People are often surprised to find out I was overweight as a child. (They might not be if they saw me around the piles of holiday cookies and candies the past few weeks.) By current standards I might only have qualified as pudgy, but at the time I was considered fat. I lost weight in high school by dieting, gained it back in college, and then began exercising while in medical school (my main form of exercise before that was avoiding gym class). For the past 35 years I have been at essentially the same weight. Which begs the question – is that due to genetics or environment? Was my overweight childhood a fate that I was able to overcome through behavioral change, or is my genetic destiny to be thin, albeit temporarily derailed by the excesses of a food-centered Long Island upbringing?
With obesity and its attendant morbidity and mortality one of the most critical public health challenges facing America and the world, this question of nature or nurture is an important one. It’s also a silly one. There is virtually no health condition that is solely genetic or environmental; everything is a result of complex interactions between the two. And while obesity is undoubtedly due to both, the modern obesity epidemic can only be explained by the environment. After all, the human genome hasn’t changed a lot in the past 40 years. Our environment has.
Now, when it comes to treating obesity, acknowledging the role of genetics is important, to prevent moralizing about “willpower” on the part of health professionals, and to establish appropriate approaches to weight loss and reasonable expectations. But with obesity, as with almost every other public health problem, prevention is better than treatment. And that won’t succeed until we understand and acknowledge the critical role of the environment.
Studies have uncovered associations between the rise of obesity and a variety of environmental factors, including not only modern behaviors like a sedentary lifestyle and larger portion sizes, but also passive elements of the environment such as proximity to sidewalks and parks; the widespread substitution of high fructose corn syrup for sugar (not all sweeteners are equally obesogenic, it seems) and the addition of sweeteners to nearly every processed food; other common food additives like emulsifiers, found in everything from mayonnaise to ice cream, that can produce harmful, obesity-promoting changes in our normal gut bacteria; and a host of endocrine-disrupting chemicals that are nearly ubiquitous.
So why do we keep seeing stories blaming our genes? I have two theories. First, as with almost everything else in the American healthcare system, the financial and other incentives are geared toward treating disease, not preventing it. And surgical and medical treatments that change your biology are probably more effective than those based on behavior change, more appealing , and more profitable. Second, those environmental factors contributing to the obesity epidemic are themselves part of multi-billion dollar industries. There is a strong incentive to distract the blame. A recent analysis of studies of the relationship between soft drinks and obesity, for example, found that industry-sponsored studies were 34 times more likely to find no association between drinking soda and obesity than those without industry funding. Such conflict-of-interest bias is not unique to this issue, but the article notes that a more typical degree of bias is a 2-5 fold relative risk in favor of a company’s products. When it comes to obesity research, even the biases are supersized. And the biggest loser is the public.