Pathogens: Cause or Effect of Social Variation?Published 6 March, 2013
The latest issue of Evolution and Human Behavior has multiple articles on the “behavioral immune system.” The idea is that infections can be defended against not only by the body’s immune system – t-cells and that sort of thing – but also by behavioral strategies that reduce the risk of infection. This includes strategies such as staying away from things that are likely to be infested with parasites, such as dead bodies, sick people, or hospitals.
This idea has been proposed to account for group-level differences. So, the idea goes, in places where there are greater risks from infection, people are more likely to use behavioral strategies to protect themselves. One of the two papers, by Terrizzi et al., looks at the relationship between variables such as “disgust sensitivity” on the one hand and ethnocentrism on the other. In places with more pathogens, people might be more likely to experience disgust – the motivational system behind the behavioral immune system – and reduce their exposure to pathogens by reducing their exposure to members of other groups. Terrizzi et al report, across a number of published studies, a “moderate” relationship. (The effect sizes they report are in the r=.25 range, for the quantitatively curious.)
The second paper, by Hackman and Hruschka, revisits some analyses of data from states in the U.S. that showed relationships between levels of pathogens in the state and a number of social behaviors, including religious commitment and collectivism. These data were previously interpreted as consistent with the ideas behind the behavioral immune system. The gist is that in places with higher pathogen threats, outgroup members represent an increased degree of risk, enhancing people’s inclinations to associate with ingroup as opposed to outgroup members. (See also Peng et al., for a related article in the same issue.)
Hackman and Hruschka offer a different interpretation, drawing on life history theory, reversing the direction of causality. Suppose that some places are riskier than others, and people facultatively adjust their behavior by adopting a faster life history strategy. (The intuition here is the nastier, more brutish and shorter life is, the better a bet it is to reproduce early and often because there is less likely to be sufficient time to reproduce later.) People pursuing faster life history strategies tend to have sex when they are younger, invest less in offspring and, importantly, become less involved in religious groups, which, some have argued, are vehicles (in the U.S.) for pursuing high-investment monomgamous reproductive strategies. A side effect of a fast life history strategy is that, because of sexual practices, sexually transmitted diseases will spread more widely. Higher pathogens, then, are the result, rather than the cause, of between-group social differences:
In light of this observation, life history theory posits a different causal link between the variables examined by F&T. Specifically, one kind of infectious disease (i.e., sexually transmitted disease) is an outcome of a fast life history strategy which should also be associated with greater likelihood of homicide and child maltreatment, less investment in religion, and an earlier sexual debut, which increases the likelihood of teenage pregnancy and of grandparents living with grandchildren (the major component of F&T measure of strength of family ties). This is in contrast to predictions from PST that infectious disease drives these different behavioral outcomes
Hackman and Hruschka point to a number of ways to distinguish between the two possibilities. For instance, the life history view predicts a special role for pathogens associated with sexually transmitted diseases; the behavioral immune system view does not. They report a number of analyses – I won’t work through them here, but I do recommend the paper to those interested in this topic – with an emphasis at looking at the relationship between pathogens and the behavioral immune system behaviors such as religious adherence, controlling for their measures of life history variables. In their words:
These analyses show that when removing the confounding effects of life history variables (i.e. fast life history proxied by early childbirth and extrinsic risk proxied by race) we find little effect of STD rates (or any measure of pathogen risk) on a suite of variables considered in prior analyses, including homicide, child fatalities, strength of family ties, and religious adherence.
I suspect proponents of the behavioral immune system will object to various elements of the analysis – anyone? – but I do like the exploration of the idea that pathogens are the effect rather than the cause in these relationships.
There was also something of a puzzle in their analysis that caught my attention. They found a positive relationship between early childbirth (an index of fast life history) and religious involvement. My prediction would have been the reverse, having been persuaded by argument I referred to above, that religious groups – in the U.S. at least – are means used by those pursuing slow life history strategies.
In any case, it seems to me that the literature on the behavioral immune system has gained a certain amount of momentum recently, and these two articles appearing in the same issue of the journal are, I think, a harbinger of a substantial amount of debate still to come.
Hackman, J., & Hruschka, D. (2013). Fast life histories, not pathogens, account for state-level variation in homicide, child maltreatment, and family ties in the US. Evolution and Human Behavior.
Terrizzi Jr, J. A., Shook, N. J., & McDaniel, M. A. (2012). The behavioral immune system and social conservatism: a meta-analysis. Evolution and Human Behavior.