The effect of diet on this atherogenic profile now became the pivotal issue. In the 1960s and most of the 1970s, the dietary goal was to lower total cholesterol. After the 1977 revelations about HDL, the best diet became the one that lowered LDL cholesterol and maybe raised HDL in the process. But if Krauss and his collaborators were right, a diet that lowers total cholesterol or LDL cholesterol can conceivably do so in a way that actually increases the proportion of small, dense LDL in the blood turning the healthy pattern A trait into the atherogenic pattern B. If we focus on LDL cholesterol alone, such a diet might appear to prevent heart disease. But if the size, density, and number of the LDL subspecies are indeed the important variables, the diet could in fact increase heart-disease risk.

Though pattern A and B traits appear to be strongly influenced by genetics, diet and other lifestyle factors play a critical role. In the late 1980s, Krauss began a series of clinical trials to explore the association between diet and the dangerous small, dense LDL. The results of his seven trials have been consistent: the lower the fat in the diet and the higher the carbohydrates, the smaller and denser the LDL and the more likely the atherogenic pattern B appears; that is, the more carbohydrates and the less fat, the greater the risk of heart disease.

On a diet that Krauss calls the “average American diet,” with 35 percent of the calories from fat, one in three men will have the atherogenic pattern B profile. On a diet of 46 percent fat, this proportion drops: only one man in every five manifests the atherogenic profile. On a diet of only 10 percent fat, of the kind advocated by diet doctors Nathan Pritikin and Dean Ornish, two out of every three men will have small, dense LDL and, as a result, a predicted threefold higher risk of heart disease. The same pattern holds true in women and in children, but the percentages with small, dense LDL are lower. Krauss and his colleagues even tested the effect of types of fat on these lipoproteins, and reported that, the more saturated fat in the diet, the larger and fluffier the LDL—a beneficial effect.*50

Though the concept of small, dense LDL as a risk factor for heart disease has been accepted into the orthodox wisdom, as has Krauss’s atherogenic profile (although now renamed atherogenic dyslipidemia), his dietary research has had no perceptible influence on discussions of the dietary prevention of heart disease. The implications are so provocative that many investigators simply ignore them. Even those clinical investigators who firmly believe that small, dense LDL is indeed the atherogenic form of LDL often refuse to comment on the dietary implications. “Well, I would rather not get into that,” said the University of Washington epidemiologist Melissa Austin, who studies triglycerides and heart disease and has collaborated with Krauss on studies of the small, dense LDL.