Good Calories, Bad Calories

While the three Eastern laboratories took three years to learn how to use an ultracentifruge for fractionating lipoproteins, Gofman proceeded with his own research, refined his understanding of how these lipoproteins predicted heart disease, and he then insisted that the analysis techniques be updated accordingly. The other investigators, however, were having considerable trouble duplicating Gofman’s original analysis, and so they refused to accept any further modifications.

In 1956, the four groups published a report in the American Heart Association journal Circulation, with a minority opinion written by Gofman and his Berkeley colleagues and a majority opinion authored by everyone else. As the majority saw it, based on the state of Gofman’s research in 1952, cholesterol was indeed a questionable predictor of heart disease risk, but the measurements of lipoproteins added little predictive power. “The lipoprotein measurements are so complex,” the majority report declared, “that it cannot be reasonably expected that they could be done reliably in hospital laboratories.” Gofman’s minority opinion, based on the state of his research in 1955, was that LDL and VLDL, the very low-density lipoproteins, were good predictors of heart disease, but that the single best predictor of risk was an atherogenic index, which took into account these two lipoprotein classes measured individually and added them together. The greater the atherogenic index, the greater the risk of atherosclerosis and heart disease.

Gofman would later be vindicated, but the majority opinion prevailed at the time: studying lipoproteins held no value in the clinical management of heart disease. Gofman and his Berkeley collaborators continued the research alone through 1963, when Gofman left to establish a biomedical-research division at the Lawrence Livermore National Laboratory and spent the rest of his career working on the health effects of radiation.

Lost entirely in the contretemps were the dietary implications of Gofman’s research. “While it is true that, for certain individuals, the amount of dietary fat is an important factor,” Gofman explained, “it turns out that there are other more significant factors that need to be considered. Human metabolism is so regulated that factors other than the actual dietary intake of one of these constituents may determine the amount of that constituent that will circulate in the bloodstream. Indeed, important observations have been made which indicate that certain substances in the diet that are not fatty at all may still have the effect of increasing the concentration of the fat-bearing lipoprotein substances in the blood.”

Though Gofman’s studies had demonstrated that the amount of LDL in the blood can indeed be elevated by the consumption of saturated fats, it was carbohydrates, he reported, that elevated VLDL—containing some cholesterol and most of the triglycerides in the blood—and only by restricting carbohydrates could VLDL be lowered.

This fact was absolutely critical to the dietary prevention of heart disease, Gofman said. If a physician put a patient with high cholesterol on a low-fat diet, that might lower the patient’s LDL, but it would raise VLDL. If LDL was abnormally elevated, then this low-fat diet might help, but what Gofman called the “carbohydrate factor” in these low-fat diets might raise VLDL so much that the diet would do more harm than good. Indeed, in Gofman’s experience, when LDL decreased, VLDL tended to rise disproportionately. And if VLDL was abnormally elevated to begin with, then prescribing a low-fat, high-carbohydrate diet would certainly increase the patient’s risk of heart disease.

This was why Gofman described the measurement of total cholesterol as a “false and highly dangerous guide” to the effect of diet on heart disease. Total-cholesterol measurements tell us nothing about the status of VLDL and LDL. Prescribing low-fat diets indiscriminately to anyone whose cholesterol appears to be elevated, or bombarding us with “generalizations such as ‘we all eat too much fat,’ or ‘we all eat too much animal fat,’” would increase heart-disease risk for a large proportion of the population. “Neglect of [the carbohydrate] factor can lead to rather serious consequences,” wrote Gofman in 1958, “first, in the failure to correct the diet in some individuals who are very sensitive to the carbohydrate action; and second, by allowing certain individuals sensitive to the carbohydrate action to take too much carbohydrate as a replacement for some of their animal fats.”