A myriad of contributing factors dictate the type and severity of alcohol-induced damage, including the dose and pattern of alcohol exposure, the developmental stage of the embryo or fetus, and individual differences in genetics and metabolism. The role of epigenetic modifications in risk and resilience to the teratogenic effects of PAE is still largely unknown, with emerging data consistent with the notion that PAE produces epigenetic changes that serve as a mediator of alcohol-induced damage. Epigenetic modifications also represent an avenue through which alcohol exposure could have a lasting negative impact on an individual throughout the lifespan.
