You're making a HUGE leap from that abstract to "black people are predisposed to being violent."
This:
Quote:
Analyses revealed that African-American males who carry the 2-repeat allele are significantly more likely than all other genotypes to engage in shooting and stabbing behaviors and to report having multiple shooting and stabbing victims.
doesn't say what you're claiming. It is strictly limited to, "African-American males who carry the 2-repeat allele," which is, "a rare allele of the MAOA gene." So a very small subset of black people might be predisposed to violence, but that is much different than all black people in general.
Even that is also a claim that is only valid within the limits of the study, which we don't know because you only published the abstract. Without being able to review the paywalled paper, it's really difficult to dig into the findings and what those caveats are.
One of them is undoubtedly environmental factors, and there is
other evidence to suggest that paternal closeness moderates the relationship between the 2R allele and delinquency. It would make sense that there is a disproportionate relationship with violence when blacks are less likely to have present father figures if that is not controlled for.
And even the author of that study
says you're drawing the wrong conclusion. Quote:
Beaver claims that 2R alone may be strong enough to account for a significant amount of violent behavior in African American men. But he doesn't think this rare gene version explains all of the variation between men who have and don't have severe antisocial traits. As he puts it, "Even if MAOA-2R is causally linked with antisocial behaviors, it is not common enough in African Americans to solely account for crime rates in blacks"
And there are others with a different perspective:
Quote:
Choe's study is the first to demonstrate that ethnic minority children African Americans, not just Caucasians with a low-expression MAOA gene variant who face harsh discipline have an increased risk for antisocial behavior. Choe's team published the effects of just the 3R variant, excluding five African American participants in their study carrying the 2R version. Curious about possibly different effects of 2R, they then reanalyzed the data to include the five black males with 2R. The findings remained the same. Combining the boys with 2R the highest risk variant and those with the less severe risky 3R did not change the differences the researchers found between the 3R and 4R variants. The five males with 2R comprised a very small sample, but the fact that both low-activity MAOA variants, 2R and 3R, interacted with an environmental factor punitive discipline at specific ages, or developmental milestones, is noteworthy. It suggests the effects of MAOA-2R on antisocial behaviors are partly mediated by non-genetic factors.
Choe stresses that genetic influences on social behaviors such as juvenile delinquency cannot be fully understood outside the context of social circumstances. He is referring not only to parenting styles, but also to the in utero environment of the unborn fetus. As he explains, compared to the white youth in his study, the African Americans were more likely to grow up in poorer, urban, dangerous neighborhoods. A high percentage of these youth are being raised by single mothers, and they grow up without the attention found in most middle-class homes. Choe acknowledges the role of genes in behavior, but he clearly thinks that environmental factors contribute substantially to ethnic differences in antisocial behaviors. As he points out, the white kids in the sample were also poor, but they lived in low-income suburban communities, not in densely concentrated inner cities. The suburbs pose less of a risk than urban communities for group delinquent behavior