Current Opinion in Psychiatry:
PERSONALITY DISORDERS: Edited by Aleksandar Janca and Charles Pull
Childhood adversity and borderline personality disorder: a focus on adolescence
Newnham, Elizabeth A.a,b,c; Janca, Aleksandard
aFrancois-Xavier Bagnoud Center for Health and Human Rights, Harvard School of Public Health, Boston, Massachusetts, USA
bDepartment of Psychiatry, University of Oxford, Oxford, UK
cSchool of Psychology
dSchool of Psychiatry and Clinical Neurosciences, The University of Western Australia, Perth, Western Australia, Australia
Correspondence to Aleksandar Janca, MD, MSc, FRCPsych, FRANZCP, Winthrop Professor and Head, School of Psychiatry and Clinical Neurosciences, The University of Western Australia, Medical Research Foundation Building, 50 Murray Street, Perth, WA 6000, Australia. Tel: +61 8 9224 0293; fax: +61 8 9224 0285; e-mail: firstname.lastname@example.org
Purpose of review: This article explores recent research in the field of childhood exposure to trauma and the development of borderline personality disorder in adolescence.
Recent findings: Adolescence is a critical period of development. Exposure to trauma, specifically sexual abuse, prior to and during puberty has specific implications for personality development and heightens risk for borderline personality disorder. Elevated symptom levels in adolescence are likely to decline across adulthood, but social and vocational impairments remain. Impulsivity, difficulties in emotion regulation, and suicidality may characterize adolescent expression of borderline personality disorder, whereas negative affect and functional impairment are more stable features of the disorder.
Summary: Preliminary findings in treatment models for adults have potential for benefit among adolescence. Further research is required to examine treatment effectiveness and efficiency. Greater attention to low-income and middle-income nations, which are disproportionately affected by adversity, is needed to determine cross-cultural validity and the impact of trauma in adolescent populations.
A safe environment and healthy interactions in early childhood and adolescence enable not only optimal cognitive and physical development, but also the psychological skills vital to later social and vocational engagement . Millions of children are exposed to trauma each year, and an emerging consensus suggests that childhood trauma and adversity are significant risk factors for the development of borderline personality disorder (BPD) and related personality traits [2▪,3,4]. Little is known about the precise role of various exposure types, the timing of traumatic experiences, or the interactive contributions of genetics and the environment in the development of BPD. A renewed focus on research into BPD in adolescence has focused on life-course development, family environment, and the relative role of genes and neurobiology to provide insights into the complex relationship between early exposure to trauma and maladaptive personality traits. This article focuses on recent studies and findings in this area so as to facilitate a more sophisticated understanding of the relationship between childhood trauma and the emergence of borderline personality traits in adolescence, a period critical to later health outcomes.
THE EARLY ENVIRONMENT
Child development occurs within a social ecology of family, peers, and community. Secure attachment with a reliable and sensitive caregiver in childhood enables the development of appropriate social behaviors, affect regulation, cognitive flexibility and coherent self-perception . Interruption to this attachment, through maltreatment, abuse, or neglect, paired with a predisposition to personality dysfunction, has potential for the development of psychopathology in adolescence and adulthood . Family conflict and mental health difficulties often occur in an environment characterized by multiple risk factors, including poverty, domestic conflict, and overcrowding. A recent examination of borderline traits by Winsper et al. [7▪] in a community sample of 6050 children and their mothers from the Avon Longitudinal Study of Parents and Children (ALSPAC) highlights the specific risk factors existing in the family environment. Using a prospective design enabled an assessment of childhood environment and parenting without concerns about memory and selective biases that have hampered prior research into BPD and childhood relationships. Family adversity was shown to have a direct impact on a child's BPD symptoms at early adolescence (11 years), and indirect effects via parental conflict, compromised parenting skills, poor cognitive functioning, and psychiatric diagnosis in the child [7▪]. An early environment of family adversity and maladaptive parenting thus heightens the risk for a child's development of BPD traits in early adolescence.
For those born into an environment of family and contextual adversity, increased risk may stem from early programming alterations of the hypothalamic–pituitary–adrenal axis due to stress during pregnancy . Additional stressors (including conflict, aggression, and violence) in the early development period may then impede the child's interpersonal skills, coherence of identity, ability to regulate emotion, and cognitive development. These factors are also likely to reduce parents’ ability to attend to the child and maintain healthy parenting. Intelligence plays a protective role [7▪], but deficits in these areas have the potential to become more pronounced in adolescence [2▪,9]. Overall, it appears that a combination of early adversity, compromised parenting, and domestic conflict set the scene for later difficulties in emotion regulation, impulsivity, and affect.
THE ROLE OF SPECIFIC ADVERSITIES
Adversity in early life has a detrimental effect on child personality development; however, the role that specific adversities play in the development of psychiatric disorders is less clear . Exposure to trauma has a dose–response effect resulting in the expression of major depressive disorder, posttraumatic stress, and anxiety disorders. Yet it appears that the pathway to BPD is characterized by a steeper increase in traumatic exposures than for other disorders [2▪]. In an investigation of the comparative patterns of adverse experience and resulting pathways to psychopathology, Pietrek et al. [2▪] assessed the role of various childhood experiences in the development of major depressive disorder, BPD, and schizophrenia. Among adult inpatients undergoing treatment, specific profiles of childhood adversity were analyzed. In comparison to healthy controls, an increase in the number of traumatic exposures over time was evident across all three groups, but significantly larger among those with BPD and major depressive disorder (MDD) than those with schizophrenia. A pronounced increase in trauma exposure just prior to puberty characterized all diagnostic groups, but patients with BPD reported a greater number of adversities across childhood than patients with either MDD or schizophrenia.
The type of traumatic exposures also differed across the three groups. Patients with BPD reported significantly more sexual abuse in their childhood than those with MDD or schizophrenia, and both BPD and MDD patients reported histories with greater physical punishment and general trauma than schizophrenia patients. Further, when looking at comorbid conditions (which were common) among the patient groups, an association was indicated in which higher rates of childhood trauma were reported by patients with comorbid BPD and MDD relative to patients with single diagnoses of MDD, BPD, or schizophrenia. The association between BPD and high rates of trauma exposure, in particular sexual abuse and punishment, is consistent with other studies of BPD development [11,12]. In a recent large-scale Norwegian twin birth cohort study, post-traumatic stress disorder (PTSD) was associated with increased risk of all personality disorders, but most strongly associated with BPD . In addition, recent findings suggest that BPD plays a mediating role in the development of suicidality among adults who experienced early life maltreatment . Among a college sample in the United States, BPD symptoms fully mediated the relationship between physical abuse and suicide potential, as well as the relationship between emotional abuse and suicide potential, but only partially mediated the association between BPD and childhood neglect. Thus, a combination of maladaptive cognitions together with an inability to regulate mood appears to mediate the link between childhood maltreatment and suicide potential in young adults .
WINDOWS OF VULNERABILITY
Comparisons of the specific timing and pathways to psychopathology suggest that windows of vulnerability exist in childhood and adolescence that play a critical role in the development of BPD. The timing of trauma exposure influences BPD symptomatology, which in turn is associated with other behavioral outcomes such as suicidality  and substance abuse . Beyond the comparative impacts of early developmental environment [7▪], recent findings suggest a role of prominent adversities in early adolescence [2▪,4]. A myriad of changes occurring during puberty perhaps heighten risk for difficulties coping with adversity and set the child on a pathway to personality change. These higher rates of BPD symptoms appear to remain relatively stable across mid-to-late adolescence , but later years see a reduction in prevalence. Assessing BPD symptoms across four age cohorts in a community sample, Arens et al. [13▪▪] demonstrated a sharp decrease in symptomatology between adolescence and young adulthood. From young adulthood, rates of BPD were maintained at lower rates for middle-aged and older-aged adults. Thus, not only is there a window of vulnerability during puberty, wherein exposure to adversity of trauma is associated with BPD symptom development, but adolescence also appears to be a period of heightened symptom expression.
To assess the course of symptoms throughout the life-span, a number of innovative prospective follow-up studies have examined BPD categorical diagnosis and dimensional symptom levels. Most suggest that BPD symptoms decline with age [14,15]. Two prospective studies demonstrated high rates of remission or reduction in symptoms over time for people with BPD in the sample, yet both also found that former patients continued to experience social and vocational functioning impairment despite remission in borderline symptoms. This reduction in BPD symptoms was shown to be consistent for categorical diagnoses as well as subsyndromal phenomenology of BPD [13▪▪]. Arens et al. [13▪▪] argued that impulsivity-type symptoms associated with BPD – suicidality, impulsive acts, self-harm – develop during adolescence and are more likely to reduce in frequency and severity over time [16,17]. A second factor composed of affective-type symptoms – dysphoria, feelings of emptiness, negative affect – represents the more chronic features of BPD and is likely to persist throughout the life-course [13▪▪]. Arens’ finding that impulsivity symptoms reduced at a sharp decline between adolescence and young adulthood, whereas affective symptoms increased with age, suggests that the pattern of symptoms characterizing BPD may change throughout the life-course. It appears that adolescence is marked by heightened vulnerability, increased rates of BPD symptoms overall, and impulsivity-type behaviors in particular, which reduce quickly over time. In contrast, from young adulthood onward, BPD symptoms are more likely to reflect depressive symptomatology, which increases with age and may result in the ongoing social and functional impairments characteristic of long-term BPD.
Answers to whether these symptoms are a result of heritability factors or environmental cues will provide important insights for intervention. An investigation of heritability and shared environment in participants from the ongoing Minnesota Twin Family Study suggested that genetic factors exerted increasing influence on BPD traits from middle to late adolescence (14–18 years) . In contrast, as the participants aged, the influence of shared environment factors such as socio-economic status, the parent–child relationship, and peer group influence, dropped to almost zero. The stability of BPD traits across the time period was largely influenced by a combination of genetic and nonshared environmental factors. As adolescents play a more active role in the selection of their environment and relationships, these factors may interact with their genetic heritability and exert influence over behavior.
Adolescence is marked by rapid changes in physiology and environment . A critical window for neural development, changes occurring in puberty affect one's abilities in core domains such as emotion regulation and decision-making . In addition, there are steep increases in responsibilities and challenging social and cognitive requirements in this period that require a sophisticated psychological skill set. Brain maturation and the reorganization of neurocircuitry that occurs in adolescence are mirrored by behavioral and personality changes. Difficulties with emotion regulation among people with BPD have been linked to a dysfunctional fronto-limbic network . Emotion regulation has, thus, been associated with a network of neural regions consisted of the amygdala, hippocampus, and prefrontal cortex and prior neuroimaging studies have indicated structural and functional abnormalities in these three areas [20,21]. However, the strong comorbidity between BPD and PTSD  clouds these findings. Smaller hippocampal and amygdala volumes have frequently been found in both BPD  and PTSD  samples, although results are variable. Seeking to distinguish the neural correlates of BPD alone, Bruehl et al.  identified increased cortical thickness in the right rostral middle frontal cortex, part of the dorsolateral prefrontal cortex in patients with BPD, but not in those with comorbid PTSD or controls. Further, and contrary to expectation, this increased thickness was associated with enhanced emotional regulation skills. Amygdala volume and thickness of the insula in those with BPD without PTSD were associated with cortical thickness of the dorsolateral prefrontal cortex, which supports the anatomical basis for fronto-limbic and fronto-insular circuitry for emotional regulation in BPD. Bruehl et al.  suggest that the thickening is due to an adaptive response that protects BPD patients and is hampered by comorbid PTSD conditions. This adaptive response accounts for the increased abilities in emotion regulation, traditionally thought to characterize BPD.
TREATMENT AND OUTCOMES
Impulsivity, suicidality, and nonsuicidal self-harm frequently associated with BPD diagnosis require a highly intensive treatment with careful monitoring of risk. Accordingly, treatment for BPD is expensive and evidence-based interventions for patients with BPD and a history of trauma are rare [25▪▪]. It is well established that adults with BPD utilize mental health services and medications at a higher rate than those with major depressive disorders or other personality disorders [26–28]. Similarly, adolescents diagnosed with BPD report high frequencies of mental health services use across both outpatient and inpatient services. Eighty-five adolescents participating in the European Research Network on Borderline Personality Disorder (EURNET-BPD; ) were assessed and among these, 87% were currently seeing a professional weekly [30▪]. Those receiving psychotherapy were significantly older and more likely to be female, but there were no significant differences in psychopathology between those in psychotherapy and those not. Further, no differences were found for a history of trauma, current impulsivity, and emotion regulation in psychotherapy use. Most adolescents with BPD reported medication use (85%), with the most commonly prescribed medications being phenothiazine antipsychotics, benzodiazepine, and selective serotonin re-uptake inhibitors (SSRIs). The high use of mental health services in this group purports to a clinical continuum between adolescence and adulthood.
The evidence base for BPD treatments suitable for use with adolescents is in its nascence. Even among adults, little evidence exists for effective treatments that address both traumatic stress and comorbid BPD. However, a recent randomized controlled trial evaluating the effectiveness of the newly developed dialectical behavior therapy for women with BPD and a history of childhood sexual abuse (DBT-PTSD) demonstrated significantly improved outcomes in posttraumatic stress symptoms with large effect sizes and no increase in harm or risk behaviors [25▪▪]. DBT-PTSD is an intensive 12-week inpatient program, that utilizes psychoeducation, mindfulness, skills training, and skills-assisted exposure, to actively treat PTSD for women with comorbid BPD. This study is the first to demonstrate the effective use of a treatment for PTSD among women who report current suicidality and self-harm with severe BPD traits [25▪▪], features that were traditionally thought to be too volatile for exposure therapy. Extension of the treatment to adolescents with complex trauma and BPD will be an important next step, with potential to reduce the impact of adult functional impairment.
Prior research in the field has been hampered by the use of cross-sectional designs, retrospective reports, and patient-only samples to explain the relationship between early life trauma and personality development. The recent publication of studies utilizing longitudinal and prospective follow-up designs and representative community samples represents a significant move forward. A longer-term focus will establish whether traits evident in childhood and adolescence are maintained in early and later adulthood. Similarly, the development and evaluation of treatment models are critically needed. Although emerging evidence suggests that DBT-PTSD is effective in treating PTSD with comorbid BPD, the extension of this treatment to adolescent samples will provide important clinical findings.
The tools used to assess BPD diagnosis and symptoms vary across the literature. It is important that future research builds on the best methods available for examining BPD in an adolescent sample to enable rigorous comparison across studies and age groups. Further, the overwhelming majority of research on trauma and BPD has been conducted in high-income settings. Despite the clear role of childhood adversity and early exposure to trauma, there is a severe lack of information on those affected by chronic childhood traumas, such as war, displacement, and disaster. A vast number of children and adolescents are affected by severe and chronic trauma, and those living in adverse conditions are at heightened risk of political conflict, violence, and disaster. Investigation into cultural expression of personality traits and the role of trauma exposure in low-income and middle-income countries will inform future research and valid treatment models. Accordingly, recent findings in BPD symptoms, risk factors, and neurological impact have built a foundation from which future research may investigate optimal treatment models, clinical implications, and cross-cultural validity for BPD among adolescents living in settings of adversity.
The first author is supported by an Early Career Fellowship from the National Health and Medical Research Council of Australia.
Conflicts of interest
There are no conflicts of interest.
REFERENCES AND RECOMMENDED READING
Papers of particular interest, published within the annual period of review, have been highlighted as:
▪ of special interest
▪▪ of outstanding interest
1. Carneiro P, Crawford C, Goodman A. The impact of early cognitive and non-cognitive skills on later outcomes. London:Centre for the Economics of Education, London School of Economics; 2007.
2▪. Pietrek C, Elbert T, Weierstall R, et al. Childhood adversities in relation to psychiatric disorders. Psychiatr Res 2013; 206:103–110.
This study compared specific childhood adversities and their effects for participants with major depressive disorder, BPD, and schizophrenia, as well as a psychiatrically healthy comparison group.
3. Allen B, Cramer R, Harris P, Rufino K. Borderline personality symptomatology as a mediator of the link between child maltreatment and adult suicide potential. Arch Suicide Res 2013; 17:41–51.
4. Amstadter A, Aggen S, Knudsen G, et al. Potentially traumatic event exposure, posttraumatic stress disorder, and Axis I and II comorbidity in a population-based study of Norwegian young adults. Soc Psychiatry Psychiatr Epidemiol 2013; 48:215–223.
5. Bowlby J. A secure base: parent–child attachment and healthy human development. New York:Basic Books; 1988.
6. Linehan M. Cognitive behavioral treatment for borderline personality disorder: theory and method. New York:Guilford Press; 1993.
7▪. Winsper C, Zanarini M, Wolke D. Prospective study of family adversity and maladaptive parenting in childhood and borderline personality disorder symptoms in a nonclinical population at 11 years. Psychol Med 2012; 42:2405–2420.
In a prospective longitudinal study of 6050 mothers and children that examined family adversity in early childhood, a significant association was found between suboptimal parenting and borderline personality symptoms at 11 years of age, partially moderated by Diagnostic and Statistical Manual, Fourth Edition (DSM-IV) diagnoses and IQ at 7–8 years.
8. Entringer S, Kumsta R, Hellhammer D, et al. Prenatal exposure to maternal psychosocial stress and HPA axis regulation in young adults. Horm Behav 2009; 55:292–298.
9. Bornovalova M, Hicks B, Iacono W, McGue M. Longitudinal twin study of borderline personality disorder traits and substance use in adolescence: developmental change, reciprocal effects, and genetic and environmental influences. Peronal Disord 2013; 4:23–32.
10. Layne C, Olsen J, Baker A, et al. Unpacking trauma exposure risk factors and differential pathways of influence: predicting postwar mental distress in Bosnian adolescents. Child Dev 2010; 81:1053–1076.
11. Battle C, Shea T, Johnson D, et al. Childhood maltreatment associated with adult personality disorders: findings from the Collaborative Longitudinal Personality Disorders Study. J Pers Disord 2004; 18:193–211.
12. Lobbestael J, Arntz A, Bernstein D. Disentangling the relationship between different types of childhood maltreatment and personality disorders. J Pers Disord 2010; 24:285–295.
13▪▪. Arens E, Stopsack M, Spitzer C, et al. Borderline personality disorder in four different age groups: a cross-sectional study of community residents in Germany. J Pers Disord 2013; 27:196–207.
This study investigated prevalence of BPD, impulsivity, and depressive symptoms in four nonclinical cohorts spanning adolescence to late adulthood (N = 2488) to assess the course of borderline personality symptoms.
14. Zanarini M, Frankenburg F, Reich D, Fitzmaurice G. Time to attainment of recovery from borderline personality disorder and stability of recovery: a 10-year prospective follow-up study. Am J Psychiatry 2010; 167:663–667.
15. Gunderson JG, Stout R, McGlashan T, et al. Ten year course of borderline personality disorder: psychopathology and function from the Collaborative Longitudinal Personality Disorders Study. Arch Gen Psychiatry 2011; 68:827–837.
16. Stevenson J, Meares R, Comerford A. Diminshed impulsivity in older patients with borderline personality disorder. Am J Psychiatry 2003; 160:165–166.
17. Meares R, Gerull F, Stevenson J, Korner A. Is self-disturbance the core of borderline personality disorder? An outcome study of borderline personality factors. Aust NZ J Psychiatry 2011; 45:214–222.
18. Steinberg L. Risk taking in adolescence. Curr Dir Psychol Sci 2007; 16:55–59.
19. Bruehl H, Preibler S, Heuser I, et al. Increased prefrontal cortical thickness is associated with enhance abilities to regulate emotions in PTSD-free women with borderline personality disorder. PLoS One 2013; 8:e65584.
20. Hayes J, Morey R, Petty C, et al. Staying cool when things get hot: emotion regulation modulates neural mechanisms of memory encoding. Front Hum Neurosci 2010; 4:230.
21. Ochsner K, Bunge S, Gross J, Gabrieli J. Rethinking feelings: an fMRI study of the cognitive regulation of emotion. Neuroimage 2002; 23:483–499.
22. Zanarini M, Frankenburg F, Dubo E, et al. Axis I comorbidity of borderline personality disorder. Am J Psychiatry 1998; 155:1733–1739.
23. Nunes P, Wenzel A, Borges K, et al. Volumes of the hippocampus and amygdala in patients with borderline personality disorder: a meta-analysis. J Pers Disord 2009; 23:333–345.
24. Karl A, Schaefer M, Malta L, et al. A meta-analysis of structural brain abnormalities in PTSD. Neurosci Biobehav Res 2006; 30:1004–1031.
25▪▪. Bohus M, Dyer A, Priebe K, et al. Dialectical behaviour therapy for posttraumatic stress disorder after childhood sexual abuse in patients with and without borderline personality disorder: a randomized controlled trial. Psychother Psychosom 2013; 82:221–233.
A randomized controlled trial of the newly developed dialectical behavior therapy for women with childhood sexual abuse related-PTSD with co-occurring BPD demonstrated early evidence of effectiveness.
26. Bender D, Skodol A, Pagano M, et al. Prospective assessment of treatment use by patients with personality disorders. Psychiatr Serv 2006; 57:254–257.
27. Bender D, Dolan R, Skodol A, et al. Treatment utilization by patients with personality disorders. Am J Psychiatry 2001; 158:295–302.
28. Comtois K, Russo J, Snowden M, et al. Factors associated with high use of public mental health services by persons with borderline personality disorder. Psychiatr Serv 2003; 54:1149–1154.
29. Corcos M, Pham-Scottez A, Speranza M. European Research Network on Borderline Personality Disorder (EURNET-BPD). American Academy of Child & Adolescent Psychiatry, 57th Annual Meeting 2010.
30▪. Cailhol L, Jeannot M, Rodgers R, et al. Borderline personality disorder and mental healthcare service use among adolescents. J Pers Disord 2013; 27:252–259.
An examination of lifetime mental health service utilization among 85 adolescents participating in the European Research Network on Borderline Personality Disorder study. The authors describe high rates of medication use and psychotherapy engagement.
adolescence; borderline personality disorder; trauma
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