Alcohol-related birth defects: an update.
Historically, mankind has at least suspected that alcohol was somehow connected with undesirable effects on progeny. In the 18th century, physicians became aware that maternal alcohol consumption resulted in excess fetal and neonatal mortality, low birth weight, and many other deleterious effects. Perhaps as a response to the temperance and Prohibition periods, scientists lost sight of or interest in the effects of alcohol in pregnancy. In the late 1960s and early 1970s, the issue surfaced again, and scientists began systematic and in-depth studies of fetal alcohol syndrome (FAS) and alcohol-related birth defects (ARBD). Epidemiologic research now suggests that FAS has outranked Down's syndrome and spina bifida in prevalence and is now the leading known cause of mental retardation. Further, it is the only one of these three that is preventable. Because a safe limit of alcohol consumption in pregnancy is not defined, abstinence during pregnancy is the most prudent preventive measure. Factors such as race, beer drinking, maternal weight gain, and low socioeconomic status are associated with a statistical increase in the incidence of FAS. In families where one child has been diagnosed as having FAS, the incidence rate can be as much as 405-fold higher than the worldwide average. Neurobehavioral deficits can occur in the offspring of drinking mothers in the absence of a diagnosis of full FAS. The deficits differ with age and seem to persist into adulthood. Mental retardation or borderline mental retardation is a nearly ubiquitous neurological deficit in diagnosed FAS. In one study, it occurred in 75 percent of the non-FAS offspring of mothers who continued to drink heavily throughout their pregnancy.From the mid-1970s, having established that alcohol is a teratogen, scientists have been trying to uncover the mechanism by which alcohol exerts its embryotoxic effects. Recent promising neuroanatomical studies have demonstrated that alcohol has a deleterious effect on neuronal migration and hence on the development of the cerebral cortex. Other studies have shown that prenatal alcohol exposure,by adversely affecting hippocampal development,may be responsible for the learning deficits so frequently encountered in FAS children. Other research has implicated prostaglandins in the mechanism of alcohol-related dysmorphology.
D000014:Abnormalities, Drug-Induced / Q000209:etiology*; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000453:epidemiology* / Q000517:prevention & control / Q000523:psychology; D006801:Humans; D007226:Infant Mortality; D007231:Infant, Newborn; D008607:Intellectual Disability / Q000139:chemically induced; D007360:Intelligence; D008431:Maternal-Fetal Exchange; D011247:Pregnancy; D014481:United States