This is what psychologists call cognitive dissonance, or the tension that results from trying to hold two incompatible beliefs simultaneously. When the philosopher of science Thomas Kuhn discussed cognitive dissonance in scientific research—“the awareness of an anomaly in the fit between theory and nature”—he suggested that scientists will typically do what they have invariably done in the past in such cases: “They will devise numerous articulations and ad hoc modifications of their theory in order to eliminate any apparent conflict.” And that’s exactly what happened with metabolic syndrome and its dietary implications. The syndrome itself was accepted as real and important; the idea that it was caused or exacerbated by the excessive consumption of carbohydrates simply vanished.

Among the few clinical investigators working on heart disease who paid attention to Reaven’s research in the late 1980s was Ron Krauss. In 1993, Krauss and Reaven together reported that small, dense LDL was another of the metabolic abnormalities commonly found in Reaven’s Syndrome X. Small, dense LDL, they noted, was associated with insulin resistance, hyperinsulinemia, high blood sugar, hypertension, and low HDL as well. They also reported that the two best predictors of the presence of insulin resistance and the dominance of small, dense LDL are triglycerides and HDL cholesterol—the higher the triglycerides and the lower the HDL, the more likely it is that both insulin resistance and small, dense LDL are present. This offers yet another reason to believe the carbohydrate hypothesis of heart disease, since metabolic syndrome is now considered perhaps the dominant heart-disease risk factor—a “coequal partner to cigarette smoking as contributors to premature [coronary heart disease],” as the National Cholesterol Education Program describes it—and both triglycerides and HDL cholesterol are influenced by carbohydrate consumption far more than by any fat.