In the Introduction to this volume, Peter K. Hatemi and Rose McDermott assert that “nature–nurture” is an “outdated juxtaposition,” an “atavistic dichotomy,” and a “dualism [that] remains absurd on its face” (p. 3). This a surprising assertion in a book titled “Man is by Nature a Political Animal.” In rejecting this dichotomy, they claim to “support the dominant interpretation across sciences which assumes the inextricable interaction between biology [by which the authors intend both genes and “physiology”] and environment in determining the growth and development of any given biological organism within a particular ecological context” (p. 3). It would be characteristic of this dichotomy to assume that genes could contribute to phenotypic variation in a manner that did not involve “inextricable interaction” between genes and the environment; likewise, it would be absurd to assume that a given physiological response could develop in a manner that did not involve environmental interaction. Such assumptions, however, are ubiquitous in this volume.

For example, Lindon J. Eaves, Hatemi, Andrew C. Heath, and Nicholas G. Martin (Chap. 4), after considering how to partition the contribution of genes versus environment to variation in political behavior, note a “potential limitation” of their models: “[T]hey are linear and additive [and] do not take into account … interactions between genes and environments” (p. 157). But if biology (which includes genes) and environment “remain codependent and interactive,” what is the value of a model that treats them as if they are not interactive? It is one thing to acknowledge the shortcomings of a model; it is another to construct a model on the basis of a principle that one simultaneously claims is “absurd on its face.” A similar “atavistic dichotomy” is found in Kevin B. Smith and John R. Hibbing's (Chap. 7) account of the development of “physiological” differences: “The evolutionary process has imbued all humans with an autonomic nervous system, but genetic variation has instilled a remarkable amount of diversity in the specific response levels of individuated nervous systems to standardized stimuli” (p. 225). Hence, diversity in autonomic responses is ascribed entirely to “genetic variation” (inasmuch as “genes build physiology” [p. 225]) in defiance of “the inextricable interaction between biology and environment.”

Consider the role of the environment in shaping the autonomic nervous system's stress response (the “fight or flight” response), inasmuch as it provides an illustration of the kind of biology–environment interaction that is conspicuously absent from this volume, as well as the evolutionary significance of such interaction. Differences in early maternal care translate into differences in the stress response of offspring, and cross-fostering studies have shown repeatedly that the key determinant is the rearing rather than the biological mother.Footnote ¹ Offspring that receive low levels of maternal care exhibit, as adults, increased levels of stress as measured behaviorally and physiologically, with females also exhibiting earlier mating behavior and lower levels of maternal care, while high maternal-care offspring exhibit, as adults, the opposite phenotypes. Significantly, these behaviors are associated with postnatal alterations to the epigenome, the complex, environmentally reactive, biochemical system that regulates the accessibility of genes to transcription factors and, thereby, the extent to which any given gene can be transcribed. The observed epigenetic changes, and corresponding changes in gene transcription rates, are consistent with increased and decreased stress responses. In other words, the environment reprograms the epigenome and the epigenome reprograms gene transcription rates.Footnote ²

This is an example of phenotypic plasticity, the ability of an organism to modify developmental trajectories and change phenotypic state or activity in response to variations in environmental conditions. Developmental phenotypic plasticity evolved because it is adaptive, promoting Darwinian fitness by enhancement of survival and reproductive success by using environmental cues to optimize the life-course strategy. A heightened stress response and diminished maternal care enhance the mother's chances of survival in a dangerous (“high stress”) environment, but by shaping the stress response and mating and rearing behavior of her offspring, she enhances their survival as well. Offspring behavioral plasticity enables the mother to adjust offspring phenotype in response to the environment she inhabits. Adversity during perinatal development can forecast an increased level of demand in the environment the offspring will occupy. Under such conditions, the animal's best interest is to enhance its behavioral (e.g., vigilance, fearfulness) and endocrine responsiveness to stress. These responses promote detection of potential threat, avoidance learning, and metabolic/cardiovascular responses that are essential under the increased demands of the stressor.

Such environmental shaping of physiological response is not to be confused with either “G × E” (“gene × environment” interaction or “gene-environment interplay” [Chap. 5]) or what Eaves and his colleagues refer to as the “ontogenetic process” (p. 154). G × E is the idea that a particular polymorphism will result in a given phenotype in one environment and a different phenotype (or no phenotype) in a different environment. The “ontogenetic process” refers to purported (and inexplicable, both in terms of physiology and adaptive value) changes in the heritability of a particular phenotype at a particular point in life as indicated by the twin-study methodology. Neither G × E nor the ontogenetic process involves phenotypic plasticity, that is, modification of developmental trajectories to meet the demands of a particular environment and, hence, neither has any apparent adaptive value. Neither epigenetics nor phenotypic plasticity—mechanisms that embody “the inextricable interaction between biology and environment”—is mentioned anywhere in this volume, although the former represents the most important development in molecular genetics and the latter the most important development in evolutionary biology over the past 50 years.

Both absurdly high heritability estimates—60% for political participation (p. 215), 60% for strength of political partisanship (p. 216), 50%–70% for attitudes toward homosexuality and gay rights—and the assumption that single polymorphisms can predict complex political behaviors (Chaps. 5, 6, 8) reinforce, rather than overcome, the traditional nature–nurture dichotomy. If we were to take such heritability estimates seriously, then we would have to conclude that humans were less biologically influenced by, and reactive to, their environments than fruit flies (heritability of aggression in fruit flies is ~10%).Footnote ³ Aggressive strains of fruit flies exhibit differences in transcription rates of more than 1,539 genes as compared to controls.Footnote ⁴ In a situation such as this, no single gene could possibly predict aggressive behavior, yet we are told that a single polymorphism can predict, for example, voting (pp. 218–19, 268).

The assumption that a single polymorphism could predict a behavior such as voting results from conceptualizing complex behaviors in the manner of “simple” genetic disorders (p. 27):

This is not a logical assumption but, rather, a profound error. Huntington's disease is a neurological disorder caused by a mutation on a gene (HTT) that is coded for the protein huntingtin. Symptoms include changes in personality and cognitive ability and, over time, the eventual loss of the ability to walk, talk, think, and reason. Can we infer from this that polymorphisms of single genes are likely to influence a wide array of complex normal behaviors associated with the healthy human brain (such as, e.g., voting)? Certainly not. An HTT gene mutation has far-reaching phenotypic consequences because the end result of an abnormal huntingtin protein is neuronal degeneration. But voting, for example, is not a monogenic disorder, or an oligogenic disorder, or a complex polygenic disorder. Normal complex human behavior is not a cluster of disorders, nor is it a cluster of distinct “behaviors,” each behavior predicted by a gene or set of genes. Rather, normal behavior is the integrated output of a highly integrated biological system interacting with a particular environment.