It isn’t too often that you hear about the beneficial aspects of obesity. So when I saw a NY Times article with the title Obesity May Have Offered Edge Over TB I was intrigued. The article discusses a commentary published this week in JAMA by Jesse Roth, MD of Albert Einstein College of Medicine of Yeshiva University. Roth suggests that the proinflammatory responses triggered by obesity may have been protective against tuberculosis. In particular, Roth makes the case that increased levels of the cytokine tumor necrosis factor (TNF), a proinflammatory marker that increases with obesity, is a potent anti-tuberculosis factor. To support his claim, Roth points out that therapeutic treatments that decrease TNF activity are associated with increased risk of tuberculosis reactivation.

Roth then goes on to discuss that the obese subgroup likely had a selective advantage over the general population, and that may be the reason why so many people are prone to metabolic diseases today. In essence, this adds a new element to the thrifty gene hypothesis, suggesting that obesity was not only protective in times of famine but it was also protective against infectious diseases such as tuberculosis.

But we must not confuse association with causation. While Roth makes some interesting speculations about the effects of obesity on tuberculosis and how selective pressure has favored this group, the evidence provided is not causal. Roth reinforces this in his concluding remarks where he writes, “it is important to recognize that theoretical constructs, no matter how logical, may yield conclusions that are not correct.” In my opinion, it is more likely that sedentary lifestyle and calorie-dense diets are the major contributors to the array of metabolic diseases we know today. Nonetheless, it is difficult to tease out the genetic versus environmental components of metabolic diseases and it is likely that both play their part in contributing to metabolic syndromes.