Is Sugar an Addictive Poison?
Hypothesis: More sugar causes both more diabetes and more obesity
The Case Against Sugar, by Gary Taubes, Knopf, 368 pp., 26.95.
Less than 1 percent of Americans—1.6 million people—were diagnosed with Type 2 diabetes in 1958. As of 2014, that figure had risen to 9.3 percent, or 29.1 million. If current trends continue, the figure could rise to more than 33 percent by 2050. Something has clearly gone wrong with American health.
The rising rate of diabetes is associated with the rising prevalence of obesity. Since the early 1960s, the percent of Americans who are obese—that is, whose body mass index is greater than 30—has increased from 13 percent to 35.7 percent today. (Nearly 70 percent of Americans are overweight, meaning their BMIs are over 25.) Roughly put, the prevailing theory is that rising fatness causes rising diabetes.
But what if both are caused by something else? That is the intriguing and ultimately persuasive argument that Gary Taubes, author Why We Get Fat (2011) and cofounder of the Nutrition Science Initiative, makes in his new book, The Case Against Sugar.
For Taubes, sugar—be it sucrose or high-fructose corn syrup—is "the principal cause of the chronic diseases that are most likely to kill us, or at least accelerate our demise," explains Taubes at the outset. "If this were a criminal case, The Case Against Sugar would be the argument for the prosecution." In making his case, Taubes explores the "claim that sugar is uniquely toxic—perhaps having prematurely killed more people than cigarettes or 'all wars combined,' as [diabetes epidemiologist] Kelly West put it."
Taubes surveys the admittedly sparse research on sugar's psychoactive effects. For example, researchers have found that eating sugar stimulates the release of dopamine, a neurotransmitter that is also released when consuming nicotine, cocaine, heroin, or alcohol. Researchers are still debating the question of whether or not sugar is, in some sense, addictive.
In the course of his exploration, Taubes devastatingly shows that most nutrition "science" is bunk. Various nutritionists have sought to blame our chronic ills on such elements of our diets as fats, cholesterol, meat, gluten and so forth. Few have focused their attention on sugar. His discussion of how nutritionists started and promoted the now-debunked notion that eating fats is a significant cause of heart disease is particularly enlightening and dismaying. Nowadays the debate over the role of fats in cardiovascular disease consists mostly of skirmishes over which fats might marginally increase risk.
Interestingly, Taubes finds that a good bit of the research on fats was funded by the sugar industry. It is not just a coincidence that the low-fat food craze took off when the U.S. Department of Agriculture issued its first dietary guidelines in 1980 advising Americans to eat less fat. The added sugar that made the newly low-fat versions of prepared foods more palatable contributed to the rise in sweetener consumption. The USDA guidelines did advise Americans cut back on eating sugar, but they also stated that, "contrary to widespread opinion, too much sugar in your diet does not seem to cause diabetes." By the way, Taubes agrees since both sucrose and high-fructose corn syrup are essentially half glucose and half fructose there is no important metabolic differences between them.
Taubes reviews the global history of sugar consumption. The average American today eats as much sugar in two weeks as our ancestors 200 years ago consumed in a year. The U.S. Department of Agriculture estimates that per-person annual consumption of caloric sweeteners peaked at 153.1 pounds in 1999 and fell to only 131.1 pounds in 2014. A 2014 analysis of data from 165 countries found that "gross per capita consumption of sugar correlates with diabetes prevalence."
So how does eating lots of sugar cause disease? Reviewing the scientific literature, Taubes suggests that the high consumption of sugar eventually produces insulin resistance in the human body. That is, cells require higher and higher levels of insulin in order to coax them into metabolizing the extra glucose floating around in our bloodstreams. As a result, in order to reduce glucose levels in the blood, the pancreas produces more and more insulin—a spiral that often leads to diabetes. Taubes also cites findings that eating sugars boosts both cholesterol and triglyceride levels in the bloodstream, compounds that are associated with higher risks of cardiovascular diseases.
What happens to the fructose component of sugar? It is not regulated by insulin. Instead the oversupply of fructose goes to the liver, where it is directly transformed into fat. According to Taubes, additional glucose appears to increase the rate at which fructose is metabolized into fat. This process may well account for a good portion of the increase in obesity rates. Fat cells are not quiescent; they release various factors that increase inflammation, contributing to all sorts of chronic maladies, including arthritis, high blood pressure, heart disease, kidney disease, and dementia. A recent Australian study found that the lives of people who are diabetic at age 50 are on average three years shorter than those folk who are not.
What's the safe threshold for consuming sugar? Based on history, Taubes suggests that diabetes is rare until annual consumption begins to exceed 70 pounds per capita. He concludes that "enough evidence exists for us to consider sugar very likely to be a toxic substance, and to make an informed decision about how best to balance the likely risks with the benefits." He admits that his case is not definitive, but many readers will come away agreeing that sugar is a likely suspect in a great many modern maladies.