4b
Theodore P. Beauchaine
An unfortunate consequence of restricting personality disorder (PD) diagnoses to those 18 years of age and older is a literature in which developmental precursors are understudied and at times undervalued. As Sharp and De Clercq (this volume) note, most efforts to understand PD development extend adult criteria downward to adolescence. These studies demonstrate that PDs exist among teens, and predict functional impairment into adulthood (e.g., Bornovalova, Hicks, Iacono, & McGue, 2013). Other studies, also summarized by Sharp and De Clercq, evaluate structural relations among PD symptoms in large samples of teens. These studies demonstrate similar patterns of PD co-occurrence and relations to Big Five personality traits as seen in adults.
Studies that identify onset age and expression of adult PD symptoms are necessary and important, but they provide limited understanding of etiopathophysiology—the complex and interactive determinants of psychopathology across the lifespan. Such determinants include genetic, neural, environmental, and cultural factors that transact with one another to eventuate in psychopathology, often beginning many years before symptom onset (e.g., Cicchetti, 1993; Sroufe & Rutter, 1984). For developmental psychopathologists, specifying etiopathophysiology is of utmost importance because it ultimately increases treatment efficacy by identifying mechanistic targets for prevention and intervention (Beauchaine, Neuhaus, Brenner, & Gatzke-Kopp, 2008). Given modest effectiveness and high drop-out rates for PD interventions delivered in adulthood (e.g., Kliem, Kröger, & Kosfelder, 2010), targeting developmental mechanisms may be essential toward reducing the extensive burden of PDs on individuals, their families, and broader social systems (Beauchaine, Hinshaw, & Bridge, 2019).
In this commentary, I present a model of antisocial and borderline PDs that describes how heritable vulnerabilities interact with environments across childhood and adolescence to affect neurodevelopment and eventuate in adult impairment. My description is necessarily brief; further details are available in our extended writings (Beauchaine, Hinshaw, & Bridge, 2019; Beauchaine, Klein, Crowell, Derbidge, & Gatzke-Kopp, 2009; Beauchaine, Zisner, & Sauder, 2017; Crowell, Beauchaine, & Linehan, 2009). Points of particular emphasis include (1) the complexity of psychopathology across development and levels of analysis; (2) the importance of multifinal outcomes – most notably ASPD for males versus BPD for females – for those reared in similar family contexts; and (3) the need to consider compromised neuromaturation of frontal brain regions implicated in self- and emotion-regulation in any developmental model of ASPD and BPD.
The Inordinate Complexity of Psychopathology
Two related goals of our research group are to elucidate neurobiological vulnerabilities to psychopathology without engaging in biological reductionism (Beauchaine & Constantino, 2017), and to specify how emotional processes, which ordinarily motivate adaptive social behavior, become disrupted in various forms of psychopathology (Beauchaine & Zisner, 2017). Over the last decade, it has become clear that neurobiological vulnerabilities to psychopathology are profoundly more complex than imagined a generation ago (Beauchaine, Constantino, & Hayden, 2018). At the same time, it has also became clear that emotion dysregulation is a transdiagnostic feature of psychopathology, and characterizes both ASPD and BPD (Beauchaine, 2015; Beauchaine et al., 2017; Crowell et al., 2009; Gratz, Dixon-Gordon, Breetz, & Tull, 2013). Although full articulation of these points would require extensive review, Figure 4.b.1 depicts the complexity of ASPD and BPD development from preschool to adulthood.
Figure 4.b.1
A neurodevelopmental model of ASPD and BPD. See text for details.
Several important points emerge from Figure 4.b.1. First, trait impulsivity, a highly heritable temperamental/personality attribute that characterizes both ASPD and BPD (as noted by Sharp and De Clercq), arises from multiple determinants, including genetic burden (e.g., normal allelic variation, de novo mutations), environmental influences (e.g., brain injury, epigenetic regulation of neurotransmitters), and neuro-hormonal functions (e.g., circulating testosterone levels) (for reviews, see Beauchaine & Constantino, 2017; Gatzke-Kopp, 2011). Notably, few of these influences are necessary or sufficient to result in functional impairment. Rather, they interact in unique combinations across individuals to confer neural vulnerability. Only a decade ago, psychopathologists were still searching for single genes to explain psychopathology. Now, it is well understood that single vulnerability alleles account for very little variance in behavioral phenotypes. For example, over 8300 single nucleotide polymorphisms (SNPs) – almost all of very small effect size – are needed to explain half of the phenotypic variance in schizophrenia liability across the population (Ripke et al., 2013). This of course includes schizotypal PD.
Second, none of these neurobiological vulnerabilities affect behavior directly. Rather, complex combinations of genetic, neuro-hormonal, and environmentally induced influences confer individual differences in neural function. In turn, neural functions give rise to psychological traits and states (e.g., anhedonia, irritability) that motivate impulsive behaviors. Thus, biological functions affect behavior by influencing temperament, personality, and emotion. PDs can therefore not be understood solely at biological levels of analysis; emotional and psychological factors must be considered (Beauchaine & Zisner, 2017).
Third, as noted by Sharp and De Clercq, behavioral expressions of vulnerability to psychopathology change in form across the lifespan, often increasing in severity and broadening across functional outcomes (Beauchaine & Cicchetti, 2016). In its developmentally “purest” form, trait impulsivity is expressed as hyperactive-impulsive ADHD in preschool, but progresses to increasingly intractable symptoms across development for those who go on to develop PDs (Figure 4.b.1). Although childhood ADHD does not determine psychopathological endpoints, it is a well-documented vulnerability to ASPD and BPD among males and females, respectively (see Beauchaine et al., 2017; Stepp, Burke, Hipwell, & Loeber, 2012).
Fourth, vulnerability traits interact with both one another and environments across childhood and adolescence to affect behavior, including personality development (Beauchaine, 2015; Beauchaine et al., 2017; Crowell et al., 2009; Finucane, Challman, Martin, & Ledbetter, 2016). Figure 4.b.1 describes how both trait impulsivity and emotion dysregulation contribute to development of ASPD and BPD. As we have reviewed elsewhere, trait impulsivity is unlikely to eventuate in PDs in the absence of co-occurring emotion dysregulation (Beauchaine et al., 2017; Beauchaine, Hinshaw, & Bridge, 2019; Crowell et al., 2009). Thus, models that include main effects of impulsivity or emotion dysregulation do not fully account for ASPD or BPD development.
Multifinality in Personality Disorders
Broadly speaking, multifinality refers to situations in which different individuals reach distinct functional endpoints given similar initial vulnerabilities. As depicted in Figure 4.b.1 and reviewed initially by our group a decade ago (Beauchaine et al., 2009), ASPD and BPD provide a compelling example of multifinality given that (1) they share genetic and temperamental vulnerabilities (e.g., Lyons-Ruth et al., 2007), (2) males with ASPD and females with BPD are often reared in the same families (e.g., Goldman, D’Angelo, & DeMaso, 1993), and (3) similar environmental influences – both familial and extra-familial – are associated with development of both PDs (e.g., Lyons-Ruth, 2008).
In the bottom panels of Figure 4.b.1, circles represent behavioral progression of early life vulnerability (ADHD) to BPD for females (light gray) and ASPD for males (dark gray). As noted above, ADHD is a documented vulnerability to both PDs (Beauchaine et al., 2017; Stepp et al., 2012). Rectangles indicate common environmental risk factors that mediate developmental progression to increasingly severe pathology across the lifespan (e.g., self-harm for girls and delinquency for boys). Although these risk factors, including coercive/invalidating families, early life abuse, deviant peer affiliations, and exposure to substances of abuse, cannot be reviewed here, they are well characterized in the ASPD and BPD literatures (see Beauchaine et al., 2017; Beauchaine, Hinshaw, & Bridge, 2019; Crowell et al., 2017). According to our developmental model, when these environmental risk factors accumulate across the lifespan, they shape and maintain emotion dysregulation, which becomes an increasingly important etiological factor in emerging PDs (Beauchaine et al., 2017; Crowell et al., 2009; Gratz et al., 2013). From this perspective, behavioral expression of vulnerability is driven more by highly heritable trait impulsivity very early in life (ADHD), with increasing influence of less heritable and highly socialized deficiencies in emotion dysregulation as PD development progresses across middle-childhood, adolescence, and adulthood. This suggests that prevention programs should focus on environmental risk factors that are known to shape emotion dysregulation before patterns of emotional responding become entrenched and extend to extra-familial relationships (see Beauchaine, Hinshaw, & Bridge, 2019).
Compromised Neuromaturation of Frontal Brain Regions
Twenty-five years of research demonstrates the importance of cortical neural function for efficient executive control, associative learning, and emotion regulation – all of which are compromised in ASPD and BPD. The prefrontal cortex (PFC) includes several functional subdivisions that are implicated in effective emotion regulation, including the dorsolateral, medial, and ventrolateral PFCs, the orbitofrontal cortex (OFC), and the insular cortex (e.g., Goldin, McRae, Ramel, & Gross, 2008). Adults with ASPD and BPD demonstrate both structural and functional compromises across many of these regions (e.g., Krause-Utz, Winter, Niedtfeld, & Schmahl, 2014; Yang & Raine, 2009). Although specific findings are beyond the scope of this commentary, ASPD and BPD are associated with smaller cortical volumes and deficient top-down frontal control over emotion, as assessed by functional connectivity.
Importantly, frontal regions are the last parts of the brain to develop fully, and are exquisitely sensitive to environmental insults. Ordinarily, prefrontal structures continue to mature into the mid-20s (Gogtay et al., 2004). However, frontal neuromaturation is compromised among delinquent and antisocial males (De Brito et al., 2009; Yang & Raine, 2009). Furthermore, children who are reared in contexts of poverty, neglect, and abuse – some of the very risk factors that facilitate development of ASPD and BPD (see Figure 4.b.1) – show cortical volumes that are nearly 10 percent smaller than those of their peers, and exhibit abnormal functional activity during associative learning into adulthood (Birn, Roeber, & Pollak, 2017; Hair, Hanson, Wolfe, & Pollak, 2015).
In some of our most recent work, we have found both reduced cortical volumes and altered neural function in the OFC among adolescent girls who were recruited for severe self-harm (Beauchaine, Sauder, Derbidge, & Uyeji, 2019; Sauder, Derbidge, & Beauchaine, 2016). As shown in Figure 4.b.1, self-harm is a precursor to BPD for many who develop the disorder (see Beauchaine, Hinshaw, & Bridge, 2019). These findings suggest that neural correlates of BPD are already emerging among teens who are at risk for the disorder, and also suggest compromised neurodevelopment, as seen in delinquent boys (De Brito et al., 2009).
As outlined above, overall impairment increases across development as neural vulnerability to emotion dysregulation accrues and adds to existing impairment imparted by heritable trait impulsivity. Evidence that (1) environmental enrichment has positive effects on cortical neuromaturation (e.g., Blair, 2016), and (2) effective intervention can improve frontal function (e.g., Beauchaine, Zisner, & Hayden, 2019) suggests the importance of targeted prevention for high-risk children. It is my hope that by taking a developmental psychopathology perspective and specifying etiopathophysiology, more effective prevention programs can be formulated that target mechanisms of PD development directly.
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Preparation of this chapter was supported by Grant DE025980 from the National Institute of Mental Health, and by the National Institutes of Health Science of Behavior Change (SoBC) Common Fund.