Author(s): Haycock PC
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Abstract Ethanol is a classic teratogen capable of inducing a wide range of developmental abnormalities. Studies in animal models suggest that differences in timing and dosage underlie this variability, with three particularly important developmental periods: preconception, preimplantation, and gastrulation. These periods of teratogenesis correlate with peak periods of epigenetic reprogramming which, together with the evidence that ethanol interferes with one-carbon metabolism, DNA methylation, histone modifications, and noncoding RNA, suggests an important role for epigenetic mechanisms in the etiology of fetal alcohol spectrum disorders (FASDs). In addition to a number of testable hypotheses, an epigenetic model suggests that the concept of a "fetal alcohol spectrum" should be expanded to include "preconceptional effects." This proposal has important public health implications, highlighting the urgency of research into the epigenetic basis of FASDs.
This article was published in Biol Reprod
and referenced in Journal of Clinical & Experimental Pathology