Alcohol use by pregnant women is regarded as teratogenic, and women are counseled to avoid alcohol during pregnancy. The American College for Obstetricians and Gynecologists’ (ACOG) Committee Opinion on At-Risk Drinking and Alcohol Dependence states unequivocally that obstetricians should give “compelling and clear advice to avoid alcohol use, provide assistance for achieving abstinence, or provide effective contraception to women who require help.”1
Despite these strong statements, the degree of teratogenicity of alcohol remains somewhat controversial, and opinions have evolved over time. For centuries, it has been known that alcohol can harm a fetus.2 For example, abnormalities in babies born to mothers using alcohol were noted during the eighteenth and nineteenth centuries.3,4
An increasing number of twentieth century studies raised serious concerns about the safety of prenatal alcohol consumption. The teratogenic effects of alcohol on the fetus were reported by Lemoine et al in 1968.5 But most physicians continued to think that the placenta provided a protective barrier that would prevent alcohol from reaching the fetus.2
In 1973, the constellation of symptoms in children with prenatal alcohol exposure was dubbed “fetal alcohol syndrome” (FAS).6 In 1981, the Surgeon General recommended warnings against alcohol use during pregnancy, and the advisory was updated in 2005 to include alcohol abstention by all women of childbearing age planning to become pregnant.2
Several studies have cast doubt on the categorical statement that alcohol consumption during pregnancy is always unsafe. A 2010 Australian study found no link between low and moderate alcohol consumption during pregnancy and alcohol-related birth defects.7 A series of Danish studies suggested that low and moderate drinking in early pregnancy had no effect in five-year-old study subjects.8 But one limitation of these studies is that the children were too young to measure the full impact alcohol can have on brain function.8
A recent study looks at the longer-term impact of moderate prenatal alcohol consumption on children, utilizing balance as a measure of neurodevelopment outcomes. Humphriss and colleagues9 conducted a population-based prospective longitudinal study of 6,915 10-year-old children who had been evaluated for balance (eg, beam walking, heel-to-toe balance on a beam, and standing on one leg), and where data was available on prenatal alcohol consumption.
Most mothers (95.5%) had consumed no-to-moderate amounts of alcohol (3 to 7 glasses per week). Importantly, no evidence was found of an adverse effect of maternal alcohol consumption on childhood balance. In fact, paradoxically, higher use was generally associated with better offspring outcomes, with some specific effects appearing “strong.” These included static balance eyes open and moderate total alcohol exposure at 18 weeks, adjusted OR 1.23 (95% CI 1.01 to 1.49); static balance eyes closed and moderate total alcohol exposure at 18 weeks, adjusted OR 1.25 (95% CI 1.06 to 1.48). A “similar pattern of association was seen for maternal alcohol use before and after pregnancy, and for paternal alcohol use during pregnancy.”
The researchers noted that the effects of prenatal exposure on offspring might be “prone to residual confounding by factors related to social position, as maternal behavior is often related to socioeconomic status (SES).” Higher total alcohol consumption was associated with “maternal-social advantage,” while binge-drinking (> 4 units per day) and abstinence were associated with maternal social disadvantage.
Since binge-drinking as well as complete abstinence were more frequently associated with social disadvantage, while more moderate use was associated with social advantage, the apparently beneficial effects of prenatal alcohol consumption might be explained by this socioeconomic disparity, rather than by the impact of alcohol per se.
To address this confounding variable, the researchers used maternal-paternal and timing of exposure comparisons in an attempt to help identify causal effects. In particular, they used an approach called “Mendelian randomization,” which “utilizes genetic variation known to influence levels of the environmental exposure under examination.” The approach is based on the assumption that since genotype (specifically, variants in alcohol dehydrogenase genes) is not usually associated with SES, it also will not be associated with socially patterned cofounding behavior. No strong associations were found between this genotype/proxy and offspring balance.