Good Calories, Bad Calories

In a more rational world, which means a research establishment not already committed to Keys’s hypothesis and not wholly reliant on funding from the institutions that had embraced the theory, the results would have immediately prompted small clinical trials of the hypothesis that raising HDL prevented heart disease, just like those small trials that had begun in the 1950s to test Keys’s hypothesis. If those confirmed the hypothesis, then longer, larger trials would be needed to establish whether the short-term benefits translated to a longer, healthier life. But the NIH administrators decided that HDL studies would have to wait. Once the Lipid Research Clinics Trial results were published in 1984, they were presented to the world as proof that lowering cholesterol by eating less fat and more carbohydrates was the dietary answer to heart disease. There was simply no room now in the dogma for a hypothesis that suggested that raising HDL (and lowering triglycerides) by eating more fat and less carbohydrates might be the correct approach. No clinical trials of the HDL hypothesis would begin in the U.S. until 1991, when the Veterans Administration funded a twenty-center drug trial. The results, published in 1999, supported the hypothesis that heart disease could be prevented by raising HDL. The drug used in the study, gemfibrozil, also lowered triglyceride levels and VLDL, suggesting that a diet that did the same by restricting carbohydrates might have a similarly beneficial effect. As of 2006, no such dietary trials had been funded.

Through the 1980s and 1990s, as our belief in the low-fat heart-healthy diet solidified, the official reports on nutrition and health would inevitably discuss the apparent benefits of raising HDL—the “good cholesterol”—and would then observe correctly that no studies existed to demonstrate this would prevent heart disease and lengthen life. By 2000, well over $1 billion had been spent on trials of cholesterol-lowering, and a tiny fraction of that amount on testing the benefits of raising HDL. Thus, any discussions about the relative significance of raising HDL versus lowering total cholesterol would always be filtered through this enormous imbalance in the research efforts. Lowering LDL cholesterol would always have the appearance of being more important.

It was the revelations that emerged from the two HDL publications in 1977 that led to the conventional wisdom about LDL, triglycerides, and HDL that we live with today. The National Heart, Lung, and Blood Institute and the American Heart Association responded to the new research by focusing on two pragmatic concerns: first, to keep the science sufficiently simple that it could be translated into equally simple guidelines for patient care, and, second, to reconcile these new observations with Keys’s hypothesis and the $250 million worth of studies that were putting it to the test. If total cholesterol was not a risk factor for heart disease above the age of fifty, as Gordon’s Framingham analysis noted, then that seemed to refute Keys’s hypothesis. One immediate goal, therefore, was to make sure that those aspects of the hypothesis that had seemed reasonably certain were not discarded prematurely on the basis of findings that might also someday turn out to be erroneous.

Since both of the new analyses had concluded that LDL cholesterol was associated with a slightly increased risk of heart disease, and since up to 70 percent of the total cholesterol in the circulation may be found in LDL, the American Heart Association and the proponents of Keys’s hypothesis now shifted the focus of scientific discussions from the benefits of lowering total cholesterol to the benefits of lowering LDL cholesterol. “Whatever the underlying disorder,” noted the Framingham investigators in 1979, “much of what has been learned in the past about the ill effects of a high serum total cholesterol can be attributed to the associated elevated levels of LD lipoprotein….”

Making LDL the “bad cholesterol” oversimplified the science considerably, but it managed to salvage two decades’ worth of research, and to justify why physicians had bothered to measure total cholesterol in their patients. One consequence of this effort was an upgrading of the adjectives used to describe the predictive ability of LDL. In 1977, Gordon and his collaborators had described LDL cholesterol as a “marginal risk factor” for heart disease. Within two years, the same authors were using the identical data to describe LDL as a “powerful predictor of risk in subjects younger than the age of 50” and as showing “a significant contribution…to coronary heart disease in persons older than the age of 50 and practically up into the eighties.” This practice has continued unabated.^*45