Think Genes Predict Social and Political Behavior? Not So Fast

My colleague Evan Charney has a very nice article in the most recent issue of the American Political Science Review:

Political scientists are making increasing use of the methodologies of behavior genetics in an attempt to uncover whether or not political behavior is heritable, as well as the specific genotypes that might act as predisposing factors for—or predictors of—political “phenotypes.” Noteworthy among the latter are a series of candidate gene association studies in which researchers claim to have discovered one or two common genetic variants that predict such behaviors as voting and political orientation. We critically examine the candidate gene association study methodology by considering, as a representative example, the recent study by Fowler and Dawes according to which “two genes predict voter turnout.” In addition to demonstrating, on the basis of the data set employed by Fowler and Dawes, that two genes do not predict voter turnout, we consider a number of difficulties, both methodological and genetic, that beset the use of gene association studies, both candidate and genome-wide, in the social and behavioral sciences.

The emphasis is mine. Having seen Evan give a fascinating presentation on this topic a few years ago, I was very happy to see (some of) his work on the topic published in such a widely read journal.

Evan also tells me that he has another paper on the topic titled “Behavior Genetics and Postgenomics” that’s forthcoming in Behavioral and Brain Sciences. Here is the abstract of that forthcoming piece:

The science of genetics is undergoing a paradigm shift. Recent discoveries, including the activity of retrotransposons, the extent of copy number variations, somatic and chromosomal mosaicism, and the nature of the epigenome as a regulator of DNA expressivity, are challenging a series of dogmas concerning the nature of the genome and the relationship between genotype and phenotype. DNA, once held to be the unchanging template of heredity, now appears subject to a good deal of environmental change; considered to be identical in all cells and tissues of the body, there is growing evidence that somatic mosaicism is the normal human condition; and treated as the sole biological agent of heritability, we now know that the epigenome, which regulates gene expressivity, can be inherited via the germline. These developments are particularly significant for behavior genetics for at least three reasons: First, these phenomena appear to be particularly prevalent in the human brain and likely are involved in much of human behavior; second, they have important implications for the validity of heritability and gene association studies, the methodologies that largely define the discipline of behavior genetics; and third, they appear to play a critical role in development during the perinatal period and, in particular, in enabling phenotypic plasticity in offspring. I examine one of the central claims to emerge from the use of heritability studies in the behavioral sciences, the principle of minimal shared maternal effects, in light of the growing awareness that the maternal perinatal environment is a critical venue for the exercise of adaptive phenotypic plasticity. This consideration has important implications for both developmental and evolutionary biology.