Lab result explainedCholesterol and lipidsLast updated November 10, 2026

VLDL cholesterol: normal range, how it is calculated, and what a high VLDL means

VLDL cholesterol (VLDL-C) · Lipid panel (usually reported as a calculated value) · reported in mg/dL (mmol/L outside the US; 1 mmol/L = 38.7 mg/dL)

VLDL cholesterol is the amount of cholesterol carried inside very low-density lipoprotein, the particle your liver uses to ship triglycerides (fat) out to the rest of the body. On most US lab reports it is not measured at all but calculated by dividing your triglyceride result by 5, which is why it often appears as "VLDL cholesterol cal" or "VLDL (calculated)". A normal VLDL cholesterol is 2 to 30 mg/dL, which simply corresponds to a triglyceride level under 150 mg/dL.

Because VLDL is the triglyceride carrier, a high VLDL and high triglycerides are the same finding, and the causes are the same: excess calories, sugar and refined carbohydrate, alcohol, abdominal weight gain and insulin resistance, with type 2 diabetes, hypothyroidism, kidney disease, some medications and inherited lipid disorders accounting for the rest. VLDL particles and the remnants they leave behind as they unload triglyceride can enter artery walls like LDL does, which is why a high VLDL adds to cardiovascular risk and why guidelines now pay attention to "remnant cholesterol" and non-HDL cholesterol rather than LDL alone.

The calculation breaks down when triglycerides are very high. Above 400 mg/dL the VLDL estimate becomes unreliable and the LDL calculation that depends on it is not reported; above 500 mg/dL the concern shifts from heart disease to acute pancreatitis. A low VLDL is not a problem. The number is most useful as a reminder that triglycerides, not just LDL, are part of your lipid picture, and it responds quickly, within weeks, to changes in diet, alcohol and weight.

VLDL-C at a glance

  • What it is: cholesterol carried in very low-density lipoprotein, the particle the liver makes to transport triglycerides; usually calculated as triglycerides divided by 5 (mg/dL).
  • Normal: 2–30 mg/dL (some labs quote 5–40). This corresponds to fasting triglycerides under 150 mg/dL. Labs differ; use the printed range.
  • Borderline: 30–40 mg/dL (triglycerides 150–199). High: 40–100 mg/dL (triglycerides 200–499). Very high: above 100 mg/dL (triglycerides 500 or more, which raises the risk of pancreatitis).
  • The calculation is only valid when triglycerides are below 400 mg/dL and the sample is fasting; above that, labs measure LDL directly or use a different equation.
  • VLDL vs LDL: VLDL is larger, carries mostly triglyceride and is made by the liver; LDL is what VLDL becomes after unloading its triglyceride, is smaller and carries mostly cholesterol. Both are counted in non-HDL cholesterol and ApoB.
  • Lowering VLDL means lowering triglycerides: cut sugar, refined carbohydrate and alcohol, lose abdominal weight, exercise, and treat diabetes or thyroid disease; prescription omega-3 and fibrates are used when levels stay very high.

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What VLDL-C measures

After a meal, and continuously from fat stores between meals, the liver packages triglycerides and some cholesterol into VLDL particles and releases them into the blood. The enzyme lipoprotein lipase, sitting on the lining of blood vessels in muscle and fat tissue, strips triglyceride out of VLDL for energy or storage. As the particle shrinks it becomes intermediate-density lipoprotein (IDL, a VLDL remnant) and finally LDL, which carries mostly cholesterol. VLDL cholesterol is therefore a snapshot of how many triglyceride-rich particles are in circulation at the moment of the blood draw.

Few labs measure VLDL directly, because that requires ultracentrifugation or nuclear magnetic resonance (NMR) lipoprotein profiling. Instead most reports calculate it with the Friedewald convention, which assumes that VLDL particles carry cholesterol and triglyceride in a fixed ratio of about 1 to 5 by weight: VLDL cholesterol (mg/dL) = triglycerides (mg/dL) divided by 5 (or divided by 2.2 in mmol/L). The same number is then subtracted, with HDL, from total cholesterol to produce the calculated LDL. This means a VLDL result contains no information beyond your triglyceride result, and anything that raises triglycerides raises it.

The ratio assumption fails when triglycerides exceed 400 mg/dL, in the rare type III dysbetalipoproteinemia (where remnants are unusually cholesterol-rich) and in non-fasting samples, where chylomicrons from the last meal inflate triglycerides. Newer equations (Martin/Hopkins and Sampson/NIH) use adjustable factors and are valid at higher triglyceride levels; some labs now use these and will report a VLDL that is not exactly triglycerides divided by 5. A 9 to 12 hour fast is still the standard preparation if VLDL or triglycerides are the question, although non-fasting lipid panels are acceptable for general risk screening.

Normal range for VLDL-C

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

GroupTypical range (mg/dL (mmol/L outside the US; 1 mmol/L = 38.7 mg/dL))Notes
Normal (optimal)2–30 mg/dLEquivalent to fasting triglycerides under 150 mg/dL. Many labs print 5–40 mg/dL; use the printed range.
Borderline high30–40 mg/dLTriglycerides 150–199 mg/dL. Usually diet, alcohol or weight related; the point at which lifestyle change is advised.
High40–100 mg/dLTriglycerides 200–499 mg/dL. Associated with insulin resistance, metabolic syndrome and higher cardiovascular risk; remnant cholesterol becomes a meaningful part of the risk.
Very highAbove 100 mg/dLTriglycerides 500 mg/dL or more. The calculation is no longer reliable above 400, and the priority becomes preventing acute pancreatitis, particularly above 880–1,000 mg/dL of triglycerides.
Non-fasting sampleOften 10–20 mg/dL higher than fastingChylomicrons from a recent meal raise triglycerides for 4 to 8 hours; a high non-fasting VLDL is confirmed with a fasting repeat.
Remnant cholesterol (VLDL plus IDL cholesterol)Total cholesterol minus LDL minus HDL; desirable below about 30 mg/dLA broader measure that includes partly digested VLDL; each 39 mg/dL (1 mmol/L) higher is associated with roughly 1.4 to 2 times the risk of ischemic heart disease in Copenhagen population studies.
Children and adolescentsNormal below 15–20 mg/dLTriglycerides under 75 mg/dL (age 0–9) or under 90 mg/dL (age 10–19) are considered acceptable.

High VLDL cholesterol

A high VLDL cholesterol means your blood is carrying more triglyceride-rich particles than it should, almost always because the liver is making too much VLDL, clearing it too slowly, or both. In most people the drivers are everyday ones: more calories than the body needs, especially from sugar, sweetened drinks, refined carbohydrate and alcohol, which the liver converts directly into triglyceride and exports as VLDL; and abdominal weight gain with insulin resistance, which both increases VLDL output and slows its clearance. A VLDL of 40 to 60 mg/dL (triglycerides 200 to 300) in someone with a larger waist, a borderline A1C and a low HDL is the typical pattern of metabolic syndrome.

Why it matters is that VLDL and its remnants are atherogenic. They are small enough to enter artery walls, they are taken up avidly by macrophages, and Mendelian randomisation studies show that genetically higher remnant cholesterol causes coronary disease about as strongly, per particle, as LDL. A high VLDL also usually travels with a low HDL and with small, dense LDL particles, the combination called atherogenic dyslipidemia. Guidelines therefore treat triglycerides above 150 mg/dL as a risk-enhancing factor and use non-HDL cholesterol (which includes VLDL cholesterol) or ApoB as the target when triglycerides are raised.

The level also points to the cause. Mild to moderate rises (30 to 100 mg/dL) are overwhelmingly lifestyle, diabetes, medication or thyroid related. Values above 100 mg/dL, meaning triglycerides over 500, usually combine a genetic tendency (familial combined hyperlipidemia or familial hypertriglyceridemia, which together affect about 1 in 100 people) with a secondary trigger such as uncontrolled diabetes, alcohol, pregnancy or estrogen. At that level the calculation itself becomes unreliable and the clinical concern switches to the risk of acute pancreatitis, which rises steeply once triglycerides exceed 1,000 mg/dL.

Common causes

  1. Excess sugar, refined carbohydrate and alcohol

    Fructose and glucose beyond immediate needs are converted by the liver into triglyceride and exported as VLDL within hours; sugar-sweetened drinks and alcohol are the two most potent dietary drivers, and binge drinking can double triglycerides for a day or two.

  2. Abdominal obesity and insulin resistance

    Insulin normally restrains VLDL production and activates lipoprotein lipase; when cells resist insulin, the liver overproduces VLDL and the blood clears it slowly. This is the mechanism behind the high VLDL, low HDL pattern of metabolic syndrome and prediabetes.

  3. Type 2 diabetes, particularly when poorly controlled

    High glucose and insulin resistance together can push triglycerides above 300 to 500 mg/dL; improving A1C often brings VLDL down by a third or more without any other change.

  4. Hypothyroidism

    Low thyroid hormone reduces lipoprotein lipase activity and LDL receptor numbers, raising VLDL, LDL and total cholesterol together. Easily missed and easily corrected; TSH is checked for any new lipid abnormality.

  5. Chronic kidney disease and nephrotic syndrome

    Reduced clearance of triglyceride-rich particles raises VLDL in advanced kidney disease, and nephrotic syndrome stimulates liver lipoprotein production, often producing very high VLDL and LDL together.

  6. Medications

    Oral estrogen (the pill, HRT), tamoxifen, isotretinoin, corticosteroids, thiazide diuretics, non-selective beta blockers, antiretroviral protease inhibitors, second-generation antipsychotics (olanzapine, clozapine), bile acid sequestrants and immunosuppressants such as cyclosporine and sirolimus all raise triglycerides and VLDL.

  7. Inherited lipid disorders

    Familial combined hyperlipidemia (about 1 in 100) raises VLDL and LDL; familial hypertriglyceridemia raises VLDL alone, often to 500 to 1,000 mg/dL of triglycerides; type III dysbetalipoproteinemia (apoE2/E2) produces cholesterol-rich remnants and is the one condition where the Friedewald VLDL estimate is misleading at any triglyceride level.

  8. Pregnancy and a non-fasting sample

    Triglycerides rise 2 to 3 fold in the third trimester as a normal adaptation, and any meal in the preceding 8 hours raises them transiently. Both inflate a calculated VLDL and are confirmed with a fasting repeat at an appropriate time.

  9. Fatty liver disease

    Non-alcoholic fatty liver disease is both a consequence and a driver of VLDL overproduction; a raised ALT with a high VLDL and a larger waist usually means the liver is storing and exporting excess fat.

Symptoms that can go with it

  • None in the vast majority; a high VLDL is found only by testing
  • Increasing waist size, fatigue after meals and cravings for sweet or starchy food, which accompany the insulin-resistant pattern
  • Severe upper abdominal pain radiating to the back, with nausea and vomiting, when very high triglycerides cause acute pancreatitis
  • Small yellow-orange bumps on the buttocks, elbows, knees or back (eruptive xanthomas) when triglycerides exceed about 1,000 to 2,000 mg/dL
  • A creamy appearance of the retinal blood vessels (lipemia retinalis) seen by an optometrist at very high levels
  • Yellowish deposits in the palm creases or over the elbows in type III dysbetalipoproteinemia
  • Symptoms of the underlying cause: cold intolerance and weight gain in hypothyroidism, thirst and frequent urination in uncontrolled diabetes

Low VLDL cholesterol

A low VLDL cholesterol, typically under 5 to 10 mg/dL, means triglycerides are low, and it is a favorable finding rather than a problem. It is common in lean, active people, in anyone eating a diet low in sugar and alcohol, and in people following very low-carbohydrate or very low-fat eating patterns. It is also the expected effect of effective triglyceride treatment such as high-dose omega-3, fibrates or good diabetes control.

Genuinely abnormal low values, with triglycerides below about 30 to 40 mg/dL along with a very low LDL, are rare and point to conditions that impair lipoprotein production or absorption: hyperthyroidism, malabsorption or malnutrition, advanced liver disease, or inherited disorders such as abetalipoproteinemia and familial hypobetalipoproteinemia. These are investigated for the underlying condition and, in the inherited forms, for fat-soluble vitamin deficiency; the VLDL number itself needs no treatment.

Common causes

  1. Healthy diet, weight and activity

    Low intake of sugar, refined carbohydrate and alcohol, a normal waist size and regular aerobic exercise all keep liver VLDL output low and clearance brisk; VLDL under 15 mg/dL is the norm in such people.

  2. Lipid-lowering treatment

    Prescription omega-3 (4 g a day lowers triglycerides 20 to 30 percent), fibrates (30 to 50 percent), niacin and, to a lesser extent, statins all lower VLDL; a low value on treatment means it is working.

  3. Hyperthyroidism

    Excess thyroid hormone speeds the clearance of triglyceride-rich particles and lowers LDL and VLDL; levels rise back when thyroid function is corrected.

  4. Malabsorption, malnutrition and advanced liver disease

    Too little dietary fat reaching the liver, or a liver too damaged to assemble lipoproteins, lowers VLDL along with cholesterol and albumin.

  5. Inherited hypobetalipoproteinemia

    Mutations in the APOB, MTTP or PCSK9 genes reduce or abolish VLDL and LDL production. Heterozygous familial hypobetalipoproteinemia (about 1 in 1,000) is usually harmless apart from fatty liver; abetalipoproteinemia is rare and causes fat malabsorption and vitamin E deficiency from infancy.

Symptoms that can go with it

  • None; a low VLDL does not cause symptoms
  • Greasy, pale stools, poor growth or unexplained weight loss with very low lipids point to malabsorption rather than to the lipid result itself

Read it alongside

  • Triglycerides — VLDL cholesterol is triglycerides divided by 5 on most reports, so the two always move together; read the triglyceride value and its fasting status first.
  • LDL cholesterol — the calculated LDL subtracts VLDL from total cholesterol, so an unreliable VLDL (triglycerides over 400) makes the LDL unreliable too; ask for a direct LDL.
  • HDL cholesterol — a high VLDL with a low HDL (under 40 in men, 50 in women) is the atherogenic dyslipidemia of insulin resistance.
  • Non-HDL cholesterol — total minus HDL; includes VLDL, remnant and LDL cholesterol and is the preferred treatment target when triglycerides are raised (goal usually 30 mg/dL above the LDL goal).
  • Apolipoprotein B — counts every atherogenic particle (VLDL, IDL, LDL and Lp(a)); the most accurate measure of risk when triglycerides are high.
  • A1C and fasting glucose or insulin — a high VLDL is often the first laboratory sign of insulin resistance; prediabetes or diabetes is found in a large proportion.
  • ALT — mildly raised with a high VLDL and a larger waist suggests fatty liver disease, which shares the same cause.
  • TSH — hypothyroidism raises VLDL and LDL together and is treated before lipid drugs are considered.

What usually happens next

  1. If the sample was not fasting, or you had alcohol or a large meal in the 24 hours before, repeat the lipid panel after a 9 to 12 hour fast before drawing conclusions.
  2. A confirmed VLDL above 30 mg/dL (triglycerides over 150) prompts a check for secondary causes: A1C, TSH, kidney function, liver enzymes, a medication review and questions about alcohol, sugary drinks and weight change.
  3. If triglycerides are over 400 mg/dL the calculated VLDL and LDL are discarded; ask for a direct LDL or an ApoB measurement so that your LDL-related risk is assessed correctly.
  4. Lifestyle changes typically lower VLDL by 20 to 50 percent within 6 to 12 weeks; a repeat panel at 3 months shows whether they are enough. Non-HDL cholesterol or ApoB, not VLDL alone, is the usual treatment target.
  5. If VLDL stays above 40 mg/dL with other risk factors, a statin is usually first (it lowers non-HDL cholesterol and events); prescription icosapent ethyl or a fibrate is added when triglycerides remain over 150 to 500 depending on overall risk.
  6. Triglycerides persistently above 500 mg/dL, or any value above 1,000, are treated promptly to prevent pancreatitis, with a very low-fat diet, no alcohol and medication, and a lipid specialist referral is reasonable to look for an inherited cause.

Diet, lifestyle and natural levers with evidence

What can move VLDL-C once the cause is known. Nothing here replaces finding the cause.

Cut added sugar, refined carbohydrate and sugary drinks

Strong evidence

Triglycerides, and therefore VLDL, respond to carbohydrate quality more than any other lipid. Meta-analyses of controlled trials show that replacing refined carbohydrate with unsaturated fat or protein lowers triglycerides by 15 to 25 percent, and that each daily serving of sugar-sweetened drink is associated with about 10 mg/dL higher triglycerides. Limiting added sugar to under 5 to 10 percent of calories and fructose-heavy drinks in particular produces falls of 20 to 50 percent in people who start high, often within 2 to 4 weeks.

Lose abdominal weight

Strong evidence

A 5 to 10 percent loss of body weight lowers triglycerides and VLDL by about 20 percent on average, and more in people with insulin resistance, by reducing the flow of fatty acids from visceral fat to the liver. In the Look AHEAD trial, intensive lifestyle intervention in people with type 2 diabetes lowered triglycerides by about 30 mg/dL more than usual care at one year. The effect is proportional to weight lost and to how much of it comes from the abdomen.

Limit alcohol

Strong evidence

Alcohol is converted to fatty acids in the liver and directly stimulates VLDL secretion. In people with raised triglycerides, stopping or sharply reducing alcohol lowers them by 20 to 80 percent, and in those with triglycerides over 500 mg/dL abstinence is advised, since alcohol is one of the commonest precipitants of pancreatitis in this group. Even moderate intake raises triglycerides measurably in people with the insulin-resistant pattern.

Omega-3 fatty acids (EPA and DHA)

Strong evidence

Marine omega-3 at 2 to 4 g a day of EPA plus DHA lowers triglycerides by 20 to 30 percent (more when starting above 500 mg/dL) by reducing liver VLDL production, according to the American Heart Association science advisory and dozens of trials. In the REDUCE-IT trial, 4 g a day of prescription icosapent ethyl (purified EPA) lowered cardiovascular events by 25 percent in statin-treated people with triglycerides of 135 to 499 mg/dL. Over-the-counter fish oil at 1 g a day lowers triglycerides only slightly.

Doses of 3 to 4 g a day can raise LDL slightly (DHA-containing products), increase bleeding tendency and, in trials, modestly increase atrial fibrillation; discuss with your clinician if you take anticoagulants or have a heart rhythm disorder.

Regular aerobic exercise

Moderate evidence

Meta-analyses of exercise trials show aerobic training lowers triglycerides by roughly 10 to 15 percent (about 15 to 30 mg/dL) independent of weight loss, by increasing lipoprotein lipase activity in muscle, with larger effects in people starting above 150 mg/dL and with higher weekly volume. In the STRRIDE trial, the equivalent of jogging about 17 to 20 miles a week lowered VLDL particle number and triglycerides significantly over 8 months, while lower volumes produced smaller changes. The effect of a single session lasts about 24 to 48 hours, so consistency matters.

Berberine

Moderate evidence

Berberine at 0.9 to 1.5 g a day for 2 to 4 months lowered triglycerides by about 25 to 45 mg/dL and LDL by about 20 to 25 mg/dL compared with placebo in meta-analyses of randomised trials in people with type 2 diabetes or dyslipidemia, partly through AMPK activation and reduced liver lipogenesis. Trials are mostly small and from China, and no outcome data exist, so it is an adjunct rather than a replacement for statin or omega-3 therapy.

Berberine inhibits CYP3A4 and CYP2D6 and can raise levels of many drugs (including cyclosporine, some statins and metformin); it causes constipation and abdominal discomfort in some people and is avoided in pregnancy, breastfeeding and newborns.

When to see a clinician promptly

  • Severe, constant upper abdominal pain spreading to the back, with nausea or vomiting, especially with known high triglycerides or after alcohol: possible acute pancreatitis, needs emergency assessment.
  • A triglyceride result above 1,000 mg/dL (VLDL above 200), which carries a substantial pancreatitis risk and needs treatment started within days, not months.
  • Triglycerides persistently above 500 mg/dL (VLDL above 100) despite diet and alcohol changes, for medication and a search for an inherited or secondary cause.
  • A high VLDL with a high A1C, a larger waist and a low HDL, to be assessed for type 2 diabetes, fatty liver and overall cardiovascular risk.
  • New yellow-orange bumps on the skin or a creamy appearance of the blood sample reported by the lab, both signs of very high triglycerides.
  • A high VLDL while pregnant, since triglycerides above 1,000 mg/dL in the third trimester are a specific pancreatitis risk and need specialist management.

Frequently asked questions

What is a normal VLDL cholesterol level?

Normal is 2 to 30 mg/dL on most US reports, which corresponds to a fasting triglyceride level under 150 mg/dL; some labs quote 5 to 40 mg/dL. Between 30 and 40 mg/dL is borderline, 40 to 100 is high and above 100 mg/dL is very high (triglycerides over 500). Because the number is calculated from triglycerides, the triglyceride result and whether you were fasting are what really determine whether it is a concern.

What does "VLDL cholesterol cal" mean on my results?

The "cal" means calculated. Most labs do not measure VLDL directly; they estimate it by dividing your triglyceride result by 5 (in mg/dL), based on the typical ratio of triglyceride to cholesterol in VLDL particles. So a triglyceride of 120 gives a VLDL cholesterol of 24, and a triglyceride of 250 gives 50. The same estimate is subtracted from total cholesterol, along with HDL, to produce your calculated LDL. It is not valid when triglycerides exceed 400 mg/dL.

What is the difference between VLDL and LDL?

Both are made by the liver and both can contribute to artery plaque, but they carry different cargo. VLDL is a large particle packed mostly with triglyceride and is the vehicle for delivering fat to tissues; as it unloads triglyceride it shrinks into IDL and then LDL, a smaller particle that is mostly cholesterol. LDL is the main carrier of cholesterol in the blood and the primary treatment target; VLDL tracks triglycerides. High VLDL and high LDL have different main causes (sugar, alcohol and insulin resistance for VLDL; saturated fat and genetics for LDL) and partly different treatments.

Is a VLDL of 35, 40 or 50 high?

A VLDL of 35 mg/dL is borderline, corresponding to triglycerides of about 175, and is usually addressed with diet, alcohol and weight changes. A VLDL of 40 (triglycerides 200) is the start of the high range and counts as a risk-enhancing factor in cholesterol guidelines. A VLDL of 50 (triglycerides 250) is clearly high and commonly goes with insulin resistance; it is worth checking A1C and thyroid function and, if other risk factors are present, discussing a statin. None of these is an emergency, and all usually fall substantially with lifestyle change within a few months.

How do I lower VLDL cholesterol?

By lowering triglycerides. The most effective steps are cutting added sugar, sweetened drinks and refined carbohydrate (20 to 50 percent reduction), limiting or stopping alcohol (20 to 80 percent in people who drink), losing 5 to 10 percent of body weight if overweight (about 20 percent) and regular aerobic exercise (10 to 15 percent). Treating diabetes or an underactive thyroid helps when they are the cause. If VLDL stays high, prescription omega-3 (icosapent ethyl 4 g a day), a statin or a fibrate are the usual medications; discuss which with your clinician.

Does VLDL cause heart disease?

Yes, VLDL and its remnants are atherogenic. They are small enough to enter the artery wall and are readily taken up by the immune cells that form plaque, and genetic studies show that lifelong higher remnant cholesterol causes coronary disease about as strongly per particle as LDL does. A high VLDL is also usually part of a cluster, with low HDL, small dense LDL, insulin resistance and high blood pressure, which multiplies risk. This is why guidelines use non-HDL cholesterol or ApoB, both of which include VLDL, as targets when triglycerides are raised.

Do I need to fast before a VLDL test?

For an accurate VLDL or triglyceride value, yes: a 9 to 12 hour fast with water only, and no alcohol for 24 hours, because a recent meal raises triglycerides (and therefore the calculated VLDL) for several hours. Non-fasting lipid panels are now acceptable for general cardiovascular risk screening, but if the non-fasting triglycerides are above 175 to 200 mg/dL, or VLDL is being used to calculate LDL, a fasting repeat is the standard next step.

Why is my LDL blank when my VLDL is high?

Because the calculated LDL depends on the VLDL estimate, and that estimate stops being reliable once triglycerides exceed 400 mg/dL (VLDL over 80). At that point the Friedewald equation would underestimate LDL badly, so labs leave it blank or flag it. The solution is a direct LDL measurement, an ApoB test or a repeat panel once triglycerides have been brought down with fasting, diet and treatment. Some labs now use the Martin/Hopkins or Sampson equations, which remain valid up to triglycerides of about 800 mg/dL.

References

  1. VLDL test. MedlinePlus Medical Encyclopedia, US National Library of Medicine (2024)
  2. Triglycerides: why do they matter?. Mayo Clinic (2022)View source
  3. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clinical Chemistry (1972)
  4. Sampson M, Ling C, Sun Q, et al.. A new equation for calculation of low-density lipoprotein cholesterol in patients with normolipidemia and/or hypertriglyceridemia. JAMA Cardiology (2020)
  5. Miller M, Stone NJ, Ballantyne C, et al.. Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation (2011)
  6. Nordestgaard BG, Varbo A. Triglycerides and cardiovascular disease. The Lancet (2014)
  7. Varbo A, Benn M, Tybjaerg-Hansen A, Jorgensen AB, Frikke-Schmidt R, Nordestgaard BG. Remnant cholesterol as a causal risk factor for ischemic heart disease. Journal of the American College of Cardiology (2013)
  8. Skulas-Ray AC, Wilson PWF, Harris WS, et al.. Omega-3 fatty acids for the management of hypertriglyceridemia: a science advisory from the American Heart Association. Circulation (2019)
  9. Bhatt DL, Steg PG, Miller M, et al.. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia (REDUCE-IT). New England Journal of Medicine (2019)
  10. Kraus WE, Houmard JA, Duscha BD, et al.. Effects of the amount and intensity of exercise on plasma lipoproteins (STRRIDE). New England Journal of Medicine (2002)
  11. Lan J, Zhao Y, Dong F, et al.. Meta-analysis of the effect and safety of berberine in the treatment of type 2 diabetes mellitus, hyperlipemia and hypertension. Journal of Ethnopharmacology (2015)
  12. 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)

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.