RESEARCH FOR PRACTICE

Abstract

Pregnant women are advised to avoid alcohol, of which no safe level has been identified. In fact, as little as one drink per day has been shown to cause untoward effects in offspring. The teratogenic effects of alcohol were first documented in 1973, when researchers discovered similar patterns in eight unrelated children of alcoholic mothers: craniofacial, limb, and cardiovascular defects, along with prenatal-onset growth deficiency and developmental delay.1 In the succeeding 27 years, alcohol's teratogenic effects have been confirmed by a large body of animal research as well as by clinical and epidemiologic studies in humans. These effects are dose-related. A recent study of 464 children followed from birth to 14 years of age revealed that greater maternal alcohol consumption was related to greater learning difficulties and behavioral problems in offspring, including antisocial behavior, substance abuse, self-reported intellectual and academic problems, and observer-reported negativity and impulsivity. This relationship between higher doses of alcohol and greater effects in offspring was evident even though the mothers generally drank socially. (A typical drinker reported consuming, on average, one drink per day prior to recognition of her pregnancy and less than half a drink per day midpregnancy.) The results also showed that drinking early in pregnancy and binge drinking were associated with the greatest risk to offspring.2 The most severe consequence of fetal alcohol exposure known to date is fetal alcohol syndrome (FAS), characterized by prenatal or postnatal growth retardation, central nervous system disturbance (neurologic abnormalities, behavioral dysfunction, intellectual impairment, and structural abnormalities such as microcephaly), and a characteristic face (elongated midface, thin upper lip, and flattened maxilla).3 In February 2000, researchers revealed that alcohol triggers widespread neurodegeneration in the developing forebrains of rats. The authors of the study suggest that the destruction of millions of neurons in the developing human brain could explain the reduced brain mass and neurobehavioral disturbances exhibited in offspring with FAS.4 The incidence of FAS is docu-