A new research report in Plos One provides support for the theory that abused children who have low level expression of the gene for monoamine oxidase A (MAOA) are more at risk of becoming violent and anti-social.
Previous research has reported that a functional polymorphism in the monoamine oxidase A (MAOA) gene promoter can moderate the association between early life adversity and increased risk for violence and antisocial behavior. In this study of a combined population of psychiatric outpatients and healthy volunteers (N = 235), we tested the hypothesis that MAOA genotype moderates the association between early traumatic life events (ETLE) experienced during the first 15 years of life and the display of physical aggression during adulthood, as assessed by the Aggression Questionnaire. An ANOVA model including gender, exposure to early trauma, and MAOA genotype as between-subjects factors showed significant MAOA×ETLE (F1,227 = 8.20, P = 0.005) and gender×MAOA×ETLE (F1,227 = 7.04, P = 0.009) interaction effects. Physical aggression scores were higher in men who had experienced early traumatic life events and who carried the low MAOA activity allele (MAOA-L). We repeated the analysis in the subgroup of healthy volunteers (N = 145) to exclude that the observed G×E interactions were due to the inclusion of psychiatric patients in our sample and were not generalizable to the population at large. The results for the subgroup of healthy volunteers were identical to those for the entire sample. The cumulative variance in the physical aggression score explained by the ANOVA effects involving the MAOA polymorphism was 6.6% in the entire sample and 12.1% in the sub-sample of healthy volunteers. Our results support the hypothesis that, when combined with exposure to early traumatic life events, low MAOA activity is a significant risk factor for aggressive behavior during adulthood and suggest that the use of dimensional measures focusing on behavioral aspects of aggression may increase the likelihood of detecting significant gene-by-environment interactions in studies of MAOA-related aggression.
The first report I came across a few years ago on a relationship between low levels of monoamine oxidase A (MAOA), abused children, and violent behavior came from a Dunedin New Zealand twins study. See my post A violence promoting gene and the follow-up and additional related info in the post Serotonin Transporter Gene Linked To Depression, Binge Drinking. Plus, see the post Initial Bullying In Late In Adolescence Causes Most Harm.
What I find interesting about the MAOA variations: The variation that makes one more violent in response to abuse basically makes humans more sensitive to environmental influence. The higher MAOA activity variation makes humans less sensitive to the environment. So the ability of humans to be influenced by the environment is under genetic control.
The fact that genetic variations cause differences in environmental sensitivity has future implications. When offspring genetic engineering enters the realm of the safely doable prospective parents are going to choose against genetic variations that cause environmental sensitivity for behavioral attributes where the parents have strongly held preferences. For example, parents who want total "Goodie Two Shoes" kids are going to choose against genetic variations that create the risk that the kids might turn out violent.
My prediction: Parents will choose genetic variations that make their kids more genetically determined, not less. Parents will choose against genetic variations that put them at 10% risk of some undesired attribute if some other genetic variations would make them at only 1% or a tenth of a percent risk of that the undesirable attribute. Similarly, parents will choose genetic variations that greatly increase the odds of various desired attributes. Basically, genetic variations that leave offspring at moderate odds (say 30% to 70%) of some outcome will get rejected in favor of genetic variations that make attributes either highly likely or highly unlikely.
|Share |||Randall Parker, 2007 June 17 06:24 PM Brain Genetics|