Why do so many of us get so fat? the answer appears obvious. “The fundamental cause of obesity and overweight,” the World Health Organization says, “is an energy imbalance between calories consumed and calories expended.” Put simply, we either eat too much or are too sedentary, or both. By this logic, any excess of calories—whether from protein, carbohydrate or fat (the three main components, or “macronutrients,” in food)—will inevitably pack on the pounds. So the solution is also obvious: eat less, exercise more.
The reason to question this conventional thinking is equally self-evident. The eat less/move more prescription has been widely disseminated for 40 years, and yet the prevalence of obesity, or the accumulation of unhealthy amounts of body fat, has climbed to unprecedented levels. Today more than a third of Americans are considered obese—more than twice the proportion of 40 years ago. Worldwide, more than half a billion people are now obese.
Besides getting fatter, we are also developing more metabolic disorders, such as type 2 diabetes, which is marked by hormonal abnormalities in the processing and storage of nutrients and is far more common in obese individuals than in lean ones.
The dissonance of an ever worsening problem despite a seemingly well-accepted solution suggests two possibilities. One, our understanding of why people get fat is correct, but those who are obese—for genetic, environmental or behavioral reasons—are unable or unwilling to heal themselves. Two, our understanding is wrong and hence so is the ubiquitous advice about how to make things better.
If the second option is true, then maybe what makes us fat is not an energy imbalance but something more akin to a hormonal defect, an idea embraced by European researchers prior to World War II. If so, the prime suspect or environmental trigger of this defect would be the quantity and quality of the carbohydrates we consume. Under this scenario, one fundamental error we have made in our thinking about obesity is to assume that the energy content of foods—whether avocado, steak, bread or soda—is what makes them fattening, not the effects that these foods, carbohydrates in particular, have on the hormones that regulate fat accumulation.
Given how often researchers refer to obesity as a disorder of the energy balance, one might assume that the concept had been rigorously tested decades ago. But a proper scientific vetting never actually happened. The experiments were too difficult, if not too expensive, to do correctly. And investigators typically thought the answer was obvious—we eat too much—and so the experiments were not worth the effort. As a result, the scientific underpinning of the most critical health issue of our era—the burgeoning rates of obesity and diabetes and their complications—remains very much an open question.
After a decade of studying the science and its history, I am convinced that meaningful progress against obesity will come only if we rethink and rigorously test our understanding of its cause. Last year, with Peter Attia, a former surgeon and cancer researcher, I co-founded a nonprofit organization, the Nutrition Science Initiative (NuSI), to address this lack of definitive evidence. With support from the Laura and John Arnold Foundation in Houston, Tex., we have recruited independent scientists to design and carry out the experiments that will meticulously test the competing hypotheses of obesity (and by extension, weight gain). The Arnold Foundation has committed to fund up to 60 percent of NuSI's current research budget and three years of operating expenses for a total of $40 million. The investigators will follow the evidence wherever it leads. If all works out as planned, we could have unambiguous evidence about the biological cause of obesity in the next half a dozen years.