Lab result explainedCholesterol and lipidsLast updated November 11, 2026

Non-HDL cholesterol: normal range, how it is calculated and what a high result means

Non-HDL cholesterol (Non-HDL-C) · Lipid panel (calculated) · reported in mg/dL (outside the US mmol/L; 1 mmol/L = 38.7 mg/dL)

Non-HDL cholesterol is all the cholesterol in your blood that is not carried in HDL, the so-called good cholesterol. It is a simple subtraction, total cholesterol minus HDL cholesterol, and it captures the cholesterol in every particle that can lodge in artery walls: LDL, VLDL, intermediate-density lipoprotein, lipoprotein(a) and chylomicron remnants. On a US report it appears as "Non-HDL-C" or "Cholesterol, non-HDL" in mg/dL, and a value under 130 mg/dL is considered desirable for most adults, with 160–189 flagged as high and 190 or above as very high.

The number exists because LDL cholesterol alone misses part of the picture. LDL-C is usually calculated from a fasting sample and becomes unreliable when triglycerides are high, whereas non-HDL cholesterol works on a non-fasting sample and already includes the triglyceride-rich particles that LDL-C leaves out. In people with high triglycerides, type 2 diabetes, metabolic syndrome or obesity, non-HDL cholesterol predicts heart attacks and strokes better than LDL-C does, which is why cholesterol guidelines in the US and Europe now list it as a secondary target and some risk calculators use it directly.

Because it is derived from numbers you already have, you can work it out yourself from any old lipid panel. A total cholesterol of 210 mg/dL with an HDL of 50 gives a non-HDL of 160, which is high even though the LDL on the same report might read a reassuring 125. The gap between the two is roughly your VLDL cholesterol, and a gap much bigger than 30 mg/dL is itself a clue that triglyceride-rich particles are contributing to your risk.

Non-HDL-C at a glance

  • What it is: total cholesterol minus HDL cholesterol; the cholesterol in all the artery-clogging (apolipoprotein B) particles combined.
  • Normal (adults): under 130 mg/dL desirable; 130–159 above optimal; 160–189 high; 190–219 very high; 220 and above often genetic (non-HDL in mmol/L x 38.7 = mg/dL).
  • Children and teens: under 120 mg/dL acceptable, 120–144 borderline, 145 or more high.
  • Targets if you already have heart disease or diabetes: under 100 mg/dL, and under 85 for the highest-risk patients in European guidance; the goal is always 30 mg/dL above the LDL goal.
  • Low non-HDL is not a problem on its own; values under 70–80 mg/dL are usually from statins, a plant-based diet or genetics.
  • Next step: if high, check triglycerides, A1C, TSH and kidney and liver function, estimate 10-year risk, and address diet, weight and activity; recheck in 6 to 12 weeks after changes.

Have your whole report? Paste it into the free Lab Explainer

Every marker explained in plain language, in context with the others, with questions to bring to your appointment. No account needed.

What Non-HDL-C measures

Cholesterol travels in the blood packaged inside lipoprotein particles. HDL particles carry cholesterol away from tissues and back to the liver and are not atherogenic. Every other class of lipoprotein, LDL, VLDL, IDL, lipoprotein(a) and chylomicron remnants, carries a single apolipoprotein B molecule and can cross into the artery wall and start or feed a plaque. Non-HDL cholesterol is the total cholesterol content of that entire apoB family, which is why it tracks apolipoprotein B levels closely (an apoB of 100 mg/dL corresponds roughly to a non-HDL of 130).

The lab measures total cholesterol and HDL cholesterol directly with enzymatic assays and subtracts one from the other, so non-HDL cholesterol has no extra cost and no additional measurement error. Unlike the Friedewald LDL calculation (total minus HDL minus triglycerides divided by 5), it does not fall apart when triglycerides rise above 400 mg/dL and it does not need you to have fasted; the 2018 ACC/AHA guideline accepts a non-fasting panel for screening precisely because total and HDL cholesterol barely change after a meal.

The difference between non-HDL and LDL cholesterol is essentially VLDL cholesterol (remnant cholesterol), which in a fasting person is about one fifth of the triglyceride value. If your triglycerides are 100 mg/dL the gap is about 20 and the two numbers tell the same story; if your triglycerides are 300 the gap is 60 or more, LDL-C alone understates your risk, and non-HDL or apoB becomes the better guide.

Normal range for Non-HDL-C

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

GroupTypical range (mg/dL (outside the US mmol/L; 1 mmol/L = 38.7 mg/dL))Notes
Adults, desirableBelow 130 mg/dLEquivalent to an LDL cholesterol under 100. Labs differ in where they print the flag; many flag 130 or 160.
Adults, above optimal130–159 mg/dLCorresponds to LDL 100–129. Common in US adults; lifestyle measures are the first response.
Adults, borderline high to high160–189 mg/dLCorresponds to LDL 130–159. Combined with other risk factors this is often where statin discussion begins.
Adults, very high190–219 mg/dLA risk-enhancing factor in the 2018 ACC/AHA guideline (alongside LDL 160–189).
Adults, severe220 mg/dL and aboveWith LDL at or above 190 this suggests familial hypercholesterolemia or another genetic lipid disorder; family members may need testing.
Children and adolescents (2–19 years)Below 120 acceptable; 120–144 borderline; 145 mg/dL and above highNHLBI/American Academy of Pediatrics cut-points. Universal screening is advised at 9–11 and 17–21.
Treatment goal, established heart disease or diabetes with risk factorsBelow 100 mg/dLNational Lipid Association target for very high risk; European guidelines use below 85 mg/dL (2.2 mmol/L).
Treatment goal, moderate riskBelow 130 mg/dLAlways 30 mg/dL higher than the matching LDL goal.

High non-HDL cholesterol

A high non-HDL cholesterol means there is more cholesterol circulating in atherogenic particles than is healthy, and the higher it is and the longer it stays there, the more plaque builds in the coronary, carotid and leg arteries. In the Multinational Cardiovascular Risk Consortium, which followed almost 400,000 people, a non-HDL of 145–185 mg/dL carried roughly double the 30-year cardiovascular risk of a level under 100, and a level above 220 carried three to four times the risk. Among people already on statins, non-HDL cholesterol predicted future events better than LDL cholesterol did.

What matters clinically is the combination of the number and your overall risk. A non-HDL of 165 in a 30-year-old with no other risk factors is a reason to change diet and recheck; the same number in a 60-year-old smoker with high blood pressure is a reason to discuss statin therapy. Clinicians plug your numbers into a 10-year risk calculator (the Pooled Cohort Equations or the newer PREVENT equations), and a non-HDL of 190–219 counts as a risk enhancer that tips borderline decisions toward treatment.

A high non-HDL with a normal LDL is a specific and common pattern. It means the excess is sitting in VLDL and remnant particles, which happens when triglycerides are high, and it points to insulin resistance, excess body fat, alcohol, untreated hypothyroidism or kidney disease rather than a pure LDL problem. In that situation the triglyceride level, A1C and waist measurement are as important as the cholesterol itself.

Common causes

  1. Diet high in saturated and trans fat

    Saturated fat reduces the liver's LDL receptors, raising LDL cholesterol; every 1 percent of calories switched from saturated to polyunsaturated fat lowers LDL by about 1.8 mg/dL. Industrial trans fats raise LDL and lower HDL, pushing non-HDL up from both sides.

  2. Excess body fat, insulin resistance and metabolic syndrome

    Visceral fat and insulin resistance drive the liver to over-produce VLDL, so triglycerides and remnant cholesterol rise while HDL falls. This is the classic cause of a high non-HDL with an unremarkable LDL.

  3. Type 2 diabetes and prediabetes

    The same VLDL overproduction plus slower clearance of triglyceride-rich particles; guidelines treat non-HDL as the preferred target in diabetes, with a goal under 100 to 130 mg/dL depending on other risk factors.

  4. Familial hypercholesterolemia and familial combined hyperlipidemia

    Inherited defects in the LDL receptor pathway (about 1 in 250 people) give LDL above 190 and non-HDL above 220 from childhood; familial combined hyperlipidemia raises both LDL and triglycerides and often runs in families with early heart attacks.

  5. Hypothyroidism

    Thyroid hormone controls LDL receptor expression; an underactive thyroid raises LDL and non-HDL by 20 to 50 mg/dL and the lipids correct once TSH is normal, which is why TSH is checked before any new lipid treatment.

  6. Kidney disease and nephrotic syndrome

    Chronic kidney disease raises triglycerides and remnants; heavy protein loss in the urine (nephrotic syndrome) makes the liver massively over-produce lipoproteins, with total cholesterol sometimes above 300 mg/dL.

  7. Alcohol and refined carbohydrate

    Both increase hepatic triglyceride synthesis and VLDL output. Sugar-sweetened drinks and more than one to two alcoholic drinks a day raise the triglyceride-rich fraction of non-HDL.

  8. Medications

    Thiazide diuretics, some beta blockers, oral corticosteroids, isotretinoin, cyclosporine, some antiretrovirals, second-generation antipsychotics, anabolic steroids and some estrogen or progestin formulations raise LDL or triglycerides.

  9. Pregnancy and menopause

    Total and non-HDL cholesterol rise 25 to 50 percent in the second and third trimesters and return to baseline a few months after delivery. After menopause LDL typically rises by 10 to 15 percent as estrogen falls.

  10. Cholestatic liver disease and anorexia nervosa

    Bile duct obstruction and primary biliary cholangitis raise cholesterol through an abnormal lipoprotein (Lp-X); severe caloric restriction paradoxically raises LDL through reduced clearance.

Symptoms that can go with it

  • None; high cholesterol itself causes no symptoms, which is why it is screened for
  • Chest pressure or tightness on exertion (angina) once coronary plaque is advanced
  • Calf or thigh pain on walking that eases with rest (peripheral artery disease)
  • Transient weakness, numbness, slurred speech or vision loss (carotid disease, TIA or stroke)
  • Yellowish deposits on the eyelids (xanthelasma) or tendon lumps on the Achilles or knuckles (tendon xanthomas), which suggest familial hypercholesterolemia
  • A white or gray ring around the cornea before age 45 (arcus), another sign of a genetic lipid disorder

Low non-HDL cholesterol

There is no lower limit of normal for non-HDL cholesterol on a standard report, and a low value is almost always good news. People on statins, ezetimibe or PCSK9 inhibitors routinely run 60 to 90 mg/dL, and the outcome trials that drove LDL to 30–50 mg/dL (non-HDL roughly 60–80) found fewer heart attacks and no excess of cancer, dementia or hemorrhagic stroke attributable to the low level itself. People who have eaten a largely plant-based diet for years, and people with inherited loss-of-function variants in PCSK9 or APOB, live with lifelong non-HDL values under 80 and have markedly less heart disease.

A non-HDL that has fallen without treatment or dietary change deserves a question rather than celebration. Unintended weight loss, an overactive thyroid, malabsorption, advanced liver disease, chronic infection or inflammation and some cancers all lower cholesterol production, and a drop of 30 mg/dL or more from your usual level with no explanation is worth mentioning to your clinician.

Common causes

  1. Lipid-lowering medication

    Statins lower non-HDL by 30 to 55 percent depending on dose, ezetimibe adds 15 to 20 percent, and PCSK9 inhibitors cut it by a further 50 to 60 percent. This is the most common reason for a value under 80 mg/dL.

  2. Plant-based or very low saturated fat diet

    Vegans average LDL 20 to 30 mg/dL lower than omnivores; the Portfolio diet (soy, nuts, viscous fiber, plant sterols) lowers LDL about 17 percent in trials.

  3. Hyperthyroidism

    Excess thyroid hormone up-regulates LDL receptors and speeds cholesterol clearance, so total and non-HDL fall; they rise again as the thyroid is treated.

  4. Malabsorption, malnutrition and chronic illness

    Celiac disease, inflammatory bowel disease, chronic pancreatitis, HIV, tuberculosis and other chronic infections reduce cholesterol absorption and synthesis.

  5. Advanced liver disease

    The liver makes most circulating cholesterol; in cirrhosis a falling cholesterol tracks loss of synthetic function and is a poor prognostic sign.

  6. Inherited hypobetalipoproteinemia and PCSK9 loss-of-function variants

    Carriers have LDL and non-HDL 30 to 40 percent below average from birth and a substantially lower lifetime risk of coronary disease; some APOB variants cause fat malabsorption and need vitamin E supplementation.

  7. Acute illness, surgery or heart attack

    Cholesterol falls by 20 to 40 percent within 24 to 48 hours of a major illness and stays low for weeks; a lipid panel drawn in hospital underestimates your usual level.

Symptoms that can go with it

  • None in the great majority; a low non-HDL from treatment or diet causes no symptoms
  • Weight loss, sweating, tremor or palpitations if hyperthyroidism is the cause
  • Diarrhea, bloating, pale stools or weight loss if malabsorption is the cause
  • Fatigue, jaundice or fluid retention if liver disease is the cause
  • Night blindness or unsteadiness in rare inherited apoB disorders from fat-soluble vitamin deficiency

Read it alongside

  • LDL cholesterol — the primary target; a non-HDL more than 30 mg/dL above LDL points to triglyceride-rich remnant particles.
  • Triglycerides — the driver of the non-HDL/LDL gap; above 150 mg/dL, non-HDL or apoB should guide decisions rather than LDL-C.
  • HDL cholesterol — the number subtracted out; a low HDL with high triglycerides is the metabolic-syndrome pattern.
  • Total cholesterol — the starting point of the calculation; total minus HDL is your non-HDL.
  • Apolipoprotein B — a direct count of atherogenic particles; apoB 130 mg/dL or more is a risk enhancer and is the best check when non-HDL and LDL disagree.
  • Lipoprotein(a) — measured once in a lifetime; a high Lp(a) adds risk that non-HDL only partly captures.
  • A1C and fasting glucose — insulin resistance is the commonest reason non-HDL is high while LDL looks fine.
  • TSH — hypothyroidism raises non-HDL and should be excluded before starting a lipid drug.

What usually happens next

  1. Calculate it from any previous panel (total cholesterol minus HDL) to see how long it has been high; the trend over years is more informative than one reading.
  2. If non-HDL is 160 or higher, ask for triglycerides, A1C, TSH, creatinine with eGFR, liver enzymes and urine albumin to find secondary causes, plus a one-time lipoprotein(a).
  3. Ask your clinician to run a 10-year risk estimate (Pooled Cohort Equations or PREVENT); whether a statin is recommended depends on that overall risk, not the cholesterol alone.
  4. A non-HDL of 220 or more, or LDL of 190 or more, raises the question of familial hypercholesterolemia: expect questions about relatives with early heart attacks and a suggestion to test first-degree family members.
  5. After starting diet changes or medication, recheck in 6 to 12 weeks; most of a statin's effect is present by 4 to 6 weeks, and dietary changes show within 4 weeks.
  6. If values disagree (high non-HDL, normal LDL), ask whether apolipoprotein B would clarify the picture; it is inexpensive and does not require fasting.

Diet, lifestyle and natural levers with evidence

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

Replace saturated fat with unsaturated fat

Strong evidence

In controlled feeding studies, replacing 5 percent of calories from saturated fat (butter, fatty meat, coconut oil, cheese) with polyunsaturated fat (nuts, seeds, fish, vegetable oils) lowers LDL cholesterol by about 9 mg/dL and non-HDL by a similar amount; the Cochrane review of 15 randomized trials found a 17 percent reduction in cardiovascular events with this swap. Eliminating industrial trans fat removes a further LDL-raising, HDL-lowering effect.

Viscous soluble fiber (psyllium, oats, barley, beans)

Strong evidence

A meta-analysis of 28 randomized trials found about 10 g of psyllium a day lowered LDL by 13 mg/dL, non-HDL cholesterol by 15 mg/dL and apoB by 5 percent over 3 weeks to 6 months. Three grams a day of oat or barley beta-glucan (about 1.5 cups of cooked oatmeal) lowers LDL by 5 to 10 mg/dL. Fiber binds bile acids in the gut, forcing the liver to pull cholesterol from the blood to make more.

Start gradually and take with plenty of water; psyllium can reduce absorption of medications taken at the same time, so separate doses by 2 hours.

Portfolio-style diet with plant sterols, nuts and soy

Strong evidence

The Portfolio diet (plant sterols 2 g, viscous fiber 10–25 g, soy protein 25–50 g and 45 g of nuts a day) lowered LDL by about 13 to 17 percent at six months in a 351-person randomized trial, more than a conventional low-saturated-fat diet. Each component works alone too: 2 g a day of plant sterols or stanols lowers LDL 8 to 10 percent, and a meta-analysis of 61 trials found each daily ounce of tree nuts lowered LDL 4.8 mg/dL and apoB 3.7 mg/dL without raising weight.

Weight loss and aerobic exercise

Moderate evidence

Each kilogram of weight lost lowers LDL by about 0.8 mg/dL and triglycerides by 1.5 mg/dL, so a 10 kg loss typically lowers non-HDL by 15 to 25 mg/dL, with the largest effect on the triglyceride-rich fraction. Exercise alone has a smaller effect on LDL (2 to 5 mg/dL) but lowers triglycerides 10 to 20 percent and raises HDL 2 to 4 mg/dL at 150 minutes a week; in the STRRIDE trial, higher-volume jogging improved the whole lipoprotein profile even without weight loss.

Red yeast rice

Moderate evidence

Red yeast rice containing about 10 mg of monacolin K (chemically identical to lovastatin) lowered LDL by 15 to 25 percent and non-HDL by a similar amount in a meta-analysis of 20 randomized trials, and reduced coronary events by 45 percent in the Chinese Coronary Secondary Prevention Study. It is effectively a low-dose statin with the same benefits and the same potential side effects.

US products vary widely in monacolin content and some contain citrinin, a kidney toxin; the same muscle and liver cautions as statins apply, and it should not be combined with a prescription statin. Tell your clinician if you take it.

Berberine

Moderate evidence

Berberine 0.9 to 1.5 g a day for 8 to 12 weeks lowered LDL by about 20 to 25 mg/dL, triglycerides by about 30 mg/dL and total cholesterol by 20 to 30 mg/dL in meta-analyses of randomized trials, mainly in people with metabolic syndrome or type 2 diabetes. It increases LDL receptor expression and also modestly improves glucose, which makes it relevant to the high-triglyceride pattern of raised non-HDL.

Causes constipation or diarrhea in some people, interacts with cyclosporine, some blood thinners and drugs metabolized by CYP3A4, and is not recommended in pregnancy or breastfeeding or for newborns (risk of kernicterus).

When to see a clinician promptly

  • Chest pain or pressure, especially on exertion or with breathlessness, sweating or pain spreading to the arm or jaw: call emergency services; high cholesterol is a background risk, not a reason to wait.
  • Sudden weakness, facial droop, trouble speaking or vision loss, even if it passes within minutes: possible stroke or TIA, treat as an emergency.
  • A non-HDL of 220 mg/dL or more, or LDL of 190 or more, at any age, to be assessed for familial hypercholesterolemia and to arrange testing for children and siblings.
  • A non-HDL of 160 or more together with diabetes, high blood pressure, smoking, kidney disease or a parent or sibling with a heart attack before 55 (men) or 65 (women), to discuss formal risk assessment and treatment.
  • Cholesterol that has risen sharply since a previous test, which may signal hypothyroidism, kidney disease or a medication effect.
  • Calf pain on walking, cold or discolored feet, or wounds on the feet that are slow to heal, which suggest peripheral artery disease.

Frequently asked questions

What is a normal non-HDL cholesterol level?

Under 130 mg/dL is desirable for most adults, which corresponds to an LDL cholesterol under 100. Levels of 130–159 are above optimal, 160–189 high and 190 or more very high. If you already have heart disease, diabetes or multiple risk factors, the goal is under 100 mg/dL, and European guidelines set it under 85 for the highest-risk patients. Labs print different flags, so check the cut-off on your report.

How do you calculate non-HDL cholesterol?

Subtract your HDL cholesterol from your total cholesterol. For example, total cholesterol 220 mg/dL minus HDL 55 gives a non-HDL of 165. It does not use the triglyceride or LDL value, which is why it works on a non-fasting sample and when triglycerides are too high for LDL to be calculated. If your report is in mmol/L, do the same subtraction and multiply by 38.7 to compare with US cut-offs.

Is non-HDL of 150, 160 or 170 high?

A non-HDL of 150 is in the above-optimal band (130–159): not high by lab criteria but above the level associated with the lowest risk, and a reason to look at diet, weight and activity. Values of 160 and 170 are in the high band (160–189), equivalent to an LDL around 130–140, and whether they need medication depends on your age, blood pressure, smoking, diabetes and family history. Ask for a 10-year risk estimate rather than judging the number alone.

What is the difference between non-HDL and LDL cholesterol?

LDL cholesterol counts only the cholesterol in LDL particles. Non-HDL adds the cholesterol in VLDL, IDL, lipoprotein(a) and remnant particles, all of which also cause plaque. In a fasting person with normal triglycerides the two differ by about 30 mg/dL and tell the same story. When triglycerides are above 150 to 200 mg/dL, or you have diabetes or obesity, non-HDL is the more accurate measure of risk and the better guide to whether treatment is working.

Why is my non-HDL high when my LDL is normal?

Because the extra cholesterol is in triglyceride-rich VLDL and remnant particles rather than in LDL. That pattern usually means high triglycerides and points to insulin resistance, excess abdominal fat, alcohol, a diet high in refined carbohydrate, untreated hypothyroidism or kidney disease. In this situation an apolipoprotein B test and an A1C are useful next steps, and the most effective levers are weight loss, cutting sugar and alcohol, and exercise.

Do I need to fast for non-HDL cholesterol?

No. Total cholesterol and HDL cholesterol change very little after eating, so non-HDL is accurate on a non-fasting sample; that is one of its main advantages over calculated LDL. Triglycerides do rise after a meal, so if your clinician also wants an accurate triglyceride or a Friedewald LDL you may still be asked to fast for 9 to 12 hours.

How quickly can I lower my non-HDL cholesterol?

Dietary changes show their full effect within about 4 weeks, so a realistic plan (replacing saturated fat, adding 10 g of psyllium or 3 g of oat beta-glucan, nuts and plant sterols) can lower non-HDL by 15 to 30 mg/dL in a month or two; weight loss adds more over months. Statins reach most of their effect by 4 to 6 weeks and lower non-HDL by 30 to 55 percent. Most clinicians recheck 6 to 12 weeks after any change.

Is non-HDL cholesterol the same as apolipoprotein B?

They measure the same particle family in different ways. Non-HDL counts the cholesterol inside atherogenic particles; apoB counts the particles themselves, one apoB per particle. They usually agree (non-HDL 130 is about apoB 100 mg/dL), but when particles are small and cholesterol-poor, as in insulin resistance, apoB can be high while non-HDL looks acceptable. ApoB is a slightly better predictor and is used to break ties, but non-HDL is free with every panel.

References

  1. Cholesterol levels. MedlinePlus, US National Library of Medicine (2024)View source
  2. Cholesterol test. Mayo Clinic (2023)View source
  3. 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)
  4. 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)
  5. Brunner FJ, Waldeyer C, Ojeda F, et al.. Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium. The Lancet (2019)
  6. Boekholdt SM, Arsenault BJ, Mora S, et al.. Association of LDL cholesterol, non-HDL cholesterol, and apolipoprotein B levels with risk of cardiovascular events among patients treated with statins: a meta-analysis. JAMA (2012)
  7. Emerging Risk Factors Collaboration; Di Angelantonio E, Sarwar N, Perry P, et al.. Major lipids, apolipoproteins, and risk of vascular disease. JAMA (2009)
  8. Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents; National Heart, Lung, and Blood Institute. Expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents: summary report. Pediatrics (2011)
  9. Jovanovski E, Yashpal S, Komishon A, et al.. Effect of psyllium (Plantago ovata) fiber on LDL cholesterol and alternative lipid targets, non-HDL cholesterol and apolipoprotein B: a systematic review and meta-analysis of randomized controlled trials. American Journal of Clinical Nutrition (2018)
  10. Jenkins DJ, Jones PJ, Lamarche B, et al.. Effect of a dietary portfolio of cholesterol-lowering foods given at 2 levels of intensity of dietary advice on serum lipids in hyperlipidemia: a randomized controlled trial. JAMA (2011)
  11. Del Gobbo LC, Falk MC, Feldman R, Lewis K, Mozaffarian D. Effects of tree nuts on blood lipids, apolipoproteins, and blood pressure: systematic review, meta-analysis, and dose-response of 61 controlled intervention trials. American Journal of Clinical Nutrition (2015)
  12. Dyslipidemia. Merck Manual Professional Version (2024)

Related markers

Related conditions

Evidence guides

Worried about your number?

Ask AskMN what your Non-HDL-C result could mean in the context of your other results, symptoms and medications. Free, unlimited, no account needed.

Ask about my Non-HDL-C

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.