It’s clear that overeating and sedentary behavior are the major culprits behind America’s obesity epidemic. An abundance of cheap, calorie-dense, supersized food coupled with mass amounts of advertising and a car-dependent lifestyle have all grown in accordance with our expanding waistlines. But there other influences, less obvious and more speculative, that are being investigated. These possible factors might be contributing to the problem and perhaps giving clues to what we can do about it.
Infectobesity
Although some experts claim that obesity spreads through social networks like a virus, a common human virus might actually contribute to the rising tide of obese populations.
Adenovirus-36 (Ad-36)—one strain in a family of about fifty adenoviruses that are responsible for colds, respiratory infections, and eye infections—was first linked to weight gain when Nikhil Dhurandhar, now a professor at Louisiana State University, noticed that chickens infected with Ad-36 became plump instead of wasting away with disease. Taking it to the lab, he has shown that when chickens and mice are infected with Ad-36, they become very fat compared with controls fed the same amount of food. Paradoxically, the obese animals had low levels of cholesterol and fatty acids in their bloodstream—the opposite of what happens with normal obesity. The viruses preferentially infected fat cells over muscle cells and could be detected up to sixteen weeks after infection.
Dhurandhar coined the phenomenon “infectobesity.” Taking the findings to human populations, he found that almost 30 percent of obese people have antibodies (an indicator of exposure) to Ad-36, whereas only 5 percent of non-obese people have them. Similar to the animal studies, the infected obese people had low levels of cholesterol and fatty acids in their blood, while the obese people without evidence of infection did not share this profile. However, it’s unclear from this study whether infection preceded obesity or came afterward.
In vitro research has shown that the virus can increase how much fat a cell holds and can predispose cells to become pre-fat cells.
Much more research needs to be done to understand how the virus acts in a human population. It’s clear that not everyone infected with Ad-36 becomes obese and not every obese person is infected with Ad-36. But it’s an interesting hypothesis and one that will surely lead to more interesting research.
The Bacterial Bulge
Viruses aren’t the only microbes that might play a role in obesity. It’s no surprise that microorganisms, which exist in greater numbers in and on our bodies than our own cells, may also alter how we extract energy from food. Many of our gut microbes have evolved symbiotically, enabling us to break down components of food, like large polysaccharides or fiber that we would not have otherwise been able to; they can also regulate genes that promote fat deposition.
In the human and mice gut, there are two main types of bacterial groups, the Bacteroidetes and the Firmicutes. Researchers have found that the proportion of the groups differ depending on whether the host is thin or fat. Normal weight mice have more Bacteroidetes than Firmicutes in their gut microflora, and obese mice have more Firmicutes.
Trying to determine whether the different compositions were a cause or an effect, a group of researchers at the Washington University School of Medicine infected germ-free mice with gut microbes from other mice. Despite eating less, the germ-free mice increased their body fat within weeks of colonization of the microbes. The microflora helped the mice extract more calories from the food they were eating; researchers hypothesize that the intestinal milieu in obese people may be more efficient in extracting energy from food.
Although it’s unclear whether the altered gut microflora is a cause or effect of obesity, researchers are trying to figure out whether weight loss can alter a person’s microflora and just how much an influence the little gut bugs have on our waistlines.
