Science journalist Gary Taubes (“Why We Get Fat” and “Good Calories, Bad Calories”) took to the pages of the journal BMJ on Tuesday to argue (yet again) that we need to rethink what’s really behind the obesity pandemic.
Taubes, who recently co-founded the nonprofit Nutrition Science Initiative in San Diego, Calif., points out that the long-standing assertion that we get fat because we consume more energy (calories) than we expend through physical activity is just an hypothesis — and one, he suggests, that has been supported by flawed, less-than-rigorous science.
“Attempts to blame obesity epidemics worldwide on increased availability of calories typically ignore the fact that these increases are largely carbohydrates and those carbohydrates are largely sugars — sucrose or high fructose corn syrup,” he writes. “And so these observations shed no light on whether it’s total calories to blame or the carbohydrate calories. Nor do they shed light on the more fundamental question of whether people or populations get fat because they’re eating more, or eat more because the macronutrient composition of their diets is promoting fat accumulation … in effect, driving an increase in appetite.”
As he has done in his earlier writings, Taubes describes the history of obesity research, pointing out that World War II was primarily responsible for the doctrinaire acceptance of the energy-balance hypothesis. In the years leading up to the war, a competing hypothesis — that obesity is a hormonal, regulatory disorder — had gained much wider acceptance, particularly in Europe.
This theory proposes that spikes in the hormone insulin from high-carbohydrate foods lead, over time, to metabolic problems that cause more adipose tissue (fat) to form on our bodies. Because the fat cells are using up so many calories, other tissues and organs in the body become deprived of energy — a factor that leads to hunger and lethargy, two telltale characteristics of obesity. But “these would be compensatory effects of the fattening process, not causes,” explains Taubes.
From the beginning, proponents of this theory believed that some people are “constitutionally” more sensitive to this lipophilic (“fat-loving”) process.
But the hormonal hypothesis “was a German and Austrian hypothesis that was lost with the anti-German sentiment after the second world war and the subsequent embracing of English, rather than German, as the lingua franca of science,” writes Taubes.
“Medicine today is often taught untethered from its history — unlike physics, for instance — which explains why the provenance of the energy balance hypothesis is little known, even by those physicians and researchers who are its diehard proponents,” Taubes adds. “Nor is it widely known that a competing hypothesis ever existed, and that this hypothesis may have done a better job of explaining the data and the observations. Knowing this history is crucial to understanding how we got into the current situation and, indeed, how we might solve it.”
Different questions, different conclusions
Because of the ascendency of the energy-balance hypothesis, obesity is now viewed as an eating disorder “to be treated and studied by psychologists and psychiatrists, while laboratory researchers [focus] on identifying the physiological determinants of hunger, satiety, and appetite,” says Taubes.
But that approach, he argues, asks the wrong question: Why do we eat too much? The better and much different question is the one asked by the hormonal hypothesis: Why do we store too much fat?
Which question we ask is important, for it leads public health officials to very different health-policy conclusions about how to go about solving the global obesity pandemic. An example, writes Taubes, can be found in our attitudes and policies about sugary beverages:
The conventional wisdom has it that sugary beverages are merely empty calories that we consume in excess, although it is possible that the metabolism of fructose (a key carbohydrate component that makes these sugars sweet) in the liver somehow circumvents leptin signaling, leading us to consume these beverages and their calories even when we’re not and shouldn’t be hungry. [Leptin is a hormone that plays a key role in regulating energy, or calorie, intake and expenditure and, thus, appetite.] The hormonal or regulatory hypothesis also focuses on the metabolism of fructose in the liver, but rather than leptin it uses evidence suggesting that fructose metabolism can induce insulin resistance, leading in turn to raised insulin levels and trapping fat in fat cells — increasing, in effect, lipophilia.
Shortcomings of current research
In his BMJ article, Taubes also discusses the shortcomings of obesity research to date, which he claims is “incapable of answering the question of what causes obesity.”
He says his new organization, the Nutrition Science Institute, intends to “fund and facilitate rigorously well controlled experimental trials, carried out by independent skeptical researchers.”
“Our hope is that these experiments will answer definitely the question of what causes obesity, and help us finally make meaningful progress against it,” he adds.
He’ll have to hurry. The U.S. Centers for Disease Control and Prevention estimates that if current trends continue, 44 percent of American adults will be not just overweight, but obese, by 2030.