Friday, January 8, 2010
No Amore for MAOA from Maori
It would be easier for me to keep up with the latest celebrity deaths if there were not such accelerating developments in genetics of violence research.
Here in the US, most liberals seem to have made up their minds that they are the true defenders of science against the evil forces of the religious right. However, in some parts of the world, liberals have clued into the fact that science threatens some of their own presumptions. With regard to the genetics of violence, New Zealand liberals are standing up for the Maori, New Zealand’s most violent ethnic group, against a specter of a scientific right. It seems to have begun with a 2006 interview with Dr. Rod Lea about the fact that about two-thirds of Maori have the moderately violence-associated 3-repeat allele of MAOA.
“Obviously, this means they are going to be more aggressive and violent and more likely to get involved in risk-taking behaviour like gambling,” he reportedly said. “It is controversial because it has implications suggesting links with criminality among Maori people. I think there is a link. It definitely predisposes people to be more likely to be criminals and engage in that type of behaviour as they grow older.”
Seven months later, The New Zealand Medical Journal featured two essays that presented no new evidence. Rather, the first by Merriman and Cameron merely criticized the assumption that a genetic association found in whites can be applied to other racial groups. The second was co-written by Dr. Lea, himself. This essay attacked the anonymous journalist who conducted the 2006 interview for distortion, “misquotes,” “misunderstandings,” “misconception,” and “negative media hype.” This essay declared that their “research agenda” “does not involve investigation of aggressive traits in Maori or any other population.” Furthermore, “the extrapolation and negative twisting of this notion by journalists or politicians to try to explain non-medical antisocial issues like criminality need to be recognised as having no scientific support whatsoever and should be ignored.”
That anyone could fail to see violent criminality as a medical issue should give emergency room doctors pause. Genetic or not, understanding this issue has life-and-death consequences. The most extreme manifestation of MAOA dysfunction, Brunner syndrome, revealed the value of dexamethasone treatment in raising MAOA levels in female carriers. Research in mice showed the potential of the experimental drugs Fenclonine, ketanserin, and tetrabenazine to lower neurotransmitter levels to normal levels. At the very least, at-risk youth could alter their diets because they may have excess tyramine from chocolate, red wine, or cheese, and restricting the amino acids phenylalanine and tryptophan could lower neurotransmitter levels without drugs.
The point made by Merriman and Cameron was a reference to a study by Widom and Brzustowicz, which was recently echoed in an essay by G Raumati Hook, who compared Preimplantation Genetic Diagnosis to Nazi eugenics. I previously pointed out how the Widom and Brzustowicz paper hid their data on African Americans because it probably showed that the extremely violence-inductive MAOA 2-repeat allele is not so rare in African Americans. Another conclusion of Widom and Brzustowicz was that maltreated white males demonstrate greater lifetime aggression if they have the 3-repeat allele rather than the 4-repeat allele, but that this is not the case for non-whites. Here again, they drew a deceptive conclusion by hiding their data. They found that white females with 3R alleles did not have higher lifetime aggression, only higher juvenile aggression. This parallels other research such as Sjöberg et al (2007) that suggest the MAOA 3-repeat allele does not increase female aggression. When Widom and Brzustowicz reported on the effect of MAOA in “non-whites,” they only gave data on men and women in combination. Their entire sample was only 39% non-white, and their non-white sample of 3-repeat allele subjects was 57% male, compared to 76% of white 3-repeat allele individuals. (2-repeat allele subjects were excluded from analysis.) It is also questionable what conclusions can be determined from the presumably diverse group of only 35 non-white men with the 3-repeat allele. Perhaps the results would have been different if the six non-white men with the 2-repeat allele were included. Nevertheless, the conclusion that a gene would behave differently in different races is a remarkable break from the traditional politically-correct assumption that race is a mere social construct. However, their conclusion about MAOA in non-whites was contradicted by studies by Weder et al and Beaver et al.
It would be difficult to overstate how intense the research focus on MAOA has become. I took the time to create a table that summarizes just the evidence comparing the 3-repeat allele to the 4-repeat allele in their effect on aggressive behavior. Even many of the scientists who study it seem to be missing the big picture, so I color-coded each study. Red studies either showed that the 4-repeat allele was more associated with aggression or that the difference was not statistically significant. Blue studies showed a significant association between the 3-repeat allele and aggression either with or without childhood maltreatment as a precipitating factor, at least in men. Purple studies had debatable results.
Some points can be drawn from this table. One is that MAOA has bucked the trend of early studies’ positive findings giving way to negating studies, which has been common among gene associations that did not bear out. Another is that aggression is just one manifestation of antisocial behavior, which could explain why many such studies found no association. Yet another is how the pace of research has increased over the years.
The table also illustrates the importance of the gene-environment combined effect on aggression, in which childhood maltreatment is also factored. Here is the same table with just those studies investigating this effect. It was originally discovered by Caspi et al, who spent decades interviewing and observing their subjects to discover maltreatment. The other studies that came out so quickly afterwards did not have time to investigate so thoroughly, and their outcomes when they successfully replicated Caspi et al tended to be less robust.
Here is the table with only studies of adult males. Those studies that are still red are either just not quite statistically significant or have explanatory qualifiers. Thus, there really should be no question that MAOA is a violence gene even with the relatively modest difference between the 3-repeat allele and the 4-repeat allele.
Now, MAOA is probably not the only gene that affects violent behavior, even if it is the most important gene for this. Reif et al found that the short allele of 5-HTTLPR enhanced the aggression effect of the 3-repeat allele of MAOA. Reif et al did not find a “main effect” of 5-HTTLPR alone on aggression, but a few other studies have. In the case of MAOA, the 3-repeat allele is much more common in Africans and Asians than in whites, but for 5-HTTLPR, the short allele is found in about 70-80% of East Asians, 40-50% of Europeans, and just 10-30% of Africans and African Americans. This should serve as a warning to watch out for any gangs of violent Asians on their way home from the library. In truth, Retz determined that the short allele only increased violence 5%. Plus, Patkar et al failed to find an effect of the short allele on aggression in African Americans, suggesting that the gene could have different effects in different races. (See above, regarding the novel consensus that race is not a social construct.)
Genetics research is rapidly moving humanity towards an understanding of violence that is complex and, for some, deeply offensive. Sadly, as violent crime claims 17,000 lives per year in the US alone, some progressives are aligning themselves against progress.