blood-sugar response in the two hours after consumption. Different individuals responded differently, and the variation from day to day was “tremendous,” as Wolever says, but the response to a specific food was still reasonably consistent. They also tested a solution of glucose alone to provide a benchmark, which they assigned a numerical value of 100. Thus the glycemic index became a comparison of the blood-sugar response induced by a particular carbohydrate food to the response resulting from drinking a solution of glucose alone. The higher the glycemic index, the faster the digestion of the carbohydrates and the greater the resulting blood sugar and insulin. White bread, they reported, had a glycemic index of 69; white rice, 72; corn flakes, 80; apples, 39; ice cream, 36. The presence of fat and protein in a food decreased the blood-sugar response, and so decreased the glycemic index.

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.

That sugar is half fructose is what fundamentally differentiates it from starches and even the whitest, most refined flour. If John Yudkin was right that sugar is the primary nutritional evil in the diet, it would be the fructose that endows it with that singular distinction. With an eye toward primitive diets transformed by civilization, and the change in Western diets over the past few hundred years, it can be said that the single most profound change, even more than the refinement of carbohydrates, is the dramatic increase in fructose consumption that comes with either the addition of fructose to a diet lacking carbohydrates, or the replacement of a large part of the glucose from starches by the fructose in sugar.

Because fructose barely registers in the glycemic index, it appeared to be the ideal sweetener for diabetics; sucrose itself, with the possible exception of its effect on cavities, appeared no more harmful to nondiabetics, and perhaps even less so, than starches such as potatoes that were being advocated as healthy substitutes for fat in the diet. In 1983, the University of Minnesota diabetologist John Bantle reported in The New England Journal of Medicine that fructose could be considered the healthiest carbohydrate. “We see no reason for diabetics to be denied foods containing sucrose,” Bantle wrote. This became the official government position. The American Diabetes Association still suggests that diabetics need not restrict “sucrose or sucrose-containing foods” and can even substitute them, if desired, “for other carbohydrates in the meal plan.”

In 1986, the FDA exonerated sugar of any nutritional crimes on the basis that “no conclusive evidence demonstrates a hazard.” The two-hundred-page report constituted a review of hundreds of articles on the health aspects of sugar, many of which reported that sugar had a range of potentially adverse metabolic effects related to a higher risk of heart disease and diabetes. The FDA interpreted the evidence as inconclusive. Health reporters, the sugar industry, and public-health authorities therefore perceived the FDA report as absolving sugar of having any deleterious effects on our health.

The identical message was passed along in the 1988 Surgeon General’s Report on Nutrition and Health and the 1989 National Academy of Sciences Diet and Health report. Here, too, the inconclusive studies and ambiguous evidence were considered insufficient to indict sugar as a dietary evil—innocent until proven guilty. These two reports also reviewed the dietary fat/heart-disease connection, which also constituted a collection of inconclusive studies and ambiguous evidence. Here, though, dietary fat was assumed guilty until proved innocent. And so the existence of ambiguous evidence was considered sufficient reason to condemn fat in the diet, particularly saturated fat, while the existence of ambiguous evidence was simultaneously considered reason enough to exonerate sugar.

This institutional absolution of sugar might have been relatively innocuous had it not been coincident with the introduction of a type of sugar refined from corn, rather than sugarcane or beets, known as high-fructose corn syrup, or HFCS, and specifically with what is technically known as HFCS-55, a sweetener that is 55 percent fructose and 45 percent glucose and was created to be indistinguishable from sucrose by taste when used in soft drinks. HFCS-55 entered the market in 1978. By 1985, half of the sugars consumed each year in the U.S. came from corn sweeteners, and two-thirds of that was high-fructose corn syrup. More important, the average consumption of sugars in total had started climbing steadily upward.

This rise in sugar consumption is one of the more perplexing dietary trends in the last century. Though Americans’ taste in starch apparently ebbed and flowed through the twentieth century, the average yearly consumption of caloric sweeteners—a category that includes table sugar, corn sweeteners, honey, and edible syrups—remained relatively constant from the 1920s, at 110–120 pounds per capita. It began to inch upward in the early 1960s, coincident with the first introduction of fructose-enhanced corn syrups. With the introduction of HFCS- 55, it increased significantly. According to USDA statistics, between 1975 and 1979 Americans consumed an annual average of 124 pounds of sugars per person. By 2000, that number had jumped to almost 150 pounds. Corn sweeteners, and particularly high-fructose corn syrup, constituted virtually every ounce of the increase. And this increase came on the heels of a period in the mid-1970s when sugar consumption per capita was decreasing, as sugar was being portrayed in the popular press as a fattening and addictive dietary nuisance.

The simplest explanation for the increase in caloric-sweetener consumption is that consumers simply failed to equate high-fructose corn syrup with the sugar that we’d been eating almost exclusively until then. Although HFCS-55 is effectively identical to sucrose upon digestion, the industry treated it, and the public perceived it, as a healthy additive, whereas sucrose carried the taint of decades of controversy. Because fructose is the predominant sugar in fruit—an apple, for instance, is roughly 6 percent fructose, 4 percent sucrose, and 1 percent glucose by

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