Dr. Joan Bushwell's Chimpanzee Refuge

It’s not a sophisticated hypothesis, but it has a certain plausibility to it: Both marathoners and household accidents related the amateur synthesizing of methamphetamine have become increasingly prevalent in the past 10 or 15 years. Assuming that these phenomena are weakly linked at best is — though sensible — far more mundane than exploring possible cause-effect relationships, however spurious or extraneous these relationships appear.
Maybe meth-making leads to marathons by causing crankheads to run around as a result of either dopamine overload or the need to flee from the authorities, leading in turn to a general yen for perambulation, improved fitness, and finally 26-mile-long footraces. Or maybe I have things backward, and meth-makers who run marathons are chronically tired from overtraining, leading to inattentiveness and the sloppy handling of volatile reagents, thereby setting the stage for untold numbers of mobile homes to explode in the wee hours of otherwise tranquil Sonoma desert mornings.
Anyway, this was one of my first thoughts when I saw this article. My proposed meth-marathon link is obviously silly on its face, but fundamentally no sillier than thinking that a virus is likely to underlie the “obesity epidemic” that has bloated richer nations in the past few decades. But obesity is of special interest to people, and mysterious pathogens enthrall scientists, so it’s somewhat understandable that even some trained scientists can ignore the whipped-cream-covered elephant sitting in their collective lap and focus instead on the phantom fleck of gold across the room.

When a health problem with no readily identified cause affects a high fraction of a society’s population, it’s rarely long before public-health officials turn to searching for infectious agents to explain it. Medical researchers have long sought viral explanations for type I diabetes, multiple sclerosis, and other common and debilitating conditions. It’s part of being open-minded, thorough, and responsible. With advances in molecular genetics techniques, many of these same diseases have been scrutinized for links to DNA, often with success.
Obesity is a different story, though. For one thing, being too fat, while unquestionably associated with numerous morbid conditions, is itself a description, not a diagnosis. Not to trivialize any serious health issue, but saying that people “die of obesity,” while not entirely misleading, is like saying that they die of alcoholism, depression, or smoking. For another, and more importantly, while the proportion of overweight people has grown substantially since the Reagan administration or so, we know, and have known for a long time, what causes any one of these people — large or lean — to gain weight: taking in more calories than they expend.
The idea that viruses may be associated with obesity has actually been kicking around for a long time, as with the 1997 edition and the 2000 edition. But the urgency and appeal of this idea takes on added strength with every new report about our collective biggetry.
I need to be fair to researchers, especially given that — because I really don’t believe that I have to — I’m not taking a hard look as science they understand better than I do. That is, I’m confidently employing my lower GI tract in writing at least some of what I’m writing today. From the linked story:

“We’re not saying that a virus is the only cause of obesity, but this study provides stronger evidence that some obesity cases may involve viral infections,” says study presenter Magdalena Pasarica, M.D., Ph.D., of the Pennington Biomedical Research Center at Louisiana State University in Baton Rouge.
“Not all infected people will develop obesity,” she notes. “We would ultimately like to identify the underlying factors that predispose some obese people to develop this virus and eventually find a way to treat it.”

Most of this pedantry borders on trivial, but needs to be expressed because of the way the media reacts to studies involving obesity. But I take issue with the implication — perhaps a result of sloppy speaking — that people can “develop” a virus. This violates all sorts of biomedical definitions. People vary widely with regard to their susceptibility to different viruses, in terms of not only serological factors (e.g., how successful the virus is a reproducing in the body) but the severity of disease penetrance (e.g., how bad the symptoms of the resultant disease is); it is, however, misleading to say that people can develop pathogens as it is to say their stomachs can develop bacon double cheeseburgers.
The arcticle notes that “30 percent of obese people were infected with the Ad-36 virus in comparison to 11 percent of lean individuals.” That’s something to look at, and those numbers need to be viewed in light of the relative numbers of people in each “group” over time, something I’m not prepared to do. But in what way? We already know that people vary greatly in their individual tendency to pack on pounds, but what is more likely to be more recent, more potent, and more subject to modification: the emergence and spread of this virus, or the obvious changes in people’s habits in the 45 years since average weight began creeping up by 25 pounds in U.S. adults?
In any event, despite the considerable and ongoing rise in the number of overweight people in the U.S. and other biggeted countries, looking for a genuine viral origin implies finding a virus with these properties:

• It has caused stores like 7-11 to begin offering “Big Gulp” soda cups in sizes as large as 64 fluid ounces — vessels which in my not-that-distant youth were available only at joke shops.

• It has led to more soft-drink machines in schools.
• It has caused people to drive more and exercise less, in many cases by ratcheting up the amount of time people spend at work.
• It has, particularly in America, eroded the concept of cities being pleasant, compact spaces for people gather and navigate on foot; entire regions have been virtually rebuilt so as to accommodate the tendency toward suburban mall-sprawl and a grossly automobile-dependent way of life.
• It has driven up competition among restaurants, leading to bigger, richer portions and far more calories ingested per “unit satiety.”

If this adenovirus were a new and significant contributor to weight gain, it seems that we could assume that the number of non-overweight people would remain more or less consistent while the people already prone to chubbiness gained the lion’s share of the extra weight we as a whole have accumulated. That is, we should see something of a “rich-get-richer” phenomenon. But we don’t; while I believe there’s been some “stretching at the edge” (i.e., that the fattest people out there are now far fatter than previously), the fact remains that since 1960, the number of people with a body-mass index over 25 has increased by 50 percent. So the bottom line may be this: Any potential antiviral agent that can offset the likelihood of weight gain in some people is going to have a very limited benefit. Even those who are both overweight and virus-carriers would hardly be given a reprieve by the elimination of the virus from their symptoms, since people can and do clearly gain weight through unrelated mechanisms.
Maybe this is just a lengthy way of saying “I call B.S.!”, but just because there’s no easy solution to the multifactorial medical, psychosocial, and economic problem that obesity has become doesn’t mean that scapegoating borderline-to-negligible factors will help anyone, and the media can be counted on to do exactly that. If scientists do reach a consensus that some communicable agent can play a role in weight gain, I’d bet my life on it not being a significant contributor and certainly on its activity requiring triggering or potentiation by an already crystal-clear collection of environmental factors.