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:
Regular physical activity or exercise
Chronic liver disease
Weight loss 
HDL-C levels are decreased in the following conditions:
Uncontrolled diabetes mellitus
Chronic renal failure
Beta-blocker therapy (short-term effect) 
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. 
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.  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.  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. 
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.  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.