Reaven supported his hypothesis with the results of observational studies that had already linked hyperinsulinemia, insulin resistance, and Type 2 diabetes to high triglycerides, heart disease, obesity, stroke, and hypertension. Three large-scale Framingham-like prospective studies of healthy nondiabetic populations—in Paris, Helsinki, and in Busselton, Australia—had also reported that, the higher the insulin levels, the greater the risk of heart disease.

As DeFronzo later remarked, the conclusion that hyperinsulinemia and insulin resistance were related to “a whole host of metabolic disorders” was an obvious one, but it required that clinical investigators measure insulin resistance in human patients, which would always be the obstacle in the science of metabolic syndrome. Measuring insulin resistance requires multiple tests of blood sugar while insulin levels are held constant and precise amounts of glucose are consumed or infused into the bloodstream. This is not the kind of test that physicians can do in a checkup, at least not without going far beyond the usual practice of sending a blood sample out to a laboratory for a battery of tests. As a result, when the National Cholesterol Education Program officially acknowledged the existence of Reaven’s Syndrome X in 2002 (renaming it metabolic syndrome), neither insulin resistance nor hyperinsulinemia was included among the diagnostic criteria, despite being the fundamental defects in the syndrome itself.

Reaven’s 1988 Banting Lecture is credited as the turning point in the effort to convince diabetologists of the critical importance of insulin resistance and hyperinsulinemia, but those investigators concerned with the genesis of heart disease paid little attention, considering anything having to do with insulin to be relevant only to diabetes. This was a natural consequence of the specialization of scientific research. Through the mid-1980s, Reaven’s research had focused on diabetes and insulin, and so his publications appeared almost exclusively in journals of diabetes, endocrinology, and metabolism. Not until 1996 did Reaven publish an article on Syndrome X in the American Heart Association journal Circulation, the primary journal for research in heart disease. Meanwhile, his work had no influence on public-health policy or the public’s dietary consciousness. Neither the 1988 Surgeon General’s Report on Nutrition and Health nor the National Academy of Sciences’s 1989 Diet and Health mentioned insulin resistance or hyperinsulinemia in any context other than Reaven’s cautions that high-carbohydrate diets might not be ideal for Type 2 diabetics. Both reports ardently recommended low-fat, high-carbohydrate diets for the prevention of heart disease.

Even the diabetes community found it easier to accept Reaven’s science than its dietary implications. Reaven’s observations and data “speak for themselves,” as Robert Silverman of the NIH suggested at a 1986 consensus conference on diabetes prevention and treatment. But they placed nutritionists in an awkward position. “High protein levels can be bad for the kidneys,” said Silverman. “High fat is bad for your heart. Now Reaven is saying not to eat high carbohydrates. We have to eat something.” “Sometimes we wish it would go away,” Silverman added, “because nobody knows how to deal with it.”