Aetiology of Borderline Personality Disorder

The causes of Borderline Personality Disorder are complex and remain uncertain. No current model has been able to integrate all of the available evidence. However, the following have been named as contributing factors to the cause of borderline personality disorder. These include:

1. Genetics;
2. Neurophysiological and neurobiological dysfunctions of emotional regulation and stress;
3. Psychosocial histories of childhood maltreatment and abuse; and
4. Disorganisation of aspects of the affiliative behavioural system, most particularly the attachment system

(The British Psychological Society & the Royal College of Psychiatrists, 2009)

Biological Factors

Biological causes could conceivably range from genetic influences to early childhood environmental impact on the development of the brain and nervous system. Emotional regulation is a core feature of borderline personality disorder and irregular function of neurotransmitters has been implicated in this. Emotional regulation involves the processing, amplification, maintenance, and attenuation of emotions generated from internal and/or environmental stimuli.

Evidence suggests that threatening or aversive stimuli activate the amygdala, which in turn activates the anterior cingulate and prefrontal cortices parts of the brain. While the anterior cingulate may play a role in the cognitive evaluation/processing of mood and affect regulation, it has also been implicated in responses to conflict that is synonymous with Borderline Personality Disorder. The orbital prefrontal cortex appears to inhibit impulsive aggression by regulating the amygdala. Such structural and functional deficit in the amygdala and hippocampus (parts of the brain that are in charge of affect regulation, attention, self-control and executive function) may contribute to the development of BPD.

Neurotransmitters particularly serotonin is also known to regulate impulses, aggression and affect. Serotonin levels have been implicated in the causality of the disorder. Dysfunction in this neurochemical has been linked to emotional instability, suicidal behaviours and impulsivity behaviours evidenced in people with the disorder (Barlow & Durand, 2009). Low levels of serotonin may also inhibit an individual to control destructive urges (The British Psychological Society & the Royal College of Psychiatrists, 2009; Barlow & Durand, 2009).

Twin studies suggest that the heritability factor of BPD does exist, with the key area being on those traits related to impulsive aggression and mood dysregulation, rather than on any direct hereditary link to borderline personality disorder itself. It is argued that personality traits such as impulsive aggression and mood dysregulation which are features of BPD are some of the traits passed on in families (Livesley, 2008). Recent studies have proposed that heritability factors of Cluster B personality disorders, as classified in the DSM-IV-TR, lies within a range of 27% to 35% suggesting that genetic factors play a less significant role in the development of borderline personality disorder than previously assumed (Reichborn-Kjennerud et al., 2007 as cited in The British Psychological Society & the Royal College of Psychiatrists, 2009).

Current evidence suggests that genetic influences on personality disorders generally, rather than on BPD specifically, acts both individually and in combination with inconsistent environmental factors (The British Psychological Society & The Royal College of Psychiatrists, 2009). Environmental factors influence the frequency and intensity of the genetic expression or phenotype of those behaviours seen as being most consistent with the disorder (Distel, Trull, Derom, Thiery, Grimmer, Martin, Willensen & Boomsma, 2008; Livesley, 2008).

Psychological Factors

Psychological factors also play a part in the aetiology of Borderline Personality Disorder (BPD). Traumatic experiences such as sexual, physical and emotional abuse experienced in childhood have all been implicated in the aetiology of BPD. These traumatic events have been said to elicit developmental arrest in vulnerable children which can contribute to the development of BPD in later life. However, abuse alone is neither necessary nor sufficient for the development of BPD. For example, predisposing factors of the child-parent relationship are likely to be mediating factors in the development of BPD whereby the quality of the family relationship, has been said to contribute to the development of BPD. Sustained abuse suffered at the hand of a family member is likely to cause disorganisation of the abused child’s attachment to that family member (Liotti, Cortina & Fari na, 2008; (Gerull, Meares, Steveson, Korner & Newman, 2008).

It has also been suggested that the caregiver’s response to the abuse may be more important than the abuse itself in long term outcome of BPD. Failures in the giving and expression of empathy occupy a place of central importance in childhood development. A limited parental capacity to display empathy following a child’s traumatic experience is likely to impair the child’s development and potentially place them at risk of dysfunctional personality development (Gerull, et al., 2008).

A family environment that is unstable and non-nurturing to the child’s perspective following a traumatic experience is unlikely to facilitate a successful adjustment after trauma. Thus the critical factor is the family environment. If the parents are unable to validate the child’s immediate reality, it is likely to hinder or distort the development of secure attachments resulting in emotion dysregulation creating vulnerability for BPD.

Social Factors

The behavioural disturbances of BPD are also considered to be, at times, due to the social environment. Family studies in particular have identified a number of factors that may be important in the development of Borderline Personality Disorder. For example, unstable, non-nurturing family environments are considered to be the key social contributor of personality dysfunction (The British Psychological Society & the Royal College of Psychiatrists, 2009). Invalidating family environments during childhood have been found to contribute to the development of emotional dysregulation.

This has been considered to be due to the parents in that environment failing to teach the child how to label and regulate emotional arousal, how to tolerate emotional distress and when to trust their own emotional responses during a time of distress (Linehan, 1993). Thus in adulthood borderline people adopt the characteristics of the invalidating environment and tend to invalidate their own emotional experiences and depend on others for accurate reflections of the external reality.

Parental under-involvement and neglect have also been seen as a contributing factor in the development of the disorder. Emotional under-involvement can contribute to the child’s difficulties in socialising and has also been shown to increase the risk of suicide (The British Psychological Society & the Royal College of Psychiatrists, 2009). Parents with BPD are regarded as “high” risk as they are likely to continue their attachment and relationship difficulties with their children.

Parents with unresolved trauma are also more likely to have attachment and relationship difficulties with their children through specific interactional patterns of avoidance and/ or dependency (Gerull, et al., 2008). If the parent acts out their past trauma in the present, this is likely to traumatise their children thereby making the intergenerational transmission of psychopathology more likely.

Based on this argument, treating a parent that suffers from BPD is critical as their pattern of disturbed attachment relationships, impulsivity, poor anger control, mood instability, egocentrism and self-defeating behaviours impairs their parenting skill and consequently will most likely put their children’s psychological wellbeing and personality development at risk (Gerull, et al., 2008).

BDP and Attachment

Attachment organisation as a theoretical construct offers a unique perspective and conceptual framework from which to understand the aetiology of borderline personality disorder. Attachment theory states that infants construct structures of implicit memory concerning the self and the attachment figure on the basis of their experience with them (Scott, Kenneth, Levy & Pincus, 2009). Usually, the child’s propensity to seek protection and comfort is met with positive responses from the significant care giver thereby promoting a secure attachment with the child. The quality of childhood relationships with significant caregivers results in mental representations or internal working models that shape our personality traits (Liotti, Cortina & Farina, 2008; Gunderson & Lyons-Ruth, 2008).

These representations are social cognitive schemata that shape the beliefs about the self as well as expectations about interpersonal relationships and the quality of attachments to significant others (i.e. secure versus insecure attachment styles). Because these representations act as guides in later social interactions, they are self-perpetuating whereby they tend to persist into adulthood as general representations of how close relationships work (Scott, Kenneth, Levy & Pincus, 2009). Borderline personality disorder is said to be triggered by significant events in the socio-relational environment of the individual that have been interpreted through social cognitive processes.

Specifically, the social cognitive processes of people with BPD have been characterised by negative appraisals of the emotions, motivations, and/or intentions of others. These types of negative social cognitive biases that may have stemmed from key relational events in childhood are generalised on to the broader socio-relational environment of the individual causing quite debilitating and insecure adult attachment patterns across most, if not all, relationships (Scott, Kenneth, Levy & Pincus, 2009). While the relationship of diagnosis of borderline personality disorder and specific attachment category is not obvious, BPD is strongly associated with insecure attachment (The British Psychological Society & the Royal College of Psychiatrists, 2009).

Prevalence

The prevalence of Borderline Personality Disorder ranges from 2 to 5% in Australia, 1 to 2% in the USA and 0.7% in Norway (Glenn & Klonsky, 2009; Lieb, Zanarini, Schmahl, Linehan & Bohus, 2004). It is reported that women are three times more likely to be diagnosed with this disorder than men and in children, the disorder is reported to be more common in girls than boys. 10% of those diagnosed with BPD attempt suicide, a rate that is higher than the general population (Glenn & Klonsky, 2009). In primary care, the prevalence of borderline personality disorder ranges from 4 to 6% (Moran et al., 2000; Gross et al., 2002 cited in The British Psychological Society & the Royal College of Psychiatrists, 2009). People with BPD are more likely to visit their General Practitioner and more likely to report psychosocial impairment compared to those without BPD.

BPD is said to be more common among those who are drug and/or alcohol dependent. Within this population, more men are diagnosed with BPD than women. Borderline Personality Disorder is also more common in those with an eating disorder and also among people presenting with chronic self-harming behaviour. Borderline clients also present more often than other individuals for evaluation or treatment with one or more comorbid DSM-IV Axis I disorders. Initially, these disorders may mask the underlying borderline psychopathology, impeding accurate diagnosis and making treatment planning difficult.

However, over time, BPD may be recognised as a consequence of the comorbid DSM-IV Axis I disorder being resistant to treatment thus causing further analysis of underlying problems and variables of influence. While there has clearly been a focus that has been maintained over the decades in the literature on the aetiology and treatment of BPD, it still appears to be under-recognised by many mental health practitioners (Moran et al., 2001 as cited in The British Psychological Society & the Royal College of Psychiatrists, 2009; Zanarini, Frankenburg, Dubo, Sickel, Trikha, Levin, & Reynolds, 1998).

Risk Factors

• Being female, 75 percent of people diagnosed with BPD are female.
• The prevalence of BPD is higher in females who have experienced sexual abuse.
• Living in a marginalised and invalidating environment
• History of abuse, neglect and invalidation.

References:

• American Psychiatric Association, (2000). Diagnostic and Statistical Manual of Mental Disorders. (4th ed.). Text Revision. Washington, DC: American Psychiatric Association.
• Barlow, D.H., & Durand, V.M. (2009). Abnormal psychology: An integrative approach (5th ed.). Belmont, CA: Wadsworth Cengage Learning.
• Gerull, F., Meares. R., Stevenson, J., Korner, A. Newman, L. (2008). The beneficial effect on family life in treating borderline personality. Psychiatry, 71, 59-70.
• Glenn, C.R., Klonsky, D. E. (2009). Emotion dysregulation as a core feature of borderline personality disorder. Journal of Personality Disorders, 23, 20-28.
• Lieb, K. Zanarini, M.C., Schmahl, C., Linehan, M.M., & Bohus, M. (2004). Borderline Personality Disorder. The Lancet, 364, 453-461.
• Linehan, M.M. (1993). Cognitive behavioural treatment of borderline personality disorder. The Gilford Press: New York: NY.
• Liotti, G., Cortina, M., Farina, B. (2008). Attachment theory and multiple integrated treatments of borderline patients. Journal of American Academy of Psychoanalysis and Dynamic Psychiatry, 36, 295-315.
• Livesley, J. (2008). Toward a genetically informed model of borderline personality disorder. Journal of Personality Disorders, 22, 42-71.

This article is an extract of Mental Health Academy’s “Borderline Personality Disorder” CPD course. The course will assist you in gaining an understanding of; the aetiology, the biological, social and psychological effects, and an outline of the diagnostic criteria for Borderline Personality Disorder including treatment options focusing on Dialectical Behaviour Therapy. Click here for more information.