Charney describes several mechanisms that will bias estimates of heritability in unpredictable directions. In addition, the mechanisms described by Charney explain the puzzling fact that research in human-behavior genetics routinely reports higher heritabilities than animal studies do. However, I argue that the concept of heritability has no real place in human research anyway.

The paper addresses the question of whether heritability can be useful in establishing genetics as an explanation for an individual’s display of some trait or behavior. After reviewing the fundamental philosophical challenge to heritability—that heritability is a population level measure—an argument is presented for rethinking the role heritability occupies in both causal and explanatory claims. It is argued that heritability can be useful for genetically based explanations of individual traits, if the conditions for proper genetic explanation are modestly reconceived, and (...) the measure is seen as an evidential tool which conforms to standard methods for determining causal factors. (shrink)

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.

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.

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.

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'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.

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.

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)

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.

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.

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.

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.

This is a critical response to "Defending Eugenics", published in MBR in 2018.

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.

The presence of gene–environment statistical interaction and correlation in biological development has led both practitioners and philosophers of science to question the legitimacy of heritability estimates. The paper offers a novel approach to assess the impact of GxE and rGE on the way genetic and environmental causation can be partitioned. A probabilistic framework is developed, based on a quantitative genetic model that incorporates GxE and rGE, offering a rigorous way of interpreting heritability estimates. Specifically, given an estimate of heritability and (...) the variance components associated with estimates of GxE and rGE, I arrive at a probabilistic account of the relative effect of genes and environment. (shrink)

Can a heritability value tell us something about the weight of genetic versus environmental causes that have acted in the development of a particular individual? Two possible questions arise. Q1: what portion of the phenotype of X is due to its genes and what portion to its environment? Q2: what portion of X’s phenotypic deviation from the mean is a result of its genetic deviation and what portion a result of its environmental deviation? An answer to Q1 provides the full (...) information about X’s development, while an answer to Q2 leaves out a large portion unexplained—that portion which corresponds to the phenotypic mean. Q1 is unanswerable, but I show it is nevertheless legitimate under certain quantitative genetics models. With regard to Q2, opinions in the philosophical and biological literature differ as to its legitimacy. I argue that not only is it legitimate, but in particular, under a few simplifying assumptions, it allows for a quantitative probabilistic answer: for normally distributed quantitative traits with no G-E correlation or statistical G × E interaction, we can assess the probability that X’s genes had a greater effect than its environment on its deviation from the mean population value. This probability is expressed as a function the heritability and the individual’s phenotypic value; we can also provide a quantitative probabilistic answer to Q2 for an arbitrary individual where the probability is a function only of heritability. (shrink)

Many cases of gene‐environment interaction, or , are misconstrued as evincing a genetic predisposition. I diagnose this misconstrual and then introduce a new concept— interactive predisposition —to correct for the mistake. I conclude by examining how recent debates over screening for individual predispositions are related to older debates about group differences between populations , drawing on the lessons of the latter to inform the former. †To contact the author, please write to: Department of Philosophy, University of Utah, Salt Lake City, (...) UT 84112; e‐mail: [email protected]. (shrink)

Philosophers of science have developed an account of causal-mechanical explanation that captures regularity, but this account neglects variation. In this article I amend the philosophy of mechanisms to capture variation. The task is to explicate the relationship between regular causal mechanisms responsible for individual development and causes of variation responsible for variation in populations. As it turns out, disputes over this relationship have rested at the heart of the nature–nurture debate. Thus, an explication of the relationship between regular causal mechanisms (...) and causes of variation and between individual development and variation offers both the necessary amendment to the philosophy of mechanisms and the resources to mediate the dispute. (shrink)

In a widely acclaimed study from 2002, researchers found a case of gene-environment interaction for a gene controlling neuroenzymatic activity (low vs. high), exposure to childhood maltreatment, and antisocial personality disorder (ASPD). Cases of gene-environment interaction are generally characterized as evincing a genetic predisposition; for example, individuals with low neuroenzymatic activity are generally characterized as having a genetic predisposition to ASPD. I first argue that the concept of a genetic predisposition fundamentally misconstrues these cases of gene-environment interaction. This misconstrual will (...) be diagnosed, and then a new concept—interactive predisposition—will be introduced. I then show how this conceptual shift reconfigures old questions and raises new questions for genetic screening. Attempts to screen embryos or fetuses for the gene associated with low neuroenzymatic activity with an eye towards selecting against the low-activity variant fall prey to the myth of pre-environmental prediction; attempts to screen newborns for the gene associated with low neuroenzymatic activity with an eye towards early intervention will have to face the interventionist’s dilemma. (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.”.

The critics of "hereditarianism" often claim that any attempt to explain human behavior by invoking genes is confronted with insurmountable methodological difficulties. They reject the idea that heritability estimates could lead to genetic explanations by pointing out that these estimates are strictly valid only for a given population and that they are exposed to the irremovable confounding effects of genotype-environment interaction and genotype-environment correlation. I argue that these difficulties are greatly exaggerated, and that we would be wrong to regard them (...) as presenting a fundamental obstacle to the search for genetic explanations. I also show that, to the extent they are cogent, these objections may prove to be even more damaging to the "environmentalist" standpoint. (shrink)

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.

The question of the influence of genes on behavior raises difficult philosophical and social issues. In this paper I delineate what I call the Developmentalist Challenge (DC) to assertions of genetic influence on behavior, and then examine the DC through an indepth analysis of the behavioral genetics of the nematode, C. elegans, with some briefer references to work on Drosophila. I argue that eight "rules" relating genes and behavior through environmentally-influenced and tangled neural nets capture the results of developmental and (...) behavioral studies on the nematode. Some elements of the DC are found to be sound and others are criticized. The essay concludes by examining the relations of this study to Kitcher's antireductionist arguments and Bechtel and Richardson's decomposition and localization heuristics. Some implications for human behavioral genetics are also briefly considered. (shrink)