Borderline Personality Disorder in Young People and

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Borderline Personality Disorder in Young People and the Prospects for Prevention and Early Intervention Andrew M. Chanen*,1,2 , Martina Jovev1, Louise K. McCutcheon1,2, Henry J. Jackson1,3 and 1,2 Patrick D. McGorry 1

ORYGEN Research Centre, Department of Psychiatry, University of Melbourne, Australia

2

ORYGEN Youth Health, Melbourne Health, Australia

3

School of Behavioural Sciences, University of Melbourne, Australia Abstract: Borderline personality disorder (BPD) is associated with substantial psychosocial impairment, morbidity, mortality and high health resource utilization. These data make a compelling case for developing prevention and early intervention strategies for BPD. This review examines the BPD diagnosis in young people, along with prospective risk factors for and precursors to the development of BPD. It then considers the prospects for and potential risks and benefits associated with prevention and early intervention for BPD. It concludes that the BPD diagnosis in young people has similar reliability, validity and prevalence to BPD in adults and that BPD in young people almost certainly has serious and pervasive negative repercussions over subsequent decades. Current data are inadequate to inform specific universal or selective prevention programs for BPD. However, they do support including BPD prevention as an outcome when evaluating universal and/or selective interventions for a variety of mental health problems and adverse psychosocial outcomes. The data are stronger for developing indicated preventive interventions but the strongest data support early intervention for the emerging BPD phenotype. Early intervention programs will need to be realistic in their aims, require change in clinician attitudes and service systems and must be mindful of the risk of iatrogenic harm.

Keywords: Borderline personality disorder, prevention, early intervention, adolescence, youth, young people. INTRODUCTION Borderline personality disorder (BPD) is characterized by a pervasive pattern of instability in affect regulation, impulse control, interpersonal relationships and self-image [1]. BPD occurs in 0.7% [2] to 1.4% [3] of the general adult population and it is the most common and the most serious of the personality disorders (PDs) in clinical practice [4]. The outcome for BPD in adulthood, while symptomatically better than expected [5-7], points toward severe and continuing disability across a broad range of functional domains [8-10], high usage of mental health resources [11-13], and high morbidity [13] and mortality [14]. These data make a compelling case for the development of empirically-tested prevention and early intervention approaches. For the purposes of this paper, we use the following World Health Organization (WHO) definitions [15]. Adolescents are aged 10 to 19 years, youth are aged 15 to 24 years and young people covers the entire age range (10 to 24 years). RATIONALE FOR PREVENTION AND EARLY INTERVENTION Diagnosing BPD in Adolescence Diagnosing PDs prior to age eighteen years has often aroused controversy [16,17]. Clinicians are frequently reluct*Address correspondence to this author at the ORYGEN Research Centre, Locked Bag 10, Parkville, Victoria, Australia 3052; Tel: +613 9342 2800; Fax: +613 9387 3003; E-mail: [email protected] 1573-4005/08 $55.00+.00

ant to do so and the DSM-IV [18], ICD-10 [19] and official practice guidelines [20] all advocate caution. The practice is also made more difficult by the lack of developmentally appropriate PD criteria or illustrations of current PD criteria in DSM-IV or ICD-10. There are also controversies among researchers regarding the borderline construct. These are beyond the scope of this paper. However, the interface between BPD and bipolar disorder or the more broadly defined bipolar spectrum [21, 22] warrants acknowledgement. In children and adolescents, the bipolar spectrum is a broadly defined phenotype, characterized by severe irritability, “affective storms”, mood lability, severe temper outbursts, symptoms of depression, anxiety, hyperactivity, poor concentration and impulsivity, with or without clear periodicity [23]. This definition has considerable phenomenological overlap with BPD but will not be a focus of this paper. Despite this, it is increasingly evident that personality pathology is a major form of psychopathology in adolescence [24-27]. Evidence supports the application of BPD (and other PD) diagnostic criteria prior to age 18 years [2730]. BPD in adolescence also has similar structure [31], phenomenology, etiology and rates of adverse childhood experiences compared to adult BPD [32], along with good concurrent validity [27, 33] and similar stability to adult BPD [34, 35]. BPD criteria also have adequate internal consistency [36]. Importantly, BPD in adolescence is associated with serious morbidity [26, 27, 29, 33] and there is evidence at the Cluster B PD level that this appears to persist for decades [37, 38]. © 2008 Bentham Science Publishers Ltd.

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Viewed from a different perspective, retrospective studies of adult inpatients [12] and outpatients [39] with BPD have found their mean age of first psychiatric contact to be 18 years (SD=6) and 17 years (SD not reported), respectively, suggesting that this group do seek treatment, even if the diagnosis of BPD is made infrequently. Is BPD a Disorder of Young People? Recent data on the point prevalence of PDs (including BPD) and their stability over time have challenged conventional assumptions about these disorders. The data available suggest that BPD is primarily a disorder of young people. Epidemiology There are few epidemiological studies of the prevalence of PDs in young people and none using representative national samples. Prevalence estimates for ‘severe’ BPD in community-dwelling teenagers in the USA range from 0.9% in the Oregon Adolescent Depression Project [40] to 3% [29] in the Children in the Community study, similar to adult rates of BPD [2, 3]. However, the rate rises to 10.8% in the Children in the Community if ‘moderate’ cases (lower symptom thresholds) are also included, reaching a peak between ages 11-14 years. Chabrol and colleagues [41] used the combination of a self-report screening instrument and the revised Diagnostic Interview for Borderlines [42] to estimate the prevalence of BPD in a sample of French high school students to be 14% – with the frequency reaching peaks at around 14 years and again in late adolescence. Finally, Moran and colleagues [43] estimated the prevalence of ICD 10 BPD in a representative sample from the state of Victoria, Australia (mean age 24 years) to be 3.5%. These data suggest that the rates of BPD phenomenology are at least as high, if not substantially higher, in young people than in adulthood but better designed epidemiological studies are required. Stability and Change By definition, personality traits have been thought to represent stable and enduring individual differences. However, over the past decade, a large body of data has accumulated supporting both continuity and change in ‘normal’ personality development up to and even beyond the first 50 years of life [44]. PDs include both acute, dysfunctional behaviors that resolve over a relatively short time frame and maladaptive temperamental traits that are relatively stable, similar to ‘normal’ personality traits [45]. By contrast, specific data on the stability of BPD in young people are sparse and often only available for Cluster B PD, rather than BPD. It appears that mean levels of BPD traits are highest in early adolescence and display moderate to high stability across the period of youth in both clinical [34] and community samples [35, 46, 47]. From this peak, they are followed by decline [47, 48] that appears to be linear [47] at least until the late 20s. Cross-sectional epidemiological studies in older samples suggest further decline with each decade, at least from the mid-30s [49] and in the National Comorbidity Survey Replication [3], age was inversely related to Cluster B PD. Rank order stability (does the person retain their rank order in the group) is also mod-

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erate to high in both clinical [34] and community samples [35, 46, 47]. It might be argued that because the natural history of BPD traits in adolescence is toward resolution, intervention is unwarranted. However, diagnostic instability does not imply ‘recovery’ [50] and the research suggests that, although mean levels of these traits decline, they cause severe impairment and disability, even in the short-term and are harbingers of prolonged psychosocial disruption [37, 38]. Psychosocial Functioning of Young People with BPD Most studies have tended to focus upon the global PD construct and specific studies of young people with BPD are sparse. The Children in the Community Study found that 1121 year-olds with BPD had the broadest range of functional impairment of all PDs, including school or work problems, psychopathology and antisocial behavior [29]. Studying a clinical sample (50% with BPD) the Yale Adolescent Follow-up Study [27] found that 12-18 year-old inpatients with PDs had significantly more functional impairment and psychopathology than those without PDs. In a cross-sectional study of 177 psychiatric outpatients aged 15-18 years, Chanen and colleagues [33] found that the BPD diagnosis during adolescence defines a group of patients with the highest levels of psychopathology and the most severe psychosocial dysfunction (a pattern similar to that found in studies of adults with BPD), compared to those with other PDs or no PD. Moreover, BPD was a significant predictor over and above axis I disorders and other PD diagnoses for psychopathology, general functioning, peer relationships, self-care and family and relationship functioning, indicating that BPD in adolescence is not reducible to axis I diagnoses. Longitudinal Outcome of BPD in Youth Since the emergence of personality problems is usually in adolescence or early adulthood, the potential for ensuing developmental disruption is high, even if the clinical features subsequently attenuate [10]. Wide-ranging prospective data from the Children in the Community Study suggest that elevated PD symptoms in adolescence have negative repercussions over the subsequent 10 to 20 years and that these repercussions are at least as serious or pervasive as those associated with axis I disorders [37, 38]. Children in the Community data for specific PDs are more limited, due to the low prevalence of individual PDs in this sample. BPD symptoms in adolescence are associated with increased risk for Axis I disorders, especially mood disorders, during early adulthood after controlling for cooccurring Axis I disorders during adolescence [26]. Also, elevated BPD symptoms in adolescence were an independent risk factor for substance use disorders during early adulthood [51]. These findings have received some support from other clinical and community-based follow-up studies [27, 52]. Adults with BPD typically experience many of their greatest difficulties in social and intimate relationships, even more so than people with other types of PDs [8, 53]. Similarly, when compared to their healthy peers, adolescents with BPD have been found to have less enduring friendships, low enjoyment of others, lack of any confidant or romantic partner and few social activities [29]. Undergraduates with

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greater BPD features also report more interpersonal problems and distress than their peers [54] and when followed-up over the subsequent 2 years, are more likely than their peers to experience interpersonal dysfunction and to have academic difficulties [55]. BPD symptoms in young women (mean age 18 years) have also been found to predict 4-year romantic dysfunction (chronic stress, conflicts, partner dissatisfaction, abuse and unwanted pregnancy), although the associations were not unique to BPD [56]. In the transition to adulthood (17 to 27 years), BPD symptoms have been found to be independently associated with sustained elevations in partner conflict [57] and BPD symptoms at age 22 years are independently associated with significant reductions in quality of life 11 years later [58]. In summary, elevated BPD symptoms in adolescence almost certainly have serious and pervasive negative repercussions over subsequent decades. Elevated BPD symptoms are prospectively associated with increased risk for axis I disorders (especially substance use and mood disorders), interpersonal problems and distress and reduced quality of life. Neurobiology of BPD in Young People Recent progress in developmental neuroscience has highlighted the substantial neurobiological changes that occur during adolescence and their links to behavioral and emotional problems [59-61]. It is widely theorized that emotion dysregulation is a core feature of BPD [62, 63] and structural and functional imaging studies in adult samples with BPD have implicated simultaneous dysfunction of frontal and limbic structures and circuits [64]. However, it is unclear whether these findings are associated with a vulnerability to BPD itself, severity or duration of BPD, treatment or with other factors, such as cumulative traumatic events, associated lifestyle factors or the co-occurrence or duration of common mental disorders [65]. Studying BPD during adolescence and young adulthood affords a unique window into the neurobiology of BPD by minimizing the impact of such ‘duration of illness’ effects upon the neurobiology of the disorder [65]. However, few studies exist. Houston and colleagues [66] found that 14-19 year-old females with BPD features did not exhibit the normal agerelated reduction in visual p300 amplitude, suggesting a pattern of abnormal brain maturation consistent with findings in samples of adults with BPD [67-69]. They also report that the maturation of right frontal brain regions was specifically affected in the adolescent BPD group, although this finding might be task-dependent. In support of this, the only magnetic resonance imaging study of adolescents with first-presentation BPD [65] found right-sided OFC grey matter volume loss compared to healthy control participants. However, they did not find significant differences for amygdala or hippocampal volumes. The authors conjectured that either the latter might only become apparent as the condition progresses or that those with smaller amygdala and hippocampal volumes are more likely to develop a chronic course. Adolescents with BPD have been found to have greater levels of perceived emotional dyscontrol than healthy control participants [70, 71] and the degree of dyscontrol is greatest

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for those with full-syndrome BPD, compared to subsyndromal BPD [70]. However, on facial affect and affective prosody recognition tasks [70], no between-groups differences were found, suggesting that these aspects of affect recognition might not be impaired in early BPD. Similarly, self-report and psychophysiological data collected while viewing emotional images in 15-24 year-olds with firstpresentation BPD did not provide evidence that the BPD participants reacted with more intense affective responses to affective stimuli than healthy control participants [71]. In fact, the BPD participants had significantly lower skin conductance responses, similar to adults with BPD [72] and showed an absence of the fear potentiated startle response during early picture processing, suggesting a state of underarousal. On an emotion regulation task, both BPD and healthy control participants showed similar startle responses when instructed to “maintain” or “suppress” their emotions. The authors conclude that, early in the course of the disorder, people with BPD demonstrate marked abnormalities in the processing of and response to affective stimuli but these appear to be related to inhibited reactivity during early processing of aversive stimuli. Garner and colleagues [73] examined pituitary gland volume in the same first-presentation BPD sample as Chanen and colleagues [65], above. They found no difference in pituitary gland volume between healthy controls and the total BPD cohort. However, within the BPD cohort, those exposed to childhood trauma tended to have smaller pituitaries. These preliminary findings suggest that exposure to childhood trauma, rather than BPD per se, might be associated with reduced pituitary gland volume, possibly reflecting hypothalamic-pituitary-adrenal axis dysfunction. This literature is rudimentary and the findings are mixed. It is still unclear whether the abnormalities described represent developmental abnormalities, consequences of the disorder itself or epiphenomena. The significance of these data for prevention and early intervention is perhaps limited to the observation that the data do not appear to suggest fixed deficits from childhood or earlier and that there might be some degree of plasticity at later developmental stages. Specialized Interventions Given the scope of the BPD problem, the emerging controlled trial literature for BPD is disproportionately small (for recent reviews see [1, 74-76]). The evidence base for pharmacotherapeutic interventions is particularly scant [1, 76]. Psychosocial intervention is currently the standard for established BPD [20] and although the gains made are mostly modest [74, 77] and universally suboptimal [1], they have begun to counteract much of the therapeutic nihilism that previously pervaded the BPD field. Several psychosocial interventions are under evaluation and more recent randomized controlled trial (RCT) data from well-designed, ‘second generation’ studies suggest good outcomes [78-80] for specialized interventions but effectiveness data are lacking. Nevertheless, it seems reasonable to conclude that effective intervention in BPD is possible and that interventions currently used in adult BPD might be successfully adapted or new ones developed for use in prevention and early intervention programs.

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Interventions for Young People The intervention literature for BPD traits and firstepisode BPD in young people is largely uninformative. To our knowledge, there are only two intervention studies in adolescents with features of BPD [81, 82] and no published RCTs addressing prevention or early intervention for BPD. An 8-week open-label trial of flupenthixol 3mg/day in 13 outpatients (11 female; mean age 17.2 years, range 14-22 years) with DSM-III-R BPD reported significant reductions in levels of impulsivity, depression, global psychopathology and significant improvement in global functioning in the 11 participants who completed the study [81]. However, absence of an RCT design and the use of an uncommon agent limit any further conclusions. A quasi-experimental study [82] assigned 29 adolescents (mean age 16.1years, SD = 1.2) with BPD features and demonstrating the “greatest need” to a modified 12-week version of Dialectical Behavior Therapy (DBT) and 82 participants (mean age 15.0 years, SD = 1.7) to treatment as usual (TAU), comprising 12 weeks of twice-weekly individual and family sessions. The DBT group had a higher rate of treatment completion but there were no significant differences in the number of suicide attempts made during treatment. PROSPECTS FOR PREVENTION AND EARLY INTERVENTION FOR BPD The idea of prevention for PDs is not new, as there exists a more advanced but independent prevention and early intervention literature for antisocial PD [83]. There have been calls for preventive interventions for BPD [1, 84] but prevention cannot occur until risk factors and developmental mechanisms have been well understood [85, 86]. Lenzenweger and Cicchetti [86] have outlined a developmental psychopathology approach to BPD with one of its aims being to inform prevention of the disorder. One problem appears to be that the term ‘prevention’ is used imprecisely in BPD. It often signifies either narrowlyfocused tertiary prevention (usually of suicidal behaviors [87, 88]) or the perhaps overwhelming task of primary prevention of BPD. Progress requires clearer specification about whether prevention refers to the timing in relation to the course of the disorder (primary, secondary or tertiary prevention) or whether it refers to the target population for intervention [89]. The latter approach restricts the term ‘prevention’ to those interventions occurring before the onset of a disorder [90] and is less concerned about whether the threshold has been reached for a case of a mental disorder. The target population approach includes a spectrum of preventive interventions ranging from universal (targeting whole population groups) through selective (targeting individuals or population subgroups at higher than average risk) to indicated preventive interventions (targeting high-risk individuals with minimal but detectable signs or symptoms that foreshadow mental disorder). In this context, early intervention is seen as early case identification and treatment, rather than prevention per se. A particular advantage of the target population approach is that it is not specifically concerned with the etiology of disorders, as complete elucidation of causal mechanisms is unnecessary for prevention. The main requirement is to identify risk factors for persis-


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tence or deterioration of problems, rather than the ‘onset’ or incidence of disorder per se. Universal and Selective Prevention for BPD There is evidence that childhood abuse or neglect, maladaptive parenting and maladaptive school experiences are risk factors for both adolescent and adult PD [37]. The data on true causal risk factors for BPD (i.e. prospectively assessed factors that precede the emergence of the BPD phenotype [90]) are meager [50]. Genetics The details of studies of the genetics of BPD and the traits underlying BPD are beyond the scope of this paper and are reviewed elsewhere [e.g. 91]. For the purpose of this paper, it is important to note that although temperamental factors might increase vulnerability to developing BPD, they are neither innately pathological nor sufficient to predict the development of BPD [92]. Prospective Risk Factors Many studies have focused upon childhood adversity and have used retrospective reports that are prone to recall biases [93]. Moreover, putative risk factors, such as childhood abuse, adverse familial environment and a family history of psychopathology are inter-correlated [94] and require disentangling. Severe childhood abuse, especially childhood sexual abuse, is common in BPD [95-97]. However, the role of childhood sexual abuse in the etiology of specific disorders, such as BPD, remains controversial, as it is neither necessary nor sufficient for the development of BPD [96, 98, 99]. Fossati and colleagues [100] estimated the common effect size for the association between childhood sexual abuse and BPD across 21 studies (comprising 2479 participants) to be r=0.279 and suggested that childhood sexual abuse is not a major psychological risk factor or causal antecedent for BPD. The only prospective studies of risk factors for symptoms of specific PDs, including BPD, come from the Children in the Community study. These include childhood abuse or neglect [99], maternal inconsistency in the presence of high maternal over-involvement [101], aversive parental behavior and low parental affection or nurturing [102]. Findings regarding specific PDs during earlier phases of the Children in the Community study require cautious interpretation because of their use of a non-standard PD assessment with somewhat low reliability and low frequencies of case-level PDs. These data are insufficient to adequately inform or justify large-scale universal or selective interventions specifically directed toward BPD. It is also challenging to translate these findings into practical targets and realistic interventions. Many risk factors are fixed exposures or even if they are variable risk factors, they are not easily amenable to change, requiring major social policy and economic changes that have a long timetable for implementation, if they are to occur at all. Also, not only are these risk factors associated with diverse outcomes other than BPD (the principle of multifinality [103]) but also the vast majority of those exposed to these risk factors, such as early trauma, do not develop psychopathology, let alone BPD [37, 98]. From this perspective, BPD is in fact a comparatively rare outcome. Finally, studies


demonstrating any benefit from universal prevention are also likely to be difficult to mount, as the number of participants required amounts to tens of thousands at least [104]. Selective prevention is more feasible but still requires large numbers of participants. Further carefully designed prospective studies of community and ‘at risk’ samples are required [50, 86] to define risk factors, pathways and mechanisms for the development of PDs, especially BPD and to describe feasible low impact and low cost interventions that might be studied. Until then, specific universal or selective prevention of BPD appears to be unrealistic. At What Point Should Intervention Specifically Target BPD? – Indicated Prevention and Early Intervention Even if broad-based universal or selective preventive interventions were to prove successful in the future, it is unlikely that any one level of prevention or any single intervention will adequately cater to the breadth and depth of the problem. Indicated prevention and early intervention could act as complementary preventive steps and with our current level of knowledge, might represent the best starting point toward developing a comprehensive prevention and early intervention strategy for BPD. Precursor Signs and Symptoms There are few signs and symptoms that predict the onset of any mental disorders with certainty [89]. It is technically imprecise to refer to the signs and symptoms from a diagnostic cluster that precede disorder but do not predict its onset with certainty as ‘risk factors’ [105], hence Eaton’s use of the term precursor signs and symptoms [89]. Disruptive behavior disorders in childhood [106, 107] or adolescence [37, 108], along with depressive symptoms [37, 40, 108] are all predictors of young adult PD. Substance use disorders during adolescence, particularly alcohol use disorders, have also been found to specifically predict young adult BPD [109, 110]. Only the Children in the Community have measured childhood or adolescent PD as a predictor of later PD. They found that PD symptoms in childhood or adolescence were the strongest long-term predictors of later PD, over and above disruptive behavior disorders and depressive symptoms [24, 37, 106, 111], although the predictions of risk are at the DSM-IV cluster level, not for individual PDs. Within this sample, a diagnosis of BPD at mean age of approximately 14 years conferred a risk ratio of 13.1 for receiving the diagnosis two years later [29]. Also, between ages 22 and 33 years, individuals at the highest end of the BPD distribution became more deviant relative to their age peers [112], perhaps representing the emerging group that conforms to descriptions of ‘adult’ BPD. These data suggest that those with elevated BPD traits in adolescence are an important group, possibly the most important group, from which adult BPD arises. However, this is unlikely to represent the only pathway to BPD [50, 86]. Targeting groups with these precursor signs and symptoms (indicated prevention) appears feasible. These data improve our capacity to focus upon clinically relevant syndromes but still not specifically upon BPD. This begs the question as to when BPD (measured dimensionally or cate-

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gorically) or the traits underlying BPD might warrant specific or specialized intervention. Paris [50] has suggested that the precursors to BPD are sub-clinical during childhood and that it is developmental increases in impulsivity associated with puberty that bring the problems associated with BPD into the clinical realm. This is supported by evidence that young people displaying BPD traits form the major group from which the young adult BPD phenotype arises [112] and that members of this group access clinical services early in the course of their disorder, even if it is infrequently recognized [12, 33, 39]. These data, combined with the strong data (above) that BPD traits in young people are no less valid or reliable than they are in adulthood and are prospectively associated with diverse functional and psychopathological poor outcomes, mean that the ‘best bet’ for immediate action appears to be early intervention for first presentation BPD traits or disorder. Similar to early intervention for first-episode psychosis, early intervention for BPD targets the diverse poor outcomes associated with BPD traits or disorder, rather than narrowly focusing upon the ‘late-stage’ DSM-IV BPD syndrome [113], as progression to symptomatically chronic BPD is uncommon [5, 6]. Successful indicated prevention and early intervention flows from a solid and high quality clinical program for the disorder in question and is arguably a prerequisite for this to occur. Indicated prevention and early intervention have been successfully applied at the Early Psychosis Prevention and Intervention Centre (EPPIC) at ORYGEN Youth Health [114-116] and have more recently begun to be applied to BPD. Chanen and colleagues1 have developed an intervention specifically for young people with BPD traits or firstpresentation BPD, based upon Cognitive Analytic Therapy (CAT [117]) and compared this with manual-based good clinical care in a randomized controlled trial in 86 15 to 18 year-old participants with two or more current DSM-IV BPD traits. Both interventions were delivered within a wellcharacterized service model and compared to a historical control group who received treatment as usual. Unpublished data from this trial indicate that CAT is an effective, timelimited early intervention for BPD and is more effective than good clinical care for the treatment of externalizing pathology or treatment as usual for the treatment of internalizing and externalizing pathology. Risks and Benefits of Prevention and Early Intervention Prevention and early intervention for BPD holds great promise but also has the potential to be undermined by unrealistic expectations. Possible aims, based upon the above data, include the reduction of borderline and/or general psychopathology, improvement of psychosocial functioning and reduced risks for axis I disorders, violence, offending behavior, suicide and self-harm and interpersonal conflict. Primary prevention of secondary disorder [118], such as substance use disorders, is a particularly appealing and pragmatic aim. Another might be the reduction of health service utilization,

1 Chanen AM, Jackson HJ, McCutcheon L, et al. Early intervention for adolescents with borderline personality disorder traits: a randomized controlled trial. Xth International ISSPD congress. The Hague, The Netherlands; 2007.

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iatrogenic complications [119] and the diversion of those with BPD from their malignant dependency upon the health system. However, “getting rid of them” must not be the aim. Indeed, this all too common attitude and the defensive practices [120] of many clinicians must be challenged. In fact, it might be important to assist those with BPD to use the health system more appropriately, given their high rates of psychiatric and medical comorbidity [13, 33]. There is evidence that training can effect change in clinician attitudes toward those with BPD [121] but no data about whether this alters clinician behavior. These potential benefits must be weighed up against potential risks. It is unclear whether broadening the net of detection and intervention will always bring benefits to those ‘cases’ that have previously gone unrecognized. BPD is a highly stigmatized label and there is the potential for iatrogenic harm, which is already seems to be common [119]. It is unclear what message should be given to young people and their families about their current problems and future prospects. The early psychosis field has engaged in wideranging debate about the merits and pitfalls of this approach [122-124]. Concerns relevant to BPD include stigma, clinicians’ pessimism and the quality of available clinical services. Another lesson from the psychoses relates to family involvement and the family-blaming mistakes of bygone eras. Early intervention might pose risks for those with subsyndromal disorder, such as unnecessary fear of illness, restriction of life goals, medication use and consequent sideeffects. However, this is based upon the assumption that those with sub-syndromal disorder are without problems. BPD traits in adolescence are associated with high levels of psychopathology and psychosocial disability that warrant early intervention on its own merits, regardless of future risks. Moreover, there is evidence suggesting that this group are clinical help-seekers from their youth [12, 33, 39], similar to those at ultra high risk for psychosis [125]. Other issues that will need to be addressed for the development of programs include the development of screening measures. Screening for treatment programs appears to be feasible in outpatient youth [126] but has not been evaluated in community samples. Also, the cost-effectiveness of preventive programs will need to be measured, should appropriate preventive and early intervention approaches prove effective. Clearly, early intervention will not be cheap at first but it might represent value for money with more focused use of existing resources and perhaps long-term cost offsets. However, cost alone should not necessarily be a barrier, as the community readily accepts the high costs of ‘end of life’ medical care. The data on the global burden of disease [127] tell us that years lived with disability is high when mental health conditions are considered because their onset is usually in young people and they often result in decades of disability and lost potential. CONCLUSIONS AND RECOMMENDATIONS Diagnosing BPD in Adolescence We conclude that the evidence supports discarding the term ‘controversial’ in relation to the BPD diagnosis in young people, recognizing that the BPD construct is no more


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or less flawed in adolescence than it is in adulthood and that it is of sufficient reliability and validity to use now, until a more satisfactory and empirically-based construct emerges in the literature. BPD is prevalent in everyday clinical practice with young people and the diagnosis identifies a group of young people with severe psychosocial dysfunction and adverse sequelae during a critical developmental period. While the data are suggestive that, from an epidemiological perspective, BPD is primarily a disorder of young people, the reasons for this remain unclear. Risk Factors and Developmental Mechanisms Improved knowledge in relation to risk factors and developmental mechanisms is required before specific primary or universal and selective preventive interventions will become feasible. The developmental psychopathology approach, outlined by Lenzenweger and Cicchetti [86], offers an organizing framework for this task. We endorse their call for studies of BPD before it emerges. In addition to prospective studies of samples selected on the basis of psychosocial risk (e.g. maltreated children), we advocate specifically selecting samples on the basis of extremes of putative temperamental characteristics preceding BPD (e.g. low effortful control and high negative affect, relational aggression, emotion dysregulation, impulsivity, affective instability and relationship dysfunction), which can be reliably measured. We add to this approach that the ‘onset’ phase of BPD offers a pragmatic and feasible window into the study of BPD that has the potential to inform our understanding of the etiology of BPD, ‘prodromal’ signs of BPD and the factors associated with maintenance or progression of BPD and associated problems. The latter is particularly relevant to indicated prevention and early intervention. Prevention and Early Intervention Clinical staging [113, 128] provides a heuristic framework for prevention and early intervention for BPD, with increasing specificity, complexity and intensity of interventions as problems evolve and intensify (see Fig. 1). Based upon available data, this would include broad-based, ‘lowtoxicity’ universal and selective interventions for a range of mental health problems and other adverse psychosocial outcomes that might include (intended or unintended) benefits for BPD, through to indicated prevention for Cluster B PDs in those displaying precursor signs and symptoms. The emerging BPD phenotype would then warrant a form of ‘late indicated’ prevention and early intervention. Primary or universal and selective prevention programs will need to be broad based, targeting key risk factors and aiming to prevent the full range of adverse outcomes associated with these risk factors, including BPD. Currently, it is practical to evaluate BPD prevention as an outcome in trials of existing successful early childhood development programs, such as Head Start [129] or universally applied parenting programs for behavior problems in children [130]. Indicated preventive programs for Cluster B PDs are achievable with a narrower range of preventive targets than for universal or selective interventions. These should explicitly comprise multiple target syndromes identified from lon-


gitudinal studies, including ‘adult’ PD syndromes, such as BPD and ASPD.

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and wide availability make it appealing. Also, the capacity to use the prescribing skills available in most medical systems makes it a pragmatic intervention alone or in combination. ACKNOWLEDGEMENTS The ORYGEN Research Centre is supported by funding from the Colonial Foundation, Melbourne, Australia. The authors would like to thank Anthony Jorm PhD, DSc for comments on an earlier version of this manuscript. REFERENCES [1] [2] [3] [4] [5] [6]

[7]

[8]

Fig. (1). Prevention and early intervention strategies for borderline personality disorder using currently available data.

The data are most compelling for the development of early intervention programs for BPD and their evaluation through well-designed clinical trials with long-term followup. The infrastructure to support such programs already exists in many health systems in industrialized countries and potential recipients of these interventions (e.g. young people with deliberate self-injury) are already help-seeking. On the face of it, the benefits of early intervention for BPD appear to outweigh any disadvantages but this question must be directly addressed in research studies. It is likely that barriers to diagnosis and access to services, such as the stigmatizing attitudes of health professionals or lack of public knowledge will also need to be targeted as a component of any intervention and change might need to be driven through ‘mental health literacy’ campaigns aimed at the general public. Such campaigns have already been successfully conducted at the general population level for depression [131] and with a youth focus for mental health problems [132]. Psychosocial interventions for adult BPD might be adapted for early intervention to cater to the unique needs of youth. However, interventions need not be restricted to conventional intensive biomedical or psychotherapeutic interventions, as early successful treatment might alter the subsequent course of disorder [113]. They might also draw upon novel, ‘low toxicity’ interventions from related fields, such as physical exercise in depression and anxiety [133] or omega-3 fatty acid, which is supported by one RCT in adult BPD [134]. Omega-3 fatty acid’s status as a ‘natural’ substance, low cost, low toxicity

[9]

[10]

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Revised: September 13, 2007

Accepted: November 13, 2007