A 2002 Science article reports on antisocial behavior in adults in relation to the activity of monoamine oxidase typeA (MAOA) and childhood maltreatment; MAOA deficiency is a strong predictor of aggressive behavior only when the child has also been maltreated (Caspi et al. 2002).
“Some meta-analyses have cast doubt on the generality of the Caspi and Moffitt results (Risch et al. 2009; see Morris et al. 2007).”
However, “in order to illustrate the approach and to raise pertinent issues, the discussion that follows uses the 2002 study. The issues raised apply to the overall research program of examining interaction between measured genetic and environmental factors even if these particular 2002-3 results turn out not to be widely replicated.”
The authors conclude that their results “could inform the development of future pharmacological treatments” (Caspi et al. 2002, 853). In the context of research on childhood experience in relation to adult behavior, the implication of that conclusion is that, if low MAOA children could be identified, prophylactic drug treatment could reduce their propensity to antisocial behavior as adults. Or, to be more precise, such treatment could reduce their vulnerability, that is, the risk that childhood maltreatment would pave the way to undesired adult outcomes.
An easy rejoinder to the authors’ conclusion would be that, if childhood maltreatment could be identified and stopped early, such action could reduce their vulnerability to low MAOA levels paving the way to undesired adult outcomes (Morris et al. 2007). Indeed, eliminating childhood maltreatment would seem to be unconditionally positive, while prophylactic drug treatment may have side effects, some of which may not emerge until later in life. The rejoinder is, however, too easy. Although the intended outcome—eliminating childhood maltreatment—may be seen as positive, the way to get to that outcome might not seem unconditionally positive. After all, detecting and preventing childhood maltreatment might require intrusion into many households, surveillance, monitoring, and intervention by state agencies, diversion of government budgets from other needs, and so on.
Notice that this discussion and the points plotted in figures of the 2002 paper involve
the averages for the respective categories of people. Within each category people show a range of antisocial behaviors. It turns out that, among children who experienced probable or severe maltreatment, the ranges overlap, that is, some of the high MAOA individuals ended up with higher antisocial behavior scores than some of the low MAOA individuals.
Adjustment of what counts as antisocial does not succeed in eliminating the potential for misclassifying which children are ones who may end up antisocial. If we counted as antisocial only those individuals whose score exceeded some value that is higher than the upper limit of the range for high MAOA individuals, this would increase the numbers of low MAOA individuals who did not end up counting as antisocial. If we lowered the cutoff score, many high MAOA individuals would end up with behavior classified as antisocial…
The issue of misclassification is especially troubling because, once the resources are invested to screen children for MAOA levels, attention would be focused on all low MAOA children. Indeed, how could treating children according to their genetic group be avoided if we do not know from a childhood MAOA assessment whether any particular individual is one who would go on, after maltreatment, to become an antisocial adult? Parents might push for additional research to identify other characteristics that differentiate among the low MAOA children and perhaps help predict who among the high MAOA children are also vulnerable. If that research took place and were successful, additional resources would have to be invested to customize the way that parents, teachers, doctors, and social workers treated the different low- and high-MAOA children and to educate everyone not simply to treat children according to which MAOA group they were a member of. In short, the implications of results based on the interaction of genetic and environmental factors depend on what action is proposed once the possibility that heterogeneity underlies those factors is taken into account.
The quotes above are from pages 132ff in Taylor, Peter J. (2014) Nature-Nurture? No: Moving the Sciences of Variation and Heredity Beyond the Gaps.
Caspi, A., J. McClay, et al. (2002). “Role of genotype in the cycle of violence in maltreated children.” Science 297(5582): 851-854.
Morris, C., A. Shen, et al. (2007). “Deconstructing violence.” GeneWatch 20(2):
Risch, N., R. Herrell, et al. (2009). “Interaction between the serotonin transporter gene (5-HTTLPR), stressful life events, and risk of depression: A meta-analysis.” Journal of the American Medical Association 301(23): 2462-2471.
(Introduction to this series of posts)