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We conduct a revaluation of the Thornhill and Fincher research project on parasites using finely-resolved geographic data on parasite prevalence, individual-level sociocultural data, and multilevel Bayesian modeling. In contrast to the evolutionary psychological mechanisms linking parasites to human behavior and cultural characteristics proposed by Thornhill and Fincher, we offer an alternative hypothesis that structural racism and differential access to sanitation systems drive both variation in parasite prevalence and differential behaviors and cultural characteristics.We adopt a Bayesian framework to estimate parasite prevalence rates in 51 districts in eight Latin American countries using the disease status of 170,220 individuals tested for infection with the intestinal roundworm Ascaris lumbricoides (Hürlimann et al., []: PLoS Negl Trop Dis 5:e1404). We then use district-level estimates of parasite prevalence and individual-level social data from 5,558 individuals in the same 51 districts (Latinobarómetro, 2008) to assess claims of causal associations between parasite prevalence and sociocultural characteristics.We find, contrary to Thornhill and Fincher, that parasite prevalence is positively associated with preferences for democracy, negatively associated with preferences for collectivism, and not associated with violent crime rates or gender inequality. A positive association between parasite prevalence and religiosity, as in Fincher and Thornhill (: Behav Brain Sci 35:61-79), and a negative association between parasite prevalence and achieved education, as predicted by Eppig et al. (: Proc R S B: Biol Sci 277:3801-3808), become negative and unreliable when reasonable controls are included in the model. We find support for all predictions derived from our hypothesis linking structural racism to both parasite prevalence and cultural outcomes.We conclude that best practices in biocultural modeling require examining more than one hypothesis, retaining individual-level data and its associated variance whenever possible, and adopting multilevel techniques suited to the structuring of the data.

Child survival is probabilistic, but the unpredictability in family formation and completed family size has been neglected in the fertility literature. In many societies, ending the family cycle with too few or too many surviving offspring entails serious social, economic, or fitness consequences. A model of risk- (or variance-) sensitive adaptive behavior that addresses long-term fertility outcomes is presented. The model shows that under conditions likely to be common, optimal, risk-sensitive reproductive strategies deviate systematically from the completed family size that would be expected if reproductive outcome is were predictable. This is termed the "variance compensation hypothesis." Variance compensation may be either positive or negative, resulting in augmented or diminished fertility. Which outcome obtained is a function of identifiable social, economic, and environmental factors. Through its effect on fertility behavior, variance compensation has a direct bearing on birth spacing and completed fertility, and thereby on problems in demography and human population biology ranging from demographic transitions to maternal depletion and child health. Risk-sensitive models will be a necessary component of a general theory of fertility.