Non-HDL cholesterol (non-HDL-C)
Non-HDL cholesterol is total cholesterol minus HDL cholesterol, so it needs no extra test and no fasting. In 68 pooled cohorts, each 43 mg/dL higher went with about 50% more coronary heart disease, and trials that lowered it cut vascular events. Published cut points run from 85 to 220 mg/dL by source, age and a person's risk.
- Status
- A calculated value printed on many lipid panel reports, not a separate test. It is total cholesterol minus HDL cholesterol [1], both of which come from the standard lipid panel, ordered by a clinician and also sold direct to consumers by some US laboratories. FDA classifies total cholesterol test systems and lipoprotein test systems as class I devices exempt from premarket notification [2].
- Measures
- The cholesterol carried by every lipoprotein except HDL, calculated as total cholesterol minus HDL cholesterol [1].
- Also called
- non-HDL-C, non-HDL cholesterol, non-HDL, non HDL cholesterol, non-high-density lipoprotein cholesterol, non-HDL chol, non-HDL chol calc, cholesterol non-HDL
- Tested for
- heart attack risk, stroke risk, cholesterol check, risk when triglycerides are high, a cholesterol check without fasting, deciding on cholesterol-lowering treatment, checking response to cholesterol-lowering drugs
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 research3
- StrongLinked to more cardiovascular disease at higher levels, about 50% more coronary heart disease for each 43 mg/dL higher across 68 pooled cohorts.
- StrongShown in trials: each 1 mmol/L (39 mg/dL) of non-HDL cholesterol lowered went with about 21% fewer major vascular events across 49 trials.
- ModerateLinked to more new type 2 diabetes at higher levels, 16% more in the higher than the lower non-HDL cholesterol group across 8 cohort studies.
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.
American Heart Association and American College of Cardiology cholesterol guideline, 2018, risk-enhancing factor
Adults aged 40 to 75 without diabetes, being assessed for risk of a first cardiovascular event · [3]
| Range | What the source calls it |
|---|---|
| below 190 mg/dL | No name given |
| 190 to 219 mg/dL | "primary hypercholesterolemia" |
| 220 or above mg/dL | No name given |
The guideline lists non-HDL cholesterol of 190 to 219 mg/dL, paired with LDL cholesterol of 160 to 189 mg/dL, as a risk-enhancing factor, with a note that 3 determinations are preferred. Its table gives no non-HDL cholesterol figure above that band. The guideline converts cholesterol to mmol/L by dividing mg/dL by 38.6 [3], and a European guideline uses 1 mmol/L to 38.67 mg/dL [4]. A 2026 guideline from the same US 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 · [4]
| Range | What the source calls it |
|---|---|
| below 85 mg/dL | "secondary goal" |
| 85 or above mg/dL | No name given |
A secondary treatment goal, not a population reference interval. The guideline's primary goals are for LDL cholesterol, and it sets each non-HDL cholesterol goal 0.8 mmol/L (30 mg/dL) above the matching LDL cholesterol goal. Printed as below 2.2 mmol/L [4]. A 2001 US panel used the same 30 mg/dL offset for people with triglycerides of 200 mg/dL or above, giving non-HDL cholesterol goals of below 130, below 160 and below 190 mg/dL across its three risk categories [1].
European Society of Cardiology and European Atherosclerosis Society guideline, 2019, high risk
Adults the guideline places at high cardiovascular risk · [4]
| Range | What the source calls it |
|---|---|
| below 100 mg/dL | "secondary goal" |
| 100 or above mg/dL | No name given |
A secondary treatment goal. Printed as below 2.6 mmol/L [4].
European Society of Cardiology and European Atherosclerosis Society guideline, 2019, moderate risk
Adults the guideline places at moderate cardiovascular risk · [4]
| Range | What the source calls it |
|---|---|
| below 130 mg/dL | "secondary goal" |
| 130 or above mg/dL | No name given |
A secondary treatment goal. Printed as below 3.4 mmol/L. The guideline gives no non-HDL cholesterol goal for people at low risk [4].
European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine consensus on laboratory reporting, 2016, fasting sample
Adults with a fasting sample, as a value for laboratories to flag on reports · [6]
| Range | What the source calls it |
|---|---|
| below 145 mg/dL | No name given |
| 145 or above mg/dL | "abnormal" |
The statement asks laboratories to flag "abnormal" results against desirable concentration cut points in place of a population reference interval. This flag value is 3.8 mmol/L, converted by multiplying by 38.6 and rounding to the nearest 5 mg/dL. The statement notes that its flag values are in some cases higher than the goals set for people at high and very high risk [6].
European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine consensus on laboratory reporting, 2016, non-fasting sample
Adults with a non-fasting sample, as a value for laboratories to flag on reports · [6]
| Range | What the source calls it |
|---|---|
| below 150 mg/dL | No name given |
| 150 or above mg/dL | "abnormal" |
A flag value of 3.9 mmol/L. The statement's table and abstract print it as 150 mg/dL, and one sentence of its text prints 155 mg/dL. The authors estimate that 50% of adults in a typical Western or Northern European country would be flagged [6].
National Heart, Lung, and Blood Institute expert panel, 2011, children and adolescents
Children and adolescents · [7]
| Range | What the source calls it |
|---|---|
| below 120 mg/dL | "acceptable" |
| 120 to 144 mg/dL | "borderline-high" |
| 145 or above mg/dL | "high" |
The panel took these values from the Bogalusa Heart Study and states they are equivalent to the pediatric cut points for LDL cholesterol. The borderline-high and high cut points represent approximately the 75th and 95th percentiles [7].
National Heart, Lung, and Blood Institute expert panel, 2011, young adults
Young adults, from data on people aged 20 to 24 · [7]
| Range | What the source calls it |
|---|---|
| below 150 mg/dL | "acceptable" |
| 150 to 189 mg/dL | "borderline-high" |
| 190 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 [7].
What has been shown to move it
Shown to lower it5
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.
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.
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].
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].
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.
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%.
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].
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]
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.
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].
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].
How it compares with the reference method
Matched the reference method1
Fasting against not fasting
Shown to match fasting results closely: non-HDL cholesterol changed by at most 0.2 mmol/L (8 mg/dL) after habitual meals in Danish adults.
The numbers and sources
- Compared with
- A fasting blood sample
- Effect
- In 33,391 Danish adults, non-HDL cholesterol did not change in response to normal food intake, while total cholesterol fell by up to 0.2 mmol/L and triglycerides rose by up to 0.3 mmol/L [20]. A joint European consensus statement, updating that analysis to 92,285 people, put the maximal mean change 1 to 6 hours after habitual meals at -0.2 mmol/L (8 mg/dL) for calculated non-HDL cholesterol and judged it not clinically significant [6]. In 1,093 hospital outpatients tested fasting and again after breakfast 3 to 4 days later, 88.8% had a change in non-HDL cholesterol within the biological variation expected in the fasting state, against 74.6% for LDL cholesterol and 78.8% for triglycerides [21].
- Population
- 33,391 adults aged 20 to 95 in the Copenhagen General Population Study [20]. 1,093 adult outpatients at a community hospital in 2016 [21].
- Sources
- [20], [6], [21]
- Caveats
- The Danish analyses compare people sampled at different times after eating, not the same people tested twice [20]. The consensus sets its non-HDL cholesterol flag 5 mg/dL higher for non-fasting samples [6].
Mixed results1
Calculated non-HDL cholesterol against reference measurements
One study found non-HDL cholesterol from routine assays placed people in the same risk category as reference methods more often than measured or calculated LDL cholesterol did.
The numbers and sources
- Compared with
- Non-HDL cholesterol calculated from reference measurement procedures at the US Centers for Disease Control and Prevention
- Effect
- With 8 direct HDL cholesterol methods, non-HDL cholesterol in people with triglycerides below 200 mg/dL had a coefficient of determination of 0.97 or above against the reference. It placed 0% to 11% of people in a lower risk category and 1% to 8% in a higher one, depending on the method. At triglycerides of 200 to 399 mg/dL, 0% to 7% were placed lower and 0% to 18% higher, a closer match than either direct or calculated LDL cholesterol gave [22]. A later review states that errors in measuring HDL cholesterol carry into calculated non-HDL cholesterol, with more impact at low concentrations, and that non-HDL cholesterol assays have been harmonized without being standardized [23].
- Population
- 175 people, 138 of them with cardiovascular disease or conditions that may affect LDL cholesterol measurement [22].
- Sources
- [22], [23]
- Caveats
- A 2011 study of 175 people, so the assays may since have changed. It states no threshold for agreement, so the result is given as numbers only [22]. The review is an essay arguing that ApoB is measured more accurately than LDL or non-HDL cholesterol [23].
What studies tie it to
Linked in research3
Heart attack, stroke and other cardiovascular disease in cohort studies
Linked to more cardiovascular disease at higher levels, about 50% more coronary heart disease for each 43 mg/dL higher across 68 pooled cohorts.
The numbers and sources
- Effect
- In 68 prospective studies, coronary heart disease rates per 1,000 person-years were 2.3 in the bottom third and 6.7 in the top third of non-HDL cholesterol. The adjusted hazard ratio per 43 mg/dL higher was 1.50 (95% CI 1.39 to 1.61) for coronary heart disease and 1.12 (1.04 to 1.20) for ischemic stroke [8]. In a consortium of 38 cohorts, 30-year cardiovascular event rates rose from 7.7% at non-HDL cholesterol below 2.6 mmol/L (about 100 mg/dL) to 33.7% at 5.7 mmol/L (about 220 mg/dL) or above in women, and from 12.8% to 43.6% in men [9]. A meta-analysis of 9 prospective studies found a relative risk of coronary heart disease of 1.79 (95% CI 1.68 to 1.91) for the highest against the lowest category [10]. Across 12 reports, the standardized relative risk of ischemic cardiovascular events was 1.34 (95% CI 1.24 to 1.44) for non-HDL cholesterol, between that of LDL cholesterol (1.25, 1.18 to 1.33) and ApoB (1.43, 1.35 to 1.51) [11].
- Population
- 302,430 people without vascular disease in 68 prospective studies [8]. 398,846 people in 38 cohorts, median follow-up 13.5 years, 54,542 cardiovascular events [9]. 448,732 people in 9 prospective studies [10]. 233,455 people with 22,950 events in 12 reports [11].
- Sources
- [8], [9], [10], [11]
- Caveats
- Observational. In the pooled cohorts the hazard ratios were at least as strong in participants who did not fast as in those who did [8]. Each study in the category comparison defined its own highest and lowest groups [10].
Cardiovascular events in trials that lowered non-HDL cholesterol
Shown in trials: each 1 mmol/L (39 mg/dL) of non-HDL cholesterol lowered went with about 21% fewer major vascular events across 49 trials.
The numbers and sources
- Effect
- In a meta-regression of 24 trials of non-statin drugs and 25 statin trials, the risk ratio for major vascular events was 0.79 (95% CI 0.76 to 0.82) per 1 mmol/L reduction in non-HDL cholesterol [12]. In an earlier analysis of 30 trials, each 1% decrease in non-HDL cholesterol with a statin went with a 4.5-year relative risk of coronary heart disease of 0.99 (95% Bayesian interval 0.98 to 1.00), and the fibrate trials did not differ from the statin trials [13]. Across 7 placebo-controlled statin trials, coronary risk fell 20.0% (95% CI 15.2 to 24.7) per standard deviation decrease in non-HDL cholesterol, 20.1% for LDL cholesterol and 24.4% for ApoB [14]. Among patients on statins in 8 trials, each standard deviation higher on-treatment non-HDL cholesterol went with a hazard ratio of 1.16 (95% CI 1.12 to 1.19) for major cardiovascular events, against 1.13 (1.10 to 1.17) for LDL cholesterol, a significant difference [15].
- Population
- 374,358 patients in 49 trials, with 46,180 major cardiovascular events [12]. 14 statin trials (100,827 people), 7 fibrate trials (21,647), 6 niacin trials (4,445) and 3 others [13]. 7 placebo-controlled statin trials [14]. 62,154 patients in 8 statin trials, of whom 38,153 were allocated to a statin [15].
- Sources
- [12], [13], [14], [15]
- Caveats
- The meta-regressions compare trials with each other, not people within a trial, and cover drugs that lower non-HDL cholesterol in different ways [12][13]. The niacin trials did not follow the pattern of the statin trials, with inconsistent results in five small trials of niacin combined with other drugs [13].
Type 2 diabetes
Linked to more new type 2 diabetes at higher levels, 16% more in the higher than the lower non-HDL cholesterol group across 8 cohort studies.
The numbers and sources
- Effect
- In a meta-analysis of cohort studies in the general population, the pooled effect size for type 2 diabetes was 1.16 (95% CI 1.079 to 1.251) for higher against lower non-HDL cholesterol. The result did not change with region, share of men, sample size or adjustment for body mass index, hypertension, waist circumference and family history of diabetes [19].
- Population
- 251,672 participants in 8 cohort studies [19].
- Sources
- [19]
- Caveats
- Observational, and the authors describe earlier studies as inconsistent and call for large prospective cohorts to confirm the finding. Each study defined its own higher and lower groups [19].
Mixed results1
Death from any cause
Mixed results: higher non-HDL cholesterol went with more deaths in people with heart disease or on statins, while pooled general-population studies found no clear link with cardiovascular death.
The numbers and sources
- Effect
- In statin-treated Danish adults, non-HDL cholesterol above the median with LDL cholesterol below it had hazard ratios of 1.18 for death from any cause (95% CI 1.02 to 1.36) and 1.78 for heart attack (1.35 to 2.34), compared with both below the median. ApoB above the median with non-HDL cholesterol below it had a hazard ratio for death of 1.21 (1.03 to 1.41) [16]. In a meta-analysis of people with coronary heart disease, high baseline non-HDL cholesterol went with a risk ratio for death of 1.24 (95% CI 1.05 to 1.46) [17]. In a meta-analysis of observational studies, elevated non-HDL cholesterol was not associated with cardiovascular death in the general population (RR 1.64, 95% CI 0.96 to 2.80) or in people with type 2 diabetes (RR 1.08, 0.57 to 2.07), while it was associated with cardiovascular disease in both (RR 1.59 and 1.99) [18].
- Population
- 13,015 statin-treated adults in the Copenhagen General Population Study, median follow-up 8 years [16]. 11,057 people with coronary heart disease in 6 studies followed 18 to 148 months [17]. 156,381 people in 13 studies [18].
- Sources
- [16], [17], [18]
- Caveats
- Observational. High and low were defined by each cohort's own median or categories [16][17]. The confidence intervals for cardiovascular death are wide [18].
Sources
- 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
- US Food and Drug Administration. 21 CFR 862.1175, Cholesterol (total) test system, and 21 CFR 862.1475, Lipoprotein test system. Electronic Code of Federal Regulations. https://www.ecfr.gov/current/title-21/section-862.1175
- 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
- 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
- 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
- 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
- Emerging Risk Factors Collaboration. Major Lipids, Apolipoproteins, and Risk of Vascular Disease. JAMA. 2009. https://doi.org/10.1001/jama.2009.1619
- Brunner FJ, Waldeyer C, Ojeda F, et al. Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium. The Lancet. 2019. https://doi.org/10.1016/S0140-6736(19)32519-X
- Liu H, Deng X, Peng Y, et al. Meta-analysis of serum non-high-density lipoprotein cholesterol and risk of coronary heart disease in the general population. Clinica Chimica Acta. 2017. https://doi.org/10.1016/j.cca.2017.05.006
- Sniderman AD, Williams K, Contois JH, et al. A Meta-Analysis of Low-Density Lipoprotein Cholesterol, Non-High-Density Lipoprotein Cholesterol, and Apolipoprotein B as Markers of Cardiovascular Risk. Circulation: Cardiovascular Quality and Outcomes. 2011. https://doi.org/10.1161/CIRCOUTCOMES.110.959247
- Marston NA, Giugliano RP, Im K, et al. Association Between Triglyceride Lowering and Reduction of Cardiovascular Risk Across Multiple Lipid-Lowering Therapeutic Classes: A Systematic Review and Meta-Regression Analysis of Randomized Controlled Trials. Circulation. 2019. https://doi.org/10.1161/CIRCULATIONAHA.119.041998
- Robinson JG, Wang S, Smith BJ, Jacobson TA. Meta-Analysis of the Relationship Between Non-High-Density Lipoprotein Cholesterol Reduction and Coronary Heart Disease Risk. Journal of the American College of Cardiology. 2009. https://doi.org/10.1016/j.jacc.2008.10.024
- Thanassoulis G, Williams K, Ye K, et al. Relations of Change in Plasma Levels of LDL-C, Non-HDL-C and apoB With Risk Reduction From Statin Therapy: A Meta-Analysis of Randomized Trials. Journal of the American Heart Association. 2014. https://doi.org/10.1161/JAHA.113.000759
- Boekholdt SM, Arsenault BJ, Mora S, et al. Association of LDL Cholesterol, Non-HDL Cholesterol, and Apolipoprotein B Levels With Risk of Cardiovascular Events Among Patients Treated With Statins: A Meta-analysis. JAMA. 2012. https://doi.org/10.1001/jama.2012.366
- 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. https://doi.org/10.1016/j.jacc.2021.01.027
- Liao P, Zeng R, Zhao X, Guo L, Zhang M. Prognostic value of non-high-density lipoprotein cholesterol for mortality in patients with coronary heart disease: A systematic review and meta-analysis. International Journal of Cardiology. 2017. https://doi.org/10.1016/j.ijcard.2016.10.106
- Cao Y, Yan L, Guo N, et al. Non-high-density lipoprotein cholesterol and risk of cardiovascular disease in the general population and patients with type 2 diabetes: A systematic review and meta-analysis. Diabetes Research and Clinical Practice. 2019. https://doi.org/10.1016/j.diabres.2018.11.002
- Han M, Shen Y, Guo X, et al. Association between non-high-density lipoprotein cholesterol and type 2 diabetes: a systematic review and meta-analysis of cohort studies. Endocrine Journal. 2025. https://doi.org/10.1507/endocrj.EJ24-0189
- 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
- Cartier LJ, Collins C, Lagacé M, Douville P. Comparison of fasting and non-fasting lipid profiles in a large cohort of patients presenting at a community hospital. Clinical Biochemistry. 2018. https://doi.org/10.1016/j.clinbiochem.2017.11.007
- van Deventer HE, Miller WG, Myers GL, et al. Non-HDL Cholesterol Shows Improved Accuracy for Cardiovascular Risk Score Classification Compared to Direct or Calculated LDL Cholesterol in a Dyslipidemic Population. Clinical Chemistry. 2011. https://doi.org/10.1373/clinchem.2010.154773
- Contois JH, Langlois MR, Cobbaert C, Sniderman AD. Standardization of Apolipoprotein B, LDL-Cholesterol, and Non-HDL-Cholesterol. Journal of the American Heart Association. 2023. https://doi.org/10.1161/JAHA.123.030405