Behavior and genetics, Part 1
The author looks at the hype around one variant of a gene found on the X chromosome, monoamine oxidase A (MAOA):
The gene comes in several varieties, distinguished primarily by their levels of activity. Because it is found on the X chromosome, females may have two different forms, while males have just one. Brunner’s aggressive Dutchmen had a rare and completely inactive variant. The so-called low-activity variant, or MAOA-L, has a slightly shorter than usual promoter – the region that controls the gene’s activity – and so produces less protein. Another common variant, MAOA-H, is more active…
Although MAOA can certainly influence our behaviour, it is no puppet-master – if anything, it is just one of many different strings. Other genes, including MAOB and COMT, affect the creation, use and breakdown of the same neurotransmitters. It is highly likely that these genes work together to affect our behaviour, and genetic studies are starting to reveal the dalliances between these dancing partners. For example, one found that women with MAOA-L are more likely to become depressed while pregnant, but only if they also carry a low-activity version of COMT.
At the very least, the “warrior gene” tag typecasts MAOA in a role that is just part of its repertoire. Behaviours are not simple traits like eye colour, and to label them as such will inevitably mislead.
Bear in mind that eye color is not nearly as simple as it’s generally presented. Few things are. There’s an awful lot of reductionism going around; the real problem comes when a simplified model–necessary for research purposes, since you can’t possibly look at everything at once–is mistaken for the whole of reality.
Yong goes on to talk about how “Nature and nurture are inextricably linked” (fancy that!):
Since then, similar interactions between nature and nurture have become part and parcel of the MAOA story. Carriers of MAOA-L are more likely to show delinquent behaviour if they were physically disciplined as children. They are also more likely to be hyperactive in late childhood if their first three years were stressful, and to develop conduct disorders if their mothers smoked cigarettes while pregnant with them. The list goes on. Likewise, Beaver found that MAOA-H carriers were more likely to commit fraud, but only if they hung around with delinquent peers.
So environments can set the degree to which genes make their presence felt, creating the stage upon which genes express themselves. The stage-set can also affect the action of genes. Smoking, for example, can reduce the activity of MAOA regardless of which variant someone has. And there is evidence from mice that a fatty diet can do the same. Genes may be able to influence our behaviour, but our behaviour also influences our genes.
So, people with particular gene variants may be more susceptible to the same environmental factors which will affect most people’s behavior in exactly the same ways. (On a less than surprising note, Spanking increases aggressive behavior in young children, period.) It’s a matter of degree. I would not be surprised to find some confirmation bias and interpretation in line with expectations, as well, looking at something as subjective as perceived behavior–very similar to what I talked about in Happiness, Part 2: In which reality is twisted.
Not having the spoons right now to track down the original research, I wonder to what extent the researchers were depending on slightly more objective measures, such as numbers of arrests for violent behaviors. This could also break down, once racial/ethnic/cultural stereotypes kick in, as is also discussed in the article. I can’t help but think yet again of some lessons which should have been learned from Buck v. Bell.
Yong goes on to discuss how this particular gene variation got hyped to reinforce some very nasty stereotypes, in particular the inherent violence of Maori people:
As far as we know, many populations have a similar level of MAOA-L carriers to Lea’s sample of Maoris, but it would be ludicrous to say that all Africans, Pacific Islanders, Japanese and Chinese men are twice as likely to be violent as Caucasians. In fact, one of the few studies on MAOA-L and aggression to look beyond white males found no link in non-white Americans (Biological Psychiatry, vol 60, p 684). The Maori case study highlights the risk of extrapolating results from behavioural genetics, particularly from one ethnic group to another.
Wow, different population groups might have different gene variant distributions. (Otherwise there wouldn’t be distinct population groups, due to “family resemblance writ large”, but hey.) And, unfortunately, things mislabeled as “warrior genes” are more socially acceptable to connect to stereotypes these days than “different visible phenotype genes”–while being just as reasonable. It’s still scientific racism.
This illustration from 1899, published in Harper’s Weekly, is described at Wikimedia Commons. How far has our society really come in some respects?
The author continues by reiterating that “Genes do not dictate behaviour”. He also observes:
Once we move beyond genetic determinism, the nature/nurture dichotomy and simplistic generalisations, the discovery of genes related to mental or behavioural disorders can only improve our knowledge of ourselves.
One thing Yong did not explicitly mention: the risk of eugenics based on dodgy understanding and research, feeding some really nasty attitudes. I have split more on that off into a second part, since the post was running long.
The same issue offered this bit of fail: Deep brain electrodes are real hope for mental illness. Ah well.