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The only factors to which Dr. Keys would give major responsibility were physical exercise (or the lack of it) and diet. He tackles the diet problem from the viewpoint of fat content. The fat in the U.S. diet, he points out, has been going up for 50 years; fats account for as much as 40% of its calories. In Sweden the proportion is 38%. But in Sardinia it is only 22%. The clincher, for Dr. Keys, is to be found among Yemenite Jews who had no coronary disease in their native habitat but have begun to develop it since they migrated to Israel and adopted its high-fat diet. Yet the amiable, blubber-eating Eskimos throw a monkey-wrench into the dietary-fat theory. In Alaska, they live for months at a time on the fat of island seal and whale, but even among their oldsters fatal atherosclerosis is rare.
Surveying the puzzling and contradictory evidence, Dr. Page offers a moderate summation: too much fat in the diet and too little are both bad. Anything below 15% is dangerous (he tried it himself for a year and found that he lost weight, energy and equanimity). Current U.S. levels are needlessly high. A nice balance: 25%. And he sees no decisive difference in the effects of vegetable and animal fats.
The Question of Cholesterol. The hottest of all arguments is over cholesterol. For the last decade or so, some researchers have been casting this fatty alcohol as the villain. It is the predominant substance found in the plaques and patches that form on the roughened inner wall (intima) of the artery, and the amount circulating in the blood is in some rough proportion to the fats in the diet. So it is temptingly simple to draw the conclusion that the dietary fat starts the trouble and the cholesterol finishes it when it has built up deposits—which may also become calcified—big enough to close a coronary artery.
Actually, the order of the steps in the formation of deposits on the artery walls is not clear. The walls become roughened. Some substance is deposited there. But, many researchers say, it may be simply a group of microscopic platelets—the elements in the blood that initiate clotting. These are too small to do any direct harm. But something else clings to their debris. According to the University of California's Dr. Henry Moon and Dr. James Rinehart, this is a sugar protein. Only after that, they say, does the cholesterol appear. And they do not believe that the sugar protein is the original villain: that, the San Francisco researchers contend, is a deficiency of vitamin B<sub>6</sub> (found in liver and egg yolk).
Across the bay in Berkeley, at U. of C.'s Donner Laboratory, Dr. John Gofman is the nation's outstanding worker with cholesterol and the substances with which it combines in the body. Researcher Gofman and his colleagues examined the combinations in which cholesterol circulates. It enters the bloodstream combined with proteins of different kinds. Cholesterol molecules in the combinations known as alpha-lipoproteins are generally of high density and seem relatively little involved in disease; the beta-lipoproteins contain the fat and flabby cholesterol molecule that is clearly implicated in atherosclerosis.