Prenatal exposure to alcohol (PEA) can cause serious disruptions in growth and maturation within the developing human brain. As early as 1973, Jones et al. coined the term fetal alcohol syndrome (FAS) characterized by a triad of features: 1) Growth deficiencies that are prenatal in origin; 2) A dysmorphic facial appearance with specific craniofacial anomalies typical of FAS (i.e., indistinct philtrum, thin vermillion border, and small palpebral fissures), and 3) Evidence for brain dysfunction126. Recently, “Fetal Alcohol Spectrum Disorders” (FASD) has been designated as a non-diagnostic, ‘umbrella’ terminology to encompass the complete spectrum of effects with or without facial dysmorphisms resulting from PEA. FASD currently affects as many as one percent of all live births in the US127.
