Lab result explainedCholesterol and lipidsLast updated November 8, 2026

Apolipoprotein B (ApoB) test: what high and low levels mean, and ApoB vs LDL

Apolipoprotein B (ApoB) · Advanced lipid panel (ordered alongside a standard lipid panel) · reported in mg/dL (some labs report g/L; divide mg/dL by 100: 90 mg/dL = 0.9 g/L)

Apolipoprotein B (ApoB) is the protein that wraps every cholesterol-carrying particle capable of lodging in an artery wall: LDL, VLDL, IDL and lipoprotein(a). Each particle carries exactly one ApoB molecule, so an ApoB blood test is a direct count of how many of these particles are circulating, rather than how much cholesterol they happen to contain. On most US reports an ApoB under 90 mg/dL is desirable, 90 to 119 is borderline, 120 to 129 is high and 130 mg/dL or more is very high; the 2018 American cholesterol guideline treats 130 or above as a risk-enhancing factor equivalent to an LDL cholesterol of 160.

ApoB matters because it is the particle count, not the cholesterol content, that drives atherosclerosis: more particles mean more collisions with and entrapment in the artery wall. For most people ApoB and LDL cholesterol rise and fall together, but in roughly one in five adults they disagree. People with high triglycerides, abdominal obesity, insulin resistance or type 2 diabetes tend to carry many small, cholesterol-poor particles, so their LDL cholesterol looks acceptable while their ApoB is high and their true risk is underestimated. Large studies show that when the two disagree, ApoB predicts heart attack and stroke better.

ApoB is measured on a standard blood sample, does not require fasting, and is standardised against an international reference material, so results are comparable between labs. It is inexpensive but still not part of a routine lipid panel in the US, which is why most people see it only when a clinician orders an advanced panel. European guidelines now recommend it as the preferred measure whenever triglycerides are high, diabetes or obesity is present, or LDL is very low, and the 2022 American College of Cardiology expert consensus gives ApoB treatment thresholds alongside LDL for people on cholesterol-lowering therapy.

ApoB at a glance

  • What it is: the structural protein on every atherogenic lipoprotein (LDL, VLDL, IDL, lipoprotein(a)); one per particle, so ApoB equals the number of harmful particles.
  • Desirable: under 90 mg/dL for most adults; under 80 mg/dL for people with established heart disease or diabetes, and under 70 mg/dL at very high risk (2022 ACC consensus and 2019 ESC/EAS guideline).
  • High: 120–129 mg/dL is high and 130 mg/dL or more is very high; 130 is the 2018 ACC/AHA risk-enhancer threshold, roughly equivalent to an LDL cholesterol of 160 mg/dL.
  • ApoB vs LDL: roughly, LDL 100 mg/dL pairs with ApoB 80, LDL 130 with ApoB 100 and LDL 160 with ApoB 120; a higher-than-expected ApoB means many small particles and higher risk than the LDL suggests.
  • Low ApoB is desirable and is the intended effect of statins and other therapy; values under about 50 mg/dL with no treatment can reflect an inherited low-cholesterol condition, hyperthyroidism, malnutrition or liver disease.
  • Next step for a high result: estimate overall cardiovascular risk, check lipoprotein(a) once, address diet, weight and activity, and discuss statin or other therapy if ApoB stays above your risk-based threshold.

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What ApoB measures

The liver packages triglycerides and cholesterol into VLDL particles, each built around one molecule of apolipoprotein B-100. As VLDL gives up triglyceride to muscle and fat, it shrinks through IDL to LDL, keeping its single ApoB throughout. Lipoprotein(a) is an LDL particle with an extra protein attached, also carrying one ApoB. The ApoB test uses an antibody to count these molecules, so the result (in mg/dL of protein) is a direct count of all potentially artery-damaging particles, 90 percent or more of which are LDL in most people. Chylomicrons from the gut carry a shorter version, ApoB-48, that is present in small numbers and barely affects the result.

A standard lipid panel measures cholesterol mass. LDL cholesterol is usually calculated, not measured, and reports how much cholesterol the LDL particles carry in total, which depends on both how many particles there are and how much cholesterol each one holds. When particles are small and cholesterol-poor, as in insulin resistance and high triglycerides, LDL cholesterol understates the particle count; when they are large and cholesterol-rich, it overstates it. Non-HDL cholesterol (total minus HDL) is a closer stand-in for ApoB because it includes VLDL cholesterol, but it still measures mass rather than number.

ApoB is measured by immunoturbidimetry or nephelometry, standardised to a World Health Organization and International Federation of Clinical Chemistry reference material, with laboratory variation of about 5 percent. Fasting is unnecessary, because ApoB changes little after meals. Results in g/L are converted to mg/dL by multiplying by 100. ApoB falls during acute illness, after a heart attack and in pregnancy's first trimester, rises in the later months of pregnancy, and is lowered by statins, ezetimibe, PCSK9 inhibitors, bempedoic acid and thyroid hormone replacement.

Normal range for ApoB

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

GroupTypical range (mg/dL (some labs report g/L; divide mg/dL by 100: 90 mg/dL = 0.9 g/L))Notes
Desirable (general adult population)Below 90 mg/dLMost US labs flag above 90 as borderline. The US adult median is about 90 to 95 mg/dL, so 'normal' here means lower risk, not average.
Borderline high90–119 mg/dLRoughly equivalent to an LDL cholesterol of 110 to 150 mg/dL; whether to treat depends on overall risk.
High120–129 mg/dLRoughly equivalent to an LDL cholesterol of 150 to 160 mg/dL.
Very high (risk-enhancing factor)130 mg/dL or aboveThe 2018 ACC/AHA cholesterol guideline lists ApoB of 130 or more as a risk-enhancing factor favouring statin treatment, equivalent to LDL of 160 mg/dL or more.
Treatment threshold: primary prevention with high risk, diabetes or LDL 190 or moreAim below 90 mg/dL2022 ACC Expert Consensus Decision Pathway; a level at or above 90 mg/dL on maximal statin is a trigger to consider adding ezetimibe or other therapy.
Treatment threshold: established cardiovascular disease, not very high riskAim below 80 mg/dLCorresponds to an LDL cholesterol below 70 and non-HDL below 100 mg/dL in the 2022 ACC consensus; the 2019 ESC/EAS guideline sets the same 80 mg/dL goal for high-risk patients.
Treatment threshold: very high risk (recurrent events or multiple high-risk conditions)Aim below 70 mg/dLCorresponds to LDL below 55 and non-HDL below 85 mg/dL. Some clinicians aim below 65 mg/dL after repeat events, mirroring the ESC 'below 65' goal for recurrence within two years.
LowBelow about 50 mg/dLExpected on statin or PCSK9 inhibitor therapy and safe. Without treatment, consider familial hypobetalipoproteinemia, hyperthyroidism, malabsorption, malnutrition or advanced liver disease.
Children and adolescentsBelow 90 mg/dL acceptable; 90–109 borderline; 110 mg/dL or above highNHLBI pediatric lipid cut-points. ApoB at or above 110 in a child prompts evaluation for familial hypercholesterolemia.

High ApoB

A high ApoB means you have an above-average number of cholesterol-carrying particles able to enter and lodge in your artery walls, and the higher the count and the longer it persists, the more plaque accumulates. Mendelian randomisation studies, which use inherited gene variants to mimic lifelong exposure, show that risk of coronary disease tracks the number of ApoB particles rather than the cholesterol or triglyceride they carry: when researchers hold ApoB constant, LDL cholesterol and triglyceride levels stop predicting risk, but when they hold those constant, ApoB still does. In the UK Biobank, each standard-deviation rise in ApoB raised heart attack risk by about 25 percent, and ApoB outperformed both LDL and non-HDL cholesterol.

The result is most informative when it disagrees with your LDL cholesterol. An ApoB that is high relative to LDL (for example LDL 115 mg/dL with ApoB 110) means your particles are small and cholesterol-poor, which is typical of abdominal obesity, high triglycerides, insulin resistance, prediabetes and type 2 diabetes. Your risk is then closer to what an LDL of 150 would suggest, and about 20 percent of adults fall into this 'discordant' group where a standard panel is reassuring and misleading. An ApoB that is low relative to LDL means large particles and somewhat lower risk than the LDL implies.

ApoB is a measure of exposure, not a diagnosis, and it is interpreted against your overall cardiovascular risk. A 35-year-old non-smoker with an ApoB of 110 and nothing else may reasonably focus on diet and weight, while someone with diabetes, a family history of early heart disease, a high lipoprotein(a) or coronary calcium on a scan is advised to treat the same number with medication. Because every ApoB-lowering drug class lowers events in proportion to the ApoB reduction, the number is also a clean target for checking that treatment is working.

Common causes

  1. Diet high in saturated and trans fats

    Saturated fat from fatty meat, butter, cheese, coconut and palm oil reduces the liver's LDL receptors, slowing particle clearance; trans fats do the same and lower HDL. Replacing 5 percent of calories from saturated fat with polyunsaturated fat lowers ApoB by around 5 to 8 percent in controlled feeding studies.

  2. Abdominal obesity, insulin resistance and type 2 diabetes

    Insulin resistance drives the liver to secrete more VLDL particles, and the resulting high triglycerides remodel LDL into small, dense, cholesterol-poor particles. This is the classic reason ApoB is high while LDL cholesterol looks acceptable.

  3. Familial hypercholesterolemia and polygenic high cholesterol

    Inherited defects in the LDL receptor, ApoB or PCSK9 genes (familial hypercholesterolemia, about 1 in 250 people) leave particles circulating two to three times longer than normal, producing ApoB of 130 to 200 mg/dL from childhood. Milder combinations of common variants account for most other high results.

  4. Familial combined hyperlipidemia

    The most common inherited lipid disorder (1 to 2 percent of people), marked by an overproduction of ApoB-containing particles, so ApoB is high while LDL cholesterol and triglycerides fluctuate; a high ApoB is the diagnostic clue.

  5. High lipoprotein(a)

    Lp(a) is an LDL particle with an extra protein attached, carries one ApoB per particle and is set almost entirely by genes. In the 20 percent of people with high Lp(a), it can contribute 10 to 30 mg/dL to the ApoB total and is not lowered by diet or statins.

  6. Hypothyroidism

    Low thyroid hormone reduces LDL receptor activity and clearance; ApoB and LDL rise together and fall with thyroid replacement, which is why TSH is checked before lipid-lowering drugs are started.

  7. Kidney disease and nephrotic syndrome

    Protein loss in nephrotic syndrome stimulates liver lipoprotein production, raising ApoB markedly; chronic kidney disease more often raises triglycerides and small dense LDL.

  8. Medications

    Thiazide diuretics at high dose, some beta-blockers, oral estrogens and progestins, anabolic steroids, isotretinoin, cyclosporine, some antiretrovirals and antipsychotics raise ApoB-containing lipoproteins.

  9. Pregnancy, menopause and ageing

    ApoB rises progressively through pregnancy and returns to baseline after delivery; it also rises by about 10 percent across the menopause transition as estrogen falls, and climbs gradually with age in both sexes.

  10. Cholestatic liver disease, Cushing's syndrome and anorexia nervosa

    Bile duct obstruction, excess cortisol and, paradoxically, severe calorie restriction each raise ApoB through altered liver lipoprotein handling.

Symptoms that can go with it

  • None; high ApoB causes no symptoms until plaque has built up over years, which is why it is found by testing
  • Yellowish deposits on the eyelids (xanthelasma), lumps over the Achilles tendons or knuckles (tendon xanthomas) or a white ring around the iris before age 45 (corneal arcus) suggest familial hypercholesterolemia
  • Chest tightness or pressure on exertion, relieved by rest, which can indicate established coronary disease
  • Calf, thigh or buttock pain when walking that eases with rest (peripheral artery disease)
  • Brief loss of vision in one eye, one-sided weakness or slurred speech, which are warning signs of stroke and need emergency care

Low ApoB

A low ApoB is, for the purposes of heart disease, good news. People born with gene variants that keep ApoB and LDL very low for life, such as loss-of-function PCSK9 variants, have 50 to 90 percent lower rates of coronary disease and no shortfall in health, and trials that drove LDL cholesterol below 30 mg/dL and ApoB below 50 with PCSK9 inhibitors on top of statins found fewer heart attacks and strokes with no increase in cancer, dementia, diabetes or other harms over several years. If you are on cholesterol-lowering treatment and your ApoB is 40 to 60 mg/dL, that is the treatment working, and there is no lower limit at which it should be stopped.

In someone taking nothing, an ApoB below about 50 mg/dL deserves a thought about why. Familial hypobetalipoproteinemia, caused by a truncating variant in the ApoB gene and carried by about 1 in 1,000 people, produces ApoB of 20 to 50 mg/dL and LDL cholesterol under 50; carriers are protected from heart disease but prone to fatty liver and, in some, vitamin E deficiency. Acquired causes include an overactive thyroid, malabsorption, malnutrition, advanced liver disease, chronic infection or inflammation, and a recent serious illness or heart attack, which lower ApoB temporarily. The rare recessive condition abetalipoproteinemia produces an undetectable ApoB from infancy with fat malabsorption and neurological problems.

Common causes

  1. Statins, ezetimibe, PCSK9 inhibitors, bempedoic acid and inclisiran

    The intended effect. High-intensity statins lower ApoB by 40 to 50 percent, ezetimibe adds 15 to 20 percent and PCSK9 inhibitors a further 50 to 60 percent, bringing many patients to 30 to 50 mg/dL.

  2. Familial hypobetalipoproteinemia

    A truncated ApoB gene lowers particle production; heterozygotes have ApoB of roughly 20 to 50 mg/dL, very low LDL, lifelong protection from atherosclerosis and an increased tendency to fatty liver.

  3. PCSK9 loss-of-function variants

    Carried by about 2 to 3 percent of African Americans, these lower LDL cholesterol by about 28 to 40 percent across life and cut coronary disease risk by up to 88 percent, with no adverse effects identified.

  4. Hyperthyroidism

    Excess thyroid hormone increases LDL receptor activity and particle clearance; ApoB and LDL fall and recover when the thyroid is treated.

  5. Malnutrition, malabsorption and anorexia with very low fat intake

    Celiac disease, pancreatic insufficiency, bariatric surgery and prolonged undernutrition reduce the substrate for lipoprotein production; severe restriction can paradoxically raise LDL in some people.

  6. Advanced liver disease

    Cirrhosis and liver failure cut the liver's capacity to make lipoproteins; a falling ApoB and cholesterol in liver disease tracks worsening synthetic function.

  7. Acute illness, heart attack, surgery and chronic inflammation

    ApoB and LDL fall by 10 to 20 percent within 24 to 48 hours of a heart attack, sepsis or major surgery and stay low for several weeks; a lipid panel drawn in hospital can understate the baseline.

  8. Abetalipoproteinemia

    A very rare recessive defect in the protein that loads lipid onto ApoB, producing an undetectable ApoB, fat malabsorption from infancy, spiky red cells and, without high-dose vitamin E and A, progressive nerve and retinal damage.

Symptoms that can go with it

  • None in the great majority; a low ApoB on treatment or from a protective gene variant causes no symptoms
  • Fatty liver, sometimes with mildly raised liver enzymes, in familial hypobetalipoproteinemia
  • Pale, bulky, greasy stools, weight loss and bloating if malabsorption is the cause
  • Weight loss, heat intolerance, tremor and palpitations if hyperthyroidism is the cause
  • Night blindness, unsteadiness or loss of sensation in the rare inherited conditions that impair fat-soluble vitamin absorption

Read it alongside

  • LDL cholesterol — the standard measure; the ratio of ApoB to LDL shows whether your particles are small and numerous (ApoB high relative to LDL) or large and few.
  • Non-HDL cholesterol — total minus HDL; tracks ApoB more closely than LDL and is available free on every lipid panel. Non-HDL above 130 mg/dL roughly matches ApoB above 100.
  • Triglycerides — when above 150 mg/dL, LDL cholesterol increasingly underestimates particle number and ApoB (or non-HDL) becomes the better guide.
  • HDL cholesterol — part of the standard panel; a low HDL with high triglycerides is the pattern in which ApoB is most likely to be unexpectedly high.
  • Lipoprotein(a) — measured once in everyone; a high Lp(a) explains part of a high ApoB, is not diet-responsive and adds independent risk.
  • A1C and fasting glucose — insulin resistance and diabetes are the commonest reasons ApoB and LDL disagree.
  • TSH — hypothyroidism raises ApoB and is corrected by treating the thyroid rather than the lipids.
  • hs-CRP and coronary artery calcium score — refine whether a borderline ApoB warrants medication by adding inflammation and plaque burden to the picture.

What usually happens next

  1. A high ApoB is read against your 10-year cardiovascular risk (the pooled cohort equations or PREVENT calculator), family history, blood pressure, A1C and smoking status; the same number means different things at different levels of overall risk.
  2. Ask for a lipoprotein(a) if you have never had one; it is measured once, explains part of a high ApoB and changes how aggressively other risk factors are treated.
  3. Secondary causes are excluded with a TSH, liver tests, kidney function and urine protein, and a review of medicines that raise lipids.
  4. Diet, weight and activity changes are given 3 to 6 months and the test repeated; a 10 to 15 percent fall is typical with sustained changes, more with substantial weight loss.
  5. If ApoB stays above your risk-based threshold (90 mg/dL for primary prevention at raised risk, 80 with established disease or diabetes, 70 at very high risk), the discussion turns to statin therapy, with ezetimibe or other agents added if the target is not reached; ApoB is rechecked 4 to 12 weeks after each change.
  6. For an ApoB at or above 130 mg/dL from a young age, or with tendon xanthomas or a family history of early heart disease, ask about testing relatives and genetic testing for familial hypercholesterolemia.

Diet, lifestyle and natural levers with evidence

What can move ApoB once the cause is known. Nothing here replaces finding the cause.

Replacing saturated fat with unsaturated fat

Strong evidence

A World Health Organization systematic review of 84 controlled feeding trials found that replacing 1 percent of daily calories from saturated fat with polyunsaturated fat lowers ApoB by about 1 mg/dL, with smaller effects from monounsaturated fat and carbohydrate; swapping 5 percent of calories (roughly butter and fatty meat for olive oil, nuts, seeds and oily fish) lowers ApoB by 5 to 8 percent. Mediterranean-style eating in the PREDIMED trial and the Portfolio diet (plant sterols, soluble fibre, soy protein and nuts) in randomised trials lowered ApoB by 8 to 12 percent against a low-fat control. Trans fats raise ApoB and should be avoided entirely.

Soluble fibre, particularly psyllium and oats

Strong evidence

A meta-analysis of 28 randomised trials found that about 10 g of psyllium a day lowered LDL cholesterol by 13 mg/dL, non-HDL cholesterol by 15 mg/dL and ApoB by about 5 mg/dL (0.05 g/L) over a median of 8 weeks, with larger effects in people starting higher. Oat beta-glucan at 3 g a day gives a similar LDL reduction of 5 to 7 percent. Soluble fibre binds bile acids in the gut, forcing the liver to pull cholesterol out of circulation to replace them.

Take with plenty of water and separate from medicines by at least 2 hours, as psyllium can reduce absorption of some drugs. Can cause bloating in the first weeks.

Weight loss when carrying excess abdominal fat

Strong evidence

Because insulin resistance drives overproduction of ApoB particles, weight loss lowers ApoB more than LDL cholesterol would predict. Meta-analyses of diet-induced weight loss trials show a fall of roughly 1 mg/dL in ApoB per kilogram lost in the first months, so a 10 percent weight loss typically lowers ApoB by 8 to 12 mg/dL and triglycerides by 20 to 30 percent; bariatric surgery lowers ApoB by 20 to 30 percent. The composition of the diet matters less than the sustained loss, though low-carbohydrate approaches lower triglycerides more and saturated-fat-heavy versions can raise LDL.

Tree nuts (about 1 to 2 oz a day)

Moderate evidence

A meta-analysis of 61 controlled trials found that each 1 oz serving of tree nuts a day lowered ApoB by 3.7 mg/dL, LDL cholesterol by 4.8 mg/dL and total cholesterol by 4.7 mg/dL, with larger effects at 2 oz a day and no weight gain when nuts replaced other snacks. Walnuts, almonds, pistachios and hazelnuts all worked; the effect comes from unsaturated fat, fibre and plant sterols displacing saturated fat and refined carbohydrate.

Plant sterols and stanols (2 g a day)

Moderate evidence

Plant sterols compete with cholesterol for absorption in the gut. A meta-analysis of 124 trials found 2 g a day lowered LDL cholesterol by about 8 to 10 percent, and trials reporting ApoB show falls of 6 to 8 percent (roughly 6 to 9 mg/dL), additive to statins. Doses above 3 g add little. Fortified spreads, yogurts and supplements are the practical sources; a normal diet provides only 0.2 to 0.4 g.

Not recommended in the rare inherited condition sitosterolemia. Effects on cardiovascular events have not been tested in outcome trials.

Red yeast rice (monacolin K)

Moderate evidence

Red yeast rice contains monacolin K, chemically identical to lovastatin. Meta-analyses of randomised trials show products supplying 3 to 10 mg of monacolin K a day lower LDL cholesterol by 15 to 25 percent and ApoB by a similar proportion, and a Chinese outcome trial of a standardised extract reduced coronary events by about 45 percent over 4.5 years in people after a heart attack.

Because it is a statin, it carries the same risks of muscle symptoms and interactions (grapefruit, some antibiotics and antifungals, cyclosporine) and must not be combined with a prescribed statin. US products are unregulated: monacolin content varies up to a hundredfold and some contain the kidney toxin citrinin. The FDA treats products with meaningful monacolin K as unapproved drugs. Discuss with your clinician rather than self-treating.

When to see a clinician promptly

  • Chest pressure, tightness or pain, especially on exertion or with breathlessness, sweating or nausea: call emergency services, since a high ApoB raises the chance this is a heart attack.
  • Sudden one-sided weakness, facial droop, slurred speech or loss of vision in one eye: emergency care for a possible stroke.
  • An ApoB of 130 mg/dL or more, or an LDL of 190 or more, at any age, which suggests familial hypercholesterolemia and calls for treatment and family screening regardless of other risk factors.
  • A high ApoB with diabetes, high blood pressure, smoking, kidney disease or a parent or sibling who had a heart attack or stroke before 55 (men) or 65 (women).
  • Calf or thigh pain when walking that eases with rest, or wounds on the feet that are slow to heal, which can indicate peripheral artery disease.
  • An unexpectedly low ApoB (below 50 mg/dL) without treatment, together with weight loss, greasy stools, tremor or abnormal liver tests.

Frequently asked questions

What is a normal ApoB level?

Most US labs call under 90 mg/dL desirable, 90 to 119 borderline, 120 to 129 high and 130 mg/dL or more very high. The US adult median is around 90 to 95 mg/dL, so an 'optimal' result is lower than average. For people who already have heart disease or diabetes, guidelines aim for under 80 mg/dL, and under 70 mg/dL for those at very high risk. Children should be under 90, with 110 or more considered high.

Is ApoB better than LDL?

As a predictor of heart attack and stroke, yes, by a modest margin, and the gap widens in people with high triglycerides, obesity, insulin resistance or diabetes. ApoB counts the harmful particles directly, while LDL cholesterol measures how much cholesterol they carry, which varies. When the two agree, either works; when they disagree, ApoB is right about the risk. The 2019 European guideline recommends ApoB as the preferred measure in those groups, and the 2018 US guideline treats ApoB of 130 or more as a risk-enhancing factor.

What ApoB level corresponds to my LDL?

In the general population, LDL cholesterol of 70 mg/dL pairs with an ApoB of about 60 to 65, LDL 100 with ApoB 80, LDL 130 with ApoB 100, and LDL 160 with ApoB 120. The 2022 ACC consensus uses LDL below 55 / ApoB below 70, LDL below 70 / ApoB below 80, and LDL below 100 / ApoB below 90 as equivalent treatment thresholds. If your ApoB is more than about 10 to 15 mg/dL above what your LDL predicts, you have many small particles and your risk is higher than the LDL suggests.

How do I lower ApoB naturally?

Swap saturated fat (butter, fatty meat, cheese, coconut oil) for olive oil, nuts, seeds and oily fish; eat 10 g a day of soluble fibre from psyllium, oats, beans and lentils; add 1 to 2 oz of nuts a day; use 2 g of plant sterols; and lose abdominal fat if you carry excess. Each of these lowers ApoB by roughly 5 to 10 percent in trials, and combined in a Portfolio-style diet they have achieved reductions of 10 to 15 percent, similar to a low-dose statin. Give it 3 months and recheck; genetics set a floor that some people cannot reach without medication.

Does exercise lower ApoB?

Modestly. Meta-analyses of aerobic exercise trials show ApoB falls of about 3 to 5 mg/dL, with larger effects when exercise produces weight loss, and resistance training gives a similar small reduction. Exercise has a bigger effect on triglycerides and HDL than on ApoB and LDL. It remains worthwhile because it lowers cardiovascular risk through blood pressure, insulin sensitivity and fitness, independently of lipids.

Is an ApoB of 100 high?

An ApoB of 100 mg/dL is in the borderline-high band (90 to 119) and corresponds to an LDL cholesterol of about 130 mg/dL. For a healthy adult with no other risk factors, it is a reason to improve diet and activity and recheck. For someone with diabetes, established heart disease, a high lipoprotein(a) or a strong family history, it is above the 80 to 90 mg/dL thresholds guidelines use and medication is usually discussed.

Do I need to fast for an ApoB test?

No. ApoB changes very little after meals, which is one of its advantages over the standard lipid panel, where triglycerides and calculated LDL are affected by food. If ApoB is drawn with a standard panel your lab may still ask you to fast for the other values, but the ApoB result itself is valid either way.

Can ApoB be too low?

Not from treatment. Trials that pushed ApoB below 50 mg/dL and LDL below 30 with PCSK9 inhibitors showed fewer cardiovascular events and no excess of cancer, cognitive problems, diabetes or other harms over several years, and people born with lifelong very low ApoB are protected from heart disease. A very low ApoB in someone taking nothing is sometimes a sign of an inherited low-cholesterol condition (which can cause fatty liver), an overactive thyroid, malabsorption or liver disease, and is worth a brief check.

References

  1. Sniderman AD, Thanassoulis G, Glavinovic T, et al.. Apolipoprotein B particles and cardiovascular disease: a narrative review. JAMA Cardiology (2019)
  2. Lloyd-Jones DM, Morris PB, Ballantyne CM, et al.. 2022 ACC Expert Consensus Decision Pathway on the role of nonstatin therapies for LDL-cholesterol lowering in the management of atherosclerotic cardiovascular disease risk. Journal of the American College of Cardiology (2022)
  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. Mach F, Baigent C, Catapano AL, et al.. 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. European Heart Journal (2020)
  5. Marston NA, Giugliano RP, Melloni GEM, et al.. Association of apolipoprotein B-containing lipoproteins and risk of myocardial infarction in individuals with and without atherosclerosis: distinguishing between particle concentration, type, and content. JAMA Cardiology (2022)
  6. Ference BA, Kastelein JJP, Ray KK, et al.. Association of triglyceride-lowering LPL variants and LDL-C-lowering LDLR variants with risk of coronary heart disease. JAMA (2019)
  7. Ference BA, Ginsberg HN, Graham I, et al.. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies: a consensus statement from the European Atherosclerosis Society Consensus Panel. European Heart Journal (2017)
  8. Mensink RP. Effects of saturated fatty acids on serum lipids and lipoproteins: a systematic review and regression analysis. World Health Organization (2016)
  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. 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)
  11. Ras RT, Geleijnse JM, Trautwein EA. LDL-cholesterol-lowering effect of plant sterols and stanols across different dose ranges: a meta-analysis of randomised controlled studies. British Journal of Nutrition (2014)
  12. Welty FK. Hypobetalipoproteinemia and abetalipoproteinemia. Current Opinion in Lipidology (2014)

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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.