Good Calories, Bad Calories

This is where the story now takes some peculiar turns. One immediate effect of the revelation about HDL, paradoxically, was to direct attention away from triglycerides, and with them the conspicuous link, until then, to the carbohydrate hypothesis. Gordon and his colleagues had demonstrated that when both HDL and triglycerides were incorporated into the risk equations of heart disease, or when obesity and the prediabetic condition of glucose intolerance were included in the equations along with triglycerides, the apparent effect of triglycerides diminished considerably. This result wasn’t surprising, considering that low HDL, high triglycerides, obesity, and glucose intolerance all seemed to be related, but that wasn’t the point. The relevant question for physicians was whether high triglycerides by themselves caused heart disease. If so, then patients should be advised to lower their triglycerides, however that might be accomplished, just as they were being told already to lower cholesterol. These risk-factor equations (known as multivariate equations) suggested that triglycerides were not particularly important when these other factors were taken into account, and this was how they would be perceived for another decade. Not until the late 1980s would the intimate association of low HDL, high triglycerides, obesity, and diabetes be considered significant—in the context of Gerald Reaven’s Syndrome X hypothesis—but by then the heart-disease researchers would be committed to the recommendations of a national low-fat, high-carbohydrate diet.

Heart-disease researchers would also avoid the most obvious implication of the two analyses—that raising HDL offers considerably more promise to prevent heart disease than lowering either LDL or total cholesterol—on the basis that this hadn’t been tested in clinical trials. Here the immediate obstacle, once again, was the institutional investment in Keys’s hypothesis. The National Institutes of Health had committed its heart-disease research budget to two ongoing studies, MRFIT and the Lipid Research Clinics Trial, which together would cost over $250 million. These studies were dedicated solely to the proposition that lowering total cholesterol would prevent heart disease. There was little money or interest in testing an alternative approach. Gordon later recalled that, when he presented the HDL evidence to the team of investigators overseeing MRFIT, “it was greeted with a silence that was very, how should I say it, expressive. One of them spoke up indicating he suspected this was a bunch of shit. They didn’t know how to deal with it.”

Indeed, the timing of the HDL revelations could not have been less convenient. The results were first revealed to the public in an American Heart Association seminar in New York on January 17, 1977. This was just three days after George McGovern had announced the publication of the Dietary Goals for the United States, advocating low-fat, high-carbohydrate diets for all Americans, based exclusively on Keys’s hypothesis that coronary heart disease was caused by the effect of saturated fat on total cholesterol. If the New York Times account of the proceedings is accurate, the AHA and the assembled investigators went out of their way to ensure that the new evidence would not cast doubt on Keys’s hypothesis or the new dietary goals. Rather than challenge the theory that excess cholesterol can cause heart disease, the Times reported, “the findings re-emphasize the importance of a fatty diet in precipitating life-threatening hardening of the arteries in most Americans,” which is precisely what they did not do. According to the Times, saturated fat was now indicted not just for increasing LDL cholesterol, which it does, but for elevating VLDL triglycerides and lowering HDL, which it does not, and certainly not compared with the carbohydrates that McGovern’s Dietary Goals were recommending all Americans eat instead.