HDL Cholesterol

Updated: Sep 07, 2021
Author: Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP, FAMIA; Chief Editor: Eric B Staros, MD 

Reference Range

High-density lipoprotein cholesterol (HDL-C) is used in the assessment of coronary or other vascular pathology risk.[1]

Normal findings for HDL-C are as follows[2] :

  • Male: >45 mg/dL or >0.75 mmol/L (SI units)
  • Female: >55 mg/dL or >0.91 mmol/L (SI units)


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

  • Hyperalphalipoproteinemia

  • Regular physical activity or exercise

  • Chronic liver disease

  • Weight loss[3]

HDL-C levels are decreased in the following conditions:

  • Obesity

  • Uncontrolled diabetes mellitus

  • Hepatocellular disease

  • Cholestasis

  • Chronic renal failure

  • Metabolic syndrome (insulin resistance, hypertriglyceridemia)

  • Malnutrition

  • Sedentary lifestyle

  • Cigarette smoking

  • Familial abetalipoproteinemia

  • Beta-blocker therapy (short-term effect)[3]


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.[4]

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.[5] 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.[6] 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.[7]

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.[3] 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.[8]

A study by Pitanga et al reported that although a positive association was found between leisure-time physical activity in adults and greater HDL-C levels, men require more physical activity than women do to demonstrate such increases. In females, it was noted, walking and moderate or vigorous physical activity correlated with raised HDL-C levels, while in males, only vigorous exercise was associated with a rise in HDL-C. It was suggested that this may be partly because men have higher resting homeostasis parameters (eg, heart rate, blood pressure, glycemic levels, caloric expenditure) than women; therefore, men may require a greater amount of physical activity to disrupt resting homeostasis and activate the physiologic means of cardiovascular protection, such as an HDL-C increase.[9]

A pooled analysis by the NCD Risk Factor Collaboration of 458 population-based studies covering 23 Asian and Western countries determined that in a number of Western nations, as well as in Japan and South Korea, the mean ratio of total-to-HDL cholesterol has declined since 1980, with the reduction in Swiss men being approximately 0.7 per decade between 1980 and 2015. (In contrast, China saw an increase in the ratio.) Also from about 1980 to 2015, HDL-C levels in Japan and South Korea saw a per-decade rise of between 0.04 mmol/L (South Korean men) and 0.17 mmol/L (Japanese women).[10]