Can a child contract obesity like the flu or tuberculosis, through proximity to someone who has it? “The etiology of obesity is multifactorial,” said a study from the Università del Piemonte Orientale in Italy, quoted in a previous Childhood Obesity News post. As science marches on, it begins to look as if obesity might have many contributing causes. The maverick German food chemist Udo Pollmer has claimed there are more than 100, though the list has proven to be Internet-elusive. But just as a thought experiment, what if there were 100 possibilities? Even if each one of them only caused 1% of obesity cases, the cumulative effect would wreak plenty of havoc.
The energy-balance formula of calories-in/calories-out is well established and has ostensibly been proven by millions of people who limit their food intake and are able to work out. It’s a difficult theory to shake. But what if, as Dr. Richard L. Atkinson of Virginia Commonwealth University believes, adenovirus-36 has something to do with obesity? The flab creeps up slowly, but the fat cells of infected lab animals grow larger and more numerous.
Dr. Jeffrey Schwimmer of the University of California, San Diego, is an expert in fatty liver disease in children and also studies obese children’s quality of life. A team he led did research on adenovirus-36, finding evidence of it in 1 out of every 7 kids in their study, and most of the kids who tested positive were in fact obese. We’re talking about an average weight difference of 50 pounds over the uninfected children. Also, David Berreby reports:
A research review by Tomohide Yamada and colleagues at the University of Tokyo in Japan, published last year in the journal PLoS One, found that people who had been infected with Ad-36 had significantly higher BMI than those who hadn’t.
A virus is not the only critter that has been accused of causing obesity. Inside a person’s body, there are 10 bacteria for every single human cell. Some are beneficial, some are harmful, and most of them, nobody knows what the heck they’re doing. Normal-weight and obese people have different kinds of gut bacteria, and we know very little about that disparity. Scripps Clinic gastroenterologist Dr. Franklin Tsai wrote:
Metagenomic studies demonstrated that certain mixes of gut microbiota may protect or predispose the host to obesity. Furthermore, microbiota transplantation studies in germ-free murine models showed that the efficient energy extraction traits of obese-type gut flora are transmissible.
Berreby notes that human testing found more of the bacterium Methanobrevibacter smithii in overweight people than in thin ones. The little bugs seem to be unusually adept in sucking the nutrients out of food. (Maybe this could help people in parts of the world where there isn’t enough to eat.)
If gut bacteria from a fat mouse are transported to the intestine of a thin mouse, the thin mouse gets fat. That’s “infectobesity,” and the same experiment would not be allowed with humans. But one of the arguments for the existence of contagious fat is that it seems to have spread from the east to the west coast of America in a pattern familiar to epidemiologists. Many health care professionals feel that “infectobesity” is a dangerous concept that might tempt people to abdicate all personal responsibility and accountability. On the other hand, if some people really and truly cannot help being fat, the world is unnecessarily cruel to them.
Your responses and feedback are welcome!
Source: “Jeffrey Schwimmer, M.D.,” UCSD.edu
Source: “The microbiome and obesity: is obesity linked to our gut flora?” NIH.gov, August 2009
Source: “David Berreby rejects the diet+exercise model of obesity epidemic causation,”
Image by Thomas Fisher Rare Book Library