And I think you're assigning me malicious motiviations, and ignoring valid research that doesn't support your own prejudices. To be painstakingly clear about w

And I think you're assigning me malicious motiviations, and ignoring valid research that doesn't support your own prejudices. To be painstakingly clear about what I'm saying here: while the 2R MAO-A allele is more common among black males than in other groups, it's only present in a single-digit percentage of even that most-affected group. Of all those men with the allele, most don't commit any crime. Only <0.01% of Americans of all races are arrested for violent crime each year. When we discuss violent criminals with a genetic predisposition to aggression, we're talking about a tiny minority of a minority of a minority, way below single-digit percentages, not all members of a particular racial group. The trouble is, that tiny minority of a minority of a minority can still skew total arrest numbers. If 0.02% of one racial group commits violent crime in a year versus 0.01% for members of another group, comparitive arrest rates will seem racially disproportionate. If that difference is seen as "police are all racist, and have a negative overall impact on black communities", bad policy may result. See recent crime spikes in American cities for examples, where de-policed minority communities have been among the hardest hit by rising violence. The good news is that MAO-A deficiency can be identified and treated pharmacologically with progesterone supplementation. Researchers have also explored CRISPR-based therapies to boost MAO-A expression. I see this condition and its treatment as analogous to Vitamin D deficiency, which for obvious genetic reasons disproportionately affects people with dark skin. If we decide we're finally allowed to talk about it, the problem can be tackled constructively and the problems caused by ignoring it will vanish. I don't believe you're sincere in your interest in the research, but in case you are, here are a few recent studies w/ relevant quotes from each abstract. Please tell me which ones you think are discredited: University of Kentucky, 2015: "Low functioning MAOA genotypes have been reliably linked to increased reactive aggression" - https://pubmed.ncbi.nlm.nih.gov/25637908/ https://pubmed.ncbi.nlm.nih.gov/25637908/ National Institute for Health and Welfare, Finland, 2015: "Our results, from two independent cohorts of Finnish prisoners, revealed that a monoamine oxidase A (MAOA) low-activity genotype (contributing to low dopamine turnover rate) as well as the CDH13 gene (coding for neuronal membrane adhesion protein) are associated with extremely violent behavior (at least 10 committed homicides, attempted homicides or batteries)." - https://pubmed.ncbi.nlm.nih.gov/25349169/ https://pubmed.ncbi.nlm.nih.gov/25349169/ University of Kansas, 2016: "In particular, converging lines of evidence have documented that these maladaptive manifestations of aggression are influenced by monoamine oxidase A (MAOA), the enzyme that catalyzes the degradation of brain serotonin, norepinephrine and dopamine." - https://pubmed.ncbi.nlm.nih.gov/26776902/ https://pubmed.ncbi.nlm.nih.gov/26776902/ University of Heidelberg, 2019: "Previous studies have linked the low expression variant of a variable number of tandem repeat polymorphism in the monoamine oxidase A gene (MAOA-L) to the risk for impulsivity and aggression" - https://pubmed.ncbi.nlm.nih.gov/31441562/ https://pubmed.ncbi.nlm.nih.gov/31441562/ University of Toronto, 2020: "Over the past two decades, research has revealed that genetic factors shape the propensity for aggressive, antisocial, and violent behavior. The best-documented gene implicated in aggression is MAOA (Monoamine oxidase A), which encodes the key enzyme for the degradation of serotonin and catecholamines. Congenital MAOA deficiency, as well as low-activity MAOA variants, has been associated with a higher risk for antisocial behavior (ASB) and violence, particularly in males with a history of child maltreatment." - https://pubmed.ncbi.nlm.nih.gov/32574581/ https://pubmed.ncbi.nlm.nih.gov/32574581/