Via this Salon article, news of paper on PLoS by Lisa Gross with the imposing title of “The Toxic Origins of Disease.”
(Sidebar:
What if scientific and medical literature were considered a public resource, available to use any way you chose at no cost; all you would have to do is give credit to the author and source as described in the Creative Commons Attribution License?
That’s from this page, which phrases it better than I can. PLoS, the Public Library of Science, solves many of the super-expensive-journal problems I had in school and the ability to google-read-cite is magnificent. I’m a big fan.)
Anyway. The paper hypothesizes that Bisphenol A, a very common polymer used to make polycarbonates and epoxy resins, causes obesity. There’s a lot of it around, and it is known to act like an estrogen receptor agonist. That’s bad:
Recent studies have confirmed that bisphenol A exposure during development has carcinogenic effects and produce precursors of breast cancer.[6] Bisphenol A has been shown to have developmental toxicity, carcinogenic effects, and possible neurotoxicity.
That’s from Wikipedia’s entry on the chemical, which is fairly conservative. OK, so we know its bad news, and maybe you should lose the Nalgene bottle for something in stainless steel. (For their part, Nalgene has their position here.) I don’t think it passed, but California was going to ban B-A from kid’s products. (Update: it died in committee.)
The Gross paper is fascinating. As you’d probably expect, the companies involved have a bit of an agenda:
By the end of 2004, they had identified 115 published studies on low doses of bisphenol A. They also found a troubling trend. Ninety percent of government studies found significant effects of bisphenol A at doses below the EPA’s lowest adverse effect level, but not a single industry study found any effect. Many of the industry studies, they pointed out, either used a rat strain with very low sensitivity to estrogen or misinterpreted failure to find effects with positive controls. Vom Saal and Hughes urged the EPA to conduct a new risk assessment on bisphenol A.
The news gets even worse:
Soto exposed pregnant rodents to “minuscule doses of bisphenol A, the same doses that humans are exposed to, according to the CDC.” In rats, this treatment produced overweight female offspring; in mice, adding the estrogenic chemical produced female offspring that behaved like males. Both rats and mice also had altered ovarian cycles. In a second round of experiments in mice, in utero bisphenol A exposures induced changes in mammary gland development that began in fetal life and persisted.
…
The changes in the breast and genital tract were expected, Soto says, but some of the behavioral effects and obesity came as a complete surprise. “We were looking at an estrogen thinking it was going to affect the reproductive system and mammary gland only, but then these two other things emerged without us ever imagining that.”
Bisphenol A might induce epigenetic changes by altering patterns of DNA methylation, a chemical modification that controls gene expression, or by activating or silencing genes at the moment of exposure during a critical period of development. Soto is pursuing these possibilities. “A single exposure during a point of vulnerability may suffice,” Soto says. “You know the thalidomide story. You can have thalidomide every day of your life and you will be fine. But [take it] at certain times during pregnancy, your child will end up with no arms.”
OK, that last bit is rather alarmist in tone. The link to obesity, however, seems to be more solid:
In the thrifty phenotype hypothesis, undernutrition in the womb programs metabolic systems to expect a postnatal world of undernutrition. From an evolutionary perspective, genes that promote insulin resistance (thereby limiting glucose uptake) and fat storage would prove advantageous in times of famine. But in a world of fast foods, empty calories, and supersized meals, the same genes would promote obesity, insulin resistance, and type 2 diabetes. Interestingly, a class of drugs used to treat type 2 diabetes (called thiazolidinediones) activates PPAR to reverse insulin resistance in muscle and liver, but in doing so increases fat mass by facilitating triglyceride uptake in adipocytes.
When vom Saal generates growth-restricted mouse pups by exposing mothers to bisphenol A, the babies go through a “ballistic postnatal growth period.” A second group of mice starts out “really heavy” and stays that way. Vom Saal’s two types of obese mice have 430 genes with different activity in their fat cells, exhibit substantial differences in glucose tolerance and leptin levels (leptin regulates appetite and energy expenditure), and lose weight at different rates.
Though understanding the underlying causes of these differences will take “multiple lifetimes of work,” vom Saal says, it’s clear that both animals end up heavy in entirely different ways, with entirely different physiological, fat metabolism, and regulatory systems. “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.”
I had previously posted about sugar, and it’s probably also true that we have a lot more obese people now that we used to. The idea that, as Leonard put it, “Does plastic make us fat?” was an important question.
One of the Gross papers’ points that struck me was that
What’s more, production of these chemicals closely tracks the rise of obesity.
Along with the explosions in autism and asthma, the sudden change in the morphology of Americans since the 70s demands answers. Why did we start to get fat (and ill) all of a sudden? What changed? The sugar/corn syrup change is probably part of it, but the correlation with bisphenol-A production is also a possibility. Correlation is not causation, of course, but I rather hope that we can overcome the vested interests and figure out what the hell happened. Papers like this are an excellent start.
