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. According to three widely held dogmas, DNA is the unchanging template of heredity, is identical in all the cells and tissues of the body, (...) and is the sole agent of inheritance. Rather than being an unchanging template, DNA appears subject to a good deal of environmentally induced change. Instead of identical DNA in all the cells of the body, somatic mosaicism appears to be the normal human condition. And DNA can no longer be considered the sole agent of inheritance. 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, epigenetic regulation, DNA variability, and somatic mosaicism appear to be particularly prevalent in the human brain and probably 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. (shrink)

Mealey's evolutionary reasoning is logically flawed. Furthermore, the evidence presented in favor of a genetic contribution to the causation of sociopathy is overinterpreted. Given the potentially large societal impact of sociobiological speculation on the roots of criminality, more-than-usual caution in interpreting data is called for.

Mealey's interesting interpretation of sociopathy is based on an inappropriate two-person game model. A multiperson, compound game version of Chicken would be more suitable, because a population engaging in random pairwise interactions with that structure would evolve to an equilibrium in which a fixed proportion of strategic choices was exploitative, antisocial, and risky, as required by Mealey's interpretation.

In the Frank (1988) model, a small increase in the number of cheaters will soon be reversed. It is not clear that this prediction holds for sociopathy. There are also many attractive evolutionary models that do not admit a small, stable proportion of cheaters. Hence, without definitive evidence about the character of early human society, we cannot conclude that sociopathy has an evolutionary origin.

Definitional slippage threatens to equate secondary sociopathy with mere criminality and leaves the status of noncriminal sociopaths ambiguous. Primary sociopathy appears to show more environmental contingency than would be implied by a strong genetic trait approach. A reinterpretation in terms of hypermasculinity and hypofemininity is compatible with the data.

According to The Bell Curve, Black Americans are genetically inferior to Whites. That's not the only point in Richard Herrnstein and Charles Murray's book. They also argue that there is something called "general intelligence" which is measured by IQ tests, socially important, and 60 percent "heritable" within whites. (I'll explain heritability below.) But the claim about genetic inferiority is my target here. It has been subject to wide-ranging criticism since the book was first published last year. Those criticisms, however, have (...) missed its deepest flaws. Indeed, the Herrnstein/Murray argument depends on conceptual confusions that have been tacitly accepted to some degree by many of the book's sharpest critics. (shrink)

We make three suggestions with regard to Mealey's work. First, her lack of a cognitive analysis of the sociopath results in underspecified mappings between sociobiology and behavior. Second, the developmental literature indicates that Mealey's implicit assumption, that moral socialisation is achieved through punishment, is invalid. Third, we advance the use of causal modelling to map the developmental relationships between biology, cognition, and behaviour.

Mealey's etiological distinction between primary and secondary sociopathy blurs the delineation between individual and group differences. She uses physiological evidence to support her claim of genetic influences, neglecting variability within social classes, frequency of delinquent behavior in upper and middle classes (measured by self-report), and discontinuity of criminal behavior across the life span. Finally, Mealey's proposals for differential intervention fall short of a future agenda, which should tailor to individual needs, not social classes.

Several hundred thousand intellectually talented 12-to 13-year-olds have been tested nationwide over the past 16 years with the mathematics and verbal sections of the Scholastic Aptitude Test (SAT). Although no sex differences in verbal ability have been found, there have been consistent sex differences favoring males in mathematical reasoning ability, as measured by the mathematics section of the SAT (SAT-M). These differences are most pronounced at the highest levels of mathematical reasoning, they are stable over time, and they are observed (...) in other countries as well. The sex difference in mathematical reasoning ability can predict subsequent sex differences in achievement in mathematics and science and is therefore of practical importance. To date a primarily environmental explanation for the difference in ability has not received support from the numerous studies conducted over many years by the staff of Study of Mathematically Precocious Youth (SMPY) and others. We have studied some of the classical environmental hypotheses: attitudes toward mathematics, perceived usefulness of mathematics, confidence, expectations/ encouragement from parents and others, sex-typing, and differential course-taking. In addition, several physiological correlates of extremely high mathematical reasoning ability have been identified (left-handedness, allergies, myopia, and perhaps bilateral representation of cognitive functions and prenatal hormonal exposure). It is therefore proposed that the sex difference in SAT-M scores among intellectually talented students, which may be related to greater male variability, results from both environmental and biological factors. (shrink)