Exposure measurements from several countries indicate that humans are routinely exposed to low levels of bisphenol A (BPA), a synthetic xenoestrogen widely used in the production of polycarbonate plastics. There is considerable debate about whether this exposure represents an environmental risk, based on reports that BPA interferes with the development of many organs and that it may alter cognitive functions and mood. Consistent with these reports, we have previously demonstrated that BPA antagonizes spine synapse formation induced by estrogens and testosterone in limbic brain areas of gonadectomized female and male rats. An important limitation of these studies, however, is that they were based on rodent animal models, which may not be representative of the effects of human BPA exposure. To address this issue, we examined the influence of continuous BPA administration, at a daily dose equal to the current U.S. Environmental Protection Agency's reference safe daily limit, on estradiol-induced spine synapse formation in the hippocampus and prefrontal cortex of a nonhuman primate model. Our data indicate that even at this relatively low exposure level, BPA completely abolishes the synaptogenic response to estradiol. Because remodeling of spine synapses may play a critical role in cognition and mood, the ability of BPA to interfere with spine synapse formation has profound implications. This study is the first to demonstrate an adverse effect of BPA on the brain in a nonhuman primate model and further amplifies concerns about the widespread use of BPA in medical equipment, and in food preparation and storage.
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Friday, October 03, 2008
Is the bisphenol (BPA) in plastic products making us dumb?
Estrogens are known to increase the number of excitatory synapses in our hippocampus and enhance both cognitive performance and spatial memory. This is why there is such interest in the possible disruptive effects of estrogenic compounds in the environment, particularly bisphenol A (BPA) that is present in some plastics. Leranth et al. now demonstrate in monkeys that a daily dose of BPA considered within the safe range for humans (50 μg/kg) completely blocks the estradiol-induced increase in axospinous synapses in three distinct fields of the hippocampus. This would be expected to have profound effects on the highly plastic excitatory (glutamatergic) circuits in both our hippocampus and prefrontal cortex. Here is their chilling abstract:
Posted by Deric Bownds at 5:30 AM
Blog Categories: brain plasticity, memory/learning, technology
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What do you think of think of the fact that the route of exposure in the Yale experiments is via subcutanious pump? Surely the point about BPA is that in an oral route of exposure, primates are able to metabolize all of the BPA. That's the theory anyway and has always been the crux of the argumentabout BPA's safety.ReplyDelete
I'd like to see the same study in primates with an oral route of exposure.
uhh... i didn't get it... could you say that in English?...ReplyDelete
I'm a designer and i'm not sure if i'm supposed to be aware of what BPA is and how it affects the human brain... somehow i feel like i need to understand this...