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OPPOSING IDEAS ON EVIDENCE OF HEART ATTACK PREVENTION
One of the reasons for blaming much of the heart attack problem on our environment is the steep rise in death rates in the past forty years or so. One objection has been that heart attack has become a ‘fashionable’ diagnosis; it suggests that death is more likely to be ascribed to a heart attack now than in 1930 (when the death certificate might have read ‘cardiac degeneration’). In English-speaking countries and Scandinavia, the grounds for diagnosing coronary disease have not changed much in the past twenty-five years. Recently Mr D. Clayton, a biostatistician at the Royal Free Hospital, London, has looked carefully at the rates for heart attack for conditions with which it might have been confused; he concluded that the mortality from coronary disease has genuinely increased since 1950. In younger men the rate has doubled.
An argument popular among certain food producers have been to say that there is no proof that their particular product contributes to heart-attack risk. In one recent instance this led to a U.S. Supreme Court action, in which the decision went against the food producer. It is true that the association between saturated-fat intake, blood cholesterol and heart attack is based on all sources of saturated fat in the diet; there is little to implicate individual foods such as eggs or cream, chocolate biscuits or coconuts! The evidence concerns saturated fat in general, and collectively points to every food which provides important amounts of it. In deciding which foods containing saturated fat are least desirable, keep in mind their content of valuable nutrients such as protein, vitamins and minerals. Milk could be made to contain a modest amount of fat, but still be rich in these components. This would be a more desirable food, say, than butter.
From time to time the suggestion has been put forward that a high blood-cholesterol level may be the consequence rather than a cause of atherosclerosis. When a scientist finds that two things often occur together, he explores all the possibilities: a could cause b, b could cause a, or both could result from something else. One argument has been that arteries are damaged by some unknown disease, and that cholesterol accumulates as it heals. This is a perfectly reasonable speculation; but no evidence has appeared to support it. In particular no one has shown that a human artery can make more than traces of cholesterol. But there is evidence that cholesterol enters the artery from the blood (most blood cholesterol is made in the liver or intestine, or comes from food). Nor has anyone shown that a ‘damaged’ artery can make enough cholesterol to cause a high level of this substance in the blood.
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