Because sucrose and high-fructose corn syrup (HFCS-55) are both effectively half glucose and half fructose, they offer the worst of both sugars. The fructose will stimulate the liver to produce triglycerides, while the glucose will stimulate insulin secretion. And the glucose-induced insulin response in turn will prompt the liver to secrete even more triglycerides than it would from the fructose alone, while the insulin will also elevate blood pressure apart from the effect of fructose. “This is really the harmful effect of sucrose,” says Mayes, “over and above fructose alone.”

The effect of fructose on the formation of advanced glycation end-products—AGEs, the haphazard glomming together of proteins in cells and tissues—is worrisome as well. Most of the research on AGE accumulation in humans has focused on the influence of glucose, because it is the dominant sugar in the blood. Glucose, however, is the least reactive of all sugars, the one least likely to attach itself without an enzyme to a nearby protein, which is the first step in the formation of AGEs. As it turns out, however, fructose is significantly more reactive in the bloodstream than glucose, and perhaps ten times more effective than glucose at inducing the cross-linking of proteins that leads to the cellular junk of advanced glycation end-products. Fructose also leads to the formation of AGEs and cross-linked proteins that seem more resistant to the body’s disposal mechanisms than those created by glucose. It also increases markedly the oxidation of LDL particles, which appears to be a necessary step in atherosclerosis.

This research on the health effects of fructose began to coalesce in the mid-1980s, just as nutritionists were disseminating the notion that fructose was particularly harmless because of its low glycemic index. And this official opinion has proven hard to sway.

Take, for example, the British Committee on Medical Aspects of Food Policy (known commonly as COMA), which in 1989 released a report entitled Dietary Sugars and Human Disease, authored by a dozen of the nation’s leading nutritionists, physiologists, and biochemists and chaired by Harry Keen, who is among the most renowned British diabetologists. The COMA report discussed the evidence, including the research of Reiser, Reaven, and others, and then concluded that the health effects of sugar were insignificant. The report did so, however, with a series of contradictory assumptions. First, Keen and his colleagues concluded that the implications of fructose-induced insulin resistance and elevated triglycerides are limited to a “relatively small group of people with metabolic disorders [that] includes people with diabetes and those with certain rare inherited disorders.” And so, with the exception of this small percentage of the population, they noted, yearly sugar consumption at 1986 levels, estimated at roughly a hundred pounds per capita in the United Kingdom, “carries no special metabolic risks.” On the other hand, they then explained, sugar consumption does carry risk for those “members of the population consuming more than about 200 g per day,” which is 160 pounds per year, or only slightly more (.4 ounce per day) than what the average American was eating in the year 2000 (not the top 10–20 percent, but the average). They next suggested that those individuals with high triglycerides, a proportion that remains unspecified but might constitute the great majority of all individuals with coronary-artery disease, should restrict their consumption of added sugars to twenty to forty pounds per year, or equivalent to the amount consumed in the U.K. in the early years of the Victorian era.