Cholesterol, ApoB & Lp(a)
What Is ApoB and Why Does It Matter?
ApoB estimates the number of cholesterol-carrying particles that can enter artery walls. It can reveal risk that LDL cholesterol alone may understate.
A standard cholesterol panel tells you how much cholesterol is being carried in your blood. Lately, a four-letter term has been turning up next to it in a lot of longevity conversations, usually said with great confidence and not much explanation. At Humanic Blue, the question is what it actually measures.
What is ApoB, and why does it matter? Apolipoprotein B is a protein found on the particles that can carry cholesterol into artery walls, and an ApoB blood test estimates how many of those particles are circulating. For anyone focused on living longer, its relevance is the heart and blood vessels. The 2026 US cholesterol guideline uses ApoB selectively, to clarify risk when a standard panel may understate it. It isn’t a replacement for LDL cholesterol, and there’s no single “optimal longevity” number.
In This Article
- ApoB counts the carriers, not the cholesterol they carry
- Why ApoB and LDL cholesterol can tell different stories
- Who the 2026 US guideline says might test it
- How to read a result, and why goals differ by risk
- Fasting, and what lowers ApoB
- What no ApoB test can promise
- The guideline goals, studies and sources behind all of this
Key Takeaways
- ApoB estimates the number of cholesterol-carrying particles that can contribute to plaque in artery walls, according to the National Lipid Association.
- When LDL-C and ApoB disagree, the National Lipid Association says heart risk generally lines up better with ApoB (or non-HDL cholesterol).
- The 2026 US guideline recommends ApoB selectively, mainly for people on cholesterol-lowering treatment who have diabetes, high triglycerides, cardiometabolic disease or known cardiovascular disease, not for every adult.
- Goals depend on risk: under 90, 70 or 55 mg/dL in the guideline’s named groups. There is no universal “optimal longevity” number.
- The European laboratory and atherosclerosis societies say fasting usually isn’t needed for an ApoB test.
- No trial shows that ApoB testing itself helps people live longer.
One particle, one ApoB
Cholesterol can’t travel through watery blood by itself. The body packages cholesterol and triglycerides inside lipoprotein particles, which act more like transport containers than loose cargo.
LDL cholesterol (LDL-C) measures the amount of cholesterol inside low-density lipoprotein (LDL) particles. ApoB measures a protein on the surface of LDL, very-low-density lipoprotein (VLDL), intermediate-density lipoprotein and lipoprotein(a), or Lp(a), particles. Each of those particles carries one ApoB molecule, so the result works as an estimate of particle number, reported in milligrams per deciliter (mg/dL). The National Lipid Association’s 2024 expert consensus, written by a panel of lipid specialists led by Daniel Soffer, MD, of the University of Pennsylvania, puts it plainly: ApoB reflects the total concentration of artery-clogging (atherogenic) lipoprotein particles in the blood. Most of its authors report consulting or research ties to makers of cholesterol-lowering drugs.
In everyday terms, LDL-C measures the cargo. ApoB counts the vehicles carrying it.
That analogy has a limit. An ApoB test reports the mass of a protein; it doesn’t literally count particles one by one. A 2023 review in the Journal of the American Heart Association, by John Contois of the laboratory-products company Sun Diagnostics and colleagues, with McGill University lipid researcher Allan Sniderman, MD, as senior author, reports that ApoB testing has had an international reference standard since the 1990s and that expert groups consider it well enough standardized for clinical care. The authors declared no conflicts. How the test is standardized
Why LDL-C and ApoB can disagree
This is where a fairly technical distinction starts to matter. Two people can carry the same amount of LDL cholesterol in a different number of particles. One may have fewer cholesterol-rich particles. The other may have more particles carrying less cholesterol apiece. Their LDL-C can match while their ApoB does not.
Clinicians call this mismatch discordance. It matters because, as the Contois and Sniderman review describes it, atherosclerosis is driven by ApoB-containing particles getting trapped in the artery wall. When LDL-C and ApoB disagree, the National Lipid Association says heart risk generally lines up better with ApoB or non-HDL-C—the cholesterol carried in all particles other than HDL.
The pattern is particularly relevant when triglycerides are elevated, or in people with diabetes and other cardiometabolic conditions. These states can produce more cholesterol-poor particles, leaving LDL-C looking less concerning than the number of particles would suggest. For people with triglycerides of 150 mg/dL or more, the 2026 US guideline prefers non-HDL-C or ApoB over LDL-C for clinical decisions.
A 2025 study from a cardiology team at Fuwai Hospital and the Chinese Academy of Medical Sciences in Beijing followed about 375,000 UK Biobank participants without heart disease who weren’t taking cholesterol drugs. People whose ApoB ran higher than their LDL-C suggested had about an 11% higher rate of heart attacks, strokes and related events. People whose ApoB ran lower had about 13% lower risk. VLDL particles and triglycerides partly explained the extra risk (European Journal of Preventive Cardiology). That’s observational evidence, a link rather than proof, and not a trial showing that ordering an ApoB test prevents events. The study details
How does counting cholesterol carriers change the interpretation of the same amount of cholesterol?
When does an ApoB test add useful information?
The 2026 American College of Cardiology and American Heart Association guideline, written with nine other US medical societies, keeps the standard lipid panel at the center of care. It calls ApoB measurement reasonable for adults already taking cholesterol-lowering treatment, particularly those with cardiovascular disease caused by plaque in arteries, cardiovascular-kidney-metabolic syndrome (overlapping heart, kidney and metabolic problems), type 2 diabetes or elevated triglycerides, once LDL-C or non-HDL-C goals have been reached and the clinician is deciding whether treatment needs to be stepped up.
For adults not on treatment, the guideline says ApoB may be reasonable to sharpen a risk estimate, help decide whether to start treatment and characterize inherited lipid disorders. An ApoB above 140 mg/dL is one of the guideline’s markers of severe hypercholesterolemia, as are an LDL-C above 190 mg/dL and a non-HDL-C above 220 mg/dL.
That’s a selective-testing recommendation, not a directive that every healthy adult needs ApoB checked repeatedly. By contrast, the guideline recommends at least one lipoprotein(a) measurement in adulthood for everyone. The two tests answer related but different questions.
What ApoB adds—and what it leaves out
The guideline and the National Lipid Association both place ApoB’s value where it resolves a specific uncertainty in the standard panel. It can reveal a high particle burden when LDL-C looks controlled and help guide treatment in selected higher-risk patients. It can’t show whether plaque is already present, separate how much of the total comes from Lp(a), or replace blood pressure, diabetes, smoking, kidney health and family history in an overall risk estimate. See the full add-and-leave-out list
In these guidelines, ApoB testing serves a specific purpose: clarifying risk or a treatment decision when the standard panel leaves uncertainty.
How should you read an ApoB result?
Start with the units. US laboratories usually report ApoB in mg/dL; some countries use grams per liter (g/L). The conversion is exact: 1 g/L equals 100 mg/dL.
Then separate a laboratory reference range from a treatment goal. MedlinePlus, a service of the US National Library of Medicine, lists a normal range of about 50 to 150 mg/dL and notes that ranges vary among laboratories. A result inside that range isn’t automatically the right treatment level for someone with established heart disease.
The 2026 US guideline makes the goal depend on risk. Where it names an ApoB goal, it’s under 90 mg/dL for lower-risk groups, under 70 for higher-risk groups and under 55 for people with cardiovascular disease at very high risk. Those numbers only mean something next to the risk group they belong to. See the guideline’s goals by risk group
Guidelines also differ by region. European cardiology and atherosclerosis societies use slightly different ApoB goals: under 100, 80 and 65 mg/dL for moderate, high and very high risk. Different numbers don’t point to a hidden biological optimum. They reflect different risk systems and guideline methods.
What separates a laboratory reference range from a goal assigned to a particular risk group?
Do you need to fast?
Usually, no. (A small mercy for anyone who has spent a morning in a lab waiting room thinking about breakfast.) A joint consensus from the European Atherosclerosis Society and the European Federation of Clinical Chemistry and Laboratory Medicine, led by Copenhagen University Hospital’s Børge Nordestgaard, found that ApoB levels are not affected by whether a person has fasted (Clinical Chemistry). MedlinePlus notes that some providers still ask people not to eat or drink for 4 to 6 hours, so it’s worth checking the instructions you’re given.
The rest of the lipid panel can still shift after a meal, especially triglycerides. The 2026 US guideline calls for a fasting profile when a nonfasting test shows triglycerides of 400 mg/dL or more, or when there’s a family history of lipid disorders or early heart disease.
ApoB also needs context rather than a list of “confounders” to explain away. The guideline asks clinicians to rule out secondary causes of abnormal lipids, which a published summary of the guideline lists as including an underactive thyroid, kidney and liver disease, diabetes, obesity, heavy drinking and medicines such as estrogens and corticosteroids; lipids also rise naturally in pregnancy. An unexpected result may therefore prompt a review of health conditions, medications and the accompanying LDL-C, non-HDL-C and triglyceride values rather than a conclusion based on ApoB alone.
What lowers ApoB?
ApoB falls when the number of circulating atherogenic particles falls. The 2026 US guideline bases treatment on overall risk and recommends evidence-based lifestyle measures and, when indicated, LDL-lowering medicines such as statins, ezetimibe, bempedoic acid or PCSK9-directed therapies.
The evidence for those add-on medicines comes from large randomized trials that counted heart attacks and strokes. In IMPROVE-IT, FOURIER and ODYSSEY OUTCOMES, which together enrolled more than 60,000 high-risk patients, adding ezetimibe or a PCSK9 inhibitor to a statin lowered LDL cholesterol further and reduced cardiovascular events. Each trial was funded by the maker of the drug it tested. Those results describe trial populations receiving specific therapies, not self-treatment targets for everyone. How the trials worked
The same guideline does not recommend dietary supplements to lower LDL-C or triglycerides, because the data on lipid lowering and heart-risk reduction are limited and inconsistent. A supplement marketed as an “ApoB hack” still has to clear the outcomes-evidence bar.
What ApoB cannot tell you
The limits above are the practical ones. One is worth drawing out: because Lp(a) carries inherited risk that an ApoB total can’t isolate, the one-time Lp(a) test answers a separate question.
Most importantly, an ApoB measurement is a risk marker and treatment guide. No trial has randomized people to “receive an ApoB test” versus “do not receive one” and shown that the test itself lengthens life. The supported claim is narrower: ApoB estimates atherogenic particle burden, improves risk classification when cholesterol measures disagree and can help clinicians judge lipid-lowering therapy. MedlinePlus adds a note of caution of its own: how much the test adds to standard cholesterol testing “is not known.”
What’s Interesting
The National Lipid Association points out that LDL-C and ApoB can be highly correlated across a population and still disagree in the individual person. That’s why the test can look redundant on a spreadsheet and useful in a clinic. Averages are great at describing crowds and less great at describing any one person in them.
It also explains why “good cholesterol, bad cholesterol” eventually became too small a vocabulary for modern lipidology. Cholesterol is cargo. Particles are carriers. The researchers behind the Contois review describe atherosclerosis as a problem of carriers getting trapped in the artery wall, which makes how many there are, and for how long, part of the story.
What This Means in Practice
Worth noting first: the goal table sorts people into risk categories, not individuals into destinies. Two people with an identical ApoB can land in different rows because of diabetes, kidney health, triglycerides or an existing heart diagnosis, which is how the same number ends up read two different ways.
If you already have an ApoB result, read it beside LDL-C, non-HDL-C and triglycerides, not in isolation. Ask which risk category and guideline your clinician is using, whether the result is discordant with your LDL-C, and whether it would change a treatment decision.
If your LDL-C is at goal but ApoB remains above the goal for your risk group, the 2026 US guideline says that may indicate residual atherogenic particle burden, particularly with diabetes, high triglycerides or established cardiovascular disease. A primary-care clinician can put the result into an overall risk estimate; a preventive cardiologist or lipid specialist is the appropriate next stop when the numbers conflict, an inherited disorder is suspected or cardiovascular disease is already present.
ApoB answers a different question from the standard triglyceride result; Triglycerides and Healthy Aging explains what that number adds.
Bottom Line
Living longer is not an outcome an ApoB test can promise. Its narrower, guideline-supported role is to reveal particle burden that may otherwise be missed and help a clinician decide whether guideline-recommended cardiovascular-risk reduction should be intensified. The question worth bringing to an appointment isn’t “What’s the lowest ApoB anyone on the internet can achieve?” It’s “What does this number add to my risk assessment, and would acting on it improve an outcome that matters?”
A NOTE FROM LONGEVITY365
We read research, consult expert perspectives and work to make complicated health information easier to understand. What you’re reading here reflects how we’ve interpreted and organized that information. It is educational content—not personal medical advice, diagnosis or treatment guidance.
We’re not perfect, and neither is the available research. Evidence changes, new studies emerge and what’s appropriate for one person may not be appropriate for another.
Use this article as a starting point for your own research and conversations with qualified professionals. Always talk with your doctor or another trusted healthcare professional before making decisions that could affect your health, particularly if you take medications, are receiving treatment, have existing health conditions, are pregnant or have other circumstances that could affect what’s appropriate for you.
Reader Questions
A few questions to carry into the comments or your next conversation. Please leave out identifying or personal medical details.
- 01What part of "What Is ApoB and Why Does It Matter" surprised you most, or made you want to ask a better question?
- 02Which distinction in the article would be most useful to carry into everyday life?
- 03What would you want Humanic Blue to unpack next from this topic?
Extra Insights & Sources
For readers who want the details behind each claim above.
What We Know
- Every LDL, VLDL, intermediate-density lipoprotein and Lp(a) particle carries one ApoB molecule, making ApoB a practical estimate of atherogenic particle number. Established. (NLA consensus; Contois et al.)
- When LDL-C and ApoB disagree, cardiovascular risk generally tracks more closely with ApoB or non-HDL-C. Supported by prospective cohorts and reflected in US clinical guidance. (NLA consensus; 2025 prospective study)
- ApoB is most likely to add information in people with high triglycerides, diabetes, cardiometabolic disease, established cardiovascular disease or very low achieved LDL-C. Supported and guideline-endorsed. (2026 ACC/AHA guideline)
- Fasting is not routinely required for ApoB measurement. Established for routine testing. (EAS/EFLM consensus)
What We Don’t Know
- There is no universal ApoB value proven to maximize lifespan in every adult. Guideline goals vary with cardiovascular risk and country. Unknown as a universal target.
- ApoB-guided treatment has not been compared with LDL-C-guided treatment in a large randomized strategy trial designed to show which testing approach prevents more events. Uncertain. The current case is built from biology, cohort comparisons and treatment trials that lowered LDL cholesterol.
- A single result cannot show a person’s cumulative lifetime exposure to ApoB-containing particles. Known limitation. Duration matters, but one blood draw is a snapshot.
How the particle count works
The National Lipid Association consensus explains that atherogenic lipoproteins differ in lipid content, size and other features, but they share one feature: each particle carries a single ApoB molecule. Because of that, the consensus says, the measured ApoB level represents the concentration of atherogenic lipoproteins in the serum. It adds that even after a meal, more than 95% of circulating ApoB is ApoB-100 in people without severe hypertriglyceridemia, so ApoB changes little between fasting and nonfasting states.
The Contois review (Journal of the American Heart Association, 2023; authors John H. Contois, Michel R. Langlois, Christa Cobbaert and Allan D. Sniderman) states that in 1994 the International Federation of Clinical Chemistry and the World Health Organization (WHO/IFCC) endorsed the standardization of ApoB measurement, and that a stable IFCC-WHO reference standard was produced. Its abstract says “Multiple expert groups have determined that the measurement of apoB is adequately standardized for clinical care” and that ApoB can be measured “inexpensively, using widely available automated methods.” The review describes “Trapping of apoB particles within the arterial wall” as “the fundamental cause of atherosclerosis.” The paper lists “Sources of Funding None. Disclosures None.” First author John Contois is affiliated with Sun Diagnostics, LLC, of New Gloucester, Maine, a developer of in vitro diagnostic products.
NLA disclosures. The NLA consensus (Journal of Clinical Lipidology, 2024; first and corresponding author Daniel E. Soffer, MD, Clinical Lipidology, University of Pennsylvania) received NLA funding for copy-editing, and authors received no payment for writing. Most of the 13 authors disclosed advisory, consulting, speaking or research relationships with pharmaceutical companies that make lipid-lowering drugs, including Amgen, Novartis, Ionis, NewAmsterdam Pharma, Esperion, Sanofi and Regeneron. One reported nothing to disclose, and two reported only employment at a research company or government and philanthropic research funding. The consensus also calls for improved access and reimbursement for ApoB testing.
The discordance study in detail
Here, HR means hazard ratio: a comparison of event rates over follow-up, where 1 means no difference, 1.11 means an estimated 11% higher rate and 0.87 means a 13% lower rate. CI means confidence interval, a range expressing statistical uncertainty. These relative comparisons do not give an individual’s chance of having an event. Cox regression is the statistical method used to compare event rates over time while accounting for measured differences between groups.
Yuan Du and colleagues (senior author Yuanlin Guo) at Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College analyzed 375,544 UK Biobank participants without baseline cardiovascular disease, not on lipid-lowering therapy and with lipid nuclear magnetic resonance data. People were grouped as concordant, discordantly high ApoB or discordantly low ApoB, based on whether their LDL-C and ApoB percentiles differed by more than 10 units. In Cox regression, the discordantly high ApoB group had a higher risk of major adverse cardiovascular events (HR 1.11; 95% CI 1.06–1.15) and the discordantly low group a lower risk (HR 0.87; 95% CI 0.83–0.93). The discordantly high group had the highest concentrations of VLDL cholesterol and VLDL particles but less cholesterol per particle. In mediation analysis, VLDL particles and triglycerides mediated 25.5% and 26.6% of the excess risk, respectively; the authors found no conclusive evidence that VLDL adds prognostic value beyond triglycerides alone. Mediation analysis estimates how much of an observed association a statistical model can account for through another measured factor. The 25.5% and 26.6% figures are model-based shares of the excess risk, not percentages of participants; they do not prove those factors caused that share. The authors concluded that ApoB is a more comprehensive marker of cardiovascular risk than LDL-C. Published online November 2025 in the European Journal of Preventive Cardiology. (Note 1)
The 2026 US guideline also lists persistently elevated ApoB of 120 mg/dL or more (alongside LDL-C of 160 to 189 mg/dL or non-HDL-C of 190 to 219 mg/dL) among its risk-enhancing factors, according to the University of Illinois Chicago Drug Information Group’s summary. That summary also paraphrases the guideline’s rationale: “Studies have shown that apoB is a more accurate predictor of ASCVD risk than LDL-C when the two measures provide differing risk estimates.” The American College of Cardiology’s announcement says ApoB “may be a more accurate risk marker than LDL-C” in people with cardiovascular-kidney-metabolic syndrome, type 2 diabetes, high triglycerides or known cardiovascular disease.
What ApoB adds and leaves out
| What the information can add | What the information cannot answer |
|---|---|
| Estimates the total burden of circulating atherogenic particles, not only the cholesterol inside LDL | Does not show whether plaque is already present or whether an artery is narrowed |
| Can reveal discordantly high particle burden when LDL-C looks controlled | Does not identify how much of the total comes from LDL, Lp(a) or triglyceride-rich remnants |
| Can help guide treatment intensification in selected higher-risk patients | Does not establish one universal treatment target for every age, sex or risk group |
| Uses a standardized, widely available blood assay that usually does not require fasting | Does not replace blood pressure, diabetes, smoking, kidney health, family history or an overall risk estimate |
The benefits and limits in this table reflect the 2026 ACC/AHA guideline and the National Lipid Association consensus.
The guideline’s goals by risk group
In the guideline language below, LLT means lipid-lowering therapy; ASCVD means cardiovascular disease caused by plaque in arteries; CKM means cardiovascular-kidney-metabolic; and TG means triglycerides. PREVENT-ASCVD is the guideline’s calculator for estimating the risk of an atherosclerotic cardiovascular event.
The 2026 ACC/AHA guideline’s recommendation on ApoB measurement (Class 2a) reads: “In adults on LLT, particularly those with ASCVD, CKM syndrome, type 2 diabetes, and/or elevated TG, measurement of apoB is reasonable to guide decisions regarding further therapeutic intensification once LDL-C and/or non–HDL-C goals are achieved.” For adults not on lipid-lowering therapy (Class 2b), measurement “may be reasonable to enhance ASCVD risk assessment, guide decisions about initiation of LLT, and characterize inherited lipid disorders.” Severe hypercholesterolemia is footnoted as “LDL-C >190 mg/dL, non–HDL-C >220 mg/dL, and/or apoB >140 mg/dL.”
Primary prevention concerns people without established atherosclerotic cardiovascular disease; secondary prevention concerns people who already have it and aims to prevent further events. The table describes guideline treatment contexts for clinicians, not targets to assign from a laboratory result alone.
| Clinical context | 2026 US ApoB goal when the guideline specifies one | What the number means |
|---|---|---|
| Primary prevention, 10-year PREVENT-ASCVD risk below 10%, with triglycerides 150–499 mg/dL | <90 mg/dL | A context-specific treatment goal, not a universal “normal” |
| Primary prevention, PREVENT-ASCVD risk at least 10%, with triglycerides 150–499 mg/dL | <70 mg/dL | Lower goal because estimated risk is higher |
| Diabetes without ASCVD risk factors or diabetes-specific risk modifiers | <90 mg/dL | Used with LDL-C and non-HDL-C goals |
| Diabetes with ASCVD risk factors or diabetes-specific risk modifiers | <70 mg/dL | Used with LDL-C and non-HDL-C goals |
| Hypertriglyceridemia, ages 40–75 with at least one ASCVD risk factor | <70 mg/dL | Applies when triglycerides are elevated |
| Clinical ASCVD at very high risk | <55 mg/dL | Intensive secondary-prevention goal |
These values come from the 2026 ACC/AHA dyslipidemia guideline’s lipoprotein-goal table (Table 3). (Note 2) The values should not be detached from the populations named beside them. The same table also lists ApoB goals for people with high triglycerides and clinical ASCVD, and “consider apoB” optional goals for some coronary-calcium and clinical-ASCVD groups.
Europe. The European Society of Cardiology and European Atherosclerosis Society retain ApoB as a secondary treatment target, with goals below 65, 80 and 100 mg/dL for very-high-, high- and moderate-risk people respectively (2019 ESC/EAS guideline). The 2025 focused update states that “Previous recommendations that have not changed are still valid,” leaving those targets in force.
Fasting. The EAS/EFLM joint consensus (Nordestgaard BG et al., 2016, published in both Clinical Chemistry and the European Heart Journal) states that HDL cholesterol, apolipoprotein A1, apolipoprotein B and lipoprotein(a) concentrations are not affected by whether a person has fasted, and recommends routine nonfasting lipid profiles. Panel members reported lecture, consulting or research payments from lipid-drug makers including Amgen, Pfizer and AstraZeneca; the EAS and EFLM paid the open-access charges. The 2026 US guideline recommends a standard nonfasting or fasting lipid profile at baseline, and a fasting profile for people with a family history of dyslipidemia or premature ASCVD, a known or suspected triglyceride disorder, or a nonfasting triglyceride level of 400 mg/dL or more.
The treatment trials in detail
- IMPROVE-IT (New England Journal of Medicine, 2015; Cannon CP et al.): 18,144 patients recently hospitalized for acute coronary syndrome received simvastatin plus ezetimibe or simvastatin plus placebo, with a median follow-up of 6 years. Time-weighted average LDL-C was 53.7 vs 69.5 mg/dL, and the 7-year primary event rate was 32.7% vs 34.7% (HR 0.936). Funded by Merck.
- FOURIER (New England Journal of Medicine, 2017; Sabatine MS et al.): 27,564 patients with atherosclerotic cardiovascular disease on statins received evolocumab or placebo for a median of 2.2 years. LDL-C fell 59%, from a median of 92 to 30 mg/dL, and primary events were 9.8% vs 11.3% (HR 0.85). Funded by Amgen.
- ODYSSEY OUTCOMES (New England Journal of Medicine, 2018; Schwartz GG et al.): 18,924 patients 1 to 12 months after an acute coronary syndrome, on high-intensity statins, with LDL-C of at least 70 mg/dL, non-HDL-C of at least 100 mg/dL or ApoB of at least 80 mg/dL, received alirocumab or placebo for a median of 2.8 years. Primary events were 9.5% vs 11.1% (HR 0.85). Funded by Sanofi and Regeneron.
The 2026 US guideline’s dietary-supplement recommendation (Class 3, No Benefit) reads: “In individuals with dyslipidemia, the use of dietary supplements is not recommended to lower LDL-C or TG based on limited and inconsistent data and/or limited benefits in lipid-lowering and reduction in ASCVD risk.”
Sources
- ACC/AHA and nine other societies (Blumenthal RS, Morris PB, et al.). 2026 Guideline on the Management of Dyslipidemia, Circulation, 2026: DOI 10.1161/CIR.0000000000001423 (PubMed 41824552; corrections published June and September 2026)
- American College of Cardiology: ACC/AHA Issue Updated Guideline for Managing Lipids, Cholesterol (March 13, 2026)
- University of Illinois Chicago Drug Information Group: Key updates from the 2026 dyslipidemia guideline (May 2026)
- Soffer DE, et al. Role of apolipoprotein B in the clinical management of cardiovascular risk in adults (NLA consensus), Journal of Clinical Lipidology, 2024: PubMed 39256087
- Contois JH, et al. Standardization of apolipoprotein B, LDL-cholesterol, and non-HDL-cholesterol, Journal of the American Heart Association, 2023: PubMed 37489721
- Du Y, et al. LDL-C and apolipoprotein B discordance and cardiovascular outcomes, European Journal of Preventive Cardiology, 2025: PubMed 41284723
- Nordestgaard BG, et al. Fasting is not routinely required for determination of a lipid profile (EAS/EFLM), Clinical Chemistry, 2016: PubMed 27235445
- Mach F, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: EAS PDF; 2025 Focused Update: EAS page
- Cannon CP, et al. IMPROVE-IT, New England Journal of Medicine, 2015: PubMed 26039521
- Sabatine MS, et al. FOURIER, New England Journal of Medicine, 2017: PubMed 28304224
- Schwartz GG, et al. ODYSSEY OUTCOMES, New England Journal of Medicine, 2018: PubMed 30403574
- MedlinePlus, US National Library of Medicine: Apolipoprotein B100
- MedScriptum: 2026 ACC/AHA Guideline for the Management of Dyslipidemia (summary of secondary causes)
Notes
Note 1: Funded by the National Natural Science Foundation of China and research grants 2021-I2M-1-008 and 2021-I2M-1-009.
Note 2: Guideline data in this article comes from published summaries, not the official report: the goal values from the University of Illinois Chicago Drug Information Group’s reproduction of the guideline’s Table 3, and the other guideline wording from the American College of Cardiology’s published summaries. Circulation has since published two corrections to the guideline (June 23 and September 8, 2026).
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