Crusio, Wim E. (1995) The sociopathy of sociobiology. Behavioral and Brain Sciences 18 (3) 552.
Commentary on Mealey, L. (1995) The sociobiology of sociopathy: An integrated evolutionary model. BBS 18 (3) 523.

The sociopathy of sociobiology

Commentary on Mealey, L. (1995) The sociobiology of sociopathy: An integrated evolutionary model. BBS 18 (3) 523.

Wim E. Crusio

Génétique, Neurogénétique et Comportement
URA 1294 CNRS, UFR Biomédicale
Université Paris V René Descartes
45, rue des Saints-Pères
75270 Paris Cedex 06

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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.

Mealey's target article provides an enormous compilation of data on vastly different subjects, varying from social psychology to evolutionary theory. Admirable as the amount of work involved with gathering, digesting, and discussing this large body of literature may be, the result is unfortunately not very enlightening. The line of reasoning has become buried under an avalanche of uncritically enumerated research findings, so that after some time the reader loses sight of exactly what the author is trying to say, based on what evidence, and what the assumptions are on which the author's interpretations are based.

In consequence, I am not quite sure what Mealey's main thesis is. As far as I see, she is trying to make two, not necessarily related, points. First, that sociopaths can be divided into two subtypes: primary and secondary sociopaths. Second, that this subdivision has come into existence because of selective forces, exerted during evolution on a genetic substrate underlying sociopathy. I trust that other commentators, that are more competent on this subject than I, will comment on the first point. I will direct my scrutiny mainly at the second one, but not without noting that neither evolution nor genetics appear to be very relevant for Mealey's arguments regarding the first point and clearly are irrelevant to the exclusively environmental recommendations presented as following from the model (sections 3.2 and 3.3).

To start with the evolutionary part, Mealey asserts that the two forms of sociopathy came into existence as a result of two different evolutionary stable strategies (ESSs; section 1.2). Although it does not become clear what role natural selection is playing here, the description of these ESSs clearly shows the logical impossibility of having two different ESSs for one single phenotype within one single population. If two different mechanisms are at work, then this implies that primary and secondary sociopathy are two different, independent phenotypes. Yet, in the last paragraph of section 2.3.1, it becomes clear that this is not what the author has in mind. I would like to see some clarification of this serious contradiction and some explanation of how natural selection may have acted in order to result in having two different ESSs for one single phenotypical continuum. In addition, might it not be necessary to consider whether and how the increasingly dramatic changes in living conditions over the last few thousands of years (and even more so in the last few centuries) may have influenced the nature of the natural selection involved, in the process perhaps rendering all this evolutionary speculation rather pointless?

The last paragraph of section 2.3.1 poses a number of other problems, too. It is argued that some persons become primary sociopaths because of their genotype. Others become secondary sociopaths because of a smaller genetic load combined with certain environmental causes (see also note 14). Perhaps this is so. Unfortunately, the evidence provided to support these ideas is very insufficient. Let me give a few examples. A number of physiological factors are discussed, for which primary sociopaths apparently differ from other people, supposedly suggesting a genetic basis for primary sociopathy. But physiological variables are phenotypes, too; there is nothing inherently different to them that would suggest they are somehow more "heritable" than other types of characters. Still, this appears to be implicitly assumed. Take the finding that upperclass, but not lowerclass, boys who subsequently became delinquent showed physical signs of hypoarousal (last paragraph of section 2.3.3), which is presented as evidence for the idea that the upper-class individuals became delinquent as the result of a particularly strong genetic predisposition. Only when hypoarousal would be a phenotype with a heritability equal to unity and perfectly correlated with sociopathy would this conclusion be warranted. The finding that almost all upper-class subjects that had been arrested came from a biological high-risk group (last paragraph of section 2.3.3) is not conclusive either. As "biological high-risk group" probably means that subjects descended from parents with an antisocial background, the familial environment of these subjects is very likely to have differed from that of control subjects, too. Mealey herself seems to recognize the importance of environmental influences, even for primary sociopaths, given the recommendations at the end of her article.

In fact, the only reasonably solid evidence provided for any genetic basis for either form of sociopathy are heritability estimates, derived from twin and adoption studies1, of around 0.60 (but see BBS commentary on Wahlsten, 1990, for a discussion of the scientific value of such estimates). However, even when rather high, this value still tells us that genotype and environment explain about equal parts of the interindividual variation observed. Summarizing, the genetic component of Mealey's model is nothing more than just some elaborate speculation.

If the present target article were dealing with, e.g., the mating behavior of black widow spiders or some other subject without direct societal impact, the author might indulge in some speculation without much possible harm. But in the present case we are dealing with people, not spiders. Scientific speculation, however interesting perhaps in itself, may easily be interpreted by politicians, journalists, or others, as stated scientific fact, the more so if the speculational nature of an author's writings is not clearly indicated as such. Sociobiologists appear to be rather prone to this kind of oversight, hence the title of my comment.


The preparation of this commentary benefitted from support by the CNRS (URA 1294), UFR Biomédicale (Université Paris V René Descartes), DRED, and the Fondation pour la Recherche Médicale.


  1. It should be noted that in all these studies at least the early part of childhood environment is confounded with possible genetic effects. Together with possible prenatal influences, this explains perhaps in part why human behavior-genetic analyses so often render heritability estimates (in the broad sense, see Mealey's note 6) that are much higher than anything reported from animal research. Note also that experimental animals are generally bred and reared in a rigourously standardized environment in order to maximize genetic effects relative to environmentally-induced variations (that is, boosting heritability).


Wahlsten, D. (1990) Insensitivity of the analysis of variance to heredity-environment interaction. Behavioral and Brain Sciences 13:109-161.