The Case Against Sugar

by Gary Taubes

If the mortality records from Philadelphia in the early nineteenth century are any indication, the city’s residents were as likely to die from diabetes, or at least to have diabetes attributed as the cause of their death, as they were to be murdered or to die from anthrax, hysteria, starvation, or lethargy.*

A dozen classes of drugs are now available to treat the disease, and the market for diabetic drugs and devices in the United States alone is over thirty billion dollars yearly.

In fact, anywhere populations begin eating Western diets and living Western lifestyles—whenever and wherever they’re acculturated or urbanized, as West noted in 1978—diabetes epidemics follow.

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.

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.

This book makes a different argument: that sugars like sucrose and high-fructose corn syrup are fundamental causes of diabetes and obesity, using the same simple concept of causality that we employ when we say smoking cigarettes causes lung cancer.

Most of us today will never know if we suffer even subtle withdrawal symptoms from sugar, because we’ll never go long enough without sugar to find out.

Sugar does induce the same responses in the region of the brain known as the “reward center”—technically, the nucleus accumbens—as do nicotine, cocaine, heroin, and alcohol.

Sweets have become the currency of childhood and of parenting.

From the seventeenth through the nineteenth centuries, sugar was the equivalent, economically and politically, of oil in the twentieth. It was the stuff over which wars were fought, empires built, and fortunes made and lost.

By the 1920s, sugar refineries were producing as much sugar in a single day—millions of pounds—as would have taken refineries in the 1820s an entire decade.

Ice-cream making might have been the one culinary talent in which the United States led the world.

For those who would immediately dismiss the possibility that sugar itself may be responsible for more premature deaths than cigarettes, we have to consider the fact that cigarettes themselves would have been far less harmful and far less addictive had it not been for sugar.

One of the common themes in the history of medical research is that a small number of influential authorities, often only a single individual, can sway an entire field of thought.

When researchers realized that the French had relatively low rates of heart disease despite a diet that was rich in saturated fats, they wrote it off as an inexplicable “paradox,” and ignored the fact that the French traditionally consumed far less sugar than did populations—the Americans and British, most notably—in which coronary disease seemed to be a scourge.

In 1960, when Stare’s nutrition department broke ground on a new five-million-dollar building, it was paid for largely by private donations, including the “lead gift,” as Stare described it, of $1.026 million from the General Foods Corporation, the maker of Kool-Aid and the Tang breakfast drink.

The way we fund science in nutrition and chronic disease research is also partly responsible for this thinking. The confluence of diet and chronic disease is not a scientific discipline in which all or many of the researchers band together to answer a few critically important questions, although I would argue that it should be. The National Institutes of Health and other research agencies fund thousands or tens of thousands of researchers to answer thousands or tens of thousands of small questions, and the hope is that out of these pieces a coherent picture will emerge. Instead, what we have is a cacophony and the assumption that if so many researchers are studying so many different pieces of the puzzle, it must be a very complex problem.

Here we’re back to those few observations that are indisputable and that we have to explain. In the second half of the nineteenth century in Western populations, and far more recently in others, obesity and type 2 diabetes emerged, eventually to become the dominant diseases of modern times. Insulin resistance characterizes both these disorders. And those who are insulin-resistant, who suffer from obesity and type 2 diabetes, are at higher risk of a host of other chronic diseases—the Western diseases, as Burkitt and Trowell described them—and these diseases, too, are associated with insulin resistance. How do we explain these observations? What has changed that could cause the emergence of these diseases worldwide and the insulin resistance that is associated with so many of them? What changes in our diets and our lifestyles can explain these changes in disease patterns? Is a simple hypothesis sufficient to do it? Is it that we’re all simply eating too much and exercising too little, which is the one simple answer that the nutritional establishment will embrace in the face of so much evidence to the contrary? Another simple answer, and a more likely one, is sugar.