What does the research show about ldl cholesterol (ldl-c)?

LDL cholesterol (LDL-C)

LDL cholesterol is the cholesterol carried in LDL particles, usually calculated, not measured. Cohort, genetic and trial evidence agree that higher levels go with more artery disease, and statin trials found about 22% fewer major vascular events per 1 mmol/L (39 mg/dL) lowered. Cut points differ by source and risk. Calculated results are least accurate when triglycerides are high.

Checked 2026-11-13

Status: Part of the standard lipid panel, ordered by a clinician and also sold direct to consumers by some US laboratories. FDA classifies LDL test systems as lipoprotein test systems, class I devices exempt from premarket notification [1]. In routine practice the result is usually estimated by an equation from the other lipid panel values, not measured [2].
Measures: The amount of cholesterol carried in low-density lipoprotein particles in blood, either calculated from total cholesterol, HDL cholesterol and triglycerides or measured directly.
Also called: LDL-C, LDL, LDL cholesterol, low-density lipoprotein cholesterol, LDL calculated, LDL chol calc, calculated LDL, direct LDL, LDL direct, LDL-C Friedewald, LDL-C Martin-Hopkins, LDL-C NIH equation
Tested for: heart attack risk, stroke risk, cholesterol check, deciding on statin therapy, checking response to cholesterol-lowering drugs, family history of high cholesterol

Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on

Linked in research2

StrongLinked to more atherosclerotic cardiovascular disease across over 200 cohort, genetic and trial studies, with risk rising with the level and the years of exposure.
StrongShown in trials: each 1 mmol/L (39 mg/dL) lowered cut major vascular events about 22% with statins, and similarly with other drugs acting through the LDL receptor.

Reported risks0

No risks sourced yet.

Reference ranges

Each range is the one its source published, in mg/dL. Also reported in mmol/L. Where sources differ, each is shown.

National Cholesterol Education Program, Adult Treatment Panel III, 2001

Adults aged 20 and older · [3]

Range	What the source calls it
below 100 mg/dL	"optimal"
100 to 129 mg/dL	"near optimal/above optimal"
130 to 159 mg/dL	"borderline high"
160 to 189 mg/dL	"high"
190 or above mg/dL	"very high" One to see a doctor about

The panel adopted this classification because the relationship between LDL cholesterol and coronary heart disease risk is continuous over a broad range. Its treatment goals depended on a person's other risk factors: below 100 mg/dL was the goal only for people with coronary heart disease or equivalent risk. The classification is based on a fasting lipoprotein profile [3].

American Heart Association and American College of Cardiology cholesterol guideline, 2018

Adults · [4]

Range	What the source calls it
below 160 mg/dL	No name given
160 to 189 mg/dL	"primary hypercholesterolemia"
190 or above mg/dL	"severe hypercholesterolemia" One to see a doctor about

The guideline does not classify LDL cholesterol below 160 mg/dL. It bases most treatment decisions for adults aged 40 to 75 with LDL cholesterol of 70 to 189 mg/dL on estimated 10-year risk, and lists 160 to 189 mg/dL as a risk-enhancing factor. At 190 mg/dL or above it advises statin therapy without calculating risk [4]. A 2026 guideline from the same bodies retires and replaces this one [5].

European Society of Cardiology and European Atherosclerosis Society guideline, 2019, very high risk

Adults the guideline places at very high cardiovascular risk · [6]

Range	What the source calls it
below 55 mg/dL	"goal"
55 or above mg/dL	No name given

A treatment goal, not a population reference interval. The guideline pairs it with a reduction of at least 50% from baseline, and prints it as below 1.4 mmol/L, converting cholesterol at 1 mmol/L to 38.67 mg/dL [6].

European Society of Cardiology and European Atherosclerosis Society guideline, 2019, high risk

Adults the guideline places at high cardiovascular risk · [6]

Range	What the source calls it
below 70 mg/dL	"goal"
70 or above mg/dL	No name given

A treatment goal, paired with a reduction of at least 50% from baseline. Printed as below 1.8 mmol/L [6].

European Society of Cardiology and European Atherosclerosis Society guideline, 2019, moderate risk

Adults the guideline places at moderate cardiovascular risk · [6]

Range	What the source calls it
below 100 mg/dL	"goal"
100 or above mg/dL	No name given

A treatment goal. Printed as below 2.6 mmol/L [6].

European Society of Cardiology and European Atherosclerosis Society guideline, 2019, low risk

Adults the guideline places at low cardiovascular risk · [6]

Range	What the source calls it
below 116 mg/dL	"goal"
116 or above mg/dL	No name given

A treatment goal. Printed as below 3.0 mmol/L [6].

European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine consensus on laboratory reporting, 2016

Adults, fasting or not, as a value for laboratories to flag on reports · [7]

Range	What the source calls it
below 115 mg/dL	No name given
115 or above mg/dL	"abnormal"

The statement asks laboratories to flag "abnormal" results against a desirable concentration cut point for people at moderate risk, in place of a population reference interval. The cut point is 3 mmol/L, which the authors converted by multiplying by 38.6 and rounding to the nearest 5 mg/dL. They estimate that 60% of adults in a typical Western or Northern European country would be flagged at this cut point [7].

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

Children and adolescents · [8]

Range	What the source calls it
below 110 mg/dL	"acceptable"
110 to 129 mg/dL	"borderline-high"
130 or above mg/dL	"high"

Values come from an earlier US pediatric cholesterol panel. The borderline-high and high cut points represent approximately the 75th and 95th percentiles for children [8].

National Heart, Lung, and Blood Institute expert panel, 2011, young adults

Young adults, from data on people aged 20 to 24 · [8]

Range	What the source calls it
below 120 mg/dL	"acceptable"
120 to 159 mg/dL	"borderline-high"
160 or above mg/dL	"high"

Values come from the Lipid Research Clinics Prevalence Study. The high cut point is the 95th percentile for 20 to 24 year olds, and the panel states these cut points are not identical to the adult classification of Adult Treatment Panel III [8].

What has been shown to move it

Shown to lower it38

BerberineStrong

Cholesterol and triglycerides

Shown to lower LDL by about 0.46 mmol/L and lower triglycerides in adults, in trials mostly from China and Hong Kong.

The numbers and sources

Effect: In 18 placebo-controlled trials (1,788 participants), berberine lowered LDL by 0.46 mmol/L (95% CI -0.62 to -0.30), total cholesterol by 0.48 mmol/L and triglycerides by 0.34 mmol/L, and raised HDL by 0.06 mmol/L. The HDL rise was seen in women and not in men [8]. A 27-trial meta-analysis found berberine combined with lipid drugs lowered cholesterol more than the drugs alone [4].
Population: Adults, mostly in mainland China and Hong Kong, for 4 to 24 weeks [8].
Sources: [4], [8]
Caveats: 15 of the 18 trials were in mainland China or Hong Kong [8].

Beta-glucanStrong

LDL cholesterol (oat beta-glucan)

Shown to lower LDL by about 0.2 to 0.25 mmol/L in adults at 3 g a day or more of oat beta-glucan.

The numbers and sources

Effect: In 28 trials, 3 g a day or more of oat beta-glucan lowered LDL by 0.25 mmol/L (95% CI 0.20 to 0.30) and total cholesterol by 0.30 mmol/L, with no change in HDL or triglycerides. Dose (3.0 to 12.4 g a day) and duration (2 to 12 weeks) did not change the result [1]. In 58 trials (3,974 people), a median 3.5 g a day lowered LDL by 0.19 mmol/L (95% CI 0.14 to 0.23), non-HDL by 0.20 mmol/L and apoB by 0.03 g/L [2].
Population: Adults, mostly with normal to raised cholesterol [1][2].
Sources: [1], [2]
Caveats: LDL heterogeneity was high in [2] (I² 79%). [1] was supported by DSM Nutritional Products and searched in-house reports at CreaNutrition, a subsidiary of an oat fiber company. FDA's health claim rests on 3 g a day or more from whole oats or barley [3].

Black seed oilStrong

Cholesterol and triglycerides

Shown to lower LDL by about 14 mg/dL and triglycerides by about 21 mg/dL in adults. HDL did not change overall.

Oil lowered total and LDL cholesterol more than powder.

The numbers and sources

Effect: In 17 RCTs, Nigella sativa lowered total cholesterol by 15.65 mg/dL (95% CI -24.67 to -6.63), LDL by 14.10 mg/dL and triglycerides by 20.64 mg/dL. HDL did not change overall (0.28 mg/dL, 95% CI -1.96 to 2.53) and rose only with seed powder. Oil lowered total and LDL cholesterol more than powder [1]. A 2025 review of 82 RCTs (5,026 participants) also reported improved total cholesterol, LDL, HDL and triglycerides [2].
Population: Adults in placebo-controlled RCTs [1]. Trials of 1 to 48 weeks [2].
Sources: [1], [2]
Caveats: The 2025 abstract lists outcomes without effect sizes [2]. Neither review measured heart attacks or strokes.

Ezetimibe and fenofibrateStrong

Ezetimibe: LDL cholesterol and ApoB

Shown to lower LDL cholesterol about 18% more than placebo when taken alone, with ApoB about 16% lower, and to lower LDL further when added to a statin.

Compared with placebo [1][2]; a statin or fenofibrate alone [3][4]

The numbers and sources

Effect: Across 8 placebo-controlled 12-week trials, ezetimibe 10 mg lowered LDL cholesterol 18.58% more than placebo (95% CI 17.48 to 19.67), total cholesterol 13.46% more and triglycerides 8.06% more, and raised HDL cholesterol 3.00% [1]. In two label trials, LDL cholesterol fell 18% and ApoB 16% on ezetimibe against a 1% rise and 2% fall on placebo [2]. Added to a statin or fenofibrate, ezetimibe lowered LDL cholesterol, total cholesterol and triglycerides further and likely raised HDL [3]. After an acute coronary syndrome, time-averaged LDL was 53.7 mg/dL on simvastatin with ezetimibe against 69.5 mg/dL on simvastatin alone [4].
Population: 2,722 people with primary hypercholesterolemia in 8 trials [1]; 1,719 adults in two trials [2]; 23,499 people in 26 trials [3]; 18,144 patients [4].
Sources: [1], [2], [3], [4]
Caveats: Lipid trials alone lasted 12 weeks [1]. Heterogeneity was substantial in the combination analyses [3].

Fiber supplementsStrong

LDL cholesterol

Shown to lower LDL cholesterol by about 0.33 mmol/L with about 10 g of psyllium a day in adults with or without high cholesterol.

The numbers and sources

Effect: Across 28 trials (1,924 participants), a median 10.2 g of psyllium a day lowered LDL cholesterol by 0.33 mmol/L (95% CI -0.38 to -0.27), non-HDL cholesterol by 0.39 mmol/L and apoB by 0.05 g/L (95% CI -0.08 to -0.03) [1]. A 2025 meta-analysis of 41 RCTs (2,049 participants) found LDL cholesterol 8.55 mg/dL lower (95% CI -12.92 to -4.19) and total cholesterol 9.05 mg/dL lower. Triglycerides and HDL did not change significantly [2].
Population: Adults with or without high cholesterol in RCTs of 3 weeks or longer [1]; adults in 41 RCTs [2].
Sources: [1], [2]
Caveats: LDL and non-HDL estimates were graded moderate quality because of inconsistency, and apoB high quality [1]. Heterogeneity in the 2025 review was considerable (I² 88% for LDL), and dose and duration did not explain it [2].

GarlicStrong

Cholesterol

Shown to lower total cholesterol about 10 to 17 mg/dL and LDL about 6 to 9 mg/dL in adults, more in those with high cholesterol.

A 2026 meta-analysis of 108 trials (7,137 adults) found total cholesterol fell 10.21 mg/dL (95% CI -13.69 to -6.74), LDL 5.90 mg/dL, and triglycerides 5.82 mg/dL, while HDL rose 2.18 mg/dL.

The numbers and sources

Effect: Across 39 trials, garlic lowered total cholesterol by 17 ± 6 mg/dL and LDL by 9 ± 6 mg/dL in people with total cholesterol above 200 mg/dL, when taken for longer than 2 months. HDL rose slightly and triglycerides did not change significantly [3]. A 2026 meta-analysis of 108 trials (7,137 adults) found total cholesterol fell 10.21 mg/dL (95% CI -13.69 to -6.74), LDL 5.90 mg/dL, and triglycerides 5.82 mg/dL, while HDL rose 2.18 mg/dL [4].
Population: Adults in 39 trials, effects reported in those with elevated cholesterol [3]. Adults in 108 trials [4].
Sources: [3], [4]
Caveats: The abstract of [3] describes earlier meta-analyses on this question as conflicting. The authors of [4] report larger effects in adults with unfavorable baseline risk factors and call for larger, longer, more rigorous trials. The two reviews disagree on triglycerides.

GlucomannanStrong

LDL cholesterol

Shown to lower LDL cholesterol by about 10%, about 16 mg/dL, in adults and children. Changes were not significant in adults with insulin resistance.

The numbers and sources

Effect: Across 14 studies with 531 participants, glucomannan lowered total cholesterol 19.28 mg/dL (95% CI -24.30 to -14.26), LDL 15.99 mg/dL (95% CI -21.31 to -10.67) and triglycerides 11.08 mg/dL (95% CI -22.07 to -0.09), with no change in HDL [1]. Across 12 studies with 370 participants, LDL fell 0.35 mmol/L (95% CI -0.46 to -0.25) and non-HDL cholesterol 0.32 mmol/L, about 10% and 7%. Apolipoprotein B did not change in 6 trials [2].
Population: Adults and children in RCTs [1][2].
Sources: [1], [2]
Caveats: Trials were small and short, with follow-up of at least 3 weeks in [2]. In 11 trials restricted to adults with insulin resistance-related conditions, lipid changes were not significant overall, with LDL and total cholesterol lower only in subgroups above 3,000 mg a day or at 4 weeks or less [3].

Green tea extractStrong

LDL cholesterol

Shown to lower LDL cholesterol slightly, about 2 mg/dL, and total cholesterol about 7 mg/dL in adults, with no HDL change.

The numbers and sources

Effect: Across 14 RCTs (1,136 subjects), green tea beverages or extracts lowered total cholesterol by 7.20 mg/dL (95% CI -8.19 to -6.21) and LDL cholesterol by 2.19 mg/dL (95% CI -3.16 to -1.21). HDL did not change [3]. Across 13 studies, LDL fell by 0.16 mmol/L (95% CI -0.22 to -0.09) [4].
Population: Adults in RCTs [3][4].
Sources: [3], [4]
Caveats: Both reviews pooled beverages with extracts.

Low-fat dietStrong

LDL cholesterol

Shown to lower LDL cholesterol slightly more than higher-fat and low-carbohydrate diets, by about 0.07 to 0.16 mmol/L.

Compared with diets with more fat

The numbers and sources

Effect: Against higher-fat diets in people not trying to lose weight, LDL fell 0.13 mmol/L (95% CI 0.05 to 0.21) and total cholesterol 0.23 mmol/L [1]. Against low-carbohydrate diets, LDL was lower on low-fat diets by 0.16 mmol/L (95% CI 0.003 to 0.33) [4], by 0.07 mmol/L at 6 to 12 months (95% CI 0.02 to 0.12) [5] and by 0.14 mmol/L at 6 months (95% CI 0.03 to 0.26) [8]. In postmenopausal women, LDL fell 3.55 mg/dL more than in the comparison group [9].
Population: Adults in the trials above [1][4][5]; 447 adults with BMI 25 or more in 5 trials [8]; 48,835 postmenopausal women [9].
Sources: [1], [4], [5], [8], [9]
Caveats: The differences are about 0.1 mmol/L, or about 4 mg/dL. In [8], the low-fat diets restricted energy and the low-carbohydrate diets did not. LDL is a risk marker, not a heart event.

Nordic dietStrong

LDL and total cholesterol

Shown to lower LDL cholesterol about 0.26 to 0.30 mmol/L against usual diets in adults with cardiometabolic risk factors.

Compared with control groups the source does not describe [1]; a usual or habitual Nordic diet, a usual Western diet or general healthy eating advice [2]; the participants' usual Western diet, in Swedish adults [3]; an average Nordic diet with the same calories [4]

The numbers and sources

Effect: In 5 RCTs (513 participants), a Nordic diet lowered total cholesterol by 0.38 mmol/L (95% CI -0.76 to -0.01) and LDL by 0.30 mmol/L (95% CI -0.54 to -0.06), with no change in HDL or triglycerides [1]. In 6 RCTs (717 participants), LDL fell 0.26 mmol/L (95% CI -0.52 to -0.00), with reductions in non-HDL cholesterol and apolipoprotein B [2]. In NORDIET, LDL fell 21% and HDL 5% over 6 weeks against usual diets [3]. In SYSDIET, non-HDL cholesterol fell 0.18 mmol/L (95% CI -0.35 to -0.01) against an average Nordic diet [4].
Population: Adults, mostly in Nordic countries, with raised cholesterol, metabolic syndrome or central obesity [1][2]; 88 Swedish adults with mild high cholesterol [3]; 200 adults with metabolic syndrome features [4].
Sources: [1], [2], [3], [4]
Caveats: Both meta-analyses pooled largely the same few trials. Heterogeneity was high (I² 89%) and certainty low for LDL in [2]. NORDIET lowered HDL along with LDL [3].

NutsStrong

LDL cholesterol and ApoB

Shown to lower LDL cholesterol by about 4.8 mg/dL per daily ounce of tree nuts, and by 10.2 mg/dL at about 67 g a day, along with ApoB.

Compared with control arms without nuts [4]; control diets the abstract does not describe [5]

The numbers and sources

Effect: Per 1 oz (28.4 g) serving a day, tree nuts lowered total cholesterol by 4.7 mg/dL (95% CI 4.0 to 5.3), LDL cholesterol by 4.8 mg/dL (95% CI 4.2 to 5.5), ApoB by 3.7 mg/dL (95% CI 2.3 to 5.2) and triglycerides by 2.2 mg/dL (95% CI 0.5 to 3.8). HDL cholesterol, apolipoprotein A1 and blood pressure did not change significantly. Effects were stronger at 60 g a day or more and did not differ by nut type. ApoB fell more in people with type 2 diabetes (11.5 mg/dL) than in healthy people (2.5 mg/dL) [4]. Pooled individual data from 25 trials found a mean 67 g a day lowered total cholesterol by 10.9 mg/dL (5.1%) and LDL cholesterol by 10.2 mg/dL (7.4%). Triglycerides fell 20.6 mg/dL in people starting at 150 mg/dL or higher and not in others [5].
Population: 2,582 adults without cardiovascular disease in 61 trials of 3 to 26 weeks [4]. 583 adults with normal or high cholesterol not on lipid-lowering drugs, in 25 trials in 7 countries [5].
Sources: [4], [5]
Caveats: Trials were short and many are shared between the two analyses. Effects were largest in people with higher starting LDL cholesterol and lower body mass index [5].

OrlistatStrong

Cholesterol and blood lipids

Shown to lower total and LDL cholesterol slightly, by about 0.3 mmol/L, with larger drops when more weight was lost.

LDL lowering was larger with more weight loss and shorter treatment.

The numbers and sources

Effect: Orlistat lowered total cholesterol by 0.30 mmol/L and LDL cholesterol by 0.27 mmol/L. HDL cholesterol fell 0.034 mmol/L and triglycerides 0.09 mmol/L. Lipoprotein(a) did not change. LDL lowering was larger with more weight loss and shorter treatment [3]. An earlier systematic review also found greater falls in total and LDL cholesterol than with control [5].
Population: 33 RCTs [3]; 28 RCTs, 17 of them with 10,041 patients over a year [5].
Sources: [3], [5]
Caveats: The changes are small. The reviews do not separate the drug from the weight lost.

OrlistatStrong

Liver enzymes in fatty liver disease

Shown to lower liver enzymes in fatty liver disease, ALT by about 9 U/L. Liver fat and scarring were not measured.

LDL cholesterol fell 5.61 mg/dL, fasting glucose 4.05 mg/dL, HOMA-IR 0.70 and BMI 0.99 kg/m².

The numbers and sources

Effect: In people with metabolic dysfunction-associated steatotic liver disease, orlistat lowered AST by 4.01 U/L (95% CI 1.97 to 6.05), ALT by 8.70 U/L (95% CI 0.90 to 16.51) and GGT by 7.74 U/L (95% CI 0.59 to 14.88) against control. LDL cholesterol fell 5.61 mg/dL, fasting glucose 4.05 mg/dL, HOMA-IR 0.70 and BMI 0.99 kg/m². Blood pressure did not change [6]. A second meta-analysis also found lower ALT, AST, HOMA-IR, BMI, cholesterol, insulin and waist circumference [7].
Population: 6 RCTs [6]; 11 studies with 582 participants [7].
Sources: [6], [7]
Caveats: Both reviews measured blood markers, not liver fat on imaging or scarring on biopsy. The trials were small and likely overlap between the reviews. The abstract of [7] does not say whether all 11 studies were randomized.

Paleo dietStrong

Cholesterol and triglycerides

Shown to lower total and LDL cholesterol and triglycerides more than comparison diets in adults, though some pooled results depended on single trials.

Compared with control diets the source does not describe [1], [3]; a diet following the Nordic Nutrition Recommendations [4]; a control group the source does not describe [5]

The numbers and sources

Effect: In people with metabolic disorders, total cholesterol fell 0.32 mmol/L (95% CI 0.15 to 0.49), triglycerides 0.29 mmol/L (95% CI 0.16 to 0.42) and LDL 0.35 mmol/L (95% CI 0.03 to 0.67) more than on control diets [5]. In 19 RCTs, total cholesterol fell 0.15, LDL 0.24 and triglycerides 0.16 more, in units the abstract does not state [3]. A third review found lower total cholesterol, triglycerides and LDL and higher HDL [1]. Triglycerides fell more than on a Nordic guideline diet at 6 and 24 months [4].
Population: Adults with metabolic disorders [5]; adults in 19 RCTs [3]; adults in 8 RCTs [1]; postmenopausal women with obesity [4].
Sources: [1], [3], [4], [5]
Caveats: In [1], lipid results changed when single studies were removed.

Soy foodsStrong

LDL cholesterol

Shown to lower LDL cholesterol by about 4.8 mg/dL, 3% to 4%, at a median 25 g of soy protein a day against non-soy protein, in pooled trials.

Compared with non-soy protein [4]; control groups the abstract does not describe [5]

In 23 trials of soy protein with its isoflavones intact, total cholesterol fell 3.77%, LDL cholesterol 5.25% and triglycerides 7.27%, and HDL cholesterol rose 3.03%.

The numbers and sources

Effect: Across 41 trials identified by the FDA, soy protein at a median 25 g a day for a median 6 weeks lowered LDL cholesterol by 4.76 mg/dL (95% CI -6.71 to -2.80) and total cholesterol by 6.41 mg/dL (95% CI -9.30 to -3.52), with no dose-response or publication bias. About 75% of trials showed a fall, though few were individually significant [4]. In 23 trials of soy protein with its isoflavones intact, total cholesterol fell 3.77%, LDL cholesterol 5.25% and triglycerides 7.27%, and HDL cholesterol rose 3.03%. Falls were larger in men and in people with high cholesterol. Tablets of extracted isoflavones did not lower total cholesterol [5].
Population: Adults with baseline LDL cholesterol of 110 to 201 mg/dL in 43 trials [4]. 23 randomized trials published 1995 to 2002 [5].
Sources: [4], [5]
Caveats: Heterogeneity was moderate (I² 55% for LDL) [4]. Most trials lasted weeks. The FDA has proposed revoking the soy protein heart claim [1], which the review authors attribute to a perceived lack of consistent LDL reduction in trials [4].

TaurineStrong

Blood sugar and blood lipids

Shown to lower fasting glucose about 6 mg/dL and triglycerides about 14 to 18 mg/dL, mostly in people with obesity, diabetes or metabolic syndrome. HDL did not change.

A second meta-analysis found fasting glucose 5.9 mg/dL lower, HbA1c 0.21% lower, triglycerides 14.4 mg/dL lower and LDL cholesterol 5.1 mg/dL lower.

The numbers and sources

Effect: Fasting glucose fell by 5.9 mg/dL (95% CI -10.7 to -1.0) and triglycerides by 18.3 mg/dL (95% CI -25.6 to -11.0). HDL cholesterol did not change [4]. A second meta-analysis found fasting glucose 5.9 mg/dL lower, HbA1c 0.21% lower, triglycerides 14.4 mg/dL lower and LDL cholesterol 5.1 mg/dL lower [5].
Population: 25 RCTs, 1,024 participants [4]; 34 RCTs [5].
Sources: [4], [5]
Caveats: Most trials were short and enrolled people with obesity, diabetes or metabolic syndrome. Neither review measured hard outcomes such as heart attacks or diabetes onset.

TurmericStrong

Cholesterol and triglycerides

Shown to lower triglycerides about 13 mg/dL and LDL about 6 mg/dL in adults with metabolic conditions. Smaller reviews found no significant LDL change.

Curcumin lowered LDL cholesterol by 5.84 mg/dL (95% CI -11.63 to -0.05), triglycerides by 13.15 mg/dL (95% CI -17.31 to -8.98) and total cholesterol by 7.76 mg/dL, and raised HDL by 2.4 mg/dL.

The numbers and sources

Effect: An umbrella review re-pooled 72 RCTs. Curcumin lowered LDL cholesterol by 5.84 mg/dL (95% CI -11.63 to -0.05), triglycerides by 13.15 mg/dL (95% CI -17.31 to -8.98) and total cholesterol by 7.76 mg/dL, and raised HDL by 2.4 mg/dL [10]. In 27 RCTs in prediabetes and diabetes, triglycerides fell 13.73 mg/dL, total cholesterol 5.24 mg/dL and LDL 5.72 mg/dL (95% CI -8.62 to -2.82), and HDL rose 2.14 mg/dL [11]. In 11 RCTs (662 people with metabolic disease), triglycerides and total cholesterol fell, while LDL and HDL did not change significantly under random-effects models [12]. With piperine added, 16 RCTs (1,038 participants) showed lower triglycerides and total cholesterol and no significant LDL change [13].
Population: Adults with noncommunicable diseases, with larger effects in type 2 diabetes [10]; adults with prediabetes or diabetes [11]; adults with metabolic disorders [12][13].
Sources: [10], [11], [12], [13]
Caveats: I² was 94% to 98% in the umbrella review [10] and above 80% in the diabetes review, which rated certainty low for every outcome [11]. The LDL drop did not reach significance in two smaller reviews [12][13]. The umbrella review found the total cholesterol and HDL changes smaller than their minimal clinically important differences [10].

Vegan dietStrong

LDL cholesterol

Shown to lower LDL cholesterol about 0.24 to 0.30 mmol/L against omnivorous or control diets in adults.

Compared with the participants' habitual diet, unchanged, in 3 trials in US and New Zealand adults, and in 8 trials a National Cholesterol Education Program diet, American Diabetes Association and Korean Diabetes Association diets, a portion-controlled diet, a Mediterranean diet, a low-fat diet, a healthy omnivorous diet or a high-carbohydrate lacto-ovo vegetarian diet [1]; an omnivorous diet [3]

The numbers and sources

Effect: Vegan diets lowered total cholesterol by 0.30 mmol/L and LDL by 0.24 mmol/L (95% CI -0.40 to -0.07), with no change in HDL or triglycerides [1]. In 30 RCTs of vegetarian or vegan diets, LDL fell 0.30 mmol/L (95% CI -0.40 to -0.19) and apolipoprotein B 12.92 mg/dL, with similar effects across intervention diet types [3].
Population: Adults with overweight or type 2 diabetes [1]; adults in 30 RCTs [3].
Sources: [1], [3]
Caveats: The larger review pooled vegan and vegetarian diets [3].

Vegetarian dietStrong

LDL cholesterol

Shown to lower LDL cholesterol about 0.3 mmol/L against omnivorous diets in adults. HDL also fell slightly in one review.

Compared with control diets the source does not describe [2]; an omnivorous control diet containing meat and dairy products [3]; an omnivorous diet [4]

The numbers and sources

Effect: In 11 trials, vegetarian diets lowered total cholesterol by 0.36 mmol/L, LDL by 0.34 mmol/L (95% CI -0.57 to -0.11) and HDL by 0.10 mmol/L (95% CI -0.14 to -0.06), with no triglyceride change [3]. In 30 RCTs, vegetarian or vegan diets lowered LDL by 0.30 mmol/L (95% CI -0.40 to -0.19) and apolipoprotein B by 12.92 mg/dL, with similar effects across intervention diet types and no triglyceride change [4]. In people with diabetes, LDL fell 0.12 mmol/L (95% CI -0.20 to -0.04) [2].
Population: Adults in randomized trials [3][4]; adults with diabetes [2].
Sources: [2], [3], [4]
Caveats: The reviews pooled lacto-ovo and vegan diets, though [4] found effects similar across diet types.

Whole grainsStrong

LDL cholesterol

Shown to lower LDL cholesterol slightly, by 0.09 mmol/L, against refined-grain control foods in pooled trials, with whole-grain oats lowering cholesterol most.

Compared with non-whole-grain control foods [8]; refined grains or placebo [9]

The numbers and sources

Effect: Whole grain intake lowered LDL cholesterol by 0.09 mmol/L (about 3.5 mg/dL, 95% CI -0.15 to -0.03) and total cholesterol by 0.12 mmol/L (95% CI -0.19 to -0.05), with no effect on HDL cholesterol. Triglycerides tended to fall (-0.04 mmol/L, 95% CI -0.08 to 0.01). Oats had the largest effect on total cholesterol (-0.17 mmol/L) [8]. In a second review, whole-grain oats improved total cholesterol (SMD -0.54, 95% CI -0.95 to -0.12) and LDL cholesterol (SMD -0.57, 95% CI -0.84 to -0.31), and whole-grain rice improved triglycerides [9].
Population: 24 randomized trials in apparently healthy adults [8]. 25 randomized trials of 2 to 16 weeks in adults with or without cardiovascular risk factors [9].
Sources: [8], [9]
Caveats: Small changes over weeks. The second review found the LDL effect for oats, not for all whole grains combined [9]. Beta-glucan from oats is on its own page.

AstaxanthinModerate

Blood sugar and blood lipids

Shown to lower fasting glucose by about 16 mg/dL and triglycerides in people with prediabetes or type 2 diabetes. Reviews disagree on LDL and total cholesterol.

The numbers and sources

Effect: In prediabetes and type 2 diabetes, astaxanthin lowered fasting glucose by 16.1 mg/dL (95% CI -29.0 to -3.3), HbA1c by 0.34 points, triglycerides by 20.9 mg/dL, total cholesterol by 12.2 mg/dL and LDL by 9.4 mg/dL, and raised HDL by 3.0 mg/dL. HOMA-IR, weight and BMI did not change [4]. At 6 to 20 mg a day, a second meta-analysis found higher HDL and lower triglycerides, with no change in LDL or total cholesterol [5]. In adults at risk of metabolic syndrome, effects on total cholesterol and systolic pressure were marginal, and LDL fell [6].
Population: 403 patients in 9 RCTs [4]; 8 studies with 11 results [5]; 321 adults in 7 RCTs [6].
Sources: [4], [5], [6]
Caveats: The reviews disagree on LDL and total cholesterol. All pooled small trials.

Beta-glucanModerate

LDL cholesterol (barley beta-glucan)

Shown to lower LDL by about 0.25 mmol/L in adults on a median 6.5 g a day of barley beta-glucan.

The numbers and sources

Effect: In 14 trials (615 people), a median 6.5 g a day of barley beta-glucan for 4 weeks lowered LDL by 0.25 mmol/L (95% CI 0.20 to 0.30) and non-HDL by 0.31 mmol/L. ApoB did not change [4].
Population: Adults in trials of 3 weeks or longer [4].
Sources: [4]
Caveats: Non-HDL heterogeneity was high (I² 98%) [4].

Beta-glucanModerate

Blood pressure

Shown to lower systolic blood pressure by about 1.4 mmHg in adults with overweight or obesity. Diastolic pressure did not change.

Across cereal beta-glucan, total cholesterol fell by 0.24 mmol/L and LDL by 0.19 mmol/L.

The numbers and sources

Effect: In people with a BMI of 25 or more, oat beta-glucan lowered systolic blood pressure by 1.38 mmHg (95% CI 0.09 to 2.66). Diastolic blood pressure did not change. Across cereal beta-glucan, total cholesterol fell by 0.24 mmol/L and LDL by 0.19 mmol/L [8].
Population: 49 studies, 3,854 people with overweight or obesity [8].
Sources: [8]
Caveats: One meta-analysis. One author is affiliated with a food science company [8].

DASH dietModerate

LDL and total cholesterol

Shown to lower LDL cholesterol slightly in adults, by 0.10 mmol/L across trials and 0.28 mmol/L in the original feeding trial.

Compared with control diets the source does not describe [3]; the DASH trial's control diet [6]; usual, low-fat and low-antioxidant diets, behavioral programs alone and usual gestational diabetes care [7]

LDL fell 11.2 mg/dL more in men than in women.

The numbers and sources

Effect: Across 20 trials, DASH lowered total cholesterol by 0.20 mmol/L (95% CI -0.31 to -0.10) and LDL by 0.10 mmol/L (95% CI -0.20 to -0.01) [3]. In the 8-week DASH feeding trial, total cholesterol fell 0.35 mmol/L (13.7 mg/dL) and LDL 0.28 mmol/L (10.7 mg/dL) against control, with no triglyceride change. LDL fell 11.2 mg/dL more in men than in women [6]. An umbrella review reported the same pooled figures as [3], with no effect on HDL or triglycerides [7].
Population: Adults in 20 trials of 2 to 24 weeks [3]; 436 adults with total cholesterol of 6.7 mmol/L or less, mean age 44.6, 60% African American [6].
Sources: [3], [6], [7]
Caveats: The umbrella review drew its lipid figures from the same meta-analysis, so the two are not independent [3][7]. The umbrella review rated most secondary outcomes very low to moderate certainty [7].

Ezetimibe and fenofibrateModerate

Fenofibrate: triglycerides, HDL and LDL cholesterol

Shown to lower triglycerides about 29% and LDL cholesterol 21% and to raise HDL 11% against placebo, with triglycerides 46% to 55% lower in severe high triglycerides.

Compared with placebo [7]

In severe high triglycerides, triglycerides fell 46.2% (baseline 432 mg/dL) and 54.5% (baseline 726 mg/dL) against -0.5% and +7.2% on placebo, while LDL cholesterol rose in both groups.

The numbers and sources

Effect: In four placebo-controlled trials of 3 to 6 months, fenofibrate at the 145 mg dose changed triglycerides by -28.9% against +7.7% on placebo, LDL cholesterol by -20.6% against -2.2%, total cholesterol by -18.7% against -0.4%, and HDL by +11.0% against +0.7%. ApoB fell 25.1% against a 2.4% rise. In severe high triglycerides, triglycerides fell 46.2% (baseline 432 mg/dL) and 54.5% (baseline 726 mg/dL) against -0.5% and +7.2% on placebo, while LDL cholesterol rose in both groups [7].
Population: 646 adults with high cholesterol or mixed dyslipidemia in 4 trials, and 147 adults with high triglycerides in 2 trials of 8 weeks [7].
Sources: [7]
Caveats: Label trials, short-term. The label reports rare severe paradoxical drops in HDL, listed under Risks [7].

Fisetin and quercetin (senolytics)Moderate

Liver enzymes and lipids in fatty liver disease (quercetin alone)

Shown to lower liver enzymes, LDL and triglycerides with quercetin alone in people with fatty liver disease, at very low to moderate certainty.

The numbers and sources

Effect: A 2025 meta-analysis of 7 RCTs (540 patients) with metabolic dysfunction-associated steatotic liver disease found that quercetin lowered ALT, AST, GGT, direct bilirubin and C-reactive protein, lowered total cholesterol, LDL and triglycerides, and raised HDL. BMI, body fat, kidney function and TNF-α did not change [10].
Population: 540 patients with fatty liver disease in 7 RCTs [10].
Sources: [10]
Caveats: GRADE certainty ranged from very low to moderate. Dose, baseline BMI and age may explain heterogeneity. The abstract gives no pooled effect sizes [10]. None of the trials measured senescent cells.

InositolModerate

Weight, blood sugar and lipids

Shown to lower BMI slightly, about 0.6 kg/m², and glucose, triglycerides and blood pressure in adults across several conditions, at low certainty for some.

The numbers and sources

Effect: In 18 RCTs (898 participants) of at least 4 weeks, inositol lowered BMI by 0.57 kg/m² (95% CI -1.10 to -0.03), waist circumference by 2.36 cm, glucose by 7.25 mg/dL, HOMA-IR by 1.21, triglycerides by 29.80 mg/dL, LDL cholesterol by 5.15 mg/dL, and systolic and diastolic pressure by 5.34 and 6.12 mm Hg [11].
Population: Adults in RCTs across several conditions [11].
Sources: [11]
Caveats: Certainty was low to very low for BMI, waist and blood pressure, and moderate for glucose, insulin and HOMA-IR. Heterogeneity was high for most outcomes, and the authors note a high risk of bias in the trials [11].

Mediterranean dietModerate

Blood pressure, cholesterol and blood sugar markers

Shown to lower blood pressure about 3/2 mmHg and LDL cholesterol and HbA1c slightly in adults, at low to moderate certainty.

Compared with no or minimal intervention, and another dietary intervention the abstract does not name [2]; a low-fat diet, a low-carbohydrate diet and the American Diabetes Association diet [7]; control diets the source does not describe [10]

In 9 RCTs (1,337 people at raised risk of diabetes or heart disease), HbA1c fell 0.18 points (95% CI -0.35 to -0.01), LDL 0.10 mmol/L and triglycerides 0.20 mmol/L.

The numbers and sources

Effect: Against no or minimal intervention, systolic blood pressure fell 2.99 mmHg (95% CI -3.45 to -2.53) and diastolic 2.0 mmHg (95% CI -2.29 to -1.71) at moderate quality, with little or no effect on LDL or HDL. Against other diets, LDL fell 0.15 mmol/L (95% CI -0.27 to -0.02) and triglycerides 0.09 mmol/L, with little or no effect on blood pressure [2]. In 9 RCTs (1,337 people at raised risk of diabetes or heart disease), HbA1c fell 0.18 points (95% CI -0.35 to -0.01), LDL 0.10 mmol/L and triglycerides 0.20 mmol/L. Fasting glucose, insulin, insulin resistance and HDL did not change [10]. Over 12 months or more, blood pressure and lipids changed about as much as on comparator diets [7].
Population: Healthy adults and adults at high cardiovascular risk [2]; adults at increased risk of type 2 diabetes and heart disease [10]; adults with overweight or obesity [7].
Sources: [2], [7], [10]
Caveats: The Cochrane review rated the lipid evidence low or very low quality for most comparisons [2]. The changes are small next to drug effects.

Milk thistleModerate

Fatty liver disease

Shown to lower liver enzymes in fatty liver disease, ALT by about 7 to 12 U/L, with low certainty and no data on deaths.

The numbers and sources

Effect: In 26 trials (2,375 patients), silymarin lowered ALT (pooled difference -12.39, 95% CI -19.69 to -5.08) and AST (-10.97, 95% CI -15.51 to -6.43), lowered total cholesterol, triglycerides and LDL, and improved steatosis on histology (OR 3.25, 95% CI 1.80 to 5.87) [5]. In a 48-week biopsy trial of 99 adults with NASH, a 30% or greater fall in disease activity score occurred in 32.7% on 700 mg three times a day and 26.0% on placebo (p 0.467). Fibrosis fell by 1 point or more in 22.4% against 6.0% (p 0.023) [6]. A 2025 Cochrane review of 17 RCTs (2,069 adults) found silymarin alone against placebo or no treatment may lower ALT by 7.21 U/L (95% CI -10.62 to -3.80, 6 trials, very low certainty). Silymarin complexes did not lower ALT, and no trial reported deaths or quality of life [7]. In a 2025 meta-analysis of 25 studies (2,283 patients), silymarin alone lowered LDL cholesterol (SMD -0.25), while ALT fell when silymarin was combined with diet or lifestyle change [8].
Population: Adults with fatty liver disease [5][7][8]. 99 adults with biopsy-proven NASH in Malaysia [6].
Sources: [5], [6], [7], [8]
Caveats: The meta-analysis authors state that the effects need confirmation [5]. The biopsy trial missed its primary outcome, and its fibrosis finding was secondary [6]. The Cochrane authors rated the evidence low to very low certainty and called benefits and harms unclear [7].

NiacinModerate

Blood lipids

Shown to raise HDL and lower triglycerides and LDL in people with vascular disease on statins, though events did not fall.

The numbers and sources

Effect: At 2 years in AIM-HIGH, median HDL rose from 35 to 42 mg/dL, triglycerides fell from 164 to 122 mg/dL and LDL fell from 74 to 62 mg/dL on 1,500 to 2,000 mg a day of extended-release niacin [1]. In HPS2-THRIVE, LDL averaged 10 mg/dL lower and HDL 6 mg/dL higher than placebo [2].
Population: 3,414 people with cardiovascular disease on simvastatin [1]; 25,673 adults with vascular disease on statin-based therapy [2].
Sources: [1], [2]
Caveats: Lipid changes did not translate into fewer events in these trials (see next block).

StatinsModerate

LDL cholesterol lowering

Shown to lower LDL cholesterol by about 51 to 56 mg/dL with atorvastatin and rosuvastatin, and triglycerides by about 25 to 32 mg/dL.

The numbers and sources

Effect: Pooled across studies, atorvastatin lowered LDL cholesterol by 51.49 mg/dL (95% CI 42.75 to 60.23) and rosuvastatin by 55.66 mg/dL (95% CI 46.32 to 65.00). Triglycerides fell by 24.76 and 31.98 mg/dL, and HDL rose by 1.85 and 3.87 mg/dL [3].
Population: Studies of atorvastatin and rosuvastatin from 2003 to 2025 [3].
Sources: [3]
Caveats: The abstract does not give study counts, doses or the comparison used. The heart attack and stroke results above are expressed per unit of LDL lowered [1].

Tai chi and qigongModerate

Blood fats in hypertension

Shown in two meta-analyses to lower LDL cholesterol and triglycerides in people with hypertension. HDL cholesterol results differed between them.

Compared with control groups the source abstract does not describe [5]; no intervention [6]

Baduanjin lowered triglycerides and LDL cholesterol and raised HDL cholesterol against no intervention.

The numbers and sources

Effect: Tai chi was associated with lower total cholesterol (WMD -0.49), triglycerides (WMD -0.49, 95% CI -0.92 to -0.07) and LDL cholesterol (WMD -0.86), and no significant effect on HDL cholesterol (P = 0.16) [5]. Baduanjin lowered triglycerides and LDL cholesterol and raised HDL cholesterol against no intervention [6].
Population: Adults with essential hypertension [5][6].
Sources: [5], [6]
Caveats: The first abstract gives no units, and its HDL interval does not contain its own point estimate [5]. The second gives no sizes for blood fats [6].

YogaModerate

Stress hormones, heart rate and blood fats, against active controls

Shown in one meta-analysis to lower cortisol, ambulatory systolic pressure, resting heart rate, fasting glucose and LDL cholesterol more than active control activities.

Compared with active control interventions [11]

The numbers and sources

Effect: Across 42 trials, practices including yoga postures were associated with lower evening and waking cortisol, ambulatory systolic blood pressure, resting heart rate, fasting blood glucose, cholesterol and LDL cholesterol, and higher high-frequency heart rate variability, compared with active controls [11].
Population: Participants in 42 randomized trials in various populations [11].
Sources: [11]
Caveats: The abstract gives no effect sizes and describes the interventions as heterogeneous. Some included mindfulness-based stress reduction alongside postures [11].

YogaModerate

Blood sugar and blood fats in type 2 diabetes

Shown in one meta-analysis to lower HbA1c by 0.47 points and fasting glucose by 24 mg/dL in adults with type 2 diabetes, with high heterogeneity.

Compared with control groups including usual care or standard treatment [12]

The numbers and sources

Effect: Pooled differences were -23.72 mg/dL for fasting blood glucose (95% CI -37.78 to -9.65, I² 82%), -0.47% for HbA1c (95% CI -0.87 to -0.07, I² 82%), -17.38 mg/dL for glucose after meals, -18.50 mg/dL for total cholesterol, +4.30 mg/dL for HDL cholesterol and -12.95 mg/dL for LDL cholesterol. Triglycerides did not differ (-12.57 mg/dL, 95% CI -29.91 to 4.76) [12].
Population: 864 adults with type 2 diabetes in 12 trials [12].
Sources: [12]
Caveats: The authors note limited methods and heterogeneity, and long-term effects were not studied [12].

CuppingLimitedStudied in men

LDL cholesterol, wet cupping

One small trial found LDL cholesterol fell after wet cupping in 47 healthy young men, with no significant change in total cholesterol, HDL or triglycerides.

Compared with no treatment [12]

The numbers and sources

Effect: Over 3 weeks after one wet cupping session, LDL cholesterol and the LDL to HDL ratio fell in the treated group against untreated controls (p < 0.0001). Triglycerides did not change, and total cholesterol (7% lower) and HDL (3% higher) did not differ significantly [12].
Population: 47 healthy men aged 18 to 25 [12].
Sources: [12]
Caveats: One small trial in young men without high cholesterol, with no sham. Wet cupping removes blood, and the authors compare it with phlebotomy [12].

Flexitarian dietLimited

Heart disease

Limited evidence: in a review of 4 trials in healthy adults, replacing part of animal protein with plant protein lowered LDL and total cholesterol. No study measured heart disease itself.

Compared with diets with a higher share of animal protein foods [9]

LDL cholesterol, total cholesterol and body weight improved in those eating the higher share of plant protein.

The numbers and sources

Effect: A 2026 systematic review found 4 dietary interventions, reported in 7 articles, that partially replaced animal protein foods with plant protein foods in healthy adults. LDL cholesterol, total cholesterol and body weight improved in those eating the higher share of plant protein. Vitamin B12 status fell on the diets with the most plant protein [9].
Population: Healthy adults with a mean or median age of 18 to 65 in randomized trials, 3 of 7 articles at low risk of bias [9].
Sources: [9]
Caveats: The abstract gives no pooled sizes of effect [9]. Cholesterol is a risk marker, not heart disease. No cohort or trial of flexitarian eating and heart attacks or heart deaths was located.

Grape seed extractLimited

Cholesterol

Limited evidence: a 50-trial review found lower total and LDL cholesterol and triglycerides, while an earlier review found no effect on lipids.

The numbers and sources

Effect: Across 50 trials, grape seed extract lowered total cholesterol (WMD -6.03, 95% CI -9.71 to -2.35), LDL cholesterol (WMD -4.97) and triglycerides (WMD -6.55). HDL did not change [5]. An earlier meta-analysis of 9 RCTs found no significant effect on lipid levels [2].
Population: Adults in RCTs [5][2].
Sources: [5], [2]
Caveats: The two reviews disagree.

HMBLimited

Adverse effects in early trials

Limited evidence: 9 short trials at 3 g a day found no change in blood chemistry or blood counts.

Total cholesterol fell 5.8%, LDL 7.3% and systolic pressure 4.4 mmHg against placebo.

The numbers and sources

How common: How often is not known: the sources give no rate.
Effect: Across 9 studies giving 3 g a day for 3 to 8 weeks, HMB did not change blood chemistry or hematology markers. Total cholesterol fell 5.8%, LDL 7.3% and systolic pressure 4.4 mmHg against placebo [14].
Population: Men and women, young and old, exercising or not [14].
Sources: [14]
Caveats: A pooled summary of nine trials, not a systematic review. No independent review of long-term safety was located.

Shown to raise it8

CoffeeStrongHow often is not known

Higher LDL cholesterol from unfiltered coffee

Shown to raise total and LDL cholesterol in trials, mainly with unfiltered brews such as boiled or French press coffee. Filtered coffee raised it very little.

The numbers and sources

How common: How often is not known: the sources give no rate.
Effect: Across 12 randomized trials averaging 45 days, coffee raised total cholesterol by 8.1 mg/dL (95% CI 4.5 to 11.6), LDL by 5.4 mg/dL (95% CI 1.4 to 9.5) and triglycerides by 12.6 mg/dL, more with unfiltered and caffeinated coffee and in people with high cholesterol [19]. An earlier pooling of 14 trials found a dose-response rise in total and LDL cholesterol with unfiltered coffee and very little with filtered coffee [20]. Five to 6 cups a day of cafetière coffee raised LDL by 0.26 mmol/L (95% CI 0.04 to 0.47) against filtered coffee over 24 weeks. Triglycerides first rose 26% and then returned near baseline [18].
Population: 1,017 participants in 12 Western trials [19]. 14 trials [20]. 46 adults aged 19 to 69 [18].
Sources: [19], [20], [18]
Caveats: The trials attribute the rise to cafestol and kahweol, oily compounds present in unfiltered coffee [21]. The lipid trials were all in Western countries [19].

EggsStrongHow often is not known

Higher LDL cholesterol in feeding trials

Shown to raise LDL cholesterol by about 8 mg/dL in randomized trials in healthy people, along with total cholesterol and apolipoprotein B.

The numbers and sources

How common: How often is not known: the sources give no rate.
Effect: Against control groups, eating more eggs raised LDL cholesterol (mean difference 8.14 mg/dL, P < 0.0001), with larger effects in trials of over two months [3]. Across 66 trials, eggs raised total cholesterol, LDL and apolipoprotein B100, did not change triglycerides, and LDL rose nonlinearly with dose [4]. Each extra 100 mg of dietary cholesterol a day raised total cholesterol by 2.2 mg/dL (95% CI 1.8 to 2.5) [2].
Population: Healthy participants in 17 randomized trials [3]. 3,185 participants in 66 randomized trials [4]. 556 participants in 17 feeding studies [2].
Sources: [3], [4], [2]
Caveats: Short trials. One review found the rise came with eating more than one egg a day for under 12 weeks [4].

Added sugarModerateHow often is not known

Blood fats and blood pressure

Shown to raise triglycerides, total and LDL cholesterol and blood pressure in trials of higher against lower sugar intake, independent of body weight.

The numbers and sources

How common: How often is not known: the sources give no rate.
Effect: Higher sugar intake raised triglycerides by 0.11 mmol/L (95% CI 0.07 to 0.15), total cholesterol by 0.16 mmol/L (95% CI 0.10 to 0.24), LDL cholesterol by 0.12 mmol/L (95% CI 0.05 to 0.19) and HDL cholesterol by 0.02 mmol/L (95% CI 0.00 to 0.03). In trials of 8 weeks or longer, systolic pressure rose 6.9 mmHg (95% CI 3.4 to 10.3) and diastolic 5.6 mmHg [11]. A liter of regular cola a day for 6 months raised triglycerides 32% and total cholesterol 11% more than milk, diet cola or water [12].
Population: 37 trials reporting lipids and 12 reporting blood pressure, each at least 2 weeks [11]. 47 overweight adults [12].
Sources: [11], [12]
Caveats: Heterogeneity was moderate to high (I² 36% to 75%) [11]. The cola trial was small.

GnRH drugs for fibroidsModerateStudied in womenVery common

Cholesterol rises

Shown to raise total and LDL cholesterol in women. On Myfembree, 13.7% with normal cholesterol rose to 200 to 239 mg/dL, against 7.7% on placebo.

LDL rose to 130 to 159 mg/dL in 9.3% against 6.5%.

The numbers and sources

How common: Very common: more than 1 in 10 people.
Effect: Among women with total cholesterol under 200 mg/dL, 13.7% on Myfembree rose to 200 to 239 mg/dL and 1.7% to 240 or above, against 7.7% and 0.6% on placebo. LDL rose to 130 to 159 mg/dL in 9.3% against 6.5% [2]. On Oriahnn, total cholesterol, LDL, triglycerides and apolipoprotein B rose, and 9 of 54 women with LDL of 130 to 159 mg/dL rose to 190 or above, against none on placebo [6]. On leuprolide, mean cholesterol rose 11 to 29 mg/dL in women with fibroids [10].
Population: Premenopausal women with fibroids in the placebo-controlled trials [2][6][10].
Sources: [2], [6], [10]
Caveats: Shifts between bands, measured at the end of 6-month trials.

Keto dietModerateVery common

LDL cholesterol and apolipoprotein B

Shown to raise LDL cholesterol over comparison diets in adults, by 0.12 to 0.35 mmol/L in most reviews and 1.08 mmol/L in normal-weight adults.

The numbers and sources

How common: Very common: more than 1 in 10 people.
Effect: LDL rose 0.12 mmol/L more than on low-fat diets over 12 months or more (95% CI 0.04 to 0.20) [1], 0.35 mmol/L more than on control diets (95% CI 0.20 to 0.50, I² 73.9%) [2], and 8.49 mg/dL more across 62 studies (95% CI 5.45 to 11.52) [5]. In 3 trials of normal-weight adults, LDL rose 1.08 mmol/L (95% CI 0.37 to 1.79) and apolipoprotein B 0.35 g/L (95% CI 0.06 to 0.65) [16]. In type 2 diabetes, LDL did not differ from control diets [7]. In one trial with weight loss held equal, LDL and apolipoprotein B did not differ from Mediterranean or very-low-fat diets [12]. Hyperlipidemia was reported in 12.8% of children treated for epilepsy [17].
Population: Adults with and without obesity [1][2][5]; normal-weight adults [16]; adults with type 2 diabetes [7]; children with epilepsy [17].
Sources: [1], [2], [5], [7], [12], [16], [17]
Caveats: Effect sizes differ several times over between populations. No trial measured heart attacks or strokes, and the authors of [5] note the lack of long-term cardiovascular outcome data.

SGLT2 inhibitorsModerateHow often is not known

LDL cholesterol rise

Shown to raise LDL cholesterol by a few percent in blood sugar trials, about 4.5% to 8.0% more than placebo on canagliflozin.

The numbers and sources

How common: How often is not known: the sources give no rate.
Effect: In pooled canagliflozin trials, LDL cholesterol rose against placebo by 4.4 mg/dL (4.5%) on 100 mg and 8.2 mg/dL (8.0%) on 300 mg [24]. In empagliflozin trials it rose by 4.6% on 10 mg and 6.5% on 25 mg against 2.3% on placebo [20]. In dapagliflozin trials it rose by 2.9% on 10 mg against a fall of 1.0% on placebo at 24 weeks. After 4 years in the dapagliflozin cardiovascular trial, LDL cholesterol had fallen by 2.5 mg/dL on dapagliflozin and 4.4 mg/dL on placebo [23]. In a network meta-analysis, canagliflozin 300 mg raised LDL cholesterol by 0.13 to 0.15 mmol/L more than the other two drugs [15].
Population: Adults with type 2 diabetes in pooled placebo-controlled trials [24][20][23]; 23,997 participants in 38 trials [15].
Sources: [24], [20], [23], [15]
Caveats: Mean changes, with no count of people affected. The cardiovascular outcome trials above measured events in the same drugs [9][10].

ZincModerate

Blood sugar

Shown to lower fasting glucose about 14 mg/dL and HbA1c about 0.55% in people with and without diabetes.

Across 18 RCTs (1,023 participants) with diabetes, gestational diabetes or prediabetes, zinc lowered serum insulin (MD -2.50, 95% CI -4.69 to -0.31) and HOMA-IR (MD -1.10, 95% CI -2.05 to -0.15), and LDL cholesterol rose slightly (MD 3.46, 95% CI 1.48 to 5.43).

The numbers and sources

Effect: Across 32 placebo-controlled interventions (1,700 participants, 14 countries), zinc lowered fasting glucose by 14.15 mg/dL (95% CI -17.36 to -10.93), 2-hour glucose by 36.85 mg/dL, HbA1c by 0.55% (95% CI -0.84 to -0.27) and hs-CRP by 1.31 mg/L [3]. Across 18 RCTs (1,023 participants) with diabetes, gestational diabetes or prediabetes, zinc lowered serum insulin (MD -2.50, 95% CI -4.69 to -0.31) and HOMA-IR (MD -1.10, 95% CI -2.05 to -0.15), and LDL cholesterol rose slightly (MD 3.46, 95% CI 1.48 to 5.43) [4].
Population: People with and without diabetes [3]; people with diabetes or prediabetes [4].
Sources: [3], [4]
Caveats: The fasting glucose effect depended on diabetes status and on the zinc formulation [3].

Carnivore dietLimitedHow often is not known

LDL cholesterol rise

Limited evidence: LDL cholesterol rose from a median of 157 to 256 mg/dL in 24 followers who shared before and after blood tests.

The numbers and sources

How common: How often is not known: the sources give no rate.
Effect: Median total cholesterol rose from 224 to 305 mg/dL (p < 0.0001) and LDL from 157 to 256 mg/dL (p 0.00024). No other blood marker changed significantly [3]. Survey respondents who reported current lipids had LDL of 172 mg/dL and HDL of 68 mg/dL [1]. A scoping review identified elevated LDL and total cholesterol across the human studies [2].
Population: 24 German followers [3]; a subset of 2,029 survey respondents [1]; 9 human studies [2].
Sources: [1], [3], [2]
Caveats: Small, self-selected groups without controls. No study measured heart attacks or strokes.

Studies disagree5

Physical activityStrong

Blood fats

Shown to lower triglycerides in pooled trials of aerobic training, with HDL cholesterol rising modestly in two reviews and not changing overall in a third.

Compared with control groups in randomized trials [8][9]; no exercise, or diet alone [10]

In sedentary adults with metabolic syndrome factors, aerobic training lowered triglycerides by 0.17 to 0.18 mmol/L, total cholesterol by 0.19 to 0.29 mmol/L and LDL cholesterol by 0.12 to 0.20 mmol/L, and raised HDL cholesterol by 0.05 to 0.10 mmol/L.

The numbers and sources

Effect: HDL cholesterol rose by 2.53 mg/dL against controls, from a minimum of about 120 minutes of exercise a week, and rose more with longer sessions [8]. In sedentary adults with metabolic syndrome factors, aerobic training lowered triglycerides by 0.17 to 0.18 mmol/L, total cholesterol by 0.19 to 0.29 mmol/L and LDL cholesterol by 0.12 to 0.20 mmol/L, and raised HDL cholesterol by 0.05 to 0.10 mmol/L [9]. In adults with overweight or obesity, aerobic exercise lowered triglycerides and did not change total, HDL or LDL cholesterol overall [10].
Population: 25 randomized trials [8]. 2,990 participants in 48 data sets of trials of at least 12 weeks [9]. 619 adults with overweight or obesity in 9 trials [10].
Sources: [8], [9], [10]
Caveats: Changes were modest. The populations differed across reviews, which may explain the HDL difference.

Green teaModerate

Cholesterol

Shown to lower total cholesterol by 2.8 mg/dL in trials of catechin-enriched green tea drinks. LDL, HDL and triglycerides did not change significantly in those trials.

Compared with water or other placebo drinks, no intervention, or green tea drinks low in catechins [4]

LDL changed by -2.61 mg/dL (95% CI -5.49 to 0.27), HDL by -0.84 mg/dL and triglycerides by -0.77 mg/dL, none significant.

The numbers and sources

Effect: In the 9 trials that gave green tea as a drink, total cholesterol fell by 2.80 mg/dL (95% CI 0.16 to 5.43). LDL changed by -2.61 mg/dL (95% CI -5.49 to 0.27), HDL by -0.84 mg/dL and triglycerides by -0.77 mg/dL, none significant. Across all 31 trials of drinks and capsules, LDL fell by 4.55 mg/dL (95% CI 2.80 to 6.31) [4].
Population: 3,321 participants in 31 randomized trials, 9 of them using a green tea drink [4].
Sources: [4]
Caveats: The drinks in these trials were green tea beverages made with extract, carrying 400 to 928 mg of catechins a day, not ordinary brewed tea. Meta-regression found no significant difference between drinks and capsules [4]. Capsule trials are on the green tea extract page.

Olive oilModerate

Cholesterol

Shown to raise HDL cholesterol slightly in trials. LDL fell with high-polyphenol olive oil, but other plant oils lowered LDL more than olive oil did.

Compared with other plant oils [9]; low-polyphenol olive oil [10][11]

The numbers and sources

Effect: Against other plant oils, olive oil raised HDL more (1.37 mg/dL, 95% CI 0.4 to 2.36) and lowered total cholesterol (by 6.27 mg/dL), LDL (by 4.2 mg/dL, 95% CI 1.4 to 7.01) and triglycerides (by 4.31 mg/dL) less. Apolipoproteins A1 and B did not differ [9]. Against low-polyphenol olive oil, high-polyphenol oil lowered total cholesterol by 4.5 mg/dL and raised HDL by 2.37 mg/dL [10]. A later pooling found higher HDL (1.13 mg/dL, 95% CI 0.45 to 1.80), lower LDL only at the highest polyphenol level (-4.28 mg/dL) and no change in total cholesterol [11].
Population: 1,089 participants in 27 randomized trials [9]. 26 randomized trials [10]. 10 randomized trials, mostly crossover, in mostly healthy Europeans [11].
Sources: [9], [10], [11]
Caveats: The changes are a few mg/dL. The comparison decides the direction: olive oil looks favorable against low-polyphenol olive oil and less favorable for LDL against other plant oils.

Red meat and processed meatModerate

Cholesterol and blood pressure in trials

Not shown to change cholesterol or blood pressure against all comparison diets combined. Against plant proteins, LDL fell less on red meat. Against fish, it fell more.

Compared with diets replacing red meat with legumes, soy or nuts, fish, poultry, mixed animal protein, refined carbohydrates or the usual diet [4]

Against fish, LDL fell 0.173 mmol/L more and HDL 0.065 mmol/L more.

The numbers and sources

Effect: Against all comparison diets combined, red meat made no significant difference to total, LDL or HDL cholesterol, apolipoproteins A1 and B, or blood pressure, and gave a smaller fall in triglycerides (0.065 mmol/L). Against high-quality plant proteins, total cholesterol fell 0.264 mmol/L less and LDL 0.198 mmol/L less. Against fish, LDL fell 0.173 mmol/L more and HDL 0.065 mmol/L more. Against refined carbohydrates, triglycerides fell 0.181 mmol/L more [4].
Population: 1,803 participants in 36 randomized trials [4].
Sources: [4]
Caveats: The result depends on what replaced the red meat. Trials measured blood markers, not heart events.

ReishiModerate

Blood sugar, cholesterol and blood pressure

Not shown to change HbA1c, fasting glucose, cholesterol or blood pressure against placebo, with one spore oil trial finding lower lipids.

In 110 adults with dyslipidemia, a spore oil extract for 12 weeks lowered total cholesterol, triglycerides and LDL and raised HDL compared with placebo.

The numbers and sources

Effect: In a Cochrane review of 5 trials (398 participants), 1.4 to 3 g a day for 12 to 16 weeks did not change HbA1c (WMD -0.10%, 95% CI -1.05 to 0.85), total cholesterol, LDL or BMI against placebo. Fasting glucose, blood pressure and triglycerides did not differ. Post-meal glucose results were inconsistent [2]. A 2025 meta-analysis of 17 RCTs (971 participants) at 200 to 11,200 mg a day for 1 to 24 weeks found no effect on blood pressure, fasting glucose or the lipid profile. BMI fell by 0.43 (95% CI 0.10 to 0.77) and heart rate by 3.92 beats a minute (95% CI 0.40 to 7.45) [3]. In 110 adults with dyslipidemia, a spore oil extract for 12 weeks lowered total cholesterol, triglycerides and LDL and raised HDL compared with placebo. The abstract gives no effect sizes [4].
Population: Adults with type 2 diabetes in the analyzed trials [2]. Healthy, at-risk and chronically ill adults [3]. Adults with dyslipidemia [4].
Sources: [2], [3], [4]
Caveats: Data in [2] came from 3 small trials, and risk of bias was unclear in 4 of 5 [2]. The 2025 review rated the certainty of evidence very low for every outcome [3]. The spore oil trial tested a different product and disagrees with both reviews on lipids [4].

Tested, and not shown to change it9

Apple cider vinegarStrong

Cholesterol

Shown to lower total cholesterol by about 6 mg/dL in adults, with no change in LDL or HDL.

The numbers and sources

Effect: ACV lowered total cholesterol by 6.06 mg/dL (95% CI -10.95 to -1.17) with no significant effect on LDL or HDL [2]. A 2025 meta-analysis of 25 trials found total cholesterol 6.72 mg/dL lower (95% CI -12.91 to -0.53, I² 50.8%), with no significant change in LDL, HDL or triglycerides [4].
Population: Adults in 9 studies [2]. 1,320 adults in 25 trials [4].
Sources: [2], [4]
Caveats: Triglyceride reductions appeared only in subgroups [2][4].

Fish oilModerate

LDL and HDL cholesterol

Mixed results: most reviews found little or no change in LDL or HDL, while subgroups saw LDL fall in some groups and rise in others.

Across mixed populations, HDL rose 1.55 mg/dL (95% CI 0.69 to 2.42), and LDL fell only in subgroups of women and of people with polycystic ovary syndrome.

The numbers and sources

Effect: The Cochrane review found little or no effect on blood lipids other than triglycerides [1]. In coronary heart disease, LDL and HDL did not change significantly, and total cholesterol fell slightly (SMD -0.12) [2]. Across mixed populations, HDL rose 1.55 mg/dL (95% CI 0.69 to 2.42), and LDL fell only in subgroups of women and of people with polycystic ovary syndrome [3]. In metabolic syndrome trials, LDL rose in low-dose subgroups (7.04 mg/dL short term, 35.5 mg/dL long term) [5].
Population: Trial participants in the four reviews above [1][2][3][5].
Sources: [1], [2], [3], [5]
Caveats: The reviews differ on direction in subgroups. The LDL rise in [5] came from few studies per subgroup.

Garcinia cambogiaModerate

Cholesterol and triglycerides

Shown to lower triglycerides about 24 mg/dL and raise HDL slightly in adults, with no LDL change. One 10-week trial found no lipid change.

LDL did not change (-1.15 mg/dL, 95% CI -16.08 to 13.78).

The numbers and sources

Effect: Across 14 trials with 623 subjects, total cholesterol fell 6.76 mg/dL (95% CI -12.39 to -0.59), triglycerides fell 24.21 mg/dL (95% CI -37.84 to -10.58) and HDL rose 2.95 mg/dL (95% CI 2.01 to 3.89). LDL did not change (-1.15 mg/dL, 95% CI -16.08 to 13.78). Changes were larger in trials longer than 8 weeks [5]. In the 10-week Korean trial, garcinia extract did not change triglycerides or total cholesterol compared with placebo [4].
Population: Adults in 14 RCTs [5]; 86 overweight adults [4].
Sources: [4], [5]
Caveats: Interventions were short and heterogeneity was significant [5].

High-protein dietModerate

Blood pressure and triglycerides

Mixed results: triglycerides fell more on higher-protein diets in two meta-analyses, while blood pressure fell slightly in one and did not differ in another.

Compared with diets with less protein

Total and LDL cholesterol, C-reactive protein and HbA1c did not change.

The numbers and sources

Effect: Across 74 trials, higher-protein diets lowered systolic (SMD -0.21, 95% CI -0.32 to -0.09) and diastolic blood pressure (SMD -0.18, 95% CI -0.29 to -0.06) and triglycerides (SMD -0.51, 95% CI -0.78 to -0.24). Total and LDL cholesterol, C-reactive protein and HbA1c did not change [6]. In energy-restricted trials, triglycerides fell 0.23 mmol/L more (95% CI 0.12 to 0.33), and blood pressure and total, LDL and HDL cholesterol did not differ [1].
Population: Adults in 74 trials [6] and in 24 weight-loss trials [1].
Sources: [1], [6]
Caveats: Restricting to studies at lower risk of bias reduced the triglyceride effect [6]. In type 2 diabetes, blood pressure changes were not significant [8].

Low-carb dietModerate

Heart risk factors

Mixed results: triglycerides and cholesterol ratio improved in some trials, while a Cochrane review found little to no difference in LDL or blood pressure over 1 to 2 years.

Compared with diets with more carbohydrate

The numbers and sources

Effect: Over 1 to 2 years, diastolic blood pressure and LDL cholesterol showed little to no difference from balanced-carbohydrate diets, with and without type 2 diabetes [1]. Over 2 years, the ratio of total to HDL cholesterol fell 20% on a low-carbohydrate diet and 12% on a low-fat diet [5]. In type 2 diabetes, triglycerides improved substantially at 6 months and less at 12 months. LDL cholesterol worsened at 12 months by an amount judged clinically important but not statistically significant [6].
Population: Adults with overweight or obesity [1][5]; adults with type 2 diabetes [6].
Sources: [1], [5], [6]
Caveats: Mean baseline LDL and diastolic pressure were in the normal range across the Cochrane trials [1]. No trial here measured heart attacks or strokes.

ResveratrolModerate

Inflammation and blood lipids

Mixed results: reviews disagree on whether CRP falls, and most found no change in LDL or triglycerides.

The numbers and sources

Effect: One meta-analysis found no change in CRP (WMD -0.144 mg/L, 95% CI -0.968 to 0.680), total cholesterol, LDL, triglycerides or glucose. HDL fell slightly (WMD -4.18 mg/dL, 95% CI -6.54 to -1.82) [4]. A later meta-analysis found lower TNF-α (WMD -0.44, 95% CI -0.71 to -0.16) and hs-CRP (WMD -0.27, 95% CI -0.5 to -0.02), with no change in IL-6 [6]. In 25 RCTs in metabolic disorders, CRP fell (SMD -0.18, 95% CI -0.33 to -0.03), and IL-6 and TNF-α did not change significantly [7]. In 6 RCTs in type 2 diabetes (533 participants), CRP fell (SMD -1.40, 95% CI -2.60 to -0.21) [8]. Apolipoprotein B (WMD 2.11 mg/dL, 95% CI -1.53 to 5.75) and apolipoprotein A-I did not change in 7 RCTs [9]. An umbrella review rated as high certainty a 0.19 mmol/L drop in total cholesterol in adults with overweight (95% CI 0.06 to 0.32) [5].
Population: 10 RCTs [4]; 17 RCTs with 736 adults [6]; adults with metabolic disorders [7]; adults with type 2 diabetes [8]; 7 RCTs [9]; meta-analyses of RCTs [5].
Sources: [4], [6], [7], [8], [9], [5]
Caveats: The reviews disagree on CRP, and the CRP effect in [8] is several times the size of that in [7]. Heterogeneity in [6] was about 50%. Evidence in [8] was low certainty. CRP is a marker, not a clinical outcome [7].

SaltModerateHow often is not known

Hormone and blood fat changes on low-sodium diets

Shown to raise renin, aldosterone, noradrenaline, total cholesterol and triglycerides slightly when sodium was cut sharply in trials. LDL and HDL cholesterol did not change significantly.

LDL cholesterol changed by 2.46 mg/dL (95% CI -1 to 5.9) and HDL by -0.3 mg/dL (95% CI -1.66 to 1.05).

The numbers and sources

How common: How often is not known: the sources give no rate.
Effect: During sodium reduction, renin rose 1.56 ng/mL/hour (82 trials), aldosterone 104 pg/mL (66 trials) and noradrenaline 62.3 pg/mL (35 trials). Total cholesterol rose 5.19 mg/dL (95% CI 2.1 to 8.3, 27 trials) and triglycerides 7.10 mg/dL (95% CI 3.1 to 11.1, 20 trials). LDL cholesterol changed by 2.46 mg/dL (95% CI -1 to 5.9) and HDL by -0.3 mg/dL (95% CI -1.66 to 1.05) [5].
Population: 917 participants for cholesterol, 712 for triglycerides and 2,904 for renin, in randomized trials of low against high sodium diets [5].
Sources: [5]
Caveats: Many trials were short and cut sodium further than guidelines ask. The review authors note these changes were more consistent than the blood pressure effect in people with normal blood pressure [5].

Beta-glucanLimited

Long-term blood sugar (HbA1c)

One trial found 6 g a day of oat beta-glucan in bread did not change HbA1c over 16 weeks in adults at risk of type 2 diabetes.

Fasting glucose, insulin and LDL cholesterol (-0.11 mmol/L, 95% CI -0.27 to 0.05) did not differ either.

The numbers and sources

Effect: In 194 adults at risk of type 2 diabetes, bread enriched to 6 g of oat beta-glucan a day for 16 weeks did not change HbA1c compared with whole-grain wheat bread (difference -0.01%, 95% CI -0.03 to 0.06). Fasting glucose, insulin and LDL cholesterol (-0.11 mmol/L, 95% CI -0.27 to 0.05) did not differ either [6].
Population: Adults aged about 58 with a mean BMI of 32 in Germany, Norway and Sweden [6].
Sources: [6]
Caveats: One trial, run as an effectiveness trial in real-life conditions, against whole-grain wheat bread, not a fiber-free control [6].

Keto dietLimited

Liver fat and insulin sensitivity

One trial found that at equal 10% weight loss, liver insulin sensitivity rose two to three times more than on Mediterranean or very-low-fat diets.

Compared with diets that did not restrict carbohydrates to the level of ketosis

LDL cholesterol, apolipoprotein B and 24-hour triglycerides did not differ between diets.

The numbers and sources

Effect: Calories were adjusted so every group lost about 10% of body weight. Muscle insulin sensitivity rose about 50% on all three diets. Liver insulin sensitivity rose two to three times more on the very-low-carbohydrate ketogenic diet (p < 0.001), and liver fat, liver fat production, HbA1c and 24-hour glucose and insulin fell most on it. LDL cholesterol, apolipoprotein B and 24-hour triglycerides did not differ between diets [12].
Population: Adults with obesity, prediabetes and fatty liver. The abstract does not give the number randomized [12].
Sources: [12]
Caveats: One small trial. Food was supplied during weight loss, so it measures the diets eaten as written. It does not apply to people without prediabetes and fatty liver.

Type in your own result

How it compares with the reference method

Matched the reference method2

Moderate

Calculated LDL cholesterol, Martin-Hopkins and Sampson-NIH equations

Shown to match measured LDL cholesterol more closely than the Friedewald equation, with 92% agreement in category for Martin-Hopkins and about half the error for Sampson-NIH.

The numbers and sources

Compared with: LDL cholesterol measured after ultracentrifugation
Effect: The Martin-Hopkins method, which adjusts the triglyceride factor to a person's triglyceride and non-HDL cholesterol values, placed 91.7% of samples in the same guideline category as measured LDL cholesterol (95% CI 91.6 to 91.8), against 85.4% for Friedewald. At estimated values below 70 mg/dL with triglycerides of 200 to 399 mg/dL, the measured value was also below 70 in 84.0% of samples, against 40.3% [17]. The Sampson-NIH equation had a root mean square error of 15.2 mg/dL against the reference method, compared with 25.7 for Martin-Hopkins and 32 for Friedewald, and a mean absolute difference of 24.9 mg/dL in people with high triglycerides, compared with 44.8 and 56.4. Its authors report accuracy at triglycerides up to 800 mg/dL similar to Friedewald below 400 mg/dL [18].
Population: 1,350,908 clinical lipid profiles, split into derivation and validation sets [17]. 8,656 patients, with further testing in outside data sets [18].
Sources: [17], [18]
Caveats: Each equation was tested by the group that developed it, and each study used a different reference procedure [17][18]. A laboratory report does not always say which equation was used.

Moderate

Fasting against not fasting

Shown to read slightly lower after eating: LDL cholesterol was at most 0.2 mmol/L (8 mg/dL) lower than fasting, 3 to 5 hours after a meal.

The numbers and sources

Compared with: A fasting blood sample
Effect: In 33,391 Danish adults, LDL cholesterol was reduced for up to 3 to 5 hours after the last meal, with a maximum change from fasting of -0.2 mmol/L [20]. A joint European consensus statement put the maximal mean change 1 to 6 hours after habitual meals at -0.2 mmol/L (8 mg/dL), judged it not clinically significant, and reported that fasting and non-fasting results are comparable in predicting cardiovascular disease [7].
Population: 33,391 adults aged 20 to 95 in the Copenhagen General Population Study [20].
Sources: [20], [7]
Caveats: A cross-sectional comparison of people sampled at different times after eating, not the same people tested twice [20]. The consensus suggests considering a fasting sample when non-fasting triglycerides exceed 440 mg/dL [7].

Mixed results3

Moderate

Calculated LDL cholesterol, Friedewald equation

Mixed results: the Friedewald equation agreed with measured LDL cholesterol in 85% of samples, and in as few as 40% at low LDL with high triglycerides.

The numbers and sources

Compared with: LDL cholesterol measured after ultracentrifugation
Effect: The Friedewald equation subtracts HDL cholesterol and one fifth of triglycerides from total cholesterol [2]. In 1.35 million US lipid profiles with triglycerides below 400 mg/dL, it placed 85.4% of samples in the same guideline category as measured LDL cholesterol. When Friedewald LDL cholesterol was below 70 mg/dL, the measured value was also below 70 in 79.9% of samples with triglycerides of 100 to 149 mg/dL, 61.3% at 150 to 199 mg/dL and 40.3% at 200 to 399 mg/dL [17]. Against the reference method in 8,656 patients, its root mean square error was 32 mg/dL, and in people with triglycerides of 400 mg/dL or above its mean absolute difference was 56.4 mg/dL [18].
Population: 1,350,908 children, adolescents and adults with clinical lipid profiles from 2009 to 2011 [17]. 8,656 patients seen at the National Institutes of Health Clinical Center, 18,715 results [18].
Sources: [2], [17], [18]
Caveats: The equation assumes a fasting sample [2]. Both comparison studies were run by the groups that developed the newer equations [17][18].

Limited

Directly measured LDL cholesterol

Mixed results: one study found 5 of 8 direct LDL methods met US accuracy goals in people without disease, and none met them in people with disease.

The numbers and sources

Compared with: Ultracentrifugation reference measurement procedure
Effect: Bias of 8 direct LDL cholesterol methods ranged from -6.8% to 1.1% in people without disease and from -11.8% to 4.1% in people with disease. Total error ranged from -13.3% to 13.5% and from -26.6% to 31.9%. Five of 8 methods met the National Cholesterol Education Program total error goals in people without disease. All failed in people with disease, which the authors attribute to a lack of specificity toward abnormal lipoproteins [19].
Population: Sera from 37 people without disease and 138 with disease, mainly dyslipidemia and cardiovascular disease [19].
Sources: [19]
Caveats: Published in 2010 on one analyzer, so the methods may since have changed. Small sample [19].

Limited

Week to week variation in one person

One small study found LDL cholesterol varied about 9% from week to week within the same healthy person, whether measured or calculated.

The numbers and sources

Compared with: The same person's fasting results on 10 weekly draws
Effect: Within-person variation was 8.7% for directly measured LDL cholesterol, 9.3% for the Friedewald equation and 9.0% for the Martin-Hopkins equation. Variation between people was 14.7%, 18.5% and 18.6% [21].
Population: 26 healthy adults (15 women) sampled weekly for 10 weeks [21].
Sources: [21]
Caveats: One laboratory and 26 people. The study states no threshold for agreement, so the result is given as numbers only [21].

What studies tie it to

Linked in research2

Strong

Heart attack, stroke and other artery disease

Linked to more atherosclerotic cardiovascular disease across over 200 cohort, genetic and trial studies, with risk rising with the level and the years of exposure.

The numbers and sources

Effect: A European Atherosclerosis Society consensus panel reviewed separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies and randomized trials. It reported a consistent, dose-dependent, log-linear association between LDL cholesterol and atherosclerotic cardiovascular disease that grows with duration of exposure, and concluded that LDL causes the disease [9]. In a pooled analysis of prospective studies, directly measured LDL cholesterol had a hazard ratio for coronary heart disease of 1.38 per 33 mg/dL higher (95% CI 1.09 to 1.73) [10]. In Mendelian randomization analyses, each 1 mmol/L (38.7 mg/dL) lower lifelong LDL cholesterol went with a 54.5% lower risk of coronary heart disease (95% CI 48.8 to 59.5), about 3 times the reduction per unit seen with a statin started later in life [11].
Population: More than 2 million participants with over 150,000 cardiovascular events [9]. 302,430 people without vascular disease in 68 prospective studies, a subset of whom had LDL cholesterol measured directly [10]. 312,321 participants in genetic studies of 9 variants in 6 genes [11].
Sources: [9], [10], [11]
Caveats: The cohort findings are observational. The consensus states that the benefit of lowering holds when the fall in LDL cholesterol is matched by a fall in LDL particle number and the treatment has no offsetting harms [9].

Strong

Cardiovascular events in trials that lowered LDL cholesterol

Shown in trials: each 1 mmol/L (39 mg/dL) lowered cut major vascular events about 22% with statins, and similarly with other drugs acting through the LDL receptor.

The numbers and sources

Effect: In 26 statin trials, each 1.0 mmol/L reduction in LDL cholesterol lowered major vascular events with a rate ratio of 0.78 (95% CI 0.76 to 0.80), including in people whose LDL cholesterol was already below 2 mmol/L [12]. Across 49 trials of 9 kinds of LDL-lowering treatment, the relative risk per 1 mmol/L (38.7 mg/dL) was 0.77 for statins (95% CI 0.71 to 0.84) and 0.75 for diet, bile acid sequestrants, ileal bypass and ezetimibe (95% CI 0.66 to 0.86). CETP inhibitors produced less risk reduction than their LDL lowering predicted (observed 1.01 against an expected 0.90) [13]. In populations starting at a median of 70 mg/dL or less, the relative risk per 1 mmol/L was 0.79 (95% CI 0.71 to 0.87) for statins and non-statins combined [14].
Population: About 170,000 participants in 26 trials, median follow-up about 5 years [12]. 312,175 participants in 49 trials [13]. A low-LDL subgroup of the statin trials plus 50,627 patients in 3 trials of non-statin drugs added to statins [14].
Sources: [12], [13], [14]
Caveats: Effects are expressed per unit of LDL cholesterol lowered, over about 5 years of treatment. The same fall in LDL cholesterol did not bring the same benefit with every drug class [13].

Mixed results2

Moderate

Death from any cause

Mixed results: one Danish cohort found more deaths at both low and high LDL cholesterol, while statin trials found 10% fewer deaths per 1 mmol/L lowered.

The numbers and sources

Effect: In 108,243 Danish adults, the association with death from any cause was U-shaped. Compared with 132 to 154 mg/dL, the adjusted hazard ratio was 1.25 (95% CI 1.15 to 1.36) below 70 mg/dL and 1.15 (1.05 to 1.27) above 189 mg/dL. The level with the lowest risk was 140 mg/dL overall and 89 mg/dL in people on lipid-lowering treatment. The pattern held for cancer and other deaths and not for cardiovascular deaths, and any increase in LDL cholesterol went with more heart attacks [15]. Across 26 statin trials, death from any cause fell 10% per 1.0 mmol/L reduction (RR 0.90, 95% CI 0.87 to 0.93), with no significant effect on deaths from cancer or other non-vascular causes [12].
Population: 108,243 people aged 20 to 100 in the Copenhagen General Population Study, median follow-up 9.4 years, 11,376 deaths [15]. About 170,000 participants in 26 statin trials [12].
Sources: [15], [12]
Caveats: The cohort finding is observational, and illness that lowers LDL cholesterol before death (reverse causation) cannot be ruled out. The trials tested lowering with a statin in people selected for trials, over about 5 years.

Moderate

Bleeding stroke at low levels

Mixed results: one cohort linked LDL cholesterol below 70 mg/dL to more bleeding strokes, while pooled trials lowering it to very low levels found no increase.

The numbers and sources

Effect: In a cohort with repeated LDL cholesterol measurements, people averaging below 70 mg/dL had more intracerebral hemorrhage than those at 70 to 99 mg/dL: adjusted HR 1.65 (95% CI 1.32 to 2.05) at 50 to 69 mg/dL and 2.69 (2.03 to 3.57) below 50 mg/dL. Risk at 100 mg/dL or above was similar to that at 70 to 99 [16]. In a meta-analysis of trials in populations starting at a median of 70 mg/dL or less and reaching a median as low as 21 mg/dL, LDL lowering was not associated with an increased risk of hemorrhagic stroke [14]. Statin trials found no significant effect on deaths due to stroke (RR 0.96, 95% CI 0.84 to 1.09) [12].
Population: 96,043 adults, mean age 51, free of stroke, heart attack and cancer at baseline, 753 hemorrhages over 9 years [16]. 50,627 patients in 3 trials of non-statin drugs plus a statin trial subgroup [14].
Sources: [16], [14], [12]
Caveats: The cohort is observational and cannot show that low LDL cholesterol caused the hemorrhages. The trials ran for a few years, so they say little about decades at very low levels.

Sources

US Food and Drug Administration. 21 CFR 862.1475, Lipoprotein test system. Electronic Code of Federal Regulations, with the FDA product classification entry for low density lipoprotein test systems (product code MRR). https://www.ecfr.gov/current/title-21/section-862.1475
Soffer DE, Marston NA, Maki KC, et al. Role of apolipoprotein B in the clinical management of cardiovascular risk in adults: An Expert Clinical Consensus from the National Lipid Association. Journal of Clinical Lipidology. 2024. https://doi.org/10.1016/j.jacl.2024.08.013
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. https://doi.org/10.1001/jama.285.19.2486
Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019. https://doi.org/10.1161/CIR.0000000000000625
Blumenthal RS, Morris PB, Gaudino M, et al. 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2026. https://doi.org/10.1161/CIR.0000000000001423
Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. European Heart Journal. 2020. https://doi.org/10.1093/eurheartj/ehz455
Nordestgaard BG, Langsted A, Mora S, et al. Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications including flagging at desirable concentration cut-points. A joint consensus statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine. European Heart Journal. 2016. https://doi.org/10.1093/eurheartj/ehw152
Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents. Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents: Summary Report. Pediatrics. 2011. https://doi.org/10.1542/peds.2009-2107C
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. https://doi.org/10.1093/eurheartj/ehx144
Emerging Risk Factors Collaboration. Major Lipids, Apolipoproteins, and Risk of Vascular Disease. JAMA. 2009. https://doi.org/10.1001/jama.2009.1619
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. Journal of the American College of Cardiology. 2012. https://doi.org/10.1016/j.jacc.2012.09.017
Cholesterol Treatment Trialists' (CTT) Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170 000 participants in 26 randomised trials. The Lancet. 2010. https://doi.org/10.1016/S0140-6736(10)61350-5
Silverman MG, Ference BA, Im K, et al. Association Between Lowering LDL-C and Cardiovascular Risk Reduction Among Different Therapeutic Interventions. JAMA. 2016. https://doi.org/10.1001/jama.2016.13985
Sabatine MS, Wiviott SD, Im K, et al. Efficacy and Safety of Further Lowering of Low-Density Lipoprotein Cholesterol in Patients Starting With Very Low Levels. JAMA Cardiology. 2018. https://doi.org/10.1001/jamacardio.2018.2258
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. https://doi.org/10.1136/bmj.m4266
Ma C, Gurol ME, Huang Z, et al. Low-density lipoprotein cholesterol and risk of intracerebral hemorrhage. Neurology. 2019. https://doi.org/10.1212/WNL.0000000000007853
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. https://doi.org/10.1001/jama.2013.280532
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. https://doi.org/10.1001/jamacardio.2020.0013
Miller WG, Myers GL, Sakurabayashi I, et al. Seven Direct Methods for Measuring HDL and LDL Cholesterol Compared with Ultracentrifugation Reference Measurement Procedures. Clinical Chemistry. 2010. https://doi.org/10.1373/clinchem.2009.142810
Langsted A, Freiberg JJ, Nordestgaard BG. Fasting and Nonfasting Lipid Levels: Influence of Normal Food Intake on Lipids, Lipoproteins, Apolipoproteins, and Cardiovascular Risk Prediction. Circulation. 2008. https://doi.org/10.1161/CIRCULATIONAHA.108.804146
Alkan Baylan F, Özcan M, Ercan Ş, et al. Biological variation estimates of direct and indirect LDL cholesterol by Friedewald and Martin-Hopkins formulas in healthy individuals. Scandinavian Journal of Clinical and Laboratory Investigation. 2026. https://doi.org/10.1080/00365513.2025.2605638

Everything in the library