What does the research show about apolipoprotein a1 (apoa1)?

Apolipoprotein A1 (ApoA1)

ApoA1 is the main protein of HDL particles. Lower levels go with more coronary heart disease in cohorts, about 62% more in the lowest than the highest third. Genetic studies and one large infusion trial did not find that higher ApoA1 lowers risk. Published cut points for a low result run from 110 to 140 mg/dL by source and sex.

Checked 2026-11-13

Status: A blood test run by clinical laboratories, ordered by a clinician. FDA lists apolipoprotein assays under lipoprotein test systems, class I devices exempt from premarket notification [1]. A European guideline describes ratios such as ApoB to ApoA1 as useful for risk estimation and not for diagnosis or as treatment targets [2].
Measures: The concentration in blood of apolipoprotein A1, the major protein of HDL particles [2].
Also called: ApoA1, Apo A1, ApoA-I, Apo A-I, APOA1, apolipoprotein A1, apolipoprotein A-I, apolipoprotein AI, apo AI, ApoB/ApoA1 ratio, apolipoprotein B to A1 ratio
Tested for: heart attack risk, cardiovascular risk, HDL particle count, the ApoB to ApoA1 ratio, family history of heart disease, low HDL cholesterol workup

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 research2

StrongLinked to more coronary heart disease at lower levels, about 62% more in the lowest than the highest third across 21 prospective studies.
StrongLinked to more heart attacks at a higher ApoB to ApoA1 ratio, about 59% higher odds per standard deviation in a 52-country case-control study.

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.

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 · [3]

Range	What the source calls it
125 or below mg/dL	"abnormal"
above 125 mg/dL	No name given

The statement asks laboratories to flag "abnormal" results against desirable concentration cut points in place of population reference intervals. It prints this one as 1.25 g/L and 125 mg/dL, and offers ApoA1 as an alternative to HDL cholesterol measurement. It estimates that 9% of adults in a typical Western or Northern European country would be flagged [3].

European Society of Cardiology and European Atherosclerosis Society guideline, 2016, men

Men · [2]

Range	What the source calls it
below 120 mg/dL	"low"
120 or above mg/dL	No name given

Not a treatment goal. The guideline states that plasma ApoA1 below 120 mg/dL for men and below 140 mg/dL for women corresponds approximately to what is considered low for HDL cholesterol. It adds that each HDL particle may carry from one to five ApoA1 molecules. The same societies published a newer guideline in 2019 [4].

European Society of Cardiology and European Atherosclerosis Society guideline, 2016, women

Women · [2]

Range	What the source calls it
below 140 mg/dL	"low"
140 or above mg/dL	No name given

Not a treatment goal. The guideline gives this as the level that corresponds approximately to what is considered low for HDL cholesterol in women, 20 mg/dL above its figure for men [2].

Reference intervals from the FINRISK 2007 study, Finland, men

Men in a reference sample of Finnish adults · [5]

Range	What the source calls it
below 110 mg/dL	No name given
110 to 200 mg/dL	"reference interval"
above 200 mg/dL	No name given

A population reference interval, printed as 1.1 to 2.0 g/L, from a reference sample of 2,828 people. It describes where most of that sample fell and was not set against later heart disease. A result above the interval lies outside it, and the study does not call such a result abnormal, so this page does not mark it as high. The same study gives a reference interval for the ApoB to ApoA1 ratio of 0.3 to 1.0 in men, a different quantity that is not placed on this scale [5].

Reference intervals from the FINRISK 2007 study, Finland, women

Women in a reference sample of Finnish adults · [5]

Range	What the source calls it
below 120 mg/dL	No name given
120 to 230 mg/dL	"reference interval"
above 230 mg/dL	No name given

A population reference interval, printed as 1.2 to 2.3 g/L. A result above the interval lies outside it, and the study does not call such a result abnormal, so this page does not mark it as high. The same study gives a reference interval for the ApoB to ApoA1 ratio of 0.3 to 0.8 in women, which is not placed on this scale [5].

Framingham Offspring Study, 1996

Adults, from white men and women in a US community cohort · [6]

Range	What the source calls it
below 120 mg/dL	No name given
120 or above mg/dL	No name given

The authors report that 1.20 g/L roughly corresponded to the 25th percentile in men and the 5th percentile in women, and that people below it were significantly more likely to have coronary heart disease. They give no name to either side of the figure. Mean ApoA1 was 134 mg/dL in 1,879 men and 154 mg/dL in 1,939 women [6].

National Heart, Lung, and Blood Institute expert panel, 2011, children and adolescents

Children and adolescents · [7]

Range	What the source calls it
below 115 mg/dL	"low"
115 to 120 mg/dL	"borderline"
above 120 mg/dL	"acceptable"

The panel took its ApoA1 values from a national US survey (NHANES III). The low cut point represents approximately the 10th percentile, so the bands describe where a child sits in the population. They were not set against later heart disease. The panel's table for young adults gives no ApoA1 values [7].

What has been shown to move it

Shown to lower it1

Ezetimibe and fenofibrateLimitedHow often is not known

Fenofibrate: paradoxical drop in HDL

Case reports: the label reports rare severe drops in HDL cholesterol, as low as 2 mg/dL, after starting fibrates, which reversed after stopping.

The numbers and sources

How common: How often is not known: the sources give no rate.
Effect: Postmarketing and trial reports describe HDL falling as low as 2 mg/dL, mirrored by a fall in apolipoprotein A1, from 2 weeks to years after starting a fibrate, with rapid recovery after stopping [7].
Population: Diabetic and nondiabetic patients in reports [7].
Sources: [7]
Caveats: Reports without a denominator. On average HDL rose in trials.

Shown to raise it2

EggsStrong

HDL cholesterol and the cholesterol ratio

Shown to raise HDL cholesterol slightly in feeding trials. The ratio of LDL or total cholesterol to HDL rose in two of three pooled analyses.

Compared with diets differing only in dietary cholesterol or number of eggs [2]; control groups eating fewer eggs [3][4]

Across 66 trials, eggs raised HDL and apolipoprotein A1 along with total and LDL cholesterol, with no change in the LDL to HDL ratio.

The numbers and sources

Effect: Each extra 100 mg of dietary cholesterol a day raised HDL by 0.3 mg/dL (95% CI 0.2 to 0.4), total cholesterol by 2.2 mg/dL and the total to HDL cholesterol ratio by 0.020 units (95% CI 0.010 to 0.030) [2]. Across 66 trials, eggs raised HDL and apolipoprotein A1 along with total and LDL cholesterol, with no change in the LDL to HDL ratio [4]. Across 17 trials in healthy people, eating more eggs raised the LDL to HDL ratio by 0.14 (P = 0.001) [3].
Population: 556 participants in 17 controlled feeding studies of at least 14 days [2]. 3,185 participants in 66 randomized trials [4]. Healthy participants in 17 randomized trials [3].
Sources: [2], [4], [3]
Caveats: The pooled analyses disagree on the ratio. Trials ran weeks to months and measured blood lipids, not heart events.

AlcoholModerate

HDL cholesterol in trials

Shown to raise HDL cholesterol by about 0.09 mmol/L in trials of adults without heart disease, with no change in triglycerides.

Compared with periods without alcohol [9]

The numbers and sources

Effect: Alcohol raised HDL cholesterol (mean difference 0.094 mmol/L, 95% CI 0.064 to 0.123), apolipoprotein A1 (0.101 g/L, 95% CI 0.073 to 0.129) and adiponectin, with a dose-response for HDL. It lowered fibrinogen (-0.20 g/L) and did not change triglycerides. Results were similar for wine, beer and spirits [9].
Population: 44 interventional studies of 13 markers in adults without known cardiovascular disease [9].
Sources: [9]
Caveats: These are blood markers, not heart attacks. The review calls them indirect support for a protective effect [9], while genetic studies of heart disease found none (see above).

Tested, and not shown to change it3

NutsStrong

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]

HDL cholesterol, apolipoprotein A1 and blood pressure did not change significantly.

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].

Red meat and processed meatModerate

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.

ResveratrolModerate

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].

Type in your own result

How it compares with the reference method

Matched the reference method1

Moderate

Fasting against not fasting

Shown to match fasting results: ApoA1 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, ApoA1 and the ApoB to ApoA1 ratio did not change in response to normal food intake, while HDL cholesterol fell by up to 0.1 mmol/L and triglycerides rose by up to 0.3 mmol/L [17]. A joint European consensus statement concluded that ApoA1 concentrations are not affected by fasting or non-fasting status [3]. In 41 Chinese volunteers sampled at five times through one day, concentrations after meals were mostly slightly lower than fasting, and within-person variation across the day was 2.4% to 4.4% for the group of measures that included ApoA1 [18].
Population: 33,391 adults aged 20 to 95, sampled at varying times since their last meal [17]. 41 healthy volunteers [18].
Sources: [17], [3], [18]
Caveats: The Danish analysis is a cross-sectional comparison of people sampled at different times after eating, not the same people tested twice [17]. The Chinese study reports one range for several lipid measures together, not a figure for ApoA1 alone [18].

Mixed results2

Moderate

Agreement between laboratories and assays

Mixed results: assays calibrated to a common reference material agreed within about 4% between laboratories in 1993, while a 2026 comparison of 8 assays concluded agreement still needs improvement.

The numbers and sources

Compared with: An international reference material, or a mass spectrometry reference measurement procedure
Effect: In an international standardization project, laboratories that transferred a common value from the reference material SP1-01 to their own calibrators measured 50 samples with a between-laboratory coefficient of variation of 2.1% to 5.6% (mean 3.6%), and the consensus mean differed from the assigned value by an average of 0.01 g/L. The World Health Organization then approved the material as its international reference for ApoA1 [19]. A 2026 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 [20]. Within single laboratories, the between-run coefficient of variation of one standardized assay was 2.9% [6].
Population: 50 fresh-frozen samples from individual donors measured by the participating laboratories [19]. 30 clinical samples measured by 8 immunoassay procedures [20].
Sources: [19], [20], [6]
Caveats: The standardization project dates from 1993, so individual assays have since changed. The 2026 abstract reports no numeric bias [20].

Limited

Variation from one test to the next

Limited evidence: one study put within-person variation of the ApoA1 to ApoB ratio at about 15% over a year, and figures for ApoA1 alone were not available to this review.

The numbers and sources

Compared with: Repeat measurements in the same person
Effect: Over one year, the median within-person variation of the ratio of ApoA1 to ApoB was 15.4%, against 6.3% for the ratio of LDL to HDL cholesterol [21]. A European study of 91 healthy people sampled weekly for 10 weeks reports that its estimates of within-person variation for ApoA1 were similar to those published earlier, and that they differed between women below and above 50 years of age [22].
Population: People followed for one year, whose number the abstract does not give [21]. 91 healthy adults in 6 European laboratories [22].
Sources: [21], [22]
Caveats: The abstracts of both studies give no within-person figure for ApoA1 alone, and the full text of the European study was behind a paywall. Neither states a threshold for agreement, so the result is given as numbers only.

What studies tie it to

Linked in research2

Strong

Coronary heart disease in cohort studies

Linked to more coronary heart disease at lower levels, about 62% more in the lowest than the highest third across 21 prospective studies.

The numbers and sources

Effect: In a meta-analysis of prospective studies in general populations, people in the bottom third of ApoA1 had a relative risk of coronary heart disease of 1.62 (95% CI 1.43 to 1.83) against those in the top third [8]. In a pooled analysis of individual records, ApoA1 and HDL cholesterol had very similar shape and size of association with coronary heart disease, and the authors concluded that either cholesterol levels or apolipoproteins can be measured for risk assessment [9]. In 27,673 initially healthy US women, the hazard ratio for cardiovascular disease in the top against the bottom fifth of ApoA1 was 0.63 (95% CI 0.52 to 0.77), against 0.52 (0.42 to 0.64) for HDL cholesterol [10]. Among patients on statins in 8 trials, each standard deviation higher ApoA1 went with a hazard ratio for major cardiovascular events of 0.79 (95% CI 0.72 to 0.82), including in those with LDL cholesterol below 50 mg/dL [11].
Population: 6,333 coronary heart disease cases in 21 studies [8]. 91,307 participants with 4,499 cases in the 22 studies with apolipoproteins measured, within 302,430 people in 68 studies [9]. 27,673 women followed 11 years, 1,015 events [10]. 38,153 trial participants allocated to a statin, 5,387 with a major cardiovascular event [11].
Sources: [8], [9], [10], [11]
Caveats: Observational, including the analysis within statin trials. The literature-based meta-analysis found heterogeneity between studies that study characteristics only partly explained [8].

Strong

Heart attack and the ApoB to ApoA1 ratio

Linked to more heart attacks at a higher ApoB to ApoA1 ratio, about 59% higher odds per standard deviation in a 52-country case-control study.

The numbers and sources

Effect: In the INTERHEART study, the ApoB to ApoA1 ratio had an odds ratio for acute myocardial infarction of 1.59 per standard deviation (95% CI 1.53 to 1.64) and a population-attributable risk of 54%, against 32% for the ratio of total to HDL cholesterol [15]. In pooled prospective studies, the hazard ratio for coronary heart disease per standard deviation was 1.49 (95% CI 1.39 to 1.60) for the ApoB to ApoA1 ratio and 1.50 (1.38 to 1.62) for the ratio of non-HDL to HDL cholesterol [9]. A literature-based meta-analysis found a relative risk of 1.86 (95% CI 1.55 to 2.22) for the top against the bottom third of the ratio [8]. In a Swedish cohort, the ratio was strongly related to fatal myocardial infarction in men and women, and ApoA1 was noted to be protective [16].
Population: 12,461 cases and 14,637 controls in 52 countries, with blood samples from 9,345 cases and 12,120 controls [15]. 91,307 participants in 22 prospective studies [9]. 3,730 coronary cases in 7 studies [8]. 175,553 people followed a mean of about 65 months, with 1,223 fatal myocardial infarctions [16].
Sources: [15], [9], [8], [16]
Caveats: Observational, and the largest study is a case-control study, which cannot show that the ratio was raised before the heart attack [15]. The ratio is a different quantity from ApoA1 and has no unit, so this page places no typed result against it. One Finnish study put its reference interval at 0.3 to 1.0 in men and 0.3 to 0.8 in women [5], and a European guideline describes such ratios as useful for risk estimation and not for diagnosis or as treatment targets [2].

Checked, no link found2

Moderate

Coronary heart disease in genetic studies

Not shown to protect against coronary disease in genetic studies: gene variants that raise ApoA1 did not go with less disease once ApoB was accounted for.

The numbers and sources

Effect: In a Mendelian randomization analysis using a variant in the APOA1 gene region, each standard deviation higher ApoA1 had an odds ratio for coronary artery disease of 1.13 (95% CI 0.98 to 1.30), while the observational hazard ratio in the same paper was 0.81 (0.75 to 0.88) [12]. In a second analysis, the odds ratio per standard deviation higher ApoA1 was 0.83 (95% CI 0.77 to 0.89) when ApoA1 was analyzed alone and 0.94 (0.76 to 1.17) after adjustment for ApoB, which itself kept an odds ratio of 1.68 (1.54 to 1.84) [13].
Population: Genetic data on 20,370 Finnish participants combined with an earlier genome-wide study, applied to 122,733 coronary cases, and 918 incident cases among 11,535 people for the observational estimate [12]. Genetic data from up to 441,016 UK Biobank participants, applied to 60,801 coronary cases and 123,504 controls [13].
Sources: [12], [13]
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 its single-trait estimates weakened under methods more robust to variants that act through several traits [13].

Limited

Heart attack, stroke and cardiovascular death in a trial that infused ApoA1

One trial found four weekly infusions of human ApoA1 after a heart attack did not significantly lower heart attack, stroke or cardiovascular death against placebo.

The numbers and sources

Effect: In the AEGIS-II trial, the composite of heart attack, stroke or cardiovascular death occurred in 4.8% of patients given ApoA1 (CSL112) and 5.2% given placebo at 90 days (HR 0.93, 95% CI 0.81 to 1.05, P = 0.24). At 180 days it was 6.9% against 7.6% (HR 0.91, 0.81 to 1.01), and at 365 days 9.8% against 10.5% (HR 0.93, 0.85 to 1.02). Adverse events were similar, with more hypersensitivity events reported with ApoA1 [14]. In a meta-analysis of people on statins, a rise in ApoA1 after starting treatment went with fewer major cardiovascular events (HR 0.93 per standard deviation, 95% CI 0.90 to 0.97), while a rise in HDL cholesterol did not (0.98, 0.94 to 1.01) [11].
Population: 18,219 patients with acute myocardial infarction, multivessel coronary disease and other risk factors, given four weekly infusions of 6 g or placebo [14]. 38,153 trial participants allocated to a statin [11].
Sources: [14], [11]
Caveats: The trial tested a short course of infused ApoA1 soon after a heart attack and was funded by the maker of the product. It did not test a lasting rise in a person's own ApoA1 [14]. The statin finding compares people within trials and is observational [11].
Why limited: This rests on one trial, of 18,219 people. Strength counts independent studies that agree, so one trial is limited at any size.

Sources

US Food and Drug Administration. 21 CFR 862.1475, Lipoprotein test system. Electronic Code of Federal Regulations, with the FDA device classification entry for apolipoproteins (product code MSJ). https://www.ecfr.gov/current/title-21/section-862.1475
Catapano AL, Graham I, De Backer G, et al. 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias. European Heart Journal. 2016. https://doi.org/10.1093/eurheartj/ehw272
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
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
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Contois J, McNamara JR, Lammi-Keefe C, et al. Reference intervals for plasma apolipoprotein A-1 determined with a standardized commercial immunoturbidimetric assay: results from the Framingham Offspring Study. Clinical Chemistry. 1996. https://doi.org/10.1093/clinchem/42.4.507
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Thompson A, Danesh J. Associations between apolipoprotein B, apolipoprotein AI, the apolipoprotein B/AI ratio and coronary heart disease: a literature-based meta-analysis of prospective studies. Journal of Internal Medicine. 2006. https://doi.org/10.1111/j.1365-2796.2006.01644.x
Emerging Risk Factors Collaboration. Major Lipids, Apolipoproteins, and Risk of Vascular Disease. JAMA. 2009. https://doi.org/10.1001/jama.2009.1619
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Boekholdt SM, Arsenault BJ, Hovingh GK, et al. Levels and Changes of HDL Cholesterol and Apolipoprotein A-I in Relation to Risk of Cardiovascular Events Among Statin-Treated Patients: A Meta-Analysis. Circulation. 2013. https://doi.org/10.1161/CIRCULATIONAHA.113.002670
Karjalainen MK, Holmes MV, Wang Q, et al. Apolipoprotein A-I concentrations and risk of coronary artery disease: A Mendelian randomization study. Atherosclerosis. 2020. https://doi.org/10.1016/j.atherosclerosis.2020.02.002
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
Gibson CM, Duffy D, Korjian S, et al. Apolipoprotein A1 Infusions and Cardiovascular Outcomes after Acute Myocardial Infarction. New England Journal of Medicine. 2024. https://doi.org/10.1056/NEJMoa2400969
McQueen MJ, Hawken S, Wang X, et al. Lipids, lipoproteins, and apolipoproteins as risk markers of myocardial infarction in 52 countries (the INTERHEART study): a case-control study. The Lancet. 2008. https://doi.org/10.1016/S0140-6736(08)61076-4
Walldius G, Jungner I, Holme I, et al. High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study. The Lancet. 2001. https://doi.org/10.1016/S0140-6736(01)07098-2
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
Yang D, Cai Q, Qi X, Zhou Y. Postprandial Lipid Concentrations and Daytime Biological Variation of Lipids in a Healthy Chinese Population. Annals of Laboratory Medicine. 2018. https://doi.org/10.3343/alm.2018.38.5.431
Marcovina SM, Albers JJ, Henderson LO, Hannon WH. International Federation of Clinical Chemistry standardization project for measurements of apolipoproteins A-I and B. III. Comparability of apolipoprotein A-I values by use of international reference material. Clinical Chemistry. 1993. https://doi.org/10.1093/clinchem/39.5.773
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
Ortolá J, Castiñeiras MJ, Fuentes-Arderiu X. Biological variation data applied to the selection of serum lipid ratios used as risk markers of coronary heart disease. Clinical Chemistry. 1992. https://doi.org/10.1093/clinchem/38.1.56
Clouet-Foraison N, Marcovina SM, Guerra E, et al. Analytical Performance Specifications for Lipoprotein(a), Apolipoprotein B-100, and Apolipoprotein A-I Using the Biological Variation Model in the EuBIVAS Population. Clinical Chemistry. 2020. https://doi.org/10.1093/clinchem/hvaa054

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