Good Calories, Bad Calories

Though this carbohydrate-induced water retention and the hypertensive effect of insulin were occasionally discussed in nutrition and dietetics textbooks—Modern Nutrition in Health and Disease, for example, which was published in 1951 and was in its fifth edition by the 1970s—they would appear solely in the technical context of water and electrolyte balance (sodium is an electrolyte), whereas the discussion of hypertension prevention would focus exclusively on the salt hypothesis. When they were discussed in obesity conferences after the 1960s, the implications were restricted to a very narrow range, usually as evidence against any metabolic advantage of carbohydrate-restricted diets. (“One claim which is often made for the low-carbohydrate diet is that 3,000 [calories]/day or more can be eaten and the patient will still lose weight if the carbohydrate intake is restricted,” explained George Bray at the Second International Conference on Obesity in 1977. “There are no convincing studies to support this claim. On the contrary…it is now well-established that a low-carbohydrate diet is followed by the excretion of water and that carbohydrate ingestion leads to retention of both salt and water.”) Since lower weight is associated with lower insulin levels, overweight hypertensives were advised to lose weight to reduce their blood pressure, but then low-calorie diets—usually low-fat and thus high in carbohydrates—would be recommended as the means to do it. On very rare occasions, “carbohydrate overeating” would be acknowledged as a nutritional factor involved in the genesis of hypertension, at least in obese patients, and then both carbohydrate restriction and salt restriction would be recommended as treatment. Those investigators, too, had come to assume that the salt hypothesis must be true.

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.