Given that natural selection is so powerful at optimizing complex adaptations, why does it seem unable to eliminate genes (susceptibility alleles) that predispose to common, harmful, heritable mental disorders, such as schizophrenia or bipolar disorder? We assess three leading explanations for this apparent paradox from evolutionary genetic theory: (1) ancestral neutrality (susceptibility alleles were not harmful among ancestors), (2) balancing selection (susceptibility alleles sometimes increased fitness), and (3) polygenic mutation-selection balance (mental disorders reflect the inevitable mutational load on the thousands (...) of genes underlying human behavior). The first two explanations are commonly assumed in psychiatric genetics and Darwinian psychiatry, while mutation-selection has often been discounted. All three models can explain persistent genetic variance in some traits under some conditions, but the first two have serious problems in explaining human mental disorders. Ancestral neutrality fails to explain low mental disorder frequencies and requires implausibly small selection coefficients against mental disorders given the data on the reproductive costs and impairment of mental disorders. Balancing selection (including spatio-temporal variation in selection, heterozygote advantage, antagonistic pleiotropy, and frequency-dependent selection) tends to favor environmentally contingent adaptations (which would show no heritability) or high-frequency alleles (which psychiatric genetics would have already found). Only polygenic mutation-selection balance seems consistent with the data on mental disorder prevalence rates, fitness costs, the likely rarity of susceptibility alleles, and the increased risks of mental disorders with brain trauma, inbreeding, and paternal age. This evolutionary genetic framework for mental disorders has wide-ranging implications for psychology, psychiatry, behavior genetics, molecular genetics, and evolutionary approaches to studying human behavior. (Published Online November 9 2006) Key Words: adaptation; behavior genetics; Darwinian psychiatry; evolution; evolutionary genetics; evolutionary psychology; mental disorders; mutation-selection balance; psychiatric genetics; quantitative trait loci (QTL). (shrink)

This response (a) integrates non-equilibrium evolutionary genetic models, such as coevolutionary arms-races and recent selective sweeps, into a framework for understanding common, harmful, heritable mental disorders; (b) discusses the forms of ancestral neutrality or balancing selection that may explain some portion of mental disorder risk; and (c) emphasizes that normally functioning psychological adaptations work against a backdrop of mutational and environmental noise. (Published Online November 9 2006).

Based on an analysis of the reports of twenty-eight national-level public commission inquiries into events involving ethno-national violence—drawn from five national contexts and arrayed over the course of the twentieth century—this article demonstrates the strikingly transnational character of these investigatory bodies’ attempts to authoritatively explain episodes of collective violence and to thereby restore governing legitimacy in the wake of violent crises. One of four distinct “logics,” or core explanatory frameworks, each associated with a particular mode of “racial power,” characterized a (...) diverse cross-national pool of violence commission reports during defined periods of the twentieth century. In revealing globally encompassing logics to what has often been framed as a national or case-specific phenomenon, the author shows how global ideational currents compose a key dimension of national political dynamics. (shrink)

If alleles that predispose to schizophrenia have reduced Darwinian fitness, their persistence in modern times is puzzling. Burns identifies the evolutionary genetics of schizophrenia as a central issue, but his treatment of it is not clear. Recent advances in evolutionary genetics can help explain the persistence of alleles that predispose to debilitating disorders such as schizophrenia, and can buttress Burns' core argument.

Crespi & Badcock (C&B) convincingly argue that autism and schizophrenia are diametric malfunctions of the social brain, but their core imprinting hypothesis is less persuasive. Much of the evidence they cite is unrelated to their hypothesis, is selective, or is overstated; their hypothesis lacks a clearly explained mechanism; and it is unclear how their explanation fits in with known aspects of the disorders.

Influences on social traits involve a tangled interplay of genetic, social, and environmental factors. Moreover, there is increasing awareness that gene–environment correlations are real and potentially measurable. Such gene–environment correlations can mislead if they are uncontrolled and genetic associations are interpreted as being purely because of direct genetic effects. This complexity is cause for more and better investigation, not a reason to refrain from researching one of the potentially important factors (genetics) influencing trait variation.