BPA and Brain Effects

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Recent Study Suggests BPA Causes Brain Effects in Primates

Recent Study Suggests BPA Causes Brain Effects in Primates, However Study has Limitations

A recent study by Leranth et al. published in Proceedings from the National Academy of Science found that administration of BPA to primates prevents a hormone induced brain response.  These subjects consisted of four small groups (3 in each group) of African green monkeys that were of reproductive age and had undergone surgery to remove the ovaries (i.e., overectomy).  For a period of 28 days, four different treatments were administered to each group of 3 monkeys via a Silastic capsule and continuous pump inserted under the skin of the back:  Control (cholesterol in a liquid vehicle), estradiol (i.e,, estrogen, dose not specified), BPA (daily rate of 50 micrograms/kilogram body weight/day), and BPA + estradiol.  Researchers measured the number of brain synapses before and after the end of the treatment.  At the end of the experiment, researchers found that monkeys treated with estradiol alone had an increase in the number of brain synapses while monkeys treated with BPA and estradiol did not have the same increase in brain synapse formation.  However, animals fed BPA alone had the same number of synapses as the control (untreated) animals, indicating BPA alone caused no effects compared with the control animals.  Rather, BPA only acted to reduce the stimulating effect of the administered estrodiol (in an ovariectomized monkey) on synapse formation.  The long term consequences of this observation are unknown.
 
There are some key points to consider in evaluating the biological relevance of this study to humans.  The dose was at least 20 times higher than the most conservatively high estimates of human BPA exposure.  Also,  the dose was NOT given orally, which means  the normal detoxification pathway for BPA, that exists in the liver, was bypassed.  Thus, this experiment is not relevant to typical human BPA exposure. Additionally, the monkeys were not hormonally normal, since their ovaries had been removed (i.e., ovariectomy). It is well known that there are interactions which occur between ovarian hormones; however, due to the ovariectomy, these effects are not present in this study.  The researchers did this to make a "cleaner" study to observe the effects of estrogen and BPA, but they lost representativeness for a human with normal hormonal function.   

As previously stated, long term effects of the observed inhibition were not addressed in this study.  Animals were killed after the 28 days of treatment and there was no surviving group of animals which could be used to see if the BPA, estrogen, or BPA + estrogen treatments had any long term consequences on brain function or relative to control animals.  Additionally, one of the three animals in the estrogen plus BPA group developed a leak in its Silastic capsule, which resulted in a very high serum estradiol level of 450 pg/mL.   The authors chose not to remove the animal from the study because they stated that "the number of spine synapses was within the range established for other animals in the experimental group."   It is difficult to say if inclusion of this primate had an effect on the study or not, but with such a small sample size (n=3), having one significant outlier is of concern.  More studies are needed to assess potential BPA effects from typical human routes of exposure (e.g., oral).

Leranth, C., et al., Bisphenol A prevents the synaptogenic response to estradiol in hippocampus and prefrontal cortex of ovariectomized nonhuman primates. Proc Natl Acad Sci U S A, 2008