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Longevity Library · Lab reference

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

System: Metabolism & Metabolomics

LDL cholesterolLDL-C · Low-density lipoprotein cholesterol

LDL cholesterol causes atherosclerosis, risk falls by about a fifth for every 39 mg/dL it is lowered with no floor found in trials, and the harm accumulates over years, so laboratories print under 100 mg/dL as optimal, guidelines set goals of under 116, 100, 70 or 55 by risk, and 190 or above is a treatment indication on its own; the number is a calculation that triglycerides can distort, and ApoB is the better count of the particles that do the damage.

LDL cholesterol is the cholesterol carried in low-density lipoprotein particles, the main particle that enters the artery wall. Genetics, more than 200 cohorts and the drug trials agree it is causal and that risk tracks lifetime exposure. The printed categories come from a 2001 US panel; on most reports it is calculated, not measured, and a high triglyceride or a very low value makes the calculation unreliable.

01 · The scale

Where the laboratory range and the evidence sit.

Lower was better in every type of study, with no floor found. Trials in about 170,000 people cut major vascular events by 22 percent per 39 mg/dL lowered, including below about 77; people born with lifelong lower LDL had half to nearly 90 percent less coronary disease; and the observational U-curve in all-cause mortality, lowest near 140 mg/dL in Copenhagen, did not hold for heart attacks and is read by its own authors as largely illness lowering cholesterol.

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  1. Common laboratory 'optimal'

    0 to 100 mg/dL · NCEP ATP III 2001

  2. Very-high-risk goal

    0 to 55 mg/dL · ESC/EAS 2019

  3. High-risk goal; US threshold for adding therapy in very-high-risk disease

    55 to 70 mg/dL · ESC/EAS 2019; AHA/ACC 2018

  4. Moderate-risk goal; adult goal in familial hypercholesterolemia

    70 to 100 mg/dL · ESC/EAS 2019; EAS 2013

  5. Low-risk goal under 116; non-fasting flag at 115

    100 to 116 mg/dL · ESC/EAS 2019; EAS/EFLM 2016

  6. Lowest all-cause mortality band in Copenhagen (observational; see caveats)

    132 to 154 mg/dL · Johannesen 2020

  7. High; risk-enhancing factor at 160 and above

    160 to 189 mg/dL · NCEP ATP III 2001; AHA/ACC 2018

  8. Very high; treatment indication on its own, possible familial hypercholesterolemia

    190 and above mg/dL · AHA/ACC 2018; EAS/EFLM 2016

  • 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 LDL cholesterol measures.

Low-density lipoproteins are the main cholesterol-carrying particles in blood, and the LDL cholesterol number estimates how much cholesterol they hold. The 2017 European Atherosclerosis Society consensus reviewed rare mutations, more than 200 prospective cohorts, Mendelian randomization studies and randomized trials, together covering more than 2 million people, over 20 million person-years and over 150,000 cardiovascular events, and concluded that LDL causes atherosclerotic cardiovascular disease: the relationship is dose-dependent and log-linear, and it grows with the duration of exposure.1Grade A

The damage is cumulative. In the consensus panel's own arithmetic, a 1 mmol/L (about 39 mg/dL) lower LDL cholesterol cuts risk by about 22 percent over five years of a trial but by about 54 percent over 40 years of lifelong exposure, which is why the age at which a number is lowered matters as much as the number.1,2Grade A

On most laboratory reports LDL cholesterol is not measured but calculated from total cholesterol, HDL cholesterol and triglycerides. The Friedewald equation assumes a fixed ratio of 5 between triglycerides and VLDL cholesterol; in 1,350,908 US lipid profiles the true ratio varied widely, and newer equations (Martin-Hopkins, Sampson) exist because the old one misclassifies people when triglycerides are high or LDL is low.3,4Grade B

03 · The laboratory range

What a laboratory calls normal.

Under 100 mg/dL printed as optimal by most US laboratories, with 100 to 129 near optimal, 130 to 159 borderline high, 160 to 189 high and 190 and above very high.

The printed categories come from the 2001 National Cholesterol Education Program Adult Treatment Panel III: optimal under 100 mg/dL, near optimal or above optimal 100 to 129, borderline high 130 to 159, high 160 to 189, very high 190 and above. The panel named LDL cholesterol the primary target of cholesterol-lowering therapy because the relationship between LDL and coronary risk is continuous from low to high, and it asked for a fasting lipoprotein profile once every 5 years in all adults aged 20 or older.5Grade A

The 2019 European dyslipidaemia guideline sets goals rather than categories: under 55 mg/dL (1.4 mmol/L) for very-high-risk adults, under 70 (1.8) for high risk, under 100 (2.6) for moderate risk and under 116 (3.0) for low risk, each paired with at least a 50 percent reduction from baseline at the higher risk levels. It states that there is no lower limit of LDL cholesterol below which benefit stops, no J-curve, and that lowering ApoB-containing particles as far as possible reduces events.6Grade A

The 2018 American guideline uses thresholds instead of goals: an LDL cholesterol of 190 mg/dL or above is an indication to start high-intensity treatment without calculating a risk score; 70 is the threshold for adding therapy in very-high-risk disease; a persistent 160 or above is a risk-enhancing factor in primary prevention; and in adults aged 20 to 39, drug therapy is needed only in selected people with 160 or above or 190 or above, with priority given to lifetime risk and lifestyle.7Grade A

04 · The evidence

What the studies support.

The Cholesterol Treatment Trialists' meta-analysis of individual data from about 170,000 people in 26 randomized trials found that each 1 mmol/L (about 39 mg/dL) reduction in LDL cholesterol cut major vascular events by 22 percent (rate ratio 0.78) and all-cause mortality by 10 percent, with the same proportional benefit in people who started below 2 mmol/L (about 77 mg/dL) and no evidence of a threshold within the range studied. Cancer incidence and cancer deaths did not rise, even at low LDL concentrations.8Grade A

The benefit does not depend on the drug. Across 49 trials and 312,175 participants, statins and non-statin approaches that work through the LDL receptor (diet, bile acid binders, ileal bypass, ezetimibe) carried the same relative risk per 1 mmol/L lowered (0.77 and 0.75), and the LDL level actually reached tracked the rate of coronary events: 1.5 percent lower per mmol/L in primary prevention trials and 4.6 percent lower in secondary prevention.9Grade A

Age does not cancel the effect. In 186,854 people from 28 trials, the 21 percent reduction in major vascular events per 1 mmol/L lower LDL cholesterol held in every age group, though the trialists note less direct evidence of benefit in people over 75 who do not already have vascular disease.10Grade A

People born with lower LDL show what a lifetime of exposure means. Across 312,321 participants and nine variants in six genes, each 1 mmol/L (38.7 mg/dL) of genetically lower LDL cholesterol carried a 54.5 percent lower risk of coronary heart disease, three times the effect of the same reduction started with a statin later in life. In the ARIC cohort, the 2.6 percent of Black participants carrying a PCSK9 nonsense mutation had 28 percent lower LDL and 88 percent less coronary disease over 15 years, and the 3.2 percent of white participants with a milder variant had 15 percent lower LDL and 47 percent less.2,11Grade B

The observational U-curve is real and needs reading carefully. Among 108,243 Danes followed a median 9.4 years, all-cause mortality was lowest at an LDL cholesterol of about 140 mg/dL (3.6 mmol/L); people under 70 had a hazard ratio of 1.25 and people over 189 had 1.15 against the 132 to 154 band. But the risk of heart attack rose with any increase in LDL, the low-LDL excess was not seen for cardiovascular death, and the authors attribute much of it to reverse causation: illness lowers cholesterol, comorbidities were commonest at the lowest levels, and the association shrank substantially once baseline disease was accounted for and the first five years of follow-up excluded. In people on lipid-lowering treatment the nadir sat at 89.12Grade B

Plaque appears below the printed ranges. In the PESA study, 1,779 middle-aged adults with no conventional risk factors (untreated blood pressure under 140/90, LDL under 160, no smoking, no diabetes) had vascular ultrasound and coronary calcium imaging; 49.7 percent already had subclinical atherosclerosis, and LDL cholesterol was independently associated with its presence and extent even in the subgroup with optimal risk factors, at an odds ratio of 1.14 to 1.18 per 10 mg/dL. This is one Spanish cohort imaged once, so it shows association, not a tested target.13Grade 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 fat with unsaturated fat

    lowers it; the outcome benefit is in trials

    In 60 controlled feeding trials, the total-to-HDL cholesterol ratio fell when saturated fat was replaced by cis-unsaturated fat and did not change when it was replaced by carbohydrate; trans fat was the worst per calorie. The Cochrane review of 15 randomized trials with about 59,000 people found that cutting saturated fat for at least two years lowered combined cardiovascular events by 21 percent with small reductions in LDL cholesterol, the larger the cholesterol fall the larger the benefit, and no effect on total mortality.14,15Grade A

  • A 'portfolio' of cholesterol-lowering foods

    lowers it by about a quarter when followed closely

    In a one-month randomized trial of 46 adults with high cholesterol, a diet combining plant sterols, soy protein, viscous fiber and almonds lowered LDL cholesterol by 28.6 percent, against 30.9 percent on a low-dose statin and 8.0 percent on a low-saturated-fat control diet, with no significant difference between the diet and the drug. It was a short, fully fed trial in motivated volunteers; the effect in ordinary life is smaller.16Grade B

  • Viscous fiber such as psyllium

    lowers it modestly

    Across 28 randomized trials with 1,924 participants, a median of about 10 grams of psyllium a day lowered LDL cholesterol by 0.33 mmol/L (about 13 mg/dL), graded moderate-quality evidence, and ApoB by 0.05 g/L.17Grade A

  • Plant sterols and stanols

    lowers it 6 to 12 percent by dose

    In 124 studies, plant sterol or stanol intakes of 0.6 to 3.3 grams a day lowered LDL cholesterol by 6 to 12 percent on average, with the effect still increasing up to about 3 grams a day, where it averaged 12 percent.18Grade A

  • Weight loss

    lowers it a little per kilogram

    Across 73 randomized trials with 32,496 overweight adults, each kilogram lost through lifestyle change lowered LDL cholesterol by about 1.3 mg/dL at 12 months, a far smaller effect than on triglycerides (4 mg/dL per kilogram); low-fat diets lowered LDL where low-carbohydrate diets mainly lowered triglycerides and raised HDL.19Grade A

  • Exercise

    lowers it a little, mostly together with diet

    Aerobic exercise alone changes LDL cholesterol inconsistently; in a review of 51 training studies, 28 of them randomized, a rise in HDL was the usual finding and LDL falls were seen less often. Combined with a prudent diet, six randomized trials in up to 559 adults lowered LDL by 9.2 mg/dL, about 7 percent, against controls. Exercise earns its place for the other things it does.20,21Grade B

  • Dietary cholesterol (eggs, shellfish, organ meats)

    raises it modestly on average, with a curve that flattens

    A meta-regression of 55 randomized feeding studies with 2,652 participants found that each additional 100 mg a day of dietary cholesterol raised LDL cholesterol by about 1.9 mg/dL on a straight-line model and about 4.5 on the nonlinear models that fit the data best, meaning the first few hundred milligrams matter most and the effect flattens at high intakes. Individual responses vary around these averages.22Grade B

  • Coconut oil

    raises it against other vegetable oils

    Across 16 clinical trials, coconut oil raised LDL cholesterol by 10.47 mg/dL and HDL by 4.00 mg/dL compared with non-tropical vegetable oils, with no effect on weight, inflammation or glucose; the result held when non-randomized and poor-quality trials were excluded.23Grade A

  • Lipid-lowering medication

    lowers it 30 to 50 percent or more by class and dose

    The guidelines' goals assume medication for people judged at risk: the American guideline asks for at least a 30 percent reduction when treatment is indicated and at least 50 percent at higher risk, and the European guideline pairs its lower goals with a 50 percent reduction from baseline. Per unit of LDL lowered, drug and non-drug routes through the LDL receptor deliver the same benefit. Whether and when to treat is a decision for a physician who knows the person's risk, not a page.7,6,9Grade A

06 · Reading it well

Caveats, and what belongs with a physician.

A calculated LDL is least trustworthy where the decisions are made. Against directly measured values in 1,350,908 US profiles, the Friedewald equation agreed with the guideline category 85.4 percent of the time and the Martin-Hopkins method 91.7 percent; among people with a calculated value under 70 and triglycerides of 150 to 199, the measured value was really under 70 in only 61.3 percent by Friedewald against 92.4 percent by the newer method. The Sampson equation, derived from 18,715 reference measurements, extends calculation to triglycerides up to 800 mg/dL. The European guideline notes that calculated LDL underestimates at triglycerides of 177 mg/dL and above, cannot be used above 400, and may mislead at very low LDL.3,4,6Grade B

LDL cholesterol and the particle count can disagree. In 12,688 US adults the median ApoB at an LDL of 100 was 80 mg/dL, but the central 95 percent spread from 66 to 99, widest when LDL was calculated by Friedewald, and even metabolically healthy people were often discordant. In 13,015 statin-treated Danes, those with high ApoB but low LDL carried 21 percent higher mortality and 49 percent more heart attacks than people with both low, while high LDL with low ApoB carried no excess. The European guideline recommends ApoB alongside LDL in diabetes, high triglycerides and very low LDL, and calls it the preferred measure for refining risk.24,25,6Grade B

One draw is an estimate. In 51 volunteers measured on three occasions, calculated LDL cholesterol varied about 8 percent from day to day, and a single measurement classified a person reliably only below about 116 mg/dL or above about 174; values between the cutoffs deserve a repeat before anything is decided.26Grade C

Fasting is not required. After an ordinary meal LDL cholesterol falls by at most about 8 mg/dL on average, so the European laboratory consensus asks for non-fasting samples to be flagged at 115 rather than 116, and the American guideline accepts fasting or non-fasting screening; the European guideline reads non-fasting values as at least as predictive.27,7,6Grade A

A very high value is often inherited. Heterozygous familial hypercholesterolemia affects about 1 in 200 to 1 in 500 people, carries up to 13-fold coronary risk, and is diagnosed in under 1 percent of those who have it in most countries. The European consensus asks for family screening when an adult has a total cholesterol of 310 mg/dL or more, early coronary disease, tendon xanthomas or sudden premature cardiac death in the family, sets adult LDL goals under 100 (under 70 with coronary disease or diabetes), and the laboratory consensus flags any LDL above 190 for referral on the same suspicion.28,27Grade A

The goals are treatment targets drawn from trials in people already judged at risk; they are not population definitions of health, the categories on the report date from 2001, and no trial has randomized healthy young adults to a lifetime LDL target. The guideline numbers differ (55, 70, 100, 116) because risk categories are drawn differently, not because the biology changes at a line.6,7,5Grade A

See a physician

  • An LDL cholesterol of 190 mg/dL or higher on any draw, or a total cholesterol of 310 or higher, which can signal familial hypercholesterolemia and is a treatment indication without a risk score.
  • 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.
  • An LDL above 160 together with diabetes, high blood pressure, kidney disease, a high lipoprotein(a), a high ApoB or a smoking history.
  • Firm lumps in the Achilles or hand tendons, yellow deposits on the eyelids, or a grey ring at the edge of the cornea before middle age.
  • A calculated LDL under 70 alongside triglycerides over 150, which is more likely a measurement problem than a reassuring number.
  • 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.

  • How low in primary prevention: the trials that found no floor were drug trials in people already at risk, and no trial has lowered LDL in healthy adults toward 55 or 70 and counted outcomes over decades.
  • The imaging data cut both ways: half of risk-factor-free middle-aged adults in PESA already had plaque, and LDL tracked it at values the laboratory calls normal, but whether treating those people changes their lives has not been tested.
  • Whether LDL cholesterol should remain the primary number at all. Genetics and the discordance cohorts say ApoB is the more accurate measure of the particles that cause harm; guidelines still write their goals in LDL because that is what the trials measured.
  • The low-LDL mortality excess in cohorts is mostly explained by illness lowering cholesterol, but a smaller association remained in the Copenhagen analysis after the authors' corrections, and its meaning is unresolved.
  • Most US reports still calculate LDL by the original Friedewald equation; which equation a laboratory uses changes the number at the low end, and the categories were never re-derived for the newer methods.

08 · In practice

How Dr. Tagge reads it in his own practice.

I read LDL cholesterol as the first look and ApoB as the count that matters. I like to see LDL under 100, and under 70 when there is family history, a high lipoprotein(a), diabetes, high blood pressure or plaque already on imaging. Those are the guideline goals for moderate and high risk; the judgment I add is that most adults are better served by reaching them earlier than later, because the arteries keep score of years as well as levels. A calculated LDL beside a high triglyceride, or a value that does not fit the rest of the picture, sends me to ApoB before I conclude anything. An LDL of 190 or more is a different conversation, about family and genes, and it comes first.

A practice judgment, labeled as one (Grade D): it is how one physician reads the number for the people he cares for, not a recommendation for you.

09

Questions

10 · Sources

28 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.

    Ference BA, Ginsberg HN, Graham I, et al.. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. European Heart Journal. 2017. PMID 28444290. DOI 10.1093/eurheartj/ehx144.

    Consensus statement · Over 200 cohorts, Mendelian randomization and trials in more than 2 million people show a dose-dependent, log-linear, causal relationship between LDL exposure and cardiovascular disease that grows with duration; 22 percent per mmol/L over 5 years, 54 percent over 40 years.

  2. 2.

    Ference BA, Yoo W, Alesh I, et al.. Effect of long-term exposure to lower low-density lipoprotein cholesterol beginning early in life on the risk of coronary heart disease: a Mendelian randomization analysis. Journal of the American College of Cardiology. 2012. PMID 23083789. DOI 10.1016/j.jacc.2012.09.017.

    Mendelian randomization · In 312,321 participants, each 1 mmol/L (38.7 mg/dL) of genetically lower LDL-C carried a 54.5 percent lower coronary risk, three times the effect of the same reduction by statin later in life.

  3. 3.

    Martin SS, Blaha MJ, Elshazly MB, et al.. Comparison of a novel method vs the Friedewald equation for estimating low-density lipoprotein cholesterol levels from the standard lipid profile. JAMA. 2013. PMID 24240933. DOI 10.1001/jama.2013.280532.

    Laboratory method study · In 1,350,908 US profiles, Friedewald's fixed factor of 5 misclassified more people (85.4 percent concordance) than an adjustable factor (91.7 percent); at triglycerides 150 to 199, a Friedewald LDL-C under 70 was truly under 70 in only 61.3 percent.

  4. 4.

    Sampson M, Ling C, Sun Q, et al.. A new equation for calculation of low-density lipoprotein cholesterol in patients with normolipidemia and/or hypertriglyceridemia. JAMA Cardiology. 2020. PMID 32101259. DOI 10.1001/jamacardio.2020.0013.

    Laboratory method study · Calculated LDL-C is less accurate at low LDL-C or triglycerides of 400 and above; a new equation derived from 18,715 reference measurements in 8,656 patients extends accurate calculation to triglycerides up to 800 mg/dL with 35 percent fewer misclassifications.

  5. 5.

    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 · LDL-C classification: optimal under 100 mg/dL, near optimal 100 to 129, borderline high 130 to 159, high 160 to 189, very high 190 and above; LDL-C the primary target of therapy; fasting profile every 5 years from age 20.

  6. 6.

    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 · LDL-C goals under 55, 70, 100 and 116 mg/dL for very-high, high, moderate and low risk, with at least 50 percent reduction at higher risk; no lower limit or J-curve; ApoB recommended with high triglycerides, diabetes or very low LDL-C; calculated LDL-C unreliable at high triglycerides or very low LDL-C; non-fasting samples acceptable.

  7. 7.

    Grundy SM, Stone NJ, Bailey AL, et al.. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA guideline on the management of blood cholesterol. Circulation. 2019. PMID 30586774. DOI 10.1161/CIR.0000000000000625.

    Guideline · LDL-C 190 mg/dL or above: start high-intensity treatment without a risk score; 70 the threshold for adding therapy in very-high-risk disease; persistent 160 or above a risk-enhancing factor; at least 30 or 50 percent reduction when treating; fasting or non-fasting screening.

  8. 8.

    Cholesterol Treatment Trialists' (CTT) Collaboration; Baigent C, Blackwell L, et al.. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010. PMID 21067804. DOI 10.1016/S0140-6736(10)61350-5.

    Systematic review and meta-analysis · Per 1 mmol/L lower LDL-C: major vascular events down 22 percent (RR 0.78) and all-cause mortality down 10 percent, including in people below 2 mmol/L, with no threshold and no rise in cancer.

  9. 9.

    Silverman MG, Ference BA, Im K, et al.. Association between lowering LDL-C and cardiovascular risk reduction among different therapeutic interventions: a systematic review and meta-analysis. JAMA. 2016. PMID 27673306. DOI 10.1001/jama.2016.13985.

    Systematic review and meta-analysis · Across 49 trials and 312,175 participants, statins (RR 0.77) and non-statin LDL-receptor routes including diet (RR 0.75) gave the same benefit per 1 mmol/L; achieved LDL-C tracked coronary event rates in primary (1.5 percent per mmol/L) and secondary (4.6 percent) prevention.

  10. 10.

    Cholesterol Treatment Trialists' Collaboration. Efficacy and safety of statin therapy in older people: a meta-analysis of individual participant data from 28 randomised controlled trials. Lancet. 2019. PMID 30712900. DOI 10.1016/S0140-6736(18)31942-1.

    Systematic review and meta-analysis · In 186,854 people, 21 percent fewer major vascular events per 1 mmol/L lower LDL-C in every age group; less direct evidence of benefit over 75 without vascular disease.

  11. 11.

    Cohen JC, Boerwinkle E, Mosley TH Jr, Hobbs HH. Sequence variations in PCSK9, low LDL, and protection against coronary heart disease. New England Journal of Medicine. 2006. PMID 16554528. DOI 10.1056/NEJMoa054013.

    Mendelian randomization · PCSK9 nonsense mutations in 2.6 percent of 3,363 Black ARIC participants: 28 percent lower LDL-C and 88 percent lower coronary risk over 15 years; a milder variant in 3.2 percent of 9,524 white participants: 15 percent lower LDL-C and 47 percent lower risk.

  12. 12.

    Johannesen CDL, Langsted A, Mortensen MB, Nordestgaard BG. Association between low density lipoprotein and all cause and cause specific mortality in Denmark: prospective cohort study. BMJ. 2020. PMID 33293274. DOI 10.1136/bmj.m4266.

    Prospective cohort · In 108,243 Danes over a median 9.4 years, all-cause mortality was U-shaped with a nadir at 140 mg/dL (89 on lipid-lowering treatment); HR 1.25 under 70 and 1.15 over 189; heart attack risk rose with any increase in LDL-C; low-LDL excess shrank after adjusting for comorbidity and excluding early deaths, read as reverse causation.

  13. 13.

    Fernández-Friera L, Fuster V, López-Melgar B, et al.. Normal LDL-cholesterol levels are associated with subclinical atherosclerosis in the absence of risk factors. Journal of the American College of Cardiology. 2017. PMID 29241485. DOI 10.1016/j.jacc.2017.10.024.

    Cross-sectional study · In 1,779 risk-factor-free PESA participants aged about 45, 49.7 percent had subclinical atherosclerosis; LDL-C was independently associated with its presence and extent (OR 1.14 to 1.18 per 10 mg/dL), even with optimal risk factors.

  14. 14.

    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, replacing saturated with cis-unsaturated fat lowered the total-to-HDL ratio; replacing it with carbohydrate did not; trans fat was most harmful.

  15. 15.

    Hooper L, Martin N, Jimoh OF, Kirk C, Foster E, Abdelhamid AS. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database of Systematic Reviews. 2020. PMID 32428300. DOI 10.1002/14651858.CD011737.pub2.

    Systematic review and meta-analysis · In 15 randomized trials with about 59,000 people, reducing saturated fat for at least two years cut combined cardiovascular events by 21 percent with small reductions in LDL cholesterol and no effect on all-cause mortality; greater cholesterol falls gave greater benefit.

  16. 16.

    Jenkins DJ, Kendall CW, Marchie A, et al.. Effects of a dietary portfolio of cholesterol-lowering foods vs lovastatin on serum lipids and C-reactive protein. JAMA. 2003. PMID 12876093. DOI 10.1001/jama.290.4.502.

    Randomized trial · In 46 hyperlipidemic adults over one month, the dietary portfolio lowered LDL-C 28.6 percent, a low-dose statin 30.9 percent and the control diet 8.0 percent, with no significant difference between diet and drug.

  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 LDL-C by 0.33 mmol/L (moderate-quality evidence) and ApoB by 0.05 g/L.

  18. 18.

    Ras RT, Geleijnse JM, Trautwein EA. LDL-cholesterol-lowering effect of plant sterols and stanols across different dose ranges: a meta-analysis of randomised controlled studies. British Journal of Nutrition. 2014. PMID 24780090. DOI 10.1017/S0007114514000750.

    Systematic review and meta-analysis · In 124 studies, 0.6 to 3.3 g/day of plant sterols or stanols lowered LDL-C by 6 to 12 percent, the effect still rising to an average 12 percent at about 3 g/day.

  19. 19.

    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 LDL-C by 1.28 mg/dL and triglycerides by 4.0 mg/dL at 12 months.

  20. 20.

    Leon AS, Sanchez OA. Response of blood lipids to exercise training alone or combined with dietary intervention. Medicine and Science in Sports and Exercise. 2001. PMID 11427777. DOI 10.1097/00005768-200106001-00021.

    Review · Across 51 training studies (28 randomized), aerobic exercise changed blood lipids inconsistently; a rise in HDL-C was the usual finding and reductions in LDL-C were seen less often.

  21. 21.

    Kelley GA, Kelley KS, Roberts S, Haskell W. Efficacy of aerobic exercise and a prudent diet for improving selected lipids and lipoproteins in adults: a meta-analysis of randomized controlled trials. BMC Medicine. 2011. PMID 21676220. DOI 10.1186/1741-7015-9-74.

    Systematic review and meta-analysis · Aerobic exercise plus a prudent diet lowered LDL-C by 9.2 mg/dL (7.2 percent) across six randomized trials in up to 559 adults.

  22. 22.

    Vincent MJ, Allen B, Palacios OM, Haber LT, Maki KC. Meta-regression analysis of the effects of dietary cholesterol intake on LDL and HDL cholesterol. American Journal of Clinical Nutrition. 2019. PMID 30596814. DOI 10.1093/ajcn/nqy273.

    Systematic review and meta-analysis · Across 55 randomized feeding studies with 2,652 participants, each extra 100 mg/day of dietary cholesterol raised LDL-C by 1.90 mg/dL (linear model) to 4.46 to 4.58 mg/dL (nonlinear models that fit best).

  23. 23.

    Neelakantan N, Seah JYH, van Dam RM. The effect of coconut oil consumption on cardiovascular risk factors: a systematic review and meta-analysis of clinical trials. Circulation. 2020. PMID 31928080. DOI 10.1161/CIRCULATIONAHA.119.043052.

    Systematic review and meta-analysis · Across 16 trials, coconut oil raised LDL-C by 10.47 mg/dL and HDL-C by 4.00 mg/dL against non-tropical vegetable oils, with no effect on glycemia, inflammation or adiposity.

  24. 24.

    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, median ApoB 49, 60, 80 and 140 mg/dL at LDL-C 55, 70, 100 and 190; at LDL-C 100 the 95 percent range was 66 to 99, widest with Friedewald LDL-C; discordance common even in metabolically healthy people.

  25. 25.

    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, high ApoB with low LDL-C carried HR 1.21 for mortality and 1.49 for heart attack; high LDL-C with low ApoB carried no excess.

  26. 26.

    Bookstein L, Gidding SS, Donovan M, Smith FA. Day-to-day variability of serum cholesterol, triglyceride, and high-density lipoprotein cholesterol levels. Impact on the assessment of risk according to the National Cholesterol Education Program guidelines. Archives of Internal Medicine. 1990. PMID 2383160.

    Laboratory method study · In 51 volunteers measured three times, calculated LDL-C varied 8 percent day to day; a single measurement classified reliably only below about 116 mg/dL or above about 174.

  27. 27.

    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 · Maximal mean post-meal change in LDL-C about minus 8 mg/dL; flag non-fasting LDL-C at 115 mg/dL and above; refer LDL-C above 190 for possible heterozygous and above 500 for possible homozygous familial hypercholesterolemia.

  28. 28.

    Nordestgaard BG, Chapman MJ, Humphries SE, et al.. Familial hypercholesterolaemia is underdiagnosed and undertreated in the general population: guidance for clinicians to prevent coronary heart disease: consensus statement of the European Atherosclerosis Society. European Heart Journal. 2013. PMID 23956253. DOI 10.1093/eurheartj/eht273.

    Consensus statement · Heterozygous FH affects about 1 in 200 to 1 in 500 with up to 13-fold coronary risk; screen when an adult has total cholesterol of 310 mg/dL or more, premature coronary disease, tendon xanthomas or sudden premature cardiac death in the family; adult LDL-C targets under 100, under 70 with coronary disease or diabetes.

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