Author Gary Taubes says that if sugar were on trial, The Case Against Sugar would be “the argument for the prosecution.” I for one would not want to be opposing counsel. Take a deep dive into modern nutrition and see where you come out. (And wait till you read what sugar has to do with cigarettes and nicotine addiction.) Taubes is also author of Why We Get Fat. This new book was published two weeks ago by Alfred A. Knopf, and Taubes will appear at the Politics and Prose bookstore in Washington tomorrow, Saturday, January 14, at 1pm. You can purchase the book there or at other local booksellers, or online at Amazon or Barnes & Noble.
PRIOR TO THE 1970s, public-health authorities and clinicians commenting on the rising tide of diabetes in the populations they studied frequently suggested what to them seemed like the prime suspect—sugar consumption. Here was a disease of carbohydrate metabolism that was becoming increasingly common as populations began consuming sugar—a kind of carbohydrate—at levels that were virtually unimaginable a century before; in some cases, just twenty or thirty years before.
As sugar consumption exploded in the United States and the United Kingdom with the industrial revolution; with the birth of the confectionary, cereal, and soft-drink industries; and with the increasing availability of chocolate bars and ice-cream treats, so did diabetes begin its inexorable climb. When sugar and sugar-rich products spread around the globe, so did diabetes. When peasant farmers throughout Africa, India, Asia, and Central and South America migrated to towns and cities to become wage earners, and changed their dietary habits accordingly—no longer eating locally grown cereals, starches, and fruits, but instead buying sugary drinks and sugar-laden treats in shops and markets—diabetes made its inevitable appearance. As Kelly West said about the emerging epidemics of diabetes in Native American populations in 1974, “Some had been nomadic hunters and meat eaters . . . while others had derived a substantial majority of their calories from fats. . . . Sugar consumption has been increasing in most, if not all, of the United States tribes in whom diabetes rates have recently increased precipitously. This same association has been observed in Eskimos of Alaska, Canada, and Greenland as well as in Polynesians.”
And on those very rare occasions when sugar consumption declined—as it did, for instance, during World War I, because of government rationing and sugar shortages—diabetes mortality invariably declined with it. “Rises and falls in sugar consumption,” wrote Haven Emerson and Louise Larimore in 1924, “are followed with fair regularity . . . by similar rises and falls in the death rates from diabetes.”
In 1974, when the sugar industry hired pollsters to survey physicians for their attitudes toward sugar, most of those physicians
said they thought sugar consumption accelerated the onset of diabetes. (One advertising executive, later asked if his children ate a particularly sugar-rich cereal for which he had modeled the ad campaign on Snoopy and the Red Baron, admitted that they never did: “You need an insulin shot if you eat a bowl of that,” he said.) In 1973, Jean Mayer of the Harvard School of Public Health, probably the most influential nutritionist of the era, was suggesting that sugar “plays an etiological role in those individuals who are genetically susceptible to the disease.” Such a statement, of course, raises the obvious question of whether anyone ever gets the disease who isn’t genetically susceptible (with the rare exceptions of those individuals who sustain injuries or tumors that affect pancreatic function). Nonetheless, at scientific meetings on sugar and other sweeteners, researchers and clinicians would debate whether or not sugar caused diabetes or only helped it along in those somehow predisposed.
By the late 1970s, though, sugar had mostly vanished from the discussion. Dietary fat had been implicated as a cause of heart disease. Nutritionists and public-health authorities responded by rejecting the idea that sugar could be responsible for the diseases that associated with heart disease, which included both obesity and diabetes.
Researchers had also come to embrace a pair of related assumptions that were poorly tested and might or might not be true. The first is that type 2 diabetes is caused by obesity, because the two diseases are so closely associated, both in populations and in individuals, and obesity typically appears first (although more than one in every ten individuals diagnosed with type 2 diabetes is neither obese nor overweight). The second assumption, as the World Health Organization puts it, is: “The fundamental cause of obesity and overweight is an energy imbalance between calories consumed and calories expended.” “The only trouble with the American diet,” as Fred Stare, the founder and head of the nutrition department at Harvard University, said in 1976 on national television, is that “we eat too damn much.” The overeating was accompanied by a decrease in physical activity, attributed to changing modes of transportation and the mechanization of labor.
Public-health authorities have considered no investigations necessary to explain the obesity and diabetes epidemics, because they have assumed that the cause is obvious. Attempts to prevent diabetes in the United States, Europe, and Asia, and among populations worldwide, are almost invariably aimed at getting these populations to eat smaller portions and fewer calories, perhaps to avoid “fatty foods,” as particularly dense sources of calories, and to increase their physical activity.
Meanwhile, the latest surge in this epidemic of diabetes in the United States—an 800 percent increase from 1960 to the present day, according to the Centers for Disease Control—coincides with a significant rise in the consumption of sugar. Or, rather, it coincides with a surge in the consumption of sugars, or what the FDA calls “caloric sweeteners”—sucrose, from sugarcane or beets, and high-fructose corn syrup, HFCS, a relatively new invention.
After ignoring or downplaying the role of sugars and sweets for a quarter-century, many authorities now argue that these are indeed a major cause of obesity and diabetes and that they should be taxed heavily or regulated. The authorities still do so, however, not because they believe sugar causes disease but, rather, because they believe sugar represents “empty calories” that we eat in excess because they taste so good. By this logic, since refined sugar and high-fructose corn syrup don’t contain any protein, vitamins, minerals, antioxidants, or fiber, they either displace other, more nutritious elements of our diet, or simply add extra, unneeded calories to make us fatter. The Department of Agriculture, for instance (in its recent “Dietary Guidelines for Americans”), the World Health Organization, and the American Heart Association, among other organizations, advise a reduction in sugar consumption for these reasons primarily.
The empty-calories argument is particularly convenient for the food industry, which would understandably prefer not to see a key constituent of its products—all too often, the key constituent—damned as toxic. The sugar industry played a key role in the general exoneration of sugar that took place in the 1970s, as I’ll explain later. Health organizations, including the American Diabetes Association and the American Heart Association, have also found the argument convenient, having spent the last fifty years blaming dietary fat for our ills while letting sugar off the hook.
The empty-calories logic allows companies that sell sugar-rich products, or products in which all the calories come from these sugars, to claim that they, too, are fighting the good fight.
Excerpted from The Case Against Sugar by Gary Taubes. Copyright © 2016 by Random House. Excerpted by permission of Alfred A. Knopf, a division of Random House LLC. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.