Antisocial personality disorder (ASPD) and borderline personality disorder (BPD) are among the most costly public health concerns confronting the US criminal justice and healthcare systems. Although ASPD affects only 3–6% of adult males and 1% of adult females (American Psychiatric Association, 2000
; Kessler et al., 1994
; Robins, Tipp, & Przybeck, 1991
), many if not most property offenses and violent crimes are committed by individuals with the disorder. Indeed, lifetime prevalence rates in incarcerated samples approach 50% (Teplin, 1994
). Thus, roughly 1 million of the 2.3 million incarcerated individuals in the US have ASPD. With the cost of imprisoning one person per year at about $25,000, ASPD accounts for $25 billion per year in corrections expenditures alone —about $200 for each US tax payer (Bureau of Justice Statistics, 2007
). This of course does not include the costs associated with crimes that led to incarceration.
Borderline personality disorder and its associated features are also quite costly (Bender et al., 2001
). According to most estimates, the prevalence rate of BPD is about 2–3% among adult females and 1% among adult males (Swartz, Blazer, George, & Winfield, 1990
), though some recent surveys yield slightly higher numbers (Grant et al., 2008
). Despite a relatively moderate prevalence rate, however, BPD is the most common Axis II disorder observed in inpatient psychiatric settings (Trull, Stepp, & Durrett, 2003
; Skodol et al., 2002
). Among adolescents with borderline traits, intentional self injury—a cardinal feature of BPD—costs the US healthcare system $150 million per year in inpatient hospitalization costs alone (Olfson et al., 2005
). Moreover, adolescents and adults who engage in self injury are at high risk for eventual suicide, with an 8–10% lifetime completion rate (e.g., APA, 2000
; Berman, Jobes, & Silverman, 2006
Although these statistics only partially capture the extent of the personal and societal costs of ASPD and BPD, they demonstrate the potential importance of furthering our understanding of both disorders in efforts to mitigate risk. As we outline in later sections, ASPD and BPD are disorders for which biological vulnerabilities interact with potentiating environments to produce debilitating and enduring personality disturbance. Understanding the precise nature of these vulnerabilities and risk factors may provide opportunities for early interventions that alter developmental trajectories toward severe psychopathology. The behavior patterns characteristic of ASPD and BPD are very difficult to treat once canalized (see e.g., Burke, 2007
; Linehan, 1993
). Thus, earlier identification of vulnerability may be necessary to prevent the significant costs of ASPD and BPD to individuals, their family members, and society (Crowell, Beauchaine, & Lenzenwger, 2008
; Crowell, Beauchaine, & Linehan, in press
In this article, we present a common developmental model of antisocial and borderline personality development that captures important biological vulnerabilities and environmental risk factors for both disorders. Though at first glance it might seem odd that we present a single model of two disorders with different symptoms and sex distributions, we are not the first authors to do so. For example, Paris (1997)
reviewed a number of common etiological factors and overlapping features of ASPD and BPD, concluding that the two disorders reflect the same underlying trait with different behavioral expressions for males versus females.
contention that ASPD and BPD share a common etiology was based on several observations. First, both disorders are characterized by significant risk for depression and suicide. As noted above, 8–10% of those with BPD eventually commit suicide (APA, 2000
). Those with ASPD are also at much higher suicide risk than the general population, with a completion rate of approximately 4–5% (Dyck, Bland, Newman, & Orn, 1988
; Robins, 1966
). Second, ASPD and BPD are both characterized by impulsivity, a trait that is about 80% heritable (e.g., Krueger et al., 2002
), conferring general rather than specific risk for psychopathology (see Beauchaine & Neuhaus, 2008
; Beauchaine, Neuhaus, Brenner, & Gatzke-Kopp, 2008
). Finally, ASPD and BPD have similar prevalence rates in the community, and nearly identical sex distributions of about 3–4:1 favoring males for ASPD and females for BPD1
. This set of observations led Paris to suggest that ASPD and BPD are sex-moderated manifestations of a single underlying pathology (see also Lyons-Ruth, 2008
In addition to the observations offered by Paris (1997)
, other findings also point toward a shared etiology for both disorders. For example, ASPD and BPD are highly comorbid in clinical samples (e.g.,Becker, Grilo, Edaell, & McGlashan, 2000
). Furthermore, affected individuals often come from the same families (Goldman, D’Angelo, & DeMaso, 1993
), and increased prevalence of ASPD is observed in the first-degree relatives of those with BPD (Schulz et al., 1989
). In addition, disturbed parent-child relationships, disrupted attachment, family discord, and traumatic experiences including abuse are common in the life histories of those with ASPD and those with BPD (e.g., Lyons-Ruth, 2008
; Norden, Klein, Donaldson, Pepper, & Klein, 1995
All of these findings are derived from symptom patterns and life histories of individuals with ASPD, individuals with BPD, and their family members. However, in the last decade much more has been learned about the molecular genetics and neurobiology of ASPD, BPD, and related traits, providing for a more comprehensive account of common vulnerabilities and risk factors for both disorders. Our primary objective in writing this article is to provide an updated model of shared etiology for ASPD and BPD that accounts for both biological vulnerabilities and environmental risk. Taken together, literature addressing the development of these personality disorders (PDs) supports the following set of conjectures, which we present here as an organizing framework for the remainder of this article:
- Both ASPD and BPD are disorders for which trait impulsivity is the principal predisposing vulnerability.
- Trait impulsivity derives primarily from heritable compromises in central dopaminergic and serotonergic function.
- For both disorders, impulsivity is potentiated by high risk family environments in which emotional lability is shaped and maintained by operant reinforcement contingencies.
- Over time, these reinforcement contingencies result in enduring patterns of emotion dysregulation—leading to ASPD and/or BPD in vulnerable individuals.
- Sex effects moderate the behavioral expression of Biology × Environment interactions to produce ASPD disproportionately in males, and BPD disproportionately in females.
In the sections to follow, we present a common developmental model of ASPD and BPD, drawing attention to etiological commonalities across disorders. In doing so, we first discuss several issues and problems associated with classifying and studying PDs, particularly among children and adolescents. Such a discussion is necessary because nosologic and diagnostic conventions affect (a) how atypical personality development is conceptualized, (b) whether diagnoses of PDs are considered in childhood and adolescence, and (c) whether or not children and adolescents with antisocial and borderline traits are studied in the same way as adults with PDs. Next, we briefly describe different approaches to studying antisocial and borderline pathologies. We then discuss impulsivity as the principal vulnerability to both PDs, before turning to the molecular genetic bases of impulsive behavior. During this discussion, we highlight important Gene × Sex interactions that may confer differential vulnerability to aggression and mood dysregulation among males versus self-injury and mood dysregulation among females. Next, we outline environmental risk factors for antisocial and borderline personality development, again pointing to commonalities across disorders.