CHICAGO – For children with attention deficit hyperactivity disorder (ADHD), possessing a variant of a gene involved in brain signaling may predict antisocial behavior and increase susceptibility to the effects of lower birth weight, according to a study in the November issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
Biological processes play a key role in the genesis of antisocial behavior with specific evidence of brain involvement and contribution of genetic and early environmental risk factors, including prenatal factors, according to background information in the article. Given the links between deficits in a brain region called the prefrontal cortical and antisocial behavior and between the enzyme catechol O-methyltranferase (COMT) and prefrontal cortical functioning, the authors suggest that a variant of the COMT gene might be associated with antisocial behavior.
Anita Thapar, M.D., of Cardiff University, Cardiff, Wales, and colleagues looked for the presence of a variant in the COMT gene in 240 British children, aged five to 14 years with ADHD or hyperkinetic disorder who are at high risk for early-onset antisocial behavior. The researchers used the children's birth weight as a marker for prenatal risk to determine the contribution of the environment to risk of developing symptoms of early-onset antisocial behavior.
The researchers found a significant association between the COMT variant and antisocial behavior; and between low birth weight and antisocial behavior. There was also a significant gene and environment (low birth weight) interaction associated with antisocial behavior.
"Early-onset antisocial behavior in a high-risk clinical group is predicted by a specific COMT gene variant previously linked with prefrontal cortical function and birth weight, and those possessing the val/val genotype are more susceptible to the adverse effects of prenatal risk as indexed by lower birth weight," the authors conclude.
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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