Personality and Intelligence

A critical evaluation of genetic contributions to psychopathy

Psychopathy can be conceptualised as a complex and multi-layered mental disorder and as such, cannot be defined as a unitary construct but one with distinct variations of trait characteristics (Lilienfeld et al., 2006; Neumann et al., 2007). The embodiment of psychopathic traits and behaviours, incorporating a lack of empathy and remorse, impulsive and antisocial behaviours, manifest as a socially malevolent and manipulative personality construct in both males and females, resulting in the inability to forge close emotional connections with others (Hare & Neumann, 2008).

Yet, subtle differences in the expression of psychopathy are seen in females, where they may be less physically aggressive than their male counterparts and instead utilise relational aggressive tactics as well as their sexuality within interpersonal relationships (Kreis & Cooke, 2011). As such, this discussion will focus on the sex differences in psychopathy, drawing on research from genetic, molecular genetics, biological and environmental contributions, to conclude that genetics contribute to a greater extent in males than females based on the available evidence. However, an implication from this is that research methods to assess female psychopathy needs refinement to mediate further research investigating psychopathy in females.

Looking at psychopathy through the lens of neuroscientific research, suggestions have intimated that the aetiology of psychopathy is determined by genetic influences and an interaction with the environment, thus transcending the nature-nurture dualism (Mariz et al., 2022). Within this field, a focus on child and adolescent twin studies, (McGue & Iacono, 2005; Viding & McCrory, 2012), seeks to establish the variability between heritability, shared and non-shared environments, explaining 100% of all phenotypic variance (Viding, Blair et al., 2005). Twin studies compare monozygotic (MZ) twins, who share 100% of their genes with dizygotic twins (DZ), who share 50% of their genes (MacGregor et al., 2000). If the similarity between MZ twins is greater than DZ twins. this difference may establish evidence for a genetic predisposition to psychopathy. However, isolating specific genes to determine the genetic contribution and unravelling genetic factors from environmental influences in psychopathy is complex (Moffitt et al., 2005).

Yet, twin studies have offered more promise in unravelling the genetic influence from the environment, than the measurement of psychopathic traits in male prison populations as conducted by Hare et al. (1990), and which has influenced psychopathy research within the social psychology domain (Jones & Paulhus, 2014), which may not be generalisable to the wider population and subject to sample bias (León-Mayer et al., 2015), Twin studies explore psychopathic traits, specifically the callous-unemotional (CU) trait, a main component of psychopathy, which if identified early in younger aged samples with antisocial tendencies, the aetiology of psychopathy may be determined before its manifestation in adulthood (Frick & White, 2008). Yet, without a definitive focus on sex differences but rather male or mixed sex samples, these differences are unclear (Blonigen et al., 2005; Viding et al, 2005). This may be mediated by violent criminality and its association with psychopathy being more prevalent in males (García et al., 2012).

Twin studies which have investigated sex differences found that heritability of CU traits was considerably lower for girls (Bezdijian et al., 2011), and this was also found in a community sample (Essau et al., 2006). However, the variance of measures used in twin study research renders inconsistent results and thus, discrepancies arise. Variance of heritability has differed considerably across studies, with CU traits ranging from 40% to 70%, with the remaining variance being mainly non-shared environments (Taylor et al., 2003; Viding & McCrory, 2012). Yet, a further consideration in these findings is the lack of consistency in the theoretical underpinnings across psychopathy measures, the divergence of semantic content in the indicators, observed traits and behaviours and incomparable sample sizes (Blonigen et al, 2005; Larsson et al., 2006). As suggestions indicate that females manifest psychopathy differently to males, such that their tactics are more covert comparably to the overt aggression of males (Crick & Grotpeter,1996), measures used in twin studies may fail to consider the sex specific manifestation of psychopathic traits.

However, sex specific heritability has been explored in twin adoption studies, which separate the genetic influence on the phenotype from the shared and non-shared environments (Plomin & Daniels, 1987). The biological parents are genetically assessed and the environmental effect evaluated through the adoptive parents. The child, adopted away from its biological parents, would only have phenotypic similarities with them due to shared genetics. Assessing the criminality of both biological parents, Beaver et al. (2011), found a significant correlation between the psychopathic traits of biological fathers with their adopted male children. Indeed, for the adopted males, the criminality of their biological father substantially increased the severity of their psychopathic traits. Interestingly, the biological mothers’ criminality was not genetically significant for their adopted male or female children. We could consider that the scales used in the study were sex generic, such that the differing manifestations was not considered and thus, unable to substantiate the phenotypic nuances of female psychopaths.

Consequently, heritability research methods are subject to limitations. A prominent assessment tool, the Psychopathy Checklist-Revised (PCL-R; Hare, Harpur et al., 1990), which employs semi-structured interviews and was developed to measures the traits and behaviours of incarcerated males, may not be relevant for twin studies. Further, the factor structure used in the PCL-R to determine male psychopaths may not be pertinent to females in institutionalised or nonclinical populations (Salekin et al., 1997). As such, self and rater report questionnaires have become more widely used.

However, these also do not account for sex differences, predominantly focusing on the trait manifestation in males and disregarding the subtle differences in females (Cooke et al., 2004). Additionally, assessment of traits and behaviours in others is subjective, whereby conflicting results may arise. Parents who rate their children’s emotional and behavioural problems through the Child Behaviour Checklist (Achenbach, 1991) or the Child Psychopathy Scale (Lynam,1997), may be distorted, if the parents are involved in different aspects of the children’s lives and thus observe different behaviours (Bartels et al., 2003). Behaviour assessed by teacher rating through the Twins Early Development Study (Viding et al, 2005). may be thought more objective, however it is still a subjective interpretation, prone to rater bias. Consequently, the observed phenotype is being assessed without a molecular genetic or epigenetic evaluation of the phenotypes, and thus a partial insight through observation may determine partial results.

Thus, to further an understanding of the genetic contribution to psychopathy, research in molecular genetics may build on the assumption that psychopathy is subject to a sexual dimorphism (Niehoff, 2014). As discussed, the disorder is multifaceted and one gene alone cannot be responsible but an interplay between genes, biology and the environment. Genes under consideration are the monoamine oxidase A, (MAOA) gene which encodes monoamine oxidise A, an enzyme that comprises dopamine, noradrenalin and serotonin neurotransmitters (Buckholtz & Meyer-Lindenberg, 2008), and SLC6A4, which encodes the serotonin transporter gene (5-HTT). A low expression allele of MAOA (MAOA-L), has been associated with psychopathic traits in males, who have experienced maltreatment in childhood, which may result in dysfunctional emotional regulation and the emergence of aggressive and violent behaviour, (Davidson et al., 2000), emphasising the gene-environment correlation. As evidenced by Sadeh et al. (2010), a further environmental correlation can be found with high levels of serotonin, a stress hormone, which plays an important role in arousal, emotion and cognition. A polymorphism in the promoter region of 5-HTT, results in variants with a short and long allele, which alters gene expression and function. Increased levels have been associated with psychopathic behaviours such as aggression and impulsivity (Lesch & Merschdorf, 2000). Homozygous carriers of the long allele with increased serotonin production, combined with a low social economic status, demonstrated high levels of the CU trait (Sadeh et al, 2010).

However, there is also a neurobiological sex difference, whereby males homozygous with the long serotonin allele, scored higher in externalising psychopathic traits than those with the short alleles, (Sadeh et al, 2010), whereas females, homozygous with short alleles scored higher psychopathic tendencies than those with the long alleles (Herman et al., 2011). There is also a sex divergence in the MAOA gene, which is X chromosome linked. Conversely to males, the MAOA-L is associated with happiness in females (Chen et al., 2013). However, those who were maltreated in childhood, presenting with a high expressing MAOA allele, are more susceptible to depression (Nikulina et al., 2012). Thus, the evidence suggests that sex differences in the expression of the MAOA gene is determined by sex hormones and environmental factors, which consequently does not confer psychopathy on females. Female hormones expressed in the amygdala and orbitofrontal cortex, regulate MAOA transcription through oestrogen and oestrogen receptors (Chakravorty & Halbreich, 1997), and appears to cause a converse expression of the MAOA gene to males, in whom the synthesis of the gene and testosterone culminate in an aggressive phenotype (Sjöberg et al., 2008). Thus, males present with externalising psychopathic traits whilst females internalise them, again emphasising the sex difference in the phenotypic behaviour of psychopathy (Blonigen et al, 2005).

Phenotypic behaviour can be influenced by the impact of the genotype on brain architecture and functional magnetic resonance imaging (fMRI) scans can help determine whether there is a gender difference in brain region functions in psychopaths. Both male and female psychopaths experience reduced limbic activation when processing emotions (Anderson & Kiehl, 2012). Two regions of the limbic system relevant to psychopathy, are the amygdala, which mediates responses to distressful emotional stimuli and the ventromedial prefrontal cortex (vmPFC), which guides behaviour in response to data received from the amygdala. Amygdala and vmPFC impairments at an early age mediates diminished integrity and renders the psychopath unable to empathise with others Thus, connectivity between the two regions is salient for behaviour which conform to societal norms (Harenski, Kim & Hamann, 2009).

Deficiencies in these regions have been found in individuals with CU traits and assessing brain reactivity through fMRI, by viewing emotionally dichotomous pictures can highlight brain region dysfunctions (Birbaumer et al., 2005). Adolescent males with high CU traits have shown reduced amygdala activation and a negative correlation between amygdala connectivity and the vmPFC (Marsh et al., 2008), in response to fearful facial expressions. Female prisoners with a high rating in unemotionality also experienced reduced amygdala responses to fearful facial expressions (Harenski et al, 2009).

A further brain area implicated in female psychopathy is the temporoparietal region, which incorporates information from the limbic system. Harenski et al (2009), found through fMRI, that temporoparietal activation to moral infractions, were higher in females than males. This leads to the suggestion that females lack affective theory of mind (Shamay-Tsoory et al., 2010), which may have its aetiology based in early childhood mistreatment (Nazarov et al., 2014). Further consideration of childhood maltreatment and the impact on the vmPFC and amygdala, amongst other brain regions, indicates the aetiology of psychopathy begins with the environment (McCrory et al., 2012).

Thus, genes interact with the environment and epigenetic alterations occur at a cellular level which can alter the phenotypic characteristics of an individual, whereby, physical abuse and malignant environments for both sexes may lead to the development of the CU trait (Frick et al., 2003). As such, inter-familial relationships are relevant to the development of psychopathic traits, for example, a nurturing familial relationship can encourage the internalisation of prosocial norms reinforcing within the child, the salience of reciprocal emotive attachments (Fowles & Kochanska, 2000). Conversely, children who have disrupted attachments through maltreatment, have shown strong correlations with psychopathy and violence compared to a control group (Weiler & Widom, 1996). If aggression is internalised and thought to be an acceptable way of dominating others, irrelevant to the suffering of the victim, then this antisocial behaviour may become the norm (Gershoff, 2002). As such, psychopathy may be determined by the environment a child is born into rather than being born a psychopath.

Yet, there are moral and ethical issues which arise from being diagnosed as psychopathic. A pertinent debate within the legal field is whether an individual who is diagnosed as a psychopath is morally responsible for their criminal actions, because their moral compass is skewed and thus, not guided by the same reasoning process as those deemed ‘normal’ (Levy, 2011). One debate puts forth that those genetically determined as being susceptible to psychopathy, may be imprisoned before they commit a crime (Levy, 2011), conversely, if a psychopath has committed a crime, they should be exempt from moral responsibility (Godman & Jefferson, 2017). Although it may be considered ethically wrong to preventatively imprison psychopaths deemed violent, these individuals should still be held responsible for their criminal acts, (Levy, 2011).

Genetic research can only determine if an individual is quantitatively susceptible to a disorder and even though the predisposition to psychopathy may be present, without an environmental trigger, the gene may lay dormant, never being expressed (Jaenisch & Bird, 2003). Yet, this elicits further concerns if genetic testing for psychopathy emerges, whereby foetus’s may be tested in utero and selective abortion may be offered (Hercher et al., 2016), bringing its own moral and ethical issues. Conversely, genetic engineering may prevent psychopathy emerging completely, filtering the disorder out of society (Nuffield Council on Bioethics, 2006). Yet, However, not all criminals are psychopaths and not all psychopaths are violent (Boduszek et al., 2019). As such, if a child is determined to be at risk, it may be pertinent to monitor them throughout their development and intervene with clinical treatment, which takes into consideration their environmental influences.

On review of the evidence, the aetiology and manifestation of psychopathy is multifaceted and a generalisation of causation from one perspective only provides a partial picture. Although research has shown that the environment is a salient factor, those environments which are abusive may not be evident or emerge through the tools used in research (Weiler & Widom, 1996). Further, with the advancement in genomics, the complexities of psychopathy may emerge, yet genetic research thus far, has provided a greater understanding of psychopathy more specifically in males (Sadeh et al, 2010). Cross-disciplinary research to determine a biopsychosocial model of psychopathy, which focuses on sex-specific manifestations, may provide the field with a more fine-grained approach to further our understanding of this complex construct. Yet, this does need to have the underlying ethos that the physiological and psychological composition of males cannot be analogised to females.

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