ABSTRACT
Fetal Alcohol Syndrome (FAS) is a devastating developmental disorder resulting from
heavy prenatal alcohol exposure. Worldwide incidence rates of FAS average about 1 case
per 1000 live births (1), which makes FAS the leading preventable cause of mental
retardation (2). The diagnosis of FAS requires a constellation of three symptom classes: (1)
growth deficiency, (2) cranio-facial abnormalities, and (3) central nervous system (CNS)
dysfunction (3-5). Research from animal models of prenatal ethanol exposure and from
observational human exposure studies has shown evidence of a dose-response relationship
to alcohol’s teratogenic capacity (6). FAS falls at the most severe end of the outcome
spectrum, and is associated with high levels of maternal alcohol consumption, such as those
associated with alcohol abuse or dependence. However, in other cases, prenatal alcohol
exposure can produce neurobehavioral dysfunction in the absence of the gross physical
abnormalities required for clinical recognition of FAS (7). The reason for this disparity of
outcome is unknown but may be related to dose or timing of exposure or other maternal or
fetal considerations. However, it is apparent that more individuals are adversely affected by
prenatal alcohol exposure than those meeting the diagnostic criteria for FAS.
