Girls who suffered childhood sexual abuse are more likely to develop alcoholism later in life if they possess a particular variant of a gene involved in the bodys response to stress, according to a new study led by researchers at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health (NIH). The new finding could help explain why some individuals are more resilient to profound childhood trauma than others.
With this study we see yet again that nature and nurture often work together, not independently, to influence our overall health and well-being, says NIH Director Elias A. Zerhouni, M.D.
This finding underscores the central role that gene-environment interactions play in the pathogenesis of complex diseases such as alcoholism, adds NIAAA Director Ting-Kai Li, M.D. A report of the study appears in the June 26, 2007 advance online publication of Molecular Psychiatry.
Previous studies have shown that childhood sexual abuse increases the risk for numerous mental health problems in adulthood. However not all abused children develop such problems, a likely indication that genetic factors also play a role. Recent studies have linked the monoamine oxidase A (MAOA) gene with adverse behavioral outcomes stemming from childhood mistreatment.
MAOA is an enzyme that metabolizes various neurotransmitters that regulate the bodys response to stress, explains first author Francesca Ducci, M.D., a visiting fellow in NIAAAs Laboratory of Neurogenetics in Bethesda, Maryland. DNA variations occur within a regulatory area the MAOA-linked polymorphic region (MAOA-LPR) -- of the MAOA gene. Two such MAOA-LPR variants occur most frequently and result in high or low MAOA enzyme activity. In a recent study, researchers found that maltreated boys who possessed the low activity MAOA-LPR variant were more likely to develop behavior problems than boys with the high activity variant.
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Contact: John Bowersox
jbowersox@mail.nih.gov
301-443-3860
NIH/National Institute on Alcohol Abuse and Alcoholism
26-Jun-2007