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Longevity Library · Lab reference

Written by Daniel Tagge, MD
Updated October 10, 2026
23 sources · Measured in mg/dL

System: Metabolism & Metabolomics

Non-HDL cholesterolNon-HDL-C · Total cholesterol minus HDL

Non-HDL cholesterol is total cholesterol minus HDL cholesterol, the cholesterol carried by every particle that can enter the artery wall, and it predicted heart disease at least as well as LDL cholesterol in more than 300,000 people without fasting; laboratories print under 130 mg/dL as desirable, guidelines set secondary goals of under 85, 100 or 130 by risk, the lowest 30-year event rates sat below 100, and 220 or above parallels an LDL of 190.

Non-HDL cholesterol is a subtraction on every standard lipid panel: total cholesterol minus HDL cholesterol, free, with no fasting and no equation. It adds up the cholesterol in LDL, VLDL, remnants and lipoprotein(a), so it tracks risk slightly better than LDL cholesterol and nearly as well as ApoB. The printed cutoff of 130 mg/dL is the 2001 LDL goal plus 30; the long-term cohorts put the lowest risk below 100.

01 · The scale

Where the laboratory range and the evidence sit.

Risk rose continuously with non-HDL cholesterol in every cohort, with the lowest rates below 100 mg/dL and no floor found. It predicted coronary disease at least as well as LDL cholesterol without fasting, slightly better in head-to-head pooling, and slightly less well than ApoB; guidelines translate that into secondary goals of under 85, 100 or 130 by risk.

085100130160190220

  1. Common laboratory 'desirable' cutoff

    0 to 130 mg/dL · NCEP ATP III 2001 (LDL goal plus 30)

  2. Very-high-risk secondary goal

    0 to 85 mg/dL · ESC/EAS 2019

  3. High-risk secondary goal; lowest 30-year event rates in the Consortium below 100

    85 to 100 mg/dL · ESC/EAS 2019; Brunner 2019

  4. Moderate-risk secondary goal; 2001 goal for coronary disease or its equivalent

    100 to 130 mg/dL · ESC/EAS 2019; NCEP ATP III 2001

  5. 2001 goal with two or more risk factors under 160; non-fasting flag at about 150

    130 to 160 mg/dL · NCEP ATP III 2001; EAS/EFLM 2016

  6. 'High' in Framingham: 22.6 percent 25-year risk when sustained from young adulthood

    160 to 190 mg/dL · Pencina 2019; Navar-Boggan 2015

  7. Risk-enhancing factor (primary hypercholesterolemia)

    190 to 219 mg/dL · AHA/ACC 2018

  8. Top Consortium category: three to four times the 30-year event rate; parallels LDL 190

    220 and above mg/dL · Brunner 2019; NCEP ATP III 2001

  • Laboratory range
  • Evidence supports
  • Guideline goal or unstudied
  • Higher risk in studies
Scale in mg/dL. Some laboratories report mmol/L; divide mg/dL by about 38.7 for mmol/L. Bands show where studies found something, not a recommendation for any one person.

02 · What it is

What Non-HDL cholesterol measures.

Non-HDL cholesterol is calculated as total cholesterol minus HDL cholesterol. The European laboratory consensus describes it as the cholesterol in LDL, remnant particles and lipoprotein(a) combined, available on any standard panel at no extra cost, from a fasting or a non-fasting sample. ApoB can be measured instead, at extra cost, because every one of those particles carries one ApoB molecule.1Grade A

The number exists because LDL cholesterol leaves things out. The 2001 US Adult Treatment Panel named non-HDL cholesterol a secondary target of therapy when triglycerides are 200 mg/dL or higher, reasoning that the VLDL cholesterol it captures is also atherogenic, and set each non-HDL goal 30 mg/dL above the matching LDL goal on the premise that a VLDL cholesterol of 30 or less is normal. The 2019 European guideline calls it a measure of the cholesterol carried by all ApoB-containing lipoproteins and recommends it, with ApoB, as part of routine lipid analysis when triglycerides are high, in diabetes, or when LDL cholesterol is very low.2,3Grade A

The causal case belongs to the particles it counts, not to the subtraction itself: the genetic studies, cohorts and trials that show LDL and ApoB cause atherosclerosis are covered in the LDL cholesterol and ApoB entries. In the Emerging Risk Factors Collaboration, once non-HDL and HDL cholesterol were accounted for, triglycerides no longer predicted coronary disease at all (hazard ratio 0.99), which is the argument for reading the whole cholesterol load rather than any one fraction.4Grade A

03 · The laboratory range

What a laboratory calls normal.

Under 130 mg/dL printed as desirable by most US laboratories; some print 130 to 159 as above desirable and 190 and above as very high, mirroring the LDL categories plus 30.

The printed cutoffs descend from the 2001 panel's rule of adding 30 mg/dL to each LDL goal: under 130 for people with coronary disease or its equivalent, under 160 with two or more risk factors, under 190 with none or one. Those were goals for people with high triglycerides, not a population reference range, and the lowest of them was written for the highest-risk group.2Grade A

The European laboratory consensus asks reports to flag a calculated non-HDL cholesterol of about 150 mg/dL or higher on a non-fasting sample and about 145 on a fasting one, cutoffs chosen for moderate risk, and notes that about half of adults in a Northern European population would be flagged at that line.1Grade A

The 2018 American guideline does not set non-HDL goals; it lists a persistent non-HDL cholesterol of 190 to 219 mg/dL, alongside an LDL of 160 to 189, as primary hypercholesterolemia and a risk-enhancing factor that favors treatment in intermediate-risk adults.5Grade A

04 · The evidence

What the studies support.

In the Emerging Risk Factors Collaboration, 302,430 people without vascular disease from 68 prospective studies were followed for 2.79 million person-years. Coronary disease occurred at 2.3 per 1,000 person-years in the bottom third of non-HDL cholesterol and 6.7 in the top third, and the adjusted hazard ratio was 1.50 for each 43 mg/dL higher; HDL cholesterol carried 0.78 per 15 mg/dL higher and triglycerides 0.99 after adjustment. The associations were at least as strong in people who had not fasted (1.72) as in those who had (1.41), and in the subset with direct measurements non-HDL cholesterol (1.42) matched directly measured LDL cholesterol (1.38). The association with ischemic stroke was about four times weaker (1.12).4Grade A

Across 12 reports with 233,455 people and 22,950 events, ApoB was the strongest of the three lipid markers for cardiovascular events (relative risk ratio 1.43 per standard deviation), non-HDL cholesterol intermediate (1.34) and LDL cholesterol weakest (1.25); the non-HDL estimate was 5.0 percent higher than LDL's and ApoB's 5.7 percent higher than non-HDL's. The authors calculated that treating everyone above the 70th US percentile by non-HDL cholesterol would prevent 300,000 more events over ten years than the same strategy by LDL cholesterol, and an ApoB strategy 500,000 more than non-HDL.6Grade A

The Multinational Cardiovascular Risk Consortium followed 398,846 people without cardiovascular disease from 38 cohorts in 19 countries for a median 13.5 years and up to 43.6, with 54,542 events. Thirty-year event rates rose stepwise with non-HDL cholesterol, from 7.7 percent in women and 12.8 percent in men below 100 mg/dL (2.6 mmol/L) to 33.7 and 43.6 percent at 220 and above, and the adjusted hazard ratios rose from 1.1 in the 100 to 145 band to 1.9 in women and 2.3 in men in the top band. The association was steepest in people under 45 at baseline (hazard ratios up to 4.3 and 4.6 in the top band) and weaker but still present after 60. In the authors' model, halving non-HDL cholesterol lowered the probability of an event by age 75 the more the earlier it was done: for example from 15.6 to 3.6 percent in women and 28.8 to 6.4 percent in men under 45 with two or more risk factors and a non-HDL of 145 to 185. That benefit is modeled from trial equations, not observed.7Grade B

The number is stable for decades, so a young adult's value is a lifetime exposure. In 2,516 Framingham Offspring participants aged 25 to 40, non-HDL trajectories were generally stable over about 30 years: 80 percent of those at 160 mg/dL or above on their first two examinations stayed high, 88 percent of those under 130 stayed under 160, and the high group had a 22.6 percent risk of cardiovascular disease over the next 25 years against 6.4 percent in the low group. In 1,478 Offspring participants free of disease at 55, coronary disease over a median 15 years ran 4.4 percent with no years above 160 before 55, 8.1 percent with 1 to 10 years and 16.5 percent with 11 to 20, a hazard ratio of 1.39 per decade of exposure after adjusting for the level at 55; 85 percent of those with prolonged exposure would not have qualified for treatment at 40 under the guidelines of the day.8,9Grade B

On treatment, non-HDL cholesterol tracked residual risk better than LDL cholesterol. In individual data from 38,153 patients randomized to a statin in 8 trials, each standard deviation higher on-treatment value carried a hazard ratio of 1.16 for non-HDL cholesterol, 1.14 for ApoB and 1.13 for LDL cholesterol, with non-HDL significantly stronger than both. In 13,015 statin-treated Danes followed a median 8 years, people with non-HDL cholesterol above the median but LDL cholesterol below it had 18 percent higher all-cause mortality and 78 percent more heart attacks than those with both low, while high LDL with low non-HDL carried no excess; high ApoB with low non-HDL still carried 21 percent higher mortality, which is why the authors rank ApoB first.10,11Grade A

For predicting a first event, non-HDL cholesterol captured almost all of the lipid signal. In 346,686 UK Biobank participants measured without fasting and followed a median 8.9 years, one standard deviation of ApoB, direct LDL cholesterol and non-HDL cholesterol carried hazard ratios of 1.23, 1.20 and 1.21, and once total and HDL cholesterol were in a risk model, adding ApoB or any LDL measure improved discrimination by at most 0.0004; among 68,649 statin users, non-HDL cholesterol and ApoB improved prediction equally (0.0030). The Emerging Risk Factors Collaboration found the same in 165,544 people: adding ApoB and ApoA-I to total and HDL cholesterol changed the C-index by 0.0006 and reclassified about 1 percent. When the UK Biobank markers were modeled together in 389,529 people, however, only ApoB remained associated with heart attack (1.27 per standard deviation), so the particle count explains the risk even where the subtraction predicts it.12,13,14Grade B

The observational U-curve in all-cause mortality exists for non-HDL as for LDL cholesterol and is drifting downward. In three Copenhagen cohorts of people not on lipid-lowering treatment (9,486 examined in 1991 to 1994, 56,796 in 2003 to 2009 and 48,105 in 2010 to 2018, followed to the end of 2022), the non-HDL cholesterol with the lowest all-cause mortality fell from 186 mg/dL (4.8 mmol/L) to 162 (4.2) as the population median fell from 174 to 150, while absolute mortality fell too. That nadir is far above every guideline goal; the LDL cholesterol entry explains why the authors of this series read the low end largely as illness lowering cholesterol rather than the reverse.15Grade C

05 · What moves it

The levers with evidence behind them.

What is listed here has been tested. The size of each effect, and the size of the study, are in the sentence, so a small effect reads as a small effect.

  • Replacing saturated and trans fat with unsaturated fat

    lowers it

    In 60 controlled feeding trials, the ratio of total to HDL cholesterol fell when cis-unsaturated fats replaced saturated fat and did not change when carbohydrate did; replacing trans fat had almost twice the effect of replacing saturated fat, and replacing fat with carbohydrate raised fasting triglycerides. Because non-HDL cholesterol is total minus HDL, the levers that move LDL cholesterol and triglycerides move it in the same direction.16Grade A

  • Viscous fiber such as psyllium

    lowers it by about 15 mg/dL

    Across 28 randomized trials with 1,924 participants, a median of about 10 grams of psyllium a day lowered non-HDL cholesterol by 0.39 mmol/L (about 15 mg/dL), LDL cholesterol by 0.33 mmol/L and ApoB by 0.05 g/L, with the non-HDL estimate graded moderate quality.17Grade A

  • Weight loss

    lowers it, mostly through the triglyceride part

    Across 73 randomized trials with 32,496 overweight adults, each kilogram lost through lifestyle change lowered triglycerides by 4.0 mg/dL and LDL cholesterol by 1.28 mg/dL at 12 months while raising HDL by 0.46; low-fat diets lowered LDL and triglycerides, low-carbohydrate diets mainly triglycerides. Non-HDL cholesterol was not reported separately, but it moves with the LDL and VLDL cholesterol those changes represent.18Grade A

  • Added sugar

    raises it modestly

    In 39 randomized trials, higher free-sugar intake raised triglycerides by 0.11 mmol/L, total cholesterol by 0.16 and LDL cholesterol by 0.12 mmol/L (about 5 mg/dL) compared with lower intake, and the effect held in trials that kept weight stable. Sugar acts on the VLDL and remnant portion of non-HDL cholesterol that LDL cholesterol alone does not show.19Grade B

  • Lipid-lowering medication

    lowers it substantially

    Medications that lower LDL cholesterol lower non-HDL cholesterol by a comparable fraction, and the guideline secondary goals assume them for people already judged at risk. The European guideline rates its non-HDL goals as moderate-grade because trials have not targeted them directly. Whether and when to treat is a decision for a physician who knows the person's risk, not a page.3Grade A

06 · Reading it well

Caveats, and what belongs with a physician.

Non-HDL cholesterol is a cholesterol mass, not a particle count. Particles differ in how much cholesterol each carries, so two people with the same non-HDL cholesterol can carry different numbers of ApoB particles, and in 12,688 US adults the spread of ApoB at a given cholesterol value was narrowest for non-HDL cholesterol, wider for LDL by the newer equations and widest for LDL by Friedewald, with discordance seen even in metabolically healthy people. When the two disagree, the Danish statin-treated cohort found that ApoB carried the risk: high ApoB with low non-HDL cholesterol still carried 21 percent higher mortality, and the authors conclude that ApoB is the more accurate marker of mortality risk than either LDL or non-HDL cholesterol.20,11Grade B

Fasting is not required, with one caveat. After an ordinary meal, calculated non-HDL cholesterol falls by at most about 8 mg/dL on average in 92,285 Danes, and the pooled cohorts found non-fasting values at least as predictive. In 26,330 women followed 11 years, though, non-HDL cholesterol predicted events more strongly when measured fasting (hazard ratio 1.29) than non-fasting (1.15), so a non-fasting value reads as a slightly blunter instrument, not a wrong one.1,4,21Grade A

One draw is an estimate. Pooling 30 studies of within-person variation, total cholesterol varied about 6.1 percent from one day to another in the same person, HDL cholesterol about 7.4 percent and LDL cholesterol about 9.5 percent; non-HDL cholesterol inherits the variation of the two numbers it is built from, so a value near a cutoff deserves a repeat before anything is decided.22Grade C

Lipoprotein(a) cholesterol is inside the number. About 30 percent of lipoprotein(a) mass is cholesterol and it is counted in total, non-HDL and LDL cholesterol, so a high non-HDL cholesterol can be partly inherited lipoprotein(a), which a once-in-a-lifetime measurement settles; the Canadian guideline now asks for that measurement in everyone, and prefers non-HDL cholesterol or ApoB to LDL cholesterol for screening whenever triglycerides exceed 1.5 mmol/L (about 133 mg/dL).1,23Grade A

The guideline numbers are secondary treatment goals inferred from LDL trials, not population definitions of health: the European goals of 85, 100 and 130 mg/dL are the LDL goals plus 30, rated moderate-grade because no trial has targeted non-HDL cholesterol, and the 2001 goals of 130, 160 and 190 were written for people with high triglycerides. No trial has randomized healthy adults to a non-HDL target.3,2Grade A

See a physician

  • A non-HDL cholesterol of 220 mg/dL or higher on any draw, which parallels an LDL of 190 under the 2001 panel's 30 mg/dL offset, sat in the top risk category of the Consortium, and was the 2013 American guideline's cue to look for genetic or secondary causes.
  • A persistent non-HDL cholesterol of 190 to 219, which the American guideline counts as primary hypercholesterolemia and a risk-enhancing factor.
  • A parent, sibling or child with a heart attack, stroke, stent or bypass before 55 (men) or 65 (women), or a relative known to have familial hypercholesterolemia.
  • A non-HDL cholesterol above 160 together with diabetes, high blood pressure, kidney disease, a high lipoprotein(a), a high ApoB or a smoking history.
  • A non-HDL cholesterol that looks fine beside a high triglyceride or a low HDL, where ApoB will say whether the particle count agrees.
  • Chest pressure, breathlessness on exertion, or pain in the calves when walking, regardless of any lipid number.

This page is education, not individual medical advice, and reading it creates no physician-patient relationship.

07 · Open questions

What the literature does not settle.

  • No outcome trial has used non-HDL cholesterol as its target; every goal is the LDL goal plus 30 mg/dL, and the European guideline grades its own non-HDL goals as moderate for that reason.
  • The Consortium's modeled benefit of halving non-HDL cholesterol early is an extrapolation from short drug trials in older people to decades in the young; no trial has tested lifelong lowering in healthy adults under 45.
  • Whether non-HDL cholesterol or ApoB should replace LDL cholesterol as the primary number. The pooled data say non-HDL beats LDL by a few percent and ApoB beats non-HDL by a few percent; the prediction studies say the extra markers add almost nothing once total and HDL cholesterol are known; the discordance studies say ApoB carries the risk when they disagree.
  • The 30 mg/dL offset assumes a normal VLDL cholesterol of 30 or less. In people with high triglycerides, insulin resistance or diabetes, the gap between LDL and non-HDL cholesterol is wider, and the fixed offset may understate their particle burden.
  • The lowest-mortality non-HDL cholesterol in Copenhagen (162 mg/dL in the most recent cohort) sits far above every goal, has been falling as the population's cholesterol falls, and is mostly explained by illness lowering cholesterol; how much of the residual association is real is unresolved.

09

Questions

10 · Sources

23 sources, read in full.

Numbered in the order they appear. Each line says what this page relies on from the paper; the link opens the record at PubMed or the publisher.

  1. 1.

    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. PMID 27122601. DOI 10.1093/eurheartj/ehw152.

    Consensus statement · Non-HDL cholesterol is total minus HDL cholesterol, equal to LDL plus remnant plus lipoprotein(a) cholesterol; maximal post-meal change about minus 8 mg/dL; flag non-fasting values at 150 mg/dL and fasting at 145; about half of adults flagged; Lp(a) cholesterol (30 percent of its mass) is included; the 2013 ACC/AHA guideline used non-HDL 220 as a cue to genetic or secondary causes.

  2. 2.

    Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001. PMID 11368702. DOI 10.1001/jama.285.19.2486.

    Guideline · Non-HDL cholesterol (total minus HDL) is a secondary target when triglycerides are 200 mg/dL or higher; its goal is 30 mg/dL above the LDL goal (under 130, 160 and 190 for the three risk categories) on the premise that VLDL cholesterol of 30 or less is normal.

  3. 3.

    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. PMID 31504418. DOI 10.1093/eurheartj/ehz455.

    Guideline · Non-HDL cholesterol (TC minus HDL-C) measures the cholesterol in all ApoB-containing lipoproteins; recommended with ApoB in routine analysis when triglycerides are high, in diabetes or at very low LDL-C; secondary goals under 85, 100 and 130 mg/dL (2.2, 2.6, 3.4 mmol/L) for very-high, high and moderate risk, set 30 mg/dL above the LDL goal and graded moderate because trials have not targeted them.

  4. 4.

    Emerging Risk Factors Collaboration; Di Angelantonio E, Sarwar N, et al.. Major lipids, apolipoproteins, and risk of vascular disease. JAMA. 2009. PMID 19903920. DOI 10.1001/jama.2009.1619.

    Systematic review and meta-analysis · In 302,430 people from 68 studies, hazard ratio 1.50 for coronary disease per 43 mg/dL non-HDL-C (2.3 vs 6.7 events per 1,000 person-years, bottom vs top third); 0.99 for triglycerides after adjustment; at least as strong without fasting (1.72 vs 1.41); non-HDL-C 1.42 vs direct LDL-C 1.38; ischemic stroke 1.12.

  5. 5.

    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. PMID 30586774. DOI 10.1161/CIR.0000000000000625.

    Guideline · Primary hypercholesterolemia (LDL-C 160 to 189 mg/dL; non-HDL-C 190 to 219 mg/dL) is a risk-enhancing factor favoring statin therapy in intermediate-risk adults; mg/dL divided by 38.6 gives mmol/L.

  6. 6.

    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. PMID 21487090. DOI 10.1161/CIRCOUTCOMES.110.959247.

    Systematic review and meta-analysis · Across 12 reports, 233,455 people and 22,950 events: ApoB RRR 1.43, non-HDL-C 1.34, LDL-C 1.25; non-HDL-C 5.0 percent above LDL-C, ApoB 5.7 percent above non-HDL-C; a non-HDL-C strategy would prevent 300,000 more events over ten years than an LDL-C strategy.

  7. 7.

    Brunner FJ, Waldeyer C, Ojeda F, et al.; Multinational Cardiovascular Risk Consortium. Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium. Lancet. 2019. PMID 31810609. DOI 10.1016/S0140-6736(19)32519-X.

    Prospective cohort · In 398,846 people from 38 cohorts (median follow-up 13.5 years, 54,542 events), 30-year event rates rose from 7.7 percent (women) and 12.8 percent (men) below 100 mg/dL to 33.7 and 43.6 percent at 220 and above; hazard ratios 1.1 to 1.9 (women) and 2.3 (men), steepest under 45 (up to 4.3 and 4.6); a modeled halving of non-HDL-C lowered the probability of an event by age 75, the more the earlier it began (15.6 to 3.6 percent in women, 28.8 to 6.4 in men under 45 with two or more risk factors at 145 to 185 mg/dL).

  8. 8.

    Pencina KM, Thanassoulis G, Wilkins JT, et al.. Trajectories of Non-HDL Cholesterol Across Midlife: Implications for Cardiovascular Prevention. Journal of the American College of Cardiology. 2019. PMID 31272554. DOI 10.1016/j.jacc.2019.04.047.

    Prospective cohort · In 2,516 Framingham Offspring participants aged 25 to 40 followed a mean 32.6 years, non-HDL-C trajectories were stable; 80 percent of those at 160 mg/dL or above stayed high and 88 percent of those under 130 stayed under 160; 25-year cardiovascular risk 22.6 percent (high) vs 6.4 percent (low).

  9. 9.

    Navar-Boggan AM, Peterson ED, D'Agostino RB Sr, Neely B, Sniderman AD, Pencina MJ. Hyperlipidemia in early adulthood increases long-term risk of coronary heart disease. Circulation. 2015. PMID 25623155. DOI 10.1161/CIRCULATIONAHA.114.012477.

    Prospective cohort · In 1,478 Framingham Offspring adults free of disease at 55, coronary disease over a median 15 years was 4.4, 8.1 and 16.5 percent with 0, 1 to 10 and 11 to 20 years of non-HDL-C at or above 160 mg/dL before 55 (HR 1.39 per decade after adjusting for the level at 55); 85 percent would not have qualified for statin therapy at 40.

  10. 10.

    Boekholdt SM, Arsenault BJ, Mora S, et al.. Association of LDL cholesterol, non-HDL cholesterol, and apolipoprotein B levels with risk of cardiovascular events among patients treated with statins: a meta-analysis. JAMA. 2012. PMID 22453571. DOI 10.1001/jama.2012.366.

    Systematic review and meta-analysis · Individual data from 62,154 patients in 8 statin trials (38,153 on statin): adjusted HR per SD of on-treatment level 1.13 for LDL-C, 1.16 for non-HDL-C and 1.14 for ApoB; non-HDL-C significantly stronger than LDL-C (P = .002) and ApoB (P = .02).

  11. 11.

    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. PMID 33736827. DOI 10.1016/j.jacc.2021.01.027.

    Prospective cohort · In 13,015 statin-treated Danes (median 8 years), high non-HDL-C with low LDL-C: HR 1.18 for all-cause mortality and 1.78 for myocardial infarction; high LDL-C with low non-HDL-C or ApoB: no excess; high ApoB with low non-HDL-C: HR 1.21 for mortality and 0.93 for infarction.

  12. 12.

    Welsh C, Celis-Morales CA, Brown R, et al.. Comparison of Conventional Lipoprotein Tests and Apolipoproteins in the Prediction of Cardiovascular Disease. Circulation. 2019. PMID 31216866. DOI 10.1161/CIRCULATIONAHA.119.041149.

    Prospective cohort · In 346,686 UK Biobank participants (non-fasting, median 8.9 years, 6,216 events), HR per SD 1.23 for ApoB, 1.20 for direct LDL-C and 1.21 for non-HDL-C; adding ApoB or any LDL-C to a model with total and HDL cholesterol changed the C-index by at most 0.0004; in 68,649 statin users non-HDL-C and ApoB each improved it by 0.0030.

  13. 13.

    Emerging Risk Factors Collaboration; Di Angelantonio E, Gao P, et al.. Lipid-related markers and cardiovascular disease prediction. JAMA. 2012. PMID 22797450. DOI 10.1001/jama.2012.6571.

    Systematic review and meta-analysis · In 165,544 people from 37 cohorts, adding ApoB and ApoA-I to total and HDL cholesterol improved the C-index by 0.0006 and reclassified about 1.1 percent of intermediate-risk adults.

  14. 14.

    Marston NA, Giugliano RP, Melloni GEM, et al.. Association of Apolipoprotein B-Containing Lipoproteins and Risk of Myocardial Infarction in Individuals With and Without Atherosclerosis: Distinguishing Between Particle Concentration, Type, and Content. JAMA Cardiology. 2022. PMID 34773460. DOI 10.1001/jamacardio.2021.5083.

    Prospective cohort · In 389,529 UK Biobank participants, ApoB, non-HDL-C and triglycerides each predicted myocardial infarction alone, but modeled together only ApoB remained (HR 1.27 per SD).

  15. 15.

    Doi T, Langsted A, Nordestgaard BG, Afzal S. LDL and non-HDL cholesterol with the lowest mortality in the general population in 1991-2018. Atherosclerosis. 2026. PMID 42208404. DOI 10.1016/j.atherosclerosis.2026.120790.

    Prospective cohort · In Copenhagen cohorts of 9,486 (1991 to 1994), 56,796 (2003 to 2009) and 48,105 (2010 to 2018) people not on lipid-lowering treatment, followed to 2022, the non-HDL-C with the lowest all-cause mortality fell from 186 mg/dL (4.8 mmol/L) to 162 (4.2) while the median fell from 174 to 150 mg/dL.

  16. 16.

    Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. American Journal of Clinical Nutrition. 2003. PMID 12716665. DOI 10.1093/ajcn/77.5.1146.

    Systematic review and meta-analysis · Across 60 controlled trials, the total-to-HDL ratio fell when cis-unsaturated fat replaced saturated fat and not when carbohydrate did; replacing trans fat had almost twice the effect; carbohydrate for fat raised fasting triglycerides.

  17. 17.

    Jovanovski E, Yashpal S, Komishon A, et al.. Effect of psyllium (Plantago ovata) fiber on LDL cholesterol and alternative lipid targets, non-HDL cholesterol and apolipoprotein B: a systematic review and meta-analysis of randomized controlled trials. American Journal of Clinical Nutrition. 2018. PMID 30239559. DOI 10.1093/ajcn/nqy115.

    Systematic review and meta-analysis · Across 28 trials with 1,924 participants, a median of about 10.2 g/day psyllium lowered non-HDL-C by 0.39 mmol/L (moderate quality), LDL-C by 0.33 mmol/L and ApoB by 0.05 g/L.

  18. 18.

    Hasan B, Nayfeh T, Alzuabi M, et al.. Weight Loss and Serum Lipids in Overweight and Obese Adults: A Systematic Review and Meta-Analysis. Journal of Clinical Endocrinology and Metabolism. 2020. PMID 32954416. DOI 10.1210/clinem/dgaa673.

    Systematic review and meta-analysis · Across 73 randomized trials with 32,496 adults, each kilogram lost through lifestyle change lowered triglycerides by 4.0 mg/dL and LDL-C by 1.28 mg/dL and raised HDL-C by 0.46 mg/dL at 12 months; low-fat diets lowered LDL-C and triglycerides, low-carbohydrate diets triglycerides.

  19. 19.

    Te Morenga LA, Howatson AJ, Jones RM, Mann J. Dietary sugars and cardiometabolic risk: systematic review and meta-analyses of randomized controlled trials of the effects on blood pressure and lipids. American Journal of Clinical Nutrition. 2014. PMID 24808490. DOI 10.3945/ajcn.113.081521.

    Systematic review and meta-analysis · Across 39 randomized trials, higher free-sugar intake raised triglycerides by 0.11 mmol/L, total cholesterol by 0.16 mmol/L and LDL-C by 0.12 mmol/L, independent of weight change.

  20. 20.

    Sayed A, Peterson ED, Virani SS, Sniderman AD, Navar AM. Individual Variation in the Distribution of Apolipoprotein B Levels Across the Spectrum of LDL-C or Non-HDL-C Levels. JAMA Cardiology. 2024. PMID 38865115. DOI 10.1001/jamacardio.2024.1310.

    Cross-sectional study · In 12,688 US adults, the spread of ApoB at a given value was highest for Friedewald LDL-C, lower for Sampson or Martin-Hopkins LDL-C and lowest for non-HDL-C; discordantly high ApoB occurred even in metabolically healthy people.

  21. 21.

    Mora S, Rifai N, Buring JE, Ridker PM. Fasting compared with nonfasting lipids and apolipoproteins for predicting incident cardiovascular events. Circulation. 2008. PMID 18711012. DOI 10.1161/CIRCULATIONAHA.108.777334.

    Prospective cohort · In 26,330 healthy women over 11 years, non-HDL-C predicted cardiovascular events more strongly fasting (HR 1.29 per SD) than non-fasting (1.15), although concentrations differed by under 5 percent.

  22. 22.

    Smith SJ, Cooper GR, Myers GL, Sampson EJ. Biological variability in concentrations of serum lipids: sources of variation among results from published studies and composite predicted values. Clinical Chemistry. 1993. PMID 8504530.

    Laboratory method study · Across 30 studies, average within-person biological variation was 6.1 percent for total cholesterol, 7.4 percent for HDL cholesterol, 9.5 percent for LDL cholesterol and 22.6 percent for triglycerides.

  23. 23.

    Pearson GJ, Thanassoulis G, Anderson TJ, et al.. 2021 Canadian Cardiovascular Society Guidelines for the Management of Dyslipidemia for the Prevention of Cardiovascular Disease in Adults. Canadian Journal of Cardiology. 2021. PMID 33781847. DOI 10.1016/j.cjca.2021.03.016.

    Guideline · For any patient with triglycerides above 1.5 mmol/L, non-HDL cholesterol or ApoB is the preferred lipid parameter for screening rather than LDL cholesterol; lipoprotein(a) once in a lifetime.

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