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Is psychopathy a harmful dysfunction?

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Abstract

In their paper “Is psychopathy a mental disease?”, Thomas Nadelhoffer and Walter Sinnott-Armstrong argue that according to any plausible account of mental disorder, neural and psychological abnormalities correlated with psychopathy should be regarded as signs of a mental disorder. I oppose this conclusion by arguing that at least on a naturalistically grounded account, such as Wakefield’s ‘Harmful Dysfunction’ view, currently available empirical data and evolutionary considerations indicate that psychopathy is not a mental disorder.

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Notes

  1. In fact, this question has received little attention across disciplines. In psychology, the notable exceptions are Krupp et al. (2012, 2013) and Leedom and Hartoonian-Almas (2012), while in philosophy, Malatesti (2014) and Reimer (2008) provide preliminary discussions of this issue.

  2. Thanks to two anonymous reviewers for suggesting to be more precise about the scope of my discussion.

  3. In general, it is important to keep in mind that mental disorders in legal proceedings are relevant to the extent that they affect legally relevant abilities of an agent (Jefferson and Sifferd 2018). So not every diagnosis of a mental disorder will be relevant for excusing some behavior. However, since antisocial behavior is strongly correlated with (or according to some it is even a part of) the construct of psychopathy (Hare 2003), then if psychopathy were a disorder, we would have strong grounds for explaining psychopaths’ tendency towards antisocial behavior as effects of legally relevant dysfunctional capacities.

  4. Here and in what follows the intended sense of “abnormality” is statistical and not normative.

  5. In addition, some studies indicate that psychopathic personality traits (Factor 1) can be exhibited without antisocial behavior (Factor 2) (see, e.g. Ishikawa et al. 2001). Accordingly, some authors make a distinction between successful and unsuccessful psychopaths (see Glenn and Raine 2014, ch. 7). However, given that this distinction is still rather contested and neuropsychologically not well-grounded (see Maes and Brazil 2013), I will not rely on it in my discussion.

  6. The most notable account is the Response Modulation Hypothesis developed by Newman and colleagues. For this and other variants of the RMH, see, e.g. Koenigs and Newman (2013).

  7. For a neurobiologically grounded model that attempts to provide a unified account of attentional and affective peculiarities correlated with psychopathy, see Moul et al. (2012).

  8. I follow Nadelhoffer and Sinnott-Armstrong (2013) in using ‘illness’, ‘disease’ and ‘disorder’ interchangeably.

  9. For a thorough discussion of different possible combinations of naturalist and normativist views about mental illness, see Kingma (2014).

  10. It might be objected that N&S-A do not give an exhaustive list of accounts of mental illness. Relevantly for the present discussion, they do not consider evolutionary or functional approaches to psychiatry, according to which some condition might be a consequence of an evolutionary adaptation and still be a disorder (see, e.g. Adriaens and DeBlock 2011; Murphy 2005; Nesse and Williams 1997). For instance, different symptoms of anxiety disorders might have been adaptive in ancestral environments which were presumably more unsecure, lacking in resources, and dangerous. But, in modern environments being overly anxious might lead to maladaptive psychological conditions and behaviors. However, I think that N&S-A rightly do not discuss such approaches to mental disorders. Evolutionary approaches to disorders, insofar as they differ from Boorse’s or Wakefield’s accounts, arguably should be construed as providing “explanatory models of dysfunctional, maladaptive behaviour (…)” (Bolton 2008, pp. 126–127, emphasis added). As such they presuppose criteria of what constitutes a mental disorder rather than determining them (see also Wakefield 1992, p. 374). Thus, in principle one might combine them with normativist, naturalist or hybrid accounts.

  11. This criticism might be resisted. However, given my focus on the Harmful Dysfunction view and space limitations, I will not discuss it. For a more recent defense of the biomedical model, see Boorse (2014). For criticisms and modifications to Boorse’s model, see, for instance, Hausman (2012) and Schwartz (2007).

  12. In other words, according to SE, the function of a trait is conferred to it by past selective processes (Neander 1991). Organisms that had these traits survived and reproduced more than other organisms that did not possess traits with these effects. For an overview of theories of biological function, see, e.g. Garson (2016), Sterelny and Griffths (1999, pp. 220–221).

  13. One question facing selected-effects theories is how far in the evolutionary past one needs to look to determine the function of a trait (see Varga 2015, p. 180, ft. 13). A plausible answer is given by the so-called ‘modern history’ account of function (Godfrey-Smith 1994; see also Sterelny and Griffiths 1999, pp. 218–220). According to this view, the function of a trait is determined by the most recent selective pressures that are responsible for maintaining the trait in a population. For its use in the explication of the concept of disorder, see Griffiths and Matthewson (2018).

  14. For recent defenses of the naturalistic accounts of disease that are structurally similar to Wakefield's HD, see Griffiths and Matthewson (2018) and Matthewson and Griffiths (2017). It should be noted, though, that unlike Wakefield (1992), whose goal is to give a conceptual analysis of the concept of disease, Griffiths and Matthewson (2018) provide an explication in the Carnapian sense or a theoretical regimentation of the concept of disease that will be useful for integrating theoretical and practical research in medicine and related fields.

  15. For other issues and complexities related to inferring the activity of natural selection from the apparent design of a feature, see Gould and Lewontin (1979), Lauder (1996) and Sterelny and Griffiths (1999, Sects. 10.3 and 10.5).

  16. It should be noted that these heritability rates do not mean that the expression of psychopathic traits is genetically determined regardless the environment (Glenn and Raine 2014, p. 23; for a discussion of heritability of antisocial behavior, see Tabery 2014, ch. 7). In fact, heritability rates indicate the proportion of variance of a phenotypic trait that can be attributed to genetic as opposed to environmental factors and these rates are always relative to populations under scrutiny. Thus, it should be kept in mind that the proper explanation of heritability of phenotypic traits, even those that have high heritability rates, will always reflect average genetic and environmental interactions in a sampled population (Tabery 2014). This means that in some individuals genetic factors, while in others environmental conditions will have a greater contribution to exhibiting psychopathic traits (Glenn and Raine 2014, p. 23).

  17. This point is raised by an anonymous reviewer because HD presupposes an etiological theory of function.

  18. Antisocial behavior is often modeled as the cheater (defection) strategy within the prisoner’s dilemma game (Harpending and Sobus 1987). However, some studies model psychopathic traits as implementing the hawk strategy in the dove-hawk game (Colman and Wilson 1997). In the empirical literature, there is evidence that psychopathic personality can be related to both the cheater and hawk strategies (see Book and Quinsey 2004).

  19. Murphy (2005, p. 270) suggests in passing that impulsivity and poor long-term planning might be seen as “adaptive cognitive styles”. I develop this point within the Life History theory in “Life-history strategy and longevity/reproduction trade-offs” Section. Thanks to an anonymous referee for pressing me to address this issue.

  20. Thanks to an anonymous referee for directing my attention to this tension in N&S-A’s discussion.

  21. The argumentation in this section should not be read as separate from the argument that psychopathic traits are maintained by a balancing selection. The LHT is a general framework for theorizing about the adaptive challenges that organisms need to solve across life-cycles to maximize their fitness. LHT presupposes that there is a heritable variability underpinning important LH traits (such as personality traits influencing one’s fitness). Frequency-dependent selection is an important mechanism that might account for such variability across different environments (Penke et al. 2007). In our case, it explains how the heritable variation underlying psychopathic and nonpsychopathic personality traits is maintained in human populations. Thanks to an anonymous reviewer for indicating the need to make clearer the connection between LHT and frequency-dependent selection.

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Acknowledgements

I wish to thank Justin Garson, Luca Malatesti, Zdenka Brzović, and Janko Međedović for reading and giving valuable comments on previous versions of this paper. I am grateful to two anonymous reviewers of Biology and Philosophy for giving extensive and very useful comments. Thanks also to the University of Rijeka for supporting early career researchers (small Grant 17.05.2.2.04). This paper is an output of project Harm, Intentions, and Responsibility (HIRe) that is financed by the Croatian Science Foundation (Grant HRZZ-UIP-2017-05-4308).

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    Marko Jurjako

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Jurjako, M. Is psychopathy a harmful dysfunction?. Biol Philos 34, 5 (2019). https://doi.org/10.1007/s10539-018-9668-5

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