I’ve been following the saga of Bisphenol-A, aka BPA, for over three years now, ever since I used it as a case study in my course “Public Science and Public Policy.” BPA is a current rage as a cause of all things evil: cancer, diabetes, obesity, heart disease and probably flatulence.
BPA in tiny amounts is in a lot of things that we eat that come out of a can. It’s a popular liner that prevents corrosion and extends shelf life, no doubt contributing to some reduction in cases of food poisoning.
In fact, it’s reasonable to say that health-conscious individuals (or, rather, individuals who think they are health-conscious) probably make some effort to minimize their BPA exposure by staying away from canned foods, and the restaurants likely to use a lot of them. They probably also watch other aspects of their diets, substituting plant protein for animal sources. More vegan=less BPA.
“Define a problem, pay a problem, and it stays a problem.”
More vegan also equals more soybeans, which just happened to be chock-full of phytoestrogens like isoflavones. You can even buy concentrated isoflavones—with the estrogen-blocking potential of hundreds of canned tomatoes—at the health foods store. Concentrated BPA, perhaps?
BPA has an additional property of being absorbed in the digestive tract, which means there is a first-pass metabolism through the liver, and the metabolite is not or only minimally active.
So, you’d think if we were going to study, say, the carcinogenicity of BPA, we’d round up some rats and feed ‘em a bunch of BPA, right?
Wrong! Recognizing the problem with first-pass metabolism, instead, we’ll inject it directly into their bloodstreams. That’s what Ana Soto, from Tufts School of Medicine did. And she got what she was looking for–signs that the rats developed cancerous or pre-cancerous conditions (though the statistics and sample size were a little dodgy).
From their classic human history “We’re All Bozos on this Bus,” the Firesign Theatre might have called this an example of Fudd’s First Law of Opposition, which states that “if you push something hard enough, it will fall over.” And so the rats fell over.
How hard were they pushed? The average human dietary exposure is about 0.3 micrograms/kilogram of body weight for infants. The rats got 250. Not through the tummy, either.
The results were published in Environmental Health Perspectives, a journal “published with support from the National Institute of Environmental Health, U.S. Department of Health and Human Services,” who also fund most of this type of research.
That’s a pretty neat deal. Apply for money from the government and then the government will publish your results. But your money goes away (and so do your many friends also riding in First Class) as soon as you start reporting serial minimal effects from putatively evil substances.
It’s kind of like the global warming game. Define a problem, pay a problem, and it stays a problem.
Some brave scholars, like Stanford’s John Ioannidis, are beginning to call out what is going on biomedicine, beginning with his famous 2005 paper, “Why Most Published Research Findings are False.” He blames a lot of it on sample size and experimental design, things clearly at issue in the BPA rat study.
But to date there’s little study of the larger rat, which is the incentive for researchers to design experiments in which, when you push something hard enough, it does fall over.