Oxidized lipids: a key to heart disease?

Oxidized lipids: A key to heart disease?

New research suggests it's the quality of cholesterol in the diet, not the quantity, that contributes most to one's risk of developing coronary heart disease and atherosclerosis (hardening of the arteries). Conventional wisdom has suggested that diets rich in lipids--a family of biological compounds including cholesterol, fatty acids, phospholipids and triglycerides (fat)--could play a major role in the development of human heart disease. But research presented April 29 in Miami at the American Chemical Society's 189th national meeting now suggests that those lipids might present a serious hazard only if and when they are transformed through oxidation.

Oxidation is any chemical reaction involving the transfer of electrons from one substance to another. Oxidizers' ability to grab electrons away from other substances makes them highly reactive chemically.

Researchers from the University of Illinois in Urbana and elsewhere report that lipids in food are likely to oxidize in a number of situations, including: when cooked meats are stored for an appreciable length of time before eating; when prepared foods--such as dehydrated eggs in cake mixes--are processed at extremely high temperatures; and when foods are cooked in recycled oil that has been heated for a long time.

"All lipids are unstable and will eventually oxidize,' explains U. of Illinois food chemist Fred A. Kummerow. Cooking just speeds the process (SN: 2/9/85, p. 88). In one test, Kummerow and his colleagues found that chicken meat began accumulating oxidized lipids within 24 hours of cooking --even though the meat had been refrigerated immediately after cooking.

The researchers also showed that oxidized lipids are toxic to arterial cells. In one in vitro test, both partially oxidized cholesterol and partially oxidized vitamin D (also a lipid) decreased these cells' ability to keep out calcium. Not only will too much calcium kill cells, but calcium deposits also characterize advanced atherosclerotic lesions.

In another test, the Illinois team counted the number of dead cells in smooth muscle from the abdominal aorta of chickens that had been fed diets high in either cholesterol or one of its oxidation products, 7-ketocholesterol. In four- and eight-week trials, roughly 2 percent of these cells were dead in chickens that had been fed a diet containing 1 percent cholesterol--about twice the rate of cell death in chicken fed no such lipid. In chickens that received the 7-ketocholesterol, almost 10 percent of the cells were dead after a four-week trial, and 22 percent in animals fed the diet for eight weeks.

Kummerow also cites work by others showing that low-density lipoproteins, protein-cholesterol agglomerations, would not enter arterial cells--a step believed necessary to deposit the lipids that help form atherosclerotic lesions--until those lipoproteins had been modified by malonaldehyde, an indicator of lipid oxidation.

Paul B. Addis of the department of food science and nutrition at the University of Minnesota in St. Paul and his colleagues report that they have recently developed the first single gas-chromatography test that will allow detection of any lipid oxide that might be present in food. He suggests that screening tests focus on 7-ketocholesterol as a flag of lipid oxidation.

While the researchers offer no formal dietary recommendations at this point, several did suggest that consumers trim the fat from the edges of meat, be aware of processed eggs and other such foods precooked at very high temperatures and store meat--particularly cooked meat-- for as short a time as possible before eating.

Cholesterol oxides were implicated in more than just heart disease. Addis notes that they have also been shown to inflame arteries and other tissues. And, he adds, the current view of atherosclerosis suggests that it develops, much like cancer, in a two-step process. Once atherosclerosis is initiated, high blood levels of cholesterol may be able to fuel its continued development, he says. But even here, he cautions against indicting normal dietary cholesterol. Where there may be a link, he says, is between dietary consumption of saturated fats and blood levels of cholesterol.

The body has developed a sophisticated antioxidant defense system. Kummerow and Addis say it's not clear whether lipid oxidants overwhelm that defense in certain individuals or attack via unprotected pathways.