To test whether the gene's short form might also raise the risk of fetal alcohol-induced problems, Schneider's team analyzed data from an ongoing, long-term study into the impacts of moderate fetal alcohol exposure on behavior and brain function in rhesus monkeys. Although fetal alcohol syndrome was first recognized in children of alcoholic mothers, attention has shifted in recent years to moderate drinking because of its potential to affect many more children, says Schneider.
"We know that 60 percent of women of child-bearing age consume alcohol and more than 50 percent of pregnancies are unplanned," she says. "So it doesn't take much to figure out that prenatal exposure to alcohol - at least in the weeks before pregnancy is detected - is substantial."
In line with this, the mother monkeys in the study's experimental group consumed the equivalent of just two alcoholic beverages five times a week during breeding and pregnancy. After the infants were born, the scientists recorded their irritability during a standard battery of developmental tests, measured their reactivity to stress when separated from their mothers at six months for weaning, and determined whether they carried the short or long form of the serotonin transporter gene promoter.
What the researchers found is that fetal alcohol-exposed infants who carried a copy of the short form were more irritable and reactive to stress than either control group infants who weren't exposed to alcohol or those who were exposed but had two copies of the gene's long form. Overall, says Schneider, the results indicate a "substantial interaction" between fetal alcohol exposure and genotype.
She and her colleagues are now conducting additional studies to see if these findings fit a larger pattern of fetal alcohol-induced problems as the monkeys grow up. At the same time, extreme irritability
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| Contact: Mary Schneider schneider@education.wisc.edu 608-265-5118 University of Wisconsin-Madison Source:Eurekalert |