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.

All of this was then summed up in the single statement—echoing the sentiments of the FDA Task Force, the National Academy of Sciences Diet and Health report, and The Surgeon General’s Report on Nutrition and Health, which preceded it—that dietary sugar consumption could not be held responsible for causing disease: “The panel concluded that current consumption of sugars, particularly sucrose, played no direct causal role in the development of cardiovascular…disease, of essential hypertension, or of diabetes mellitus….”

Four years later, The American Journal of Clinical Nutrition dedicated an entire issue to the deleterious effects of dietary fructose. A common refrain throughout the issue was the need for research that would establish at what level of sugar consumption the effects discussed—the elevation of blood pressure and triglycerides, increased insulin resistance, and even accelerated formation of advanced glycation end-products—would lead to disease. “Further studies are clearly needed to determine the metabolic alteration that may take place during chronic fructose or sucrose feeding,” as the Swiss physiologists Luc Tappy and Eric Jéquier wrote.