjustment for both HDL-C and non-HDL-C. The passage does not establish that adjustment for HDL-C alone produced the attenuation described in the claim. (LLM, conf=0.86)

  cites [72] Di Angelantonio, 2009, Major lipids, apolipoproteins, and risk of vascular disease, JAMA sourceExperimental — accuracy not yet measured

In the paper

“They found that the strength of an SNP's effect on TG levels correlated strongly with the magnitude of effect on CAD, after adjustment for the SNP's effects on LDL-C and HDL-C”

What the sources say

• Supported

  The Abstract states that the strength of a SNP’s effect on triglycerides correlates with its effect on CAD risk even after accounting for its effects on LDL-C and/or HDL-C. It also reports a strong association across 185 SNPs after adjustment for both LDL-C and HDL-C (P = 1×10−9). (LLM, conf=0.95)

  cites [116] Do, 2013, Common variants associated with plasma triglycerides and risk for coronary artery disease, Nat Genet source

In the paper

“a well-known limitation of Mendelian randomization analyses is that they are susceptible to genetic pleiotropy”

What the sources say

• Supported

  In “The Mendelian randomization study design,” the paper identifies pleiotropy as a possible shortcoming: a DNA variant may affect disease risk through mechanisms other than the biomarker being tested, undermining the causal inference. This directly supports the cited limitation. (LLM, conf=0.94)

  cites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res source

In the paper

“Two large randomized controlled trials (RCTs) evaluating the efficacy of extended-release niacin vs placebo on background statin therapy in individuals with established ASCVD did not demonstrate a reduction in vascular events”

What the sources say

• Partly supported

  The Study Design and Study Population sections describe a randomized, placebo-controlled trial of 3,414 patients, and the Discussion reports no significant reduction in cardiovascular events with extended-release niacin added to intensive statin therapy. This paper establishes the result for one trial, not two: its Discussion says the other large niacin trial, HPS2-THRIVE, was still in follow-up. (LLM, conf=0.88)

  cites [18] Boden, 2011, Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy, N Engl J Med sourceExperimental — accuracy not yet measured
• ?Could not verify

  The Discovery Cohorts and APOC3 loss-of-function results sections describe genetic associations with coronary heart disease, not niacin treatment trials. Searches for extended-release niacin, placebo, background statin therapy, and vascular events found no passage in our copy addressing the two claimed randomized trials. (LLM, conf=0.78)

  cites [19] Crosby, 2014, Loss-of-function mutations in APOC3, triglycerides, and coronary disease, N Engl J Med sourceExperimental — accuracy not yet measured

In the paper

“Volanesorsen (previously known as ISIS-APOC-III RX ) is a second-generation ASO developed to inhibit apoCIII”

What the sources say

• Partly supported

  The RESULTS passage describes ISIS 304801 as a second-generation antisense oligonucleotide designed to reduce APOC3 mRNA, supporting the drug class and intended target. Our copy does not identify ISIS 304801 as volanesorsen or ISIS-APOC-III RX, so it does not establish the name equivalence in the citing sentence. (LLM, conf=0.84)

  cites [170] Gaudet, 2015, Antisense inhibition of apolipoprotein C-III in patients with hypertriglyceridemia, N Engl J Med sourceExperimental — accuracy not yet measured

In the paper

“Mendelian randomization studies of variants associated with TGs are commonly affected by the pleiotropic effects of single-nucleotide polymorphisms (SNPs) on multiple metabolic pathways affecting plasma lipids, including HDL-C and LDL-C”

What the sources say

• Supported

  In “Plasma triglyceride-rich lipoproteins as causal,” the paper says Mendelian randomization studies using triglyceride-associated SNPs are difficult to interpret because most such SNPs have pleiotropic relationships with lipids. It specifies that 87 of 94 triglyceride-associated lead SNPs were also associated with LDL-C and/or HDL-C. (LLM, conf=0.94)

  cites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res source
• ?Not checked — no full text of the sourcecites [115] Ference, 2018, Causal effect of lipids and lipoproteins on atherosclerosis: lessons from genomic studies, Cardiol Clin source

In the paper

“was nonsignificant after adjustment for non-HDL-C”

What the sources say

• Partly supported

  The Results > Triglyceride section reports a null association between triglycerides and coronary heart disease after adjustment: HR 0.99 (95% CI, 0.94–1.05). However, that result followed adjustment for both HDL-C and non-HDL-C; the passage does not establish that adjustment for non-HDL-C alone made the association nonsignificant. (LLM, conf=0.86)

  cites [72] Di Angelantonio, 2009, Major lipids, apolipoproteins, and risk of vascular disease, JAMA sourceExperimental — accuracy not yet measured

In the paper

“TGs were not associated with stroke after adjustment for lipids”

What the sources say

• Supported

  The Methods (Statistical Analyses; page not provided) say hazard ratios were progressively adjusted for lipid measures. The Results (Triglyceride; page not provided) report adjusted triglyceride hazard ratios close to 1 for ischemic, hemorrhagic, and unclassified stroke, with confidence intervals spanning 1. This supports the claim as a finding of no statistically significant association after adjustment. (LLM, conf=0.92)

  cites [72] Di Angelantonio, 2009, Major lipids, apolipoproteins, and risk of vascular disease, JAMA source

In the paper

“This finding supported the notion that plasma TG levels are an independent causal risk factor for CAD”

What the sources say

• Partly supported

  The Abstract (page unavailable) reports that genetic effects on triglycerides correlate with CAD risk after accounting for effects on LDL-C and HDL-C, supporting the cited finding. But it concludes that triglyceride-rich lipoproteins may causally influence CAD, not that plasma triglyceride levels themselves are an independent causal risk factor. (LLM, conf=0.86)

  cites [116] Do, 2013, Common variants associated with plasma triglycerides and risk for coronary artery disease, Nat Genet sourceExperimental — accuracy not yet measured

In the paper

“In the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study, addition of fenofibrate to statin therapy did not result in significant beneficial effects on CVD risk”

What the sources say

• Supported

  The Results > Clinical Outcomes section reports no statistically significant reduction in the primary cardiovascular outcome when fenofibrate was added to simvastatin (hazard ratio 0.92; P = 0.32). No page number is provided in our copy. (LLM, conf=0.94)

  cites [146] Ginsberg, 2010, Effects of combination lipid therapy in type 2 diabetes mellitus, N Engl J Med source

In the paper

“We now understand apoCIII as a pleiotropic regulator of TGRL metabolism through LPL-dependent and LPLindependent pathways”

What the sources say

• Supported

  The Discussion explicitly calls APOC3 a central and pleiotropic regulator of triglyceride-rich lipoprotein metabolism. It describes its previously recognized effect on the LPL-dependent pathway and reports evidence that it also regulates metabolism through LPL-independent pathways. (LLM, conf=0.95)

  cites [49] Gaudet, 2014, Targeting APOC3 in the familial chylomicronemia syndrome, N Engl J Med source

In the paper

“a subgroup of patients with atherogenic dyslipidemia may have derive CV benefit from the combination of fenofibrate and simvastatin”

What the sources say

• Supported

  The Discussion reports that patients with high triglycerides and low HDL cholesterol appeared to benefit from fenofibrate, and concludes that adding fenofibrate to a statin may benefit patients with type 2 diabetes and substantial dyslipidemia. The claim preserves the paper’s tentative wording; the studied population was patients with type 2 diabetes. (LLM, conf=0.93)

  cites [146] Ginsberg, 2010, Effects of combination lipid therapy in type 2 diabetes mellitus, N Engl J Med source

In the paper

“Mendelian randomization studies further support the notion that HDL-C may not be causally related to CHD risk”

What the sources say

• Supported

  The section “Plasma HDL cholesterol as a non-causal biomarker” says genetic analyses have generally failed to support a causal role for HDL-C in CHD. It reports a Mendelian randomization study in which genetically influenced HDL-C showed no significant change in myocardial infarction risk. The triglyceride-rich lipoproteins section also reports a negligible isolated HDL-C genetic effect on CHD risk. (LLM, conf=0.94)

  cites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res source
• Partly supported

  The Discussion reports that HDL-C-raising genetic variants did not reduce myocardial infarction risk and suggests that plasma HDL-C’s association with myocardial infarction may be indirect. This supports the claim’s cautious causal interpretation, but the study tested myocardial infarction, not the broader category of coronary heart disease outcomes. (LLM, conf=0.85)

  cites [111] Voight, 2012, Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study, Lancet sourceExperimental — accuracy not yet measured

In the paper

“Again, there was no significant difference in allcause mortality”

What the sources say

• Supported

  Table 2 reports death from any cause in 220 placebo patients (17.4%) and 198 gemfibrozil patients (15.7%), with P=0.23. This supports the claim that the VA-HIT trial found no statistically significant difference in all-cause mortality. (LLM, conf=0.95)

  cites [136] Rubins, 1999, Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol, N Engl J Med source

In the paper

“three large RCTs of cholesterol ester transfer protein inhibitors (dalcetrapib, evacetrapib, and torcetrapib) did not improve CV outcomes despite substantial increases in plasma HDL-C levels”

What the sources say

• ?Not checked — no full text of the sourcecites [20] Barter, 2007, Effects of torcetrapib in patients at high risk for coronary events, N Engl J Med source
• Partly supported

  The Results and Discussion report that dalcetrapib substantially raised HDL cholesterol without improving major cardiovascular outcomes. The introductory text (p. 2090) reports increased HDL cholesterol but excess morbidity and mortality with torcetrapib. The paper does not report cardiovascular-outcome results for evacetrapib; it appears only as a lipid-level trial in the References. (LLM, conf=0.90)

  cites [21] Schwartz, 2012, Effects of dalcetrapib in patients with a recent acute coronary syndrome, N Engl J Med sourceExperimental — accuracy not yet measured
• Supported

  The introduction (p. 1934) reports that torcetrapib raised HDL cholesterol by about 70% but was associated with higher rates of death and cardiovascular events, while dalcetrapib raised HDL cholesterol by 30% without lowering cardiovascular-event rates. The Discussion reports that evacetrapib raised HDL cholesterol substantially without reducing cardiovascular events. (LLM, conf=0.93)

  cites [22] Lincoff, 2017, Evacetrapib and cardiovascular outcomes in high-risk vascular disease, N Engl J Med source

In the paper

“if a DNA variant is known to have a direct influence on the biomarker level or activity of a protein that influences the biomarker level and that biomarker is causal for disease, then the DNA variant should be associated with the disease risk without the possibility of reverse causality”

What the sources say

• Partly supported

  The Mendelian randomization study design section says that a variant directly affecting a causal biomarker should be associated with disease risk, consistent with the variant’s effect on the biomarker. It also describes the design as “fairly impervious” to reverse causation, which supports the point but is less absolute than saying reverse causality is impossible. (LLM, conf=0.84)

  cites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res sourceExperimental — accuracy not yet measured

In the paper

“The FFA formulation has greater bioavailability compared with the ethyl esters”

What the sources say

• Supported

  The Discussion reports that earlier studies found greater EPA or DHA bioavailability from free fatty acids than from ethyl esters. It also cites a study finding markedly enhanced omega-3 free-fatty-acid bioavailability over ethyl esters in overweight patients on a low-fat diet. (LLM, conf=0.91)

  cites [151] Schuchardt, 2011, Incorporation of EPA and DHA into plasma phospholipids in response to different omega-3 fatty acid formulations--a comparative bioavailability study of fish oil vs. krill oil, Lipids Health Dis source

In the paper

“Fibrates or fibric acid derivatives exert their lipidmodifying effects by activating the peroxisome proliferator-activated receptor (PPAR)-a, a nuclear receptor that increases expression of LPL, apoAI, and other lipid-related genes”

What the sources say

• Supported

  The section “FADS Polymorphisms and Plasma Levels of Omega-3 Fatty Acids” states that fenofibrate activates PPAR-alpha, a nuclear receptor that increases transcription, expression, and activity of LPL and apoAI, among other genes. It also contrasts omega-3 fatty acids with fibrates in their dependence on PPAR-alpha. No page number is provided in the supplied passages. (LLM, conf=0.91)

  cites [13] Rosenson, 2014, Genetics and causality of triglyceride-rich lipoproteins in atherosclerotic cardiovascular disease, J Am Coll Cardiol source

In the paper

“The biomarker is likely not causal for the disease if similar association between the DNA variant and disease risk as seen in observational studies is not apparent”

What the sources say

• Partly supported

  The Mendelian randomization study design section says that a missing expected association between a DNA variant and disease risk argues against the biomarker being causal. The source makes this inference conditional on the variant influencing the biomarker and the study being adequately powered; the citing sentence omits those conditions. (LLM, conf=0.82)

  cites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res sourceExperimental — accuracy not yet measured

In the paper

“10%-15% reduction in plasma TG levels with Mediterranean diet”

What the sources say

• ?Not checked — no full text of the sourcecites [38] Watts, 2013, Demystifying the management of hypertriglyceridaemia, Nat Rev Cardiol source
• ?Not checked — no full text of the sourcecites [134] Appel, 2005, Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial, JAMA source
• Partly supported

  Table 2 (page unavailable) reports triglyceride levels of 114 mg/dL in the lowest Mediterranean-diet-score quintile and 103 mg/dL in the highest—about 9.6% lower. The study supports an association near the low end of the claimed range, but does not establish a 10%–15% reduction caused by the diet. (LLM, conf=0.88)

  cites [135] Rumawas, 2009, Mediterranean-style dietary pattern, reduced risk of metabolic syndrome traits, and incidence in the Framingham Offspring Cohort, Am J Clin Nutr sourceExperimental — accuracy not yet measured

In the paper

“Rodent studies have demonstrated that inhibition of apoB synthesis did not increase hepatic steatosis compared with inhibition of MTP”

In the paper

“Moreover, remnants, due to their larger size, carry more cholesterol per particle than LDL”

In the paper

“Mexican Americans have the highest prevalence of hypertriglyceridemia across all categories of TG levels, followed by non-Hispanic whites and non-Hispanic blacks”

In the paper

“Patients with chronic kidney disease frequently have elevated TG levels due to diminished activity of LPL, reduced clearance of TGRL, and increased VLDL secretion”

In the paper

“Numerous epidemiological studies and meta-analyses have demonstrated a positive association of TGs with risk of ASCVD”

In the paper

“In fact, postprandial TG concentrations have been shown to be an equal, if not superior, predictor of future CVD events compared with fasting levels”

In the paper

“Thus, this TGRLinduced inflammatory response is characterized by monocyte adhesion to the endothelium and neutrophil activation”

In the paper

“Despite severe hypertriglyceridemia, these individuals do not develop atherosclerosis in the absence of other CV risk factors”

In the paper

“Studies suggest that there are differential effects of apoB vs MTP inhibition on hepatic steatosis”

In the paper

“However, despite substantial reduction in LDL-C, patients continue to have recurrent ASCVD events.”

In the paper

“In the general population, TG distribution is skewed with a tail toward the highest levels compared with normal distribution of other lipid parameters such as total cholesterol, LDL-C, and HDL-C”

In the paper

“On the other hand, TGRLs can be taken up by arterial wall macrophages directly without oxidative modification”

In the paper

“In most individuals, these differences in plasma fasting and nonfasting TG level are small and therefore likely clinically insignificant.”

In the paper

“Observational and genetic epidemiology consistently demonstrate that individuals with low plasma levels of LDL-C over the life course have lower rates of ASCVD compared with those with average or high levels of LDL-C”

In the paper

“Moreover, a robust evidence base has accumulated in recent years that also suggests remnant lipoproteins are important contributors to atherosclerosis and development of CVD”

In the paper

“All this may confound the causal association between elevated TG levels and ASCVD.”

In the paper

“This increased flux of FFA in the circulation also enhances intestinal chylomicron secretion leading to elevated TG levels”

In the paper

“The higher risk of events in women compared with men has been attributed to confounding from higher levels of alcohol intake in men”

In the paper

“The attenuation of LPL activity is largely due to increased concentrations of apoCIII, an endogenous inhibitor of LPL, observed in uremic states”

In the paper

“Observational and genetic epidemiological data strongly support a causal role of triglycerides (TGs) and the cholesterol content within triglyceride-rich lipoproteins (TGRLs) and/or remnant cholesterol (RC) in the development of ASCVD.”

In the paper

“A growing amount of evidence suggests that triglycerides (TGs) and/or the cholesterol content within triglyceride-rich lipoproteins (TGRLs) may contribute to this residual risk”

In the paper

“Hypertriglyceridemia may be an important contributor of this residual risk.”

In the paper

“Insulin plays a key role in the regulation of apolipoprotein (apo) B metabolism, in which it stimulates degradation of newly synthesized apoB, limiting VLDL formation”

In the paper

“On the other hand, genetic or therapeutic antagonism of apoB production can lead to hepatic steatosis through suppression of VLDL secretion”

In the paper

“Large TG-rich chylomicrons and VLDL particles cannot penetrate the arterial wall to be retained within the subendothelial space and engulfed by vascular macrophages”

In the paper

“Thus, the TGs themselves, although possibly potentiating atherogenesis, may not directly lead to plaque formation.”

In the paper

“The absence of hepatic steatosis with apoB inhibition is thought to be due to accumulation of lipids in the ER, which stimulates ER autophagy, leading to fatty acid (FA) oxidation and protection from fat accumulation”

In the paper

“The use of the Friedewald equation for LDL-C estimation, which depends on fasting lipoprotein measurements, resulted in early guideline recommendations to use fasting lipid profiles”

In the paper

“Alternatively, direct LDL-C measurements can also be used to more accurately calculate RC in the setting of significantly elevated TG levels.”

In the paper

“On the other hand, TGRLs and their remnants are thought to be equally or more atherogenic than LDL.”

In the paper

“However, evidence from Mendelian randomization studies and a series of failed randomized controlled cardiovascular (CV) outcomes trials suggests that HDL-C, although a useful biomarker of risk, may not be a causal risk factor for ASCVD”

In the paper

“Once trapped in the subendothelial space, LDL particles must be modified (e.g., oxidative modification) before they can be taken up by scavenger receptors on the surface of macrophages, leading to the formation of foam cells and development of atherosclerotic plaque”

In the paper

“Excess alcohol consumption is associated with increased adipocyte lipolysis and flux of FFAs to the liver, resulting in increased very-low-density lipoprotein (VLDL) production”

In the paper

“Therefore, an estimation of RC may be more important than the TG level itself.”

In the paper

“LPL-mediated hydrolysis of TGRL produces lipolytic products such as oxidized FFAs”

In the paper

“neither of these large niacin trials sought to recruit patients with hypertriglyceridemia”

In the paper

“Genetic studies, and in particular Mendelian randomization studies, provide a robust tool to establish causality because they capture a life-time effect of an exposure”

In the paper

“These findings were surprising to many and challenged the canonical view of apoCIII as primarily an inhibitor of LPL”

In the paper

“Importantly, subjects enrolled in the trial were on baseline statin therapy with well controlled LDL-C”

What the sources say

• ?Not checked — no full text of the sourcecites [165] Bhatt, 2019, Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia, N Engl J Med source

In the paper

“EPA-only formulations do not increase LDL-C levels compared with DHA-containing formulations”

What the sources say

• ?Not checked — no full text of the sourcecites [149] Jacobson, 2012, Effects of eicosapentaenoic acid and docosahexaenoic acid on low-density lipoprotein cholesterol and other lipids: a review, J Clin Lipidol source

In the paper

“Subsequent metaanalyses have also demonstrated similar findings regarding the benefits of fibrates in patients with true dyslipidemia”

What the sources say

• ?Not checked — no full text of the sourcecites [143] Jun, 2010, Effects of fibrates on cardiovascular outcomes: a systematic review and meta-analysis, Lancet source
• ?Not checked — no full text of the sourcecites [144] Jakob, 2016, Fibrates for primary prevention of cardiovascular disease events, Cochrane Database Syst Rev source
• ?Not checked — no full text of the sourcecites [145] Wang, 2015, Fibrates for secondary prevention of cardiovascular disease and stroke, Cochrane Database Syst Rev source

In the paper

“the Bezafibrate Infarction Prevention (BIP) study did not show a clinical benefit of bezafibrate compared with placebo for the primary composite outcome (fatal or nonfatal MI or sudden death) in patients with CHD”

What the sources say

• ?Not checked — no full text of the sourcecites [138] The BIP Study Group, 2000, Secondary prevention by raising HDL cholesterol and reducing triglycerides in patients with coronary artery disease. The Bezafibrate Infarction Prevention (BIP) study, Circulation source

In the paper

“DNA variants can be used to assess if a biological marker (e.g., TG) that has an epidemiological association for risk of disease (e.g., CHD) is likely causal for the disease”

In the paper

“there is now general consensus that adjustment of TGs by non-HDL-C is inappropriate”

In the paper

“it is now generally accepted that HDL-C, although associated with ASCVD, is not in the causal pathway”

In the paper

“As such, Mendelian randomization studies are an effective way to understand the causal role of TGRLs and CVD”

In the paper

“Thus, apoCIII is a promising target for pharmacologic modulation of TGRL metabolism”

In the paper

“The aforementioned observational epidemiology linking TGs and RC to ASCVD is largely consistent”

In the paper

“30%-50%”

What the sources say

• ?Not checked — no full text of the sourcecites [15] Shapiro, 2016, From lipids to inflammation: new approaches to reducing atherosclerotic risk, Circ Res source

In the paper

“~5% reduction in plasma TG levels with resistance training”

What the sources say

• ?Not checked — no full text of the sourcecites [38] Watts, 2013, Demystifying the management of hypertriglyceridaemia, Nat Rev Cardiol source

In the paper

“Findings from observational and genetic epidemiological studies are consistent and strongly support a causal role of TGRL and/or RC as risk factors for ASCVD”

In the paper

“despite substantial reduction in atherosclerotic risk with statins and additional LDL-C-lowering therapies, patients continue to be at a substantial residual risk for recurrent events”

In the paper

“In the Reykjavik study, TG concentrations in the highest tertile were associated with increased odds of CHD (OR, 2.04; 95% CI, 1.78 to 2.32) after adjustment for age and sex compared with the lowest tertile.”

What the sources say

• ?Not checked — no full text of the sourcecites [68] Sarwar, 2007, Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies, Circulation source

In the paper

“5%-10% reduction in initial body weight reduces TG levels by 25%”

What the sources say

• ?Not checked — no full text of the sourcecites [38] Watts, 2013, Demystifying the management of hypertriglyceridaemia, Nat Rev Cardiol source
• ?Not checked — no full text of the sourcecites [132] Van Gaal, 1997, The beneficial effects of modest weight loss on cardiovascular risk factors, Int J Obes Relat Metab Disord
• ?Not checked — no full text of the sourcecites [133] Dattilo, 1992, Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis, Am J Clin Nutr source

In the paper

“Similar findings were seen in the EPIC-Norfolk cohort.”

What the sources say

• ?Not checked — no full text of the sourcecites [68] Sarwar, 2007, Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies, Circulation source

In the paper

“0.27 mg/dL per kg weight loss”

What the sources say

• ?Not checked — no full text of the sourcecites [38] Watts, 2013, Demystifying the management of hypertriglyceridaemia, Nat Rev Cardiol source
• ?Not checked — no full text of the sourcecites [132] Van Gaal, 1997, The beneficial effects of modest weight loss on cardiovascular risk factors, Int J Obes Relat Metab Disord
• ?Not checked — no full text of the sourcecites [133] Dattilo, 1992, Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis, Am J Clin Nutr source

In the paper

“30%-50%”

What the sources say

• ?Not checked — no full text of the sourcecites [15] Shapiro, 2016, From lipids to inflammation: new approaches to reducing atherosclerotic risk, Circ Res source

In the paper

“Minimal reduction in TG in individuals with baseline TG ,150 mg/dL”

What the sources say

• ?Not checked — no full text of the sourcecites [131] Stein, 1998, Comparison of statins in hypertriglyceridemia, Am J Cardiol source

In the paper

“Further adjustment for risk factors and other lipid measures attenuated the risk (OR, 1.43; 95% CI, 1.23 to 1.65).”

What the sources say

• ?Not checked — no full text of the sourcecites [68] Sarwar, 2007, Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies, Circulation source