Lucas Matthews and I substantially revised my SEP entry on Heritability. This version includes discussion of the missing heritability problem and other issues that arise from the use of Genome Wide Association Studies by Behavioral Geneticists.

Androphilia refers to sexual attraction and arousal to adult males, whereas gynephilia refers to sexual attraction and arousal to adult females. The Kin Selection Hypothesis posits that genes for male androphilia can persist if androphilic males offset the fitness costs of not reproducing directly by enhancing indirect fitness. In theory, by directing altruistic behavior toward kin, androphilic males can increase the reproduction of kin, thereby enhancing indirect fitness. Evidence supporting the KSH has been documented in Samoa. Samoan transgendered, androphilic males, (...) known locally as fa’afafine, are socially accepted by the majority of Samoans. In contrast, no supportive evidence has been garnered from other cultures that are characterized by less social tolerance toward male androphiles. Tests of the KSH in Canada might be more likely to yield findings consistent with Samoa because Canadian social and political attitudes toward male androphiles are markedly more tolerant and accepting. Here, we compared the willingness of Canadian androphilic men, gynephilic men, and androphilic women to invest in nieces and nephews as well as in non-kin children. Consistent with the KSH and findings from Samoa, androphilic men exhibited a significantly greater cognitive dissociation between altruistic tendencies directed toward kin versus non-kin children relative to gynephilic men and androphilic women. The present study, therefore, provides some tentative support for the KSH from a culture other than Samoa. Findings and future directions for research are considered within the context of the existing cross-cultural literature. (shrink)

The spectre of determinism stalks many of the concerns surrounding the impact of genetic research into both disease and normal behaviour. The ability accurately to predict a person's actions would certainly have profound implications for notions of individuality and free will. But to what extent will the current explosion in genetic research provide more accurate predictors than have been available for millennia in the form of wealth, social status and perceived family resemblance? The genetic research program is at too early (...) a stage to answer this question with confidence, but various indicators tend to point in the same direction: the predictive ability of genetic analysis will generally be low. This conclusion runs counter to widely perceived popular notions. The deconstruction of genetic determinism is an essential safeguard against the real concern that genetic information may be used for discrimination by unscrupulous powers. (shrink)

The validity of the classification of “primary sociopaths” as a qualitatively distinct group in the general population is questioned. Cenetic variation in the experience and expression of emotions may play a role in the development of antisocial behavior. However, research clearly documents that socialization environments powerfully modify the expression of genetic biases in a manner that increases or decreases the risk for “sociopathy.”.

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.

As more criminals are imprisoned, other individuals change their behavior to replace them, as predicted by the theory of strategic behavior. The physiological correlates of sociopathy suggest that research in cognitive neuroscience can lead toward a solution. Promising pathways include building upon current knowledge of self-deceit, the independence of positive and negative emotions, the lateralization of risk and caution, and the conditions promoting prosocial behavior.

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.

Mealey's sociopathy model is an exemplar of popular diathesis-stress models. Although such models, when presented in descriptive language, offer the illusion of integrative explanation, their actual scientific value is very limited because they fail to make specific, quantitative, falsifiable predictions. Conceptual and quantitative weaknesses of such diathesis-stress models are discussed and the requirements for useful models are outlined.

The psychological mechanisms implicated in psychopathy do not limit their activity to those behaviors that support a cheater strategy in social games. They result in a number of other clearly maladaptive behaviors that do not directly involve other individuals. Thus, any gains that might arise from the use of a cheater strategy in social situations are probably lost elsewhere.

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.

Strengths of Mealey's target article are its implementation of results from game-theoretic analyses and its potential links with other formal developments. In recent dynamic decision/choice models, reduced salience of avoidance tendencies, said to typify primary sociopaths, has quantifiable consequences for response latencies and choices. Also, formal models of stress effects on information processing predict selected effects of hypoarousability.

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.

Behavioral biologists have long sought to link behavioral units (e.g., aggression, depression, sociopathy) with biological units (e.g., genes, neurotransmitters, hormones, neuroanatomical loci). These units, originally contrived for descriptive purposes, often lead to misunderstandings when they are reified for purposes of causal analysis. This genetic and biochemical explanation for sociopathy reflects such problems.

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.

Recent evidence that psychopathy is a nonarbitrary population, such that the trait may be categorical rather than continuous, is consistent with Mealey's distinction between primary and secondary psychopaths. Thus, there are likely to be at least two routes to criminality, and psychopathic and nonpsychopathic criminals are likely to respond differently to interventions.

If sociopathy is a biological adaptation, it probably evolved in small social groups in which individuals lacked the social mobility required for a con-man strategy to work. On the other hand, conflicts between groups may have provided a large niche for sociopathy throughout human history.

We propose that Mealey's model is limited in its description of sociopathy because it does not provide an adequate role for the main organ mediating genes and behavior, namely, the brain. Further, on the basis of our research, we question the view of sociopaths as a homogeneous group.

Mealey proposes two categorical classes of sociopath, primary and secondary. I criticize this distinction on the basis that constructs of this kind have proved unrealistic in personality taxonomy and that dimensional systems capture reality much more successfully. I suggest how such a system could work in this particular context.

We doubt that primary sociopathy is adaptive, for three reasons: First, its prevalence is too low to require an adaptive explanation. Second, a common sequela of damage to the orbito-frontal lobes is Any pattern of behavior that can be produced by brain damage is unlikely to be adaptive. Third, we argue that most human social behavior is not under tight genetic control, but is produced by open-ended calculation of fitness-contingencies.

The key questions arising from Mealey's analysis are: Do environmental factors such as early maternal rejection also contribute to the emotional deficits observed in psychopaths? Are there psychophysiological protective factors for antisocial behavior that have clinical implications? Does a disinhibited temperament and low arousal predispose to primary psychopathy? Would primary or secondary psychopaths be most characterized by prefrontal dysfunction?

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.

Problems of definition and identification in the integrated evolutionary model of sociopathy are suggested by Schoenfeld's (1974) criticism of the field of race differences in intelligence. Moral judgments by those labeled primary and secondary sociopaths may offer a way to validate the assumptions of the model.

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.

Further understanding at neuroscientific and personality levels should considerably advance our ability to deal with individuals that have strong sociopathic tendencies. An analysis of neurodynamic responses to emotional stimuli will eventually be able to detect sociopathic tendencies of the brain. Such information could be used to enhance the options available to individuals at risk without limiting their personal freedoms.

Four questions are raised about Mealey's genetic argument: (1) Where is the evidence that secondary sociopathy is less heritable than primary sociopathy? (2) What is the genetic correlation between the two types of sociopathy? (3) How does genotype-environment interaction relate? (4) How strong are the links between our evolutionary past and current heritability?

Psychopathy has as its central traits socialization, sensation seeking, and impulsivity. These are combined in a supertrait: Impulsive Unsocialized Sensation Seeking (ImpUSS). Secondary types are defined by combinations of ImpUSS and neuroticism or sociability. All broad personality traits have both genetic and environmental determination, and therefore different etiologies (primary as genetic, secondary as environmental) for primary and secondary sociopathy are unlikely.

This commentary extends arousal theory to suggest an explanation for the well-established inverse correlation between church attendance and involvement in crime. In addition, the results of two surveys of social scientists are reviewed to reveal just how little impact the biosocial/sociobiological perspective has had thus far on social science.