Does plastic make us fat?
A ubiquitous chemical in common plastic may play a role in the obesity epidemic. The chemical industry is unamused.
The basic story line of "The Toxic Origins of Disease," a superb exposé in the June issue of PLoS Biology by science writer Liza Gross, fulfills a classic archetype. Publicly funded scientists determine that a commonly used substance may be harmful to human health. The industry that produces said substance responds in an all-out assault to undermine their data. Cue a lobbying firm that cut its teeth representing tobacco companies and the cast of characters is perfect.
In this case, the chemical at issue is bisphenol A, a basic building block of polycarbonate plastic, and, according to Gross, "one of the highest-volume chemicals in commercial production." A bevy of publicly funded researchers have found evidence that low doses of bisphenol A interfere with embryonic development in animals by exposing them to higher levels of hormones, such as estrogen, than normal. The chemical industry has fought back by commissioning scores of studies that find exactly the opposite. This leads to some lovely statistical info-nuggets: A survey conducted in 2005 found that of "115 published studies concerning effects of low doses of bisphenol A in experimental animals, 94 percent of publicly funded studies found evidence of harm while 100 percent of chemical industry studies found no evidence of harm."
Gross' treatment of the struggle over bisphenol A is a case study in how to do hard-science muckracking. She is sensitive to the nuances involved in exploring complex biological interactions that involve numerous variables, rigorous in her presentation of the chemical industry's push-back, and through it all, thoroughly compelling. I've been a fan of the Public Library of Science's efforts to break the stranglehold that closed-access journals have over the publication of scientific research since its inception, but aggressive journalism like this raises the ante several notches higher.
The efforts of the chemical industry to combat findings that a ubiquitous synthetic chemical (traces of which can be found in the urine of just about every living human being in the United States ) might cause developmental and reproductive defects in humans, even when ingested in low doses, are not surprising. But there is one aspect to this story that is quite eye-opening.
There appears to be evidence that the damage done by bisphenol A during embryonic development may be scrambling the signals that fat cells normally receive during prenatal and neonatal development. After the initial distortion, the affected fat cells never work properly again. Affected animals are unable to properly metabolize their normal diets, leading to obesity. And guess what? The introduction of bisphenol A into the human environment in significant quantities tracks pretty closely, in timing, to the advent of the so-called obesity epidemic in the United States.
The equation that connects bisphenol A to obesity is complex. It's not a simple matter of 1 plus 1 equaling 2. Gross concludes "The Toxic Origins of Disease" by quoting Fred vom Saal, one of the first scientists to discover the possible harm caused by exposure to low doses of bisphenol A.
In this case, the chemical at issue is bisphenol A, a basic building block of polycarbonate plastic, and, according to Gross, "one of the highest-volume chemicals in commercial production." A bevy of publicly funded researchers have found evidence that low doses of bisphenol A interfere with embryonic development in animals by exposing them to higher levels of hormones, such as estrogen, than normal. The chemical industry has fought back by commissioning scores of studies that find exactly the opposite. This leads to some lovely statistical info-nuggets: A survey conducted in 2005 found that of "115 published studies concerning effects of low doses of bisphenol A in experimental animals, 94 percent of publicly funded studies found evidence of harm while 100 percent of chemical industry studies found no evidence of harm."
Gross' treatment of the struggle over bisphenol A is a case study in how to do hard-science muckracking. She is sensitive to the nuances involved in exploring complex biological interactions that involve numerous variables, rigorous in her presentation of the chemical industry's push-back, and through it all, thoroughly compelling. I've been a fan of the Public Library of Science's efforts to break the stranglehold that closed-access journals have over the publication of scientific research since its inception, but aggressive journalism like this raises the ante several notches higher.
The efforts of the chemical industry to combat findings that a ubiquitous synthetic chemical (traces of which can be found in the urine of just about every living human being in the United States ) might cause developmental and reproductive defects in humans, even when ingested in low doses, are not surprising. But there is one aspect to this story that is quite eye-opening.
There appears to be evidence that the damage done by bisphenol A during embryonic development may be scrambling the signals that fat cells normally receive during prenatal and neonatal development. After the initial distortion, the affected fat cells never work properly again. Affected animals are unable to properly metabolize their normal diets, leading to obesity. And guess what? The introduction of bisphenol A into the human environment in significant quantities tracks pretty closely, in timing, to the advent of the so-called obesity epidemic in the United States.
The equation that connects bisphenol A to obesity is complex. It's not a simple matter of 1 plus 1 equaling 2. Gross concludes "The Toxic Origins of Disease" by quoting Fred vom Saal, one of the first scientists to discover the possible harm caused by exposure to low doses of bisphenol A.
"We think that environmental chemicals like bisphenol A are likely to target subpopulations of individuals that are rendered very sensitive to these chemicals by virtue of their genes, genetic background, maternal -- fetal interactions .... and the amount of hormones they're exposed to."
The connection between fetal growth restriction, environmental estrogens, and obesity risk may be especially relevant for infertile couples, who are increasingly opting for in vitro fertilization [IVF]. For various reasons, many IVF babies are born premature and growth-restricted. Vom Saal worries that exposing this "highly sensitive subgroup" of babies to environmental chemicals that lead to accelerated postnatal growth will permanently alter their capacity to metabolize even normal diets and predispose them, like the mice in his experiments, to a lifetime of obesity.
Vom Saal acknowledges that trying to unravel all the "phenomenally complex" interactions and components that contribute to obesity is "like chipping away at the pyramid," but he has no doubt that animal studies on bisphenol A's effects have relevance to humans. "This chemical is harming snails, insects, lobsters, fish, frogs, reptiles, birds, and rats," vom Saal says, "and the chemical industry is telling people that because you're human, unless there's human data, you can feel completely safe."
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