More Genes and Politics

Larry Arnhart has an informative and detailed post on the debate  I highlighted last week about the possible genetic determinants of voting behavior. The whole post is worth a read. Here is the key passage:

In both of these debates, the opposing sides employ the rhetoric of arguing against a “straw man.”  Charney criticizes his opponents for being genetic determinists.  His opponents criticize him and others like him for being environmental determinists.  And yet no one here is defending either genetic determinism or environmental determinism.  Charney agrees that genes matter.  His opponents agree that environment matters.

The debate over the Fowler and Dawes article is confusing, because Fowler and Dawes imply two different kinds of claims—one is very astonishing and the other is very modest.  The very astonishing claim is that two genes predict voter turnout, and this is the claim that Charney easily refutes.  The very modest claim is that these two genes might matter a little in influencing voter turnout, but these two genes by themselves cannot actually predict voter turnout, and in fact these two genes are probably much less important than other factors.  Charney comes close to agreeing with this very modest claim when he says: “DNA is one component of a complex, integrated, interactive, and dynamic biological-environmental-ecological process through which biological organisms come to manifest divergent phenotypes.”  Charney, Fowler, and Dawes all agree that particular genes influence but do not specify behavior, because genes interact with other genes, with other biological factors, and with the physical and social environment.

One Response to More Genes and Politics

  1. Evan Charney March 23, 2012 at 9:47 pm #

    I would like to clarify what we are, and are not, arguing our article “Candidate Genes and Political Behavior.”

    We nowhere in this article argue on the basis of a contrast between “genetic determinism” on the one hand and “environmental determinism” on the other, nor do we claim that Fowler is arguing that it’s “all in the genes” or that having a certain polymorphism determines that one will or will not vote. What we dispute is precisely what Fowler claims: that one or two common gene variants could so influence a complex behavior as to be capable of predicting that behavior, even if manner in which it influences that behavior is “miniscule” (although I am not sure how something that has a miniscule effect could be predictive).

    The assumption that a single polymorphism could PREDICT (or be a risk-factor for, no matter how small the risk) complex behaviors (such as all political behavior) runs contrary to a growing consensus that most human traits with a heritable component involve proteins coded in thousands of genes. For example, current estimates are that upwards of 7000 genes may be necessary to explain 45% of the variation in height, a highly heritable trait. Variation in aggression in fruit flies involves variation in levels of proteins encoded in thousands of genes, interacting with each other in complex ways (epistasis), and the same genes implicated in variation in aggression are implicated in every other conceivable physiological process (pleiotropy). Yet aggression is only ~0.1% heritable. Given this, no single gene could possibly be predictive of behavioral variation. Nor does any single gene play a predetermined role as a “risk-factor,” no matter how small a risk factor it is. Behaviors are not like monogenic or polygenic disorders (e.g., cystic fibrosis).

    Ultimately, the dichotomy between genes and environment is a false one because it is becoming increasingly clear that what differentiates humans from other species is not the number and kind of genes we possess (humans have fewer genes than corn) but patterns of gene expression. Gene expression is regulated by the epigenome, which is highly environmentally responsive, effectively blurring the distinction between genes and environment.

    I would also like to emphasize the following (emphasized in the article):

    The same set of polymorphisms of the MAOA gene (MAOA-μVNTR) that Fowler and Dawes claimed were associated with voting have also been associated with, e.g., agreeableness, alcoholism, Alzheimer’s disease, anorexia nervosa, attachment, attention deficit hyperactivity disorder, attitudes toward longshot risks, auditory evoked potentials, autism, binge drinking, body mass index, bone mineral density, borderline personality disorder, chronic fatigue syndrome, contraception use, credit card debt, epilepsy, extraversion, facial expression recognition, fearfulness, fibromyalgia, financial risk taking, fraudulent behavior, gambling (both performance and pathological), gang membership, harm avoidance, hypertension, insomnia, intelligence, memory, migraines, narcolepsy, neuroticism, obesity, obsessive compulsive disorder, openness, pain perception, panic disorder, Parkinson’s disorder, persistence, postpartum depression, restless legs syndrome, reward dependence, schizophrenia, smoking, sudden infant death syndrome, suicide, telomeric length, temperomandibular disorder, time perception, and Tourette syndrome.
    The other gene polymorphism Fowler and Dawes identified as being associated with voting, i.e., the linked polymorphic region of the serotonin transporter gene (5-HTTLPR), have been associated with e.g., agreeableness, alcoholism, Alzheimer’s disease, anger/aggression, anorexia nervosa, antisocial behavior, apthmous stomatitis, attachment, attention deficit hyperactivity disorder, autism, binge drinking, bipolar disorder, blood glucose control in diabetics, blushing, body mass index, borderline personality disorder, brain activation by colorectal distension, brain activation in processing errors, breast cancer, bulimia, caudate nucleus volume, chronic fatigue syndrome, choosing between greater rewards and punishments, cleft lip, conscientiousness, contraception use, cooperativeness, creativity, creative dance performance, criminal behavior, decision making under ambiguity/risk, deductive reasoning, depression, type II diabetes, early onset myocardial infarction, emotion appraisal, emotion induced retrograde amnesia, epilepsy, extraversion, fearfulness, fibromyalgia, frontotemporal lobar degeneration, fibromyalgia, pathological gambling, gastric emptying, harm avoidance, heroin use, hyperprolactinemia, hypertension, attitudes toward individualism and collectivism, insomnia, intelligence, interpersonal sensitivity, interpretive bias, irritable bowel syndrome, job satisfaction, job stress, loneliness, longevity, maternal sensitivity, migraines, neurodermatitis, neuroticism, novelty seeking, number of sexual partners, obesity, obsessive compulsive disorder, openness, optimism, oral lichen planus, osteoporosis, pain perception, panic disorder, parenting, Parkinson’s disease, persistence, periodontal disease, postpartum depression, posttraumatic stress disorder, premature ejaculation, premenstrual dysphoria disorder, psoriasis, resiliency to victimization, reward dependence, schizophrenia, seasonal affective disorder, sexual frequency, shyness, sleep apnea, smoking, social phobia, startle response, stress response, sudden infant death syndrome, suicide, sustained attention, tardive dyskinesia, time perception, utilitarian moral judgments, verbal fluency in ecstasy users, and well-being.

    What is going on here is data mining on a massive scale, and this has occurred for at least two reasons: The widespread use of data sets that contain behavioral information (usually in the form of self-reporting) as well as genotype information of specific polymorphisms in a handful of genes; creative hypotheses based upon the results of earlier studies (a partial list of associations that have been made with specific polymorphisms on four genes and a bewildering array of phenotypes is available at: