In one of the first studies to link molecular genetic variants to adolescent delinquency, sociological research published in the August issue of the American Sociological Review identifies three genetic predictors--of serious and violent delinquency--that gain predictive precision when considered together with social influences, such as family, friends and school processes.The paper:
[. . .]
The three genetic polymorphisms that predict delinquency include:
1. the 30-base pair (bp) promoter-region with a variable number tandem repeat (VNTR) in the monoamine oxidase A (MAOA) gene,
2. the 40-bp VNTR in the dopamine transporter 1 (DAT1) gene and
3. the Taq1 polymorphism in the dopamine D2 receptor (DRD2) gene. MAOA regulates several brain neurotransmitters important in behavioral motivation, aggression, emotion and cognition (e.g., serotonin, dopamine, norepinephrine).
The Integration of Genetic Propensities into Social-Control Models of Delinquency and Violence among Male YouthsMy guess is genetic differences such as these (along with IQ) will ultimately be shown to account for a much larger fraction of cross-racial variation in crime than racial differences in circulating testosterone levels (which seem far from fixed). I don't have population frequency data for the specific polymorphisms mentioned above, but the SNP rs979606 in MAOA, for example, varies in the familiar Asian <> European <> African pattern. Update: Racial differences are also apparent in DRD2 Taq1 genotypes and the DAT1 40 bp VNTR, though their meaning is not clear to me yet.
Authors: Guo, Guang; Roettger, Michael E.; Cai, Tianji
Source: American Sociological Review, Volume 73, Number 4, August 2008 , pp. 543-568(26)
This study, drawing on approximately 1,100 males from the National Longitudinal Study of Adolescent Health, demonstrates the importance of genetics, and genetic-environmental interactions, for understanding adolescent delinquency and violence. Our analyses show that three genetic polymorphisms—specifically, the 30-bp promoter-region variable number tandem repeat (VNTR) in MAOA, the 40-bp VNTR in DAT1, and the Taq1 polymorphism in DRD2—are significant predictors of serious and violent delinquency when added to a social-control model of delinquency. Importantly, findings also show that the genetic effects of DRD2 and MAOA are conditional and interact with family processes, school processes, and friendship networks. These results, which are among the first that link molecular genetic variants to delinquency, significantly expand our understanding of delinquent and violent behavior, and they highlight the need to simultaneously consider their social and genetic origins.
Another relevant paper:
Neuropsychopharmacology (2008) 33, 425–430; doi:10.1038/sj.npp.1301417; published online 11 April 2007
A Non-Additive Interaction of a Functional MAO-A VNTR and Testosterone Predicts Antisocial Behavior
Rickard L Sjöberg et al.
A functional VNTR polymorphism in the promoter of the monoamine oxidase A gene (MAOA-LPR) has previously been shown to be an important predictor of antisocial behavior in men. Testosterone analogues are known to interact with the MAOA promoter in vitro to influence gene transcription as well as in vivo to influence CSF levels of the MAO metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) in human males. We examined the possible joint effects of testosterone (measured in CSF) and MAOA-LPR genotype on antisocial personality disorder and scores on the Brown–Goodwin Aggression scale in 95 unrelated male criminal alcoholics and 45 controls. The results confirm that MAOA genotype and CSF testosterone interact to predict antisocial behaviors. The MAOA/testosterone interaction also predicted low levels of CSF MHPG, which tentatively suggests the possibility that the interaction may be mediated by a direct effect on gene transcription. If replicated these findings offer plausible explanations for previous inconsistencies in studies of the relationship between testosterone and male human aggression, as well as for how MAOA genotype may influence aggressive behavior in human males.
antisocial personality disorder, antisocial behavior, MAO-A gene, testosterone, gene by hormone interaction, MHPG