Personality and Mental Health

(2014)

Published online in Wiley Online Library (wileyonlinelibrary.com) DOI 10.1002/pmh.1279
Commentary

RICHARD C. HOWARD, Institute of Mental Health, Nottingham, UK

Psychological androgyny

The concept of psychological androgyny refers to the co-occurrence in the same individual, regardless of his or her biological sex, of a comparable degree of socially desirable masculine (‘instrumental’) and feminine (‘expressive’) qualities. It has attracted considerable attention from social, personality, and developmental psychologists since the early 1970s when Bem (1974) first formulated the idea that an individual’s gender role identity—and not biological sex—is the ‘lens’ through which she or he interprets, classifies, and processes people, behaviours, attributions, and other things (Wharton, Day, Mohr, Gerace, & Howells, 2014). The literature on androgyny indicates that there are considerable individual differences, as well as differences across cultures (e.g. Ward, 2000), in the degree to which a person’s gender role identity aligns with (i.e. is congruent with) his or her biological sex. Bem (1975) viewed androgyny in a positive light, considering it advantageous for individuals to internalize both masculine and feminine psychological attributes since this was conducive both to their psychological well-being and their ability to adapt to changing situational constraints. The determinants of androgyny remain obscure and understudied, but likely reflect a complex interaction, developmentally, between biological (e.g. genes, sex steroids) and psychosocial influences.

While psychological androgyny has been extensively studied in normal samples, and to a limited extent in clinical samples (Burchardt & Serbin, 1982), it has not to date been studied in individuals, either community resident or incarcerated, with personality disorders. However, a study that investigated relationships between self-reported antisocial traits and masculinity and femininity using Bem’s (1974) Sex Role Inventory (SRI) in a student sample found positive and inverse relationships, respectively, between antisocial traits and SRI masculinity and femininity (Hamburger, Lilienfeld, & Hogben, 1996). Extrapolating this result to patients with ASPD, it might be inferred that such patients would show a high level of masculine traits, and a low level of feminine traits. Consistent with this, the readiness to express anger, a defining feature of both ASPD and BPD, has been found to reflect gender role—a greater degree of masculine traits—rather than male sex (e.g. Wharton et al., 2014). However to date no study has been conducted comparing gender role with biological sex in either ASPD or BPD.

A major drawback of studies carried out to date by gender role researchers is that they have focused exclusively, and overwhelmingly in student samples, on stereotypically male and female traits that are positive and desirable, for example the feminine traits ‘compassionate’, ‘tender’, and ‘affectionate’ and the male traits ‘dominant’ and ‘forceful’. They have neglected the possibility that negative, i.e. maladaptive, male and female personality traits might also co-occur in the same individual, where they might represent a pathological expression of androgyny.

Does androgyny have a ‘dark side’?

All normal personality traits might be said to have their ‘dark side’, and traits of personality disorder, as has been argued by numerous authors, can be thought of as maladaptive variants of normal personality (Millon & Grossmann, 2006; Parker & Barrett, 2000; Trull & Durrett, 2005; Widiger, Clark, & Livesley, 2009). Thus for example anankastic traits can be seen as the dark side of a normal tendency to strive for perfection. ‘Hostile dominance’, the characteristic interpersonal style of the antisocial individual (Blackburn, Logan, Renwick, & Donnelly, 2005) can be seen as the dark side of a normal tendency to assert oneself and stand one’s ground in situations of interpersonal conflict. One is bound to ask, therefore, whether androgyny might not also have its dark side. Traits associated with a general predisposition to externalizing, including aggressive and violent behaviour and substance dependence, are considerably more common in males than in females, while traits associated with internalizing, in particular traits associated with neuroticism or ‘negative affectivity’, are considerably more common in females (Caspi et al., 2014; Eaton et al., 2012). In other words, there is a gender-linked tendency for males to externalize, and for females to internalize. Caspi et al. (2014) recently examined data from the Dunedin longitudinal study and confirmed the propensity for males to externalize and for females to internalize, but found no sex differences in the tendency to general psychopathology (the p factor, which ‘…has thought disorder symptoms at its pinnacle’ (p. 132)). These authors noted that independently of a liability to general psychopathology, externalizing and internalizing are highly gendered styles. But individuals, regardless of their sex, in whom antisocial PD (ASPD) and borderline PD (BPD) co-occur, show a combination of both (male) externalizing and (female) internalizing tendencies (Howard, Khalifa, & Duggan, 2014). Evidence is presented below in support of the view that the combination of traits shown by those showing ASPD/BPD comorbidity represents a pathological form of androgyny in which the combination of both male/externalizing and female/internalizing traits, together with a high level of general psychopathology (in which thought disorder features prominently), results in a particularly severe form of personality pathology. First, however, a caveat is in order regarding use of the term ‘co-morbidity’ throughout this commentary. It is not implied that ASPD and BPD represent true disorders that can occur ‘co-morbidly’ with each other, nor that antisocial/borderline co-morbidity represents a ‘super disorder’. Rather, as suggested by the network perspective proposed by Borsboom and Cramer (2013), the symptoms/traits of ASPD and BPD together represent a complex network of causally interconnected thoughts, feelings, and behaviours that are linked not just with each other, but also with traits/symptoms of other disorders. According to this network perspective, those symptoms/traits shared by both ASPD and BPD, e.g. impulsivity, hostility, would hypothetically act as ‘bridge symptoms’ that enable causal relationships to be established between the symptoms/traits of ASPD, BPD, and other disorders.

 

Antisocial/borderline PD comorbidity: a severe and dangerous form of PD?

It is well established in the literature first, that the prevalence of both ASPD and BPD is high in criminal populations (Fazel & Danesh, 2002), particularly in those who have committed serious violent and sexual offences (Schroeder et al., 2013); second, that—at least in clinical and forensic samples—ASPD is more prevalent in males than in females (3% vs 1%: American Psychiatric Association, 1994) and BPD more prevalent in females (75% female according to DSM-IVTR [APA, 2000]); and third, that in forensic samples ASPD and BPD frequently occur together in a ‘devastating combination’ (Coid, 1992, p. 89) that represents ‘ a very particular constellation of abnormalities of mental state with a wide range of disorderly conduct’ (Mullen, 1992, 238). Consistent with this, antisocial/borderline comorbidity has been found to be significantly associated with a greater degree of violence both in community samples (Freestone, Howard, Coid, & Ullrich, 2012; Howard, Huband, Mannion, & Duggan, 2008) and in male offenders with PD (Howard et al., 2014). Patients showing ASPD/ BPD comorbidity can be considered as showing a particularly severe form of PD in so far as they show both a high level of DSM Axis 1 comorbidity, particularly anxiety disorder, alcohol dependence and severe childhood conduct disorder, and a high level of Axis II (PD) comorbidity (Freestone et al., 2012; Howard, Huband, & Duggan, 2012). Freestone et al. (2012) also found greater psychosis scores (pl.) in their ASPD/BPD comorbid group, suggesting that this comorbidity may be associated with a high degree of thought disorder, and hence general psychopathology, a suggestion that has received support in a recent study of forensic psychiatric patients with PD (Howard, Hepburn, & Khalifa, 2014).

In the general (UK) population the prevalence of co-occurring ASPD and BPD is very low (0.3%: Coid et al., 2006), but is markedly increased in forensic samples where it varies with the degree of dangerousness of the particular sample studied, increasing as one ascends a hierarchy of dangerousness (see Duggan & Howard, 2009, Figure 2.2). Moreover, the prevalence of antisocial/borderline comorbidity in females overtakes that found in males as one ascends the hierarchy. Thus among a sample of UK prisoners who met criteria for ‘dangerous and severe PD’, the highest level of dangerousness, nearly 80% of women compared with 62% of men showed ASPD/BPD comorbidity (Coid et al., 2007). At a lower level in the hierarchy, 24% of women, compared with 16% of men, among a random sample of low-security men and women admitted for assessment to a U.S. correctional facility were found to meet criteria for both ASPD and BPD (Black, Gunter, Loveless, Allen, & Sieleni, 2010). Still lower down the hierarchy, in a UK non-forensic sample of treatment-seeking patients with PD, ASPD/BPD comorbidity occurred in about 9% overall and to an equal degree in both men and women (Howard et al., 2008; Howard, Huband, & Duggan, 2012). In summary, therefore, antisocial/borderline comorbidity occurs more densely in samples with a higher degree of presumed dangerousness and, at the highsevere end, to a greater degree in women than in men. The conclusion that may be drawn from these findings is that antisocial/borderline comorbidity represents a particularly toxic combination of both internalizing and externalizing personality traits which, together with thought disorder (general psychopathology, Caspi et al.’s (2014) p factor), is associated with a specific set of both genetic and environmental risk factors (Torgersen et al., 2008). Since, as reviewed above, there is a male bias towards exhibiting externalizing traits, and a female bias in favour of internalizing traits, this combination (i.e. externalizing plus internalizing plus thought disorder) might be considered a pathological phenotypic expression of androgyny in which maladaptive and predominantly male externalizing traits coexist in the same individual with maladaptive and predominantly female internalizing traits. Next we consider how this supposition might offer insights into the developmental origins of adult antisociality and outline the beginnings of such a developmental model.

Developmental origins of pathological androgyny

The developmental trajectory leading to severe adult antisocial behaviour undoubtedly starts at conception and continues as a cascade of influences occurring throughout early and late childhood and adolescence (Howard & McMurran, 2013). The predisposition to externalizing behaviours appears to be strongly genetically influenced (Krueger et al., 2002). Both child sexual abuse and childhood conduct disorder predispose to personality disorder in general, but both are reported to be non-specific with regard to the type of personality disorder that eventuates in adulthood (Bernstein, Cohen, Skodol, Bezirganian, & Brook, 1996; Moran et al., 2011). The critical question then is: how do these genetic and childhood predispositions translate into the specific constellation of personality features that, by late adolescence and early adulthood, characterize those showing ASPD co-morbidly with BPD?

A possible answer to this question suggests that severe adult antisocial behaviour, and violence in particular, might result, during adolescence, from the interactive effects of pubertal sex hormones and adolescent alcohol abuse on region-specific brain development (Howard, 2009). This hypothesis, further elaborated by Howard and McMurran (2013), highlights a distinction drawn by Albert and Steinberg (2011) between two neural systems, a social-emotional reward system and a cognitive control system, each having a different developmental trajectory. Coincident with the dramatic structural and functional changes in the human brain following puberty, the social-emotional reward system develops in a curvilinear fashion, reaching maximum strength in early/mid-adolescence. In contrast, the cognitive control system develops in slow and linear fashion throughout adolescence extending into early adulthood (see Howard & McMurran, 2013, Figure 5.1). There is a time window during mid-adolescence (roughly between ages 13 and 15 years) when the social-emotional reward system shows maximum strength and there is heightened motivation for reward-seeking, unconstrained by a still immature cognitive control system that shows maturational lag. According to Albert and Steinberg (2011), synaptic pruning and increased myelination in late adolescence and early adulthood support a gradual improvement in the efficiency of the cognitive control system, which continues to develop beyond age 20. Driven by the motivation to seek rewards, risk taking occurs maximally during the mid-adolescent period, and part of that risk taking involves experimentation with drugs and alcohol. Those with strong externalizing tendencies manifested in childhood conduct disorder, particularly when this co-occurs (in 20–50% of cases) with callous-unemotional traits that are associated with a reward-oriented response style and low levels of fear and anxiety (reviewed by Frick & Ray, 2014), would be expected to show a heightened strength of the social-emotional reward system, leading them to seek out excitement and to engage in risky behaviours, including risky use of alcohol. Significantly, the mean age of onset of adolescent alcohol abuse in adolescents with a history of conduct disorder is around 16 years, and adolescent alcohol abuse was found to mediate the relationship between childhood conduct disorder and adult antisocial personality, both in a community sample (Howard, Finn, Gallagher, & Jose, 2012) and in a forensic PD sample (Khalifa, Duggan, Howard, & Lumsden, 2012). Evidence reviewed by Lisdahl, Gilbart, Wright, and Schollenbarger (2013) suggests that both intermittent binge drinking and the development of alcohol use disorder can result in significant cognitive, structural, and functional brain changes in both male and female adolescents. Structural brain abnormalities seen in adolescents with alcohol use disorder include reduced hippocampal and prefrontal cortical volumes, particularly in those areas of prefrontal cortex that mediate executive control of cognitive processes (Doallo et al., 2014). Importantly, these structural brain changes are not only moderated by gender (Medina et al., 2008; Squeglia et al., 2012), but are associated with earlier onset of alcohol use (Doallo et al., 2014). Thus the consequence of excessive alcohol use in early and midadolescence will putatively be impaired and/or delayed development of neural substrates of the cognitive control system, whose disruption will then result in a chronic inability to control emotional impulses. Emotional dysregulation has been found to mediate the effects of both borderline PD and antisocial traits on violence (Newhill, Eack, & Mulvey, 2012). This suggests that the inability to self-regulate emotionally is one factor that might explain the link between PD (particularly antisocial/borderline PD co-morbidity) and violence. However, a cognitive disturbance (thought disorder) must also be considered as a factor contributing to the association of ASPD/BPD comorbidity and violence. Howard, Hepburn & Khalifa (2014) reported that delusional thinking fully mediated the relationship between internalizing traits and violence in a forensic sample of PD patients, which is consistent with Caspi et al.’s (2014) report that general psychopathology (p) accounted for the relationship between internalizing and violent convictions in the Dunedin longitudinal study cohort.

Future research directions

Two potential directions for future research are indicated by the foregoing. First, the lack of studies examining gender role in incarcerated populations, particularly those with personality disorder, represents a notable gap in the PD literature that deserves to be filled. Such studies would permit the direct testing of the hypothesis proposed here, that antisocial/borderline PD comorbidity in association with delusional thinking represents a pathological form of androgyny, since individuals displaying this combination would clearly be predicted to display high levels of both masculinity and femininity across a broad spectrum of gender-linked personality traits, both adaptive and maladaptive. Perhaps the biggest challenge is to explain how, in the course of development, adaptive gender-linked internalizing and externalizing traits become, so to speak, perverted through association with general psychopathology to generate this maladaptive and socially damaging form of androgyny. Results from the Dunedin longitudinal study reported by Caspi et al. (2014) suggest that brain integrity in early (age 3) development plays an important role in this respect, but it is also possible that brain function is further compromised as a consequence of adolescent alcohol and drug use, as outlined above. The co-occurrence of childhood conduct disorder with early-onset alcohol abuse appears to identify an important sub-group of individuals who, as children, show particularly severe conduct disorder symptomatology, as well as a high degree of antisocial/borderline comorbidity and severe violence as adults (Khalifa et al., 2012). A separate literature dealing with callousunemotional traits suggests the presence of these traits designates a sub-group of children and adolescents with serious conduct problems who differ on important emotional, cognitive and contextual characteristics, implicating distinct causal processes leading to their antisocial behaviour in contrast to antisocial youth who are normative on callous-unemotional traits (Frick & Ray, 2014). It will be the task of future research to verify the current proposal that a distinct developmental pathway leads from severe conduct disorder co-occurring with callous-unemotional traits to early-onset alcohol (and other drug) abuse and thence, via compromised brain function, to an adult outcome of severe personality disorder characterized by both antisocial and borderline pathology.

Second, there is a need for longitudinal studies tracking cohorts of both normal and “at risk” (e.g. conduct disordered) children from pre-puberty through puberty and adolescence in order to verify the suggested interaction between pubertal sex steroids, early-onset alcohol use, and region-specific brain development. Pubertal status at a given age appears to be a particularly pertinent variable, since Castellanos-Ryan, Parent, Vitaro, Tremblay, and Séguin (2013) have described a developmental pathway characterized by differences in the level of pubertal maturation reached by age 12. Pubertal status was indirectly associated with adolescent substance use partly through increases in sensation seeking, providing indirect support for the Albert and Steinberg (2011) dual-systems model alluded to above.

 

Conclusion

Androgyny is a concept that has been developed and studied in the context of normal populations, including across different cultures (e.g. Ward, 2000), but has not been applied to the study of personality disorders. This represents a significant gap in the literature. It is proposed that psychological androgyny is particularly applicable to those who, manifesting a combination of antisocial and borderline PDs, lie at the extreme of the severity dimension of PD. It is further proposed that the androgyny construct can inform the study of the neurodevelopmental origins of this severe form of PD.

References

Albert, D., & Steinberg, L. (2011). Peer influences on adolescent risk behaviour. In M. T. Bardo, R. Milich, & D. H. Fishbein (Eds.), Inhibitory Control and Drug Abuse Prevention (pp. 211–226). New York: Springer.

American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: APA.

American Psychiatric Association [APA]. (1994). Diagnostic and Statistical Manual of Mental Disorders (4th ed.). Washington DC: APA.

Bem, S. L. (1974). The measurement of psychological androgyny. Journal of Consulting and Clinical Psychology, 42, 155–162.

Bem, S. L. (1975). Sex role adaptability: one consequence of psychological androgyny. Journal of Personality and Social Psychology, 31(4), 634–643.

Bernstein, D. P., Cohen, P., Skodol, A., Bezirganian, S., & Brook, J. S. (1996). Childhood antecedents of adolescent personality disorders. American Journal of Psychiatry, 153, 907–913.

Black, D. W., Gunter, T., Loveless, P., Allen, J., & Sieleni, P. (2010). Antisocial personality disorder in incarcerated offenders: Psychiatric comorbidity and quality of life. Annals of Clinical Psychiatry, 22(2), 113–120.

Blackburn, R., Logan, C., Renwick, S. J. D., & Donnelly, J. P. (2005). Higher-order dimensions of personality disorder: Hierarchical structure and relationships with the fivefactor model, the interpersonal circle and psychopathy. Journal of Personality Disorders, 19(6), 597–623.

Borsboom, D., & Cramer, A. O. J. (2013). Network analysis: An integrative approach to the structure of psychopathology. Annual Review of Clinical Psychology, 9, 91–121.

Burchardt, C. J., & Serbin, L. A. (1982). Psychological androgyny and personality adjustment in college and psychiatric populations. Sex Roles, 8(8), 835–851.

Caspi, A., Houts, R. M., Belsky, D. W., Goldman-Mellor, S. J., Harrington, H., Israel, S., Meier, M. H., Ramrakha, S., Shalev, I., Poulton, R., & Moffitt, T. E. (2014). The p factor: one general psychopathology factor in the structure of psychiatric disorders? Clinical Psychological Science, 2, 119–137.

Castellanos-Ryan, N., Parent, S., Vitaro, F., Tremblay, R. E., & Séguin, J. R. (2013). Pubertal development, personality, and substance use: a 10-year longitudinal study from childhood to adolescence. Journal of Abnormal Psychology, 122(3), 782–796.

Coid, J. (1992). DSM-III diagnosis in criminal psychopaths: A way forward. Criminal Behaviour and Mental Health, 2, 78–94. Coid, J., Yang, M., Roberts, A., Ullrich, S., Moran, P., Bebbington, P., Brugha, T., Jenkins, R., Farrell, M., Lewis, G., & Singleton, N. (2006). Violence and psychiatric morbidity in a national household population – a report from the British Household Survey. American Journal

of Epidemiology, 164, 1199–1208.

Coid, J., Yang, M., Ullrich, S., Zhang, T., Roberts, A., & Roberts, C. (2007). Predicting and understanding risk of re-offending: the prisoner cohort study. Research Summary, Ministry of Justice, London.

Doallo, S., Cadaveira, F., Corral, M., Mota, N., LópezCaneda, E., Rodríguez Holguín, S. (2014). Larger Mid-Dorsolateral Prefrontal Gray Matter Volume in Young Binge Drinkers Revealed by Voxel-Based Morphometry. PLoS One, 9(5), e96380. doi: 10.1371/journal.pone.0096380

Duggan, C., & Howard, R.. (2009). The “functional link” between personality disorder and violence: A critical appraisal. In M. McMurran, & R. C. Howard (Eds.), Personality, Personality Disorder and Violence (pp. 19–37). Chichester: J. Wiley & Sons.

Eaton, N. R., Keyes, K. M., Krueger, R. F., Balsis, S., Skodol, A.

E., Markon, K. E., Grant, B. F., & Hasin, D. S. (2012). An invariant dimensional liability model of gender differences in mental disorder prevalence: evidence from a national sample. Journal of Abnormal Psychology, 121, 282–288.

Fazel, S., & Danesh, J. (2002). Serious mental disorder in 23 000 prisoners: A systematic review of 62 surveys. The Lancet, 359, 545–550.

Freestone, M., Howard, R. C., Coid, J., & Ullrich, S. (2012). Adult antisocial syndrome co-morbid with borderline personality disorder is associated with severe conduct disorder, substance dependence and violent antisociality. Personality and Mental Health, 7(1), 11–21.

Frick, P. J., & Ray, J. V. (2014). Evaluating callous-unemotional traits as a personality construct. Journal of Personality. doi: 10.1111/jopy.12114

Hamburger, M. E., Lilienfeld, S. O., & Hogben, M. (1996). Psychopathy, gender, and gender roles: implications for

antisocial and histrionic personality disorders. Journal of Personality Disorders, 10(1), 41–55.

Howard, R. C. (2009). The neurobiology of affective dyscontrol: implications for understanding ‘dangerous and severe personality disorder’. In M. McMurran & R.C. Howard (Eds.), Personality, Personality Disorder and Violence (pp. 157–174). Chichester: Wiley-Blackwell.

Howard, R. C., Finn, P. R., Gallagher, J., & Jose, P. E. (2012). Adolescent-onset alcohol abuse exacerbates the influence of childhood conduct disorder on late adolescent and early adult antisocial behaviour. Journal of Forensic Psychiatry & Psychology, 23, 7–22.

Howard, R. C., Hepburn, E., & Khalifa, N. (2014). The relationship between personality disorder comorbidity, delusional thinking and violent conduct in a forensic psychiatric sample. Submitted, under review.

Howard, R. C., Huband, N., & Duggan C. (2012). Adult antisocial syndrome with co-morbid borderline pathology: association with severe childhood conduct disorder. Annals of Clinical Psychiatry, 24, 127–134.

Howard R. C., Huband, N., Mannion, A., & Duggan, C. (2008). Exploring the link between personality disorder and criminality in a community sample. Journal of Personality Disorders, 22, 589–603.

Howard, R. C., Khalifa, N., & Duggan, C. (2014). Antisocial personality disorder comorbid with borderline pathology and psychopathy is associated with severe violence in a forensic sample. Journal of Forensic Psychiatry and Psychology. doi: 10.1080/14789949.2014.943797

Howard, R. C., & McMurran, M. (2013). Alcohol and violence in developmental perspective. In M. McMurran (Ed.), Alcohol-Related Violence: Prevention and Treatment (pp. 81–102). Chichester: Wiley-Blackwell.

Khalifa, N., Duggan, C., Howard, R., & Lumsden, J. (2012). The relationship between childhood conduct disorder and adult antisocial behavior is partially mediated by early-onset alcohol abuse. Personality Disorders: Theory, Research, and Treatment, 3, 423–432. doi: 10.1037/a0027017

Krueger, R. F., Hicks, B. M., Patrick, C. J., Carlson, S. R., Iacono, W. G., & McGue, M. (2002). Etiologic connections among substance dependence, antisocial behavior, and personality: Modeling the externalizing spectrum. Journal of Abnormal Psychology, 111, 411–424.

Lisdahl, K. M., Gilbart, E. R., Wright, N. E., & Schollenbarger, S. (2013). Dare to delay? The impacts of adolescent alcohol and marijuana use onset on cognition, brain structure, and function. Frontiers in Psychiatry. doi: 10.3389/fpsyt.2013.00053

Medina, K. L., McQueeny, T., Nagel, B. J., Hanson, K. L., Schweinsburg, A. D., Tapert, S.F. (2008). Prefrontal cortex volumes in adolescents with alcohol use disorders: unique gender effects. Alcoholism: Clinical and Experimental Research, 32, 386–394.

Millon, T., & Grossmann, S. D. (2006). Millon´s evolutionary model for unifying the study of normal and abnormal personality. In S. Strack (Ed.), Differentiating normal and abnormal personality (2nd ed., pp. 3–49). New York: Springer Publishing Company.

Moran, P., Coffey, C., Chanen, A., Mann, A., Carlin, J. B., & Patton, G. C. (2011). Childhood sexual abuse and abnormal personality: a population-based study. Psychological Medicine, 41, 1311–1318.

Mullen, P. E. (1992). Psychopathy: A developmental disorder of ethical action. Criminal Behaviour and Mental Health, 2, 234–244.

Newhill, C. E., Eack, S. M., & Mulvey, E. P. (2012). A growth curve analysis of emotion dysregulation as a mediator for violence in individuals with and without borderline personality disorder. Journal of Personality Disorders, 26, 452–467.

Parker, G., & Barrett, E. (2000). Personality and personality disorder: Current issues and directions. Psychological Medicine, 30, 1–9.

Schroeder, M., Iffland, J.S., Hill, A., Berner, W., & Briken, P. (2013). Personality disorders in men with sexual and violent criminal offense histories. Journal of Personality Disorders, 27, 519–530.

Squeglia, L. M., Sorg, S. F., Schweinsburg, A. D., Wetherill, R. R., Pulido, C., Tapert, S.F. (2012). Binge drinking differentially affects adolescent male and female brain morphometry. Psychopharmacology, 220, 529–539.

Torgersen, S., Czajkowski, N., Jacobson, K., Reichborn-

Kjennerud, T., Røysamb, E., Neale, M. C., & Kendler, K. C. (2008). Dimensional representations of DSM-IV cluster B personality disorders in a population-based sample of Norwegian twins: a multivariate study. Psychological Medicine, 38, 1617–1625.

Trull, T. J., & Durrett, C. A. (2005). Categorical and dimensional models of personality disorder. Annual Review of Clinical Psychology, 1, 355–380.

Ward, C. A. (2000). Models and Measurements of Psychological Androgyny: A Cross-Cultural Extension of Theory and Research. Sex Roles, 43, 529–552.

Wharton, M., Day, A., Mohr, P., Gerace, A., & Howells, K.

(2014). The impact of masculinity on anger arousal in ambiguous situations. Journal of Relationships Research, 5, e1. doi: 10.1017/jrr.2014.1

Widiger, T. A., Clark, L. A., & Livesley, W. J. (2009). An integrative dimensional classification of personality disorder. Psychological Assessment, 21, 243–255.

Address correspondence to: Richard C. Howard, Institute of Mental Health, Nottingham, UK. Email: richard.howard@nottingham.ac.uk