Obesity continues to infiltrate the news. Last week, we reported on one study linking the obesity epidemic to the consumption of sugar-sweetened beverages and another study documenting the increase in obesity among infants. Now this week the feature article in the NY Times Sunday magazine is all about “infectobesity,” the radical new theory that some forms of obesity may have infectious causes. This article has quickly become the most-read article in the NY Times, which isn’t at all surprising to us, but just goes to show the level of interest in the topic. Now if only something could be done about it!
While overeating is certainly one factor behind obesity, it is most likely not the only cause. Over the past decade, more than 50 genes have been found to contribute to obesity. Yet, if genes and eating control our weight, how is it possible for identical twins with identical genes and diets to have vastly different weights? The answer could lie in microorganisms living inside of us.
Out of all the cells in the human body, only one out of 10 is a human cell. Everything else is microbial. Beginning with our journey down the birth canal, we are constantly exposed to various microbes which populate our gut. These microbes aid in our digestion and absorption of nutrients. They create capillaries, produce vitamins, make enzymes which metabolize bile acid and cholesterol, break down plant polysaccharides, and extract and stores calories. Although we all have these microbes in our guts, the makeup of our microbe populations is different based on the microbes to which we are exposed and the antibiotics which we take. These small differences in the make up of our microbe populations can translate into huge differences between people. As Jeffrey Gordon of Washington University explains, although a bowl of Cheerios should theoretically have 110 calories no matter who eats it, different people will actually absorb different amounts of calories due to differences in their gut flora. “A diet has a certain amount of absolute energy,” he says, “but the amount that can be extracted from that diet may vary between individuals — not in a huge way, but if the energy balance is affected by just a few calories a day, over time that can make a big difference in body weight.”
In animal studies, microbe-free mice were found to be leaner than their normal counterparts. Without gut microbes, they could not extract calories from some of the food they ate, so the food passed through their bodies without being used or converted to fat. Thus, although they ate more food than the normal mice, the germ-free mice had 60% less fat. However, when gut microbes from normal mice were transplanted into the germ-free mice, the germ-free mice quickly gained weight and soon resembled their normal peers. In another experiment, Gordon compared normal-weight mice to mice with a genetic mutation that made them fat. Like humans, the microflora in both sets of mice predominantly consisted of two types of bacteria, Bacteroidetes and Firmicutes. However normal mice had more of the Bacteroidetes and the obese mice had far more Firmicutes. The role of these different proportions is still unclear, but Gordon and colleagues have been collecting stool samples from normal-weight and obese humans to determine whether a lean-type and obese-type microflora exists and whether weight loss results in a change in a person’s microflora..
In addition to bacteria, viruses may be another infectious cause of obesity. Nikhil Dhurandhar happened upon this idea while studying autopsies of chickens infected with the SMAM-1 virus. He noticed that these chickens had excess abdominal fat, which seems counterintuitive to their wasting away. Even more intriguing, the chickens had low levels of cholesterol and triglycerides despite their excess fat. The same thing happened to humans infected with the virus. Several human adenoviruses, which are closely related to the SMAM-1 chicken virus, have produced the same effects in humans, including AD-36, AD-5, and AD-37. It is still unclear exactly how these viruses cause obesity. They may affect fat cells directly, leading to increased fat cell numbers and sizes or they may impair the brain’s appetite control mechanism. Alternatively, viral infections may result in obesity via an indirect effect through inflammation.
Critics of infectobesity feel that there are other, more plausible, biological causes of obesity, such as the thrifty genotype hypothesis. According to this theory, humans who were able to store food during years of plenty for use during periods of scarcity had an evolutionary advantage. However, now that food abounds, that advantage has turned into a disadvantage.
However, if microbes do turn out to be relevant, it could change the way the public thinks about obesity. This new research will challenge the idea that fat people are lazy and not as virtuous as thin people. It might also help non-obese people understand how difficult it is for obese people to lose weight and maintain that weight loss. However, the danger of any biological explanation of obesity – be it genetics or microbes – is that people will fall into the predeterministic trap and dismiss behavior as irrevelent. Since we are still years away from developing therapies to deliberately manipulate the gut microflora or interfere with the offending microbes, behavior modification remains the most effective weapon that we have in the fight again obesity, whatever its cause.