Causes of Borderline Personality Disorder – Etiology
As with many other psychiatric disorders, Borderline Personality Disorder (BPD) is widely regarded as the product of complex interactions among multiple factors, including genetic, neurochemical, neuroanatomical, and psychological factors. It is important to emphasize that there is considerable diversity in the literature with regard to etiological understandings of BPD, and that many conclusions remain speculative.
Evidence suggests that BPD runs in families. Through the study of biological relatives of people with BPD, it has been proposed that BPD is 4 to 20 times more prevalent among relatives of those with BPD compared to relatives of individuals not diagnosed with BPD (Links et al. 1988; White at al. 2003). Torgersen and colleagues (2000) provided support for the genetic vulnerability of BPD by studying monozygotic and dizygotic twins. In their study, the concordance rate of BPD among monozygotic twins was 35% compared to a 7% concordance rate among dizygotic twins. The high concordance rate of BPD found in monozygotic twins is strongly suggestive of genetics playing a role in the etiology of BPD.
There is some support for neurochemical vulnerability in people with BPD. Specifically, two neurotransmitters have caught the attention of researchers: serotonin and norepinephrine. Serotonin has been found to be associated with aggression and impulsivity, whereby as levels of serotonin decrease, aggression and impulsive behaviours increase. Thus, it has been suggested that the characteristic aggressive and impulsive behaviours of BPD are the result of decreased or low levels of serotonin in the brain (Rinne et al. 2000). In much the same way, norepinephrine has been found to be related to aggressive behaviours in BPD. Coccaro et al. (2003) found that males with lower levels of norepinephrine were more likely to be diagnosed with BPD and more likely to have a lifetime history of aggression.
Researchers have also found anatomical and physiological brain differences between those with and without BPD. Hyperactivity of the amygdala, a brain structure in charge of autonomic responses associated with fear, arousal, and emotional responses, has been found in people with BPD (Wingenfeld et al. 2010). Additionally, decreased functioning of the prefrontal and preorbital cortex in patients with BPD has been related to a decreased capacity of affect control (Kernberg and Michels 2009). These findings might explain the sensitivity to environmental stressors and the deep impact that these stressors have in the interpersonal relationships and affects of individuals with BPD.
Consistently, individuals diagnosed with BPD report trauma and adversity as characteristic of their early lives. These individuals tend to differ from those without mental health concerns and from people diagnosed with other personality or mood disorders on reports of physical abuse, sexual abuse, and neglect during childhood (Ogata et al. 1990; Perry and Herman 1993; Weaver and Clum 1993; Zanarini et al. 2000). Similarly, people with BPD report more maternal and paternal abandonment, more parental conflict, and higher rates of being raised by relatives or in foster homes (Bandelow et al. 2005). Patients with BPD can further be differentiated from other psychiatric patients on the basis of their lack of resolution and capacity to think about or reflect on traumatic experiences (Fonagy et al., 1996). It appears that patients with BPD suffer the effects of trauma without being able to cognitively process their experiences and that this combination, beginning early in life, promotes a type of vicious circle in which their ability to think about and regulate their emotional experience is impaired.
The emotional and interpersonal instability characteristic of BPD may be the result of a failure to create secure attachments early in life. Bowlby (1973) suggested that there is continuity between the quality of our early relationships with caregivers and our adult interpersonal relationships. Early attachment behaviour enables infants to maintain proximity and contact with caregivers, which serves to promote the formation of an affectionate bond between infant and caregiver, ensuring safety and survival. Based on the repeated experience of the caregiver’s timely soothing responses, infants develop the expectation that important others are sources of help and comfort, along with the eventual capacity to regulate their own emotional states. These developments, the products of secure early attachment relationships, are both impaired among patients with BPD.
Integrating parallel streams of thought from the fields of psychoanalysis, developmental psychology, and cognitive neuroscience, comprehensive theories of BPD have been developed by leading authorities in the field including Kernberg (1984), Fonagy (1991), and Linehan (1993). Although differing in certain aspects, these theories all attend to the issue of mentalization. The concept of mentalization describes the way humans make sense of their social world by imagining the mental states (e.g., beliefs, motives, emotions, desires, and needs) that underpin their own and others’ behaviours in interpersonal interactions. Fonagy (1991) has elaborated a theory of how the capacity to mentalize develops in early childhood and, alternatively, how deviations from this normal developmental path result in severe forms of adult psychopathology, most notably BPD.
Fonagy and colleagues (e.g., Fonagy, Gergely, Jurist & Target, 2002) suggest that, in order to cope with a neglectful or abusive caregiver, children may defensively inhibit thinking about the intentions of others because it is too painful to think about an attachment figure’s wish to cause them harm. Furthermore, in cases of abuse or neglect, the absence of care signals danger and lack of safety that in turn triggers the child’s attachment system. Thus, the child seeks physical proximity to the caregiver but at the same time is defensively psychologically distant. This contradictory position can lead to distortions in the development of self-regulatory abilities and an overall sense of self.
An Integrative Perspective
Oldham (2009) provided an eloquent and succinct summary of contemporary research on BPD, which integrates recent advances in our understanding of BPD. As Oldham explains, contributions of clinical and basic science research have helped us recognize that the “stress-vulnerability” model of disease is a useful guide for considering a biopsychosocial concept of BPD. Researchers have identified core heritable endophenotypes (a special kind of biomarker) of affective dysregulation and impulsive aggression (Siever et al. 2002). Additional findings that brain abnormalities can be identified by brain imaging techniques, and that inherent hyperactivity of the amygdala has been detected lend further support to the idea that borderline pathology is at least partially “hard-wired” (Donegan et al. 2003). The heritable “priming” for emotional overactivity, coupled with an impairment in the usual cortical capacity to downregulate or inhibit this limbic-driven emotionality or impulsivity (New et al. 2007), can interfere with the normal attachment process during development (which can be magnified when there is inadequate parental support). Such a disposition can arrest or distort integration of aspects of self and others, resulting in early onset and persistence of profound interpersonal difficulties that characterise those with BPD.