The effect of alcohol on development has been extensively studied in many different animal species (Cudd, 2005). In particular, a single exposure to EtOH during the pre-implantation period was shown to enhance post-implantation fetal death and resorption and to retard normal embryo development (Padmanabhan and Hameed, 1988). In humans, fetal alcohol exposure (FAE) is also correlated with low birth weight, growth, and morphological abnormalities (Day et al., 1989), and in higher rates of spontaneous abortions (Kline et al., 1980; Windham et al., 1997). Numerous other reports have demonstrated genetic, cellular, and biochemical association of alcohol with teratogenesis (Armant and Saunders, 1996; Goodlett and Horn, 2001; Resnicoff et al., 1994; Wozniak et al., 2004). The wide range of physiological and morphological defects associated with FAE suggests that the etiology of FASDs involve a high degree of cellular and molecular heterogeneity. Gastrulation period is considered to be the most sensitive to teratogenic insult, suggesting that differentiating cells might be especially vulnerable to the teratogenic effects of EtOH (Armant and Saunders, 1996).
