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. 1 Ngā mea kōaro o ngā wā tamarikitanga, Te taumahatanga o aua mea Me ētahi mahi whakaora hinegaro mō ngā wāhine Māori Adverse childhood experiences, HPA axis functioning and culturally enhanced mindfulness therapy among Māori women in Aotearoa New Zealand. A dissertation presented in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Psychology at Massey University, Palmerston North, New Zealand Miriama Deborah Ketu-McKenzie 2019 Ko Tongariro me Tararua ngā pāe maunga, Ko Taupo-nui-ā-Tia te moana Ko Manawatū te awa Ko Te Arawa me Tainui ngā waka Ko Ngāti Tūwharetoa me Ngāti Raukawa ngā iwi Ko Ngāti Rongomai, Ngāti Hine, Ngāti Whakatere, me Ngāti Takihiku ngā hapū Ko Rongomai, Korohe, Whakawehi-Poutu, me Kereru ngā marae Ko Claude Turetangata Ketu raua Ko Aniwaniwa Oterangi McGregor ōku mātua tūpuna Ko Claude Ketu rāua ko Faye Schultz ōku matua Ko Anaru McKenzie tōku hoa rangatira Tokotoru ngā tamariki, Ko Thomas Turetangata, Ko Rachel Ringahuia, Ko Esther Aniwaniwa Oterangi Ketu-McKenzie Ko Miriama Ketu-McKenzie ahau Tihei Mauri ora 2 Nā tō rourou, nā taku rourou ka ora ai te iwi With your food basket and with my food basket, the people will thrive 3 ABSTRACT Chronic health conditions such as obesity, type II diabetes, cardiovascular disease, depression and anxiety are prevalent among Māori women in New Zealand, as are adverse experiences in childhood and chronic stress. Recent studies have shown a link between adverse childhood experiences (ACEs) and chronic health problems later in life. Many of those studies propose that dysregulation in the stress response system - specifically the hypothalamic-pituitary-adrenal (HPA) axis - mediates that link. Cortisol is the primary corticosteroid released by the HPA axis and is commonly used as a biomarker for assessing HPA axis functioning. Mindfulness-Based Stress Reduction (MBSR) is a therapy that uses a range of breathing techniques, stretches, formal meditations and awareness exercises designed to help regulate the stress response by changing the way the brain manages and relates to stress. Due to its Eastern roots, MBSR therapy assumes an holistic view of health that mirrors some of the key concepts promoted in Te Ao Māori. This research tested the HPA axis functioning of eight adult Māori women who had experienced high ACEs, and explored associations between cortisol dysregulation, visceral obesity (a risk factor for many chronic health conditions) and psychological distress. This research also tested the clinical effectiveness and cultural responsiveness of an MBSR course that had been enhanced to suit a Māori audience. Participants provided pre, mid and post-treatment salivary cortisol samples that measured changes to their acute stress cortisol response, as well as changes to their daily cortisol slope, their cortisol awakening response and their overall cortisol levels. They also provided pre and post-treatment waist circumference measurements. Self-report data assessing depression and anxiety levels, PTSD levels, stress eating habits, perceived stress levels and mindful awareness levels, was collected, as was qualitative data in the form of pre and post-treatment interviews. The results indicated that culturally enhanced MBSR therapy was well received with this sample of Māori women and that the participants reported a wide range of benefits as a result of practicing mindfulness meditation. 4 5 ACKNOWLEDGEMENTS This project would have been impossible to complete without the aid and support of the Rose Hellaby Postgraduate Scholarship, the Karahipi Tumuaki Scholarship, Te Rau Puawai, Pūrehuroa and the Massey University Doctoral Scholarship committees. I was gifted support from those organisations under the premise that I would endeavour to make the way smoother for those who might follow in my footsteps. To that end, I dedicate this work to the rangatahi, me ngā tauira Māori o tenei rā. To my early supervisors Dr. Mei Wah Williams and Associate Professor John Podd, I offer my complete and sincere thanks for the time, attention and faith you invested in me and this work. Though circumstances meant you were unable to see the project across the finish line, your gentle wisdom and guidance is still very present throughout. He mihi māhana ki a kōrua. To my post-relocation supervision team, Dr. Michael Philip, Dr. Wendy Holley-Boen and Dr. Stephen Hill, your commitment to walk beside me as I waded through the ‘swampy lowlands’ of this project made all the difference. You joined this research team knowing only that a student was in need of supervisors, and you didn’t run away when you discovered that I was also juggling a newborn, a toddler and 5-year old. For that, I am most grateful. Your faith in my ability to see this project through to completion in spite of the challenges, was integral to maintaining my momentum. Wendy, I offer special thanks to you for encouraging me to be bold and to honour the social justice aspects of this work. Michael, I acknowledge you for being kind to my mistakes and for encouraging me to follow the path that was right for this piece, not the path that was most convenient, well-tread or most widely accepted. This work is better off because of your combined input. Thank you. 6 There are many, whose time, expertise, mana and networks contributed to the timely completion of this project. Specifically though, I would like to acknowledge Dr. Karl Iremonger at the University of Otago and Dr. Kingsley Nirmilaraj at Tauranga Hospital for providing expert advice and opinions on the collection and interpretation of the cortisol data. I would also like to acknowledge the team at Te Manu Toroa Kaupapa Māori Health Care Service and Natasha & Grant Rix, for their unmitigated support during the early phases of this project. Special thanks also to Francie & Cindy Diver, Fran & Zoe at Kōhatu, Moana Theodore, Moana Wesley, King’s High School, Southern DHB, Aunty Kathy, Hamish & Stephanie, Leann, Wendi Raumati and Olly Ohlson, who generously shared their networks, their wisdom and their resources in the service of this mahi. Also to Ben Hutchison, Kirby-Jane Hallum, Andrew McKenzie and Richard Huber, who contributed their time, energy and acting skills to the project, at considerable expense to their moral comfort. He mihi nunui ki a koutou katoa. To my whānau in Shannon – Nana, Koro, Aunty Diane, Aunty Mae, Aunty Nina, Aunty Lani, Aunty Ellen, Uncle Robert, Uncle Moses and especially Dad – thank you for being my link to Te Ao Māori, Te Ao Mārama, me Te Ao Turoa. It is from you that I have drawn the motivation, courage and energy to pursue better outcomes for tangata Māori. Thank you for your quiet support over the years. To my whānau in Morrinsville – Naomi, Nathan, David, Paiahua, Te Uru Maranga, Whetu Marama, Aunty Maxine and Mum – thank you for keeping my feet on the ground, thank you for inspiring me to keep walking when I forgot why I had set out in the first place, thank you for being a home base to which I could return whenever the journey became too difficult. To Richard and Louise McKenzie, I owe profound gratitude for providing me with the one thing I lacked most during this process, time. Richard, your encouragement and belief has meant a great deal. Louise, you sacrificed many hours of freedom to 7 watch the kids while I hid away and wrote. Your knowledge of Te Ao Māori is embedded in these pages. I cannot adequately express the depth and sincerity of my thanks to you for your contribution. To the wāhine who participated in this project, you are the heroes of this research. It is your stories, your courage in telling those stories, your faith in this process and your resilience in the face of adversity that has made this a work worth reading. To Kovido, the man who led us through unknown terrain – thank you for taking a leap of faith and fronting this challenge head on. You were a rare find and I am ever grateful to you for being someone who so effortlessly walks the talk. Finally, to my children – Thomas, Rachel, and Esther. This PhD has been in the background of your lives since before you were even born. I can never get back the time I have spent working on my computer instead of attending to your needs. I can only hope that life will be kind enough to give me many more hours enjoying your company and being present for our moments together. To Andrew, it is your friendship and love that this process has tested the most. You were a catalyst for believing I could even attempt higher education. Thank you for being there. I hope time will show that the benefits of undertaking this research outweighed the costs. I promise you will have my undivided attention for many years to come. 8 9 Table of contents List of Figures 19 Glossary of Māori words 20 Chapter 1 - Pākeha New Zealanders live longer than Māori 22 1.1 Outline and Aims 22 1.2 Personal context 22 1.3 Health and social disparities between Māori and Pākeha New Zealanders 24 1.4 Factors influencing disparity 26 1.5 My own positioning 27 1.6 A word on language 27 1.7 Thesis structure 28 1.8 The present study 29 1.9 Chapter outline 31 Chapter 2 - Chronic stress contributes to early death 32 2.1 Outline and Aims 32 2.2 The stress response system 32 2.2.1 The short term-stress response 32 2.2.2 The long term stress response 34 2.2.3 An introduction to cortisol 35 2.2.4 Prolonged cortisol exposure 35 2.2.5 Cortisol awakening response (CAR) 36 2.2.6 Cortisol daily slope (DS) 37 2.2.7 Cortisol response to acute stress (AS) 38 2.3 Stress definitions 39 2.4 Effects of stress 40 2.5 The adverse childhood experiences study (ACE) 41 2.5.1 The extended ACE Pyramid 43 2.5.2 Personal context 45 2.6 The allostatic load model 45 2.6.1 Homeostasis 45 2.6.2 Allostasis 46 2.7 Summary 47 Chapter 3 - From historical trauma to early death 48 3.1 Outline and aims 48 3.2 Tier One: Historical trauma 48 3.2.1 Historical trauma contributes to adverse social conditions 50 3.2.2 Personal context: From land loss to poor social conditions 51 10 3.3 Tier Two: Social conditions 52 3.3.1 Social conditions contribute to adverse childhood experiences 53 3.3.2 Personal context: From poor social conditions to high ACEs 54 3.4 Tier Three: Adverse childhood experiences 54 3.4.1 Adverse childhood experiences contribute to allostatic load 57 3.4.2 Personal context: From high ACEs to allostatic load 59 3.5 Tier Four: Allostatic load 59 3.5.1 Allostatic load contributes to coping behaviour 63 3.5.2 Personal context: From allostatic load to coping 65 3.6 Tier Five: Coping 66 3.6.1 Coping behaviour contributes to the burden of chronic disease 68 3.6.2 Personal context: From coping mechanisms to early death 68 3.7 Tier Six: Burden of chronic disease 69 3.7.1 Burden of chronic disease contributes to early death 71 3.7.2 Personal context 71 3.8 Tier seven: Early death 72 3.8.1 Personal context 72 3.9 Summary 73 Chapter 4 - Systemic contributors to early death 74 4.1 Outline and aims 74 4.2 An overview of inequity 74 4.3 Barriers at the level of governance 75 4.4 Barriers in the way health care is structured 77 4.4.1 Potential solutions 78 4.5 Barriers due to conflicting views of health 78 4.5.1 Potential solutions 81 4.6 Barriers due to the absence of spirituality 82 4.6.1 Potential solutions 84 4.7 Barriers due to lack of tikanga Māori 85 4.7.1 Potential solutions 85 4.8 Barriers at the level of individual health professionals 86 4.8.1 Potential solutions 87 4.9 Summary 88 Chapter 5 - Mindfulness therapy for Māori 90 5.1 Outline and aims 90 5.2 Meditation and the relaxation response 90 5.3 Mindfulness meditation 91 5.3.1 Mindfulness Based Stress Reduction (MBSR) 91 5.3.2 Benefits of MBSR therapy 92 11 5.3.3 Mindfulness meditation reduces risk factors for chronic disease 94 5.4 Criticism of mindfulness 95 5.5 MBSR fits well with Māori worldviews 96 5.5.1 MBSR is informed by an holistic view of health 97 5.5.2 MBSR therapy promotes spirituality 97 5.5.3 MBSR is group based therapy 98 5.5.4 MBSR is experiential therapy 99 5.5.5 MBSR concepts overlap with concepts in Te Ao Māori 100 5.5.6 MBSR can be adapted for minority groups 100 5.5.7 MBSR promotes non-judgmental practitioners 101 5.5.8 MBSR bridges between Māori and bio-medical model 102 5.6 Summary 103 Chapter 6 – The present study 105 6.1 Outline and aims 105 6.2 Research question one 105 6.3 Research question two 106 6.4 Research question three 107 6.5 Rationale for selecting Māori women with childhood adversity 108 6.6 Rationale for focus on chronic stress 109 6.7 Rationale for focus on cortisol profiles 110 6.8 Rationale for focus on visceral obesity 112 6.9 Rationale for focus on psychological distress 113 6.10 Rationale for focus on MBSR 114 6.11 Methodology and design 115 6.12 Summary 118 Chapter 7 – Cultural enhancements to MBSR 119 7.1 Outline and aims 119 7.2 Standardised MBSR therapy 119 7.3 Culturally enhancing MBSR therapy – Consultation 119 7.3.1 Integrating tikanga Māori and MBSR therapy 120 7.4 The therapist 121 7.5 Study Settings 122 7.6 Outline of course content and cultural enhancements 122 7.7 Class One 123 7.7.1 Cultural enhancement of Class One: Hau and Mauri 123 7.8 Class Two 125 7.8.1 Cultural enhancement of Class Two: Te taha hinengaro 125 7.9 Class Three 125 7.9.1 Cultural enhancement of Class Three: Te taha tinana 126 12 7.10 Class Four 126 7.10.1 Cultural enhancement of Class Four: Ha, a kui mā, a koro mā 126 7.11 Class Five 127 7.11.1 Cultural enhancement of Class Five: Te taha wairua 127 7.12 Class Six: 128 7.12.1 Cultural enhancements of Class Six: Te taha whānau 128 7.13 Full day workshop: Silent retreat 128 7.14 Class Seven 129 7.14.1 Cultural enhancements to Class Seven: Atawhai and Aroha 129 7.15 Class Eight 129 7.15.1 Cultural enhancements of Class Eight: Te Whare Tapa Whā 130 7.16 Summary 130 Chapter 8 – Method 131 8.1 Outline and aims 131 8.2 Participant characteristics 132 8.3 Ethical considerations 133 8.4 Outcome Measures 135 8.5 Measuring mindful awareness 137 8.5.1 Mindful Attention and Awareness Scale (MAAS) 137 8.6 Measuring chronic stress 138 8.6.1 Social Readjustment Rating Scale (SRRS) 138 8.6.2 Perceived Stress Scale (PSS) 139 8.7 Measuring cortisol dysregulation 140 8.7.1 Cortisol awakening response (CAR) 140 8.7.2 Cortisol daily slope (DS) 141 8.7.3 Cortisol response to acute stress (AS) 141 8.8 Measuring visceral obesity 143 8.8.1 Waist circumference (WC) 143 8.8.2 Dutch Eating Behaviour Questionnaire (DEBQ) 144 8.9 Measuring psychological distress 145 8.9.1 Depression, Anxiety and Stress Scale (DASS) 145 8.9.2 PTSD Checklist – Civilian Version (PCL-C) 146 8.10 Measuring how culturally enhanced MBSR was received 147 8.10.1 Semi-structured interviews 147 8.11 Study procedure 149 8.11.1 Baseline assessment phase 149 8.11.2 Treatment phase 150 8.11.3 Post-treatment assessment phase 150 8.12 Summary 150 13 Chapter 9 - Results: Individual case studies 152 9.1 Outline and aims 152 9.2 Case Study One: Ripeka 152 9.2.1 Findings from research question one: Baseline results 153 9.2.1.1 Mindful awareness 153 9.2.1.2 Chronic stress 154 9.2.1.3 Cortisol dysregulation 154 9.2.1.4 Visceral obesity 154 9.2.1.5 Psychological distress 155 9.2.2 Findings from research question two: Response to the course 155 9.2.3 Findings from research question three: Clinical change 159 9.2.3.1 Mindful Awareness 159 9.2.3.2 Chronic stress 159 9.2.3.3 Cortisol dysregulation: 160 Cortisol awakening response (CAR) 160 Cortisol daily slope (DS) 160 Acute stress response (AS) 161 9.2.3.4 Visceral obesity 162 9.2.3.5 Psychological distress 162 9.2.4 Summary 163 9.3 Case Study Two: Ani 164 9.3.1 Findings from research question one: Baseline results 165 9.3.1.1 Mindful awareness 165 9.3.1.2 Chronic stress 165 9.3.1.3 Cortisol dysregulation 166 9.3.1.4 Visceral obesity 166 9.3.1.5 Psychological distress 166 9.3.2 Findings from research question two: Response to the course 166 9.3.3 Findings from research question three: Clinical change 170 9.3.3.1 Mindful Awareness 170 9.3.3.2 Chronic stress 170 9.3.3.3 Cortisol dysregulation: 171 Cortisol awakening response (CAR) 171 Cortisol daily slope (DS) 172 Acute stress response (AS) 172 9.3.3.4 Visceral obesity 173 9.3.3.5 Psychological distress 173 9.3.4 Summary 174 9.4 Case Study Three: Hararutu 176 9.4.1 Findings from research question one: Baseline results 177 14 9.4.1.1 Mindful awareness 177 9.4.1.2 Chronic stress 177 9.4.1.3 Cortisol dysregulation 178 9.4.1.4 Visceral obesity 178 9.4.1.5 Psychological distress 178 9.4.2 Findings from research question two: Response to the course 178 9.4.3 Findings from research question three: Clinical change 181 9.4.3.1 Mindful Awareness 181 9.4.3.2 Chronic stress 181 9.4.3.3 Cortisol dysregulation: 182 Cortisol awakening response (CAR) 182 Cortisol daily slope (DS) 182 Acute stress response (AS) 183 9.4.3.4 Visceral obesity 183 9.4.3.5 Psychological distress 184 9.4.4 Summary 185 9.5 Case Study Four: Kiri 186 9.5.1 Findings from research question one: Baseline results 187 9.5.1.1 Mindful awareness 187 9.5.1.2 Chronic stress 187 9.5.1.3 Cortisol dysregulation 187 9.5.1.4 Visceral obesity 188 9.5.1.5 Psychological distress 188 9.5.2 Findings from research question two: Response to the course 188 9.5.3 Findings from research question three: Clinical change 190 9.5.3.1 Mindful Awareness 190 9.5.3.2 Chronic stress 190 9.5.3.3 Cortisol dysregulation: 191 Cortisol awakening response (CAR) 191 Cortisol daily slope (DS) 192 Acute stress response (AS) 192 9.5.3.4 Visceral obesity 193 9.5.3.5 Psychological distress 193 9.5.4 Summary 194 9.6 Case Study Five: Arohia 195 9.6.1 Findings from research question one: Baseline results 196 9.6.1.1 Mindful awareness 197 9.6.1.2 Chronic stress 197 9.6.1.3 Cortisol dysregulation 197 9.6.1.4 Visceral obesity 197 15 9.6.1.5 Psychological distress 197 9.6.2 Findings from research question two: Response to the course 198 9.6.3 Findings from research question three: Clinical change 202 9.6.3.1 Mindful Awareness 202 9.6.3.2 Chronic stress 202 9.6.3.3 Cortisol dysregulation: 203 Cortisol awakening response (CAR) 203 Cortisol daily slope (DS) 204 Acute stress response (AS) 204 9.6.3.4 Visceral obesity 205 9.6.3.5 Psychological distress 205 9.6.4 Summary 206 9.7 Case Study Six: Wairata 208 9.7.1 Findings from research question one: Baseline results 209 9.7.1.1 Mindful awareness 209 9.7.1.2 Chronic stress 210 9.7.1.3 Cortisol dysregulation 210 9.7.1.4 Visceral obesity 210 9.7.1.5 Psychological distress 210 9.7.2 Findings from research question two: Response to the course 210 9.7.3 Findings from research question three: Clinical change 211 9.7.3.1 Mindful Awareness 211 9.7.3.2 Chronic stress 211 9.7.3.3 Cortisol dysregulation: 212 Cortisol awakening response (CAR) 212 Cortisol daily slope (DS) 212 Acute stress response (AS) 213 9.7.3.4 Visceral obesity 213 9.7.3.5 Psychological distress 214 9.7.4 Summary 215 9.8 Case Study Seven: Marama 216 9.8.1 Findings from research question one: Baseline results 217 9.8.1.1 Mindful awareness 217 9.8.1.2 Chronic stress 217 9.8.1.3 Cortisol dysregulation 217 9.8.1.4 Visceral obesity 218 9.8.1.5 Psychological distress 218 9.8.2 Findings from research question two: Response to the course 218 9.8.3 Findings from research question three: Clinical change 220 9.8.3.1 Mindful Awareness 220 16 9.8.3.2 Chronic stress 220 9.8.3.3 Cortisol dysregulation: 221 Cortisol awakening response (CAR) 221 Cortisol daily slope (DS) 222 Acute stress response (AS) 222 9.8.3.4 Visceral obesity 223 9.8.3.5 Psychological distress 223 9.8.4 Summary 224 9.9 Case Study Eight: Ngāpaki 225 9.9.1 Findings from research question one: Baseline results 226 9.9.1.1 Mindful awareness 226 9.9.1.2 Chronic stress 226 9.9.1.3 Cortisol dysregulation 226 9.9.1.4 Visceral obesity 227 9.9.1.5 Psychological distress 227 9.9.2 Findings from research question two: Response to the course 227 9.9.3 Findings from research question three: Clinical change 230 9.9.3.1 Mindful Awareness 230 9.9.3.2 Chronic stress 230 9.9.3.3 Cortisol dysregulation 231 Cortisol awakening response (CAR) 231 Cortisol daily slope (DS) 231 Acute stress response (AS) 232 9.2.3.4 Visceral obesity 233 9.2.3.5 Psychological distress 233 9.9.4 Summary 234 Chapter 10 – Discussion 235 10.1 Outline and aims 235 10.2 Research questions one 235 10.2.1 Summary 237 10.3 Research question two 238 10.3.1 Perceived benefits 238 10.3.2 Qualities of the teacher 239 10.3.3 Group based therapy 240 10.3.4 Mindfulness as a spiritual practice 240 10.3.5 An holistic approach 241 10.3.6 Congruence with Māori concepts 241 10.3.7 Summary 242 10.4 Research question three 242 10.4.1 Summary 244 17 10.5 Strengths and limitations of the study 245 10.5.1 Design limitations 245 10.5.2 Design strengths 247 10.5.3 Cortisol measurement limitations 248 10.5.4 Cortisol measurement strengths 248 10.5.5 Construct validity limitations 249 10.5.6 Construct validity strengths 250 10.5.7 Cultural limitations 250 10.5.8 Cultural strengths 251 10.6 Implications and future research 252 10.7 Conclusion 253 10.8 Personal reflection 255 Appendix A - AUCg cortisol awakening response 286 Appendix B - AUCg cortisol daily slope 287 Appendix C - AUCg acute stress test 288 Appendix D - Letter of ethical approval 289 Appendix E - Saliva sampling instructions 290 Appendix F - Information Sheet 291 Appendix G - Consent form 295 Appendix H - ACE Questionnaire 296 18 List of Figures 1.1 Life expectancy rates for Māori and non-Māori New Zealanders.......................25 2.1 The hypothalamus-pituitary-adrenal axis…………………………………………..33 2.2 Daily cortisol slope..............................................................................................38 2.3 Adverse childhood experiences (ACE) pyramid.................................................43 2.4 Extended ACE Pyramid......................................................................................44 3.1 Three common hypo-cortisolemic curves ………………………………………....57 3.2 Diurnal salivary cortisol concentrations in chronic fatigue syndrome…………...58 3.3 Types of allostatic load……………………………………………………………….60 List of Tables Table 1: Participant demographics……………………………………………………….... Individual Case Studies Table 1: Baseline results……………………………………………………………………. Figure 1: Mindful awareness scores……………….…………………………………....... Figure 2: Perceived stress scores ………………………………………………………… Figure 3: Baseline CAR…………………………………………………………………….. Figure 4: Mid-treatment CAR………………………………………………………………. Figure 5: Post-treatment CAR……………………………………………………………… Figure 6: Baseline DS………………………………………………………………………. Figure 7: Mid-treatment DS………………………………………………………………… Figure 8: Post-treatment DS……………………………………………………………….. Figure 9: Stress perceptions during baseline TSST……………………………………... Figure 10: Cortisol response to baseline TSST………………………………………….. Figure 11: Stress perceptions during post-treatment TSST…………………………….. Figure 12: Cortisol response to post-treatment TSST…………………………………... Figure 13: Eating behaviour scores……………………………………………………….. Figure 14: Depression, anxiety and stress scores……………………………………….. Figure 15: Post-traumatic stress scores…………………………………………………... 19 Glossary of Māori words Māori Indigenous New Zealander Pākeha New Zealander of European descent Aotearoa The Māori name for New Zealand Te Reo Māori The Māori language Whānau Family, extended family, kin networks Tangi Traditional Māori funeral that lasts 3-days Whanaungatanga Togetherness, relationship Tangata whaiora Mental health consumer Te tiriti o waitangi Māori version of the Treaty of Waitangi Reo me ona tikanga Māori language and traditions Te kohanga reo Māori language immersion early childhood care The waitangi tribunal Entity charged with addressing Treaty breaches Tāne Men, man, male Marae Māori meeting ground Karanga Ceremonial call performed by women Ia He, she, him, her, it Tipuna Ancestor(s) Koro Grandfather, old man Kaupapa maori Māori approach, Māori agenda Te rau puawai Mentorship programme for Māori studying health He korowai oranga The Māori health strategy Te whare tapa wha Model of Māori health Whare House Te taha tinana The physical side of being Te taha wairua The spiritual side of being Te taha hinengaro The mental side of being Te taha whanau The social side of being Io Supreme being Mauri Life principle, energy Ātua Gods, deities Papatuanuku Earth mother Ranginui Sky father Whakapapa Ancestry, lineage, genealogy, history Hui Meeting, gathering Kaumatua Elder, wise person Tikanga Māori traditions, protocols, practices, rituals Pōwhiri Traditional Māori welcome onto a marae Karakia Prayer, incantation Mihimihi Formal way of greeting another Kai Food, eating Manaakitanga Sharing, kindness, hospitality, collaboration Awhi Support, help Whakamā Shame, embarrassment Tangata whenua People of the land (Māori) Tohunga Expert, healer 20 Kura kaupapa Māori immersion special character school Waiata Song, singing Awhinatanga Ongoing support Pepeha Way of introducing yourself in Māori Karakia kai Blessing the food before eating it Koha Gift Kaitiaki Guardian Wharenui Māori meeting house Hau Breath of spirit Hongi Ritual involving pressing noses together Te ao māori The Māori world Tinana Body Ha a kui ma a koro ma Breath of our ancestors living on through us Ha taonga tuku iho Breath handed down across generations Utu Reciprocity Aroha Love Hariru Greeting one another with hongi or handshake Tapu Sacred Whakamā Shame 21 Chapter 1 - Pākeha New Zealanders live longer than Māori 1.1 Outline and Aims This chapter introduces the research project and uses personal experience to provide context for the investigations that follow. The chapter briefly discusses the current health status of Māori in relation to Pākeha New Zealanders, it introduces 1 2 the content of each subsequent chapter and provides a summary of the research questions explored within this study. 1.2 Personal context As the third born daughter of a Māori man and a Pākeha woman, I have spent many years making connections between the many disparate worlds that inform my existence. My mother is the middle of three children who grew up in 1950’s rural Aotearoa New Zealand at a time when all pubs closed at 6:00pm, and some 3 refused to serve drinks to Māori (Christoffel, 2013; Hutt, 2003). My father is the eldest of eight children who were also raised at that time - a time when te reo Māori 4 was not even recognised as an official language of Aotearoa New Zealand (New Zealand Government, 2018). On my mother’s side of the family, we recently lost an aunt who lived to the age of 105 and an uncle who lived to the age of 98. Mum’s own mother (my grandmother) lived until the age of 82. However Dad’s mother, (my Nana), like 15 of her 20 siblings, died before the age of 60 at a time when the average Pākeha New Zealander was expected to live for at least 70 years (Ministry of Health, 2018e). Te reo Māori was the first language spoken by both of my paternal grandparents, yet my father barely heard a word of it growing up, because when his parents were at school, they, like many other Māori, had been beaten by their teachers for speaking Te reo Māori and for engaging in traditional Māori practices (Selby, 2014). 1 Māori = Indigenous New Zealander 2 Pākeha = New Zealander of European descent 3 Aotearoa = The Māori name for New Zealand 4 Te Reo Māori = The Māori language, made an official language of New Zealand in 1987 22 Thus, he never learned to speak his native language. However, Dad was raised with traditional, collectivistic Māori values, which placed family loyalty above all other pursuits. This largely explains why 60 years later, he and six of his siblings still live in or near their hometown of Shannon, Horowhenua (pop.1506) (Statistics New Zealand, 2013). Through my father, I am connected to a large whānau of Māori, most of whom are 5 expected to live an average of seven years less than the family members on my mothers’ side - simply because they are Māori (Ministry of Health, 2018e). The statistics imply that most of their deaths will be preceded by chronic disease (Ministry of Health, 2018f). As an adolescent, I watched as over the course of several years, my father changed from being a relatively healthy 41 year old Māori male, to becoming obese, being diagnosed with Type II diabetes, developing hypertension and heart disease, and battling serious mental health issues. He was eventually diagnosed with Cushing’s Disease – an illness characterised by excess levels of the steroid hormone, cortisol (Adina et al., 2018). Following this, he underwent transphenoidal surgery to remove a pituitary adenoma, which stopped his body from producing too much cortisol - after which most of his symptoms were reversed. In the twenty years since his operation it has become widely known that cortisol plays an important part in regulating almost every major system in the body. Notably, cortisol is produced in response to waking, in response to exercise, and in response to acute stress (Bianchi & Esposito, 2012). Three years prior to becoming sick, my father had resigned from his job and taken over the leadership of a prominent local church. At the same time, he had enrolled as a student at Bible college. Notably, his change in vocation prompted a significant drop in income for the family, for the church leadership position was an unpaid one. One month after starting his position at the church, his grandmother died. Eight weeks after that, his wife gave birth to their fourth child. Ten days after the baby 5 Whānau = Family, extended family, kin networks 23 arrived, his mother died suddenly, and being a church minister, he presided over her tangihanga. Suffice it to say, he experienced more stress in that one year than 6 some might experience in a decade. In the years since his surgery, Dad has for the most part, enjoyed reasonable health. However, two years ago he was diagnosed with end stage renal failure, as well as prostate cancer, and he now spends four and a half hours per day attached to a dialysis machine. He is 65 years old. Consistent with the nationwide Māori health statistics, chronic disease and premature death has featured prominently in my Māori family history and continues to do so. Even while writing the final draft of this thesis we received news that Dad’s youngest brother had died suddenly of a stroke. He was 51. The average life expectancy of a Māori man is presently 73 years. The average life expectancy of a Pākeha man is 80 years (Ministry of Health, 2018e). 1.3 Health and social disparities between Māori and Pākeha New Zealanders Health and social disparities between Māori and Pākeha New Zealanders mirror those of indigenous in other countries (Oetzel et al., 2017). Like First Nations people in Canada, aboriginal people in Australia and the Torres Strait Islands, American Indian, Native Alaskan and Native Hawaiian men and women in the United States, the indigenous people of Aotearoa New Zealand are also over-represented in the prison population, in rates of unemployment, in levels of homelessness and poverty, in low rates of educational attainment and, in high rates of alcoholism, drug addiction, and mental health problems (Anderson et al., 2006; Jackson-Pulver, Haswell, Ring, Waldon, & Clark, 2010; Reading & Wien, 2009; Ring & Brown, 2003). However, nowhere are disparities more clearly seen than in the life expectancy rates between the two ethnic groups. 6 Tangihanga = Māori funeral ceremony that typically lasts for three days. 24 Figure 1.1 Life expectancy rates for Maori and non-Maori. Dotted line shows adjustments for undercounting during the years 1980-1999. Reprinted from Ministry of Health (2018e). Historically, such knowledge has been used to argue that negative indigenous health and social outcomes must be genetic in origin (Lundy, 2002; Paradies, Montoya & Fullerton, 2007) or that indigenous peoples experience poor health simply because they make poor lifestyle choices, such as eating nutrient-deficient foods and smoking (Whelan & Wright, 2013). Such explanations are convenient because they absolve those in power of the responsibility to prioritise the wellbeing of indigenous communities (Abdolhosseini et al., 2016). In the case of Māori however, the genetic argument simply does not hold. Early records suggest that prior to colonisation, Māori showed exemplary health characterised by ‘great muscular strength’ (Nicholas & Marsden, 1817, p.230) and an absence of any ‘eruption upon the skin or the least mark which indicated that such a mark had formerly existed’ (Kippis, 1842, p.81). Moreover, the life expectancy of Māori in the early 1800’s of approximately 30 years, was considered equal to or greater than that of Europeans (Pool, 2011). But within 100 years of regular colonial contact, the life expectancy from birth for Māori women had decreased to 23 years, while the life expectancy from birth for Pākeha women had increased to 55 years of age (Pool & 25 Jackson, 2011). Although most of this disparity is attributable to communicable diseases, 128 years later in 2018, Māori women still live an average of seven years less than non-Maori and most of that disparity is because of preventable, chronic disease (Ministry of Health 2018e; Ministry of Health, 2018f). 1.4 Factors influencing disparity While it is widely accepted that the health and social disparities in New Zealand are in some way linked to the devastating effects of British colonisation (frequently known as historical trauma ), the exact mechanisms through which colonisation continues to exert its effects upon Māori are not explicitly known. This has caused some health professionals to question the relevance of historical trauma as a contributing agent (Oetzel et al., 2017). Life-style choices and poverty are obvious targets for justifying disparities because Māori are three times more likely than non-Maori to smoke cigarettes and two times more likely to drink heavily (Ministry of Health, 2018a; Ministry of Health, 2018k). Māori are also two times more likely to become obese and they are also more likely to self harm (Ministry of Health, 2018i; Ministry of Health, 2018j). Combined with statistics showing that disproportionately more Māori are homeless, unemployed or living in crowded housing conditions (Marriott & Sim, 2014), it is easy to assume that the reason Māori do not live as long as their Pākeha counterparts is because of their neglectful health behaviours and unfortunate life circumstances. However, a growing body of evidence indicates that there may be another factor underlying many of these health disparities. Emergent research from Australia suggests that chronic exposure to psychosocial stress might be one of the defining differences between indigenous and non-indigenous peoples the world over (Berger et al., 2017). In addition, chronic psychosocial stress may be the point at which historical trauma, social conditions and health risk behaviours all converge to promote chronic disease, ultimately leading to early death. 26 1.5 My own positioning My father’s illness sparked a long term interest in the steroid hormone cortisol and in the role it plays in maintaining physical and mental health. Indeed, that experience largely contributed to my decision to become a Clinical Psychologist. Having recently completed a clinical psychology training programme however, I am now trained to view the world through a clinical lens that encourages researchers to be impartial, to view behaviours as clusters of symptoms, then to frame them as evidence of psychopathology and see people as individuals who are solely responsible for the quality of their lives and health. While the clinical paradigm has many merits and has helped countless individuals find resolution to their health problems, it is also a paradigm that contrasts with the collectivistic cultural orientation in which I was raised - an orientation that places relationships and whanaungatanga ahead of cost-saving and career advancement. 7 I did not want this study to perpetuate models of health that blame Māori for their social status. Nor did I want to ignore the contribution that adopting health risk behaviours has had on the health of many Māori. For that reason, this study represents a unique integration of both Western and indigenous ways of seeing the world, and ways of gathering and analysing knowledge. My position recognises the value of multiple methods of data collection. To that end, this study uses biological markers of health to assess physiological well-being and combines that with knowledge and insight gained from self-report psychological measures as well as in-depth interviews, which honor the lived experience of each participant. My hope is that by conducting research in this way, the relationships built during this study will last well beyond the life of this project. 1.6 A word on language In the service of promoting bi-cultural research practices, this thesis utilises both English and Māori terms, some of them interchangeably. Terms that are commonly 7 Whanaungatanga = From the root word whānau meaning togetherness, relationship 27 used throughout include wāhine (the Māori word for woman or women), kōrero , (which means talk or speech), and whānau, (the word Māori use to denote family). The term Pākeha is used to denote a New Zealander of European descent. The term non-Māori is used when referring to a New Zealander who is not Māori, but who may not necessarily be of European descent. In recognition of the fact that our country has two names, the term Aotearoa New Zealand is used throughout. Translations of all Māori terms are provided in the glossary, and definitions of Māori words that are used infrequently, can be found in footnotes at the bottom of the page on which they are used. Of note for this work, the term psychopathology has been largely discarded in favor of the term psychological distress , to challenge the assumption that mental illness resides solely within the individual and necessarily represents a ‘fault’ within them. In line with a growing number of clinicians who are adopting more compassionate language when working with tangata whaiora , psychological distress is used herein 8 to describe persistent and distressing mental experiences which often follow from extremely adverse life circumstances - regardless of whether or not they meet DSM-5 criteria for mental disease (Drapeau, Marchand, & Beaulieu-Prevost, 2012). 1.7 Thesis structure Unlike most scientific PhD dissertations, this thesis breaks form by placing the personal context alongside discussions of societal-level problems. This thesis also begins and ends with direct references to myself and my family. While this might invite criticism from those immersed in traditional modes of scientific research, it is worth noting that the status quo is failing the indigenous people of Aotearoa New Zealand, and that continuing to conduct and present research the way it has always been done, may not necessarily be in the best interest of many Māori. Therefore, this study offers a novel approach to both research presentation and service delivery that prioritises Māori well-being ahead of Western ideals of impartiality. 8 Tangata whaiora = Mental health consumer 28 1.8 The present study The present study is comprised of two parts - both of which build on knowledge gained from watching my father’s health journey. The first part explores links between stress exposure and poor health outcomes, and draws on emergent evidence which suggests that stress is not equally distributed across sectors of society i.e., those who are socially disadvantaged are not only exposed to more stress throughout the lifespan but they are often also more vulnerable to the adverse psychological and physiological effects of that stress (Gibson et al., 2014; Hammen, 2006). The second part acknowledges that poor health is only a partial contributor to the problem of chronic disease and early death among Māori. For alongside the health disparities, there are differences in the quality of health care offered to Māori, as well as differences in the way that health services are delivered to Māori. Several researchers have documented that the pathway for Māori through the public health system is longer and slower than it is for non-Maori (Reid & Robson, 2006; Jansen & Smith, 2006) because Māori face barriers at every level of the health-care system (Russell, Smiler, & Stace, 2013). The present study attempts to address these issues using multiple investigations to examine different aspects of the problem. One investigation looks at associations between adverse childhood experiences, cortisol dysregulation, and psycho-physiological determinants of health. The other investigation tests the effectiveness of a novel mind-body intervention that has been infused with Māori tikanga. This study uses the adverse childhood experiences (ACE) model to detail the progression from historical trauma through to chronic disease and early death. It also uses the allostatic load model to argue that factors such as historical trauma, health-risk behaviours and childhood adversity all converge on a common theme, namely chronic, cumulative psychosocial stress. Building on the hypothesis that 29 chronic activation of the neuroendocrine stress response system contributes to long-lasting physiological damage, this study also tests the effectiveness of a culturally enhanced mindfulness intervention designed to reduce stress activation by calming the arousal response. To that end, this study presents the findings from an experiment in which eight Māori women with histories of childhood adversity completed a culturally enhanced mindfulness based stress reduction course. At its essence, this is a Māori centred research project that draws on my experience as a wāhine of both Māori and Pākeha descent, as a Clinical Psychologist who was raised with highly collectivistic values, as a member of a whānau bereft of elders, and as a New Zealander who has worked in three different government agencies that all provided inadequate services for Māori. My experience has taught me that there is an urgent need for research that can offer immediate benefits to Māori, and for health services that prioritise Māori wellbeing. For those reasons the following project sought to answer the following three research questions. 1. How frequently would the following outcomes co-occur in Māori women who have reported a high number of adverse childhood events (ACEs): a. chronic life stress b. cortisol dysregulation c. visceral obesity d. psychological distress 2. How would a group of Māori women with high ACE scores respond to a culturally enhanced Mindfulness Based Stress Reduction course? 3. How would a culturally enhanced mindfulness-based intervention influence the psychological and physiological profiles of Māori women with high ACE scores? 30 1.9 Chapter outline Chapter 2 offers a brief foundation for understanding key concepts such as stress, the stress response system and cortisol dysregulation. It also introduces the two main models upon which this study is built, namely the adverse childhood experiences (ACE) pyramid and the allostatic load model. Chapter 3 takes recent figures released from Statistics New Zealand and uses them to show how the two models are useful in understanding disparities between Māori and non-Māori today. Chapter 4 outlines problems within the New Zealand health-care system that contribute to high rates of chronic disease and early death among Māori. Chapter 5 offers potential solutions to those problems and introduces the concept of mindfulness meditation. Chapter 6 outlines the research questions in more detail and provides an overview of the methods used to answer each question. Chapter 7 presents the structure and content of the culturally enhanced mindfulness intervention tested within this project. Chapter 8 details the methods used in conducting the study. Chapter 9 presents the case studies of the eight Māori women who participated in the project. Chapter 10 draws together their results and discusses them in context of the research questions. It also outlines the strengths and limitations of the project and points to future directions for research. Chapter 10 ends with a personal reflection that discusses the process of completing this project. 31 Chapter 2 - Chronic stress contributes to early death 2.1 Outline and Aims This chapter provides an overview of stress and the stress response system and discusses the importance of the body’s primary steroid hormone, cortisol. It also introduces the adverse childhood experiences (ACE) pyramid and the allostatic load model, both of which aid understanding of how chronic stress can contribute to early death. 2.2 The stress response system The human stress response system is comprised of two neuroendocrine systems that serve complimentary functions aimed at maintaining homeostasis (balance) within the body (Fink, 2016; Friedman, 2002; Kalat, 2007). When those systems are compromised - as sometimes happens under conditions of extreme stress - the health consequences can be devastating (McEwen, 2016). Those two systems are the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal axis (HPA axis) (Kalat, 2007). Where the SNS is fast acting and provides an immediate, brief, emergency response to stress, the HPA axis is slower acting and dominates in conditions of prolonged stress (Fink, 2016; Kalat, 2007). 2.2.1 The short term-stress response Whenever humans appraise a situation as threatening, their emergency response system (the SNS) is activated (McEwen, 2016). That activation triggers the release of a complex sequence of hormones that includes the catecholamine agents epinephrine and norepinephrine, as well as corticotrophin-releasing-factor (CRF). CRF prompts the pituitary gland (located at the base of the brain) to release adrenocorticotrophin hormone (ACTH), which then triggers the adrenal glands to secrete cortisol (Buckingham, Cowell, Gillies, Herbison, & Steel, 1997). 32 Cortisol prepares the body for fight/flight/faint/freeze behaviours by flooding the bloodstream with glucose (sugar), which then supplies the large muscles of the body with an immediate source of energy (Kalat, 2007). Cortisol also inhibits insulin production, which encourages the body to use up the excess glucose (Friedman, 2002). Cortisol helps the body to fight inflammation by suppressing functions that are not immediately essential (such as reproduction) and inhibiting the release of cytokines (proteins that tell other cells to fight infection), which in the short term, has an anti-inflammatory effect (Friedman, 2002; Sapolsky, Romero, & Munck, 2000). Cortisol elevations enhance memory formation, which is thought to help an individual remember situations that have proved to be threatening or dangerous (Sapolsky, 2002). Cortisol also causes the arteries to narrow, which contributes to the blood being pumped harder and faster (Friedman, 2002). This increase in vascular responsiveness enables the body to move more quickly (McEwen, 2016). Negative feedback loops ensure that when the stressful situation has resolved, hormone levels return to normal, which protects the body and the brain from damage caused by prolonged steroid exposure (Buckingham, Cowell, Gillies, Herbison, & Steel, 1997). Figure 2.1 The hypothalamic-pituitary-adrenal axis. Reprinted from Kalat (2007). 33 In the event of a near miss car accident, one might recognise this cascade of events is happening when their heart starts thumping loudly, their hands become clammy as blood is drawn away from the extremities and directed towards their vital organs, they feel light-headed or faint, and/or they experience that familiar ‘rush’ of adrenalin, which provides a surge of energy that enables them to run from, or fight the imminent danger. This sequence of events is usually experienced psychologically as either anxiety or excitement (Kalat, 2007). Notably, many people experience those same sensations when standing in front of a group of people giving a talk. The reason for this, is that even though the risk of imminent physical threat is generally low when speaking in public, for humans, social acceptance and belonging is as critical to our survival as physical safety is, and there are few situations where one is more vulnerable to being evaluated negatively than when they have the full attention of an audience (Dickerson & Kemeny, 2004). Thus, the human brain appraises situations that present a major physical threat (e.g., a car crash) and situations which present a major social evaluative threat (e.g., public speaking) in similar ways (Zoccola, Woody, Dickerson, & Hooker, 2018). Once a threat to survival has been appraised, a physiological, neuroendocrine response is triggered regardless of whether that threat is physical or psychosocial (Dickerson & Kemeny, 2004). This has implications for groups of people who tend to experience more of both types of threat than others, such as Māori. 2.2.2 The long term stress response As mentioned, the second part of the stress response system - the HPA axis - dominates under conditions of ongoing stress, such as living with an abusive partner (Kalat, 2007). The HPA axis regulates levels of cortisol in the bloodstream (Sapolsky, 2002). Recall that cortisol is vital for maintaining many of the body’s regulatory functions. As such, cortisol can influence weight gain, obesity, blood sugar levels and diabetes development, as well as impact the immune system, gastrointestinal and cardiovascular health (Sapolsky, Romero, & Munck, 2000). 34 2.2.3 An introduction to cortisol Cortisol exerts many effects over the body. It can influence the types of food a person is likely to crave when they feel stressed, as well as how much of that food they are then likely to eat (Dallman, Pecoraro, & Warne, 2006). Cortisol levels can influence the way in which food is metabolised making it more likely that food will be stored as fat (Tomiyama, Dallman, & Epel, 2011). Cortisol can also influence where on the body that fat is stored (namely, around the middle), which is particularly hazardous, because too much of that type of fat (visceral obesity) drastically increases the risk of developing metabolic diseases like Type II diabetes - a chronic health condition in which Māori are especially overrepresented (Dallman, Pecoraro, & Warne, 2006; Ministry of Health, 2017a). 2.2.4 Prolonged cortisol exposure While exposure to an acute stressor triggers a highly adaptive increase in cortisol levels (resulting in high blood sugar, increased insulin resistance, enhanced inflammatory capability, reduced cytokine release, enhanced memory and increased vascular responsiveness), prolonged cortisol exposure damages the machinery of the body and the brain (McEwen, 2016). Long term cortisol exposure suppresses the immune system, making the body less resilient to bugs and increasing cancer risk (McEwen, 2008), it damages hippocampal neurons leading to memory loss (Sapolsky, Uno, Rebert, & Finch, 1990), it causes plaque to build up in the arteries increasing risk of heart disease and stroke (Cortisol, 2018), it increases insulin resistance and maintains high blood sugar contributing to weight gain and Type II diabetes (McEwen, 2008). It can also irritate the lining of the stomach, increasing the risk of developing gastrointestinal illnesses (Wallace et al., 2011). Thus, high cortisol levels can be said to be adaptive only in the short term. Under conditions of chronic or repeated stress, the stress response system may sometimes ‘wear out’ in order to prevent damage to the brain and body resulting in 35 stress-induced hypo-cortisolism , or it may maintain high levels of cortisol, which results in hyper-cortisolism – the condition my father had. Chronically high levels of cortisol are commonly associated with mood and anxiety-related issues, visceral obesity, high blood pressure and insulin resistance (Tabarin, 2018). Chronically low levels of cortisol are associated with post-traumatic stress disorder, visceral obesity, chronic fatigue syndrome, fibromyalgia, chronic pain, depression, and rheumatoid arthritis (Heim, Ehlert, & Hellhammer, 2000; Maripuu, Wikgren, Karling, Adolfsson, & Norrback, 2016). Thus, when cortisol levels become dysregulated too often and for too long, the body is placed at increased risk of becoming obese, developing certain cancers, developing Type II diabetes, hypertension, heart disease and cerebrovascular disease (McEwen, 2008). Those are all chronic health conditions that disproportionately affect Māori (Ministry of Health, 2017b). Moreover, cancer, diabetes, heart disease and stroke account for 77% of all Māori deaths (Ministry of Health, 2018f). The implication of this, is that over three quarters of premature Māori deaths are preventable, and might be linked to chronic stress and subsequent disruption of the neuroendocrine stress response system. Cortisol dysregulation can be measured using saliva samples, which are non-invasive and provide an accurate way of assessing HPA axis functioning (Bozovic, Racic, & Ivcovic, 2013). The three HPA axis measurements most commonly used in neuroendocrine research are the cortisol awakening response , the diurnal slope and the cortisol response to acute stress . 2.2.5 Cortisol awakening response (CAR) In healthy individuals, cortisol levels start to rise during the late stages of sleep, then rapidly increase in response to waking (Miller, Shapiro, Han, Margolin, & Arbel, 2018). This is known as the cortisol awakening response (CAR). Levels typically increase from 50-160%, reaching their daily peak approximately 30-40 minutes after 36 waking (Miller et al., 2016). Approximately 60-75 minutes after reaching that peak, cortisol levels return to baseline across the day (Wolkowitz & Rothschild, 2003). As yet, the exact function of the CAR remains unclear. However it is speculated that the rise in cortisol levels helps to stimulate waking (Ice & James, 2007). Among stress researchers there is wide agreement that the CAR represents a discrete aspect of the circadian rhythm of cortisol that appears to be moderately stable within individuals over time. However the CAR can vary in relation to short-term influences such as acute stress or shift-work, as well as long term influences such as chronic stress, burnout and depression (Luecken & Gallo, 2008). A blunted cortisol awakening response (<50% increase in levels in the first 30 minutes of waking) is typical of a hypo-cortisolemic profile and is often associated with work stress (Fries et al., 2005), atypical depression (Bremmer et al., 2007), chronic fatigue syndrome (Torres-Harding et al., 2008) fibromyalgia (Riva, Mork, Westgaard, Ro, & Lundberg, 2010), post traumatic stress disorder (Heim, Meinlschmidt, & Nemeroff, 2003) hyperthyroidism, rheumatoid arthritis (Edwards & Guilliams, 2010), visceral obesity (Tomiyama, Dallman, & Epel, 2011), burnout (Juster et al., 2011) and metabolic syndrome (Luecken & Gallo, 2008). 2.2.6 Cortisol daily slope (DS) Another measure of HPA axis functioning is the daily cortisol slope. In healthy individuals following normal daily schedules, cortisol levels reach their morning peak 30-40 minutes after waking then fall throughout the day, reaching an evening nadir between 2000hr and 0200hr (see Figure 2.2) (Luecken & Gallo, 2008). This diurnal pattern of cortisol provides important clues as to the functioning of the HPA axis. Specifically, a lack of steepness (flattening) in the decline of cortisol levels from morning to evening has been shown to reliably reflect a variety of disorders, including those mentioned above in section 2.2.5 (Ice & James, 2007). 37 Figure 2.2. Average cortisol levels over three days for 48 volunteers aged over 65 and living in the Twin Cities Greater Metropolitan area, Minnesota, USA. Reproduced from Luecken & Gallo, (2008). 2.2.7 Cortisol response to acute stress (AS) In healthy individuals cortisol levels show a rapid increase upon exposure to acute stress (Luecken & Gallo, 2008). Within five minutes of exposure to a stressor, ACTH levels start to rise. They peak approximately 11-20 minutes from the time of stressor onset. In concert with this, cortisol levels also increase, reaching a plasma peak 20-40 minutes after stress exposure (Dickerson & Kemeny, 2004). This rise often appears in saliva samples approximately ten minutes after stress exposure (Bozovic, Racic, & Ivkovic, 2013). After termination of the stressor, cortisol levels return to baseline - a process which takes approximately one hour (Leucken & Gallo, 2008). In hypo-cortisolism, cortisol levels fail to rise leading to an inadequate physiological stress response. Other patterns of dysregulation include failure of cortisol shut-down once the stressor has resolved, and excessive output of cortisol in response to acute stress exposure (hyper-cortisolism) (McEwen, 2016). To summarise, cortisol dysregulation in the form of hyper-cortisolism (too much) or hypo-cortisolism (too little) can often follow exposure to chronic stress. Both conditions are associated with visceral obesity (fat around the middle of the body) and psychological distress. Cortisol dysregulation can be measured by examining 38 the cortisol awakening response, the cortisol daily slope and the cortisol response to acute stress, using saliva samples. 2.3 Stress definitions Defining stress is a complex task because stress means different things to different people, at different times, under different circumstances (Fink, 2016). When the term stress was first published by Hans Selye in the mid-1930’s, it was used to reference both the cause and effect of stress (Szabo, Tache, & Samogyi, 2012). Because of the confusion that caused, clear distinctions were later drawn between factors considered to be stressors (e.g., demands) and the body’s physiological response to stress. Yet in spite of this, confusion remains. For while some researchers define stress by describing its nature and its qualities (e.g., psychosocial stress, traumatic stress) others define stress in terms of how it affects the body (e.g., good stress, tolerable stress and toxic stress (Dickerson & Kemeny, 2004; McEwen, 2016). Commonly, stress is divided into categories such as major life events and daily hassles (Wethington, 2016) . Major life events can include both happy events such as a wedding, and sad events like the loss of a spouse (Holmes & Rahe, 1967). Daily hassles are comprised of stressors like driving to work in traffic (Wethington, 2016). Chronic stress can be used to reference stress experiences that are ongoing, such as never having enough money to pay the rent, as well as to frequently occurring stressors such as repeated exposure to physical abuse (Dallman, Pecoraro, & Warne, 2006). Chronic stress can also refer to adverse experiences in childhood, which continue to influence the stress response system long after initial exposure (Felitti et al., 1998). While all of these forms of chronic stress are known to activate the HPA axis, chronic psychosocial stress in particular (i.e., stress which involves social evaluative threat or interpersonal stress) is thought to uniquely influence the HPA axis, as opposed to the SNS (Dickerson & Kemeny, 2004). 39 Key attributes of any stressful experience are uncontrollability and unpredictability (McEwen, 2016). Thus, recent definitions of stress have included situations in which ‘one’s environmental demands exceed one’s perception of the ability to cope’ (Fink, 2016, p.5). Stress has also been defined as the ‘state of an organism when reacting to challenging new circumstances’ (Friedman, 2002, p.423), which, like Selye’s definition, refers only to biological reactions. Integrating both ideas, Kim and Diamond (2002) propose that stress comprises three elements: 1) an observable increase in neuronal activity as measured by neurochemical levels, motor activity or electroencephalogram, 2) subjective perceptions of the experience as aversive and 3) a sense of lack of control. Thus, they offer the following definition, which can be applied across species and paradigms to describe stress – whether real or perceived, environmentally or exogenously driven: Stress: ‘a condition in which an individual is aroused and made anxious by an uncontrollable aversive challenge’ (p.454). The current research uses Kim and Diamond’s (2002) definition because it encompasses components that are central to all of the previous definitions. 2.4 Effects of stress How stress affects an individual depends on many factors including the age at which they are exposed to the stress (Berens et al., 2017), how frequently the stress occurs (McEwen, 2016), how prolonged and severe, the stress is (Felitti et al., 1998), how much support the person has around them when the stress occurs (Dickerson & Kemeny, 2004; Lazarus, 2006) and how resilient or sensitised they are to that particular type of stress (McCarty, 2016). The exact nature of the stress is also a factor, for exposure to a psychosocial stressor (such as sexual assault) will often have different long-term consequences for the stress response system as compared with surviving a natural disaster, because of the difference in meaning attached to those events. Thus, the way in which stress is appraised and interpreted also influences how stress is then managed (Lazarus, 2006). 40 McEwen (2016) has proposed the terms good stress , tolerable stress and toxic stress to describe the effects that different kinds of stress can have on the body. Good stress is the kind experienced when one is exposed to a new challenge that ultimately fosters growth, such as starting a new course. Tolerable stress refers to experiences that induce a moderate amount of challenge, but which the individual adapts to because they have adequate resources. For example, needing to fix a broken down car but having the money and time to do so. Toxic stress refers to experiences where the demands clearly outweigh the individual’s resources to cope, such as a child experiencing parental abuse and being unable to access support (Felitti et al., 1998). Toxic stress is the kind that most contributes to allostatic load, as discussed further in Chapter 3. The younger the brain, the more damaging the effects of toxic stress (McEwen, 2016). This study hypothesizes that chronic stress is a particularly salient feature in the lives of many Māori women for a number of reasons: 1) because Māori tend to belong to large families and hold collectivistic values, which means they are likely to be at increased risk of experiencing a high number of major life event s (weddings, funerals, births), as well as frequent daily hassles ; 2) because Māori women are twice as likely as Pākeha women, to experience domestic violence in adulthood (i.e., chronic stress) (Ministry for women, 2015); and 3) because Māori women report high rates of sexual and violent abuse in childhood (Hirini, Flett, Long, & Millar, 2005) (i.e., toxic stress). Additionally, Māori women are more likely to be living in poverty than Pākeha women (Marriott & Sim, 2014) and they are more likely to experience the daily paradigm clash of holding collectivistic values in a society that is highly individualistic (Ketu-McKenzie, 2011), both of which can be viewed as chronic psychosocial stressors. 2.5 The adverse childhood experiences study (ACE) Evidence of a relationship between childhood adversity and chronic disease was firmly established by the adverse childhood experiences (ACE) study published in 1998 (Felitti et al., 1998). The ACE study was a project in which 8,506 American 41 patient volunteers answered a ten item questionnaire about adverse childhood experiences. The survey asked participants to mark ‘1’ in a checkbox if, prior to the age of 18, they had lived through experiences from seven different categories of adversity. Those categories included witnessing violence against their mother, directly experiencing psychological, physical or sexual abuse, and/or living with household members who were suicidal, substance abusers, imprisoned, or mentally ill. Those experiences were chosen because they represent psychosocial stressors – i.e., the type of stress considered to be most toxic for a child and the kind most likely to exert long-lasting physiological effects (Dube et al., 2003) After analysing the completed surveys, the ACE study authors reported a powerful graded exposure relationship between adverse experiences in childhood and risk factors for the leading causes of premature death. In short, the higher the number of adverse childhood experiences a person endorsed, the more likely they were as adults to experience alcoholism, drug abuse, depression, and to attempt suicide (Felitti et al., 1998). Additionally, the higher a person’s ACE score, the more likely they were to smoke cigarettes, be physically inactive, be severely obese, have had more than fifty sexual partners across their lifetime, and to have contracted a sexually transmitted disease. Moreover, the higher a person’s ACE score, the more likely they were to develop ischemic heart disease, cancer, chronic lung disease, skeletal fractures and liver disease - in other words, the more likely they were to develop the leading causes of early death (Dube et al., 2003; Felitti, 1998). Notably, the ACE study participants were largely comprised of white Americans, not African-American or Hispanic individuals. Given that several studies have shown that Māori experience a high number of those same adverse events in childhood, and that the associated later life conditions and health-risk behaviours reported in the ACE study are also disproportionately represented among Māori, the ACE framework could provide a 42 useful way of understanding the current health status of Māori (Marie, Fergusson, & Boden, 2009; Ministry of Health, 2018f). Based on their findings, Felliti et al. (1998) proposed ‘the ACE pyramid’ to explain the mechanisms through which early life adversity might lead to the development of chronic disease and early death. Figure 2.3 ACE pyramid showing proposed progression from ACE to early death via adoption of health risk behaviours. Reprinted from Felitti et al. (1998). The ACE pyramid (see Figure 2.3) posits that adverse childhood experiences can disrupt neurodevelopment, which can then lead to impairments in social, emotional and/or cognitive processes, which can in turn lead to the formation of health risk behaviours (such as stress eating), which in turn increase the likelihood of premature death, either directly (in the case of suicide) or indirectly, through the development of a chronic health disorder (such as Type II diabetes) (Felitti et al., 1998). 2.5.1 The extended ACE Pyramid In the 20 years since the original ACE pyramid was published, developments in the areas of molecular genetics, epigenetics, and fMRI technology, as well as increased 43 acceptance of socio-ecological perspectives in health have led to an acknowledgement that for some populations, adverse childhood experiences can begin long before a child is even born (Center, 2015). In recognition of this, an extended ACE pyramid was proposed by RYSE Center in Richmond, California in 2015. Figure 2.4. Model of Extended ACE pyramid constructed by RYSE Center, Richmond, California. Reprinted by permission. The extended ACE pyramid (see Figure 2.4) includes two more tiers placed below adverse childhood experiences to acknowledge the influence that historical trauma and social conditions can have on the occurrence of adverse childhood events. Building on scientific advancements, the extended ACE pyramid also provides more accurate labels for some of the existing tiers. For instance, complex trauma has been added to the third tier alongside adverse childhood experiences , acknowledging that the deleterious effects of ACEs are amplified when they result in complex trauma (van der Kolk, 2005). On the fourth tier, allostatic load has been added to social and cognitive impairment , acknowledging emergent research which suggests that long standing changes in the stress response system 44 might mediate the relationship between ACEs and poor health (McEwen, 2016). Adoption of health risk behaviours has been re-labelled coping, acknowledging that the relationship between chronic stress and adoption of health risk behaviours is perhaps more usefully viewed as attempts to cope with and attenuate the chronic stress response (Center, 2015; Tomiyama, Dallman, & Epel, 2011). Lastly, the tier closest to the top has been changed from disease, disability and social problems to burden of disease, distress, criminalisation, stigmatisation, acknowledging that ACEs likely contribute to more social problems than just chronic disease i.e., they might also contribute to anti-social behaviours. Running alongside the extended ACE pyramid is an arrow labelled microaggressions, implicit bias, epigenetics , which acknowledges that the progression from historical trauma to chronic disease and early death is likely to be mediated by additional factors that require further investigation. The current project applies the extended ACE pyramid to Māori living in Aotearoa New Zealand. 2.5.2 Personal context While completing this project my father chose to complete the ACE survey. His ACE score was 9 out of 10. 2.6 The allostatic load model The allostatic load model extends knowledge that activation of the stress response system is adaptive in the short term but that prolonged or repeated activation leads to poor health outcomes in the long term. This concept (and the concept of homeostasis) is central to understanding allostatic load and overload (McEwen, 2016). 2.6.1 Homeostasis Homeostasis is often described as the body’s equilibrium or set point . It refers to the stable set of internal conditions the body maintains in order to preserve balance 45 (Friedman, 2002). Homeostasis is commonly referenced in relation to heart rate and body temperature. For instance, homeostasis of body temperature in humans means that the body seeks to maintain a body temperature of 37 degrees celsius at all times. When the body’s internal temperature starts to increase, a series of responses (e.g., sweating) are triggered that serve to return the body to its set point temperature of 37 degrees celsius (Kalat, 2007). 2.6.2 Allostasis While homeostasis maintains stability and the parameters of life, allostasis is the process through which the body achieves stability through change (McEwen, 2016). Using the temperature example again, if a person’s internal temperature drops below 37 degrees celsius, their blood vessels will constrict to prevent unnecessary heat loss and involuntary shivering might ensue in order to generate heat that can warm the body and thus return it to homeostasis (Friedman, 2002). Allostasis is what enables the body to adapt to a challenge and then return to its pre-set equilibrium following challenge exposure. While a certain amount of adaptation is normal, frequent demand on the stress response system can cause lasting damage (McEwen, 2016). A common metaphor used to describe the process of allostasis, is that of a car constantly braking and accelerating in order to maintain a stable speed. For a finely tuned engine, such behaviour can cause wear and tear on the motor, damaging its internal machinery - as allostasis does to the body (Friedman, 2002). The cumulative effect of allostatic processes on the body is known as allostatic load and common examples of it include weight gain, fatigue, hypertension and depression (McEwen, 2016). Excessive exposure to allostatic processes can lead to pathophysiological conditions, or allostatic overload . Common examples of allostatic overload include Type II diabetes, ischemic heart disease, metabolic syndrome, high cholesterol, chronic pain, chronic fatigue and arthritis - in short, the same 46 chronic diseases that are prevalent in the Māori population and which contribute to early death (McEwen, 2016; Ministry of Health, 2018f). 2.7 Summary The relationship between stress and illness is enormously complex. Exposure to stress invokes a whole-body, neuroendocrine response which is adaptive in the short term but which leads to wear and tear on the body in the long term, resulting in allostatic load. Because frequency of exposure to stress is unique for every person, allostatic load is accumulated at different rates for people across the lifespan. This makes untangling the psychological and physiological correlates of chronic stress a difficult endeavour. To illustrate, although post traumatic stress disorder is considered a ‘psychological disorder’, it also has circulatory, respiratory and musculoskeletal associations - as does depression. Although the allostatic load model cannot account for every illness encountered by Māori, it provides a useful framework for understanding how stress negatively affects health. Combined with findings from the adverse childhood events study, which found a strong link between high ACE scores and the very same chronic diseases that affect Māori, the allostatic load model offers a novel explanation as to why Pākeha New Zealanders live longer than Māori. 47 Chapter 3 - From historical trauma to early death 3.1 Outline and aims This chapter applies the extended ACE pyramid and the allostatic load model to Māori today. It follows the format of the tiers described by the extended ACE pyramid in Chapter 2, from historical trauma to early death and presents a brief summary of Māori history along the way. This chapter intersperses personal examples with national statistics to enhance understanding and give context to each of the tiers of the extended ACE pyramid. 3.2 Tier One: Historical trauma Historical trauma is a specific form of stress that refers to the ‘cumulative emotional and psychological wounding over the lifespan and across generations, emanating from massive group trauma experiences’ (Wirihana & Smith, p.198; Yehuda et al., 2009). For Māori, the term historical trauma has been used to reference both the genetic changes that resulted from colonisation by the British during the 1800’s, as well as the systemic consequences of colonisation, such as institutionalised, interpersonal and internalised racism (Reid & Robson, 2006; Walters et al., 2011). Historical trauma has also been used in reference to alterations in Māori identity resulting from the decline of the Māori language, loss of cultural practices/knowledge , disconnection between Māori and the environment due to land loss/economic and workforce requirements, and the loss of entire communities due to the land