Kenyon is unusual in this kind of laboratory research in that she had already interpreted the results of her research as relevant to her own life. As Kenyon tells it, the day she realized that glucose shortened the lives of her worms, she decided to restrict her own consumption of carbohydrates to a bare minimum. She lost thirty pounds, she says; her blood pressure, triglycerides, and blood-sugar levels all dropped; and her HDL increased. Kenyon recognizes her experience as anecdotal, but it certainly influenced her suspicion that carbohydrates would also cause chronic disease in humans through their effect on insulin and insulin-like growth factor.

A more common approach to this research implicating insulin and IGF in the causation of chronic disease is to avoid any possible dietary implications and focus solely on the connotations for drug or gene therapies. This was the approach used by Dennis Selkoe and Rudolph Tanzi, who concluded their April 2004 report on insulin and Alzheimer’s by suggesting that the results “have attendant therapeutic implications.” The only therapeutic implication they discussed was the possibility of creating “compounds” that increase the activity of insulin-degrading enzyme—the equivalent of reducing insulin levels—and so inhibiting the accumulation of Alzheimer’s plaques in the brain.

This same approach was used by Ronald Kahn and his collaborators when they discussed the lean, long-lived transgenic mice they had created by knocking out the insulin receptors on the fat cells of the mice. The publication of the research in Science was accompanied by a press release from the Joslin Diabetes Center, of which Kahn is president, focused almost exclusively on the “dream of 60 million overweight American adults,” which it described as the desire to “throw away those diet books and eat whatever you want without becoming fat, and—as a bonus—not develop diabetes and live longer as well.” The press release implied that this dream might be accomplished by the insights gleaned from these transgenic mice, and Kahn was quoted discussing therapeutic implications, although once again diet was not one of them. “Perhaps one day if we are able to find a drug to reduce or block insulin action in fat cells in humans, we might be able to prevent obesity, as well as Type 2 diabetes and other metabolic diseases,” Kahn wrote. “And who knows, they might also live longer too.” Diabetologists implicitly take the same tack whenever they discuss the need for their diabetic patients to “normalize” blood sugar, while recommending that this be accomplished primarily with “intensive insulin therapy” rather than restricting the carbohydrate content of their diets.