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.
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.
Another non-traditional explanation of weight gain is the environmental abundance of estrogen-mimicking chemicals, which are found in everything from shampoo to plastic water bottles.
Known as obesogens, these foreign chemicals are thought to disrupt normal developmental control over energy balance and fat storage. Although still an emerging hypothesis, researchers know that widely used chemicals such as bisphenol A (BPA) can disrupt endocrine function. Toxicology data, all of it done on laboratory animals, has found that low doses of BPA, which is used in plastics, lining of cans, and baby bottles, can lead to adipogenesis, or fat cell accumulation. Other potential adverse effects of BPA have led places like San Francisco to ban it.
Another potential class of obesogens is organotins, which are widely persistent organic pollutants. Because of their effect on the reproductive systems of marine wildlife, there is an international ban on their use in ship paint. However, they’re still used in other applications, but their affects on humans health haven’t been studied.
Much more research on the role of obesogens in obesity needs to be done. A 2006 article on obesogens and health notes, “the roles of environmental chemicals in the etiology of complex diseases such as obesity, type 2 diabetes, and cardiovascular disease are currently poorly understood.”
Not time to seal yourself in a (paper) bubble just yet.
While certainly these theories are just that—theories, still in discovery mode—they do present interesting hypotheses for why some people might pack on the pounds while others don’t. While we know that food, exercise, and genetics are the crux of body size, we’ve also found other factors—exposure to advertising, living in an unsafe neighborhood, and sleep patterns—that contribute to weight gain. Like with many diseases, there could be many routes to the same outcome. But until they’re figured out, I’ll stick with the tried and true: exercising and eating my veggies.