Negative Bisphenol A Effects on the Epigenome Blocked by Nutritional Supplements
Dolinoy, et. al. Proc. Natl. Acad. Sci. USA 104:13056-13061 (2007) Fulltext [RL Jirtle] [D Dolinoy]
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23 July 2007: The hypothesis of fetal origins of adult disease proposes that early developmental exposures involve epigenetic modifications, such as DNA methylation, that influence adult disease susceptibility (Jirtle and Skinner). In utero or neonatal exposure to bisphenol A (BPA), a high-production-volume chemical used in the manufacture of polycarbonate plastic, is associated with higher body weight, increased breast and prostate cancer, and altered reproductive function (Maffini et al.).
This study shows that maternal exposure to this endocrine-active compound shifts the coat color distribution of viable yellow agouti mouse offspring toward yellow by decreasing DNA methylation of the Agouti gene during early stem cell development. Moreover, maternal dietary supplementation, with either methyl donors like folic acid or the phytoestrogen genistein, can negate the negative effects of BPA on the epigenome.
Thus, compelling evidence is presented that exposure to BPA during pregnancy changes offspring phenotype by stably altering the epigenome, an effect that can be counteracted by maternal dietary supplements. These findings strongly support the inclusion of epigenetic effects of xenobiotic chemicals like BPA into the risk assessment process, as well as the investigation of nutritional supplementation as a parental preventive approach to counteracting environmental influences on the epigenome.
