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.

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.

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.

Sociopaths are “outstanding” members of society in two senses: politically, they draw our attention because of the inordinate amount of crime they commit, and psychologically, they hold our fascination because most ofus cannot fathom the cold, detached way they repeatedly harm and manipulate others. Proximate explanations from behavior genetics, child development, personality theory, learning theory, and social psychology describe a complex interaction of genetic and physiological risk factors with demographic and micro environmental variables that predispose a portion of the population (...) to chronic antisocial behavior. More recent, evolutionary and game theoretic models have tried to present an ultimate explanation of sociopathy as the expression of a frequency-dependent life strategy which is selected, in dynamic equilibrium, in response to certain varying environmental circumstances. This paper tries to integrate the proximate, developmental models with the ultimate, evolutionary ones, suggesting that two developmentally different etiologies of sociopathy emerge from two different evolutionary mechanisms. Social strategies for minimizing the incidence of sociopathic behavior in modern society should consider the two different etiologies and the factors that contribute to them. (shrink)

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.

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.

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?

Mealey's analysis of secondary sociopathy has much in common with Belsky, Steinberg, and Draper's (1991) evolutionary theory of socialization. Both draw attention to the potential influence of early rearing in the promotion of a cold, detached, manipulative, and opportunistic style of relating to others and, in so doing, raise the question of whether secondary sociopathy represents a facultative reproductive strategy.

Unlike some psychiatric illnesses, criminal lifestyles are not reproductive dead ends and may represent frequency-dependent adaptations. Sociopaths may gain reproductively from their greater relative to nonsociopaths. This mating-effort construct should be assessed directly in future studies of sociopathy. Collaboration between biologically oriented and environmentally oriented researchers is needed to investigate the biosocial basis of sociopathy.

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.

Mealey's excellent target article rests on several assumptions that may be questioned, including the overarching assumption that sociopathy reflects the failure of a small minority of males to cooperate with the larger group. I suggest that violent competition in ancestral bands cheatinggame was the primary evolutionary precursor of sociopathy. Today's violent sociopath is far more a than a failed cooperator.

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.

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.

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.

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.

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.

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?

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 sociobiological model of sociopathy could profit from attachment theory, in particular, the theory and research on the basis of the Adult Attachment Interview (Main & Goldwyn 1985–1993). Findings of an adult attachment study in a forensic psychiatric setting are summarized. Three attachment-oriented strategies for families, schools, and forensic settings are proposed to help reduce or prevent secondary sociopathy and criminal recidivism.

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.

Recent studies lend support to the two-pathway model of the evolution of sociopathy with evidence that: 1) psychopathy (primary sociopathy) is a discrete type and 2) in general, sociopaths have relatively high levels of reproductive success. Hare's Psychopathy Checklist may provide a start for the revision of terminology that will be necessary to distinguish between primary and secondary trajectories.

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.

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.

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 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.

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.

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.

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 distinguishes two types of sociopathy: (1) or obligate, and (2) 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.

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.

Understanding the bases of complex behavioral phenotypes, such as sociopathy, is assisted by an evolutionary approach, in addition to other theoretical perspectives. Unraveling genetic and environmental factors underlying variant forms of sociopathy remains a key challenge for behavioral science investigators. Twin research methods (e.g., longitudinal analyses; twins reared apart) offer informative means of assessing novel hypotheses relevant to sociopathic behaviors.

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.

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.

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.

Emotion is critical in Mealey's conceptual arguments. However, several of her assertions about the role of emotion in sociopathy are problematic. Questions are raised regarding the link between lack of anxiety and low levels of secondary emotions such as love and sympathy, the argument that sociopaths are low in anxiety but high in neuroticism, and the designation of anxiety as a secondary emotion.

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 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.

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.

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.

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 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. (shrink)

Mealey's data do not support her dichotomous model of primary and secondary sociopathy; this data supports the view that there is a continuum of degrees of sociopathy, from zero to the maximal manifestation. There are multitudes of factors that can contribute to sociopathy and the countless different mixes of them can produce multiple degrees and variations of sociopathic behavior.

Two specific aspects of Mealey's model are questioned: (1) the application of the concept of Evolutionarily Stable Strategy to all alternative strategies, including those that involve reduced lifetime reproductive success; and (2) the evidence for the dual role of testosterone, which is based mainly on studies of a modulating effect on aggression.