Apolipoprotein B (ApoB)
ApoB reflects the number of cholesterol-carrying particles tied to artery disease. In pooled cohorts, each standard deviation higher went with about 43% more cardiovascular events, and genetic studies and drug trials agree in direction. Published cut points run from 60 to 130 mg/dL depending on the source and a person's risk. Fasting does not change the result.
- Status
- A blood test run by clinical laboratories, ordered by a clinician and also sold direct to consumers by some US laboratories. FDA classifies apolipoprotein assays as lipoprotein test systems, class I devices exempt from premarket notification [1].
- Measures
- The concentration of apolipoprotein B in blood, which reflects the number of LDL and other atherogenic lipoprotein particles because each particle carries a single ApoB molecule [2].
- Also called
- ApoB, Apo B, APOB, apolipoprotein B, apolipoprotein B-100, ApoB-100, Apo B-100, apolipoprotein B100
- Tested for
- heart attack risk, cardiovascular risk, cholesterol particle number, risk when triglycerides are high, checking response to cholesterol-lowering drugs, family history of heart disease
Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on
Linked in research4
- StrongLinked to more cardiovascular events at higher levels, about 43% more per standard deviation in pooled cohorts, a stronger link than for LDL cholesterol.
- StrongShown in trials: each 10 mg/dL lowered went with about 7% fewer major cardiovascular events, except with drugs that act outside the LDL receptor.
- ModerateShown to track coronary heart disease in genetic studies, with about 23% lower odds for each 10 mg/dL lower lifelong ApoB.
- LimitedOne cohort of statin-treated adults linked high ApoB with low LDL cholesterol to 21% more deaths and 49% more heart attacks than when both were low.
Reported risks0
No risks sourced yet.
Reference ranges
Each range is the one its source published, in mg/dL. Also reported in g/L. Where sources differ, each is shown.
American Heart Association and American College of Cardiology cholesterol guideline, 2018
Adults aged 40 to 75 without cardiovascular disease, when ApoB has been measured · [3]
| Range | What the source calls it |
|---|---|
| below 130 mg/dL | No name given |
| 130 or above mg/dL | "elevated" |
The guideline lists "elevated apoB" of 130 mg/dL or above as a risk-enhancing factor to weigh in a discussion about statin therapy, and states that this level corresponds to an LDL cholesterol of 160 mg/dL or above. It names measurement as relevant mainly when triglycerides are 200 mg/dL or above. It gives no term for results below 130 [3]. A 2026 guideline from the same bodies retires and replaces this one [4].
European Society of Cardiology and European Atherosclerosis Society guideline, 2019, very high risk
Adults the guideline places at very high cardiovascular risk · [5]
| Range | What the source calls it |
|---|---|
| below 65 mg/dL | "secondary goal" |
| 65 or above mg/dL | No name given |
A treatment goal, not a population reference interval. The guideline sets ApoB as a secondary goal after LDL cholesterol and gives no term for results at or above the goal [5].
European Society of Cardiology and European Atherosclerosis Society guideline, 2019, high risk
Adults the guideline places at high cardiovascular risk · [5]
| Range | What the source calls it |
|---|---|
| below 80 mg/dL | "secondary goal" |
| 80 or above mg/dL | No name given |
A treatment goal, not a population reference interval. The same guideline sets a different goal for each risk category [5].
European Society of Cardiology and European Atherosclerosis Society guideline, 2019, moderate risk
Adults the guideline places at moderate cardiovascular risk · [5]
| Range | What the source calls it |
|---|---|
| below 100 mg/dL | "secondary goal" |
| 100 or above mg/dL | No name given |
A treatment goal, not a population reference interval. The guideline gives no ApoB goal for people at low risk [5].
National Lipid Association expert clinical consensus, 2024, very high risk
Adults at very high risk: several major cardiovascular events, or one major event plus several high-risk conditions · [2]
| Range | What the source calls it |
|---|---|
| below 60 mg/dL | No name given |
| 60 or above mg/dL | "at or above the treatment threshold" |
A threshold at which the consensus suggests considering more intensive lipid-lowering therapy. It was not tested in a trial. The authors derived it from the average ApoB that matched an LDL cholesterol of 55 mg/dL in a US survey and in two drug trials, rounded to the nearest ten [2].
National Lipid Association expert clinical consensus, 2024, high risk
Adults at high risk: cardiovascular disease, diabetes, or an estimated 10-year risk of 20% or more · [2]
| Range | What the source calls it |
|---|---|
| below 70 mg/dL | No name given |
| 70 or above mg/dL | "at or above the treatment threshold" |
Derived from the average ApoB that matched an LDL cholesterol of 70 mg/dL, not from a trial that enrolled or treated people by ApoB [2].
National Lipid Association expert clinical consensus, 2024, borderline to intermediate risk
Adults with an estimated 10-year cardiovascular risk of 5% to under 20%, or LDL cholesterol of 190 mg/dL or above · [2]
| Range | What the source calls it |
|---|---|
| below 90 mg/dL | No name given |
| 90 or above mg/dL | "at or above the treatment threshold" |
Derived from the average ApoB that matched an LDL cholesterol of 100 mg/dL. In untreated US adults surveyed from 2005 to 2016, the median ApoB was 90 mg/dL, the 5th percentile 54 and the 95th percentile 137, so about half of untreated adults sit at or above this threshold [2].
European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine consensus on laboratory reporting, 2016
Adults, fasting or not, as a value for laboratories to flag on reports · [6]
| Range | What the source calls it |
|---|---|
| below 100 mg/dL | No name given |
| 100 or above mg/dL | "abnormal" |
The statement asks laboratories to flag "abnormal" results against desirable concentration cut points in place of population reference intervals. It prints the cut point as 1.00 g/L and 100 mg/dL, and notes that its flagging values are in some cases higher than the goals set for people at high and very high risk. It estimates that 59% of adults in a typical Western or Northern European country would be flagged at this cut point [6]. In 3,824 Framingham Offspring Study participants, mean ApoB was 103 mg/dL in men and 96 mg/dL in women, and 120 mg/dL was roughly the 75th percentile in men [7].
National Heart, Lung, and Blood Institute expert panel, 2011, children and adolescents
Children and adolescents · [8]
| Range | What the source calls it |
|---|---|
| below 90 mg/dL | "acceptable" |
| 90 to 109 mg/dL | "borderline-high" |
| 110 or above mg/dL | "high" |
The panel took its ApoB values from a national US survey of children (NHANES III). The borderline-high and high cut points represent approximately the 75th and 95th percentiles, so the bands describe where a child sits in the population. They were not set against later heart disease [8].
What has been shown to move it
Shown to lower it8
LDL cholesterol (oat beta-glucan)
Shown to lower LDL by about 0.2 to 0.25 mmol/L in adults at 3 g a day or more of oat beta-glucan.
In 58 trials (3,974 people), a median 3.5 g a day lowered LDL by 0.19 mmol/L (95% CI 0.14 to 0.23), non-HDL by 0.20 mmol/L and apoB by 0.03 g/L.
The numbers and sources
- Effect
- In 28 trials, 3 g a day or more of oat beta-glucan lowered LDL by 0.25 mmol/L (95% CI 0.20 to 0.30) and total cholesterol by 0.30 mmol/L, with no change in HDL or triglycerides. Dose (3.0 to 12.4 g a day) and duration (2 to 12 weeks) did not change the result [1]. In 58 trials (3,974 people), a median 3.5 g a day lowered LDL by 0.19 mmol/L (95% CI 0.14 to 0.23), non-HDL by 0.20 mmol/L and apoB by 0.03 g/L [2].
- Population
- Adults, mostly with normal to raised cholesterol [1][2].
- Sources
- [1], [2]
- Caveats
- LDL heterogeneity was high in [2] (I² 79%). [1] was supported by DSM Nutritional Products and searched in-house reports at CreaNutrition, a subsidiary of an oat fiber company. FDA's health claim rests on 3 g a day or more from whole oats or barley [3].
Ezetimibe: LDL cholesterol and ApoB
Shown to lower LDL cholesterol about 18% more than placebo when taken alone, with ApoB about 16% lower, and to lower LDL further when added to a statin.
Compared with placebo [1][2]; a statin or fenofibrate alone [3][4]
In two label trials, LDL cholesterol fell 18% and ApoB 16% on ezetimibe against a 1% rise and 2% fall on placebo.
The numbers and sources
- Effect
- Across 8 placebo-controlled 12-week trials, ezetimibe 10 mg lowered LDL cholesterol 18.58% more than placebo (95% CI 17.48 to 19.67), total cholesterol 13.46% more and triglycerides 8.06% more, and raised HDL cholesterol 3.00% [1]. In two label trials, LDL cholesterol fell 18% and ApoB 16% on ezetimibe against a 1% rise and 2% fall on placebo [2]. Added to a statin or fenofibrate, ezetimibe lowered LDL cholesterol, total cholesterol and triglycerides further and likely raised HDL [3]. After an acute coronary syndrome, time-averaged LDL was 53.7 mg/dL on simvastatin with ezetimibe against 69.5 mg/dL on simvastatin alone [4].
- Population
- 2,722 people with primary hypercholesterolemia in 8 trials [1]; 1,719 adults in two trials [2]; 23,499 people in 26 trials [3]; 18,144 patients [4].
- Sources
- [1], [2], [3], [4]
- Caveats
- Lipid trials alone lasted 12 weeks [1]. Heterogeneity was substantial in the combination analyses [3].
LDL cholesterol
Shown to lower LDL cholesterol by about 0.33 mmol/L with about 10 g of psyllium a day in adults with or without high cholesterol.
The numbers and sources
- Effect
- Across 28 trials (1,924 participants), a median 10.2 g of psyllium a day lowered LDL cholesterol by 0.33 mmol/L (95% CI -0.38 to -0.27), non-HDL cholesterol by 0.39 mmol/L and apoB by 0.05 g/L (95% CI -0.08 to -0.03) [1]. A 2025 meta-analysis of 41 RCTs (2,049 participants) found LDL cholesterol 8.55 mg/dL lower (95% CI -12.92 to -4.19) and total cholesterol 9.05 mg/dL lower. Triglycerides and HDL did not change significantly [2].
- Population
- Adults with or without high cholesterol in RCTs of 3 weeks or longer [1]; adults in 41 RCTs [2].
- Sources
- [1], [2]
- Caveats
- LDL and non-HDL estimates were graded moderate quality because of inconsistency, and apoB high quality [1]. Heterogeneity in the 2025 review was considerable (I² 88% for LDL), and dose and duration did not explain it [2].
LDL cholesterol and ApoB
Shown to lower LDL cholesterol by about 4.8 mg/dL per daily ounce of tree nuts, and by 10.2 mg/dL at about 67 g a day, along with ApoB.
Compared with control arms without nuts [4]; control diets the abstract does not describe [5]
ApoB fell more in people with type 2 diabetes (11.5 mg/dL) than in healthy people (2.5 mg/dL).
The numbers and sources
- Effect
- Per 1 oz (28.4 g) serving a day, tree nuts lowered total cholesterol by 4.7 mg/dL (95% CI 4.0 to 5.3), LDL cholesterol by 4.8 mg/dL (95% CI 4.2 to 5.5), ApoB by 3.7 mg/dL (95% CI 2.3 to 5.2) and triglycerides by 2.2 mg/dL (95% CI 0.5 to 3.8). HDL cholesterol, apolipoprotein A1 and blood pressure did not change significantly. Effects were stronger at 60 g a day or more and did not differ by nut type. ApoB fell more in people with type 2 diabetes (11.5 mg/dL) than in healthy people (2.5 mg/dL) [4]. Pooled individual data from 25 trials found a mean 67 g a day lowered total cholesterol by 10.9 mg/dL (5.1%) and LDL cholesterol by 10.2 mg/dL (7.4%). Triglycerides fell 20.6 mg/dL in people starting at 150 mg/dL or higher and not in others [5].
- Population
- 2,582 adults without cardiovascular disease in 61 trials of 3 to 26 weeks [4]. 583 adults with normal or high cholesterol not on lipid-lowering drugs, in 25 trials in 7 countries [5].
- Sources
- [4], [5]
- Caveats
- Trials were short and many are shared between the two analyses. Effects were largest in people with higher starting LDL cholesterol and lower body mass index [5].
LDL cholesterol
Shown to lower LDL cholesterol about 0.24 to 0.30 mmol/L against omnivorous or control diets in adults.
Compared with the participants' habitual diet, unchanged, in 3 trials in US and New Zealand adults, and in 8 trials a National Cholesterol Education Program diet, American Diabetes Association and Korean Diabetes Association diets, a portion-controlled diet, a Mediterranean diet, a low-fat diet, a healthy omnivorous diet or a high-carbohydrate lacto-ovo vegetarian diet [1]; an omnivorous diet [3]
In 30 RCTs of vegetarian or vegan diets, LDL fell 0.30 mmol/L (95% CI -0.40 to -0.19) and apolipoprotein B 12.92 mg/dL, with similar effects across intervention diet types.
The numbers and sources
- Effect
- Vegan diets lowered total cholesterol by 0.30 mmol/L and LDL by 0.24 mmol/L (95% CI -0.40 to -0.07), with no change in HDL or triglycerides [1]. In 30 RCTs of vegetarian or vegan diets, LDL fell 0.30 mmol/L (95% CI -0.40 to -0.19) and apolipoprotein B 12.92 mg/dL, with similar effects across intervention diet types [3].
- Population
- Adults with overweight or type 2 diabetes [1]; adults in 30 RCTs [3].
- Sources
- [1], [3]
- Caveats
- The larger review pooled vegan and vegetarian diets [3].
LDL cholesterol
Shown to lower LDL cholesterol about 0.3 mmol/L against omnivorous diets in adults. HDL also fell slightly in one review.
Compared with control diets the source does not describe [2]; an omnivorous control diet containing meat and dairy products [3]; an omnivorous diet [4]
In 30 RCTs, vegetarian or vegan diets lowered LDL by 0.30 mmol/L (95% CI -0.40 to -0.19) and apolipoprotein B by 12.92 mg/dL, with similar effects across intervention diet types and no triglyceride change.
The numbers and sources
- Effect
- In 11 trials, vegetarian diets lowered total cholesterol by 0.36 mmol/L, LDL by 0.34 mmol/L (95% CI -0.57 to -0.11) and HDL by 0.10 mmol/L (95% CI -0.14 to -0.06), with no triglyceride change [3]. In 30 RCTs, vegetarian or vegan diets lowered LDL by 0.30 mmol/L (95% CI -0.40 to -0.19) and apolipoprotein B by 12.92 mg/dL, with similar effects across intervention diet types and no triglyceride change [4]. In people with diabetes, LDL fell 0.12 mmol/L (95% CI -0.20 to -0.04) [2].
- Population
- Adults in randomized trials [3][4]; adults with diabetes [2].
- Sources
- [2], [3], [4]
- Caveats
- The reviews pooled lacto-ovo and vegan diets, though [4] found effects similar across diet types.
Blood pressure and other heart risk markers
Shown to lower systolic blood pressure by about 1.6 mmHg for plant sterols and stanols as a class. HDL, blood sugar and weight did not change.
The numbers and sources
- Effect
- Plant sterols and stanols lowered systolic blood pressure by 1.55 mmHg (95% CI 0.42 to 2.67), diastolic by 0.84 mmHg, apoB by 0.06 g/L and hs-CRP by 0.25 mg/L. HDL cholesterol, fasting glucose, HbA1c, body weight, waist and fat mass did not change [5].
- Population
- Adults of mixed health status in trials pooled across 14 meta-analyses. Blood pressure came from one of them [5].
- Sources
- [5]
- Caveats
- Class-level evidence, not beta-sitosterol alone. These are risk markers, not heart attacks or strokes. Certainty was moderate to high for most outcomes, downgraded for inconsistency, imprecision or publication bias [5].
Fenofibrate: triglycerides, HDL and LDL cholesterol
Shown to lower triglycerides about 29% and LDL cholesterol 21% and to raise HDL 11% against placebo, with triglycerides 46% to 55% lower in severe high triglycerides.
Compared with placebo [7]
ApoB fell 25.1% against a 2.4% rise.
The numbers and sources
- Effect
- In four placebo-controlled trials of 3 to 6 months, fenofibrate at the 145 mg dose changed triglycerides by -28.9% against +7.7% on placebo, LDL cholesterol by -20.6% against -2.2%, total cholesterol by -18.7% against -0.4%, and HDL by +11.0% against +0.7%. ApoB fell 25.1% against a 2.4% rise. In severe high triglycerides, triglycerides fell 46.2% (baseline 432 mg/dL) and 54.5% (baseline 726 mg/dL) against -0.5% and +7.2% on placebo, while LDL cholesterol rose in both groups [7].
- Population
- 646 adults with high cholesterol or mixed dyslipidemia in 4 trials, and 147 adults with high triglycerides in 2 trials of 8 weeks [7].
- Sources
- [7]
- Caveats
- Label trials, short-term. The label reports rare severe paradoxical drops in HDL, listed under Risks [7].
Shown to raise it2
Higher LDL cholesterol in feeding trials
Shown to raise LDL cholesterol by about 8 mg/dL in randomized trials in healthy people, along with total cholesterol and apolipoprotein B.
Across 66 trials, eggs raised total cholesterol, LDL and apolipoprotein B100, did not change triglycerides, and LDL rose nonlinearly with dose.
The numbers and sources
- How common
- How often is not known: the sources give no rate.
- Effect
- Against control groups, eating more eggs raised LDL cholesterol (mean difference 8.14 mg/dL, P < 0.0001), with larger effects in trials of over two months [3]. Across 66 trials, eggs raised total cholesterol, LDL and apolipoprotein B100, did not change triglycerides, and LDL rose nonlinearly with dose [4]. Each extra 100 mg of dietary cholesterol a day raised total cholesterol by 2.2 mg/dL (95% CI 1.8 to 2.5) [2].
- Population
- Healthy participants in 17 randomized trials [3]. 3,185 participants in 66 randomized trials [4]. 556 participants in 17 feeding studies [2].
- Sources
- [3], [4], [2]
- Caveats
- Short trials. One review found the rise came with eating more than one egg a day for under 12 weeks [4].
LDL cholesterol and apolipoprotein B
Shown to raise LDL cholesterol over comparison diets in adults, by 0.12 to 0.35 mmol/L in most reviews and 1.08 mmol/L in normal-weight adults.
In 3 trials of normal-weight adults, LDL rose 1.08 mmol/L (95% CI 0.37 to 1.79) and apolipoprotein B 0.35 g/L (95% CI 0.06 to 0.65).
The numbers and sources
- How common
- Very common: more than 1 in 10 people.
- Effect
- LDL rose 0.12 mmol/L more than on low-fat diets over 12 months or more (95% CI 0.04 to 0.20) [1], 0.35 mmol/L more than on control diets (95% CI 0.20 to 0.50, I² 73.9%) [2], and 8.49 mg/dL more across 62 studies (95% CI 5.45 to 11.52) [5]. In 3 trials of normal-weight adults, LDL rose 1.08 mmol/L (95% CI 0.37 to 1.79) and apolipoprotein B 0.35 g/L (95% CI 0.06 to 0.65) [16]. In type 2 diabetes, LDL did not differ from control diets [7]. In one trial with weight loss held equal, LDL and apolipoprotein B did not differ from Mediterranean or very-low-fat diets [12]. Hyperlipidemia was reported in 12.8% of children treated for epilepsy [17].
- Population
- Adults with and without obesity [1][2][5]; normal-weight adults [16]; adults with type 2 diabetes [7]; children with epilepsy [17].
- Sources
- [1], [2], [5], [7], [12], [16], [17]
- Caveats
- Effect sizes differ several times over between populations. No trial measured heart attacks or strokes, and the authors of [5] note the lack of long-term cardiovascular outcome data.
Tested, and not shown to change it5
LDL cholesterol
Shown to lower LDL cholesterol by about 10%, about 16 mg/dL, in adults and children. Changes were not significant in adults with insulin resistance.
Apolipoprotein B did not change in 6 trials.
The numbers and sources
- Effect
- Across 14 studies with 531 participants, glucomannan lowered total cholesterol 19.28 mg/dL (95% CI -24.30 to -14.26), LDL 15.99 mg/dL (95% CI -21.31 to -10.67) and triglycerides 11.08 mg/dL (95% CI -22.07 to -0.09), with no change in HDL [1]. Across 12 studies with 370 participants, LDL fell 0.35 mmol/L (95% CI -0.46 to -0.25) and non-HDL cholesterol 0.32 mmol/L, about 10% and 7%. Apolipoprotein B did not change in 6 trials [2].
- Population
- Adults and children in RCTs [1][2].
- Sources
- [1], [2]
- Caveats
- Trials were small and short, with follow-up of at least 3 weeks in [2]. In 11 trials restricted to adults with insulin resistance-related conditions, lipid changes were not significant overall, with LDL and total cholesterol lower only in subgroups above 3,000 mg a day or at 4 weeks or less [3].
LDL cholesterol (barley beta-glucan)
Shown to lower LDL by about 0.25 mmol/L in adults on a median 6.5 g a day of barley beta-glucan.
ApoB did not change.
The numbers and sources
- Effect
- In 14 trials (615 people), a median 6.5 g a day of barley beta-glucan for 4 weeks lowered LDL by 0.25 mmol/L (95% CI 0.20 to 0.30) and non-HDL by 0.31 mmol/L. ApoB did not change [4].
- Population
- Adults in trials of 3 weeks or longer [4].
- Sources
- [4]
- Caveats
- Non-HDL heterogeneity was high (I² 98%) [4].
Cholesterol and blood pressure in trials
Not shown to change cholesterol or blood pressure against all comparison diets combined. Against plant proteins, LDL fell less on red meat. Against fish, it fell more.
Compared with diets replacing red meat with legumes, soy or nuts, fish, poultry, mixed animal protein, refined carbohydrates or the usual diet [4]
The numbers and sources
- Effect
- Against all comparison diets combined, red meat made no significant difference to total, LDL or HDL cholesterol, apolipoproteins A1 and B, or blood pressure, and gave a smaller fall in triglycerides (0.065 mmol/L). Against high-quality plant proteins, total cholesterol fell 0.264 mmol/L less and LDL 0.198 mmol/L less. Against fish, LDL fell 0.173 mmol/L more and HDL 0.065 mmol/L more. Against refined carbohydrates, triglycerides fell 0.181 mmol/L more [4].
- Population
- 1,803 participants in 36 randomized trials [4].
- Sources
- [4]
- Caveats
- The result depends on what replaced the red meat. Trials measured blood markers, not heart events.
Inflammation and blood lipids
Mixed results: reviews disagree on whether CRP falls, and most found no change in LDL or triglycerides.
Apolipoprotein B (WMD 2.11 mg/dL, 95% CI -1.53 to 5.75) and apolipoprotein A-I did not change in 7 RCTs.
The numbers and sources
- Effect
- One meta-analysis found no change in CRP (WMD -0.144 mg/L, 95% CI -0.968 to 0.680), total cholesterol, LDL, triglycerides or glucose. HDL fell slightly (WMD -4.18 mg/dL, 95% CI -6.54 to -1.82) [4]. A later meta-analysis found lower TNF-α (WMD -0.44, 95% CI -0.71 to -0.16) and hs-CRP (WMD -0.27, 95% CI -0.5 to -0.02), with no change in IL-6 [6]. In 25 RCTs in metabolic disorders, CRP fell (SMD -0.18, 95% CI -0.33 to -0.03), and IL-6 and TNF-α did not change significantly [7]. In 6 RCTs in type 2 diabetes (533 participants), CRP fell (SMD -1.40, 95% CI -2.60 to -0.21) [8]. Apolipoprotein B (WMD 2.11 mg/dL, 95% CI -1.53 to 5.75) and apolipoprotein A-I did not change in 7 RCTs [9]. An umbrella review rated as high certainty a 0.19 mmol/L drop in total cholesterol in adults with overweight (95% CI 0.06 to 0.32) [5].
- Population
- 10 RCTs [4]; 17 RCTs with 736 adults [6]; adults with metabolic disorders [7]; adults with type 2 diabetes [8]; 7 RCTs [9]; meta-analyses of RCTs [5].
- Sources
- [4], [6], [7], [8], [9], [5]
- Caveats
- The reviews disagree on CRP, and the CRP effect in [8] is several times the size of that in [7]. Heterogeneity in [6] was about 50%. Evidence in [8] was low certainty. CRP is a marker, not a clinical outcome [7].
Liver fat and insulin sensitivity
One trial found that at equal 10% weight loss, liver insulin sensitivity rose two to three times more than on Mediterranean or very-low-fat diets.
Compared with diets that did not restrict carbohydrates to the level of ketosis
LDL cholesterol, apolipoprotein B and 24-hour triglycerides did not differ between diets.
The numbers and sources
- Effect
- Calories were adjusted so every group lost about 10% of body weight. Muscle insulin sensitivity rose about 50% on all three diets. Liver insulin sensitivity rose two to three times more on the very-low-carbohydrate ketogenic diet (p < 0.001), and liver fat, liver fat production, HbA1c and 24-hour glucose and insulin fell most on it. LDL cholesterol, apolipoprotein B and 24-hour triglycerides did not differ between diets [12].
- Population
- Adults with obesity, prediabetes and fatty liver. The abstract does not give the number randomized [12].
- Sources
- [12]
- Caveats
- One small trial. Food was supplied during weight loss, so it measures the diets eaten as written. It does not apply to people without prediabetes and fatty liver.
How it compares with the reference method
Matched the reference method1
Fasting against not fasting
Shown to match fasting results: ApoB did not change after normal food intake in 33,391 Danish adults.
The numbers and sources
- Compared with
- A fasting blood sample
- Effect
- In the Copenhagen General Population Study, ApoB did not change in response to normal food intake, while LDL cholesterol fell by up to 0.2 mmol/L and triglycerides rose by up to 0.3 mmol/L [17]. A joint European consensus statement concluded that ApoB concentrations are not affected by fasting or non-fasting status [6].
- Population
- 33,391 adults aged 20 to 95, sampled at varying times since their last meal [17].
- Sources
- [17], [6]
- Caveats
- A cross-sectional comparison of people sampled at different times after eating, not the same people tested twice [17]. A US consensus limits the statement to people without severe hypertriglyceridemia [2].
Mixed results1
Agreement between laboratories and assays
Limited evidence: US survey data put most ApoB assays within 4 mg/dL of target, while a 2026 comparison of 8 assays concluded agreement still needs improvement.
The numbers and sources
- Compared with
- A reference measurement procedure, or the target value of a proficiency survey
- Effect
- A US expert consensus reports that in the College of American Pathologists accuracy-based lipid survey, bias for most ApoB tests is below 4 mg/dL and the coefficient of variation usually ranges between 5% and 6% [2]. In the Dutch national quality assessment program, 28% of laboratories exceeded the program's bias limit for ApoB, against 68% for LDL cholesterol [18]. A comparison of 8 immunoassay procedures with a mass spectrometry reference procedure found the immunoassay results correlated well with the reference, and concluded that harmonization among the immunoassays still needs improvement [19]. In an older study, the between-run coefficient of variation of one standardized assay was 6.60% [7].
- Population
- Laboratories taking part in US and Dutch proficiency programs [2][18]. 30 clinical samples measured by 8 immunoassay procedures [19].
- Sources
- [2], [18], [19], [7]
- Caveats
- The survey figures are quoted from two papers that do not give the number of laboratories or samples, and one of them is an essay arguing that ApoB is adequately standardized [18]. The 2026 abstract reports no numeric bias [19].
What studies tie it to
Linked in research4
Heart attack and other cardiovascular events
Linked to more cardiovascular events at higher levels, about 43% more per standard deviation in pooled cohorts, a stronger link than for LDL cholesterol.
The numbers and sources
- Effect
- A meta-analysis of 12 reports found a standardized relative risk of fatal or nonfatal ischemic cardiovascular events of 1.43 for ApoB (95% CI 1.35 to 1.51), 1.34 for non-HDL cholesterol (1.24 to 1.44) and 1.25 for LDL cholesterol (1.18 to 1.33) [9]. In UK Biobank adults not taking lipid-lowering drugs, ApoB, non-HDL cholesterol and triglycerides were each associated with a first heart attack. When they were assessed together, only ApoB remained associated (adjusted HR 1.27 per standard deviation, 95% CI 1.15 to 1.40), and the same was found in statin-treated trial patients with atherosclerosis [10]. In 68 prospective studies, the hazard ratio for coronary heart disease per standard deviation was 1.49 (95% CI 1.39 to 1.60) for the ratio of ApoB to apolipoprotein A-I and 1.50 (1.38 to 1.62) for the ratio of non-HDL to HDL cholesterol [11].
- Population
- 233,455 people with 22,950 events in 12 reports [9]. 389,529 UK Biobank participants followed a median 11.1 years, and 40,430 trial patients followed a median 2.5 years [10]. 302,430 people without vascular disease in 68 studies, a subset of whom had apolipoproteins measured [11].
- Sources
- [9], [10], [11]
- Caveats
- Observational. ApoB, LDL cholesterol and non-HDL cholesterol are highly correlated, which makes their separate contributions hard to tell apart [12]. The largest pooled analysis reported ApoB only as a ratio to apolipoprotein A-I [11].
Coronary heart disease in genetic studies
Shown to track coronary heart disease in genetic studies, with about 23% lower odds for each 10 mg/dL lower lifelong ApoB.
The numbers and sources
- Effect
- In Mendelian randomization analyses, gene variants that lower triglycerides (in LPL) and gene variants that lower LDL cholesterol (in LDLR) were associated with the same lower odds of coronary heart disease per 10 mg/dL lower ApoB: OR 0.771 (95% CI 0.741 to 0.802) and 0.773 (0.747 to 0.801). After adjusting for ApoB, the associations of triglycerides and of LDL cholesterol with coronary heart disease became null [13]. A second multivariable analysis found that only ApoB kept a robust effect (OR 1.92 per standard deviation higher, 95% CI 1.31 to 2.81), while the LDL cholesterol estimate reversed (OR 0.85, 95% CI 0.57 to 1.27) [12].
- Population
- 654,783 participants in 63 cohort or case-control studies, including 91,129 with coronary heart disease [13]. Genetic data from up to 441,016 UK Biobank participants, applied to 60,801 coronary cases and 123,504 controls [12].
- Sources
- [13], [12]
- Caveats
- Gene variants act from birth, so these estimates describe lifelong differences, not a change made later in life. The authors of one analysis note that lipid traits are highly correlated, which limits conclusions about any single one [12].
Cardiovascular events and death in trials that lowered ApoB
Shown in trials: each 10 mg/dL lowered went with about 7% fewer major cardiovascular events, except with drugs that act outside the LDL receptor.
The numbers and sources
- Effect
- Across 29 randomized trials, each 10 mg/dL decrease in ApoB went with a relative risk of 0.93 for major adverse cardiovascular events (95% CI 0.90 to 0.97), 0.93 for cardiovascular death (0.88 to 0.98) and 0.95 for death from any cause (0.92 to 0.99). For major events the relative risk was 0.88 (0.83 to 0.93) with statins and 0.96 (0.94 to 0.99) with non-statin drugs that clear ApoB through the LDL receptor. Drugs that lower ApoB by other routes (CETP inhibitors, fibrates, niacin, omega-3 fatty acids) showed no reduction (1.02, 0.81 to 1.30), and the reduction in death from any cause was limited to statins [14]. An earlier analysis of 25 trials found each 10 mg/dL decrease went with 9% less coronary heart disease, 6% less major cardiovascular disease and no decrease in stroke. Across all drug classes, the fall in ApoB did not consistently predict risk better than the fall in LDL or non-HDL cholesterol [15].
- Population
- 332,912 patients in 29 trials of at least 1,000 people and 1 year [14]. 131,134 participants in 25 trials: 12 of statins, 4 of fibrates, 5 of niacin and 4 others [15].
- Sources
- [14], [15]
- Caveats
- Both analyses compare averages between trials, not individuals within them. None of the trials behind current treatment thresholds enrolled people by ApoB, and ApoB was often measured in only part of a trial population [2].
Death and heart attack when ApoB and LDL cholesterol disagree
One cohort of statin-treated adults linked high ApoB with low LDL cholesterol to 21% more deaths and 49% more heart attacks than when both were low.
The numbers and sources
- Effect
- Compared with both values below the median, ApoB above the median with LDL cholesterol below it had hazard ratios of 1.21 for death from any cause (95% CI 1.07 to 1.36) and 1.49 for heart attack (95% CI 1.15 to 1.92). High LDL cholesterol with low ApoB was not associated with a higher risk of either outcome [16].
- Population
- 13,015 statin-treated adults in the Copenhagen General Population Study, median follow-up 8 years [16].
- Sources
- [16]
- Caveats
- Observational, in one Danish cohort. High and low were defined by the cohort's own medians, which the abstract does not report [16].
Sources
- US Food and Drug Administration. 21 CFR 862.1475, Lipoprotein test system. Electronic Code of Federal Regulations, with the FDA product classification entry for apolipoproteins (product code MSJ). https://www.ecfr.gov/current/title-21/section-862.1475
- Soffer DE, Marston NA, Maki KC, et al. Role of apolipoprotein B in the clinical management of cardiovascular risk in adults: An Expert Clinical Consensus from the National Lipid Association. Journal of Clinical Lipidology. 2024. https://doi.org/10.1016/j.jacl.2024.08.013
- 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: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019. https://doi.org/10.1161/CIR.0000000000000625
- Blumenthal RS, Morris PB, Gaudino M, et al. 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2026. https://doi.org/10.1161/CIR.0000000000001423
- 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. https://doi.org/10.1093/eurheartj/ehz455
- Nordestgaard BG, Langsted A, Mora S, et al. Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications including flagging at desirable concentration cut-points. A joint consensus statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine. European Heart Journal. 2016. https://doi.org/10.1093/eurheartj/ehw152
- Contois JH, McNamara JR, Lammi-Keefe CJ, et al. Reference intervals for plasma apolipoprotein B determined with a standardized commercial immunoturbidimetric assay: results from the Framingham Offspring Study. Clinical Chemistry. 1996. https://doi.org/10.1093/clinchem/42.4.515
- Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents. Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents: Summary Report. Pediatrics. 2011. https://doi.org/10.1542/peds.2009-2107C
- Sniderman AD, Williams K, Contois JH, et al. A Meta-Analysis of Low-Density Lipoprotein Cholesterol, Non-High-Density Lipoprotein Cholesterol, and Apolipoprotein B as Markers of Cardiovascular Risk. Circulation: Cardiovascular Quality and Outcomes. 2011. https://doi.org/10.1161/CIRCOUTCOMES.110.959247
- 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. JAMA Cardiology. 2022. https://doi.org/10.1001/jamacardio.2021.5083
- Emerging Risk Factors Collaboration. Major Lipids, Apolipoproteins, and Risk of Vascular Disease. JAMA. 2009. https://doi.org/10.1001/jama.2009.1619
- Richardson TG, Sanderson E, Palmer TM, et al. Evaluating the relationship between circulating lipoprotein lipids and apolipoproteins with risk of coronary heart disease: A multivariable Mendelian randomisation analysis. PLOS Medicine. 2020. https://doi.org/10.1371/journal.pmed.1003062
- 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. https://doi.org/10.1001/jama.2018.20045
- Khan SU, Khan MU, Valavoor S, et al. Association of lowering apolipoprotein B with cardiovascular outcomes across various lipid-lowering therapies: Systematic review and meta-analysis of trials. European Journal of Preventive Cardiology. 2020. https://doi.org/10.1177/2047487319871733
- Robinson JG, Wang S, Jacobson TA. Meta-Analysis of Comparison of Effectiveness of Lowering Apolipoprotein B Versus Low-Density Lipoprotein Cholesterol and Nonhigh-Density Lipoprotein Cholesterol for Cardiovascular Risk Reduction in Randomized Trials. The American Journal of Cardiology. 2012. https://doi.org/10.1016/j.amjcard.2012.07.007
- Johannesen CDL, Mortensen MB, Langsted A, Nordestgaard BG. Apolipoprotein B and Non-HDL Cholesterol Better Reflect Residual Risk Than LDL Cholesterol in Statin-Treated Patients. Journal of the American College of Cardiology. 2021. https://doi.org/10.1016/j.jacc.2021.01.027
- Langsted A, Freiberg JJ, Nordestgaard BG. Fasting and Nonfasting Lipid Levels: Influence of Normal Food Intake on Lipids, Lipoproteins, Apolipoproteins, and Cardiovascular Risk Prediction. Circulation. 2008. https://doi.org/10.1161/CIRCULATIONAHA.108.804146
- Contois JH, Langlois MR, Cobbaert C, Sniderman AD. Standardization of Apolipoprotein B, LDL-Cholesterol, and Non-HDL-Cholesterol. Journal of the American Heart Association. 2023. https://doi.org/10.1161/JAHA.123.030405
- Dikaios I, Cobbaert CM, Delatour V, et al. Correlation and Commutability Study between an LC-MS-Based Reference Measurement Procedure and Immunoassays Measuring Apolipoprotein A-I and Apolipoprotein B. Clinical Chemistry. 2026. https://doi.org/10.1093/clinchem/hvag063