Prenatal alcohol exposure predisposes the offspring to neurofacial deficits and growth retardation resulting in a spectrum of mild to severe deficits, which comprise the Fetal Alcohol Spectrum Disorders (FASD) (Idrus & Thomas, 2011). Dysregulation of methylation pathways is an important causative factor for FASD development. In a mouse model of FASD, alcohol exposure during early neurulation caused global methylation pattern differences (Liu et al., 2009). Alcohol has been shown to inhibit DNA methylation and affect programming of neural stem cells thereby affecting their differentiation and causing disruptions in early embryonic development (Zhou et al., 2011). Prenatal alcohol exposure was shown to increase DNMT1 and MeCP2 expression and reduce hypothalamic pro-opiomelanocortin (POMC) gene expression (Bekdash, Zhang, & Sarkar, 2013).
