Etiological Hypotheses of BPD
In order to extrapolate developmental hypotheses drawn, in part, from a literature on adults, one must illustrate that there is some degree of continuity from early temperamental predispositions to later adult personality. Indeed, although evidence suggests that diagnosable BPD does not emerge until late adolescence, there is a rich developmental literature linking early temperament with later personality (for a review, see Halverson, Kohnstamm, & Martin, 1994
). Moreover, both empirical and theoretical work suggests that many aspects of adult personality emerge early in childhood and are driven largely by biological predispositions (Caspi, 2000
; Kagan & Snidman, 2007
). For example, Caspi and colleagues found that temperamental variables at age 3 predict adult personality structure, the emergence of psychopathology, and antisocial behaviors in adulthood (Caspi, 2000
; Caspi et al., 2003
). In particular, youth who were identified as undercontrolled were subsequently at greater risk for developing externalizing disorders, whereas those who were inhibited were at greater risk for developing internalizing disorders (Caspi, 2000
). Thus, it appears that temperamental differences that can be observed early in life are linked to adult personality, patterns of interpersonal relations, and the development of psychopathology (see also Beauchaine & Neuhaus, 2008
; Kagan, 2008
). In the remainder of this article we synthesize research on known biopsychosocial correlates of BPD with the developmental literature in proposing five testable hypotheses.
Hypothesis 1: Poor impulse control and emotional sensitivity are early biological vulnerabilities for BPD.
When viewed cumulatively, studies conducted to date suggest that BPD is associated with deficits in both impulse control and emotion regulation. Family studies reveal significant familial aggregation of both impulse control disorders and mood disorders among those diagnosed with BPD (White et al., 2003
). This makes BPD unique when compared with other disorders of childhood, such as ADHD and depression, which appear to involve more circumscribed biological vulnerabilities that are more often restricted to dysfunction in specific neural systems (Beauchaine, 2001
). Yet, like BPD, some disorders do appear to result from biological vulnerabilities across multiple neural systems. Examples include CD and ASPD, which are associated with dysfunction in mesolimbic and mesocortical structures that subserve impulse control and with disruption in medullary functions that subserve emotion regulation and emotional expression (see Beauchaine, 2001
; Beauchaine, Gatzke-Kopp, & Mead, 2007
; Marsh, Beauchaine, & Williams, 2008
). Thus, we draw from these related literatures in our exploration of potential biological underpinnings of BPD.
Research on externalizing psychopathology suggests that impulsivity is highly heritable, although its specific expression is linked with environmental opportunities (Beauchaine & Neuhaus, 2008
; Beauchaine et al., 2008
; Cadoret, Leve, & Devor, 1997
; Hinshaw, 2002
; Krueger et al., 2002
). In fact, the emergence of more severe behavioral and emotional dysregulation among impulsive children appears to be largely dependent on environmental risk exposure (Jaffee et al., 2005
; Lynam et al., 2000
; Patterson et al., 2000
). Emotional lability and dysregulated anger appear to be particularly sensitive to environmental experience and may be overlaid onto temperamental impulsivity as a consequence of repeated negative reinforcement within the family (see above). Stressors in early development appear to alter already compromised dopaminergic, noradrenergic, and serotonergic pathways and may also contribute to hormonal alterations in the developing brain (for a review, see King, Tenny, Rossi, Colamussi, & Burdick, 2003
). Heightened sensitivity to environmental stress may therefore mediate the relation between biological vulnerabilities and the emergence of disorders such as BPD.
Although there is limited research on the development of emotion dysregulation in BPD, research on the development of CD and ASPD suggests that broad emotion dysregulation emerges across the preschool and the middle school years among vulnerable (e.g., impulsive) children (Beauchaine et al., 2007
). Data to support this assertion come from a series of psychophysiological studies with externalizing preschool children (Crowell et al., 2006
), middle school children (Mead et al., 2004
), and adolescents (Beauchaine et al., 2001
). These studies indicate that differences in psychophysiological markers of emotion dysregulation (e.g., RSA) are present among impulsive middle school children and adolescents but are not yet apparent among impulsive preschoolers. This suggests that at least some of the biological vulnerability for emotion dysregulation is shaped and later maintained by environmental influences. This interpretation is consistent with Linehan’s theory of emotion dysregulation evolving in invalidating environments and with findings indicating that (a) emotion regulation (and RSA) are socialized within families (Calkins, 1997
; Shipman & Zeman, 2001
) and (b) about 50% of RSA—a consistent marker of emotional adjustment—is environmentally determined (Kupfer et al., 2005
). Finally, early emotion regulation abilities, which are marked by high RSA, appear to buffer children from developing psychopathology in adverse rearing environments (e.g., Katz & Gottman, 1997
). Thus, emotion dysregulation, though partly heritable, is also sensitive to environmental input. As a result, high-risk family environments may contribute to the development of dysregulated affect among impulsive and/or emotionally sensitive children. This leads to our second hypothesis.
Hypothesis 2: Broad emotion dysregulation is fostered and maintained within an invalidating developmental context.
Although we suggest that the emotionally sensitive child is vulnerable to developing BPD, this vulnerability is likely exacerbated within an invalidating caregiving environment (Linehan, 1993
). Within this context, a child’s expressions of emotion are often rejected by the family and life’s problems are oversimplified. Consequently, the child is not taught how to modulate emotional arousal or cope with distress. Because emotional expressions are poorly tolerated within the caregiving environment, the child does not learn how to label and understand his or her emotional experiences, and the interpretation and communication of emotions is made increasingly difficult. Furthermore, in an invalidating environment, extreme emotional displays are often needed to generate helpful responses from caregivers. Thus, the family haphazardly punishes communication of negative emotions while intermittently reinforcing extreme emotional outbursts and actions.
A parallel model of the development of emotion dysregulation in CD and ASPD has received considerable empirical support. This literature outlines the processes through which emotional lability is shaped within the families of children with ADHD, leading to the development of CD among those raised in high-risk family environments but not among those raised in protective family environments (Beauchaine et al., 2007
; Patterson, Chamberlain, & Reid, 1982
; Patterson, DeBaryshe, & Ramsey, 1989
; Patterson, Dishion, & Bank, 1984
; Snyder, Edwards, McGraw, & Kilgore, 1994
; Snyder, Schrepferman, & St. Peter, 1997
). As articulated by Patterson and colleagues, repeated escalating exchanges between impulsive at-risk children and their parents serve as training for emotionally labile interaction patterns. Negative social exchanges (involving both punishment and negative reinforcement of emotional outbursts; see above) shape the behavior of both the parent and the child. Over time, this pattern results in increased frequency, intensity, and affective valence of negative interactions. The child learns that highly aversive behaviors and labile expressions of emotion are effective in obtaining desired ends, and this further disrupts parenting efforts.
Common to both the Linehan and Patterson models is the notion that family processes lead to increasingly more extreme emotional displays on the part of both the parent and the child. It is through such processes that emotional lability is shaped within the family context. In the case of antisocial pathology, this model of emotional lability has been confirmed in longitudinal studies where negative reinforcement of aggression predicts the later emergence of antisocial and emotionally labile behavior (Snyder et al., 1997
). Furthermore, reinforcement of aggressive and emotionally labile interaction styles likely contributes to the development of antisocial behavior by fostering ineffective means of dealing with social conflict. Emotionally labile patterns of interacting are common to BPD as well. Thus, the literature demonstrating that operant processes shape emotional lability across development provides empirical support for Linehan’s (1993)
biosocial model and for our third hypothesis.
Hypothesis 3: Reciprocal transactions between biological vulnerability and environmental risk potentiate emotion dysregulation and lead to more extreme behavioral dyscontrol.
It is important to emphasize, as we have in , that an invalidating developmental context is likely shaped by specific characteristics of both the caregiver and the child and their interactions over time. As reviewed above, certain child characteristics, such as impulsivity, are biologically driven and present early in development. An example from the developmental literature includes the “difficult child” exemplar described by Thomas, Chess, and colleagues (Thomas, Chess, & Birch, 1968
; Thomas, Chess, Birch, Hertzig, & Korn, 1963
). After nearly 50 years of research, the difficult child construct has been revised substantially; researchers have identified three broad dimensions of infant temperament: extraversion/surgency, negative affectivity, and effortful control (e.g., Rothbart & Rueda, 2005
). Effortful control, which contributes to both emotional and behavioral regulation, is defined as “the ability to inhibit a dominant response to perform a subdominant response, to detect errors, and to engage in planning … and self regulation” (Rothbart & Rueda, 2005
, p. 169). Accumulating data indicate that the neural substrates of effortful control overlap with those implicated in BPD and externalizing behavior problems, among them the prefrontal cortex and the anterior cingulate cortex (Rothbart & Rueda, 2005
). Children at risk for BPD are also likely to be high on negative affectivity, which is characterized by discomfort, frustration, shyness, sadness, and nonsoothability.
As implied above, hypothesized contributions of the caregiver include (a) a tendency to invalidate emotions and an inability to model appropriate expressions of emotion, (b) an interaction style that negatively reinforces emotional arousal, and (c) a poor fit between the child’s temperament and parenting style. This final point is emphasized here because it highlights the Biology × Environment transactions that shape both child and caregiver behaviors. In theory, a child with low biological vulnerability may be at risk for BPD if there is an extreme discrepancy between child and caregiver characteristics or if the family’s resources are extremely taxed (e.g., alcoholism, sibling with cancer). Such situations have the potential to perpetuate invalidation, because the demands of the child often exceed the ability of the environment to meet those demands (Linehan, 1993
). The converse is also likely; a biologically vulnerable child may be protected in a well-matched environment where strong family supports are in place. Such multifinal outcomes led Linehan to propose three primary types of families that increase risk for BPD: the disorganized family (e.g., one that is pervasively neglectful or maltreating), the perfect family (e.g., one in which expressing negative emotions is taboo), and the normal family (one characterized primarily by poorness of fit). It must be noted that caregiver characteristics are not necessarily fixed or preexisting. Rather, the caregiver is also a product of complex biological, social, and psychological transactions, including evocative effects of the child on parenting style.
Hypothesis 4: There are early behavioral indications of risk for BPD.
In this review we have emphasized that the developmental trajectory leading to BPD likely begins with biologically driven temperamental vulnerabilities. However, these early vulnerabilities have low predictive specificity and most likely indicate risk for a plethora of partially overlapping psychological conditions. By middle childhood, emotionally dysregulated and impulsive youth are most likely to meet or partially meet diagnostic criteria for a mood disorder comorbid with impulsive behaviors. Therefore, youth with comorbid internalizing and externalizing psychopathology likely represent one population at heightened risk for later BPD. This hypothesis is consistent with evidence suggesting that the combination of internalizing and externalizing psychopathology increases risk for both suicidal and nonsuicidal self-injury (e.g., Verona, Sachs-Ericsson, & Joiner, 2005
), which occur commonly among adults diagnosed with BPD. Indeed, as reviewed above, there is an extremely high rate of self-inflicted injury among those with BPD, of whom approximately 40%–90% engage in nonsuicidal self-injury or make a suicide attempt at some point in their life (American Psychiatric Association, 2004
). Moreover, retrospective evidence suggests that nearly 1/3 of adults with BPD reported first engaging in self-injury before the age of 12 and another 1/3 began such behaviors during adolescence (Zanarini et al., 2006
). This suggests that it is a minority of those with BPD whose first episode of self-injury occurs after a BPD diagnosis can be ascertained reliably.
There is also considerable overlap between characteristics observed among self-injuring youth and those diagnosed with a personality disorder (for a review, see Miller, Rathus, & Linehan, 2007
). Over two decades of research supports a relation between adolescent self-inflicted injury and personality disorders, particularly borderline and antisocial pathology (Brent et al., 1994
; Clarkin, Friedman, Hurt, Corn, & Aronoff, 1984
; Marton et al., 1989
; Marttunen, Aro, Henriksson, & Lönnqvist, 1994
; Pfeffer et al., 1991
; Runeson & Beskow, 1991
). In a review of 14 studies of completed suicide, Linehan, Rizvi, Welch, and Page (2006)
found that 40%–53% of individuals met criteria for a personality disorder. Linehan et al. also reported a high correspondence between suicide and personality disorders among youth. Moreover, self-inflicted injury was an identifiable behavior that captured features of both impulsivity and emotion dysregulation. As with other impulsive and/or addictive behaviors, self-injury represents a failure to inhibit a dominant response in the service of more distal goals or objectives. Yet evidence also suggests that it serves an emotion regulation function (e.g., Zlotnick, Donaldson, Spirito, & Pearlstein, 1997
) and is often used as a strategy to reduce emotional distress. For these reasons, among youth who have not been identified previously, the manifestation of self-injurious behaviors indicates the need to assess for additional risk factors for a borderline diagnosis.
Hypothesis 5: Traits and behaviors indicative of BPD emerge earlier than a full diagnosis and may exacerbate risk for BPD.
According to the developmental model presented here, a taxed caregiving environment perpetuates emotional and behavioral dysregulation in the biologically vulnerable child. Theorists have proposed that early neurocognitive impairment may be one such vulnerability that moderates the relationship between an insecure/disorganized attachment and a later BPD diagnosis (e.g., Judd, 2005
). Thus, traits and behaviors may manifest as early as birth and likely shape the developmental context within which BPD emerges. This process is dynamic and continues into adolescence and adulthood. For example, by adolescence, extremely dysregulated behaviors (e.g., self-inflicted injury, disordered eating, substance abuse) may also impact the parent–child relationship by lessening trust and increasing conflict and rigidity. Indeed, evidence suggests that there are high levels of parent–child conflict among self-injuring adolescents. Moreover, the interaction between low peripheral serotonin and high family conflict appears to increase risk for self-injurious behaviors among adolescent girls (Crowell et al., 2008
). However, self-injury is certainly not the only maladaptive behavior that may occur in the developmental progression leading to BPD. In cases where self-injury is not present in the etiological formulation, it is possible that other repetitive maladaptive behaviors serve a similar function (e.g., purging or drug abuse). Although clinically it is important to understand each individual’s behavioral repertoire, from an etiological perspective the manifest behavior is not as important as the function that behavior serves. In our model, we not only assert that problematic behaviors serve an emotion regulation/avoidance strategy but also suggest that these behaviors exacerbate risk for BPD via evocative effects on interpersonal relationships and via interference with healthy emotional development.