Distributing the origins of human will

In The New York Times David P. Barash writes about how parasites might influence our behavior. This should not be too shocking an idea to readers of this weblog, I’ve blogged about Toxoplasma gondii before, on which there has been a raft of publications over the past 10 years or so. My main issue is that like much of behavior genomics I wonder about the possibility of any terminus and conclusion to this line of inquiry (as opposed to being fodder for high publicity publications indefinitely). For any given personality trait we know that a small proportion (on the order of 10 percent) of the predicted variation within the population is due to variation in family environment (i.e., the impact of parent-specific choices). Of the remaining fraction it is about evenly split between genetic effects (i.e., the genes you inherit from your parents, and the consequent dispositions) and “other/non-shared environmental effects.”

This last is really just a residual; we don’t know what’s going on within the model. In The Nurture Assumption Judith Rich Harris posited that much of the remaining environmental component was peer effects. But there are other possibilities. Perhaps strangely, this environmental component could in part be types of genetic variation not captured by the genetic effect proper (e.g., epistasis). Or, it could be developmental noise, which might be biologically fixed rather early on in life. More recently people have wondered if it could be epigenetic variation. And of course, it could be parasites.

If I had to bet money I suspect that most of the heritable genetic variation for most behavioral traits will be widely distributed across the genome. In other words, many genes of small cumulative effect. This means that in many cases we won’t have a ‘silver bullet’ ‘X [trait] gene.’ But why should we limit this to genetic effects? Why would we expect a few classes of parasites to be responsible for most of the behavioral variation due to parasites? Or one particular environmental input as the root cause of cross-cultural variation (e.g., some have adduced that differences between Eastern and Western cultures might be due to the alphabetic literacy of the latter)? To some extent this is building a case for pessimism about the power of reductionism in smoking out causal chains. On the one hand we may be able to robustly and confidently partition components of variation. And yet we may have difficultly in ascertaining the exact details of the haze of causal factors which sum up together to produce the phenotypes we see around us. I have no problem with this, but it seems that for broad acceptance of any given effect (genetic or environmental) it is often important to point to a specific gene or environmental causal agent.

Source: Discover Magazine – Gene Expression