One important implication of Jenkins and Wolever’s glycemic-index research is that it provided support for Cleave’s speculations on the saccharine disease. The more refined the carbohydrates, the greater the blood-sugar and insulin response. Anything that increases the speed of digestion of carbohydrates—polishing rice, for instance, refining wheat, mashing potatoes, and particularly drinking simple carbohydrates in any liquid form, whether a soda or a fruit juice—will increase the glycemic response. Thus, the addition of refined carbohydrates to traditional diets of fibrous vegetables or meat and milk, or even fish and coconuts, could be expected to elevate blood-sugar and insulin levels in the population. And this would conceivably explain the appearance of both atherosclerosis and diabetes as diseases of civilization, through the physiological abnormalities of metabolic syndrome—glucose intolerance, hyperinsulinemia, insulin resistance, high triglycerides, low HDL, and small, dense LDL.

Jenkins and Wolever’s research, first published in 1981, led to a surprisingly vitriolic debate among diabetologists on the value of the glycemic index as a guide to controlling blood sugar. Reaven argued that the concept was worthless if not dangerous: saturated fat, he argued, has no glycemic index, and so adding saturated fat to sugar and other carbohydrates will lower their glycemic index and make the combination appear benign when that might not quite be the case. “Ice cream has a great glycemic index, because of the fat,” Reaven observed. “Do you want people to eat ice cream?” Reaven also disparaged the glycemic index for putting the clinical focus on blood sugar, whereas he considered insulin and insulin resistance the primary areas of concern. The best way for diabetics to approach their disease, Reaven insisted, was to restrict all carbohydrates.

Paradoxically, the glycemic index appears to have had its most significant influence not on the clinical management of diabetes but on the public perception of sugar itself. The key point is that the glycemic index of sucrose is lower than that of flour and starches—white bread and potatoes, for instance—and fructose is the reason why. The carbohydrates in starches are broken down upon digestion, first to maltose and then to glucose, which moves directly from the small intestine into the bloodstream. This leads immediately to an elevation of blood sugar, and so a high glycemic index. Table sugar, on the other hand—i.e., sucrose—is composed of both glucose and fructose. To be precise, a sucrose molecule is composed of a single glucose molecule bonded to a single fructose molecule. This bond is broken upon digestion. The glucose moves into the bloodstream and raises blood sugar, just as if it came from a starch, but the fructose can be metabolized only in the liver, and so most of the fructose consumed is channeled from the small intestine directly to the liver. As a result, fructose has little immediate effect on blood-sugar levels, and so only the glucose half of sugar is reflected in the glycemic index.