Signals change on 'good' cholesterol Study links HDL to heart disease

July 23, 1993|By Los Angeles Times

LOS ANGELES -- For almost 52 million Americans with high cholesterol, the complex causes of heart disease were long ago reduced to a simple formula of good cholesterol and bad cholesterol. The higher the ratio of good cholesterol to bad cholesterol, the greater the chances of staying healthy.

Now experiments with genetically engineered mice show that some high-density lipoproteins -- the so-called good HDL cholesterol long thought to prevent heart disease -- may actively cause it.

Researchers at the University of California, Los Angeles, have demonstrated that mice with high levels of a common HDL are more likely to develop atherosclerosis than normal mice.

Even mice on a low-fat diet had a higher incidence of heart disease if that specific HDL protein was present, the researchers determined.

Their finding, published in today's issue of the journal Science, calls into question the growing consensus among medical professionals that HDL is a key defense against a heart disease that kills half a million Americans every year. It leaves many health-conscious people where they started when the cholesterol debate began: trying to decide how much of what is too much.

"What this study shows is that HDL proteins are not all alike," said medical geneticist Aldons Lusis, one of five UCLA scientists who conducted the research, sponsored by the National Institutes of Health.

"Some may protect against atherosclerosis and some may not. Some may be associated with increased risk," he said.

"This is probably something people don't want to hear because it means that it all is more complicated and not so straightforward," he said.

Cholesterol, a natural substance found in all the body's cells, is carried through the bloodstream in protein capsules. If it accumulates along artery walls, it can constrict the flow of blood and heighten the probability of a heart attack.

Low density lipoproteins (LDL) carry cholesterol from the liver throughout the body. High LDL levels are regarded as a major risk factor for heart disease.

HDL proteins remove excess cholesterol from the bloodstream and carry it to the liver where it is removed. Low levels of HDL have been associated with high risk of atherosclerosis.

In the effort to combat heart disease, HDL cholesterol has recently attracted considerable attention.

Earlier this year, a panel of experts convened by the National Heart, Lung and Blood Institute formally urged physicians to test for HDL as a "negative" risk factor that would reduce the chances of developing heart disease.

The National Cholesterol Education Program in June urged doctors treating patients with high cholesterol to select medications that raise HDL levels. Many popular drugs prescribed to treat high cholesterol benefit in part from their ability to increase levels of HDL blood proteins.

Several groups have been experimenting with synthetic HDL proteins in the hope they can come up with an effective treatment for heart patients.

Some researchers even speculated that moderate drinking, which some studies suggest appears to reduce coronary disease, might owe its beneficial effect to the ability of ethyl alcohol to increase levels of HDL in the bloodstream.

If borne out by additional research, the UCLA study adds an unexpected variable which may lead clinicians to reconsider the role of HDL in heart disease.

"Eventually, there will probably be dietary and diagnostic implications. But we don't know enough to apply it immediately," Mr. Lusis said.

There are two common HDL proteins: apoA-I, which apparently does confer some resistance to coronary artery disease, and apoA-II, the subject of the UCLA study, which appears to do just the opposite.

Earlier studies with genetically engineered mice at the Lawrence Berkeley Laboratory provided direct evidence that one HDL blood protein, apoA-I, can protect against heart disease.

Baltimore Sun Articles
Please note the green-lined linked article text has been applied commercially without any involvement from our newsroom editors, reporters or any other editorial staff.