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Cholesterol-oxides debate isn't over.

Cholesterol/oxides debate isn't over

In recent years researchers have accumulated a growing body of evidence linking oxidized cholesterol and the development of artery-clogging atherosclerosis. Most of the cholesterol in fresh animal products is nonoxidized. The oxygen-based reactions that convert cholesterol to its oxides speed up dramatically once meats or animal products (including oils and eggs) are heated. And even the refrigeration or freezing of cooked cholesterol products will not slow oxidation back to the precooked rate, a finding suggesting that eating leftovers could be considerably more harmful than eating freshly cooked food. A number of researchers now suspect that from the standpoint of heart disease, these oxides may be far more dangerous than fresh cholesterol (SN: 5/4/85, p.278).

But data from an 11-week experiment with rabbits at the University of Wisconsin in Madison now suggest the opposite. Says Stephen L. Taylor, "Our study very clearly shows that cholesterol causes more [atherosclerotic] lesions and more severe lesions than do cholesterol oxides.' Not surprisingly, he adds, "our work has caused a great deal of consternation among all those others [in cholesterol/oxides research].'

The rabbits were fed 166 milligrams per kilogram of body weight daily of oxide-free cholesterol, cholesterol oxides only, a mix of both, or neither. Afterwards the researchers surveyed the entire arterial tree of each animal for signs of atherosclerosis. All rabbits, even those receiving no cholesterol or cholesterol oxides, developed some atherosclerosis. However, the animals receiving a diet laced with pure cholesterol developed the most severe and invasive lesions, according to a report in the November ATHEROSCLEROSIS. Those receiving a diet with both cholesterol and its oxides developed somewhat less atherosclerosis. And those whose diets included the oxides but no pure cholesterol developed only slightly worse atherosclerosis than those receiving neither cholesterol nor its oxides.

"We're not quite sure why our findings differ so dramatically from everyone else's,' Taylor says. But one difference, he says, may be the way the sterols (cholesterol and/or its oxides) were delivered--throughout the day as part of the entire diet, not in one huge dose.

Another possible difference, he says, is the degree to which his sterols were purified. His "cholesterol only' does contained less than 1 percent impurities. In some earlier studies, he says, contamination of a sterol does could be as high as 38 percent.

"What our data indicate,' Taylor says, "is that the process of atherosclerosis has been slowed down in the case of the cholesterol oxides, not speeded up.' As a result, he believes "attention should be refocused on the real problem--cholesterol.'

Several other researchers believe the jury is still out on the relative atherogenicity of oxides. For example, Fred A. Kummerow, a food chemist at the University of Illinois in Urbana-Champaign, says that although "this work appears to have been carefully done, I have a hard time accepting its findings.' He says his own work in chickens has just as convincingly shown that some oxides--such as 7 keto-cholesterol--are far more atherogenic than cholesterol.

C. Bruce Taylor, who retired from cholesterol/oxides research at the Veterans Administration Medical Center in Albany, N.Y., also finds the Wisconsin study unconvincing. He criticizes its failure to survey how the animals managed their sterol supplements with blood-cholesterol measurements, and the omission in the oxides dose of cholestane triol--a cholesterol oxide now known to be highly atherogenic.

Moreover, points out Paul B. Addis at the University of Minnesota in St. Paul, though it's not uncommon to use rabbits in these studies, their inability to metabolize these sterols makes them a poor model of human atherogenicity. In sum, he says, "I think more research is needed to resolve this issue.'
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Publication:Science News
Date:Dec 13, 1986
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