Since the late 1970s, investigators have demonstrated the existence of other hormonal mechanisms by which insulin raises blood pressure—in particular, by stimulating the nervous system and the same flight-or-fight response incited by adrenaline. This was first reported by Lewis Landsberg, an endocrinologist who was then at Harvard Medical School and would later become dean of the Northwestern University School of Medicine. Landsberg showed that, by stimulating the activity of the nervous system, insulin increases heart rate and constricts blood vessels, thereby raising blood pressure. The higher the insulin level, the greater the stimulation of the nervous system, Landsberg noted. If insulin levels remained high, so Landsberg’s research suggested, then the sympathetic nervous system would be constantly working to raise blood pressure. The heart-disease research community has paid attention to Landsberg’s work, but has considered it relevant only for the obese. Because obesity is associated with higher insulin levels, and because it’s now believed that obesity causes higher insulin levels (whereas obesity itself is allegedly caused by the consumption of excess calories of all types), any possible link to carbohydrate consumption or “carbohydrate overfeeding” is overlooked. Even Landsberg has concentrated almost exclusively on the obesity-insulin-hypertension connection and ignored the idea that the increase in insulin levels due to excessive carbohydrate consumption, or due to the consumption of refined and easily digestible carbohydrates, might have a similar effect.

One question that will be addressed in the coming chapters is why medical investigators and public-health authorities, like Landsberg, will accept the effects of insulin on chronic diseases as real and potentially of great significance, and yet inevitably interpret their evidence in ways that say nothing about the unique ability of refined and easily digestible carbohydrates to chronically elevate insulin levels. This is the dilemma that haunts the past fifty years of nutrition research, and it is critical to the evolution of the science of metabolic syndrome. As we will discuss, the observation of diseases of civilization was hardly the only evidence implicating sugar and refined carbohydrates in these diseases. The laboratory research inevitably did, too. Yet the straightforward interpretation of the evidence—from carbohydrates to the chronic elevation of insulin to disease—was consistently downplayed or ignored in light of the overwhelming belief that Keys’s dietary-fat hypothesis had been proved correct, which was not the case.