A D V E R T I S E M E N T
COURTESY OF BRUCE BLUMBERG
Exercise all you want, but it’s pollution that may be a factor in weight gain, according to UC Irvine associate professor Bruce Blumberg.
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Despite the nagging of diet experts, fitness instructors, public health officials, doctors, nurses and moms, the tide of obesity that has practically engulfed Western civilization over the past two decades shows no sign of reaching its ebb.
In the United States, the percentage of adults who are obese — defined by the National Institutes of Health as a body-mass index exceeding 30 — has doubled since 1990, climbing from 12 percent to a whopping 24 percent in 2005, closely tracking Oregon figures, according to the Oregon Health Division.
For the most part, the blame for the obesity epidemic has fallen on diet and exercise, with particular emphasis on familiar evils such as the proliferation of junk food, the advent of the remote control, trans fat, ever-longer commutes and even the disappearance of physical education in schools.
But now some researchers have identified a new suspect: pollution.
Attributing obesity to diet and exercise is “practically scientific dogma at this point,” says Bruce Blumberg, associate professor of developmental and cell biology at UC Irvine. But, he continues, “diet and exercise are simply not adequate to explain the explosion of obesity in Western countries.”
Instead, Blumberg believes the obesity epidemic actually is due, in part, to industrial pollution — specifically to low levels of toxic compounds he calls “obesogens.”
Just as exposure to carcinogens can trigger cancer, Blumberg and other researchers say exposure to obesogens can trigger a dramatic increase in the amount of fat produced in a person’s body, leading to excess weight and obesity.
The precise mechanism by which these obesogens operate remains dimly understood. They belong to a class of compounds known as “endocrine disrupters” because they block or pervert the operation of the hormones that govern crucial biological processes such as growth, reproduction, sexual development and behavior.
Five years ago, Blumberg was studying the biological effects of various marine pollutants — in particular, tributyl tin, or TBT, a pesticide notorious for its toxic properties, such as bizarre mutations in the shells of mollusks and the sex organs of sea snails.
Blumberg and his co-workers exposed female frogs to extremely low levels of TBT; as expected, TBT did indeed cause sexual mutation among frogs. But what was really striking, he says, was that the hapless amphibians got fat — really fat.
“To be honest, I will have to say we stumbled on this,” he says.
Although most of the research on endocrine disrupters has focused on their potential effects on sexual development, fat production also is regulated by the hormone system and is, theoretically at least, just as susceptible to disruption.
Blumberg injected mice with TBT and observed similar results: fat rodents. Even more significant, the compound triggered obesity in ridiculously min-uscule quantities. In fact, Blumberg and his colleagues demonstrated effects from TBT at 27 parts per billion — the rough equivalent of 4 tablespoons in an Olympic-sized swimming pool.
Blumberg concluded that the fattening effects of TBT and a group of similar compounds known as organotins are so profound that even trace amounts could trigger an increase in weight. “The introduction of organotins is likely to be a contributing factor to the obesity epidemic,” Blumberg says.
Toxicology experts concur that some compounds are so potent that they can indeed trigger changes at minute concentrations, at least in the test tube.
“It sounds absurd, but it’s not inconsistent with what we see in the lab,” says Fred Berman, director of the Toxicology Information Center at the Center for Research on Occupational and Environmental Toxicology at Oregon Health & Science University.
The disruptive effects of organotins stem from their propensity to stimulate a particular hormone receptor that plays a key role in maintaining the body’s metabolism, in effect telling the body which kind of cells are in short supply and need to be grown.
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