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The rationale for lowering the total fat content of the diet to 30 percent was the tangential expectation that such a diet would help us control our weight. In 1984, the year of the NIH Consensus Conference, Robert Levy and Nancy Ernst of the NHLBI had described the state of the science this way: “There has been some indication that a low-fat diet decreases blood cholesterol levels,” they wrote. “There is no conclusive proof that this lowering is independent of other concomitant changes in the diet (for example, increased dietary fiber or complex carbohydrate…or decreased cholesterol or saturated fatty acid level)…. It may be said with certainty, however, that because 1 g fat provides about 9 calories—compared to about 4 calories for 1 g of protein or carbohydrate—fat is a major source of calories in the American diet. Attempts to lose weight or maintain weight must obviously focus on the content of fat in the diet.” Though this was an untested conjecture (however obvious it might seem), the official healthy diet of the nation was now a low-fat diet. A new generation of diet doctors, the most influential of whom was Dean Ornish, were even prescribing 10-percent-fat diets, if not lower.

Another striking aspect of the low-fat diet recommendations is how little any individual might benefit from lowering his cholesterol.*19 Keys and others had argued that heart disease had to be prevented because its first symptom was often a fatal heart attack. But in twenty-four years of observation, the Framingham Heart Study had detected no relationship between cholesterol and sudden cardiac death. The likelihood of suffering a fatal first heart attack was no less for those with a cholesterol level of 180 mg/dl than for those with 250. “The lack of association between serum cholesterol level and the incidence of sudden death suggests that factors other than the atherosclerotic process may be of major importance in this manifestation of coronary artery disease,” explained Thomas Dawber.

There is also little to gain from lowering cholesterol even in less catastrophic manifestations of the disease. This was made clear in 1986, when Stamler published a reanalysis of his MRFIT data in JAMA. As Stamler reported it, the MRFIT investigators had continued to track the health of the 362,000 middle-aged men who had originally been screened as potential candidates for MRFIT, including death certificates. Stamler reported that the cholesterol/heart-disease association applied at any level of cholesterol, and so anyone would benefit from lowering cholesterol.

Using the MRFIT data, however, it is possible to see how large or small that benefit might be (see chart, below). For every one thousand middle-aged men who had high cholesterol—between, say, 240 and 250 mg/dl—eight could expect to die of heart disease over any six-year period. For every thousand men with cholesterol between 210 and 220, roughly six could expect to die of heart disease. These numbers suggest that reducing cholesterol from, say, 250 to 220 would reduce the risk of dying from a heart attack in any six-year period from .8 percent (eight in a thousand) to .6 percent (six in a thousand). If we were to stick rigorously to a cholesterol-lowering diet for thirty years—say, from age forty to seventy, at which point high cholesterol is no longer associated with an increased risk of heart disease—we would reduce our risk of dying of a heart attack by 1 percent.

The data from the MRFIT trial showing the relationship between heart-disease mortality and cholesterol levels in the blood.

The data from the MRFIT trial showing the relationship between total mortality—i.e., death by all causes—and cholesterol levels in the blood.

Whether we would actually live longer by lowering our cholesterol is, of course, a different question. People die from myriad causes. Though Stamler neglected to include total mortality data in his JAMA article, a second group of MRFIT investigators did include it in an article published in The Lancet just a month earlier.

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