Disease and liberalisation


Jason Collins


September 28, 2011

Ronald Bailey has written an article for Reason on Randy Thornhill and Corey Fincher’s work linking disease and liberalisation. Bailey writes:

Thornhill and Fincher argue that the risk of infectious disease affects elites’ willingness to share power and resources, the general social acceptance of hierarchical authority, and the population’s openness to innovation. Their central idea is that ethnocentrism and out-group avoidance function as a kind of behavioral immune system. Just as individuals have immune systems that fight pathogens, groups of people evolve with local parasites and develop some resistance to them. People who are not members of one’s group may carry new diseases to which the group has not developed defenses. “Thus,” Thornhill and Fincher write, “xenophobia, as a defensive adaptation against parasites to which there is an absence of local adaptation, is expected to be most pronounced in regions of high parasite stress.” …

Thornhill and Fincher believe that more recent advances in medicine and public health are implicated in the post-1950s wave of liberalization that swept over the United States and Western Europe. The advent of penicillin, the arrival of polio vaccines, the elimination of malaria, the chlorination of drinking water, and the reduction in food-borne illnesses all combined to dramatically reduce disease. The authors suggest that if people experience few infections as they grow up, they perceive strangers and novel ways of life as safe; tolerance and the embrace of social, economic, and technological innovation follow. They note that areas of the world in which disease rates remain high have not experienced such liberalization.

Disease sounds a plausible reason for avoiding out-groups, but what is the incentive of an elite to share resources and power in the absence of disease? And can ethnocentrism and out-group avoidance be more simply explained by kin selection or strategic considerations?

Bailey notes the policy implications of this theory:

If Sachs, Thornhill, Fincher, and  Gelfand are right, reducing a country’s disease burdens should promote the rise of liberal institutions. “If the parasite hypothesis of democratization is supported by additional research,” Thornhill and Fincher write, “humanitarian efforts to reduce human rights violations and to increase human liberties and democracy in general will be most effective if focused on the most fundamental causal level of infectious disease reduction.”

I agree with the objective, but is this causal link in the right direction? Do people with a low disease burden support liberal institutions, or do liberal institutions create the framework under which disease can be controlled?

If I had to argue for the former, I would probably use Garrett Jones’s hypothesis that high-IQ is a significant factor in determining the level of trust in a society. If there is a link between disease and IQ, as Thornhill and Fincher have argued, the effect of disease reduction on liberalisation would be largely via the IQ mechanism.

However, I am not convinced of this causal link. More generally, the direction of causation is the central issue with the suite of articles linking parasites to religion, IQ, liberalisation and armed conflict (and I think there are others) that Thornhill and Fincher have produced over the last few years. What Thornhill and Fincher have successfully shown is that parasite loads and a host of characteristics of poorer nations are correlated.

Ultimately, I expect that the causal mechanisms between disease, IQ and institutions largely flow from IQ and institutions to disease. That is not to say that disease cannot reduce IQ - it undoubtedly does in some instances and is possibly part of the feedback loop during development. However, an IQ to disease causal relationship provides a mechanism by which disease declines - high IQ groups develop more liberal institutions, have much more wealth and can more effectively control disease. If causation flows in the other direction, it leaves open why disease prevalence varies greatly between areas that, based on climate, geography and history, should have similar levels of disease.