HDL cholesterol: what low and high HDL levels mean and how to raise it
HDL cholesterol (HDL-C) · Lipid panel · reported in mg/dL in the US; mmol/L elsewhere (1 mmol/L = 38.7 mg/dL; 40 mg/dL = 1.0 mmol/L, 60 mg/dL = 1.6 mmol/L)
HDL cholesterol is the cholesterol carried in high-density lipoprotein particles, which collect excess cholesterol from tissues and artery walls and return it to the liver, which is why it is called the 'good' cholesterol. An HDL under 40 mg/dL (1.0 mmol/L) in men or under 50 mg/dL (1.3 mmol/L) in women is low and is one of the five criteria for metabolic syndrome; 40 to 59 is acceptable; and 60 mg/dL (1.6 mmol/L) or more has traditionally been counted as protective. Most US labs flag anything under 40.
The two most common reasons HDL is low are insulin resistance (the cluster of abdominal weight gain, high triglycerides and rising glucose that precedes type 2 diabetes) and smoking, with inactivity close behind. Genetics sets each person's baseline, and women run about 10 mg/dL higher than men from puberty until menopause. Anabolic steroids and some other drugs lower it sharply; regular alcohol, endurance exercise and estrogen raise it.
HDL has a complicated reputation. In population studies, each 1 mg/dL higher HDL is linked to 2 to 3 percent lower coronary risk, and a low HDL is a reliable marker that something metabolic is wrong. But drugs that raise HDL by 20 to 100 percent (niacin and the CETP inhibitors) failed to prevent heart attacks in large trials, and people with gene variants that raise HDL are not protected. Current thinking is that a low HDL points to risk that comes from elsewhere (triglyceride-rich particles, insulin resistance, inflammation), and that raising the number by itself is not a goal. Fixing the causes of a low HDL is.
HDL-C at a glance
- What it is: cholesterol carried in HDL particles, which remove cholesterol from tissues and artery walls (reverse cholesterol transport).
- Low: under 40 mg/dL (1.0 mmol/L) in men, under 50 mg/dL (1.3 mmol/L) in women. Average is about 45–50 in men and 55–60 in women. Multiply mmol/L by 38.7 to convert.
- High: 60 mg/dL (1.6 mmol/L) or more, historically counted as a 'negative' risk factor. Very high levels (over about 90–100) do not add protection and in some studies carry higher mortality.
- Low HDL is usually a marker of insulin resistance, high triglycerides, smoking or inactivity rather than a problem in itself; it is not a treatment target in US or European guidelines.
- Niacin and CETP-inhibitor drugs raise HDL substantially but did not reduce heart attacks or strokes in trials, so no medication is prescribed to raise HDL.
- Next step: treat the causes. Exercise (about +2.5 mg/dL), quitting smoking (+4), losing weight (+0.35 per kg) and replacing refined carbohydrate with unsaturated fat each raise HDL modestly and lower risk through other routes.
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What HDL-C measures
High-density lipoproteins are the smallest and densest lipoprotein particles, built around apolipoprotein A-I made by the liver and intestine. Newly formed HDL is nearly empty of cholesterol; it picks up cholesterol from cells, including the cholesterol-laden macrophages inside artery plaques, through transporters such as ABCA1, and ferries it back to the liver for excretion in bile. HDL also carries antioxidant and anti-inflammatory enzymes. This return journey, reverse cholesterol transport, is the mechanism behind HDL's protective reputation.
The lab measures the cholesterol inside HDL particles, not the particles themselves or how well they work. Modern analysers use a direct homogeneous assay that masks the other lipoproteins and measures HDL cholesterol enzymatically; older methods precipitated LDL and VLDL first. Either way, the result is the cholesterol content of HDL, which tracks reasonably with particle number but says nothing about function. Research measures of HDL function, such as cholesterol efflux capacity, predict heart disease better than HDL cholesterol, but are not yet clinical tests.
HDL cholesterol does not need fasting and is one of the more stable lipid measures, varying about 5 to 7 percent between weeks in the same person. It falls temporarily by 20 to 40 percent during acute illness, after surgery or a heart attack, and is lowered by high triglycerides because the two particles exchange contents (via cholesteryl ester transfer protein, CETP). It rises slowly with sustained exercise or weight loss over months, so a recheck sooner than 8 to 12 weeks after a change rarely shows much.
Normal range for HDL-C
Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.
| Group | Typical range (mg/dL in the US; mmol/L elsewhere (1 mmol/L = 38.7 mg/dL; 40 mg/dL = 1.0 mmol/L, 60 mg/dL = 1.6 mmol/L)) | Notes |
|---|---|---|
| Low, men | Under 40 mg/dL (1.0 mmol/L) | NCEP ATP III 'major risk factor' threshold and the metabolic syndrome criterion for men. About 1 in 4 US men is below it. |
| Low, women | Under 50 mg/dL (1.3 mmol/L) | Metabolic syndrome criterion for women; women run roughly 10 mg/dL higher than men, so the same value means more in a woman. |
| Acceptable | 40–59 mg/dL (1.0–1.5 mmol/L) | Where most adults sit. Average US values are about 47 mg/dL in men and 58 in women. |
| High (protective range) | 60 mg/dL (1.6 mmol/L) or higher | Counted as a negative risk factor in older US guidelines; the 2018 ACC/AHA guideline uses HDL only within the overall risk calculator. |
| Very high | Above about 90–100 mg/dL (2.3–2.6 mmol/L) | No additional benefit; large cohort studies show higher all-cause mortality above about 97 mg/dL in men and 135 in women. Often genetic (CETP or hepatic lipase variants) or alcohol-related. |
| Children and adolescents | Over 45 acceptable; 40–45 borderline; under 40 low | NHLBI 2011 paediatric cut-offs. |
| During acute illness or after surgery | Falls 20 to 40 percent for several weeks | Not representative; repeat 8 weeks after recovery. |
High HDL cholesterol
An HDL of 60 mg/dL or more has long been read as good news, and up to about 80 to 90 mg/dL that is broadly supported by population data: people in this range have fewer heart attacks, partly because high HDL travels with low triglycerides, leanness, physical activity and not smoking. Older US guidelines let a high HDL 'cancel out' one other risk factor. In practice a high HDL in a healthy, active person needs no action.
Very high HDL is more ambiguous. Danish and Canadian cohort studies of more than 100,000 people found a U-shaped curve: mortality was lowest around 73 mg/dL in men and 93 in women, and rose again above roughly 97 (men) and 135 (women), with the excess coming from both cardiovascular and non-cardiovascular deaths. Genetic studies agree: variants that raise HDL (in CETP, hepatic lipase or the SR-B1 receptor) do not lower coronary risk, and the SR-B1 variant raises it despite HDL levels of 100 or more, apparently because cholesterol is stuck in HDL rather than being delivered to the liver. A very high HDL should therefore not be taken as licence to ignore LDL, blood pressure or glucose.
Outside genetics, the common drivers of a high HDL are regular alcohol (dose-related; about 4 mg/dL per 30 g of alcohol a day), endurance exercise, estrogen (natural or prescribed), and a few medications. Primary biliary cholangitis, a chronic liver disease, is a less common cause and shows up with raised alkaline phosphatase. A sudden rise in a previously average HDL is worth a question about alcohol intake and new medications.
Common causes
Inherited high HDL
Loss-of-function variants in CETP (common in people of Japanese ancestry), hepatic lipase deficiency and some apolipoprotein variants raise HDL to 80 to 150 mg/dL. These families are not consistently protected from heart disease; the SR-B1 (SCARB1) variant is associated with more coronary disease despite very high HDL.
Alcohol
A meta-analysis of 42 trials found 30 g of alcohol a day (about two drinks) raised HDL by about 4 mg/dL. Heavier drinking raises it further, but also raises triglycerides, blood pressure and the risk of cancer and liver disease, and genetic studies suggest alcohol gives no net protection to the heart.
Endurance exercise
Distance runners and cyclists typically run 10 to 20 mg/dL higher than sedentary peers of the same weight. Exercise raises HDL partly by lowering triglycerides and increasing lipoprotein lipase activity.
Female sex and estrogen
Estrogen increases apolipoprotein A-I production, so women run about 10 mg/dL higher than men from puberty to menopause. Oral estrogen (contraceptive or menopausal hormone therapy) raises HDL by 10 to 15 percent; transdermal estrogen much less.
Medications
Niacin (raises HDL 15 to 35 percent), fibrates (5 to 15 percent), statins (5 to 10 percent), the anticonvulsants phenytoin, carbamazepine and phenobarbital, and oral estrogen all raise HDL.
Primary biliary cholangitis
This autoimmune liver disease characteristically raises HDL as well as total cholesterol, with a high alkaline phosphatase and positive antimitochondrial antibodies; the high cholesterol does not seem to carry the usual cardiovascular risk.
Leanness and recent sustained weight loss
HDL dips during active weight loss and then rises above baseline once weight stabilises, by about 0.35 mg/dL for every kilogram lost.
Symptoms that can go with it
- None; high HDL causes no symptoms
- Itching, fatigue or jaundice if primary biliary cholangitis is the cause
- Flushing and itching within an hour of a dose if niacin is the cause
- A raised GGT or MCV on the same blood tests, which point to alcohol as the driver
- A very high HDL with other risk factors should still prompt attention to LDL, blood pressure and glucose, since it does not offset them
Low HDL cholesterol
A low HDL, under 40 mg/dL in men or 50 in women, is one of the most consistent markers of cardiovascular risk in population studies: in the Framingham cohort, people with an HDL under 35 had about twice the coronary risk of those over 55, independent of LDL. It is also one of the five criteria for metabolic syndrome (with a large waist, triglycerides of 150 or more, blood pressure of 130/85 or more and fasting glucose of 100 or more), and three of the five make the diagnosis. Most people with a low HDL have at least one of the others.
The reason low HDL predicts risk is largely that it is a readout of insulin resistance and high triglycerides. When triglyceride-rich particles are abundant, CETP swaps their triglyceride for HDL's cholesterol, HDL becomes triglyceride-rich and is broken down faster, and the HDL cholesterol level falls. That is why HDL is low in abdominal obesity, prediabetes, type 2 diabetes and fatty liver, and why it rises when triglycerides fall. Smoking lowers it by a further 4 to 6 mg/dL through a separate effect on HDL metabolism. Inactivity, very low-fat high-carbohydrate diets and several medications complete the usual list.
What a low HDL does not mean is that you should take something to raise it. Niacin raises HDL by 15 to 35 percent, yet in the AIM-HIGH (3,414 patients) and HPS2-THRIVE (25,673 patients) trials it prevented no heart attacks or strokes when added to a statin and caused more side effects; the CETP inhibitors raised HDL by 30 to 130 percent with no benefit or, for torcetrapib, harm. The 2018 US cholesterol guideline accordingly uses HDL only as an input to the risk calculator and sets no HDL target. The useful response to a low HDL is to treat what caused it, which means lowering triglycerides, waist size and glucose, stopping smoking and being active, and to make sure LDL and blood pressure are controlled, since those are the levers that change outcomes.
Common causes
Insulin resistance, metabolic syndrome and type 2 diabetes
The most common cause. High triglyceride-rich VLDL particles exchange triglyceride for HDL cholesterol via CETP, and the triglyceride-rich HDL is cleared faster. Low HDL with triglycerides over 150 mg/dL almost always means insulin resistance.
Smoking
Smokers have HDL about 4 to 6 mg/dL lower than non-smokers, and a meta-analysis of cessation studies found HDL rose by about 4 mg/dL within weeks of quitting, with no change in LDL.
Physical inactivity and excess abdominal fat
Sedentary people have lower lipoprotein lipase activity and higher triglycerides. HDL rises about 2.5 mg/dL with regular aerobic exercise and about 0.35 mg/dL per kilogram of sustained weight loss.
Very-low-fat, high-refined-carbohydrate diets
Replacing fat with refined carbohydrate lowers HDL by about 0.4 mg/dL per 1 percent of calories switched and raises triglycerides; replacing saturated fat with unsaturated fat does not lower HDL, while trans fats lower it.
Anabolic steroids and testosterone
Oral anabolic steroids can cut HDL by 40 to 70 percent within weeks, one of the most dramatic lipid effects of any drug; injected testosterone replacement lowers it more modestly (around 10 percent). HDL recovers within months of stopping.
Other medications
Non-selective beta-blockers (about 10 percent fall), thiazide diuretics at high dose, androgenic progestins, isotretinoin (about 15 percent), some antiretrovirals and the immunosuppressant cyclosporine lower HDL.
Acute illness, surgery and inflammation
HDL is a negative acute-phase reactant and falls 20 to 40 percent during infection, after surgery or a heart attack, and in active inflammatory disease such as rheumatoid arthritis or lupus. It recovers with the illness.
Chronic kidney disease, nephrotic syndrome and liver disease
Kidney disease impairs HDL maturation; nephrotic syndrome and advanced liver disease reduce apolipoprotein A-I production.
Inherited low HDL
Rare mutations in apolipoprotein A-I, ABCA1 (Tangier disease, with orange tonsils and HDL near zero) or LCAT cause lifelong very low HDL. Familial hypoalphalipoproteinemia (HDL under 25 to 30 across a family) is more common and may or may not raise coronary risk depending on the gene.
Multiple myeloma and other paraproteins
Abnormal antibody proteins can interfere with the HDL assay or bind HDL, producing a spuriously low or truly low value; suspected when HDL is unexpectedly very low in an older adult with anemia or kidney impairment.
Symptoms that can go with it
- None; low HDL causes no symptoms of its own
- Features of the metabolic syndrome that usually accompanies it: a waist over 40 inches (men) or 35 inches (women), high blood pressure, rising glucose
- Fatigue after meals, skin tags or dark velvety skin at the neck and armpits (acanthosis nigricans), signs of insulin resistance
- Chest pressure on exertion or calf pain on walking, if atherosclerosis has already developed
- Enlarged orange-yellow tonsils, clouded corneas and nerve symptoms in the rare Tangier disease
Read it alongside
- Triglycerides — the two move in opposite directions; a triglyceride-to-HDL ratio over 3.5 (both in mg/dL) is a practical marker of insulin resistance and small, dense LDL.
- LDL cholesterol and non-HDL cholesterol — the actual treatment targets; a low HDL raises the priority of getting these down but is not treated itself.
- Total cholesterol-to-HDL ratio — under 3.5 is ideal and over 5 raises risk; a useful summary when HDL is unusually high or low.
- Fasting glucose, A1C and fasting insulin — low HDL with triglycerides over 150 is usually insulin resistance, and these tests confirm where you are on that path.
- Apolipoprotein B — counts atherogenic particles; often high in low-HDL, high-triglyceride states even when LDL cholesterol looks acceptable.
- Apolipoprotein A-I — the main HDL protein; low with low HDL suggests fewer particles, while a normal apoA-I with low HDL cholesterol suggests cholesterol-depleted particles typical of high triglycerides.
- Alkaline phosphatase and liver enzymes — a high HDL with a high alkaline phosphatase raises the question of primary biliary cholangitis; low HDL with high ALT suggests fatty liver.
- hs-CRP — chronic inflammation lowers HDL and raises risk independently.
What usually happens next
- Look at the whole panel: a low HDL with triglycerides over 150 mg/dL points to insulin resistance, and the practical response is weight, waist, activity, glucose and triglycerides rather than HDL itself.
- Ask for your 10-year cardiovascular risk estimate, which includes HDL; the decision about statins or blood pressure treatment flows from that, not from HDL alone.
- Review medications and habits that lower HDL: smoking, anabolic steroids or testosterone, beta-blockers, high-dose thiazides, progestin-only contraceptives, isotretinoin. Mention any that could be changed.
- Give lifestyle changes 3 to 6 months before rechecking; HDL moves slowly, and expect gains of 2 to 10 mg/dL from combined exercise, smoking cessation, weight loss and swapping refined carbohydrate for unsaturated fat.
- If HDL is under 25 to 30 with normal triglycerides and no obvious cause, or very low HDL runs in your family, ask about apolipoprotein A-I measurement and a lipid clinic referral; rare genetic causes are worth naming even if treatment is the same.
- Do not start niacin or any 'HDL-raising' supplement without discussing it: niacin raises the number but did not reduce heart attacks in large trials and has real side effects.
Diet, lifestyle and natural levers with evidence
What can move HDL-C once the cause is known. Nothing here replaces finding the cause.
Regular aerobic exercise
Strong evidenceA meta-analysis of 25 randomised trials (1,404 adults) found aerobic exercise raised HDL by an average 2.5 mg/dL, with a minimum effective dose of about 120 minutes a week or 900 kcal of exercise energy expenditure, and each extra 10 minutes per session adding about 1.4 mg/dL. Duration of sessions mattered more than intensity. People with a high body mass index or high total cholesterol responded less, and the HDL rise is accompanied by larger falls in triglycerides, which is where much of the benefit lies.
Stopping smoking
Strong evidenceA meta-analysis of 27 studies found HDL rose by about 4 mg/dL (0.1 mmol/L) after quitting, with no change in LDL or total cholesterol, and a randomised trial of smokers found the increase was present at one year even in those who gained weight. Smokers run 4 to 6 mg/dL lower than non-smokers, so quitting essentially restores the deficit. Cardiovascular risk halves within one to two years of stopping, through many mechanisms beyond HDL.
Weight loss, once weight is stable
Strong evidenceA meta-analysis of 70 weight-loss studies found that during active weight loss HDL dips slightly (about 0.07 mg/dL per kg), but once weight stabilises it rises by about 0.35 mg/dL for every kilogram lost, so a 10 kg loss maintained for a few months raises HDL by about 3.5 mg/dL. The accompanying fall in triglycerides (about 1.3 mg/dL per kg) and waist size are the main reasons low HDL improves. Testing during the losing phase can be misleading.
Replace refined carbohydrate and trans fat with unsaturated fat
Moderate evidencePooled analysis of 60 controlled feeding trials found that replacing 1 percent of calories from carbohydrate with monounsaturated fat raised HDL by about 0.3 mg/dL, while trans fat lowered HDL and raised LDL. In the PREDIMED trial, a Mediterranean diet rich in olive oil and nuts improved HDL function (cholesterol efflux capacity) more than it raised the HDL number. Practically, this means olive oil, nuts, avocado and oily fish in place of white bread, sweets and sugary drinks, and avoiding partially hydrogenated oils, which are now rare in US foods.
Prescription-strength nicotinic acid, 1 to 2 g a day, raises HDL by 15 to 35 percent, lowers triglycerides by 20 to 50 percent and LDL by 5 to 25 percent, and in the pre-statin Coronary Drug Project of the 1970s it reduced heart attacks. But in the two large modern trials where it was added to a statin, AIM-HIGH (3,414 patients, HDL rose from 35 to 42 mg/dL) and HPS2-THRIVE (25,673 patients), it prevented no heart attacks or strokes and caused more serious adverse events, including new diabetes, infections and bleeding. The FDA withdrew approval for niacin-statin combinations in 2016. It is included here because people search for it, not as a recommendation.
Flushing, itching, raised blood glucose, gout flares, liver injury (particularly with sustained-release products) and muscle problems when combined with statins. Over-the-counter 'no-flush' niacin (inositol hexanicotinate) does not raise HDL. Nicotinamide, the B3 form in multivitamins, has no lipid effect.
When to see a clinician promptly
- Chest pressure or pain, breathlessness, or pain spreading to the arm, neck or jaw, with or without a known lipid problem: possible heart attack, call emergency services.
- Sudden one-sided weakness, facial droop, slurred speech or loss of vision: possible stroke, call emergency services.
- A low HDL together with a waist over 40 inches (men) or 35 (women), triglycerides over 150, blood pressure over 130/85 or fasting glucose over 100: this is metabolic syndrome and warrants a plan to prevent diabetes and heart disease.
- HDL under 25 to 30 mg/dL in you or several family members, or orange-tinted tonsils, which suggest an inherited HDL disorder worth specialist assessment.
- A sharp fall in HDL after starting a new medication or supplement, particularly anabolic steroids or testosterone, which can cut HDL by half.
- A very high HDL (over 100 mg/dL) with a raised alkaline phosphatase, itching or fatigue: possible primary biliary cholangitis.
Frequently asked questions
What is a good HDL level?
At least 40 mg/dL (1.0 mmol/L) for men and 50 mg/dL (1.3 mmol/L) for women, which are the thresholds below which HDL counts as a risk factor. An HDL of 60 mg/dL or more has historically been considered protective. Above about 90 to 100 there is no extra benefit and some studies show higher mortality, so 'higher is better' stops being true at the top of the range. The average is about 47 in US men and 58 in US women.
Is an HDL of 35 low?
Yes. An HDL of 35 mg/dL is below the 40 threshold for men and well below the 50 threshold for women, and in the Framingham study people under 35 had roughly twice the coronary risk of those over 55. On its own it does not call for medication, but it is a strong hint of insulin resistance, especially if triglycerides are over 150 mg/dL or your waist is large, and it is a reason to check glucose, A1C and blood pressure and to make sure LDL is well controlled.
How can I raise my HDL?
Four measures have good evidence: regular aerobic exercise (about +2.5 mg/dL on average, more with longer sessions), quitting smoking (about +4 mg/dL), losing weight and keeping it off (+0.35 mg/dL per kilogram lost), and replacing refined carbohydrate and trans fat with olive oil, nuts and oily fish. Lowering triglycerides raises HDL too, so cutting sugar and alcohol excess helps. None of these produces a dramatic rise, but each lowers cardiovascular risk through other routes, which is what matters. No supplement or drug raises HDL in a way that has been shown to prevent heart attacks.
Is an HDL of 80 or 100 too high?
An HDL of 80 is high and, in an active non-drinker with normal triglycerides, is simply good. At 100 and above, large cohort studies find the protection disappears and mortality starts to rise, particularly in men, and genetic studies show that very high HDL from gene variants does not prevent heart disease. The practical message is not that high HDL is dangerous but that it does not offset other risks, so LDL, blood pressure and glucose still need attention. If a very high HDL is new, think about alcohol intake, hormone therapy and liver tests.
Does alcohol raise HDL, and is that good?
Alcohol does raise HDL, by about 4 mg/dL per two drinks a day in trials, and this was long cited as the explanation for the 'French paradox'. Newer genetic studies and better-designed cohorts find no cardiovascular protection from moderate drinking once confounding is removed, while alcohol raises triglycerides, blood pressure, atrial fibrillation risk and cancer risk. No guideline recommends starting or increasing alcohol to raise HDL.
Should I take niacin to raise HDL?
No, not for that reason. Niacin raises HDL by 15 to 35 percent, but when it was added to statin treatment in two large trials totalling almost 30,000 patients it prevented no heart attacks or strokes and caused more diabetes, infections and bleeding, and the FDA withdrew approval for niacin-statin combinations in 2016. These trials, together with the failure of the CETP inhibitors, are why no drug is prescribed to raise HDL. Niacin still has a narrow role for very high triglycerides under specialist supervision.
Why is my HDL low when I eat healthily and exercise?
Genetics sets a large part of your baseline, and some people have lifelong HDL in the 30s with no metabolic problem; if your triglycerides are under 100 and your glucose normal, a low HDL carries much less meaning. Other common explanations are smoking (including vaping nicotine), testosterone or anabolic steroid use, beta-blockers, a very low-fat diet heavy in refined carbohydrate, recent illness, or testing during active weight loss, when HDL dips before it rises.
What is the triglyceride to HDL ratio?
Divide triglycerides by HDL, both in mg/dL. A ratio under 2 is ideal, 2 to 3.5 is average and over 3.5 suggests insulin resistance and a predominance of small, dense LDL particles; it was validated as a screening marker for insulin resistance in a US study of overweight adults. The cut-offs are less reliable in people of African ancestry, who tend to have lower triglycerides at the same degree of insulin resistance. If using mmol/L, the equivalent thresholds are about 0.9 and 1.5.
References
- HDL: the 'good' cholesterol. MedlinePlus, US National Library of Medicine (2024)View source
- Grundy SM, Stone NJ, Bailey AL, et al.. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA guideline on the management of blood cholesterol. Circulation (2019)
- Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA (2001)
- Voight BF, Peloso GM, Orho-Melander M, et al.. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet (2012)
- AIM-HIGH Investigators. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. New England Journal of Medicine (2011)
- HPS2-THRIVE Collaborative Group. Effects of extended-release niacin with laropiprant in high-risk patients. New England Journal of Medicine (2014)
- Madsen CM, Varbo A, Nordestgaard BG. Extreme high high-density lipoprotein cholesterol is paradoxically associated with high mortality in men and women: two prospective cohort studies. European Heart Journal (2017)
- Rohatgi A, Khera A, Berry JD, et al.. HDL cholesterol efflux capacity and incident cardiovascular events. New England Journal of Medicine (2014)
- Kodama S, Tanaka S, Saito K, et al.. Effect of aerobic exercise training on serum levels of high-density lipoprotein cholesterol: a meta-analysis. Archives of Internal Medicine (2007)
- Maeda K, Noguchi Y, Fukui T. The effects of cessation from cigarette smoking on the lipid and lipoprotein profiles: a meta-analysis. Preventive Medicine (2003)
- Dattilo AM, Kris-Etherton PM. Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis. American Journal of Clinical Nutrition (1992)
- Rimm EB, Williams P, Fosher K, Criqui M, Stampfer MJ. Moderate alcohol intake and lower risk of coronary heart disease: meta-analysis of effects on lipids and haemostatic factors. BMJ (1999)
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