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 proposes two categorical classes of sociopath, primary and secondary. I criticize this distinction on the basis that “type” 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.

Mealey distinguishes two types of sociopathy: (1) “primary,” or obligate, and (2) “secondary,” or facultative. Either sociopathy evolved twice, or one form is derived from the other, e.g., through: (1) genetic assimilation generating polymorphism in the relative strength of biases favoring the development of otherwise facultative strategies, or (2) independently heritable but strategically relevant characteristics biasing the optimal selection of facultative strategies.

Sociobiological explanation requires both a reliable and a valid definition of the sociopathy phenotype. Mealey assumes that such reliable and valid definition of sociopathy exists in her “Integrated Evolutionary Model.” A review of psychiatric literature on the diagnosis of antisocial personality disorder clearly demonstrates that this assumption is faulty. There is substantial disagreement among diagnostic systems (e.g., RDC, DSM-III) over what constitutes the antisocial phenotype, different systems identify different individuals as sociopathic. Without a valid definition of sociopathy, sociobiological theories like Mealey's should be viewed as entirely speculative.

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 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.

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.

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 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.

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.

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.

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.

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.

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 “pseudopsychopathy.” 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.

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.

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?

Questions are raised about several issues discussed by Mealey: (1) the nature of the distinction between primary and secondary sociopaths, (2) some difficulties with a general arousal theory of criminality, and (3) the possible role of countervailing forces in the development of sociopathy. An important area that calls for attention is the patterning of different specific emotions in the lives of sociopaths as compared to other groups.

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.

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?