Multifinality in the development of personality disorders: a Biology x Sex x Environment interaction model of antisocial and borderline traits

Abstract

Although antisocial personality disorder (ASPD) is more common among males and borderline PD (BPD) is more common among females, some authors have suggested that the two disorders reflect multifinal outcomes of a single etiology. This assertion is based on several overlapping symptoms and features, including trait impulsivity, emotional lability, high rates of depression and suicide, and a high likelihood of childhood abuse and/or neglect. Furthermore, rates of ASPD are elevated in the first degree relatives of those with BPD, and concurrent comorbidity rates for the two disorders are high. In this article, we present a common model of antisocial and borderline personality development. We begin by reviewing issues and problems with diagnosing and studying PDs in children and adolescents. Next, we discuss dopaminergic and serotonergic mechanisms of trait impulsivity as predisposing vulnerabilities to ASPD and BPD. Finally, we extend shared risk models for ASPD and BPD by specifying genetic loci that may confer differential vulnerability to impulsive aggression and mood dysregulation among males and impulsive self-injury and mood dysregulation among females. Although the precise mechanisms of these sex-moderated genetic vulnerabilities remain poorly understood, they appear to interact with environmental risk factors including adverse rearing environments to potentiate the development of ASPD and BPD.

Figure 1

A heterotypically continuous developmental trajectory to antisocial personality disorder (ASPD) that begins with hyperactivity and impulsivity in preschool. ADHD = attention-deficit/hyperactivity disorder; ODD = oppositional defiant disorder; CD = conduct disorder; SUDs = substance use disorders.

Figure 2

Simplified synthesis and metabolism pathways for dopamine (left panel) and serotonin (right panel). These pathways suggest a number of points at which dopaminergic and serotonergic function might be affected by, for example, genes that encode for neurotransmitter activity or conversion enzyme activity. Though not pictured, DA is also converted into norepinephrine by dopamine-β-hydroxylase, which is in turn converted into epinephrine by phenylethanolamine-N-methyltransferase.

Figure 3

A biosocial model of antisocial and borderline personality development. In the left panel, genetic vulnerability interacts with environmental risk to produce oppositional behavior and chronic emotion dysregulation, eventuating in antisocial behavior among boys and borderline traits among girls. In the right panel, a protective environment buffers vulnerable children from developing emotional and behavioral dysregulation. Adapted from Beauchaine et al., 2007.