Drinking alcohol during pregnancy can lead to teratogenesis, the development of embryonic defects. The estimated incidence of Fetal Alcohol Spectrum Disorders (FASD), referring to a wide array of alcohol-exposure effects, is approximately on1% of live births in the US. Yet not all women who drink during pregnancy give birth to children with observable deficits. A mouse study has found that genetics may help to explain alcohol-related susceptibility and resistance.
Chris Downing, a research associate at the University of Colorado and corresponding author for the study stated that many factors have been shown to play a role in the development of FASD, including the amount, timing and pattern of maternal alcohol consumption, maternal age and parity, maternal ethnicity and socioeconomic status, cultural factors, maternal smoking and other drug abuse, and maternal diet/nutrition. In addition, studies with humans and mice have shown that both maternal and fetal genotypes in conjunction with the environment play a role in susceptibility and resistance to the detrimental effects of in utero alcohol exposure.
According to Downing “Using mice, we can control for all of these confounding variables. Within an inbred strain, all mice are virtually genetically identical, greater than 99.9%. When one looks at more than one inbred strain of mice, and all mice are housed and treated the same, differences between strains are taken as evidence of a genetic effect.”
Downing and his colleagues looked at alcohol teratogenesis in five inbred strains of mice: Inbred Short-Sleep (ISS), C57BL/6J (B6), C3H/Ibg (C3H), A/Ibg (A), and 129S6/SvEvTac (129). Pregnant mice were given either 5.8 g/kg alcohol or maltose-dextrin on day nine (roughly equivalent to days 28-31 of human gestation) of pregnancy. They were subsequently sacrificed on day 18, and their fetuses examined for gross morphological malformations.
The B6 mice that were exposed to alcohol in utero had fetal weight deficits, as well as digit, kidney, brain ventricle and vertebral malformation. In contrast, 129 mice showed no teratogenesis, while the remaining three strains showed varying degrees of teratogenesis.
Downing concludes that “certain strains were sensitive to some effects of prenatal alcohol and resistant to others. The fact that inbred strains differed showed that genetics plays a role.”
Downing added that these findings can be extrapolated to humans, because genetic effects on prenatal alcohol phenotypes in mice have been demonstrated, and the mouse and human genomes are remarkably similar, it suggests genetics plays a role in humans as well. He recommends that researchers need to begin to systematically investigate genetic factors mediating susceptibility and resistance to the effects of prenatal alcohol exposure.
Source: Results will be published in the July issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.