Bedside Snapshot
- Normal (Adult)
- Men ≥40 mg/dL (≥1.0 mmol/L); women ≥50 mg/dL (≥1.3 mmol/L). Fasting not required
- Critical Values
- No universal critical value: interpret by trend and clinical context
- High Suggests
- Female sex, exercise, weight loss
- Heavy alcohol use
- Genetic variants (CETP, SR-BI)
- Extreme (≥116 mg/dL men, ≥135 mg/dL women): higher all-cause mortality
- Low Suggests
- Sepsis, infection or ACS (acute-phase drop)
- High triglycerides, obesity, diabetes, metabolic syndrome
- Smoking, inactivity, testosterone therapy
- Rare genetic HDL deficiency
- Act Now If
- No HDL-C value needs emergency treatment. A very low HDL-C in an acutely ill patient marks severity: treat the cause. Triglycerides >880 mg/dL on the same panel: pancreatitis risk, refer
- Watch Out For
- A panel drawn during infection, sepsis or ACS understates HDL-C; repeat after recovery: at least 3 weeks after infection (NHLBI pediatric guidance), longer after sepsis, critical illness or MI
Reference & Critical Ranges
Lab-specific ranges: Your lab sets the range, not this page. Intervals vary by laboratory, analyzer and population. Use the range printed on your report. The values below are typical.
Reference ranges
| Population | Conventional | SI | Notes |
|---|---|---|---|
| Adult men | ≥40 mg/dL | ≥1.0 mmol/L | Low is <40 mg/dL. The European Atherosclerosis Society (EAS) and European Federation of Clinical Chemistry (EFLM) suggest labs flag ≤40 mg/dL in both sexes |
| Adult women | ≥50 mg/dL | ≥1.3 mmol/L | Low is <50 mg/dL, the metabolic syndrome cut point for women. Some labs flag only <40 mg/dL |
| Pregnancy | No pregnancy-specific range | — | HDL-C typically rises during pregnancy (peaks around mid-gestation), so a low value is not explained by pregnancy. Pregnancy is a recognized cause of secondary dyslipidemia; assess long-term risk outside pregnancy |
| Older adult | Same as adult | — | No separate range |
| Children and adolescents | Acceptable >45 mg/dL; borderline 40–45; low <40 | >1.2; 1.0–1.2; <1.0 mmol/L | National Heart, Lung, and Blood Institute (NHLBI) pediatric cut points; low is about the 10th percentile |
| Young adults (20–24 years) | Acceptable >45 mg/dL; borderline 40–44; low <40 | >1.2; 1.0–1.1; <1.0 mmol/L | NHLBI young-adult cut points for pediatric clinicians |
Severity & critical values
| Level | Conventional | SI | What it means / typical findings |
|---|---|---|---|
| Low | <40 mg/dL (men); <50 mg/dL (women) | <1.0 mmol/L; <1.3 mmol/L | Marker of higher atherosclerotic cardiovascular disease (ASCVD) risk, usually with high triglycerides and insulin resistance. Also falls in acute illness |
| Normal | ≥40 mg/dL (men); ≥50 mg/dL (women) | ≥1.0 mmol/L; ≥1.3 mmol/L | — |
| High | Up to about 90 mg/dL | Up to about 2.3 mmol/L | In population studies, coronary risk falls as HDL-C rises to about this level. Madsen 2017 found lowest all-cause mortality near 73 mg/dL in men and 93 mg/dL in women |
| Very high | >90 mg/dL | >2.3 mmol/L | No further fall in coronary risk. Ask about alcohol intake and family history |
| Extreme | ≥116 mg/dL (men); ≥135 mg/dL (women) | ≥3.0 mmol/L; ≥3.5 mmol/L | Higher all-cause mortality in large population cohorts (U-shaped curve); cause not established |
| Critical | No universal critical value | — | Interpret by trend and clinical context |
Critical values: There is no universal critical value, so read the trend and the clinical picture. A new, very low HDL-C in an acutely ill patient is the illness talking (sepsis, acute coronary syndrome). It is not a lipid disorder.
Conversion: mg/dL × 0.0259 = mmol/L (mmol/L × 38.67 = mg/dL)
Non-HDL cholesterol
Non-HDL-C = Total cholesterol − HDL-C
In children and adolescents, non-HDL-C below 120 mg/dL is acceptable. Adult goals depend on risk category, so see Non-HDL Cholesterol.
Friedewald LDL cholesterol (mg/dL)
LDL-C = Total cholesterol − HDL-C − (Triglycerides ÷ 5)
The Friedewald formula is valid only when triglycerides are <400 mg/dL (<4.5 mmol/L). Above that, labs measure LDL-C directly. Any error in HDL-C carries into both calculations.
Causes of Abnormal Results
Low (HDL-C <40 mg/dL in men, <50 mg/dL in women)
| Mechanism | Common causes | Bedside clue |
|---|---|---|
| Acute-phase response | Sepsis, acute bacterial or viral infection, acute coronary syndrome (ACS) | Acutely ill patient; a fall from a previously normal value. Low HDL-C in sepsis is associated with death |
| Excess triglyceride-rich lipoproteins / insulin resistance | Obesity, metabolic syndrome, type 2 diabetes, polycystic ovary syndrome (PCOS) | High triglycerides on the same panel; central obesity; high glucose or HbA1c |
| Liver disease | Cholestatic and chronic liver disease (reduced hepatic synthesis of HDL components) | Abnormal liver tests; jaundice or pruritus |
| Lifestyle | Cigarette smoking or smoke exposure; physical inactivity | Social history |
| Sex hormones | Testosterone therapy (for example gender-affirming therapy); menopause (modest fall in HDL-C) | Medication history; HDL-C falls on therapy or after menopause |
| Other drugs (secondary dyslipidemia; effect on HDL-C varies) | Beta-blockers, isotretinoin, corticosteroids, some oral contraceptives, select antiretrovirals and chemotherapy agents | Medication list; lipids changed after starting the drug |
| Kidney disease | Chronic kidney disease (CKD); nephrotic syndrome (secondary dyslipidemia) | Low estimated glomerular filtration rate (eGFR), proteinuria, edema |
| Rare genetic disorders | Familial hypoalphalipoproteinemia, apolipoprotein A-I (apoA-I) mutations, Tangier disease (ABCA1 defect; HDL virtually absent), lecithin-cholesterol acyltransferase (LCAT) deficiency and fish-eye disease | Very low HDL-C without high triglycerides or an acquired cause; family history. Only some forms cause premature ASCVD |
Low HDL-C in the sick patient: Sepsis and other acute illness push HDL-C down, and HDL loses its protective work along with it. Read the number as a severity marker. Do not call the patient dyslipidemic off an acute-phase sample. Repeat the panel once they recover.
High (HDL-C >90 mg/dL; extreme ≥116 mg/dL in men, ≥135 mg/dL in women)
| Mechanism | Common causes | Bedside clue |
|---|---|---|
| Physiologic | Female sex, regular exercise, weight loss | Healthy, active patient with normal triglycerides |
| Exposure | Heavy alcohol use | Drinking history; may explain part of the excess mortality seen with extreme HDL-C |
| Drugs | Niacin, fibrates, cholesteryl ester transfer protein (CETP) inhibitors | The rise in HDL-C does not mean lower risk |
| Genetic: slower HDL catabolism | CETP variants; scavenger receptor B1 (SR-BI) variants; hepatic lipase variants | Family clustering. SR-BI and hepatic lipase variants raise HDL-C with normal or higher coronary risk |
Very high is not extra protection: Past about 90 mg/dL, coronary risk stays flat. Extreme HDL-C tracks with higher all-cause mortality and infection. Do not wave off high LDL-C, smoking, diabetes or hypertension because HDL-C looks high.
Interpretation & Bedside Approach
Step-by-step approach
- Is it real and representative? Fasting is not needed. Ask whether the patient was acutely ill when the sample was drawn. Infection, sepsis and ACS all pull lipid values down.
- How sick is the patient? HDL-C never changes emergency management. In the ED or ICU, a very low value tells you how sick the patient is. Treat the underlying illness, not the number.
- Acute vs chronic, and the trend: Compare with a value from a well period. After a mild infection, wait at least 3 weeks before measuring for risk assessment (NHLBI pediatric guidance, extrapolated to adults). After sepsis, critical illness, ACS or major surgery, allow longer. Local practice often lands at 6–8 weeks. That is not a guideline interval. After ACS, draw on admission and repeat later.
- Read the whole panel: HDL-C and triglycerides move in opposite directions. Calculate non-HDL-C (total cholesterol − HDL-C). Nonfasting triglycerides >440 mg/dL (5 mmol/L): consider a fasting repeat; >880 mg/dL (10 mmol/L): pancreatitis risk, refer.
- Classify with current criteria: Low HDL-C is one of five harmonized metabolic syndrome components (2009). In adults aged 30–79, HDL-C and total cholesterol feed the AHA PREVENT equations (2023), which the 2026 ACC/AHA dyslipidemia guideline uses. For children, use the NHLBI cut points.
- Escalate or dispose: No acute action here. Hand off to primary care for cardiovascular risk follow-up. Refer to a lipid specialist for unexplained HDL-C near zero, or for extreme values with a family history. Advise lifestyle measures (aerobic exercise, smoking cessation, weight loss). They raise HDL-C and improve the whole lipid profile. Still, HDL-C is not pursued as a separate treatment target.
Patterns
| Pattern | Suggests |
|---|---|
| Low HDL-C + high triglycerides + central obesity or high glucose | Insulin resistance or metabolic syndrome; check glucose or HbA1c, blood pressure and waist |
| New low HDL-C in a febrile, hypotensive or post-MI patient | Acute-phase response; severity marker; repeat after recovery |
| HDL-C near zero, normal triglycerides, no acquired cause | Rare genetic HDL deficiency (Tangier disease, LCAT deficiency, apoA-I mutation); refer |
| Low HDL-C in a patient on testosterone | Expected hormone effect |
| Very high HDL-C + heavy drinking | Alcohol effect; address alcohol use |
| High HDL-C + high LDL-C or non-HDL-C | Risk is set by the atherogenic particles; high HDL-C does not offset it |
Metabolic syndrome (harmonized definition, 2009): any 3 of 5
| Component | Threshold |
|---|---|
| Waist circumference | Population- and country-specific cut points |
| Triglycerides | ≥150 mg/dL (1.7 mmol/L) or drug treatment for high triglycerides |
| HDL-C | <40 mg/dL (1.0 mmol/L) in men, <50 mg/dL (1.3 mmol/L) in women, or drug treatment for low HDL-C |
| Blood pressure | Systolic ≥130 and/or diastolic ≥85 mmHg, or antihypertensive treatment |
| Fasting glucose | ≥100 mg/dL or drug treatment for high glucose |
Do not treat the number: Niacin, fibrates and most CETP inhibitors raise HDL-C. Added to statins, they have not consistently reduced cardiovascular events. The 2026 ACC/AHA guideline sets treatment goals for LDL-C and non-HDL-C, not HDL-C.
Special Populations
| Population | What changes | Clinical implication |
|---|---|---|
| Neonates & infants | Lipid screening is not routine before 2 years | Targeted screening may start at 2 years with a family history of premature ASCVD or familial hypercholesterolemia |
| Children & adolescents | Own cut points (acceptable >45 mg/dL, low <40 mg/dL). Low HDL-C usually comes with obesity, inactivity or smoke exposure | Universal screening at 9–11 years (NHLBI also once at 17–21 years), nonfasting non-HDL-C first. HDL-C rises with exercise and weight loss |
| Pregnancy | Pregnancy is a cause of secondary dyslipidemia. HDL-C, LDL-C and triglycerides typically rise, with HDL-C peaking around mid-gestation | A low HDL-C is not explained by pregnancy; do not use pregnancy values for long-term risk; reassess after pregnancy |
| Older adults | No clinically meaningful difference in range | PREVENT was developed for ages 30–79 years |
| CKD / dialysis | Low HDL-C is associated with lower kidney function; nephrotic syndrome causes secondary dyslipidemia | PREVENT includes eGFR; HDL-C is one of several inputs |
| Critically ill | HDL-C falls with sepsis, infection and ACS | Severity marker only; defer risk assessment until recovery |
| Transgender patients on hormones | Testosterone lowers HDL-C (about 8.5 mg/dL after 2 years or more). Estrogen therapy showed no consistent HDL-C change, but triglycerides rose | Low-quality evidence; interpret against the patient's on-treatment baseline |
Race-free risk: PREVENT is sex-specific and leaves race out. HDL-C and total cholesterol go in as measured. No ancestry adjustment to HDL-C is needed.
Interfering Factors & Pitfalls
Collection & handling
| Factor | Effect | Why | Avoid / fix |
|---|---|---|---|
| Nonfasting sample | No meaningful change | HDL-C is not affected by fasting status | Nonfasting is the default; fast only if nonfasting triglycerides are >440 mg/dL |
| Drawn during acute illness | ↓ | Acute-phase response in infection, sepsis and ACS | Repeat at least 3 weeks after a mild infection (NHLBI pediatric guidance); after sepsis, ACS or surgery, repeat once recovered, commonly 6–8 weeks (local practice, not guideline-derived) |
Medications & supplements
| Factor | Effect | Why | Avoid / fix |
|---|---|---|---|
| Testosterone | ↓ | Sex-hormone effect on HDL metabolism | Interpret against the on-treatment baseline |
| Niacin, fibrates, CETP inhibitors | ↑ | Raise HDL-C without proven event reduction | Do not read the rise as lower cardiovascular risk |
Physiologic / biologic
| Factor | Effect | Why | Avoid / fix |
|---|---|---|---|
| High triglycerides | ↓ | True inverse relation with triglyceride-rich lipoproteins and remnants | Read HDL-C with triglycerides and non-HDL-C |
| Heavy alcohol use | ↑ | Alcohol raises HDL-C | Ask about intake when HDL-C is very high |
Assay & calculation
| Factor | Effect | Why | Avoid / fix |
|---|---|---|---|
| HDL-C error in derived values | False + or False − in calculated LDL-C and non-HDL-C | Both subtract HDL-C from total cholesterol | Use measured LDL-C when triglycerides are ≥400 mg/dL |
| Cholesterol content, not function | — | HDL-C does not measure cholesterol efflux or other HDL functions | Function assays are research tools, not routine tests |
Common misinterpretations
- "High HDL-C cancels high LDL-C": it does not. Act on LDL-C, non-HDL-C and overall risk instead.
- "Raise HDL-C with a drug to lower risk": Drugs that raise HDL-C have not consistently reduced events on top of statins.
- "Low HDL-C in the ICU means a lipid disorder": usually it is the acute-phase response. Not a lipid disorder.
- "The patient must fast": Not for HDL-C. Nonfasting is the default.
Physiology & Test Basics
What it measures
HDL cholesterol (HDL-C) is the cholesterol carried inside high-density lipoprotein particles. Think of it as cargo. It does not measure how well HDL works. Total cholesterol counts the cholesterol in every lipoprotein. LDL-C counts the cholesterol in LDL. Non-HDL-C (total minus HDL-C) counts the cholesterol in all atherogenic apolipoprotein B (apoB) particles.
Physiology & regulation
- Formation: apoA-I, the main HDL protein, picks up phospholipid and cholesterol from cells through the ABCA1 transporter. That step is rate-limiting.
- Maturation: LCAT esterifies cholesterol, which moves it into the particle core.
- Exchange: CETP trades HDL cholesteryl esters for triglycerides carried on apoB lipoproteins.
- Clearance: through SR-BI, the liver pulls HDL cholesterol back in (reverse cholesterol transport).
- Other roles: HDL also works as an anti-inflammatory and an antioxidant, protects the endothelium and supports innate immunity. One example is neutralizing bacterial lipopolysaccharide.
- Risk marker, not cause: genetic studies do not support HDL-C as a cause of ASCVD. Low HDL-C mostly reflects excess triglyceride-rich remnants.
How it is measured
Serum (red or gold top) or plasma, depending on the lab. Automated analyzers measure HDL-C directly. It is part of the standard lipid panel, and some point-of-care lipid devices report it too. Fasting is not required.
Why it matters
HDL-C feeds the PREVENT risk equations, the metabolic syndrome definition, and the calculated LDL-C and non-HDL-C. In emergency and critical care, it is rarely acted on. A lipid panel drawn during sepsis or ACS will understate HDL-C. A very low value marks a sicker patient.
Clinical Pearls
ACS admission panel: Draw the lipid panel on admission, no fasting needed. ACS pulls lipid values down. Plan a repeat panel after recovery, before you judge long-term risk.
Nursing: no fasting needed: Do not hold breakfast for a lipid panel. In diabetes, nonfasting testing is preferred. Fasting adds hypoglycemia risk.
Transport: note the timing: A lipid panel in the transfer packet, drawn during sepsis or ACS, is not the patient's baseline. Hand it off as an acute-phase value. It never changes transport decisions.
Low HDL-C plus high triglycerides: Low HDL-C with high triglycerides should send you looking for the rest of the metabolic syndrome: waist, blood pressure, glucose or HbA1c.
Extreme HDL-C: At ≥116 mg/dL in a man or ≥135 mg/dL in a woman, do not relax. Ask about alcohol and consider genetic causes.
Testosterone lowers HDL-C: Expect HDL-C to fall in patients on testosterone therapy. Compare with their on-treatment baseline.
No drug to raise HDL-C: Niacin, fibrates and CETP inhibitors raise HDL-C. Added to statins, they have not consistently reduced cardiovascular events. Treatment targets LDL-C and non-HDL-C. Fibrates are used for severe hypertriglyceridemia.
References
- Writing Committee Members; Blumenthal, R. S., Morris, P. B., Gaudino, M., Johnson, H. M., et al. (2026). 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, 153(17), e1154–e1276. https://doi.org/10.1161/CIR.0000000000001423
- Khan, S. S., Matsushita, K., Sang, Y., Ballew, S. H., Grams, M. E., Surapaneni, A., et al. (2024). Development and validation of the American Heart Association's PREVENT equations. Circulation, 149(6), 430–449. https://doi.org/10.1161/CIRCULATIONAHA.123.067626
- von Eckardstein, A., Nordestgaard, B. G., Remaley, A. T., & Catapano, A. L. (2023). High-density lipoprotein revisited: Biological functions and clinical relevance. European Heart Journal, 44(16), 1394–1407. https://doi.org/10.1093/eurheartj/ehac605
- Nordestgaard, B. G., Langsted, A., Mora, S., Kolovou, G., Baum, H., Bruckert, E., et al. (2016). 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, 37(25), 1944–1958. https://doi.org/10.1093/eurheartj/ehw152
- Madsen, C. M., Varbo, A., & Nordestgaard, B. G. (2017). Extreme high high-density lipoprotein cholesterol is paradoxically associated with high mortality in men and women: Two prospective cohort studies. European Heart Journal, 38(32), 2478–2486. https://doi.org/10.1093/eurheartj/ehx163
- Maraka, S., Singh Ospina, N., Rodriguez-Gutierrez, R., Davidge-Pitts, C. J., Nippoldt, T. B., Prokop, L. J., & Murad, M. H. (2017). Sex steroids and cardiovascular outcomes in transgender individuals: A systematic review and meta-analysis. Journal of Clinical Endocrinology & Metabolism, 102(11), 3914–3923. https://doi.org/10.1210/jc.2017-01643
- Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents; National Heart, Lung, and Blood Institute. (2011). Integrated guidelines for cardiovascular health and risk reduction in children and adolescents: Full report (landmark guideline). National Institutes of Health. https://www.nhlbi.nih.gov/health-topics/integrated-guidelines-for-cardiovascular-health-and-risk-reduction-in-children-and-adolescents/integrated-guidelines-for-cardiovascular-health-and-risk-reduction-in-children-and-adolescents-full-report
- Alberti, K. G., Eckel, R. H., Grundy, S. M., Zimmet, P. Z., Cleeman, J. I., Donato, K. A., et al. (2009). Harmonizing the metabolic syndrome: A joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity (landmark definition). Circulation, 120(16), 1640–1645. https://doi.org/10.1161/CIRCULATIONAHA.109.192644
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