HDL - The quiet cholesterol?

Main Category: Cholesterol
Article Date: 24 Feb 2004 - 0:00 PST

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The first connection between cholesterol and atherosclerosis was made by German scientists in 1910.

It wasn't until the mid-1950s that John W. Gofman, MD, a University of California - Berkley biophysicist, observed that elevated levels of high-density lipoprotein (HDL) cholesterol were associated with reduced risk of heart attack.

The Framingham Heart Study described the effects of HDL cholesterol in 1977 and subsequently established low HDL-C levels as an independent predictor of coronary risk.

New guidelines issued by the National Cholesterol Education Program (NCEP) in 2001 changed the definition of "low" HDL to <40 mg/dL from the previously established level of <30 mg/dL. (NCEP says HDL >60 mg/dL is considered protective against heart disease.)

The Centers for Disease Control estimates that about half of all Americans have total cholesterol over 200 mg/dL, making dyslipidemia one of the most prevalent medical conditions in the U.S.

Many coronary artery disease (CAD) patients, however, do not have substantially elevated total or LDL cholesterol. Although LDL generally receives primary attention for clinical management, low HDL cholesterol is often the predominant lipid abnormality.

It has been estimated that for every 1 mg/dL increase in HDL, risk for a CAD event is reduced by 2% in men and 3% in women. "Even the very first cholesterol management guidelines identified low HDL as a risk factor," says Daniel J. Rader, MD, associate professor of medicine and pathology at the University of Pennsylvania School of Medicine.

"It hasn't gotten the same attention as LDL partly because there haven't been good medicines for raising it. Low HDL is certainly a major coronary risk factor and currently presents a big unmet medical need."

The NCEP's Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP-III) says that about 50% of the variability of serum HDL cholesterol levels derives from genetic factors.

The other 50% comes from acquired factors including elevated serum triglycerides, overweight and obesity, physical inactivity, cigarette smoking, type 2 diabetes, very high carbohydrate intakes, and the use of some drugs including anabolic steroids, thiazides, progestational agents, and certain beta-blockers.

Although not identifying a specific goal level for HDL-raising therapy, ATP-III does say, "…nondrug and drug therapies that raise HDL cholesterol levels and are part of management of other lipid and nonlipid risk factors should be encouraged."

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