A consideration of the genetics of sociopathy suggests the following. The author's Evolutionary Stable Strategy (ESS) types 2 to 4 are more likely than types 1 and 5 in crimes of violence, and there may not be an ESS for crimes of property or for sociopathy. Correlations between sociopathy and crimes of property are also more likely due to environmental than to genetic variants, and correlations between sociopathy and crimes of property are due more to environmental than genetic variants.

We received 23 spirited commentaries on our target article from across the disciplines of philosophy, economics, evolutionary genetics, molecular biology, criminology, epidemiology, and law. We organize our reply around three overarching questions: (1) What is a cause? (2) How are randomized controlled trials (RCTs) and within-family genome-wide association studies (GWASs) alike and unalike? (3) Is behavior genetics a qualitatively different enterprise? Throughout our discussion of these questions, we advocate for the idea that behavior genetics shares many of the same pitfalls (...) and promises as environmentally oriented research, medical genetics, and other arenas of the social and behavioral sciences. (shrink)

Evolutionary analysis suggests that policies based on deterrence may cope effectively with primary sociopathy if the threat of punishment fits the crime in the cost/benefit calculus of the sociopath, not that of the public. On the other hand, policies designed to offset serious disadvantage in social competition may help inhibit the development of secondary sociopathy, rather than deter its expression.

Independent samples of women were surveyed to test Trivers and Willard’s hypothesis that the mother’s condition and her ability to invest in her offspring affect the (secondary) sex ratio of her offspring. Patterns of sex ratios (number of males per 100 females) were analyzed in conjunction with four attributes of a mother’s microenvironment: level of health in her community, family structure, relative access to resources, and her birthing history. The results inferentially support the hypothesis that the microenvironment of the woman (...) would act to bias the sex ratio of her offspring. These specific data lend support to Trivers and Willard’s general hypothesis. (shrink)

Endorsing Mealey's analysis, it is pointed out that increasing rates of crime and violence are due to increasing proportions of children being reared in circumstances radically different from the extendedfamily environment to which we are evolntionarily adapted, that is, they are reared without fathers.

The well-established finding that siblings growing up in the same family turn out to be very different from one another has puzzled psychologists and behavior geneticists alike. In this theoretical note we describe the possible ontogeny and phylogeny of a sibling differentiation mechanism. We suggest that sibling competition for parental investment results in sibling differentiation on a number of characteristics, producing different developmental trajectories within families. Variations in developmental trajectories within families may have had fitness advantages in ancestral environments because(a) (...) sibling competition for extrafamilial resources would be reduced and(b) these variations would be suited to environments containing a variety of niches or to changing environments. Predictions derived from this model and an example of an application to attachment theory are presented. (shrink)

Although Mealey's account provides several interesting hypotheses, her integration across disparate samples renders the value of her explanation for psychopathy ambiguous. Recent evidence on Psychopathy Checklist-identified samples (Hare, 1991) suggests primary emotional and cognitive deficits inconsistent with her model. Whereas high-anxious psychopaths display interpersonal deficits consistent with Mealey's hypotheses, low-anxious psychopaths' deficits appear more sensitive to situational parameters than predicted.

We consider four mechanisms by which apparent discontinuities in the distribution of antisociality could arise: (1) executive genes or hormonal systems, (2) multiplicative interactions of predisposing factors, (3) environmental tracking into a limited number of social roles, and (4) cross-generational gene—environment interactions. A more explicit consideration of complex self-organizing dynamic systems may help us understand the maintenance of antisocial subpopulations.

Although serotonin, testosterone, and genes contribute to sociopathy, the relationships are probably indirect and subject to modifiers (e.g., present only under certain conditions of rearing and temperament). Age at menarche may be a marker variable as well as a causal factor. Since the genders differ in all four areas, sex differences in sociopathy represent a very complex interaction of these factors.

Mealey's work has several interesting implications: It refutes the charge that sociobiology paints a cynical portrait of human nature and adopts a one-sided reductionism; it exemplifies a general theoretical scheme for constructing evolutionary biopsychosocial models of human behavior; and it has the practical effect of promoting and informing early intervention in children at risk for psychopathic disorder.

In this brief commentary the author concentrates on the treatment perspectives of Mealey's model. The main weakness of the model is that it does not provide a satisfactory theoretical connection between treatment and different types of target behavior. Even within the primary-secondary distinction, there are large individual differences that should not be overlooked in the planning of treatment.