Abstract

The fetal alcohol syndrome (FAS) is a pattern of physical malformations observed in the offspring of women who drink alcohol during pregnancy. The most serious effect of in utero exposure to alcohol is mental retardation. Although the physical characteristics associated with the FAS have been attributed to the direct effects of alcohol, conditions secondary to alcohol intake (e.g., altered nutrition) cannot be eliminated as etiological factors in the impairment in cognitive function. Although animal models have been developed to study the question of direct versus indirect causation, there is little agreement in the results of these studies, and the methodology used leaves much to be desired in terms of adequate controls. Concern over the deleterious effects of alcohol on the developing fetus can be traced back to the time of Aristotle, who observed that drunken women often bore children who were feebleminded (Warner & Rosett, 1975). Although this observation has been rediscovered several times hence, most notably during England's gin epidemic of the 18th century (Warner & Rosett, 1975), it was not until the early 1970s that the relationship between prenatal exposure to alcohol and birth defects drew serious scientific and medical attention. Current findings suggest that prenatal exposure to alcohol is associated with a distinct pattern of congenital malformations that have collectively been termed the fetal alcohol syndrome (FAS). Among the characteristics of this syndrome are intrauterine and postnatal growth deficiency, a distinctive pattern of physical malformations, including microcephaly, shortened palpebral fissures (the size of the eye opening), joint, limb, and cardiac anomalies, and behavioral/cognitive impairment such as fine motor dysfunction and mental retardation. Although the actual number of children born with the FAS is not known, recent estimates place the number at one to two live births per

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