Good Calories, Bad Calories

Another shift in emphasis was to incorporate HDL and some combination of triglycerides, LDL, and total cholesterol into the calculation of a “lipid profile” of heart-disease risk, a process that was initiated with the very first articles by Gordon and his collaborators. These lipid profiles allowed for the continued use of LDL or total cholesterol in the calculation of heart-disease risk, even though they added little or no predictive power to the use of HDL alone.

Ironically, these lipid profiles also provided the rationale for physicians to keep measuring total cholesterol in their patients, even though it had now been confirmed, as Gofman had noted a quarter-century earlier, that it was a dangerously unreliable predictor of risk. The reason is that LDL cholesterol itself happened to be particularly difficult to measure.^†46 It was not the kind of measurement that physicians could easily order up for their patients. And since it didn’t seem to matter in these lipid profiles whether it was total or LDL cholesterol that was included along with HDL—either way, HDL was the dominant predictor of risk—then, “from a practical point of view,” as Gordon and his colleagues noted, “total cholesterol can substitute for LDL cholesterol” in calculating risk. Total cholesterol could be measured easily in the clinic, so physicians would continue to measure it. The evidence had dictated a complete turnabout in the science, and then pragmatic considerations had turned it about again, until the clinical management of patients and the public perception were back exactly where they had started.

The revelations about HDL had equally little influence on the institution of a national low-fat, high-carbohydrate diet. Whether or not triglycerides were an independent risk factor, once the protective nature of HDL was confirmed, then Gofman’s argument of 1950 was also reaffirmed: there were at least two potential diet-related ways of preventing heart disease, and any treatment that improved the situation with one risk factor had to avoid exacerbating the situation with the other. In the 1960s, Gofman, Ahrens, Albrink, and Fredrickson, Levy, and Lees had all discussed the dangers of replacing the fat in the diet with carbohydrates because this would elevate triglycerides. Now the dangers of lowering HDL became the issue. “In the search for an optimal therapy for avoiding or correcting atherosclerosis,” as the Framingham investigators noted in 1979, “the ideal lipid response would appear to be the one that raises HD lipoprotein as it lowers LD lipoprotein. Therapeutic maneuvers that affect only one of these lipoprotein particle systems in a favorable way, while adversely affecting the other, may be less promising….”

Diets that lowered cholesterol by replacing saturated fat with polyunsaturated fats would have accomplished such a balancing act, but there was legitimate concern that polyunsaturated fats were carcinogenic, and so the AHA had simply recommended fat reduction in general. This meant replacing the fat calories with carbohydrates. But the “good cholesterol” in HDL would be diminished by eating more carbohydrates. By the 1980s, discussions of heart-disease prevention typically avoided this dilemma by neglecting to mention the effect of carbohydrates on HDL.^*47 Instead, people were told to raise their HDL through exercise and weight loss, and then prescribed, as the American Heart Association did, low-fat, high-carbohydrate diets as the means to lose that weight.

In 1985, Scott Grundy and his colleague Fred Mattson provided what appeared to be the ideal compromise—a dietary means both to lower LDL cholesterol and to raise HDL cholesterol without consuming more carbohydrates or saturated fats. This was monounsaturated fats, such as the oleic acid found in olive oil, and it served to keep the focus on the fat in the diet, rather than the carbohydrates. In the 1950s, Keys had assumed that monounsaturated fats were neutral, because they had no effect on total cholesterol. But this apparent neutrality, as Grundy reported, was due to the ability of these fats simultaneously to raise HDL cholesterol and lower LDL cholesterol. Saturated fats raise both HDL and LDL cholesterol. Carbohydrates lower LDL cholesterol but also lower HDL. Grundy and Mattson’s discovery of the double-barreled effect of monounsaturated fats, and particularly oleic acid, reignited the popular interest in the Mediterranean diet as the ideal heart-healthy diet, though it seemed to be heart-healthy only in some Mediterranean regions and not in others, and such diets, as even Grundy conceded, had never been tested. When they finally were tested in two clinical trials in the 1990s—the Lyon Diet Heart Trial and an Italian study known as GISSI-Prevenzione—both supported the contention that the diet prevented heart attacks, but neither provided evidence that it did so by either raising HDL or lowering LDL, which was how it was now alleged to work.