Saturday, November 1, 2014

What is the Cause of the Obesity Epidemic?

The other day I noted how USDA diet recommendations have contributed to obesity. Today, I saw this article at Aeon Magazine on the obesity epidemic that makes an interesting observation:

...  over the past 20 years or more, as the American people were getting fatter, so were America’s marmosets. As were laboratory macaques, chimpanzees, vervet monkeys and mice, as well as domestic dogs, domestic cats, and domestic and feral rats from both rural and urban areas. In fact, the researchers examined records on those eight species and found that average weight for every one had increased. The marmosets gained an average of nine per cent per decade. Lab mice gained about 11 per cent per decade. Chimps, for some reason, are doing especially badly: their average body weight had risen 35 per cent per decade. Allison, who had been hearing about an unexplained rise in the average weight of lab animals, was nonetheless surprised by the consistency across so many species. ‘Virtually in every population of animals we looked at, that met our criteria, there was the same upward trend,’ he told me. 
It isn’t hard to imagine that people who are eating more themselves are giving more to their spoiled pets, or leaving sweeter, fattier garbage for street cats and rodents. But such results don’t explain why the weight gain is also occurring in species that human beings don’t pamper, such as animals in labs, whose diets are strictly controlled. In fact, lab animals’ lives are so precisely watched and measured that the researchers can rule out accidental human influence: records show those creatures gained weight over decades without any significant change in their diet or activities. Obviously, if animals are getting heavier along with us, it can’t just be that they’re eating more Snickers bars and driving to work most days. On the contrary, the trend suggests some widely shared cause, beyond the control of individuals, which is contributing to obesity across many species.
 The author also notes that weight gain is not spread evenly across sexes or income levels--in fact, women and people from lower incomes are more likely to obese.

The author suggests environmental factors may be playing an important role. For instance, some chemicals (e.g., "bisphenol-A (or BPA) that is used in many household plastics has the property of altering fat regulation in lab animals") cause people and animals to fatten up.
BPA has been used so widely — in everything from children’s sippy cups to the aluminium in fizzy drink cans — that almost all residents of developed nations have traces of it in their pee. This is not to say that BPA is unique. In any developed or developing nation there are many compounds in the food chain that seem, at the very least, to be worth studying as possible ‘obesogens’ helping to tip the body’s metabolism towards obesity. For example, a study by the Environmental Working Group of the umbilical cords of 10 babies born in US hospitals in 2004 found 287 different industrial chemicals in their blood. Beatrice Golomb, professor of medicine at the University of California, San Diego, has proposed a long list of candidates — all chemicals that, she has written, disrupt the normal process of energy storage and use in cells. Her suspects include heavy metals in the food supply, chemicals in sunscreens, cleaning products, detergents, cosmetics and the fire retardants that infuse bedclothes and pyjamas.
Other chemicals are also be looked at to see if the alter fat regulation. Another possibility is that by getting so much better at controlling out environment--specifically, regulating temperature via furnaces and air conditioners--we burn less fat. Using artificial light to disrupt the night/day cycle has the same effect. Also:

There is also the possibility that obesity could quite literally be contagious. A virus called Ad-36, known for causing eye and respiratory infections in people, also has the curious property of causing weight gain in chickens, rats, mice and monkeys. Of course, it would be unethical to test for this effect on humans, but it is now known that antibodies to the virus are found in a much higher percentage of obese people than in people of normal weight. 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. 

As with viruses, so with bacteria. Experiments by Lee Kaplan and colleagues at Massachusetts General Hospital in Boston earlier this year found that bacteria from mice that have lost weight will, when placed in other mice, apparently cause those mice to lose weight, too. And a study in humans by Ruchi Mathur and colleagues at the Cedars-Sinai Medical Center in Los Angeles, published in the Journal of Clinical Endocrinology and Metabolism earlier this year, found that those who were overweight were more likely than others to have elevated populations of a gut microorganisms called Methanobrevibacter smithii. The researchers speculated that these organisms might in fact be especially good at digesting food, yielding up more nutrients and thus contributing to weight gain. 

The researcher who first posited a viral connection in 1992 — he had noticed that the chickens in India that were dead of an adenovirus infection were plump instead of gaunt — was Nikhil Dhurandhar, now a professor at the Pennington Biomedical Research Centre in Louisiana. He has proposed a catchy term for the spread of excess weight via bugs and viruses: ‘infectobesity’.
 The author warns that the true answer may be a combination of factors.

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