Summary
Until recently, studies pertaining to the effect(s) of prenatal alcohol on fetal and postnatal development have largely focussed on teratogenic outcomes. These studies have generally utilized excessive alcohol exposure models, and examined resultant outcomes that are gross and can be measured in the offspring as a fetus or at birth. Very few studies have addressed the possible long term, or programming, effects of prenatal alcohol exposure. Even observational studies in humans with fetal alcohol syndrome have been limited, as noted by Day and Richardson, consisting of “too few studies to assess accurately the effect of drinking on development beyond the neonatal period”. These authors go on to speculate that the effects observed in humans represent only, “the more severe end of a continuum of effects”. As we learn more about the origins and various mechanisms of human fetal programming, animal studies of fetal exposure to socially relevant amounts of alcohol are likely to grow in importance. Alcohol exposure is an important contributing factor to small birth weight in human populations and may also contribute to the production of the small birth weight phenotype. In addition, because the effects of moderate fetal alcohol exposure resemble the phenotype of other animal models of fetal programming, there is an experimental advantage to using alcohol to generate the phenotype and investigate the underlying initiating and mediating mechanisms. Alcohol exposure can be targeted to a single time point or spread over a longer period, and the dose can be easily titrated. For these and other reasons that will become apparent only as we learn more, the studies of developmental programming of adult disease and those of the subtle pathophysiological effects of moderate maternal alcohol consumption are bound to become increasingly linked.
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Schwartz, J., Carey, L.C. (2006). Programming Effects of Moderate and Binge Alcohol Consumption. In: Wintour, E.M., Owens, J.A. (eds) Early Life Origins of Health and Disease. Advances in Experimental Medicine and Biology, vol 573. Springer, Boston, MA. https://doi.org/10.1007/0-387-32632-4_15
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DOI: https://doi.org/10.1007/0-387-32632-4_15
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