This weekend, The New York Times Magazine featured an article entitled, “Fat Factors,” suggesting that a previously unconsidered factor may be to be blame for your weight—microogranisms.
The article’s author, Robin Marantz Henig, describes recent research indicating yet another biological theory of weight—we already have about 50 “guilty” obesity genes, some of which regulate appetite, satiety cues, and activity level. But now, scientists are exploring the possibility that intestinal microbes (e.g., bacteria, fungi, etc.) may play a role in how fat you come to be. And, lest you have any lingering doubts about an uncertain future, Jeffrey Gordon, the director of the Center for Genome Sciences at Washington University, informs us: “‘Microbes colonize our body surfaces from the moment of our birth. . . . They are with us throughout our lives, and at the moment of our death they consume us.’”
According to Henig’s article, microbes (microflora) accomplish a multitude of gastro-intestinal tasks, including the production of vitamins and enzymes, as well as the facilitation of digestion. Henig writes that they “help extract calories from the food we eat and help store those calories in fat cells for later use—which gives them, in effect a role in determining whether our diets will make us fat or thin.” Thus, my 450-calorie meal may be different than yours. It’s possible that I will extract and store 400 of these calories, you only 300, based on varying levels of intestinal microbes, thus complicating the classic calories-in-versus-out method of weight-loss or -maintenance. And, the formulaic 3,500-calorie reduction requisite for a one-pound weight-loss? Again, not so rigid when microbes are involved.
The Times article details animal studies, suggesting that bacterial microflora and/or exposure to certain viruses (“infectobesity”) lead to increased incidence of obesity. In other words, catching a virus can make you fat. Correlational studies in humans seem to support this notion—those with certain viral antibodies are more likely to be obese. Viruses may lead to increases in fat-cell counts and size or may toy with the brain’s satiety center.
While data are still preliminary, researchers are already toying with antibody tests (documenting exposure to one of the implicated viruses), and as you might imagine, antiviral-drug administration looms in the horizon. What I find most interesting about this report are its psychological and sociocultural correlates. Here, we have yet another biological theory of weight (the existence of obesity genes, preceding it) and yet, we still hold strong to the belief that obesity is a psychological condition, an individual failure of will-power, conviction, and self-regard, when in fact, there are plenty of “overweight” people who eat no more than their thinner counterparts. More and more, research is debunking that myth. Henig details an interesting example discussed by Rudolph Leibel, a Columbia University obesity researcher, “. . . if you take two nonobese people of the same weight, they will require different amounts of food depending on whether or not they were once obese. . . formerly fat people need to eat less than never-fat people to maintain the exact same weight.” The possibility of a microbial factor in the incidence of obesity lends weight to the notion that losing weight may be more of an uphill battle than previously thought.
And there seems to be good reason for this. Transport overweight people back in time, and they’re likely to fare better than those who are thin. As Henig notes, the “thrifty-genotype” hypothesis of weight suggests that historically, there was an evolutionary advantage to packing on the pounds. Now, technologically advanced beyond famine and draught, there’s no such need for biological stores, but let’s not underestimate the power of context—put obese people in another time and another place, and they’re royalty, exalted for their natural inclination toward getting fat and “keeping it on.” They survive, while the skinny perish, somehow unable (or not having the discipline) to eat enough.