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HDL Cholesterol 

  • Author: Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP; Chief Editor: Eric B Staros, MD  more...
Updated: Jan 16, 2014

Reference Range

High-density lipoprotein (HDL) cholesterol is used in the assessment of coronary or other vascular pathology risk.

The reference range of high-density lipoprotein cholesterol (HDL-C) is 40-50 mg/dL in men and 50-60 mg/dL in women.



High-density lipoprotein cholesterol (HDL-C) levels are increased in the following conditions:

HDL-C levels are decreased in the following conditions:


Collection and Panels

Specimen type: Plasma or serum

Container: Green-top (heparin) tube, red-top tube, or gold-top 7-mL serum-separating tube (SST; sometimes called marble-top tubes or yellow-topped tubes, referring to the stoppers, which are either gold or red-gray)

Specimen volume: 0.5 mL

Other instructions: The patient should fast at least 12-14 hours before the blood draw for the lipid panel

Panels: Lipid panel




High-density lipoprotein cholesterol (HDL-C), which consists mostly of cholesterol, phospholipid, and protein, is produced and secreted by the liver and intestine.[2]

HDL-C transports cholesterol from tissues to the liver. In this reverse cholesterol transport process, it performs a "clean-up" function. This process is called reverse cholesterol transport because cholesterol synthesized in peripheral tissues is eventually returned to the liver for its disposal from the body.

HDL-Cs have many surface proteins. Apo-A1 and apo-A2 proteins on HDL-C are derived by direct secretion from the liver.[3] ApoA-I synthesis is necessary to produce HDL-C. Mutations in the apoA-I gene that cause HDL-C deficiency are associated with accelerated atherogenesis. Overexpression of apoA-I in the mouse model protects against experimentally induced atherogenesis.[4] Additionally, HDL-C may protect against atherogenesis by mechanisms not directly related to reverse cholesterol transport. These functions include putative anti-inflammatory, anticoagulant, antioxidative, platelet anti-aggregatory, and profibrinolytic activities.[5]

High levels of HDL-C are desirable because of their inverse relation with coronary risk. HDL-C is called good cholesterol because it is inversely related with the incidence of atherosclerosis.


HDL-C is used in the assessment of coronary or other vascular pathology risk.


HDL-C levels are decreased in association with recent illness; starvation and stress; smoking; obesity and lack of exercise; medications such as thiazide diuretics, steroids, and beta-blockers; hypertriglyceridemia; and in elevated immunoglobin levels.

HDL-C levels are increased in association with moderate ethanol consumption, insulin, and estrogen.[1] Additionally, regular aerobic exercise, smoking cessation, decrease in body mass index, and statin therapy (mild) increase HDL-C levels. Statins or HMG-CoA reductase inhibitors modestly increase HDL-C levels. The mild rise in HDL-C levels from these drugs may be related to inhibition of rho-signaling pathways with activation of peroxisome proliferator-activated receptor (PPAR)–alpha. Increases in HDL-C levels may also be attributable to decreasing plasma cholesteryl ester transfer protein (CETP) activity by statins.[6]

Contributor Information and Disclosures

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP Associate Professor of Medicine, St Louis University School of Medicine

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP is a member of the following medical societies: American College of Physicians, American Medical Informatics Association, Royal College of Physicians and Surgeons of Glasgow, Royal College of Surgeons of Edinburgh, Healthcare Information and Management Systems Society

Disclosure: Nothing to disclose.

Chief Editor

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

  1. Williamson MA, Snyder LM, Wallach JB. Wallach's interpretation of diagnostic tests. 9th ed. Wolters Kluwer/Lippincott Williams & Wilkins Health: Philadelphia; 2011.

  2. Botham KM MP. Lipid Transport & Storage. Murray RK BD, Botham KM, Kennelly PJ, Rodwell VW, Weil PA, ed. Harper's Illustrated Biochemistry. 28th ed. New York McGraw-Hill: 2009.

  3. L W. Xanthomatoses and Lipoprotein Disorders. Wolff K GL, Katz SI, Gilchrest BA, Paller AS, Leffell DJ,, ed. Fitzpatrick's Dermatology in General Medicine. 7th ed. New York: McGraw-Hill: 2008.

  4. TP B. Drug Therapy for Hypercholesterolemia and Dyslipidemia. Brunton LL CB, Knollmann BC, ed. Goodman & Gilman's The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill; 2011.

  5. deGoma EM, deGoma RL, Rader DJ. Beyond high-density lipoprotein cholesterol levels evaluating high-density lipoprotein function as influenced by novel therapeutic approaches. J Am Coll Cardiol. 2008 Jun 10. 51(23):2199-211. [Medline].

  6. Rader DJ. Raising HDL in Clinical Practice: Clinical Strategies to Elevate HDL. New York:. Available at http://Medscape: Accessed: March15, 2012.

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