Copyright is owned by the Author of the thesis. Permission is given for a copy to be downloaded by an individual for the purpose of research and private study only. The thesis may not be reproduced elsewhere without the permission of the Author. The Surviving Emotional Storms Programme: A service user informed programme developed from an exploratory study of help-seeking experiences of NZ tertiary students with Borderline Personality Disorder. A thesis presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Psychology at Massey University, Auckland New Zealand. Jennifer Jean Beckett 2023 ii Abstract In this qualitative thesis, 14 university students were interviewed about their lived experience of having Borderline Personality Disorder. Participants discussed arduous journeys in search of effective treatment and described their increasing risk while trying to access help, alongside their experiences when able to access publicly funded treatment. Results from thematic analysis highlighted a super-theme of a continuous invalidation loop, discussed from an ecological and attachment perspective. This started with early help-seeking invalidation in participants’ microsystems, with the loop then broadening across systems over time, and help seeking attempts. This included contact with the mental health system, which was suggested to be a perpetuating factor in the development and maintenance of Borderline Personality Disorder. The help-seeking invalidation loop was briefly interrupted when participants were diagnosed, which occurred for most, directly after a suicide attempt. Diagnosis brought temporary relief, when participants armed themselves with knowledge about the condition including prognosis and treatment. The validation from informed diagnosis aided an externalisation process to occur, enhancing connections with self and others. However, accessing treatment proved difficult, crisis and respite was perceived as invalidating and when in treatment participants’ attempts at connection were often thwarted. Results from the thematic analysis guided the design and delivery of a group intervention. The intervention was administered using an action research methodology to university students either diagnosed with Borderline Personality Disorder or with borderline traits. The intervention, an adaptation from traditional dialectic behavioural therapy, iii integrated the results from the thematic analysis. To address the super-theme findings, attachment theory was interspersed throughout the intervention, utilizing aspects of narrative and acceptance and commitment therapies. The intervention was adapted and evolved from participant feedback over six cycles of 12-session intervention groups. In each group participants reported reduced severity of borderline symptoms and increased mindfulness ability. The research took place prior to and during the global pandemic and Covid-19 mandatory lockdowns in NZ, during which the research was expanded to finish with an online intervention accessed by students across NZ. iv Acknowledgements I am immensely grateful to the extraordinary women who have shared their stories so openly about the personal experiences they had on their journey to access help. I can only hope that I have been able to honour your brave stories and use them to help and empower others. I would also like to express my deep gratitude for all the people who participated in the group interventions and shared their first-hand knowledge so generously. I would like to acknowledge my supervisors. Thanks to Dr Linda Jones, for enabling me to start this research journey. You held a torch at the starting point; your support and enthusiasm will never be forgotten. I would like to especially thank Dr Kirsty Ross, who took over that torch early in the research. Your amazing encouragement and expertise have guided me through, thank you! I also wish to thank Dr Ross Flett for his practical support for this research project. I would like to acknowledge my clinical supervisor, Marie Corbett, with special thanks. Marie is a woman of magic, she creates and holds safe spaces for others, and has supported me so that I could do this research and clinical work with some respite. A kindred spirit with a sense of humour; thank you Marie! I am grateful to Dr Maxine Stephenson, who has been incredibly generous with her time and expertise in reading through and discussing my work with me. Thank you for being so quick to help and so giving of your time, you are such a lovely person. v Thank you, Claire Komatas, for all your practical, generous group and thesis help and encouragement, and to Emma Wenman, for your fresh eyes and practical help and assistance. Thank-you Nadine, Emma M, Diyani, and Lyn, for your contributions to the group interventions and facilitation. I am grateful to the talented Ruby Jude, who created the original illustration of Mooj. Jenny Hardyment, I cannot thank you enough for your practical diagram help, and for all your bubbly support over the years of walks and talks and encouragement along the way. Thanks to my parents Lois and Bernie, my family, and friends who are the kind of awesome people that I can disappear from, into the world of thesis for months at a time, and yet the connections still burn as brightly as if we had talked yesterday, Alexis, Emily, Julie, and Julia. Thanks to Dave, who has come into my life again during the last year of a massive research project, and all the chaos and time limitations that come with that. Thanks to Jahmon and Cara and my beautiful grandbabies, both born during this research; Colton and Mason. This thesis is dedicated to Leslie Jean Ravenhall, long gone, but always in my heart. vi Table of Contents Abstract ........................................................................................................................... ii Acknowledgements ......................................................................................................... iv Table of Contents ............................................................................................................ vi List of Tables ................................................................................................................... ix List of Figures .................................................................................................................. ix Introduction ................................................................................................................... 11 Chapter 1: Introducing Borderline Personality Disorder ................................................... 18 History of BPD Diagnosis: Sociogenic Conversion ..................................................................... 19 Current Definition of BPD ....................................................................................................... 23 Prevalence of BPD .................................................................................................................. 26 Aetiology of BPD .................................................................................................................... 27 Neurocognitive and Biological Risk Factors ................................................................................................. 28 Cognitive Deficits with Biological Foundations ............................................................................................ 30 Personality Traits ......................................................................................................................................... 32 Developmental Factors ................................................................................................................................ 34 Psychological and Environmental Factors.................................................................................................... 35 Attachment .................................................................................................................................................. 37 Genetic and Environmental Interplay in BPD Etiology ................................................................................. 37 Abnormal Parenting and Parents’ Genetics ................................................................................................. 38 Biopsychosocial Model of BPD Development .............................................................................................. 39 Chapter 2: How do we intervene when things go wrong? Treatment for BPD .................. 42 Cognitive Behavioural Therapy ............................................................................................... 43 Acceptance and Commitment Therapy.................................................................................... 44 Dialectic Behavioural Therapy ................................................................................................ 49 Change and Acceptance Dialectics .............................................................................................................. 50 Therapist and patient dynamics................................................................................................................... 52 Barriers to DBT Treatment Effectiveness ..................................................................................................... 61 Qualitative Research on DBT Experiences of People with BPD ................................................................... 61 Stigma and Treatment ................................................................................................................................. 64 Attachment-Informed DBT .......................................................................................................................... 69 Mentalization-Based Therapy ................................................................................................. 72 Research Questions ................................................................................................................ 76 Aims ............................................................................................................................................................. 76 Objectives .................................................................................................................................................... 77 Chapter 3: Methodology ................................................................................................. 79 Introduction ........................................................................................................................... 79 Research Methodology ........................................................................................................... 80 vii Research Paradigm ................................................................................................................. 81 Research Design ..................................................................................................................... 85 Stage 1: Foundational Interviews ................................................................................................................ 85 Methods. ................................................................................................................................................. 86 Data Analysis. .......................................................................................................................................... 86 Ethical Approval. ...................................................................................................................................... 88 Participant Selection/Sampling/Recruitment. ......................................................................................... 91 Participant Demographics. .................................................................................................................. 91 Procedure. ........................................................................................................................................... 91 Data Collection and Analysis. .................................................................................................................. 92 Stage 2: Intervention Design, Implementation and Evaluation ................................................................... 93 Methods. ................................................................................................................................................. 94 Ethical Approval. ...................................................................................................................................... 95 Participant Selection, Sampling, and Recruitment. ................................................................................. 95 Participant Demographics. .................................................................................................................. 96 Procedure. ........................................................................................................................................... 96 Data collection and analysis. ................................................................................................................... 98 Ethical Considerations. .......................................................................................................................... 100 Reliability, Validity, and Trustworthiness .............................................................................. 102 Conclusion ........................................................................................................................... 103 Chapter 4: Reflexive Thematic Analysis ......................................................................... 106 Introduction ......................................................................................................................... 106 Introducing the Participants ................................................................................................. 107 Process ................................................................................................................................ 107 Results ................................................................................................................................. 109 Overarching super-theme: Invalidation Navigates the Help-Seeking Journey, Through Multiple Pathway Points and Roadblocks ............................................................................................................................... 111 Theme 1: An Early Beginning of Symptoms and Suffering (Pathway Point) .............................................. 119 Theme 2: The Risk Escalation Part of the Journey: Escalated Risk and Suicide Attempts Prompt Diagnosis ................................................................................................................................................................... 136 Theme 3: Process of Diagnosis as Invalidating .......................................................................................... 143 Theme 4: Diagnosis Seen as the Missing Piece of the Puzzle, Provided Relief, Hope, Sense-Making, a Language, and the Starting Point for Self-Improvement. .......................................................................... 156 Theme 5: Seeking Treatment After Diagnosis was Difficult, Invalidating, and Full of Gaps that Blocked Effective Treatment in the Mental Health System. ................................................................................... 165 Theme 6: Making It to the Treatment: The Good, the Bad, and the Ugly ................................................. 182 Discussion ............................................................................................................................ 201 Super-Theme.............................................................................................................................................. 201 Theme 1 ..................................................................................................................................................... 202 Theme 2 ..................................................................................................................................................... 207 Theme 3 ..................................................................................................................................................... 210 Theme 4 ..................................................................................................................................................... 212 Theme 5 ..................................................................................................................................................... 215 Theme 6 ..................................................................................................................................................... 217 Conclusion ........................................................................................................................... 220 Chapter 5: Thematic Analysis meets Action Research: The Intervention Adaptation ....... 226 viii Introduction ......................................................................................................................... 226 Action Research ................................................................................................................... 226 Cycle 1 ................................................................................................................................. 227 Phase 2: Action Planning ............................................................................................................................ 228 Chapter 6: Action Research Continuation ...................................................................... 265 Cycle 1 ................................................................................................................................. 265 Phase 3: Taking Action ............................................................................................................................... 265 Phase 4: Evaluation .................................................................................................................................... 271 Phase 5: Specified Learning: Problem Reassessed ..................................................................................... 301 Cycle 2 ................................................................................................................................. 304 Phase 1: Defining/Diagnosing the Problem ............................................................................................... 304 Phase 2: Action Planning ............................................................................................................................ 305 Phase 3: Taking Action ............................................................................................................................... 307 Phase 4: Evaluation .................................................................................................................................... 307 Phase 5: Specified Learning and Problem Reassessed ............................................................................... 324 Cycle 2 ................................................................................................................................. 326 Phase 1: Defining/Diagnosing the Problem ............................................................................................... 326 Phase 2: Action planning ............................................................................................................................ 326 Phase 3: Taking Action ............................................................................................................................... 328 Phase 4: Evaluation .................................................................................................................................... 329 Phase 5: Specified Learning: Problem Reassessed ..................................................................................... 336 Cycle 4 ................................................................................................................................. 338 Phase 1: Problem Definition/Diagnosis ..................................................................................................... 338 Phase 2: Action Planning ............................................................................................................................ 338 Phase 3: Taking Action ............................................................................................................................... 339 Phase 1 - Revisited: Problem Definition ..................................................................................................... 342 Phase 2 - Revisited: Action Planning .......................................................................................................... 343 Phase 3 - Revisited: Taking Action ............................................................................................................. 344 Phase 4: Evaluation .................................................................................................................................... 346 Phase 5: Specified learning ........................................................................................................................ 356 Cycle 5 ................................................................................................................................. 356 Phase 1: Problem Definition ...................................................................................................................... 356 Phase 2: Action Planning ............................................................................................................................ 358 Phase 3: Taking Action ............................................................................................................................... 358 Cycle 5, Cohort 5 ........................................................................................................................................ 359 Cycle 5, Cohort 6 ........................................................................................................................................ 359 Phase 4: Evaluation .................................................................................................................................... 360 Cohort 5. ................................................................................................................................................ 360 Cohort 6. ................................................................................................................................................ 361 Phase 5: Problem Reassessed .................................................................................................................... 369 Chapter 7: Final Discussions and Conclusions ................................................................ 371 Chapter Overview ................................................................................................................ 371 References.................................................................................................................... 389 APPENDICES ................................................................................................................. 480 ix List of Tables Table Page 1. Stage 1 RTA Identified Themes and Sub-Themes…………………………. 126 List of Figures Figure Page 1. The ACT Hexaflex model of Psychological Flexibility……………… 46 2. DBT Skills Training Modules and Change and Acceptance Dialectics………………………………………………………………... 52 3. Gerald Susman’s 5-stage Participatory Action Research Model…. 91 4. Bronfenbrenner’s Ecological Systems Theory Model………………. 113 5. Chronological Road Map of Participants’ Help-Seeking Journey… 115 6. The Help-Seeking-Validation-Loop………………………………….. 215 7. Introduction to Mooj and the Survival Skills Program Workbook…. 240 8. Workbook Page: Mooj is Lost at Sea……………………………….. 242 9. Workbook Page: The World According to Mooj…………………….. 242 10. Workbook Page: Other People According to Mooj…………………. 243 11. Workbook Page: Significant Relationships According to Mooj……. 244 12. Workbook Page: Mooj’s Rock………………………………………… 245 13. Workbook Page: Mooj’s Weigh Downs……………………………… 246 14. Workbook Page: Mooj’s SURVIVAL Lifejacket…………………….. 248 15. Mooj’s Hexaflex Diamond…………………………………………….. 249 16. Workbook Page: The Distress Thermometer……………………….. 255 17. Workbook Page: Sensory Modulation through Touch (TIPP): Intense 30 Second Reset……………………………………………... 256 18. Workbook Page: Mooj Summarizes the TIPP Skills………………. 257 19. Workbook Page: Attachment Psychoeducation……………………. 259 20. Workbook Page: Attachment Styles and Psychoeducation……….. 260 21. Group Table with Workbooks and Art Supplies…………………….. 266 22. Group M & M Mindfulness Exercise…………………………………. 270 23. Comparison of Cohort 1 Pre- and Post-Group Intervention BEST Scores…………………………………………………………………… 272 x 24. Comparison of Cohort 1 Pre- and Post-Group Intervention BEST Positive Behaviour Scores……………………………………………. 272 25. Comparison of Cohort 1 Pre- and Post-Group Intervention Mindfulness Self-Assessment Scores Scores…………………………………………………………………… 274 26. Comparison of Cohort 2 Pre- and Post-Group Intervention BEST Scores…………………………………………………………………... 308 27. Comparison of Cohort 2 Pre- and Post-Group Intervention BEST Positive Behaviour Scores…………………………………………….. 309 28. Comparison of Cohort 2 Pre- and Post-Group Intervention Mindfulness Self-Assessment Scores……………………………….. 309 29. Comparison of Cohort 3 Pre- and Post-Group Intervention BEST Scores…………………………………………………………………. 330 30. Comparison of Cohort 3 Pre- and Post-Group Intervention BEST Positive Behaviour Scores…………………………………………….. 330 31. Comparison of Cohort 3 Pre- and Post-Group Intervention Mindfulness Self-Assessment Scores……………………………….. 331 32. PowerPoint Slides Created for the Online Survival Skills Group………………………………………………….......................... 346 33. Comparison of Cohort 4 Pre- and Post-Group BEST Scores…….. 348 34. Comparison of Cohort 4 Pre- and Post-Group Intervention BEST Positive Behaviour Scores……………………………………………. 349 35. Comparison of Cohort 4 Pre- and Post-Group Intervention Mindfulness Self-Assessment Scores……………………………….. 349 36. Comparison of Cohort 5 Pre- and Post-Group BEST Scores…….. 361 37. Comparison of Cohort 5 Pre- and Post-Group Intervention BEST Positive Behaviour Scores……………………………………………. 362 38. Comparison of Cohort 5 Pre- and Post-Group Intervention Mindfulness Self-Assessment Scores……………………………….. 362 39. Comparison of Cohort 6 Pre- and Post-Group BEST Scores…….. 363 40. Comparison of Cohort 6 Pre- and Post-Group Intervention BEST Positive Behaviour Scores……………………………………………. 363 41. Comparison of Cohort 6 Pre- and Post-Group Intervention Mindfulness Self-Assessment Scores……………………………….. 364 11 Introduction New Zealand (NZ) has one of the highest rates of youth suicide in the world (Mental Health Foundation of New Zealand, 2023). Ranking the second highest in the developed world, with 14.9 deaths per 100,000, NZ’s youth suicides sit at more than double the average rate (UNICEF, 2020). Mental Health Foundation Chief Executive Shaun Robinson called the number of youth deaths’ “a sobering reflection on the failure of New Zealand to come together to prevent suicide”, stating that a focus on suicide awareness is not enough, and the time has come to focus on prevention (Bond, 2017). Within NZ’s youth population, some are at greater risk of suicide than others. Despite immense research and funding, suicide prevention has been targeted toward identifying and treating such conditions as depression, yet our suicide statistics continue to be of great concern. I am a registered psychologist and have spent the past 13 years working with university students at a leading NZ university. In this role, I have regularly consulted with students at-risk of suicide and who are self-harming, and who often had a history of prior suicide attempt(s). I am intimately aware of the challenges of meeting the rising demands for therapy within a small multidisciplinary team, positioned in primary care. I wanted a better understanding of this population of at-risk students, beginning with how many of those seeking counselling within the university setting were experiencing suicidal ideation and/or behaviours, and the key reasons why. 12 My preliminary investigation indicated that during 2018, at least 1 in 5 students reported feeling suicidal at the time of requesting university counselling, within my university setting. This included the students who filled in an online counselling request form, but not for those who walked in during a crisis. The acuity of students presenting for help can be extremely high and complex. Those presenting to emergency departments in metal health crisis can wait up to ten hours for an assessment, and are either seen briefly and discharged, or put on waiting lists for evidence-based treatments for up to a year (Lambie, 2020). The tsunami of need that universities are being faced with is not fully being met in the community and acute crisis services. After long hospital waits, students are often sent back to university halls of residences (Redmond, 2018). The NZ Union of Students’ Association says that the well-known wait times discourage students from seeking help in the first instance, and that the growing number of students needing mental health support in recent years has become untenable (Redmond, 2018). Many of the at-risk students that I had contact with had symptoms characteristic of Borderline Personality Disorder (BPD) and emerging BPD traits. This aligns with findings from Lambie (2020), that emotional and interpersonal dysregulation were a significant factor in suicide risk in NZ. This thesis aimed to explore the experiences of the tertiary student BPD sub-population, to platform the development of a consumer informed intervention to bridge the access to treatment gap and reduce BPD severity, such as self-harm and suicide risk. BPD is a personality disorder characterised by impulsivity, difficulty regulating intense emotions, interpersonal and self-identity difficulties. People with BPD often self-harm 13 (Linehan, 1993), have chronic suicidal tendencies (Lieb et al., 2004), and are sensitive to their emotions. Emotions are frequently experienced as intense, and difficult to calm down from (Linehan, 2015). This has been described as an ongoing rollercoaster of emotions, which can be highly distressing for those living with it, and those around them (Van Zutphen et al., 2018). Therefore, while people with depression may react with suicide ideation and behaviours in response to intense low mood (Arria et al., 2009), people with BPD frequently have this response to a variety of intense emotions. Consequently, approximately 75% of people with BPD attempt suicide (Links, et al., 2013), and have increased mortality compared to the general population (Sharp & Romero, 2007). This places intense pressure on health care systems, when people with BPD come into regular contact with health services related to suicide attempts and self-harm (Zanarini et al., 2001). Females are three times more likely to be diagnosed with the condition (Sansone & Sansone, 2011). Despite BPD being widely studied, those with BPD continue to suffer, struggle to access effective help (Lawn & McMahon, 2015), and face discrimination (Ring & Lawn, 2019). Though limited public treatment is available for people with BPD in NZ, in my working experience, referrals to the public mental health and crisis system are frequently met with extensive waitlists and referred back to the referrer (in this case, the university). I have accompanied many students to the emergency department for hospitalisation due to self-harm and/or suicide attempts (sometimes occurring on campus). These referrals frequently resulted in discharge straight back to the university medical centre, sometimes on the same day of a suicide attempt. My clinical experiences reflect findings by Lambie (2020), that people in NZ who visit emergency departments with suicide ideation are seen briefly by emergency services, and then either discharged 14 (without treatment of the problems causing suicidal and self-harm behaviours), or put on waitlists for evidence-based treatments for up to a year. This highlights issues around safety and risk management, particularly for students who reside on campus. These risks became even more crucial and topical over the course of this research, as the Ministry of Education (MoE) published a new code of practice for the pastoral care of tertiary and international students which highlighted NZ universities’ responsibility in managing student risk (MoE, 2021). The new code, prompted after a NZ tertiary student’s suicide on campus, provoked urgent discussion around the risk and responsibility of students under the care of tertiary education settings. The code states that universities must be able to identify at-risk students and have clear pathways for assisting these students, with access to appropriate mental health services on campus and in the community. This put universities in a difficult situation, especially as community resources are limited, and there are gaps in resources to refer students to, such as the long public waitlists with strict entry requirements. My work experience ignited both my concern and research interest in the substantive gaps in our mental health system between risk, need, and service delivery, specifically within the arena of tertiary students with BPD. The Treatment Gap This research aims to bridge the gap between long waitlists and access to effective intervention for tertiary students with BPD and BPD traits, reducing the associated risk of being on a long public waitlist. 15 When students cannot be transferred into the care of the public mental health system (and are instead discharged back to the University), Health and Counselling services are expected to manage more risk yet lack the resources to do so. These challenges were heightened with the Pastoral Care Code and with the Covid-19 global pandemic, which caused upheaval and stress for both students and university staff. As well as the universities holding that risk, psychologists working in these departments are also pulled into the gap. Psychologists in NZ are registered under the Health Practitioners Competence Assurance Act (HPCA) (2003) and, under this code, are responsible for managing referrals safely, until another organisation can accept the referred person. While some students face very long waitlists for public evidence- based treatments, others are not eligible to be on the waitlists at all. This places further demand on psychologists working within the university settings. An alternative option is for these students is to pay for private therapy, something many students cannot afford. Some students referred for emergency help are discharged from the hospital after a suicide attempt without a mental health support plan (Redman, 2018). Research indicates that risk may increase for people with BPD after contact with emergency services (Links & Bergmans, 2004), meaning students may be at even greater risk when discharged back to university accommodation and services, that, without an intervention program, are not equipped to manage the risk they are now mandated to take responsibility for. 16 Given similar challenges, some overseas university counselling centres have increased the availability of evidence-based therapies for students including DBT skills training group interventions (Chugani et al., 2013; Meaney-Travares & Hasking, 2013; Uliaszek et al., 2016). This can assist by extending the help available to students who may only be able to access a brief number of individual sessions, by increasing groups that support their wellbeing. Chapters 1 and 2 review the literature relevant for this research. Chapter 1 introduces borderline personality disorder, starting with a historical overview of the condition. The current definition of BPD is then outlined, including the diagnostic criteria, followed by a discussion of the aetiological factors. In Chapter 2 current treatment interventions for BPD are reviewed, linked with the aetiological theories they align with. Strengths and weaknesses are identified for these interventions, followed by a proposed intervention design, which combines several evidence-based therapies to sit within an attachment framework. This chapter also explores stigma research and the importance of including BPD experience and feedback in an intervention design and evaluation. Chapter 3 outlines the chosen methodology, describing how the research was carried out, encompassing the study design, the researcher’s stance, and ethical considerations. Chapter 4 introduces the participants interviewed for thematic analysis and the thematic analysis results and discussions. Chapter 5 describes how the thematic analysis was married to action research and spotlights the transformation of the thematic analysis results into the practicality of the group intervention program 17 design. The content and delivery of the program discussed, including excerpts from the program, such as the development of a character who gives voice to some of the themes from people with BPD being utilized within the intervention. Chapter 6 outlines the evaluation and refinement of the intervention using action research cycles, spanning a total of six 12-week groups with 59 participants, and further adaptations of the intervention, driven by participant feedback in the form of pre- and post-group intervention measures, in-between session participant feedback, and clinical observation. Chapter 7 summarises and synthesizes discussions and findings from both stages of this research and includes considerations for future research. 18 Chapter 1: Introducing Borderline Personality Disorder Personality is a multifaceted and complex construct that has been a subject of human interest throughout time. The word personality originates from the Latin word persona, interpreted as mask (Engler, 2014). We may relate the concept of a mask to hiding one’s true self; however, in ancient Greek times, a persona was a mask worn by an actor to express and highlight specific personality traits of a character (Jevons, 1916). Much like the ancient Greek masks, people with BPD often exhibit strong facial expressions to communicate their feelings to others (Dammann, 2020; Hepp et al., 2019). Researchers suggest that this may be a display of the emotional hyper- reactivity that they feel within themselves (Renneberg et al., 2005; Sansone & Sansone, 2010). A key focus of this research is the exploration of this population’s attempts to communicate and connect with others. This thesis exemplifies the experiences of people with BPD having to intensify expressions of distress to be seen and heard to access help, within an invalidating environment. However, before delving into deeper understandings of communication issues in BPD in later chapters, an overview of what is known about the psychology of BPD will be provided. This chapter considers factors that contribute to what psychiatry considers to be abnormal personality, specifically borderline personality disorder (BPD). This chapter 19 begins with a brief outline of the historical roots of BPD and then locates BPD within its current classification amongst other personality disorders. Issues pertaining to BPD’s definition and classification are identified. Finally, the aetiology of BPD will be discussed, aetiology being the background for intervention, which is the focus of Chapter 2. History of BPD Diagnosis: Sociogenic Conversion To contextualise the history of BPD, it is important to have a general understanding of the societal influence on the expression of mental health. BPD is historically a controversial diagnosis that affects many more women than men (APA, 2013), with symptoms of distress being relational to the environment (Linehan, 2015). Mental health symptoms are shaped socially, with symptoms of distress shown to change over time, culture, and history (Triandis & Suh, 2002). Shorter (1992) suggests that psychopathology may draw from a collective bank of symptoms, created by culture and society. A classic example of this is hysteria, which, like BPD, was predominately diagnosed in females. Symptoms such as chest pains, tightness in the throat and muscles, aches, pains, and shortness of breath, were all said to be hysterical symptoms in women (Showalter, 1997). Hysteria was originally thought to be caused by the wandering womb, that women’s wombs were moving to various parts of the body, causing physical symptoms (Starcevic & Lipsitt, 2001). An illness often afflicting young unmarried women and widows, it was said to be that the wandering womb was looking for semen (Pilowsky, 1997). The treatment was marriage, sex, and pregnancy (Shapiro & Rosenfeld, 1987). 20 Considering the restrictive status and lives of women during these times, somatic aches, pains, and physical stress symptoms may have been a way in which women could express their dissatisfaction and distress (Simon, 1978). This reflects the culture of the time, which was rife with sexism, power dynamics, women’s fixed roles, and lack of scientific advancement to understand physiology (Pilowsky, 1997). Like BPD, hysteria was influenced by earlier concepts of the condition, which influenced thoughts on aetiology and treatment. According to Paris and Lis (2012) the development of BPD may have similarly been shaped by sociocultural and historical factors, along with a failure to acknowledge the social context of women’s adversity, and a pathologizing of women’s distress (Shaw & Proctor, 2005; Ussher, 2013). Culture and society, which now includes current social media technology reliance, have a powerful influence on mental health conditions, such as BPD. Müller-Vahl et al. (2022) published an article in which they report symptoms of the first outbreak of what they call a new type of mass sociogenic illness, solely spread by social media. They have coined the term mass social media-induced illness and view this as “the 21st century expression of a culture-bound stress reaction of our postmodern society, emphasising the uniqueness of individuals, valuing their exceptionality, promoting attention-seeking behaviours and perpetuating our permanent identity crisis” (Müller- Vahl et al., 2022, p. 256). BPD is a complex condition that historically has been difficult to conceptualise, define, and gain acceptance for as a classification. BPD was first described in 1938 by Adolph Stern, a psychoanalyst who noticed a group of patients with a set of symptoms that he 21 described as being on the border between neurosis and psychosis (Stern, 1938). He observed that these borderline patients did not seem to improve with the treatment therapies available at that time (Paris, 2008). BPD was not initially embraced as a widely accepted concept, and research was scarce for some time after Stern coined the term Borderline Personality Disorder (New & Triebwasser, 2017). Some of this may have been due to the term being misleading, as it is not fully aligned with BPD symptoms in the way that anxiety and depressive disorders are quite descriptive in their names, for example. This may be due to a lack of alternative diagnostic names. Other names have been suggested for consideration, but dismissed, such as for example, Emotional Dysregulation Disorder (Livesley, 2017). Prospective names have not been able to umbrella all BPD diagnostic criteria. BPD was not accepted as a diagnostic category by the American Psychiatric Association’s (APA) Diagnostic and Statistical Manual of Mental Disorders (DSM) until the release of the DSM-III in 1980 (Al-Alem & Omar, 2008; APA, 1980), nor the International Classification of Diseases (ICD) until the ICD-10 was published in 1992 (Kulacaoglu & Kose, 2018; World Health Organization, 1992). Not being accepted into official classification systems meant there was less research and experience for clinicians to diagnose and attempt treatment protocols, while other conditions were advancing and evolving in their knowledge base and clinical practice (Masland et al., 2023; Zimmerman & Gazarian, 2014). Though not formally classified between the late 1930s to early 1970s, the number of people presenting with BPD symptoms increased over time, exhibiting diagnostic 22 criteria yet to be formally recognised (Millon & Davis, 1993). Paris (2008) asserted that there is very little historical evidence of the current BPD symptoms that people express now, such as self-harming through cutting, and taking repeated overdoses. Instead, these were more hysterical symptom expressions, until the 1940s onward. This may have been the point where culture and society were changing, and hysterical symptoms merged or converted into a more modern version of what is now considered BPD. According to Becker (1997) BPD- is the new hysteria- a social construction, a diagnosis of dysregulation of the times and a patriarchal response to women’s struggle for identity and independence in Western culture. Wirth-Cauchon (2001) similarly argued BPD stems from women’s reconciliation of conflicting and contradictory societal expectations that are upon them. Interestingly, given the shared historical symptom distress similarities of BPD with hysteria, BPD was added to the DSM at the same time hysteria was taken out (Cramer, 2019). Decades later, new specific theories of BPD were put forward, and measurement systems offered. In 1976, psychoanalyst Kernberg described his concept of the borderline personality organisation. The first empirical research for BPD began in 1975, when Gunderson and Singer created a structured diagnostic interview for BPD, the Diagnostic Interview for Borderlines (DIB), and published this for use, with the aim to provide operational criteria for diagnosing BPD. The DIB is a semi-structured interview that accessed five symptom areas, which included social adaptation, impulsiveness, affects, psychotic symptoms and interpersonal relations (Gunderson & Singer, 1975). The DIB can discriminate BPD from other conditions, such as, schizophrenic, and neurotic depressives, as they were known as at that time (Kolb & Gunderson, 1980). 23 Five years after the DIB was published for use, BPD was accepted into the DSM-III (APA, 1987) as a personality disorder diagnosis and, later, the ICD-10 (World Health Organisation, 1992). BPD’s classification has had minimal changes in all the subsequent versions of the DSM. The DSM-III (APA, 1987) described eight symptom criteria, of which five or more criteria needed to be met for a diagnosis to be made. The DSM-IV, DSM-IVR, and current edition, the DSM-5-TR, have kept the eight criteria and added a ninth criterion (APA, 1994, 2000, 2022). As the BPD classification in each edition of the DSM (APA, 1987, 1994, 2000, 2013, 2022) adapted, so did assessment measures. In 1989, Zanarini and her colleagues revised Gunderson and Singer’s diagnostic interview (DIB-R), increasing its ability to distinguish BPD from other personality disorders (Zanarini et al., 1989). With each updated edition of the DSM, working groups plan and revise changes. The DSM-1V (APA, 1994) and DSM-1VR (APA, 2000) used a multi-axial system to guide clinicians to consider Axis 1 conditions (general mental health conditions and conditions often diagnosed in infancy and childhood), while Axis 2 consisted of the range of personality disorders (APA, 2013). This has not continued in the current DSM-5 (APA, 2013, 2022). In summary, the development of BPD is considered by some to be socially constructed, influenced, and maintained within an evolving society. It has been a difficult construct to define, accept, and include in psychology’s classification systems, and it sits in our current DSM-5-TR as a personality disorder. Current Definition of BPD 24 The DSM-5-TR (APA, 2022) has evolved over time alongside scientific understandings of personality disorders, having improved in terms of breadth of mental health conditions, and scientific advances. Personality disorders remain classified in their own section. The DSM-5-TR defines a personality disorder as An enduring pattern of inner experience and behaviour that deviates markedly from the expectations of the individual’s culture, is pervasive, and inflexible, has an onset in adolescence or early adulthood, is stable over time and leads to distress or impairment (APA, 2022, Personality Disorders section, para, 1). BPD is one of ten diagnosable personality disorders classified within the DSM-5-TR, divided into three clusters: Cluster A, Cluster B, and Cluster C, with BPD sandwiched in the middle cluster. Cluster A includes paranoid, schizoid, and schizotypal personality disorders. Cluster B is where BPD is located, among antisocial, histrionic, and narcissistic personality disorders. Cluster C includes avoidant, dependant, and obsessive-compulsive personality disorders (APA, 2022). Alongside the general definition of personality disorders, BPD has a specific set of criteria classified in the DSM-5-TR (APA, 2022, Borderline Personality Disorder section, F60.3): Diagnostic Criteria A pervasive pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity, beginning by early adulthood and present in a variety of contexts, as indicated by five (or more) of the following: 1. Frantic efforts to avoid real or imagined abandonment. 2. A pattern of unstable and intense interpersonal relationships characterised by alternating between extremes of idealisation and devaluation. 25 3. Identity disturbance: markedly and persistently unstable self-image or sense of self. 4. Impulsivity in at least two areas that are potentially self-damaging (e.g., spending, sex, substance abuse, reckless driving, binge eating). 5. Recurrent suicidal behaviour, gestures, or threats, or self-mutilating behaviour. 6. Affective instability due to a marked reactivity of mood (e.g., intense episodic dysphoria, irritability, or anxiety usually lasting a few hours and only rarely more than a few days). 7. Chronic feelings of emptiness. 8. Inappropriate, intense anger or difficulty controlling anger (e.g., frequent displays of temper, constant anger, recurrent physical fights). 9. Transient stress-related paranoid ideation or severe dissociative symptoms. To meet DSM-5-TR criteria, patients must meet five out of nine criteria. Issues and critiques with this categorization of BPD relate to clinical presentations. For example, the criteria are very broad and could be experienced for several reasons, including the experience of trauma. The overlap with trauma will be discussed further in Chapter 3. People can also have some borderline traits without meeting or maintaining full diagnostic criteria. The criteria indicate BPD as having an onset in adolescence or adulthood; however, a growing body of research suggests that earlier onset of symptoms in childhood is particularly relevant in BPD (Bemporad et al., 1982; Bozzatello et al., 2020; Gratz et al., 2009). Diagnosis of BPD can be made earlier than age 18, if there is a 1-year pattern of immature personality development with disturbances in at least five of the nine domains of BPD (APA, 2022). With regards to 26 flexible versus fixed personality wording in the DSM-5-TR, ‘inflexible’ within the above criteria is incongruent with research which points to the impact of the environment on learning, which holds that personality can be flexible and ever changing through life experiences (Caspi et al., 2004; Triandis & Suh, 2002). Current trait theory, such as the Big Five Factor Mode (Digman, 1990), suggests that though personality traits are enduring, there is flexibility both in age/stage and in primary, cardinal, and secondary traits. This puts into question the definition of personality disorder. If someone has a personality disorder, by this definition, it seems there an insinuation that they cannot be shaped by treatment, environment, and learning. It brings into question, does the term personality even belong in the diagnostic name? Perhaps being named under such category adds to the stigma of BPD, discussed in later chapters. The DSM-5-TR classification of BPD, like with many other disorders listed, has a reliance on culturally normative criteria, despite the criticism that cultural norms rely too highly on society’s influence (Sadock & Sadock, 2003). Given this, and the societal stigma on BPD, which can include institutional stigma influencing mental health professionals, questions arise as to whether institutional stigmatization about personality disorders may have permeated into the DSM-5-TR classification itself. Prevalence of BPD BPD is a highly prevalent, chronic, and life-threatening psychiatric disorder, that affects millions of people worldwide. This severe and pervasive personality disorder affects 1.1-2.5% of the population, with approximately 70% of those diagnosed being women (APA, 2013). In NZ, the Mental Health Foundation estimates that approximately 2% of our general population meet diagnostic criteria for BPD, and that approximately 20% of mental health service users meet the criteria (Mental Health 27 Foundation New Zealand, 2022). It is associated with high rates of suicide (Oquendo et al., 2007), and high-risk behaviours including deliberate self-harm, (e.g., cutting, burning) and recurrent suicide ideation and attempts (Linehan, 1993). Approximately 75% of BPD sufferers attempt suicide (Oldham, 2006; Oumaya et al., 2017; Soloff et al., 2000) and up to 10% complete suicide (Lieb et al., 2004; Paris & Zweig-Frank, 2001). People with BPD have severe impairments in functioning, such as unstable interpersonal relationships, impulsivity, emotional dysregulation, and disrupted sense of self (Linehan, 2020). Given this, they often use mental health services intensively (Meuldijk et al., 2017) making up approximately 15-20% of psychiatric inpatient admissions and outpatient mental health services (Korzekwa et al., 2008; Zimmerman et al., 2008) and costs to society are consequently high (Van Asselt et al., 2007). Given this, timely access to effective interventions for people with BPD is of utmost importance. BPD onset is often viewed as emerging during adolescence and early adulthood, when it is most often diagnosed (Sharp & Fonagy, 2015). Research indicates that the mean age of onset is 18, with the condition said to peak in adolescence and remain stable across time until a slight decline in older adults (Sharp & Fonagy, 2015). It is important to consider some of the aetiological theories of BPD, to understand early prevention and treatment options. Aetiology of BPD The DSM-5-TR (APA, 2022) classifies diagnoses according to observed symptoms, rather than describing aetiology. Thus, it does not indicate specific causes for the 28 observed symptoms, nor suggest treatment intervention. As with other personality disorders, aetiology for BPD is complex, with differing perspectives on its development (Sharp & Romero, 2007). Livesley (2017) has suggested that we are in an exciting stage where treatments for BPD are changing ideas about the conceptualisation of BPD is and its causes. Predisposition-stress models fall under neo-Kraepelinian theory, which views psychological and social factors as generalised stressors that can trigger an underlying predisposition into a disorder such as BPD (Zuckerman, 1999). This theory hypothesizes that each disorder has biological predispositions that reflect specific vulnerabilities (Paris, 2007). Thus, biological vulnerability explains the specific disorder that someone may develop, under certain psychological and social stress. In a large study by Reichborn-Kjennerud, et al. (2013) hereditary vulnerability factors were found to account for approximately 55% of people who meet the criteria for BPD. This research suggests several primary traits are associated with BPD but that the genetic architecture probably involves a single common genetic factor which then influences all the primary traits of BPD to some extent. Understanding and consideration of biological and later environmental factors have clinical implications for treatment interventions as some of these etiological factors need to be accounted for in treatment. Neurocognitive and Biological Risk Factors 29 Though the exact biological mechanisms underlying BPD are yet to be fully understood, strong evidence suggests biological factors contribute to the development of BPD. Extensive research has demonstrated the centrality of mood dysregulation and impulsivity (Bohus, et al., 2004; Skodel et al., 2002) in people with BPD, including self-reports of people with BPD experiencing greater frequency and intensity of emotional experience (Stiglmayr et al., 2001). Siever and Davis (1991) were the first to hypothesize that underlying BPD were core dimensions of impulsivity and affective instability. These two dimensions have been frequently found in the relatives of people with BPD (Paris, 1994; Silverman et al.,1991). A heritability study using twins highlighted genetic influencers that could explain up to 42% of the variation in BPD (Distel, 2008). Biological factors have been linked to the development of BPD in a wide variety of ways, such as temperament. Temperament is a key influencer in the development of personality traits which are said to be influenced by biological factors (Cloninger, 1994; Stepp et al., 2014). Those with BPD often exhibit specific temperamental traits that may contribute to the development of the disorder. For example, Trull et al. (2010) found that people with BPD often have high levels of negative affectivity and impulsivity - two central features of BPD diagnostic criteria. Distel et al. (2008) found that people with BPD have high levels of novelty seeking, another temperamental trait associated with the development of BPD. A meta-analysis by Bornovalova et al. (2013) found that people with BPD have higher levels of emotional dysregulation and impulsivity compared to control groups. These findings together suggest that temperament-based traits may be potential biological determinants for BPD. 30 Cognitive Deficits with Biological Foundations Some studies also show a relationship between biologically based cognitive deficits and brain abnormalities in the development of BPD. According to Gunderson and Lyons-Ruth (2008) people with BPD are more likely to have cognitive deficits that have biological foundations. Subtle neurological deficits have been found, for example, in the frontal lobes, which are involved in impulsivity, low self-monitoring, and cognitive inflexibility (Meekings & O’Brien, 2004; Lieb et al., 2004). The areas of the brain that have been implicated with BPD are the amygdala and prefrontal cortex, and hippocampus (Lieb et al, 2004). Soloff et al. (2003) found altered baseline metabolism in the prefrontal cortex of people with BPD; Donegan et al. (2003) found altered activation in the amygdala in response to facial expressions; and Herpetz et al. (2001) also found this in response to emotional stimuli. This makes sense in relation to the diagnostic criteria, as both heightened emotional sensitivity and intensity is linked to hyperactivity in the amygdala (Herpetz et al, 2001) and hypoactivity of the prefrontal cortex is linked with difficulties in regulating emotional responses (Goodman et al., 2008). Later in this chapter, the role of trauma will be introduced, but it is important to signal here that trauma has been linked with biological changes in the brain (Rogosch & Cicchetti, 2004). Moreover, deficits in neurobiological mechanisms, and reduced serotonergic functioning, have been identified in brain imaging studies of those with BPD (James & Taylor, 2008). This makes sense as serotonergic functioning is related to impulsivity (Coccaro et al., 1997). Neuroimaging studies have shown reduced serotonin levels with impulsive and aggressive 31 behaviours, and unstable mood states (Gurvits et al., 2000). People with BPD have been shown in neuro-imaging studies to have reduced hippocampal and amygdala volumes compared to the general population (Driessen et al., 2000; Tebartz van Elst et al., 2003); however, it is unclear if reduced volumes were caused by BPD or were premorbid. BPD has been associated with altered Hypothalamic-pituitary-adrenal axis (HPA) axis functioning. The HPA axis is complex set of interactions between the hypothalamus, pituitary gland, and adrenal glands which work together to regulate the body's response to stress (Sheng et al., 2021). When stress is registered by the body, the hypothalamus releases a hormone (corticotropin-releasing hormone) which then signals the pituitary gland to release adrenocorticotropic hormone. This hormone then activates the adrenal glands to produce a stress hormone called cortisol, which is responsible for preparing the body for fight or flight response (Sheng et al., 2021). Studies have shown that people with BPD have an over-active HPA axis, leading to increased cortisol levels when reacting to stress. For example, Drews et al. (2018) conducted the first meta-analysis (covering 804 publications) to explore this extensively. Results found that following psychosocial stress, people with BPD have elevated and continuous cortisol output. These findings have important clinical implications for the treatment of people with BPD. Hyperactivity in the HPA axis may, in part, be responsible for emotional dysregulation and impulsivity characteristics in BPD. These findings highlight the importance of taking biological aetiology into consideration when designing 32 interventions for BPD such as to include psychoeducation on stress awareness and managing stress responses with the rationale behind it presented. This research also highlights and validates why it may be so difficult for people with BPD to manage intense emotions, because their biological systems are hyperactive, making sense of the references to the emotional rollercoaster of BPD. In other words, it is more difficult for people with BPD to manage stress and the intense emotions that come with stress, as both psychological and physical differences are at play. Research has shown that childhood trauma is common in people with BPD (Bornovalova et al., 2013; Brier & Zaidi, 1989). Childhood trauma can cause permanent changes to the HPA axis, leading to increased cortisol reactivity and heightened stress responses (Shär et al., 2022). A recent meta-analysis by Shär et al. (2022) suggested blunted cortisol stress reactivity occurred in people who had experienced childhood trauma. Alterations in HPC axis functioning and therefore cortisol have been proposed as possible mechanisms that link childhood maltreatment experiences, BPD, and health disparities (Shär et al., 2022). Personality Traits The trait theory of personality proposes that personality can be understood by identifying and measuring traits, which are seen to be stable and enduring (Fleeson & Jayawickreme, 2015). Perhaps the most popular trait theory of personality is the 5- factor model (Digman, 1990), also referred to as the OCEAN (Goldberg, 1993). This view holds that people can be described by five core varying traits: openness to new experiences, conscientiousness, extroversion, agreeableness, and neuroticism 33 (Digman, 1990). Research has demonstrated moderate stability in these traits across the lifespan (Funder, 2001; Terracciano et al., 2005), with some traits increasing and decreasing over time. For example, research has shown that conscientiousness increases in young and middle adulthood as people are better equipped to manage relationships and careers (Donnellan & Lucus, 2008). The Big Five has been demonstrated to exist across ethnicities, cultures and ages with some researchers suggesting biological and genetic components to these traits (Jang et al., McCrae & Costa, 1997). The key point with the trait theory of personality is the notion that we have stable and enduring characteristics that are not prone to significant change. BPD is said to be mostly stable across time (Paris, 2020), and trait-based conceptualizations and assessments of BPD have shown that there may be stable traits related to BPD (Cattell & Mead, 2008). The DSM-5-TR (2022) offers an alternative model to diagnose and classify the personality disorders which appear closely tied to the OCEAN. The alternative approach, for example, level of disturbance in self and interpersonal functioning such as empathy, and pathological traits such as negative affect and antagonism (APA, 2022). One critique of trait theory is that it can underestimate the role of the environment and situational factors on people. This critique is supported by Mischel and Shoda’s (1995) research, which suggests that people’s behaviour can be the result of a combination of both personality traits and situational factors. In addition, trait theory may fail to fully account for the development of personality over time as people evolve with life experiences (Roberts & DelVecchio, 2000). 34 Developmental Factors Personality can be conceptualised developmentally, through the procession of a series of stages, within standardised norms, accomplishing the tasks of each stage. For example, the first task of Erikson stages is trust versus mistrust (McLeod, 2023). The theory is that a healthy personality learns to trust others if the infants’ needs are consistently met by their caregiver. If the caregiver is responsive to the infants needs during this stage (attentively feeding, changing, soothing, holding) then the infant is said to gain a generalised view of others being safe to trust, the world being stable, and the first step of a healthy on-track personality is set for course (Skodol et al., 2002). However, there are a variety of things that can go wrong. The caregiver may not be responsive due to post-natal depression, ill physical or mental health, the infant may be in an incubator, there may be external situations impacting attentiveness such as parental loss, adoption, lockdowns, wars, and other traumatic events. If normal progression through one stage is interrupted, the next stage and developmental task may also be impacted, setting off-course for healthy personality development. The infant may learn to respond to inconsistent caregiving by crying louder, for longer, and becoming highly distressed on a regular basis, before being able to elicit a caregiver’s response (McLeod, 2013). A strong body of research suggests that repeated distress, especially early in life, can impact nervous system development and sensitivity. This aligns with biological aetiology discussed, that people with BPD and those who have experienced early trauma, have been found to have hyperresponsiveness of the HPA axis (Rinne et al., 2002). This example of a developmental stage difficulty and biological consequences 35 impacting on emotion and behaviour is relevant to BPD as it ties in with key diagnostic criteria, such as emotional dysregulation, sensitivity, trust, and relational (attachment) issues. Psychological and Environmental Factors As discussed, approximately 80-91% of people diagnosed with BPD have often experienced trauma (sexual, physical, and/or emotional) during their childhoods (Bornovalova et al., 2013; Brier & Zaidi, 1989; Elzy, 2011; Herman et al., 1989; Zanarini, 2000; Zanarini et al., 1997). Therefore, the experience of trauma has been suggested as an explanatory factor for the aetiology of BPD. These may be big event traumas such as sexual abuse or an accident, or a series of on-going accumulative subtle invalidating experiences. Trauma is more commonly reported in BPD compared to many other mental health disorders (Zanarini et al., 1989). People with BPD are more likely to have experienced childhood sexual abuse, (Sansone et al., 2005) which has the strongest association with BPD, independent of other psychological risk factors such as neglect or loss (Ogata et al, 1990; Paris, 1994). Adult survivors of childhood abuse often live with significant life-altering consequences, including psychiatric disorders. The highest accounts of these are Post Traumatic Stress Disorder, mood and substance disorders, and BPD (Green et al., 2010). 36 The symptoms associated with childhood abuse significantly overlap with BPD criteria (Browne & Finkelhor, 1986; van der Kolk, 1991) such as emotional dysregulation, dissociation, disturbed sense of self, interpersonal difficulties, depressed mood, suicidality, problems in intimate relationships such as trust and attachment issues, substance abuse issues, dissociation, and self-harm (Perez-Fuentes et al., 2013) The high proportion of females having BPD may also be explained by gender differences in the sexual abuse of children. Studies taking account of the severity of the abuse, such as if the perpetrator was a family member, frequency, duration, and the nature of the sexual act(s), more strongly related to BPD than the act alone (Gilbert et al., 2009; Porter et al., 2020). This is of clinical relevance to account for in treatment of BPD. Adverse childhood experiences (ACEs) are forms of invalidation that interfere with normal emotional and social development which are associated with a variety of negative health outcomes, including developing mental disorders such as BPD (Agrawal et al., 2004; Cloitre et al., 2005; Levy, 2005; Hughes et al., 2017; Kleindienst et al., 2020). Linehan (1993, 2020), the creator of a gold-star treatment for BPD, has stated that invalidation plays a central role in the aetiology and maintenance of BPD, and therefore is highly relevant in the treatment of this condition. Recently, Schulze et al. (2022) investigated the relationship between ACE’s, BPD, and attachment insecurity. From their findings, they suggest that emotional abuse in childhood may bridge the relationship between ACE and the development of BPD, and that this is at least partially explained by insecure attachment. They found identity disturbance, a BPD central criterion, was strongly associated with insecure attachment, and that identity disturbance and efforts to avoid abandonment were most highly linked to the 37 trait of affect instability than any other BPD trait. This really highlights the impact of early trauma and invalidation in the development of BPD. When attachment is problematic or unsuccessful in a child’s early years, insecure attachment can develop (Crow & Levy, 2019), which will now be discussed. Attachment Bowlby’s model of attachment has clear implications for both healthy and dysfunctional personalities. When early attachments are poor, personality is negatively affected (Barone et al., 2011). Chapter 2 explores attachment theory intervention, and so is only briefly mentioned here in relation to aetiology of BPD. Many researchers suggest that disturbed attachments play a key role in the development of BPD (Carvalho Fernando et al., 2014; Crow & Levy, 2019; Levy, 2005). Agrawal et al. (2004) reviewed 13 studies that had linked BPD and attachment, finding a strong association between BPD and insecure, disrupted attachment. Their research demonstrated that people interviewed all shared the dialectic of longing for intimacy and anxiety about being rejected. The absence of secure early attachments, according to Fonagy et al. (2002), causes mentalization deficits that lead to the development of BPD. Genetic and Environmental Interplay in BPD Etiology In a large-scale study focused on both genetic and environmental risk factors of BPD, Reichborn-Kjennerud et al. (2013) reviewed the nine criteria of BPD in the DSM-5. They found an overall single common genetic factor that influences all BPD criteria to 38 varying degrees. Some criteria showed a high biological and genetic base. However, they also discovered that interpersonal factors accounted for 70.1% of unique environmental influences on the unstable relationship criterion. This suggests that specific environmental factors account for much of the liability to unstable relationships (Reichborn-Kjennerud et al., 2013) which highlights the role that attachment and trauma may play. These findings complement those from Schultze et al. (2022), previously discussed, where emotional abuse (invalidation) was found to be the bridge between the nine BPD criteria and ACEs. Abnormal Parenting and Parents’ Genetics People with BPD experience a higher rate of early separation and loss of their parents in childhood than others (Paris, 1994; Soloff & Millwards, 1983). Though early parental loss and separation fit into the aetiology section of attachment, abnormal parenting, including genetic predispositions for mental health, have been said to play a possible role in BPD development. Studies report those with BPD are more likely to have a family history of mental illness. From a biological perspective, first-degree relatives of those with BPD are more likely to have BPD, Antisocial Personality Disorder, Alcoholism, or Depressive Disorders (Gunderson & Lyons-Ruth, 2008; Skodol, 2012; Zanarini et al., 2001). These conditions involve impulse control and affect instability, personality traits that may be genetic (Skodol, 2012). However, the psychological impact of being brought up living with a parent who has any of these conditions could lead to neglect, trauma, early separation, or loss. For example, depression in a parent can lead to neglect (Friedman & Billick, 2015). When 39 measuring the quality of relationships between people with BPD and their parents, Boucher et al. (2017) found that BPD participants consistently reported a lack of parental care and empathy, inability to meet their emotional needs, inconsistent treatment, inconsistent parental norms and values, a lack of maternal warmth, and/or ridged overprotection. According to Paris (1994), psychological risk factors may instead act as precipitants for a predisposition, based on biological vulnerabilities. The point here is that other environmental and biological interrelated risk factors are suggested in the development of BPD, that may have clinical relevance for treatment, such as psychoeducation on these factors. Biopsychosocial Model of BPD Development Linehan (1993) created a specific therapy for BPD, Dialectical Behavioural Therapy (DBT), which synthesizes etiological factors together in a biopsychosocial model of BPD. Linehan’s model is a comprehensive theory that accounts for both aetiology and maintaining factors of BPD, focusing on the interplay between biological, psychological, and social factors. Her theory acknowledges the biological vulnerability aspects of BPD, such as emotional dysregulation and impulsivity (Chapman, 2019), which interacts with environmental factors such as trauma, and invalidation. An invalidating environment is one where a child’s feelings, thoughts, and behaviours are dismissed or invalidated (Linehan, 1993). Being invalidated leads to reduced emotional regulation ability and the development of maladaptive coping strategies, such as the avoidance of emotions and behaviours that go with this, for example, self- harm (Paris & Lis, 2013). Linehan’s (1993) model is key to this thesis, as much of the research continues with this theme of ongoing invalidation, and its impact on 40 treatment. Linehan’s model considers social and cultural factors that can contribute to BPD, such as stigmatization, gender roles, and discrimination (Linehan, 2020), which in themselves can increase the risk of trauma and invalidation. This aligns with the view presented that the expression and manifestation of mental health conditions, such as hysteria and BPD, can be socially constructed by the culture of the time. In summary, since Stern’s construct of BPD, the term has progressed from psychoanalytic colloquialism to a valid psychiatric diagnosis which acknowledges the complex interplay of genetics, temperament, and the environment (Courtney-Seider et al, 2013). Since the inclusion of BPD in the DSM-III (APA, 1987), research has vastly improved our knowledge of the developmental risk factors for BPD. Despite this, there has still been a general lack of consensus for a model of BPD that agrees on the aetiology of BPD (Siever et al., 2002; Linehan, 2020). Risk factors include biological, environmental, and psychological factors such as trauma, attachment, parental, and family genetics, and social factors. In line with the predisposition stress model, BPD pathology can be viewed as grounded in biological variability and exacerbated by environmental and psychological factors. None of these risk factors taken on their own can individually account for the development of BPD, a complex and multifaceted disorder. The best fit for understanding its development may be the synthesizing of etiological factors into a flexible biopsychosocial model of BPD, such as that has been proposed by both Linehan (1993) and Paris (1994). Some people with BPD do poorly with treatment for a variety of reasons, and one suggested possibility for this is the lack of the inclusion of all aspects of 41 biopsychosocial aetiology into treatment (Paris, 1994). Invalidation, through trauma or more subtle invalidating environments, are factors that knit through BPD aetiology, and diagnostic criteria. These relate to attachment theory, which is not attended to directly as a treatment objective in DBT but is added to the adaptation of the treatment intervention in this study. Chapter 2 links the aetiology of BPD with treatment and explores these issues. 42 Chapter 2: How do we intervene when things go wrong? Treatment for BPD BPD can be treated with several evidence-based interventions. Thirty years ago, Marsha Linehan published her Dialectic Behavioural Skills (DBT) manual as a specific treatment for BPD (Linehan, 1993). Over the past 30 years, different BPD treatments have been developed. These interventions, though well researched, may be impractical to apply without adaptation within a NZ university setting. Given the literature reviewed in Chapter 1, a new intervention for BPD would ideally align with and address the complex aetiological factors and the nine BPD diagnostic criteria. A major aim of this thesis is to develop a new BPD treatment, by, in part, the adaptation of existing treatments. An objective is to take the strengths of several evidence-based interventions, and to address their shortcomings, and the need for briefer intervention, by combining therapies and applying first-hand knowledge from the thematic analysis component of this research to create a new intervention. Therefore, this chapter reviews several prominent BPD treatments and highlights gaps where these treatments may not fully align with BPD criteria or fit with access to early intervention for tertiary populations aims. This chapter presents an overview of Cognitive Behavioural Therapy (CBT), Dialectic Behavioural Therapy (DBT), Acceptance and Commitment Therapy (ACT), and Mentalization Based Therapy (MBT). These interventions will be viewed under a lens of the diathesis-stress and ecological models. For young people with emerging BPD, 43 relationships with the adults in their worlds may be the vector for navigating predispositions to help tolerate distress and build resilience. Therefore, it will be argued that synthesising several evidence-based therapies together with attachment theory will be beneficial. Cognitive Behavioural Therapy Cognitive Behavioural Therapy (CBT) is a short-term, present-focused psychotherapy, that focuses on the relationship between thoughts (cognitions), and behaviour (Beck et al., 1979). There is evidence for its effectiveness for a wide range of mental health conditions including depressive disorders (Oud et al., 2019), anxiety disorders, including obsessive-compulsive disorder (Kaczkurkin & Foa, 2022), panic disorder (Otto & Deveney, 2005), generalized anxiety disorder (Stefan et al., 2019), social anxiety disorder (Alden et al., 2018), phobias (Antony & Rowa, 2005) and post- traumatic stress disorders (Otte, 2022). CBT aims to restructure and change how a person thinks and behaves. CBT, given its success in treating many conditions, has been applied as a potential treatment for BPD. Linehan had been trained in behaviourism and then CBT; as an expert in BPD, she believed that CBT, although helpful for some BPD criteria, required adaptation for BPD patients, as studies of CBT treatment for BPD show mixed results (Linehan, 1993). For example, a large, randomized control study found that CBT was more effective than treatment as usual (TAU) for self-harm in general, but less effective for people with the diagnosis of BPD who self-harm (Tyrer et al., 2003). In 44 contrast, another study showed CBT to be superior for treating BPD than TAU, despite a short treatment duration of 16 weeks (Davidson et al., 2006). In a large-scale study, Davidson added 27 sessions of CBT to borderline patients’ TAU and results indicated that the addition of CBT to usual treatment showed some gradual and sustained improvements in state anxiety and dysfunctional beliefs (Davidson et al., 2006). In a 4-year follow-up to their previous study, Davidson and colleagues reported that treatment gains were maintained (Davidson et al., 2010). Conversely, a recent meta-analysis by Fisher (2022) has suggested that therapies such as Dialectical Behavioural Therapy and Mentalization Based Therapy appear superior to CBT. Acceptance and Commitment Therapy Like CBT, Acceptance and Commitment Therapy (ACT) has a theoretical background which stems from radical behaviourism. It has emerged from challenges of cognitive and behavioural therapies, as well as challenges in the assumptions of knowledge itself (Hayes, 2016). However, unlike CBT, ACT falls under the umbrella of functional contextualism, a philosophy of science that assumes that we know the world only through our interactions in it (and with it) and that our interactions in the world are historically and contextually limited (Hayes, 2016). This aligns with the biopsychosocial model of BPD discussed in Chapter 1, which includes social learning and the influence of society and culture as etiological and maintaining factors, such as feminist views of BPD replacing hysteria as an outlet of distress from societal pressure (Shaw & Proctor, 2005; Ussher, 2013). 45 In brief, the generalised goal of ACT is to increase psychological flexibility, represented by the principles in the six facets of Steven Hayes’ Hexaflex Model (Hayes et al., 2004), shown in Figure 1. Under the philosophy of functional contextualism in ACT, specific behaviours are located within their context and assessed by their function (Arch et al., 2012). For example, if applied to a BPD context, the function of a behaviour, such as self-harm, would be openly explored. From an ACT perspective, cutting oneself in response to emotional pain might be seen as serving the function of experiential avoidance, to avoid the experience of fully feeling an upsetting emotion. Functional contextualism aids in clarifying psychological issues that may be 46 perpetuating a person’s problematic behaviour (Hayes, 2016). Treatment can then be aimed at reducing experiential avoidance. Because ACT has a contextual foundation, therapeutic concepts are viewed differently. Where CBT might focus on substituting what is positioned as unhelpful thoughts through detecting, challenging, and replacing thoughts to change behaviours, ACT is concerned with the function and context of thoughts and behaviours (Bach & Moran, 2008). Because ACT locates this instead to the function and context, as said, the function of self-harm may fall under experiential avoidance. If the BPD patient has the urge to engage in self-harm to avoid the full experience of Note. From “Improving Mental Wellbeing Among University Students Via a Smartphone Application Based on Acceptance and Commitment Therapy” [Master's thesis, University of Waikato] (p. 10), F. Li, 2018, Research Commons (https://researchcommons.waikato.ac.nz/bitstream/handle/10289/11925/thesis.pdf?seque nce=4&isAllowed=y). Figure 1 The ACT Hexaflex Model of Psychological Flexibility 47 feeling emotionally overwhelmed, then the function is avoidance of emotion. Therefore, instead of struggling or arguing with the thought, (of CBT), ACT aims to help the person to sit with distressing thoughts, and to provide some strategies to aid this (Apsche et al., 2014). ACT encourages staying with thoughts and emotions, without needing to change them, control them, or avoid them, and instead make choices based on one’s values rather than avoidance. Research supports ACT’s effectiveness as a treatment for a range of disorders - including anxiety disorders (Hayes, 2016), psychosis (Bloy et al., 2011) and everyday non-clinical populations (Hayes, 2016). Longitudinal studies show the successful long- term effectiveness of ACT for anxiety and depression (Forman, et al., 2012). There is, to date, very few studies using ACT alone to treat BPD. Morton et al. (2012) compared a brief 12-session group ACT therapy to TAU. Participants meeting 4/9 criteria for BPD were randomly assigned to either the TAU group, or TAU plus ACT 12-week add-on, in a community setting. Results indicated a significant decrease in BPD symptoms for participants who received the ACT add-on sessions, while the TAU group showed no significant changes. Treatment gains were sustained at a 3-month follow-up; arguably, this treatment may be more accessible for people, given the 12- week commitment, rather than traditional longer-term therapies for BPD. Adaptation of ACT for the treatment of BPD has shown promising results. Research by Gratz and Gunderson (2006) utilized an adapted ACT treatment component for BPD. They added 14 group sessions of ACT to TAU and reported positive effects on BPD symptoms of self-harm and intense emotions. Their research had a combination 48 of several therapies (DBT, emotion-focused therapy (EFT), behaviour therapy, and ACT) to decrease experiential avoidance. Gratz and Gunderson (2006) noted that the 6/14 sessions that primarily focused on ACT generated the most enthusiasm from group participants. In a more recent study, elements of different treatment modalities from a contextual behavioural perspective including ACT, DBT, and Functional Analytic Psychotherapy (FAP) were integrated to form a group treatment. Participants with BPD were assigned to an ACT group, a DBT group, or the combined ACT, DBT, and FAP group (Reyes- Ortega et al., 2019). Pre- and post-group measures were taken of BPD symptom severity, emotional dysregulation, experiential avoidance, and attachment. All the brief contextual behavioural therapy groups demonstrated effectiveness; they all decreased symptom severity, emotional dysregulation, and negative interpersonal attachment. No group condition stood out as being more effective than the others. The researchers attribute these changes from all groups to the reduction in experiential avoidance and learning mindfulness skills. Another study provided a rationale for including ACT values work as a component in the treatment for BPD (Cameron et al., 2014). The argument is that retention rates for people with BPD receiving treatment are high. Cameron and colleagues suggest that ACT values work can help to increase motivation and adherence to treatment, thus having the possibility to increase retention rates (Cameron et al, 2014). Another unique contribution ACT could offer to people with BPD is working around self-as-context, which is one of the four core processes of ACT, shown on the Hexaflex 49 model (see Figure 1). This seems a relevant treatment adjunct for BPD, given the identity disturbance and unstable sense of self that people with BPD have (Linehan, 1993), and continue to carry even after treatment, into older-adult life (Morgan et al., 2013). Self-as-context can be developed in mindfulness and defusion exercises, such as noticing yourself and noticing your thoughts and feelings, to get a sense of the self that exists beyond thoughts and feelings. Research points to ACT as a promising treatment for BPD, at least in conjunction with other treatment programs. Although ACT is not specifically designed to treat BPD, given the way it places problematic behaviours in the context rather than with the person, it fits in well with an ecological and stress-diathesis model that considers the environment, history, society, and language. ACT is transdiagnostic, which may be a further good fit for BPD, given the historical uncertainty around the BPD diagnosis itself, and the arguments of whether it is better redefined as a trauma disorder or redefined as traits (Classen et al., 2006). All said, ACT seems to be a promising treatment addition for BPD. ACT shares a synergy with DBT, another third wave therapy that emphasizes acceptance and mindfulness. Next, the two main interventions for BPD will be described and discussed, with their strengths and limitations outlined, for the purpose of considering possible adaptations for the new intervention for this study. Dialectic Behavioural Therapy 50 Linehan created DBT, which at this time is the only evidence-based treatment recommended for BPD by the Cochrane library (Lambie, 2020). Given her recently made public declaration that she personally identified as having BPD traits, and experienced psychiatric inpatient stays (Linehan, 2020), she seemed to have an insider’s perspective on what might help. Consequently, she was able to tailor DBT to address many BPD criteria, such as extreme emotional reactivity, and high sensitivity to perceived rejection, and risk behaviours (Bayles et al., 2014). She designed DBT treatment by adapting CBT to add specific skills to increase mindfulness and distress tolerance, to help regulate emotions and improve communication skills. This adaptation carries over the collaborative stance of the therapist from CBT, and adds therapist validation, to acknowledge and validate that people with BPD experience emotional pain, directly challenging the stigma that the patient is, for example, self-harming for attention (Apsche et al., 2005). Linehan’s biopsychosocial model of BPD outlined in Chapter 1 emphasises invalidation and the invalidating environment being both an etiological and maintaining factor for DBT. Therefore, she links this with her DBT intervention through therapist validation stance and strategies. Therapy targets include change and acceptance dialectics that underpin the four modules of DBT skills training; mindfulness, distress tolerance, emotional regulation, and interpersonal effectiveness skills (Bayles et al., 2014). The skills modules will be discussed and expanded on in-depth in Chapter 5 and Chapter 6 when the DBT adapted intervention is outlined. Change and Acceptance Dialectics 51 Linehan (1993) found that a blend of cognitive therapy and acceptance and change dialectics showed improved outcomes for her patients with BPD (Linehan, 1993, 2015). DBT was primarily targeted to the borderline population, with the dialectic pertaining to change and acceptance. Dialectics is the concept that everything is made up of opposites or opposing forces, and that change will occur when one opposing force is stronger than the other, and both parts are acknowledged (Linehan, 1993). A key component of dialectical thinking is that for any perspective, alternative perspectives exist. This highlights the possibility that one’s perspective may then be out of balance, thus contributing to emotional distress (Fruzzetti & Payne, 2020). Figure 2 illustrates the change and acceptance dialectics underlying the four DBT skills modules. On one hand, there is an underlying stance in DBT that the patient is doing the very best at the time with what coping skills they have. At the same time, the dialectic is that this is often not good enough to keep people with BPD safe, so there is a need for change (Linehan, 1993). The change and acceptance dialectics are a major task for all parties, both for the therapist to teach and the patient to master. DBT therapists are both accepting and pushing for change, and aim to do so in a skilful way, as people with BPD can be fearful of rejection from the therapist (Linehan, 2015). Therefore, both the dialectics and the relationship dynamics are essential in the delivery of the dialectics. 52 Therapist and patient dynamics Contingency Learning. In DBT, the therapist plays a teaching role (e.g., DBT skills training and psychoeducation), and they use their relationship dynamic as part of the therapy. Contingency management is central to change dialectics and is derived from operant conditioning theory to either reinforce or punish certain behaviours (Skinner, 1988). The DBT therapist can use positive reinforcement (for example, a chocolate fish in group skills training to reward homework compliance), or disincentives such as the DBT 24-hour rule. The DBT 24-hour rule is that if a patient attempts suicide or self-injury, the access to their primary therapist is cut off for 24 hours, excluding group contact so that this behaviour is not accidentally reinforced with additional caregiving that may perpetuate risk (Linehan, 1993). Increased Figure 2 DBT Skills Training Modules and Change and Acceptance Dialectics Note. From “Dealing With Distress: An Introduction to Healthy Coping Strategies”, C. Vivyan, 2009, Get Self Help (https://www.getselfhelp.co.uk/docs/DealingwithDistress.pdf). Copyright 2009 Carol Vivyan, permission to use for therapy. 53 contingency management is shown to be especially helpful for the simultaneous treatment of co-morbid post-traumatic stress disorder, and for helping people with BPD into work (Carmel et al., 2016). Contingency management is key to addressing therapy-interfering behaviours (Linehan, 1993; Martin & Pear, 2019). Therapy Interfering Behaviours (TIBs). Linehan (2015) coined the DBT term therapy interfering behaviours, pertaining to both the patient and therapist. Psychology has been described as a mixture of art and science (Shapiro & Carlson, 2009), which is relevant for addressing therapy-interfering behaviours, as DBT can be described as a ‘dance’ with the push-pull behaviours, and the therapist has an opportunity to be creative with how to attend to this dance (Chapman & Rosenthal, 2016). For example, the Ekman Faces studies indicate that people with BPD respond differently than other populations when shown various facial expressions; people with BPD tend to find even neutral and smiling faces as initially threatening (Unoka, 2011). The DBT therapist needs to be mindful of their own face and tone, at the same time reflecting the person’s reactions and expressions, and simultaneously having difficult conversations. For example, many people with BPD have exaggerated facial expressions that show their intense reactions to situations (Renneberg et al., 2005). Some DBT strategies aim to help bring awareness to, and reduce the intensity of, facial expressions, such as the Mona Lisa half-smile DBT exercises (Linehan, 1993). Therapist Validation in Relationship. In CBT, the therapist’s collaborative stance is the focus on the therapist-patient relationship. DBT expands this with the therapist using key validation skills (Fruzzetti & Ruork, 2019). Validation is an essential 54 DBT strategy that can be a tool in communicating the acceptance and change of dialectics. Successful validation may include paying attention to the patient’s behaviour in context and authentically communicating their understanding, by understanding that the patient’s feelings are valid and understandable. validation principles are woven into both the DBT skills training (e.g., self-validation skills); as well as being a key component in the therapist-patient relationship in individual DBT, alongside shaping the change and acceptance dialectic (Fruzzetti & Ruork, 2019). Linehan (1993) likens teaching DBT skills in individual therapy sessions to pitching a tent during a hurricane. People with BPD frequently struggle with ongoing chaos and a roll