Where Inner and Outer Worlds Meet: Psychological Research in the tradition of George W. Brown

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Where Inner and Outer Worlds Meet

The importance of George Brown’s contribution to medical sociology through his longitudinal studies of psychiatric disorder and its relationship to social context is widely recognised. This collection of seventeen chapters exemplifies a particular way of working as a medical sociologist which focuses on the understanding of the meaning of social experiences as the key to an individual’s health status. It combines the biographical richness of qualitative research with the ability to carry out quantitative analyses and thus reach conclusions on the basis of statistical significance. The contributors mainly focus on conditions of depression and anxiety, relating these to the meaning of people’s experiences or ‘life events’ prior to their onset. Within this framework different authors focus on more specific meanings including both demographic aspects such as gender, parity, lifestage, employment, refugee/immigration status, humiliation, entrapment, loss and also more interpersonal stresses such as neglect, abuse and critical or unsupportive relationships. This is a book which offers a rich treasury of information for all researchers interested in understanding the complex relationship between our inner and outer worlds: it captures the essence of George Brown’s unique way of working. Tirril Harris is Senior Research Fellow, Socio-medical Research Centre, Academic Department of Psychiatry, Guys, Kings and St Thomas Schools of Medicine (Research Officer to Professor George W. Brown).

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Where Inner and Outer Worlds Meet Psychosocial research in the tradition of George W. Brown

Edited by Tirril Harris

London and New York

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First published 2000 by Routledge 11 New Fetter Lane, London EC4P 4EE Simultaneously published in the USA and Canada by Routledge 29 West 35th Street, New York, NY 10001 Routledge is an imprint of the Taylor & Francis Group This edition published in the Taylor & Francis e-Library, 2005. “To purchase your own copy of this or any of Taylor & Francis or Routledge’s collection of thousands of eBooks please go to www.eBookstore.tandf.co.uk.” © 2000 Tirril Harris All rights reserved. No part of this book måy be reprinted or reproduced or utilised in any form or by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying and recording, or in any information storage or retrieval system, without permission in writing from the publishers. British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library . Library of Congress Cataloguing in Publication Data Where inner and outer worlds meet: psychosocial research in the tradition of George W. Brown / edited by Tirril Harris. p. cm. Includes bibliographical references and index. ISBN 0-415-20268-X (hardcover) 1. Social psychiatry. 2. Depression, Mental–Etiology. 3. Life change events. 4. Adjustment (Psychology) I. Brown, George W. (George William), 1930– II. Harris, Tirril O. RC455 .W49 2000 616.89–dc21 ISBN 0-203-99204-0 Master e-book ISBN

ISBN 0-415-20268-X (Print Edition)

00–042214

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Contents

List of figures List of tables List of contributors Preface 1 Introduction to the work of George Brown

viii ix x xiv 1

TIRRIL HARRIS

PART 1

Social psychiatry and social science 2 George Brown’s contribution to psychiatry: the effort after meaning

53

55

JIM BIRLEY AND DAVID GOLDBERG

3 Bringing meaning back into social psychiatric research: making subjective meanings objective

61

DAVID MECHANIC

4 George Brown: the science of meaning and the meaning of science

71

PAUL BEBBINGTON

PART 2

Measurement of key psychosocial factors in research 5 Lessons from using semi-structured interviews with seriously ill patients

79

81

ELIZABETH DAVIES

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vi Contents

6 Expressed emotion: measuring relationships

97

JULIAN LEFF

7 Contextual measures and subjective appraisal

111

LOUISE LEMYRE

PART 3

Model building 8 Negative life events and family negativity: accomplishments and challenges

121

123

MICHAEL RUTTER

9 Towards a dynamic stress-vulnerability model of depression: the role of neuroticism, life events and gender

151

JOHAN ORMEL AND JAN NEELEMAN

10 The timing of lives: loss events over the life course and the onset of depression

171

PAUL SURTEES AND NICK WAINWRIGHT

11 The childhood experience of care and abuse (CECA): an exploration with adolescent refugees

195

MICHEL TOUSIGNANT, EMMANUEL HABIMANA, COLETTE BIRON, ESTHER SIDOLI-LEBLANC AND MATHILDE BRAULT

12 Gender differences in the experience and response to adversity

211

TOM CRAIG AND SOUMITRA PATHARE

13 The long-term effects of childhood adversities on depression and other psychiatric disorders

227

RON KESSLER

14 Evolved socio-emotional systems and their role in depressive disorders

245

MARTIN EALES

PART 4

Psychosocial factors in conditions other than depression

261

15 Life stress and bipolar disorder: is the dimension of social rhythm disruption specific to onset of manic episodes?

263

ELLEN FRANK, DAVID KUPFER AND SUSAN MALKOFF-SCHWARTZ

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Contents vii

16 The study of life events has clarified the concept of psychosomatic disorders

275

FRANCIS CREED

PART 5

Postscript

289

17 Some thoughts on the future of social psychiatry

291

GEORGE W. BROWN

Index

319

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Figures

1.1 1.2 8.1 8.2 8.3 8.4 8.5 8.6 9.1 10.1 10.2 10.3 10.4 10.5 10.6 12.1 17.1

Provoking agents and vulnerability factors for depression Irregular or disruptive severe events related to depression Severe events and difficulties in early adult life Parental personality disorder and hostility, and persistent child disturbance Effect of life events on variance in depressive symptoms MZ pair differences in life events and MZ pair differences in depression Family negativity and antisocial behaviour Family negativity and depression The dynamic stress-vulnerability model Some possible representations of self-reported adverse event effects Self-reported adaptation by gender to loss Self-reported upset to loss and adaptation to loss by lifestage MDD following maternal loss by age at time of loss MDD onset following marital loss with no event by gender interaction MDD onset following marital loss with allowance for event by gender interaction Simplified schema of Brown and Harris model of depression Percentage of women with at least one severe event in 12 months

11 25 131 132 135 137 138 139 153 177 181 182 186 187 188 212 303

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Tables

1.1 1.2 5.1 5.2 10.1 11.1 11.2 11.3 12.1 12.2 14.1 16.1 16.2 16.3 16.4 17.1

Premarital pregnancy as a key junction point in the lifespan model Typical forms of data presentation Inter-rater reliability for 13 interviews Scales where inter-rater reliability failed (Kappa <0.40) Odds of MDD (during the 12 months pre-assessment) CECA frequencies of high scores Prediction of DSM-III-R caseness from CECA variables Prediction of DSM-III-R diagnoses from CECA variables Onset of depression following severe events Couples study: onset of depression by domain of provoking crisis Proposed subtypings or dimensions of depression Proportions of those who had experienced a marked relationship difficulty Proportions of those who had experienced a severe event Those who experienced a severe event prior to the onset of a physical illness Specific types of life event in patients with physical illnesses Childhood abuse or neglect and depression

19 41 85 86 184 202 203 203 219 220 254 278 279 282 283 300

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Contributors

Tirril Harris is Research Fellow in the Socio-Medical Research Centre, Academic Department of Psychiatry, at the St Thomas site of the Guy’s, King’s and St Thomas’ School of Medicine, London. She has worked closely with George Brown for thirty years, collecting and analysing data and running training courses in the team’s research instruments. She also works in private practice as a psychoanalytical psychotherapist. Jim Birley is a psychiatrist, formerly Dean of the Institute of Psychiatry, London. His interests have particularly included psychosocial aspects of psychiatric aetiology and his work on schizophrenia with George Brown was one of the key early studies. Professor Sir David Goldberg former director of the Institute of Psychiatry, London, has championed a psychosocial perspective on psychiatry throughout his career. He is particularly well known for his work in training general practitioners in the detection and management of depression and anxiety. David Mechanic is Professor of Medical Sociology at the Institute for Health, Health Care and Ageing Research, at Rutgers University, New Jersey, USA. While he has contributed widely to all fields of medical sociology, his special interest has been in the determinants and effects of illness behaviour and treatment-seeking. Paul Bebbington is Professor of Social and Community Psychiatry at the Royal Free and University College London Medical School. His interests have spanned many areas of social psychiatry from gender to life events. He is currently involved in the second round of the National Morbidity Survey for Psychiatric Disorder, and studies of assertive outreach for schizophrenia and dialectical behaviour therapy for personality diorders. Elizabeth Davies is Specialist Registrar in Public Health at the Department of Palliative Care and Policy, Guy’s, King’s and St Thomas’ School of Medicine, London, having recently moved there from the Health Care Evaluation Unit,

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Contributors xi St George’s Hospital Medical School. Her current interests are in the area of health services research, particularly communication and quality of life. Julian Leff is Professor of Social and Cultural Psychiatry at The Institute of Psychiatry, London. He has published widely on cultural aspects of psychiatry but is even better known for his work devising and evaluating interventions with families of patients suffering from schizophrenia, based on the understanding of expressed emotion or EE. Louise Lemyre is Associate Professor, School of Psychology, University of Ottawa, Canada. Her specialisation is in psychosocial stress in health settings. Her interests lie in normal populations in real life situations. She has developed and validated the Psychological Stress Measure which has been translated into five languages and is used for stress monitoring in hospital as well as work contexts. She also teaches social psychology and health psychology. Professor Sir Michael Rutter, FRS, was founder director of both the Social, Genetic and Developmental Research Centre and the Medical Research Council Child Psychiatry Research Unit at the Institute of Psychiatry, London. His research has spanned the study of psychosocial and genetic risk factors, with a particular focus on the ways in which nature-nurture interplay is involved in normal and abnormal lifespan development. Johan Ormel is Professor of Social Psychiatry at the University of Groningen, Holland. His research has been wide-ranging, including both clinical and epidemiological studies of diagnosis, prognosis, treatment and cost-effectiveness (mostly in primary care settings). His work has also encompassed aetiological epidemiological studies (especially personality and life stress) as well as the consequences of common mental disorders. Jan Neeleman trained in psychiatry at the Institute of Psychiatry, and in epidemiology at the School of Hygiene and Tropical Medicine, both in London. His main interests concern suicidal behaviour, substance use and psychosomatic medicine. He is presently a Senior Lecturer in psychiatric epidemiology and Consultant Psychiatrist at the University of Groningen where he runs a Pioneer research programme focusing on the physiological basis of frailty and general liability to ill-health. Paul Surtees is a Member of the Scientific Staff, MRC Biostatics Unit, Institute of Public Health, University of Cambridge and also Honorary Clinical Psychologist to Addenbrookes NHS Trust, Cambridge. His research interests include the role of social factors, particularly adverse experience, in the onset and course of affective disorder and investigation of social and psychological determinants of chronic disease and mortality. Nick Wainwright is Statistician at the MRC Biostatics Unit, Institute of Public Health, University of Cambridge. His current research interests focus on

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xii Contributors statistical methods as applied to models of social adversity and health change, with emphasis on time order, time-varying exposure effects and onsets of affective disorder. Michel Tousignant is Director of the Research Laboratory in Human and Social Ecology, University of Quebec in Montreal. He is author of Les origines sociales et culturelles troubles psychologiques (1992, Presses Universitaires de France) and co-editor of Ethnicity, Immigration and Psychopathology (1997, Plenum Press). His current work is on life events and suicide. Emmanuel Habimana is Professor of Psychology, University of Quebec in Trois-Rivieres. He has done research on ‘envy, spirit possession and mental illness in Rwanda ‘. He is now working on ‘envy and giftedness’. Colette Biron is Consulting Psychologist at Douglas Hospital, Montreal. Esther Sidoli-Leblanc is Psychologist at Douglas Hospital, Montreal. Mathilde Brault is in private practice in psychology and research associate at the Centre de Recherche Fernand-Seguin, Montreal. Tom Craig is Professor of Community Psychiatry at the St Thomas site of Guy’s, King’s and St Thomas’ School of Medicine, King’s College, London. For many years he was psychiatric adviser to George Brown’s research team. His work has included studies on psychosocial aspects of gastro-intestinal disorder, on somatisation disorder, homelessness and gender aspects of life-span developmental models of psychiatric disorder. Soumitra Pathare, a consultant psychiatrist, lives and works in Pune, a city of 2.5 million in western India, having worked at St Thomas’ Hospital, London, for several years. He qualified as a psychiatrist from the University of Mumbai (Bombay) in 1991 and obtained his PRCPsych in 1994. His clinical interests are in designing rehabilitative services for the chronic mentally ill in a developing country (India) and designing services for extending mental health care to under-served populations in India. His research interests include studying the role of social and developmental factors in the aetiology of depression and research into increasing public awareness and reducing stigma associated with mental illness in developing countries. Ronald Kessler is a Professor in the Department of Health Care Policy at Harvard Medical School. He is the recipient of Research Scientist and MERIT awards from the National Institute of Mental Health. He is the Principal Investigator of the National Comorbidity Survey, the first study to administer a psychiatric diagnostic interview to a representative sample of the US. He is also the codirector, with Bedirhan Ustun, of the WHO World Mental Health 2000 (WMH 2000) surveys, a series of psychiatric epidemiology surveys carried out in representative samples in over two dozen countries throughout the world.

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Contributors xiii Martin Eales is Consultant Psychiatrist, Somerset Partnership NHS and Social Care Trust, and Honorary Senior Lecturer, Division of Psychiatry, University of Bristol. His current research interests focus on developing artificial models of emotion activation systems. Ellen Frank is Professor of Psychiatry and Psychology at the University of Pittsburgh School of Medicine, Department of Psychiatry. In addition, she is Director of the Depression and Manic-Depresssion Clinic at the Western Psychiatric Institute and Clinic. She has almost two decades of experience in the maintenance treatment of recurrent affective disorders and in the research evaluation of both pharmacological and psychotherapeutic maintenance therapies. David Kupfer is Thomas Detre Professor and Chair of the Department of Psychiatry at the University of Pittsburgh School of Medicine. For more than twenty years, his research has focused primarily on the conceptualisation, diagnosis and treatment of mood disorders. He has written extensively on the use of medication in recurrent depression, the causes of depression and the relationship between biological rhythms, sleep and depression. Susan Malkoff-Schwartz received her doctorate in clinical psychology from the University of Pittsburgh. Dr Schwartz coordinated the research conducted in the Life Events and Depression research unit under the direction of Dr Ellen Frank. She was instrumental in developing and implementing a unique rating scheme for understanding social rhythm disruption in patients diagnosed with bipolar disorder. Francis Creed is Professor of Psychological Medicine at the University of Manchester Medical School. His early work on life events and appendectomy inspired George Brown’s team and others to use their psychosocial measures with physical as well as psychiatric illness, and his team has since spawned a host of parallel studies. He has also been involved in a number of projects extending such work into the area of intervention. George Brown is Professor Emeritus of the University of London, and continues to work at the Socio-Medical Research Centre which he founded and which is now based in the Academic Department of Psychiatry at the St Thomas’ site of the Guy’s, King’s and St Thomas’ School of Medicine.

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Preface

The appearance of this book is an occasion which highlights just how many people there are who must be thanked for the establishment of the research tradition to be celebrated here. Without the long-term support of the Medical Research Council it is difficult to see how the programme of work discussed could have continued and expanded in the way it did. Thanks must go first and foremost to them, with gratitude expressed also to the Economic and Social Science Research Council who have funded some of the key ‘parallel’ samples, such as the two Hebridean Island surveys, and the two studies of the teenage sons and daughters of mothers seen a decade or so earlier on an MRC programme grant. Indeed, although the MRC was responsible for funding the investigation of most of the Camberwell general population sample, it was the ESRC (or SSRC as it was then known) which in 1969 had borne the initial risk of financing the first 120 interviews, before it was clear that it really was possible to collect such intimate material without jeopardising the validity of any conclusions based upon it by provoking a high refusal rate in response to what, in those days, might well have been considered intrusive questioning. Moreover, a special debt is owed to the Foundations Fund for Research in Psychiatry, New Haven, who at an early stage, before our MRC funding was established, rescued us from financial difficulties. More recently, we have also been given considerable support from the USA by the John D. and Catherine T. MacArthur Foundation, who funded the upgrading of our training packages, and stimulated the development of more specialised versions of our instruments for the adolescent and elderly age groups. Over the years other funders have helped with our parallel projects: the KnowHow Fund helped us train psychiatrists in Moscow in the use of our research instruments; the British Council helped us build links with workers in Egypt; the Rowntree Foundation, the Baring Trust, the King’s Fund and the Mental Health Foundation helped the Family Welfare Association to expand their small befriending service in the way our aetological model predicted would prove a viable intervention for chronic depression so that we could evaluate their work. The Mental Health Foundation had already funded work where our psychosocial model had been extended to examine psychosomatic disorder, my study of patients with menorrhagia and secondary amenorrhea.

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Preface xv Clearly our next debt is to the members of our research teams and to our colleagues who have formed part of our consensus meetings, some of whom can be directly thanked for their additional efforts as contributors to this volume. After thirty years work, there have been so many of us that not all can be mentioned by name but many are explicitly acknowledged in the main text of the book where the evolution of our psychosocial measures is described. However, little attention is paid there to issues of psychiatric diagnosis and it is thus fitting to express our gratitude here to all those psychiatrists who have helped us refine our approach to the dependent variables in parallel with our perspective on the independent ones. A particularly important contribution came from colleagues associated with the development of the Present State Examination (PSE), John Copeland and John Cooper, and later John Wing, Julian Leff and Sheila Mann. They helped us define ‘cases’ of depression in the general population in those early days before the ICD system of WHO and the DSM system of the American Psychiatric Association were properly worked out. Later we were fortunate to have funds for a psychiatric colleague within our own team, and Elaine Murphy and Tom Craig carried on the ‘Bedford College caseness’ tradition, systematising the rating procedure to take account of time order and comorbidity a decade before they became fashionable, and preparing a manual of anchoring examples in the style of our psychosocial instruments. However, the foundations of this systematisation had been laid by two other colleagues outside the programme funding: Ray Prudo, who joined us in the Hebrides and helped us broaden our understanding of anxiety disorders, and a visitor from Australia, Robert Finlay-Jones, who galvanised us into statistical analysis of our hundreds of PSE schedules in order to produce the Finlay-Jones checklist for ‘caseness of depression’. Years later, it is encouraging to reflect on the close similarity between these and the DSM criteria for major depression. As I have conveyed, it is not feasible to list all the social scientist colleagues who have contributed, but special mention must be made of Margot Jeffreys who gave the team a comfortable base in the Medical Sociology section of the Bedford College department of Social Policy for many years. What can be underlined, however, is how much this style of research into the meaning of people’s experiences depends on the participation of each member of the consensus group sharing their views. With each programme grant, team members faced different samples and thus different ranges of experiences which required different degrees of empathy to rate. They also had to face different situations in the interview situation, where sometimes respondents became worryingly distressed and sometimes they reported harrowing circumstances with an almost equally worrying calm. Sometimes, especially in the later projects where information about childhood was collected, team members would find that material disclosed by interviewees brought back distressing memories of their own past which had to be contained while they finished the interview. It must be recorded that the team members faced all these trials successfully and for this they deserve George’s and my greatest thanks. Our next debt of gratitude must be to the publishers who saw fit to produce the proposed volume, despite the cyclical change in opinions in the profession about Festschrifts and their roles. Edwina Welham has shown unstinting support to a

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xvi Preface project which she took on because she valued the historical link between George Brown’s work and her publishing house. Both Tavistock Publications, which produced Social Origins of Depression in 1978, and Unwin Hyman, the British publishers of Life Events and Illness in 1989, later became part of Routledge, whose inspired book lists at the frontiers between sociology, psychology and psychotherapy owe much to the shared vision of Edwina and her predecessors at Tavistock, John Harvard Watts and Gill Davies; all these imprints have now been incorporated in Taylor and Francis. I am very grateful to Nell Gatehouse who was willing to adapt her timetable most flexibly to help with the preparation of the typescript. I must also thank Sheila Williams for her patience in offering help with computing, and Laurence Letchford, whose computing advice over the years has been invaluable. It seems that the evolution of the team’s actual measures has been influenced almost as much by his creative way of working as it has by the research workers. This has been especially true of the tricky business of ensuring the correct time order for independent and dependent variables by sensitive design of rating schedules. In fact it has become customary for many of our colleagues who have also benefited from Laurence’s help to joke with us about the Julian and Gregorian calendars in recognition of his particular coding system. Finally, the greatest debt of all must be to the many hundreds of women and men who have talked with us about their outer lives and their inner feelings and reflections. I hope they will not feel their trust has been betrayed. Tirril Harris 2000

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1

Introduction to the work of George Brown Tirril Harris

This book is intended as a tribute. It aims to provide an exposition of a particular way of working as a social scientist. As will emerge, that way of working focuses on ‘meaning’ as the vehicle of understanding how social frameworks affect their members. This requires any general theoretical exposition to be grounded in the detailed aspects of the data which can reveal such meaning. Empathy on the part of the investigator is used to grasp meaning with the proviso that such an intuitive grasp must not override the need for statistical confirmation of causal links that emerge. The research itself has always begun with questions of direct concern for psychiatry and has led to a wide range of theoretical interpretations that in turn have been influenced by a range of disciplines. While in many ways the description ‘grounded theory’ neatly fits this approach, more pedantic interpretations of that epithet leave it ambiguous as to whether this is an appropriate label. Nevertheless, terminology apart, to focus in detail on the research of one of the leading exponents of this approach, George Brown, is one clear way to convey this style of work and this is the task of this first chapter. Later chapters fill out the picture by describing recent work by close colleagues operating in the same tradition. It is fitting to begin with a brief history of the studies in social psychiatry carried out by Brown and colleagues before proceeding to summarise those characteristic features which distinguish them and contribute to their value. Listing the evolution of these research topics highlights the inexorable way in which discovering associations between psychiatric disorder and external demographic variables pushes the social scientist to think about internal mediating processes and to contemplate the bridge between outer and inner worlds. Brown’s work may fairly be divided into two broad phases both of which follow this course: the first between 1956 and 1967 at the Institute of Psychiatry’s Medical Research Council Social Psychiatry Unit, focusing on schizophrenia, and the second based at London University’s Bedford College (latterly Royal Holloway), targeting clinical depression, and continuing since 1967. For both these disorders, a number of preventive interventions have been stimulated by the research.

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2 Introduction

The evolution of Brown’s work Schizophrenia and expressed emotion It is hardly surprising that Brown’s earliest work at the Institute of Psychiatry fitted well within the traditions of sociology then current. An analysis of death certificates, and mental hospital and County Constabulary records, provided contrasting pictures of, on the one hand, the quasi-urban mining valley of the Rhondda and, on the other, the nearby rural Vale of Glamorgan, with more psychiatric cases in the former, particularly among the ‘non-miners’, but crimes of violence occurring with equal frequency in both areas (Carstairs and Brown, 1958). The authors’ stimulating discussion of their findings already reveals an awareness of the importance of nosocomial factors and of the potentially crucial role of ‘social pressures’ in explaining such ‘recorded’ rates of psychiatric disorder. But it was not for fifteen years that Brown was able to move on to pursue such epidemiological themes by examining the role of life stress and treatment seeking in the interview-diagnosed onset of psychiatric disorder in a random female population sample (Brown, Ni Brolchain and Harris, 1975). In 1956, British psychiatry was entering a period of remarkable upheaval and growth that was to lead within a decade to the widespread running down or closure of many of its large mental hospitals. An authoritative Maudsley Monograph by Vera Norris had at this very juncture anticipated the need for more hospitals to cope with overcrowding. Indeed, in the years immediately preceding Brown’s joining the unit in 1956, patients with a diagnosis of schizophrenia were still retained in considerable numbers for two years, at which point their chances of leaving hospital in any one year became increasingly slim. Hospitals had large wards for highly disturbed patients but most longstay patients were largely inactive, and quite often largely mute and withdrawn. The main brief of the unit, as defined by its honorary director, Aubrey Lewis, was to consider issues raised by this longstay population, most of whom had a diagnosis of schizophrenia. Old records were studied to build up a picture of possible changes over time in admission and discharge. But this simple picture was supplemented by the insights into actual underlying mechanisms which emerged with Brown’s discovery that for many years a careful record had been kept at Cane Hill Hospital of all visits to each patient, and each such ledger sheet, when full, was filed with the patient’s clinical notes. He was able to establish that any schizophrenic patient unvisited in their first eight weeks was at a particularly high risk of becoming longstay. The intriguing possibility was that this could be linked in some way to the marked lowering of the rate of continuous retention for two years that had occurred at some hospitals with the introduction of the major tranquillising drugs in the mid 1950s. Brown predicted that those involved in the changes would in the main be the unvisited patients, and this was confirmed at Cane Hill and a second large hospital, Banstead, serving London. A case was therefore made that part of the impact of the new drugs had been to influence the attitudes of medical and nursing staff – a possibility later confirmed when it was shown that a handful of reforming medical

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Tirril Harris 3 superintendents had achieved comparable high rates of discharge well before the introduction of the new drugs (Wing and Brown, 1970). A good deal of the unit’s research at this time concerned services for schizophrenic patients (e.g. Parkes, Brown and Monck, 1962). A particularly substantial contribution was the intensive longitudinal study of particular patients over an eight-year period made with John Wing in three mental hospitals (Wing and Brown, 1970). In this inquiry into institutionalisation and schizophrenia, they were able to confirm their hunch that the amount of ‘unoccupied time’ experienced by a patient was in part a consequence of his or her place in a particular system of care and was a major factor producing symptoms such as ‘muteness’ and poverty of speech. They also found an important effect with the degree of social restrictiveness on the patient’s ward which was independent of the effect of unoccupied time. With this in mind, Brown describes the good luck they had when, a year or so after their initial visit to one of the hospitals, they discovered that many longstay patients had been allocated to new wards during a major organisational change and how this was done in terms of where they had once lived in the hospital’s catchment area. This meant that the current placement could be treated as if it were part of a random design, not due to selection on the basis of some aspect of the patient’s mental state. The original finding was confirmed, but now it was unlikely that the clinical changes (for better and worse) associated with the levels of restrictiveness of the new wards could be due to selection bias (Brown, 1973). The study had involved the careful description of a number of aspects of the lives of the patients, including a meticulous listing of all their personal possessions. It documented not only changes in these terms, but also how the reforms in each of the three hospitals could, in time, stop or even be reversed, and as a result how clinical gains made earlier could be lost. However, it was hard data concerning readmissions rather than discharges or patterns of care within the hospital – patients coming back to hospital away from relatives rather than relatives coming up to hospital to see patients – that became the take-off point for his most important insights about schizophrenic relapse. The best account of the work on onset and relapse in schizophrenia is probably that by Brown himself as he examines the role of induction and deduction in the discovery of what has come to be known as ‘expressed emotion’ (Brown, 1985). Three substantial projects were involved. The first, begun in 1956, studied the relatively rare male patients who had been discharged from seven mental hospitals between July 1949 and June 1956 after at least a two-year stay: the housekeepers of the domestic group to which the patients had gone on leaving hospital were interviewed to determine duration of discharge period until relapse and level of social adjustment. Data collection followed a procedure that was, albeit in a more streamlined form, to become the hallmark of his work. The conduct of the interview was not formalised, but interviewers used a checklist to ensure all 160 items had been covered. Each team member had to take part in interviewing, with weekly meetings for discussion of possible ambiguities in the recording of particular items. Surprisingly, for schizophrenic patients who formed the majority, unsuccessful outcome, defined as return to hospital within one year, bore little relation to

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4 Introduction age or length of prior hospital stay but was associated with failing to find employment and with returning to live with parents or wives rather than living in hostels or lodgings, even when level of residual symptomatology at discharge was controlled (Brown, Carstairs and Topping, 1958). The resulting analysis was extensive but one example is sufficient to convey its nature. Unemployment as such was not always highly associated with relapse. When only those patients living with a mother were considered, risk of relapse was considerable if both had remained at home unemployed. But all other possible arrangements were related to low chances of relapse. This move from consideration of a formal status such as ‘unemployed’ to concern with context in interpersonal terms was the hallmark of much of the research that was to follow. At this point Brown was captivated by the ability of Lazarsfeldian-type crosstabulation to open up a complex data set, and the way this could lead to insights about possible mechanisms. He considers the logic involved to be the formative intellectual input of his early research career. But this went with the hard lesson that insights were more than likely to remain just that, since within the bounds of one study it was always possible to think of alternative explanations. It is possible that the dramatically different outcomes of unemployed patients whose mothers stayed at home and those who were employed could be due to the mothers who chose to stay home more often sensing their son’s greater vulnerability to relapse. While it was often possible to explore such speculations within the same data set (for example, by considering the level of symptomatology and the mother’s work history) at best this served to increase the degree of confidence about whether or not the idea was worth pursuing. Hence his early emphasis on replication and the conception of social research as a series of linked inquiries, gradually affording insights into a web of causal factors – and hopefully eventually permitting sufficient confidence to intervene in a situation in an experimental or quasi-experimental way in the light of such insights. (In this instance this had to wait a further twenty years for the work of Leff and Vaughn.) The second project, begun in 1959, was planned to follow the insights of the first, but now with any schizophrenic patient leaving hospital, since by this point it was clear that it was the question of readmission rather than chronic stay that would dominate psychiatric attention. The study looked prospectively at what appeared to be a crucial factor in relapse – the quality and quantity of contact in the home to which the patients returned. It involved 128 male patients and utilised new scales concerning emotional expression especially developed for the task, based on measures of emotional involvement, hostility and dominance when patient and family were seen together (Brown, Monck, Carstairs and Wing, 1962). The main hypothesis was confirmed: patients returning to homes characterised by ‘high emotional involvement’ were more likely to deteriorate, even when clinical condition at discharge was controlled. (The term ‘expressed emotion’ was not employed for another ten years.) The subsidiary hypothesis – that, for patients living with such relatives, the fewer the hours spent with them the more they would be protected – was confirmed for those who were moderately or severely disturbed at discharge.

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Tirril Harris 5 The final study, begun in 1966, was intended as a replication. Again it was mainly prospective and had been preceded by two years devoted to the development of additional and more refined measures of family life, involving collaboration with Michael Rutter and a number of his colleagues (Brown and Rutter, 1966; Rutter and Brown, 1966). Eight types of interview were carried out for each carefully diagnosed patient and family, and ten if the patient was readmitted before follow up nine months after discharge. The main results of the second project were replicated and in certain important respects extended among the thirty-five of the 101 patients who relapsed (Brown, Birley and Wing, 1972). The emotion that played the crucial role was now more precisely specified in an ‘expressed emotion’ index, with ‘number of critical comments about patient made by key relative’ as the crucial component, while ‘emotional over-involvement’ played a more subsidiary role. The measures were now based on talking to relatives alone. Warmth was not included in the EE index but was shown to relate to a much reduced chance of relapse among those homes low on criticism and over-involvement. Work impairment and behavioural disturbance were only related to relapse because of their association with level of expressed emotion. A major contribution of the developmental research, which was probably only possible because of everyone’s close involvement in the minutiae of each tape-recorded interview, was the distinction between critical and dissatisfied comments. It was only after the discussion of many interviews and more than a year into the development work that the distinction was made between the two highly correlated measures. Once criticism was taken into account, dissatisfaction, however extensive, proved to be unrelated to relapse. It was how the content was expressed – its vocal aspects – that was central. It is difficult to see how such a subtle distinction could have been both sensed and then operationalised without the kind of intuitive approach advocated by Brown, and the difficulty in making this distinction probably goes some way to explain the problem there has been in developing a questionnaire-based alternative to the EE index. It exemplifies how he embraced the investigator as the ideal means of clarifying psychosocial material – and supported his view that one of the shortcomings of much current research was the failure to link as a matter of course alternative questionnaire-type instruments with such measures. The impact of this ‘expressed emotion’ could be mitigated to some extent by phenothiazine medication and by spending less than thirty-five hours a week in face-to-face contact with the critical relative. Other factors independently linked to relapse were age under forty-five, male sex, prior admission, unskilled manual occupation, failure ever to achieve a satisfactory sexual adjustment and a clear-cut and typical schizophrenic diagnosis (as opposed, for example, to atypical psychosis or paranoid state). Particularly enlightening was the project’s use of the timebased data of the one-year follow up to suggest a two-way effect: that the level of patient’s disturbance could influence the level of expressed emotion, with the conclusion that what was involved was a circular effect (whether vicious or benign). A similar caution was exhibited in the refusal to comment on claims that factors in the relatives’ personality and handling of the patient as a child contributed to the first onset of schizophrenia. This allegiance to strict scientific canons, despite the

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6 Introduction favourable reception of the report by the radical audiences of the time, was to be repeated with Brown’s later work on depression. Three years later he was as careful not to be colonised by feminist views of depression as he was now to stand apart from the antipsychiatrist perspective of schizophrenia being promulgated by Laing, Esterson and followers (Laing and Esterson, 1964). The report of this third data set ends with careful consideration of possible practical recommendations which were later followed through by Julian Leff, Chris Vaughn and other colleagues (Leff et al., 1982). In the midst of this work on the role of the quality of relationships, Brown used his impressions of the relapse process to pursue another avenue investigating the role of life events in precipitating schizophrenic episodes (Brown and Birley, 1968). As with his sense of the importance of the emotional climate in the home, his concern with life events emerged directly from the detailed accounts he had collected about the circumstances surrounding relapse. He was impressed how often the onset of a clear-cut florid episode (and sometimes this was the first) could occur within a matter of days of an event that on common sense grounds would be expected to lead to emotional arousal. The events were typically negative (such as witnessing a murder when working as a doorman at a nightclub), but a few were positive and had been clearly linked on the patient’s part with the experience of joy and elation. In terms of the research itself, ‘events’ were seen as experiences likely to produce significant emotion in most people – and this emotion (and parallel biological processes) was hypothesised as the crucial mediating factor. In order to prevent bias, events were rigorously defined by a pre-established set of rules which ensured that the study did not include minor incidents that might be given special weight by a patient or relative because the illness had closely followed. Setting up such a threshold involved discussion with Jim Birley of hundreds of examples of possible events – often at some length. The seriousness with which this was taken can be gauged by recalling the discussion over whether to include an eye falling out of a pet goldfish – it was not! The key point is that, as with the EE index, the task of measurement was firmly in the hands of the investigators. It was they who, on the basis of as detailed an account as possible of the event, decided whether or not an incident was to be included and thereby set up rules for future interviews. For obvious methodological reasons the person’s report of their emotional response was not taken into account. The study of a consecutive series of fifty recent admissions where onset/relapse could be accurately dated to within a week found that 60 per cent of the patients had experienced an event during the three weeks before onset compared with only 19 per cent among a comparison group of 325 persons questioned about the three weeks before interview. However, for the patient series, during three earlier three-week periods an average of only 23 per cent experienced such an event – a figure close to the percentage in the comparison series whose experience remained the same over the whole series of four three-week periods. A key feature of this work with the instrument that was later to evolve into the ‘Life Events and Difficulties Schedule’ (LEDS), was the definition of ‘independent’ events, such as the doorman witnessing a murder, that by their nature could not be seen as possibly brought about by the insidious onset of the psychotic

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Tirril Harris 7 illness. These were contrasted with others within the patient’s potential control such as a job change or a house move, that might be seen as influenced in some way by the symptoms. (Events such as being sacked from a job were excluded altogether as much too likely to be linked to some aspect of the illness.) The fact that the patient-comparison group difference in experience of events held when only ‘independent events’ were examined suggested that a real increase in the rate of events had been involved – one which was unlikely to have been brought about by abnormal behaviour on the patient’s part. A further report concluded that there were no differences in experience of an event by age, sex, symptomatology and diagnostic category. However, among the subgroup of patients who gave a history of stopping, or considerably reducing, their phenothiazine medication the proportion experiencing an event in the three weeks before onset was less than half that among the other patients (31 per cent and 72 per cent respectively) and not significantly different from the comparison group (Birley and Brown, 1970). The paper concludes with the remark that ‘it is thus rather curious that there is now better evidence for the importance of precipitating events in schizophrenia than there is for affective states’ and comments that this maybe due to methodological difficulties involved in assessing onset in affective illness – ‘a problem upon which we are engaged at present.’ It thus ushers in the next phase of Brown’s work. The lifespan model of depression In 1967, Brown moved from the Institute of Psychiatry to the Social Research Unit headed by Margot Jeffreys at Bedford College. When Bedford College was amalgamated with Royal Holloway and moved out to Surrey in 1984, his research team moved to an annexe of the college in Bedford Square, with the fortuitous result that changes in the nomenclature of the research instruments were minimal: the Bedford College measures became the Bedford Square measures, which they have remained despite his move to the department of psychiatry at St Thomas’ Hospital in 1999. The description that follows of the evolution of the model of depression that emerged adheres quite closely to that of various key instruments that were also developed in this period. Proximal provoking agents Life events before onset were the first building block which Brown was to use in the edifice of his model of depression, paralleling work on depression that was beginning at the same time (Paykel et al., 1969). The version of the LEDS that had been used in the schizophrenia work was expanded to include difficulties (ongoing problems such as poor housing and bad marriages) where there were often no associated events in the period of the inquiry. Also included were many other dimensions besides ‘independence’ that might capture some aspects of the meaning of the experience. These dimensions ranged from straightforward qualities such as the focus (or main actor) to more complex features such as degree of prior warning or routine change implied by the event.

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8 Introduction However, the methodological problem afflicting work on affective disorder more profoundly than that on schizophrenia was that of avoiding circularity in dealing with meaning. For the earlier work it had been possible to deal with the likelihood of emotional arousal following an event in a highly general sense; but this would be unlikely to be enough for depressive conditions where there had been a common recognition among psychiatrists that there was a reactive form triggered by some kind of stress. It was therefore essential to deal more squarely with the meaning of experiences that were likely to be depressing or anxiety-provoking, but still not using the respondent’s report of their reaction to those events. Following the insights of Schutz about Verstehen, Brown approached the issue by setting the event in the context of the interviewee’s prior concerns, plans and purposes that stem from activity caught up in roles: how, for example, being turned down for rehousing by a local authority thwarts a woman’s wish, amply reflected in her behaviour, to move from an overcrowded and damp flat, to give her children ‘a better start in life’. The measure most central to the question of meaning was long-term contextual threat or unpleasantness judged in terms of such plans and concerns. This, if rated severe, was to prove the crucial aspect of events that related to a depressive onset (Brown et al.,1973). It was distinguished on the one hand from short-term contextual threat (unpleasantness only within the first few days after an event) and, on the other hand, for methodological reasons, from reported threat both short- and long-term. The rating of severity was a 4-point scale which was later dichotomised to reflect ‘severe’ and ‘non-severe’ levels. Whereas reported threat was a rating of the degree of emotional response described by the particular individual, contextual threat was an estimate of the likely emotional reaction of a typical person with biographical circumstances similar to that of the interviewee. Contextual ratings were made by consensus meetings of raters kept unaware of the person’s self-report or of whether or not the event was followed by any psychiatric symptomatology. However, while ratings were always made blind, once agreement was reached raters were made aware of what subjective material had been reported. As examples accumulated this feedback had some influence on the standards employed for the blind contextual ratings. Almost certainly as part of this feedback over the years some thresholds changed. This resulted not only from a sensing that the earlier ratings had been in error but also because of secular changes in values. For example, it was so common for women to report relief after elective termination for an unwanted pregnancy in a marriage where there already were children that by the mid 1970s there had to be a revision of the initial criteria that a rating could not fall below the top 2 points on long-term threat. Examples of the various scale-points used in rating events and difficulties were collected in ‘dictionaries’ that were used as reference works: however, in recognition of the uniqueness of individual experience it has always been permissible to depart from a particular standard conveyed by such examples in the light of some unusual contextual feature. For the most part, however, raters have been guided by the examples provided (with these growing in considerable number over time).

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Tirril Harris 9 Vulnerability factors While the initial work on depression followed his own prior sampling strategy of using mental hospital patients (in this instance, the Maudsley Hospital), Brown had always hoped to extend the work to include a comparison group of a random sample of the population surrounding the hospital. This author joined his team as part of a programme to make this possible, working half time with one of the first grants awarded by the Social Science Research Council, to establish that collecting such intimate data was perfectly possible in the general population. Participation was high – perhaps partly due to the decision to concentrate on women where there was reason to believe they stood a greater chance than men of becoming depressed. This was also the first occasion on which one of the new family of semi-structured clinical interviews, the Present State Examination developed by John Wing and colleagues (Wing et al., 1974), had been used in a general population inquiry. Sampling was on the basis of rateable household units in the old borough of Camberwell, with one woman randomly selected from each household when the interviewer arrived on the doorstep. The first small sample consisted of 220 households with a refusal rate of 17 per cent (Brown, Ni Brolchain and Harris, 1975). Later a replication study added another 238 women, and data on the whole group of 458 was published alongside the Maudsley patient data under the title Social Origins of Depression (Brown and Harris, 1978). What perhaps had not been anticipated was the high rate of clinical depression found in the community (that is depression comparable to conditions seen in a local out-patient psychiatric department). About half of these seventy-six cases had lasted more than twelve months so their life-event experience collected at interview postdated their onset; and because the focus was upon psychosocial experiences that might influence onset these women were excluded from most analyses. But this allowed the other half (the ‘onset cases’) to be used, along with the remaining 382 women, in analyses of ‘aetiological’ factors contributing to onset without contamination by the determinants of treatment-seeking which must inevitably threaten to distort psychiatric patient samples. The evolution of the vulnerability model on the basis of the Camberwell population sample was a prime example of Brown’s move from outer to inner world, and back again. It followed six steps: 1 2

3 4

The substantial link found in the patient series between severe events/major difficulties (provoking agents) and depressive onset was confirmed. Associations were documented between depression and various demographic-type factors such as lower social class and the presence of children in the home. Associations between these factors and the experience of a provoking agent were established. Most crucially, only those with a provoking agent were considered to see whether those agents alone were mediating the link between the demographic factors and depression. Since the association between depression, social class

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10 Introduction

5

6

and life-stage still remained, provoking agents clearly could not be the sole factor to play this crucial mediating role. A fifth step was therefore taken to explore the role of other psychosocial experiences linked both to depression and these same demographic factors (social class or presence of children). Four were identified. Two involved roles: lack of employment outside the home and presence of more than three children under 15 rendered women more likely to respond to a provoking agent with depression. Two involved close relationships: lack of an intimate confiding relationship with someone at home (usually a partner) and loss of mother before age 11 through death or long-term separation. These last two were particularly powerful ‘vulnerability factors’. In fact they were asociated with the demographic factors identified and were therefore strong candidates as critical mediating variables. The final step was to propose a speculative model to account for these findings.

This early version of the model used concepts from a number of disciplines to show how inner and outer worlds might meet, and though it has been elaborated in the ensuing twenty years it has remained the cornerstone of an increasingly elaborate model. The challenge was to bring some understanding of the correlation of low social class and symptomatology such as poor appetite and anergia. And here a start had been made. Where the link between social class and the presence of a severely threatening event (and to a lesser extent a severe difficulty) was concerned, the experience of the meaning for the most part appeared to have largely involved loss, if this was broadly defined to include not just loss of person, role or material object but also loss of a cherished idea. Beck’s influential cognitive perspective had already highlighted a triad of attitudes seeming to characterise the symptoms of depressive illness – that the world appeared pointless, the self worthless and the future hopeless. Brown and Harris speculated that the essence of vulnerability to depression might be an attitude that would resonate with this triad; that it was a tendency to generalise the feelings of hopelessness which would, to some degree, be provoked in anyone experiencing one of these losses; that such a generalising tendency would be part of a wider disposition of low self-esteem and low mastery which would link with the four vulnerability factors as shown in Figure 1.1; that social support and advice obtained in response to intimate confiding would tend to promote mastery, and the support figure’s sympathy might reflect an image of someone deserving of concern, thus raising self-esteem. It also seemed possible, following attachment theory (Bowlby, 1969, 1973), that loss of a mother early in life would mean the loss of such a supportive figure just when the foundations of the self-image were being laid and the subsequent mother-surrogate might not always be able to help the child make up for this. The concept of ‘role-identity’ (McCall and Simmons, 1966) was invoked to explain how the other two vulnerability factors fed into the model: those women with a number of such role identities would be better able to resist the tendency to generalise hopelessness because they would have a wider range of alternative

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Tirril Harris 11

PROVOKING AGENTS Severe event/ difficulty

Specific helplessness

Generalised helplessness

DEPRESSION VULNERABILITY FACTORS Lack of intimate confiding Loss of mother before 11 Three or more children under 15 Lack of outside employment

Low self esteem/ Low mastery

Figure 1.1 Provoking agents and vulnerability factors for depression.

sources of value or self-validation. Thus while most women were wives and mothers, those who also had identities involving work, friendship, neighbourhood or leisure activities would be better buffered against a loss in the domestic arena. The presence of three or more children requiring baby-sitting would be likely to prove a greater handicap to acquiring such alternative role identities than a smaller family. As a lorry-driver’s ex-wife with no children noted ‘I don’t think I could have weathered my husband leaving me if I hadn’t just started that job in reception. They were all so complimentary to me there that it boosted my self-esteem (sic) and tided me through’. This example is typical of the way that Brown developed his theoretical models: by keeping close to the data he had ready access to the insights which individuals had about themselves, and by collecting his data in the way he did he could then turn such insights into testable theory. In fact when the model was first reported, one assessor raised objections on the grounds that working-class women did not talk of self-esteem. (They do, but probably more often in terms of lack of confidence). Whether or not respondents did or did not have language for, and insight about, the process was a subsidiary issue: what was crucial was whether Brown and his colleagues had correctly identified something to which the links between environment and affective disorder could plausibly be attributed. Confirmation came from later studies. Replicating and refining the model Work over the next two decades can basically be said to have confirmed and amplified this basic model. Any brief account of these developments must inevitably fail to do them justice. Often there was important work, both replicating and refining prior findings, which, though inspired by the Bedford College/Square model, was carried out by other teams and in a chapter of this kind focusing on

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12 Introduction Brown’s own work it will be impossible to do justice to them. Developments fall into eleven broad groupings: I

DEVELOPING A MEASURE OF SELF-ESTEEM AND CONFIRMING ITS PREDICTED ROLE

The main problem with testing the suggested role of self-esteem was that low selfesteem was generally accepted as a common sequel to depression. A longitudinal study was accordingly required where self-esteem would be measured at an initial contact and any onset of depression at the time of a one-year follow-up interview. The development of the Self-Evaluation and Social Support Measure (SESS) to be used in a prospective study took five years' work with colleagues Mary Lou Kevlin and Patricia O’Connor. The self-evaluation measure, which was one part of a much larger instrument, took account of relevant statements made at any point in a lengthy interview – some in response to direct questions and others quite spontaneously. Account was taken not only of those involving self-acceptance, as do most such indices, but also of the subject’s feelings about a range of her attributes such as intelligence, efficiency, attractiveness or sympathy with others and how salient each was for her. Her estimate of her performance in roles such as parent, wife, friend, worker, darts player and so on was also taken into account, and again how important each role was for her. The semi-structured nature of the data collection allowed the possibility that a woman should define as highly salient for her an attribute that few others would name, or derive feelings of self worth from, such as being willing to put up with tiring demands. In this way the measure respected the individuality of a woman’s inner world. Extensive analyses of these scales resulted in just two 4-point scales covering negative and positive evaluation of self (NES and PES). The Islington project, in which these were first used, began in 1980 and selected to study only women with children at home, most of whom were ‘working class’, since the Camberwell survey had shown them to be more likely to suffer from depression. Of the 404 women first interviewed, 353 were followed up, of whom fifty were already depressed at the time of first contact. Among the 303 others, thirty-two became depressed, all but three after a provoking event. Such an event risk was nearly three times higher among those with NES (Brown et al., 1986). Later work from colleagues in Edinburgh confirmed this picture (Miller et al., 1989). The role of PES as a protective factor was considerably less powerful. II

DEVELOPING A MEASURE OF HUMILIATION/ENTRAPMENT EVENTS AS AN EXTERNAL

‘MATCH’ OF THE INTERNAL VULNERABILITY FACTOR OF LOW SELF-ESTEEM OR LOW MASTERY

Already at the time of the Camberwell survey it could be seen that the severe events before depressive onset tended to involve losses but no explicit contextual-type rating had been developed distinguishing these from those involving danger, hassle or other types of severe events. A two-year visit to Brown’s team by Robert FinlayJones, who wished to compare depressive and anxiety onsets, provided the opportunity for the systematisation of such ratings, with a beautiful cross-over result:

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Tirril Harris 13 severe events involving loss mainly preceded depression and those involving danger mainly preceded anxiety onsets, while joint onsets of both conditions were often preceded by experiences of both loss and danger, either from two separate events or from both features occurring in the same event – for example, the revelation that the loss of husband by death had left the subject with unexpected news of dangerously unmanageable debts (Finlay-Jones and Brown, 1981). Use of this rating in Islington showed nearly a three-fold increase in depressive onset after a severe loss compared with other severe events (and a thirty-fold increase compared with those without a severe event, see Brown, Bifulco and Harris, 1987). One of the most interesting types of loss was that of a cherished idea. One woman became depressed shortly after learning that her name had been taken off one housing list and put on another where she would have to wait even longer, thus losing the cherished idea that she might be rehoused within the year. Many of these ideas were hopes for an exit from a situation of entrapment, or trusts which were destroyed by revelation of secrets, or ideas of others’ trust and love shattered by a humiliation. An initial attempt to develop a specific rating of ‘severe failure’ events was much improved a few years later when, guided by the work of Price and colleagues (1994) and by Paul Gilbert (1992), Brown began to look to evolutionarily based response patterns as a source of explanation, and developed the humiliation/entrapment rating of severe events. He had for some time believed the crucial role of critical comments in psychotic relapse was related to an evolutionarily-based tendency to find them particularly punishing (just as a smile is innately rewarding) and he was sympathetic to the idea that the ‘meaning’ involved in responding to a life event often had a significant biological component – that the brain had evolved as a meaning-making apparatus on which both culture and more personal experience are to be built. In this sense he had distanced himself from much of the postmodernist relativism increasingly influencing British sociology. As will be seen later, the success of the measures in quite different cultures supported this idea of a basic ‘human nature’ capable in any culture, for example, of experiencing humiliation or the unpleasantness of ‘critical comments’. Re-analysis of the Islington sample a decade later using blind raters showed humiliation-entrapment events to be much more depressogenic than other severe losses, while a third group of other severe events involving danger/severe hassle or minor loss proved the least likely to lead to onset: proportions followed by onset in those three groups of event sequences were respectively 31 per cent (41/131), 13 per cent (13/100) and 3 per cent (4/146) (Brown, Harris and Hepworth, 1995). The findings have since been replicated in a patient series (op.cit.) and in a black township in Harare (Abas and Broadhead, 1997). This willingness to chew over data collected many years earlier and come up with new insights is one of Brown’s noted characteristics to which we will return. One by-product of this new rating was a further analysis of single parenthood and employment in the Islington sample. It became clear that experiences of entrapment and humiliation were the key factor explaining how situations of both financial hardship and the work strain associated with full-time work were

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14 Introduction producing double the rate of depressive episodes among single mothers (Brown and Moran, 1997). III

PURSUING THE PROTECTIVE ROLE OF INTIMATE CONFIDING AND

ACTIVE EMOTIONAL SUPPORT

The longitudinal design of the Islington project gave opportunities for a more sensitive exploration of the Camberwell intimacy result. Aided particularly by colleagues Andrews and Bifulco, Brown set out to test whether the intimacy result (which was replicated) could in some way be attributed to reporting bias, such that those who had become depressed described support received more unfavourably than those without disorder – not because it had in reality been less supportive but because their symptoms coloured their view of things. By looking at confiding at first interview and onset in follow up, this could be ruled out. Results, however, fell short of statistical significance; and, indeed, confiding at the time of first interview only emerged as clearly important among the quarter of the sample who were single mothers where the confidante was usually a close female friend or relative. But Brown’s view has been that if research is on the right track such failures are as likely as not to be the forerunners of significant new insights. And so it proved. The crucial point of the single mother result was that support provision had been remarkably stable: if they had it at first interview they almost always had it during any subsequent crisis. The picture for the married was a good deal less predictable, especially where support from partners was concerned. Further ratings were therefore developed to take account of support actually received with severe crises occurring during follow up. These ratings followed the philosophy of the LEDS that material should be collected in detail about behaviour of support figures and rated according to how most women would judge it – in this case the supportiveness of each close tie. Results suggested that the failure of first-interview ratings to predict onset was not due to the reporting bias of the original retrospective intimacy measure but to actual changes in behaviour between the two interviews. Women with good support at first who were ‘let down’ in terms of support by their support figure were in fact even more likely to have become depressed than those with consistently unsupportive environments (Brown et al., 1986). The severe event itself – for example, learning of a husband’s infidelity – was often the reason for the failure of support. The new ‘crisis support’ scales distinguished various aspects over and above confiding. Most crucial was active emotional support, with the other person making him- or herself available to varying degrees to listen and react with concern and advice. If present to a moderate or marked degree, this seemed to reduce considerably a woman’s chances of becoming depressed following a severe event. But of interest was the fact that the predictive power of such good support decreased in the presence of just one accompanying negative response. A mother’s sympathy about an unwanted pregnancy might in this way be rendered undermining rather than protective if accompanied at some point by a negative response conveying ‘you have only yourself to blame’. A husband’s outward commiseration over rent arrears

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Tirril Harris 15 could be rendered worthless by his continued gambling. Later re-analysis of the written descriptions of the nature of the other person’s responsiveness produced further refinements which distinguished different manners of support failure: criticism as compared with the less demeaning but still unhelpful inability to empathise; failures due to conflicts of loyalty as opposed to the support figure being too preoccupied with her own problems to give time to be with the respondent; as well as various other responses (Harris, 1992). One of the key debates in the social support literature had involved the counterposition of inner perception and outer ‘reality’. A team in Canberra using the standardised ISSI (Interview Schedule for Social Interaction) had concluded from their prospective study that it was the perceived adequacy of support (ADAT) rather than the objective characteristics of the support itself (i.e. its availability or AVAT) which accounted for any protective role (Henderson, Byrne and DuncanJones, 1981). In other words, the ISSI had not highlighted something about the impact of the outer world, but merely identified those with a ‘plaintive set’ or an inner world predisposing them on the one hand to perceive the support of others as unsatisfactory and on the other hand to becoming depressed. Among the new Bedford Square ratings there was also a ‘perceived helpfulness of support’. This indicated the reverse: those who perceived as helpful a type of response which the interviewer-consensus judged most women would have found merely lukewarm (that is low on active emotional support) were more likely to have become depressed than the majority who reported such responses as only somewhat helpful (Andrews and Brown, 1988). In seeking to account for this, links were made with childhood experience, and it emerged that the women who perceived inadequate support as helpful had more often than the rest experienced early inadequate parenting (see section v below). This is reminiscent of some of the case histories described in the writings of attachment theory (Bowlby, 1969, 1973, 1980) where patients cling to the idea of a parent as basically supportive, despite describing to the therapist parental behaviour of a neglectful, or even abusive, type. One discussion of the discrepancy of the Canberra and Islington results was a chapter jointly authored by Henderson and Brown discussing ways of measuring support (Henderson and Brown, 1988). Here it was agreed that the ISSI’s ‘perceived adequacy of support’ (ADAT) might well be reflecting something of the actual behaviour of the support figure(s) rather than simply reflecting an intrapersonal attribute such as plaintive set. In other words, the subjective measure might be doing a better job of measuring what occurred in the external world than the index designed to do this – ‘availability of contact’ (AVAT). The latter was a score reflecting the range of contacts available, although the London research had suggested good quality support from just one core person could be protective. However, the argument for the importance of what occurred in the external world clearly does not rule out a significant contribution from the internal world. Indeed, the London results on perceived helpfulness clearly indicated that this contextual ‘outer’ perspective needed to be supplemented by some measure of the inner world, an intrapersonal style that characterised a way of relating to others; Toni

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16 Introduction Bifulco later carried the torch for this (see vi below). Of course, the impact of such an intrapersonal style may be due in good part to the way that others respond. IV

COPING STYLE

Another area explored in the Islington project was coping style. It seemed possible that the semi-structured interview might throw light from a new angle on the traditional distinctions between practical and emotional coping. The predictive power of Brown and Harris’ initial coping schedule was much enhanced when Bifulco prized apart the strategies of cognitive avoidance, downplaying and denial usually blurred under the heading of ‘minimisation’. The distinction between the last two was particularly important and resembled the distinction between the defence mechanisms of suppression and repression (Haan, 1963; Vaillant, 1976). Following a severe event downplaying was protective against depressive onset whereas denial was associated with a higher rate (Bifulco and Brown, 1996). Downplaying involved focusing on aspects of the problem which could make it appear less negative, for example by comparing one’s situation with a similar crisis experienced by another acquaintance which was worse: for example the mother of a child with cerebral palsy saying ‘well at least he is not Downs or autistic, so he is quite clever and gets on well with people’. With downplaying the respondent is fully conscious that a considerable problem exists, but with denial such a realisation seems absent to the extent that the respondent may manifest a suspicious indifference to its impact. The report was cautious about these results on the grounds that descriptions of coping were retrospective, and thus – unlike the harder measures of life events – might be influenced by subsequent mental state (Bifulco and Brown, 1996). Self-blame and helplessness were also identified as ‘poor’ or depressogenic coping. V

PURSUING THE MEANING OF EARLY LOSS OF MOTHER:

THE KEY ROLE OF NEGLECT AND ABUSE

In 1978, a special study was begun in Walthamstow, North London, to follow up the Camberwell finding that early loss of mother was a vulnerability factor. Women were selected in terms of: 1 2 3

childhood death of mother or of father childhood separation of at least twelve months from mother or from father no experience of these throughout childhood, including separations of less than twelve months.

Depression was examined in terms of both one-year and life-time prevalence. The Camberwell loss-of-mother result was replicated, but loss of mother between ages 11 and 17 also appeared to be linked to adult depression. Death of father again in no way rendered adult depression more likely. However, interpreting the

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Tirril Harris 17 role of separation from father was less easy as there was a non-significant trend (Harris, Brown and Bifulco, 1986). A detailed interview had been developed to explore the processes across the lifespan that intervened between childhood loss and adult mental state, and this led to the development of a two-strand model (Harris, Brown and Bifulco 1990b). What emerged was the likely continuous interplay between factors external to the individual, such as various negative experiences linked with low social class membership, parental loss and other independent life events along the environmental strand, and internal factors along the intrapsychic strand, such as helplessness or attitudinal constraints concerning confiding. But easily the most important factor in understanding the link of loss of mother and depression was the quality of replacement care by a surviving parent or surrogate ones after the loss. The refinement of this measure was typical of Brown’s style of working. The measures of relevance for quality of care that were initially included were parental warmth, rejection, companionship, punitiveness and discord. While these confirmed the original hypotheses for the group with separation from mother, those with death of mother showed only a non-significant trend. But reading through the descriptive accounts of the women’s experiences as children gave a distinct impression that women with adult depression had fared much worse after their mother’s death than those without depression. Brown constructed two new variables, with detailed rating rules. He then trained other team members to apply these and the whole sample was rated without knowledge of adult mental state. One, ‘structural rejection’ included aspects of rejection that had not been considered severe (only mild) by the straightforward rejection measure because they involved family structure and geography – such as father, grandparents and aunts sending the child to a children’s home – rather than the rejection of face-to-face interactions. However neither this, nor the other variable ‘failure to belong’ (which recorded the degree to which the woman felt she had failed to belong with the replacement parents) quite reached statistical significance. However, Toni Bifulco was using the death of mother and no loss comparison groups for her doctoral thesis and had included some extra variables which turned out to be associated with adult depression, and when those with separations from mother and father were also considered much the same associations emerged (Harris, Brown and Bifulco, 1986). One was parental indifference, and one low parental control or lax supervision/discipline, the combined variable being dubbed ‘lack of care’. An additional support for the importance of this factor came from the group with no loss of parent where, despite its much lower rate, depression, was also associated with lack of care, which in this instance was, of course, from the real parents. Parental loss was important because it was much more often associated with ‘lack of care’, particularly starting after the loss. The refinement of this measure occurred at the time of the third visit to the Islington sample, so it was possible to test it on another group. The finding was in fact replicated (Bifulco, Brown and Harris, 1987). However, this sample also afforded further refinements: with Brown’s encouragement, two other team members had introduced new questions at this third interview with Andrews being

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18 Introduction especially interested in women’s experience of violence and Adler in their experience of sexual abuse. Both turned out to relate to adult depression, particularly if occurring in childhood (Andrews and Brown, 1988; Bifulco, Brown and Adler, 1991). At this stage the lack of care measure was superseded by a more powerful one combining parental indifference with experience of severe sexual or physical abuse, known in brief as ‘childhood adversity’ measured by the CECA (Childhood Experience of Care and Abuse) (Bifulco, Brown and Harris, 1994). It proved a powerful predictor not only of depressive prevalence, but also of chronicity (Brown and Moran, 1994; Brown, Harris, Hepworth and Robinson, 1994) and of all DSM-III-R anxiety conditions except simple phobia and mild agoraphobia (Brown and Harris, 1993). VI

THE LIFESPAN MODEL, THE TRANSITION TO ADULTHOOD AND

THE CONVEYOR BELT TO EARLY ADULT ADVERSITY

Once childhood adversity had been identified as important in its own right (as well as mediating the link of adult depression with parental loss), it was possible to begin to chart the various routes to adult depression. Before outlining this, however, it needs to be pointed out that the Walthamstow project took place before the measure of negative evaluation of self was fully developed and that the internal world was approximated by a measure of helplessness/mastery (Harris, Brown and Bifulco, 1990a). Although primarily focused on in the current period, information about helplessness was also sought and rated for other times such as prior to first depressive onset (if any) and a crude rating also made with reference to childhood. The addition of these ‘internal’ measures revealed the likely complexity of the routes from childhood adversity to adult depression. One crucial junction point was becoming pregnant premaritally – that is, before having established a stable cohabiting relationship (Brown, 1982) as represented in Table 1.1. In terms of the past such a pregnancy was associated with the external measure childhood adversity and with the internal measure of childhood helplessness. In terms of the future it related in the same way to external adversity (that is experiencing provoking agents) and to the internal measures of helplessness and low self-esteem (Harris, Brown and Bifulco, 1990b). Particularly clear was its current association with severe interpersonal life events and difficulties and lack of emotional support with severe stress in general (Harris, Brown and Bifulco, 1987). This, of course, made sense given that the pregnancy had often trapped women in a partnership which they might well not have otherwise chosen; (or, if chosen, not have remained within for so long). A characteristic insight of Brown’s here was to note a paradoxical feature of the interplay of individual experience and demographic influence. The latter is usually seen as the background and origin of the former, and yet here the influence appeared to be reversed: the individual experience played a role in determining later demographic status. Women with a premarital pregnancy were less likely than the rest of the sample to experience the upward social mobility that affected those living in Walthamstow during their lifetimes, and, as a result of staying in the working class, they were thus more subject to

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Tirril Harris 19 Table 1.1 Schematic table illustrating premarital pregnancy as a key junction point in the lifespan model Level of Childhood explanation

Transitional launching period

Demographic Individual external

Early

Later

Psychiatric state in adulthood

Remaining working class Parental neglect and/or abuse

Mixed: origins both internal and external Individual internal

Adulthood

Helplessness/ low self-esteem/ insecure attachment

Severe material/ economic life events Premarital pregnancy

Poor support

Helplessness/ low self-esteem/ insecure attachment

Helplessness/ low self-esteem/ insecure attachment

Severe interpersonal events

Depression

Depression

adversity in adulthood. This also made sense given that the men with whom the premarital pregnancies had been conceived were likely to have been forced prematurely into earning in order to support a family and thus perhaps been less able to complete any apprenticeship or training that could lift them out of the working class. It seemed as if the young women who had suffered childhood adversity had found themselves on a conveyor belt to a relatively deprived adulthood with a concomitant greater risk of episodes of depression and anxiety. But the final word was one of hope: it was possible to get off the conveyor belt, and especially to be helped off by a supportive caregiver later, usually a partner in adulthood, but occasionally a new surrogate parent. Whereas many theorists with over-deterministic convictions would have reached for as yet unmeasured internal variables to explain how some had managed to both find and then to respond to such support figures, Brown introduced the notion of luck into the aetiological model: ‘There is a need to take heed of Machiavelli’s dictum on the inevitable role of Fortuna in human affairs, the bitch goddess of unpredictability’ (Brown, Harris and Bifulco, 1986, p.289). Certainly, when comparing one life history with another, it often seemed complete chance that one woman had had the good luck to meet someone who was ready to be supportive and faithful, while another had ended up with someone without either of these qualities. More recently, the Bedford Square team has brought more of the inner world into the model of depression by introducing Bowlby’s notion of internal working models of relationships, following the hypothesis that insecure attachment style would play a key mediating role between childhood external experience and adult

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20 Introduction mental state. At first, measures of dispositions such as hostility, dependence and nurturance were combined to approximate Bowlby’s categories (Bowlby, 1980) of compulsive self-reliance, caregiving and ambivalence and the predicted mediating role was confirmed (Harris and Bifulco, 1991). Later, a measure of adult–adult attachment style, the Attachment Style Interview (ASI), was specifically developed (Bifulco et al., 2000) to correspond with the categories ‘secure’, ‘dismissive’, ‘preoccupied’ and ‘fearful’ that are probably now more familiar than Bowlby’s own in the world of attachment research (see George, Kaplan and Main,1985; Bartholomew and Horowitz, 1991; Hazan and Shaver, 1987). Women not exhibiting standard (or secure) attachment styles were more vulnerable to onset (Bifulco et al., 2000) and less likely to recover from chronic depression (Harris, Brown and Robinson, 1999b) than those rated standard. VII

LIFE EVENTS, SOCIAL SUPPORT AND REMISSION

The note of optimism struck by charting how a standard attachment style can help women off such a conveyor belt to adversity has also typified more recent work at Bedford Square on remission from depression. The context of remission emerged as the mirror-image of that surrounding onset. For episodes lasting twenty weeks or more, remissions were more often than not preceded by reduction in a severe difficulty or by a fresh start event. The latter were defined not as any markedly positive event but as those which promise to end an ongoing state of deprivation (Brown, Adler and Bifulco, 1988). Thus marriage to a loved boyfriend by someone who had experienced a relatively trouble-free courtship, or an examination distinction for someone who has always done well, would not be considered fresh starts whereas becoming engaged after years of single parenthood, or starting fulltime higher education after years in a poorly paid job, would qualify. One interesting implication of this definition is that such ‘positive’ experiences proved to be much more common among the deprived and disadvantaged – a clear contrast with the more common sense expectation that positive events were more likely among the non-deprived. (Earlier exploratory research had found that positive events in any one year for many were largely of a ‘routine’ kind such as a foreign holiday, a new grandchild or buying a washing machine – certainly not the kind of events involved in fresh starts or difficulty reduction.) Another somewhat paradoxical result was that around a third of fresh start events were also rated severely threatening – yet another example of the multiple meanings picked up by the LEDS. Indeed, in this sense there is the possibility that on occasions a severe event provoking a depressive episode, say the departure of a violent and feckless husband, may already contain the ‘fresh start’ that will bring about a recovery. Later work contrasted the pattern of ‘fresh starts’ preceding depressive recovery with remission from anxiety after ‘anchoring’ events. The latter were defined as reflecting a likely increase in security following becoming fixed or anchored in a role or situation that involved increased regularity or predictability of an activity or a relationship (Brown, Lemyre and Bifulco, 1992). As a final test of the hypotheses arising out of these findings, Brown mounted an intervention study with Harris.

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Tirril Harris 21 Raising the funds themselves to finance social workers who would train volunteer befrienders and offer them backup support, they selected women who had been seriously depressed for at least twelve months and randomly allocated them to befriended or waiting-list-control status. While fresh start experiences again featured as of key importance, along with standard attachment style and an absence of very poor coping, befriending was also required to model remission (Harris, Brown and Robinson, 1999a and b). Moreover, among the befriended those whose volunteer had given them not merely good, but markedly good, active emotional support did best of all. VIII

GENDER DIFFERENCES AND ROLE IDENTITIES

Although there was a small group of male patients included in the first sample from the Maudsley Hospital which Brown studied when he first turned his attention to depression, until the 1990s his aetiological work almost exclusively involved women. The thirty-five original male patients had shown a broadly similar pattern of results as far as provoking life events were concerned. Two projects begun in 1989 were especially designed to involve men. The first, with adults, selected 100 couples who had recently experienced a shared severe event or difficulty in order to compare the ways in which the women would respond differently from their male partners. In order to study situations that were as similar as possible despite gender, couples were not included where the event was only severe for one and not for the other (for example, the death of one spouse’s sibling would rarely be severe for the other spouse). The expected two-fold difference between men and women in rates of depression was found, but it now proved possible to relate this to features of the events themselves. It was only among the forty-seven couples with an event involving a child, reproduction or housing that this higher rate of depression among women was found, and it was possible to see that this stemmed from their greater commitment and involvement in such domains. For thirteen of these forty-seven crises, ‘role salience’ was rated a good deal less given the relatively greater involvement of the male partner in the home, and here there was no difference in depressive onset. For the remaining couples, the proportion of men responding with depression to financial and marital provoking agents was no lower than among women (Nazroo, Edwards and Brown, 1996). Gender differences in social support were also interesting: while a supportive marriage was protective for both, women expressed greater need for support within marriage and were also more likely to seek support from close relationships outside the marriage. Receiving support from outside marriage, which was protective for women, was associated with higher depression among men (Edwards, Nazroo and Brown, 1997). The authors speculate that this may be due to men feeling more demeaned by confiding their emotions, and so postponing support seeking until they are under more emotional pressure to do so, that is, perhaps, until depressive symptoms have already begun. The other study, of ninety-six young men who were sons of some of the women included in the 1980 Islington sample, broadened the focus to include conduct

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22 Introduction disorder as well as depression and anxiety (Brown and Hepworth, 1993). It was run in parallel with a study of seventy-six daughters selected in the same way (Andrews, Brown and Creasey, 1990). The experience of severe events during a twelve-month period was much the same for both the sons and the daughters (50 per cent and 52 per cent respectively), as was the overall experience of psychiatric disorder (13 per cent and 12 per cent respectively). However, the type of disorder differed between the genders, with 11 per cent of daughters and no sons suffering from depression, anxiety or eating disorder, while 7 per cent of sons and no daughters met criteria for conduct disorder. This confirmed much earlier notions that women tend to develop ‘internalising’ disorders while men develop ‘externalising’ ones (Cleary, 1987). However, contrary to this expectation, the prevalence of addictive disorders such as alcohol/drug abuse and gambling, which are usually considered to be ‘externalising’, was no different between the sexes, possibly a generational feature. Interesting differences in experience of childhood adversity also emerged and their role in explaining these differences in diagnostic types was considered. Daughters had experienced more sexual abuse than sons (and the increased rate was largely among relatives from whom the boys had undergone no sexual abuse at all) and they had suffered more than twice the rate of antipathy from their mother before age 17, both of which could be seen as precursors of the damaged self-image postulated by Brown’s model as mediating between childhood adversity and adult disorder. By contrast, the sons more often reported low levels of parental supervision and containment which might be expected (and was found) to go with their higher levels of conduct and antisocial personality disorder. As would be expected, given that many of the sons were brothers to the daughters, rates of another factor believed to produce later disorder in offspring, chronic or recurrent depression in the mothers, were similar in the two groups. IX

CROSS-CULTURAL DIFFERENCES: IMPLICATIONS FOR GENETICS

Consistent with Brown’s undergraduate degree in anthropology, he has throughout his career sought to explore his ideas and measures in other societies. This became possible when foreign colleagues who had trained in the use of his team measures took them home, translated them and carried out data collection. In Holland Giel (and later Ormel) and in Austria Katschnig were some of the first to take the LEDS across the Channel in the early 1970s, with Lora, Fava and Faravelli following in Italy in the next decade, and Gorwood and Amiel-Lebigre in France in the 1990s. Crossing the Atlantic came more slowly, and was given a definite boost when the MacArthur Foundation funded a week-long workshop on the LEDS in Pittsburgh in 1989 – an invitation which was later to be repeated for the SESS and CECA measures respectively in 1992 and 1994. But the cross-cultural implications of Brown’s work can be more clearly seen in the studies where he himself was more directly involved. There are three of these, although his close supervision of a small study in Nairobi in 1977 (Vadher and Ndetei, 1981) also deserves mention for the success of the blind team consensus in distinguishing

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Tirril Harris 23 those polygamous marriage events which were likely to be depressogenic from those more clearly in keeping with traditional values and thereby with only minor or no long-term contextual threat where rates of depression were low. The first study, of women in the Scottish Outer Hebrides islands in the mid 1970s, inspired by the suggestion of Una Maclean, was directly led by Brown ‘in the field’ – a favourite phrase which he more usually employed to describe visits to the less exotic areas around Camberwell Green. Members of the London team had to learn new probes about lifestock management, storms at sea, weaving and the kelp (seaweed) industry as they spent several weeks in the north collecting data. Psychiatric supervision was given by Ray Prudo, who managed a much longer stay on a second island, Lewis, the following year. Depression was less prevalent than in inner London, as were severe events (Brown and Prudo, 1981), but particularly interesting was the lesser prevalence on the islands of certain types of severe events. These, under the influence of Alexander Leighton’s work on socially disintegrated communities in Canada (Leighton et al., 1963) were characterised as ‘disruptive’ and included severe events that in some way challenged the smooth running of the social fabric, such as interpersonal conflicts, divorces, burglaries, assaults, relatives’ suicide attempts, and job dismissals. These were contrasted with less ‘irregular’ severe events such as deaths, illnesses and seasonal migrations. Within the islands there was a differential distribution both of disruptive events and of clinical depression, with those more integrated into traditional island culture (in terms of crofting occupation and dedicated church attendance) less depressed than those less religious and living in the plentiful rural council housing provided by the Highlands and Islands Board. The latter women not only manifested a good deal more depression but also had a higher experience of disruptive events (Prudo, Harris and Brown, 1984). This mirrored the social class results in London when the Camberwell events were re-rated in terms of disruptiveness and their relationship with depression re-analysed by occupational grading. Another interesting comparison involved the prevalence of psychiatrically relevant anxiety without depression which was not only higher in the Hebrides than in Camberwell, but also higher among those islanders who were more integrated into their traditional way of life – the latter judged by regular churchgoing and living on an active farm. Many of the anxiety states were the residues of former comorbid depressive and anxiety conditions starting many years earlier with the death of a close relative (Prudo et al., 1981). However, it struck Brown that this unusual sensitivity to death in the Highland community might not necessarily be influenced only by the strictness of the presbyterian religion. It might as much result from the high rate of outmigration to Glasgow and to Canada by its bolder members, having left a higher proportion of constitutionally anxious persons behind, while conversely Camberwell might have a lower proportion of such anxiety-prone individuals being diluted by the high rate of bolder in-migrants who flow into the inner London boroughs. Nevertheless, despite this constitutional caveat, the apparent cross-over result between anxiety and depression with varying degrees of adherence to the old Hebridean culture was a springboard for a reinterpretation of Durkheim’s distinction between regulation and integration in traditional society: It was suggested that

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24 Introduction whereas the integration and attachment provided by the crofting extended family might protect against the isolation that often produces depression, the strict regulation of the Free Church of Scotland might engender more anxiety about wrongdoing (Prudo, Harris and Brown, 1984). Brown’s role in the second study was less direct, but still strong. Data was collected by Spanish colleagues who were ex-masters students of his in the town of Bilbao and two rural populations, one Basque-speaking and one Spanish-speaking. In order to keep a close understanding of the differing cultural context and its possible implications for rating standards, members of the London team participated in ‘remote’ consensus meetings, that is responding by telephone and letter and visiting Spain on several occasions to offer supervision. In addition, at the time of write-up, Brown gave considerable input, though not a co-author (Gaminde et al., 1993). Again the same rural-urban difference in rates of depression was paralleled by a similar difference in rates of severe and disruptive events, with the Basque-speaking villages presenting an even more extreme contrast to the city of Bilbao than the Spanish-speaking rural women. Again, within the Spanish-speaking rural population with a rate comparable to the Outer Hebrides, ‘integration’ into the traditional way of life was related to a lower rate of depression. Although funds for the third study – in Zimbabwe – did not allow for ongoing supervision by Brown during data collection, the colleagues involved returned to England with their data and it was therefore possible to institute consensus rating checks with him before the final write-up of the analysis into which he gave a substantial input (Abas and Broadhead, 1997). Particular care had been taken to assemble a group of health workers to form a local consensus team to adapt the London ratings for Harare. Among such adaptations notable were the different stress valences of the menopause (rarely distressing in London but commonly ‘severe’ in Harare) and the importance of questioning whether anyone believed a spell had been cast by someone to cause any severe events identified, since accusations of witchcraft were not uncommon and always served to increase the contextual unpleasantness. Here the sample was totally located in Harare so there was no scope for an urban–rural comparison. But the very high rates, on the one hand of severe and disruptive events, and on the other hand of depression, re-echoed the pattern that had already emerged when comparing Scotland and Spain with London. In all these studies, although considerable emphasis was placed on taking account of local values, the parallel use of London standards turned out to agree remarkably well with the ‘local’ ratings. For example, in Harare when London standards were used only 5 per cent of events rated severe by local standards were missed. The same degree of convergence held when humiliation/entrapment events were later rated. Indeed, the much higher rate of depression experienced in Harare compared with London was clearly related to their much higher rate of such events. Figure 1.2 shows the rate of severe events by type in a number of populations. The fact that these differences so closely parallel the rate of clinical depression became a lynchpin in debate about the role of genetic factors in the aetiology of depression. It is not that genetic differences between populations are ruled out altogether as explaining differences in depression between them, but that they are

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Percentage

Rate per 100 women

Tirril Harris 25 90 80 70 60 50 40 30 20 10 0 5 10 15 20 25 30 35

87

Irregular/disruptive events 31

21

11

8

0 2.4

15.1

10.6

10.3

11.0 Case depression

30.0 Zimbabwe

London

Bilbao

Outer Hebrides

Spanish rural

Basque rural

Figure 1.2 Irregular or disruptive severe events related to depression.

highly unlikely to be capable of explaining such large differences in rates: in short, given that variations in rates of depression between populations parallel so closely the variations in those psychosocial factors established as of aetiological importance for depression, there is much less room left for a genetic explanation (Brown, 1996). X

DIAGNOSTIC ISSUES, PSYCHOSOCIAL FACTORS AND

MELANCHOLIC-PSYCHOTIC DEPRESSION

One important feature of Brown’s work on psychosocial factors was its bearing on certain diagnostic debates, and a second sample of psychiatric patients studied in the late 1980s fuelled these ideas. The two patient data sets were clearly well suited as bases from which he could contribute to the well-known debate concerning differences between neurotic depression and the so-called ‘endogenous’ symptom patterns in terms of environmental precipitation. (Brown had collaborated with John Copeland to collect symptom data on the Maudsley series in 1968, but the Present State Examination (PSE) had been used with the North London sample in 1985.) A key opponent in this debate was Paul Bebbington who also reported on two patient series and a curious cross-over took place: initially Brown and colleagues, chief among whom on this issue was Ni Brolchain, used discriminant function analysis of symptoms to maintain there was little evidence for such differences in experience of LEDS-defined provoking agents, except perhaps a modest tendency for those at the very extreme ‘psychotic’ end of the dimension to have fewer severe events, but as many major difficulties (Brown,

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26 Introduction Ni’ Brolchain and Harris, 1979). Paykel and colleagues had earlier reached a somewhat similar conclusion (Paykel, 1974). Around this time Bebbington and colleagues, using the ID-Catego system with the PSE, reported many fewer with severe events among those in the D and RD categories considered closer to melancholia (Bebbington, Tennant and Hurry, 1981). In a critique of this paper, Brown argued that this finding might be the misleading result of a number of decisions about sampling and measurement that had been taken (Brown and Harris, 1982). In a later paper using a different sample but the same ID-Catego diagnoses, Bebbington’s group reported no differences in experience of marked and moderate events, acknowledging their departure from their earlier position (Bebbington et al., 1988). Meanwhile, Brown had also collected data from another hospital sample, and after promoting discussions within the MacArthur Foundation Network on Depression he published in the Archives of General Psychiatry in parallel with other network members (Frank et al., 1994). These new findings permitted a revised view of this controversy and may well help to explain some of the puzzling inconsistency of previous data sets: taking a six-month pre-onset period it seemed that first episodes of melancholic or psychotic depression were very similar to all neurotic depressive episodes in terms of the proportion that were ‘provoked’, but that subsequent melancholic-psychotic episodes were significantly less often preceded by a severe event (Brown, Harris and Hepworth, 1994). Given that different treatment agencies would be likely to receive different proportions of patients with first and later episodes, the pictures of provocation for melancholic-psychotic depression would be bound to differ by setting – for example, tertiary referral centres would be likely to contain more with recurrence and so show a lower proportion with preceding severe events if the investigators failed to control for episode number. Brown related these findings to work by another MacArthur Foundation Network member, Robert Post, who had suggested an underlying neurophysiological process involving sensitivity or scarring, particularly in relation to bipolar disorder (Post et al., 1986). XI

INTEGRATING BIOLOGICAL MEASURES INTO THE PSYCHOSOCIAL MODEL

As already implied, Brown’s work is ongoing, and cannot yet all be reported. However, it is important to flag up a new area – the integrating of measures of salivary cortisol into the model of depression. This is being done in collaboration with Joe Herbert at the department of anatomy at Cambridge University. Relations between cortisol, psychiatric status, lifestress, support and coping are being explored both cross-sectionally and prospectively. The work parallels studies of cortisol, life events and depression among adolescents undertaken by Ian Goodyer and Joe Herbert. Other disorders While it is clear that the bulk of Brown’s work has been around schizophrenia and depression, he has not hesitated to affirm the potential relevance of his

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Tirril Harris 27 aetiological model for other conditions, including physical disorders, especially those traditionally considered ‘functional’. Here the colleagueship of Francis Creed proved of some importance: Creed approached Brown’s team in the late 1970s for training to explore his hypothesis that patients undergoing appendicectomy without ‘true’ appendicitis would prove to have experienced more stressful life events. Around the same time, Brown embarked on a study which identified the relevance of LEDS provoking agents for onset of a range of physical disorders brought to general practice surgeries (Murphy and Brown, 1980). This was followed by his direct involvement in work with gastrointestinal (GI) disorder (Craig and Brown, 1984) and coronary heart disease (Nielson, Brown and Marmot, 1989). While the full lifespan was not investigated, these two studies illustrate the flexibility with which Brown’s style of work with the preonset period can be used to tease meaningful associations out of the data. Those with gastrointestinal disorders with no clear organic basis had a higher rate than the healthy comparison group (and those with organic GI conditions), not only of the provoking agents relevant for depression, but also of major and minor depressive symptomatology occurring after the event but before the onset of the physical condition. Moreover, exploration of the nature of the non-severe events preceding the abdominal pain in the ‘organic’ GI group gave insight about a new ‘goal-frustrating’ aspect of events, and Craig worked hard to systematise this novel LEDS dimension. As a result it was available for use in the study of myocardial infarction (MI) where a statistically significant difference was also found (mostly involving work events), with 31 per cent in the MI and only 6 per cent of the comparison group experiencing such an event in the key pre-onset period. However, the MI study also adopted a flexible approach to the definition of this key pre-onset period, recognising the long duration required for the occurrence of the hypothesised intervening physiological process (the build-up of atheroma). A ten-year period was covered and showed that a continuous length of exposure to work stress and overload was of crucial significance rather than the problems merely being concentrated in a narrower time-band around MI. Furthermore, in terms of exploring interactions between stress and previously identified vulnerability to heart disease (for example, Type A personality), the data suggested an interaction between scoring positive on the workload index and having a high Bortner type A rating. Brown’s influence on the work of others The volume edited by Brown and Harris in which the GI and the MI studies were reported (Brown and Harris, 1989) contains further examples of how his overall approach has had considerable influence on research by others. For example, the idea of systematising a new LEDS dimension is discussed there by Harris in chapter 10 in connection with the onset of secondary amenorrhea and challenging events, while a new dimension of ‘conflict over speaking out’ is described by House and Andrews in chapter 13 in connection with onset of functional dysphonia. Later LEDS work with eating disorders systematised a dimension of

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28 Introduction ‘pudicity’, or events involving major shame around a sexual theme, which were more common before restricting anorexia than before bulimia nervosa and rare in the comparison group (Schmidt et al., 1997). Such systematisations of new dimensions rarely occurred without Brown’s close involvement and is so characteristic of his working style that it is discussed in greater detail below. In general Brown’s influence has arisen not only through his encouragement of younger colleagues but also more directly through the trainings that he and his team members have been able to offer; and this has only been possible because of the longterm funding available for his research team. His move from the staff of Bedford College to become a member of the external scientific staff of the Medical Research Council in 1979, and the MRC’s continued renewal of his programme grant during the 1980s and 1990s, allowed members of his team to provide training and supervision in a whole range of measures they had developed. Originally, as with his style of data collection and consensus rating, this was very much a close face-to-face educational process, though backed by written manuals. Latterly, help to upgrade these courses by producing more effective training packages was also made available by the MacArthur Foundation. As the model of disorder grew to encompass more elements both stretching further back over the lifespan and moving further in to the respondent’s inner world of attachments, coping and commitments, the possibility arose that interviews might take more than eight hours. It therefore became imperative to streamline the measures, and recent developments include the Shortened LEDS (SLEDS) and the MiniCECA, as well as collaborative work with Kessler and Wethington on a fully structured questionnaire (or SLI) for use by ordinary survey workers based on LEDS principles (Wethington, Brown and Kessler, 1996). The range of Brown’s influence upon the work of others is as broad as the range of his own work, from the spate of interventions focused upon the expressed emotion of relatives of schizophrenic patients (Leff et al., 1982) to investigations of progression from HIV to full AIDS syndrome (Evans et al., 1997) and relapse in breast cancer. Whereas the former have nearly always replicated each other’s findings, the jury is still out on the last issue of breast cancer. The two LEDS reports already published reached different conclusions, one retrospective study with positive results for LEDS severe events (Ramirez et al., 1989) and the other prospective with no association (Barraclough et al., 1992). Two further prospective studies of breast cancer relapse using both the LEDS and the coping interview are now in progress. Meanwhile, two other studies have suggested that LEDS severe events are of relevance in the initial onset of breast cancer (Chen et al., 1995; Geyer, 1991), and a third has reported negative results (Protheroe et al., 1999). Other work using the LEDS with physical disorder includes studies of insulindependent diabetes (Robinson and Fuller, 1985), multiple sclerosis (Grant et al.,, 1989), and stroke (House et al, 1990).

Brown’s style of work Something of Brown’s style of work will already have begun to emerge. The most pertinent comment perhaps was made by his psychiatric colleague at the

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Tirril Harris 29 Maudsley, Douglas Bennett, who attributed his success to his insistence on keeping very close to the data. Although occasionally maddening for his colleagues, this is indeed his unspoken prescript and is true at every stage of the research process. A second, equally essential, prescript is the crucial importance of the time order between variables, particularly between the dependent variable and any independent one. This stems from his commitment to understanding aetiology, and thus the temporal ordering essential for the attribution of causality, but of course requires a special closeness to the data, particularly when additional factors are included in the modelling process. In order to get a flavour of how this closeness has allowed him to pursue the principles of grounded theory with a particular thoroughness, it is illuminating to describe his typical approach to each stage of research. Before doing this, however, it may be useful to say something about Brown’s views on grounded theory. Brown’s approach to the theory of grounded theory The original protagonists of grounded theory (Glaser and Strauss, 1967) were writing thirty years ago in a context where the discipline of sociology seemed in danger of stultification, either at the hands of the then dominant functionalist or structuralist ‘logico-deductive’ theories (represented by Parsons, Merton and Blau) or by the somewhat mindless verificational empiricism represented by large-scale survey research. A central feature of the grounded theory approach, whereby theory evolves during actual research through the interplay between observation, data collection and analysis, is ‘a general method of constant comparative analysis’ (ibid: vii). Theory was to be carefully induced from diverse data, although theory based on previous research might be carried into current studies and elaborated (Vaughan, 1992) or modified as incoming data are meticulously played against them. Glaser and Strauss used their own research with dying patients to give examples of the practice of this method. In a paper on grounded theory Brown argued that they might have gone too far in proposing a relaxation of the safeguards of verificational studies. He goes on to suggest that the main reason they manage to avoid concern with traditional methodological issues, and yet have assurance in the worth of the resulting theory, was because it was grounded in a certain type of data (Brown, 1973). The type of first-hand observations Glaser and Strauss were able to make – of how nurses behaved differently to young and old patients or to black as compared to white patients – could impart a reasonable conviction that these attributes had some influence on the nurses’ behaviour. Moreover, in conversation the nurses might even tell the research worker why they were behaving as they were. But some phenomena involve much greater discontinuity, either in time or space or in the level of systems studied. For example, once psychiatric patients are committed to hospital by their relatives it is no longer possible to observe the impact of their illness upon those relatives in the home: this can only be reconstructed by questioning and confidence in any theory in such circumstances must therefore at least partly depend on meeting certain methodological criteria about such questioning, and meeting

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30 Introduction them at an early stage of the research. ‘Rescue operations are not always possible, and it is foolhardy to rely on a vague hope that something can be done at the analysis stage’ (op.cit. p.13). In arguing for what he called ‘a proper balance’ between verification and exploration/theoretical formulation, Brown was not rejecting the basic tenets of grounded theory, merely aiming to supplement them with useful methodological tools. His approach was thus able to combine the breadth of the statistical analyses of epidemiology with the depth of the type of case history advocated by Glaser and Strauss – a combination well suited to reveal the links between inner and outer worlds. Grounded theory in practice As already mentioned, Brown’s chief method of pursuing grounded theory in practice is to stay close to his data so that he can think flexibly about what may be going on and capture it more thoroughly. This can be seen at all stages of the research process. Data collection This flexibility can be achieved, along with the systematic structure required for analyses of comparable data across persons and groups, if data collection follows a semi-structured interview format, which has neither the rigidity and respondent bias of questionnaires nor the unmanageability of open-ended conversation. Brown viewed such a training as almost an academic discipline, especially in so far as the recording of time order was concerned. Whether or not his anthropology background was responsible for the instruction he gave his colleagues, he instilled in us the sense of how important use of language and specific terms could be for ‘creating a “sharedness of meanings” in which both interviewer and respondent understand the contextual nature of the interview’ (Fontana and Frey, 1994, p.371). However, he emphasised the key need for respondents to be encouraged to talk freely about issues in any way relevant to the research. If this was achieved it did not matter that a particular question might have been misunderstood; indeed, such a misunderstanding might well give some insight into the concerns of the respondent. What was required was for the interviewer to continually review what was being said in the light of what had been said earlier and to explore any ambiguities. And here it was helpful to see much of this in terms of a series of stories – of which the interviewer had to make sense and which could be returned to at any point during the interview, along the lines ‘but earlier I had the sense that… Is that right?’ In Brown’s experience respondents were usually happy to collaborate in this way to obtain a full and accurate account as long as these were issues of relevance to them. If not, it was the job of the interviewer to seek their indulgence. There was also a need to keep other issues in continual review – for example, the emotion with which things were said (and especially the tone of voice); how the respondent was feeling about the interview itself; whether a ‘no’ to a question was

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Tirril Harris 31 said in a way that gave some hint that further tactful questioning might be useful; whether in asking a question it should be linked to something said earlier and so on. However, while coherent stories should be sought about facts, this certainly should not hold for emotions and attitudes which indeed might appear to change radically during the course of the interview itself. Such ‘ambivalence’ had to be accepted for what it was, with no attempt to uncover ‘true’ feelings. Thus, before narrative became a focus of a good deal of sociological research, Brown was emphasising the importance of conducting the interview as much as possible like a conversation rather than an inquiry. He was also concerned that as far as possible the interview should, out of common courtesy, be a ‘good’ experience for the respondent. But perhaps because of his growing awareness of the long road between knowledge and application, Brown also saw the need for the work to be strong scientifically – then at least the effort and distress would not have been in vain. But fortunately there can be little doubt that for the great majority the conversational approach was not found distressing and often was welcomed. Here we should bear in mind that the respondent typically exerted some real control: for example, if it was apparent that one topic was particularly important for him or her (say some issue surrounding a son’s or daughter’s admission to hospital), this issue would be brought forward from its chosen place on the interview schedule. The interviewer (where possible) used a tape recorder, rather than take notes, since this would not only permit satisfactory eye contact between research worker and respondent but also allow the information to be given at the latter’s own pace. Where the research itself was concerned Brown remained satisfied with audio- rather than video-recording, although he anticipated all four of Gorden’s important nonverbal elements of the interview: ‘proxemic communication – the use of interpersonal space to communicate attitudes, chronemic communication – the use of pacing of speech and length of silence in conversation, kinesic communication – any body movements or postures, and paralinguistic communication – all the variations in volume, pitch, and quality of voice’ (Gorden, 1980). The first and third of these, being visual, would only be available to the interviewer and could not be recorded on an audio-cassette. It should be added that Brown has often referred to his excitement on reading Richardson’s book (Richardson, 1965) around the time he was helping to develop the Camberwell Family Interview for the EE measure – a book which like none other truly reflected his views about research interviewing. Brown’s faith that such interviews would rarely be experienced as intrusive, despite the fact that respondents were at times talking about particular private experiences for the first time, was built on years of hearing interviewees express surprise at how much they had gained from (and even enjoyed) the experience – often finding it useful in helping them to reflect on their lives. But his faith was also based upon the care his workers were made to take to be courteous and attentive while not leaving aside the social neutrality of science. As younger colleagues acquired more feedback from interviewees, they would develop the same empathy for their subjects and their contexts. This, more than any other factor, would allow them to learn from the data and provoke team discussions that produced new

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32 Introduction hypotheses grounded in the material. For this reason he always maintains that, as in the Social Psychiatry Research Unit, in every study the principal investigator should be involved to some degree in data collection and it should certainly not just be farmed out to ‘hired hands’ as if it were a menial task. It should perhaps also be mentioned that he rather enjoyed the freedom allowed by the semi-structured nature of the interviewing where probes are used very much at the interviewer’s initiative. Sometimes he would even tease some of the research staff who had left something unprobed for not having enough curiosity – a feature of his emphasis on the need to feel interest in everything said during an interview: the interviewer should never relax. Measures and their development Appreciation of meaning and context is the keynote of Brown’s approach to measurement. Not only is this dealt with extensively in many of the other chapters of this volume, but some key features have already been discussed above in connection with his work on expressed emotion and his findings on depression, notably concerning measures of the degree of contextual threat/unpleasantness of life events. These will therefore only be summarised here in terms of three critical features: the background philosophical requirement to minimise bias, the types of ratings developed and their use in practice. CONTROL OF BIAS

From the first, Brown has pursued a modified form of positivism in the sense he has believed that the impingement of the external world can be described in terms of meaning independently from that individual’s interpretation of that impingement, but in a way that approximates to their experience; and that this could be done sufficiently accurately for causal conclusions to be entertained when individuals were considered in aggregate – for example, in contrasting those with and those without a severe event. This has been achieved by investigators using what have become known as ‘contextual ratings’. In practice there is a good deal of variability in the degree to which context is considered in the different types of rating, although in all what a person reports about feelings is ignored. In other words, a ‘contextual’ estimate of the environment can be made which will have a validity quite separate from the subjective appraisal of those involved. Brown’s guiding light has been the need to control for possible bias, arguing that questionnaire users might pride themselves on reducing investigator bias but could do little to prevent the respondent bias that stems from undigested subjective reporting (Brown, 1974a). Thus two women with a comparable experience – a minor incident involving the car behind them breaking only a side light – might give different responses to a checklist item on whether they had experienced any car accident in the study period, according to their basic level of general anxiety, with the less anxious one ticking ‘no’. Thus any association that might emerge between car accidents and panic attacks might be misleading due to a more fundamental link

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Tirril Harris 33 between prior generalised anxiety inflating the reports of such incidents. With probes by the investigator about the context of each accident, it would be possible to make a good enough estimate of the comparability of the two accidents, for example in terms of the obvious aspects such as the amount of damage, personal injury, resulting argument and less obvious ones such as whether the car was being driven without the owner’s permission or subsequent lack of insurance cover. In other words, the investigator, not the subject, would decide when to tick ‘yes’ or ‘no’. The key rating taking account of ‘objective evidence’ of relevant plans and concerns in contextual severe long-term threat was described earlier. However, the motive for the creation of such ratings has not been simply methodological. They are useful in several other ways. What, for example, if an external factor, such as a close friend’s emotional support, served to prevent a lover’s infidelity from being experienced as humiliating? A completely accurate measure would militate against our ability to show the protectiveness of such support as the event would not be classified as stressful. This is avoided by a measure reflecting the potential for such an event to be humiliating. Therefore, while not wishing to downplay the general aim of Bedford Square contextual measures to be as accurate as possible, their probabilistic nature can in this sense increase their theoretical relevance. Furthermore, the difficulty of obtaining an accurate assessment based on self reports needs to be recognised. Let us say the behaviour just outlined was experienced as humiliating but that in a matter of weeks a new lover had been acquired and the woman was able to look back on the crisis in a less negative light. This final appraisal may dominate any subjective account. Two final advantages are worth noting. First, Leventhal has discussed the need to see emotion in contextual terms – pointing out how depressed mood in elderly women often relates to illness in their partner and in men to their somatic status and how this helps to explain the gender difference in predicting health outcomes from this ‘emotion’. The LEDS contextual approach helps bypass such problems of the meaning of particular emotions by concentrating more on the emotion-provoking situation rather than the ‘emotion’ itself. Second, a threatening event will typically ‘lead’ to the experience of a number of ‘emotions’ as a person comes to terms with its implications. This has presented formidable problems for psychologists wishing to study event appraisal (Frijda, 1993). Fortunately, the LEDS is able to deal with any number of possible meanings – involving, for example, not only the humiliation of a lover’s infidelity, but also the event as a key loss (she had been hoping to live with him), as a danger (she had just learned that she was pregnant) and so on. It is just this flexibility of the contextual approach that has over the years enabled a range of possible meanings to be documented and this in turn has led to the establishment of specific links – for example, between ‘danger’ and anxiety disorders, ‘fresh starts’ and recovery from depression, ‘goal frustration’ and abdominal pain, and ‘challenge’ and secondary amenorrhea. The various measurement systems developed under Brown’s guidance (not just the LEDS) are now based on manuals of examples which enable research workers to reach satisfactory inter-rater reliability. The origins of these ground rules emerged in good part from the regularly held consensus discussions. Right from his early work on

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34 Introduction schizophrenia, Brown appreciated the value of team debate in refining the concepts that needed measuring, and such consensus meetings continue despite the existence of manuals, as a fail-safe system for idiosyncratic experiences of a kind not yet described in these ‘dictionaries’. Furthermore, unlike the interviewer, other members of consensus meetings, when asked to rate an item, can be kept blind to the scores on other variables hypothesised to relate to this item and some control on investigator bias is therefore available. Training in the use of his measures particularly involves training in the unbiased presentation of material to consensus meetings. SUPPLEMENTING CONTEXTUAL RATINGS

Emphasis has been placed on the probabilistic aspect of contextual ratings given their originality and the fact that their nature and purpose has so frequently been misunderstood. It is therefore important to build on the point already made that the whole range of ratings, especially in the SESS, attempt to reflect as accurately as possible attitudes and emotions and, indeed, often take account of self-reports of feelings in their assessments. In a prospective inquiry such subjective material is much less open to the various sources of invalidity and can be an invaluable supplement to contextual measures collected retrospectively at follow up, say, of events. Thus in the Islington inquiry, women were encouraged at the time of first contact to talk about various role domains such as motherhood, marriage and employment, and were rated on a four-point scale in terms of the interest, involvement and enthusiasm they conveyed. A ‘marked’ rating was not common and on average the women had only 1.5 such ratings for six role domains. These ratings could be easily compared with later life events in terms of whether there was a match: a marked commitment to motherhood would ‘match’ the later event of learning of a son’s arrest for drug dealing. In practice, such matching for commitment proved to increase threefold the chances of a severe event being followed by a depressive onset (Brown, Bifulco and Harris, 1987). In terms of an investigatorbased approach to measurement, there are two clear implications. First, the use of a crude estimate of the concerns and plans of the respondent as part of the contextual ratings of threat has been justified. Second, it underlines the approximate and conservative nature of the contextual ratings, but how none the less they have been good enough to get research under way and enable the development of a reasonably convincing aetiological model. DEVELOPMENT OF RATING SCALES

Brown’s approach to rating is basically categorical. Again I will take the measure of events as an example, but the argument holds throughout the various instruments. As already noted, events can be described in many ways and these qualities can vary in degree. Unlike the wide-ranging scales often found with checklist questionnaires where scores often extend beyond ten points, Brown’s scales have been deliberately kept to four or five points, usually representing differing

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Tirril Harris 35 degrees of the dimension at stake – for example ‘marked’, ‘moderate’, ‘some’ and ‘little or no’ loss, danger or humiliation. They thus represent broad categories for which it is easier to obtain inter-rater reliability than with the narrower ones of say the nine-point scales found with some interviews such as the Adult Attachment Interview (George, Kaplan and Main, 1985). There is no requirement that the Bedford Square scales embody equal intervals. The manuals typically give examples of the top and bottom of the range to be placed within the specified scalepoint. They are also deliberately allotted digits of a value opposite to the quantitative implications of their descriptions, with ‘4’ signifying ‘little or none’ and ‘1’ denoting ‘marked’ so as to check investigators from crudely ‘adding’ items, thus wrongly treating the dimensions as interval rather than ordinal scales. How much the understanding of how to develop a valid and reliable rating scale of this type has always been integral to Brown’s teaching is reflected in a recent chance reunion of mine with a former student of his, now well established in a quite different academic unit concerned with psychoanalytic studies. Clearly delighted to gossip about the Bedford College of twenty years ago, he recalled both the intellectual demands Brown made on him during preparation of his thesis and how much he had learnt from his approach. He cited in particular a post-graduate seminar devoted to how to develop a rating scale; how this typically took many months and many versions with its metalevel message about how, in such a drawnout process, it was never too late to make amendments and to capture what might start as mere hunch in a measure that could then be put to the test. An eight-page document describing the origins of the ‘expectedness’ rating for a life event was distributed. It followed the process through five stages: how its testing in practice first led to the production of two scales from the perspective of the day of the event – ‘expectedness of event occurring’ and ‘expectedness of its timing’ – and later a third in terms of the expectedness of the ‘warning’ of its occurrence and later still whether this was specific or only general warning. The document shows the evolution of such labels as new interviews were carried out, and illustrates the typical process whereby ‘in trying to solve rating problems there is a tendency to overcomplicate scales and often this is followed by a ‘reaction’ in which simplifications are made’. As a background to this process he also underlined how once a scale was developed, inter-rater reliability was essential, how during its development progress typically came from disagreements and how insights could arise from trying to understand the basis for these. The danger in such developmental work was a tendency to underplay disagreements once a certain level of agreement had been reached. For example, the fundamental distinction in the EE work between ‘critical comments’ and ‘dissatisfaction (without criticism)’ only emerged fairly late in the developmental process when the implications of occasional puzzling differences in rating were faced and a reason hammered out. Indeed, one can add that, even with an established instrument, listening to a minority view at a consensus meeting can be enlightening and lead to useful amendments to current standards.

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36 Introduction USE OF RATINGS IN PRACTICE

As implied earlier, the use of such scales is based on examples of precedents set out in manuals, with accompanying explanatory comments about why the rating was not one point higher or lower. The following instance from the life-event manual, section 7101 (Start of new heterosexual relationship) illustrates this procedure. The initial case identifying number is followed by two digits representing short- and long-term contextual threat, then a letter ‘S’, ‘O’ or ‘J ‘representing focus (subject-, other- or joint-focused). The final rating of independence gives both the scale-point digit and a short-hand label of its meaning. The accompanying explanations are in italics. ISL330 2, 2, Jb Independence: 6 (intentional) Subject is a separated woman in her mid-30s, who left her jealous and violent husband 11 months prior to meeting her new boyfriend. This man is in complete contrast to her ex-husband, being kind, gentle and considerate. Since the separation, her ex-husband has been hanging around daily by her front door watching her and the children. He has access to the children, but this has not as yet been a source of conflict. Meeting the new boyfriend is rated ‘2–moderate’ on long-term threat because of the jealous husband in the background and not because of the characteristics of the new boyfriend or the relationship with him. Although by the end of the 10 to 14 days period the husband has not actually caused any trouble (hence the ‘b’ rating rather than a more threatening rating of ‘a’) his presence in the neighbourhood is menacing, and his past behaviour suggests that he might become violent either towards her, the new boyfriend or the children. FJ297 3, 3, J Independence: 6 (intentional) Subject is a 32-year old woman separated from her husband. She begins a relationship with her hairdresser also separated from his wife. No associated problems. Although there are no problems evident in the relationship, the complication of both being separated without formal divorce raised the threat rating to ‘3– some’. P125 3, 3, J Independence 6 (intentional) Subject is aged 26 and divorced from her husband. She meets a man who becomes her first steady boyfriend since the separation. There are no current problems associated with her previous marriage, but her 8-year-old daughter reacts in quite a hostile way to the new boyfriend. The ‘3-some’ on threat reflects the daughter’s reaction.

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Tirril Harris 37 PP020 3, 4, J Independence: 6 (intentional) Subject is a divorced woman in her 30s. She puts an advert in a ‘lonely hearts’ column of a magazine. She gets 4 immediate responses by post, and arranges to see her first date. There are no problems on this, but they do not arrange to meet again. The ‘3–some’ rating on short-term threat reflects the possible danger associated with going out with a complete stranger, the only prior contact with whom has been by post and telephone. FJ236 4, 4, J Independence: 6 (intentional) Subject starts a relationship with a man who is permanently separated from his wife who lives abroad. She is single and lives alone. No obvious problems. In this example although the partner is separated not divorced, it is a legal separation which will make any divorce proceedings easier, and the fact that the ex-wife lives abroad means that she will be less likely to interfere in the current relationship. It therefore does not reach a ‘3-some’ on threat. As mentioned earlier, the systematisation of additional scales can on occasions occur after the data has been gathered, sometimes many years later. This is only possible, however, because Brown’s practice has always been to insist on accompanying the quantifiable ratings with full longhand descriptive accounts of the relevant narrative, and to preserve the audio-cassettes so they will be available should it seem necessary to mine for further details. It is therefore possible to read through these descriptions, develop new insights and hunches and undertake consensus discussions which refine a new scale, which can then be subject to the necessary tests of inter-rater reliability. Such was the case with the dimensions of ‘pudicity’ and ‘conflict over speaking out’ referred to earlier. With the former, a Bedford Square worker, responsible for producing a supplement to the adult life-event dictionary with special examples of teenagers’ experience, was given access to the written descriptions of all the events in Schmidt and Treasure’s samples of eating disorder patients (Schmidt et al., 1997) and was struck by the relatively higher number of certain types of event compared to the other teenage samples she was reading through for the same purpose. These events appeared to involve sexually shaming situations, often with public disapproval of the respondent’s sexuality. A typical Bedford Square four-point scale was then elaborated in consultation with Treasure and Schmidt, with a lengthy memorandum amounting almost to a mini-manual concerning ‘pudicity’, with anchoring examples of its different degrees and explanations as to why, for example, one event was rated only ‘3-some’ whereas the previous one had been rated ‘2-moderate’. Two further workers from Bedford Square were then ‘trained’ in the scale thresholds and joined the original worker in rating a list of detailed descriptions of some sixty events, none of which had, of course, been used in the training memorandum. This was the inter-rater reliability exercise. A similar procedure was followed during the elaboration of the dimension of ‘conflict over speaking out’– perhaps the most complex dimension the LEDS has

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38 Introduction attempted to systematise (Andrews and House, 1989). Essentially such situations involve the conflict of divided loyalties or a dilemma where speaking out in either direction is likely to bring trouble – for example, a woman whose colleagues were pressing her to voice a complaint against her immediate manager whom they all suspected of embezzlement. Here, however, it proved much harder to achieve reliability. While Andrews and House had highly concordant ratings with Brown and Harris on new events hitherto not rated by any of the four, the other Bedford Square raters at first seemed all over the place. Further discussion revealed that their training in the new rating had not been explicit enough about something the four creators of the scale had taken for granted as part of the context: namely, that women who found themselves in such situations would be in some sense selfselected for high commitment to the persons’ roles likely to be involved rather than a completely random series of personality types. The degree of conflict they would be likely to feel would be correspondingly higher than for the perhaps less punctilious, less committed, ‘average’ woman upon whom the new trainees were basing their ratings in the spirit of the ordinary LEDS threat/unpleasantness scale. Once the need to take account of this likely context of the event was built into the training it was possible to achieve high inter-rater reliability with a further set of raters blind to onset of functional dysphonia. To sum up then, Bedford College measures combine elaborate systematisation with a flexibility that permits continual creative refinement such that insights about the outer world can be matched ever more closely with those about the inner world. This willingness to chew over data collected many years earlier and come up with new insights has been one of Brown’s noted characteristics, enabled only by the form in which data was recorded with detailed longhand descriptions. It is a clear example of that interplay between intuitive hunch and tested experience which can then be fed back into further replication and refinement – the hallmark of grounded theory. Utilising differing samples and designs One of the corollaries of Brown’s interdisciplinary perspective was his ease in using different samples. Starting from the traditional social psychiatry study of patients and branching out to their relatives, he moved to a more epidemiologicalbased approach with the Camberwell representative sample of women, originally seen as a comparison group for the depressed Maudsley patients. This allowed a move from a simple case-control investigation to a fuller vulnerability, or stressdiathesis, analysis. But this initial work on depression was cross-sectional with the time element introduced by careful retrospective questioning. Having used this to elaborate a basic model of depression Brown not only needed to test it in a prospective study (as in the earlier schizophrenic research), but could also afford to cut costs by concentrating on the more vulnerable rather than using unselected samples. Thus, his first prospective study focused on working-class women with children, a group the earlier Camberwell research had identified as particularly at risk for depression. This produced data which refined the notion of vulnerability,

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Tirril Harris 39 bringing it in closer to the internal world of the women in the form of the presence of important negative elements in their close relationships and this was the selection criterion for his next prospective studies which focused on coping and salivary cortisol. Other samples chosen for other purposes were selected on the dependent variable (for example chronic depressives only in the befriending project) or on a crucial independent variable such as childhood death or separation from parent, or the recent experience of a severe event such as for the couples sample where the men and women had to be compared in terms of their reactions to a shared severe event. While the range of selections served to provide a variety of perspectives on the same theme, it also sensitised Brown to key pitfalls that can attend analyses of such samples and about which he was keen to warn other research workers, namely: the limitations of studying only high risk women, for example those with at least one vulnerability factor. To the degree that these are correlated with a further putative risk factor the impact of the latter will be attenuated or even rendered non-existent. Thus if the impact of childhood adversity on depression is largely via the vulnerability factor which has been the basis for selecting the sample, say negative elements in core relationships, then a clear link between childhood adversity and depression would not be expected in that sample, and should not, therefore, be considered a replication failure. (Bifulco et al., 1998, p.48). Another pitfall Brown identified in the process of comparing results in differing samples was the misleading nature of many prospective studies, in the sense that they usually still required retrospective questioning to deal with what happened during the follow-up period itself and since time order was usually critical within this period a questionnaire approach was unlikely to be satisfactory. Here his insistence on thorough examination of time order throughout the whole study period was critical. Following through the Camberwell finding that lack of confiding in partner was a key vulnerability factor, the longitudinal Islington sample focused on confiding in partner at first interview as a moderator of provoking agent(s) during the twelve-month follow up and failed to produce a statistically significant result (see above). One response could have been to withdraw prematurely defeated, admitting a replication failure. But, as discussed earlier, fortunately it was possible to use the follow-up data which retrospectively charted the crisis support offered to the respondent by her partner using contextual-type measures. This threw a different light on the matter: it became clear that confiding was something that could change dramatically during periods of time far shorter than the twelve-month follow up and that this, rather than the situation at first interview, was bound to play the crucial mediating role between stressor and risk of depression. Thus a woman with high emotional confiding/support with partner at first interview may find herself ‘let down’ when she wishes to get support from him over a severe event during follow up when for some reason he can no longer give it. For example, one couple who, at first interview, seemed quite supportive

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40 Introduction to each other, were unable to talk to each other at all about the death of their child in a road accident during follow up and the wife suffered onset of depression. Once the frequency of the experience of being let down became apparent it put into question the whole range of assumptions upon which longitudinal work is based. This implies the need to supplement such prospective studies with retrospective time-order-sensitive checks to monitor any such changes between successive data collection points. But, of course, the only way this can be properly done is to adopt a style of data collection with a strict requirement to establish time order and to use contextual-type measurement in order to minimise reporting bias. But such complexity and a return to ‘retrospective’ measures inevitably raises again the issue of validity. Here Brown has consistently taken the view that, in most instances, one piece of research can give only a certain level of confidence in its findings. It is best seen in terms of whether a further study is justified (which typically will be even more expensive) and the form it should take. The complexities surrounding social support all along made it clear intervention-type enquiries would be required and this is just what the RCT concerning befriending sought to do. Analysis and presentation of data Brown has at times joked about his time working as an engineering draughtsman on leaving school as having had a crucial influence on his research career. Certainly he has always been acutely aware that results need to be presented in a form that is easy to grasp, and this has led him to favour the simplicity of categorical variables. He has often expressed puzzlement about why almost every important measure he has helped to develop has worked effectively as a dichotomy; to take just a handful of examples: 8 weeks or more unvisited in hospital (schizophrenic admissions inquiry); 7 critical comments and 35 hours or more face-to-face contact (expressed emotion research); severe event (Camberwell inquiry); negative evaluation of self (Islington inquiry); severe interpersonal difficulty (Chronicity analyses); lack of care (Walthamstow early loss study). He has been aware of the importance of showing a dose-response relationship, but when this has emerged it has typically been by forming an index from the individual dichotomous ratings. There is, for example, some suggestion of such a doseresponse when summing the dichotomous ratings that form the childhood adversity index: parental indifference, household violence to subject and sexual abuse. His position can be summarised as favouring the simpler categorical (typically dichotomised) approach as a matter of choice, unless the alternative can be shown to be clearly superior. In fact, because of diagnostic habits, the use of a categorical approach rather than dimensional scores is also associated with most diagnostic research in psychiatry. Certainly presenting percentages, followed by the raw

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Tirril Harris 41 Table 1.2 Typical forms of data presentation A The favoured 2

2 table

Percentage of women with remission from chronic depression by fresh start experience and allocation of befriending (n= 86, rct) Befriending Fresh start experience Allocation

Yes

No

Total

Yes No per cent remission per cent remission

Total per cent remission

cell a 82 (18/22)

cell b 48 (10/21)

65 (28/43)

cell c 75 (12/16)

cell d 19 (5/27)

43 (17/43)

79 (30/38)

31 (15/48)

B The use of an index Percentage of women with remission from chronic depression by score on an index of (i) fresh start experience, (ii) standard attachment style, (iii) absence of very poor coping and (iv) allocation of befriending (N = 121, including second-year befriendees who were first year controls) Index score All four factors present

Percentage remission 100

(7/7)

Three factors present

83

(25/30)

Two factors present

47

(20/43)

One factor present

20

(7/35)

Nil

17

(1/6)

Total in sample

50

(60/121)

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42 Introduction numbers – numerator and denominator – in brackets (see Table 1.2 A), helps readers feel closer to the data than would the corresponding regression table which would give less sense of effect size and proportions. It is also much easier to get a sense of what might be happening when a reader can refer back to anchoring examples of what is involved in rating something above the categorical threshold, say, of severe distress, and then relate this to the finding of a 20 per cent overall reduction in such distress, whereas the implications of a statement that there has been an average ‘0.4’ point reduction on a twelve-point scale of distress is much more difficult to grasp. Even in multivariate analyses, Brown has a characteristic manner of getting a message across simply by using indices. Thus instead of producing a 16-cell four-by-four table of the type corresponding to the two-by-two version in Table 1.2 A, he would give one simple column in terms of an index showing a score of the number of the four independent variables present (Table 1.2 B). Thus most of the four-point scales mentioned earlier have later been used as dichotomous categories, the usual division falling between point ‘2’ (moderate) and point ‘3’ (some). Occasionally odd-numbered scales – say with five- or threescale points – have been introduced, but these have often been amended later to allow dichotomisation at the midpoint. For example, for some time the scale of confiding in husband, which had been originally the simple yes/no of the Camberwell intimacy rating, was rated on a five-point scale, but it appeared that the crucial predictive split fell somewhere around the middle of point ‘3’ and in order to analyse dichotomously data had to be re-rated as it were on a six-point scale around this mid-point. Thus in its current version confiding is a four-point scale. It is sometimes tempting to think that Brown prides himself on having an idiosyncratic approach to data analysis and presentation. He loves to reminisce about the days of Hollerith cards and has no hesitation in broadcasting his suspicions of computers (at least when not backed up by extensive parallel analyses working from the raw data itself). Moreover, he sees it as the hallmark of a Bedford Square report that two-by-two tables should be presented in such a way that the cell with the highest depression will be the top left cell, or cell a. This runs counter to most people’s way of thought which follows the binary mode where ‘0’ represents ‘no’ and ‘1’ represents ‘yes’. Here, with two variables expected to be depressogenic, the highest proportion with depression would be found in the bottom right cell, or cell ‘d’. It must be said, however that his idiosyncracies have proved highly productive. His own verdict on himself has been to highlight the importance of a ‘sense of puzzlement’ and of the ‘personal belief in pursuing anomalies’ (Brown, 1985:8–9). In always supplementing computer analyses with hand-written lists of cases, often brightly coloured, where each hue indicates the presence or absence of a key variable, he ensures that he stays close to the data and often notices anomalies that would not strike those not working at the level of the individual cases. Perhaps the greatest pleasure he obtains from the new computerisation of survey analyses is the ease with which error-free lists can be produced – and it is very rare for him to publish any computer-based tabulations without having performed a parallel analysis by hand based on such lists. Where complex algorithms have been used to derive variables, the pencil and paper analysis has usually come first as he

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Tirril Harris 43 argues firmly that it is impossible to avoid error (sometimes of shocking proportions) if the complex computerised procedures are not ‘checked’ by such parallel workings. (The latter are, of course, always checked by a final computer-based analysis.) Once having identified something puzzling in the data – for example, that those with a severe event emerging from a severe long-term difficulty were much more likely to become depressed than those with a ‘new’ severe event – going back to the longhand descriptions can be productive. But this activity can only be successful if the sleuth is armed with a range of plausible theory. The outcome is usually a refinement of the original rating, which sharpens the prediction but must then be replicated in a further sample. A typical example of such a procedure can be seen in the Walthamstow study where, working from his close knowledge of each woman respondent, he elaborated a new variable ‘manner of coping with premarital pregnancy’ as even more predictive of adult depression than undergoing such a pregnancy in the first place. Those who elected for an induced abortion, or who turned to another man other than the child’s father as a long-term partner, had a surprisingly low rate of adult depression, while those who settled down with the child’s father faute de mieux showed the highest rate of all. Once this discrimination became built in to the data set, further analyses revealed its link with the woman’s inner world in terms of her helplessness/mastery, both in childhood and in adulthood (Harris, Brown and Bifulco, 1987, 1990a, b). Once again the additional grounding of the work was pointing to a bridge between inner and outer worlds. Use of statistics Enough should by now have been said to indicate how Brown’s confidence in his willingness to challenge ongoing orthodoxy of thought is grounded both in his data and in the consensus ratings of his teams. This confidence has extended, on occasion, even to rethinking statistical lore. This aspect of Brown’s contribution is much less well recognised than his substantive findings about psychiatric disorder, but it illustrates his originality of thought, albeit guided by statistically expert colleagues. There are three main issues where he has entered the field of debate: the first, the brought forward time, is arguably less original than the others, although in terms of conventional bibliographical references it might appear more so because it has its own label – own marketing brand. A

THE BROUGHT FORWARD TIME (BFT)

This index was first developed intuitively as a means of estimating the aetiological role of life events that in principle could range from triggering an onset that would have occurred before long in any case to a situation where the disorder would not have occurred for a long time, and perhaps not at all, without the event. Its strength (and also its main weakness) is that it is based on the highly conservative assumption that every onset would occur at some point in the future. Going on from this, Brown’s insight was that the frequency in a population of the

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44 Introduction events known to be capable of provoking a depressive onset (i.e. severe events) could be used to make an estimate of the degree to which an event ‘brought forward’ or anticipated the onset. It is intuitively apparent that the higher the proportion of those with a disorder brought about by an event and the lower the rate of such events in the population as a whole the more important events must be in their causal role. Julian Peto gave the idea the correct mathematical basis, arriving at much the same result as reached by Brown (Brown, Harris and Peto, 1973). Unlike the index of attributable risk per cent which gave an effect size for a factor occurring in a specified fixed period, the BFT explicitly took account of the different times over which various sick groups reported raised rates of the putative causal factor as compared with the well group. It was able to distinguish the likely ‘triggering’ effect of a life event for schizophrenic relapse from the ‘formative’ effect of a severe event for the start of a depressive episode. However, its weakness was that while finding a formative effect (as with depression) could be taken seriously, the built-in assumptions were so conservative that finding a triggering effect could not rule out the possibility that the events played a formative role. Brown came to believe that where schizophrenic episodes were concerned it was necessary to explore more deeply the possibly unique meaning a particular provoking event had for a particular patient. This was important because the very wide range of events that could be involved meant that the BFT index would inevitably indicate a triggering effect. This problem is still with us, although the idea of a more specific dimension (the intrusiveness of life events for the schizophrenic patient) has indicated one possible way to proceed. B

THE MEANING OF STATISTICAL INTERACTION

The original exposition of the vulnerability model had cited an ‘interaction’ between provoking agent and vulnerability factor which a number of critics have challenged as incorrect on the grounds that it was not statistically significant, at least when logistic regression was employed. An early comment (Everitt and Smith, 1979) claimed there was truth on both sides and the dispute just represented the difference between additive and multiplicative statistical interaction. Brown’s line on this topic has hardened over the years as successive generations have sought to engage him in debate. With the help of Martin Eales, he entered the offensive against the built-in conditions of multivariate statistics which make them inappropriate for testing the vulnerability hypothesis, namely that they use as their starting-point the assessment of whether the vulnerability factor shows a significant main effect. This is not the same as determining whether the variable has an effect in the absence of the stressor – the one crucial requirement of the hypothesis (Brown and Harris, 1986). The chapter cites Bishop, Fienberg and Holland’s classic account of loglinear analysis (1975) where they discuss an approach developed by Worcester (1971). This approach represents one way of avoiding the narrow restriction to using hierarchical models by which one is prohibited in suggesting models where a three-factor interaction term is posited in the absence of one or both of the main effects. The contribution to the debate contained in this chapter

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Tirril Harris 45 has so far received no further commentary. Meanwhile in a paper entitled ‘Now you see it now you don’t’ (Brown, Harris and Lemyre, 1991), Brown has thrown light on this issue from another direction by discussing the implications of recognising thresholds and categories (as opposed to using a continuous dimension which permits multiple regression instead of loglinear or logistic analyses). The paper reworks the same data in several different ways: first as a two by two by two vulnerability table, then using continuous scores for the dependent variable (total PSE score of depression along with non-specific symptoms, core depressive symptom subscore, Index of Definition), sometimes controlling for initial symptom score but sometimes not, sometimes omitting and sometimes including those with chronic cases of depression. One analysis uses binary as opposed to logistic regression. The conditions under which the vulnerability result does or does not emerge as significant provoke comments about the specificity of symptom patterns and ‘noise’ in their measurement. The use of continuous dimensional measures, with the consequent failure to exclude ‘chronic’ disorders because there is no ‘caseness threshold’, is revealed as obscuring insights which can be gained with a categorical approach. The paper is typical of Brown’s willingness to rethink tenets that others take as set in stone, and then to look at the issue from many different angles. C

THE ANALYSIS OF COMORBIDITY

One of the problems in analysing comorbidity is that there are two (at least) dependent variables, say anxiety and depression, and that they can be expected to occur together by chance. Here Martin Eales was once again a source of crucial insight. By using loglinear analysis, rather than logistic regression which focuses on one dependent (categorical) variable, he made it possible to analyse the effects of two key risk factors (childhood and adult adversity) on anxiety and depression simultaneously (Brown, Harris and Eales, 1993). For this it was essential not to include the interaction term representing the association between anxiety and depression themselves. It was possible to estimate how much comorbidity would be expected by chance by multiplying the overall rate of depression by the overall rate of anxiety. This could then be decomposed into the baseline comorbidity expected among those with experience of neither risk factor, which, when subtracted from the total chance comorbidity, would leave the proportion due to increased prevalence as a result of the two identified risk factors in the sample. Similarly, among the nonchance comorbidity, that due to the presence of a risk factor as a common antecedent of both disorders could be distinguished from the remaining unexplained comorbidity. This was where the loglinear analysis proved so useful, because it enabled an estimate of the expected number of comorbid cases for any particular model by adding cell estimates in that model for the four cells positive on both anxiety and depression. The size of the common antecedent comorbidity could then be calculated by comparing the expected number of comorbid cases before and after the inclusion of the terms representing

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46 Introduction the risk factor – in this case only childhood adversity, since the best model specified that adult adversity related only to depression not anxiety.

Concluding comments To attempt to summarise a near life-time’s work in a chapter must always be a risky endeavour, but even more so when the range of work is so extensive as in Brown’s case. Almost inevitably I will have omitted some of his contributions which others deem important and certainly I have rushed the exposition of others in a way that some may feel intellectually indigestible. I have also had only limited space to devote to the potential relevance of his work to interventions. What this chapter may therefore obscure is quite simply the pleasure of Brown’s work, the excitement it gives him, such that he always arrives at his desk before half past eight in the morning, and the fun it can be to chase an idea with him despite the lateness of the hour. Such a chase might start from him asking:‘Do you remember that woman on the Isle of Lewis who went to Glasgow and had a similar event?’ and move on, via a quote from a Thomas Hardy poem, to a hunch about something similar which he felt might be occurring in the current data set. Then armed with computer listings he might go back to reread the relevant written descriptions in each file and rethink each subject’s experience in the light of the new idea. Later, everything will have to be systematised, but for the moment the acts of scientific pursuit and of imagination are as one.

References Abas, M., and Broadhead, J. (1997) ‘Depression and anxiety among women in an urban setting in Zimbabwe’, Psychological Medicine, 27, 59–71. Ainsworth, M.D., and Wittig, B.A. (1969) ‘Attachment and the exploratory behaviour of one-year olds in a strange situation’ in B.M.Foss (ed.) Determinants of Infant Behaviour, Vol 4, London: Methuen. Andrews, B., and Brown, G.W. (1988a) ‘Social Support, onset of depression and personality: an exploratory analysis’, Social Psychiatry, 23, 99–108. ——, and Brown, G.W. (1988b) ‘Marital violence in the community. A biographical approach’, British Journal of Psychiatry, 153, 305–12. ——, Brown, G.W. and Creasey, L. (1990) ‘Intergenerational links between psychiatric disorder in mothers and daughters: the role of parenting experiences’, Journal of Child Psychology and Psychiatry, 31, 1115–29. Andrews, H., and House, A., (1989) ‘Functional Dysphonia’ in G.W.Brown and T.O.Harris (eds) Life Events and Illness, New York: Guilford Press. Barker, C., Pistrand, N., and Elliott, R., (1994) ‘Research methods in Clinical Counselling Psychology’, Chichester: John Wiley Barraclough, J., Pinder, P., Cruddas, M., Osmond, C., Taylor, I., and Perry, M., (1992) ‘Life events and breast cancer prognosis’, British Medical Journal, 304, 1078–81. Bartholomew, K., and Horowitz, L.M., (1991) ‘Attachment Styles among young adults: A test of a four-category model’, Journal of Personality and Social Psychology, 61, 226–4.

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Tirril Harris 47 Bebbington, P., Tennant, C., and Hurry, J., (1981) ‘Adversity and the nature of psychiatric disorder in the community’, Journal of Affective Disorders, 3, 345–66. ——, Brugha, T., MacCarthy, B., Potter, J., Sturt, E., Wykes, T., Katz, R., and McGuffin, P., (1988) ‘The Camberwell Collaborative Depression Study. I. Depressed probands: Adversity and the Form of Depression’. Beck, A. T., (1967) Depression: Clinical experimental and theoretical aspects, London: Staples Press. Bifulco, A., and Brown, G.W. (1996) ‘Cognitive coping response to crises and onset of depression’, Journal of Social Psychiatry and Psychiatric Epidemiology, 31, 163–72. ——, Brown, G.W., and Harris, T.O., (1987) ‘Childhood loss of parent, lack of adequate parental care and adult depression: a replication’, Journal of Affective Disorders, 12, 115–28. ——, Brown, G.W., and Adler, Z. (1991) ‘Early sexual abuse and clinical depression in adult life’, British Journal of Psychiatry, 159, 115–22. ——, Brown, G.W., and Harris, T.O. (1994) ‘Childhood Experience of Care and Abuse (CECA): A Retrospective Interview Measure’, Child Psychology and Psychiatry, 35, 1419–35. ——, Brown, G.W., Moran, P., Ball, C., and Campbell, C. (1998) ‘Predicting clinical depression in women: the role of past and present vulnerability’, Psychological Medicine, 28, 39–50. ——, Moran, P., Ball, B., and Bernazzani, O., (2000) ‘Adult attachment style and depression: a new measure of the ability to make supportive relationships’. Submitted to British Journal of Medical Psychology. Birley, J.L.T., and Brown, G.W. (1970) ‘Crises and life changes preceding the onset and relapse of schizophrenia: clinical aspects’, British Journal of Psychiatry, 116, 327–33. Bishop, Y.M.M., Fienberg, S.E., and Holland, P.W., (1975) ‘Discrete Multivariate Analysis: theory and practice’, Cambridge, Massachusetts and London: MIT Press. Bowlby, J. (1969) Attachment and loss. Vol 1: Attachment, New York: Basic Books. —— (1973) Attachment and loss. Vol 2: Separation: Anxiety and Anger, New York: Basic Books. —— (1980) Attachment and loss. Vol 3: Loss: Sadness and depression, New York: Basic Books. Brown, G.W. (1963) ‘Changing patterns of care of the schizophrenic patient’, British Journal of Psychiatric Social Work, 7, 5. —— (1973) ‘Some thoughts on grounded theory’, Sociology, 7, 1–16. —— (1974a) ‘Meaning, measurement, and stress of life events’ in B.S. Dohrenwend and B.P. Dohrenwend (eds) Stressful life events: their nature and effects. USA: John Wiley and Sons. —— (1974b) ‘Life events and the onset of depressive and schizophrenic conditions’ in E.K.E. Gunderson and R.H.Rahe (eds) Life Stress and Illness, Springfield, Illinois: C.C. Thomas. —— (1982) ‘Early loss and depression’ in C.M. Parkes and J. Stevenson-Hinde (eds) The Place of Attachment in Human Behaviour, New York: Basic Books; London: Tavistock Publications. —— (1985) ‘The discovery of “Expressed Emotion”: Induction or Deduction?’ in J. Leff and C. Vaughan (eds), Expressed Emotion in Families: Its Significance for Mental Illness, New York: Guilford Press. ——, (1996) ‘Genetics of depression: a social science perspective’, International Review of Psychiatry, 8, 387–401.

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48 Introduction ——, and Bifulco, A. (1990) ‘Motherhood, employment and the development of depression: A replication of a finding?’, British Journal of Psychiatry, 156, 169–79. ——, and Birley, J.L.T. (1968) ‘Crises and life changes and the onset of schizophrenia’, Journal of Health and Social Behaviour, 9, 203–14. ——, and Harris, T.O. (1978) Social Origins of Depression: A Study of Psychiatric Disorder in Women, London: Tavistock Publications; New York: Free Press. ——, and Harris, T.O. (1982) ‘Disease, distress and depression: a comment’, Journal of Affective Disorders, 4, 1–8. ——, and Harris, T.O. (1986) ‘Establishing Causal Links: The Bedford College Studies of Depression’ in H. Katschnig (ed.) Life Events and Psychiatric Disorders, Cambridge: Cambridge University Press. ——, and Harris, T.O. (1989) Life events and Illness, New York: Guilford Press; London: Unwin and Hyman. ——, and Harris, T.O. (1993) ‘Aetiology of anxiety and depressive disorders in an innercity population. 1. Early adversity’, Psychological Medicine, 23, 143–54. —— and Hepworth, C., (1993) ‘Launching from adolescence to adulthood: a study of the impact of family life’, Report to the ESRC Ref: R000 23 2042. ——, and Moran, P. (1994). ‘Clinical and psychosocial origins of chronic depressive episodes. I: a community survey’, British Journal of Psychiatry, 165, 447–56. —— and Moran, P. (1997) ‘Single mothers, poverty and depression’, Psychological Medicine, 27, 21–33. ——, and Prudo, R. (1981) ‘Psychiatric disorder in a rural and an urban population: 1. Aetiology of depression’, Psychological Medicine, 11, 581–99. ——, and Rutter, M. (1966) ‘The measurement of family activities and relationships: a methodological study’, Human Relations, 19, 241–63. ——, and Wing, J.K. (1962) ‘A comparative clinical and social survey of three mental hospitals’, Sociological Review Monograph, 5. ——, Carstairs, G.M., and Topping, G. (1958) ‘Post-hospital adjustment of chronic mental patients’, Lancet, 2, 685. ——, Parkes, C.M., and Wing, J.K. (1961) ‘Admissions and readmissions to three London mental hospitals’, Journal of Mental Science, 107, 1070. ——, Monck, E.M., Carstairs, G.M., and Wing, J.K. (1962) ‘Influence of family life on the course of schizophrenic illness’, British Journal of Preventative Social Medicine, 16, 55. ——, Bone, M., Dalison, B., and Wing, J.K. (1966) Schizophrenia and Social Care, Oxford: Oxford University Press. ——, Birley, J.L.T., and Wing, J.K. (1972) ‘The influence of family life on the course of schizophrenic illness: a replication’, British Journal of Psychiatry, 121, 241–58. ——, Sklair, F., Harris, T.O., and Birley, J.L.T. (1973a) ‘Life events and psychiatric disorders: 1. Some methodological issues’, Psychological Medicine, 3, 74–8. ——, Harris, T.O., Peto, J. (1973b) ‘Life events and psychiatric disorders: 2. Nature of causal link’, Psychological Medicine, 3, 159–76. ——, Ni’ Bhrolchain, M., and Harris, T.O. (1975) ‘Social class and psychiatric disturbance among women in an urban population’, Sociology, 9, 225–4. ——, Ni’ Bhrolchain, M., and Harris, T.O. (1979) ‘Psychotic and neurotic depression: 3. Aetiological and background factors’, Journal of Affective Disorders, 1, 195–211. ——, Andrews, B., Harris, T.O., Adler, Z., and Bridge, L. (1986) ‘Social support, selfesteem and depression’, Psychological Medicine, 16, 813–31.

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Tirril Harris 49 ——, Harris, T.O. and Bifulco, A. (1986) ‘Long-term effect of early loss of parent’ in M. Rutter, C.Izard, and P.Read (eds) Depression in Childhood: Developmental Perspectives, New York: Guilford Press. ——, Bifulco, A., and Harris, T.O. (1987) ‘Life events, vulnerability and onset of depression: some refinements’, British Journal of Psychiatry, 150, 30–42. ——, Adler, Z., and Bifulco, A. (1988) ‘Life events, difficulties and recovery from chronic depression’, British Journal of Psychiatry, 152, 487–98. ——, Andrews, B., Bifulco A., and Veiel. H. (1990) ‘Self-esteem and depression: 1. Measurement issues and prediction of onset’, Social Psychiatry and Psychiatric Epidemiology, 25, 200–9. ——, Harris, T.O. and Lemyre L. (1991) ‘Now you see it, now you don’t – some considerations on multiple regression’ in D. Magnusson, L.R. Bergman, G. Rudinger and B. Torestad (eds) Problems and methods in longitudinal research: stability and change, Cambridge: Cambridge University Press. ——, Lemyre, L., and Bifulco, A.T., (1992) ‘Social factors and recovery from anxiety and depressive disorders: a test of the specificity hypothesis’, British Journal of Psychiatry, 161, 44–54. ——, Harris, T.O., and Eales, M.J. (1993) ‘Aetiology of anxiety and depressive disorders in an inner-city population. 2. Comorbidity and adversity’, Psychological Medicine, 23, 155–65. ——, Harris, T.O., and Hepworth, C. (1994) ‘Life events and “endogenous” depression: a puzzle re-examined’, Archives of General Psychiatry, 51, 525–34. ——, Harris, T.O., Hepworth, C. and Robinson, R. (1994) ‘Clinical and psychosocial origins of chronic depressive episodes. II: a patient enquiry’, British Journal of Psychiatry, 165, 457–65. ——, Harris, T.O., and Hepworth, C. (1995) ‘Loss, humiliation and entrapment among women developing depression: A patient and non-patient comparison’, Psychological Medicine, 25, 7–21. Carstairs, G.M., and Brown, G.W. (1958) ‘A census of psychiatric cases in two contrasting communities’, Journal of Mental Science, 104, 72. Chen, C.C., David, A.S., Nunnerley, H., Michell, M., Dawson, J.L., Berry, H., Dobbs, J., Fahy, T., (1995) ‘Adverse life events and breast cancer: case-control study’, British Medical Journal, 311, 1527–30. Cleary, P.D.(1987) ‘Gender differences in stress-related disorders’ in R.C.Barnett, L.Biener, and G.K.Tsaruch (eds) Gender and Stress, New York: Free Press. Craig, T.K.J., and Brown, G.W., (1984) ‘Goal Frustration and life events in the aetiology of painful gastrointestinal disorder’, Journal of Psychosomatic Research, 28, 411–21. Edwards., A.C., Nazroo, J., and Brown, G.W. (1997) ‘Gender Differences in Marital Support following a Shared Life Event’, Social Science and Medicine, 1–9. Evans, D.L., Leserman, J., Perkins, D.O., Stern, R.A., Murphy, C., Beiyao Zheng, M.S., Gettes, D., Longmate, J.A., Silva, S.G., van der Horst, C.M., Hall, C.D., Folds, J.D., Golden, R.N., and Pettito, J.M., (1997) ‘Severe Life Stress as a predictor of early disease progression in HIV infection’, American Journal of Psychiatry, 154, 630–4. Everitt, B.S.and Smith, A.M.R. (1979) ‘Interactions in contingency tables: a brief discussion of alternative definitions’,. Psychological Medicine, 9, 581–3. Finlay-Jones, R., and Brown, G.W., (1981) ‘Types of stressful life event and the onset of anxiety and depressive disorders’, Psychological Medicine, 11, 803–15. Fontana, A. and Frey, J.H., (1994) ‘Interviewing: The Art of Science’ in Denzin, N.K., and Lincoln, Y.S., (eds) Handbook of Qualitative Research, California: Sage Publications.

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50 Introduction Frank, E., Anderson, B., Reynolds, C.F., Ritenour, A. and Kupfer, D.J., (1994) ‘Life events and the research diagnostic criteria endogenous subtype’, Archives of General Psychiatry, 51, 519–24. Frijda, N.H., (1993) ‘The place of appraisal in emotion’, Cognition and Emotion 7, 357–87. Gaminde, I, Uria, M., Prado, D., Querejeta, I. and Ozamiz, A. (1993) ‘Depression in three populations in the Basque Country – a comparison with Britain’, Social Psychiatry and Psychiatric Epidemiology, 28, 243–51. Geyer, S (1991) ‘Life events prior to manifestation of breast cancer: a study concerning eight years before diagnosis’, Journal of Psychosom Res., 35,355–63. Gilbert, P., (1992) Depression: the Evolution of Powerlessness, Hove: Lawrence Ehrlbaum. Glaser, B., and Strauss, A., (1967) The Discovery of Grounded Theory: Strategies for Qualitative Research, Chicago: Aldine. George, C., Kaplan, N., and Main, M, (1985) ‘The attachment interview for adults’, unpublished manuscript, University of California, Berkeley. Gorden, R.L., (1980) Interviewing: Strategy, techniques and tactics, Homewood, IL: Dorsey. Grant, I., MacDonald. W.I., Patterson. T., and Trimble, M.R., (1989) ‘Multiple Sclerosis’ in G.W.Brown and T.O.Harris (eds) Life Events and Illness, New York: Guilford Press. Haan, N., (1963) ‘Proposed model of ego functioning: coping and defence mechanisms in relation to IQ change’, Psychological Monographs, 77, 1–23. Harris, T.O. (1989) ‘Disorders of menstruation’ in G.W.Brown and T.O.Harris (eds) Life Events and Illness ,New York: Guilford Press. —— (1992) ‘Some reflections on the process of social support: the nature of unsupportive behaviours’ in: H.O.F.Veiel and U. Baumann (eds) The meaning and measurement of Social Support, Washington: Hemisphere Publishing Corporation, 171–89. —— and Bifulco, A. (1991) ‘Loss of parent in childhood, and attachment style and depression in adulthood’ in C.M. Parkes and J.S. Hinde (eds) Attachment Across the life cycle, London: Tavistock; New York: Routledge. ——, Brown, G.W., and Bifulco, A. (1986) ‘Loss of parent in childhood and adult psychiatric disorder: The role of lack of adequate parental care’, Psychological Medicine, 16, 641–59. ——, Brown, G.W., and Bifulco, A.T. (1987) ‘Loss of parent in childhood and adult psychiatric disorder: The role of social class position and premarital pregnancy’, Psychological Medicine, 17, 163–83. ——, Brown, G.W., and Bifulco, A. (1990a) ‘Depression and situational helplessness/mastery in a sample selected to study childhood parental loss’, Journal of Affective Disorders, 20, 27–41. ——, Brown, G.W., and Bifulco, A. (1990b) ‘Loss of parent in childhood and adult psychiatric disorder: a tentative overall model’, Development and Psychopathology, 2, 311–28. ——, Brown, G.W., and Robinson, R (1999a) ‘Befriending as an intervention for chronic depression among women in an inner city. I: Randomised Controlled Trial’, British Journal of Psychiatry, 174, 219 -25. ——, Brown, G.W., and Robinson, R (1999b) ‘Befriending as an intervention for chronic depression among women in an inner city.II: Role of fresh-start experiences and baseline psychosocial factors in remission from depression’, British Journal of Psychiatry, 174, 225–33. Hazan, C., and Shaver, P., (1987) ‘Romantic love conceptualised as an attachment process’, Journal of Personality and Social Psychology, 52, 511–24.

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Tirril Harris 51 Henderson, A.S., and Brown, G.W. (1988) ‘Social support: the hypothesis and the evidence’ in A.S. Henderson and G.D. Burrows (eds) Handbook of Social Psychiatry, Amsterdam: Elsevier, 73–85. ——, Byrne, D.G., and Duncan-Jones, P (1981) Neurosis and the Social Environment, Sydney: Academic Press. Horowitz, F.D., (1994) ‘The need for a Comprehensive New Environmentalism’ in R. Plomin and G.E. McClearn (eds) Nature, Nurture and Psychology, Washington: American Psychological Association, 341–54. House, A., Dennis, M., Mogridge, L., Hawton, K., and Warlow, C., (1990) ‘Life events and difficulties preceding stroke’, Journal of Neurology, Neurosurgery and Psychiatry, 53, 1024–8. Laing, R.D., and Esterson, A., (1964) Sanity, Madness and the Family, London: Tavistock Books. Leff, J., Kuipers, L., Berkowitz, R., Eberlein-Vries, R., and Sturgeon, D., (1982) ‘A controlled trial of social intervention in the families of schizophrenic patients’, British Journal of Psychiatry, 141, 121–34. Leighton, D.C., Harding, J.S., Maclin, D.B., MacMillan, A.M., and Leighton, A.H., (1963) The Character of Danger, New York: Basic Books. Leventhal, H., Leventhal, E.A., and Schaeffer, P (1988) ‘Vigilant Coping and Health Behaviour: a lifespan problem’ in M.Ory and R.Abeles (eds) Ageing, Health and Behavior. Baltimore: Johns Hopkins. McCall, G.J., and Simmons, J.L., (1966) Identities and Interactions, New York: Free Press. Miller, P.M., Kreitman, N.B., Ingham, J.G., and Sashidharan, S.P., (1989) ‘Self-esteem, life stress and psychiatric disorder’, Journal of Affective Disorders, 17, 65–75. Murphy, E., and Brown, G.W. (1980) ‘Life events, psychiatric disturbance and physical illness’, British Journal of Psychiatry, 136, 326–38. Nazroo, J.Y., Edwards, A.C., and Brown, G.W. (1996) ‘Gender differences in the onset of depression following a shared life event: a study of couples’, Psychological Medicine, 27, 9–19. Nielson, E., Brown, G.W., and Marmot, M., (1989) ‘Myocardial Infarction’ in G.W.Brown and T.O.Harris (eds) Life Events and Illness, New York: Guilford Press. Norris, V., (1959) Mental Illness in London: a Statistical Enquiry into Admissions to Mental Hospitals (Maudsley Monograph No: 6) Oxford: Oxford University Press. Parkes, C.M., Brown, G.W., and Monck, E.M. (1962) ‘The general practitioner and the schizophrenic patient’, British Medical Journal, 1, 972. Paykel, E.S., (1974) ‘Recent Life Events and Clinical Depression’ in E.K.E.Gunderson and R.H.Rahe, Life Stress and Illness, Springfield, Illinois: C.C.Thomas ——, Myers, J.K., Diendelt, M.N., Klerman, G.l., Lindenthal, J.J., and Pepper, M.M.(1969) ‘Life events and depression: a controlled study’, Archives of General Psychiatry, 21, 753–60. Post, R.M., Rubinow, D.R. and Ballenger, J.C., (1986) ‘Conditioning and sensitisation in the longitudinal course of affective illness’, British Journal of Psychiatry, 149, 191– 201. Price, J., Sloman, L., Gardner, Jr, R., Gilbert, P., and Rohde, P., (1994) ‘The social competition hypothesis of depression’, British Journal of Psychiatry, 164, 309–15. Protheroe, D., Turvey, K., Horgan, K., Benson, E., Bowers, D., House, A., (1999) ‘Stressful life events and difficulties and onset of breast cancer: case-control study’, British Medical Journal, 319, 1027–30.

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52 Introduction Prudo, R., Brown, G.W., Harris, T.O., and Dowland, J. (1981) ‘Psychiatric disorder in a rural and an urban population: 2. Sensitivity to loss’, Psychological Medicine, 11, 601–16. ——, Harris, T.O., and Brown, G.W. (1984) ‘Psychiatric disorder in a rural and an urban population: 3. Social integration and the morphology of affective disorder’, Psychological Medicine, 14, 327–45. Ramirez, A., Craig, T.K.J., Watson, J.P., Fentiman, I.S., North, W.R.S., and Rubens, R., (1989) ‘Stress and the relapse of breast cancer’, British Medical Journal, 298, 291–3. Richardson, S.A., Dohrenwend, B.S., and Klein, D., (1965) Interviewing: its Forms and Findings, New York: Basic Books. Robinson, N. and Fuller, J.H. (1985) ‘The role of life events and difficulties in the onset of diabetes mellitus’, Journal of Psychosom. Res., 29, 583–91. Rutter, M., and Brown, G.W. (1966) ‘The reliability and validity of measures of family life and relationships in families containing a psychiatric patient’, Social Psychiatry, 1, 38–53. Schmidt, U.H, Tiller, J.M., Andrews, B., Blanchard, M., and Treasure, J., (1997) ‘Is there a specific trauma precipitating onset of an eating disorder?’, Psychological Medicine, 27, 523–30. Schutz, A., (1971) ‘Concept and theory formation in the social sciences’ in A. Schutz Collected papers (Vol 1, 48–98), The Hague: Nijhoff. Vadher, A., and Ndetei, D.M., (1981) ‘Life events and depression in a Kenyan setting’, British Journal of Psychiatry, 139, 134–7. Vaillant, G.E., (1976) ‘Natural History of Male Psychological Health: V. The relation of choice of ego mechanisms of defence to adult adjustment’, Arch. Gen. Psychiatry, 33, 535–45. Vaughan, D (1992) ‘Theory elaboration: the heuristics of case analysis’ in H.Becker and C.Ragin (eds) What is a Case? (173–202), New York: Cambridge University Press. Wethington, E., Brown, G.W., and Kessler, R.C. (1996) ‘Interview Measures of Life Events’ in L. Gorden, S. Cohen and R.C. Kessler (eds). Measuring Stress: A Guide for Health and Social Scientists, Oxford: Oxford University Press. Wing, J.K., and Brown, G.W. (1961) ‘Social treatment of chronic schizophrenia: a comparative study of three mental hospitals’, Journal of Mental Science, 107, 847. ——, and Brown, G.W. (1970). Institutionalism and Schizophrenia: a comparative study of three mental hospitals, Cambridge: Cambridge University Press. ——, Cooper, J.E., and Sartorius, N. (1974) The Measurement and classification of psychiatric symptoms: an instruction manual for the Present State Examination and CATEGO programme, London: Cambridge University Press. Worcester, J. (1971) ‘The relative Odds in the 2x2x2 contingency table’, American Journal of Epidemiology, 93, 145–9.

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Part I

Social psychiatry and social science

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2

George W. Brown’s contribution to psychiatry The effort after meaning Jim Birley and David Goldberg

What would psychiatry have been like if it hadn’t been for George Brown? Some things would have been just the same. The biological juggernaut would still have rolled, we would know just as much about neuro-transmission, neuro-imaging, neuro-pharmacology and genetics; and there would have been the same meticulous attention paid to nosology. But what would we have known about the importance of social factors in schizophrenia and depression? In both these, George has left the field looking very different – and he has inspired a whole generation of other investigators to repeat his studies, and demonstrate the way that theory devised in England works in other, very different environments. Studies of life events, emotional expression, childhood experience of abuse and exact measures of social disadvantage have all been pioneered by George, but have also been taken forward by psychiatrists and other social investigators. Early on in his career with the MRC Social Psychiatry Unit, George did an apparently simple piece of research on patients with schizophrenia. He examined the visitor’s book (which, by law, had to be carefully recorded) in two mental hospitals over two periods in 1950/1 and 1955/6. In the first period, when 37 per cent of all patients stayed for more than two years after admission, those who had received no visitors during the first two months of their stay were much more likely to stay longer than two years – 83 per cent compared to 25 per cent. In the second period, both hospitals had a more active discharge policy with only a smaller proportion detained for more than two years. In one, where 21 per cent were still longstay, the difference between those visited and not visited remained, but not significantly so (27 per cent versus 18 per cent). In the other, with a more active policy (7 per cent longstay), the difference remained significant – 16 per cent versus 4 per cent. George discussed the possible interpretation of his findings, with appropriate modesty, but the point to emphasise for a psychiatrist was that here was a social variable, capable of predicting outcome as strongly as many ‘symptomatic’ or other familiar psychiatric variables, which had been overlooked – and George’s study has been forgotten, although it may still be relevant to the revolving doors and overloaded acute units of present day community psychiatry.

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56 Jim Birley and David Goldberg Social factors were not something to be taken seriously by most psychiatrists. They were treated more as a convenient ‘lump’ of variables which was left over to explain things which could not be explained by ‘real’ psychiatric variables – diagnosis, symptomatology, family history, age and type of onset. But the studies that John Wing and George published together in Institutionalism and Schizophrenia (1960) demonstrated convincingly that the symptomatology of chronic schizophrenia was profoundly influenced by the patient’s social environment, and that the ‘natural history’ of the disease reflects the ‘natural history’ of the institution. The measures that were proposed in that book for the social correlates of institutionalised patients were clearly George’s work, and represented a radically different tradition from the descriptions reported by other observers such as Goffman or Russell Barton. Received opinion has always had difficulty in accepting George’s views. The original paper on precipitating events and schizophrenia (1968) was rejected by the British Journal of Psychiatry on the grounds that it was too far-fetched to think that schizophrenia could be caused by psycho-social events. George has courageously pursued the hypothesis that social events and situations can, if they follow certain sequences, cause a psychiatric illness and can also be implicated in recovery. This hypothesis received only a little encouragement from studies of schizophrenia where the ‘weight of causality’, as measured by the ‘brought forward time’ (Brown, Harris and Peto, 1973) was small. If social factors seem not to make a major contribution to the cause of schizophrenia (and the jury is still out on this question), George’s early studies provided plenty of evidence that they affect the course of the illness very profoundly. From the ward atmosphere of the institutions, George moved to the family atmosphere in people’s homes. This, and the degree of exposure of the patient to it, are now recognised as important variables which can be altered by appropriate interventions. George’s studies have led to a large amount of research on this topic, out of which have developed family interventions which have been given the ‘Cochrane accolade’ of evidence-based efficiency. George’s work on the influence of expressed emotion – in particular critical comments by key family members – on the course of schizophrenia have led directly to a wave of further research studies on family life and schizophrenia – now culminating in the Thorn training programme for psychiatric community nurses. This new role of the community nurse will probably do more good for people suffering from schizophrenia and for their families than any other single change in community mental health services. His first studies of depression, both in the community and the clinic, were more encouraging, suggesting the importance of severe loss events and a predisposition of vulnerability often brought about by losses early in life. It is the further investigations in this field, covering both depression and anxiety, and their different aetiologies, which George has pursued so imaginatively and persistently. Thirty years ago, depressive illnesses were divided into endogenous and reactive varieties: no social causes were sought for the former, the secret to the aetiology being sought in genetic loading in the family history – with an implication of multiple recessive

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George W. Brown’s contribution to psychiatry 57 characteristics – or perhaps mutations, if this was negative. George’s early research showed conclusively that each type of depression was equally likely to follow a loss event, and the conventional dichotomy was eventually discarded by clinicians. The dichotomy that replaced ‘reactive versus endogenous’ was the milder ‘neurotic versus psychotic’ depression. George showed that the difference between these was mainly one of severity (Ni’ Bhrolchain, Brown and Harris, 1979), a conclusion that was replicated in a later study using different techniques (Goldberg, Bridges, Duncan-Jones and Grayson, 1987). Other studies related different prevalence rates for anxiety and depression to different social circumstances in the populations studied (Prudo, Harris and Brown 1984). However, George’s most enduring work in the field of affective disorders is likely to be the light he and his co-workers have thrown on the determinants of vulnerability to depressive illness. His team has shown that while both childhood and adult adversity led to depression, only childhood adversity led to anxiety in adult life: the social antecedents of the two affects had to be considered separately (Brown and Harris, 1993; Brown, Harris and Eales, 1996). More recent work has dealt with the importance of humiliation and entrapment as life situations predisposing women to depressive illness (Brown, Harris and Hepworth, 1995). George’s method has been careful empirical demonstration, linked to a philosophy that similar events can have different meanings for different individuals, so that ‘checklist’ approaches to life events are exposed as shallow and incapable of accurate prediction. Some of his research has led to direct and obvious benefit to the mental health services and their patients. But this work is but the tip of an iceberg of substantive research whose approach has been neglected by psychiatrists although George’s methods – careful interviews and analysis of the resultant findings – are, or should be, the methods which all psychiatrists use. The most obvious explanation for this is related to Karl Popper’s experiment with his student classes. He told them ‘to observe’ – much to their bewilderment. All observation requires a hypothesis about what one is observing. The average psychiatrist does observe the interaction and interplay of events on his or her patients, but does not collect data in a systematic way. Systematic data collection itself presupposes hypotheses on how it should be used. George follows, and has further developed, the Social Psychiatry Unit’s fine tradition of developing both theory and methodology together. He has paid particular attention to the time sequence of events and has categorised them in an empirical manner so that trained interviewers can record them in a reliable way as judged by inter-rater agreements. This is the approach which psychiatrists use for recording the clinical state of the patient, but not so assiduously for the social state and history – although it has been thought about, using Adolf Meyer’s life chart, for instance. Inter-rater reliability, by itself, is of little use unless what is assessed has some validity, and it is on this point that George has been so original. Psychiatrists have regularly asked their patients about upsetting events, but have generally left them to define what these were. George prepared a pre-selected list of possible events – not in itself an original idea. He pays tribute to Holmes’ and Rahe’s pioneering studies but does not support the use of the arbitrary scores which they gave to

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58 Jim Birley and David Goldberg events. He pointed out that an event can have enormously different ‘meanings’ – a pregnancy, for instance, or a child leaving home. It is the meanings which matter and these can only be assessed in context by obtaining as much relevant information as possible about the subject, both past and present, in order to be able to assess the events’ significance. But this assessment was judged by others (George’s team) and not by the person’s own interpretation or reaction, nor by the psychiatrist’s knowledge of an ensuing illness. By his insistence that meaning must be re-introduced to the interpretation of psychopathology, George has both humanised social psychiatry and rendered it capable of scientific respectability. It is perhaps his most enduring legacy to psychiatry. The development of this approach, with theory and methodology going hand in hand, has led to a series of important publications and to an accumulation of carefully collected and rated observations which allow for many further testings of theory. Just as the earlier studies led to important developments of assessment and treatments in psychiatry, so George’s more recent work, over the past twenty years, will influence psychiatry in the future, both in theory and in practice. He came to a field where social factors were largely ignored or glossed over and he has left it at a stage where no serious commentator can doubt the importance of social factors, each one of which has been carefully documented. It is paradoxical to accuse someone as original and creative of being too conventional, but if there is a shortcoming it is his acceptance of conventional nosology and his preference for dichotomising social variables which are clearly continuous. Where nosology is concerned he relaxes somewhat, it is true, and allows his subjects to be non-cases, mildly depressed or ‘case depression’, or non-case, mildly anxious and ‘case anxiety’ or any combination of these two affects. Indeed, it was this approach which allowed him to view subclinical depression and anxiety as vulnerability factors for later ‘caseness’ of depression. George ignores genetic factors in his theorising about depression and does not approve of vulnerability factors like neuroticism, even though the evidence for the importance of this variable is fairly persuasive. He has also said little about personality styles as a determinant of vulnerability. He avoids structural equation modelling and multi-wave sweeps of the same population over many years. His work has been mainly confined to working-class women and he therefore has little to say about middle-class women and men, which is a pity since it is becoming clear that alcohol problems share common roots with anxiety and depression, and are often a predominately male way of dealing with difficulties. However, his choosing to focus on working class women is due to the higher prevalence of depression in this group and, since his methods are highly labourintensive, he has really had little choice in this matter. His refusal to consider dimensional models of symptoms ensured that psychiatrists and other clinicians were comfortable with his approach, and this made it more likely that his research would be funded. As it was, he faced enormous critical onslaught from psychiatrists during the early years after he left the Maudsley: at least he could point out that he was using the same clinical concepts that they were, and so his research could not be lightly discounted.

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George W. Brown’s contribution to psychiatry 59 At present, the theories of biological psychiatry have an immense influence on psychiatrists, but there are serious gaps in the ‘biology’ which is used, with its overwhelming emphasis on physical reductionism, to the exclusion of ecology and psychological behaviour, whether individual or social. George’s approach, with its painstaking attention to detail, coupled with the accumulation of data and imaginative insights into how it might be analysed, is much closer to the methods used by Charles Darwin than are the complex statistical programmes of genetic analysis and hereditability. These analyses recognise environmental factors as important, but rather as the residual factors unaccountable by genetics. But an interaction between the two is now recognised and accepted by all current researchers. George has made environmental factors his special study and especially the home environment (past and present) of his subjects. Biological psychiatry will only come of age as the rightful descendant of Darwin when the environment is given as detailed an analysis as the chromosomes. Working with George is like studying with an inspiring, demanding, goodhumoured and infuriating trainer. He makes the same high demands on his colleagues as he does on himself. Perhaps his most infuriating characteristic is his creativity. Just when a careful edifice of argument and logical conclusions has been constructed, he knocks it down and wants to try a different, perhaps more interesting, approach. A good deal of research can be rather boring, pursuing ideas which are not particularly new, along lines which are fairly familiar – the ‘paradigms’ of Thomas Kuhn. George overflows with ideas. He does not horde them. Indeed he tests them, and his colleagues, to destruction and the experience is never boring. This same generosity permeates his many interests beyond the social sciences, including literature, music, painting, poetry and, in particular, sculpture. For George himself is a sculptor and his search for truth is, in our view, rather like that of a sculptor, searching for the essence hidden in the wood or stone, and working with its grain. All the best works of art remain as fresh and stimulating as when they were finished. George’s papers have the same quality. They do not ‘age’. His studies on Expressed Emotion and Schizophrenia (1972) continue to inspire important research and practice today. His brilliant essay on ‘The Mental Hospital as an Institution’ (1973) was ‘re-visited’ twenty years later by Professor Peter Huxley who found it highly relevant to many aspects of current community care. It is equally relevant, not only to those many parts of the world where traditional institutions still dominate the psychiatric scene, but to any service where institutional habits and attitudes are still powerful obstacles to change: that is just about everywhere.

References Brown, G.W. (1959) ‘Social factors influencing length of stay of schizophrenic patients’, British Medical Journal, 2, 1300–2. —— (1973) ‘The mental hospital as an institution’, Social Science and Medicine, 7, 407–24.

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60 Jim Birley and David Goldberg —— and Birley, J.L.T. (1968) ‘Crises as life changes and the onset of schizophrenia’, Journal of Health and Social Behaviour, 9, 203–14. —— and Harris, T.O.(1993) ‘Aetiology of anxiety and depressive disorders in an inner city population: 1 Early adversity’, Psychological Medicine, 23, 143–66. —— and Wing, J.K. (1960) Institutionalism and Schizophrenia, Cambridge: Cambridge University Press. ——, Birley J.L.T. and Wing, J.K. (1972) ‘The influence of family life on the course of schizophrenic illness: a replication’, British Journal of Psychiatry, 121, 241–58. ——, Harris. T.O. and Peto, J., (1973) ‘Life events and psychiatric disorders: 2. The nature of the causal link, Psychological Medicine, 3, 159–76. ——, Harris, T.O. and Eales, M.J. (1996) ‘Social factors and co-morbidity of depressive and anxiety disorders’, British Journal Psychiatry, 168, suppl 30: 50–7. ——, Harris, T.O. and Hepworth, C. (1995) ‘Loss, humiliation and entrapment among women developing depression: a patient and non-patient comparison’, Psychological Medicine 25, 7–22. Goldberg, D.P., Bridges, K., Duncan-Jones, P. and Grayson, D. (1987) ‘Dimensions of neurosis seen in primary care settings’, Psychological Medicine 17, 461–70. Huxley, P. (1993) ‘Resettlement and community care: the mental hospital as an institution revisited’, Psychiatric Bulletin, 17, 279–82. Ni’ Bhrolchain, M., Brown, G.W. and Harris, T.O. (1979) ‘Psychotic and neurotic depression: 2. Clinical characteristics’, British Journal Psychiatry, 134, 94–107. Prudo, R., Harris, T.O. and Brown, G.W. (1984) ‘Psychiatric disorder in a rural and an urban population: 3. Social integration and the morphology of affective disorder’, Psychological Medicine, 14, 327–45.

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3

Bringing meaning back into social psychiatric research Making subjective meanings objective David Mechanic

In the post World War II period, and for the decades of the 1950s and 1960s, psychodynamic thinking dominated psychiatric thinking and research in the United States (Grob, 1991). There was much popular speculative theory about ‘psychosomatic’ processes but little rigorous investigation. Much emphasis in American psychiatry was on early developmental processes and the role of personality in disease. British psychiatry, and European psychiatry more generally, followed a stricter medical model. There was not much epidemiological work at the time, but what little there was, was highly descriptive and not very exciting, typically counting disease events in relation to conventional socio-demographic categories. The concepts of ‘stress’, ‘social support’, ‘coping’ and many others we now take for granted had not yet become serious focuses for research and there were few plausible or researchable models of intervening pathways. There was, however, a substantial tradition for analytical epidemiological work in sociology as represented in the classic study of suicide by Emile Durkheim (English edition, 1951) and important early ecological studies such as Faris and Dunham’s (1939) classic study of the distribution of hospital admissions of mental illness from varying areas of Chicago. Ecological studies were open to serious methodological criticisms, as were other studies measuring hospital admission in contrast to independent assessments of psychiatric morbidity. During World War II, American researchers, responding to military screening needs, developed the Army NeuroPsychiatric Screening Adjunct, which later became the basis for efforts to measure psychiatric morbidity in the community (Mechanic, 1999, p.48–51). By the 1950s, there were three alternative streams in a developing psychiatric epidemiology reflecting salient theoretical and methodological issues that were to set the context for George Brown’s efforts when he joined the Institute of Psychiatry’s Social Psychiatry Research Unit in 1956. The efforts to develop community screening instruments during the war informed two major epidemiological efforts initiated by Rennie and Srole in New York (the Midtown Manhattan Study, Srole et al., 1962), and by the Leightons in Nova Scotia (Leighton et al., 1963). The weaknesses of these studies in validly measuring psychiatric morbidity were matched by the difficulties of the second approach adopted by Essen-Möeller (1956) and later Hagnell (1966) in Sweden in which a psychiatrist made unstandardised clinical judgments of people in the community. In any case, having

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62 David Mechanic psychiatrists make thousands of clinical assessments in the field did not seem very practical for the development of this new research enterprise. The third major development, in the tradition of Durkheim, was the path-breaking investigation in New Haven of social stratification and mental illness, using laboriously gathered data from hospital, clinic and psychiatrists’ treatment records to define the mentally ill population (Hollingshead and Redlich 1958). Two other streams of research in this period were to have important influence on thinking about the role of stress in disease and its incorporation into epidemiological investigation. In the 1940–60 period, Harold Wolff, a highly talented professor of medicine and neurology at the Cornell University Medical College, and his colleagues carried out a broad range of medical studies relating stress and disease and in 1953 Wolff published a summary of some of these studies in his book, Stress and Disease (Wolff, 1953). Over the years, many talented medical researchers interested in psychosomatic processes worked in Wolff’s laboratory and went on to have much influence on research in the stress field, among them Thomas Holmes, who entered the field by working on stress and tuberculosis. In 1956, Hans Selye published his volume on The Stress of Life (Selye, 1956) providing a seemingly plausible biological framework for linking social stressors to disease occurrence, a volume which helped encourage interest in the study of stress. In the 1960s, attention in the MRC Social Psychiatry Research Unit under John Wing’s leadership was focused on increasing the validity and reliability of psychiatric assessment, addressing the central problem that had plagued all efforts in psychiatric epidemiology and much clinical research as well. Successive versions of the Present State Examination were being developed and tested, focused initially on the diagnosis of schizophrenia but then applied more widely. Work in the unit, and Brown’s later work at Bedford College, was premised on careful diagnostic assessment following the PSE criteria. Although there were later controversies as to whether the depressed women seen in the community were comparable to those seen in psychiatric settings, the depression studies, unlike many American community studies, were based on PSE criteria for establishing a diagnosis. In 1967, Holmes and Rahe published their Social Readjustment Rating Scale (SRE) designed to measure stress, a measure that Tom Holmes had been developing and collecting data on for many years (Holmes and Rahe, 1967). This stress scale was based on the theory, implicit in the earlier work of Wolff and Selye, that changes in life circumstances called for physical and psychological readjustments that strained the organism and contributed to disease. Thus, Holmes and his coworkers believed that both positive and negative changes that called for readjustment could contribute to morbidity. The Social and Readjustment Rating Scale, however, was not constructed in a manner that allowed this hypothesis to be tested empirically. The scale was a long list of generally described life change events, weighted by scores indicating the relative level of expected adjustment required by the event. The approach had many other methodological difficulties as well, (Mechanic, 1975, 1978) but it encompassed some important innovations that contributed to the epidemiological study of stress.

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Bringing meaning back into research 63 Most important was that Holmes and his co-workers understood that simply measuring perceptions of stress was unreliable and their scale was intended to capture ‘objective’ stress as measured by the occurrence of actual events weighted by the magnitude of readjustment believed to be required by these events among samples of the general population. This was a crude form of contextual analysis which Brown later developed to an art, but it was a tendency in the right direction. A second major advantage (or disadvantage, depending on your perspective) of the scale was the ease of using it, and it very quickly was adopted and incorporated into numerous population and clinical studies. Brown was a vigorous critic of the Holmes–Rahe approach (Brown, 1974) which he often equated with what he viewed as the American approach to research – taking the fast and easy route. Recognising the low reliability of social measurement, he and Michael Rutter had earlier embarked on efforts to improve measurement of family relationships and activities which resulted in an important paper, Human Relations, in 1966 and contributed to building their approach to measurement over the years (Brown and Rutter, 1966). Brown’s criticism of the SRE reflected his efforts, beginning with his work on schizophrenia with Jim Birley (Brown and Birley, 1968), to capture meaning in research without threats to validity. In this study, they avoided the easy path of eliciting perceptions of the stressfulness of events and instead defined events a priori which they believed were likely to produce marked emotional arousal in most people. Thus, they excluded events that would be innocuous to most people, ‘although they might be disturbing to a few for idiosyncratic reasons (Brown, 1974, p.227)’. ‘We set out to establish whether phenomena had occurred quite irrespective of how the person felt about them (Brown 1974, p. 227).’ They also gave attention to classifying events that were more or less independent of personal behaviour to take account of the fact that people are active agents and that disturbed persons often create their own crisis-producing life environments. This was also the initial effort to carefully document the importance of dating when events actually occurred, an idea that was to have major importance in subsequent work. The concept of respondent as active agent, seemingly so obvious today, was not a particularly dominant research idea at the time. Clinicians and thoughtful members of the public naturally understood that disturbed people often created the circumstances of their undoing, but researchers typically and conveniently ignored this. There was little sensitivity to selection effects in medical research and the idea of randomised controlled trials were then seen by most psychiatrists, indeed most physicians, as a precious idea and vigorously resisted. The more we have come to understand how life contexts evolve, the more obvious it has become that even events we commonly conceive of as capricious and random have a higher probability of occurrence among some persons than others because of life style and other personal decisions that increase exposure and vulnerability (Mechanic, 1998). This is an idea we continually rediscover. For example, in the area of social support, we are now again learning that individuals from very early life have varying capacities to attract social support from others (Werner and Smith, 1992).

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64 David Mechanic

Measuring meaning objectively Those who know Brown’s work and his persistent efforts to measure meaning objectively might be surprised at his receptivity to psychodynamic insights from clinical colleagues and from literature. As a voracious reader, George often selected illustrations in his writings and lectures from classic works and these were often inspirations for his creativity. From the start, he was perfectly clear about his objective: It is unnecessary to see the measurement of meaning as inevitably tied to the respondent’s account of feelings or his account of his reasons for feelings and actions. Clearly these are desirable – but if, as in our present case, they are suspect, a description of circumstances and behavior will enable us to make a reasonable estimate of the meaning of an event. I use the term reasonable in the sociologist’s sense that the aggregate results of such a procedure when carried out for many individuals will approximate to the truth and be free of the kind of systematic bias that vitiates hope of explanatory inquiry. (Brown, 1974, p. 225) George appreciated that understanding gleaned from an objective standpoint is not quite the same as being in the head of the individual. But he believed that events could be understood objectively by taking account as much as possible of the ‘biographically determined circumstances’. The method that evolved sought to reduce bias by strict rules that established the events and the persons to be taken account of before collecting any data. The interview that identified the events was itself free-flowing with a lengthy follow up about the circumstances surrounding each event and much was elicited spontaneously about the event as the interview went forward. The contextual ratings eventually made by the research team took into account the particular circumstances surrounding each event without considering the respondents’ accounts of their reactions to these events. The system of ratings was developed and elaborated over many years, becoming increasingly complex and time intensive. This approach is described in detail by Harris and others in this volume, and there is no need for more detail here. One limitation of the approach was its intensity and some researchers wondered whether the method was cost effective. This has been a sore point with George and a source of his frequent criticism of American researchers’ carelessness about issues of validity. But a fuller appreciation of this debate requires some understanding of Brown’s notion of the importance of validity for political reasons.

The politics of the study of meaning Through much of the period under review, particularly in the UK, research in psychiatric epidemiology was dominated by a medical perspective and by physicians. When first at the Institute of Psychiatry in 1965 I was impressed by the

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Bringing meaning back into research 65 hierarchical power structure and the extent to which one professor – Sir Aubrey Lewis – ruled the roost. Michael Shepherd, then Aubrey’s protégé, emulated his dominance and I attended Aubrey’s and Michael’s rounds somewhat in the guise of an ethnographer. They were both erudite figures but what impressed me most was their unveiled dominance and the extent to which they were feared. A few years later I was returning to London from a psychiatric epidemiology meeting in Aberdeen with Sir Aubrey and he questioned me about the department I then chaired at Wisconsin. When I told him about the seventy-some professors in my department, he turned to me incredulously and asked how I could exercise intellectual leadership over so many. I had to explain that this was not the way things worked in America. Such was the environment George grew up in, and it was not always easy for the lone sociologist. It was still difficult for social researchers to be taken seriously by doctors, but it was to the credit of Sir Aubrey that he saw the value in social and epidemiological inquiry. It should not be surprising that establishing credibility with his psychiatrist colleagues was not a trivial matter as Brown developed his research programme at Bedford College. In the early years, garnering funding for applied sociology in psychiatry was difficult – social science funding committees insisted on adhering to the fashions and theoretical cannons of the discipline while medical committees had difficulty seeing the place and value of social research. British (Maudsley) psychiatry was unimpressed (perhaps even repelled) with psychodynamic developments in the United States and was not particularly friendly toward their brethren at the Tavistock – especially Ronald Laing, who had become somewhat of a public celebrity. So, in the early years, funding a credible programme that focused on meaning (typically seen as a ‘soft’, ‘fuzzy’ and unscientific phenomenon) was a struggle. George’s insistence on addressing life events and meaning in so formal a fashion was in part political. As he noted: … the need for valid measurement is in part political. There is a wide-spread reluctance among the medical profession to take seriously the case that life events play an important etiological role in psychiatric or physical illness. This is perhaps understandable given their training and professional interests. In such a situation valid measurement may serve as much to refute criticism as to increase the actual association between life events and illness. Methodological demands are bound to be greatest in areas of research that threaten vested professional, scientific, or political interests. (Brown, 1974, p. 234) Politics is no small matter in medical research and a related anecdote conveys the medical resistance encountered by novel approaches. In the early 1970s, Archie Cochrane was making his strong case for randomised controlled trials and, with some colleagues, embarked on a trial comparing hospital and home care following myocardial infarction (Mather et al., 1971). Cochrane was to meet with his medical colleagues who were less than enamoured with the RCT methodology.

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66 David Mechanic The results at that stage showed a slight numerical advantage for those who had been treated at home. I rather wickedly compiled two reports: one reversing the number of deaths on the sides of the trial. As we were going into the committee, in the anteroom, I showed some cardiologists the results. They were vociferous in their abuse: ‘Archie, ’ they said, ‘We always thought you were unethical. You must stop this trial at once.’ I let them have their say for some time and then apologized and gave them the true results, challenging them to say as vehemently, that coronary care units should be stopped immediately. There was dead silence… (Quoted in Doll, 1997, p. 8)

Illness, behaviour and related issues Much of the early work on stress and illness depended on existing physician, clinic and hospital records, and was the basis for many interesting observations and hypotheses. Harold Wolff and Lawrence Hinkle, for example, did much of their stress work on a large number of employees of a telephone company for whom there were extensive medical records over several years. In these investigations they were introducing the then novel notion that: [Man’s] attempts to adapt to life situations which do not fill his needs, which frustrate his aspirations, or which place heavy and conflicting demands upon him are very often associated with an increased susceptibility to all forms of illness, regardless of nature or etiology. (Hinkle and Wolff, 1957, p. 132) They introduced much data to justify this idea, but the data were derived from illness records and the assumption that any bias in recognition of illness or the inclination to seek care was unimportant. In reading these studies, it seemed plausible that persons who were dissatisfied with their jobs and their lives might be more inclined to seek sickness as an excuse and to justify exemption from work and other obligations. My first major study in 1957 was initiated to evaluate the Hinkle–Wolff assumption and to ascertain how variations in perceptions, needs and role definitions led individuals to differentially recognise and respond to illness and seek care through varying pathways (Mechanic and Volkart, 1961). I was able to show that medical records were socially constructed and not simply mirrors to sickness; the conclusions based on such record data, while not necessarily incorrect, could not possibly be substantiated in this way (Mechanic, 1963). This was the beginning of illness behavior and help-seeking as a field of study (Mechanic, 1995). Over subsequent decades, the research enterprise has become far more methodologically sophisticated and sensitive to the sources of error and bias. The quality of interviewing has improved dramatically and cognitive testing now allows us to assess how respondents understand our questions and whether the measures we use tap what they purport to measure (Schwartz and Sudman, 1996). Sampling has improved immeasurably and investigators increasingly use prospective designs

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Bringing meaning back into research 67 which avoid the retrospective reconstructions of reality that were so common in earlier research efforts. Longitudinal investigation is intended to make causal sequencing more clear but even these refinements are limited because of the complexity and richness of life trajectories. Two specific problems are common in analysis. Even the best longitudinal studies are, at best, a sample of cross-sections which make it difficult to capture important causal patterns that occur iteratively and in close temporal proximity. Interviews completed at intervals of years or even months lose much of the patterns of everyday events that influence important health outcomes (Mechanic, 1979, 1989). As a consequence, we often find that large epidemiological investigations, and even longitudinal studies, have less explanatory power than some smaller but intensive qualitative studies. Furthermore, because the statistical controls typically used in longitudinal analyses require a focus on studying changes in response or outcomes, as compared with the determinants of initial patterns and dispositions, it is often impossible to account for the most important differences whose pathways are already established prior to the initial measurements. These types of issues have contributed to significant disagreements between the proponents of quantitative and qualitative research. Although most agree about the value of constructively linking the quantitative and qualitative perspectives, this has rarely occurred. The methodology involving the LEDS is an unusually successful example of crossing this divide in health research by retaining the depth and richness of the best qualitative work but analysing it in a framework that retains rigour and objectivity, and avoids the types of retrospective bias in reporting that diminishes many studies. If we are to achieve the understanding we seek, our approaches must capture the dynamic nature of meaning systems as they evolve with change in circumstances. The typical survey does this poorly for the reasons noted above, but the LEDS, combined with the elaborately developed scoring system to characterise events and reactions, was an original and productive innovation for capturing meaning while taking advantage of serendipity. George Brown’s insistence on staying close to his data and taking the time and effort to interview his respondents and know them and their families thoroughly has been a source of many important insights and much of his success. His early work on ‘expressed emotion’, for example, is now an important building block for psychoeducational programmes around the world in the management of schizophrenia and other disorders. What struck me most about George after first meeting him, and reinforced repeatedly over the years, has been his ability to think, as we Americans now put it, ‘outside the envelope’. This talent has clearly served him well.

References Brown, G. (1974) ‘Meaning, measurement, and stress of life events’, in B.S. Dohrenwend and B.P. Dohrenwend (eds) Stressful Life Events: The Nature and Effects, New York: John Wiley and Sons, 217–43.

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68 David Mechanic —— and Birley, J.L. (1968) ‘Crises and life changes and the onset of schizophrenia’, Journal of Health and Social Behaviour, 9, 203–14. —— and Rutter, M. (1966) ‘The measurement of family activities and relationships: a methodological study’, Human Relations, 19, 241–63. Doll, R. (1997) ‘A Reminiscence of Archie Cochrane,’ in A. Maynard and I. Chalmers (eds) Non-random Reflections on Health Services Research: On the 25th Anniversary of Archie Cochrane’s Effectiveness and Efficiency, London: BMJ Publishing Group. Durkheim, E. (1951) Suicide: A Study in Sociology, trans. J.A. Spaulding and G. Simon, New York: Free Press. Essen-Möeller, E. (1956) ‘Individual traits and morbidity in a Swedish rural population’, Acta Psychiatrica et Neurologica Scandinavica, 100, Supplement. Faris, R.E.L. and Dunham, H.W. (1939) Mental Disorders in Urban Areas, Chicago: University of Chicago Press. Grob, G.N. (1991) From Asylum to Community: Mental Health Policy in Modern America, Princeton: Princeton University Press. Hagnell, O. (1966) A Prospective Study of the Incidence of Mental Disorder, Stockholm: Svenska Bokförlaget Norstedts-Bonniers. Hinkle, L.E., Jr. and Wolff, H.G. (1957) ‘Health and the social environment: experimental investigations’, in A.H. Leighton, J. Clausen and R.N. Wilson (eds) Explorations in Social Psychiatry, New York: Basic Books. Hollingshead, A.B. and Redlich, E.C. (1958) Social Class and Mental Illness: A Community Study, New York: John Wiley and Sons. Holmes, T.H. and Rahe, R.H. (1967) ‘The social readjustment rating scale’, Journal of Psychosomatic Research, 11, 213–18. Leighton, D.C. et al., (1963) The Character of Danger: Psychiatric Dangers in Selected Communities, New York: Basic Books. Mather, H.G. et al., (1971) ‘Acute myocardial infarction: home and hospital treatment’, British Medical Journal 3, 334–8. Maynard, A. and Chalmers, I. (eds) (1997) Non-random Reflections on Health Services Research: On the 25th Anniversary of Archie Cochrane’s Effectiveness and Efficiency, London: BMJ Publishing Group. Mechanic, D. (1963) ‘Some implications of illness behavior for medical sampling’, New England Journal of Medicine, 269, 244–7. —— (1975) ‘Some problems in the measurement of stress and social readjustment’, Journal of Human Stress, 1, 43–8. —— (1978) Medical Sociology, 2nd ed., New York: Free Press. —— (1979) ‘Correlates of physician utilisation: why do major multivariate studies of physician utilisation find trivial psychosocial effects?’, Journal of Health and Social Behaviour, 20, 387–96. —— (1989) ‘Medical sociology: some tensions among theory, method and substance’, Journal of Health and Social Behaviour 30, 147–60. —— (1995) ‘Sociological dimensions of illness behaviour’, Social Science and Medicine, 41, 1207–16. —— (1998) ‘Stress-moderating and -amplifying factors’ in B.P. Dohrenwend (ed.) Adversity, Stress, and Psychopathology, New York: Oxford University Press, 371–5. —— (1999) Mental Health and Social Policy: The Emergence of Managed Care, 4th edition, Boston: Allyn and Bacon. —— and Volkart, E.H. (1961) ‘Stress, illness behavior and the sick role’, American Sociological Review 26, 51–8.

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Bringing meaning back into research 69 Schwartz, N. and Sudman, S. (1996) Answering Questions: Methodology for Determining Cognitive and Communicative Processes in Survey Research, San Francisco: JosseyBass. Selye, H. (1956) The Stress of Life, New York: McGraw-Hill. Srole, L. et al., (1962) Mental Health in the Metropolis: The Midtown Manhattan Study, New York: McGraw Hill. Werner, E.E. and Smith, R.S. (1992) Overcoming the Odds: High Risk Children from Birth to Adulthood, New York: Cornell University Press. Wolff, H. (1953) Stress and Disease, Springfield, Ill: Thomas.

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4

George W. Brown The science of meaning and the meaning of science Paul Bebbington

George Brown has made several great contributions to his chosen field. Although they can be separated into theoretical and methodological aspects, they are in fact linked: the methodological innovations, which have had a major impact on social psychiatry, are inevitably driven by theory. The methodological developments could be regarded merely as an energetic devotion to the creation of many useful research instruments and techniques, but the most striking thing about them is that they bridge an ancient gap between the natural and social sciences. In doing so, they call in question the reality of this traditional division. In order to evaluate Brown’s place in social psychiatry, one must recapitulate philosophical debates that were central to the developments of sociology, and psychiatry and psychology, in the last century, and which were ongoing when his career was in its early stages. These debates seem less salient now: the battles have receded, being heard now only as a distant and sporadic clashing. However, they were important in their time, and it is not clear that the casus belli has been resolved. von Wright (1971) expressed the matter succinctly: the social and behavioural sciences ‘have become the battleground for the two opposed trends in philosophy of scientific method’. He described these two trends as the Aristotelian and Galilean. The Aristotelian tradition seeks explanations in teleological terms, while the Galilean is essentially mechanistic. The Galilean tradition was advanced in the nineteenth century by the work of Comte and Mill. These writers espoused three articles of belief: the idealisation of the methodology of mathematics and physics; an adherence to causal explanation; and methodological monism, the view that the methods of the natural and human sciences are the same. This is actually an oversimplification. Thus, teleological explanations are apparent in the natural sciences as well as in the social. Indeed, teleological ideas were incorporated in mechanical systems from the eighteenth century, when a number of self-regulating machines were in use. Alfred Russell Wallace (1859) actually employed these concepts as an analogy of the effects of natural selection in his key paper. What truly underlies the debate between the two traditions is the role of the concepts of ‘meaning’ and of ‘understanding’. Some authorities have argued that human behaviour is irreducible to general laws precisely because of the fact that it

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72 Paul Bebbington is ‘meaningful’. By this they imply that it is not merely purposive, it is purposive within a system of socially determined ends. Thus Winch (1958) claimed that the essence of human behaviour is that it is rule-governed. He argued that any human action derives its significance from shared beliefs about what it is to act. For Winch (1958), the concept of rule-governed behaviour is intimately related to that of ‘making a mistake’. Thus the possibility of carrying out a correct action implies a system of rules within which it is to be judged. He argued that the possibility of mistakes and of choice poses grave difficulties for falsificationist science. Winch claimed that we are unable to make scientific laws about the behaviour of an agent whose actions determine the rules under which the agent acts (see also Shotter, 1975, and Wetherick, 1979). To assert that behaviour is meaningful implies that we can understand it. A major issue is whether such understanding, which is the basis of lay attempts to explain behaviour and which shares the language of causality, may validly be given the logical form of causal explanation. Thus, we can understand meaningful behaviour: can this be the basis for causal explanation, or are understanding and explanation irreducibly separate ways of grasping the world? This concern is central to Brown’s approach to sociological method. One of the great debates in psychiatry in the 60s and 70s concerned this issue of the nature of explanation. This was at a time when Popper’s (1932, trs. 1963) view about the demarcation of scientific knowledge from other sorts of knowledge was influencing a number of psychiatrists (e.g. Wing, 1978). This was apposite because Popper had developed his ideas about the proper methodology of science in response to his experience in working with Alfred Adler in Vienna, as a very young man indeed. Popper took refutability as the gold standard for a scientific theory. He himself pointed out that psychoanalytic theory is couched in terms that are irrefutable. ‘It was precisely this fact – that they always fitted, that they were always confirmed – which in the eyes of their admirers constituted the strongest argument in favour of these theories. It began to dawn on me that this apparent strength was in fact their weakness’ (Popper, 1963). Popper himself was of the opinion that psychoanalytic theories ‘… describe some facts, but in the manner of myths. They contain most interesting psychological suggestions, but not in testable form’. He was very clear that such pre-scientific myths might be developed and become testable. However, in their present form, they cannot claim to be backed by empirical evidence in the scientific sense. Nevertheless, they ‘… may easily be in some genetic sense, the result of observation’. In saying this, he clearly asserts some empirical content to psychoanalytic theory. Popper’s views were used in the debate over whether psychoanalysis could be regarded as a science (Cioffi, 1970; Farrell, 1970). The protagonists of psychoanalysis either claimed that psychoanalysis was an empirical science, or, as Rycroft (1968) argued, that the purpose of psychoanalytic theory was not causal explanation, but an attempt at understanding. Rycroft says: ‘The procedure [Freud] engaged in was not the scientific one of elucidating causes, but the semantic one of making sense of it.’ This leads us on to the writings of Karl Jaspers, who was also influential during this period.

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The science of meaning 73 In fact, the separation between explanation and understanding has a very long history. It goes back at least as far as the mid-nineteenth century, when the German philosopher-historian Droysen (1858) distinguished between the methods of philosophy, of science and of history. The knowledge arrived at in those disciplines he expressed in the words erkennen (to know), erklären (to explain) and verstehen (to understand). These terms and the distinction they represent were introduced into sociology by Max Weber (trs.1962), and into psychiatry by Karl Jaspers (trs. 1963). While Weber did not regard the erklären and verstehen as polar opposites, Jaspers certainly did. Jaspers was dismissive of the effect of his seminal 1913 article and of his General Psychopathology published in the same year. ‘All I had done was to link psychiatric reality with the traditional humanities.’ He brought the distinction between causal explanation and understanding into the foreground. ‘In the natural sciences we find causal connections only, but in psychology our bent for knowledge is satisfied with the comprehension of quite a different sort of connection. Psychic events ‘emerge’ out of each other in a way which we understand, attacked people become angry and spring to their defence, etc.’ (Jaspers, trs. 1963). For Jaspers, these meaningful connections were merely analogous to real causal connections. Understanding was something immediate and irreducible and, he claimed, not acquired inductively by experience. Thus, he stated: ‘The meaningful connections of psychological events have also been called ‘causality from the inside’ and this term has characterised the unbridgeable gap which exists between this, which can be called ‘causal’ only as an analogy, and the real causal connections, the ‘causality from outside’ (Jaspers, 1974). He said: ‘The rules of causality are obtained inductively and culminate in theories about what lies at the root of the given reality. Particular cases are then subsumed under them. Genetically understandable connections, however, are ideal-typical connections; they are self-evident and not inductively obtained. Because we note the frequency of a meaningful connection, it does not mean the meaningful connection becomes the rule’ (Jaspers, 1963). Jaspers was ready to admit that psychic events are open to causal explanation, but he implied that they might only be effects and that causation had to be ‘extraconscious’. Jaspers himself claimed that Freud’s work was a psychology of meaning, and not of causal explanation, ‘as Freud thinks’. The separation between causality and meaning emphasised by Jaspers, has, as we have seen, been used to defend psychoanalysis from the Popperians. However, there are inconsistencies in what Jaspers himself said about the distinction. He envisaged the possibility of extending understanding ‘to remote connections which at first sight might seem incomprehensible’ (Jaspers, 1963). By doing this, he admitted the importance of hypothetical considerations in generating understanding. This undermines his view that genetically understandable connections are self-evident. I would argue that self-evidence is in fact the belief that we have in the commonsense models of the mind that we all possess to some degree. Jaspers was clearly a reductionist: he insisted that causal links can only proceed up the hierarchy of concepts. However, Jaspers’ admission of the role of

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74 Paul Bebbington hypotheses in generating understanding crucially undermines his position. There is a tension between hypothesis testing and the emotional component of belief. The latter is what Cardinal Newman called the ‘grammar of assent’ and what Einstein, in the context of theory in physics, referred to as einfühling. Einstein talked of: ‘The search for those highly universal laws from which a picture of the world can be obtained by pure deduction.’ However, he went on: ‘There is no logical path leading to these … laws. They can only be reached by intuition and empathy’ (quoted in Popper, 1963). Thus, the flash of insight is a measure of our conviction, and does not reflect on the attributes of that which we apprehend. By separating causal and meaningful connections, Jaspers set up a situation in which it was possible to dismiss the study of the relationships between social contexts and states of mind – this sort of research came to be seen as lower order at best and dubious at worst. The natural consequence was a move towards making psychiatry a biological and reductionist discipline. We have certainly seen this consequence in action at various periods in the history of psychiatry. Brown and his colleagues have however acted as a major counterweight, certainly in the UK and to an extent in the US. It is because of Brown’s early researches (e.g. Brown et al., 1962, 1972; Brown and Birley, 1968; Wing and Brown, 1970) that the idea of a social component in the explanation of the characteristics of schizophrenia was disinterred and rehabilitated. For me, the most interesting part of Brown’s work relates to the evaluation of the impact of life events. The staging posts of this continuing methodological innovation are Brown’s consideration of what is likely to constrain people’s responses to events. It is clear that people do respond to life events, particularly unpleasant ones, but that these responses vary. This leads straight into the realms of Jaspers’ verstehende Psychologie – how do we understand the individual’s responses to events? However, Brown was interested in the further question of the extent to which events explain people’s responses. The problem is that the very definition of a life event is tied up with our understanding of its effects. While things happen in people’s lives all the time, it is only certain types of happening that are regarded as life events. The attributes that researchers identify that enable a happening to qualify as an event are derived from the researcher’s own theories of mind. Thus, life events virtually always have to have either a quality of change or a quality of unpleasantness (these qualities may obviously be related). The problem here is that not only do researchers have a theory of mind, but they share it with their research subjects. Obviously there are variations in the details of individuals’ theories of mind, but, nevertheless, the similarities are quite general. If this is the case, why should we not take the respondent’s own estimation of the life event as veracious? The problem is that respondents not only have a theory of mind, but they seek to apply it to account for their own predicament. This is the search after meaning (Bartlett, 1932). Following the distinction made by Windelband (1894) between nomothetic and idiographic sciences, it is clear that the search after meaning is essentially an idiographic procedure. Nomothetic sciences aim at generality: they seek to establish general laws which, taken together

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The science of meaning 75 with the specification of initial conditions, have the object of prediction. Idiographic sciences, such as history, seek to explain individual given facts. Thus, idiographic sciences work backwards from explananda to explanans. Prediction holds a special place in the methodology of science which retrodictive explanation cannot. This arises from what Popper (1976) termed ‘the retransmission of falsity’. When we follow a valid argument from premises to a conclusion which proves false, one or other premise must also be false. However, there are no truth constraints on the premises which may be postulated to explain a given fact. Indeed, Popper (1976) suggested that this represents a logical basis for the distinction between nomothetic and idiographic sciences. This raises the question of whether, in their search for meaning, subjects have any privileged access to the truth. If not, subjective accounts of the impact of a life event on somebody’s mood state cannot be taken at face value. This itself has been the subject of debate. Thus, Harré (1976) did not allow the possibility of rejecting the subject’s account, while Gauld and Shotter (1977) seemed prepared to. Pettit (1979) assumed ‘that an agent does not have any special kind of knowledge of his concern and beliefs’. If we accept that a subject’s own use of feeling-explanation is in itself the use of a theory of mind, disagreement with the subject is obviously allowable. Explanations that people render of their feelings while under the influence of hypnotic suggestion confirm this. It does seem clear that not only is it allowable to reject a subject’s own account of the relationship between context and feelings, but that it might be mandatory in seeking to establish an empirical relationship between variables such as life events and mood states. This was the position at which Brown arrived in the 1960s, when he started to develop his methods of assessing life events. At that time, attempts had already been made to define life events and indeed to quantify them. In order to remove the subjective element as far as possible from the evaluation of life events, authors such as Holmes and Rahe (1967) constructed a priori lists of life events which could be used as the basis of eliciting a life event history. Quantative values could be attributed to these life events. This was done by using a rating sample, that is by averaging the ratings of a sizeable group of people. However, the life events in the list of Holmes and Rahe (1967), and in others like it, were not in fact events per se, but rather rubrics under which events could be subsumed. Because event lists had to be of finite length for practical reasons, and because the list had to be reasonably exhaustive, each rubric could cover events occurring in a range of contexts. Thus, in the effort to remove the subjective element of evaluation, the adherents of the inventory approach to life event assessment were throwing out much of the information that would allow a meaningful evaluation of the impact of actual events. Brown’s novel solution to this problem was to develop a measure whereby events could be evaluated in their contexts. This was the development of the famed Life Events and Difficulties Schedule (Brown and Harris, 1978). This is a semistructured interview that seeks to elicit narratives in relation to events. Thus, not only is the nature of the event identified, but also its context. These narratives, once they have been elicited by an interviewer, are presented in the form of a vignette to

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76 Paul Bebbington a panel of raters. The raters have documented guidance on aspects of the rating procedure, but essentially what they do is to apply their own theory of mind, shaped by the common culture of the researchers, to the event and its circumstances. Thus the question they ask themselves is: ‘In this set of circumstances how likely would an event of this type be to elicit a strong emotional response?’ It should be noted that the premises involved in theories of mind may be quite complicated, and the overall impact of the event may be assessed in the context of quite detailed information about circumstances past and present. In this procedure, what Brown has succeeded in doing is to take an idiographic analysis and use it to build a variable that can be used nomothetically. He has thus bridged the divide between meaning and explanation. Defining life events in this way resulted in a clear association between such events and the development of depressive disorder (Brown and Harris, 1978). However, the problem with the initial evaluative procedure was that the assessment of the event incorporated many elements of theories of mind. Over the years, Brown and his colleagues have refined their approach, mainly by taking out the evaluation of life events contexts that could be rated separately. The first attempts to do this were apparent in the early reports (Brown et al., 1975, 1977). Thus, the original ‘vulnerability model’ suggested that the impact of life events would be enhanced by certain additional contexts. These were early loss of mother, nonemployment, involvement in the hurly-burly of child care, and the inability to access adequate social support. Clearly, these are things which most people would understand as being of importance. By using them as separately defined variables, Brown could refine the predictive power of the model which he and his colleagues were building to account for depression. This process of refinement continues. Thus, Brown and his colleagues have examined qualitative distinctions in the sorts of life events associated with depression and with anxiety (Finlay-Jones and Brown, 1981). They have also refined the study of early events, such as parental loss, in such terms as the lack of adequate parental care in the follow-up period. They have developed elaborate ideas about the pathways linking early events with later social and mental health outcomes (Harris et al., 1986, 1987, 1990). The use of additional dimensions with which to assess life events has also been part of this process of refinement. Thus the early ratings of threat were relatively simple, but these have become more elaborate measures of the life event connotations of loss, humiliation and entrapment (Brown et al., 1995). Details of this process of development will appear elsewhere in this book, but I adduce them in order to illustrate Brown’s approach to the refinement of meaning. Elements in lay theories of mind are teased out and go towards the establishment of models which may then be tested empirically. This process has links with other developments in psychology and social psychiatry. The last twenty years of the twentieth century saw psychology recover its mind. Cognitive theory has come to the fore to account for both affective and psychotic disorders. It is a truism that all social theories in psychiatry are also cognitive and that all cognitive theories are social (Bebbington, 1985). Nevertheless, in

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The science of meaning 77 the individual theory their dual nature is not always acknowledged. Our group’s model of psychosis is clearly both social and cognitive (Garety et al., 2000). Theory of mind has itself become the object of study, so that we are developing theories about theories of mind (Doody et al., 1998; Zelazo et al., 1999). The refinement of the quantitative assessment of life events has its application in our group’s own work on schizophrenia. It is clear from the experience of people engaged in cognitive behaviour therapy with psychosis that many patients with, for example, persecutory delusions, have experienced events which in their characteristics were likely to induce exactly a sense of isolation and persecution. Preliminary work using essentially a Brownian strategy has corroborated this idea (Raune et al., 2000). Thus, Brown’s effort to create a nomothetic science out of material that was traditionally regarded as idiographic, has coincided with and encouraged a great deal of research examining the interface between social and psychological phenomena. That is no mean legacy.

References Bartlett, F.C. (1932) Remembering: a Study in Experimental and Social Psychology, London: Cambridge University Press. Bebbington, P.E. (1985) ‘Three cognitive theories of depression’, Psychological Medicine, 15, 759–71. —— and Birley, J. L. T. (1968) ‘Crises and life changes and the onset of schizophrenia’, Journal of Personality and Social Psychology 50, 1013–20. —— and Harris, T.O. (1978) Social Origins of Depression: A Study of Psychiatric Disorders in Women, London: Tavistock. ——, Monck, E. M., Carstairs, G. M. and Wing, J. K. (1962) ‘Influence of family life on the course of schizophrenic illness’, British Journal of Preventive and Social Medicine 16, 55–68. ——, Birley, J. L. T. and Wing, J. K. (1972) ‘Influence of family life on the course of schizophrenic disorders: A replication’, British Journal of Psychiatry 121, 241–58. ——, Ni’ Bhrolchain, M. and Harris, T. O. (1975) ‘Social class and psychiatric disturbance among women in an urban population’, Sociology 9, 225–54. ——, Harris, T.O. and Copeland, J.R. (1977) ‘Depression and loss’, British Journal of Psychiatry, 130, 1–18. ——, Andrews, B., Harris, T.O., Adler, Z. and Bridge, L. (1986) ‘Social support, selfesteem and depression’, Psychological Medicine, 16, 813–31. ——, Harris, T.O. and Hepworth, C. (1995) ‘Loss, humiliation and entrapment among women developing depression: a patient and non-patient comparison’, Psychological Medicine, 25, 7–21. Cioffi, F. (1970) ‘Freud and the idea of a pseudoscience’ in R. Borger and F. Cioffi (eds) Explanation in the Behavioural Sciences, Cambridge:Cambridge University Press. Doody, G.A., Gotz, M., Johnstone, E.C., Frith, C.D. and Owens, D.G. (1998) ‘Theory of mind and psychoses’, Psychological Medicine, 28, 397–405. Droysen, J.G. (1858) Grundriss der Historik, quoted in von Wright (1971). Farrell, B.A. (1970) ‘Psychoanalytic theory’ in S.G.M. Lee and M. Herbert (eds) Freud and Psychology, Harmondsworth, Middlesex: Penguin Books.

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78 Paul Bebbington Finlay-Jones, R. and Brown, G.W. (1981) ‘Types of stressful life events and the onset of anxiety and depressive disorders’, Psychological Medicine, 28, 803–15. Garety, P., Kuipers, E., Freeman, D., Fowler, D. and Bebbington, P.(2000) ‘A cognitive model of the positive symptoms of psychosis’, submitted to Psychological Medicine. Gauld, A. and Shotter, J. (1977) Human Action and its Psychological Investigation, London: Routledge and Kegan Paul. Harré, R. (ed.) (1976) Life Sentences, London: Wiley. Harris, T.O., Brown, G.W. and Bifulco, A. (1986) ‘Loss of parent in childhood and adult psychiatric disorder: the role of lack of adequate parental care’, Psychological Medicine, 16, 41–659. ——, Brown, G.W. and Bifulco, A. (1987) ‘Loss of parent in childhood and adult psychiatric disorder: the role of social class position and premarital pregnancy’, Psychological Medicine, 17, 163–83. ——, Brown, G.W. and Bifulco, A. (1990) ‘Depression and situational helplessness/ mastery in a sample selected to study childhood parental loss’, Journal of Affective Disorders, 20, 27–41. Holmes, T.H. and Rahe, R.H. (1967) ‘The social readjustment rating scale’, Journal of Psychosomatic Research , 11, 213–18. Jaspers, K. (1963) General Psychopathology, translated from the German 7th edition by Hoenig, J and Hamilton, M.A., Manchester: Manchester University Press. Jaspers, K. (1974) ‘Causal and meaningful connections between life history and psychosis’, in. S.R. Hirsch and M. Shepherd (eds) Themes and Variations in European Psychiatry, Bristol: John Wright and Sons. Pettit, P. (1979) ‘Rationalization and the art of explaining action’, in N. Bolton (ed.) Philosophical Problems in Psychology, London: Methuen. Popper, K.R. (1932 translated 1963) Conjectures and Refutations, London: Routledge and Kegan Paul. —— (1976) ‘The logic of the social sciences’, in T. Adorno (ed.) The Positivist Dispute in German Sociology, London: Heinemann. Raune, D., Bebbington, P. and Kuipers, E. (2000) ‘The attributes of life events and the content of delusions’, in preparation. Rycroft, C. (1968) ‘Causes and meaning’, in C. Rycroft (ed.) Psychoanalysis Observed, Harmondsworth, Middlesex: Panguin Books. Shotter, J. (1975) Images of Man in Psychological Research, London: Methuen. von Wright, G.H. (1971) Explanation and Understanding, Ithaca. NY: Cornell University Press. Wallace, A.R. (1859) ‘On the tendency of varieties to depart indefinitely from the original type’, Journal of the Linnean Society, 3, 53–62. Weber, M. (1962) Basic Concepts in Sociology, translated by H.P. Secher, London: Owen. Wetherick, N.E. (1979) ‘The foundations of psychology’, in N. Bolton (ed.) Philosophical Problems in Psychology, London: Methuen. Winch, P. (1958) The Idea of a Social Science, London: Routledge and Kegan Paul. Windelband, W. (1894) Geschichte und Naturwissenschaft quoted in von Wright (1971). Wing, J. K. (1978) Reasoning about Madness, London: Oxford University Press. —— and Brown, G.W. (1970) Institutionalism and Schizophrenia. A Comparative Study of Three Mental Hospitals 1960–68, Cambridge: Cambridge University Press. Zelazo, P.D., Astington, J.W., Olson, D.R. (eds) (1999) Developing Theories of Intention: Social Understanding and Self-control, Mahwah, NH, USA: Lawrence Erlbaum Associates, Inc.

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Part II

Measurement of key psychosocial factors in research

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5

Lessons from using semistructured interviews with seriously ill patients Elizabeth Davies

Introduction In this chapter I give a personal account of using an approach to data collection influenced by instruments such as the Camberwell Family Interview (CFI) and the SESS (Self Evaluation and Social Support) to study seriously ill patients and their close relatives or carers. It is sometimes overlooked in discussing the ‘hardness’ of instruments such as the LEDS that George Brown and his colleagues have devoted a great deal of their time developing instruments to reflect as sensitively as possible subjective states covering a range of emotions and highly personal concerns. The study I recount concerned patients suffering from malignant cerebral glioma – a form of brain cancer with a particularly poor prognosis – and I was concerned to study the quality of life after radiotherapy treatment. I planned to see patients and relatives, as far as possible, soon after their initial diagnosis and then at three monthly intervals. I first describe the background to the study and the choice of a semi-structured interview to approach sensitive aspects of this situation. My aim was to quantify aspects of patients’ and relatives’ experience using rating scales developed as an integral and lengthy part of the research itself. I then outline how the scales were created and discuss a number of practical and ethical issues that emerged during the study. Studies of the effectiveness of treatment do not usually gather detailed interview-based data, and some fiercely critical letters followed the initial papers published in 1996 in the British Medical Journal. Although this has been subsequently balanced by positive comment, I suggest that part of the reason for the controversy was the ambivalence many in medicine felt to what is seen as the dangerous subjectivity of interview data. Such a response is intriguing as an interview approach is far closer to good everyday clinical practice than the perennial questionnaire employed in most such research, and widely regarded as the more ‘objective’. In this context I consider the future use of interview-based measures in quality of life studies.

Background Malignant cerebral glioma is the most common form of malignant brain tumour and represents a significant part of the work of a neurosurgical unit. The

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82 Elizabeth Davies prognosis is poor and the median survival after surgery alone only about three months. Radiotherapy is the main treatment option and two randomised controlled trials have shown that six weeks of this treatment prolongs median survival after surgery to around nine months (Walker et al., 1978; Kristiansen et al., 1981). Even with radiotherapy two years from the diagnosis only 5–15 per cent of patients remain alive (Green et al., 1983). This relatively modest effect and the absence of detailed data on the palliation of symptoms, quality of life or possible adverse effect, had raised doubts about the treatment amongst some neurologists. In 1986, a retrospective analysis of case records in one UK centre was published showing they did not always refer their patients on for radiotherapy. The authors suggested that such an approach might be ethically justified since their patients’ outcome seemed similar to treated patients (Wroe et al., 1986). The study recounted in this chapter, carried out between 1990 and 1994, set out therefore to describe the clinical course, the quality of life, and the views of patients and relatives about the value of treatment. Why choose an interview? Previous research had mostly consisted of randomised controlled trials of treatment or neuropsychological and psychiatric studies describing psychological or cognitive syndromes caused by brain damage. The reactions of patients or their families to the diagnosis had been little studied (Lishman, 1987). The study needed, therefore, to explore the decision patients and relatives made about treatment while often aware of the strong possibility of disability and death. Initial contacts with patients simply served to confirm my belief that using questionnaire-based measures of quality of life alone would be inappropriate, leaving aside any question of their likely validity, and that the conversational style of an instrument such as the SESS would be more able to ensure the kind of flexible and sensitive questioning that was clearly required. Another reason for choosing an interview approach was the fact that cognitive problems due to brain damage could be expected to influence a patient’s ability to fill out questionnaires or answer structured questions. A semi-structured interview retained the facility to assess the extent of cognitive problems and adapt questions to the patient’s understanding. In practice, it was possible to interview, without too much difficulty, seventy-five of the eighty-three patients undergoing radiotherapy. The rest, however, were too confused. Some who were interviewed did have language and cognitive problems but these did not prevent them talking understandably about what they found important. Establishing an early rapport also made it seem easier to remain in touch as the illness progressed. Inevitably, however, at advanced stages of the disease the interview was often largely limited to an assessment of the problems the patient was having, and finally to relying on relatives’ accounts of problems. The need for such an approach was also underlined by the initial interviews which made clear the immediate and often dramatic effect that a tumour could have on physical, psychological and social function, making the experiences of

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Interviewing seriously ill patients 83 these patients often of a different order from those of other cancer patients. Certainly some insight into the consequences of such changes seemed essential if the research was to lead to better psychosocial management or better information and support for families. From the start I placed considerable weight on the possibility of such knowledge. To explore at length the experiences of such patients and families was daunting, and I felt unable to justify this intrusiveness for the sake of research alone.

Developing the interview Interviews were mostly conducted at home, tape-recorded and then transcribed. I began with open-ended interviews with six patients and relatives, asking what was important for them and identifying themes that would need to be explored in the main enquiry. These interviews also increased my confidence about the feasibility of the proposed research. Discussing transcripts with experienced interviewers suggested areas or cues I had missed or instances where I had been insensitive in my questioning. Throughout I noted questions that had appeared to be helpful in tapping particular concerns and probes which had provided clarification. For example, to find out what a patient or relative understood about the prognosis I first asked them to describe how they came to suspect that anything was wrong. As they recounted the events of the diagnosis I would ask questions along the lines of ‘Do you remember exactly what that doctor said?’ or ‘Were they able to find out any more about the outlook in your particular case?’ My approach was to allow the patient or relative to begin to discuss the diagnosis using the past tense so that they might possibly distance any distress they had felt. Once the framework of events had been established, and I was clear about their understanding, I might bring the discussion of reactions and implications into the present. If their current perspective was not yet clear I might ask ‘Do you feel any differently about it now?’ I was often surprised how far patients’ perceptions differed from my own, and I quickly learnt never to assume that patients or relatives were aware of the particularly poor prognosis. I also decided it was not my place (even though medically qualified) to volunteer this information during interviews. Development was not limited to a defined phase. Although a satisfactory interview schedule had emerged after the first batch of interviews, and the rating scales were broadly developed by the thirtieth interview, it was necessary at this point to attempt to finalise them as one interviewer was appointed. The four or five points on these scales were attempts to reflect the range of responses about particular issues – for example, how far patients appeared to be unaware of the poor prognosis. For this, as interviews had accumulated, a single scale proved to be inadequate to reflect the complexity of the issue. And by this point two scales had been developed to reflect awareness of the prognosis – ‘thoughts about the possibility of death’ and ‘belief in cure’– the former the extent to which the patient or relative mentioned or implied during the interview that they might die; the latter the extent to which they appeared to believe treatment was likely to produce a cure. A further series of scales broadly followed the Bedford College

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84 Elizabeth Davies scheme for coping measures which had been applied to patients with breast cancer (Pinder et al., 1992). Thoughts or beliefs were rated separately from the coping process we surmised the patient or relative to be using. As the initial work had progressed new scales were developed and others amended, both demanding the return to earlier interviews to make fresh ratings. And new examples of particular scale points emerged all the time. It was therefore a process combining intuition, classification, and constant revision. My aim was to identify types of experience emerging out of the accounts that were obtained rather than imposing some kind of preformed framework upon them, whilst all the time being on the lookout for ‘new’ aspects not ‘fitting’ the rating scales that had already been outlined. At around this stage of the work, a second worker was appointed to help with interviewing. This added impetus to the developmental work as coherent descriptions of each scale and extensive examples of scale points had to be in place for training. There was a great deal of discussion, and revisions and additions continued for some time. As a part of training, independent ratings of recorded interviews were made and many of the amendments resulted from discussion of rating discrepancies. At this stage we were also anticipating a formal test of the inter-rater reliability of the scales. The investment of time This to-ing and fro-ing and the final check on inter-rater reliability was timeconsuming. The interviewers received detailed feedback about their initial interviews together with discussion of all ratings they had made. The team as a whole discussed each new interview. This, as already noted, allowed new insights or ideas to be shared; it also enabled the interviewers to talk about any difficulties experienced. There was, therefore, a deliberate initial openness to the possibility of revision of scales and the reworking of earlier ratings until the stages of the reliability exercise itself were carried out well into the project. There was clearly an overlap between developmental work and actual data collection, but my feeling is that without this it would have been much more difficult to feel secure enough about the quality of the ratings to start data collection with any conviction. Inter-rater reliability is shown in Tables 5.1 and 5. 2. Table 5.1 shows there was good agreement about the two scales concerned with awareness of the prognosis – ‘Belief in cure’ and ‘Thoughts about the possibility of death’. By contrast we fell short of acceptable reliability for what were arguably some of the most interesting coping scales – ‘denial’, ‘felt uncertainty’ and ‘seeking meaning’ (see Table 5.2). We seemed more successful in reaching agreement about what our respondents believed but less so about the underlying dynamics. For example, our rating scale for denial tried to take account of an apparent lack of sadness or anxiety shown by a patient recounting the poor prognosis, the fact that they appeared to attach no importance to such information or recounted stories that didn’t ‘make sense’. Despite our fascination with the phenomenon, endless discussion and attempts to simplify the scales, our differing backgrounds in medicine, psychotherapy or

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Interviewing seriously ill patients 85 Table 5.1 Inter-rater reliability for 13 interviews (Kappa*) Detail

4-point scale 2-point scale

Satisfaction with medical care Felt concern of doctor Felt openness of doctor Felt support from general practitioner Felt overall coordination in care Felt coherence in information Felt ability of the system to deal with distress

0.72 — 0.72 0.70 0.62 1.00

0.61

Awareness of the likely prognosis Belief in cure Thoughts about the possibility of death

— 0.70

0.77

Overall satisfaction with radiotherapy Negative comments about radiotherapy Overall satisfaction with surgery Distress over hair loss

— 0.76 — 0.67

0.86

Coping strategies Anger Acceptance Positive appraisal Control Avoidance

0.75 0.60 0.70 0.64 0.65

Problems caused by the illness in everyday life Hobbies or interests Household tasks Social life Self-care Cognitive ability

— — — — —

Social support Perceived support from relative or carer Perceived religious support Overall distress

0.67 0.81 0.66

Satisfaction with treatment

1.00

0.88 0.80 0.86 0.60 1.00

*I have listed Kappa for reliability on the 2-point scales only when it was not possible to achieve good agreement on 4 points.

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86 Elizabeth Davies Table 5.2 Scales where inter-rater reliability failed (Kappa < 0.40) Satisfaction with treatment Positive comments about surgery Positive comments about radiotherapy Coping strategies Felt independence Denial Seeking meaning Felt uncertainty Problems caused by the illness in everyday life Work Social support Discussion of the diagnosis with carer or relative

psychology, and our personalities, seemed to give us different thresholds for what we regarded as ‘more than the normal amount of denial’. By contrast, we were reasonably successful in rating ‘avoidance’ and ‘positive appraisal’, probably because these ratings rely more on what people say they are doing . Respective examples are ‘I put it to the back of my mind’ or ‘There are worse off than me, I try to put a brave face on it’. Although our failures were disappointing they probably ensured that the successful scales did not reflect the idiosyncratic perspective of one of us and that there would be little difficulty in conveying what was involved to others. I was aware throughout of the need to avoid the charge of the inherent ‘subjectivity’ of the scales, although it was the very subjective nature of experience that by and large we set out to capture. Leaving aside the formal issue of inter-rater reliability, it was equally important for us as a team to ‘believe’ in the scales – not least that we were doing something to bring to life the somewhat shadowy concept of quality of life. During the early stages doubt was never far away; and when the first patient died I was left wondering about the point of the exercise. Hindsight suggests that the problem was that an investigator-based approach keeps the interviewer continually immersed in their data with the possibility of new doubts arising about the work of particular measures – or at best a continual need for reassurance that they were working as they should. Certainly our measures rarely took on the kind of ‘hardness’ of the questionnaire-based instrument that often seems to impress the medical mind. We were, of course, aware of questionnaires covering some aspects of quality of life for cancer patients; but our doubts were not always eased by our failure to recognise with any confidence what aspects of experience they were attempting to reflect. Nor were our clinical colleagues not directly involved in data collecting always of help. Questions such as ‘will you be able to predict those who will have the best quality of life?’ made little sense when we were struggling to document the complexity that appeared to be present in our interviews. It was too soon to reach for

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Interviewing seriously ill patients 87 such simplification.1 I return later to the question of how far the use of questionnaires can avoid such heart searching. Those not involved in the study would also often ask whether we found it ‘depressing’ to be seeing people who were so ill and so many of whom would die. Without doubt it was an emotionally demanding study. However, I found it more difficult mid-way into the study, having evidence of shortfalls in psychosocial and palliative care and sensing the kind of help that patients needed, without at that stage being able to argue for its provision. I was therefore determined to represent the experiences of these patients in a way that might have some chance of improving care.

Practical and ethical aspects of the study The acceptability of interviewing Because of the nature of the illness, we were concerned as interviewers to avoid creating additional distress. We approached patients several weeks after the diagnosis, explaining that we wished to interview them several times over the coming year about their satisfaction with care and treatment. We also asked to see a close relative or carer separately, since they might have a different perspective, and we asked each patient to discuss our request for them to join the study. A week later, when we telephoned, as many as ninety-two of a consecutive series of 105 patients agreed to an initial interview. Eighty-nine had close relatives and all but four of these also agreed to be seen. We asked permission to tape-record interviews, emphasising that ‘all information would be confidential… and will not be written in the medical notes’. We also emphasised that data would be stored and reported anonymously, and we repeated this at each subsequent interview. All but one carer agreed to the interview being recorded. Three interviewers conducted altogether 451 interviews, each lasting about 75 minutes. Despite the distressing experiences covered, we judged, from their comments and demeanour, that almost two-thirds (284/451) gained some comfort or satisfaction from the contacts. Some said they appreciated the chance to repay the health service or give feedback about unsatisfactory management. Some were flattered that their views were valued. For example: ‘Well, thank you for being interested enough to listen to my story. I do hope you find it some use.’ Or, ‘Fine. No. No problems at all. No problem. I’m pleased you have contacted me.’ Others found the interview an opportunity to reflect privately: ‘It’s nice having someone I can talk to, not a relative, a staff member or friend, but someone outside of the situation whom I can tell things I wouldn’t tell anyone else.’ However, in twenty-one of the 451 contacts, it was clear, even if not directly stated, that the patient or relative had disliked the experience. They became uncomfortable, changed the subject or asked pointedly if we had any more questions. Some found a particular issue difficult and, in trying to encourage them, the interviewer seemed to have probed too far. The worst of these instances left a strong impression: ‘I agreed to see you because I was so impressed with the care I

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88 Elizabeth Davies have got and I would like to help in any way I can. Maybe it’s inevitable, but I must say it’s actually been quite upsetting and I feel you’ve reduced me somewhat.’ The impression that most patients and relatives were happy to co-operate appears to be confirmed by the high follow-up rate achieved. Where we had first seen a relative, in all but 5 per cent of cases a patient or relative agreed to see us again. The apparent acceptability tallies with other workers. A questionnaire follow-up by Funch and Marshall (1981) reported that only 5 per cent of the cancer patients they had contacted wished they had not participated and Fallowfield (1987) reported that 85 per cent of women with breast cancer found interviews helpful. A more specific worry about our approach was the fact that many studies suggest that communication between family members about life-threatening illness is difficult and rarely completely open (Glaser and Strauss, 1965; Hinton, 1980). Partly with this in mind we decided to ask to see patients and relatives separately. We wanted to be able to ask relatives about cognitive change without the possibility of the patient listening to a distressing account of his or her condition. In fact, only six relatives requested that they be interviewed with the patient, and three of these, as far as we could judge, wanted to help patients with severe speech problems. Later in the study, two other relatives admitted having disliked separate interviews, making only five clearly objecting to this approach. Only one patient conveyed he did not wish to be seen alone. For some relatives it seemed the request elicited relief that the interview would allow them to speak freely. Joint interviews, when they did occur, were more difficult to manage, particularly when a couple disagreed. Interviewers would find themselves veering away from sensitive topics or trying to defuse a situation. Others have commented on the unpredictability of such interviews (Larossa et al., 1981). The value of seeing each patient and relative or carer separately was borne out by the frequency of a disparity in awareness of the prognosis discussed later. Had joint interviews been conducted, this finding would have emerged less strongly, and, given that many families appeared not to have discussed the prognosis explicitly, deliberately raising this in joint interviews would probably have altered the situation. For some families, such discussion might have been a welcome intervention; for others, it could have been extremely distressing. The interview as an intervention One possible objection to in-depth interviewing is that it prompts people to seek out information their doctors have decided not to disclose. To assess this, we noted the nature of every question asked of the interviewer. In twenty-three of the 451 contacts, respondents simply wished to know whether their views were typical. Twenty-four of the patient interviews and twenty-three with relatives contained straightforward questions about the practicalities of treatment. Relatives were more likely to ask questions (57/205) than patients (42/246) and were over twice as likely to ask about prognosis – twenty-three versus nine. Generally, most had already asked medical staff the same questions. We first reflected these questions back, asking why they sought alternative views. We encouraged them to

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Interviewing seriously ill patients 89 speak again with their doctors and conveyed that as research workers we were not in a position to deal with such questions. However, if a patient or relative was persistent, we felt it dishonest and unproductive to feign ignorance. No patient for whom we confirmed the poor prognosis withdrew from the study. Furthermore, we got no hint from either our interviews or contact with staff that such answers had created difficulties for clinicians, or altered subsequent management. A further objection to in-depth interviewing may be that the interviewer can only elicit sensitive information by adopting the role of counsellor, albeit unwittingly. Undoubtedly during our interviews we used some counselling techniques (such as reflecting questions back), but our relationship differed in several basic aspects. First, we were always visitors to the home, and rather than defining the situation, needed to adapt to it. Second, we saw patients every three months, an interval a good deal less frequent than outpatient appointments and far less than for counselling. However, while the study did no more than set out to try to avoid creating additional distress, the depth of enquiry and the continuity provided by seeing the same interviewer did on occasions mean that respondents placed importance on a developing relationship. For example, one relative (Chappell, 1997), who has since written about her experience comments: A detached but interested observer can bring up aspects of life that are worth evaluating and admitting. The enquiry went beyond considerations that my husband and I could have considered together … Effectively, this acted as counselling for us both … I suddenly realised the value of being able to share our thoughts within a professional context. The whole of that period without such back-up would indeed have felt much bleaker. We frequently found ourselves being thanked for listening, and were typically shown considerable hospitality. Eleven relatives gave small gifts, or wrote after the patient’s death. All in all, we felt we were afforded highly privileged access that was a consequence of the perceived legitimacy of doing something that might improve the situation for others yet to suffer from the illness. The reward for the respondents was to contribute to this end, encouraged by the undivided attention and often straightforward sympathy of the interviewer. One unexpected problem that emerged was whether the interviewer should ever contemplate intervening in a difficulty recounted in an interview. We were often aware of a worsening in a patient’s condition, and there were fourteen instances where, after obtaining patient or relative consent, I felt it appropriate to approach the clinical team. Eleven instances concerned the aggressive behaviour, worsening cognitive deficit or distress of the patients and three the distress of a relative. In five instances, this resulted in a change in management. In only one of the other instances did we attempt to do more: a second opinion was sought after a family appealed directly to us for help. The case and the conclusions are described in detail elsewhere (Davies et al., 1998). Although likely to be rare, this possibility should certainly be anticipated, discussed with clinicians and planned for by future workers.

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90 Elizabeth Davies

Some findings The study showed that as they began radiotherapy seventy-one of the seventy-five patients who could initially be interviewed understood that they suffered from a brain tumour. However, only one quarter (19/75) appeared to be aware of the poor prognosis. Of the rest, equal numbers were unaware or only partly aware, and aware patients were more distressed. Relatives, by contrast, were three times more likely to be aware of the poor prognosis and as a group were more distressed. Although twenty-nine of the seventy-five patients made negative comments about radiotherapy, in our first contact with them after the start of the treatment only thirteen were completely dissatisfied. As we followed up patients, we found evidence of a possible trade-off between quality and length of life. In terms of their reports of ability in hobbies and interests, household tasks, social life, self care or cognitive problems, only 40 per cent of patients achieved a period of stability or remission following radiotherapy (Davies et al., 1996b). Severely disabled patients appeared to gain little benefit whilst most of those less disabled we judged, using interview and clinical data, to have experienced significant adverse effects such as deterioration or tiredness (Davies et al., 1996a). However, despite this initial dissatisfaction expressed by patients about radiotherapy, we could not find evidence that this increased and it remained at about the same onefifth throughout. We suggested that part of the explanation for patients’ limited awareness seemed to lie in the fact that their relatives and doctors had protected them. Also, that the coping strategies of patients, and perhaps some cognitive deficits, served to produce a strong hope for a better outcome. This made it difficult to explore directly with patients the possible trade-off between quality and length of life. We concluded that to conceptualise questions of trade-off as rational choices ignored the social and emotional context of life-threatening illness and that hope itself may be an important component of quality of life in such situations (Davies et al., 1996b).

Reactions from a medical audience The ‘sin of subjectivism’ As noted earlier, the first publications in the British Medical Journal drew a mixed response. In an accompanying editorial, Gregor and Cull (1996) suggested that cognitive and language deficits may have affected the ability of patients to take part in the interviews. They observed that the study ‘showed many of the problems that beset qualitative work’, referring to a recent paper by Mays and Pope (1995) which had called for more rigour in qualitative research. Quality of life assessment should, they felt, be grounded in clinical trials using established questionnaire measures and formal neuropsychological testing. They also suggested that the interpretation of side effects was based only on selected evidence and needed to be reviewed. In later correspondence Brada and colleagues (1997),

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Interviewing seriously ill patients 91 writing from the MRC Brain Tumour Working Party, suggested the results on side effects and their implications were ‘unpublishable’ and ‘ a travesty to evidence-based medicine to which the BMJ claims allegiance’. Guerrero et al. (1997) described the method as a ‘non-validated subjective rating scale’ and Salander and colleagues (1997) contested the concept of awareness of prognosis and the accuracy of its assessment. Other informal feedback suggested scepticism that interviews could elicit what patients ‘really thought’ about their prognosis because of the strong tendency to denial. There were also comments that qualitative and quantitative methods had been inappropriately mixed. To me, it is interesting how reminiscent this response is to some of the early criticisms of the results of LEDS research. Clearly there remains a strong perception that qualitative and quantitative approaches are different and should remain so. For some, socalled qualitative methods and interview research appear only to gain acceptance in so far as they provide initial insights or ‘interesting’ data. The dominant view still appears to be that a questionnaire measure can be developed to provide an objective answer to relevant clinical questions and the approach is inherently superior. Using data from patient interviews to deduce adverse effects and question the concept of treatment itself was perhaps also seen as a threat to professionalism. However, it was not all criticism. The introductory ‘Editor’s Choice’ in the British Medical Journal had introduced the paper as one that ‘reeks of the real world’. This comment has since been echoed by a number of experienced clinicians commenting informally along the lines that the results were fascinating, and that they matched their personal experience, ‘told it how it was’, ‘talked about real people’, and disclosed the ‘difference between appearance and reality’. One generously even described the method as a ‘human scientific approach’. This was heartening and now several years later it seems possible to conclude that we made a reasonable job of feeding back to the profession the feelings of patients and relatives and possibly to increase awareness of the importance of psychosocial and palliative care. One consequence was the use of the material to develop national clinical guidelines for best practice for treatment and psychosocial and palliative care (Davies and Hopkins, 1997) followed by a trial to implement these guidelines in three Scottish centres. Resources for developmental work The general success of the ‘qualitative’ investigator-based measures developed by Brown and his colleagues to predict ‘hard’ outcome measures now shows the futility of a general rejection of such methods. It could be said that the basic problem is more mundane: the approach is undoubtedly more labour-intensive and therefore more expensive than questionnaire research. For the average medical practitioner or funding body the results emerged too slowly. The two clinicians who conceived the study – Dr Charles Clarke and the late Dr Anthony Hopkins – had both felt that interview data made more intuitive sense and had no doubts about the approach adopted. Their clinical experience was that the key issues to tackle were those of

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92 Elizabeth Davies doctor-patient communication and the nature of family relationships. Although showing a touching faith in the value of the approach, even their patience was clearly stretched by the time taken for data collection and analysis – five years in all. There will always be a need to develop more cost-effective measures and there is no reason why this should not involve questionnaires as long as their development is closely linked with the kind of material I have outlined. Some attempt at this was made in our work; but perhaps due to my lack of experience an effort to shorten the interview and use a range of ratings was undertaken rather late in the day. Almost certainly, as in this enquiry, early forays in an area using such an investigator-based, conversational approach, are time consuming. Whether or not this is inevitable is less important than the recognition that there must in future be efforts to shorten the ‘instrument’. Since the issues tackled are relevant to much that occurs in hospital medicine there is reason to believe that in future a good deal of initial developmental work can be circumvented and a more restricted range of scales employed.

Comparing interview results with data from questionnaires Developing questionnaire items It is unfortunate that our interview data cannot be directly compared with questionnaire measures tackling the same issues, but at the time these did not exist. Osoba and colleagues (1996) recently developed a twenty-four-item questionnaire for patients with brain cancer. Items were suggested by discussions with health professionals and a patient and relative support group. They are grouped to reflect ‘emotional distress’, ‘uncertainty’, ‘visual disorder’, ‘motor dysfunction’ and ‘communication deficit’ with headaches, seizures, drowsiness, leg weakness, bladder control and treatment side-effects covered by single items. Most relate to neurological symptoms rather than to awareness of the prognosis, family coping or ability to function in key roles. The measure was assessed for test/re-test reliability on a sample of 105 patients and the authors confirmed that patient responses correlated with clinicians’ independent ratings of neurological status, motor deficit, dysphasia and confusion. They found that patients with dysphasia and motor deficit reported more emotional distress (measured in this case by a single item about feeling frustrated, agitated and angry), and that patients’ ratings on the ‘uncertainty’ scale correlated with increasing disability. The uncertainty scale included items about uncertainty about the future, worsening outlook on the future, setbacks in the condition and the disruption of family relationships. The authors also found that those with dysphasia and motor deficit were more likely to have deteriorated physically at follow up (Osoba et al., 1996). A later report showed relatives tended to rate patients as having more problems than patients rated themselves (Sneew et al., 1997). This measure clearly conveys something of the patient’s perception of his or her symptoms, but reveals little about their impact or meaning or how patients and

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Interviewing seriously ill patients 93 relatives deal with differences of opinion. The authors suggest, for example, that the correlation between uncertainty and disability may be because of items covering ‘setbacks’ and ‘disruption to family life’ within the uncertainty scale, and ‘these items may have a physical component’. Given the lack of any background material, such suggestions can at best be plausible possibilities. In this respect, a small qualitative interview study of only four patients with low-grade glioma (Koivukangas and Koivukangas, 1988) argued more persuasively for the importance of conceiving of quality of life in terms of ability to take part in usual social activities and roles. The authors suggested that this should be seen contextually in relation to the past and future roles of each patient. Another more recent study used interviews with nineteen patients with high-grade glioma to describe a range of cognitive manoeuvres that patients used to deal with the threat of the diagnosis. Using a psychoanalytic framework to analyse their findings, these authors judged that most of these patients were aware of the poor prognosis (Salander et al., 1996). I have no doubt about my view that a questionnaire-based enquiry would have been quite inappropriate for the profoundly sensitive issues in the study I have outlined. However, while this may often be the case, I think it is possible to conceive of an effective social science where questionnaire and interview methods can complement each other. The interviewer-based enquiry is often costly but its strengths are in the observation, insight and understanding it affords. The Expressed Emotion measures developed by George Brown and his colleagues in the 1960s show this potential. But where, as is usual, it is impossible to observe what we wish to study, it is possible in many instances to recreate a picture of what occurred by the encouragement of ‘stories’, and, of course, the observance of the feelings as they are recounted. Many benefits follow – including the ability to tackle time order and the ability to subsequently develop new ratings. The questionnaire also has its strengths. It is often excellent as a screening instrument, for example, for psychiatric disorder when followed by a more detailed investigation. It may also be useful as a predictive tool. Some measures of quality of life or perceived health are better predictors of outcome or even death than conventional measures of disease severity. However, such successes tend to be extended too far. Because of its ease of use and ability to generate data quickly, the questionnaire may become the core measure of the ‘condition’ and attempts made to correlate this with other questionnaire measures. As a method, it cannot explore the processes that might be involved in a particular feeling or state or give insight into causal mechanisms. Questionnaire measures of quality of life are often needed for trials of new treatments or interventions where interviews may not be feasible for the large numbers of patients involved. Although calls have been made to develop questionnaire measures out of interview data (Maguire and Selby, 1989), it seems all too often that this developmental phase is omitted. Items are instead derived from existing measures or from aspects that researchers think should be included and measures are not grounded in the experiences of the group they are intended to represent. Rather than validating the measure against interview data, scores are compared with measures of symptoms, disease stage or severity or another questionnaire

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94 Elizabeth Davies measure, thereby defeating the object of measuring the separate entity of quality of life. Most readings of the quality of life literature complain of the conceptual and methodological difficulties that abound and the variety of ways which different workers have attempted to operationalise quality of life. Given the profound importance of the issue, a combined agenda of interview and questionnaire research seems long overdue in the study of quality of life.

Acknowledgements This work was supported by the Cancer Research Campaign (Grant no. CP1017) and was carried out in the Department of Neurological Sciences, St. Bartholomew’s Hospital, London and the former Research Unit of the Royal College of Physicians of London. I thank Sue Hall and Maureen O’Connor for all their help interviewing patients and developing the scales and Dr Charles Clarke and the late Dr Anthony Hopkins for their support.

Note 1

Dr Jim Birley rather nicely summed up this stage as ‘doing research without knowing what the answer is going to be’, and reassuringly said he found it refreshing to find someone who ‘hadn’t got what they were going to find packaged up from the beginning’.

References Brada, M., Thomas, D., Rampling, R., Crawford, P., Burnet, N., Byrne, P. and Sokal, M. (1997) ‘Modern radiotherapy can give good quality survival for six months’, letter, British Medical Journal, 314, 899. Chappell, J. (1997) ‘Breaking bad news: the perspective of relatives’ in Davies, E. and Hopkins, A. (eds) Improving care for patients with malignant cerebral glioma, London: RCP. Davies, E. and Hopkins, A. (1997) ‘Good practice in the management of adults with malignant cerebral glioma: clinical guidelines’, British Journal of Neurosurgery, 11(4), 318–30. Davies, E., Clarke, C.R.A. and Hopkins, A.P. (1996a) ‘Malignant cerebral glioma I: Survival, disability and morbidity following radiotherapy’, British Medical Journal, 313, 1507–12. Davies, E., Clarke, C.R.A. and Hopkins, A.P. (1996b) ‘Malignant cerebral glioma II: Patient and relative perspectives on the value of radiotherapy’, British Medical Journal, 313, 1512–6. Davies, E., Hall, S., Clarke, C.R.A., Bannon, M.P. and Hopkins, A.P. (1998) ‘Do research interviews cause distress or interfere in management? Experience from a study of cancer patients’, Journal of the Royal College of Physicians of London, 32, 406–41. Editor’s Choice (1996) ‘The real world of brain tumours and mentally ill prisoners’, British Medical Journal, 312, (18 Dec).

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Interviewing seriously ill patients 95 Fallowfield, L.J. (1987) ‘Quality of life: the objective measurement of subjective responses to cancer and its treatment’, Cancer Topics, 6, 99–100. Funch, P.P. and Marshall, J.R. (1981) ‘Patient attitudes following participation in a health outcome survey’, American Journal of Public Health, 71, 1396–8. Glaser, B.G. and Strauss, A.L. (1965) Awareness of Dying, London: Weidenfeld and Nicolson. Green, S.B., Byar, D.P., Walker, M.D. et al. (1983) ‘Comparisons of carmustine, procarbazine and high dose methylprednisolone as additions to surgery and radiotherapy for the treatment of malignant glioma’, Cancer Treatment Reports, 67(2), 121–31. Gregor, A. and Cull, A. (1996) ‘Radiotherapy for malignant glioma’, British Medical Journal, 313, 1500–1. Guerrero, D., Hines, F., Sardell, S. and Brada, M. (1997) ‘Patients should be treated in specialist units’, British Medical Journal, 314, 899. Hinton, J. (1980) ‘Whom do dying patients tell?’, British Medical Journal 281, 1328–30. Koivukangas, P. and Koivukangas, J. (1988) ‘Role of quality of life in therapeutic strategies in brain tumours’, Health Policy; 10, 241–57. Kristiansen, M., Hagen, S., Kollevold, T. et al. (1981) ‘Combined modality therapy of operated astrocytomas grades III and IV. Confirmation of the value of irradiation and lack of differentiation of bleomycin on survival time’, Cancer, 47, 647–54. Larossa, R., Bennett, L.A. and Gelles, R.J. (1981) ‘Ethical dilemmas in qualitative family research’, Journal of Marriage and the Family, May, 303–13. Lishman, W.A. (1987) The psychological consequences of cerebral disorder, Oxford: Blackwell Scientific. Maguire, P. and Selby, P. (1989) ‘Assessing quality of life in cancer patients’, British Journal of Cancer, 60, 437–40. Mays, N. and Pope, C. (1995) ‘Rigour and qualitative research’, British Medical Journal, 311, 109–12. Osoba, D., Aaronson, N.K., Sneew, K., Hsu, M.A., Yung, W.K.A., Brada, M. and Newlands, E. (1996) ‘The development and psychometric validation of a brain cancer quality of life questionnaire for use in combination with a cancer-specific questionnaire’, Quality of life Research, 5, 139–50. Pinder, K.L., Ramirez, A.J., Bifulco, A., Harris, T.O. (1992) Coping with cancer. A schedule for measuring cognitive responses to a diagnosis of cancer, London:ICRF Clinical Oncology Unit, Guys Hospital and MRC Department of Social Policy and Social Science, Royal Holloway and Bedford New College. Salander, P., Bergenheim, T. and Henriksson, R. (1996) ‘The creation of protection and hope in patients with malignant brain tumours’, Society of Scienctific Medicine, 42, 985– 96. Salander, P., Bergenheim, T. and Henriksson, R. (1997) ‘Patients’ awareness of prognosis may be confounded by successful coping mechanisms’, letter, British Medical Journal, 314, 900. Sneew, K.C.A., Aaronson, N.K., Sprangers, M.A.G., Detmar, S.B., Wever, L.D.V. and Schorngel, J.H. (1997) ‘Value of caregiver ratings in evaluating the quality of life of patients with cancer’, Journal of Clinical Oncology, 15(3), 1206–17. Walker, M.D., Alexander, E., Hunt, W.E. et al. (1978) ‘Evaluation of BCNU and/or radiotherapy in the treatment of anaplastic gliomas. A co-operative clinical trial’, Journal of Neurosurgery, 48, 333–43.

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96 Elizabeth Davies Wroe, S.J., Foy, P.M., Shaw, M.D.W., Williams, I.R., Chadwick, D.W, West C. and Towns, G. (1986) ‘Differences between neurosurgical and neurological approaches in the management of malignant brain tumours’, British Medical Journal, 293.

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6

Expressed emotion Measuring relationships Julian Leff

The mental hospital – in the beginning The Medical Research Council Social Psychiatry Unit was set up under Sir Aubrey Lewis’s directorship in 1948. When George Brown joined the unit in 1956, the mental hospital was still at the centre of psychiatric services, although some pioneering superintendents had begun to discharge longstay patients who were stable and not conspicuously disabled. This change in policy at local level was of great interest to the members of the research unit since it antedated the introduction of the antipsychotic drug chlorpromazine, and hence represented a social innovation. The enthusiasm of the pioneers was somewhat dampened when it became evident that some of the patients discharged with such hopes had to be readmitted, but this setback represented a challenging question for the research team. What could it be in the lives of the patients resettled in the community that unbalanced their mental equilibrium? A study was mounted of 229 men discharged from psychiatric hospitals, 156 of them with a diagnosis of schizophrenia. Measurements were made of a large number of variables that might explain the readmission rate (Brown, Carstairs and Topping, 1958). In the event, the strongest link with readmission was the type of home to which patients were discharged. Unexpectedly, patients who left hospital to live with their parents or wives were more likely to need readmission than those who resided in lodgings or with brothers or sisters. It was also discovered that patients living with their mother had less chance of returning to hospital if they and/or their mother went out to work (Brown,1959). While this result could readily be explained as a consequence of the degree of the patient’s disability, it also hinted at the possibility of a deleterious effect of prolonged contact between patient and relative (Brown, 1985).

The trouble with families One did not have to search far for an explanation, since a psychoanalytic literature was already building up that identified the pathogenic family as the prime cause of schizophrenia (e.g. Fromm-Reichmann, 1948; Lidz and Lidz, 1949). However, none of these theoreticians had provided convincing evidence for their views (Hirsch and Leff, 1975). George Brown realised that it was crucial to develop a

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98 Julian Leff reliable method of measuring emotional relationships in families, including those between husbands and wives as well as parent–child relationships. It was astonishing that nothing of this kind existed in the 1950s, partly due to the fact that family therapy was only introduced during that decade. Brown was joined by Michael Rutter, whose interest lay in the emotional impact of neurotic parents on their children. Together they developed a method of measuring emotions and relationships from audio-taped interviews with patients and their relatives. The main development work was done with married couples, and only later on was the work extended to include the parents of people with schizophrenia (Brown, 1985). The schedule they constructed was dubbed the Camberwell Family Interview (CFI). At first they conducted interviews with the relative individually and then with the relative and patient jointly. As they gained experience with the technique, they retained only the interview with the relative which produced the most useful data.

The measuring instrument The concept was named Expressed Emotion (EE) – in some ways an unfortunate choice since its association with a poor outcome for schizophrenia has led some professionals to infer that all emotions should be suppressed. This incorrect interpretation has given EE a bad press when, in fact, only negative emotions are used to constitute the index of EE, while warmth has a beneficial effect on people with schizophrenia. By now, however, the term and its acronym have become enshrined in the literature, in psychiatric culture, and even in examinations, so that it is too late to substitute a more accurate label. The expressiveness of the voice The main components of EE are critical comments, hostility, over-involvement and warmth. Positive comments are also measured but no study has shown them to be useful. The rating of critical comments, hostility and warmth is heavily dependent on the way in which the respondent uses their voice to express feelings, whereas the judgement of over-involvement also takes into account reported behaviour. It is evident that the ways in which the voice is used to convey emotion vary by individual, by region, by culture and by language. How, then, can the assessment be standardised? The answer is that each respondent acts as his or her own standard while cultural factors are inevitably taken into account. In everyday life, we can very quickly accommodate to a person’s style of emotional expression. In the CFI, this is probably also done without much thought, but it is, of course, essential to listen to a section of the recording to establish the interviewee’s usual range of vocal expression, attending to rate, volume, pitch and tonal changes. It is then possible to judge when a passage is more highly charged with emotion. Because the rater’s judgement is based on the particular subject’s habitual style of vocal delivery, the technique can be used in any culture and even works in tonal languages such as Chinese (Putonwa) where changes in tone are

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Expressed emotion: measuring relationships 99 used to alter the meaning of phonemes (Xiong et al., 1994). I doubt that the originators of the technique were aware of the remarkable cultural flexibility that they had built into the instrument, since it did not become fully evident until the first study in a non-European language was successfully completed (Leff et al., 1990). What emotions is EE measuring? A question that is often asked is what emotions are represented by the components of the EE scale, since critical comments, hostility, over-involvement and warmth are not in themselves primary emotions as identified, for example, by Ekman and colleagues (1968). The vocal qualities that characterise critical comments clearly convey anger. Consequently, a count of critical comments is an indication of how angry the respondent gets with the patient. A high proportion of respondents, about one third of the London samples, make no critical comments at all, and hence are assumed to be tolerant of the patient’s symptoms and behaviour. A handful of respondents lie at the extreme upper end of the distribution, making forty or fifty critical comments in the course of the CFI, equivalent to a ‘machine gun’ rate. Observations of direct interactions between patients and their relatives confirm that critical relatives get involved in angry exchanges with the patient which they seem unable to avert or to step aside from (Hooley and Hahlweg, 1986). These sequences of escalating anger are likely to end in physical violence, and it is characteristic of some high EE families that they call in the police. By contrast, low EE relatives rarely get caught up in angry exchanges. They do not seem to be provoked to anger by the patients. Furthermore, they have developed effective strategies to defuse tense situations. These often involve distracting the patient with a task that will take him or her out of their presence. For example, one mother would ask her son to take the dog for a walk when he began to show signs of anger. Hostility is defined as a sequence of critical comments about a variety of the patient’s behaviour expressed spontaneously by the respondent. Hence it represents an intense degree of anger. Another form of hostility is recognised when the respondent criticises the patient’s personal qualities, as opposed to their behaviour. This amounts to rejection of the patient, not in itself an emotion, but a consequence of uncontrollable anger and frustration. Over-involvement is rated as present when any one of four qualities characterise the relative’s responses: over-emotionality, over-protectiveness, excessive selfsacrifice, and over-identification with the patient. Apart from the first, these are not emotions but behaviours. Work with over-involved relatives during a number of years has made it clear that the emotional wellsprings of these behaviours are anxiety and guilt. Over-involvement is most commonly shown by mothers, and occasionally by fathers, but rarely by other kin. Indeed, it was only when George Brown extended his preliminary investigations with married couples to the parents of schizophrenic patients that he became aware of the need to develop a scale for over-involvement (Brown, 1985). Parents whose child develops schizophrenia always feel responsible for the patient’s illness. This is understandable, since any

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100 Julian Leff psychological disturbance in a child is likely to prompt the parents to question where they went wrong. Unrelieved guilt leads to reparative attempts to make things better for the child, and in its extreme form can mean taking over and doing everything for the sick person. Unfortunately, this has the effect of undermining the person’s skills and confidence, so that in the long run over-protectiveness impedes the person’s recovery. It also fosters dependence of the sick person on their relative. The patient then becomes anxious about the prospect of having to cope without the constant attention of their relative, and develops an over-protective attitude towards them. A symmetrical relationship results, in which each partner is anxious about and over-protective of the other. The measurement of warmth depends heavily on vocal qualities with smiling being a common accompaniment; in the CFI it often conveys an empathic attitude by the relative. Such relatives are more able to identify aspects of the patient’s behaviour which are a product of the illness, and to make allowance for them. By contrast, critical relatives typically fail to recognise that schizophrenia often incapacitates the patient in areas of daily life. Patients who are unable to get up in the morning, who fail to wash regularly, or who do not participate in household tasks are criticised for being lazy and selfish. This is reflected in the fact that 70 per cent of critical comments were found to focus on these negative symptoms of schizophrenia rather than on the florid symptoms of delusions and hallucinations (Leff and Vaughn, 1985). Relatives who are high on warmth are not only rarely critical but also provide emotional support to the patient. The ways in which some relatives are able to actively assist the patient to cope with the illness are explored in more detail later in this chapter.

The link between EE and the course of schizophrenia The first study to employ the EE measure and relate it to the course of schizophrenia was conducted by Brown, Birley and Wing (1972). This built on the findings of an earlier study (Brown et al., 1962), but included women as well as men with schizophrenia, and also used the newly developed Present State Examination (PSE) and the associated CATEGO programme (Wing, Cooper and Sartorius, 1974). Patients were followed up for nine months after they returned home from hospital. Relapse was defined as a recurrence of schizophrenic symptoms in those who were free of them on discharge, or an exacerbation of persisting symptoms. Readmission to hospital has not been used as an indication of a poor outcome because it depends on a multitude of factors, including the degree of tolerance of the patient’s behaviour by the relatives, and local policies on community care. Relapse of schizophrenia was found to be more likely if the relative made more than six critical comments, expressed any hostility, or scored above two on the over-involvement scale. However, if the relative scored low on these negative emotions, but high on warmth (four or five), relapse was less likely to occur. This study also confirmed the protective effect of low social contact with a relative who scored high on the negative emotions. An index of EE was constructed from the scores on critical comments, hostility and over-involvement. If one relative in the

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Expressed emotion: measuring relationships 101 household scored high, the household was characterised as high EE. However, when there were two parents present they were usually congruent with respect to their EE levels. The findings of this study were successfully replicated some years later, but a group of patients with depressive neurosis was added to determine whether the association was specific to schizophrenia (Vaughn and Leff, 1976). We found that almost all the depressed patients were living with spouses, whereas only half of the schizophrenic patients were. Spouses of depressed and schizophrenic patients were equally critical, but over-involvement was virtually confined to parents, as Brown had discovered during the development of the EE measure. Whereas we found six critical comments to be the threshold that produced the greatest separation in relapse rates of schizophrenia between high and low EE households, for the depressed patients the best cut-off was two critical comments. We interpreted this as meaning that depressed patients are even more sensitive to criticism than people with schizophrenia. It was another fifteen years before we took up the thread of this story, because we were preoccupied with advancing the research on schizophrenia. Meanwhile, numerous replications of the association between EE and relapse of schizophrenia were appearing in print. This was largely due to the establishing by Christine Vaughn of a regular training course in administering the CFI and rating EE. The course is held twice a year for about ten trainees, each of whom has to submit a research protocol before being accepted for training. The course lasts two weeks, and trainees have to reach an inter-rater reliability of 0.8 or above on all component scales to be accredited as EE raters. This degree of quality control is essential to ensure that researchers around the world employ comparable methods of assessment. There have now been more than thirty published studies of relatives’ EE and the course of schizophrenia. Kavanagh (1992) reviewed twenty-six of these and found that the median relapse rate was 48 per cent for patients living in high EE households and 21 per cent for those in low EE households. A more recent aggregate analysis by Bebbington and Kuipers (1994) of data from 1,346 patients confirmed the association between relatives’ EE and relapse, and also the protective effect of low face-to-face contact for patients in high EE homes. They also examined the effect of gender and found that, although women with schizophrenia had a better outcome than men, the associations held true for both sexes. The odds ratio for relapse in high EE compared with low EE homes was 4.30 for men and 4.37 for women. The link between relatives’ EE and schizophrenic relapse is one of the most firmly established relationships in the field of psychiatry. However, the direction of cause and effect cannot be determined by naturalistic studies. Attempts have been made to explore the possibility that relatives’ EE is a response to the patient’s disturbed behaviour. Brown et al., (1962) excluded patients with severe symptoms or markedly embarrassing behaviour rated on discharge, and found that the association between relatives’ emotional attitudes and patients’ relapse persisted. Numerous subsequent studies have replicated this finding, making it unlikely that the patients’ behaviour or symptoms mediate the relationship between relatives’ EE and outcome. However, any one of a number of factors could be responsible.

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102 Julian Leff

Studies of interventions in families One approach to this problem is to intervene in the family with the aim of changing the emotional atmosphere in the home. If this were successful and were to be accompanied by a reduction in the relapse rate, it would constitute a strong argument for a direct effect of EE on the course of schizophrenia. Following our successful replication of the study by Brown, Birley and Wing (1972), we embarked on an intervention study with the primary intention of elucidating the relationship between EE and relapse, but recognising that an efficacious intervention would represent a new form of treatment for schizophrenia. Our strategic aims were to reduce high EE to low, and/or high contact to low: either should lead to a reduced relapse rate if the family emotional environment was directly influential. We developed an intervention consisting of education about schizophrenia, problem solving, improving communication, reducing EE and contact, expanding the family’s social networks, and lowering expectations (Kuipers, Leff and Lam, 1992). In the context of a randomised controlled trial, in which all patients were in high social contact with high EE relatives, the intervention proved effective in changing three quarters of the experimental families in the desired direction (Leff et al., 1982). The patients in the experimental families had a relapse rate of only 8 per cent over nine months compared with the control group rate of 50 per cent. In a second trial, we compared work with individual families in their own homes, including the patient, with a relatives group, from which patients were excluded. We found that the relatives group was better at reducing EE, while the family sessions were better at reducing social contact. At a two year follow-up, the patients had comparable relapse rates, which were significantly lower than those of patients in the first trial who received medication alone (Leff et al., 1990). These two studies provide reasonably strong evidence for a direct influence of the emotional atmosphere in the home on the patient’s illness (Leff, 1989). There have now been more than ten similar trials published, the results of which strongly support the efficacy of family interventions in improving the course of schizophrenia over and above the effects of maintenance medication. The Cochrane collaboration has now endorsed this conclusion (Anderson and Adams, 1996). Thus, after more than three decades, the study of family emotions started by George Brown has led to the creation of a new and efficacious treatment for schizophrenia.

Relatives’ EE and other psychiatric conditions Our original finding of an association between the EE of the spouse and the course of depressive neurosis has since been replicated in one study in Oxford (Hooley, Orley and Teasdale, 1986), and in another in Egypt (Okasha et al., 1994). This is reminiscent of the findings of Brown and colleagues about the importance of a severe interpersonal difficulty at onset and chronicity of depression (Brown and Moran, 1994: Brown et al., 1994). However, a recent study in Cambridge failed to replicate the association (Hayhurst et al., 1997).

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Expressed emotion: measuring relationships 103 Historically, the next condition to which measurement of EE was applied was eating disorders. Fischmann-Havstad and Marston (1984) working in Los Angeles, found that obese women who had lost weight were more likely to regain weight if their spouse was critical of them. There was a link with the work on depressive neurosis in that the same level of critical comments, two or above, predicted a poor outcome for both conditions. This was followed by research on anorexia nervosa which established associations both with dropping out of treatment and with the outcome of this disorder (Szmukler et al., 1985; Le Grange et al., 1992; van Furth et al., 1996). Work by Miklowitz et al., (1986, 1988) has established a relationship between relatives’ EE and relapse of bipolar disorders with the relevant threshold at six critical comments. Recently there have been publications linking relatives’ EE with childhood emotional and conduct disorders (threshold… dichotomised at 0 versus 1 plus, Schwartz et al., 1990), with the course of alcoholism (threshold 4, Fichter et al., 1997; threshold 6, O’Farrell et al., 1998), and with the outcome of psychological treatment for post-traumatic stress disorder (threshold 6, Tarrier et al., in press). The ubiquitous influence of relatives’ EE on a wide variety of psychiatric disorders has a number of important implications. First, it is evident that relatives’ EE cannot be a specific cause of relapse of schizophrenia since it is associated with so many other conditions. It appears likely that relatives develop high EE attitudes in response to any chronic or relapsing psychiatric illness. Second, it is not possible to postulate that high EE attitudes are an expression of a gene or genes for schizophrenia which family members share with the patient. This was unlikely from the start of the research, since George Brown began developing the measure with non-schizophrenic patients and their families, and subsequent work has confirmed his understanding. Third, once an association between EE and the outcome of any illness has been firmly established, there is an opportunity to test experimentally an intervention designed to change EE.

An intervention for depression Although we were intrigued by our original findings linking relatives’ EE with the course of depression (Vaughn and Leff, 1976), the research on schizophrenia absorbed all our energies until the 90s. A small number of studies on this topic were published subsequently, although it did not attract the same level of interest as the work on schizophrenia. However, a meta-analysis by Butzlaff and Hooley (1998) showed that the effect size for EE was significantly greater for mood disorders than for schizophrenia. Using a cut-off of three critical comments, the mean effect size for mood disorders was 0.45 compared with 0.30 for schizophrenia (t=1.93, p=.03). Of course, we had set out on our depression intervention study years before these results were published, but they add a post hoc justification to our boldness in proceeding on the basis of a handful of naturalistic studies. Whereas with the families of schizophrenic patients, a small group of us had started from scratch to develop a new form of intervention, in the case of depression we already had some idea of the kind of intervention we wanted to test. At the invitation of

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104 Julian Leff colleagues at the Marlborough Family Service, we joined a group of family therapists who were interested in evaluating their particular approach to working with families. After many months of discussion, a study was mounted which included a number of measures of family function. As it turned out, only EE showed dramatic changes in response to family therapy, with significant reductions in both critical comments and over-involvement (Asen et al., 1991). The therapy used with the experimental families was based on systems theory, with the assumption that the presenting problem was an indication of malfunction in the family system, which needed to be addressed as a whole rather than focusing on the one ‘sick’ member. Applied to a depressed person living with a critical partner, this approach rejects the role of the patient as salient, and focuses on the dysfunctional relationship. There are obvious links with the identification by Brown and Harris (1978) of vulnerability factors for the development of depression, one of which is the absence of a confiding relationship. However, the systemic approach goes further in negating the concept of a sick person and their healthy, though unsupportive, partner. This is not a fashionable view of depression in the current climate of biological theories about brain transmitters and vast publicity exercises by pharmaceutical companies to promote a multitude of antidepressant drugs. Interestingly, the public is far more impervious to these campaigns than the medical profession. Our original intention was to compare three different forms of intervention: antidepressant medication, couple therapy and individual cognitive therapy. The latter was included since it purports to tackle the problem of low self-esteem, which George Brown and colleagues have postulated to underlie vulnerability to depression (Brown et al., 1990). Unfortunately, the drop-out rate from the cognitive therapy was so high (eight out of eleven subjects) that we had to discontinue this arm of the trial. It is worth emphasising that, whereas in the studies of schizophrenia we added the family intervention to maintenance antipsychotic medication, in the case of depression, we were postulating that couple therapy would be an efficacious alternative to medication, both for treatment and prophylaxis. This implies a different conceptualisation of the two conditions. We view schizophrenia as basically the manifestation of a biological fault which, however, renders the sufferer very sensitive to their social environment. Thus medication is an essential bedrock of treatment, on which the family intervention is constructed. By contrast, pitting couple therapy against medication implies that any biological basis for depressive neurosis can be ignored in treatment. The trial was designed to include two phases – a treatment phase lasting up to one year followed by a prophylactic phase continuing for a further year. Therefore, subjects were randomised to a regime of antidepressant drugs or twelve to twenty sessions of couple therapy during the first year, after which both forms of treatment were discontinued and the subjects were followed up for a second year without treatment. The rationale for this is that a number of different forms of treatment, including drugs, cognitive therapy, interpersonal therapy, and marital therapy, have been shown to be efficacious in improving the symptoms of depression, but there is a high rate of recurrence. Therefore, the acid test of a treatment is whether it can prevent further episodes of depression.

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Expressed emotion: measuring relationships 105 We recruited subjects from both north and south London, as we had a research base at the Marlborough Family Unit as well as at the Maudsley hospital. We wished to include only patients living with a critical partner, defined as making two or more critical comments on the CFI. In the event, only five partners out of over 100 scored less than this and were excluded. Randomisation resulted in forty patients being assigned to couple therapy and thirty-seven to antidepressant medication. During the course of the first year of treatment, 56 per cent of subjects dropped out of drug treatment compared with only 15 per cent from couple therapy, indicating a strong preference for the latter. At the one year follow-up, patients in the couple therapy arm had improved more in terms of depressive symptoms than those on medication (Leff et al., in press). At the end of the second year, during which no treatment was given, the advantage of couple therapy was sustained. Thus, couple therapy was more efficacious than drugs in treating depressive symptoms and in preventing recurrence of depression in a subsequent year. It was also more acceptable to the patients and their partners than medication. We attempted to identify the mechanism by which couple therapy achieved its superior effect, by measuring self-esteem and EE at baseline and at the two-year follow-up. Self-esteem improved significantly and critical comments decreased significantly over the course of the trial, but to an equal extent in the two groups. This surprising result means that the greater benefit of couple therapy compared with drugs cannot be ascribed to its ability to reduce critical comments or increase self-esteem, although these may be important accompaniments of recovery from depression in general. Since no work was done with the couples in the drug group, the reduction in the partner’s critical comments could be simply an effect of time or be a consequence of an improvement in the patient’s behaviour and symptoms. Whatever the explanation, it is clear that there is a major difference between the findings for schizophrenia and those for depression. The family intervention for schizophrenia seems to have achieved its effect by reducing EE and/or social contact, whereas a reduction in EE does not explain the efficacy of couple therapy for depression. Further studies of intervention with depressed patients and their partners are needed before we can be sure of this conclusion, but it does at least suggest that other hypotheses concerning the factors that maintain depression should be considered. For example, severe marital difficulties which, according to the LEDS, prolong depressive episodes (Brown et al., 1994), do not inevitably involve critical comments, but can include extreme coldness and refusal to discuss troubling issues. Couple therapy may reduce this witholding behaviour on the part of the spouse. Moreover, even for couples where the stressor provoking the depression did not directly involve the marital relationship, increasing insight during therapy on the part of the spouse into the role of this provocation may mean his/her increased support with this stressor leading to one of the fresh start events identified as key precursors of depressive remission both in naturalistic (Brown et al., 1988) and in intervention (Harris et al.,1999) studies.

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106 Julian Leff

Relatives’ EE and physical illnesses In recent years EE has been measured in relation to physical illnesses. Associations with outcome are not nearly as impressive as in psychiatric conditions: two studies of diabetes, one in Britain (Stevenson et al., 1991) and the other in the US (Koenigsberg et al., 1993), have produced contradictory findings. A study of inflammatory bowel disease found that patients needing to have their bowel removed were much more likely to live with low EE relatives (Vaughn et al., in press). This is probably explained by the compassion evoked in relatives by severe illnesses which could not be controlled by medication. A study from a group in Milan has shown an association between relatives’ EE and the frequency of epileptic fits (Bressi et al., in press). More confirmatory evidence is required before interventions are planned, but some of these findings suggest that there may be opportunities to improve the course of physical illnesses by working with the patients' families.

EE in professional carers George Brown’s interest in the study of the emotional environment in the family was stimulated by the beginning of the deinstitutionalisation movement. Since those early days the majority of the psychiatric hospitals in England and Wales have been closed. Many of the former longstay patients are now living in group homes in the community, staffed by professional carers. This situation has come about because few relatives maintained contact with longstay patients during the decades they were in the asylums (Leff et al., 1996). Some of the group homes have high staffing levels, up to 1:1, and staff are necessarily in intimate social contact with the residents. In some ways the atmosphere in these houses is more like that of a family than a ward. Therefore it is not surprising that staff can develop high EE attitudes, although these take the form of criticism rather than over-involvement (Ball et al., 1992; Moore and Kuipers, 1992; Snyder et al., 1994; Willetts and Leff, 1997). The significance of these findings is that paid carers can become as angry with the patients as can family members, despite their professional training and stance. Furthermore, the behaviours that anger them are just the same as those that upset family members, namely the negative symptoms of severe mental illness. In view of the parallels between staff in group homes and relatives, we designed a training programme for staff which was firmly based on the intervention for families, although considerably briefer. We found that a programme of ten sessions was effective in altering staff attitudes: in particular they acquired a broader range of coping strategies and were more able to see things from the patient’s perspective (Willetts and Leff, 1997). This is equivalent to an increase in empathy, which is a key characteristic of low EE relatives.

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Expressed emotion: measuring relationships 107

Overview In writing about the discovery of Expressed Emotion, George Brown (1985) recorded his ‘incredulity that we could really have uncovered such a strong effect’. While his doubts must by now be stilled by the accumulation of an impressive body of evidence for the association of EE with the course of numerous psychiatric conditions, his surprise at what else has emerged from the research on EE must have grown exponentially. As described above, two completely new and efficacious forms of treatment have been developed on the basis of the EE measures – one for schizophrenia, the other for depression. Furthermore, the association of EE with the outcome of other psychiatric conditions and with some physical illnesses offers the hope that other innovative family interventions may be created in the future. Our experience with family work for schizophrenia and couple therapy for depression has taught us that each intervention needs to be tailored to the specific needs of the client group and the family constellations associated with it. The brilliant success of these endeavours largely rests on George Brown’s inspired recognition that family emotional relationships play a crucial role in the evolution of illness.

References Anderson, J. and Adams, C. (1966) ‘Family interventions in schizophrenia’, British Medical Journal, 313, 505–6. Asen, K., Berkowitz, R., Cooklin, A., Leff, J., Loader, P., Piper, R. and Rein, I. (1991) ‘Family therapy outcome research: A trial for families, therapists and researchers’, Family Process, 30, 3–20. Ball, R. A., Moore, E. and Kuipers, L. (1992) ‘Expressed emotion in community care staff’, Social Psychiatry and Psychiatric Epidemiology, 27, 35–9. Bebbington, P. and Kuipers, L. (1994) ‘The predictive utility of Expressed Emotion in schizophrenia: an aggregate analysis’, Psychological Medicine, 24, 707–18. Bressi, C., Bressi, S., Cerveri, G. et al., (in press) ‘Epilepsy and family expressed emotion: correlation with the clinical course and psychological variables’. Brown, G. W. (1985) ‘The discovery of Expressed Emotion: induction or deduction?’ in J. Leff and C. Vaughn (eds) Expressed Emotion in Families: Its Significance for Mental Illness, 7–25, London: Guilford. —— and Harris, T.O. (1978) Social Origins of Depression: a Study of Psychiatric Disorder in Women, London: Tavistock. —— and Moran, P. (1994) ‘Clinical and psychosocial origins of chronic depressive episodes. I: a community survey’, British Journal of Psychiatry, 165, 447–56. ——, Carstairs. G .M. and Topping, G. (1958) ‘Post hospital adjustment of chronic mental patients’, Lancet, ii, 685–9. ——, Monck, E. M., Carstairs, G.M. and Wing, J. K. (1962) ‘Influence of family life on the course of schizophrenic illness’, British Journal of Preventive and Social Medicine, 16, 55–68. ——, Birley, J. L. T. and Wing, J. K. (1972) ‘Influence of family life on the course of schizophrenic disorders: a replication’, British Journal of Psychiatry, 121, 241–58.

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108 Julian Leff ——, Adler, Z. and Bifulco, A.T. (1988) ‘Life events, difficulties and recovery from chronic depression’, British Journal of Psychiatry, 152, 487–98. ——, Bifulco, A. and Andrews, B. (1990) ‘Self-esteem and depression III. Aetiological issues’, Social Psychiatry and Psychiatric Epidemiology, 25, 235–43. ——, Harris, T.O., Hepworth, C., and Robinson, R. (1994) ‘Clinical and Psychosocial origins of chronic depressive episodes. II: a patient inquiry’, British Journal of Psychiatry, 165, 457–65. Butzlaff, R. L. and Hooley, J. M. (1998) ‘Expressed emotion and psychiatric relapse: A meta-analysis’, Archives of General Psychiatry, 55, 547–52. Ekman, P., Sorenson, E. R. and Friesen, W. V. (1968) ‘Pan-cultural elements in facial displays of emotion’, Science, 164, 86–8. Fichter, M. M., Glynn, S. M., Weyerer, S, Liberman, R. P. and Frick, U. (1997) ‘Family climate and expressed emotion in the course of alcoholism’, Family Process, 36, 202–21. Fischmann-Havstad, L.and Marston, A .R. (1984) ‘Weight loss maintenance as an aspect of family emotion and process’, British Journal of Clinical Psychology, 23, 265–71. Fromm-Reichmann, F. (1948) ‘Notes on the development of treatment of schizophrenics by psychoanalytic psychotherapy’, Psychiatry, 11, 263–73. Harris, T.O., Brown, G.W. and Robinson, R. (1999) ‘Befriending as an intervention for women with chronic depression in an inner city. II: The role of fresh-start experiences and baseline psychosocial factors in remission from depression’, British Journal of Psychiatry. 174, 225–33. Hayhurst, H., Cooper, Z., Paykel, E. S., Vearnals, S. and Ramana, R. (1997) ‘Expressed emotion and depression: A longitudinal study’, British Journal of Psychiatry, 171, 439–43. Hirsch, S. R. and Leff, J. P. (1975) Abnormalities in Parents of Schizophrenics, Maudsley Monograph No. 22, London: Oxford University Press. Hooley, J. M. and Hahlweg, K. (1986) ‘The marriages and interaction patterns of depressed patients and their spouses: Comparison of high and low EE dyads’ in M. J. Goldstein, I. Hand and K. Hahlweg (eds) Treatment of Schizophrenia: Family Assessment and Intervention, 85–95, Berlin: Springer. ——, Orley, J. and Teasdale, J.D. (1986) ‘Levels of Expressed Emotion and relapse in depressed patients’, British Journal of Psychiatry, 148, 642–7. Kavanagh, D. (1992) ‘Recent developments in expressed emotion and schizophrenia’, British Journal of Psychiatry, 160, 601–20. Koenigsberg, H. W., Klausner, E., Pelino, D., Rosnick, P. and Campbell, R. (1993) ‘Expressed emotion and glucose control in insulin-dependent diabetes mellitus’, American Journal of Psychiatry, 150, 1114–15. Kuipers, E., Leff, J. and Lam, D. (1992) Family work for schizophrenia: a practical guide, Gaskell: London. Leff, J. P. (1989) ‘Controversial issues and growing points in research on relatives’ Expressed Emotion’, International Journal of Social Psychiatry, 35, 133–45. —— and Vaughn, C. (1985) Expressed emotion in families: its significance for mental illness, Guilford: New York. ——, Kuipers, L., Berkowitz, R., Eberlein-Fries, R. and Sturgeon, D. (1982) ‘A controlled trial of social intervention in the families of schizophrenic patients’, British Journal of Psychiatry, 141, 121–34. ——, Wig, N., Ghosh, A., Bedi, H., Menon, D. K., Kuipers, L., Korten, A., Ernberg, G., Day, R., Sartorius, N. and Jablensky, A. (1987) ‘Expressed emotion and schizophrenia in North India. III. Influence of relatives’ expressed emotion on the course of schizophrenia in Chandigarh’, British Journal of Psychiatry, 151, 166–73.

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Expressed emotion: measuring relationships 109 ——, Berkowitz, R., Shavit, N., Strachan, A., Glass, I. and Vaughn, C. (1990) ‘A trial of family therapy versus a relatives’ group for schizophrenia, two year follow-up’, British Journal of Psychiatry, 157, 571–7. ——, Trieman, N. and Gooch, C. (1996) ‘Team for the Assessment of Psychiatric Services (TAPS) Project 33: Prospective follow-up study of longstay patients discharged from two psychiatric hospitals’, American Journal of Psychiatry, 153, 1318–24. ——, Vearnals, S., Brewin, C. R. et al., (in press) ‘The London Depression Intervention Trial: An RCT of antidepressants versus couple therapy in the treatment and maintenance of depressed people with a partner: clinical outcome and costs’, British Journal of Psychiatry. Le Grange, D., Eisler, I., Dare, C. and Hodes, M. (1992) ‘Family criticism and selfstarvation: a study of expressed emotion’, Journal of Family Therapy, 14, 177–92. Lidz, R. W. and Lidz, T. (1949) ‘The family environment of schizophrenic patients’, American Journal of Psychiatry, 106, 332–45. Miklowitz, D. J., Goldstein, M. J., Nuechterlein, K. H., Snyder, K. S. and Doane, J. A. (1986) ‘Expressed emotion, affective style, lithium compliance and relapse in recent onset mania’, Psychopharmacology Bulletin, 22, 628–32. ——, Goldstein, M. J., Nuechterlein, K. H., Snyder, K.S. and Mintz ,J. (1988) ‘Family factors and the course of bipolar affective disorder’, Archives of General Psychiatry, 45, 225–31. Moore, E. and Kuipers, L. (1992) ‘Behavioural correlates of EE in staff patient interactions’, Social Psychiatry and Psychiatric Epidemiology, 27, 298–303. O’Farrell, T. J., Hooley, J., Fals-Stewart, W. and Cutter, H. S. G. (1998) ‘Expressed emotion and relapse in alcoholic patients’, Journal of Consulting and Clinical Psychology, 66, 744–52. Okasha, A., El Akabawi, A. S., Snyder, A. S., Wilson, A. K., Youssef, I. and El Dawla, A. S. (1994) ‘Expressed emotion, perceived criticism, and relapse in depression: a replication in an Egyptian community’, American Journal of Psychiatry, 151, 1001–5. Schwartz, C. E., Dorer, D. J., Beardslee, W. R., Lavori, P. W. and Keller, M. B. (1990) ‘Maternal expressed emotion and parental affective disorder: risk for childhood depressive disorder, substance abuse, or conduct disorder’, Journal of Psychiatric Research, 24, 231–50. Snyder, K. S., Wallace, C. J., Moe, K. and Liberman, R. P. (1994) ‘Expressed emotion by residential care operators and residents’ symptoms and quality of life’, Hospital and Community Psychiatry, 45, 1141–3. Stevenson, K., Sensky, T. and Petty, R. (1991) ‘Glycaemic control in adolescents with Type 1 diabetes and parental Expressed Emotion’, Psychotherapy and Psychosomatics, 55, 170–5. Szmukler, G. I., Eisler, I., Russell, G. F. M. and Dare, C. (1985) ‘Anorexia nervosa, parental “expressed emotion” and dropping out of treatment’, British Journal of Psychiatry, 147, 265–71. Tarrier, N., Sommerfield, C. and Pilgrim, H. (in press) ‘The effect of the relatives’ level of expressed emotion (EE) on the outcome of psychological treatment of PTSD patients’, Journal of Traumatic Stress. van Furth, E. F., van Strien, D. C., Martina, L. M. L., van Son, M. J. M., Hendrickx, J. J. P. and van Engehand, H. (1996) ‘Expressed emotion and the prediction of outcome in adolescent eating disorders’, International Journal of Eating Disorders, 20, 19–31. Vaughn, C. and Leff, J. P. (1976) ‘The influence of family and social factors on the course of psychiatric illness: a comparison of schizophrenic and depressed neurotic patients’, British Journal of Psychiatry, 129, 125–37.

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110 Julian Leff ——, Leff, J. and Sarner, M. (in press) ‘Relatives Expressed Emotion and the course of inflammatory bowel disease’, Journal of Psychosomatic Research. Xiong, W., Phillips, M. R., Hu, X., Wang, R., Wang, Q., Dai, J., Kleinman, J. and Kleinman, A. (1994) ‘Family-based intervention for schizophrenic patients in China: randomised controlled trial’, British Journal of Psychiatry, 165, 239–47. Willetts, L. E. and Leff, J. (1997) ‘Expressed emotion and schizophrenia: the efficacy of a staff training programme’, Journal of Advanced Nursing, 26, 1125–33. Wing, J. K., Cooper, J. E. and Sartorius, N. (1974) The Description and Classification of Psychiatric Symptoms: An Instruction Manual for the PSE and CATEGO System, London: Cambridge University Press.

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7

Contextual measures and subjective appraisal Louise Lemyre

In the tradition of North American psychological research on stress, paper and pencil measurements have been long-time favourites. Given problems of validity and reliability of checklists and self-reports, Lazarus and Folkman’s book in 1984 Stress, Appraisal and Coping had come to many as a consolation for the difficulty of measuring life hardships in a consistent fashion: the quintessence of the stress experience laid in the subjective appraisal of threat. Certainly the work by Lazarus and Folkman has been a landmark in the field of psychological stress in America. It inspired a great number of research studies and fed the growing attention given to the role of cognition and emotion in mental health (Cronkite and Moos, 1984; Kanner et al., 1981; Vinokur and Caplan, 1986). It also brought an answer to some shortcomings and critics of life event checklists (Tausig, 1982; Zimmerman, 1983). It offered an alternative to the wide use of either counting raw numbers of ticked items or adding up generalised normative change weights (Holmes and Rahe, 1967). However, the popularity of the appraisal approach to stress engulfed much of the research in contamination and circularity (Delongis et al., 1982; Dohrenwend et al.,1984; Hobfol, Schwarzer and Koo, 1996; Ensel and Lin, 1991; Monroe, 1982). In physics, it is common practice to describe movements with respect to relative frames of references, especially so in the context of multiple motions. It has proven crucial to our understanding of impact. How well can we appreciate the speed of a train from the word of the traveller walking in one of its coaches? A better description of the situation is achieved by adding the reference frame of the engineer on the tracks or that of a bystander on the platform. Similarly, the dynamics of mental health, life-events, behaviours and cognition may also benefit from a multi-referential description. Influenced by Kurt Lewin’s (1951) Person–Environment formula, for my understanding of the stress process I needed an external frame of reference against which I could appreciate people’s appraisal of their life situation. I was interested in what conditions stressed people more than others. How did emotion, perception and cognition change with the course of events? Was it people’s view that changed or the circumstances they were in (Bandura, 1997) ? Did people ‘distort’ as most cognitivists put it, have ‘negative views’ or ‘positive illusions’ (Beck, 1976; Hammen and Mayol, 1982; Sarason, 1975; Taylor, 1983)? What part was ‘reality’

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112 Louise Lemyre playing? How accurate was people’s appraisal? How reliable? How consensual? The issue was not to find an ‘absolute stressing metric’ but to disentangle subjective appraisal from factual evidence so that by some triangulation one could better appreciate the role of individual differences, without necessarily evoking mental illness (Lemyre, 1987). In my quest for another referencing system, the work of George Brown and his colleagues provided me with a powerful tool for many of my queries. Social Origins of Depression (Brown and Harris, 1978) came as a revelation . Although my own interest lay more in the stress process in the normal population, I had found a meaningful psychosocial thesis of pathology. It was a comprehensive, integrative, articulated and powerful view of the forces in one’s life story: the rarest and finest combination of psychology, sociology, psychiatry and epidemiology. I had also found an accessible, feasible, realistic methodology. Maybe it was not perfect, maybe it was not 100 per cent accurate, but it was consistent and independent. After my post-doctoral training with the Bedford Square unit, I started to use the Life Event and Difficulty Schedule (LEDS) and its derived complements (for social support and coping) in my work on the cognitive apprehension process in stress, relating contextual and subjective evaluations of life circumstances. Appraisal became my dependent variable and the LEDS contextual ratings the anchor in assessing the environment input.

Subjective appraisal of joint events in couples The question of individual differences in appraisal has been difficult to document. How much of the variance is due to variation in the stressors being examined versus idiosyncrasies of either perception or reporting? Colette Biron (1993), one of my doctoral students, and I used the LEDS with couples consulting at fertility clinics. We relied on the interviews done independently with each spouse to: a b c

identify stressors common to both partners have their version of each stressor get their respective subjective appraisal in a self-reported format on scales matching in content the main ratings of the LEDS.

All interviews were rated blind to the other spouse version. We then identified stressors which were contextually rated as ‘joint’ events that should have been reported by both partners. Data supported the validity of the LEDS: 84 per cent of those rated as joint events were indeed reported by both partners, more so for ‘severe events’. We compared subjective appraisal ratings of the two partners for joint events that had been given the same contextual severity. (In some instances, joint events were given different severity ratings for each spouse.) We also analysed the differences in terms of whether those joint events were fertility-related or not. Appraisal was measured using a ten-item subjective appraisal rating scale yielding three main appraisal components: perceived impact (relating to threat, negativity, loss,

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Contextual measures and subjective appraisal 113 severity, undesirability); perceived mastery (relating to control, positivity, challenge); and perceived uncertainty (challenge, danger, unknown, lack of control). A significant main effect showed that indeed severe events were rated with more impact than non-severe events. Moreover, there was a gender effect. Women reported less mastery and more perceived uncertainty than their partners about both fertility and non-fertility events of the same contextual threat. There was also an interaction effect: discrepancies between genders were stronger for chronic difficulties than for events. Women reported higher impact for chronic difficulties, even for contextually mild difficulties, and much more so than their partners. Men reported on the whole that chronic difficulties had little impact. Using multiple regression we found women’s distress was related to the interaction between contextual severity and their appraisal of impact and of uncertainty. The only significant predictor for male distress was appraisal of mastery, independently of contextual severity. The LEDS provided us with a unique tool to compare responses of spouses to a common situation. The contextual approach ensured that where ratings were comparable, there was an objective and replicable standard that could be related to their subjective responses. As just noted, the subjective impact of events blindly rated as objectively non-severe, was greater for women and much more so for chronic difficulties at all levels of severity. There was also a main effect for gender on appraisal of mastery and a trend towards a similar effect for appraisal of uncertainty. It also looked as though appraisal played a different role in non-severe circumstances than in severe conditions. Thus investigation of cognition, distortion or illusion should not presume a linear relationship. Only the rating system of the LEDS, where contextual and subjective threat/unpleasantness are distinguished, could have provided us with such discriminating results. Nazroo, Edwards and Brown (1997) carried out a somewhat similar study of couples especially selected because they had experienced a common severe life event. Instead of emphasising differences in subjective response, they focused on the development of clinically relevant depression, and found the marked excess of depression among women was due to their greater sensitivity to severe events involving children, procreation and housing. Rates of onset following all other types of severe event were comparable between the genders. In both studies the LEDS therefore provided a scaffolding from which gender difference in response could be fruitfully explored.

Subjective and contextual evaluations in anticipation of events The longitudinal design of the infertility study also provided us with an opportunity to investigate anticipated events. Life event research has concentrated on the impact of events occurring in a defined period, mostly in the past six, twelve or more months (Dohrenwend and Dohrenwend, 1974; Kessler et al., 1991; Thoits, 1982). But on occasion events that are anticipated may also be of relevance. Some work on anticipation has been done by Frankenhauser (1980), Antonovsky

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114 Louise Lemyre (1979), Arthur (1987) and Gjesme (1983) but only in very specific experimental settings. Much is still to be learnt about the process of anticipating events (Gardner et al., 1992; Mechanic, 1962). George Brown and colleagues had allowed in the LEDS coding system for forecast events. A threat rating is made for any intimation of a major change likely to happen. Also, the LEDS includes a danger scale which relates to the threat of a future development in an event. With Manon Truchon (1995), we expanded on the LEDS coding system to: a

b

create investigator-based ratings for situations that might be expected to be anticipated, given the context. (For example, a housing move for a couple in fertility treatment living in a studio, or a financial difficulty if the woman was the only bread-earner with no work compensation benefits.) include events that were subjectively anticipated by the respondent irrespective of the degree to which the current circumstances justified this, and rate them on contextual severity with a special code. Along with these was an estimate of the likelihood of occurrence in the next year.

Although this exercise was unprecedented, agreement between partners interviewed independently about such reported anticipated future events was 67 per cent. Inter-rater agreement on severity of threat and the other major scales yielded a value of ‘kappa’ similar to that for events that had actually occurred. On a test/retest sub-sample, 90 per cent of anticipated severe events were repeated. The expanded LEDS thus appeared to provide reliable means of gathering data on anticipated events. Overall, the events anticipated reflected those that had already occurred. Proportions of events were similar across domains for past events and future events except for the health domain. Although in terms of the past twelve months health events had been the most frequently reported, they were the least anticipated for the next twelve months. The overall number of anticipated future events was correlated to the number reported in the prior twelve months. However, proportionally more positive events were anticipated than had occurred in the past twelve months. Women anticipated far more events than men. Finally, the number of events anticipated related to feelings of current stress even when the contribution of recently occurring events was controlled. This line of work, although at present somewhat tangential to the main thrust of research, attests in its own special way to the power and flexibility of the LEDS system. Over the last twenty or so years, it has become clear that one of its major assets is the way in which new scales can be developed and – it might be added – encouraged by the richness of the data collected by routine LEDS usage. In my experience, there is no sense of being locked into an unmalleable instrument; and where a new problem is being tackled it is an ideal platform from which to develop insights and new scales (Costello and Devins, 1988). Furthermore, the conceptualisation of the contextual frame of reference permits a systematic derivation for each psychosocial variable of its mirror images, first from the respondent’s perspective and second, from the observer’s perspective (i.e. the investigator).

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Contextual measures and subjective appraisal 115

Figure and background changes: peripheral versus focal stressor The LEDS also provided us with a window on to the appraisal process that takes place in the context of an unfolding event. One study allowed us to gain some insights on how appraisal of one stressor depends on the co-existence of other stressors. With Lise Fillion (1993), women who were going through a biopsy for suspected breast cancer were interviewed before surgery, after diagnosis and at about six months follow-up, about their life as a whole. One of our interests was how far their appraisal of LEDS-type events and difficulties would change in time and be modified by the tumour’s status. Women described in a LEDS format interview the discovery of the suspicious lump in their breast as well as their other events and difficulties. These were rated according to the LEDS guidelines by a team of trained assistants. Women also filled in at each study point a subjective appraisal rating scale relative to: a b

their tumour their worst other stressor.

Thirty women with a malignant tumour were matched on age, income, education and marital status with one of sixty with a benign mass. Among the striking results was the fact that levels of reported stress were lower at follow-up for the cancer group than the benign group. Moreover, although for the great majority of women the contextual (i.e. objective) severity of their worst other stressor – called here the peripheral stressor – did not change through the study period, their appraisal of this continuing difficulty did change – generally in the direction of lesser stress. There was also an interaction effect associated with tumour status. For the benign group, the peripheral stressor lost perceived importance during the diagnosis period but regained its level of preoccupation after the biopsy results. For the malignant group, the peripheral stressor remained at a lower level. These results speak of the relativity of the appraisal process. They probably accurately indicate how cognitions change according to the context but they also, on a more pessimistic note, underline their unreliability as a metric when a person is living through a developing crisis.

Variation in appraisal for a constant context Similarly, with Lisa Sweet (1999) we used the LEDS in the earlier stage of breast cancer screening with women age 50 and more, without specific risk factors (no personal nor family history of cancer), participating in a mass prevention programme. Among 800 women who filled appraisal ratings at three different points in time (T1: prior to screening; T2: awaiting results; T3: post results). Three months later, 120 were seen at a follow-up interview (T4). Half of these had received within days of their screening a false positive result based on either their

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116 Louise Lemyre clinical palpation or mammogram. The other half had received a perfectly negative screen result. All were actually cleared from any detectable malignancy within a few weeks and were known to be healthy at time of interview. Despite the fact that those with a negative screen result were at the same level of contextual severity throughout the screen process, their appraisals varied a good deal – both between the women and across time. As expected, subjective severity tended to diminish with time and there was for many women a positive change even before the screen results were known. Again, appraisal appeared to be a highly labile process and to use it as the sole indicator of the stressfulness of a situation, as is commonly done, may, on the basis of these findings, be misleading. Our results also call attention to some paradoxical effects of the screening procedure for breast cancer in the sense that in some instances it inappropriately and prematurely reassured women on their personal health while it led to over-estimated populational risk.

‘I know what I do’ or ‘I know what to do’: rating reported coping In the same study with Joanne Savoie (1999), we looked at coping using a LEDStype technique of rating coping. Congruent with a meta-analysis of the literature (Carver and Scheier, 1994; Endler and Parker, 1990; Pearlin, 1991), four coping scales were rated, based on accounts of behaviours and plans: cognitive approach, cognitive avoidance, behavioural approach and behavioural avoidance. Compared to the moderately low reliability of self-reported coping questionnaires, this measure (the LEDS-Cope) obtained good stability. Inter-rater agreement was around .90, test/retest was very high at .95. However, the concordance between the respondent’s self-rating and the investigator’s rating of the person’s coping was very low, correlating only .30. Women reported more active coping than judged by investigator-based ratings. Conversely, they reported less avoidant coping than was estimated. Analyses comparing groups and times revealed significant differences only on the contextual measures and not on subjective appraisal. For example, women who had been screened as positive were rated with less behavioural approach coping at T2 and T3 and with more avoidance post-results. Self-reported coping strategies did not differ in a consistent fashion between times or across screen results nor predict distress. To our knowledge this is one of the first studies contrasting a self-reported measure of coping with an investigator-based one. It proved very helpful in pinpointing the subtleties of the construct of coping and the difficulties in its measurement. Coping scales have been known to show weaknesses but few studies have actually targeted those deficiencies. The differences between self-reports and investigatorbased ratings are a matter of hypotheses themselves. It could be that people are unreliable reporters, bad observers of themselves, too susceptible to the effects of social desirability, biased towards the positive illusion of being a good coper, or just telling us that they know what they should do almost in an effort to actually

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Contextual measures and subjective appraisal 117 induce in themselves the desirable answer. It is yet to be further explored. The investigator-based system of Brown and colleagues is a golden tool for doing it.

The use of investigator-based measures such as the LEDS The fundamental characteristic of the LEDS is that it relies on ratings independent of the respondent. The investigators make the judgments. The power of the approach is its flexibility and ability to tackle a surprising range of difficult questions. Certainly, since it still relies on information provided by the respondent, it is open to potential bias. This is true. But to the extent that the questioning attempts to reconstruct actual coping and other behaviour in the course of discussing the development of the crisis, it may well provide a reasonable approximation of what occurred. Direct observations would be preferable but are rarely possible. The flexibility of the LEDS also allows the derivation of new scales custom-made for particular objectives, and the procedure to be followed in developing new scales is now well rehearsed and documented (see chapters 1 and 5 in this volume). One only needs to define the scales and establish their reliability. But I should be honest. There is a love-hate relationship with the LEDS-system! It costs so much in time, effort, details and agonies. Yet once you have found this level of refinement of information, you cannot go back to bulk undifferentiated data. I cannot live without it!

For a Galilean psychology In conclusion, I would like to advocate an understanding of psychological processes with more built-in relativity. Especially for psychologists who tend to put the burden of mental health on the psyche of the person, it is good to be made more aware and reminded of the weight and inertia of life adversities. Contextual severity has a main effect. Subjective appraisal may add an interaction effect. We should also convey how mental health is a two-way road. Once distress has set in the course of appraisal is modified. Following Copernicus, I would like to challenge the common belief that the Self is the centre of the psychological universe. I rather conceive the Self in orbit around life circumstances whose severity determines the gravitational force. Our role might be to describe constellations that allow comets to change their course. In this perspective, the etiological model elaborated by Brown and colleagues which articulates a structural chain with an affective chain to describe a final common pathway leading to depression (Akiskal and McKinney, 1973) is a sophisticated integration of sociological factors, psychological processes and psychiatric states. Like Galileo’s telescope, the LEDS is the tool to disentangle the various forces involved in the system and help identify the various components. To understand the complexity of the galaxy of life experiences we need more empirical observations about the sequencing of events, emotions, behaviours and cognition. It calls for a double axis paradigm: subjective and contextual.

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118 Louise Lemyre

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Contextual measures and subjective appraisal 119 Kanner, A. D., Coyne, J. C., Schaeffer, C. and Lazarus, R. S. (1981) ‘Comparison of two modes of stress measurement: daily hassles and uplifts versus major life events’, Journal of Behavioral Medicine, 4, 1–39. Kessler, R. C., Price, R. H., and Wortman, C.B. (1985) ‘Social factors in psychopathology: Stress, social support, and coping processes’, Annual Review of Psychology, 36, 531–72. ——, Kendler, K.S., Heath, A., Neale, M.C., and Eaves, L.J. (1991) ‘Social support, depressed mood and adjustment to stress: a genetic epidemiologic investigation’, Journal of Personality and Social Psychology, 62, 257–72. Lazarus, R. S ., and Folkman, S. (1984) Stress, appraisal, and coping, New York: Springer. Lemyre, L. (1987) Stress et appréhension cognitive, unpublished doctoral thesis, Université Laval, Quebec, Canada. Lewin, K. (1951) Field theory in social science, New York: Harper.Free Press. Mechanic, D. (1962) Students under stress, New York: Free Press of Glencoe. Monroe, S. M. (1982) ‘Life events assessment: Current practices, emerging trends’, Clinical Psychology Review, 2, 435–53. Nazroo, J.Y., Edwards, A.C. and Brown, G.W. (1997) ‘Gender differences in the onset of depression following a shared life event: a study of couples’, Psychological Medicine, 27, 9–19. Pearlin, L.I. (1991) ‘The study of coping’ in J. Eckenrode (ed.) The Social Context of Coping, New York: Plenum Press. Sarason, I. S. (1975) ‘Anxiety and self-preoccupation’ in I.S. Sarason and C.D. Spielberger (eds) Stress and Anxiety, vol 2. 27–43, Washington: Hemisphere. Savoie J., (1999) Contextual and Subjective Indices of Coping Strategies in Breast Cancer Screening: A Longitudinal Study, unpublished doctoral thesis, University of Ottawa, Canada. Sweet, L., (1999) Stress, Subjective Appraisal and Anticipation in the Context of Breast Cancer Screening: A Longitudinal Study, unpublished doctoral thesis, University of Ottawa, Canada. Tausig, M. (1982) ‘Measuring life events’, Journal of Health and Social Behavior, 23, 52–64. Taylor, S. E. (1983) ‘Adjustment to threatening events: A theory of cognitive adpatation’, American Psychologist, 1161–73. Thoits, P. A. (1982) ‘Life stress, social support and psychological vulnerability: Epidemiological considerations’, Journal of Community Psychology, 10, 341–62. Truchon, M. (1995) Evenements de vie anticipés et stress psychologique chez des couples en démarche reproductive, unpublished doctoral thesis, Université Laval, Quebec, Canada. Truchon, M. and Lemyre, L., (1995) ‘Les événements anticipés comme stresseurs’, Santé mentale au Québec, 20, 2, 77–98. Vinokur, A., and Caplan, R.D. (1986) ‘Cognitive and affective components of life-events: Their relations and effects on well-being’, American Journal of Community psychology, 14, 351–70. Zimmerman, M. (1983) ‘Methodological issues in the assessment of life events: A review of issues and research’, Clinical Psychology Review, 5, 339–70.

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Part III Model building

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8

Negative life events and family negativity Accomplishments and challenges Michael Rutter

The research agenda of the psychopathological effects of negative life events and family negativity was, to a very considerable extent, set by George Brown and his colleagues during the 1960s and 1970s (Brown, 1972; Brown, Sklair, Harris and Birley, 1973; Brown, Harris and Peto, 1973). Of course, an interest in these topics, and a concern over their effects, goes back a very long way. What marks out George’s contribution as providing a quantum leap ahead is the way in which he took the topic and systematically set about determining what research was needed in order to test the rather inchoate, but important, ideas then prevailing about the possible role of life stresses and adversities in the origins and course of mental disorder. George would undoubtedly claim that he set about this task from the perspective of medical sociology but, in actuality, what he did cannot sensibly be reduced to the concepts and methods of one discipline. In my view, there are four key qualities that marked George out as different from most of his colleagues then, and still do today. First, of course, there was a very firm recognition of the potential importance of psychosocial influences and, hence, a determination to take these seriously and rigorously test their effects. Second, there was, as there has been throughout George’s career, an abiding concern for clarity of conceptualisation. A general notion was never good enough for George; he had to translate it into something that had both theoretical and practical implications and to do so in a way that was testable. Third, there was a consistent asking of provocative questions about the meaning of experiences and about the mechanisms involved in mediation of risk and protective processes. Fourth, there was a very firm commitment to the need for good hard-headed measurement. Sociologists were once described as people who studied disadvantaged data, but George sought to ensure, that even if his subjects were disadvantaged (the fact that usually they were reflected his concerns), his data were not. Social and behavioural sciences today are going through one of their recurrent periods of agonising over a supposed neglect of qualitative research methods (Feagin, 1999). Although, curiously, this is something that I have never discussed with George, I have no doubt that he would exhibit impatience over a false dichotomy. If you are to study the real meaning of experiences, research is going to have to use qualitative approaches but, equally, if hypotheses on the consequences of the meaning of

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124 Michael Rutter experiences are to be taken seriously, quantification will be crucial (Coverdill et al., 1994; Kidder and Fine, 1987; Seale, 1999).

Development of the Camberwell Family Interview I first got to know George in 1962 when I joined the MRC Social Psychiatry Unit. The two of us quickly realised that we shared many research interests and were similarly committed to the need to span good conceptualisation, a concern for meaning, and a respect for rigorous measurement. We worked closely together to develop what subsequently came to be known as the Camberwell Family Interview. This proved to be a highly rewarding partnership that was great fun and which worked remarkably well in producing good research tools. Working with George was not always easy because he is an argumentative fellow, not unduly troubled by self-doubt (as I think he would be the first to admit). What made it all immensely interesting and worthwhile, however, was the fact that both of us felt impelled to understand the phenomena we were investigating and were dedicated to the production of practical tools of measurement. George was always full of creative ideas and he would press his point of view hard. Despite that, he has always been immensely responsive to other people, very interested in their ideas as well as his, and he loved the serious game of intellectual ‘battle’ that is designed to provide understanding and to solve important problems. Looking back on the development of the Camberwell Family Interview, I think that it achieved several important things. Most crucially, perhaps, it established that it was possible to devise reliable and valid methods of measuring qualities such as warmth and hostility which at first sight might seem rather intangible and difficult to pin down. It worked, I think, because of several key features. First, it started with an explicit recognition that both attitudes and behaviour were important but that each required a somewhat different approach to measurement (Brown and Rutter, 1966; Rutter and Brown, 1966). Second, it combined a systematic standardised approach to the reporting of events and experiences and the use of observations on how people talked about other family members as a way of deriving quantitative measures of important features of their relationship and their interactions. The former led, in George’s case, to the development of the Life Events and Difficulties Schedule (LEDS) (Brown and Harris, 1978) and, in my case, to measures of marital discord and family negativity (Quinton, Rutter and Rowlands, 1976) and then later to a child version of a LEDS-style approach measuring acute and chronic stresses and adversities (Sandberg et al., 1993). The latter (observational approach) led to the development of the concept and measurement of negative expressed emotion (EE) that has proved to be a most remarkably robust predictive measure in relation to psychopathology (Leff and Vaughn, 1985). Subsequently, others developed a much briefer measurement of the same phenomenon using the so-called five-minute speech sample (Magaña et al., 1986; Moore and Kuipers, 1999). Similarly, we developed a more naturalistic version of the five-minute speech sample in which neutral questions are used to encourage parents to talk about their children, proving much more acceptable and

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Negative life events and family negativity 125 less stressful for families than expecting them to talk for five minutes without prompts (Sandberg et al., in preparation). The success of EE probably derives from three main features. First, there is an appreciation that people were likely to be less defensive about their real feelings if these simply derive from the way they talked about someone rather than from explicit statements about their feelings. Second, the measure was person-specific and, therefore, much more likely to reflect something particular about a relationship rather than a general stylistic quality. The fact that EE did that was a strength. Third, it appreciated that these feelings needed to be assessed on the basis of the way individuals talked about someone when there was not a focus on psychopathology. This was because it was important to seek to measure a feature of the relationship rather than something that was solely a reflection of talking about negative behaviours. At about the same period of time, George was involved in his collaborative study of mental hospitals in which the objective was to determine the extent to which the qualities of the mental hospital as a social institution influenced the course of serious psychiatric disorder (Brown and Wing, 1962). I played no role in that research but the findings influenced me through the demonstration that somewhat comparable methods of measurement could be applied to the social life of institutions as applied to social relationships in the family. Indirectly, this played a part in the shaping of my later investigation of schools as social institutions (Rutter et al., 1979).

George’s impact on life events research The early research into the effects of life events on psychopathology was dominated by the use of checklists of one kind or another that brought together a most heterogeneous mix of events, some of which were outside the individual’s control and some of which were obviously likely to have been caused by the person’s own behaviour. Case-control comparisons in terms of life event scores constituted the usual approach. Important steps in the development of interview approaches to life events were being taken by Paykel and others (Paykel, 1983; Paykel et al., 1969), but it would be fair to say that the revolution in life events research was largely due to the innovations of George Brown and Tirril Harris (1978). A systematic standardised interview approach was developed in order to obtain systematic information about the range of life events that might be important with respect to psychopathology. Five main conceptual/strategic steps were fundamental in taking forward its use (Rutter and Sandberg, 1992): •

The concept of ‘contextual threat’ provided an incisive means of sorting out possibly crucial differences among the different types of life event. It was argued that people affectively and cognitively process their experiences and that hence it was essential to consider the personal meaning of life events, rather than seek to measure them objectively in a vacuum. Means were developed to assess both the short-term and long-term psychological threat as they applied to the individual.

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126 Michael Rutter •

•

•

•

To avoid criterion contamination, it was essential that the assessment of threat be done through means that did not rely on people’s self-reports of whether or not they were upset by a particular experience. The importance here derived from the fact that it is a normal human tendency to search for meaning in experiences and if people have developed a mental disorder following some experience, they are quite likely to attribute the onset to the experience even if it had played no causal role. The way round this was provided by relying on standardised approaches to the assessment of threat, the ratings being done by a panel of researchers but using information on personal social context. There was an appreciation that through their actions people could well bring about stressful life events or experiences. From a methodological point of view, it was crucial to differentiate between life events that were independent of the person’s psychopathology and those that might be dependent on the person’s own behaviour. There was no assumption that dependent life events brought about by the person’s own behaviour might not have important consequent effects but, for methodological reasons, it was essential to differentiate between independent and dependent life events if the causal hypothesis was to be put to the test in a rigorous fashion. George recognised that causal inferences were always likely to be weak so long as they relied only on showing that life events of a negative kind were more common in patient samples than in control groups from the general population. The timing of life events in relation to the timing of the onset of psychiatric disorder was seen as a useful way forward. If life events truly precipitated mental disorder, it might be expected that such events carrying a high level of long-term contextual threat would be most likely to recur in the period immediately preceding onset. This is indeed what was found and the fact that it was provided important support for the causal inference. Finally, it was appreciated that the great majority of negative life events and experiences were not followed by the onset of psychiatric disorder (later data indicated that only about 1 in 5 women who experience a severely threatening event develop a clinically significant depressive disorder) (Brown, Bifulco and Harris, 1987). It was necessary to consider why this might be the case. George postulated that the answer might lie in some people having an enhanced vulnerability as a result of prior experiences of a sensitising kind.

Since then, Brown and Harris have developed each of these themes with, in particular, a more detailed classification of different sorts of life events (with a particular focus on humiliation and entrapment) and a much greater focus on the role of vulnerability factors in the form of both childhood adversities and a depressogenic cognitive style (Brown, 1998). There were also other methodological improvements but these five features were probably the ones that did most to revolutionise life events research, because they brought about a major transformation in the ways in which life events were thought about, measured, and assessed. The consequence has been an immense burgeoning of studies relating life events to the onset of all manner of disorders (Brown and Harris, 1989).

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Negative life events and family negativity 127

Some key queries on the effects of life events The considerable corpus of research undertaken by Brown and Harris, their colleagues and students or ex-students, has played a major role in the development of a general acceptance that life events constitute important precipitants of psychiatric disorder. This has become most firmly established in the case of depression, but most people have concluded that they play a somewhat similar role in other forms of psychopathology. Using the challenging approach that George first adopted in undertaking research into life events, let me re-examine some of the key issues regarding the postulated causal role of both negative life events and more long-standing family negativity as important contributors to the causation of psychiatric disorder. In undertaking this overview of some of the key queries, I make main use of research with which I have been involved, but I also consider evidence from other studies. The causal inference George’s focus on the timing of life events in relation to the onset of disorder unquestionably constituted a most useful step forward in testing the causal inference. However, over the years, it has become clear that there are several problems in the use of case-control designs for this purpose, by far the most commonly used research strategy (Robins, 1998; Kessler, 1997). George anticipated a number of these issues and addressed some of them in his use of longitudinal data (see, for example, Andrews and Brown, 1995). I think that it is likely that he accepts most of the points that follow. First, in sharp contrast to the amount of work that has gone into measurement of the timing of life events, there has been a paucity of research examining what is entailed in the onset of psychiatric disorder. Although depressive conditions (along with other mental disorders) can sometimes begin very acutely with the sudden emergence of many symptoms all beginning at much the same time, this is not the usual pattern. Often the onset of frank mental disorder has been preceded by a longer period of rumbling low level symptomatology. Often, too, there are several potentially relevant points of clinical transition (see Brown and Harris, 1978). Thus, there is the point at which it is first apparent that a person’s mental state is different from what has been usual for them; there is the point at which symptoms start interfering with either work performance or leisure activities or both; there is the point at which help is first contemplated or sought; and there may be a point at which a person becomes incapacitated by the disorder and is unable to work or needs to be admitted to hospital. Surprisingly little attention has been paid to how a decision is taken as to which of these constitutes ‘the’ onset, or on the consequences of taking different approaches to onset. There is also a need to be concerned with the fact that both the timing of the life event and the timing of the onset of disorder usually derive from the same informant. It is standard practice for these to be separately rated but the information that provides the basis for rating nevertheless derives from the same person, providing the opportunity for criterion contamination (Bank et al., 1990).

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128 Michael Rutter A further problem with case-control designs is that, necessarily, the betweengroup difference with respect to life events is influenced by other risk factors with which the life events happen to be associated (Sandberg et al., submitted). Thus, these include life events occurring at other times, more long-standing adverse life experiences, and indeed any other kind of genetic or environmental risk factor. The focus on timing helps but only in so far as it is shown that there is not a between-group difference with respect to other time periods and to the extent that the coincidences of timing are not due to rater bias. A further problem derives from the fact that so many disorders are chronic or recurrent (Judd, 1997). It may be that this is more so with respect to clinic samples than general population samples but it would be reasonable to suppose that the most important question is why there is such individual variability in the extent to which there is a liability to experience psychopathology over time. The effects in provoking onset of disorder have some indirect relevance to overall liability but some half of the population experience a depressive disorder at some time during their life and the proportion suffering from any form of mental disorder is higher than that. On the other hand, the proportion suffering persistent or recurrent psychopathology involving substantial social impairment is much lower. Surprisingly little research has examined the possible role of life events in relation to lifetime liability, although George has studied the role of both early childhood adversities (such as neglect or abuse) and ongoing interpersonal difficulties as predictors of chronicity (Brown and Moran, 1994; Brown et al., 1994b). My own research has only touched on these issues and has done so exclusively in relation to child psychopathology. Nevertheless, the findings have been provocative. Thus, we found that the agreement on the timing of onset was decidedly poor unless it had taken place during a quite brief recent time period (Angold et al., 1996). We also found that it was quite common for different symptoms to emerge at different times, with the consequence that it was possible for there to be several different onsets in relation to different aspects of the disorder (Rutter and Sandberg 1992). Also, at least in cases seen at a community clinic, quite a few disorders had already been present for longer than eighteen months before children were seen at the clinic. The data are far too few for any firm conclusions but they certainly point to the need for a more critical approach to the study of the onset of psychiatric disorder. In the case of children, it is possible to deal with the problem of criterion contamination by using both parent and child reports and considering life events on the basis of one informant and the onset of disorder on the basis of the other (Sandberg et al., submitted; Silberg et al., 1999). That constitutes a rigorous way of getting rid of the problem of criterion contamination but, at the same time, it does mean that there are two sources of error of measurement and not just one. The problem that case-control comparisons carry with them the ‘baggage’ of risk factors other than life events was dealt with in the study of Sandberg et al. (submitted) by looking at life events at different time periods both before and after onsets. In other words, the temporal comparisons were within-individual, rather than between groups. The results showed no significant effects of life events across informants

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Negative life events and family negativity 129 and, even within informants, effects only on the basis of child reports (Sandberg et al., submitted). The sample studied contained only a tiny handful of depressive disorders and it is possible that the findings might be quite different if they had been the focus of study. On the other hand, the general methodological issues remain and it is clear that greater use needs to be made of longitudinal studies in which the occurrence of major life events at one point in time can be considered in relation to the onset of psychiatric disorder at some later point in individuals who did not show disorder at the time the study started. There are very few studies of this kind (Tennant, 1983) and nearly all concern specific life events such as bereavement (Carnelly et al., 1999; Kessler, 1997; Paykel and Cooper, 1992). The few available findings are generally supportive of a causal impact on psychopathology but they confirm that most threatening life events do not result in psychiatric disorder. Of course, that is typical of the findings for risk factors of all kinds and the low incidence of provoked disorders in no way undermines the causal importance of life events, but it does underline the need to determine the mechanisms involved in individual differences – both with respect to exposure and susceptibility to life stresses and adversities. Individual differences in risk exposure In the early years of life events research, scarcely any attention was paid to the crucially important observation that individuals differed enormously in risk exposure. Some people’s lives seemed absolutely full of both acute and chronic stressful life experiences. By contrast, other people sail through with remarkably little in the way of serious stress. Stress is very far from randomly distributed and it is necessary to determine what mechanisms are involved in individual differences in environmental risk exposure. At least two very different processes need to be considered: 1 2

societal influences and broad living conditions influences deriving from people’s own behaviour (Rutter et al., 1995).

Broad living conditions In the late 60s and early 70s, we focused on the possible role of broad living conditions. The starting point was the finding that rates of emotional and behavioural disorders in young people were about twice as high in inner London as they were on the Isle of Wight (Rutter et al., 1975; Rutter and Quinton, 1977). The findings showed that this area difference in rates of psychopathology was not a function of biases relating to in- or out-migration but it was largely attributable to differences in family risk factors such as discord and disruption. It seemed that there was something about inner city life that put strains on families and it was this effect, rather than effects impinging directly on the children, that seemed largely responsible for the increased risk of psychopathology. Our focus here was on broad

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130 Michael Rutter aspects of family negativity rather than life events as such, and our starting point was risks for the children, rather than adults. Nevertheless, the findings are likely to have much broader implications. The last decade of the twentieth century saw an upsurge in an interest about the effects of living conditions on rates of psychopathology (Sampson, 1997; Brooks-Gunn et al., 1997). The main focus has been on area differences in antisocial behaviour, and the findings have suggested the importance of a lack of social cohesion as a key feature of the area effect. It does not need spelling out that, if confirmed, this would be likely to have implications also for depression and other forms of psychopathology. Other research has focused on housing policy and on the ways in which particular housing estates come to experience social disintegration (Power, 1997). Racial discrimination and racial harassment, regrettably, remain features of our society (Brown, 1984; Madood et al., 1997) and, although little studied as such, it is likely that this has implications for rates of exposure to stressful life events and experiences. Influences deriving from personal behaviour Robins’ (1966) now-classic long-term follow-up study of children who had attended a child guidance clinic in mid-America during the inter-war years was probably the first systematic research to show the huge importance of people’s own behaviour in shaping their life experiences. Boys who had shown conduct problems in childhood had a much increased rate of a wide range of adverse life experiences – including rebuffs from friends, lack of social support, being dismissed from jobs, and repeated marital breakdown. Our own research tackled the same issue using, as our starting point, the survey of 10-year-olds in Inner London that was used for our comparative study with the Isle of Wight. Champion et al. (1995) followed up the sample when they had reached their late twenties. A teacher questionnaire measure of emotional and behavioural disturbance at age 10 was used in order to have a measure that was free from possible bias in parental reporting and which applied to behaviour outside the home. The follow-up compared the rate of both acute life events and long-term difficulties or experiences that carried high levels of long-term threat and which Brown and Harris (1978, 1989) had shown carry the highest risk for the onset of depression in adult life. Rates were compared according to the presence or absence of conduct problems and of emotional disturbance at age 10. The findings (see Figure 8.1) were striking in showing that both forms of behaviour in childhood were associated with an increased rate of negative events and experiences some eighteen years later, the effect being much stronger in the case of antisocial behaviour than of emotional difficulties. We combined several long-term longitudinal studies in order to examine the same issue with respect to the likelihood that a person would marry or cohabit with someone showing problem behaviour in childhood/adolescence as shown by antisocial features or substance misuse (Quinton et al., 1993). We focused on this feature because we had found earlier that this was an important factor in

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Negative life events and family negativity 131

Mean number of events/difficulties

6

conduct/mixed

5

emotional disturbance

4

no disturbance

3 2 1 0

Severe events

Severe difficulties

Figure 8.1 Severe events and difficulties in early adult life.

the likelihood that there would be marital discord or disruption – an experience demonstrated to make it more likely that antisocial behaviour would continue in adult life (Zoccolillo et al., 1992; Laub et al., 1998) and which is one of the key events/experiences that increase the risk for depression (Brown and Harris, 1978, 1990). We found a powerful indirect chain effect by which the person’s own behaviour, adverse family influences, and participation in a deviant peer group all played an important role. Although the individual effect of each of these when considered in isolation was quite modest, their cumulative effect was strong. Moreover, these are not independent experiences. Pawlby et al. (1997a, b) showed that adolescents from high risk family backgrounds differed greatly from general population controls in their peer group experiences. This interplay is likely to have arisen through several different routes. However, our own earlier study of children reared in residential group homes showed the extent to which their experiences were followed by a feeling of a lack of control over their lives and, hence, a failure to exert planning in relation to key life decisions (Quinton and Rutter, 1988). School influences also played a part in this process, with good experiences in that environment seeming to serve as a degree of protection. Gene-environment correlations During the 90s, behaviour geneticists have drawn attention to the extensive evidence of gene-environment correlations with respect to a wide range of behaviour and experiences (Plomin and Bergeman, 1991; Plomin, 1995; Kendler, 1997; Rutter et al., 1997a; Thapar et al., 1998). This arises through three rather different routes: passive, evocative and active gene-environment correlations.

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132 Michael Rutter

% children with persistent disturbance

50 45

parental personality disorder

40

no personality disorder

35 30 25 20 15 10 5 0

Moderate/marked

None/little

Figure 8.2 Parental personality disorder and hostility, and persistent child disturbance.

Passive gene-environment correlations reflect the fact that parents pass on to their children genes as well as creating environments for them. Correlations arise because parents with genetically influenced psychopathology show an increased likelihood of providing an adverse rearing environment. Evocative correlations reflect the fact that through their own genetically influenced behaviour, people elicit responses from other people and thereby influence their interactions with them. Individuals showing psychopathology are more likely than other people to elicit negative interactions. Active correlations arise from the fact that, through their behaviour, people shape and select their own environments. By how they act, some people put themselves in situations that are risky in one way or another and which are more likely to give risk to negative life experiences. We tackled the first risk route indirectly by comparing the families of parents newly referred for a psychiatric disorder and parents in the general population (Rutter and Quinton, 1984; Rutter et al., 1997). We found that many adversities were much more frequent in the families with a mentally ill parent. Thus, marital discord was much more common and so was hostility or criticism focused on an individual child (see Figure 8.2). This was especially the case when the parental psychopathology included a personality disorder. This was not a genetically sensitive design and hence it was not possible to quantify the genetic contribution to this correlation but obviously there would be some genetic influence. What was important about the finding, however, was the indication that the genetic mediation could well come through personality features rather than through any direct effect

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Negative life events and family negativity 133 of the acute mental disorder. This has implications for the ways in which the independence/dependence of life events and experiences is conceptualised. It is crucial that independence be assessed in terms of any behaviour of the individual and not just symptomatology of the disorder under investigation (Sandberg et al. 1993). The initial LEDS conceptualisation focused on independence from the symptomatology of the disorder being studied (Brown and Harris, 1978) but over the years its measurement of independence has broadened in the ways suggested here (see Brown and Harris, 1986). The other important implication of the finding is the indication that acutely negative life experiences are likely to be more common in individuals who also suffer from chronic psychosocial adversities (see Brown and Harris, 1986). In that study, we did not focus specifically on acute life events, but it may be inferred that the same is likely to apply to them as well as to family negativity. Indeed, that is what has been found (Adrian and Hammen, 1993). In that connection, a key issue concerns the extent to which the risks for disorder stem from the life events and how far from the psychopathology from which they derive (Daley et al., 1997). More recently, using data from the Virginia Twin Study of Adolescent Behavioral Development, we have examined the role of correlations deriving from the individual’s own behaviour (i.e. evocative or active correlations) in relation to life events and depressive symptomatology in 8–16 year olds (Silberg et al., 1999). In order to do this it was essential both to focus on life events with a demonstrated empirical association with depression, and to focus on life events that could apply to just one twin and that were potentially open to the influence of gene-environment correlations. This led to a subset of life events (measured by parent and child questionnaire) with events such as failing a grade or falling out with a friend. For the reasons already considered, it was also essential to avoid the possibility of criterion contamination so that the analyses used parent measures on the life events and child measures on the psychopathology. The findings showed a significant genetic contribution to the liability to experience life events, a heritability of 49 per cent to 91 per cent as measured across two waves of data collection. To some extent, the genetic influences on life events and depression were the same and to some extent they were different. There was a negligible genetic contribution to depressive symptomatology in pre-pubertal children but there was a significant, albeit small (circa 30 per cent) genetic contribution to liability to depressive symptomatology in adolescent girls. The overall pattern of findings from genetic modelling suggested that the rise in depression seen in girls during the adolescent age period involved the operation of this gene-environment correlation. The rise in depression was most evident in both sexes when there were negative life events but the genetic contribution primarily came in with respect to girls. Other studies have similarly shown a genetic effect on the liability to experience negative life events (Thapar et al., 1998; Kendler et al., 1993). The same applies to parental negativity (Kendler et al.,1997; Ge et al.,1996; O’Connor et al., 1998). Thus, in the Colorado Adoption Study, O’Connor et al. found that adopted children whose biological mother (who did not rear them) showed antisocial behaviour were more likely to experience negativity from their

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134 Michael Rutter adoptive parents and that this came about because of the children’s own disruptive behaviour. One important feature of this study, however, was that the association between adoptive parental negativity and disruptive behaviour in the child remained just about as strong after excluding the operation of genetic factors, at least in so far as these were indexed by the biological parental phenotype. The implication was that either this represented a true environmental effect or the evocative effect of the children’s behaviour derived from characteristics that were determined by other environmental influences, or both. In other words, the findings are confirmatory that there are real effects of children on their parents (as also shown by a range of other studies – see Bell and Chapman 1986, Rutter et al., 1997b), but that it should not necessarily be assumed that these mainly reflect gene-environment correlations. That is only part of the story. Individual differences in susceptibility to environmental risks An absolutely consistent finding in the literature has been the very considerable variability in people’s responses to negative life events and adverse life experiences (Rutter,1999; in press, a). Regardless of the severity or nature of the environmental hazard, huge individual differences in vulnerability have been found. In recent years, molecular geneticists have begun to examine the role of genetic factors in this marked individual variation in susceptibility. Strong genetic effects have been found in relation to environmental factors as diverse as head injury (Teasdale et al., 1997), malaria (Knight et al., 1999; Wahlgren, 1999), and smoking (Talmud et al., in press). Quantitative genetic findings in the field of antisocial behaviour have similarly shown the importance of gene-environment interactions (Bohman, 1996; Cadoret et al., 1995). Individuals with genetic vulnerabilities tend to be those who are most susceptible to environmental hazards. In the Virgina Twin Study, we tested for this possibility directly in relation to the role of negative life events in the liability to depression and anxiety symptomatology. In a twin study, it is not possible to undertake satisfactory tests for interactions if there are also gene-environment correlations. Accordingly, it was necessary to focus on those life events that had an empirical association with depression/anxiety but which were of a kind that made it unlikely that gene-environment correlations could apply. In view of our earlier findings, we also focused on older girls (Silberg et al., submitted). This subset of life events included experiences such as a new stepbrother or sister or father losing a job. The findings showed that there was no genetic effect on these life events. The way in which it is necessary to test for gene-environment interaction in a twin study is to determine if the heritability is greater in the presence of the environmental risks (in this case negative life events). The results showed that it was. The heritability for depressive symptomatology was 27 per cent in the absence of life events and 39 per cent in the presence of two or more life events. The same applied in relation to anxiety, the comparable figures being 19 per cent and 44 per cent. At first sight, the finding seems paradoxical because genetically influenced

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% of variance from genetic components for depressive symptoms in child

Negative life events and family negativity 135 30 25 20 15 10

‘baseline’ genes gene–environment interaction

5 0

None

One Life events

Two or more

Figure 8.3 Effect of life events on variance in depressive symptoms.

susceptibility to environmental hazards is being inferred on the basis of a greater genetic effect in the presence of the environmental hazards and this seems the wrong way round. It is not, in fact, but that is because heritability includes the interaction term. This is shown graphically in Figure 8.3. The baseline genes are the same in the presence or absence of life events but the interaction term increases substantially and significantly in the presence of life events. The finding is important in showing that genetic factors constitute part of the reason why people vary in their response to life events but it is also important because it indicates that genetic effects often operate in indirect ways. That is, their effect is dependent on the cooccurrence of negative life events. The results underline the fact that nature and nurture are not as independent and clearly separable as they are sometimes thought to be. The ways in which the interaction operates also serves as a reminder that the effect that derives from the combination of genes and environment acting together is misleadingly entirely included in the genetic term in the traditional behaviour genetic analyses whereas it is neither exclusively genetic nor exclusively environmental; it is both. Using a different research strategy in a twin design, Kendler et al. (1995) similarly showed that twins with a genetic susceptibility were more likely to develop a major depressive disorder following a life event than those without that susceptibility. They had to rely on a more indirect inference about genetic vulnerability but the findings were closely parallel to ours. We also examined the role of gene-environment correlations in parental negativity, again using the Virginia Twin Study Data (Carbonneau et al., submitted). Twins in monozygotic pairs were more likely than those in dizygotic pairs to experience similar levels of parental negativity, as measured by the TIRE. When there is a tendency for parental hostility or criticism to be focused on one particular

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136 Michael Rutter child in the family, it is necessary to consider why it is this child that has been targeted. Our findings, like those of others, indicate that genetically influenced behavioural features of the child play a considerable role in that targeting. Chronic adversities and susceptibility to negative life events Several issues arise with respect to chronic adversities and acute life events. As already noted, the two tend to be associated, at least in clinical samples. We need to ask whether the risks mainly derive from the chronic adversities or from the acute events; whether the risks associated with chronic adversities require the additional operation of acute events; whether psychopathology is more likely to develop after life events that are associated with, or derive out of, chronic adversity; and whether acute life events that are not accompanied by chronic adversity also carry psychopathological risks. One way of approaching this set of issues was to use a case-control design. We found that case-control differences were much stronger with respect to chronic adversities than they were with life events that were not accompanied by chronic adversity (Sandberg et al. 1993). It was also found, however, that this combination of chronic and acute risks was particularly a feature of psychiatric samples (Sandberg et al., 1998). In a separate study of the role of life events in provoking asthmatic attacks, acute life events that were independent of chronic adversity were more evident. It may be relevant that the psychiatric clinic sample that we used applied to a very socially disadvantaged area and many of the disorders experienced by the children were recurrent or chronic. Also, very few cases of depressive disorder were included. It could be that life events independent of chronic adversity might be more important with respect to depressive disorders arising for the first time in adolescence. There has been surprisingly little systematic research into the role of chronic adversities in sensitising children to the effects of acute events. An early study of ours (Quinton and Rutter, 1976) suggested chronic adversity might make children more liable to develop disorder following admissions to hospital in the pre-school years but the study was not primarily set up to investigate the possibility and the findings were suggestive rather than decisive. The matter requires more systematic investigation. Is the causal effect of life events truly environmentally mediated? Psychosocial researchers, including George Brown (1996), have been somewhat reluctant to accept the importance of genetic influences on psychopathology and even more reluctant to accept the need to take seriously the possibility that the effects of psychosocial factors may be partially genetically, rather than environmentally, mediated. The converse, however, has also been true. That is, many behaviour geneticists have been reluctant to accept the possibility that psychosocial influences may indeed have an important, environmentally mediated, effect on the liability to psychopathology (Scarr, 1992 and 1997). The need, surely, is to put aside preconceptions and undertake research that can put environmental hypotheses to the test. That is what we have tried to do. One strategy is to examine differences within monozygotic

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% of adolescents within life events groups

Negative life events and family negativity 137 30 25 20

Within-pair difference in life events

15

2 or more points difference

10

1 point difference

5 0

no difference 1 point

2 or more points

within MZ pair difference in depression (child report) Figure 8.4 MZ pair differences in life events and MZ pair differences in depression.

(MZ) pairs (Pike et al., 1996a). Because MZ pairs share all their genes, any differences within-pair must be due to non-genetic influences. The research tactic, therefore, involves determining whether, within MZ pairs, the postulated psychosocial risk factor is associated with the psychopathology being investigated. This is a harsh test because it necessarily excludes the impact of environmental risks brought about through gene-environment correlations. As we have seen, that constitutes an important route by which environmental risks develop. Nevertheless, if environmental effects are evident in this design, it is clear that the possibility of genetic mediation has been effectively excluded. In the Virginia Twin Study (Silberg et al., 1999), we used this strategy with respect to life events and depressive symptomatology. In order to exclude the artefact of method variance, as already noted, the measures of life events and of child psychopathology that we used derive from different informants. As illustrated in Figure 8.4, significant within-pair differences were found. Kendler et al. (1999) found the same with respect to stressful life events and the onset of major depression in adults. Both sets of findings are strongly indicative of an environmentally mediated causal effect of life events on depression. The same applied with respect to parental negativity and antisocial behaviour (Carbonneau et al., submitted). Pike et al. (1996b) similarly found an effect of parental negativity on antisocial behaviour, using a composite spanning different informants in order to avoid criterion contamination (with a different measure of negativity from that used by Carbonneau et al.). Significant within-pair correlations were again found between parental negativity and antisocial behaviour (.28 to .34). The effects were less clear cut in the case of depression but were also evident to some degree, albeit short of

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138 Michael Rutter Fathers’ negativity

Mothers’ negativity

Siblings’ negativity

G = 0.34

G = 0.39

G = 0.13

Es = 0.23

Es = 0.16

Es = 0.37

En = 0.07

En = 0.05

En = 0.01

Children’s antisocial behaviour G = path coefficient for genetic route Es = path coefficient for shared environmental effect En = path coefficient for non-shared environmental effect Figure 8.5 Family negativity and antisocial behaviour.

statistical significance (.15 to .16). Two inferences derive from this set of findings. First, they provide a strong demonstration that there is a truly environmentally mediated effect of life events and of family negativity. Second, they also show that part of the difference between MZ and DZ pairs must derive from environmental, as well as genetic, factors. That is because the combination of the finding of a gene-environment correlation and a within-MZ-pair effect violates the equal environments assumption (see Rutter et al., submitted). The violation probably does not make much difference to the estimation of genetic effects but it certainly does make a difference to the detection of specific environmental effects, something that has been largely ignored in the behaviour genetics literature up to now. It requires greater attention in the future. An alternative genetic research strategy is to use bivariate analyses in which the environment is treated as a phenotype. By employing across-twin, across-trait analyses, it is possible to determine the extent to which the effect of a psychosocial factor is truly environmentally mediated. This strategy has the additional advantage that it serves to eliminate the effects of random measurement error. Pike et al. (1996b) used this strategy very effectively to examine the effects of family negativity on both antisocial behaviour and depressive symptomatology (see Figures 8.5 and 8.6). As expected, the findings showed that the effects involved both environmental and genetic mediation. What was really striking, however, was that family negativity, even when measured as a child-specific variable, had an environmental effect that was largely shared, rather than non-shared. That finding runs directly counter to behaviour genetic claims (Plomin and Bergeman, 1991) and it is regrettable that the paper was written in a way that downplayed this finding (it is not even mentioned in the abstract). It is necessary to appreciate that the earlier behaviour genetic claims on the supposedly far greater importance of non-shared

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Negative life events and family negativity 139 Fathers’ negativity

Mothers’ negativity

Siblings’ negativity

G = 0.21

G = 0.24

G = 0.00

Es = 0.13

Es = 0.05

Es = 0.25

En = 0.04

En = 0.05

En = 0.00

Children’s depression G = path coefficient for genetic route Es = path coefficient for shared environmental effect En = path coefficient for non-shared environmental effect Figure 8.6 Family negativity and depression.

environmental effects failed to take into account that the non-shared environmental term included measurement error. When that was taken into account, and particularly when looking at behaviour as manifest over time, the findings were rather different (Rutter et al., 1999). It has been very important to ensure the use of childspecific measures but the findings show that the categorical distinction between shared and non-shared environmental effects is nothing like as clear as some behaviour geneticists have argued. We need to consider the ways in which familywide psychosocial risks have effects that may both impinge equally on all the children and also may be differentially targeted on just one. Testing this possibility requires the use of somewhat different research designs from those that have been employed up to now. In the Virginia Twin Study, we also looked at possible shared environmental effects of family dysfunction on antisocial behaviour using an extended twinfamily design (Meyer et al., 2000). The findings showed an environmentally mediated effect that was equivalent to an approximate doubling of the risk for antisocial behaviour in the children. The same strategy was used by Kendler et al. (1996) to show a substantial shared environmental effect of parental loss on the liability to the later development of alcoholism in adult life. So far, there has been relatively little research testing environmental risk hypotheses in ways that take account of the possibility of genetic mediation. Nevertheless, the findings have been consistent in showing that, although genetic factors do play a part in mediation, there is also a true environmentally mediated risk associated with both negative life events and family negativity. Moreover, other research designs may also be used to test environmental risk hypotheses (see Rutter et al., submitted) and the findings are again consistent, confirming the reality of environmental risk mediation (Rutter, in press, b).

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140 Michael Rutter

Challenges for the future The field of psychosocial research would not have been the same without the creative impact of George Brown’s thinking and of the impressive corpus of empirical research findings from his team. These findings are clear cut in showing the clinical importance of both the life events and the family negativity that George focused on as risk factors for psychopathology. Also, both the investigator-based standard interview methods that he pioneered and the negative expressed emotion measure have stood the test of time and remain extremely useful research tools. In this concluding section of the chapter, I consider the challenges that remain. Inevitably, as is the way of science, the solving of some questions has been followed by an opening up of an even broader range of questions that have to be tackled. Methodological issues Three main methodological needs stand out. First, there is concern over the extent to which findings on the effects of life events in provoking the onset of psychopathology rest on data from a single informant. The opportunities for artefact deriving from criterion contamination are obvious. In research with children, the agreement between parents and children has been only modest. The one large scale epidemiological study with data from both parents and adolescents did not examine parent-child agreement on the timing of life events (Monck and Dobbs, 1985) and the issue has not been tackled systematically in the case of adults. Multi-informant, multi-modal methods of assessment have become a standard requirement in psychological research (Bank et al., 1990; Patterson et al., 1992) and it needs to be brought to the study of life events and of family negativity. With children and adolescents, more use could be made of paternal reports and, with adults, use needs to be made of reports from a cohabiting partner. Second, it is necessary to appreciate the limitations of case-control designs for studying the temporal connections between life events and the onset of disorder. Studies of temporal associations within individuals (i.e. examining the patterning over time, both before and after onset) have a role. Prospective longitudinal studies would, however, provide a stronger research strategy. Third, there needs to be continuation of the efforts to further streamline measurement (Rutter, in press, b). The point is that many of the most important research questions require both large samples and measurement of other key variables. The five-minute speech sample (Magaña et al., 1986; Moore and Kuipers, 1999) constituted a useful step forward in the measurement of expressed emotion. As used with children, the psychosocial assessment of children’s experiences (PACE) provides a more naturalistic approach in which the interviewer is able to help the informant talk through the use of neutral prompts and questions. The measure has been found to agree well with assessments based on a whole interview and to show good stability over time (Sandberg et al., in preparation). Shorter versions of interview assessments of life events are needed and, for many purposes, it may be useful to focus on a more limited range of common high risk events (Brugha and Cragg, 1990). Although questionnaire measures are clearly less satisfactory than

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Negative life events and family negativity 141 investigator-based interviews, they are needed for large-scale surveys and efforts are needed to avoid the limitations of so many of the measures in the field. Effects on lifetime liability Up to now, most of the research in the field of life events has focused on effects on the timing of onset of disorder. Initially, that constituted an important methodological step forward because of its advantages in testing causal hypotheses. It remains of some interest but it is even more important to examine the role of life events and of family negativity on the liability to psychopathology as manifest over time. Many disorders are recurrent or chronic and we need to know the role of psychosocial influences on that ongoing liability to psychopathology. In that connection, it is particularly important to examine the relative importance of acute life events and chronic psychosocial adversities and, most especially, the interplay between them. Life event researchers have long recognised that there was a need to consider both long-term experiences and acute events but rather few studies have systematically set out to determine the relative importance of their roles in the cause and course of psychopathology. In that connection, attention needs to be paid to the possibility that the role of psychosocial influences on the first development of psychiatric disorder may be greater than on recurrence of episodes. Post (1992) suggested that the concept of ‘kindling’, by which the onset of disorder brings about changes within the individual that lead to later recurrence, may apply to depressive disorders (see also Brown et al., 1994a). There is a growing body of evidence that the concept may have some validity (Kendler et al., in press). Effects of life events and family negativity on the organism Psychosocial researchers have, up to now, given less priority than needed to the study of what psychosocial influences do to the organism. It is necessary to pose the question because, if the effects are carried forward in time, what mechanisms are implicated? For the most part, it has been thought that changes in social cognitive sets and attributions are crucial (Brown and Harris 1990; Teasdale and Barnard, 1993). It is indeed highly likely that that is part of the story, although it has to be said that research so far has not put the postulated causal chain effect to the test in rigorous fashion. Other possibilities, however, also need to be considered (Rutter, 1989). The alternatives include effects on interactional styles, on behavioural patterns, on the neuro-endocrine system and on brain structure and function. The evidence on the last two possibilities largely derives from animal studies involving rather severe environmental manipulations (Hennessy and Levine, 1979; O’Brien, 1997) and it is not known with any certainty how far these routes are important with respect to more ‘ordinary’ experiences of life events and family negativity in humans. The question of what are the effects on the organism is one of the most neglected and most important issues in the field of psychosocial research and it is important that it receive greater attention in the future.

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142 Michael Rutter Origins of individual variations in environmental risk exposure If people are to take seriously the causal role of psychosocial experiences in the cause and course of psychopathology (and they should), it is necessary to consider why people vary so greatly in their exposure to environmental risks. Research has begun to tackle this crucially important issue, and the findings already indicate the need to consider both the societal influences and the role of the person’s own behaviour in shaping and selecting environments. Good leads are available in the literature but we know surprisingly little about the details of the mechanisms involved; we know even less about the ways in which the interplay between nature and nurture is important in the carry-forward of environmental effects. Behaviour geneticists have rightly emphasised the important role of gene-environment correlations but the interplay between persons and their environments involves far more than this. The point is that, through their behaviour, people do influence what happens to them and this happens whether or not behaviour has largely been brought about by genetic or environmental influences. In this connection, it is necessary to return to the issue of the extent to which life events are independent of the individual. This notion was first introduced because it was crucial to take it into account in research strategies if causation was to be tested in a critical fashion. That remains important and, indeed, it is necessary to extend the notion to reflect the fact that people influence their environments through features that are as much related to their personality functioning as to their acute symptomatology. In view of the important extent to which there are associations between personality disorder and acute psychiatric conditions (Klein et al., 1993), it is necessary that the measurement of independence extends more broadly than it has sometimes in the past. Nevertheless, there are other ways in which the same methodological need may be met (see Rutter et al., submitted) and it is crucial to realise that experiences that are directly brought about by people’s own behaviour can nevertheless have an important causal effect (see Kendler et al., 1999). The example of smoking well illustrates the point (Rutter et al., 1993) and, in the field of psychopathology, this has been well shown in relation to the effects of a harmonious marriage in making it less likely that antisocial behaviour continues in adult life (Rutter et al., 1997 b; Laub et al. 1998). Susceptibility to life events and family negativity From the earliest days of research into life events and family negativity, the huge individual variation in response has been obvious. Research findings have pointed to the likely role of both genetic factors and earlier adverse experiences in creating an increased or decreased vulnerability but evidence on both remains quite limited. Also, very little is known of the personal characteristics that mediate susceptibility to adverse experiences. There is some evidence that neuroticism, rather than low self-esteem, indexes liability to affective disorder (Roberts and Kendler, 1999), although this conclusion may be influenced by how self-esteem is measured (see Andrews and Brown, 1993). Whether this constitutes the key feature in relation to individual differences in response to negative

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Negative life events and family negativity 143 life events and experiences remains uncertain, but there are indications that it may do so (Van Os and Jones, 1999). Psychosocial researchers have tended to favour some aspect of a cognitive set as the mediating variable but that is also unestablished. The topic of the mechanism involved in susceptibility to life events and family negativity constitutes a priority area. Therapeutic implications and mechanisms Finally, there has been little attention so far to the therapeutic implications of the findings, other than in the field of expressed emotion and schizophrenia (Leff and Vaughn, 1985; Bebbington and Kuipers, 1994). The evidence is persuasive that appropriately targeted interventions can serve to reduce family negativity but the research designs have done much less to test the postulate that the reduction in negativity is the mediating feature of the therapeutic benefits in relation to psychopathology. That requires the testing of dose-response relationships examining the connections between changes in negativity and changes in psychopathology within treated groups. Also, although it has been clear for a long time that negative expressed emotion constitutes a risk factor for many forms of psychopathology, there has been much less research outside the field of schizophrenia. The therapeutic implications of the life events findings have received even less attention. The main emphasis has been on the likely benefits of interventions using cognitive behavioural approaches, and there is some evidence of their value (Clark and Fairburn, 1997), but, to what extent is it important that such methods take account of life events and experiences and does the presence of such risk factors in the individual make a difference to therapeutic outcome? We do not know. The research needs and opportunities are obvious. Brown and his colleagues (Harris et al., 1999 a, b) well recognised this point in their study of befriending. The results showed the value of this form of intervention but, interestingly, the benefits were not mediated by the hoped-for therapeutic effects on ‘fresh-start’ positive life events. Although the latter were the most powerful predictors of remission, befriending had not increased their frequency.

Conclusions The field of research into life events and family negativity that owes so much to the conceptual clarity and methodological rigour contributed by George Brown remains as important today as it was at the time George entered the field. It is very much a tribute to his programmatic research that there is now a general acceptance of the importance of these risk factors for psychopathology. However, as George would be the first to point out, we have passed the point of usefulness of yet another case-control study using traditional designs. Together with his longtime colleague Tirril Harris, and other collaborators, George’s own research has continued to dig away at some of the many difficult questions that remain. However, there are still very considerable challenges ahead and new research strategies are going to be needed. Sometimes, I feel a concern that, with all the

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144 Michael Rutter excitement of the revolution in biological psychiatry and in molecular genetics, there may be a lack of really creative innovative psychosocial researchers to take the field forward in the future. But, in asking who are the younger parallels of George Brown entering the field today, perhaps there should be a feeling of reassurance that the older George Brown remains very active in research and, hopefully, some of the answers to the questions posed in this chapter will come from his own future studies.

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Negative life events and family negativity 145 —— and Harris, T.O. (1990) ‘Loss of parent in childhood and adult psychiatric disorder: A tentative overall model’, Development and Psychopathology, 2, 311–28. —— and Moran, P. (1994) ‘Clinical and psychosocial origins of chronic depressive episodes. I: A community survey’, British Journal of Psychiatry, 165, 447–56. —— and Rutter, M. (1966) ‘The measurement of family activities and relationships: A methodological study’, Human Relations, 19, 241–63. —— and Wing, J.K. (1962) ‘A comparative clinical and social survey of three mental hospitals’, Sociological Review Monograph, 5. ——, Harris, T.O. and Peto, J. (1973) ‘Life events and psychiatric disorders: II. Nature of causal link’, Psychological Medicine, 3, 159–76. ——, Sklair, F., Harris, T.O. and Birley, J.L.T. (1973) ‘Life events and psychiatric disorders: I. Some methodological issues’, Psychological Medicine, 3, 74–8. ——, Bifulco, A. and Harris, T.O. (1987) ‘Life events, vulnerability and onset of depression: some refinements’, British Journal of Psychiatry, 150, 30–42. ——, Harris, T.O. and Hepworth, C. (1994a) ‘Life events and “endogenous” depression: A puzzle re-examined’, Archives of General Psychiatry, 51, 525–34. ——, Harris, T.O., Hepworth, C. and Robinson, R. (1994b) ‘Clinical and psychosocial origins of chronic depressive episodes. II: A patient enquiry’, British Journal of Psychiatry, 165, 457–65. Brugha, T.S. and Cragg, D. (1990) ‘The list of threatening experiences: The reliability and validity of a brief life events questionnaire’, Acta Psychiatrica Scandinavica, 82, 77–81. Cadoret, R.J., Yates, W.R., Troughton, E., Woodworth, G. and Stewart, M.A. (1995) ‘Genetic-environmental interaction in the genesis of aggressivity and conduct disorders’, Archives of General Psychiatry, 52, 916–24. Carbonneau, R., Rutter, M., Silberg, J.L., Simonoff, E., Hewitt, J.K. and Eaves, L.J. (submitted) ‘Assessment of genetic and environmental influences on differential ratings of within family experiences and relationships in twins’. Carnelly, K.B., Wortman, C.B. and Kessler, R.C. (1999) ‘The impact of widowhood on depression: Findings from a prospective study’, Psychological Medicine, 29, 1111–23. Champion, L.A., Goodall, G. and Rutter, M. (1995) ‘Behavioural problems in childhood and stressors in early adult life. I: A 20-year follow-up of London school Children’, Psychological Medicine, 25, 231–46. Clark, D.M. and Fairburn, C.G. (eds) (1997) Science and practice of cognitive behaviour therapy, Oxford: Oxford University Press. Coverdill, J.E., Finlay, W. and Martin, J.K. (1994) ‘Labor management in the southern textile industry’, Sociological Methods and Research, 23, 54–8. Daley, S.E., Hammen, C., Burge, D., Davila, J., Paley, B., Lindberg, N. and Herzberg, D.S. (1997) ‘Predictors of the generation of episodic stress: A longitudinal study of late adolescent women’, Journal of Abnormal Psychology, 106, 251–9. Feagin, J.R. (1999) ‘Soul searching in sociology: Is the discipline in crisis?’, Chronicle of Higher Education: Opinion and Arts, Oct 15th 1999, B4. Ge, X., Conger, R.D., Cadoret, R.J., Neiderhiser, J.M., Yates, W., Troughton, E. and Stewart, M.A. (1996) ‘The developmental interface between nature and nurture: A mutual influence model of child antisocial behavior and parenting’, Developmental Psychology, 32, 574–89. Harris, T.O., Brown, G.W. and Robinson, R. (1999a) ‘Befriending as an intervention for chronic depression among women in an inner city: I. Randomised controlled trial’, British Journal of Psychiatry, 174, 219–24.

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146 Michael Rutter ——, Brown, G.W. and Robinson, R. (1999b) ‘Befriending as an intervention for chronic depression among women in an inner city: II. Role of fresh-start experiences and baseline psychosocial factors in remission from depression’, British Journal of Psychiatry, 174, 225–32. Hennessey, J.W. and Levine, S., (1979) ‘Stress, arousal and the pituitary-adrenal system: A psychoendocrine hypothesis’ in J.M. Sprague and A.N. Epstein (eds) Progress in psychobiology and physiological psychology, New York: Academic Press, 133–78. Judd, L.L. (1997) ‘The clinical course of unipolar major depressive disorders’, Archives of General Psychiatry, 54, 989–91. Kendler, K.S., Neale, M.C., Kessler, R., Heath, A. and Eaves, L. (1993) ‘A twin study of recent life events and difficulties’, Archives of General Psychiatry, 50 ,789–96. ——, Kessler, R.C., Walters, E.E., MacLean, C., Neale, M.C., Heath, A.C. and Eaves, L.J.. (1995) ‘Stressful life events, genetic liability, and onset of an episode of major depression in women’, American Journal of Psychiatry, 152, 833–42. ——, Neale, M.C., Prescott, C.A., Kessler, R.C., Heath, A.C., Corey, L.A. and Eaves, L.J. (1996) ‘Childhood parental loss and alcoholism in women: A causal analysis using a twin-family design’, Psychological Medicine, 26, 79–95. ——, Sham, P.C; MacLean, C.J. (1997) ‘The determinants of parenting: An epidemiological, multi-informant, retrospective study’, Psychological Medicine, Vol 27(3), 549–63. ——, Karkowski, L.M. and Prescott, C.A. (1999) ‘Causal relationship between stressful life events and the onset of major depression’, American Journal of Psychiatry, 156, 837–41. ——, Karkowski, L.M., and Gardner, C.O. (in press) ‘Stressful life events and prior episodes in the etiology of major depression in women: an evaluation of the “kindling” hypothesis’, American Journal of Psychiatry. Kessler, R.C. (1997) ‘The effects of stressful life events on depression’, Annual Review of Psychology, 48,191–214. Kidder, L.H. and Fine, M. (1987) ‘Qualitative and quantitative methods: When stories converge’ in M. M. Mark and R.L. Shotland (eds) Multiple methods in program evaluation. New directions for program evaluation, no. 35 55–75, San Francisco: Jossey-Bass. Klein, M.H., Kupfer, D.J. and Shea, M.T. (1993) Personality and depression: A current view, New York: Guilford Press. Knight, J.C., Udalova, I., Hill, A.V.S., Greenwood, B.M., Peshu, N., Marsh, K., and Kwiatkowksi, D. (1999) ‘A polymorphism that affects OCT-1 binding to the TNF promoter region is associated with severe malaria’, Nature Genetics, 22, 145–50. Laub, J.H., Nagin, D.S. and Sampson, R.J. (1998) ‘Trajectories of change in criminal offending: good marriages and the desistance process’, American Sociological Review, 63, 225–38. Leff, J.P. and Vaughn, C. (1985) Expressed emotion in families: its significance for mental illness, New York: Guilford Press. Madood, T., Berthoud, R., Lakey, J., Nazroo, J., Smith, P., Virdee, S. and Beishon, S. (1997) Ethnic minorities in Britain: Diversity and disadvantage, London: Policy Studies Institute. Magaña, A.B., Goldstein, M.J., Karno, M., Niklowitz, D.J., Jenkins, J. and Falloon, I.R.H. (1986) ‘A brief method for assessing expressed emotion in relatives of psychiatric patients’, Psychiatric Research, 17, 203–12.

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Negative life events and family negativity 147 Meyer, J.M., Rutter, M., Silberg, J.L., Maes, H.H., Simonoff, E., Shillady, L.L., Pickles, A., Hewitt, J.K., Eaves, L.J. (2000) ‘Familial aggregation for conduct disorder syptomatology: the role of genes, marital discord and family adaptability’, Psychological Medicine. Monck, E., and Dobbs, R. (1985) ‘Measuring life events in an adolescent population: Methodological issues and related findings’, Psychological Medicine, 15, 841–50. Moore, E. and Kuipers, E. (1999) ‘The measurement of expressed emotion in relationships between staff and service users: the use of short speech samples’, British Journal of Clinical Psychology, 38, 345–56. O’Brien, J.T. (1997) ‘The “glucocorticoid cascade” hypothesis in man. Prolonged stress may cause permanent brain damage’, British Journal of Psychiatry, 170, 199–201. O’Connor, T. G., Deater-Deckard, K., Fulker, D., Rutter, M., Plomin, R. (1998) ‘Early adolescence: Antisocial behavioral problems and coercive parenting’, Developmental Psychology, 34, No. 5, 970–81. Patterson, G.R., Reid, J.B. and Dishion, T.J. (1992) Antisocial boys, Eugene, Oregon: Castalia. Paykel, E. (1983) ‘Methodological aspects of life events’, Journal of Psychosomatic Research, 27, 341–52. Paykel, E.S. and Cooper, Z. (1992) ‘Life events and social stress’ in E. S. Paykel (ed.) Handbook of affective disorders (2nd ed.), New York, USA: Guilford Press, 149–70. ——, Myers, J.K., Dienelt, M.N., Klerman, G.L., Lindenthal, J.J. and Pepper, M.P. (1969) ‘Life events and depression: a controlled study’, Archives of General Psychiatry, 21, 753–60. Pawlby, S.J, Mills, A. and Quinton, D. (1997a) ‘Vulnerable adolescent girls: Opposite sex relationships’, Journal of Child Psychology and Psychiatry, 38, 909–20. Pawlby, S.J., Mills, A., Taylor, A. and Quinton, D. (1997b) ‘Adolescent friendships mediating childhood adversity and adult outcome’, Journal of Adolescence, 20, 633–44. Pike, A., Reiss, D., Hetherington, E.M. and Plomin, R. (1996a) ‘Using MZ differences in the search for non-shared environmental effects’, Journal of Child Psychology and Psychiatry, 37, 695–704. Pike, A., McGuire, S., Hetherington, E.M., Reiss, D. and Plomin, R. (1996b) ‘Family environment and adolescent depression and antisocial behavior: A multivariate genetic analysis’, Developmental Psychology, 32, 590–603. Plomin, R. (1995) ‘Genetics and children’s experiences in the family’, Journal of Child Psychology and Psychiatry, 36, 33–68. —— and Bergeman, C.S. (1991) ‘The nature of nurture: Genetic influences on “environmental” measures’, Behavioral and Brain Sciences, 10, 1–15. Post, R. (1992) ‘Transduction of psychosocial stress into neurobiology of recurrent affective disorder’, American Journal of Psychiatry, 149, 999–1010. Power, A. (1997) Estates on the edge: The social consequences of mass housing in Northern Europe, London: Macmillan. Quinton, D. and Rutter, M. (1976) ‘Early hospital admissions and later disturbances of behaviour: an attempted replication of Douglas’ findings’, Developmental Medicine and Child Neurology, 18, 447–59. —— and Rutter, M. (1988) Parenting breakdown: The making and breaking of intergenerational links, Aldershot: Avebury. ——, Rutter, M. and. Rowlands, O. (1976) ‘An evaluation of an interview assessment of marriage’, Psychological Medicine, 6, 577–86.

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148 Michael Rutter ——, Pickles, A., Maughan, B. and Rutter, M. (1993) ‘Partners, peers and pathways: Assortative pairing and continuities in conduct disorder’, Development and Psychopathology, 5, 763–83. Roberts, S.B. and Kendler, K.S. (1999) ‘Neuroticism and self-esteem as indices of the vulnerability to major depression in women’, Psychological Medicine, 29, 1101–9. Robins, L.N. (1966) Deviant children growing up, Baltimore: Williams and Wilkins. —— and Robertson, J. (1998) ‘Exposure to “fateful” events: A confounder in assigning causal roles to life events’ in B.P. Dohrenwend (ed.) Adversity, stress and psychopathology, New York and Oxford: Oxford University Press. Rutter, M. (1989) ‘Pathways from childhood to adult life’, Journal of Child Psychology and Psychiatry, 30, 23–51. —— (1999) ‘Resilience concepts and findings: implications for family therapy’, Journal of Family Therapy, 21, 119–44. —— (2000) ‘Resilience reconsidered: conceptual considerations and empirical findings’ in J. Schonkof and S. Meisels (eds) Handbook of early childhood intervention, Cambridge and New York: Cambridge University Press. —— (in press) ‘Psychosocial influences: Critiques, findings and research needs’, Development and Psychopathology. —— and Brown, G.W. (1966) ‘The reliability and validity of measures of family life and relationships in families containing a psychiatric patient’, Social Psychiatry, 1, 38–53. —— and Quinton, D. (1977) ‘Psychiatric disorder – ecological factors and concepts of causation’ in McGurk, H. (ed.) Ecological factors in human development, Amsterdam: North-Holland, 173–87. —— and Quinton, D. (1984) ‘Parental psychiatric disorder: Effects on children’, Psychological Medicine, 14, 853–80. —— and Sandberg, S. (1992) ‘Psychosocial stressors: Concepts, causes and effects’, European Child and Adolescent Psychiatry, 1, 3–13. ——, Cox, A., Tupling, C., Berger, M. and Yule, W. (1975) ‘Attainment and adjustment in two geographical areas. I: The prevalence of psychiatric disorder’, British Journal of Psychiatry, 126, 493–509. ——, Maughan, B., Mortimore, P., Ouston, J. with Smith, A. (1979) Fifteen thousand hours: Secondary schools and their effects on children, London: Paul Chapman Publishers. ——, Silberg, J. and Simonoff, E. (1993) ‘Whither behavior genetics? A developmental psychopathology perspective’ in R. Plomin and G.E. McLaren (eds) Nature, nurture and psychology, Washington, DC: APA Books, 433–56. ——, Champion, L., Quinton, D., Maughan, B. and Pickles, A. (1995) ‘Understanding individual differences in environmental risk exposure’ in P. Moen, G.H. Elder Jr. and K. Lüscher, (eds) Examining lives in context: Perspectives on the ecology of human development, Washington, DC: American Psychological Association. ——, Dunn, J., Plomin, R., Simonoff, E., Pickles, A., Maughan, B., Ormel, J., Meyer, J. and Eaves, L.J. (1997a) ‘Integrating nature and nurture: Implications of person-environment correlations and interactions for developmental psychopathology’, Development and Psychopathology, 9, 335–64. ——, Maughan, B., Meyer, J., Pickles, A., Silberg, J., Simonoff, E. and Taylor, E. (1997b) ‘Heterogeneity of antisocial behavior: Causes, continuities and consequences’ in R.Dienstbier and D.W. Osgood (eds) Nebraska Symposium on Motivation: Vol 44. Motivation and Delinquency, Lincoln, NE: University of Nebraska Press, 45–118.

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Negative life events and family negativity 149 ——, Silberg, J., O’Connor, T., Simonoff, E. (1999) ‘Genetics and child psychiatry: I Advances in quantitative and molecular genetics’, Journal of Child Psychology and Psychiatry, 40, 3–18. ——, Pickles, A., Murray, R. and Eaves, L. (submitted) ‘Testing hypotheses on specific environmental risk mechanisms for psychopathology’. Sampson, R.J., Raudenbush, S.W., and Earls, F. (1997) ‘Neighborhoods and violent crime: A multilevel study of collective efficacy’, Science, 277, 918–24. Sandberg, S., Rutter, M., Giles, S., Owen, A., Champion, L., Nicholls, J., Prior, V., McGuinness, D and Drinnan, D. (1993) ‘Assessment of psychosocial experiences in childhood: Methodological issues and some substantive findings’, Journal of Child Psychology and Psychiatry, 34, 879–97. ——, McGuinness, D., Hillary, C. and Rutter, M. (1998) ‘Independence of childhood life events and chronic adversities: A comparison of two patient groups and controls’, Journal of American Academy of Child and Adolescent Psychiatry, 37, 728–35. ——, Rutter, M, Pickles, A, McGuinness, D., Angold, A. (submitted) ‘Do high threat life events really provoke the onset of psychiatric disorder in children?’. ——, Rutter, M. and Järvi, J. (in preparation) ‘A brief assessment of expressed emotion (EE): Correlates and temporal stability’. Scarr, S. (1992) ‘Developmental theories for the 1990s: Development and individual differences’, Child Development, 63, 1–19. —— (1997) ‘Behavior-genetic and socialization theories of intelligence: Truce and reconciliation’ in Sternberg, R.J. and Grigorenko, E.L. (eds) Intelligence, heredity and environment, New York: Cambridge University Press, 3–41. Seale, C. (1999) The quality of quantitative research: introducing qualitative methods, London: Sage. Silberg, J., Pickles, A., Rutter, M., Hewitt, J., Simonoff, E., Maes, H., Carbonneau, R., Murrelle, L., Foley, D. and Eaves, L. (1999) ‘The influence of genetic factors and life stress on depression among adolescent girls’, Archives of General Psychiatry, 56, 225–32. ——, Rutter, M., Neale, M. and Eaves, L. (in press) ‘Genetic moderation of environmental risk for depression and anxiety in adolescent girls’, British Journal of Psychiatry. Talmud, P.J., Bujac, S.R., Hall, S., Miller, G. J. and Humphries, S. E. (in press) ‘Substitution of asparagine for aspartic acid at residue 9 (D9N) of lipoprotein lipase markedly augments risk of ischaemic heart disease in male smokers’, Atherosclerosis. Teasdale, J.D. and Barnard, P.J. (1993) Affect, cognition and change: Re-modelling depressive thought, Hove, England: Erlbaum. Teasdale, G. M., Nicoll, J. A. R., Murray, G. and Fiddes, M. (1997). ‘Association of apolipoprotein E polymorphism with outcome after head injury’, Lancet, 350, 1069–71. Tennant, C. (1983) ‘Editorial: Life events and psychological morbidity: The evidence from prospective studies’, Psychological Medicine 13, 483–6. Thapar, A., Harold, G. and McGuffin, P. (1998) ‘Life events and depressive symptoms in childhood – shared genes or shared adversity? A research note’, Journal of Child Psychology and Psychiatry, 39, 1153–8. Van Os, J. and Jones, P.B. (1999) ‘Early risk factors and adult person-environment relationships in affective disorder’, Psychological Medicine, 29, 1055–67. Wahlgren, M. (1999) ‘Creating deaths from malaria’, Nature Genetics, 22, 120–1. Zoccolillo, M., Pickles, A., Quinton, D. and Rutter, M. (1992) ‘The outcome of childhood conduct disorder: Implications for defining adult personality disorder and conduct disorder’, Psychological Medicine, 22, 971–86.

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9

Towards a dynamic stress-vulnerability model of depression The role of neuroticism, life events, and gender Johan Ormel and Jan Neeleman

Introduction In the mid-1970s, George Brown sought to teach me (Ormel) two important lessons. First, he argued that the meaning of stressful life events (SLEs) and longterm difficulties (LTDs) was critical for understanding their relationship with depression so that life stress should not be measured merely by means of checklists. He succeeded in convincing me. Second, he argued that meaning should be inferred from the event, the context in which it occurs, and occasionally from key aspects of the person’s life history which may have background relevance for the experience of the current event. This time he did not convince me, at least not entirely. I still doubt what key aspects can be safely included in the contextual event ratings. Not that I hesitate to take into account, when a woman is sent by her family doctor for the diagnosis of her own breast lump, the fact that her mother’s premature death was caused by breast cancer. My hesitation concerns, in particular, biographical events which were, in part or entirely, due to the behaviour and decisions of the respondent. After all, biography reflects other determinants of depression than events, like personality, and associated coping and appraisal styles. Thus, using biography to rate events might be to confound them with other factors of aetiological importance. This is critical in studies which try to unravel causal associations between personality, experiences, and depression – the topic of this chapter. More specifically, we describe in this chapter some of the work done in Groningen on neuroticism, life events, and depression. We start with an outline of the Dynamic Stress-Vulnerability Model to provide a framework for the interpretation of the empirical findings. Next we discuss the gradual differentiation between the concepts of vulnerability and risk factors, followed by the Groningen research findings. Finally we suggest that LEDS methodology can be used to study the ‘aetiology of present vulnerability’.

The dynamic stress-vulnerability model Stress-vulnerability models are central to the study of determinants of depression risk (Brown and Harris,1978; Goldberg et al., 1990; Rodgers, 1991; Monroe and

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152 Johan Ormel and Jan Neeleman Simons 1991). Their common core is that pathogenic effects of stress are more pronounced when its recipients are more vulnerable. In this chapter we aim to introduce a dynamic version of the stress-vulnerability model. This dynamic model (DSV-model) describes how personal biography, environment, events and psychopathology influence each other (see Figure 9.1). DSV proposes that individual mental health, expressed, for example, by habitual levels of anxiety, depression, (anti)social and impulsive behaviour, is relatively stable over time just like somatic functions such as blood pressure and pulse which remain within a narrow range over time. Despite temporal fluctuations of these habitual (symptom) levels, due to event exposure (Duncan-Jones et al., 1990; Ormel and Schaufeli, 1991), over a longer period mental health is in a dynamic equilibrium with the environment. People differ not only with respect to their habitual symptom level but also with respect to the degree at which it fluctuates following event exposure. The former inter-individual difference is attributable to persons’ psychobiological and social features. Stated differently, habitual symptom levels reflect psychobiological and social vulnerability and resilience . In contrast, fluctuations of symptom levels within individual biographies are due to experience of negative and positive events and circumstances (events). The nature of the events people experience is determined by random chance but also by individuals’ freedom to act and the control they have over their environment. Freedom to act (or scope for action) is limited by exogenous social and physical features of individuals’ environment. Environmental control reflects more endogenous, person-linked factors, and refers to individuals’ capacities to modify their environments in a desired direction, given their freedom to act. Jointly, freedom to act and environmental control determine how many persons can select and modify their environments. Thus, low social status implies relatively little freedom to act and social competence relatively more environmental control. However, even when freedom to act and environmental control are high, individuals do not necessarily select risk-free environments. Certain individuals may be inclined to choose environments where stress, of a social, occupational or relational nature, is particularly likely to occur. Whether mental health indeed declines following the experience of stressful events depends on (Lazarus and Folkman, 1984; Cohen, 1988; Cohen et al., 1995): their formal features (degree of unexpectedness, uncontrollability, etc.); how subjects appraise them; and how subjects cope with them. The DSV-model assumes that psychobiological and social vulnerability factors act on risk, largely via their influences on what people experience and how they appraise and cope with these experiences. Hence, the concept of vulnerability in the DSV-model refers to instrumental (or present) vulnerability (Ormel and deJong, 1999) to emphasise the proximal mechanisms of exposure, appraisal and coping through which vulnerability acts. Instrumental vulnerability is seen as the result of the interactions between an individual’s genetic vulnerability (encoded in the genome – susceptibility) and experiences (intra-uterine, childhood, adolescence). Although instrumental vulnerability may change at any time during adulthood, these changes are

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A dynamic stress-vulnerability model 153 (1)

(1)

Behaviour/experiences

Psychobiological vulnerability

Environmental control

Social vulnerability

(exogenous determinants)

appraisal

(2)

Perceived loss, threat, etc.

(2)

– conflictual family environment – low SES – urbanisation – poverty

coping

(4) (3)

Action space

Stressful events situations (objective features)

(endogenous determinants)

– deviant temperamental styles (eg. neuroticism, impulsivity) – dysfunctional physiological systems (eg. vegetative nervous system dysbalance, HPA-axis dysregulation) – (social cognitive deficits)

(Bad) luck

(4) Mental (ill) health

(3)

Figure 9.1 The dynamic stress-vulnerability model.

generally incidental and temporary. During childhood and adolescence, however, within-subject changes in instrumental vulnerability are more frequent and lasting. Subjective versus objective meaning A major contribution of Brown and colleagues was their distinction between subjective and contextual meaning of events. While the subjective meaning reflects the outcome of an individual’s appraisal process, the contextual meaning refers to a more ‘objective’ meaning in which both the event and contextual properties are taken into account but not the individual’s personality. Raters judge the likely contextual meaning in terms of loss, danger, fresh start, or whatever dimension of meaning is the focus, by asking themselves to what extent the event reflects that dimension, e.g. loss, for persons with the very same socio-demographic characteristics and observable goals as the individual who experienced the event. Thus, the ‘objective’ meaning refers to the likely meaning for an individual given his circumstances of living and goals. Features determining the objective meaning The ‘objective’ meaning of events is determined by their form and their content. Among the formal properties of events, their degree of (un)expectedness and (un)controllability have received attention in connection with research on post-traumatic stress conditions. Dependent on the victims’ position on the

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154 Johan Ormel and Jan Neeleman external-internal locus of control dimension, events, which are less controllable and more unexpected, induce more post-traumatic stress (Solomon et al., 1989). On the basis of their content, negative life events have been distinguished, according to the degree to which they imply loss as opposed to danger (Brown et al., 1995). Positive life events have been distinguished in delogjamming, anchoring and fresh start events (Brown et al., 1988; Brown et al., 1992). Regarding the contextual properties it is best to distinguish personal from macro contextual features. Important features of the personal context are the socio-demographic characteristics of the individual (sex, age, education, profession, etc.) and his goals and plans. For instance, the objective meaning of becoming pregnant can change completely depending on the woman’s plans, goals, and socio-demographic characteristics. However, the ‘objective’ meaning is also dependent on the macro context (Neeleman, 1997). The threat implied by psychosocial risk factors such as job loss or poverty is larger in periods or regions where employment and prosperity are the norm. The central role of meaning in the pathogenesis of mental ill health and its context-dependence are relatively specific to psychosocial determinants of (mental) health. Noxious effects of tobacco on health exist irrespective of somebody’s perceptions of them and of whether or not smoking is the norm or not. In general, psychosocial determinants carry higher mental health risks with them when they are rare and appraised as more threatening or stigmatising than when they are more prevalent. The appraisal process: subjective meaning As described above, the appraisal process yields the subjective meaning of events. Obviously, the same factors that determine the objective meaning play a role in the subjective meaning, although not with the same weights, as the objective meaning refers to the ‘average’ person within a particular context. Subjective meaning depends also on numerous individual characteristics, including personality and various idiosyncratic needs and norms. The coping process The coping process refers to emotional, cognitive and behavioural ways of dealing with events and their consequences. It may be adequate (leading to neutralisation of the threat), inadequate (the threat persists or increases) or – whilst apparently adequate – carry a cost of increased risk of mental ill health. Avoidance of anxiety-provoking situations may prevent anxiety in the short term but may foster a fully fledged phobia in the long run. The situation determines whether a coping strategy is adequate or not (Lazarus, 1993). Problem-focused coping is adequate when the environment is amenable to change, i.e. when there is freedom to act. Emotional coping (e.g. ignoring or denial) is more adaptive when circumstances cannot be altered i.e. when freedom to act is limited.

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A dynamic stress-vulnerability model 155 Continuous interplay The DSV-model is characterised not only by the dynamic nature of the equilibrium of mental health it proposes, but also by the continuous interplay between its various parameters such as individual genetic make-up, personality and socioeconomic status as they develop over time, and the occurrence of life events. The DSV-model allows additive, mediating as well as interactive, effects between vulnerability factors and events with regard to the outcome of interest. Collectively, vulnerability and experiences determine the liability to onset and remission, and hence the risk (or probability) of crossing a diagnostic threshold either way. Events with a relatively high risk of pushing someone across the threshold might be denoted as onset-provoking or remission-promoting agents. In addition, and contrary to the traditional image of the individual as the passive recipient of environmental experiences, the DSV-model emphasises the active control of the individual by selection, modification and even (re-)creation of (stressful) experiences. Whether or not ill health develops, and in which shape, depends on disorder-specific sensitivities in neurophysiological systems, characteristics of the coping process and how experiences are appraised.

Onset of Depression Life stress and onset Most evidence on the aetiological role of life events derives from retrospective case control comparing experience of and exposure to events between depressed subjects or those receiving mental health care for depression and non-depressed or non-treated controls. It has emerged that onset of depression is preceded by unpleasant events in around 75 per cent of cases whilst only around a quarter of subjects without depression onset experience such events in a comparable period (Brown and Harris, 1989; Jenaway and Paykel, 1997). Willige et al. (1995) used, in the Groningen Primary Care Study, a case control design to examine the role of life stress in the onset of emotional disorders as seen in twenty-five Groningen GPs’ surgeries. Severe life events (SLEs) and recently (less than two years) arisen long-term difficulties (LTD), both assessed with the LEDS, were both risk factors for onset of psychopathology as assessed with the PSE and classified according to the Bedford College criteria. LTDs which had been in existence for over two years did not affect risk of disorder, not even as vulnerability factors, e.g. by modifying (strengthening) effects of SLEs. The effects of SLEs and recent LTDs were additive. Around 60 per cent of anxiety and depressive disorders were preceded by at least one of the two versus 24 per cent in the control group. Co-occurrence of SLE and recent LTD increased the probability of an anxiety disorder ten-fold, of a depressive episode seven-fold, and of a mixed episode of anxiety and depression five-fold. Much rarer than case-control are cohort studies comparing the prospective incidence of depression between individuals exposed to stresses such as sacking,

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156 Johan Ormel and Jan Neeleman bereavements and threatening somatic illness, and individuals not so exposed (Surtees et al., 1995). However, the rare ones there have been generally support the findings of case control studies. Neuroticism and onset Various prospective studies have found that neuroticism and related temperaments and traits predict onset of emotional disorders (Caspi et al., 1996; Krueger., 1996; Hirschfeld et al., 1983, 1997; Kendler et al, 1993; Clayton,1994). Boyce et al. (1991) suggested that the risk of depression is mainly related to interpersonal sensitivity, which they believe has five components: interpersonal awareness, need for approval, separation anxiety, timidity and fragile inner-self. In the Groningen Well-being Study of a random population sample of 296 adults, neuroticism measured in 1970 predicted psychological distress at four successive follow-ups in the next two decades (Ormel and Wohlfarth, 1991; Sanderman, 1988). Psychological distress was measured in the Groningen Well-being Study by means of various measures, including a short semi-structured interview (rating frequency, duration and severity of some anxiety and depression symptoms), Bradburn’s self-report Negative Affect scale, and, in the last two measurement waves, Goldberg’s thirty-item general health questionnaire. Approximately 10 per cent of the sample was rated as having suffered from depressed mood for more than two weeks in the past four weeks. For worrying this percentage was 16 per cent. Mediation and modification effects of neuroticism In the Groningen Well-being Study, SLEs and LTDs mediated part of the effect of baseline neuroticism on psychological distress measured many years later (Ormel and Wohlfarth, 1991). Interestingly, the mediation was limited to person-dependent events and difficulties, i.e. provoking agents which were brought about by the individual’s own decisions or behaviour. Exposure to person-independent stresses was not associated with baseline neuroticism. We also found that neuroticism modified the effect of life stress on psychological distress (Ormel and Wohlfarth, 1991). Improvement and deterioration of circumstances of life during a one-year period had a much stronger impact on change in distress level in those with high baseline neuroticism (26 per cent of sample; beta = 0.51) compared to those with low scores (43 per cent; beta = 0.13). Note that neuroticism was measured six years prior to the assessment waves of symptoms, events, and difficulties. Neuroticism and life stress mediate genetic effects Genetic factors may act on risk factors for depression instead of on the disorder itself. There is evidence for genetic influence on risk factors of depression. Flint et al. (1995), for example, identified three loci in the mouse genome associated with emotional reactivity (neuroticism), a risk factor for anxious and depressive disorders in humans. It has further been shown that practically all major personality

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A dynamic stress-vulnerability model 157 traits are partially controlled by genetic factors. Studies of twins and adopted children have estimated that 40–60 per cent of the variations in neuroticism in a given population can be attributed to genetic factors (Loehlin, 1992; Heath et al., 1992). Exposure to life stress is also partly controlled by genetic factors. A range of studies have found genetic influences on life experiences (Kendler et al., 1993, 1995; Plomin et al., 1990; McGuffin et al., 1991; Foley et al., 1996). Since life events do not have genes, the direct genetic effects on life events and difficulties may be hard to understand. The answer lies in the assumption that the environment is not independent of the individual, but partially selected and created by the individual. This is borne out by the finding that genetic effects seem limited mainly to events over which the subjects had some control, i.e. events that resulted from their own decisions and behaviour. It is hypothesised that genes influence the environment through their affect on temperament, social abilities, and subsequently on personality. This presupposes that personality influences life event exposure, which indeed has been upheld by a number of studies, including work done in Groningen. Neuroticism, for example, is associated with the occurrence of unpleasant events and problems. Ormel and Wohlfarth (1991), Fergusson and Horwood (1987), Heady and Wearing (1989), Magnus et al. (1993) and Saudino et al. (1997) provided evidence that exposure to certain events is associated with age, neuroticism, extraversion, openness to new experiences, and position in society. Neuroticism is a predictor mainly of negative events, extraversion of positive events, and openness to experiences predicts both positive and negative ones. Neuroticism and low social status above all seem to predict the incidence of interpersonal, financial and ‘political and legal’ stress. An as yet unresolved question is whether depression, neuroticism and exposure to stressors are influenced by the same genetic factors. Kendler and KarkowskiShuman (1997), however, found a strong genetic correlation between neuroticism, exposure to stress under control of the individual, and depression. This suggests that the genes that predispose the individual to depression are in part identical to those which control neuroticism and, via neuroticism, influence exposure to certain stress. It should be noted however that the meaning of the genetic correlation between neuroticism and depression depends on how neuroticism is interpreted. There is definitely no agreement on this. As a matter of fact, the items with which neuroticism is typically measured refer to chronic negative feelings and cognitions, which in part resemble symptoms of mood and anxiety disorders. The elderly – a special group? While the significance of neuroticism, SLEs and LTDs in the aetiology of unipolar depression is well established for young and middle-aged persons, in particular women, little is known about the role of these risk factors, and their interrelationships, in the aetiology of depression in later life. This is unfortunate, as the prevalence of (mild) depression is considerable in the elderly, and the elderly are both absolutely and proportionally a growing age group. The uncertainties involve not only the main effects of these risk factors but also mediation and

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158 Johan Ormel and Jan Neeleman modification. To address these issues we did a case-control study, nested in a large community survey of elderly people held in 1993 (Brilman et al. submitted; Ormel et al., submitted). We compared eighty-three incident depressive cases with eighty-three controls, both recruited during 1996–8. We assessed onset, history, and type of depression (PSE 10), as well as date of occurrence and severity of SLEs and LTDs (LEDS). Neuroticism was measured premorbidly in 1993. 1

2

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SLEs, LTDs and neuroticism increased risk of onset of depression three to twenty-three-fold. Common types of events were loss of physical and mental capacities, and loss of close ties and social contacts due to illness, death, or institutionalisation of the respondent, his/her partner or significant others (e.g. child or friend). Elderly persons with a depression had experienced an excess of these losses in the three months preceding onset compared to controls in a comparable period. These findings are in line with the high prevalence of health-related stress in later life (Bieliauskas, 1995; Davies, 1994; Prince et al., 1997) and its association with depressive symptoms found in earlier studies (Beekman et al., 1997; Prince et al., 1997, 1998). We did not find any mediation by life stress of the effects of neuroticism. Similarly, the risk of ongoing LTDs on depression was not mediated by SLEs. The occurrence of SLEs in this old-age sample was independent of neuroticism and LTDs. Whilst this seems at odds with a characteristic of the DSV-model, namely that vulnerability acts, in part, via stress generation, it may be due to the nature of life stress in the elderly. Whereas depressogenic stress in younger age groups often arises from interpersonal conflicts (arguments, letting down, conflicts at home or at work), financial hardship, work problems or unemployment, common stresses in older people involve loss of physical and mental capacities, of relationships and social contacts, due to illness and aging. Since poverty is uncommon in the Netherlands due to good social security, pensions and subsidised housing, events associated with poverty are rare. Consequently, older people may be predominantly exposed to losses that are outside their control, and thus independent of their vulnerabilities as indicated by neuroticism and ongoing LTDs. Although SLEs were also capable of triggering depressive episodes in those with low neuroticism and no LTDs, neuroticism and LTDs tended to amplify the effects of SLEs. In the presence of high neuroticism or an LTD of at least moderate severity, the (added) depressogenic effect of SLEs was threefold stronger than in the absence of high neuroticism or LTDs. This expands similar findings for neuroticism (Ormel and Wohlfarth, 1991; Kendler et al., 1995; Bolger and Schilling, 1991) to the elderly. The amplification of the effect of a SLE by an ongoing LTD has not been demonstrated before, although it comes close to Brown and Harris’ (1989) observation that a severe event which matches an existing difficulty has a three-fold increased risk in women compared to a severe event without a matching difficulty. The modifying role of difficulties may help to shed some light on the question why an ongoing LTD triggers onset of depression at that particular point in time in persons who did

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A dynamic stress-vulnerability model 159

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not experience a severe event. It might be that the timing of onset relates to the occurrence of a relatively mild event whose effect is amplified by an ongoing LTD. The severity of the depression did not affect the results. The univariate effects of all predictors were just as large in the subgroup of symptomatic and minor depression as in the subgroup of major depression. Expanding earlier work of Brown et al. (1994) and Frank et al. (1994) to the elderly, history of depression turned out to be important. Neuroticism had a stronger, and SLEs a weaker effect on the risk of recurrent depression compared to first lifetime episodes, albeit the effects were significant in both subgroups. These differences fit the notion of accumulation of vulnerability due to prior mental ill health, resulting in increased sensitivity for mild events, which may obscure the fact that severe events have an even stronger impact. As about half of recurrent episodes were minor, the aetiological differences between first and recurrent episodes are not limited to severe depressions, but apply to milder variants as well. We do not know whether the difference in vulnerability is due to genetic differences or vulnerability accumulation by earlier episodes, a process also described as kindling and sensitisation (Post 1992). A considerable proportion of episodes was not preceded by a health or nonhealth-related SLE in the three months preceding onset. Of the cases, 47 per cent did not experience a SLE of at least mild severity, of whom 31 per cent did not even have a high neuroticism score at baseline. Thus the onsets of some late-life depressions seem unrelated to SLEs and neuroticism, which might reflect the higher proportion of organic affective states among the elderly compared to the young (Rabins et al., 1991).

Remission of depression The role of events in remission of depression has received less attention. A first question is whether the SLEs and LTDs that contributed to the onset have influence on prognosis. Results are mixed. Some studies found that depressions which were triggered by life stress remitted quicker than depressions with a ‘spontaneous’onset (Monroe et al., 1985; Reno and Halaris, 1990; Tennant et al., 1981). Others have been unable to confirm this (Lloyd et al., 1981; Murphy, 1983). However, the presence of LTDs such as chronic disabling somatic illness and interpersonal conflicts delay remission (Kedward, 1969; Sims, 1975; Brown and Moran, 1994), which suggests that life events may also affect prognosis of depression when they have degenerated into chronic difficulties. A separate issue concerns the possible effects on prognosis of life events supervening during episodes. Findings have been mixed. Studies of mild depressions in population or primary care samples suggest that SLEs delay (Wittchen, 1988; Giel et al., 1978) and positive life change (PLC) brings forward remission (Tennant et al., 1981; Brown et al., 1988, 1992; Davies et al, 1983; Parker et al., 1985; Needles and Abramson, 1990; Ronalds et al.,1997; Oatley and Perring, 1991; Leenstra et

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160 Johan Ormel and Jan Neeleman al.,1995). PLCs refer to life events and other life changes that restore hope, increase sense of security, or provide relief from ongoing stresses. PLC is neither a necessary or sufficient condition for remission. Against this background, Oldehinkel and co-workers (in press) examined in the Groningen Primary Care Study whether some of those factors that have been implicated in the course and outcome of depression like symptom severity, neuroticism, selfesteem, social support, and attributional style (Brugha et al., 1997; Katon et al., 1994; Lara et al., 1997; Needles and Abramson, 1990; Brown et al., 1988; Brown et al., 1990; Keller et al., 1992; Ronalds et al., 1997) act – wholly or in part – by modifying effects of PLC. One hundred and four primary care patients with a recent onset of depressive disorder were followed for three and a half years. Detailed diagnostic information was obtained by the PSE, which was administered three times; dates of transitions in diagnostic status between measurements were established with Course Interviews. PLC was assessed with the LEDS (Brown et al, 1992), yielding dates of occurrence and multidimensional contextual ratings of events and difficulties. Only episodes lasting longer than three months were considered (N=86; 69 per cent females, mean age 36.6). PLC was associated with time to remission in females (hazard ratio 2.3) but not males. In a multivariate model containing PLC as a time-varying covariate alongside fixed covariates measured at baseline, in addition to PLCs’ effects, significant associations with time to remission were found for age, severity of premorbid difficulties, neuroticism, selfesteem, available network size, and four coping strategies (tension reduction, withdrawal, self-reassurance, and mobilising social support). Time to remission was relatively short for young people, and for those with low severity of premorbid difficulties, low neuroticism, high self-esteem, a large available network, and a coping strategy aimed at reducing tension, mobilising social support, self-reassurance, and no withdrawal. The interaction between gender and PLC continued to exist despite full adjustment, so that the PLC raised the instantaneous probability of remission 4.4-fold in females whilst no effect was apparent in males. In addition, it emerged that the impact of PLCs was larger in the presence of high neuroticism scores. Gender and PLC It is highly intriguing that effects of PLC on time to remission should be limited to women, since most studies on the relationship between life stress and depression employed females only (e.g., Bifulco et al., 1998; Brown et al., 1988; Brown and Moran, 1997; Fergusson and Horwood, 1984, Kendler et al., 1997; Lora and Fava, 1992; Mazure, 1998). Oldehinkel’s results are in line with Cooke’s (1986), who failed to find a (simple) relationship between life stress and ‘anxiety-depression’ in males, but at odds with others. These gender differences may be associated with gender-related role differences which are at their peak among persons in their early thirties (Jorm, 1987). This is also suggested by research in couples who had recently experienced a life event which was potentially depressogenic for both of them, which found that women had a greater risk of a depressive episode;

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A dynamic stress-vulnerability model 161 but only following events in the traditionally female domain (e.g. events involving children or household), and only when the couples showed clear gender differences in associated roles (Nazroo et al., 1997). Consistent with this, male depressed patients have been found to report more problems of work than male controls (Nanko and Demura, 1993). Role areas of particular concern to males may be less subject to resolution by positive change than role areas which are important for females. An additional explanation for Oldehinkel’s findings is that the LEDS, developed using female samples, is perhaps less sensitive to life change that is relevant for men such as status-related events. Neuroticism and PLC The interaction of PLC with neuroticism, observed by Oldehinkel, suggests that highly neurotic people benefit more from PLC. If replicated in other populations, this finding would support the DSV-model which postulates that life changes, negative as well as positive, have more impact on well-being in neurotic people than in less vulnerable persons.

Events that might change vulnerability In the context of research on post-traumatic stress disorder, evidence is accumulating that life-threatening experiences (traumas) have the potential to create lasting vulnerability to emotional disorder. The neurobiological basis of the added vulnerability is now being revealed by neuroimaging and neuropsychological studies in patients with PTSD (Charney et al., 1993). The amygdala, locus ceruleus and frontal lobes are among the cerebral structures implicated. It is in them that severe or lasting trauma causes persistent changes in the regulatory circuitry of the ‘emotional brain’, with various effects on HPA-axis functioning and autonomic nervous system (Kagan, 1994). Epidemiological concepts which may help explain how vulnerability may change over time are turning points (e.g. attachment to the labour force and cohesive marriage; both strengthen social bonds in adulthood), sensitising and steeling experiences (Rutter, 1996; Andrews et al., 1993; Caspi and Moffit, 1993; Laub and Sampson, 1993; Harris et al., 1990). It is easier to imagine intuitively how such experiences can bring about longterm change in exposure to stressors than to grasp how they can change the organism. For example, a cohesive marriage or cohabitation with a non-deviant partner can reduce exposure to environmental risk factors. But does it act on the psychobiology of the person? And, if so, how? Has the biological substrate been altered? Alternatively, are the effects on styles of appraisal and coping? Or do they represent different sides of the same coin? We hypothesise that at least four factors interact to determine the degree to which events may sensitise or steel the organism (Ormel and deJong, 1999). First, the event should represent a significant challenge, which can turn out as a failure (loss) or a success (gain). Its significance as a challenge depends on its potential to

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162 Johan Ormel and Jan Neeleman affect future physical and/or social well being (Ormel et al., 1996). Especially important is the potential loss or gain of resources for its production such as selfefficacy, a key-relationship, planning capacities, and income. Other factors that help determine the outcome of the challenge are attribution of control, social support, and genetic vulnerability. Social support, in particular the active-emotional variant of it, is important in two respects. In case of failure, social support that helps buffer blows to self-esteem may prevent sensitising. In case of success, social support that helps to increase the sense of mastery and self-esteem may result in steeling. Genetic vulnerability may enhance the sensitising effect and weaken the steeling effect in subjects with high genetic vulnerability as compared to persons with low genetic vulnerability (other things being equal). With varying exposure to events throughout life time and different levels of the factors that determine whether events steel or sensitise individuals or turn their trajectory in a different direction, inter-individual differences in vulnerability might become larger with increasing age. If this process of increasing variance does exist, it is probably counteracted by selective mortality amongst the most vulnerable. Sensitising and steeling experiences may set the stage for long-term change in instrumental vulnerability by changing one or more of the proximal etiologic mechanisms such as exposure to life stress, appraisal style, or coping style. The change in exposure to life stress can be brought about by either a change in environment or by a change in action space and environmental control. It is not surprising that loss of physical function and loss of contact with close ties form the bulk of losses in later life. According to Social Production Function theory, physical capacities and close ties are important resources for achieving major instrumental goals of physical and social well being (Lindenberg and Frey 1993; Ormel et al. 1997; Steverink et al. 1998). Steverink et al. have argued that in later life the production of well-being through means such as status, behavioural confirmation and ‘stimulation’ becomes more difficult, relative to means such as affection and ‘comfort’. It is precisely the latter two that are threatened by loss of contact with close ties and loss of physical function.

Conclusion The Groningen findings fit the DSV-model. The data discussed in this chapter suggest: 1 2 3

both main and additive interaction effects of SLEs, LTDs, and neuroticism on risk of depression; both main and additive interaction effects of PLC and neuroticism on time to recovery from depression; and effects of neuroticism on life stress exposure, i.e. mediation of the influence of neuroticism on depression via life stress.

Another way of expressing this mediation is that neuroticism speeds up the occurrence of SLEs. The reason that this mediation effect was only observed in non-

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A dynamic stress-vulnerability model 163 elderly and not in older people, is probably due to the uncontrollability of prevalent, disease-related forms of loss in later life. There is often a contribution made by the person, if passive, to the seemingly uncontrollable humiliations suffered by younger people, while the physical afflictions of old age may come really out of the blue. Low controllability of life stress reduces the opportunity for action space and environmental control to prevent or modify it. If neuroticism can be interpreted as a marker of psychobiological sensitivity to stress, and ongoing difficulties as an indicator of social vulnerability, both vulnerability within the skin and vulnerability outside the skin tend to amplify the depressogenic effects of SLEs. Our findings expand the original stress-vulnerability model developed by Brown and Harris (1978) by showing that life events are also capable of triggering a depressive episode in the absence of vulnerability, at least in older people, although the effects are substantially larger in psychobiologically and socially vulnerable older people. To date, we have not studied the plasticity of psychobiological vulnerability by experience, another important assumption of the DSV-model. However, we have started a fifteen-year longitudinal study of a cohort of 2,500 10-year olds, the TRAILS study, which will examine the plasticity of vulnerability (and, of course, resilience). A major objective of TRAILS is to test hypotheses concerning the determinants of vulnerability change, including all kinds of experiences and indicators of past vulnerability. LEDS methodology will play an important role in the assessment of experiences and their qualities. Important indicators of vulnerability will be neuroticism, impulsivity, social capital, family loading and (social) cognitive deficits. The observation by Oldehinkel et al. (in press) that the association of time to recovery with PLC appeared negligible for males, while the instantaneous probability of remission increased over four-fold after a positive life change in females is puzzling, and in need of replication. Depression has a multifactorial aetiology with genetic and environmental contributions. The substantial, genetic influences on neuroticism and depression are rarely predominant. Moreover, the prevalence of depression shows substantial cross-cultural variation (Brown, 1996) which is, in part, related to variation in the frequency with which LTDs, SLEs and PLCs occur in different cultures and at different times. The prevalence of depression in a particular population at a particular time may be related largely to social characteristics of that population at that time, while the question of who in that population develops depression may be largely genetically determined (Ormel et al., in press). Genetic effects on depression risk are mediated in part by neuroticism, which, in turn, acts partly by influencing exposure to, and modifying effects of, experiences on onset and remission of depression. Such interactions between individuals’ genetic make-up, their personality and biography and their environment are important phenomena with potential relevance for primary and secondary prevention of depression. However, they can only be clarified if their various components are clearly distinguished and not confounded, for instance, by taking more than only person-independent key aspects of a person’s biography into account in the rating of events.

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164 Johan Ormel and Jan Neeleman

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A dynamic stress-vulnerability model 167 Lora, A. and Fava, E. (1992) ‘Provoking agents, vulnerability factors and depression in an Italian setting: a replication of Brown and Harris’s model’, Journal of Affective Disorders, 24, 227–35. Magnus, K., Diener, E., Fujita, F. and Pavot, W. (1993) ‘Extraversion and neuroticism as predictors of objective life events: A longitudinal analysis’, Journal of Personality and Social Psychology, 65, 5, 1046–53. Mazure, C.M. (1998) ‘Life stressors as risk factors in depression’, Clinical Psychology: Science and Practice, 5, 291–313. McGuffin, P., Katz, R., and Rutherford J.(1991) ‘Nature, nurture and depression: a twin study’, Psychological Medicine, 21, 329–35. Monroe, S.M., Thase, M.E. and Hersen, M. (1985) ‘Life events and the endogenousnonendogenous distinction in the treatment and post-treatment course of depression’, Comprehensive Psychiatry, 26, 175–86. —— and Simons, A.D. (1991) ‘Diathesis-stress theories in the context of life stress research: Implications for the depressive disorders’, Psychological Bulletin, 110, 406– 25. Murphy, E. (1983) ‘The prognosis of depression in old age’, British Journal of Psychiatry, 142, 111–19. Nanko, S. and Demura, S. (1993) ‘Life events and depression in Japan’, Acta Psychiatrica Scandinavica, 87, 84–187. Nazroo, J. Y., Edwards, A. C. and Brown, G. W. (1997) ‘Gender differences in the onset of depression following a shared life event: a study of couples’, Psychological Medicine, 27, 9–19. Needles, D. J. and Abramson, L. Y. (1990) ‘Positive life events, attributional style, and hopefulness: testing a model of recovery from depression’, Journal of Abnormal Psychology, 99, 156–65. Neeleman, J. (1997) The social and epidemiological context of suicidal behaviour, Groningen: Van Denderen. Oatley, K. and Perring, C. (1991) ‘A longitudinal study of psychological and social factors affecting recovery from psychiatric breakdowns’, British Journal of Psychiatry, 158, 28–32. Oldehinkel, A.J., Ormel, J. and Neeleman, J. (in press) ‘Predictors of time to remission from depression in primary care patients: do some people benefit more from positive life change than others?’, Journal of Abnormal Psychology. Ormel, J. (1980) Moeite met leven of een moeilijk leven: Een vervolgonderzoek naar de invloed van psychosociale belasting op het welbevinden van driehonderd Nederlanders, Proefschrift Rijksuniversiteit Groningen, Groningen: Konstapel. —— and de Jong, A. (1999) ‘On vulnerability to common mental disorders. An evidencebased plea for a developmental perspective’ in M. Tansella and G. Thornicroft (eds) Common mental disorders in primary care, London: Routledge. —— and Schaufeli, W. (1991) ‘Stability and change of psychological distress and their relationship with self-esteem and locus of control’, Journal of Personality and Social Psychology 60, 288–99. —— and Wohlfarth, T. (1991) ‘How neuroticism, long-term difficulties, and changes in quality of life affect psychological distress. A longitudinal approach’, Journal of Personality and Social Psychology, 60, 744–55. ——, Lindenberg, S., Steverink, N. and Verbrugge, L.M. (1996) ‘Subjective well-being and social production functions’, Social Indicators Research, 46, 61–90.

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168 Johan Ormel and Jan Neeleman ——, Lindenberg, S., Steverink, N. and Von Korff, M. (1997) ‘Quality of Life and Social Production Functions: a framework for understanding health effects’, Social Science and Medicine, 45, 1051–63. ——, Neeleman, J. and Wiersma, D. (in press) ‘Determinanten van psychische gezondheid in I.A.M. Maas and J. Jansen (eds) Volksgezondheid toekomst verkenning. Psychische (on)gezondheid: determinanten en de effecten van interventies, Bilthoven: RIVM. ——, Oldehinkel, A.J. and Brilman, E.I. (submitted) ‘The aetiology of depression in later life. A prospective, population-based study of neuroticism, ongoing difficulties, life events, and type of depression’. Parker, G., Tennant, C. and Blignault, I. (1985) ‘Predicting improvement in patients with non-endogenous depression’, British Journal of Psychiatry, 146, 132–9. Plomin, R., Lichtenstein, P., Pedersen, N.L., McClearn and G.E., Nesselroade, J.R. (1990) ‘Genetic influence on life events during the last half of the life span’, Psychology and Ageing 5, 25–30. Post, R.M. (1992) ‘Transduction of psychosocial stress into the neurobiology of recurrent affective disorder’, American Journal of Psychiatry, 149, 999–1010. Prince, M.J., Harwood, R.H., Blizard, R.A., Thomas, A. and Mann, A.H. (1997) ‘Social support deficits, loneliness and life events as risk factors for depression in old age. The Gospel Oak Project VI’, Psychological Medicine, 27, 323–32. ——, Harwood, R.H., Blizard, R.A., Thomas, A. and Mann, A.H. (1997) ‘Impairment, disability and handicap as risk factors for depression in old age. The Gospel Oak Project V’, Psychological Medicine, 27, 311–21. ——, Harwood, R.H., Thomas, A. and Mann, A.H. (1998) ‘A prospective population-based cohort study of the effects of disablement and social milieu on the onset and maintenance of late-life depression. The Gospel Oak Project VII’, Psychological Medicine, 28, 337–50. Rabins, P., Pearlson, G. and Aylward, E. (1991) ‘Cortical magnetic resonance imaging in elderly patients with major depression’, American Journal of Psychiatry, 148, 617–20. Reno, R.M. and Halaris, A.E. (1990) ‘The relationship between life stress and depression in an endogenous sample’, Comprehensive Psychiatry, 31, 25–33. Rodgers, B. (1991) ‘Models of stress, vulnerability and affective disorder’, Journal of Affective Disorders, 21, 1–13. Ronalds, C., Creed, F., Stone, K., Webb, S. and Tomenson, B. (1997) ‘Outcome of anxiety and depressive disorders in primary care’, British Journal of Psychiatry, 171, 427–33. Rutter, M. (1996) ‘Transitions and turning points in developmental psychopathology: As applied to the age span between childhood and mid-adulthood’, International Journal of Behaviour Development, 19, 603–26. Sanderman, R. (1988) Life events, mediating variables and psychological distress: a longitudinal study, thesis, University of Groningen. Saudino, K.J., Pedersen, N.L., Lichtenstein, P., McClearn, G.E. and Plomin, R. (1997) ‘Can personality explain genetic influences on life events?’, Journal of Personality and Social Psychology, 72, 1, 196–206. Sims, A. (1975) ‘Factors predictive of outcome in neurosis’, British Journal of Psychiatry, 127, 54–62. Solomon, Z., Mikulincer, M. and Benbenishty, R. (1989) ‘Locus of control and combatrelated post-traumatic stress disorder: the intervening role of battle intensity, threat appraisal and coping’, British Journal of Clinical Psychology, 28, 131–44. Steverink, N., Lindenberg, S. and Ormel, J. (1998) ‘Towards understanding successful ageing: patterned change in resources and goals, Ageing and Society, 18, 441–67.

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A dynamic stress-vulnerability model 169 Surtees, P.G. (1995) ‘In the shadow of adversity: the evolution and resolution of anxiety and depressive disorder’, British Journal of Psychiatry, 166, 583–94. Tennant, C., Bebbington, P. and Hurry, J. (1981) ‘The short-term outcome of neurotic disorders in the community: the relationship of remission to clinical factors and to ‘neutralising’ life events’, British Journal of Psychiatry, 139, 213–20. Willige, G. van de, Ormel, J. and Giel, R. (1995) ‘Etiologische betekenis van ingrijpende gebeurtenissen en langdurige moeilijkheden voor het ontstaan van depressie en angststoornissen: een nadere uitwerking’, Tijdschrift voor Psychiatrie, 37, 689–703. Wittchen, H.U. (1988) ‘Natural course and spontaneous remission of untreated anxiety disorders: results of the Munich follow-up study (MFS) in I. Hand and H.U. Wittchen (eds) Panic and Phobias 2. Treatment and variables affecting course and outcome.

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10 The timing of lives Loss events over the life course and the onset of depression Paul Surtees and Nick Wainwright

Introduction Progress in the methods of assessment of adverse event histories over the pastquarter century has enabled advances in understanding the form and pattern of health change following such experiences; particularly concerning changes in psychiatric health. Such work has shown, for example, through the increasingly finemapping of particular event attributes to individual circumstances, that certain events appear to carry special salience for such health change (Brown et al., 1995, Lam et al., 1996). The origin of many of these ideas can be traced to the papers published by George Brown and colleagues during the early 1970s that addressed the concerns of those researchers initially sceptical of the causal role of adverse experience for the onset of psychiatric disorder (Brown et al., 1973a; Brown et al., 1973b; Brown, 1974). These publications provided the foundation to much of the work that has followed: giving increased attention to study design (the appropriateness of particular comparison groups), to event assessment methodology (the choice of equivalent time periods for comparison groups), to definitions of episode status and of onset timing, and subsequently stimulating ideas concerning the causal mechanisms through which adverse exposure might be seen to influence health change (originating from ideas of brought forward time). Alternative approaches to the assessment of adverse event histories have been developed over the last two to three decades, most notably those that depend upon a list approach in contrast to interview based methods (see Turner and Wheaton, 1995; Wethington et al., 1995 for recent reviews), and differences in the ideas that underpin assessment have evolved. These concern, for example, the extent to which event exposure ratings either should or should not be endowed with contextrelated information that may subsequently be seen to perturb evaluation of social vulnerability (see Dohrenwend, 1998). These interview techniques, of which the Life Events and Difficulties Schedule (LEDS: Brown and Harris, 1978) set a new standard, have provided a means through which a detailed narrative of adverse experience can be recorded and rated using scales of increasing subtlety. However, their use is limited by the total assessment time they require (that typically extends over many hours including post-interview rating) and the implications this has for study costs and research design. Such considerations have contributed to the

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172 Paul Surtees and Nick Wainwright inapplicability of the interview-style methods either in those studies charged with investigating the role of adverse experience in very large-sample study designs or where an extended event risk period (for example, of several years) may be of special interest. Both these requirements are combined in epidemiological studies seeking to establish the role of adverse experience in the incidence and course of (chronic) physical disease During the last five years or so, appeals have been made for the integration of ideas that underpin life stress research with those drawn from work in life-span developmental psychology, upon which life course theory has been founded (e.g. see George, 1993; Pearlin and Skaff, 1996; Elder et al., 1996; Karel, 1997). Both research traditions have a common interest in the timing of event transitions within lives and with mapping their immediate and longer-term impact, whether this concerns evaluation of the role of event sequences experienced over relatively narrow time-frames and consequent changes in health or, in the case of life course methods, a concern with the dynamics of lives over time – ‘a sequence of socially defined, age-graded events and roles that the individual enacts over time’ (Elder, 1998: 941). Typically, life stress research has been, and continues to be, pursued with the aim of improving understanding of the relationship between adverse experience and the onset of (for example, psychiatric) disorder, through studies assessing adverse experience over relatively brief time-frames (usually six months to a year). Whilst such designs reflect the difficulty of accurately assessing extended event histories, the importance of a life course perspective has been (at best) minimised (with, for example, early childhood events considered in relation to health effects following adversity in adult life), or more usually completely neglected (Elder et al., 1996, Pearlin and Skaf, 1996). Against this background, significant attempts have been made recently to extend the time-frames of adverse event history assessment in order to provide a clearer foundation for understanding the role of stress in life course dynamics (e.g. Ensel and Lin, 1996, Ensel et al., 1996). This work has examined the duration over which adverse events have health effects and the relationship between events experienced many years previously (distal events) in association with other events experienced more recently (proximal events) with health outcomes. Such work has required the development of new event history assessment techniques that attempt to map an individual’s personal trajectory through time, recording significant events and transitions within distinct life domains (e.g. relationships, work, education, etc.). Repeated use, at intervals, of these assessment approaches (e.g. the Life History Calendar) has provided a means through which the evolution of life change can be mapped over extended periods of individual lives as dynamic episodes rather than through a history of static incidents (e.g. Caspi et al., 1996; Lin et al., 1997). Recent life stress and life course research has suggested that improved understanding of the role of adverse experience in health change may be achieved through unifying aspects of the two perspectives. Such perceived advantage stems from the view that a life course perspective provides a framework within which normative and non-normative (age-graded) experiences can be evaluated in terms of clearly defined outcomes. The development of models of the impact of

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Loss events and the onset of depression 173 sequences of adverse events, experienced over relatively short-term study periods, in relation to episodes of depression, has, for example, suggested evidence for the additivity and subsequent decay of event effects (e.g. see Surtees 1989, Surtees et al., 1997) and provided the basis for precise tests of vulnerability (Surtees and Wainwright, 1996; Surtees and Wainwright, 1999). Additivity, here having been assessed in terms of the increased likelihood of depressive disorder according to the number of adverse events experienced. Of special interest, therefore, is whether broadly equivalent support for these ideas can be found based upon eventhistory data drawn from the study of extended time periods and, if so, whether the adoption of a life course perspective to these data could provide new insights into modelling of the life stress process over the life course.

Plan of the chapter The following discussion is focused on investigating the process through which event exposure may lead to depressive disorder onset. Initially, an approach to adversity (and affective disorder history) assessment is described within the context of a large-scale nutritional epidemiology study. Second, the role of time and time-interactions are discussed in the context of survival analysis with particular emphasis on the use of discrete-time methods. A strategy is then outlined for evaluating the temporal influence of event exposure on subsequent onsets of disorder. Third, results of an initial exploration of these data are discussed focusing upon individuals’ reports of the impact of, and adaptation to, selected (maternal and marital loss) events experienced over the life course. Finally, results are presented from a discrete (grouped) time survival analysis with particular attention given to the time-varying influence of loss experience on adult depressive disorder onset.

Study context: EPIC Recent reports have focused the attention of researchers and policy makers alike on the disability attributable to chronic disease (e.g. WHO, 1997; Murray and Lopez, 1997). This work has highlighted the extent to which cardiovascular disease and cancer are amongst the leading causes of mortality, morbidity and disability globally and particularly so for the developed nations. These reports have also shown mood disorders to be a leading cause (globally) of disability and, whilst concluding in 1990 that unipolar major depression was ranked fourth in terms of a measure of disease burden (the disability adjusted life year), it is considered likely to be ranked first (globally) by the year 2020 (WHO, 1997). These current (and growth) perspectives on the health burden attributable to mood disorders are further elaborated by an accumulating literature implicating a history of mood disorders as conferring heightened risk of subsequent chronic physical disease and mortality (Eaton et al., 1996; Everson et al., 1996; Glassman and Shapiro, 1998; Kaplan and Reynolds, 1988; Kouzis et al., 1995; Morris et al., 1993; Shekelle et al., 1981). In recognition of results from nutritional epidemiology studies that have consistently shown a relationship between diets rich in fruit and vegetables and a reduction in risk of

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174 Paul Surtees and Nick Wainwright certain site-specific cancers, the European Prospective Investigation into Cancer and Nutrition (EPIC) project was implemented during the early 1990s (see Riboli and Kaaks, 1997), to capitalise upon known diet diversity across Europe. This project is a multi-centre prospective cohort study addressing the importance of nutritional and other factors on chronic disease development in nine European countries with populations distinguished by variations in dietary habits and cancer risk. The EPIC in Norfolk study is designed to measure the incidence of chronic disease in a population sample of around 25,000 people aged 45–74 years at recruitment. The sample has been obtained through general practitioners, with data collected on diet, haematological indices, physical activity, reproductive history, medical and family history and lifestyle through a variety of questionnaires and other procedures (Bingham, 1997; Bingham et al., 1997; Day et al., 1999). Psychosocial factors in the study are assessed through the Health and Life Experiences Questionnaire (HLEQ) and include a restricted assessment of the mood status of a respondent over their lifetime. This is assessed through a structured self-assessment approach to psychiatric symptoms embodying rules from the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV, APA, 1994), but limited only to major depressive disorder (MDD) and generalised anxiety disorder (GAD). The HLEQ mood section was designed to identify those thought likely to meet putative (anxiety or depressive) DSMIV diagnoses at any time in their lives, to provide evidence of chronicity and to provide estimates (where appropriate) of onset and offset timings. Initial analysis has suggested that prevalence estimates of MDD within the EPIC sample (2.3 per cent for two weeks, 4.2 per cent for 12-months and 13.9 per cent over the lifetime), are closely comparable to those obtained recently by interview in the UK and to those lifetime MDD rates determined through international studies (Surtees et al., 2000).

Measurement of adversity over the life course Three approaches to the assessment of adverse experience are employed in the HLEQ. The first is based upon experiences up to age 16 and includes measures of parental care, circumstances or behaviour during that time (e.g. parental divorce, prolonged unemployment, drink or drug abuse), prolonged periods of separation from mother and other adverse experiences (physical abuse by someone close, experience of a frightening event, being sent away from home because of own actions/behaviour). Second, the lifetime occurrence of a set of pre-defined adverse events is also assessed but limited by the constraints of questionnaire assessment to those experiences most likely to be accurately remembered over a lifetime; namely serious illnesses, injuries or assaults, relationship events (separation, divorce, termination of pregnancy), work events (retirement, redundancy or being sacked) and loss experiences (of first degree relatives). Additional questions are asked concerning events involving the police (resulting in a subsequent court appearance), and of any other unpleasant (or disappointing) events that were very important in the respondent’s life. A further question concerns the experience of positive and fulfilling events considered to have had a beneficial influence on their life. Event timing (year of occurrence), and degree of subjective upset felt immediately following

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Loss events and the onset of depression 175 each event, coded on the four-point scale: (1) not at all, (2) a little, (3) moderately, (4) extremely, are also assessed. As earlier work suggested support for statistical models of the relationship between adverse event effects and the onset of depression through allowance for decay in their effects over time (e.g. Surtees, 1989), a further question concerned the extent to which a respondent felt that they had recovered from the effects of the event at the time of assessment, coded through a fourpoint scale: (1) completely, (2) mostly, (3) a little, (4) not at all. Third, a non-prescriptive calendar approach was designed to enable recording of longer-term, more enduring adverse circumstances experienced over the life course. This approach is presented to each respondent as a Personal Life Chart (PLC) through which respondents are asked to record the times of prolonged difficulty in their lives and to date and describe them briefly. Only general guidance is given to participants concerning areas of life where such difficulties may have been experienced (such as emotional, financial, social). The approach was designed primarily to encourage disclosure of all prolonged times of personal difficulty, regardless of their basis. This format therefore provides a brief way of representing periods of relative personal difficulty across lifetimes in the EPIC population and stems from the methodological framework of the LEDS (Brown and Harris, 1978) approach to the assessment of long-term difficulties; adapted here for use within a questionnaire format and to record experiences across a lifetime. A rating scheme has been developed to enable the free-text descriptions of the broad universe of experiences charted to be reliably classified by area and according to the focus of each difficulty. Inevitably, retrospective event history data arising from the combined use of these three approaches to assessment can provide, at best, only a limited temporal skeleton of those outstanding and prolonged adverse experiences across a lifetime. Whilst this approach is in some contrast to what would be obtained through use of interview methods, there is no reasonable alternative to using a questionnaire technique in the context of such a large population study as EPIC.

Exploration of ideas and analytic strategy Brown and colleagues presented arguments to elucidate the nature of the causal link between adverse events and the onset of psychiatric disorder, illustrating these through ideas that conceived of adverse events as being either of triggering or formative importance for onset and through invoking the concept of brought forward time; an… ‘estimate of the average time from an onset produced by an event to the time when a spontaneous onset would have occurred had no events intervened’ (Brown et al., 1973b: 165). Central to these ideas is the opinion that an individual’s morbid risk is a function of some unobserved (latent) process that can be perturbed through the experience of new events, but that the morbid risk may be most reasonably understood to diminish over time, in the absence of subsequent adverse experience. Further development of these original ideas since publication has followed, through a greater concentration upon the details of developing the assessment of event histories (e.g. with refinement of the LEDS and through other approaches such as in the Structured Event Rating System, SEPRATE: see Wethington et al.,

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176 Paul Surtees and Nick Wainwright 1995; Dohrenwend, 1998) rather than in attempts to advance understanding of the way in which adverse experience relates to disorder onset through the development and testing of statistical models of that process. This can only follow through identification of the principles that underpin the link and subsequently through testing of models of their representation. As a consequence, the ability to relate complex event histories to changes in health state still remains limited. Particular interest analytically has focused upon those few attributes of the event-illness relationship that would appear to be of central importance for constructing the first steps towards a generic (modelling) solution relating a history of adverse event exposures to changing health states and outcomes. These concern recognition that there is a dose-response component to the relationship (that events of severe impact have greater health consequences than those of more minor impact), that under some circumstances adverse event effects appear to be additive (e.g. Surtees et al., 1997), that the adverse effects of events appear to decay over time (e.g. Surtees, 1989), that the duration over which morbid risk levels are raised, following event exposure, may extend over many decades and may vary according to the life stage at event exposure (e.g. see Kessler and Magee, 1993; Kessler et al., 1997) and according to prior history of the health outcome of interest (see Kessler et al., 1996; Kessler, 1997). These characteristics that appear to govern the relationship between adverse experience and depression have been further elaborated through investigation of ‘incubation’ or delay between event occurrence and subsequent onset of affective disorder (Bebbington et al., 1993), through preliminary attempts to account for the temporal patterning of events prior to outcome or onset (Surtees and Ingham, 1980; Frank et al., 1996), and through the more recent and increasing application of discrete (grouped) time survival approaches (see below) to the analysis of event history relationships (see Willett et al., 1998).

Time-dependent covariates and time-varying effects The techniques of survival analysis lend themselves naturally to the investigation of models of the relationship between a history of adverse event exposures and the subsequent onset of disorder. Such analysis provides the basis for the investigation of many of the issues raised above within a framework where time, and how it is permitted to enter into these survival models, takes on pivotal importance. There is increasing recognition of the need to consider not just the main effects of risk factors but also whether and how these effects might interact with time (Willett and Singer, 1997; Willett et al., 1998). First, risk factors for each individual in a study can be either fixed, taking a single value that remains unchanged throughout the study period (e.g. gender) or time-dependent, changing value continuously (e.g. age) or passing through a number of states over the study period (e.g. marital status, occurrence of life events). Second, the effects of these risk factors may themselves be time-varying (the effect may be confined to a particular time period that is of fixed duration or show signs of decaying influence with elapsed time), and third, the main effect of risk factors may vary with age (showing a greater or lesser effect depending on the individual’s current age/life- stage).

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Loss events and the onset of depression 177

A

B

t

C

t

D

t

t Figure 10.1 Some possible representations of self-reported adverse event effects (A) raw data, an event occurs at a particular age (or calendar time), (B) event effect shown as enduring and undiminished over time, (C) event effect enduring but with progressively diminishing adverse effect over two subsequent discrete time periods, and (D) progressive and differential adaptation to event effects over time according to exposure context and to individual differences in stress adaptive capacity.

The nature of these time-dependencies is particularly relevant when studying the effects of life events in relation to onsets of disorder. A history of prior adverse experience could be expressed as a time-dependent covariate whose value changes to reflect each new event occurrence. Interactions may be present to modify the influence of events on onsets, either as a function of age (life-stage), or by other factors that confer vulnerability or resilience to the negative effects of events. The main event effect may also either vary with time (e.g. decay) or be dependent in some way on the prior history of events experienced (e.g. additivity, scarring). It is clearly important to try to establish the functional form (over time) of these main event effects before any interactions (with age or other modifying factors) are

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178 Paul Surtees and Nick Wainwright considered (Kessler et al., 1996). Consequently, there are a variety of different ways of specifying parameters for the effects of time-varying predictors in order to investigate how such representations provide improved understanding of relationships. These ideas are illustrated sequentially in Figure 10.1 for a single adverse event with primary attention given to the time of occurrence of the event relative to age or calendar time (Figure 10.1A). A priori we have no information on how this event might influence subsequent risk of disorder, although we might choose to construct a simple time-dependent covariate that takes value 0 until occurrence of the event and 1 thereafter (Figure 10.1B), i.e. the individual moves into a higher (or lower) risk group following event occurrence. However, this is only one of a family of simple timedependent covariates that could have been constructed, each of which involves important assumptions about how the event influences disorder. Even the simple representation of Figure 10.1B contains the implicit assumption that the individual, having moved into a higher risk group, remains in a state of increased risk from then on. This assumption is perhaps of little importance in the short term but takes on greater importance for studies over much longer time periods (particularly those looking at the whole life-course) as it seems unreasonable to expect a single event experienced many years previously to have a uniform and unchanging influence. We might more reasonably expect the influence of the event to be either over after a certain amount of time or at least to diminish in intensity. Figure 10.1C shows a time-dependent covariate constructed to incorporate two separate periods of altered risk, with initial high impact and subsequent decay towards original levels. Equivalently, we could specify a smooth exponential decay so as to vary according to certain (vulnerability) factors (e.g. gender) as in Figure 10.1D. These illustrations represent just a few possible ways in which an adverse event might enter a model as a time-dependent covariate. In some instances, the representation of Figure 10.1B will suffice but in others it will be important to consider alternatives. The functional form of time-varying effects and the importance of choosing an appropriate representation has been discussed, notably in the context of models for extended exposures to radiation and the aetiology of cancers (Thomas, 1988; Curtis and Thomas, 1992) with ideas such as cumulative, threshold and saturation of exposure levels, and also in relation to loss events (Jagger and Sutton, 1991) and psychiatric endpoints (Kessler et al., 1996). The inclusion of time-dependent covariates such as in Figure 10.1B is now fairly routine in standard statistical software packages. More importantly, we can construct a time-dependent covariate to represent step decay or exponential decay (as in Figure 10.1, C and D) or indeed to represent any functional form (of decay or otherwise) and there is no difference in the way these covariates are included in models as long as their values are known or specified in advance. The only additional programming required is in the construction of the exposure history as a time-dependent covariate. In terms of exponential decay this means that it is straightforward to fit the curves of Figure 10.1D as long as the decay parameter (e.g. with a half-life of six months/one year/two years, etc.) is specified in advance. Each different representation entails different assumptions about the nature of that influence and consequently produces important differences both in model results and in their interpretation.

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Loss events and the onset of depression 179

Discrete-time survival methods There has been a recent and increasing trend towards the application of discretetime survival approaches to the analysis of life event history relationships (Kessler and Magee, 1993; Willett and Singer, 1993; Kessler et al., 1997; Kendler and Karkowskishuman, 1997; Kendler et al., 1998; Willett et al., 1998). These methods are the natural choice where time is measured with respect to a discrete set of units (e.g. time until conception as the number of menstrual cycles) but are also used as an approximation to continuous time methods where data are grouped over time, for example, within monthly or yearly intervals (Allison, 1982). An appealing feature of these discrete (grouped) time methods is that they are computationally straightforward and allow great flexibility for the inclusion of time-dependent covariates and the testing of interactions over time. Timedependent covariates can be included with equal ease within Cox proportional hazards models and different functional representations for exposure histories can also be evaluated (Jagger and Sutton, 1991). However, the Cox model is not necessarily well suited to providing a detailed description of the time-varying effects of covariates (Aalen, 1989; Willett and Singer, 1997) and it remains easier to examine the changing effects of predictors over time within the discrete (grouped) time approach (Kessler and Magee, 1993; Surtees and Wainwright, 1999). These methods have been used in their standard form, not only to include risk factors such as age and marital status as time-dependent covariates, but also to examine more complex issues of time-dependency. Analyses have looked at the time-varying nature of adverse event effects through examination of different duration of effects and over different time lags (Kendler et al., 1998; Kessler et al., 1996); issues concerning the additivity of multiple event exposures and threshold levels of impact (Kendler et al.,1998); ideas of changing effects over the life-course through the inclusion of cross-product interaction terms with age (Willett et al.,1998; Willett and Singer, 1997; Kessler and Magee, 1993) and to examine the shape of these changing effects through inclusion of more complex terms to look for evidence of simple distance effects or scarring (Kessler et al., 1997).

Proposed strategy for examining temporal variation in event effects Work discussed elsewhere used nested comparisons of simple functional forms of time-dependent covariates (of different duration and at different time lags) to test ideas of decay in, and vulnerability to, the effects of adverse experience (Surtees and Wainwright, 1999). The strategy discussed here aims to combine these ideas with the use of more complex functional forms of time-dependent covariates constructed as indices of exposure and with particular emphasis on representations involving exponential decay (Surtees, 1989). Initial analysis uses combinations of simple time-dependent covariates to establish the strength and functional form (over time) of event effects. These provide for:

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180 Paul Surtees and Nick Wainwright • • •

a constant effect following event occurrence (as shown in Figure 10.1B) a constant effect but for a fixed duration only (e.g. one, two, three, … years) separate effects of one year duration at various time lags following event occurrence.

The nested comparison is such that if one representation of event effect (e.g. a constant effect with fixed duration of two years) contributes significantly to a model already mapping that of another specification (e.g. a constant effect of continuing duration) but not vice-versa, then this is considered as strong evidence that the latter provides a better representation of the temporal form of the event effect (Surtees and Wainwright, 1999). A sequential analysis may find, for example, first that the event effects are of fixed duration and second that the effects are significantly different in successive time periods following event occurrence. This would lead to a model that uses two time-dependent covariates and estimates the event effect to be of the form of Figure 10.1C. Having established a loose representation of the changing influence of events over time in terms of these step functions, an appropriate functional form is chosen and constructed as a single time-dependent covariate. In this example, exponential decay is the natural choice and the decay period is chosen, by inspection, to map the estimated values observed from the step functions of Figure 10.1C. This strategy takes advantage of the fact that any pre-specified functional form of time-varying covariate can be introduced into the discrete-time survival models without additional complexity, while noting that any number of functional forms and variations of those forms could be chosen. For this reason, specific tests with simple functions are used to inform both the choice of function and of any associated parameters (e.g. decay period). Once the temporal form of this main event effect has been established, analysis then proceeds to investigate how this might vary by other modifying risk factors and by life-stage.

Sample The following discussion of these ideas is based upon participants contacted through the first five general practices working with the EPIC project serving a mixture of rural and urban districts within Norfolk. At recruitment to EPIC, all participants were healthy, middle aged or older, and actively agreed to join in the study knowing that their health status would be followed up for the rest of their lives. Illustration of relationships are based upon an available (interim) sample of 3,491 individuals (55.9 per cent female) aged between 48 and 79 years at the time of questionnaire completion, representing around 77 per cent of those still eligible to be mailed (after allowance for deaths) since recruitment.

Exploration of self-reported adaptation to the experience of loss Maternal, together with marital, loss experience has provided a natural focus for

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Loss events and the onset of depression 181

Marital loss

Maternal loss A

Female Male

3 2 1

4

Adaptation

Adaptation

4

B

Female Male

3 2 1

0

10

20 30 40 Years since event

0

10 20 30 Years since event

40

Figure 10.2 Self-reported adaptation by gender to (A) maternal loss and (B) marital loss (through death or divorce).

the study of the health consequence of adversity. Evidence from such work has shown marked gender differences in health status following marital loss and mortality rates to reach their maximum during the first six months of bereavement (for both sexes). Whilst women report an excess of morbidity, mortality is increased amongst men and such risk appears to be raised for up to fifteen years following bereavement (e.g. Osterweis et al., 1985; Bowling, 1987; Jagger and Sutton, 1991; Schaefer et al., 1995). These results, from epidemiologically oriented analyses, are complemented by other work founded on social and psychiatric perspectives that has reported a raised risk of adult psychiatric disorder (particularly depression) following loss of mother in childhood (e.g. Harris et al., 1986; Bifulco et al., 1992) and the way in which psychiatric morbidity evolves during the immediate post-marital bereavement period (Surtees, 1995). Other work has highlighted intriguing findings concerning the symptoms of traumatic marital grief as subsequent predictors of outcomes that include raised blood pressure, heart trouble and cancer (Prigerson et al., 1997) and of gender differences in those effects (Chen et al., 1999). Recent results (Penninx et al., 1998), suggesting that chronic depression, after adjustment for other factors, was associated with an increased risk of cancer, provide further evidence for the apparent links between adverse experience, psychiatric morbidity (particularly depression) and the onset and development of chronic physical disease. Loss experience over the life course can be seen therefore to occupy a pivotal role for the development of an improved understanding of the impact of adverse experience on health change and a basis for the specification and refinement of psychosocial models seeking to explain differential vulnerability to adverse experience. Given evidence on (marital) loss and the subsequent period of heightened risk for health change, the EPIC (interim HLEQ) data were examined for evidence of a

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182 Paul Surtees and Nick Wainwright

Marital loss

Maternal loss 4

Degree of upset

Degree of upset

4 3 2

A

1

20

30

40

50

60

Age

3

B

1

20

2 1

30

40

50

60

Age

4

<50 ≥50

C

2

70

Adaptation

Adaptation

4

3

70

<50 ≥50

D

3 2 1

0

10

20

30

Years since event

40

0

10

20

30

40

Years since event

Figure 10.3 Self-reported upset to (A) maternal loss and (B) marital loss (through death or divorce) and adaptation to such losses (C and D) by lifestage (aged ≥ 50 vs < 50).

progressive adaptation to such loss experience and whether or not gender appeared to differentiate adaptive capacity to such exposure. Figure 10.2A shows mean selfreported adaptation scores by loss of mother, plotted by elapsed time since that loss, and reveals the extent to which adaptation was reported by gender for the 69 per cent of respondents who had experienced loss of mother (excluding losses during childhood as defined by loss at age ≤16). The results show quite distinct and sustained differences in self-reported adaptation over a time period in excess of thirty years. Similarly, Figure 10.2B shows mean self-reported adaptation scores following loss of spouse (defined here to include all losses through divorce/separation or death). Nearly 15 per cent of the sample reported experiencing death of spouse and nearly 20 per cent divorce, yielding a combined group of nearly 32 per cent who had experienced one or both of the events over the life course. The figure suggests a gradual adaptation to these event experiences over an assessment period (again) of greater than thirty years. Both figures suggest support for a general recovery from adverse event effects over time, with the results by gender indicating a differential adaptation to the effects of both maternal and marital loss events; women reporting consistently slower adaptation than men over periods in excess

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Loss events and the onset of depression 183 of thirty years. Self-reported impact scores (degree of upset) also varied significantly by gender, with women reporting higher impact than men for both maternal loss and loss of spouse events (mean score 3.7 vs 3.4 and 3.6 vs 3.3, respectively). Figure 10.3 shows the mean reported event impact scores and adaptation for both maternal and marital loss events (Figures 10.3A and C maternal loss; Figures 10.3B and D marital loss). Relative to age at the time of event occurrence, these results reveal evidence for the differential impact of (and adaptation to) these loss events by life stage; for example, impact of death of mother exhibited a decreasing trend with increasing age when experienced (being reported as more upsetting for those respondents who were younger at the time) and conversely, loss of spouse (through death or divorce) showed an increasing trend in reported impact with age. Adaptation to the effects of maternal loss events was reported as being more rapid for those aged ≥ 50 years than for those younger at the time of event experience; with adaptation to marital loss events by those same exposure age groups being reversed. Note that these age effects have been observed in both directions; a result that strengthens the case that they are not simply artificially induced through differential rates of retrospective recall.

Exploration of MDD risk by age, gender and loss experience Table 10.1 shows odds ratios for recent (twelve month) depression. Consistent with established findings, a strong gender difference was found with females reporting nearly twice as many episodes of MDD as males, along with a significant age effect, where those aged 62–79 years reported fewer episodes than those aged 48–61. Fewer episodes were reported by those whose mothers died prior to the time of assessment, but this difference failed to reach statistical significance. Conversely, there was a marked and significant increase in episodes amongst those who had ever experienced marital loss. Results also revealed evidence for additivity in event effects in that the increase in the odds of MDD was greater in those who had experienced more than one such loss than in those who experienced only one. There was also evidence for progressive adaptation to event experiences with a marked increase in MDD episodes in those who had experienced loss of spouse within the five years prior to assessment, a lesser but significant increase for those whose loss experience was greater than five but less than ten years previously and no such difference in those whose loss was experienced more than ten years previously. Evidence for life-stage effects was also shown in relation to loss of spouse; those who experienced marital loss when aged ≥ 50 reporting a greater number of MDD episodes than those who were younger at the time of loss. The odds of recent MDD by death of mother (and by either recency or age at time of loss) revealed no significant relationships (results not shown). Together, these exploratory results show evidence for progressive (and variable) adaptation to event effects and of life-stage effects through differential impact by age. However, they are based upon self-report measures (both of event impact and of adaptation) and focus exclusively on only the most recent episodes of depression. Clearly for a life-course perspective to contribute to a gain in

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184 Paul Surtees and Nick Wainwright Table 10.1 Odds of MDD (during the 12 months pre-assessment) according to demographic factors and adverse experiences by lifestage Factor

Odds of 12 month MDD

Gender

1.7 [1.2–2.4]

Age (> median, 62 yrs.)

0.6 [0.4–0.8]

Maternal loss

0.7 [0.5–1.1]

Marital loss: Ever vs never 1 vs 0 events > 1 vs 0 events Recency of marital loss: Within the last 5 years vs never Between 5 and 10 years ago vs never More than 10 years ago vs never Age of S at marital loss: ≥ 50 vs never < 50 vs never

2.0 [1.4–2.8] 1.7 [1.1–2.4] 3.4 [2.1–5.5] 5.3 [3.3–8.3] 2.1 [1.1–3.8] 1.2 [0.7–1.8 2.4 [1.6–3.6] 1.8 [1.2–2.7]

understanding of the process through which adverse events precipitate (or bring forward) onsets of disorder at different life stages, analysis must take account of time order. In particular, where event effects vary with elapsed time and where age effects are suspected of being important, it remains essential to take full account of the relative timing of event occurrences with disorder onset.

The model A discrete (grouped) time survival analysis was employed with person-years as the unit of measurement. Outcome was time until first onset of depression, with each individual contributing one observation for each year at risk from age 17 up to age at onset or censoring. The logistic model was adopted and SPlus (Chambers and Hastie, 1992) used to fit multiple regression models with a mixture of fixed and time-dependent covariates. Baseline hazard was modelled through inclusion of time-dependent covariates to represent both age and period effects (in five year bands). Results are discussed here in terms of odds ratios (along with corresponding 95 per cent confidence intervals) and χ2 tests of differences in residual deviance are used to compare nested models in the usual way. Primary interest focuses on the differences in event rates reported in the years leading up to onset or censorship; hence non-cases (controls) were censored at equivalent times (agematched) relative to the assessment of cases. This strategy ensures that event histories for cases and controls are compared for similar time periods relative to assessment and provides a natural adjustment for the bias that might arise through differential rates of retrospective recall (Kessler et al., 1996). The timing of events was recorded to the nearest year, so it was impossible to distinguish time

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Loss events and the onset of depression 185 order for events and onsets reported in the same year. For the analysis here, all events occurring prior to, or in the same year as onset, are included. The sensitivity of results to the inclusion or omission of these events is discussed later.

Results A total of 505 marital loss events and 939 maternal losses were experienced prior to onset of MDD or censorship. Of the onsets, 412 met (putative DSM-IV) MDD criteria for a first episode and were dated from amongst HLEQ returns by a total of 3,353 respondents contributing a total of 83,688 person-years for analysis. Exclusions to analysis included those where MDD status and/or timing of first onset episode were unknown, (76 and 30 respectively), and a further 32 who reported first episode onsets prior to age 17. Risk of onset was again found to be increased for females (OR 1.6, 95 per cent C.I. [1.3–1.9]) and this was included along with age and period effects in all subsequent models.

Temporal influence of life events Use of a standard time-dependent covariate with incremental change at each new event occurrence (as in Figure 10.1B), suggested a significantly increased risk of MDD onset following loss of spouse (OR 2.0 [1.5–2.6]) but no increased risk following maternal loss (1.0 [0.7–1.2]). However, as discussed above, this assumes that the events have constant and enduring influence that is not necessarily appropriate on the time-scale considered here. A more detailed examination, following the principles described above, revealed a best fitting model for the temporal influence of marital loss events to contain a combination of two-step functions (as in Figure 10.1C), with a very strong effect for loss of spouse found in the year of loss (OR 14.8, 95 per cent C. I. [10.5–20.8]), and a lesser, but still appreciable effect in the year immediately following event occurrence (2.8 [1.4–5.8]). These results are consistent with an exponential type decay process, that in discrete time is given by xt = et + δ. xt–1, 0 < δ < 1, where et is an indicator of new event occurrences, xt is the resulting index of adversity and where half-life is given by -loge(2)/loge(δ) representing the time until increased risk of disorder following event occurrence has reduced to half its initial value, measured on the (log) scale on which parameters are estimated in the regression equations. The magnitudes of the effects above suggest an underlying process with δ = 0.4 (a half-life of 9 months), computed through a simple function written in the C programming language. Replacing the two-step functions of Figure 10.1C with this exponential decay process results in a model of almost equivalent fit. The temporal patterning of the influence of maternal loss on subsequent onsets of MDD was less clear cut yielding insufficient evidence to distinguish between models with: year 1 effect only (OR: 2.9 [1.7–4.8]); year 1 and 2 effects (equal impact), OR: 2.3 [1.5–3.5]; and year 1 and 2 effects with decay, OR’s 2.9 [1.7–4.8] and 1.7 [0.8–3.2], respectively. Each representation essentially provides an equivalent fit but for symmetry with the loss of spouse results, an exponential decay

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186 Paul Surtees and Nick Wainwright

Odds of MDD by maternal loss

x

12 10 8 6 x

4

x x

x

x

2

x

0

17–20

26–30

x

36–40 46–50 Age

x

x

56–60

x

x

66–70

Figure 10.4 Increased odds of MDD following maternal loss by subject’s age at time of loss. (Observed and estimated values shown as points and solid line, respectively).

representation was taken with δ = 0.5 (calculated as above). Having established an appropriate representation for the main event effects, analysis then proceeded to investigate whether these effects showed variations either by life-stage or by gender.

Variation in event effects by life-stage No significant interactions were found between the main effect of marital loss and age, but a significant linear age interaction (p < 0.01) was found for maternal loss. Observed odds ratios by 5-year age-band are plotted in Figure 10.4 along with estimated odds from the model with a linear age-interaction (solid line). The observed odds ratios act as visual justification for the appropriateness of the fitted curve that in turn provides statistical confirmation of the strength of this effect. This can be seen as a life-stage effect with greatest impact of maternal loss for those respondents who were younger at the time of such loss.

Variation in event effects by gender No significant interactions were found to suggest that the main event effect of maternal loss varied by gender, but significant interactions were found for loss of spouse. The existing model for marital loss included a main effect for gender but no event-gender interaction. An exploratory model used two-step functions to represent the temporal variation in event effect and estimated hazards for this model (on the logit scale) are shown in Figure 10.5A by gender and relative to

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Loss events and the onset of depression 187 Female

logit (hazard)

Male

0

1 2 3 Years since event

4

Female

B

Male

logit (hazard)

A

0

1 2 3 Years since event

4

Figure 10.5 Predicted hazard of MDD onset following marital loss (through death or divorce) with no event by gender interaction. Event effects are represented as either (A) step functions or (B) as exponential decay.

the occurrence of a single loss of spouse event (at time 0). This model implies a uniform increased risk of onset by gender but that the main effect of loss of spouse is the same for males as it is for females. In terms of the exponential decay model (δ = 0.4), the main effect of loss of spouse has the same pattern for all respondents, regardless of gender and this is illustrated in Figure 10.5B. To examine this in more detail, separate models were fitted by gender using the same principles as above, and these revealed quite different results. A one parameter model was found to be sufficient for females with odds of MDD in the year of loss 17.2 [11.5–25.5] whereas a three parameter model was preferred for males with odds 10.4 [5.3–20.6] in the year of loss, 6.6 [2.8–15.5] in the subsequent year, and 4.4 [1.6– 12.5] two years following loss. A full model, allowing three parameters for the main effect of loss of spouse and including all gender interactions, revealed no significant difference in the year of loss but significant interactions for the subsequent two years (p = 0.02 and p = 0.03, respectively). Estimated hazards (on the logit scale) for these models are shown in Figure 10.6A and suggests that different adaptive processes are at work with decay δ = 0.001, say for females, (almost no effect after year 1) and δ = 0.8 (half-life around three years) for males. This exponential decay model is displayed in Figure 10.6B. Significant gender interactions were found, above, but an explicit test of this differential adaptation is available through a nested comparison of these two exponential decay models (Figures 10.5B and 6B) that employ time-dependent covariates to represent the main event effect, in the first case constructed with δ = 0.4 for all respondents and in the second, to incorporate differential adaptation (δ = 0.001 and δ = 0.8). This second time-dependent covariate was significant when added to a model already containing the first (χ2 = 7.7 on 1 df, p < 0.01) but not vice versa (χ2 = 2.5 on 1 df, p = 0.11) and this can be seen as strong evidence in support of a model with separate decay parameters, i.e. differential adaptation to the marital loss events. There was also a suggestion that the initial loss event impact was higher for females but this was not statistically significant.

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188 Paul Surtees and Nick Wainwright

Female

logit (hazard)

Male

0

1 2 3 Years since event

4

Female

B

Male

logit (hazard)

A

0

1 2 3 Years since event

4

Figure 10.6 Predicted hazard of MDD onset following marital loss (through death or divorce) with allowance for event by gender interaction. Event effects are represented as either (A) step functions or (B) as exponential decay.

Comment This chapter has been concerned with the development of ideas underpinning the role of adverse experience in the subsequent onset of affective disorder. This already narrow objective was further refined through concentrating only upon the experience of two specific loss events in the sample studied. This focus was adopted in order to illustrate the way in which competing analytic models can be specified to precisely represent, and be employed to test, substantive ideas concerning the duration of event effects, their differential effects and models of the process of adaptation to adverse experience. Exploratory results suggested progressive (and variable) adaptation to loss event effects and of life-stage effects through differential impact by age (based on self-report measures). In addition, marital loss experience was shown to imply an increased risk of current (twelve month) MDD with this risk being more pronounced for multiple events, for events experienced more recently and for those respondents who were older at the time of loss. Discrete (grouped) time survival models, employed in relation to the first adult onset of a depressive episode, revealed strong evidence for the increased risk of such disorder following (both marital and maternal) loss events and that the effects of these events were well modelled as exponential decay processes with the magnitude of effect halving every nine and twelve months respectively. The impact of maternal loss events was found to vary significantly by age, being greatest in those respondents who were younger at the time of loss. Marital loss events showed strong evidence for differential adaptation by gender, with the period of increased risk limited to the year of event occurrence for women and a much slower adaptive process for men (with half-life of about three years). There was some conflict between the exploratory results and those from the survival models that take a more complete account of the timing of events and first onsets. This can be seen as further justification for the need to take proper account of temporal order and of possible variations in covariate effects over time and age.

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Loss events and the onset of depression 189 All events in the year of onset were included in analysis and, while many of these events occurred prior to onset, some will have been experienced during the few months following onset. We would expect this to be less than half of all such events given consistent evidence in the literature for an increased event rate immediately prior to onset. A full sensitivity analysis would randomly assign a proportion of these events to have occurred after onset and would exclude these events from analysis. As investigation here has concentrated on the ideas behind the modelling of temporal variation in covariate (adverse event) effects, this analysis was not performed. However, the most cautious of sensitivity analyses would have been to exclude all events reported in the same year as episode onset. From the results reported, we can see that while the strength of relationships was greatly reduced for events reported strictly prior to onset, significant relationships do remain and these suggest an increased risk of MDD onset following event exposure. Hence, while it is possible that results are contaminated by some events occurring after onset and exclusion of these events (if known) could weaken results, it is unlikely that the core findings relating to the nature and strength of the event effects would be altered. A strategy for investigating the temporal variation in event effects was adopted here whereby a loose representation of the time-varying influence of events was established through a set of preliminary analyses and then a single time-dependent covariate was constructed to match the evidence gained from these models. Analysis then proceeded to investigate how this might vary by other modifying risk factors and by life-stage. The models presented concentrate on representations involving exponential decay and on issues of differential adaptation and of variation in event effects by other modifying factors. It is clear, first, that the strategy adopted affords opportunities to investigate other hypotheses through relatively simple extensions, for example, by allowing and testing other functional forms to represent ideas such as additivity, ceiling effects (or residual scarring subsequent to adverse exposure) and, second, that parameters associated with the temporal variation in event effects (e.g. of decay period/half-life) that are currently prespecified (though informed by exploratory analyses) could be estimated as part of the main model. The latter would involve a marked increase in analytic complexity and would suggest a move perhaps towards consideration of new ways of representing the complex inter-relationships between events and disorder (Surtees and Wainwright, 1998) and the possible use of Markov Chain Monte Carlo techniques (see Gilks et al., 1996) along with ideas from the more recent development of dynamic survival models (Gamerman, 1991; Fahrmeir and Wagenpfeil, 1996; Fahrmeir and Knorr-Held, 1997). However, simple exploratory models remain important as they can reveal both the form and strength of relationships without resort to computationally more intensive procedures. The results discussed therefore have shown the importance of looking in detail at the role of time and the way in which time-dependent covariate effects are introduced into the models. They have further suggested that even when models are (computationally) relatively straightforward, different representations of time-dependent effects can have important consequences on parameter estimates, particularly in models seeking to

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190 Paul Surtees and Nick Wainwright evaluate relationships over extended periods of time (i.e. over the life-course). When events were assumed to have a single and enduring impact on onsets of depression, no significant relationships were apparent for maternal loss events, whereas when models were used that incorporated a decay component these events were seen to impact significantly on first onsets of depression and the strength of relationships for marital loss events was also greatly increased. Clearly, whilst the relatively simple representation of relationships discussed provides one foundation to the development of modelling strategies, others, such as those suggested, may be required to model circumstances of greater complexity. This complexity stems partly from converging research themes that are increasingly adopting a life-course perspective, have intertwined objectives, and are concerned with, for example, establishing the relative (temporal) salience of biological, nutritional and social factors for adult health. Such work has shown the persistence into adulthood of the health effects of early biological (and nutritional) insults and parental divorce (Kuh and Ben-Shlomo, 1997; Cherlin et al., 1998); results that may be further elaborated through consideration of adverse experience in adulthood, of individual differences in stress adaptive capacity and of sequential changes in health. Analytic frameworks are needed therefore that permit evaluation of early circumstances in the context of subsequent adversity exposure in relation to health change and mortality. Whilst advances in understanding the role of adversity in disease aetiology continue to depend upon the sound assessment of event exposure histories, increasingly such advances depend also upon the design and implementation of statistical models that map more precisely (than hitherto) those event attributes and processes progressively identified as governing their relationship with health change.

Acknowledgements The EPIC study in Norfolk is coordinated from Cambridge (UK). The project researchers in Cambridge are: Sheila Bingham, MRC Dunn Clinical Nutrition Centre; Kay-Tee Khaw, Department of Clinical Gerontology; Nicholas Day, Robert Luben, Suzy Oakes and Ailsa Welch, Strangeways Research Laboratories. The project researchers associated with the psychosocial component of EPIC in Cambridge are: Carol Brayne, Department of Public Health and Primary Care; Felicia Huppert, Department of Psychiatry; Lucy Clifton, Strangeways Research Laboratories; Paul Surtees and Nick Wainwright, MRC Biostatistics Unit and Institute of Public Health. The psychosocial component of EPIC in Norfolk is funded by the Medical Research Council. EPIC in Norfolk is supported by: British Heart Foundation, Cancer Research Campaign, Europe against Cancer Programme of the Commission of the European Communities, Imperial Cancer Research Fund, Medical Research Council, and the Ministry of Agriculture, Fisheries and Food.

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Loss events and the onset of depression 191

References Aalen, O.O. (1989) ‘A linear regression model for the analysis of life times’, Statistics in Medicine, 8, 907–25. Allison, P.D. (1982) ‘Discrete-time methods for the analysis of event histories’ in S. Leinhardt (ed.) Sociological Methodology, San Francisco: Jossey-Bass, 61–98. American Psychiatric Association, APA. (1994) Diagnostic and statistical manual of mental disorders, Fourth Edition, Washington DC: American Psychiatric Association. Bebbington, P., Der, G., MacCarthy, B., Wykes, T., Brugha, T., Sturt, P. and Potter, J. (1993) ‘Stress incubation and the onset of affective-disorders’, British Journal of Psychiatry, 162, 358–62. Bifulco, A., Harris, T. and Brown, G.W. (1992) ‘Mourning or early inadequate care? Reexamining the relationship of maternal loss in childhood with adult depression and anxiety’, Development and Psychopathology, 4, 433–49. Bingham, S.A. (1997) ‘Dietary assessments in the European prospective study of diet and cancer (EPIC)’, European Journal of Cancer Prevention, 6, 118–24. ——, Gill, C., Welch, A., Cassidy, A., Runswick, S.A., Oakes, S., Luben, R., Thurnham, D.I., Key, T.J.A., Roe, L., Khaw, K-T. and Day, N.E. (1997) ‘Validation of dietary assessment methods in the UK arm of EPIC using weighed records, and 24–hour urinary nitrogen and potassium and serum vitamin C and carotenoids as biomarkers’, International Journal of Epidemiology, 26, (Suppl. 1), S137– S151. Bowling, A. (1987) ‘Mortality after bereavement: a review of the literature on survival periods and factors affecting survival’, Social Science and Medicine, 24, 117–24. Brown, G.W. (1974) ‘Meaning, measurement, and stress of life events’ in B. S. Dohrenwend and B. P. Dohrenwend (eds) Stressful Life Events: Their Nature and Effects, New York: Wiley, 217–43. —— and Harris, T.O. (1978) Social Origins of Depression, London: Tavistock Publications. ——, Sklair, F., Harris, T.O. and Birley, J.L.T. (1973a) ‘Life events and psychiatric disorders Part 1: some methodological issues’, Psychological Medicine, 3, 74–87. ——, Harris, T.O. and Peto, J. (1973b) ‘Life events and psychiatric disorders Part 2: nature of causal link’, Psychological Medicine, 3, 159–76. ——, Harris, T.O. and Hepworth, C. (1995) ‘Loss humiliation and entrapment among women developing depression, a patient and non-patient comparison’, Psychological Medicine, 25, 7–21. Caspi, A., Moffitt, T.E., Thornton, A., Freedman, D., Amell, J.W., Harrington, H., Smeijers, J. and Silva, P.A. (1996) ‘The Life History Calendar – A research and clinical assessment method for collecting retrospective event-history data’, International Journal of Methods in Psychiatric Research, 6, 101–14. Chambers, J.M. and Hastie, T.J. (1992) Statistical Models in S, Pacific Grove: Wadsworth and Brooks-Cole. Chen, J.H., Bierhals, A.J., Prigerson, H.G., Kasl, S.V., Mazure, C.M. and Jacobs, S. (1999) ‘Gender differences in the effects of bereavement-related psychological distress in health outcomes’, Psychological Medicine, 29, 367–80. Cherlin, A.J., Chase-Lansdale, P.L. and McRae, C. (1998) ‘Effects of parental divorce on mental health throughout the life course’, American Sociological Review, 63, 239–49. Curtis, S.B. and Thomas, D.C. (1992) ‘Dose time response models for radiation carcinogenesis’, Advances in Radiation Biology, 16, 45–76.

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192 Paul Surtees and Nick Wainwright Day, N., Oakes, S., Luben, R., Khaw, K-T., Bingham, S., Welch, A. and Wareham, N. (1999) ‘EPIC-Norfolk: study design and characteristics of the cohort’, British Journal of Cancer, 80, (Suppl. 1), 95–103. Dohrenwend, B.P. (1998) Adversity, Stress and Psychopathology, New York: Oxford University Press. Eaton, W.W., Armenian, H., Gallo, J., Pratt, L. and Ford, D.E. (1996) ‘Depression and risk for onset of Type-II diabetes. A prospective population-based study’, Diabetes Care, 19, 1097–102. Elder G.H. Jr. (1998) ‘The Life Course and Human Development’ in R.M. Lerner (ed.) (general editor W. Damon) Handbook of Child Psychology, Vol. 1: Theoretical Models of Human Development, New York: Wiley, 939–91. ——, George, L.K. and Shanahan, M.J. (1996) ‘Psychosocial Stress over the Life Course’ in H.B. Kaplan (ed.) Psychosocial Stress: Perspectives on Structure, Theory, LifeCourse, and Methods, San Diego: Academic Press, 247–92. Ensel, W. M. and Lin, N. (1996) ‘Distal stressors and the life stress process’, Journal of Community Psychology, 24, 66–82. Ensel, W.M., Peek, M.K., Lin, N. and Lai, G. (1996) ‘Stress in the life course: A life history approach’, Journal of Aging and Health, 8, 389–416. Everson, S.A., Goldberg, D.E., Kaplan, G.A., Cohen, R.D., Pukkala, E., Tuomilehto, J. and Salonen, J.T. (1996) ‘Hopelessness and risk of mortality and incidence of myocardial infarction and cancer’, Psychosomatic Medicine, 58, 113–21. Fahrmeir, L. and Knorr-Held, L. (1997) ‘Dynamic discrete-time duration models: Estimation via Markov Chain Monte Carlo’, Sociological methodology, 27, 417–52. —— and Wagenpfeil, S. (1996) ‘Smoothing hazard functions and time-varying effects in discrete duration and competing risks models’, Journal of the American Statistical Association, 91, 1584– 94. Frank, E., Tu, X.M., Anderson, B., Reynolds, C.F., Karp, J.F., Mayo, A., Ritenour, A. and Kupfer, D.J. (1996) ‘Effects of positive and negative life events on time to depression onset – an analysis of additivity and timing’, Psychological Medicine, 26, 613–26. Gamerman, D. (1991) ‘Dynamic Bayesian models for survival data’, Applied Statistics, 40, 63–79. George, L.K. (1993) ‘Sociological perspectives on life transitions’, Annual Review of Sociology, 19, 353– 73. Gilks, W.R., Richardson, S. and Spiegelhalter, D.J. (eds) (1996) Markov Chain Monte Carlo in Practice, London: Chapman and Hall. Glassman, A.H. and Shapiro, P.A. (1998) ‘Depression and the course of coronary artery disease’, American Journal of Psychiatry, 155, 4–11. Harris, T.O., Brown, G.W., and Bifulco, A. (1986) ‘Loss of parent in childhood and adult psychiatric disorder: the role of lack of adequate parental care’, Psychological Medicine, 16, 641–59. Jagger, C. and Sutton, C.J. (1991) ‘Death after marital bereavement – is the risk increased?’, Statistics in Medicine, 10, 395–404. Kaplan, G.A. and Reynolds, S.P. (1988) ‘Depression and cancer mortality and morbidity: prospective evidence from the Alameda County Study’, Journal of Behavioral Medicine, 11,1–13. Karel, M.J. (1997) ‘Aging and depression: vulnerability and stress across adulthood’, Clinical Psychology Review 17, 847–79.

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Loss events and the onset of depression 193 Kendler, K.S. and Karkowskishuman, L. (1997) ‘Stressful life events and genetic liability to major depression: genetic control of exposure to the environment’, Psychological Medicine, 27, 539–47. ——, Karkowski, L.M. and Prescott, C.A. (1998) ‘Stressful life events and major depression: risk period, long-term contextual threat, and diagnostic specificity’, Journal of Nervous and Mental Disease, 186, 661–9. Kessler, R.C. (1997) ‘The effects of stressful life events on depression’, Annual Review of Psychology, 48, 191–214. —— and Magee, W.J. (1993) ‘Childhood adversities and adult depression: basic patterns of association in a US national survey’, Psychological Medicine, 23, 679–90. ——, Magee, W.J. and Nelson, C.B. (1996) ‘Analysis of Psychosocial Stress’ in H.B. Kaplan (ed.) Psychosocial Stress: Perspectives on Structure, Theory, Life-Course, and Methods, San Diego: Academic Press, 333–66. ——, Davis, C.G. and Kendler, K.S. (1997) ‘Childhood adversity and adult psychiatric disorder in the US National Comorbidity Survey’, Psychological Medicine, 27, 1101– 19. Kouzis, A., Eaton, W.W. and Leaf, P.J. (1995) ‘Psychopathology and mortality in the general- population’, Social Psychiatry and Psychiatric Epidemiology, 30, 165–70. Kuh, D. and Ben-Shlomo, Y. (eds) (1997) A Life Course Approach to Chronic Disease Epidemiology, Oxford: Oxford University Press. Lam, D.H., Green, B., Power, M.J. and Checkley, S. (1996) ‘Dependency, matching adversities, length of survival and relapse in major depression’, Journal of Affective Disorders, 37, 81–90. Lin, N., Ensel, W.M. and Lai, G. W-f. (1997) ‘Construction and use of the life history calendar: reliability and validity of recall data’ in I. H. Gotlib and B. Wheaton (eds) Stress and Adversity over the Life Course: Trajectories and Turning Points, New York: Cambridge University Press, 249–72. Morris, P.L.P, Robinson, R.G., Andrzejewski, P., Samuels, J. and Price, T.R. (1993) ‘Association of depression with 10-year post-stroke mortality’, American Journal of Psychiatry, 150, 124–9. Murray, C.J.L and Lopez, A.D. (1997) ‘Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study’, Lancet, 349, 1436–42. Osterweis, M., Solomon, F. and Green, M. (eds) (1985) ‘Epidemiologic perspectives on the health consequences of bereavement’, in Bereavement Reactions, Consequences, and Care, Washington DC: National Academy Press, 15–44. Pearlin, L.I. and Skaff, M.M. (1996) ‘Stress and the life course: a paradigmatic alliance’, Gerontologist, 36, 239–47. Penninx, B.W.J.H., Guralnik, J.M., Pahor, M., Ferrucci, L., Cerhan, J.R., Wallace, R.B. and Havlik, R.J. (1998) ‘Chronically depressed mood and cancer risk in older persons’, Journal of the National Cancer Institute, 90, 1888–93. Prigerson, H.G., Bierhals, A.J., Kasl, S.V., Reynolds, C.F. III, Shear, M.K., Day, N., Beery, L.C., Newsom, J.T. and Jacobs, S. (1997) ‘Traumatic grief as a risk factor for mental and physical health morbidity’, American Journal of Psychiatry, 154, 616–23. Riboli, E. and Kaaks, R. (1997) ‘The EPIC Project: rationale and study design’, International Journal of Epidemiology, 26 (Suppl.1), S6–S14. Schaefer, C., Quesenberry, C.P. Jr. and Soora Wi. (1995) ‘Mortality following conjugal bereavement and the effects of a shared environment’, American Journal of Epidemiology, 141, 1142–52.

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194 Paul Surtees and Nick Wainwright Shekelle, R.B., Raynor, W.J., Ostfeld, A.M., Garron, D.C., Bieliauskas, L., Liu, S.C., Maliza, C. and Paul, O. (1981) ‘Psychological depression and 17-year risk of death from cancer’, Psychosomatic Medicine, 43, 117–25. Surtees, P.G. (1989) ‘Adversity and psychiatric disorder, a decay model’ in G.W. Brown and T.O. Harris (eds) Life Events and Illness, New York: Guilford Press, 161–95. —— (1995) ‘In the shadow of adversity; the evolution and resolution of anxiety and depressive disorder’, British Journal of Psychiatry, 166, 583–94. Surtees, P.G. and Ingham, J.G. (1980) ‘Life stress and depressive outcome: application of a dissipation model to life events’, Social Psychiatry, 15, 21–31. —— and Wainwright, N.W.J. (1998) ‘Adversity over the life course: assessment and quantification issues’, Stress Medicine, 14, 205–11. —— and Wainwright, N.W.J. (1996) ‘Fragile states of mind, neuroticism, vulnerability and the long-term outcome of depression’, British Journal of Psychiatry, 169, 338–47. —— and Wainwright, N.W.J. (1999) ‘Surviving adversity: event decay, vulnerability and the onset of depression’, European Archives of Psychiatry and Clinical Neuroscience, 249, 86–95. ——, Wainwright, N.W.J., Gilks, W.R., Brugha, T.S., Meltzer, H. and Jenkins, R. (1997) ‘Diagnostic boundaries, reasoning and depressive disorder. II. Application of a probabilistic model to the OPCS general population survey of psychiatric morbidity in Great Britain’, Psychological Medicine, 27, 847–60. ——, Wainwright, N.W.J. and Brayne, C. (2000) ‘Psychosocial aetiology of chronic disease: a pragmatic approach to the assessment of lifetime affective morbidity in an EPIC component study’, Journal of Epidemiology and Community Health, 54, 114–22. Thomas, D.C. (1988) ‘Models for exposure-time-response relationships with applications to cancer epidemiology’, Annual Review of Public Health, 9, 451–82. Turner, R.J. and Wheaton, B. (1995) ‘Checklist Measurement of Stressful Life Events’ in S. Cohen, R.C. Kessler and L.U. Gordon (eds) Measuring Stress. A Guide for Health and Social Scientists, New York: Oxford University Press, 29–58. Wethington, E., Brown, G.W. and Kessler, R.C. (1995) ‘Interview Measurement of Stressful Life Events’ in S. Cohen, R.C. Kessler and L.U. Gordon (eds) Measuring Stress. A Guide for Health and Social Scientists, New York: Oxford University Press, 59–79. Willett, J.B. and Singer, J.D. (1993) ‘Investigating onset, cessation, relapse, and recovery: why you should, and how you can, use discrete-time survival analysis to examine event occurrence’, Journal of Consulting and Clinical Psychology, 61, 952–65. —— and Singer, J.D. (1997) ‘Using discrete-time survival analysis to study event occurrence across the life course’, in I.H. Gotlib and B. Wheaton (eds) Stress and Adversity over the Life Course, Cambridge: Cambridge University Press, 273–94. ——, Singer, J.D. and Martin, N.C. (1998) ‘The design and analysis of longitudinal studies of development and psychopathology in context: statistical models and methodological recommendations’, Development and Psychopathology, 10, 395–426. World Health Organization (WHO) (1997) The World Health Report 1997. Conquering Suffering Enriching Humanity, Report of the Director-General, Geneva: World Health Organization.

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11 The childhood experience of care and abuse (CECA) An exploration with adolescent refugees Michel Tousignant, Emmanuel Habimana, Colette Biron, Esther Sidoli-Leblanc, and Mathilde Brault This chapter has two goals. The first is to consider the association of the three components of the Childhood Experience of Care and Abuse (CECA) with psychopathology among adolescents from refugee families living in the province of Quebec, Canada. The second is to discuss the use of the CECA in a transcultural setting and to illustrate the advantages and appropriateness of its contextual approach in research with informants from thirty-five different countries. The CECA has been less often associated with the important contribution of George Brown and his collaborators to psychiatric epidemiology than have measures of current psychosocial experience such as the LEDS. We would like to underline in this chapter the central part played by vulnerability originating from early family experience in their aetiological model. The CECA is a semi-structured interview used to collect retrospectively material about the main dimensions of parental behaviour up to the age of seventeen likely to be associated with adult psychopathology (Bifulco, Brown and Harris, 1994; Bifulco and Moran, 1998). Its development was considerably influenced by the need to assess the quality of care following experiences of loss and separation which many of the women initially investigated had experienced in childhood during the Second World War (Harris, Brown and Bifulco, 1986; Brown, Harris and Bifulco, 1986; Bifulco, Brown and Harris, 1987).

Literature review There is ample documentation of the predictive importance of family variables for adolescent psychopathology. And this may well be even greater for refugee families whose members so often rely on each other for support (Murphy, 1955). However, we know relatively little about adolescents from refugee families despite evidence that, as a group, they are at high risk for mental health problems (Canadian Task Force on the Mental Health of Immigrants and Refugees, 1988). Recent studies have documented the prevalence of psychiatric diagnoses in selected groups but little information is provided about the family conditions associated with them. Relatively high rates of disorder have been reported but with a decrease in prevalence with length of stay in their adopted country (Sack et al., 1993; Sack et al.,

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196 Michel Tousignant and colleagues 1994; Krupinsky and Burrows, 1986). A prospective inquiry of a Southeast Asian sample in the western United States has shown that there was still a high rate of PTSD six years after original contact but a sharp decrease of depressive and anxiety states. In this study of adolescents, more than two-thirds had a diagnosis, PTSD; major depressive disorder and generalised anxiety disorder being the most prevalent conditions (Kinzie et al., 1986; Sack et al., 1986). Other studies conducted on Southeast Asian and Chilean adolescents from refugee families have confirmed this high risk for emotional disorders compared to local samples (Muecke and Sassi, 1992; Hjern, Angel and Hojer, 1991). Various components of the CECA have been associated with later psychopathology in adults. Lack of care during childhood, in the form of indifference or lack of supervision of control, has repeatedly been shown to be associated with a doubling of the risk of adult depression (Harris, Brown and Bifulco, 1986; Brown, Harris and Bifulco, 1986). Parental antipathy, as well as physical and sexual abuse, have also been shown to relate to caseness in a sample of adolescents and young adult women (Andrews, Brown and Creasey, 1990). The bulk of research has used different instruments and has been in agreement about the importance of family life but the literature is too great to review here. Suffice it to say that externalising disorders have been particularly associated with disciplinary behaviour. For example, poor and inconsistent parental supervision was related to conduct disorders in a clinical sample of 7- to 12-year-old boys (Frick et al., 1992). Corporal punishment was also associated with the use of violence among black adolescents (DuRant et al., 1994). Little systematic information has been gathered about family life in refugee families. Using the focus group approach with women, Ho (1990) reported that Southeast Asian groups acknowledged that physical discipline with the use of small sticks was common, though the Vietnamese said they did not approve of using any kind of object. These women also acknowledged the fact that boys enjoyed much more freedom than girls. The goal of this study was to identify family experiences of care and abuse associated with adolescent psychopathology in refugee families. The main questions were: 1 2 3

What is the prevalence of the main types of experience recorded by the CECA in a multicultural population of refugee families? Is high control more predictive of caseness than other variables? Are CECA scales associated to specific diagnoses?

Methodology Sample A random sample of 203 adolescents from refugee families in the province of Quebec, Canada, was interviewed. They had come from thirty-five different countries and represented four main geographical sources of refugees (Latin America, Eastern Europe, Middle East and Southeast Asia) to Western countries

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The childhood experience of care and abuse 197 since the mid-1970s. The age span was 14–18 years. More than half arrived after the age of 6 and only fifteen were born in Canada. The sample was drawn from high school rolls in communities with high rates of refugees. These rolls included the father’s country of origin and we selected adolescents from countries that had experienced a civil war during the last fifteen years. After sending an introductory letter, we checked by phone with the adolescent whether the family had migrated mainly for political reasons. The rate of sucessfully completed interviews was 62 per cent. See Tousignant et al. (1999) for more information on the socio-demographic characteristics.

Instruments Childhood Experience of Care and Abuse (CECA) The CECA covers the period of childhood and adolescence up to age 17 (Bifulco, Brown and Harris, 1994). Similar questions cover mother and father as well as any other carers if the period during which they provided care lasted three months or more. Interviews lasted on average forty-five minutes. The CECA training manual (Bifulco et al., 1994a) provides guidelines and coding examples. In a previous study by the first author, all but one scale reached an inter-rater reliability of at least 0.78 (kw). In another study, a high agreement between sisters was reached about their respective experience of abuse and neglect and information from interviews about parental death was confirmed by death certificate records (Bifulco et al., 1997). The present study included the CECA original variables of negligence/indifference; supervision; discipline; physical abuse; sexual abuse; and family discord. High control was considered present if at least one of the supervision and discipline scores was high. Lack of care included either severe indifference or low control. More recent measures such as antipathy, role reversal, favouritism and scapegoating were also used. The original ratings were done by the main author, but all severe or deviant scores had to be agreed on by a consensus group. The validity of the CECA has been discussed in various publications which have provided information on the rationale of the method and the concepts, the predictive validity and inter-rater reliability (Bifulco, Brown and Harris, 1994). The instrument covers separately the relationship of the child with the mother and with the father as well as with all other surrogate parental figures. There is the possibility of recording a change in ratings with the date of occurrence. Following the tradition of the contextual method, the interview contains actual examples of relevant behaviour and avoids basing ratings on general statements alone. One of the main limitations of using standardised instruments is the difficulty faced in transferring their use to other cultures. The strict translation of an item can serve to make it odd and even alien to many non-Western people. It is also our experience that care must be taken in confronting an adolescent with actual details of deviant parental behaviour because of the discomfort such a direct approach can provoke. Moreover, languages do not always offer linguistic equivalents and back

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198 Michel Tousignant and colleagues translation cannot cope with this problem. On the other hand, if an English or a French version is administered, the respondent from a different cultural background can associate meanings other than the one originally intended by the authors. In some previous work, we have shown that items of a standardised instrument like the Health Opinion Survey were often interpreted in highly diverse ways within a French-speaking sample from Montreal (Tousignant, Brosseau and Tremblay, 1987). The semi-structured format avoids many of these pitfalls because the interviewer can use paraphrases to convey the meaning of a question; where possible the adolescent is encouraged to talk at some length about everyday events in a conversational manner. It is also much easier using a semi-structured approach to keep some control over the experience of intrusiveness. It is possible to start, for example, with fairly neutral questions about family life, to encourage accounts of actual behaviour and perhaps only fairly late in a sequence of queries to ask more direct questions, and then often only as a follow-up to a point already made by the respondent. There was, however, an important difference in the application of the CECA. It had usually been used with adult women some years after they had left their family of origin. In this study, adolescents were still experiencing many of the family events they were reporting. There were two dangers: one was that the respondent would bias the information about earlier periods in childhood according to what was now happening at home; the other was a possible reluctance to disclose sensitive material about ongoing family life – not least to an interviewer from a different culture. In many traditional cultures, there is a feeling that family problems should not be mentioned to outsiders. We were therefore apprehensive that answers to the investigation of family life would be restricted to polite and evasive replies. We made the early decision to meet the adolescent at home which soon proved to be a mistake. Even though we asked to see them alone, some made clear that their parents were within earshot and that a closed door was not a sufficient safeguard of privacy. The university office proved, by and large, a more welcome setting for most of the adolescents but not for some parents who remained apprehensive. Indeed, some adolescents were accompanied by their fathers even if we had forewarned them that they would have to wait in a separate room for quite a long period. A few adolescents had been asked to phone home at frequent intervals during the interview. Compared with another Quebec study (Tousignant, Bastien and Hamel, 1993) involving suicidal adolescents and a control group, the volume of the material and the degree of confidence was similar in this refugee study. First of all, these adolescents from refugee families, with a few exceptions, had been attending school in Quebec for a minimum of three years. This appeared to have been long enough for them to accept that personal concerns could be shared with friends and professionals. Second, at times we sensed the possibility that the CECA’s encouragement of detailed discussion of family behaviour may have contributed to a process of independence from parents by sharing personal experiences with a neutral third party. Others were clearly proud to tell how their families had successfully survived the trauma of war and the adversities of unemployment and poverty in Canada.

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The childhood experience of care and abuse 199 Seven interviewers worked on this project and, as a team, we were able to use Spanish, Arabic, Kinirwanda or German as necessary. All of us had some experience or training in clinical psychology or in qualitative research methods. Ratings Norms of parental behaviour vary so much across cultures that the family situations did not correspond at times with the illustrations in the CECA manual based on English protocols. For instance, parents in some cultures accept without question that physical punishment is legitimate and desirable, and even the sign of a caring parent, when a child is getting out of control; or that, in order to safeguard her reputation, the place of an adolescent daughter is at home. For this reason, we made a rule that each high or deviant score would have to be confirmed by a consensus group of five persons. The fact that three members of our team were from or had lived in North and sub-Saharan Africa and central America helped us to take account of the cultural context. We were generally conservative in attributing a high score when we were in presence of borderline cases. In an analysis not reported here, the ratings of high and normal control were highly correlated with the adolescent’s subjective evaluation of the legitimacy of the parental behaviour, even though both had been rated independently. Parental control Most of the disagreements over rating involved supervision and discipline, the two scales measuring parental control. It was sometimes difficult to decide whether a parental behaviour not conforming to Western values, and apparently shared by a significant minority of the relevant cultural group, should be considered deviant or putting a child at risk. We took the position that our role was not to decide whether a culture was right or wrong but to make a judgment whether behaviour sufficiently uncommon in a Western context to be considered deviant would raise the chance of producing developmental problems and increased vulnerability to psychopathology, given the adolescents’ transplantation to Canada with the shift in everyday experiences that this was bound to involve. From the adolescents’ accounts, we found there were clearly often wide divergences between their own and their parents’ outlooks and, given this, we found that the alternative emic approach, that is, rating in terms of the standards shared by the culture in question, was not easy to follow. First, adolescents were daily subjected in school to loud rock music, media values, and to the relativism of a multicultural society. Most conveyed that they were building their identity by integrating in various ways lessons from their country of origin with the North American way of life. Second, their parents were also involved in a process of acculturation and most hoped for a full participation of their children in Canadian culture, even though what they said to their children was often filled with contradictions. In short, it proved nearly impossible to establish where the culture of the adolescents was located.

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200 Michel Tousignant and colleagues It was, therefore, finally decided to follow the London CECA guidelines but to lean on the conservative side when rating for ‘high’ supervision or discipline. In the case of physical abuse and neglect however, the CECA standards proved straightforward. We added a new scale to reflect whether the parental behaviours were regarded as legitimate by the adolescent. In general, high supervision was exercised by limiting outside social contacts or dating, by listening to phone conversations, and by refusing permission to go out. By and large, such behaviour was negatively perceived by the adolescents except by some living in fundamentalist Muslim families. Daughters secluded at home did not find there the rich social lore of a female universe characteristic of their country of origin. Often, they spent their time watching television. They were also apparently envious of school friends with more freedom. Some felt ashamed of the fact that their parents picked them up after school. A score of high supervision was not given if the adolescent had been permitted some opportunity for basic socialisation. But we gave a high score if an adolescent was not allowed to go out after the evening meal, especially during the summer vacations. An example of high supervision was a girl allowed to attend a Saturday school dance but escorted back home by her father at 10 pm just after the music had started. Discipline was easier to code. High discipline was often associated with chronic physical abuse. There were few instances of a child being repeatedly hit without any apparent element of sadism or disregard on the part of the parents. Parents guided by moral considerations rather than by feelings of frustration by and large used milder forms of punishment. We also sensed that harsh punishment in families from some cultural backgrounds might have been related less to a particular cultural tradition than to the general context of civil war eroding values and making violence more acceptable. Outright violent behaviour was most common among the group from Salvador, a country where people had probably been more directly exposed to violence than in any other country in our sample. Unfortunately, this remains no more than a hunch as there are no comparisons for the prewar period. Role reversal Refugee families are often poor and adolescents are expected to bring home money from working after school. Moreover, because many parents are not fluent in French or English, their children take on responsibilities unusual for their age, such as looking for a job for their father. Such instances made it necessary to reconsider the definition of role reversal established by the London CECA. We took the position that the child had to replace, or to take a responsibility usually reserved to, a parent in order to score high on role reversal. Many daughters took on a substantial share of the domestic chores, but a high score was only given if it appeared to us that the mother was unloading many of her core responsibilities. There were relatively few instances of a parent sharing intimate confidences with a child; in general, we sensed that the frontier between generations was too strong

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The childhood experience of care and abuse 201 in most of the cultures for this to occur although there were a number of instances where children felt that they had to protect their parents, who could not speak French adequately, and to keep in contact with them during the day in case something occurred with which they could not cope. Some children were also used as translators and brokers in difficult situations. Some, for example, were asked to accompany their parents to a physician and even at times to help them take a decision about major surgery or gynecological problems. Favouritism of other Our research started just at the time when the favouritism/scapegoating scales had recently been introduced in London, but for the most part we obtained sufficient material for a rating although we have taken more account of the perception of the child than in London. On the whole, parents favoured boys in the sense they were largely free from domestic chores and were given much more freedom than daughters in life outside the home. As will be seen, the rating of favouritism of other turned out to be unexpectedly important in relation to psychopathology. Diagnostic Interview Schedule for Children – 2.25 For diagnostic purposes, we used the French translation of the disk – 2.25 employed by the Quebec Health of Children Survey and validated on a Quebec sample (Breton et al., 1999). This instrument has been tested with modified versions and shown to have high inter-rater reliability and acceptability to patients (Shaffer et al., 1993). The concurrent criterion validity test using a semi-structured clinical interview on similar information found moderate levels of agreement with this standardised instrument (Piacentini et al., 1993). Some readers may not be familiar with the diagnosis of overanxiety used for children in the DSM-III-R. This diagnosis is often centred on performance and on fear of being embarrassed. It was mainly prevalent among girls from Southeast Asia.

Results Table 11.1 presents the frequencies and rates of the component scales of the CECA for each gender and for the total sample. The results obtained for a random sample of women with a child living at home in the London Borough of Islington are given as a point of reference (Bifulco, Brown and Harris, 1994). This latter sample was largely working class and included around a quarter who were lone parents. It is therefore possible that their rates of negative experiences in childhood and adolescence are somewhat greater than would be obtained in a representative sample of the female population of London. Bearing in mind the London sample dealt only with women, the overall results show more similarities than differences. Rates of parental indifference, control, physical abuse and antipathy are similar, with the Canadian sample tending to show somewhat lower figures. Discord in the home is comparable, with slightly

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202 Michel Tousignant and colleagues Table 11.1 CECA frequencies of high scores by sex and total, and comparison with Islington sample in London Refugee sample CECA variable

Target parent

Boys %

Indifference

London women

Girls N

Total

%

N

%

N

%

M

6

6

12

13

9

19

—

P

6

6

14

15

10

21

—

P/M

11

11

18

19

15

30

17

M

11

11

17

17

9

18

—

P

2

2

13

13

8

15

—

M

2

2

13

13

7

15

—

P

8

8

14

14

11

22

—

Control

P/M

9

9

26

26

17

35

18

Antipathy

M

6

6

21

21

13

27

17

P

8

8

13

13

10

21

20

M/P

11

11

13

13

17

24

—

M/P

20

20

20

20

20

40

18

0

0

2

2

1

2

9

29

30

32

33

31

63

38

M

10

10

17

17

13

27

—

P

6

6

11

11

8

17

—

Favouritism of other

M/P

9

9

23

24

16

33

—

Scapegoating

M/P

3

7

—

Supervision

Discipline

Physical abuse Sexual abuse Discord Role reversal

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The childhood experience of care and abuse 203 Table 11.2 Prediction of DSM-III-R caseness from CECA variables (logistic regression analysis) CECA variable

Boys r

Girls OR

Total

r

OR

Indifference

0.10

0.11

Control

0.09

0.30**

Antipathy

0.21*

3.9

0.18

Physical abuse

0.21*

3.3

0.20*

Discord

0.16

0.23*

Favouritism

0.36**** 9.9

Role reversal

0.12

r

OR

0.13 4.1

0.26****

4.0

0.21**

3.2

2.8

0.20***

2.9

3.1

0.20***

2.7

0.34**** 5.2

0.36****

6.9

0.11

0.11

Notes: * P<.05 ** P<.01 *** P<.001 **** P<.0005

Table 11.3 Prediction of DSM-III-R diagnoses from CECA variables (logistic regression analysis) Diagnosis

Predicting Variable

Phobia

Indifference

Overanxiety

Antipathy

Depression

Wald

df

p<

OR

3.41

1

0.010

3.33

9.28

1

0.050

4.14

Control Favouritism

5.36 13.30

1 1

0.050 0.001

5.77 16.70

Conduct disorders

Discord Favouritism

4.02 5.06

1 1

0.050 0.050

3.48 4.40

Overall caseness

Control Favouritism of other sex

4.99 10.46

1 1

0.050 0.001

2.69 5.00

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204 Michel Tousignant and colleagues more in Islington. A notable difference is the almost complete absence of sexual abuse among the refugee female adolescents. This might well relate to the strict surveillance of their activities. The rate of favouritism of other is 14 per cent and girls are mostly the victims. Role reversal by mothers is more frequent than that by fathers, at 13 per cent. In the univariate analyses (logistic regression), all CECA variables except two (indifference and role reversal) are associated with caseness (Table 11.2). Antipathy and high supervision (control) only reach the .05 level. All the other measures are highly significant, above the 0.005 level. In the bottom two rows of Table 11.3, the results of the logistic regression analysis show two variables associated with overall caseness: first, a highly significant interaction effect of favouritism of another child by sex – girls have relatively higher rates than boys when they report being victim of favouritism. High control is the only other variable significant. When analysing each diagnosis separately, favouritism of another child is highly associated with major depression and, to a lesser degree, with conduct disorder. Favouritism notwithstanding, there is at least one variable specifically associated with each diagnosis, though only at the 0.05 level. The second variable associated with depression is high control and high discord is related to conduct disorder. Antipathy is related to overanxiety and indifference to simple phobia.

Discussion The high rate of caseness in this sample was 21 per cent when excluding simple phobia, which was almost twice the rate of a provincial sample of 13–14 year-olds (11 per cent) (Tousignant et al., 1999). We could therefore expect a high rate on the CECA scales. The interference of the parents in the social activities of many adolescents, some even being refused permission to participate in them at all, had already led us to suspect we would find a high rate of control. The rate of 17 per cent was much higher than the rate obtained previously with a Montreal sample (Tousignant, Bastien and Hamel, 1993). High control was at 6.5 per cent and this sample included a high number of immigrants. The high control was mostly present in the female group. Boys were treated no differently in this respect than the Quebec children. It was often reported in the course of the interviews that boys had much more freedom. This differential treatment is often observed in agricultural societies where women’s lives are restricted to the domestic space. The rate of physical abuse was also quite high at 20 per cent. Most incidents of physical abuse involved leaving marks on the body visible the next day. Most were done with a belt or a stick. One mother burned her child on the lip for having lied. There was, however, only one instance of violence involving a severe injury. It is interesting to note that violence originated as often from the mother as from the father. The climate of violence was not restricted to the parent-child relationship. Violence between parents was also high, at 20 per cent, with family discord 31 per cent.

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The childhood experience of care and abuse 205 The rate of physical abuse towards children recorded in this sample was similar to that reported about their own childhoods by the Islington inner-city women. In carrying out the interviews we gained the impression that for the most part the amount of physical abuse was probably no different from that found in the country of origin, although in one instance we felt that the level of violence in the home may have been exacerbated by the climate of civil violence that had prevailed in their home country. By contrast, there was little sexual abuse in this sample, just 1 per cent related to a parent. (In this instance, the father of an 11-year-old girl had walked naked in her presence, visibly and not by accident, though without masturbating or attempting to seduce. It seemed that this behaviour would have been judged highly improper in this culture, so the consensus group classified it as an instance of exhibition. This father acted strangely in general and his real intentions were hard to identify.) This rate of sexual abuse may appear low considering the intrusive behaviour of parents and it needs to be borne in mind that the reports of higher rates from Islington women occurred well after they had left home. We certainly cannot claim that this rate is a correct estimate but neither have we any reason to suggest that it would be much higher had we proceeded differently. Most interviews with adolescent girls were carried out by young women with clinical experience. The interview also covered relationships with boyfriends and girls were quite open in discussing this topic as well as family violence. One of the highlights of the results is the high rate of favouritism of other. Around a quarter of girls felt that others were favoured far more than themselves in contrast to only 9 per cent of the boys. This pattern almost certainly reflected the greater freedom given to boys in the home cultures but the girls in the sample often no longer saw this as entirely legitimate. Many certainly found the situation harder to accept when the values of the school environment emphasised sex equality and when the other students were relatively free to organise their leisure activities as they wished, especially with regard to boyfriends. It was also clear that many immigrant parents feared that the sexual relationships of the children might transgress religious standards. In other instances, they were clearly concerned such relationships should not cross ethnic boundaries. In some families, the favouritism shown by parents was sufficiently marked for scapegoating and rejection to be rated, especially when it was made clear that one or both parents would have much preferred their child to be a boy rather than a girl. There was a high rate of role reversal, with 13 per cent involving the mother and 8 per cent the father. However, this was not associated with psychopathology. In summary, adolescents from refugee families differ from the London sample mainly on the measures directly or indirectly involving parental control, physical abuse and favouritism. These behaviours were more frequent towards girls, with the exception of physical abuse. There was also considerable conflict in these families, as shown by the high rates of family discord and violence between spouses. Most CECA scales were significantly related to caseness. But role reversal and indifference showed only nonsignificant tendencies. The rate of diagnoses for informants scoring high on these two scales was similar to the rates found for other

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206 Michel Tousignant and colleagues measures but the lower frequencies made the test more conservative. Though lower in frequency than high control or family discord, favouritism was associated with a particularly high rate of caseness. In its most extreme form, scapegoating, all but one were cases. However, there were too few instances to keep this latter variable in the analysis. In a multivariate analysis, favouritism of other was the factor with the highest level of significance and high control was second. There was also a sex by favouritism of other interaction along with a lesser contribution of control. One may ask why favouritism of other much more than control, and control rather than physical abuse? High control was generally more persistent than physical abuse, often covering the entire span of childhood and adolescence. Beatings were often reported to be restricted to the pre-adolescent stage. It is also possible that physical abuse may make the child more vulnerable only in the presence of high control. In this regard, 80 per cent of cases of physical abuse were associated with high control (28/35) and the correlation was .88. By comparison, the correlation between physical abuse and indifference was .35. Favouritism of other was present in nine boys and twenty-four girls and the percentage of psychopathology was 55 per cent for both sexes. The strong effect of favouritism of other may reflect the role of contradictions in parental behaviour. As long as harsh physical punishment is perceived as a just retribution, equally distributed among the disobedient children, there is a sense of legitimation which can sometimes be backed by the culture. In comparison, in the Montreal sample, harsh punishment originated more often from sadistic parents or surrogate parents, and was often accompanied by indifference. The same argument can be applied to high control. It may be an inconsistent control that is more detrimental to self-esteem. If a child can see that his experience is the same as that of his brothers and sisters, he may come to feel that existence is harsh but just. It is when this sense of justice is diminished by an arbitrary attitude that the child may feel victimised and nurture a strong resentment. Turning to the issue of specific diagnoses, favouritism of other and high control were both needed to model depression. As mentioned earlier, favouritism of other may have a deleterious impact on self-esteem and induce a sense of powerlessness. We refer to the LEDS research which has shown that it was not so much loss as such that provoked depression as humiliation and entrapment (Brown, Harris and Hepworth, 1995). In this case, favouritism has probably led to some kind of rejection and humiliation with the implicit message that some children in the family have more worth than the others. High control may lead to a feeling of entrapment and powerlessness. Concerning the relationship between over-anxiety and antipathy, we had the impression that the instances of antipathy reflected parental tenseness rather than rejection or dislike. This situation would not so much affect self-esteem but make children apprehensive about reactions of bad temper. We found associations of both favouritism of other and family discord with conduct disorder. If favouritism of other translates into the breaking of a moral code, it makes sense that it would foster conduct disorders. On the other hand, there seems to be a logical relationship between family discord and this diagnosis (Rutter,

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The childhood experience of care and abuse 207 Quinton and Hill, 1990). It is implicit in both that the use of power is a more efficient way of coping with problems than negotiation. At first sight these findings may appear puzzling: the high frequency of favouritism of other among girls may seem to contradict the generally expected greater frequency of conduct disorder among boys, which was again found here. (There were nine boys and four girls with conduct disorder.) However, there was also considerable comorbidity between depression and conduct disorder, even among boys. Finally, there is a need to comment on the unexpected association of simple phobia with indifference. This result may have been the product of a chance correlation. On the other hand, as cases of phobia were more frequent among females from Southeast Asia, it is tempting to indulge in speculation: there were many single mothers in this group apparently overwhelmed by their responsibilities. It may be that the extreme experiences of war and exile led, on the one hand, to the phobic symptoms of the children, and, on the other, to the apathy and indifference of the mothers, without the two being in a cause-effect relationship.

Conclusion Even if the CECA takes longer to administer than most scales of parent-child relationships, it covers the main dimensions of lack of care and abuse. This is a definitive advantage over most measures which tend to study only one dimension; it is possible to sort out which variables are more instrumental in the development of a specific psychopathology or problem. For instance, we know relatively little about parent-child characteristics of adolescents and adults who have committed suicide (Wagner, 1997) and the CECA would be a good instrument to use retrospectively with a third party. Altogether, the CECA and its contextual approach is much more flexible and adaptable to a multicultural setting than standard instruments. These adolescents from refugee families felt quite at ease with the conversational tone and were not shy to confide on family matters. The fact that some parental behaviours like harsh punishment are now negatively perceived in Western countries, while still being sanctioned by some cultures, presents an interesting challenge. In this regard, this study has shown that we should stick to the original scoring rules and verify empirically whether most high scores are associated with psychopathology.

Acknowledgements This study was supported by grants from the Social Sciences and Humanities Research Council of Canada, FCAR (Quebec ministry of education) and FODAR (University of Quebec). The writing was done while the first author was visiting professor at the National Institute of Advanced Studies, Indian Institute of Sciences, Bangalore, India. We thank the following for their assistance: Claire Malo, Bérengère Denis and Francine Perrault.

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208 Michel Tousignant and colleagues

References Andrews, B., Brown, G.W., and Creasey, L. (1990) ‘Intergenerational links between psychiatric disorder in mothers and daughters: The role of parenting experiences’, Journal of Child Psychology and Psychiatry, 31, 1115–29. Bifulco, A. and Moran, P. (1998) Wednesday’s Child, London: Routledge. ——, Brown, G.W. and Harris, T. (1987) ‘Childhood loss of parent, lack of adequate parental care and adult depression: a replication’, Journal of Affective Disorder, 12, 115–28. ——, Brown, G.W. and Harris, T.O. (1994) ‘Childhood Experience of Care and Abuse (CECA): A retrospective interview measure’, Journal of Child Psychology and Psychiatry, 35, 1419–35. ——, Brown, G.W., Neubauer, A. and Harris, T.O. (1994) Childhood Experience of Care and Abuse (CECA). Childhood interview training package, London: Royal Holloway College. ——, Brown, G.W., Lillie, A. and Jarvis, J. (1997) ‘Memories of childhood neglect and abuse: Corroboration in a series of sisters’, Journal of Child Psychology and Psychiatry, 38, 365–74. Breton, J.J., Bergeron, L., Valla, J.P., Berthiaume, C., Gaudet, M., Lambert, J., St-Georges, M., Houde, L. and Lépine, S. (1999) ‘Quebec Child Mental Heath Survey: Prevalence of DSM-III-R mental health disorder’, Journal of Child Psychology and Psychiatry, 40, 375–84. Brown, G.W., Harris, T.O. and Bifulco, A. (1986). ‘Long-term effects of early loss of parent’ in M. Rutter, C.E. Izzard, P.B. Read (eds) Depression in Young People: Developmental and Clinical Perspectives, New York: Guilford Press. ——, Harris, T.O. and Hepworth, C. (1995) ‘Loss, humiliation and entrapment among women developing depression: A patient and non-patient comparison’, Psychological Medicine, 25, 7–21. Canadian Task Force on the Health of Immigrants and Refugees (1988) After… the Door has Opened, Canada: Secretary of State, Multiculturalism, Health and Welfare. DuRant, R.H., Cadenhead, C., Pendergrast, R.A. Slavens, G. and Linder, C.W. (1994) ‘Factors associated with the use of violence among urban black adolescents’, American Journal of Public Health, 84, 612–17. Frick, P.J., Lahey, B.B., Loeber, R., Stouthamer-Loeber M., Christ, M.A. and Hanson, K. (1992) ‘Familial risk factors to oppositional defiant disorder and conduct disorder: Parental psychopathology and maternal parenting’, Journal of Consulting and Clinical Psychology, 60, 49–55. Harris, T., Brown, G.W. and Bifulco, A. (1986). ‘Loss of parent in childhood and adult psychiatric disorder: the role of lack of adequate parental care’, Psychological Medicine, 16, 641–59. Hjern, A., Angel, B. and Hojer, B. (1991) ‘Persecution and behavior: A report of refugee children from Chile’, Child Abuse and Neglect, 15, 239–48. Ho, C.K. (1990) ‘An analysis of domestic violence in Asian American communities: A multicultural approach to counselling’ in L. Brown (ed.) Diversity and Complexity in Feminist Therapy, New York: Haworth Press. Kinzie, J.D., Sack, W.H., Angell, R.H., Manson, S. and Rath, B. (1986) ‘The psychiatric effects of massive trauma on Cambodian children: I. The children’, Journal of the American Academy of Child and Adolescent Psychiatry, 25, 370–6. Krupinsky, J. and Burrows, G. (1986) The Price of Freedom, Oxford: Pergamon.

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The childhood experience of care and abuse 209 Muecke, M.A. and Sassi, L, (1992) ‘Anxiety among Cambodian refugee adolescents in transit and in resettlement’, Western Journal of Nursing Research, 14, 267–91. Murphy, H.B.M. (1955) Flight and Resettlement, Geneva: UNESCO. Piacentini, J., Shaffer, D., Fisher, P., Schwab-Stone, M., Davies, M. and Gioia, P. (1993) ‘The Diagnostic Interview Schedule for Children-Revised Version (DISC-R): III. Concurrent criterion validity’, Journal of the American Academy of Child and Adolescent Psychiatry, 32, 658–65. Rutter, M., Quinton, D. and Hill, J. (1990) ‘Adult outcome of institution-reared children: Males and females compared’ in L.N. Robins and M. Rutter (eds) Straight and devious pathways from childhood to adulthood, Cambridge: Cambridge University Press. Sack, W.H., Angell, R.H., Kinzie, J.D. and Rath, B. (1986) ‘The psychiatric effects of massive trauma on Cambodian children: I. The family, the home, and the school’, Journal of the American Academy of Child and Adolescent Psychiatry, 25, 377–82. ——, Clarke, G., Him, C., Dickason, D., Goff, B., Lanham, K. and Kinzie, J.D. (1993) ‘A 6year follow-up study of Cambodian refugee adolescents traumatized as children’, Journal of the American Academy of Child and Adolescent Psychiatry, 32, 431–7. ——, McSharry, S., Clarke, G.N., Kinney, R., Seeley, J. and Lewinsohn, P. (1994) ‘The Khmer Adolescent Project: I. Epidemiologic findings in two generations of Cambodian refugees’, Journal of Nervous and Mental Disease, 182, 387–95 Shaffer, D., Schwab-Stone, M., Fisher, P., Cohen, P., Piacentini, J., Davies, M., Edelbrock, C. and Regier, D. (1993) ‘The Diagnostic Interview Schedule for Children-Revised Version (DISC-R), I: preparation, field testing, interrater reliability, and acceptability’, Journal of the American Academy of Child and Adolescent Psychiatry, 32, 643–50. Tousignant, M., Brosseau R. and Tremblay, L. (1987) ‘Sex bias in mental health surveys: Do women tend to report less serious symptoms than men’, Psychological Medicine, 17, 203–15. ——, Bastien M.F., Hamel, S. (1993) ‘Suicidal attempts and ideations among adolescents and young adults: The role of father and mother care and parents’ separation’, Social Psychiatry and Psychiatric Epidemiology, 28, 256–61. ——, Habimana, E., Malo, C., Sidoli-LeBlanc, E., Biron, C. and Bendris, N. (1999) ‘The Quebec Adolescent Refugee Project. Psychopathology and Family Variables in a Sample from 35 Nations’, Journal of the American Academy of Child and Adolescent Psychiatry, 38, 11, 1426–32. Wagner, B.M. (1997) ‘Family risk factors for child and adolescent suicidal behavior’, Psychological Bulletin, 121, 246–98.

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12 Gender differences in the experience and response to adversity Tom Craig and Soumitra Pathare

Introduction Sex differences in the prevalence of common affective disorders have been well documented in most Western populations. For example, the American National Comorbidity Survey based on a nationwide probability sampling frame of 8,000 men and women found a female preponderance of 1.7 for lifetime DSM-III-R Major Depressive Disorder and the British National Survey of Psychiatric Morbidity found a female excess of 1.5 for depression and 1.8 for mixed states of depression and anxiety. The excess is most marked during the reproductive years, emerging at adolescence and peaking in the mid-30s. In prepubertal children there is a male preponderance of depression, the female excess emerging during adolescence. The female excess, particularly for milder disorders, is greatest in early adulthood and subsequently declines. Whether it ever disappears entirely is debatable, with some studies showing a persistent elevation and others finding a male excess in late life. These differences are not explained by artefacts such as the different styles of reporting distress or by greater psychiatric consultation by women. Nor has the excess been adequately explained in terms of biological factors though it is clear that these are implicated for disorders at the more severe end of the spectrum and for bipolar disorder. The emergence of a female excess at adolescence and (in some studies) its disappearance in later life, has led to much speculation concerning a hormonal aetiology. But attempts to relate the emergence of depression at puberty to changes in hormonal status have been largely inconclusive and it is difficult to disentangle the biological from the psychological and social changes associated with menarche. Similarly, several prospective studies of the menopause have failed to find convincing associations either in clinic populations or in general population surveys of women around the menopause. Some of the best evidence for biological processes comes from investigations of depression associated with childbirth. Post-partum blues are probably related to the abrupt changes in sex hormones post-partum and it appears that women who experience the blues are more likely to develop clinical depression a few weeks later, implying a biological aetiology for some post-partum depression. There is also evidence that parity is an important factor as the prevalence of severe depression among nulliparous women

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212 Tom Craig and Soumitra Pathare Early cohabitation Pre-marital pregnancy

Childhood adversity (Parental indifference/abuse)

Unreliable spouse Low crisis support

Entrapment and other severe crises

Onset

Psychological vulnerability Negative self-evaluation Sub-clinical symptoms Insecure attachment

Figure 12.1 Simplified schema of Brown and Harris model of depression.

is very similar to that for men. While parity has also been found to be associated with increased prevalence of moderately severe depression in community samples, this effect is largely explained by exposure to the environmental adversity that goes along with marriage and motherhood. In short, it seems likely that we need to turn to social and psychological factors for an explanation for the non-psychotic, moderate depression that comprises the majority of cases in community surveys and psychiatric out-patient clinics.

An aetiological framework In Figure 12.1 we show a simplified version of the aetiological model of depression developed by Brown and Harris. This model provides a helpful framework for exploring differences in men and women that might go some way to explaining the observed difference in rates of disorder. According to this model, which was developed almost exclusively from studies of women, the immediate precursor of most episodes of depression is a stressful experience involving aspects of loss, humiliation or entrapment (chapter 1). These crises are particularly likely to result in depression in the presence of ‘psychological’ vulnerability (negative evaluation of self or chronic sub-clinical symptoms of anxiety/depression) or of ‘environmental’ vulnerability (inadequate support particularly from a partner or a very close other at the time of the crisis). The risk of onset is also increased amongst those with histories of childhood adversity involving marked parental neglect, or physical or sexual abuse. Such childhood adversity is linked to adult vulnerability via a chain of events which include premarital pregnancy and marriage to unsupportive partners and which culminate in negative interactions with partners and unsatisfactory experiences at work, and, in some circumstances, in difficulty calling upon support in times of crisis. Taking this model as a starting

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Gender differences in adversity 213 point, it is apparent that one might look for differences between men and women at several points along this complex causal chain.

The role of adverse childhood experience There is now reasonably convincing evidence that adverse childhood experiences (involving severe parental indifference, and physical and sexual abuse) more than double the risk of women suffering depression in adulthood. There are few studies exploring gender differences between childhood adversity and adult disorder, but those that do suggest that childhood experiences are more predisposing to depression in women than in men. Sexual abuse is particularly associated with adult disorder and occurs far more commonly to girls. But even if men escape depression, they may still be liable to other consequences of their early experience. A number of studies suggest that boys may be more sensitive to parental marital breakdown than girls, responding with distress, behavioural disorder and mental health problems, though the evidence is not uniform nor the effect particularly strong. Of greater significance is the evidence that poor quality parenting, particularly harsh and punitive discipline, is implicated in the development of externalising behaviour problems such as conduct disorder) (Farrington and Hawkins, 1991; Patterson, Reid and Dishion, 1992). Deater-Deckard and Dodge (1997) review the evidence for a causal link between childhood aggression (and hence conduct disorder and possibly later adult externalising behaviour problems) and harsh parental discipline. Using data from a longitudinal study of the development of aggressive behaviour in a random sample of 585 boys and girls, they showed that ratings of parents’ harsh discipline when the children were age 5 were predictive of later aggressive behaviour at school and with later conduct disorder. Interestingly, harsh discipline by mothers was more strongly correlated with externalising behaviour problems among girls than among boys with the opposite being true for harsh discipline administered by fathers. This suggests that the imitation of parent behaviour by a child may be greater when the child sees the parent as a role model and where the parent is the same sex as the child. But critics of this hypothesis point out that harsh discipline is seldom administered by opposite-sex parents, particularly fathers to daughters, and it is even possible that opposite-sex punishment is more likely to suppress aggressive behaviour than same-sex punishment. In an impressive longitudinal study in Christchurch, New Zealand, Fergusson and colleagues followed up a birth cohort of 1,256 children with a range of social measures at birth, 4 months and annually to age 15 using parental interviews, child interviews, teacher information and official records. They examined the relationship between exposure to parental separation and a range of later outcomes including early onset sexual activity, substance abuse, conduct disorder, mood and anxiety disorder. The study confirmed an association between parental separation and later risk of problem behaviours though the association was modest and partially explained through correlation with a number of factors which both increased risk of parental separation and increased risk of adolescent problems – economic deprivation, parental substance abuse and parental conflict. No gender specific

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214 Tom Craig and Soumitra Pathare effects were observed. In a further analysis, they showed that at age 15, children with multiple problem behaviours were much more likely to have come from backgrounds characterised by a wide range of social, economic, parental and child rearing adversity. The children in the most disadvantaged 5 per cent of the cohort had risks of becoming multiple problem teenagers that were over 100 times that of children who were in the most advantaged 50 per cent of the cohort. It was rare for a multiply disadvantaged child to escape later problems. Resilience appeared to relate to having a higher IQ score at age 8, having lower affiliations with delinquent peers, lower exposure to family adversity and lower rates of ‘novelty seeking’ at age 16. Girls were no more likely to be resilient than boys. Girls were, however, more likely to report depressive symptoms than boys. In girls, but not in boys, depressive symptoms were highly correlated with maternal depressive symptoms measured at an earlier point in the study (when the children had been aged 8–13). This correlation could be largely explained by the fact that the marital discord, family adversity and social disadvantage which led to depression in the mothers were also responsible for the increased vulnerability to depression in their daughters as well. The children of depressed women also had significantly higher rates of oppositional and conduct disorder than those whose mothers were not depressed – an association which, once again, appeared to be mediated by social and contextual factors. Conduct disorder in childhood is associated with the early use of psychoactive substances and thus with adult substance abuse and dependency. The striking over-representation of males with addictive disorders seems related to the fact that they have much higher rates of conduct disorder and tend to begin using substances at an earlier age and are also more likely to be involved in deviant adult peer group networks than women. In another important longitudinal follow-up study of disadvantaged boys and girls, David Quinton and colleagues used data from four studies of young people first collected in childhood and followed up into their mid-20s. Childhood measures included an assessment of conduct disorder, planning behaviours in relation to future sexual cohabitation, and to employment and assessment of the level of deviance of the peer groups joined in the first few years after leaving school. Adult functioning was assessed in terms of the quality of social relationships, the presence of antisocial behaviour and substance abuse. A key focus was the examination of the course and outcome of conduct disorder in men and women and the importance of supportive cohabiting relationships in promoting a switch from conduct disorder to stable adult adjustment. The study reported several results of interest to gender. There was a movement out of disorder for both boys and girls who had supportive relationships in early childhood but such relationships were relatively rare in these socially disadvantaged populations. The chain of environmental links between childhood and adulthood differed in important ways for men and women. Girls who had been taken into statutory care were more likely than those not in care to develop conduct disorder, to lack family support, to show lower levels of planning, to cohabit and to have their first pregnancies earlier, ending up with deviant partners and poorer outcomes on all adult measures. In contrast, men

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Gender differences in adversity 215 who had been in care showed no increased tendency to cohabit earlier than general population males. Early cohabitation was only important for women, and the men were more likely to cohabit later with non-deviant women and were less likely to use marriage as a means of escaping an unhappy home. Thus they were less likely to find themselves entrapped in unrewarding relationships, that, from Brown’s perspective, play such an important part in depression. It appears, therefore, that childhood adversity is a general risk factor increasing the vulnerability to both internalising and externalising disorders in adulthood. What is less clear is whether there may be a gender difference in adult vulnerability to particular disorders following childhood adversity – women being more likely to develop depression and men to develop externalising disorders of conduct and substance dependency, given broadly equivalent exposure to childhood deprivation. We set out to explore this possibility in a recent study of mixed sibling pairs (Pathare and Craig, submitted). The study was an initial, exploratory, cross-sectional investigation of ninety-five brother-sister pairs within five years of each other’s age who had grown up together in the same household and thus, in a very crude sense, shared a common background in terms of economic (dis)advantage and household arrangements, including parental marital stability. Sibling pairs were recruited through the sister as this was thought to be likely to improve the response rate of men. A postal questionnaire was sent to all women aged 21–40 registered with local general practitioners and consecutive respondents meeting selection criteria were invited to interview. This consecutive series was supplemented by a ‘high risk’ group selected on the basis of a positive response to the Childhood Experience of Care and Abuse Questionnaire (CECA-Q Bifulco, 2000) so as to obtain an approximately 2: 1 ratio of women with adverse and non-adverse childhood experiences. The brother-sister pairs were then interviewed using a variety of semi-structured assessments of childhood experience, attachment (Attachment Style Interview – Bifulco, 2000), and lifetime psychiatric disorder (SCID-IV – First et al., 1996). In the combined series, a third of the women and a quarter of the men had experienced some form of adversity in childhood. There was a considerable degree of concordance between brothers and sisters for childhood adversity with, for example, 90 per cent (75/83) concordant for the presence or absence of parental neglect. But despite the high level of agreement concerning the presence of childhood adversity, there was very little concordance for the experience of depression in adulthood, even when pairs concordant and discordant for adversity were analysed separately. In contrast, there was a modest concordance for adult substance dependency that was confined to the siblings who were also concordant for adversity. Women had a higher prevalence of life-time depression than men. This higher prevalence was most apparent among women with childhood adversity who were eight times more likely to have experienced depression than their male counterparts (OR 7.8; 95 per cent CI 1.9–34.9). Childhood adversity was also found to be associated with a history of chronic and recurrent depression in women but not in men. In contrast to the findings for depression, childhood adversity was a risk for lifetime prevalence of addictive disorder in both men and women. Once again, there

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216 Tom Craig and Soumitra Pathare were differences in base rates, this time with men reporting a higher rate of disorder than women even in the absence of childhood adversity (men 18 per cent [11/63], women 3 per cent (2/62); odds ratio 6.35, 95 per cent CI 1.2 to 43.6) and while men with childhood adversity had three times the rate of addictive disorder than men without adversity, women with adversity had eleven times the rate of those without adversity (3 per cent vs 33 per cent). Thus childhood adversity was more strongly associated with both depression and addictive disorder in women than in men. But at this stage it would be unwise to conclude that shared childhood environments are not important. From Brown’s studies, it seems likely that while childhood adversity is a powerful risk factor for depression in women, there has also to be at least one adult psychosocial risk in the environment to precipitate an episode. Put another way, childhood adversity operates as a vulnerability factor for depression, serving to increase the risk of breakdown only once ‘activated’ by later crises. The studies of externalising disorder, on the other hand, suggest that childhood adversity is a direct risk, at least for conduct and behavioural disorder from an early age. If childhood adversity is a vulnerability factor for adult depression, what are the mediating variables that persist across time and interact later with the immediate precipitant of depression? One way by which childhood experience is thought to influence adult functioning is via the capacity to make and benefit from stable supportive relationships. This ‘attachment’ theory posits that early childhood experiences of care provide a template for future relationships (Bowlby, 1977). Children exposed to childhood adversity are expected to be more likely to develop insecure attachment styles and are thus more likely to have difficulties in adult relationships. For our purposes, non-standard or insecure attachment styles can be distinguished from standard attachment and classified according to the extent of desire for engagement in personal relationships. Two styles are characterised by a high desire for engagement – an enmeshed style in which there is a high need for relationships coupled with a marked intolerance of separation and a fearful style in which this desire for closeness is constrained by fears of rejection. Similarly, two styles characterised by high self-reliance and a low desire for contact with others can be distinguished – an angry-dismissive style with hostile and mistrustful attitudes and a withdrawn style characterised by high self-reliance, and low desire for close relationships but without anger or fearfulness. Insecure attachment of the enmeshed/fearful styles has been associated with depression and low self esteem (Hazan and Shaver, 1990; Roberts, Gotlib and Kassel, 1996) while dismissive/withdrawn styles have been found to be associated with conduct disorder and substance abuse in adolescents (Rosenstein and Horowitz, 1996). In our study of mixed sibling pairs, we hypothesised that the pathway from childhood adversity to depression and to substance use disorders might be by way of such insecure attachment styles. We hypothesised that men with histories of childhood adversity would be more likely to display dismissive/withdrawn styles, while women with such adversity would be more likely to have enmeshed/fearful styles. Furthermore, we speculated that regardless of gender, adult depression

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Gender differences in adversity 217 would be associated with the enmeshed/fearful style and substance use disorders with a dismissive/withdrawn attachment style. These hypotheses were broadly supported. Childhood adversity was significantly associated with the presence of non-standard adult attachment styles that differed between men and women. Women were somewhat more likely to have an enmeshed/fearful style but the most striking difference was with respect to dismissive/withdrawn styles with nearly twice as many men as women displaying this type of attachment (29 per cent vs 15 per cent). Individuals with enmeshed/fearful styles had four times the rate of depression compared to individuals with standard attachment ( 9 per cent vs 35 per cent) while those with dismissive/withdrawn style had six times the rate of addictive disorder seen in those with standard attachment (3 per cent vs 18 per cent) and twice the rate of those with an enmeshed/fearful style (9 per cent vs 18 per cent). For addictive disorder, only dismissive/withdrawn attachment style played a role, thus supporting our hypothesis that addictive disorder is associated with dismissive style of attachment, regardless of gender. However, for depression, both being female and having an enmeshed/fearful attachment style had independent effects suggesting that there must be some factor other than childhood adversity or attachment style that is ‘driving’ the female excess of depressive disorder.

Gender differences in exposure to life events In depression, one adult environmental risk factor that turns up time and again is a poor quality marriage. In the deprived inner city areas, where much of Brown’s work has been conducted, it is apparent that women, even if not singled out by their own developmental pathway (including disordered attachment style) to select deviant males, will be at a statistically higher risk of partnering such males, while, conversely, men will have a somewhat greater chance of marriage to a stable supportive partner. Women are yoked to men’s lives in ways which are likely to increase their exposure to stress – not only do they carry the greater burden of motherhood but they also share their partner’s financial and employment events (which may be greater for deviant males) thus having an overall increased risk of exposure to stress. Deviant males, characterised perhaps by shallow or dismissive attachments, conduct disorder and substance abuse, may nevertheless, actually be protected against depression by a supportive partner and by the very nature of their attachments (or lack of them). One popular hypothesis suggests that sex difference in depression might be the result of women’s greater exposure to stress as a result of the caring roles they adopt in Western society. This role strain hypothesis is said to be particularly important for married women where sex differences in rates of depression are greatest (Gore and Mangione, 1983). For the most part, however, there is little evidence to suggest that women experience a greater amount of stress than do men. Studies have not found women to report either more events or higher cumulative life event scores (Bebbington et al., 1981; Bebbington, Tennant and Hurry, 1991; Dohrenwend, 1973) though they may report being more affected by events

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218 Tom Craig and Soumitra Pathare (Kessler, 1979) and there are sex differences in coping behaviours, particularly in the use of problem-solving strategies (Pearlin and Schooler, 1978). There is, however, another related theme. We are judged by others and judge ourselves in terms of how well we live up to the expectations encompassed by the roles we play in society. A failure to live up to the expectations of a particular role is associated with emotions of shame, guilt and, possibly, depression. Individuals who face a crisis in a single overvalued role that forms the basis of much of their self-identity should be particularly prone to depression as might those whose practical circumstances limit access to roles which have little actual or perceived value. Men and women differ both in the roles they carry out in society and in the status afforded to these roles, as well as in the salience of the role to the individual’s sense of self and well being. So, for example, in Britain, it is women who still carry the main obligation for the care and nurture of family and friends and whose core roles involve childcare and homemaking while for men, the most salient roles involve financial provision. This suggests that women’s greater vulnerability to depression might be specifically tied to their greater exposure to events affecting family and friends and which, broadly speaking, match women’s attunement to the needs of others and their role as main carers for family and friends (Kessler and McLeod, 1984). Brown’s Islington studies certainly seem to support the general notion that events which confirm a failure in a core role are important generators of depression: women were much more likely to develop depression following a severely threatening event if the event matched a role to which they were highly committed (Brown, Bifulco and Harris; 1987). This vulnerability to a specific class of events is also broadly in keeping with the notion of identity-relevant stressors (Thoits, 1991). This notion derives from the view that people build up a sense of who they are through the roles they play in life and that stressors that disrupt salient roleidentities are particularly likely to lead to depression. Since men and women are likely to differ in terms of the aspects of their life which most contribute to their sense of identity and self-esteem, so they are also likely to differ in terms of the likely events which provoke depression. Note that, on its own, this does not provide an answer to why rates of depression should differ between the sexes, only that the provoking crises may differ in interesting ways. For this to account for differences in the incidence or prevalence of depression, one would have to show that the events which are most associated with depression are also most commonly encountered by women, perhaps because of their particular responsibility and involvement in domestic roles. There are two studies that appear to support this notion. The later elaborations of Brown and Harris’s model have drawn attention to the contextual dimensions of humiliation and entrapment as being the attributes of life events which best predict depression, both in community and patient series (Brown, Harris and Hepworth, 1995). A recent study of a high risk homeless population lends additional support. In this study, 161 homeless young people with an average age of 18 were assessed for psychiatric disorder and exposure to a variety of environmental stressors. The LEDS was used mainly as a means of describing their chaotic lifestyle but the study also provided the opportunity to explore the impact of homelessness and

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Gender differences in adversity 219 Table 12.1 Onset of depression following the occurrence of humiliation/entrapment and other severe events among homeless young people and Islington women Humiliation/entrapment % onset

Other severe event % onset

Men

20 (2/10)

4 (2/48)

Women

25 (8/32)

8 (2/25)

Women

31 (41/131)

7 (17/246)

Homeless

Islington

related crises on the onset and course of psychiatric disorder. The onset rate of depression was around 4 per cent over the two-year study period for men and 12 per cent for women. All onsets, in both men and women, were preceded by at least one severe event. Table 12.1 shows the proportion of young men and women who reported an onset of depression by whether or not this followed a severe event involving humiliation/entrapment (H/E) and compares these results with those of Islington women. The results of the two studies are very similar despite differences in age and the potentially more chaotic lifestyle of homeless young people. Around a quarter of the young women and one in five of the men who experienced a humiliation/entrapment event developed depression compared with fewer than one in ten of those with severe events involving other qualities. But, while humiliation/entrapment seems to be at the heart of crises for both sexes, women were, in fact, far more likely to report events that were rated this way than were the men in this sample (55 per cent of all severe events in women involved humiliation/ entrapment vs only 17 per cent of severe events for the men). This was partly, but not entirely, explained by pregnancy and childbirth events among the women, 40 per cent (16/40) of whom reported one or more medically confirmed pregnancies. Of these, ten had their babies or were intending to do so but only one was still in contact with the father, the rest all having been abandoned by him. In contrast, 14 per cent of the men reported a pregnancy in a partner and all had broken off contact with the young woman on hearing the news of her pregnancy (Craig, 1996; Craig and Hodson, 2000). Such highly disturbed populations are an insecure base from which to explore the wider relevance of gender differences in response to stressful experience. However, Nazroo, Edwards and Brown (1997) report another even more compelling account of differences in relative impact of events. In this study, ninety-seven couples were recruited on the basis of having recently jointly experienced an event or ongoing difficulty of a severity likely to lead to depression. In addition to LEDS measures of the crises, respondents were questioned in detail about four role-related sets of activity – childcare, housework, financial provision and financial management. Ratings were made of the extent

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220 Tom Craig and Soumitra Pathare Table 12.2 Couples study: onset of depression by domain of provoking crises Women

Men

Domain of crisis

(n) % onset

(n) % onset

Children

(7/21) 33

(2/21) 10

Housing

(6/16) 25

Reproduction

(4/10) 40

(1/10) 10

Financial

(4/44) 9

(8/44) 18

ns

Other

(7/24) 29

(4/24) 17

ns

Total

(26/115) 23

(15/115) 13

<0.06

32

(0/16)

P (1df)

0

6

<0.005

of the respondents’ commitment to each role and of the extent to which respondents felt more or less responsible for each activity compared with his/her partner (relative responsibility) and also whether they were more or less involved in carrying them out (relative involvement). Finally, each crisis was examined to see the extent to which it matched these areas of commitment, responsibility and involvement. The authors hypothesised that any increased risk of depression among women would hold only for those events which were typically salient for female roles; any depression among men would involve life events that on the whole were more salient to male roles; finally, that there would be no difference in the rate of depression in those couples where there was little difference in the actual role salience of the crisis as reported by both partners. The ninety-seven couples experienced a total of 129 shared crises. Of all the couples, thirty-four women and twenty men reported an episode of depression in the study period. Although the expected excess rate of depression amongst the women was observed, this excess was entirely confined to crises involving children, housing or reproductive events (Table 12.2) i.e. just those crises that a priori might be expected to be most salient for women. There was also a doubling of men’s risk of depression following financial crises, though this was not statistically significant. Women were more likely to have greater involvement and responsibility for childcare and housework and for the management of household finances, with men holding more involvement and responsibility for financial provision and, in keeping with this, women were more likely to blame themselves for children, household and reproduction crises while men were more likely to blame themselves for financial crises. A final analysis explored the actual variability in role performance using the ratings of role salience for children, household and reproductive crises. This analysis showed that gender differences in the onset of depression following a crisis were restricted to those crises with greater salience for the woman. When the man also had significant involvement, the gender difference in onset was not observed. Women were also more likely to blame themselves

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Gender differences in adversity 221 for crises involving children, housing and reproduction and men were more likely to under-report these crises. In conclusion, this study supports both the cost of caring (Kessler and McLeod, 1984) and the role-identity (Thoits, 1991) interpretations of the gender difference in depression.

Sex differences in accessing and providing support There is now good evidence that for women, support from a partner or very close other is associated with reduced risk of depression (Brown, 1996; Brown et al., 1986). The failure of a previously supportive tie to give emotional support at the time of a crisis results in a particularly high risk of breakdown (Brown et al., 1986). It is not difficult to see how one might get from the sort of assortative pairing implied by Quinton’s study higher rates of depression in women that are associated with a failure of support at times of crisis. There is much less research on the role of support in men. Intimacy with a partner has been shown to be protective for men following the loss of employment and men seem to be more likely to become psychologically disturbed following the death of their spouse (Stroebe and Stroebe, 1983). The type of support that is protective may differ between the sexes. So, for example, Brugha and colleagues (1990) found that the protective aspects of the social network differed between men and women, with men seemingly protected by more distant acquaintances while, in women, satisfaction with support and aspects of her immediate family and close friends seemed most important. Other studies have also commented that casual, more extensive networks without emotional intimacy may be more protective for men (Bolton and Oatley, 1987; Gore and Colten, 1991); and that within marriage, men are more likely to receive than to give emotional support (Vanfossen, 1981). In a companion paper to the ‘couples’ study described earlier, Edwards, Nazroo and Brown (1998) examined gender differences in the quality of marriage and of the support received from partner or other close tie at the time of a crisis and the relationship of this support to depression. In this study, marital support proved protective for both men and women but women showed an excess rate of depression across all levels of marital support. This suggests that gender differences in quality of marriage cannot explain sex differences in depression. A logistic regression was used to model the contributions of quality of marriage, type of event and gender to onset of depression. This confirmed that marital support was protective for men and women and that it was the greater sensitivity of women to children, housing and reproductive crises that accounted for gender differences in rates of depression. A further analysis explored the contribution of the quality of marriage to the felt need for support expressed by men and women separately. Men were more likely to express indifference to the crisis and were less likely to feel a need to confide. Men were also less likely to seek external support, with half as many men as women reporting a very close relationship outside marriage. Having such a close friendship outside marriage reduced the risk of depression in women but not in men, who had an even higher rate of onset when it was present. This is a finding

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222 Tom Craig and Soumitra Pathare reminiscent of other investigations that have suggested that men who receive help from friends might even be at higher risk of breakdown (Husaini et al., 1982), perhaps reflecting both that for men to seek such help reinforces feelings of failure and inadequacy and also that they only seek help with the most disturbing events.

Conclusions In this chapter, we have explored the relevance of Brown and Harris’s model of depression to understanding gender differences in the prevalence of affective disorder. Taking childhood adversity as the key starting point, research is beginning to unravel subtle differences in the downstream pathways for vulnerable men and women that include intriguing variations in attachment, rates of exposure to depressogenic crises and in confiding and other help-seeking behaviour. While this has taken us some way, there are still many unanswered questions. Why do men and women exposed to essentially similar childhood adversity develop distinctly different attachment styles? Can the model account for observed differences between men and women in all societies? To what extent are these behaviours a result of differences in the socialisation of boys and girls and to what extent are they determined by biology? The success of the enterprise to date owes a great deal to the ideas, methods and measures developed by George Brown – his painstaking attention to detail, emphasis on the importance of establishing time order in measurement and the development of measures that have been taken up by researchers around the globe. It seems highly likely that his achievements will continue to underpin future research for many decades to come.

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224 Tom Craig and Soumitra Pathare ——, Horwood, L. J. and Lynskey, M. T. (1994) ‘Parental separation, adolescent psychopathology and problem behaviors’, Journal of the American Academy of Child and Adolescent Psychiatry, 33, 1122 – 31. First, M. B., Gibbon, M., and Spitzer, R. L. (1996) Structured Clinical Interview for DSMIV Axis I disorders (Version 2), New York: Biometrics Research Department, New York State Psychiatric Institute. Gater, R. A., Dean, C. and Morris, J. (1989) ‘The contribution of childbearing to the sex difference in first admission rates for affective psychosis’, Psychological Medicine, 19, 719–24. Gore, S. and Colten, M. E. (1991) ‘Gender stress and distress: social – relational influences’ in J. Eckenrode (ed.) The Social Context of Coping, New York: Plenum Press. —— and Mangione, T. W. (1983) ‘Social roles, sex roles and psychological distress: additive and interactive models of sex differences’, Journal of Health and Social Behavior, 24, 300–12. Green, B. H., Copeland, J. R., Dewey, M. E., Sharma, V. and Saunders, P. A. (1992) ‘Risk factors for depression in elderly people: a prospective study’, Acta Psychiatrica Scandinavica, 86, 213–17. Hannah, P., Adams, D., Lee, A., Glover, V. and Sandler, M. (1992) ‘Links between early post-partum mood and post-natal depression’, British Journal of Psychiatry, 160, 777–80. Harris, T. O., Brown, G. W. and Bifulco, A. (1987) ‘Loss of parent in childhood and adult psychiatric disorder: The role of social class position and premarital pregnancy’, Psychological Medicine, 17, 163–83. Hazan, C. and Shaver, P. (1990) ‘Love and work: an attachment theoretical perspective’, Journal of Personality and Social Psychology, 59, 270–80. Hetherington, E. M., Cox, M. and Cox, R. (1982) ‘Effects of divorce on parents and children’ in M. Lamb (ed.) Non-traditional Families, Hillside, New Jersey, 233–88. Erlbaum. Huesmann, L. R. (1997) ‘No Simple Relation’, Psychological Inquiry, 8, 200–4. Hunter, M. S. (1990a) ‘Emotional well-being, sexual behaviour and hormone replacement therapy’, Maturitas, 12, 299–314. —— (1990b) ‘Somatic experience of the menopause: a prospective study’, Psychosomatic Medicine, 52, 357–67. Husaini, B. A., Neff, J. A., Newbrough, J. R., and Moore, M. C. (1982) ‘The stress buffering role of social support and personal competence among the rural married’, Journal of Community Psychology, 10, 409–26. Jorm, A. F. (1987) ‘Sex and age differences in depression: a quantitative synthesis of published research’, Australian and New Zealand Journal of Psychiatry, 21, 46–53. Kessler, R. C. (1979) ‘Stress, social status and psychological distress’, Journal of Health and Social Behavior, 20, 259–72. —— and McLeod, J. D. (1984) ‘Sex differences in vulnerability to undesirable life events’, American Sociological Review, 49, 620–31. ——, McGonagle, K. A., Swartz, M., et al (1993) ‘Sex and depression in the National Comorbidity Survey, I: lifetime prevalence, chronicity and recurrence’, Journal of Affective Disorders, 29, 85–96. McGee, R., Feehan, M., Williams, S., and Anderson, J. (1992) ‘DSM-III disorders from age 11 to age 15 years’, Journal of the American Academy of Child and Adolescent Psychiatry, 31, 50–9.

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Gender differences in adversity 225 McKinlay, J. B., McKinlay, S. and Brambilia, D. (1987) ‘The relative contributions of endocrine changes and social circumstances to depression in mid-aged women’, Journal of Health and Social Behaviour, 28, 345–53. Meltzer, H., Gill, B., Petticrew, M., and Hinds, K. (1995) OPCS Surveys of Psychiatric Morbidity in Great Britain, Report 1, The prevalence of psychiatric morbidity among adults living in private households, London: HMSO. Nazroo, J. Y., Edwards, A. C. and Brown, G. W. (1997) ‘Gender differences in the onset of depression following a shared life event: a study of couples’, Psychological Medicine, 27, 9–19. Nolen-Hoeksema, S. (1987) ‘Sex differences in unipolar depression: evidence and theory’, Psychological Bulletin, 101, 259–82. Oakeley-Browne, M. A., Joyce, P. R., Wells, J. E., Bushnell, J. A. and Hornblow, A. R. (1995) ‘Adverse parenting and other childhood experience as risk factors for depression in women aged 18–44 years’, Journal of Affective Disorders, 34, 13–23. Pathare, S. and Craig, T. K. J. (2000) paper submitted to British Journal of Psychiatry. Patterson, G. R., Reid, J. B. and Dishion, T. J. (1992) Antisocial Boys, Eugene: Castalia. Pearlin, L. I. and Schooler, C. (1978) ‘The structure of coping’, Journal of Health and Social Behavior, 22, 337–56. Porter, B. and O’Leary, K. D. (1980) ‘Marital discord and childhood behavior problems’, Journal of Abnormal Child Psychology, 8, 287–95. Quinton, D. and Rutter, M. (1988) Parenting breakdown: the making and breaking of intergenerational links, Aldershot, Hants: Avebury. ——, Pickles, A., Maughan, B. and Rutter, M. (1993) ‘Partners, peers and pathways: assortative pairing and continuities in conduct disorder’, Development and Psychopathology, 5, 763–83. Roberts, J. E., Gotlib, I. H. and Kassel, J. D. (1996) ‘Adult attachment security and symptoms of depression: the mediating roles of dysfunctional attitudes and low selfesteem, Journal of Personality and Social Psychology, 70, 310–20. Robins, L. N. and McEvoy, L. (1990) ‘Conduct problems as predictors of substance abuse’ in L. Robins and M. Rutter (eds) Straight and devious pathways from childhood to adulthood, Cambridge: Cambridge University Press, 182–204. Rosenstein, D. S. and Horowitz, H. A. (1996) ‘Adolescent attachment and psychopathology’, Journal of Consulting and Clinical Psychology, 64, 244–53. Stroebe, M. S. and Stroebe, W. (1983) ‘Who suffers more? Sex differences in health risks of the widowed’, Psychological Bulletin, 93, 279–301. Thoits, P. A. (1991) ‘On merging identity theory and stress research’, Social Psychology Quarterly, 54, 101–12. Vanfossen, B. E. (1981) ‘Sex differences in the mental health effects of spouse support and equity’, Journal of Health and Social Behavior, 22, 130–43. Veijola, J., Puukka, P., Lehtinen, V., Moring, J., Lindholm, T. and Vaisanene, E. (1998) ‘Sex differences in association between childhood experiences and adult depression’, Psychological Medicine, 28, 21–7. Weissman, M. M., Leaf, P. J., Tischler, G. L., et al (1988) ‘Affective disorders in five United States communities’, Psychological Medicine, 18, 141–53. Whitaker, A., Johnson, J., Shaffer, D., Tapoport, J., Kalikow, K., Walsh, B. T., Davies, M., Braiman, S. and Dolinsky, A. (1990) ‘Uncommon troubles in young people: prevalence estimates of selected psychiatric disorders in a non-referred adolescent population’, Archives of General Psychiatry, 47, 487–96.

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13 The long-term effects of childhood adversities on depression and other psychiatric disorders Ron Kessler

George Brown and Tirril Harris’s influential book The Social Origins of Depression (1978) was published the year I began my post-doctoral training in psychiatric epidemiology. The book was not only required reading in our training programme, but also the source of great inspiration to all of us in the programme. Many of the psychiatric epidemiologists of my generation, myself included, credit the intellectual excitement generated by that book and by George and Tirril’s subsequent writings as major factors in our decision to continue in the field. In my own case, the encouragement and friendship George so generously bestowed on me have also been additional important sources of inspiration. One of the most intriguing of the many lines of research on the social origins of depression that George has pioneered concerns the long-term effects of childhood adversities. Stimulated largely by George’s initial work in this area, a number of studies now exist that have consistently found associations between specific childhood adversities and adult depression (e.g. Mullen et al., 1996; Oakley-Browne et al., 1995; Rodgers, 1994; Romans et al., 1995; Stein et al., 1996). Although limited by the fact that they are largely based on retrospective reports, these studies provide very useful information for purposes of excluding otherwise plausible hypotheses and focusing subsequent research in confirmatory prospective studies. The value of these studies has been compromised, however, by three limitations. The first of these three is that the effects of childhood adversities on initial onset and subsequent course of depression have usually not been distinguished. This has created uncertainty regarding causal pathways. One very plausible and widely held notion advanced by George and his colleagues is that childhood adversities create enduring intrapsychic vulnerabilities that lead to heightened emotional reactivity to adult stress (Harris, Brown and Bifulco, 1990). For example, loss events early in life might lead not only to early-onset depression but also to disturbed attachment styles that create a depressogenic reaction to loss events throughout life. If this is the case, we would expect that childhood adversities are associated not only with risk of lifetime depression but also with illness course (e.g. recurrence, number of episodes, and speed of episode recovery). Clinical studies carried out by Brown et al. (1994) as well as by others (e.g. Zlotnick et al., 1995) have reported results consistent with this expectation. However, other studies have found that most childhood adversities are related to first onset but not to

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228 Ron Kessler course of adult disorders (e.g. Faravelli, Paterniti and Scarpato, 1995; Pollack et al., 1996). Resolution of these inconsistent results requires a distinction to be made between the predictors of first onsets and predictors of recurrent episodes of depression in representative community samples. This distinction is seldom made in published studies. Second, most studies of childhood adversities have focused on adult depression as the only outcome variable (Brown and Moran, 1994; Kunugi et al., 1995; OakleyBrowne et al., 1995; Rodgers, 1994; Zlotnick et al., 1995), implicitly assuming that these effects are uniquely depressogenic. But this might not be so. George’s work shows this quite clearly in documenting comparable effects of some adversities on both depression and anxiety (Brown, Harris and Eales, 1993). Some work on this issue suggests that there may be specificity in the effects of childhood adversities (Briere and Runtz, 1990; Mullen et al., 1996; Portegijs et al., 1996; Rutter, 1989). However, other studies suggest that the adult consequences of different childhood adversities are not very distinct (Bushnell, Wells and Oakley-Browne, 1992; Mullen et al., 1993). Resolution of these inconsistent results requires that analyses be carried out that adjust for lifetime comorbidities among disorders. This is seldom done in published studies. Third, many studies of childhood adversities have focused on only a single adversity and made interpretations of results assuming that the effects are unique to that particular adversity. This is especially common in studies on the long-term effects of childhood sexual abuse (e.g. Romans et al., 1995). The authors of these studies strongly suggest that it is sexual abuse rather than the cluster of adversities usually associated with sexual abuse that leads to adverse mental health outcomes, even though these related adversities are seldom measured or assessed for their effects. The same problem can be found in studies on the long-term effects of other childhood adversities, such as lack of care (e.g. Plantes et al., 1988), parental divorce (e.g. Rodgers, 1994), and parental substance abuse (e.g. Velleman and Orford, 1993). The assumption of unique effects is almost certainly false. Indeed, George and his colleagues have clearly shown this in their studies of childhood loss, where they have documented that associated abuse and neglect are often involved as complicating factors (Harris, Brown and Bifulco 1986; 1990). A few studies have investigated the comparative effects of different adversities and the ways in which these effects combine to promote adult depression. These studies are uniform in concluding that childhood adversities usually occur in clusters, making it difficult to pinpoint any one particular adversity as the critical determinant of subsequent adult depression (Mullen et al., 1996; Portegijs et al., 1996; Romans et al., 1993). This is an important omission, because clarification of unique and common effects is needed both for purposes of increasing our understanding of causal processes and for purposes of targeting intervention efforts. The aim of this chapter is to review recent work carried out by my colleagues and myself to address these three limitations using data from large-scale community surveys carried out in the US. I begin with a review of our work on differential predictors of first onset and recurrence of depression. I then discuss our work on

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Long-term effects of childhood adversities 229 outcomes other than depression. Finally, I summarise our ongoing work on the separate and joint effects of multiple adversities.

Distinguishing effects on onset and course of depression The causal pathways involved in the long-term effects of childhood adversities have been investigated by a number of researchers (e.g. Rutter, 1989; Sroufe and Rutter, 1984). George Brown’s group has been responsible for one of the most influential and sustained of these investigations in a series of papers on the longterm effects of early parental loss (Harris, Brown and Bifulco, 1986; 1990). Several important mediating effects have been documented in these studies. Some of these effects involve environmental pathways. For example, several forms of childhood adversity have been shown to predict insecure adult attachments (e.g. Brown et. al., 1986; McLeod, 1991) which, in turn, have been linked to vulnerability to adult depression (Brown and Harris, 1978). Other mediators involve intrapsychic pathways. For example, some forms of childhood adversity have been shown to predict intrapsychic vulnerabilities in adulthood such as helplessness, low self-esteem, and interpersonal dependency (e.g. Testa et al., 1990) which, in turn, have been linked to vulnerability to adult depression (Barnett and Gotlib, 1988). It is important to note that most work in this area has concentrated on the predictor of index episode of depression rather than on first onsets. There is a risk of specification error in this approach. To explain this concern, it is important to note that childhood adversities are known to be associated with risk of childhood and adolescent depression (e.g. Fleming and Offord, 1990; Goodyer, 1990). It is also known that early-onset depression is associated with high recurrence risk (e.g. Harrington et al., 1990; Lewinsohn, Hoberman and Rosenbaum 1988). Taken together, these results suggest that the observed relationships between childhood adversities and adult depression might be due to a mediating effect of early-onset depression on adult recurrence. Yet, most research on the long-term effects of childhood adversities neglects the investigation of this possibility. This is true even though theoretical discussions point to the possibility that early-onset depression can shape the subsequent adult environment in ways that might incorrectly be interpreted as evidence for mediating effects of adult environmental variables (Rutter, 1989). A good illustration of this potential problem is found in studies that have documented a putative mediating effect of insecure adult attachment on the association between childhood parental loss and adult depression (e.g. Harris, Brown and Bifulco, 1990). The results of these studies have led some researchers to conclude that success in forming secure adult intimate relationships can negate any adverse effect of childhood parental loss on adult depression (Parker and Hadzi-Pavlovic, 1984). However, it is important to recognise that an equally plausible alternative is that lack of success in forming secure adult attachments and current depression might both be predicted by a history of early depression. This distinction is an important one from an intervention perspective. The mediation hypothesis

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230 Ron Kessler predicts that successful interventions aimed at improving the intimate relationships of adults who lost their parents in childhood will remove any elevated risk of adult depression that exists among these people. The misspecification hypothesis predicts that the elevated risk of adult depression will not be removed by such interventions because secure adult attachments are markers of risk rather than actual risk factors (Kraemer et al., 1997). It is possible to adjudicate in a provisional way between these contending hypotheses involving dated mediators such as marital status by obtaining retrospective information about age at first onset of depression. This information could be used to construct a control variable for history of depression prior to the age of marriage. This control variable, in turn, could then be used to adjust for the effect of history of prior depression in evaluating the mediating effect of marital quality, assessed prior to the onset of an index episode of depression, on the association between childhood parental loss and that episode. If such an analysis showed that prior depression is a significant predictor of the index episode of adult depression and that marital quality is no longer significant in predicting the index episode, the most plausible interpretation would be that marital quality is a marker of a more fundamental risk factor rather than itself a risk factor of adult depression. A more general approach to this analysis problem would be to decompose the effect of childhood parental loss, or other childhood adversities, on current depression into effects on first onset (in the total sample) and illness course (in the sub-sample of people with a lifetime history of depression). This is the approach we took in our initial analyses of this problem. Our first analyses were based on data collected in a large two-wave household survey of the US adult population that included retrospective reports about eight childhood adversities and a brief screening measure of Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III) major depression. The survey, entitled the Americans Changing Lives (ACL) survey, was carried out in face-to-face interviews with a nationally representative sample of 3,617 adults aged 25 and older. See House et al. (1990) for details about the ACL. Neither childhood adversity nor adult depression was an area of major interest to the ACL investigators. As a result, measures of these constructs were based on a brief set of screening questions. Childhood adversities were assessed with a series of yes-no questions about the occurrence of each of the following eight experiences prior to the time the respondent was 16 years of age: • • • • • • • •

death of mother death of father serious parental marital problems parental divorce family violence serious family drinking problems family mental illness absence of a close and confiding relationship with any adult.

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Long-term effects of childhood adversities 231 Depression was assessed with a re-worded version of the stem question from the depression section of the Diagnostic Interview Schedule (DIS) Version III-A (Robins et al., 1981). Questions were also included to date the age at first onset of depression, lifetime number of depressive episodes, the timing of the most recent depressive episode, and the duration of the most recent depressive episode. Our initial analyses of these data used information about childhood adversities obtained in the baseline ACL to predict twelve-month prevalence (i.e. either first onset or recurrences) of depression in the follow-up survey. A measure of lifetime history of depression obtained in the baseline survey was included as a control variable in the prediction equation. The analysis began by replicating previous research in documenting associations between the eight childhood adversities and recent (twelve-month) episodes of major depression. Five of the eight adversities were found to be significantly associated with depression in the past twelve months (family drinking problems, family mental illness, family violence, parental marital problems, and parental divorce) with odds-ratios (ORs) in the range l.4 to 2.6 (Kessler and Magee, 1993). The investigation of the possibility that these associations were due to indirect influences through history of depression began with an analysis of first onset based on discrete-time survival analysis. We found that seven of the eight childhood adversities had significant effects on life history of depression (the exception being parental divorce). Five of these seven had effects that decreased significantly with age in predicting first onset episodes. All five of the latter (family violence and mental illness, early death of either mother or father, and lack of a close relationship with an adult) significantly predicted early onset depression (defined as a first episode of depression by age 20). The ORs for first onsets after age 20, in the subsample of respondents who were never depressed in the first twenty years of their life, in comparison, were all quite weak, with only one of the five (family violence) continuing to be associated with a significant risk of first onset. The next part of the analysis examined whether various forms of childhood adversity influence recurrence of depression. This was done by estimating a series of logistic regression models in the sub-sample of respondents with a history of depression prior to the year before the follow-up interview to predict the recurrence of an episode of depression at any time during that twelve-month period. The results showed that only three of the eight adversities (family history of mental illness, family history of violence, and parental divorce) significantly predicted recurrence. Consistent with previous research (Coryell, Endicott and Keller, 1991; Sorenson, Rutter and Aneshensel, 1991), no significant main effect was found for age at first onset on recurrence risk, nor did the effects of any of the childhood adversities on recurrence vary as a function of either current age or age at first onset. An issue that occurred to us in evaluating these initial results was that some childhood adversities might interact with early-onset depression to create subsequent environmental experiences that exacerbate initial symptoms and reduce resources for long-term resolution and recovery. There is some evidence consistent with this possibility in the literature on the long-term effects of adolescent

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232 Ron Kessler conduct disorder and substance abuse (Maughan, Gray and Rutter, 1985). We know very little about such interactions, in comparison, as they apply to the continuity of depression into adulthood. An initial attempt to provide information of this sort in the ACL data considered the effect of twelve potential mediators of the relationship between childhood family violence and adult depression. Childhood family violence was selected because it was the only childhood adversity in the ACL to have an independent effect on adult recurrent depression in the sub-sample of respondents with a history of prior depression after controlling for comorbidities among the adversities. All of the mediators were measured in the baseline ACL interview. They were used to study recurrence of depression in the twelve months prior to the re-interview among respondents who had a lifetime history of depression as of the baseline interview but who were not depressed at the time of interview. The mediators included three measures of sociodemographic characteristics that might be influenced by childhood family violence and might be consequential for adult major depressive episode (educational attainment, income, and marital status), three measures of social networks and social support, three measures of personality (extroversion, neuroticism, and personal efficacy), and three measures of chronic stress (financial stress, chronic interpersonal stress, and chronic health problems). Most of these potential mediators had previously been shown to be affected by childhood adversities (Amato and Keith 1991; Brown and Harris, 1978; Browne and Finkelhor, 1986; Hojat, Borenstien and Shapurian, 1990; McLeod, 1991; Rodgers, 1990). There is also evidence from the broader epidemiologic literature that all of these mediators are significantly associated with prevalence of depression in adulthood (Brown and Harris, 1978; McGonagle and Kessler, 1990; Weissman et al., 1991). The examination of mediator effects began by estimating a pair of regression equations for each of the twelve potential mediators. The first equation investigated whether there was a significant effect of childhood family violence on the mediator. The second equation investigated whether there was a significant effect of the mediator on recurrent depression net of family violence. Only one of the twelve potential mediators – chronic interpersonal stress – passed this pair of tests. This variable was found to be consistently significant in sub-samples, arguing against the otherwise plausible interpretation that one significant association out of twelve could occur by chance (Kessler and Magee, 1994). But what causal processes made this mediating effect occur? One plausible possibility is that childhood violence increased emotional vulnerability to some more proximate risk factor of recurrent depression, a possibility consistent with the notion that childhood adversity can promote adult depression by increasing emotional vulnerability to adult stressful experiences (Rutter, 1989). The vulnerability factors that have most frequently been hypothesised to explain this stress-exacerbating effect are enduring features of the self, such as self-efficacy and conceptions of others in relation to oneself that can influence maintenance of support networks (Harris, Brown and Bifulco, 1990; Masten, Best and Garmezy, 1990; Metalsky and Joiner, 1992). This possibility was investigated by estimating a

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Long-term effects of childhood adversities 233 series of models in which we determined whether any of the baseline potential mediators interacted with childhood family violence to predict recurrent depression. The only significant interaction to emerge from this exploratory analysis was again associated with chronic interpersonal stress. Furthermore, as with the main effect, this interaction was consistently significant in sub-samples, arguing that it is a genuine effect rather than due to a single chance occurrence in a set of twelve separate tests. Analysis of the interaction showed that childhood family violence was associated with recurrent adult depression only in the presence of high chronic adult interpersonal stress. This is reminiscent of George Brown’s finding that low selfesteem is associated with childhood adversity only via current negative elements in relationships (Brown et al., 1990). ACL respondents with a history of childhood family violence who did not subsequently have adult interpersonal stress had no higher rates of adult depression than respondents with neither a history of childhood family violence nor adult interpersonal stress. There are at least two plausible interpretations of this finding. One interpretation is that the interaction was due to selection rather than to causation. This could occur if the vulnerability to recurrent depression associated with childhood family violence also causes chronic interpersonal stress, in which case the existence of these stressors would be more a marker of vulnerability than an exacerbating factor. An indirect test of this interpretation was carried out by estimating interactions of childhood family violence with age at onset of depression, number of lifetime episodes of depression, and ‘density’ of depression, defined in terms of average number of episodes per year since first onset. If selection was at work, we would have expected that these measures of the severity and course of depression would have had powerful interaction effects that reduced the interaction between family violence and interpersonal stress. As it turned out, this was not the case. The interaction between childhood family violence and interpersonal stress remained statistically significant and unchanged in magnitude when these additional interactions were used as controls, arguing against the selection interpretation. The second plausible interpretation is that the interaction between childhood family violence and interpersonal stress comes about because childhood family violence is associated with vulnerability factors that increase emotional reactivity to adult stress. If this is true, these vulnerability factors must be quite specific to interpersonal stress, because childhood family violence was not found to interact with other measures of chronic stress in the ACL. If true, this specificity would be in some ways heartening, because it would imply that interventions that focused on the interpersonal relationships of those at risk due to early exposure to violence might be more effective than interventions that attempted to change more global conditions of their lives. Some small amount of previous research has been done on specific vulnerabilities of this sort (see Metalsky and Joiner, 1992) and there are several ways they could come into play in the interaction between childhood family violence and interpersonal stress. One is that childhood family violence might create disturbed

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234 Ron Kessler attachment styles (Alexander, 1992) which, in turn, increase emotional reactivity to interpersonal stress (Barnett and Gotlib, 1988). Another is that childhood family violence might increase the tendency to make more extreme appraisals or to use more maladaptive coping strategies to manage interpersonal stress. Consistent with this possibility, previous research has shown that denial, repression, regression, and dissociation are frequently adopted by those exposed to extreme childhood adversity (Coons and Milstein, 1984). These coping strategies may have survival value during childhood in the context of insecure and disorganised family relationships, but are maladaptive in adult interpersonal contexts (Sroufe and Rutter, 1984). Another possibility is that adult interpersonal stress may reactivate depressogenic memories of childhood violence (Millon, 1990). Depending on the mechanisms involved, it is conceivable that the link between childhood family violence and recurrence of depression could be broken by interventions aimed either at modifying attachment styles or at providing social skills training. The latter might be useful either in reducing exposure to interpersonal stress or changing coping and appraisal processes in a way that would enhance the efficacy of conflict resolution styles or reduce emotional reactivity to interpersonal stress.

Effects on other mental health outcomes The ACL results were useful in suggesting that we were correct in our original concern about the importance of history of depression as a mediator and modifier of the relationship between childhood adversity and adult depression. However, the results were limited by imprecision in the measures. It was all the more striking, in light of this fact, that while we documented fairly substantial gross associations between most of the childhood adversities and recent episodes of depression, these associations were consistently attenuated when the analysis was confined to respondents with a history of depression. This led us to believe that specification in terms of history was truly important. However, we realised that this pattern of results needed to be replicated in data sets with more adequate measures. Soon after completing the ACL analyses, we had an opportunity to lay the groundwork for replication and expansion as part of the design of the US National Comorbidity survey (NCS), a survey designed to obtain nationally representative data on the prevalence, risk factors, and consequences of psychiatric morbidity and comorbidity (see Kessler et al., 1994 for details on the NCS). Based on the results of the ACL analysis, we included a long series of questions about childhood adversity in the part II sub-sample of the NCS. This sub-sample consisted of 5,877 respondents in the age range 15–54 who were interviewed face to face about their lifetime and recent history of many different DSM-III-R mental disorders. One group of NCS childhood adversity questions used the Family History Research Diagnostic Criteria method to generate diagnoses of maternal and paternal psychopathology (depression, generalised anxiety disorder, alcoholism, drug dependence, and antisocial personality disorder) during the respondent’s childhood years. Another group assessed the parenting styles of the respondent’s

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Long-term effects of childhood adversities 235 mother and father in terms of warmth and over-protectiveness with scales developed by Parker and Parker (1991). A third group assessed verbal and physical violence of the respondent’s parents towards each other and towards the respondents using scales developed by Straus (1990). A final group of questions asked about a wide range of potentially traumatic childhood events such as separation from a parent, death of a loved one, and sexual abuse. NCS measures of adult psychiatric disorders were based on a modified version of the Composite International Diagnostic Interview (CIDI; World Health Organization, 1990). The CIDI is a fully structured diagnostic interview that generates diagnoses according to the definitions and criteria of both DSM-III-R and the International Classification of Diseases, tenth revision (ICD-10). Rather than focus exclusively on depression, the CIDI was used to generate diagnoses of a wide range of DSM-III-R disorders. These included mood disorders (major depression, dysthymia, mania), anxiety disorders (generalised anxiety disorder, panic disorder, phobia, post-traumatic stress disorder), substance use disorders (alcohol abuse, alcohol dependence, drug abuse, drug dependence), and other disorders (conduct disorder, adult antisocial behaviour, schizophrenic, and other nonaffective psychoses). Good reliability and validity of these assessments were documented in a series of international studies carried out as part of the WHO Field Trials of the CIDI (Wittchen, 1994) as well as in an NCS clinical reappraisal study (Kessler et al., 1998). Our initial analyses of these data used information on age at onset of the separate NCS/DSM-III-R disorders and episode prevalence during the twelve months prior to the interview to replicate and extend the ACL analyses. This began by examining bivariate associations of over thirty different measures of childhood adversity in predicting twelve-month prevalences of the separate NCS disorders. Two important results emerged. First, the vast majority of dichotomously measured childhood adversities were found to be significantly and positively associated with recent prevalences of not only depression but also almost all other adult disorders assessed in the NCS, with ORs ranging between 1.3 and 4.6. Second, the adversities differed in the adult disorders that they affected most powerfully. For example, while the experience of being in a life-threatening accident as a child had its strongest effect on adult agoraphobia (OR = 3.9), exposure to childhood family violence had its strongest effect on adult depression (OR = 4.2). Next, we investigated the effects of childhood adversities on first onset of the NCS disorders. As in the more limited investigation of the ACL data, results showed that the vast majority of the adversities were significantly associated with first onset of each of the lifetime disorders. In addition, we found that the majority of these effects decreased significantly with age. Most adversities were significant predictors of early-onset disorders (defined as disorders that began earlier than age 20). In comparison, only a minority of the adversities also predicted first onset of later-onset disorders. The significant effects on later-onset disorders were generally weaker than the effects on early-onset disorders (Kessler, Davis and Kendler, 1997). We then examined whether various forms of childhood adversity influence twelve-month persistence of the NCS disorders among respondents with a lifetime

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236 Ron Kessler history. Results showed that for the most part they do not when each adversity is examined on its own. Furthermore, we could find no evidence that the effects of the adversities on recurrence varied as a function of either current age or age at onset.

The joint effects of multiple adversities The NCS data were also used to study the joint effects of multiple adversities on adult mental disorders. The first step in doing this was to estimate multivariate prediction equations of the joint effects of all the adversities considered in the above bivariate models. A striking result emerged from these analyses: that the effects of most adversities became statistically insignificant in the multivariate models. Further analysis showed that this occurred because most of the adversities were strongly interrelated. This made it difficult to distinguish individual effects. More detailed analyses were then carried out to determine whether it is possible to create composite risk scores of the significant childhood adversities (e.g. Truett, Cornfield and Kannel, 1967). We found that this could not be done due to the fact that there are powerful and complex interactions among the adversities in predicting most adult disorders. These interactions were examined using an empirical search strategy that created optimally predictive interactive risk profiles among multiple predictor variables. Preliminary results suggested that a number of these profiles exist and that most of them involve some combination of disturbed attachment relationships and traumatic experiences involving either interpersonal loss or interpersonal violence. We are still in the process of investigating these profiles. Several general results can be reported from these analyses. One is that, despite the fact that most of the childhood adversities we considered were highly interrelated, the numbers of respondents with pure adversities were large enough for separate analysis of most individual adversities. This was documented by comparing respondents who experienced no childhood adversities with others who experienced one and only one childhood adversity. Most of the individual adversities were found to be significantly related to early-onset of the vast majority of the mental disorders assessed in the NCS. Contrary to our initial expectations, very little evidence of specificity was found. For example, most childhood loss events were as strongly related to the onset of anxiety disorders as they were to the onset of mood disorders. It is noteworthy, as reported at the end of the last subsection, that evidence of specificity was found in unrestricted analyses of the total sample. Our failure to find continued evidence of specificity in the analysis of respondents who experienced only one adversity might be due to the small number of respondents with only one adversity. At the same time, it is noteworthy that Brown, Harris and Eales (1993) also found very little evidence of specificity in an independent sample. Clearly, replication is required in other datasets to evaluate the consistency of this result. Another general result is that two broad patterns of interaction were found in the multivariate analyses. The first is a pattern in which the cumulative effects of two

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Long-term effects of childhood adversities 237 or more adversities are greater than the effects of only one adversity, but less than the sum of the effects of the composite adversities. In the extreme, we were unable to detect any incremental effects of a sixth or seventh type of adversity on the mental health of respondents who experienced five or more childhood adversities. This is perhaps not surprising in light of the fact that the adversities included in our analysis are nothing more than dichotomous indicators of the rich realities of the adversities to which our respondents were exposed to during childhood. The other broad pattern of interaction involved events in which the occurrence of one adversity undoes another adversity. Perhaps the most important example concerns the long-term effects of parental divorce. This is an important example because parental divorce has increased so dramatically since the end of World War II in the US (Bumpass and Castro, 1987; Cherlin, 1981) that today nearly 50 per cent of all children in this country experience it (Bumpass, 1984). A review of the considerable body of research that has emerged to examine the impact of parental divorce on children suggests that it has a variety of adverse effects on mental health that persist into adulthood (Chase-Lansdale, 1990; Wertlieb, 1997). Almost all of these analyses were based on simple comparisons between children of divorce and children in two-parent homes without adjusting for the fact that children of divorce are much more likely than others to have been exposed to other adversities. Our analyses addressed this problem by adjusting for multiple adversities. We found that the impact and sign of the effect of parental divorce on early-onset psychiatric disorder varies depending on the other adversities associated with the disturbed parental marriage. When the divorce occurred in the absence of other adversities, it was associated with a significantly elevated risk of early-onset psychiatric disorders. This effect decreased as the number of associated adversities increased. At the extreme, when the divorce was associated with prior marital violence that was terminated as a result of the marital break-up, we found that parental divorce is associated with good mental health outcomes for the child. This is especially so when the father is reported to be violent and an alcoholic, the mother was free of depression or other mental disorders, and the mother was the custodial parent after the break-up. Perhaps this experience can be seen as an example of what George Brown (1993) has referred to as a severe event that is also a ‘fresh start event’, with a consequent positive impact on mental state.

Discussion The results reviewed here raise concerns about the interpretation of previous studies of the adult consequences of childhood adversities. The greatest concern involves the first of the three issues addressed here, regarding the distinction between effects on first onset and effects on course. It is doubtless the case that childhood adversities are strongly related to adult mental disorders. However, the interpretations of results in studies regarding mediating processes, which have been pioneered by George Brown and his collaborators, are made more difficult to confirm due to the fact that the analyses usually did not distinguish between effects on first onset of depression and effects on the onset of recurrent episodes

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238 Ron Kessler of depression. The critical issue is that the presumed mediators in these analyses might, in fact, be markers rather than risk factors. If so, then inferences drawn from these studies regarding intervention targets could be incorrect. This is a serious problem as we move from analytic to experimental epidemiological studies of the social origins of mental disorders. In one respect, the concern raised here about the distinction between onset and course is merely one example of the more general problem of unmeasured common causes in nonexperimental studies. It is never possible to exclude the possibility of confounding in studies of this sort. The purpose of nonexperimental studies is to refine our incomplete understanding of causal processes by excluding otherwise plausible causal hypotheses until the range of remaining possibilities is narrow enough to lend itself to experimental investigation. In this regard, nonexperimental studies can be expected to generate insights, but not definitive explanations. Yet it is important to appreciate that the distinction between onset and course holds a special place in the consideration of unmeasured common causes. This is true because our ultimate goal in nonexperimental studies is to pinpoint modifiable intervention targets. A critical issue in this task concerns targeting of intervention timing in the natural history of the disorder. If a childhood adversity has an effect on early first onset, but not on later onset or course, then the focus of intervention has to be on the part of the life course prior to first onset, not later in the life course. If, on the other hand, childhood adversity also influences later onsets, then we need to search for mediators of these effects that could then become intervention targets for primary prevention efforts later in the life course. If childhood adversity also influences recurrence or speed of episode recovery, then we need to search for mediators that can become targets in secondary or tertiary prevention effects. Most of the childhood adversities that my colleagues and I have examined up to now appear to have effects that are confined to early first onset. This is not to say that the presumed mediators pinpointed in previous studies of the long-term effects of childhood adversities are not important risk factors of later-onset psychiatric disorders or course; they might be. However, the analysis approach used in the previous studies provides much less convincing evidence for the existence of true mediation than a naive interpretation would lead us to think. This is because this approach fails to distinguish between onset and course and fails to evaluate the possibility that childhood adversities have their main effects on early onset rather than on later onset or on course. It is important to note in this regard that the vast majority of episodes of depression that occur in adulthood are recurrences. As a result, it is important that future research on risk factors for adult depression explicitly recognise that the de facto focus is on the predictors of episode recurrence and that the investigation should be explicitly limited to people with a prior history of depression. Intervention implications for secondary prevention of recurrence will be much easier to infer if the research design is refined in this way so as to avoid the confounding effect of unmeasured prior history.

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Long-term effects of childhood adversities 239 The results reviewed in this chapter on the second of the three issues my colleagues and I have examined in our studies of childhood adversity – that the effects of these stressors extend well beyond depression – are important in at least two respects. The first involves the cost-benefit ratio of early intervention among youth with childhood adversities. The finding that most adversities predict a wide range of early-onset disorders means that there would be many benefits of early intervention. The second involves the hypothesis discussed earlier in this chapter that unmeasured common causes might explain the relationships between childhood adversities and adult psychopathology. Perhaps the most plausible possibility of this sort is that genetic factors create both family adversities and psychiatric disorders that create the false impression of adversities causing adult disorders. Consistent with this possibility, twin research shows that there is a significant genetic component in most common psychiatric disorders (Kendler et al., 1995), which means that genetic liability to these disorders is transmitted by inheritance from parent to child. We also know that parental psychiatric disorder can take a variety of behavioural forms that create adversities for children, including family violence, financial problems, and marital disruption (Kendler et al., 1993). Together, these effects could induce an association between adversity and disorder even if childhood adversity has no causal impact on adult disorder. Our results, showing broad-based effects of many adversities on a number of different types of psychopathology, are important in arguing against the hypothesis of genetic influence. The reason is that genetic influences are not common across the same wide range of disorders for which effects of childhood adversities have been documented. This means that there can be no simple selection process on the basis of unmeasured genetic vulnerability that creates these associations. It is important to realise that this observation does not exclude the possibility that genetic vulnerability exacerbates the effects of childhood adversities. Interactions of this sort almost certainly exist. However, the existence of these interactions means that adversities are nonetheless important causal risk factors. Finally, our results regarding the overlapping effects of multiple adversities, have important implications both for theory and intervention development. In terms of theory, these results show that caution is needed in interpreting the results of research that focuses on a single adversity and a single form of psychopathology. Specific associations should not be interpreted as unique. Our results regarding the overlapping effects of multiple adversities are important for intervention development because they caution against programmes designed to ameliorate the effects of very narrowly targeted adversities. Childhood adversities often come in bundles. And the joint effects of commonly occurring bundles represent an important, heretofore neglected, topic of research. Programmes aimed at tackling the problem of family violence, the problem of childhood sexual abuse, or the problem of neglect are likely to fail unless they are sensitive to the fact that these individual adversities are often embedded in larger adversity clusters. Another important result for intervention planning purposes is the finding in both the ACL and NCS that the effects of childhood adversities on adult psychopathology are largely due to effects on early first onset rather than

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240 Ron Kessler persistence of disorder. If this is true, it means that many of the factors that mediate the effects of childhood adversities on adult psychopathology are either in place prior to the first onset of disorder or are mediated by the effect of early-onset on persistence. An important implication is that ideas about the timing of interventions and intervention targets need to be rethought to recognise that children exposed to many forms of adversity have a window of vulnerability to psychopathology that seems to end with the transition into adulthood. It is important to acknowledge that all of these results must be considered provisional due to the fact that the measures on which they are based come from retrospective reports and fairly superficial assessments. It would be valuable to replicate these results in data sets that were based on the very detailed semi-structured interviewer-based interviews that George Brown has developed and refined over the years. The challenge in doing this is that the complex interactive approach my colleagues and I have used to analyse our data requires very large sample sizes (over 3,000 respondents in the ACL and close to 6,000 in the NCS). We were able to afford to obtain such large samples because our data collections consisted of interviews that averaged only about ninety minutes to complete. The much more probing interviews administered by George’s group take much longer to complete. As a result, George’s studies all involve samples of several hundred people rather than the thousands we need to address the questions we have in our work. It is true that the greater precision in the interviews George’s group carries out helps combat the problem of comparatively small sample sizes. However, even with this increased precision, the statistical power in samples of the size George has collected is totally inadequate to address research questions involving the complex interactions I have discussed here. An important goal for future research, then, is to refine the types of interviews George has developed so that they can feasibly be administered to larger samples.

Acknowledgements Preparation of this chapter was supported by US Public Health Service grants R01 MH MH52861 and K05 MH00507. The author appreciates the thoughtful comments of Tirril Harris on an earlier version of this chapter.

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Long-term effects of childhood adversities 241 Brown, G.W. (1993). ‘Life events and affective disorder: replications and limitations’, Psychosomatic Medicine, 55, 248–59. —— and Harris, T.O. (1978) Social Origins of Depression: A Study of Psychiatric Disorder in Women, New York: Free Press. —— and Moran, P. (1994) ‘Clinical and psychosocial origins of chronic depressive episodes. I: A community survey’, British Journal of Psychiatry, 165, 447–56. ——, Andrews, B., Harris, T., Adler, Z. and Bridge, L. (1986) ‘Social support, self-esteem, and depression’, Psychological Medicine, 16, 813–31. ——, Bifulco A., Veiel, H.O., and Andrews B. (1990) ‘Self-esteem and depression. II. Social correlates of self-esteem’, Social Psychiatry and Psychiatric Epidemiology, 25, 225–34. ——, Harris, T.O., and Eales, M.J. (1993) ‘Aetiology of anxiety and depressive disorders in an inner-city population. 2. Comorbidity and adversity’, Psychological Medicine, 23, 155–65. ——, Harris, T.O., Hepworth, C. and Robinson, R. (1994) ‘Clinical and psychosocial origins of chronic depressive episodes. II: A patient enquiry’, British Journal of Psychiatry, 165, 457–65. —— and Finkelhor, D. (1986) ‘Initial and long-term effects: A review of the research’ in D. Finkelhor (ed.) Sourcebook on Childhood Sexual Abuse, Beverly Hills, CA: Sage Publications. Bumpass, L.L. (1984) ‘Children and marital disruption: A replication and update’, Demography, 21, 71–82. —— and Castro, T. (1987) ‘Recent trends and differentials in marital disruption’, Center for Demography and Ecology Working Paper, 87–20, Madison, Wisconsin: University of Wisconsin. Bushnell, J.A., Wells, J.E. and Oakley-Browne, M.A. (1992) ‘Long-term effects of intrafamilial sexual abuse in childhood’, Acta Psychiatrica Scandinavica, 85, 136–42. Chase-Lansdale, P.L. (1990) ‘The impact of divorce on life-span development: short and long-term effects’ in P.B. Baltes, D.L. Featherman and R.M. Lerner (eds) Life-Span Development and Behavior, Hillsdale, New Jersey: Lawrence Erlbaum. Cherlin, A. (1981) Marriage, Divorce, Remarriage: Changing Patterns in the Postwar United States, Cambridge, Massachusetts: Harvard University Press. Coons, P.M. and Milstein, V. (1984) ‘Rape and post-traumatic stress in multiple personality’, Psychological Reports, 55, 839–45. Coryell, W., Endicott, J. and Keller, M.B. (1991) ‘Predictors of relapse into major depressive disorder in a nonclinical population’, American Journal of Psychiatry, 148, 1353–8. Faravelli, C., Paterniti, S. and Scarpato, A. (1995) ‘5-year prospective, naturalistic followup study of panic disorder’, Comprehensive Psychiatry, 36, 272–7. Fleming, J.E. and Offord, D.R. (1990) ‘Epidemiology of childhood depressive disorders: a critical review’, Journal of American Academy of Child and Adolescent Psychiatry, 29, 571–80. Goodyer, I.M. (1990) ‘Family relationships, life events and childhood psychopathology’, Journal of Child Psychology and Psychiatry, 31, 161–92. Harrington, R., Fudge, H., Rutter, M., Pickles, A. and Hill, J.P. (1990) ‘Adult outcomes of childhood and adolescent depression’, Archives of General Psychiatry, 47, 465–73. Harris, T., Brown, G.W. and Bifulco, A. (1986) ‘Loss of parent in childhood and adult psychiatric disorder: the role of lack of adequate parental care’, Psychological Medicine, 16, 641–59.

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242 Ron Kessler ——, Brown, G.W. and Bifulco, A. (1990) ‘Loss of parent in childhood and adult psychiatric disorder: a tentative overall model’, Development and Psychopathology, 2, 311–28. Hojat, M., Borenstien, B.D. and Shapurian, R. (1990) ‘Perceptions of childhood dissatisfaction with parents and selected personality traits in adulthood’, Journal of General Psychology, 117, 241–53. House, J.S., Kessler, R.C., Herzog, R., Mero, R.P., Kinney, A.M. and Breslow, M.J. (1990) ‘Age, socioeconomic status, and health’, The Milbank Quarterly, 68, 383–411. Kendler, K.S., Neale, M.C., Kessler, R.C., Heath, A.C. and Eaves, L.J. (1993) ‘A twin study of recent life events and difficulties’, Archives of General Psychiatry, 50, 789–96. ——, Walters, E.E., Neale, M.C., Kessler, R.C., Heath, A.C. and Eaves, L.J. (1995) ‘The structure of the genetic and environmental risk factors for six major psychiatric disorders in women’, Archives of General Psychiatry, 52, 374–83. Kessler, R.C. and Magee, W.J. (1993) ‘Childhood adversities and adult depression: basic patterns of association in a US National Survey’, Psychological Medicine, 23, 679–90. —— and Magee, W.J. (1994) ‘Childhood family violence and adult recurrent depression’, The Journal of Health and Social Behavior, 35, 13–27. ——, McGonagle, K.A., Zhao, S., Nelson, C.B., Hughes, M., Eshleman, S., Wittchen, H.U. and Kendler, K.S. (1994) ‘Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States: results from the National Comorbidity Survey’, Archives of General Psychiatry, 51, 8–19. ——, Davis, C.G., and Kendler, K.S. (1997) ‘Childhood adversity and adult psychiatric disorder in the US National Comorbidity Survey’, Psychological Medicine, 27, 1101– 19. ——, Wittchen, H.-U., Abelson, J.M., McGonagle, K., Schwarz, N., Kendler, K.S., Knäuper, B. and Zhao, S. (1998) ‘Methodological studies of the Composite International Diagnostic Interview (CIDI) in the US National Comorbidity Survey’, International Journal of Methods in Psychiatric Research, 7, 33–55. Kraemer, H.C., Kazdin, A., Offord, D., Kessler, R.C., Jensen, P. and Kupfer, D.J. (1997) ‘Coming to terms with the terms of risk’, Archives of General Psychiatry, 54, 337–43. Kunugi, H., Sugawara, N., Aoki, H., Nanko, S., Hirose, T. and Kazamatsuri, H. (1995) ‘Early parental loss and depressive disorder in Japan’, European Archives of Psychiatry and Clinical Neuroscience, 245, 109–13. Lewinsohn, P.M., Hoberman, H.M. and Rosenbaum, M. (1988) ‘A prospective study of risk factors for unipolar depression’, Journal of Abnormal Psychology, 97, 251–64. Masten, A.S., Best, K.M. and Garmezy, N. (1990) ‘Resilience and development: contributions from the study of children who overcome adversity’, Development and Psychopathology, 2, 425–44. Maughan, B., Gray, G. and Rutter, M. (1985) ‘Reading retardation and antisocial behavior: a follow-up into employment’, Journal of Child Psychology and Psychiatry, 26, 741–58. McGonagle, K.M. and Kessler, R.C. (1990) ‘Chronic stress, acute stress, and depressive symptoms’, American Journal of Community Psychology, 18, 681–705. McLeod, Jane D. (1991) ‘Childhood parental loss and adult depression’, Journal of Health and Social Behavior, 35, 205–20. Metalsky, G.I. and Joiner, T.E., Jr. (1992) ‘Vulnerability to depressive symptomatology: a prospective test of the diathesis-stress and causal mediation components of the hopelessness theory of depression’, Journal of Personality and Social Psychology, 63, 667–75. Millon, T. (1990) ‘The disorders of personality’ in L.A. Pervin (ed.) Handbook of Personality, New York: The Guilford Press.

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Long-term effects of childhood adversities 243 Mullen, P.E., Martin, J.L., Anderson, J.C., Romans, S.E. and Herbison, G.P. (1993) ‘Childhood sexual abuse and mental health in adult life’, British Journal of Psychiatry, 163, 721–32. ——, Martin, J.L., Anderson, J.C., Romans, S.E. and Herbison, G.P. (1996) ‘The long-term impact of the physical, emotional, and sexual abuse of children: a community study’, Child Abuse and Neglect, 20, 7–21. Oakley-Browne, M.A., Joyce, P.R., Wells, J.E., Bushnell, J.A. and Hornblow, A.R. (1995) ‘Adverse parenting and other childhood experience as risk factors for depression in women aged 18–44 years’, Journal of Affective Disorders, 34, 13–23. Parker, G. and Hadzi-Pavlovic, D. (1984) ‘Modification of levels of depression in mother-bereaved women by parental and marital relationships’, Psychological Medicine, 14, 125–35. —— and Parker, H. (1991) ‘Female victims of child sexual abuse: adult adjustment’, Journal of Family Violence, 6, 183–97. Plantes, M.M., Prusoff, B.A., Brennan, J. and Parker, G. (1988) ‘Parental representations of depressed outpatients from a USA sample’, Journal of Affective Disorders, 15, 149–55. Pollack, M.H., Otto, M.W., Sabatino, S., Majcher, D., Worthington, J.J., McArdle, E.T. and Rosenbaum, J.F. (1996) ‘Relationship of childhood anxiety to adult panic disorder: correlates and influence on course’, American Journal of Psychiatry, 153, 376–81. Portegijs, P.J.M., Jeuken, F.M.H., van der Horst, F.G., Kraan, H.F. and Knottnerus, J.A. (1996) ‘A troubled youth: relations with somatization, depression and anxiety in adulthood’, Family Practice, 13, 1–11. Robins, L.N., Helzer, J.E., Croughhan, J. and Ratcliff, K.L. (1981) ‘National Institute of Mental Health Diagnostic Interview Schedule: its history, characteristics and validity’, Archives of General Psychiatry, 38, 381–9. Rodgers, B. (1990) ‘Behavior and personality in childhood as predictors of adult psychiatric disorder’, Journal of Child Psychology and Psychiatry, 31, 509–18. —— (1994) ‘Pathways between parental divorce and adult depression’, Journal of Child Psychology and Psychiatry, 35, 1289–308. Romans, S.E., Walton, V.A., McNoe, B., Herbison, G.P. and Mullen, P.E. (1993) ‘Otago Women’s health survey 30-month follow-up: I. onset patterns of non-psychotic psychiatric disorder’, British Journal of Psychiatry, 163, 733–8. ——, Martin, J.L., Anderson, J.C., O’Shea, M.L. and Mullen, P.E. (1995) ‘Factors that mediate between child sexual abuse and adult psychological outcome’, Psychological Medicine, 25, 127–42. Rutter, M. (1989) ‘Pathways from childhood to adult life’, Journal of Child Psychology and Psychiatry, 30, 23–51. Sorenson, S.B., Rutter, C.M. and Aneshensel, C.S. (1991) ‘Depression in the community: an investigation into age of onset’, Journal of Consulting and Clinical Psychology, 59, 541–6. Sroufe, L.A. and Rutter, M. (1984) ‘The domain of developmental psychopathology’, Child Development, 55, 17–29. Stein, M.B., Walker, J.R., Anderson, G., Hazen, A.L., Ross, C.A., Eldridge, G. and Forde, D.R. (1996) ‘Childhood physical and sexual abuse in patients with anxiety disorders and in a community sample’, American Journal of Psychiatry, 153, 275–7. Straus, M.A. (ed.) (1990) Physical Violence in American Families: Risk Factors and Adaptations to Violence in 8,145 Families, New Brunswick, New Jersey: Transaction Publishers.

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244 Ron Kessler Testa, M., Miller, B.A., Downs, W.R. and Panek, D. (1990) ‘Long-term effects of childhood victimization: the moderating impact of social support’, presented at the Annual Meeting of the American Society of Criminology in Baltimore, Maryland, November 7–10. Truett, J., Cornfield, J. and Kannel, W. (1967) ‘A multivariate analysis of the risk of coronary heart disease in Framingham’, Journal of Chronic Diseases, 20, 511–24. Velleman, R. and Orford, J. (1993) ‘The adult adjustment of offspring of parents with drinking problems’, British Journal of Psychiatry 162: 503–16. Weissman, M.M., Bruce, M.L., Leaf, P.J., Florio, L.P. and Holzer, C., III. (1991) ‘Affective disorders’ in L.N. Robins and D.A. Regier (eds) Psychiatric Disorders in America, New York: The Free Press. Wertlieb, D. (1997) ‘Children whose parents divorce: life trajectories and turning points’, in I.H. Gotlib and B. Wheaton (eds) Trajectories and Turning Points: Stress and Adversity Over the Life Course, New York: Cambridge University Press. Wittchen, H.-U. (1994). ‘Reliability and validity studies of the WHO Composite International Diagnostic Interview (CIDI): A critical review’, Journal of Psychiatric Research, 28, 57–84. World Health Organization (1990) Composite International Diagnostic Interview (CIDI, Version 1.0), Geneva, Switzerland: World Health Organization. Zlotnick, C., Ryan, C.E., Miller, I.W. and Keitner, G.I. (1995) ‘Childhood abuse and recovery from major depression’, Child Abuse and Neglect, 19, 1513–16.

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14 Evolved socio-emotional systems and their role in depressive disorders Martin Eales

Introduction George Brown’s work contains a constant interplay between close attention to empirical detail and theoretical development, extended by a remarkable ability to translate and develop new ideas into empirically-based concepts. This is well illustrated in the links between certain areas of his work and theories of human socio-emotional behaviour framed in terms of evolved, species-typical, core motivational systems. This chapter discusses how this material has been incorporated and refined within his research into the aetiology of depression, and, in turn, how it can fertilise further theoretical development.

Depression and affectional behaviour The development of attachment theory by Bowlby (1958, 1969–1980) has had a major impact on thinking within psychotherapy, developmental psychology, and ethology (e.g. Bretherton and Waters, 1985; Heard and Lake, 1986, 1997; Kraemer, 1992; Bartholomew and Perlman, 1994; Suomi, 1995). Its background model of evolved, functionally specialised core behaviour systems, although modernised in terminology and theoretical background, shares many features with older accounts such as that of McDougall (1945/1908). This is combined with a detailed, empirically-based account of the attachment system as a prototypical example; a functional system serving to secure and maintain caregiving contact by others, and manifested in proximity-seeking and care-eliciting behaviours, separation distress, and the fostering of exploratory behaviour by the presence of the caregiver (‘safe base’ phenomena). In human beings, at least, aspects of attachment behaviour observable in infancy become internalised and integrated with more complex cognitive processes as development proceeds, and remain important organisers of interpersonal emotion and behaviour in close relationships into adult life (Bowlby, 1969; Heard and Lake, 1986; Hazan and Shaver, 1987; Bartholomew and Perlman, 1994). Since the work of Ainsworth (e.g. Ainsworth, Bell and Stayton, 1971), much research into attachment has focused on individual differences in attachment behaviour, their explanation and their implications for later development. In contrast, there has been relatively

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246 Martin Eales little further research into the core mechanisms that make up the more constant or universal aspects of attachment behaviour. For example, the explanation of attachment processes in terms of the coordinated activation of lower-level emotion systems remains a somewhat neglected area (although see McDonald, 1992). Bowlby’s account of attachment behaviour described an initial phase of agitated protest and search behaviour after separation from an attachment object, followed later, if contact was not restored, by a state of ‘despair’ and behavioural inactivation. Some aspects of these states clearly resemble features of clinical depressive and anxiety disorders. The suggestion that the resemblances arise from the same behavioural substrate is persuasive, particularly where depressive or anxiety disorders have developed following interpersonal loss or separation (Bowlby, 1969–80, Volume 2, Part III and Volume 3; Bowlby, 1977; Parkes, 1972). There is also accumulating evidence that individual differences in attachment style or in cognitive models of attachment relationships may provide trait markers predicting responses to future loss (reviewed by Blatt and Zuroff, 1992). However, the focus of attachment theory on one particular motivational system has tended to foster self-contained explanations, in which the possible role of other systems is ignored – for example, the possibility that more severe and pathological reactions to loss depend on the admixture of other, non-affectional, types of behavioural response (as suggested by Freud, 1957/1917). A related limitation of theories of depression that draw on attachment theory is their tendency to treat attachment behaviour as if it forms the basis for all responses to social bond disruption, and as if it covers the whole range of affectional behaviour, including caregiving as well as attachment. Where they have not been passed over cursorily, affectional behaviours associated with the caregiving role have often been discussed purely in terms of their responsiveness to others’ attachment needs (e.g. Heard and Lake, 1997), or treated as an appendage of the attachment system, for example, in attempts to correlate individual differences in caregiving behaviour with the person’s own attachment style (Kunce and Shaver, 1994). There is some justification for this conflation of the two systems, as there is evidence that caregiving and care-eliciting (i.e. attachment) behaviours in humans share certain response components. For example, overlapping ranges of facial expression and autonomic response are seen in the areas of both negative affect (distress/sadness and pity/sympathy/‘concern’) and positive affect (warmth) linked with each pattern of behaviour (Eisenberg, McCreath and Ahn, 1988; Eisenberg et al., 1989; McDonald, 1992). The implication, that they depend on an overlapping set of emotional-motivational mechanisms, is biologically unusual, as in most other species, caregiving behaviour by parents and care-seeking behaviour in young – in species where these are present – appear to involve mutually adapted but otherwise independent sets of behavioural mechanisms (for reviews, see Krasnegor and Bridges, 1990; Rosenblatt and Snowdon, 1996; a similar assumption is made in the human case by Bowlby, 1969, 1984; and by Gilbert, 1989). Such overlapping is probably not unique to humans, however, as display symmetry in caregiving/attachment relationships has been noted in other closely related species such as chimpanzees, both in expressions of warmth and in expressions of

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Evolved socio-emotional systems 247 distressed/concerned contact-seeking (e.g. van Lawick-Goodall, 1968, pp. 249ff.). The commonalities between the two sets of behaviour are reinforced in human beings by the fact that affectional relationships between adults or older children are not consistently polarised in one direction but often involve a mutuality or reversibility of role in which elements of caregiving and attachment may both be expressed towards the other party. Nonetheless, attachment and caregiving behaviours differ sharply in the factors by which they are activated and in some of their associated responses. The need to distinguish them is illustrated particularly clearly by the different meanings of interpersonal loss where the person lost is a caregiver (e.g. where a child loses a parent) or is a dependent party (e.g. where a parent loses a child). The interpretation of depression as a response to loss of a supportive attachment figure hardly applies in the second case. Yet grief is no less typical. Moreover, just as pity and distress share certain common features, while differing in other ways, grief in caregivers shares numerous qualities with other types of grief, while differing, at least quantitatively, in others. The frequency and prominence of guilt feelings in bereaved parents has been noted by numerous authors (e.g. Owen, Fulton and Markusen, 1978; Singh and Raphael, 1981). In a detailed comparison of responses to loss by death of spouses or children, Lehman, Wortman and Williams (1987) showed that guilt feelings were more frequent and persistent in those who had lost a child; this could not be explained as a confound of severity of depression, as depression overall was greater among bereaved spouses. It needs to be recognised that attachment is only one half of a wider system of affectional behaviour, and that some types of affective disturbance linked with the disruption of affectional bonds have little to do with attachment per se. A more complete understanding of the functioning of this wider system requires more attention to caregiving behaviour and its associated patterns of emotional arousal – which are more ancient, in evolutionary terms, than attachment behaviour – than has been given so far. Most research and theory relevant to this area belongs to a very different paradigm (e.g. Hoffman, 1981; Eisenberg, 1986), and there has been little real progress in understanding human caregiving behaviour as a specialised functional system since McDougall’s discussion of the ‘tender emotion’ almost a century ago (McDougall, 1945/1908, pp. 56 ff.).1 Depression and loss in George Brown’s work Research into life events and depression in community and clinical samples carried out at Bedford College beginning in the 1970s (Brown, Harris and Ni’ Bhrolchain, 1975; Brown and Harris, 1978; Brown, Harris and Copeland, 1977) emphasised the importance of recent life events carrying long-term threat, and specifically loss events, in the onset of depression. Many aspects of the research could be seen as consistent with the perspective of attachment theory, and it was cited at length by Bowlby (1980). Parallels with attachment theory were actually closer in the second factor of their aetiological model of depression, that is, in the area of psychosocial

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248 Martin Eales vulnerability to depression, than in qualities of the provoking events. The protective role of a confiding relationship with a husband or boyfriend, in studies of female samples, has been confirmed repeatedly in subsequent research (reviewed in Harris, 1992 and Brown, 1992; evidence in men is comparable but much less extensive, e.g. Eales, 1988; Edwards, Nazroo and Brown, 1998). This finding, taken together with the lack of any consistent evidence that social support from wider social networks has a similar protective influence, suggests that support from an attachment figure, or confirmation of a relationship providing attachment security, is a critical protective factor. The effect is not confined to events involving interpersonal loss, but it does appear to be relatively specific to depressive disorders; and what evidence there is suggests that a confiding relationship does not protect in the same way against the onset of anxiety disorders (Finlay-Jones, 1989). Another vulnerability factor identified in the early Camberwell studies, loss of mother before the age of 11, was seized upon by some as supporting certain other aspects of attachment theory. Subsequent research indicates that a large part of the effect of early life experience on later risk of depression is mediated by population-dependent effects on subsequent relationships and life history – for example, where early loss is correlated with subsequent premarital pregnancy and early marriage, both risk factors for adult depression in women (Harris, Brown and Bifulco, 1990). This does not exclude a formative influence of early experience on depression-relevant personality characteristics, although lack of consistent care following the loss (e.g. by substitute caregivers) appears more important than loss per se. The emphasis on loss as a common ingredient in depressogenic events appeared to present a further point of contact with attachment theory. Interpersonal losses and separations (or threats of these) were an important group of events provoking onset of depression in urban settings (e.g. Brown and Harris, 1978; Paykel et al., 1969), and were found to be even more central as provoking agents in the Hebrides studies, where culturally normative patterns of affectional behaviour appeared to influence the impact of losses within the extended family (Prudo et al., 1981). However, the concept of loss used was wider than that relevant to attachment theory. It was based on the more general notion of ‘deprivation of sources of value or reward’ (Brown and Harris, 1978, p. 233), and included all severe events where there was loss of a source of personal value in relation to high-level plans or aspirations. While the source of value lost could be an attachment figure, or some other person, it could equally be an item of a quite different kind, as in disappointed ambition, damaged reputation, or loss of financial security. There were precedents for this extended concept of loss, in behavioural theories of depression based on loss of reward (e.g. Lewinsohn, 1974), and in cognitively oriented approaches to emotion and motivation in which low-level affective phenomena are seen in terms of a simple global distinction between positive or negative emotional valence. However, the main justification for the more inclusive concept of loss used by Brown and Harris was that it accounted more fully for the range of life events associated with onset of depression. Finlay-Jones formalised this broader concept of loss and showed that such events were of much greater importance for depression

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Evolved socio-emotional systems 249 than ‘danger’ events, in which there was a threat of future loss. The latter are more important in provoking episodes of anxiety disorder (Finlay-Jones, 1989). Although attachment theory offers important insights into many depressive phenomena, it evidently cannot provide an overall explanatory model for the results outlined here unless it is supplemented by considerable speculative overlay. This would remain the case even if it were extended to include affectional behaviour more generally, including caregiving behaviour. One way to increase the scope of explanatory models is to appeal to generalised cognitive processes (e.g. Beck, 1976; Brown and Harris, 1978). Another is to consider other specialised motivational systems that may be relevant to depressive states.

Depression and agonistic behaviour ‘Agonistic behaviour’ refers to patterns of behaviour which originate in the context of intraspecific conflict or competition (including competition that is anticipated and pre-empted or avoided). It includes, on the one hand, various forms of assertive behaviour, including threat, some forms of aggression, and social displays that convey and affirm superior status over others and, on the other hand, forms of behaviour that function to appease threat and/or to concede place or status to others, generically labelled submissive or appeasement behaviours. The simplest and most frequent response by a weaker party to threat – or anticipated threat – is instrumental avoidance or escape. Submissive displays with specialised expressive features generally occur where there are other, concurrent, motivations to approach or at least to stay in the vicinity of the other party.2 An obvious and widely distributed example is the occurrence of submissive behaviours in the context of courtship and sexual behaviour, which is seen in many different animal groups (Hinde, 1970, pp. 360–95; Eibl-Eibesfeldt, 1970, pp. 116–34). In species where a wider range of cooperative behaviour is adaptively important, the scope for prosocial, relationship-building or -maintaining consequences of appeasement behaviours and their derivatives is greatly magnified, and the situations in which they occur extend beyond those in which conflict or potential conflict between individuals is an obvious focus of interaction (de Waal, 1986). Comparative evidence suggests that the group of human emotional-motivational states which includes shame and related emotions (embarrassment, humiliation, and so on), unified by a common or overlapping set of expressive features and situational predictors, is homologous with the spectrum of passive submissive/appeasement behaviours seen in non-human primates. Aspects of this homology have been recognised by many authors, including those who have pointed to resemblances between shame-spectrum emotions and certain animal behaviors in physical form, functional significance, or both (Darwin, 1980/1838, p. 10; McDougall, 1945/1908, pp. 53–6; Fox, 1967; Barkow, 1975, 1976; Gilbert, 1989; see also Öhman, 1986; Leary and Meadows, 1991; Leary, Britt, Cutlip and Templeton, 1992), and those who have identified the function of shame or related emotions as that of interpersonal appeasement or submission, without drawing explicit parallels with other species (e.g. Strathern, 1975; Semin and Manstead,

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250 Martin Eales 1982; Scheff, 1988; Castelfranchi and Poggi, 1990; Barrett, 1995). The culturally universal association of shame-spectrum emotions with certain types of human courtship/sexual interaction matches precisely the widespread occurrence of submissive behaviours in this context in other species. There are clearly also species differences, and shame-spectrum emotions in human beings differ considerably from their animal counterparts in some ways; for example, they are subject to much greater cognitive elaboration, and their capacity to be elicited by internalised signals expands their time-frame beyond short-term situational activation of the kind seen in other species to include anticipatory, recurrent or persistent activation. Some further species differences are mentioned below. Recent theoretical interest in the role of agonistic behaviours in human psychiatric disorder stems mainly from the work of Price (1969), Gardner (1982) and Gilbert (1989, 1992; see also Price et al., 1994), although some aspects of the subject were formulated clearly much earlier by McDougall (1926, pp. 352 ff.). McDougall interpreted mood disorders in terms of abnormal activity of a cognitive-affective ensemble (the ‘sentiment of self-regard’) linked with evolved behaviour patterns (‘instincts’) of self-assertion and submission, which he had correctly seen as homologous with agonistic behaviours in other animals (McDougall, 1945/1908, pp. 53–6 and 162–72). Since McDougall’s time, the area has been relatively neglected, in comparison with the extensive interest shown in attachment behaviours. Agonistic behaviours have often been seen as primitive forms of behaviour, more or less successfully suppressed by other systems – seen as more advanced, more distinctively human, perhaps even more desirable – responsible for cooperative or affectional behaviour (e.g. MacLean, 1990; Gilbert, 1992; Heard and Lake, 1997), and the prosocial, relationship-maintaining aspects of submissive behaviours have been generally overlooked. Furthermore, some authors have over-emphasised the connection between agonistic behaviour and dominance rank. Here the distinction between the interactional and relationship levels of analysis has been blurred, obscuring the fact that social power in human groups depends to a large extent on context-variable coalition behaviour that is much more extensive and complex than that seen in any other species. The perceived social threats to which human appeasement behaviours (i.e. shame-spectrum emotions) respond often have little to do with interpersonal dominance, and concern instead the position of an individual vis-à-vis a social group – which may be extensive, undefined, or imaginary – rather than any other particular individual. As with attachment/affectional behaviour discussed earlier, work by Brown and colleagues has provided evidence for the relevance of this area of behaviour to depressive disorders. Brown, Harris and Hepworth (1995) developed measures of two new event dimensions, humiliation, based on a contextual rating of the meaning of the event as ‘rendering a person devalued in relation to others or self’, and entrapment, based on a contextual rating of the meaning of the event as underlining the likely continuation of a pre-existing marked difficulty. They showed that a high proportion of severe events preceding depressive onset in their community sample could be partitioned into those involving humiliation-entrapment (71 per cent) or pure interpersonal loss (16 per cent).3 In the six months following a severe

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Evolved socio-emotional systems 251 event in one or other of these categories, 29 per cent of subjects in the community sample suffered onset of depression, whereas after severe events not involving humiliation-entrapment or interpersonal loss, the onset rate was only 4 per cent. It is notable therefore that in this empirically-based analysis, as in the analysis of depressogenic events in terms of motivational systems, a more specific notion of interpersonal loss re-emerges from the more generalised, ‘cognitive’ concept of loss. The significance of these two new event types or dimensions remains to be clarified. For example, applying the same definition of humiliation in male samples would probably reveal a wider range of relevant events than those that emerged among Brown, Harris and Hepworth’s (1995) female subjects. Many other events that involve ‘loss’ broadly conceived have implications for perceived reputation, social status, or social comparison (e.g. Eales 1988, 1989). The concept would realistically include a wide range of achievement-related adverse events in which agonistic processes are involved either directly (e.g. social comparison processes with an inherently competitive content) or indirectly (e.g. self-assessment against internalised standards arousing patterns of emotional response learned in earlier experiences of antagonistic interaction with authority figures). There is every reason to believe such extensions will be possible (see also the discussion of ‘atypical’ events in chapter 1).

Processes limiting domain-specificity of motivational systems Brown, Harris and Hepworth (1995) do not consider the states provoked by humiliation-entrapment events and those provoked by pure interpersonal loss as reflecting, even potentially, distinct types of depression. Instead they are treated, in effect, as different aetiological pathways that subsequently merge in a final pathway shared by all types of depression. The implication that disturbances of different behavioural systems should have the same or similar outcomes runs contrary to the assumptions of ‘evolutionary psychology’ that evolved behavioural or motivational mechanisms are domain-specific, an argument that has been made with great force by some of its proponents (Tooby and Cosmides, 1992). However, even among those who recognise the importance of evolved behavioural mechanisms, the emphasis on domain-specificity has been questioned (McDonald, 1991; Shapiro and Epstein, 1998). Domain-specificity is limited both by ‘vertical’ integration with domain-general processes or mechanisms, and by ‘horizontal’ integration or cross-talk between specialised mechanisms that have systematically inter-related elicitors or consequences. Both of these are likely to be relevant to the interaction of affectional and agonistic behaviour patterns in depression. The domain-general mechanisms referred to most often are cognitive processes that can be applied to different areas of behaviour in the service of different systems or motivations. These are presupposed in accounts of negative thinking linked with depression (Beck, 1976), including the cognitive model presented in

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252 Martin Eales the earlier work of Brown and Harris (1978). Even if seen as hybrids between a generalised processing resource and more specialised emotional or motivational systems, they are less self-contained than is suggested by the assumption of strict domain-specificity, and may combine elements linked with different motivational systems. For example, the ‘working models’ of attachment figures or relationships considered by Bowlby (1969) are usually referred to as belonging to the ‘attachment system’, but descriptions often incorporate material about non-affectional social behaviours, for example, expectations about agonistic responses on the part of the attachment figure. Other relevant domain-general mechanisms might include primitive mechanisms mediating responses to rewarding or aversive stimuli (Schneirla, 1959; Davidson et al., 1990). These may be linked with multiple more complex specialised emotions or behaviour systems, providing a further avenue where aetiologically differentiated types of affective disturbance may have convergent consequences. In addition to domain-general mechanisms, there are examples in many species where specialised systems do not function as separate, independent processes, but interact with each other. In various primate species (and some other social mammals, including dogs), care-eliciting display behaviours that typically occur as components of attachment behaviour may also occur as responses to perceived threat, serving an appeasement function through the response incompatibility between agonistic and caregiving behaviour in the other party (van Hooff, 1967). Conversely, ‘submissive’ displays that are characteristically seen as responses to threat may also occur as care- or contact-seeking behaviours, for example in infant chimpanzees in response to maternal rejection during weaning (Clark, 1977), and in adult chimpanzees seeking contact with a more dominant individual after recent conflict (van Lawick-Goodall, 1968; Bygott, 1979; de Waal, 1982). Analogous observations could be made about the occurrence of sexual behaviours in the context of affectional or agonistic interaction, and of affectional or agonistic behaviours in the context of sexual interaction. Cross-talk of this kind between different behavioural domains appears particularly richly developed in humans and closely related species. Shame itself illustrates this: although its origin in agonistic behaviour is evident from the form of its associated expressive behaviours and the full range of its elicitors, when maturely developed it is often closely linked with affectional behaviours. Rejection in a close relationship is one of its commoner elicitors. In fact many human socioemotional phenomena show a dual aspect in which a circumstance can elicit an agonistic response, or an affectional response, or sometimes both. For example, feelings stimulated by approval or disapproval can be mainly affectional – e.g. passive warmth, or distress over apprehended bond disruption – or mainly agonistic – e.g. pride or shame – or both. Similarly, helplessness may foster appeasing or care-seeking behaviours (or both) in the subject, and may elicit a caregiving response, or bullying cruelty (or neither) in another person. For this reason, there may be little to be gained by asking whether perceptions of helplessness or powerlessness associated with depression are primarily agonistic phenomena, to be understood in terms of defeat responses, or affectional or attachment-

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Evolved socio-emotional systems 253 related phenomena, to be understood in terms of feelings of vulnerability and need for care. They may be related to either, or both, of these, in different individuals and different circumstances.

Variability in depressive states related to distinct behavioural, motivational or emotional processes The most obvious implication of these limitations on domain-specificity for the modelling of depressive states is that they counteract the formation of discrete syndromes based on disturbance in single specialised behaviour systems: generalisation of disturbance across linked systems or mechanisms will lead to convergence in the characteristics of depressive states regardless of their specific origins. If this convergence were complete, the overall effect would be the same as that if all depressive states arose from a single domain-general process, either as the locus of a primary disturbance or as a common final pathway in which various aetiological processes converge. Depressive states would be homogeneous, varying only in severity. If convergence were less complete, variability among depressive states might, with appropriate analysis, yield correlations between system-specific aetiological factors and observable indicators of system-specific functional disturbances (e.g. certain groups of symptoms, and potentially other, e.g. physiological, variables). The aetiological dichotomy between humiliation-entrapment and pure loss identified by Brown, Harris and Hepworth (1995) bears some resemblance to the much wider proposals by a number of authors that psychosocial processes relevant to the aetiology of depression can be divided into two discrete types or dimensions, related to different motivational systems, different types of provoking event, and different aspects of personality vulnerability (Table 14.1). The theoretical basis of these subtypings varies greatly, but the common ground between them in the differentiation of types of provoking event, and somewhat less consistently in the described predisposing personality factors, has been noted previously (Blatt and Zuroff, 1992; Hardy, 1998). Most authors making this distinction have also suggested that the two aetiological dimensions are associated with important differences in symptomatology: clinical features such as demonstrative distress, anxiety, intolerance of being alone, feelings of helplessness, and care- and reassurance-seeking behaviour being cited as typical of depression linked with social bond disruption, and features such as self-criticism, guilt, preoccupation with personal failure or inferiority, and social withdrawal as typical of depression linked with failure/loss of control issues. As yet there is limited substantiation for these (largely theory-derived) distinctions. Studies using questionnaire-based measures of life events and of personality factors have examined differential sensitivity to adverse events of different types in individuals with particular personality styles: correlations have generally been in the predicted directions, but more consistently for high sociotropy and bond disruption events than for high autonomy and failure/loss of control events (Hammen et al., 1989; Robins and Block, 1988; Robins, 1990). A similar conclusion was

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254 Martin Eales Table 14.1 Proposed subtypings or dimensions of depression based on differentiated psychosocial aetiology Typical provoking event type

disruption of close relationships by loss separation, rejection

perceived failure, disruption of sense of control/mastery

Suggested predisposing personality factors

trait dependency

trait self-criticism

Blatt et al., 1982

‘sociotropy’

‘autonomy’

Beck 1983

anxious/insecure attachment style

avoidant attachment style

Blatt and Zuroff 1992

‘anaclitic’ depression

‘introjective’ depression

Blatt 1974

‘disruption of interpersonal relatedness’

‘disruption of selfdefinition’

Blatt and Zuroff 1992

loss/disruption in relation to ‘dominant other’

frustration or failure Arieti and Bemporad 1978 involving a ‘dominant goal’

‘sociotropic’ depression

‘autonomous’ depression

Proposed depressive subtypes

Beck 1983

drawn from a larger set of studies reviewed by Blatt and Zuroff (1992), although many of these did not study depressed subjects but involved self-prediction (or self-report) of event-related distress in non-clinical samples. More could be done in this area. There is evidence from elsewhere in the Bedford College programme that certain attributes confer differential vulnerability to specific types of adverse experience, although the examples so far have been features of individuals’ social environments or past experience rather than personality attributes. Examples include the elevated risk of depression where a severe event ‘matches’ in content a pre-existing social difficulty or identified role conflict (Brown, Bifulco and Harris, 1987; Eales, 1988), and increased sensitivity to loss by death in populations with particular patterns of interpersonal attachment (Prudo et al., 1981). Extending this to consider differential sensitivity to specific event types conferred by personality attributes would be important irrespective of whether in turn these can be related to different types of depression. Differences in symptom profile in depressed subjects have been examined against questionnaire measures of sociotropy and autonomy. Here the predicted correlations have once again been more consistent for sociotropy/dependency than

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Evolved socio-emotional systems 255 for autonomy (Blatt et al., 1982; Robins, Block and Peselow, 1989; Robins and Luten, 1991). However, none of these studies have attempted to distinguish aetiological from pathoplastic phenomena (e.g. where personality may predict individual differences in interpersonal behaviour occurring in response to the experience of depression). Evidence for differences in symptom profile between depressive states provoked by different types of event is largely absent. Overall, this research offers some support for a pathway to depression involving high dependency needs and adverse events involving interpersonal loss, but evidence for the second dimension is less clear (Nietzel and Harris, 1990). This may reflect the fact that whilst sociotropy or dependency can be readily related to a biologically meaningful system – the attachment system – the concepts of autonomy or self-definition are less easy to relate to the activity of a specific functional system. On the one hand, as outlined earlier, guilt and self-criticism appear to be common in loss reactions among caregivers, where they may be related to disturbed or disrupted caregiving behaviour. On the other hand, some forms of these same phenomena, in particular forms of self-criticism that are accompanied by a sense of vulnerability to the critical regard of others, withdrawal in the wake of failure, and the experience of shame, are more readily related to agonistic behaviour patterns. Disturbances of these two types of behaviour are likely to have differing correlates (e.g. in event type and personality vulnerability) which will obscure the picture if they are aggregated within a single category. Further research in this area also needs to take into account the non-domain-specific processes discussed earlier. For example, events involving failure or loss of control often have implications for relationships with others, and engender apprehensions about bond disruption, rejection etc., that may dilute any correlation with other category- or dimension-specific factors. It is also important to treat the two aetiological ‘types’ as dimensions rather than exclusive categories. A particular adverse event, or the personality profile of a particular individual, may involve elements from both dimensions (Blatt et al., 1982). Although the formulation of humiliation-entrapment as a global event category by Brown, Harris and Hepworth (1995) was justified to simplify the analysis in order to provide an initial demonstration of the importance of this type of behaviour, many of these events arose in close affectional relationships, and are likely to have involved disruption of multiple behavioural processes. Further analysis may profit from treating these as event dimensions so that joint and separate effects with other event dimensions can be analysed.

Conclusion Many previous theories of depression drawing on ethology or evolutionary psychology have had a monopolistic character, focusing on one type of explanation to the exclusion of others, or seeking to identify one mechanism or process as the ‘primary’ disturbance. In contrast, material reviewed in this chapter has outlined evidence pointing to the value of explicit modeling of multiple systems and the interactions between them. In some ways this is reflected in the development of

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256 Martin Eales George Brown’s approach itself. His early aetiological model of depression was oriented mainly around generalised cognitive processes as a common final pathway (Brown and Harris, 1978). But his subsequent work refers, in effect, to a composite model involving multiple partially independent processes, some of them generalised and some specialised: cognitive processes have, as before, retained centre stage, but alongside these there is a recognition of the role of attachment-related emotional phenomena (Bifulco et al., 2000), agonistic behaviour patterns (Brown, Harris and Hepworth, 1995), and low-level physiological processes that may be primed by stress responses (Brown, Harris and Hepworth, 1994), each based on specific research findings from the Bedford College programme. Refining the description of the functional systems involved, and developing a detailed model of how they interact, are important tasks that remain.

Notes 1

2

3

McDougall’s understanding of emotional states relevant to caregiving behaviour was limited by the lumping together of (negative/aversive) states of pity or sympathy and (positive/rewarding) states of nurturant warmth, with their quite different forms of expression, as instances of one and the same emotion. He also considered initially that distress in helpless individuals was nothing more than an imitative reference to this ‘tender emotion’ in prospective caregivers. It was only in the 14th (1919) edition of his Introduction to Social Psychology that he recognised distress and its associated display behaviours as a component of a system of care-eliciting or care-seeking behaviours that had evolved with its own separate function. By this time other aspects of his theory had been elaborated too far to accommodate the wide-ranging revisions that this implied. Interpreting the affective content of pity/sympathy as merely an imitative response to distress in others (e.g. Hatfield, Cacioppo and Rapson, 1993) involves a similar but opposite mistake. The exception to this is where escape or avoidance of a threatening party is not possible. Although common under abnormal conditions of captivity, in most species this appears to occur rarely under free-ranging conditions. Among their patient series, the figures for humiliation-entrapment and interpersonal loss alone were 62 per cent and 14 per cent respectively. It should be noted that the hierarchical event classification used entailed that many events included in the humiliation-entrapment category involved concurrent interpersonal loss – e.g. separations resulting from rejection in close relationships – and these figures therefore underestimate the true significance of interpersonal loss.

References Ainsworth, M.D.S., Bell, S.M. and Stayton, D.J. (1971) ‘Individual differences in strangesituation behaviour of one-year-olds’ in H.R. Schaffer (ed.) The Origins of Human Social Relations, London: Academic Press. Arieti, S. and Bemporad, J. (1978) Severe and mild depression: the psychotherapeutic approach, New York: Basic Books. Barkow, J. (1975) ‘Prestige and culture: a biosocial interpretation’, Current Anthropology, 16, 553–72. Barkow, J. (1976) ‘Attention structure and the evolution of human psychological characteristics’ in M. R. A. Chance and R. R. Larsen (eds) The Social Structure of Attention, London: Wiley, 203–219.

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Evolved socio-emotional systems 257 Barrett, K. C. (1995) ‘A functionalist approach to shame and guilt’ in J. P. Tangney and K. W. Fischer (eds), Self-Conscious Emotions, New York: Guilford Press, 25–63. Bartholomew, K. and Perlman, D. (1994) Attachment processes in adulthood (Advances in Personal Relationships, Volume 5), London: Jessica Kingsley Publishers. Beck A.T. (1976) Cognitive therapy and the emotional disorders, New York: International Universities Press. Beck, A.T. (1983) ‘Cognitive therapy of depression: new perspectives’ in P.J. Clayton and J. Barrett (eds) Treatment of Depression: old controversies and new approaches, New York: Raven Press. Bifulco, A.T., Moran, P.M., Ball, C. and Bernazzani, O., (2000) ‘Adult attachment style and onset of depression: the attachment style interview (ASI)’ submitted. Blatt, S.J. (1974) ‘Levels of object representation in anaclitic and introjective depression’, Psychoanalytic Study of the Child, 29, 107–57. Blatt, S.J. and Zuroff, D.C. (1992) ‘Interpersonal relatedness and self-definition: two prototypes for depression’, Clinical Psychology Review, 12, 527–62. Blatt, S.J., Quinlan, D.M., Chevron, E.S., McDonald, C. and Zuroff, D. (1982) ‘Dependency and self-criticism: psychological dimensions of depression’, Journal of Consulting and Clinical Psychology, 50, 113–24. Bowlby, J. (1958) ‘The nature of the child’s tie to his mother’, International Journal of Psychoanalysis, 39, 350–73. Bowlby, J. (1969–1980) Attachment and Loss (3 vols), London: The Hogarth Press. Bowlby, J. (1977) ‘The making and breaking of affectional bonds: 1. Aetiology and psychopathology in light of attachment theory’, British Journal of Psychiatry, 130, 201–10. Bowlby, J. (1984) ‘Violence in the family as a disorder of the attachment and caregiving systems’, American Journal of Psychoanalysis, 44, 9–27. Bretherton, I. and Waters, E. (eds) (1985) ‘Growing points in attachment theory’, Monographs of the Society for Research in Child Development, Vol. 50, Chicago: University of Chicago Press. Brown, G.W., (1992) ‘Social support: an investigator based approach’ in H.O.F.Veiel and U. Baumann (eds) The meaning and measurement of social support, Washington: Hemisphere Publishing Corporation, 235–57. Brown, G.W. and Harris, T.O. (1978) Social Origins of Depression, London: Tavistock. Brown, G.W., Bifulco, A. and Harris, T.O. (1987) ‘Life events, vulnerability and onset of depression: some refinements’, British Journal of Pysychiatry, 150, 30–42. Brown, G.W., Harris, T.O. and Copeland, J.R. (1977) ‘Depression and loss’, British Journal of Psychiatry, 130, 1–18. Brown, G.W., Harris, T.O. and Hepworth, C. (1994) ‘Life events and endogenous depression: a puzzle re-examined’, Archives of General Psychiatry, 51, 525–34. Brown, G.W., Harris, T.O. and Hepworth, C. (1995) ‘Loss, humiliation and entrapment among women developing depression: a patient and non-patient comparison’, Psychological Medicine, 25, 7–21. Brown, G.W., Ni’ Bhrolchain, M. and Harris, T.O. (1975) ‘Social class and psychatric disturbance among women in an urban population’, Sociology, 9, 225–54. Bygott, J.D. (1979) ‘Agonistic behavior, dominance and social structure in wild chimpanzees of the Gombe National Park’ in D. Hamburg and E. R. McCown (eds), The Great Apes, Menlo Park, California: Benjamin Cummings, 405–27. Castelfranchi, C. and Poggi, I. (1990) ‘Blushing as discourse: was Darwin wrong?’ in W. R. Crozier (ed.) Shyness and embarrassment: perspectives from social psychology, Cambridge: Cambridge University Press, 230–54.

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258 Martin Eales Clark, C.B. (1977) ‘A preliminary report on weaning among chimpanzees of the Gombe National Park’ in S. Chevalier-Skolnikoff and F.E. Poirier (eds), Primate Biosocial Development, New York: Garland, 235–60. Darwin, C. (1980/1838) ‘The ‘M’ Notebook’ in H.E. Gruber and P.H. Barrett (eds) Darwin on Man, Book 2, Chicago: University of Chicago Press. Davidson, R.J., Ekman, P. Saron, C.D., Senulis, J. and Friesen, W.V. (1990) ‘Approachwithdrawal and cerebral asymmetry: emotional expression and brain physiology’, Journal of Personality and Social Psychology, 58, 330–41. Eales, M.J. (1988) ‘Depression and anxiety in unemployed men’ Psychological Medicine, 18, 935–45. Eales, M.J. (1989) ‘Shame among unemployed men’, Social Science and Medicine, 28, 783–89. Edwards, A., Nazroo, J.Y. and Brown, G.W., (1998) ‘Gender differences in marital support following a shared life event’, Social Science and Medicine, 46, 1077–85. Eibl-Eibesfeldt, I. (1970) Ethology: the biology of behavior, New York: Holt, Rinehart and Winston. Eisenberg, N. (1986) Altruistic emotion, cognition and behavior, Hillsdale, New Jersey: Lawrence Erlbaum. Eisenberg, N., McCreath, H. and Ahn, R. (1988) ‘Vicarious emotional responsiveness and prosocial behavior: their interrelations in young children’, Personality and Social Psychology Bulletin, 14, 298–311. Eisenberg, N., Fabes, R. A., Miller, P. A., Fultz, J., Shell, R., Mathy, R. M. and Reno, R. R. (1989) ‘Relation of sympathy and personal distress to prosocial behavior: a multimethod study’, Journal of Personality and Social Psychology, 58, 55–66. Finlay-Jones, R. (1989) ‘Anxiety’ in G.W. Brown and T.O. Harris (eds), Life Events and Illness, New York: Guilford Press. Fox, R. (1967) ‘In the beginning: aspects of hominid behavioral evolution’, Man, 2, 415–33. Freud, S. (1957/1917) ‘Mourning and melancholia’, Standard Edition of the Complete Psychological Works of Sigmund Freud, Vol. 14, London: Hogarth Press, 237–58. Gardner, R. (1982) ‘Mechanisms in manic-depressive disorder: an evolutionary model’, Archives of General Psychiatry, 39, 1436–41. Gilbert, P. (1989) Human Nature and Suffering, Hove: Lawrence Erlbaum Associates. Gilbert, P. (1992) Depression: The evolution of powerlessness, Hove: Lawrence Erlbaum Associates. Hammen, C., Ellicott, A., Gitlin, M. and Jamison, K.R. (1989) ‘Sociotropy/autonomy and vulnerability to specific life events in patients with unipolar depression and bipolar disorders’, Journal of Abnormal Psychology, 98, 154–60. Hardy, G.E. (1998) ‘A psychodynamic-interpersonal model of depression based on attachment theory’ in S. Checkley (ed.) The management of depression, London: Blackwell. 125–41. Harris, T.O., Brown, G.W. and Bifulco, A. (1990) ‘Loss of parent in childhood and adult psychiatric disorder: a tentative overall model’, Development and Psychopathology, 2, 311–28. Harris, T.O. (1992) ‘Some reflections on the process of social support and the nature of unsupportive behaviours’ in H.O.F.Veiel and U. Baumann (eds) The meaning and measurement of social support, Washington: Hemisphere Publishing Corporation, 171–89. Hatfield, E., Cacioppo, J., and Rapson, R.L. (1993) Emotional contagion, Cambridge: Cambridge University Press. Hazan, C. and Shaver, P.R. (1987) ‘Romantic love conceptualised as an attachment process’, Journal of Personality and Social Psychology, 52, 511–24.

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Evolved socio-emotional systems 259 Heard, D. and Lake, B. (1986) ‘The attachment dynamic in adult life’, British Journal of Psychiatry, 149, 430–9. Heard, D. and Lake, B. (1997) The challenge of caregiving for attachment behaviour, London: Routledge. Hinde, R.A. (1970) Animal Behaviour, 2nd ed, London: McGraw-Hill. Hoffman, M.L. (1981) ‘Is altruism part of human nature?’, Journal of Personality and Social Psychology, 40, 121–37. van Hooff, J. (1967) ‘The facial displays of the catarrhine monkeys and apes’ in D. Morris (ed.) Primate Ethology, London: Weidenfeld and Nicolson, 7–68. Kraemer, G.W. (1992) ‘A psychobiological theory of attachment’, Behavioral and Brain Sciences, 15, 493–541. Krasnegor, N.A. and Bridges, R.S. (eds) (1990) Mammalian parenting: biochemical, neurobiological and behavioral determinants, New York: Oxford University Press. Kunce L.J. and Shaver, P.R. (1994) ‘An attachment-theoretical approach to caregiving in romantic relationships’ in K. Bartholomew and D. Perlman (eds) Attachment processes in adulthood (Advances in Personal Relationships, Volume 5), London: Jessica Kingsley, 205–37. van Lawick-Goodall, J. (1968) ‘The behaviour of free-living chimpanzees in the Gombe National Park’, Animal Behaviour Monographs, 1, 161–311. Leary, M.R. and Meadows, S. (1991) ‘Predictors, elicitors, and concomitants of social blushing’, Journal of Personality and Social Psychology, 60, 254–62. Leary, M.R., Britt, T. W., Cutlip, W. D., and Templeton, J. L. (1992) ‘Social blushing’, Psychological Bulletin, 112, 446–60. Lehman, D.R., Wortman, C.B. and Williams, A.F. (1987) ‘Long-term effects of losing a spouse or child in a motor vehicle crash’, Journal of Personality and Social Psychology, 52, 218–31. Lewinsohn, P.M. (1974) ‘A behavioral approach to depression’ in R.J. Friedman and M.M. Katz (eds) The Psychology of Depression: Contemporary Theory and Research, New York: Winston-Wiley. McDonald, K. (1991) ‘A perspective on Darwinian psychology: the importance of domaingeneral mechanisms, plasticity, and individual differences’, Ethology and Sociobiology, 12, 449–80. McDonald, K. (1992) ‘Warmth as a developmental construct: an evolutionary analysis’, Child Development, 63, 753–73. McDougall, W. (1945/1908) An introduction to social psychology, 26th edition, London: Methuen. McDougall, W. (1926) An outline of abnormal psychology, London: Methuen. MacLean, P.D. (1990) The Triune Brain in Evolution, New York: Plenum Press. Nietzel, M.T. and Harris, M.J. (1990) ‘Relationship of dependency and achievement/autonomy to depression’, Clinical Psychology Review, 10, 279–97. Öhman, A. (1986) ‘Face the beast and fear the face: animal and social fears as prototypes for evolutionary analyses of emotion’, Psychophysiology, 23, 123–45. Owen, G., Fulton, R. and Markusen, E. (1978) ‘Death at a distance: a study of family survivors’, Omega – Journal of Death and Dying, 13, 191–224. Parkes, C.M. (1972) Bereavement: studies of grief in adult life, London: Tavistock. Paykel, E.S., Myers, J.K., Dienelt, M.N., Klerman, G., Lindenthal, J.J. and Pepper, M.P. (1969) ‘Life events and depression: a controlled study’, Archives of General Psychiatry, 21, 753–60.

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260 Martin Eales Price, J. (1969) ‘Neurotic and endogenous depression: a phylogenetic view’, British Journal of Psychiatry, 114, 119–20. Price, J., Sloman, L., Gardner, R., Gilbert, P. and Rohde, P. (1994) ‘The social competition hypothesis of depression’, British Journal of Psychiatry, 164, 309–15. Prudo, R., Brown, G.W., Harris T.O. and Dowland, J. (1981) ‘Psychiatric disorder in a rural and an urban population: 2. Sensitivity to loss’, Psychological Medicine, 11, 601–16. Robins, C.J. (1990) ‘Congruence of personality and life events in depression’, Journal of Abnormal Psychology, 99, 393–7. Robins, C.J. and Block, P. (1988) ‘Personal vulnerability, life events, and depressive symptoms: a test of a specific interactional model’, Journal of Personality and Social Psychology, 54, 847–52. Robins, C.J. and Luten, A. (1991) ‘Sociotropy and autonomy: differential patterns of clinical presentation in unipolar depression’, Journal of Abnormal Psychology, 100, 74–7. Robins, C.J., Block, P. and Peselow, E.D. (1989) ‘Relations of sociotropic and autonomous personality characteristics to specific symptoms in depressed patients’, Journal of Abnormal Psychology, 98, 86–8. Rosenblatt, J.S. and Snowdon, C.T. (eds) (1996) Parental care: evolution, mechanisms and adaptive significance, Advances in the Study of Behavior, Volume 25, San Diego: Academic Press. Scheff, T.J. (1988) ‘Shame and conformity: the deference-emotion system’, American Sociological Review, 53, 395–406. Schneirla, T.C. (1959) ‘An evolutionary and developmental theory of biphasic processes underlying approach and withdrawal’, Nebraska Symposium on Motivation, 1–43. Semin, G.R. and Manstead, A.S.R. (1982) ‘The social implications of embarrassment displays and restitution behavior’, European Journal of Social Psychology, 12, 367–77. Shapiro, L., and Epstein, W. (1998) ‘Evolutionary theory meets cognitive psychology: a more selective perspective’, Mind and Language, 13, 171–94. Singh, B. and Raphael, B. (1981) ‘Post-disaster morbidity of the bereaved: a possible role for preventive psychiatry’, Journal of Nervous and Mental Disease, 169, 203–12. Strathern, A. (1975) ‘Why is shame on the skin?’, Ethnology, 14, 347–56. [reprinted in J. Blacking (ed.) The Anthropology of the Body, London: Academic Press, 1977.] Suomi, S.J. (1995) ‘Influence of attachment theory on ethological studies of biobehavioral development in non-human primates’ in S. Goldberg, R. Muir, and J. Kerr (eds), Attachment Theory: Social, developmental and clinical perspectives, Hillsdale, New Jersey: The Analytic Press. Tooby, J. and Cosmides, L. (1992) ‘The psychological foundations of culture’ in J. Barkow, L. Cosmides and J. Tooby (eds), The Adapted Mind: Evolutionary Psychology and the Generation of Culture, Oxford: Oxford University Press. de Waal, F. (1982) Chimpanzee politics, London: Unwin. de Waal, F.B.M. (1986) ‘The integration of dominance and social bonding in primates’, Quarterly Review of Biology, 61, 459–79.

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Part IV

Psychosocial factors in conditions other than depression

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15 Life stress and bipolar disorder Is the dimension of social rhythm disruption specific to onset of manic episodes? Ellen Frank, David J. Kupfer, and Susan Malkoff-Schwartz The search for the aetiology and most efficacious treatment of affective illnesses, including manic-depressive (bipolar), should involve the integration of biologic, genetic, and psychosocial components. Within the last decade, several investigative groups have demonstrated a relationship between life stress and exacerbations in the course of bipolar disorder (e.g. Ellicott et al., 1990; Joffe et al., 1989; Hammen and Gitlin, 1997). Although some of these investigations have evaluated life events in a manner that is philosophically consistent with the work of the Bedford College group, very few have employed the full Life Events and Difficulties Schedule (LEDS – Brown and Harris, 1978a) protocol. Furthermore, methodologic limitations are common in the literature of life stress and onset of bipolar disorder (see Johnson and Roberts, 1995). In many past studies, for example, stressful life events were ascertained by chart review (e.g. Ambelas, 1979, 1987; Ambelas and George, 1986; Clancy et al., 1973; Davenport and Adland, 1982; Leff et al., 1976) and episode onset was determined by date of hospital admission (Ambelas, 1979, 1987; Kennedy et al., 1983; Mayo, 1970). In others, whether events were a consequence of bipolar illness was not assessed (Glassner et al.,1979; Glassner and Haldipur,1983; Hall et al., 1977; Joffe et al., 1989; Thompson and Hendrie, 1972) and control groups were not employed (Davenport and Adland, 1982; Dunner et al., 1979; Leff et al., 1976; Mayo, 1970). Even among investigations that employed self-report questionnaires and/or semi-structured interviews to identify severely threatening life events, dated episodes from onset of first symptoms, omitted illness-related events, and used appropriate control groups, results are inconsistent. Specifically, pre-onset rates of severe life events have been found to be significantly greater than those among control subjects or during control periods in some (Bebbington et al., 1993a; Hunt et al.,1992) but not all (Chung et al., 1986; McPherson et al., 1993; Sclare and Creed, 1990) carefully conducted investigations. Moreover, depressive onsets in addition to manic onsets were investigated in only two of these studies (Hunt et al., 1992; McPherson et al.,1993). Since it has been well documented that severe life events are important factors in the onset of unipolar depression (Brown and Harris, 1978b, 1989), it is surprising that the role of stress in the onset of depressive

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264 Ellen Frank and colleagues bipolar episodes has been studied so infrequently. The role of severe life events in the onset of bipolar disorder, then, remains equivocal, especially for depressive onsets. We have conducted two investigations of the role of stressful life events in onset of bipolar episodes using the LEDS methodology. These investigations have occurred in the context of a randomised controlled trial of acute and maintenance treatment of patients with bipolar I disorder. This trial compares the efficacy of a newly developed psychotherapy, Interpersonal and Social Rhythm Therapy (IPSRT – Frank et al., 1994) with standard clinical management in appropriately medicated patients presenting in an acute episode of mania or depression. Subjects are treated to remission and then provided with prophylactic maintenance treatment for a period of two years. In this chapter we will describe our application of LEDS methodology in this study sample to address the following questions: 1 2

whether stressful life events relate differentially to the onset of manic versus depressive and cycling bipolar episodes and whether other aspects of life events besides threat/severity could be associated with onset of bipolar episodes.

Social rhythm disruption Because our psychotherapeutic intervention was based on a theory that posits that disruptions in social routine may be implicated in the provocation of depressive and, particularly, manic recurrences, we developed a rating scheme for LEDSdefined life events which assesses the extent to which an event would be expected to lead to disruption in social routines or rhythms. We have hypothesised that the degree of disruption in social routines associated with an event may play a significant role in the onset of affective episodes, regardless of the psychological threat (severity) associated with that event (Ehlers et al., 1988; Ehlers et al., 1993). The idea of ‘social rhythm disruption (SRD) events’ was borne out of the hypothesis that disturbances in social rhythms or routines may lead to disruptions in circadian rhythms, which then may potentiate the onset of affective episodes in vulnerable individuals (Ehlers et al., 1993). This theory evolved from observations that social routines (e.g. timing of sleeping, eating and exercise) help to entrain circadian rhythms (Aschoff, 1981; Ehlers et al., 1988) and, further, that disruptions in circadian rhythms have been linked with the pathogenesis of both depression and mania (Goodwin and Jamison, 1990; Leibenluft and Frank, in press; Wehr and Wirz-Justice, 1981). SRD events have been called social zeitstorers (time disturbers), and include such hypothesised sources of circadian rhythm dysfunction as transmeridian flight, shift work, having a newborn baby in the home, and marital separations (Ehlers et al., 1993). SRD events could also be of low threat according to standard LEDS rating criteria. For example, a job reassignment that involved no change in responsibilities or co-worker group, but required a twohour change in wake-up time would be low on conventional LEDS ratings of threat, but high on social rhythm disruption.

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Life stress and bipolar disorder 265 We developed SRD ratings because we felt that a clearer understanding of the influence of social rhythm disruptions on bipolar episode onsets would be an important contribution to our understanding of the biologic and psychosocial precipitants of affective episode onset, and would inform both treatment and ongoing research in the etiology of bipolar episode onsets. The cyclical nature of bipolar disorder and diurnal fluctuations in mood observed in depressed patients suggested that disruptions in biological rhythms may be instrumentally involved in the pathogenesis of affective disorders (Ehlers et al., 1993). The application of LEDS methodology to the examination of the relation between social rhythm disruption and onset of bipolar disorder demonstrates a unique opportunity to apply a psychosocial measure to help elucidate psychobiologic mechanisms involved in the initiation of bipolar episodes.

Two studies of life events, social rhythm disruption, and bipolar disorder The two studies of life events, SRD, and bipolar disorder that we conducted involved male and female patients recruited from medical referrals, self-referrals, and public information campaigns, who were participants in the randomised controlled trial of acute and maintenance treatment of patients with bipolar I disorder discussed above (MH 29618, E. Frank P.I.). Diagnoses at study entry, and episode onset dates based on the presence of the first depressive or manic symptom, were ascertained by structured clinical interviews (Schedule for Affective Disorders and Schizophrenia – Lifetime version (SADS-L—Spitzer, 1978) or Structured Clinical Interview for Axis I DSM-IV Disorders (SCID – First et al., 1995) conducted by social workers or research nurse clinicians. Classifications of the course of index episodes from onset until study entry were also made during these interviews. Accordingly, index episodes were classified into one of seven possible episode types (primarily manic, primarily depressed, manic cycling to depressed, depressed cycling to manic, manic and cycling, depressed and cycling, and mixed). Upon study entry, subjects were required to have a lifetime diagnosis of bipolar 1 disorder and to be currently experiencing a Definite Major Depressive Episode or Definite Manic Episode per Research Diagnostic Criteria (RDC – Spitzer et al., 1978) or SCID criteria. In addition to the current index episode, subjects had to have had at least two prior episodes of bipolar disorder, with at least one of those episodes occurring within five years of the index episode. A period of remission of at least twelve weeks between index episode onset and the most recent past bipolar episode was also required. Other inclusion criteria included scoring > 7 on the Raskin Severity of Depression Scale (Raskin et al., 1969; Prien et al., 1984) and > 15 on the seventeen-item Hamilton Rating Scale for Depression (HRS-D – Hamilton, 1960); or > 7 on the Raskin Severity of Mania Scale (Raskin et al., 1969; Prien et al., 1984) and > 15 on the Bech-Rafaelsen Mania Scale (Bech et al., 1979; Bech et al., 1986). Exclusion criteria included:

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266 Ellen Frank and colleagues 1 2

3 4 5 6 7

meeting conventional criteria for rapid-cycling (> four episodes per year) meeting RDC criteria for any psychiatric diagnoses other than mania or depression in the past two and a half years (with the exception of anxiety disorders and phobias) having a history of chronic drug or alcohol abuse within the past three years meeting criteria for schizophrenia, schizoaffective disorder, organic affective syndrome, or unspecified functional psychosis meeting full criteria for borderline or antisocial personality disorder having serious medical illness in women, being pregnant or refusing to use contraception.

Subjects entered the study in an acutely ill state, and were randomly assigned to one of four treatment strategies combining appropriate pharmacotherapy with various combinations of modified interpersonal psychotherapy (IPSRT) and/or medication clinic visits. Patients were seen weekly until stabilised for four weeks, after which they were seen biweekly for twelve weeks and then monthly for two years. At the time of the life events interview, all subjects were remitted but still in treatment in accordance with the larger study protocol. Informed consent was given by all subjects. Stressful life events occurring during the period between interview date and one year prior to onset of the index episode were assessed using the Bedford College Life Events and Difficulties Schedule (LEDS – Brown and Harris, 1978a). The LEDS interview was conducted after patients had been in treatment for more than twelve weeks and had achieved remission of acute symptomatology. Such symptom stabilisation was operationalised as the attainment of scores of < 7 on the HRS-D and Bech-Rafaelsen Mania Scale for a duration of at least three weeks. LEDS interviews were conducted by interviewers with bachelor’s or master’s degrees who were trained either by George Brown and Tirril Harris at Bedford College, London, or by their trainees at Western Psychiatric Institute and Clinic, Pittsburgh, Pennsylvania. LEDS interviewers by necessity were aware of patient status at the time of the interview, but unaware of specific pre-onset and control periods under study, and were not involved in clinical assessment or treatment of study participants. Life events were rated for severity during a consensus panel meeting attended by the initial interviewer plus one or two additional trained LEDS raters. Members of the consensus panel were unaware of onset date and periods of study. According to conventional LEDS definitions, ‘severe events’ were all life events rated 1, along with those rated 2 and directly focused on the subject, on a four-point scale of long-term threat (the threat of an event ten to fourteen days after it occurs). Severe events were also rated on the degree to which they could be considered a manifestation of prodromal symptomatology of a full-blown bipolar episode. Accordingly, any event that was thought to be a consequence of current bipolar symptoms was not included in analyses. Events were also rated on independence, that is, the degree to which their occurrence was independent of the subject’s

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Life stress and bipolar disorder 267 influence. Events rated either independent or possibly independent were included in analyses. Each stressful life event identified by the LEDS was further subjected to the additional rating of Social Rhythm Disruption (SRD). More specifically, once occurrences of any severity had been identified by the LEDS as meeting criteria for events or incidents, the event or incident narrative that was written as part of the LEDS chart was then reviewed and rated for SRD. The SRD rating was developed in our research group, and reflects the degree to which a given event potentially and acutely affects the sleep-wake cycle. Each LEDS-identified event or incident, then, was rated for the degree to which, because of its timing or social disruptiveness, it was thought to be likely to interfere with an individual’s sleep or daily routines. For example, events that likely contribute to acute sleep disruption (e.g. going to the emergency room at 1 am; overseas travel) or those that involve a desynchronisation in routine that could lead to sleep disruption or change in sleep/wake cycle (e.g. becoming unemployed; starting full-time college) would receive high SRD ratings (Malkoff-Schwartz et al., 1998). Similar to LEDS ratings, SRD ratings are determined by consensus, are made with regard to the particular subject’s biographical context, and are guided by delineated criteria and examples. Also similar to life stress ratings, SRD ratings range from one (marked) to four (little or no disruption). A conservative approach was taken to the rating of SRD events, such that significant potential change in sleep disruption or routine was necessary for an event or incident to receive an SRD rating above four. Any LEDS event rated 1–3 on SRD was included in analyses, and illness-dependent events were excluded from analyses. In two reliability assessments of ratings of subsets of SRD events conducted in our research group, the SRD ratings have been shown to have high inter-rater reliability (Kappa = .94 and .87). Depending on context, the following criteria were generally used to rate SRD: events that involve staying awake all night or marked disruption in routine (e.g. starting a night shift job; new baby in household) are rated SRD=1; events that involve disrupted sleep in the middle of the night, going to sleep much later or rising much earlier than usual, or moderate disruption in routine (e.g. being hospitalised overnight; any vacation or travel involving a time zone change of over two hours; ending cohabiting with partner) are rated SRD=2; events that involve going to sleep somewhat later or rising somewhat earlier than usual, or some disruption in routine (e.g. having outpatient medical procedure requiring early morning admission to hospital; starting full-time college classes) are rated SRD=3; events that involve disruptions of social routines or sleep that are only probable (e.g. starting and ending non-cohabiting relationships) or tend to be routinising (e.g. starting a fulltime job after being unemployed) are rated SRD=4 (Malkoff-Schwartz et al., 1999). Study 1 The first preliminary study (Malkoff-Schwartz et al., 1998) was conducted in order to examine the role of social rhythm disruption events and severely

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268 Ellen Frank and colleagues threatening events in the onset of depressive and manic bipolar episodes. The specific aim of this study was to determine whether the proportion of subjects experiencing at least one SRD or severe event during an eight-week pre-onset period would be significantly greater than the proportion of subjects experiencing such types of life stress during an eight-week episode-free control period. Whether manic and depressive onsets would be differentially associated with pre-onset rates of SRD or severe events was also investigated. Control periods were selected to be as close as possible to the last eight weeks of the pre-onset year, but were moved earlier in time if definite bipolar symptomatology was occurring during the optimal control period. As a result, the average control period was between weeks 41–48 prior to onset. Because we were interested in studying the provocation of clearly manic and clearly depressive episodes, we selected for this preliminary investigation the first thirty-nine subjects who 1 2 3

had an index episode characterised by a single polarity from the onset of the episode until study entry (N=20 manic and 19 depressed), had achieved remission of their index episode, had completed the LEDS interview.

One-tailed McNemar’s tests were used for within-subject analyses (pre-onset versus control period), and two-tailed Fisher’s exact X2 tests were used for between-subject analyses (manic versus depressed patients, pre-onset period). Analyses revealed that, when all bipolar subjects were considered together, 41 per cent of bipolar subjects experienced at least one SRD event in the pre-onset period, compared to 21 per cent who had at least one SRD event in the control period (p=.05). Considering manic and depressed subjects separately, 65 per cent of manic subjects experienced at least one SRD event in the pre-onset period, versus 20 per cent who experienced at least one SRD event in the control period (p=.01). In contrast, for depressed patients, 16 per cent had SRD events in the preonset period, while 21 per cent had SRD events in the control period (p=.50). Between-group comparisons confirmed a unique association between SRD and onset for manic episodes, as more manic than depressed subjects had at least one SRD event during the pre-onset period (p=.003). Looking next at traditionally defined severe events, 21 per cent of all bipolar subjects combined were found to have had at least one severe event in the pre-onset period, compared to 8 per cent with at least one severe event in the control period (p=.06). When considered separately, 25 per cent of manic and 16 per cent of depressed subjects experienced at least one severe event in the pre-onset period, compared to 10 per cent of manic and 5 per cent of depressed subjects who experienced a severe event in the control periods (ps=.19 and .25 for manic and depressed subjects, respectively). Finally, manic and depressed subjects did not differ in rates of subjects with at least one severe event in the eight-week pre-onset period (p=.69). The results of this preliminary investigation suggested that severe events may be important in the onset of bipolar episodes regardless of polarity, whereas social

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Life stress and bipolar disorder 269 rhythm disruption, a measure of potential sleep disruption, is specific to the onset of mania. The interesting findings in this investigation that subjects with manic onsets had significantly more pre-onset events involving social rhythm disruption relative to both their own episode-free control periods and to pre-onset periods of patients with depressive episodes were regarded as support for the hypothesis that acute sleep disruption is related to onsets of mania. Although it had been hypothesised that social rhythm disruptions that could ultimately affect the sleep/wake cycle could lead to onset of affective episodes in vulnerable individuals (Ehlers et al., 1993; Wehr and Wirz-Justice, 1981), this was the first time that the measurement of such social rhythm disruption in community-dwelling patients had been attempted. The findings were regarded as consistent with the hypothesis posited by Wehr and colleagues (Wehr et al., 1987) that psychosocial factors that appear to trigger manic onsets could do so via their capacity to cause sleep deprivation, and that sleep reduction may be the final common pathway for the onset of mania. These findings were also consistent with our clinical observations that manic episodes appear to be more directly associated with acute life events than bipolar depressive episodes. The role of life events in the precipitation of depressive episodes, however, remained unclear. Study 2 The second investigation (Malkoff-Schwartz et al., 1999) expanded on the results of the first, and was conducted in order to determine whether other types of bipolar episode onsets (e.g. depressive and cycling) or unipolar depressive episode onsets would be related to SRD and severe events similarly to manic onsets. We also aimed to examine the timing between SRD or severe events and episode onsets. Subjects in this investigation were sixty-six bipolar patients (thirty-nine of whom were the same as in the preliminary investigation) who were participants in the randomised trial of maintenance therapies in bipolar disorder for patients aged 21–65 described above; and forty-four unipolar depressed patient participants in a study of biological and social rhythms for individuals with recurrent depression aged 20–50 (MacArthur Foundation grant, D. Kupfer PI). Patients in the unipolar protocol received interpersonal therapy (IPT – Klerman et al., 1984) alone, followed by pharmacotherapy if remission was not achieved with IPT. In both research protocols, research nurse clinicians or social workers conducted structured clinical interviews (SADS-L or SCID) to determine initial diagnoses, index episode onset dates, and onset and offset dates of past affective episodes. Study inclusion criteria and methodology for the bipolar patient sample was the same as described above. In the unipolar study, subjects were eligible for study participation if they were experiencing a Definite Major Depressive Episode per RDC criteria, and if they scored over fifteen on the seventeen-item HRS-D at study entry. Additionally, subjects must have had at least one prior episode of unipolar depression within two and a half years of the index episode, and a remission period between index episode onset and the most recent past unipolar episode of at least ten weeks. Informed consent was given by all subjects.

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270 Ellen Frank and colleagues Since, in the first investigation, pre-onset severe and SRD events were not found to be associated with bipolar depressive onsets, and since it is likely that depressive onsets take longer to develop than manic onsets, in this second investigation we decided to consider both eight- and twenty-week pre-onset periods (i.e. weeks 1–8 and 1–20 prior to onset, respectively). We also selected eight- and twenty-week episode-free control periods from the one-year pre-onset period of each subject that were as close as possible to the beginning of the pre-onset year (ideally during weeks 45–52 and 33–52 prior to onset). Aiming for this time period would help ensure that control periods were as comparable as possible to corresponding preonset periods with respect to season of the year. The actual eight- and twenty-week control periods occurred, on average, during weeks 38–45 and 43–50 prior to onset (respectively), reflecting adjustments made to control periods when other affective episodes were occurring during optimal control periods. The four groups of subjects in this investigation were: bipolar manic (N=21), bipolar depressed (N=21), bipolar cycling (N=24), and unipolar depressed subjects (N=44). One-tailed McNemar’s tests were used for within-subject analyses (pre-onset versus control period), and two-tailed Fisher’s exact X2 tests were used for between-subject analyses (between-group comparisons at the pre-onset period). Logistic regression analyses were conducted when necessary to include categorical and continuous covariates in the between-subject analyses. We also employed backward survival analyses using the Kaplan-Meier life table method (Kaplan and Meier, 1958) to examine the timing of SRD or severe events in episode onsets. This method has previously been used to examine how life events temporally relate to episode onset (Bebbington et al.,1993b; Sherrill et al., 1997). The median time (backward in time) from onset to the first pre-onset SRD or severe event was compared between the groups with the log rank test. We found that 62 per cent of manic subjects experienced at least one SRD event in the pre-onset period, versus 29 per cent of the same subjects in an eight-week control period (p=0.02). In addition, during eight-week pre-onset periods, more manic (62 per cent) than bipolar depressed (19 per cent), bipolar cycling (8 per cent), and unipolar depressed subjects (25 per cent) experienced at least one SRD event (p’s=0.01, 0.0003, and 0.006, respectively). Similarly, more manic (68 per cent) than bipolar cycling (12 per cent) and unipolar depressed subjects (39 per cent) experienced at least one SRD event during 20–week pre-onset periods (p’s=0.0008 and 0.05, respectively). Survival analyses revealed that manic subjects experienced SRD events closer to onset than the subjects in the other affective groups (p=0.0001). In fact, 50 per cent of manic subjects experienced at least one SRD event within six weeks of onset. Results of analyses of severe events indicated that more manic (47 per cent) than bipolar cycling (12 per cent) and unipolar depressed subjects (19 per cent) experienced at least one severe event during the twenty-week pre-onset period (p’s=0.03 and 0.06, respectively). No other comparisons were statistically significant. Finally, between-group severe event and SRD analyses were re-run controlling for baseline group differences in age and number of prior affective episodes. Most results remained unchanged.

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Life stress and bipolar disorder 271 With the inclusion of unipolar depressed and bipolar cycling comparison groups, and by adding a twenty-week pre-onset period to eight-week pre-onset periods of study, the results of this second investigation confirmed a unique association between social rhythm disruption and onset of manic episodes of bipolar disorder. An association between onset of manic episodes and severe events occurring within twenty weeks of onset was also observed. Taken together, these findings suggest that SRD and severely threatening life events may be uniquely related to onset of bipolar manic episodes relative to onsets of other types of affective episodes. Surprisingly, despite the strong literature support for an association between severe events and onset of unipolar depression (e.g. Brown and Harris, 1978b; 1989), we did not observe such an association in this investigation. Perhaps an analysis of the role of severe difficulties could have fruitfully supplemented this finding, while the inclusion of a non-psychiatric control group might have shed light on the association between severe life events and onset of unipolar depression by revealing whether Pittsburgh is an area with a particularly low rate of severe events compared to other sites cited in the literature.

Conclusions The results of both studies confirm an association between life events characterised by social rhythm disruption and onset of manic episodes, and identify an association between severely threatening life events and onset of manic episodes. These findings contribute to our understanding of the biologic and psychosocial precipitants of affective episodes, and inform both treatment and ongoing research in the etiology of bipolar episode onsets. For example, the SRD observations suggest that psychotherapies that encourage stabilisation of social rhythms (e.g. IPSRT) may help to prevent or mitigate manic recurrences. Further, the findings help to advance our understanding of the timing of episode onsets in recurrent affective illnesses such as bipolar disorder, by indicating specifically that the onset of episodes of bipolar mania may be uniquely sensitive to environmental events. Lastly, the identification of a link between social rhythm disruption and onset of bipolar episodes helps to advance our understanding of the etiopathogenesis of bipolar disorder, by suggesting a link between psychosocially related disruptions in sleep and onset of manic episodes. We find it gratifying that the application of a new rating protocol to life event narratives generated by the LEDS has enabled us to further our understanding of the interplay between biological rhythms and affective episode onset. We believe this speaks for the unique nature of the LEDS as an instrument and a technique that allows for constant expansion and increasing levels of complexity in understanding the multifaceted relationship between life events and both conventional medical and psychiatric illnesses. We look forward to the many opportunities a robust, reliable instrument such as the LEDS can provide as we continue to pursue our understanding of the role of life events in bipolar disorder.

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272 Ellen Frank and colleagues

Acknowledgements The research reported in this chapter was supported by the NARSAD Distinguished Investigator Award (EF), NIMH grants MH-29618 (EF) and MH-30915 (DJK), and the MacArthur Foundation Network on the Psychobiology of Affective Disorders (Drs. Kupfer and Frank).

References Aschoff, J. (1981) Handbook of Behavioral Neurobiology, Volume 4, Biological Rhythms, New York: Plenum Press. Ambelas, A. (1979) ‘Psychologically stressful events in the precipitation of manic episodes’, British Journal of Psychiatry, 135, 15–21. —— (1987) ‘Life events and mania: A special relationship’, British Journal of Psychiatry, 150, 235–40. Ambelas, A. and George, M. (1986) ‘Predictability of course of illness in manic patients positive for life events’, Journal of Nervous and Mental Disease, 174, 693–95. Bebbington P., Wilkins, S., Jones, P., Foerster, A., Murray, R., Toone, B. and Lewis, S. (1993a) ‘Life events and psychosis: initial results from the Camberwell Collaborative Psychosis Study’, British Journal of Psychiatry, 162, 72–9. Bebbington, P.E., De, G., MacCarthy, G., Wykes, T., Brugha, T., Sturt, P. and Potter, J. (1993b) ‘Stress incubation and the onset of affective disorders’, British Journal of Psychiatry, 362, 358–62. Bech, P., Bolwig, T.G., Kramp, P. and Rafaelsen, O.J. (1979) ‘The Bech-Rafaelsen Mania Scale and the Hamilton Depression Scale’, Acta Psychiatrica Scandinavica, 59, 420–30. ——, Kastrup, M. and Rafaelsen, O.J. (1986) ‘Mini-compendium of rating scales for states of anxiety, depression, mania, and schizophrenia with corresponding DSM-III syndromes’, Acta Psychiatrica Scandinavica 73, suppl. 326, 7–36. Brown, G.W. and Harris, T.O. (1978a) The Bedford College Life-Events and Difficulty Schedule: Directory of Contextual Threat Ratings of Events, London: Bedford College, University of London. —— and Harris, T. (1978b) Social Origins of Depression: A Study of Psychiatric Disorder in Women, New York: Free Press. —— and Harris, T. (1989) ‘Depression’ in G.W. Brown and T. Harris (eds) Life Events and Illness, New York: Guilford Press. Chung, R.K., Langeluddecke, P. and Tennant, C. (1986) ‘Threatening life events in the onset of schizophrenia, schizophreniform psychosis and hypomania’, British Journal of Psychiatry, 148, 680–85. Clancy, J., Crowe, R., Winokur, G. and Morrison, J. (1973) ‘The Iowa 500: precipitating factors in schizophrenia and primary affective disorder’, Comprehensive Psychiatry, 14, 197–202. Davenport, Y.B. and Adland, M.L. (1982) ‘Postpartum psychoses in female and male bipolar manic-depresesive patients’, American Journal of Orthopsychiatry; 52, 288–97. Dunner, D.L., Patrick, V. and Fieve, R.R. (1979) ‘Life events at the onset of bipolar affective illness’, American Journal of Psychiatry, 136, 508–11. Ehlers, C.L., Frank, E. and Kupfer, D.J. (1988). ‘Social zeitgebers and biological rhythms: A unified approach to understanding the etiology of depression’, Archives of General Psychiatry, 45, 948–52.

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Life stress and bipolar disorder 273 Ehlers, C.L., Kupfer, D.J., Frank, E. and Monk, T.H. (1993) ‘ Biological rhythms and depression: The role of zeitgebers and zeitstorers’, Depression, 1, 285–93. Ellicott, A., Hammen, C., Gitlin, M., Brown, G. and Jamison, K. (1990) ‘Life events and the course of bipolar disorder’, American Journal of Psychiatry, 147, 1194–198. First, M.B., Spitzer, R.L., Gibbon, M. and Williams, J.B.W. (1995) Structured Clinical Interview for DSM-IV Axis I Disorders – Patient Edition (SCID-I/P), Version 2.0, New York: Biomedics Research Department, New York State Psychiatric Institute. Frank, E., Kupfer, D.J., Ehlers, C.L., Monk, T.H., Cornes, C., Carter, S. and Frankel, D. (1994) ‘Interpersonal and social rhythm therapy for bipolar disorder: Integrating interpersonal and behavioral approaches’, The Behavior Therapist, 17, 143–49. Goodwin, F.K. and Jamison, K.R. (1990) Manic-Depressive Illness, Oxford: Oxford University Press. Glassner, B. and Haldipur, C.V. (1983) ‘Life events and early and late onset of bipolar disorder’, American Journal of Psychiatary, 140, 215–17. ——, Haldipur, C.V. and Dessauersmith, J. (1979) ‘Role loss and working-class manic depression’, Journal of Nervous and Mental Disease, 167, 530–41. Hall, K.S., Dunner, D.L., Zeller, G. and Fieve, R.R. (1977) ‘Bipolar illness: A prospective study of life events’, Comprehensive Psychiatry, 18, 497–505. Hamilton, M. (1960) ‘A rating scale for depression’, Journal of Neurology, Neurosurgery and Psychiatry, 23, 56–62. Hammen, C. and Gitlin, M. (1997). ‘Stress reactivity in bipolar patients and its relation to prior history of disorder’, American Journal of Psychiatry, 154, 856–57. Hunt, N., Bruce-Jones, W. and Silverstone, T. (1992) ‘Life events and relapse in bipolar affective disorder’, Journal of Affective Disorders, 25, 13–20. Joffe, R.T., MacDonald, C.M. and Kutcher, S.P. (1989) ‘Life events and mania: A casecontrolled study’, Psychiatry Research, 30, 213–16. Johnson, S.L. and Roberts, J.E. (1995). ‘Life events and bipolar disorder: Implications from biological theories’, Psychological Bulletin, 117, 434–49. Kaplan, E.L. and Meier, P. (1958). ‘Nonparametric estimation from incomplete observations’, Journal of the American Statistical Association, 53, 457–81. Kennedy, S., Thompson, R., Stancer, H.C., Roy, A. and Persa, E. (1983) ‘Life events precipitating mania’, British Journal of Psychiatry, 142, 398–403. Klerman, G.L., Weissman, M.M., Rounsaville, B.J. and Chevron, E.S. (1984) Interpersonal Psychotherapy of Depression, New York: Basic Books. Leff, J.P., Fischer, M. and Bertelson, A.C. (1976) ‘A cross-national epidemiological study of mania’, British Journal of Psychiatry, 129, 428–42. Leibenluft, E. and Frank, E. (in press) ‘Circadian rhythms in affective disorders’ in J.S. Takahashi, F. Turek and R.Y. Moore (eds) Handbook of Behavioral Neurobiology: Circadian Clocks, New York: Plenum Publishing. Malkoff-Schwartz, S., Frank, E., Anderson, B., Sherrill, J.T., Siegel, L., Patterson, D. and Kupfer, D.J. (1998) ‘Stressful life events and social rhythm disruption in the onset of manic and depressive bipolar episodes: A preliminary investigation’, Archives of General Psychiatry, 55, 702–7. ——, Frank, E., Anderson, B.P., Hlastala, S.A., Luther, J.F., Sherrill, J.T., Houck, P.R. and Kupfer, D.J. (1999) ‘Social rhythm disruption and stressful life events in the onset of bipolar manic, depressed, and cycling, and unipolar depressed episodes’, poster presented at the Third International Conference on Bipolar Disorder, Pittsburgh, PA. Mayo, J.A. (1970) ‘Psychosocial profiles of patients on lithium treatment’, International Pharmacopsychiatry, 5, 190–202.

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274 Ellen Frank and colleagues McPherson, H., Herbison, P. and Romans, S. (1993). ‘Life events and relapse in established bipolar affective disorder’, British Journal of Psychiatry, 163, 381–85. Prien, R.R., Kupfer, D.J., Mansky, P.A., Small, J.G., Tuason, V.B., Voss, C.B. and Johnson, W.E. (1984) ‘Drug therapy in the prevention of recurrences in unipolar and bipolar affective disorders’, Archives of General Psychiatry, 41,1096–104. Raskin, A., Schulterbrandt, J., Reatig, N. and McKeon, J.J. (1969) ‘Replication of factors of psychopathology in interview, ward behavior, and self-report ratings of hospitalised depressives’, Journal of Nervous and Mental Diseases, 148, 87–98. Sclare, P. and Creed, F. (1990) ‘Life events and the onset of mania’, British Journal of Psychiatry, 156, 508–14. Sherrill, J.T., Anderson, B., Frank, E., Reynolds, C. F. III, Tu, X. M., Patterson, D., Ritenour, A. and Kupfer, D. J. (1997) ‘Is life stress more likely to provoke depressive episodes in women than in men?’, Depression and Anxiety, 6, 95–105. Spitzer, R.L. (1978) Schedule for Affective Disorders and Schizophrenia – Lifetime Version (SADS-L), New York: New York State Psychiatric Institute. Spitzer, R. L., Endicott, J. and Robins, E. (1978) ‘Research Diagnostic Criteria: Rationale and reliability’, Archives of General Psychiatry, 35, 773–82. Thomson, K.C. and Hendrie, H.C. (1972). ‘Environmental stress in primary depressive illness’, Archives of General Psychiatry, 26, 130–32. Wehr, T.A. and Wirz-Justice, A. (1981) ‘Internal coincidence model for sleep deprivation and depression’ in W.P. Koella (ed.) Sleep 1980, Basel, Switzerland: Karger. ——, Sack, D.A. and Rosenthal, N.E. (1987) ‘Sleep reduction as a final common pathway in the genesis of mania’, American Journal of Psychiatry, 144, 201–04.

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16 The study of life events Clarifying the concept of psychosomatic disorders Francis Creed

Introduction The concept of a number of ‘psychosomatic disorders’ (e.g. peptic ulcer, rheumatoid arthritis) used to imply that psychological and social variables were important only in certain, distinct disorders. This narrow approach has been replaced by a broader concept of ‘psychosomatic research’, namely, the concurrent study of biological, psychological and social variables in health and disease (World Health Organization, 1964). This chapter illustrates how the Life Events and Difficulties Schedule (LEDS) has been invaluable in providing a reliable and valid measure of social variables. The chapter is divided into sections concerning the aetiology of two major forms of disorders: first, patients presenting with medically unexplained symptoms, and second, recognised physical illnesses with clear pathological changes. The chapter indicates how psychological and social variables are now being considered alongside biological ones in terms of aetiology and course of disorder. Measurement of life events in physical disorders There are a number of ways in which measuring life events before the onset of physical illness presents fewer problems compared to investigations of psychiatric illness. First, some physical illnesses may have a sudden, datable onset of symptoms – such as myocardial infarction, appendicitis, or stroke. Such onsets are more precisely defined than the onsets of depressive or psychotic illness. It is sometimes possible to interview these patients within a few days or weeks of the onset of illness. (Of course onsets of some other physical illnesses such as cancers are even less easy to date.) Second, comparison subjects may be available who have experienced similar symptoms, but who belong to a different diagnostic group (e.g. chest pain that can and cannot be explained by a heart attack). Third, the issue of ‘independence’ may be less problematic. Although ending a longstanding relationship with a partner/spouse may be the result of depression, rather than its cause, this same life event is less likely to be the result of a physical illness, which develops subsequently.

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276 Francis Creed Medically unexplained symptoms Increasing attention is being paid to medically unexplained symptoms, namely those symptoms which mimic common physical illness but where the symptoms cannot be explained by any recognisable physical illness. Common examples are chest pain resembling angina or abdominal pain suggesting stomach ulcer or bowel disease. Medically unexplained symptoms are common, forming up to 25 per cent of new presentations to general practitioners and 30–40 per cent of new medical out-patients at hospital clinics and are very expensive to the NHS because of repeated visits to doctors, investigations and medication (Hamilton et al., 1996; Wessley et al., 1999). Research using the LEDS has greatly increased our understanding of some of these disorders. Physical illnesses with associated tissue damage The previously described concept of ‘psychosomatic disorders’ held that diseases such as peptic ulcer or rheumatoid arthritis were brought on by stress. Recent advances of biomedical science have indicated the importance of infective or genetic factors and there has often been a tendency to dismiss the importance of the contribution of proximal stress. It is here that the WHO definition of psychosomatic is useful – the relationship between biological, psychological and social variables underlies the concept of multifactorial causation of disease, e.g. heart disease.

The onset of medically unexplained abdominal pain and life stress Appendicectomy The first study using the LEDS chose patients undergoing appendicectomy. It had previously been recognised that a proportion of young females undergoing appendicectomy had a normal appendix removed and no other physical illness to explain their abdominal pain – i.e. medically unexplained abdominal pain. Previous studies had indicated that these young females were more anxious or more likely to report social problems than those who had definite appendicitis. It had not been possible, however, to link the anxiety and the abdominal pain sufficiently clearly to deduce causality. The use of the LEDS meant that an objective and accurate measure of recent stressful life events could be applied. The LEDS interview could be undertaken a few days after the operation, which was not long after the onset of the abdominal pain. Since the LEDS interview was so soon after the operation (on average three to five days) the patient, the interviewer and the group of researchers rating the severity of events were all blind to the eventual diagnosis (Creed, 1981). The results showed a striking difference between the groups. Sixty per cent of patients whose appendix was categorised as ‘not acutely inflamed’ had experienced a severely threatening life event in the thirty-eight weeks prior to the onset

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The study of life events 277 of their abdominal pain compared to 25 per cent of those with appendicitis and 20 per cent of the healthy comparison group (p < 0.01). A number of checks on these data were possible (Creed, 1989). First, the appendicectomy patients were followed up one year after the operation and during the post-operative year the rate of life events fell to that of the community comparison group. Second, it was possible to interview a number of siblings of the appendicectomy patients who had experienced significantly fewer life events than the appendicectomy patients over the same period preceding the operation. Lastly, the results were checked using data for women of the same age obtained in the original Camberwell study (Brown and Harris, 1978). Twenty-five per cent of these community comparison women had experienced a severe event during the preceding thirty-eight weeks, a figure very similar to the 27 per cent and 20 per cent of the appendicitis and matched community comparison subjects, respectively (Creed, 1989). Irritable bowel syndrome, functional dyspepsia, peptic ulcer and colitis The appendicectomy study was repeated in patients presenting to a gastroenterology clinic. The patients were those who had abdominal pain, which had started during the six months prior to clinic attendance and in whom the date of the onset of the pain could be established (Craig and Brown, 1984). They were interviewed before the diagnosis was ascertained. The diagnosis was either of a physical illness with specific pathological changes (e.g. peptic ulcer) or of a descriptive nature as the symptoms could not be explained by specific pathology (e.g. irritable bowel syndrome or functional dyspepsia). The results were remarkably similar to the appendicectomy study – 57 per cent of the medically unexplained abdominal pain group reported a severe event in the preceding thirty-eight weeks compared to 23 per cent of those with an organic diagnosis (peptic ulcer or colitis) and 15 per cent of the matched community comparison groups (Craig, 1989, p.240). The findings in these two studies of abdominal pain patients were compared to LEDS data collected from patients admitted to hospital following deliberate selfharm, a group well-known for their recent social problems (Creed, Craig and Farmer, 1988). Seventy per cent of the deliberate self-harm patients had experienced a severe life event during the thirty-eight weeks prior to the self-harm and this was not significantly different from the 60 per cent of appendicectomy patients and 57 per cent of clinic patients with irritable bowel syndrome and functional dyspepsia. The commonest difficulties in all these groups concerned close relationships. Table 16.1 shows the proportion of each group who had an ongoing chronic marked difficulty involving a close relationship (usually spouse or close family member). Such difficulties are uncommon in the healthy population but occurred in about one third of the medically unexplained abdominal pain groups.

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278 Francis Creed Table 16.1 The proportion of each group who had experienced a marked relationship difficulty Gastroenterology clinic patients

Appendicectomy patients

Peptic ulcer and colitis (n = 56)

11%

Appendicitis (n = 63) 13%

IBS and functional dyspepsia (n = 79)

38%

Normal appendix (n = 56)

Comparison subjects

4%

Community comparison

30%

D.S.H. patients

29%

8%

Source: Creed, Craig and Farmer, 1988.

Severe life events, abdominal pain and depression It is possible that patients with medically unexplained abdominal pain, who had experienced stressful life events and/or chronic difficulties had concurrent depression. If this were so, then the relationship between environmental stress and the onset of pain might not be a direct one but only via depression. Table 16.2 shows the proportion of each group who had experienced a severe event by depressed and non-depressed subjects. Of community comparison subjects and patients with medically explained pain who did not have depression (peptic ulcer, appendicitis etc.) 25 per cent or fewer had experienced a severe life event in the preceding thirty-eight weeks. For those with depression or anxiety, the proportions were higher throughout ranging from 78 per cent to 40 per cent This compared to two-thirds of the clinic or deliberate self-harm patients and 40 per cent of the appendicectomy patients, who also had a depressive or anxiety disorder. Interestingly, 53–65 per cent of patients with medically unexplained abdominal pain, who did not have current psychiatric disorder, had experienced a recent severe event. This clarified the relationship between social stress and onset of abdominal pain – it was not simply through the intervening variable of depression/anxiety. The relationship with recent stress was similar whether depression/anxiety was present or not. On the basis of this result psychological treatment trials have been developed, in which all patients with severe irritable bowel syndrome or functional dyspepsia have been included, not just those with anxiety or depression. The results demonstrate that psychotherapy can help such patients and the abdominal pain improves in two-thirds of patients (Guthrie et al.,1991). Further studies confirming the relationship between life events and abdominal pain Other studies in different settings produce similar results. Vassilas (1990), using a modified version of the LEDS, found a significant excess of threatening events

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The study of life events 279 Table 16.2 The proportion of subjects in the three groups who had experienced a severe event during the 38 weeks before onset/interview. Each group is divided into those who did, or did not, have depressive or anxiety disorder at the time of interview Gastroenterology clinic patients

Appendicectomy patients Yes

D.S.H. patients

Depression/anxiety

Yes

No

Peptic ulcer and colitis (n = 56)

67%

17%

Inflamed 40% appendix (n = 63)

25%

IBS and functional dyspepsia (n = 79)

70%

65%

Noninflamed 78% appendix (n = 56)

53%

Comparison subjects 64%

11%

Community comparison

16%

40%

No

Yes

No

68%

73%

both in patients having a normal appendix removed and in self-poisoning patients compared to a community comparison group. Ford and colleagues (1987), using the LEDS in the gastroenterology clinic, found that the weighted life event scores for the IBS patients were twice that of the events experienced by patients with organic disease. Bennett et al., (1998), also using the LEDS, found that continuing chronic difficulties form the single most important predictor of outcome in irritable bowel syndrome, even when controlling for the effects of severe bowel symptoms, emotional distress, age and gender. The only other important predictor was anxiety, but this was only important in patients who did not have continuing chronic difficulties. The use of the LEDS has, therefore, clarified the relationship between environmental stress and the onset and perpetuation of abdominal pain that is medically unexplained. This finding appears to conform to the traditional psychosomatic paradigm. Severe life events are associated with the onset of abdominal pain for which no pathology can be found. It is possible that the stress leads to painful contractions of the colon in those who are constitutionally predisposed to respond in this way. In addition, where psychiatric symptoms are present, depression or anxiety may also contribute to altered colonic motility (Latimer et al., 1981) as well as to a lowered pain threshold. This does not mean, however, that we can ignore biological variables. It has recently been shown that infective causes are important and irritable bowel syndrome may occur after an episode of gastroenteritis (Neal, Hebden and Spiller, 1997). The prediction of IBS following gastroenteritis appears to be based partly on psychological variables (neuroticism) and partly on biological variables (continued infection). Life events have not yet been studied in this context (Gweek et al., 1996 and 1999). It is likely that biological and psychosocial variables interact in the chronic fatigue syndrome. A slightly different picture has emerged from a prospective study of glandular fever than from that in medically unexplained abdominal pain

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280 Francis Creed (Bruce-Jones et al., 1994). Social adversity was closely associated with depressive disorders two and six months after the onset of glandular fever but severe life events were not directly related to the development of the post-infectious fatigue syndrome or delayed physical recovery – the factors underlying these have yet to be clarified. It may emerge that there are two models concerning the relationship between stress and medically unexplained symptoms. The first involves a direct relationship between the stress and the development of pain; in the second, stress is only important indirectly in so far as the experience of severe life events leads to depression. Functional dysphonia and menorrhagia Two other studies of disorders of medically unexplained symptoms indicate these different relationships. One concerned women with functional dysphonia, where no tissue damage was involved, yet severe events simply defined were not related to onset (Andrews and House, 1989). However, events characterised contextually by ‘conflict over speaking out’ occurred significantly more commonly in women with functional dysphonia than controls (Table 16.4). In these situations, raters judged that any woman would feel torn between conflicting obligations (e.g. work versus caring for an elderly relative) but could not speak out for fear of the consequences. There seemed therefore to be a direct association between this kind of life event and the onset of the dysphonia. Results in menorrhagia were similar to those for functional abdominal pain: 56 per cent of menorrhagia patients, 28 per cent of secondary amenorrhea, and 29 per cent of community comparison subjects had experienced a severe event over the year prior to onset (Harris, 1989). Women with menorrhagia frequently experienced onset of depression following the severe life event and before onset of the menorrhagia. Depression appears in many instances to have mediated the link between the severe life event and the onset of the physical symptoms.

Life events and physical illness involving tissue damage Goal frustration events There has long been controversy as to whether peptic ulcer should be regarded as a ‘psychosomatic’ disorder. It has been shown repeatedly that such patients have increased anxiety/depression compared to healthy comparison subjects but no study had been able to demonstrate convincingly whether the anxiety plays a part in its cause rather than simply being secondary to the ulcer pain and concern about the illness. In the Craig and Brown study of patients attending a gastroenterology clinic, peptic ulcer patients were found to have experienced an excess of a particular type of life events – the so-called ‘goal-frustrating’ life event, in which an important life goal is frustrated by the occurrence of the stressor. Such experiences had occurred to 54 per cent of the peptic ulcer patients, 24 per cent of the irritable bowel/

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The study of life events 281 functional dyspepsia patients and 9 per cent of the community comparison group (Craig and Brown, 1984). Examples of goal-frustrating events include a man’s failure to gain compensation after repeated failure at court to sue the builder of his faulty house; and the disappearance of a woman’s lover shortly before the culmination of a well-established plan to separate from her husband and move in with him (Craig, 1989). This association of goal frustration with peptic ulcer has been replicated in an Australian study (Ellard et al., 1990). However, the experience of goal frustration may not be specific to peptic ulcer as a similar relationship has been reported in myocardial infarction patients. Peptic ulcer has now been associated with Helicobacter pylori infection and treatment by eradicating this agent is extremely effective. At first sight this appears to contradict the finding concerning exposure to goal frustration life events. However, the relationship between H. pylori and ulcer is not straightforward. Although over 90 per cent of duodenal ulcers and 70 per cent of gastric ulcers are infected with H. pylor, only a minority of infected patients develop ulcers and other factors determining the resistance of the host need to be considered (Go, 1997). The clinical outcome of H. pylori infection is most likely a result of complex interactions among host, bacterial and environmental factors. Concurrent organic and psychiatric disorder As shown in Table 16.2, the experience of a severe life event and/or chronic difficulty may be followed by the development of both physical illness and the depressive disorder. This was shown by Murphy and Brown (1980), whose study of new onsets of physical illness in the community avoided possible biases brought about by treatment seeking. The onset of physical illness was not generally associated with the experience of a recent severe event except in the group of patients who also had a concurrent psychiatric illness. The authors proposed a model in which life event stress led to depression, which might affect some physiological functioning and lead to organic disease. However, this model only explained the onset of physical illness in a minority of patients; the majority of patients with a new onset of a physical disease did not have a concurrent psychiatric disorder and had not experienced a recent severe life event. This is, in fact, the finding that has emerged so far from most studies of onset of physical diseases, where the onset is readily defined (Table 16.3). Two illnesses have less easily dateable onset – breast cancer and multiple sclerosis. Myocardial infarction The first study, using an early version of the LEDS, indicated no clear association with severe life events simply defined (Connolly, 1976), but suggested that a subgroup characterised by goal frustration might differ in frequency between MI sufferers and healthy controls. A more recent LEDS study (Neilson, Brown and Marmot, 1989) similarly indicated that during the year before MI, 22 per cent of patients had experienced a severe event compared to 25 per cent of controls. This

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282 Francis Creed Table 16.3 Percentage of subjects experiencing a severe event prior to the onset of a physical illness compared to comparison group (38–52 weeks taken unless specified) % of cases with severe event

% of controls

Myocardial infarction (Nielson, 1989)

22%

25%

Appendicitis (Creed, 1981)

25%

19%

Organic gastro-intestinal conditions (Craig and Brown, 1984)

23%

15%

Multiple sclerosis (Grant, 1989)

77%

35%

Stroke (House, 1990)

24%

12%

Secondary amenorrhea (Harris, 1989)

28%

29%

Breast cancer (Protheroe et al., 1999) (5-year-period)

60%

62%

lack of a difference in terms of severely threatening events is very similar to that mentioned previously concerning organic gastrointestinal disease in the absence of depressive disorders (Table 16.2). The proportions for goal frustration in the two prior years were, however, significantly different (31 per cent of MI patients versus 6 per cent of controls) and indicate, perhaps, that this type of event is not specific to peptic ulcer. The same study also found a considerable excess (40 per cent versus l5 per cent) of work, housing and financial difficulties extending over a ten-year period prior to MI. A combined index of work-related difficulties (long hours, little vacation time and other stresses) discriminated best between MI and controls but the study raised the possibility that these might be a result of the subjects’ type A behaviour. Smoking and alcohol consumption were not associated with workload stress and it appeared that smoking and work stress were both making independent etiological contributions (Neilson et al., 1989 p.335). Stroke The Oxford stroke study (House et al., 1990) used the LEDS and excluded events and difficulties involving physical health problems affecting the subject. The proportion of subjects experiencing a severe event was 24 per cent among stroke patients in the year prior to stroke and 8 per cent in the subsequent year; the corresponding figure for controls was l2 per cent. Since the higher rate of stressful life events extended back over six months prior to the stroke, the authors speculated that the stressful event might accelerate the arteriosclerotic process, possibly by increased blood pressure or by increasing blood viscosity or coaguability. Penrose (1972) proposed a similar hypothesis to explain the link between life events and subarachnoid haemorrhage. Two groups of patients with subarachnoid haemorrhage could be discerned. Those without a berry aneurysm who had no

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The study of life events 283 Table 16.4 Specific types of life event (of all severities) in patients with physical illnesses Case

Controls

Peptic ulcer – goal frustration (Craig, 1989)

54%

9%

Myocardial infarction –goal frustration (over 2 years – Nielson, 1989) (over 3 months – Nielsen, 1989) (Connolly, 1976; re-analysed in Nielsen, 1989)

31% 14% 12%

6% 3% 1%

Secondary amenorrhoea – challenge (1 year) (over 1 month) (Harris, 1989)

58% 38%

32% 4%

Functional dysphonia – conflict over speaking out (event or difficulty) (Andrews and House, 1989)

54%

16%

excess of life events prior to their bleed and those with a berry aneurysm who had an excess of life events. Penrose suggested that the increased stress was responsible for the haemorrhage, possibly because of increased blood pressure. Arthritis Rheumatoid arthritis (RA) has also been considered a ‘psychosomatic’ condition, including the so-called ‘rheumatoid personality’. Several small studies indicated the experience of traumatic life events prior to the onset of RA but one study using the LEDS found that only 18 per cent of recent onset cases had experienced a severe event during the six months preceding onset (Conway, 1994). This finding is in line with results for most organic diseases that have been studied so far, suggesting that the stress is relatively unimportant compared to genetic and infective factors. Multiple sclerosis The findings in one study of multiple sclerosis (MS) differ from the general pattern of results concerning physical disease (Grant et al., 1989). MS patients were interviewed several years after the onset of the disease and 62 per cent reported a severe event during the six months prior to onset compared to 15 per cent of the control group (p < 0.001). Relationships and housing problems showed the clearest difference between patients and controls. If these results are repeated, it may indicate that a different mechanism is involved in the onset of MS compared to myocardial infarction, stroke, and, possibly, rheumatoid arthritis. Stressful life events might be related to a change in the immunological status of MS patients, but the exact date of the immunological changes (as opposed to the onset of symptoms) cannot be determined in the light of present knowledge.

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284 Francis Creed Common cold There is good recent evidence that LEDS-measured stress is associated with increased susceptibility to infection (Cohen et al., 1998). Experimental innoculation with the common cold virus led to the development of a cold in those exposed to ongoing severe difficulties, especially those relating to un- or under-employment or enduring difficulties with close family or friends. This study provides a basis for suggesting that the experience of severe chronic difficulties is linked to the onset of physical illness when infective or immune processes are involved. Breast cancer There has long been speculation that cancer is precipitated by stress but only recently has this idea been put to the test using rigorous methods. The results are still not clear though there is an increasing body of evidence that demonstrates no direct link between the experience of stress and the development or relapse of breast cancer. Five studies have used the LEDS. Two studies have shown a positive relationship between severe events and onset of breast cancer (Geyer, 1991; Chen et al., 1995) but the largest and most careful study has demonstrated no association (Protheroe et al., 1999). Similarly, an association between severe events and relapse of breast cancer in a retrospective case-control study was shown by Ramirez et al. (1989) but a more recent study with four times as many subjects shows no association (Barraclough et al., 1992). The Barraclough study also showed no association between depression and relapse of breast cancer but contradictory again is the recent study showing that depression does predict an increased chance of relapse, albeit in a very small number of patients (Watson, 1999). Critiques of this work have questioned whether the appropriate biologically plausible hypothesis has been tested (McGee, 1999). Further work in this area needs to consider any role of stressful life events alongside biological variables and probably to examine different relationships in subgroups of patients. Low birthweight babies and miscarriage The role of stressful life events has been determined in relation to low birthweight babies. For those born premature, a severe life event or difficulty during pregnancy contributed, together with a previous history of low birthweight baby and bleeding during pregnancy. For babies which had been growing slowly during the pregnancy, it was lack of social support which independently contributed together with smoking and a previous low birthweight baby (Mutale et al., 1991). In the case of miscarriage, there is a significant relationship with a severe life event during the three months preceding miscarriage (35 per cent versus 15 per cent for continued pregnancies) (O’Hare and Creed, 1995). Further work is required to clarify more precisely the role of these social factors in relation to the biological processes that may contribute to miscarriage. Social stress may be associated with

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The study of life events 285 dietary or affective processes; alternatively it may affect physiological processes such as blood flow to the uterus. Diabetes and behavioural variables There are two LEDS studies concerning the control of diabetes (Wrigley and Mayou, 1991; Lloyd et al.,1999). Both show that the experience of severe life events and/or marked chronic difficulties are associated with poor control, either assessed using measures of glycaemic control or admission through poor control. These studies indicate that a behavioural link, such as stress leading to impaired dietary control, may be involved rather than a direct effect of stress on physiological or other biological processes. However, further research is required as there is some evidence that stress is related to the onset of diabetes – presumably as part of a multi-factorial model, which might also involve infective and immune processes (Robinson and Fuller, 1985).

Conclusion This chapter has indicated how the study of psychosomatic relationships has developed considerably as a result of the use of the LEDS in appropriate studies. The work so far has indicated the different potential models linking stressful life events and onset or exacerbation of disease. Work is now beginning to extend into the biological or physiological mechanisms by which stress is related to disease processes. The next generation of this work needs to measure biological variables in great detail alongside social and psychological variables, measured in similar detail. Such work is almost certain to use and continue to develop the interviews developed at Bedford College under the direction of George Brown.

References Andrews, H. and House, A. (1989) ‘Functional dysphonia’, in G.W. Brown and T.O. Harris (eds) Life events and illness, New York: Guilford Press. Barraclough, J., Pinder, P., Cruddas, M., Osmond, C., Taylor, I. and Perry, M. (1992) ‘Life events and breast cancer prognosis’, British Medical Journal, 304, 1078–81. Bennett E. J., Tennant, C.C., Piesse, C., Badcock, C-A., Kellow, J.E. (1998) ‘Level of chronic life stress predicts clinical outcome in irritable bowel syndrome’, Gut, 43, 256–62. Brown, G. W. and Harris, T. O. (1978) Social origins of depression: A study of psychiatric disorder in women, London: Tavistock. Bruce-Jones, W.D., White, P.D., Thomas, J.M. and Clare, A.W. (1994) ‘The effect of social adversity on the fatigue syndrome, psychiatric disorders and physical recovery, following glandular fever’, Psychological Medicine, 24, 651–59. Chen, C.C., David, A.S., Nunnerley, H., Michell, M., Dawson, J.L., Berry, H. et al. (1995) ‘Adverse life events and breast cancer: a case control study’, British Medical Journal, 311, 1527–30.

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286 Francis Creed Cohen, S., Frank, E., Doyle, W.J., Skoner, D.P., Rabin, B.S. and Gwaltney, J.M. (1998) ‘Types of stressors that increase susceptibility to the common cold in health adults’, Health Psychology, 17, 214–23. Connolly, J. (1976) ‘Life events before myocardial infarction’, Journal of Human Stress, 2, 3–17. Conway, S.C, Creed, F.H. and Symmons, D.P.M. (1994) ‘Life events and the onset of rheumatoid arthritis’, Journal of Psychosomatic Research, 38, 837–48. Craig, T.K. (1989) ‘Abdominal pain’ in G.W. Brown and T.O. Harris (eds) Life events and illness, New York: Guilford Press. Craig, T.K., and Brown, G.W. (1984) ‘Goal frustrating aspects of life event stress in the etiology of gastrointestinal disorder’, Journal Psychosomatic Research, 28, 411–21. Creed, F. (1981) ‘Life events and appendectomy’, Lancet, 1, 1381–5. Creed, F. (1989) ‘Appendectomy’ in G.W. Brown and T.O. Harris (eds) Life events and illness, New York: Guilford Press. Creed, F., Craig, T., and Farmer, R. (1988) ‘Functional abdominal pain, psychiatric illness, and life events’, Gut, 29, 235–42. Ellard, K., Beaurepaire, J., Jones, M., Piper, D. and Tennant, C. (1990) ‘Acute chronic stress in duodenal ulcer disease’, Gastroenterology, 99, 1628–32. Ford, M J., Miller, R.M.C.C., Eastwood, J. and Eastwood, E.A. (1987) ‘Life events, psychiatric illness and the irritable bowel syndrome’, Gut, 28, 160–5. Geyer, S. (1991) ‘Life events prior to manifestation of breast cancer: a limited prospective study, covering eight years before diagnosis’, Journal of Psychosomatic Research, 35, 355–63. Go, M.F. (1997) ‘What are the host factors that place an individual at risk for Helicobacter pylori-Associated Disease?’, Gastroenterology, 113, S15–20. Grant, 1., McDonald, W. I., Patterson, T., and Trimble, M. R.(1989) ‘Multiple sclerosis’ in G. W. Brown and T. O. Harris (eds) Life events and illness, New York: Guilford Press. Guthrie, E., Creed, F., Dawson, D., and Tomenson, B. (1991) ‘A controlled trial of psychological treatment for the irritable bowel syndrome’, Gastroenterology, 100, 450–7. Gwee, K. A., Graham, J. C., McKendrick, M. W., Collins, S. M., Marshall, J. S. Walters, S. J., Read, N. W. (1996) ‘Psychometric scores and persistence of irritable bowel after infectious diarrhoea’, Lancet, 347, 150–3. ——, Leong, Y. L., Graham, J. C., McKendrick, M. W., Collins, S. M., Walters, S. J., Underwood, J. E., Read, N. W. (1999) ‘The role of psychological and biological factors in post-infective gut dysfunction’, Gut, 44, 400–6. Hamilton, J., Campos, R. and Creed, F. (1996) ‘Anxiety, depression and management of medically unexplained symptoms in medical clinics’, Journal of Royal College of Physicians, 30, 18–20. Harris, T.O. (1989) ‘Disorders of menstruation’ in G. W. Brown and T. O. Harris (eds) Life events and illness, New York: Guilford Press.. House, A., Dennis, M., Mogridge, L., Hawton, K. and Warlow, C. (1990) ‘Life events and difficulties preceding stroke’, Journal of Neurology, Neurosurgery and Psychiatry, 53, 1024–8. Latimer, P., Sarna, S., Campbell, D., et al. (1981) ‘Colonic motor and myoclectric activity: A comparative study of normal subjects, psychoneurotic patients with irritable bowel syndrome’, Gastroenterology, 80, 893–901. Lloyd, C.D., Dyer, P.H., Lancashire, R.J., Harris, T.O., Daniels, J.E. and Barnett, A.H. (1999) ‘Association between stress and glycaemic control in adults with type 1 (insulindependent) diabetes’, Diabetes Care, 22, 1278–83.

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The study of life events 287 McGee, R. (1999) ‘Does stress cause cancer?’, editorial, British Medical Journal, 319, 1015–16. Murphy, E., and Brown, G.W. (1980) ‘Life events, psychiatric disturbance and physical illness’, British Journal of Psychiatry,136, 326–38. Mutale, T., Creed, F.H., Maresh, M., and Hunt, L. (1991) ‘Life events and low birthweightanalysis of infants pre-term and small for gestational age’, British Journal of Obstetrics and Gynaecology, 98, 166–72. Neal, K.R., Hebden, J., and Spiller, R. (1997) ‘Prevalence of gastrointestinal symptoms six months after bacterial gastroenteritis and risk factors for development of the irritable bowel syndrome: postal survey of patients’, British Medical Journal, 314, 779–82. Neilson, E., Brown, G.W., and Marmot, M. (1989) ‘Myocardial infarction’ in G. W. Brown and T.O. Harris (eds) Life events and illness, New York: Guilford Press. O’Hare, T. and Creed, F. (1995) ‘Life events and miscarriage’, British Journal of Psychiatry, 167, 799–805. Penrose, R. (1972) ‘Life events before sub-arachnoid haemorrhage’, Journal of Psychosomatic Research, 16, 329–33. Protheroe, D., Turvey, K., Horgan, K., Benson, E., Bowers, D. and House, A. (1999) ‘Stressful life events and difficulties and onset of breast cancer: case-control study’, British Medical Journal, 319, 1027–30. Ramirez, A., Craig, T.K., Watson, J.P., Fentiman, I.S., North, W.R.S. and Rubens, R.D. (1989) ‘Stress and relapse of cancer’, British Medical Journal, 298, 291–3. Robinson, S. and Fuller, J.H. (1985) ‘Role of life events and difficulties in the onset of diabetes mellitus’, Journal of Psychosomatic Research, 29, 583–91. Vassilas, C. A. (1990) ‘Differentiating life stresses prior to admission to hospital for appendicectorny and suicide’, Journal of Psychosomatic Research, 34, 699–707. Watson, M., Haviland, J.S., Greer, S., Davidson, J. and Bliss, J.M. (1999) ‘Influence of psychological response on survival in breast cancer: a population-based cohort study’, Lancet, 354, 1331–16. Wessley, S., Nimnuan, C. and Sharpe, M. (1999) ‘Functional somatic syndromes: one or many?’ Lancet, 354, 936–9 World Health Organization (1964) Psychosomatic disorders. Thirteenth report of the WHO Expert Committee on Mental Health, Geneva: World Health Organization. Wrigley, M. and Mayou, R. (1991) ‘Psychosocial factors and admission for poor glycaemic control: a study of psychological and social factors in poorly controlled insulindependent diabetic patients’, Journal of Psychosomatic Research, 35, 355–43.

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Part V

Postscript

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17 Some thoughts on the future of social psychiatry George W. Brown

The anthropological literature makes clear that a gift can be a serious matter. The honour-bound culture of the Icelandic sagas was particularly extreme where to give a gift that could not be reciprocated was to risk homicide (Miller, 1993). Those readers who know Tirril will find it easy to accept that her particular gift is weightier than it should be, given her persistent extirpation of her own major contribution to much of the research she outlines. The generosity of the chapter by Jim Birley and David Goldberg simply adds to my predicament. I can only reply in all truth that the work they outline would certainly not have emerged in the form it has without the kind of unstinting and continuous support of the kind they have given. Just one of many examples: David Mechanic, whose chapter follows theirs, initiated financial support from America after the MRC had decided in 1971 not to continue funding the last part of our initial grant to study depression, with the scarcely veiled message that our preliminary report was flawed in a fundamental way. His support and the enthusiasm of members from the American Foundation Fund for Research in Psychiatry who visited us surprisingly soon after, which included Neil Smelser and James Anthony, plucked us out of very deep trouble. In response to such generosity and the intellectual distinction of the contributions to this volume I am thankful that I have a slender excuse for the inadequacy of my response by noting our editor has given me a matter of only days to say something of the future. My comments reflect the ideas that occurred to me as I have read through the chapters. The sections roughly follow the order of the issues that have arisen as the research outlined in the opening chapter has developed. I remain excited by many of the issues that have been raised. And here I find myself at odds with a recent editorial in Psychological Medicine that sees psychiatric epidemiology as becalmed (Henderson and Blackwood, 1999). The collaboration with molecular genetics that is seen as a solution may prove fruitful. But why the disenchantment? Is it possible that it relates to the increasing dominance of large scale enquiries in psychiatric epidemiology with all the limits this places on subtlety of measurement? I must confess that, with some notable exceptions, what has emerged from these in recent years from such enquiries rarely appears to do much more than to follow in the footsteps of the insights of more intensive enquires. Our challenge, as I see it, is to bring together the two research traditions.

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292 George W. Brown

Proximal aetiological effects Meaning and context Durkheim’s Le Suicide remains the key sociological text for social psychiatry just because, despite its intellectual brilliance, it so patently failed to close the gap between the macrolevel and the individual. This failure is where we all begin. In chapter 4, Paul Bebbington ably reminds us of the classic debates concerning this gap in the fields of philosophy and sociology. Life-event research because of its systematic documenting of the changes in everyday life has been one of the means of closing it. The early work on life events and schizophrenia simply asked whether events had occurred before a relapse (Brown and Birley, 1968; Birley and Brown,1970). Subsequent research concentrated on the question of their meaning, taking into account the impact on any plan and concern caught up in the event. Contextual threat ratings were used and, since I deal with various types of meaning, I refer to this one involving such plans and concerns as role based since it deals with the extent an event is likely to have threatened a heavily invested activity. Some of the meaning of such an event will derive from its impact on a picture a person has formed of him or herself – either intentionally or by accident – in interaction with others. It can be seen as a form of capital; what George Park refers to as character: ‘… the current store of reputational and positional gains which he has built up, or to which he has fallen heir. So far as man is an effective social agent, we conceive it will be an overriding concern in all his involvements to maintain his character: defending what he has gained and adding, where he think he can add, to its ostensible value’ (1974, p. 97). But there was already evidence in the initial research that we would need to deal with at least one other broad source of meaning: the fact that a florid onset of schizophrenia could swiftly follow an event such as witnessing a murder of a stranger while shopping indicated the involvement of a motivational-emotional system with no necessary link with role-based meaning. Martin Eales in chapter 14 discusses such special purpose processing systems and makes clear that a rolebased investment often involves specialised systems such as caregiving. Women in London, for instance, differ a great deal in their commitment to the role of mother (Boulton, 1983). In terms of the aetiology of psychiatric disorders some kind of preattunement to various kinds of social display based on such systems is likely to be involved (see Buck, 1999 for an extensive discussion of such systems): that, for example, we are likely to find the critical comments of the EE index (or correlated facial displays) punishing as we find a smile rewarding (Öhman, 1986). The fact that investigator-based measures such as the Life Events and Difficulties Schedule (LEDS) and Expressed Emotion (EE) have been shown to work across quite different cultures is less surprising if they reflect a common human nature arising out of a long evolutionary history. Perhaps the most interesting recent development in terms of such special purpose systems is the apparent key role of life events involving humiliation and entrapment

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The future of social psychiatry 293 in provoking episodes of depression. However, the success in bringing together two types of meaning (social role-based reflecting ego-involvement and biological special purpose systems) also hints at possible limitations of the present version of the LEDS. The findings concerning humiliation and entrapment emerged from the study of women with a child living at home. In a later study in North London of depressed women between 18 and 60 treated by psychiatrists, we were struck by the fact that the provoking severe events occurring to those without children often appeared to be of lesser severity than among the Islington mothers where a major crisis in an active core relationship was usually involved. One event occurring before onset to a single patient in her fifties was the fact that she had been prevented from going to work for several months after construction scaffolding fell on her without leaving a substantial injury. This was not the kind of provoking event we had become used to finding. Reading through the descriptive accounts it became apparent that such events may have increased a person’s awareness of the restricted nature of her life. The accident occurred to someone living alone whose sexual relationship gave her little by way of intimacy or support and who had no other close tie. It had been rated as severely threatening, though not leading to any permanent handicap, because of its financial implications. When talking about it, she conveyed concern about her ‘marginal’ status , ‘It made me wonder who would look after me when I couldn’t work’. Other such events hinted at the possibility that a sense of exclusion, of not belonging, was involved – again a response that might well have evolutionary roots (Gilbert, 1989; Gardner, 1988). Another patient was French and for five years had been working in London and leading a lonely life, returning to the family farm for a summer holiday each year. Again, she had a clearly inadequate sexual relationship. The provoking severe event was a brother writing some months after her father’s death to convey that the family had decided that since she was now so far from the family, it was unnecessary for her to inherit part of the family property. It would not be surprising if she responded to this with a sense of exclusion, of not belonging. Martin Eales discusses how the social threats provoking shame-spectrum emotions often concern the position of an individual vis-à-vis a (real or imaginary) social group. Also, the two examples would not probably be atypical events from his perspective as they are core elicitors of both a) agonistic-related states e.g. shame-spectrum emotions stimulated by rejection and exclusion and b) attachment-related distress (‘not being looked after’). It remains an open question how far, if we had seen such women before the occurrence of these events, we would have been able to document the extent to which they had invested (if only in fantasy) in a more attractive way of life. At the very least, the development of retrospective ratings to do the same job would require a good deal of work to discover ways of recognising premonitory signs of such concerns. In chapter 7, Louise Lemyre has described intriguing ways in which she has proceeded down this road in order to take more account of personal meaning, using the LEDS to provide an ‘objective’ scaffolding of contextual ratings of threat to explore reports of experience. This kind of work also promises to provide useful feedback for the LEDS itself, in the sense of new insights that can be used to strengthen the criteria for making contextual judgements.

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294 George W. Brown The literature on life events and children using LEDS-type measures is already extensive (e.g. Goodyer, 1995; Sandberg et al., 1993). This is a particularly interesting development since the balance of the different types of meaning so far elaborated may tend to differ for children with the greater salience of behavioural systems and chronic stress at that age compared with role-based meaning. It is also possible that for the study of some non-depressive disorders it will be necessary to develop ways of dealing with a variety of special purpose systems that are only minimally associated with role-based meaning. The original and simpler form of the LEDS did just this by focusing on events capable of leading to significant emotional arousal (including joy). The strange bedfellows that resulted may have been predictive of schizophrenic relapse because they correlated with a basic physiological response, say, with raised dopamine levels. In chapter 15, Ellen Frank and David Kupfer give an excellent example of such a development – where potentially sleep-depriving events were shown often to precede manic episodes in bipolar patients. Francis Creed has nicely reviewed the various extensions of the LEDS to physical disorders and associated somatic conditions in chapter 16. His review as a whole conveys that it is the functional disorders such as a non-inflamed appendix that are most clearly related to LEDS-type events. Research with breast cancer presents a picture of conflicting findings. However, some clear links with physical disorders have emerged and, as he points out, issues surrounding the role of infection may be prominently involved. Hans Ormel in chapter 9 raises the interesting issue of how far ‘experiences’ in a person’s past should be taken as part of the context in rating an event since they may reflect other determinants of aetiological importance such as personality. The problem here is that a person’s world is not so easily partitioned. The fact that some aspect of personality contributed to a marital separation in the past does not detract from the fact that this may have a direct effect on the way a second one is experienced. However, in practice, I suspect the LEDS ratings rarely pay enough attention to the past to make this an important source of bias. I am confident, for instance, that the rating of the likely threat of the second marital separation would be usually entirely determined by the consideration of the immediate circumstances surrounding it. The matter could easily be settled. Given the flexibility of the instrument, it would merely require a rating of threat to be made where the consensus team were blind to any such information. Indeed, given that some might think the LEDS might actually pay more attention to a person’s past, it would also be possible to make a parallel set of ratings deliberately setting out to take account of all relevant events in the past. The trouble is that this would be likely to involve untested assumptions – for example, would the number of earlier separations beyond a certain figure tend to raise or reduce threat? On the whole, I believe the present emphasis on the use of more or less contemporary material to estimate the likely strength of relevant plans and concerns is the safest route to take about the past. Finally, mention should be made of Paul Surtees and Nick Wainwright’s approach (chapter 10). This introduces the notion that meaning is not only determined by aspects of events that are cognitively and emotionally appraised, but also

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The future of social psychiatry 295 by more mechanical features such as time since occurrence. Surtees’ work on event decay, or, as he originally called it, ‘dissipation’ (Surtees and Ingham, 1980), represents an important additional feature of the LEDS research. His move to extend it to cover longer periods across the lifespan is challenging. However, these models still need to be integrated with the analysis of LEDS difficulties, whose exacerbations, reductions and offsets are actually recorded and can be used to inform the simple event-focus of Surtees’ models. Such an approach has been started by a group in Spain (Livianos-Aldana et al., 1999). Implicit in the inclusion of difficulties in the second edition of the LEDS was the assumption that they would reflect something of the differential rates of ‘decay’ (or rather non-decay) of events. This was confirmed by the finding of a greatly raised risk of depression following a matching difficulty event (i.e. a severe event that occurred in a role domain such as work or motherhood that matched an ongoing severe difficulty in the same domain) which suggests their relevance in the sense that risk of onset remained high during the course of a difficulty but with another severe event required to potentiate this risk and bring about any onset (Brown, Bifulco and Harris, 1987). Genetics of depression Behavioural genetics deals with the genetic variability of individuals rather than with human nature in the sense of the non-variable component of special purpose motivational-emotional systems. But whatever emphasis is given to the type of genetic input there can be no dispute that the brain in a biological sense is a meaning-making apparatus (Gilbert, 1989). In this sense the suspicion of genetics on the part of social scientists that Michael Rutter points out in chapter 8 is an anachronism. However, there is still much to be settled concerning what may be seen as an individual against a population perspective on any genetic contribution. The crux of the matter is the calculation of heritability (h2). This has controversial features – for example, as Michael Rutter notes, that by fiat the calculation of the term includes any interplay with the environment. It is highly likely that, at least for common psychiatric conditions, it will turn out that an environmental input will also be involved. But this is easily dealt with by an appropriately cautious commentary and I will pursue the matter no further, particularly as Michael Rutter reviews key pieces of current research. More central is the general failure of genetic research to provide an adequate ecological base for its conclusions. Much psychopathology is associated with highly deprived environments and this needs to be reflected in sampling those selected for study. Stoolmiller (1999) has recently discussed the implications of a failure to deal with a full range of environments. He concentrates on adoption studies since these are generally accepted as the only secure way of estimating the role of shared versus non-shared environment. He notes the extreme conclusions that have been drawn about the lack of a role for a shared environment, defined as a common experience within the home – for example, one recent conclusion by a behavioural geneticist states that ‘children would develop into the same sort of adults if we left

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296 George W. Brown them in their homes, their schools, their neighbourhoods, and their culture or subcultural groups, but switched all the parents around’ (Harris, 1995, p.461). It is just this kind of extravagance that encourages scepticism about behavioural genetics on the part of social scientists. Stoolmiller documents the highly selected nature of the parents of adopted children in terms of the relative absence of marked deprivation comparee with those not adapted and how this serves to reduce the estimate of the role of shared environment. This truncated selection also explains the striking paradox that adoption studies also provide some of the strongest evidence for the role of shared environment. When data is dealt with in terms of group differences between adopted and non-adopted a sizeable shared environment emerges. Locurto (1990) in a review concluded that adoption appeared to raise IQ by 12 points. (It is of interest here that a recent twin study of verbal IQ has confirmed the importance of the environment using an indirect and probably mild indicator of deprivation: among the men from highly educated families h2 was 0.74 and for less well educated families it was only 0.26 [Rowe et al., 1999]). Until recently, such inconsistency between the results from individual and group comparisons of adoption designs has been dealt with by an obscure ‘two-realms’ hypothesis allowing both positions to be held. Stoolmiller argues for its implausibility and demonstrates that it is only possible to take such a position if the implications of the dramatic restriction in a range of environments in terms of adversity in adoption studies are ignored. Group differences therefore provide an important complement to traditional genetic indices. For example, whatever the estimates of heritability obtained in each of the six populations discussed in chapter 1 (Brown, 1996), it would be necessary to consider the implications of the ten-fold difference in the prevalence of depression ranging from 2.5 per cent in a Basque-speaking rural Spanish community to 30 per cent in a Shona-speaking black township in Harare, bearing in mind the differences are closely followed by parallel ones in the rate of severe events. The high figure for Harare has also been repeated in a survey of black women in rural South Africa (Rumble et al., 1996) and, more surprising, an even higher rate in a study of rural Pakistan (Mumford et al., 1996, 1997). It is difficult to avoid the conclusion that psychosocial factors must have determined these dramatic differences in rates across populations. Indeed, they probably reflect one of the consequences of fast rates of technological and environmental change and the kind of sociocultural disintegration that can accompany these (Leighton et al., 1971). Paradoxically, such high rates point to a possibly more incisive approach. More substantial genetic contributions may well emerge with differentiation by diagnostic type (particularly those that are rare) and outcome (especially chronic course). In terms of the latter, however, another study in rural Pakistan has not only reported very high rates of depression, but that nearly all were chronic conditions (Husain, Creed and Tomenson, 2000). I should add that behavioural geneticists are fully aware of the importance of a population perspective (e.g. Rutter, Giller and Hagell, 1998). My old colleague, Jack Tizard, often gave the telling example of height – that its high heritability does not explain the large secular increases in height that have taken place in

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The future of social psychiatry 297 Western societies. The failure to emphasise the existence of two perspectives has probably been partly due to the fact that studies using genetically informative designs rarely have comparative material and therefore lack data that would naturally lead to such contrasts. However, although there are doubtless methodological problems, the example I gave earlier of verbal IQ and parental socioeconomic status, suggests more could be done in terms of internal comparisons. Cultural differences One of the surprising aspects of investigator-based measures has been their usefulness in quite disparate cultures. (The Islington finding concerning humiliation and entrapment events, for example, was almost exactly replicated in the Zimbabwe survey of Shona-speaking women (Broadhead and Abas, 1998) and Michel Tousignant in his discussion of refugee children documents the usefulness of the CECA, dealing with childhood experiences of abuse and neglect. This success runs counter to the relativistic stance of much current anthropological writing (e.g. Shweder and Levine, 1984). It has, of course, been necessary to take account of some cultural differences – for example, the LEDS had to reflect the high value placed on male children in Zimbabwe and the rejection of a wife that could follow her failure to produce a son; however, the changes that have been required so far have been modest. The finding by Ekman, Sorenson and Frieson (1969) that isolated tribal people in New Guinea could both recognise and express pancultural facial display, as noted by Buck (1999), has probably more than any single study led to the renaissance of research on emotion. Much of the excitement of cross-cultural research is likely to come from the challenge of inconsistencies within aetiological models that have proved to have general applicability. For example: studies in Spain and Italy have confirmed the relevance of the London-based model of depression, but at the same time did not find motherhood to be a risk factor (Gaminde et al., 1993; Fava et al., 1981). And although EE measures predicted relapse of schizophrenic patients in India, there was a puzzling positive correlation between critical comments and warmth of core relatives (Wig et al., 1987); and despite very high rates of depression among rural Pakistani women the rate of marital difficulties was extraordinarily low (Husain and Creed, 1999). All such findings raise intriguing questions: could the last, for example, relate to reluctance on the part of the women to discuss their marriage which hid the true rate of marital difficulties? Or to the existence of a culturally defined emotional distance between couples, with support being provided by same-sex relatives, that, with recent changes in these traditional avenues, had permitted the unusual coexistence of both low marital dissatisfaction and low overall support? Diagnostic issues The failure to deal satisfactorily with the inherent variability of conditions such as depression is one of the disappointments of much current research – leaving aside the penchant for psychologists to deal merely with fluctuations in mood among

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298 George W. Brown their students. There is a particular need to grasp the implications of the highly selected nature of depressive conditions treated by psychiatrists – for example, personality disorder is common among female depressed patients, but relatively rare among those defined as cases in the general community (e.g. Alnaes and Torgersen, 1991; Klein et al., 1993). We need research informed by clinically relevant questions rather than driven by the constraints of existing resources or the demands of fashionable technologies. A particularly worrying development has been the widespread acceptance, since the ECA Catchment Area studies in the US in the 1970s (Robins and Regier, 1991), of clearly less than ‘gold standard’ psychiatric measures. It needs to be accepted that measurement of psychiatric conditions is a highly demanding business and that if we are attempting to break new ground nothing less than the best investigator-based interview instruments should be enough. Progress requires increasingly collaborative research. Here life-event research already offers some possible leads. For example, what is the genetic relevance of the fact that among the North London depressed patients, even when melancholic-psychotic conditions were excluded, 10 per cent of the women had no evidence of anything untoward about their lives in terms of the LEDS (Brown, Harris and Hepworth, 1995)? The important question of comorbidity is also one to which a life-event perspective, interpreted in the broadest sense, can contribute. The experience of childhood neglect and abuse relates to a doubling of the risk of both adult depression and anxiety (DSM-III-R anxiety disorders excluding mild agoraphobia and phobic conditions), and in addition contributes to the joint occurrence of the two (Brown, Harris and Eales, 1993). An interesting development, with some echoes of the work of Paul Bebbington and his colleagues on a cognitive approach to psychotic symptoms, has emerged from research concerned with the high incidence of depression among schizophrenic patients. Initial results suggest that the appraisal of entrapment in the psychotic illness itself (i.e. perceived loss of control regarding it) plays a significant role independent of treatment and illness variables (Rooke and Birchwood, 1998).

A lifespan perspective Research has now documented the importance of a range of current environmental factors other than life events, with social support probably playing a crucial role in depression – though apparently not for anxiety (Finlay-Jones, 1989). David Mechanic (chapter 3) notes how ‘in longitudinal enquiries there can be a failure to deal with the determinants of initial patterns and dispositions and in terms of outcomes of interest often it is impossible to account for most of the important differences whose pathways are already established prior to initial measurements’. This predicament is reflected in the way over the years LEDStype research has been forced to push back in time to take detailed account of childhood experience. Of course, a great deal of other research has also been concerned with similar issues. In general with the length of the causal chains involved it has been more difficult to gain confidence about the mechanisms entailed, and

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The future of social psychiatry 299 much research has concentrated on the less demanding task of isolating risk factors – it must be said often with highly impressive results (e.g. Fergusson, Horwood and Lynskey, 1994). Ron Kessler in chapter 13 nicely illustrates the difficulties that have to be faced in translating such work into confident conclusions about details of the causal chains involved. He suggests that our early efforts concerning the role of childhood neglect and abuse may have been subject to misspecification bias and has emphasised instead the critical role of an early onset of depression in increasing risk in adult life. His view has been influential: for example, a recent discussion of the nature of depression states: ‘Given the overwhelming importance of the history of depression, one cannot assume that most onsets of an episode of depression can be explained by a set of interpersonal circumstances in which anyone would get depressed’ (Coyne, 1999, p.371). The effect of such a view is to downplay the role of the adult environment. While, in my judgement, current evidence suggests this is unwarranted, it is a timely reminder of how much about the origins of depression remains to be firmly established. There appear to be four broad possibilities concerning the role of early depression, bearing in mind that they are not necessarily mutually exclusive: 1

2

3 4

Early depression as a marker for environmental factors. It is well established that early depression (say before age 20) is related to adverse prior circumstances and often severe parental abuse or neglect. These experiences may in turn lead to long-term emotional vulnerability, such as a propensity toward low self-esteem or attachment problems. In this way early depression may simply reflect the fact that childhood adversity and resulting adult vulnerability tend to persist (and reinforce each other), which in turn can lead to further episodes. (See Tirril Harris’ discussion of external and internal strands). Early depression as a mediating variable. Early depression itself may directly influence placement on a trajectory of adversity – for example, by leading to drug abuse and a resulting chaotic way of life. Early depression as a marker for constitutional/genetic risk. Early depression as a risk factor in its own right. Our own research with melancholic-psychotic episodes of depression has suggested that after the first episode the proportion of episodes with a provoking event drops markedly (Brown, Harris and Hepworth, 1994), indicating the kind of kindling or sensitisation mechanism that has been suggested to play a role in the rapid cycling of bipolar conditions (Post, 1990). It is possible early onset of any depression may make such a process more likely.

The last two perspectives would seem to reflect Ron Kessler’s basic position. Each of the four can be elaborated: for example, an elaboration of the first would be that because a dichotomous indicator of early adversity is necessarily crude, early depression may be no more than a marker for the degree of such adversity and its adverse effect on the resulting life course.

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300 George W. Brown Table 17.1 Childhood abuse or neglect, depression before 20 and post-20 experience of depression Childhood neglect Depression or abuse prior 20

(n)

Post-20 depression (%) Chronic Non-chronic Nil

No

No

(52)

8

27 35

Yes

(9)

11

No

(86)

37

(46)

56

100%

30

100%

37

100%

33 70

Yes

100%

33 44

Yes

65

26

37 63

Any fully convincing choice between the various possibilities will require highly detailed sequential lifespan material. To this end my colleagues have been collecting data over the last ten years. However, short of this, it is possible, like Ron Kessler, to formulate hypotheses capable of making a prima-facie case for one or other position. In his chapter, he summarises as critical for his position (i.e. 3 and 4 above) the fact that the associations of various childhood adversities and recent episodes were attenuated when analysis was restricted to those with a history of depression (excepting the final twelve months). Unfortunately this fails to take account of the fact that many adult depressive disorders occur to women lacking any early adversity or early depression. Since for them an adult episode often reflects persistent severe difficulties such as a violent marriage or lone motherhood, members of a group selected on this basis but without childhood adversity are likely to have a raised rate of depression in the final twelve months, and the analytic strategy therefore artificially reduces the association between childhood adversity and late depression. If early depression is an independent risk factor then it will be associated with a high rate of adult depression even among those lacking childhood adversity. As a preliminary test of this alternative hypothesis I have used data from a study of sisters, 80 of whom were selected randomly and 118 on the basis that at least the first sister had experienced abuse or neglect before the age of 17 (Bifulco et al., 1997). Early depression was defined as occurring before 20. (Five women too young to qualify for investigation of any experience after age 20 are excluded from this particular analysis.) As expected there were associations between early adversity and early depression and between both and post-20 depression defined as Bedford College caseness or DSM major depressive episode, either lasting at least one year (i.e. chronic) or one of lesser length (non-chronic). The hypothesis concerning early depression in its own right was not supported on two counts (Table 17.1). First, such women only had a raised risk when childhood adversity was also

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The future of social psychiatry 301 present. Equally important, few women experienced early depression without childhood adversity, indicating that the overall importance of early depression on its own in contributing to adult depression could not in any case be great because it occurred so rarely. The alternative position was supported since the association of early and adult depression disappeared once childhood adversity was controlled (rows 1 versus 2 and 3 versus 4) but not the reverse (rows 1 versus 3 and 2 versus 4). Another feature is that the role of both factors was much more important in determining chronic as compared with more short-lived depressive episodes. But I must emphasise this example is intended as illustrative; it represents an opening skirmish in what is likely to be prolonged debate. The issue of early depression gains importance from its relevance for one of the key unresolved questions in social psychiatry – the frequently documented sex differences in type of behavioural and psychiatric disorder. The basic facts are well known. Conduct disorder occurs at least twice as frequently in males, and later antisocial personality disorder even more frequently. Conversely females through much of their life suffer more than males from internalising disorders, and particularly depression. There are signs of some convergence in recent years, but large scale enquiries still report large differences. On balance where depression is concerned evidence at present suggests a social explanation (e.g. Bebbington, 1996). At the same time there is intriguing evidence for significant, albeit indirect, biological inputs. Evidence is accumulating around three issues. First, is the role of family experience in childhood and adolescence including that of abuse and neglect. In chapter 12, Tom Craig reviews some of the current evidence for the latter. A group in Pittsburgh (that includes Ellen Frank) has reviewed the possible role of social and hormonal mechanisms that stimulate affiliative needs for females at puberty (Cyranowski et al., 2000). Their focus is particularly on the precipitous rise in depression rates for adolescent girls that is already apparent at 15. Their account is fully compatible with my emphasis on role-based meaning together with the greater risk of girls experiencing humiliation and rejection in the context of major changes in their core social relationships. Like Tom Craig, they also note how strained or insecure attachment arising out of parental ties may play a key role. Here I would emphasise the way such insecure attachment styles may both encourage early and ill-advised sexual relationships and contribute to greater vulnerability should they go wrong. A second issue is the degree to which a coming together of a not dissimilar set of risk factors in adult life can produce sex differences independently of any early experience. There is now good reason to believe this is so. On both issues comparative research is likely to be important. The extent of sex differences in such adultonly depression is likely to relate to macrolevel societal changes. On current evidence these are likely to contribute to the present large sex differences, but where there is a convergence in gender roles there may be a reduction among sub-groups in a population (e.g. Wilhelm and Parker, 1989; Nazroo, Edwards and Brown, 1987). Also, Michel Tousignant’s findings (chapter 11) in refugees from different cultural groups remind us that it would be informative to study sex differences in adolescent depression where traditional sex roles are still in place.

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302 George W. Brown A third key issue concerns the significance of the different patterning of disorder of one sex for the other. What, for example, are the implications for women of the extraordinary increase of antisocial behaviour among young men over the last fifty years in all developed countries with the exception of Japan (Rutter and Smith, 1995)? The huge literature on the origins of conduct disorder and subsequent antisocial behaviour among young men points to the central role of family experience, particularly family discord, separation or divorce and quality of parenting with evidence that family transitions tend to disrupt the latter (Capaldi and Patterson, 1991). Genetic factors are certainly also involved, probably most clearly via the link of conduct disorder with hyperactivity which has a significant genetic loading.

The proximal and distal environments and the origins of life events In Chapter 8, Michael Rutter refers to a series of recent papers supporting the idea that there is a significant genetic contribution to life event occurrence and elsewhere he has noted: ‘Where life events come from is the least investigated of all key issues and yet, from both theoretical and policy or practice viewpoints it is the most crucial’ (Rutter and Sandberg, 1992, p.10). It may therefore be useful to summarise something of what is known about the source of humiliation-entrapment (H-E) events, and not least how this might be linked to the differing pattern of disorders of men and women that I have just discussed. I have little doubt that any one H-E event is likely to be the result of multiple factors: the violent attack on a lone mother by her husband whom she had not seen for a year may appear at first glance to have come ‘out of the blue’. But what about the fact that she chose to marry him despite having experienced his violence and that she had recently started a relationship with someone who had been a close friend of her husband? Under this kind of scrutiny it might well be possible to argue that the majority of H-E events can be linked, at least in a tenuous fashion, to earlier choices and doubtless at times ultimately to our genes. However, while this needs to be kept in mind, it does not rule out the importance of searching for major sources of influence. Tirril Harris drew attention, in her opening account of LEDS research, to the large differences in the rates of severe events across six very disparate populations. It has also been possible to consider in a similar way in some of these the proportion experiencing at least one H-E event in a twelve-month period. Among women with at least one child at home proportions ranged from 27 per cent in Harare, 23 per cent in Islington, 13 per cent in Camberwell and 4 per cent in the Outer Hebrides (Brown, 1996). The nature of the events themselves suggests some role for macrolevel changes – for example, some H-E events in Harare were clearly linked to the frequency of migration of labour and an increase in sexually transmitted disease. Figure 17.1 goes further by dividing urban Camberwell by social class and rural Outer Hebrides by the degree of integration into the local traditional way of life. For women between 18 and 65 much the most

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The future of social psychiatry 303

A 30 25 20

Urban–Harare Humiliation/ entrapment Urban–Camberwell

% 15

10

Rural–Outer Hebrides

5 0 25 20

B Loss/danger

% 15

10 5 0

20

C Death

% 15

10 5 0

Working

Middle

Social class (172)

(240)

(218)

Low

Middle

High

Social integration (58)

(108)

(40)

Figure 17.1 Percentage of women with at least one severe event in 12 months.

clear differentiation of severe events occurs among those classed as H-E events with a thirty-fold difference between Harare and the most integrated women in the Outer Hebrides in the proportion with at least one such event. Differences in the experience of the wider category of loss or danger were much less, with only the most integrated rural women having a notably lower rate. (Loss included loss of a role, resources or a cherished idea about self or someone close, as well as loss of a person, with danger typically the threat of these.) Deaths of close ties were considered separately and were only more common (at double the rate) in Harare. (Of course, if deaths are combined with other kinds of loss, experience of loss among Harare women far exceeds that of other women.) These results undoubtedly reflect a host of secular changes often involving basic institutions such as in present day Europe increased marital breakdown, fewer children, and a greater amount of a lifetime spent living alone. Such changes can therefore be expected, as well as increasing H-E events, to have an impact on rates of the ‘atypical’ severe events I discussed earlier involving feelings of isolation and not belonging or being looked after.

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304 George W. Brown A second set of relevant findings concerns a division of a population in terms of a correlate of socioeconomic status, lone motherhood. Such women had much increased in numbers in the ten years separating the Camberwell and Islington surveys and had double the risk of a depressive episode when compared with other mothers. This was entirely explained in a statistical sense by their much greater risk of experiencing an H-E event (Brown and Moran, 1997). Considering H-E events in terms of type sheds further light on matters. For example, a comparison of H-E events occurring to lone and other mothers showed that most fell into three broad categories: 1 2 3

events involving separation, violence or infidelity from a lover, ex-partner or current partner (19 per cent lone versus 10 per cent other mothers) childhood events almost all involving some kind of ‘delinquency’ (14 per cent versus 7 per cent) a mixed group largely linked with entrapment in material deprivation (13 per cent versus 4 per cent).

In overall terms 39 per cent versus 18 per cent experienced at least one of the three categories, with such events accounting for four-fifths of the total H-E events. The comparative data already outlined produced one unexpected and related finding. The rate of H-E events involving a partner, ex-partner or lover was a good deal higher in Harare than Islington despite the frequency of marital problems in the latter; but quite unexpected was a much lower rate of H-E events involving children in Harare (Jeremy Broadhead, August 1999, personal communication). As with Michael Rutter’s consideration of the Isle of Wight data, I had expected the problems of children to be driven essentially by family problems in Harare as well as in Islington. At present it is only possible to speculate that the traditional kinship structure in Harare was still effective enough to provide some needed protection for children, which in turn reduced the chances of creating H-E events for their mothers. Obviously the matter of origins can be taken still further. Continuing with the example of children, a number of studies (including our own) suggest that children of lone mothers have a higher incidence of psychopathology (e.g. Dornbusch et al., 1985; Coughlin and Vuchinich, 1996). In Islington this is associated with a raised rate of H-E events for the mother – indeed, part of the definition of conduct disorder is the occurrence of these very events – such as discovering a child has been playing truant and glue sniffing. A range of factors is likely to contribute to male antisocial behaviour, including the quality of the local school system (poor in Islington at the time of our survey), quality of contact with the father and the nature of the discipline and supervision provided by the mother – which in turn related to her level of depression and so on. So far I have dealt with cross-sectional inquiries, but a lifespan approach is equally illuminating. A key study, using the LEDS, followed up after fifteen years a sample of children originally selected at age 10 as behaviourally ‘disturbed’ or ‘not disturbed’ by means of a teacher questionnaire. In their late twenties the

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The future of social psychiatry 305 disturbed group showed twice the rate of severe events, with no difference in nonsevere events. This difference involved events rated both independent of the individual’s actions and those dependent on them. The same overall finding held for ongoing severe difficulties. Indeed, the difference only held for events linked to a chronic difficulty (Champion, Goodall and Rutter, 1995). A pair of studies carried out by Bernice Andrews and Cathy Hepworth of the 15–25-year-old daughters and sons of the Islington women first interviewed some ten years earlier has revealed a similar picture for severe events in the sense that experience of childhood abuse or neglect, or a mother’s experience of partner violence or marked discord, was related to a doubling of the risk of such events among their children ten years later. There was also evidence of a sex difference. The daughters experienced a greater number of H-E events. It was also possible to show, by in addition taking into account the impact of severe events on others, that in this inner-city setting a male was twice as likely to create an H-E event for a woman as vice versa. All three longitudinal studies, therefore, in their different ways, raise the issue of gender and ‘victimisation’. However, the work reviewed so far stops short of the question of how far an individual might have contributed to bringing about events. Early concern with this issue was essentially methodological, aimed to see whether the basic life event-onset link held for clearly ‘independent’ events. Since then more complex schemes have been introduced. Most attempts deal only with the more or less contemporary situation and have reached the perhaps not unsurprising conclusion that for the most part Islington women had not played a major role in bringing about the humiliating and entrapping circumstances they had been caught up in. For example, a close examination of severe marital difficulties among Islington women judged the majority of partners involved to be ‘grossly undependable’ (Brown et al., 1986). The exceptions are more interesting. These were particularly apparent in the depressed patient series who showed evidence of personality disorder (excepting those of a schizoid, or fearful kind). Severe events where the woman’s behaviour appeared to have played a direct role occurred more commonly among those with dramatic personality disorder – 58 per cent (15/26) of the severe events preceding their onset in contrast to 18 per cent (11/61) among the other depressed patients. In more general terms, there can be no question of the importance of taking into account personal characteristics in seeking the origin of particular H-E events even if this is likely to have a clear bidirectional component. Also relevant is the evidence that those with conduct disorder in childhood are more likely to have partners deviant in terms of antisocial behaviour (Rutter et al., 1995). But here the role of propinquity needs to be kept in mind: a young girl leaving a violent home at 16 to live in a hostel for the homeless may well decide to live together with a boy from a similar deprived background with all going well till she has her first child. Choices are often heavily circumscribed. In our current research we have little doubt that most women who have experienced violence in a marriage or cohabitation show every sign of trying to avoid it on a second occasion – sadly often without success (Andrews, 1992). Following the lead of Uri Bronfenbrenner, often the

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306 George W. Brown local ecological niche of women can be seen in terms of entrapment. And entry into such a niche can emerge directly from an adolescent’s entrapment in a neglectful or abusive parental home. And in such circumstances individuals will not only experience H-E events, they will also at times create them for others. And here recent work can be seen to have spelt out in more detail and in general population samples the implications of Lee Robins’ classic work linking conduct disorder with adult events such as marital separations, violence and heavy drinking. The matter should not, however, be overstated: in Islington only around half of the H-E events created by young men for others were brought about by those with earlier conduct disorder. There is bound to be tension between group and individual perspectives concerning the origins of life events. The importance of macrolevel factors cannot be doubted; nor can there be a question that genetic and constitutional factors play some role in influencing who experiences such events. One key issue must be the nature of personality characteristics that interact with environmental factors to produce events. To take an extreme example, the rate of highly disturbing and traumatic events occurring to children in some urban centres in the US, such as witnessing a drug-motivated murder, is extraordinarily high (Freeman et al., 1993; Fitzpatrick and Boldizar, 1993). Personality characteristics along the lines of ‘novelty seeking’ may well relate to the time spent by a child on the streets and his chance of being involved in such an event. Ordinary variability in such a characteristic may therefore be expected to correlate with who experiences ‘misadventures’. Given there is a genetic contribution to such a characteristic, the rate of any resulting H-E events might be seen as partly genetically determined. However, where the variability in a personality characteristic has remained stable in a population but the rate of such events has been increasing, their origins are probably best seen as essentially ‘social’. In instances where a personality characteristic, say ‘life course persistent antisocial behaviour’ (Moffit, 1993), has also increased in prevalence, perhaps in response to increasing family instability, more emphasis on a genetic contribution might be warranted – but, of course, in interaction with environmental changes. The issue of origins becomes uncomfortably complex when reduced to the question of individual complicity, and there is something to be said for concentrating attention on questions of possible practical relevance. As already noted, ‘positive events’ appear to play a major role in remission of depression (Brown, Lemyre and Bifulco, 1992; Brown, 1993) and they are of obvious interest in any consideration of the role of personal characteristics in event production. Here it is perhaps relevant that our initial attempt to study such events failed abysmally. An exploratory study of a random sample of non-depressed women found the kind of block-buster event we envisaged, such as falling in love, finding a new confidante or some singular achievement, were extremely uncommon. Events we were told about were largely of the kind of buying a new car or domestic appliance, or in one instance ‘seeing a stag on the skyline during a holiday in Scotland’. It took several years after this debacle for us to realise that the events that we had in mind of importance were in good part a function of the very states of deprivation and adversity we had

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The future of social psychiatry 307 been studying as aetiological factors. If one is lonely and isolated, the finding of a new confidante or a boyfriend is a real possibility – although, sadly in the longer term, it may lead to disappointment. This suggests a key research issue is to document more systematically the link between deprivation and positive experience, bearing in mind that key changes are sometimes anticipated by small ones – starting driving lessons while depressed followed a few months later by taking a parttime job. Once again, a lifespan perspective is relevant. Following up our original Islington women some eight years later, Bernice Andrews found that there had been definite changes in self-esteem and almost all this had been in a favourable direction (Andrews and Brown, 1995). More often than not the change had been associated with what were positive life events such as a violent husband eventually leaving home, or a woman returning to work or entering further education. One surprising feature of such findings is that the possible role of treatment – physical and psychotherapeutic – in helping to create events, large and small, is a totally uninvestigated question. Such research may produce surprises. It is possible, for example, that the potential for any intervention to encourage such events may help to explain the surprising non-specific nature of many current treatments.

Other sources of meaning It is now reasonably clear that more than a severe event usually needs to be present for a depressive onset of clinical relevance to occur; and most life-event research in recent years has been concerned with studying this background risk in psychosocial terms. It has proved possible to characterise women in terms of psychological and environmental risk factors in a way that nearly half will develop an episode in the following year (Brown, Bifulco and Andrews, 1990; Bifulco et al., 1998). (There is evidence that effective social support with the crisis itself is a key mediating factor here (e.g. Brown, 1992; Harris, 1992; Edwards, Nazroo and Brown, 1998).) While this simple two-fold index is an unusually powerful predictor, it still leaves plenty of room for the introduction of other risk (and protective) factors. One issue is obviously the relationship between such ongoing vulnerability and the chances of experiencing a life event, particularly of a humiliation-entrapment kind. Around half of H-E events emerge out of severe difficulties that had persisted for at least one year, and this is sufficient to provide a significant link since they correlate highly with vulnerability. An ongoing marital difficulty involving persistent quarrelling and occasional violence (environmental vulnerability) is often associated with low self-esteem (psychological vulnerability) and over time leads to crises such as the discovery of infidelity (H-E event). Low self-esteem that forms part of psychosocial vulnerabiltiy is just one example of a third source of relevant meaning – a memory-linked emotional schema (such as helplessness, memories of incidents of abuse) that can be brought into play following a severe event (Brown, 2000). Given the mounting evidence for this third source, my earlier emphasis on the importance of specific meaning with its biological roots needs to be seen in context, in the sense that it joins with other

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308 George W. Brown sources of meaning. A key to the origins of human depression (in contrast to animal models) is probably the much greater cognitive elaboration that our brain makes possible. As noted by Martin Eales, in this way the time-frame of a special system response can be expanded beyond short-term situational activation. For this reason we have a much reduced chance compared with animals of escaping from events of a humiliating and potentially entrapping nature, bearing in mind the majority of severe events leading to onset of depression involve close social ties (Brown, Harris and Hepworth, 1995). Also relevant in such entrapment is the fact that compared with other primates we have a greater facility for the development of emotional commitments to close ties that are not readily put aside (MacDonald, 1992); and the effect of this is reinforced where ‘axiomatic’ roles, such as motherhood, are involved (Park, 1974). The unravelling of the origins of depressive disorders is both inexhaustibly complex and fascinating just because it can involve the conjunction of these three broad types of meaning – role-based, special purpose and memory-linked together with mediating factors such as social support. This is not the occasion to comment further on memory-linked meaning – a matter that deserves a commentary at least as lengthy as that given to life events. Perhaps the greatest immediate challenge is to link the raised risk of adult depression associated with early abuse and neglect with the way dysfunctioning of the attachment system can be played out across long periods of a person’s life. It is already clear that where early experience is concerned, a range of disorders other than depression needs to be considered. One finding to emerge from the study of lone mothers in Islington is that mixed states of depression involving anxiety in the form of either panic, severe agoraphobia, GAD or social phobia accounted for their greater rate of depression. And that the three key risk factors for such mixed states in the population as a whole were childhood abuse or neglect, earlier marital violence or current lone mother status (Brown and Moran, 1997). It is also clear that Hans Ormel’s concern with the predictive role of neuroticism needs to be pursued under this general umbrella. The key challenge here is to distinguish its overlap with phenomena such as self-esteem and low grade psychiatric symptomatology that are known to fluctuate over time and to distil a component of neuroticism that is more stable irrespective of its origin.

Design and measurement Michael Rutter has reviewed at some length issues concerning design and measurement and I feel compelled to add a footnote to only one of his points – the limitations of a case-control design. This design is limited by the fact it focuses attention on the event-disorder link and it neglects why this event at this time was of aetiological importance; an issue only partially dealt with by considering the role of ongoing vulnerability. Fortunately, if the research is based on a population sample, it is a simple matter to exit from a design to consider all events occurring in a given period and pursue the question of what qualities characterise the particular events that precede the onset of a disorder in comparison with the others in

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The future of social psychiatry 309 that time-frame. This was, in fact, the way we documented the depressogenic quality of H-E events in comparison with other severe events. I restrict further comments to a few highly selected issues. Unfortunately, measurement in the social sciences is inextricably linked to a question of resources – both in terms of the time to complete a thesis or the overall time allowed for the research by a grudging funding body, and also in terms of the financial allocation requested for such work – often a trivial sum in most grant applications. Investigator-based measures are expensive both to develop and to employ, as Elizabeth Davies conveys in detail in chapter 5, and it would be silly to expect much by way of increase in their sole use. However, it is not silly to urge for their greater integration into an ongoing programme of research, and it does seem worthwhile to argue that traditional large scale survey-type enquiries should not be undertaken without prior intensive work or without a small scale enquiry nested within the larger one. One reason is that questionnaire-type enquiries without such safeguards can cut themselves off from the real world and literally manufacture findings. James Nazroo (1995), in the context of an enquiry of life events occurring to couples, questioned in depth about marital violence. The results were unequivocal – men were far more given to such violence as properly defined. And yet there is a widespread belief that there is sexual symmetry in such violence (see, for example, Moffitt and Caspi, 1998). A thorough review of this literature makes it clear that this conclusion is largely the result of the widespread use of a checklist of selfreported ‘acts’ perpetrated or experienced (Dobash et al., 1992). The instrument in its attempt to avoid self-serving and biased reporting, fails to deal with context. It is confined to questions of the kind whether they have ‘pushed’ their partners, have ‘slapped’ them and so forth. Any person who acknowledges a single such instance is deemed a perpetrator of violence regardless of the context, consequences or meaning to those involved. It is difficult to believe that the instrument could have survived the feedback from more intensive enquiry. Margolin (1987) who did just this, for example, reported instances such as the ‘kicking’ which took place in bed in more of a kidding than a serious fashion, and another instance where the wife, who had been scored for serious violence and the husband for low level violence, had for years passively accepted his repeated abuse but had on only one occasion retaliated by hitting him over the head with a wine decanter (1987, p.82). In chapter 5 on interviewing, Elizabeth Davies has touched on such issues, and also poignantly conveyed the doubtful morality of studying deeply threatening situations with standardised questionnaires. The question of context raised by this particular measure of marital violence is central to measurement in the social sciences (e.g. Scheff, 1997). Sometimes such a placing of a ‘part’ in a larger ‘whole’ is done more or less automatically. For example, some respondents are just more ebullient in talking about someone when compared to others considered to show the same degree of warmth on the EE rating, but in a more muted fashion. In everyday life we quickly make this kind of correction and it was certainly not something my colleagues attempted to teach during our training sessions. But, as Paul Bebbington conveys, the issue of what context to take into account is often more controversial. On some occasions, as

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310 George W. Brown seen in the LEDS measurement of events, tight control over this is in order. But whatever the research design some constraint is usually necessary if only because the same ‘event’ may carry several meanings. In the research on the role of positive events, we found that as many as a quarter of the positive events occurring before remission had also been rated severely threatening (Brown, Lemyre, and Bifulco, 1987). One woman in the context of a long drawn out acrimonious dispute with her husband had been bullied by him and his solicitor into accepting a divorce settlement concerning their family home. The event was considered severely threatening (and humiliating) in the context of her long resistance and their bullying behaviour. At the same time from a more forward-looking perspective it was rated as ‘delogjamming’ (and positive) in the sense that it resolved a bitter dispute and with the considerable financial resources that were released she had the opportunity to start to plan what she would do with her life. The adequacy of the degrees of embeddedness in context achieved by a particular enquiry is a matter of judgement. For example, Scheff, whose primary interest is in the detailed microanalysis of speech, considers the EE measures of criticism and over-involvement atheoretical and wanting (op.cit., p.28). Perhaps a fairer judgement would be in terms of whether a measure is embedded enough for progress in the research undertaken – in this instance the prediction of a florid psychotic relapse. Further elaboration will almost certainly then be possible. Michael Goldstein’s group at the University of California did just this with EE measures. In one study, for example, they showed that high-EE relatives were more likely to respond with criticism to the first unusual thought verbalised by the patient; and when this occurred the probability of a second unusual thought was augmented (Magana et al., 1986). It might be objected this is an example of the pursuit of context via the study of process rather than in the elaboration of a particular measure. But the two activities are mutually reinforcing – the issue of context is perhaps best seen as a matter of interweaving between attempting to fix meaning within a particular measure and extending context via the study of process. One problem with checklist instruments is, of course, the difficulty they have in dealing with context. But it needs to be recognised that they can on occasions nonetheless be highly effective. In terms of large scale studies of birth cohorts, they have been of central importance in opening up the whole field of inquiry into developmental trajectories. They can also reveal challenging issues worth more exploration – it is now established, for instance, that the response to a couple of questions about perceptions of health are highly effective in predicting morbidity and mortality several years later, even when controls for state of current health have been made (Idler, 1992). And once an investigator is reasonably sure of what is going on, such a checklist may well be accurate enough to be useful in a large scale enquiry. Choice of measurement methods should depend on these kinds of consideration. What should not play a role are the quite spurious claims about the inherent weakness and subjectivity of an investigator-based approach. Finally, there are two key issues in psychiatric research concerning longitudinal enquiries. Despite their greater cost there is an important place for retrospective measures based on intensive interviewing. There is now evidence for the accuracy

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The future of social psychiatry 311 of the retrospective questions of the CECA measuring child neglect and abuse (Bifulco et al., 1997) and the LEDS covering retrospectively a ten-year period (Neilson, Brown and Marmot, 1989). It is often overlooked that a prospective enquiry, if it is restricted to dealing with the situation at the time of a particular prior interview, leaves whole blocks of time uncovered (see David Mechanic, chapter 3). Also given the increasing salience of studies of childhood abuse and neglect there are practical and legal problems about collecting such material during childhood itself. Current evidence suggests that a fair job can be made of reconstructing an accurate picture at a much later point in time. Another problem concerning longitudinal enquiries is the very high rates of attrition that are possible in large scale studies even when well funded. Here, I believe there is a place for a parallel smaller scale enquiry – a one-off cross-sectional one is likely to be more effective in representing the ‘difficult to follow up’ who will certainly include many of the most deprived and will enable some estimate to be made of the extent of possible error due to any extensive drop out from the main inquiry.

Intervention studies Ron Kessler points out that the issue of the validity of a theory is critical in so far as we wish to intervene in the real world. I would add that as a research programme progresses and the awesome complexities of the world become ever clearer, such interventions acquire a double allure: as well as possibly throwing more light on the processes we have been attempting to understand, they might enable us to justify the privilege of doing research. I suspect, for example, that where the subtle interplay of social support and sense of self-worth is concerned, confidence about its role may only come from experimental enquiries of the kind initiated by Tirril Harris in the area of chronic depression and befriending (Harris, Brown and Robinson, 1999a,b). But to justify intervention we need reasonably convincing models. And here it needs to be borne in mind that a ‘factor’, such as number of critical comments in the EE index, may have quite different implications according to the disorder that is being investigated. In the original research it was conceived of as playing a direct role – literally that the spiralling tension resulting from such displays within the family could provoke a florid schizophrenic relapse. However, I believe the important extension of the EE index by Christine Vaughn and Julian Leff (1976) to study depression (and the use of a much lower threshold for critical comments) requires a quite different framework. The fact that fewer critical comments are predictive of relapse suggests to me not that such patients are more sensitive to criticism but that the new threshold is a marker for rather different family processes. The importance of the lower threshold could then come about in many ways – for example, perhaps a husband’s sense that his behaviour has contributed to his wife’s depression has restricted his criticism, but is irrelevant for his plan to leave her (the event that provokes her relapse). I suspect that given Julian Leff’s involvement in evaluating marital therapy (see chapter 6), he might go along with this resiting of the EE index.

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312 George W. Brown There are grounds for optimism about the impact of perspectives involving ‘meaning’ upon clinical practice. In recent years psychologists working in the cognitive-behavioural tradition have increasingly sought to amend their theoretical framework in these terms. Teasdale and Barnard (1993) have argued that at least two levels of meaning representation need to be considered (in addition to lower level modality-specific forms of representation) in any model of psychopathology. Brewin and Power (1999) adopt a similar critique of single-level approaches to meaning and have outlined a taxonomy of themes characterising appraisal mechanisms associated with psychopathology, highlighting their links with childhood adversity. They have taken the perspective further into understanding the process of therapeutic change and extol the therapeutic importance of ‘the construction of a successful narrative’ (op.cit., p.154) since, from the multi-level perspective on meaning, this may have a positive impact in a number of quite different ways, both altering conscious appraisals and blocking the reactivation of unconscious representations. Such a viewpoint has distinct echoes of many of the chapters in this volume. Tirril Harris and I have been pessimistic about the possibility of extending the present LEDS-based aetiological model of depression into effective RCT trials because of what for us is a rigid interpretation of this design which has seemed to insist on evaluating the effectiveness of essentially one ‘thing’ for each experimental arm. With so many potential factors playing a role in the perpetuation and relapse of depressive conditions it has seemed to us counterproductive to concentrate on ‘one’ kind of intervention. What seemed to be required was the possibility of offering a sm`rgasbord of interventions, the choice of which would be made to match the individual aetiological pathways to depression of each patient, and largely basing this in general practice. Fortunately, the preliminary report of a recent MRC working party on RCT designs conveys that opinion is changing and that there is increasing recognition of a need to move towards more complex designs. But while it is fully appropriate that psychiatry continues to see its role as intervening in terms of the individual, social psychiatric research with common disorders does present psychiatry with something of a dilemma. A condition such as depression, even in its chronic form, is so common in parts of the UK (let alone other parts of the world) that it represents a major public health problem – and certainly not one psychiatry can hope to deal with on its own. I have a sense that there is a growing realisation that the issue of numbers must be faced – with an attempt to reach a much broader consensus of the way forward – and perhaps the place to begin is to search for ways of stimulating ‘natural’ ways of giving support within a population. I become increasingly doubtful about the assumption that the only way forward, where common psychiatric disorders are concerned, is solely via some kind of professional or quasi-professional contact.

References Alnaes, R.A., and Torgersen, S., (1991) ‘Personality and personality disorders among patients with various affective disorders, Journal of Personality Disorders, 5, 107–21.

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The future of social psychiatry 313 Andrews, B. (1992) ‘Attribution processes in victims of marital violence: Who do women blame and why?’ in J.H. Harvey, T.L. Orbuch and A.L. Weber (eds.) Attribution, Accounts and Close Relationships, New York: Springer-Verlag, 170–93. Andrews, B., and Brown, G.W. (1995) ‘Stability and change in low self-esteem: the role of psychosocial factors’, Psychological Medicine, 25, 23–31. Bebbington, P. (1996) ‘The origins of sex differences in depressive disorder: bridging the gap’, International Review of Psychiatry, 8, 295–332. Bifulco, A., Brown, G.W., Lillie, A., and Jarvis, J. (1997) ‘Memories of childhood neglect and abuse: corroboration in a series of sisters’, Journal of Child Psychology and Psychiatry, 38, 365–74. Bifulco, A., Brown, G.W., Moran, P., Ball, C., and Campbell, C. (1998) ‘Predicting clinical depression in women: the role of past and present vulnerability, Psychological Medicine, 28, 39–50. Birley, J.L.T., and Brown, G.W. (1970) ‘Crises and life changes preceding the onset and relapse of schizophrenia: clinical aspects’, British Journal of Psychiatry, 116, 327–33. Boulton, M.G. (1983) On being a mother: a study of women with pre-school children, London and New York: Tavistock Publications. Brewin, C.R. and Power, M.J. (1999) ‘Integrating psychological therapies: processes of meaning transformation’, British Journal of Medical Psychology, 72, 143–57. Broadhead, J., and Abas, M. (1998) ‘Life events and difficulties and the onset of depression amongst women in an urban setting in Zimbabwe’, Psychological Medicine, 28, 29–38. Brown, G.W. (1992) ‘Social support: an investigator-based approach’ in H.O.F. Veiel and U. Baumann (eds) The meaning and measurement of social support, Washington, DC: Hemisphere Publishing Corporation, 235–57. —— (1993) ‘Life events and affective disorder: replications and limitations’, Psychosomatic Medicine, 55, 248–59. —— (1996) ‘Genetics of depression: a social science perspective’, International Review of Psychiatry, 8, 387–401. —— (2000) ‘Emotion and clinical depression: an environmental view’ in M. Lewis and J. Havilland-Jones (eds) Handbook of Emotions Second Edition, New York: Guilford Publications. ——, and Birley, J.L.T. (1968) ‘Social precipitants of severe psychiatric disorder’ in E.H. Hare and J.K. Wing (eds) Psychiatric Epidemiology, Oxford: Oxford University Press. —— and Moran, P. (1997) ‘Single mothers, poverty and depression’, Psychological Medicine, 27, 21–33. ——, Bifulco, A., Harris, T., and Bridge, L. (1986) ‘Life stress, chronic subclinical symptoms and vulnerability to clinical depression’, Journal of Affective Disorders, 11, 1–19. ——, Bifulco, A., and Harris, T.O. (1987) ‘Life events, vulnerability and onset of depression: some refinements’, British Journal of Psychiatry, 150, 30–42. ——, Bifulco, A., and Andrews, B. (1990) ‘Self-esteem and depression: 3 aetiological issues’, Social Psychiatry and Psychiatric Epidemiology, 25, 235–43. ——, Lemyre, L., and Bifulco. A. (1992) ‘Social factors and recovery from anxiety and depressive disorders: a test of the specificity hypothesis’, British Journal of Psychiatry, 161, 44–54. ——, Harris, T.O., and Eales, M.J. (1993) ‘Aetiology of anxiety and depressive disorders in an inner-city population. 2. Comorbidity and adversity’, Psychological Medicine, 23, 155–65.

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314 George W. Brown ——, Harris, T.O., and Hepworth, C. (1994) ‘Life Events and “endogenous” depression: a puzzle re-examined’, Archives of General Psychiatry, 51, 525–34. ——, Harris, T.O., and Hepworth, C. (1995) ‘Loss, humiliation and entrapment among women developing depression: A patient and non-patient comparison’, Psychological Medicine, 25, 7–21. Buck, R. (1999) ‘The biological affects: a typology’, Psychological Review, 106, 301–36. Capaldi, D.M., and Patterson, G.R. (1991) ‘Relation of parental transitions to boys’ adjustment problems: 1. A linear hypothesis. 2. Mothers at risk for transitions and unskilled parenting’, Developmental Psychology, 27, 489–504. Champion, L.A., Goodall, G., and Rutter, M. (1995) ‘Behaviour problems in childhood and stressors in early adult life. A 20-year follow-up of London school children’, Psychological Medicine, 25, 231–46. Coughlin, C., and Vuchinich, S. (1996) ‘Family experience in pre-adolescence and the development of male delinquency’, Journal of Marriage and the Family, 58, 491–501. Coyne, J.C. (1999) ‘Thinking interactionally about depression: a radical restatement’ in T. Joiner and J.C Coyne (eds) The Interactional Nature of Depression, Washington: American Psychological Association, 365–92. Cyranowski, J.M., Frank, E., Young, E., and Katherine Shear, M. (2000) ‘Adolescent onset of the gender difference in lifetime rates of major depression’, Archive of General Psychiatry, 57, 21–7. Dobash, R.P., Dobash, R.E., Wilson, M., and Daly, M. (1992) ‘The myth of sexual symmetry in marital violence’, Social Problems, 39, 71–91. Dornbusch, S.M., Carlsmith, J.M., Bushwall, S.J., Ritter, P.L., Leiderman, H., Hastorf, A.H., and Gross, R.T. (1985) ‘Single parents, extended households, and the control of adolescents’, Child Development, 56, 326–41. Durkham, I. (1897) Le Suicide, Paris: Falcon; trs (1952) London: Routledge and Kegan Paul. Edwards, A.C., Nazroo, J., and Brown, G.W. (1998) ‘Gender differences in marital support following a shared life event’, Social Science and Medicine, 46, 1077–85. Ekman, P., Sorenson, E.R., and Friesen, W.V. (1969) ‘Pan-cultural elements in facial displays of emotion’, Science, 164, 86–8. Fava, G.A., Munari, F., Pavan, L., and Kellner, R. (1981) ‘Life events and depression’, Journal of Affective Disorders, 3, 159–65. Fergusson, D.M., Horwood, L.J., and Lynskey, M. (1994) ‘The childhood of multiple problem adolescents: a 15-year longitudinal study’, Journal of Child Psychiatry, 35, 1123–40. Finlay-Jones, R. (1989) ‘Anxiety’ in G.W. Brown and T.O. Harris (eds) Life Events and Illness, New York: Guildford Press, 95–112. Fitzpatrick. K.M., and Boldizar, J.P. (1993) ‘The prevalence and consequences of exposure to violence among African-American youth’, Journal of American Academy of Child and Adolescent Psychiatry, 32, 424–30. Freeman, L.N., Mokros, H., and Poznanski, E.O. (1993) ‘Violent events reported by normal urban school-aged children: characteristics and depression correlates’, Journal of American Academy of Child and Adolescent Psychiatry, 419–23. Gardner, R. (1988) ‘Psychiatric syndromes as infra-structure for intra-specific communication’ in M.R.A. Chance (ed.) Social Fabrics of the Mind, Hillsdale, New Jersey: Erlbaum, 197–226.

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The future of social psychiatry 315 Gaminde, I., Uria, M., Padro, D., Querejeta, I. and Ozamiz, A. (1993) ‘Depression in three populations in the Basque country – a comparison with Britain’, Social Psychiatry and Psychiatric Epidemiology, 28, 243–51. Gilbert, P. (1989) Human Nature and Suffering, Hillsdale, New Jersey: Erlbaum. Gilbert, P. (1992) Depression: The Evaluation of Powerlessness, Hove (UK): Erlbaum. Goodyer, I.M., (1995) ‘Life events and difficulties: their nature and effects’, in I. Goodyer (ed.) The depressed child and adolescent: developmental and clinical perspectives, Cambridge: Cambridge University Press. Harris, J.R. (1995) ‘Where is the child’s environment? A group socialisation theory of development’, Psychological Review, 102, 458–89. Harris, T.O. (1992) ‘Some reflections of the process of social support; and nature of unsupportive behaviours’ in H.O.F. Veiel and U. Baumann (eds) The meaning and measurement of social support, Washington, DC: Hemisphere Publishing Corporation, 171–89. ——., Brown, G.W., and Robinson, R. (1999a) ‘Befriending as an intervention for chronic depression among women in an inner city. 1: Randomised controlled trial’, British Journal of Psychiatry, 174, 219–25. ——, Brown, G.W., and Robinson, R. (1999b) ‘Befriending as an intervention for chronic depression among women in an inner city. 2: Role of fresh-start experiences and baseline psychosocial factors in remission from depression’, British Journal of Psychiatry, 174, 225–33. Henderson, A.S. and Blackwood, D.H.R. (1999) ‘Molecular genetics in psychiatric epidemiology: the promise and challenge’, Psychological Medicine, 29, 1265–71. Husain, N., Creed, F., and Tomenson, B. (2000) ‘Depression and social stress in Pakistan’, Psychological Medicine, 30, 395–402. Idler, E.L. (1992) ‘Self-assessed health and mortality: a review of studies’, International Review of Health Psychology, 1, 33–54. Klein, M.H., Kupfer, D.J., and Shea, M.T. (1993) Personality and depression: a current view, New York: Guildford Press. Leighton, D.C., Hagnell, O., Leighton, A.H., Harding, J.S., Kellert, S.R., and Danley, R.A. (1971) ‘Psychiatric disorder in a Swedish and a Canadian community: an exploratory study’, Social Science and Medicine, 5, 189–209. Livianos-Aldana, L., Rojo-Moreno, L., Cervera-MartRnez, G., Dominguez-Carabantes, J.A. (1999) Temporal evolution of stress in the year prior to the onset of depressive disorders’, Journal of Affective Disorders, 53, 253–62. Locurto, C. (1990) ‘The malleability of IQ as judged from adoption studies’, Intelligence, 14, 275–92. MacDonald, K. (1992) ‘Warmth as a developmental construct: an evolutionary analysis’, Child Development, 63, 753–73. Magana, A.B., Goldstein, M.J., Karno, M., Miklowitz, D.J., Jenkins, J., and Falloon, I.R.H. (1986) ‘A brief method for assessing expressed emotions in relatives of psychiatric patients’, Psychiatry Research, 17, 203–12. Margolin, G. (1987) ‘The multiple forms of aggressiveness between marital partners: how do we identify them?’, Journal of Marital and Family Therapy, 13, 77–84. Miller, W.I. (1993) Humiliation and other essays on honour, social discomfort and violence’, London: Cornell University Press. Moffitt, T.E. (1993) ‘Adolescent-limited and life-course persistent antisocial behaviour: a developmental taxonomy’, Psychological Review, 100, 674–701.

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316 George W. Brown Moffitt, T.E., and Caspi, A. (1998) ‘Annotation: implications of violence between intimate partners for child psychologists and psychiatrists’, Journal of Child Psychology and Psychiatry, 39, 137–44. Mumford, D.B., Nazir, M., Jilani, F., and Baig, I.Y. (1996) ‘Stress and psychiatric disorder in the Hindu Kush: a community survey of mountain villages in Chitral, Pakistan’, British Journal of Psychiatry, 168, 299–307. ——, Saeed, K., Ahmad, I., Latif, S., Mubbashar, M.H. (1997) ‘Stress and psychiatric disorder in rural Punjab: a community survey’, British Journal of Psychiatry, 170, 473–8. Nazroo, J.Y. (1995) ‘Uncovering gender differences in the use of marital violence: the effect of methodology’, Sociology, 29, 475–94. ——, Edwards, A.C., and Brown, G.W. (1987) ‘Gender differences in the onset of depression following a shared life event : a study of couples’, Psychological Medicine, 27, 9–19. Neilson, E., Brown, G.W., and Marmot, M. (1989) ‘Myocardial infarction’ in G.W Brown and T.O. Harris (eds) Life Events and Illness, New York: Guildford Press, 313–42. Öhman, A. (1986) ‘Face the beast and fear the face: animal and social fears as prototypes for evolutionary analyses of emotion’, Psychophysiology, 23, 123–45. Park, G. (1974) The Idea of Social Structure, New York: Anchor Books, Anchor Press/Doubleday. Post, R.M. (1990) ‘Sensitisation and kindling perspectives on the course of affective illness: toward a new treatment with the anticonvulsant Carbamazepine’, Pharmopsychiatry, 12, 3–17. Robins, L.N. (1966) Deviant Children Grown Up: A sociological and psychiatric study of sociopathic personality, Baltimore: Williams and Wilkins. ——, and Regier, D.A. (1991) Psychiatric Disorders in America: The epidemiological catchment area study, New York: The Free Press; Oxford: Maxwell Macmillan International. Rooke, O., and Birchwood, M. (1998) ‘Loss, humiliation and entrapment as appraisals of schizophrenic illness: a prospective study of depressed and non-depressed patients’, British Journal of Clinical Psychology, 37, 259–68. Rowe, D.C., Jacobson, K.C., and Van den Oord, J.C.G. (1999) ‘Genetic and environmental influences on vocabulary IQ: parental education level as moderator’, Child Development, 70, 1151–62. Rumble, S., Swartz, L., Parry, C. and Zwarenstein, M. (1996) ‘Prevalence of psychiatric morbidity in the adult population of a rural South African village’, Psychological Medicine, 26, 997–1007. Rutter, M., and Sandberg, S. (1992) ‘Psychosocial stressors: concepts, causes and effects’, European Child and Adolescent Psychiatry, 1, 3–13. ——, and Smith, D.J. (1995) Psychosocial Disorders in Young People, New York: John Wiley and Sons Inc. ——, Champion, L., Quinton, D., Maughan, B., and Pickles, A. (1995) ‘Understanding individual differences in environmental risk exposure’ in P.Moen, G.H. Elder Jr. and K.Lüscher (eds) Examining lives in context: Perspectives on the ecology of human development, Washington, DC: American Psychological Association, 61–93. ——, Giller, H., and Hagell, A. (1998) Antisocial Behaviour by Young People, New York: Cambridge University Press.

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The future of social psychiatry 317 Sandberg, S., Rutter, Giles, S., Owen, A., Champion. L., Nicholls, J., Prior, V., McGuiness, D. and Drinnan, D, (1993) ‘Assessment of psychosocial experiences in childhood: methodological issues and some substantive findings’, Journal of Child Psychology and Psychiatry, 34, 879–97. Scheff, T.J. (1997) Emotions, the social bond, and human reality, UK: Cambridge University Press. Shweder, R. and LeVine, R. (eds) (1984) Culture Theory: Essays on mind, self, and emotion, New York: Cambridge University Press. Stoolmiller, M. (1999) ‘Implications of the restricted range of family environments for estimates of heritability and nonshared environment in behaviour-genetic adoption studies’, Psychological Bulletin, 125, 392–409. Surtees, P.G., and Ingham, J.G. (1980) ‘Life stress and depressive outcome: application of a dissipation model to life events’, Social Psychiatry, 15, 21–31. Teasdale, J.D. and Barnard, P.J. (1993) Affect, cognition, and change: Re-modelling depressive thought, Hove: Erlbaum. Vaughn, C.E. and Leff, J.P. (1976) ‘The influence of family and social factors on the course of psychiatric illness: a comparison of schizophrenic and depressed neurotic patients’, British Journal of Psychiatry, 129, 125–37. Wig, N., Menon, D.K., Bedi, H., Ghosh, A., Kuipers, L., Leff, J., Korten, A., Day, R., Sartorius, N., Ernberg, G., and Jablensky, A. (1987) ‘Expressed emotion and schizophrenia in North India, 1: cross-cultural transfer of ratings of relatives’ expressed emotion’, British Journal of Psychiatry, 151, 156–60. Wilhelm, K. and Parker, G. (1989) ‘Is sex necessarily a risk factor to depression’, Psychological Medicine, 19, 401–13.

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Index

Abas, M. 13, 24, 297 abdominal pain 276–7 accidents 32–3; life threatening 235 achievement-related events 251, 255 action space 162 addictive disorder 215–6, see also substance abuse, externalising disorder gender and 217 Adler, Z. 18, 20, 72 adversity, childhood 16–18, 45–6, 196, 213, 227–40, 299; composite scores of in childhood 237; chronic 124, 133, 136; need to control for multiple in childhood 228, 236; social 214, 280 agonistic behaviour 249; responses 252; connection with dominance rank overemphasised 250 agoraphobia 23, 235 Ainsworth, M. 245 Akiskal, H. 117 alcoholism, 139 Alexander, P. 234 Alnaes, R. 298 Ambelas, A. 263 amenorrhea, secondary 33, 282, 283 American approach to research 63, 64, 111 Americans Changing Lives (ACL) survey 230, 239; size of 240 analysis 2, 40–3, 76, 230 anchoring, rating of 20, 154 Andrews, B. 14, 17, 22, 127, 142, 305, 307 Andrews, H. 27 angina 276 anticipation of events 113–14 antipathy 196; and overanxiety 206 antipsychiatry 6 antisocial behaviour 130–1, 134, 138, 214; personality disorder 266 Antonovsky, A. 113

anxiety 13, 18, 32–3, 45, 298 appeasement, function of 252; versus assertive behaviour 249 appendicectomy 276 appraisal, style of 111, 151, 154, 234, 312; as dependent variable 112; relativity of 115 Arieti, S. 254 Aristotelian approach 71 arteriosclerosis 282 arthritis 275, 276, 283 Aschof, J. 264 ASI (Attachment Style Interview) 20, 215 asthma 136 attachment, theory 15, 245, 247, 252, 256; insecure/nonstandard attachment styles and psychopathology 212, 216, 228, 236, 301, 308; link of secure attachment with intimate social support 248; mutuality of with caregiving 246; only part of a wider affectional system 247 attitudes versus behaviour 124 attributable risk percent 44 back translation 197–8 Bandura, A. 111 Banstead Hospital 2 Barnard, P. 141, 312 Barnett, P. 229, 234 Barraclough, J. 28, 284 Bartholomew, K. 245 Bebbington, P. 26, 101, 143, 176, 217, 263, 270, 292, 298, 301, 309 Bech-Rafaelsen Mania Scale 265, 266 Beck, A. 10, 111, 249, 251, 254 Bedford College (Royal Holloway) 1, 7, 11, 35, 62, 247, 256, 266, 285 befriending 20–21, 311 behaviour as well as attitudes 124

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320 Index Bemporad, J. 252 Bennett, D. 29 Berry aneurysm 282–3 Best, K. 232 bias, control of 6, 32, 34 Bifulco, A. 13, 14, 15, 16, 17, 20, 72, 160, 181, 195, 215, 218, 227, 228, 229, 232, 248, 254, 255, 256, 300, 306, 307, 310, 311 Bilbao, Spain 2 biographical circumstances 8, 76, 151 bipolar disorder 263–71 Birchwood, M. 298 Birley, J. 5, 6, 63, 74, 292 Biron, C. 112 birth weight, low 284 Blatt, S. 246, 253, 254, 255 bleeding during pregnancy 284 blindness 34 blood flow to uterus 285 blushing 250 bond disruption 17, 247, 255 Boulton, M. 292 Bowlby, J. 10, 15, 216, 245, 246, 247, 252 Boyce, P. 156 Bretherton, I. 245 Brewin, C. 312 Brilman, E. 158 British Medical Journal 81, 91 Broadhead, J. 13, 24, 297, 304 Bronfenbrenner, U. 305 Brought Forward Time 43–4, 171, 175 Bruce-Jones, W. 280 Brugha, T. 140, 160 Bumpass, L. 237 Cadoret, R. 134 Camberwell Family Interview (CFI) 81, 98, 124; survey 9–11, 38, 42, 277, 302 Canadian Task Force, on mental health of immigrants and refugees 196 Canberra 15 cancer 174; breast cancer 28, 115, 284 Cane Hill Hospital 2 Carbonneau, R. 135, 137 cardiovascular disease 174; see also myocardial infarction care-eliciting display behaviour 252 caregiving, mutuality of with attachment 246 carers 81, 85, 86, 88 Carstairs, M. 2, 4 case-control designs 38, 127, 136, 140, 155, 308; limitations of 143 Caspi, A. 156, 172, 309

cause, causal chains 18–20, 153, 299; unmeasured common causes 238 CECA (Childhood Experience of Care and Abuse) 195–207, 297; administered retrospectively to adults 198; and psychopathology 205; intercultural flexibility of the instrument 207; prevalence figures for 201–2; validity and reliability 197, 311; CECA-Q 215 cerebral glioma, 81 Champion, L. 130, 305 checklist instruments 30, 57, 63, 309, 310 Chen, N. 284 childbirth, and depression 211 Christchurch, New Zealand, study of adolescents 213 chronic fatigue 279–80 chronicity of disorder 20, 128, 159 Chung, R. 263 circadian rhythms, 264 Clark, D. 143 Clayton, P. 156 coagulability 282 Cochrane accolade 56, 65, 102 cognitive avoidance 86 CBT (Cognitive Behavioural Therapy) 143 Cohen, S. 284 cohort studies 155 cold, common 284 colitis 277 Colorado Adoption Study 133 comfort 162 commitment 35, 218 comorbidity 45, 298 Composite International Diagnostic Interview (CIDI) 235 composite risk scores, 236 conduct problems/disorder 130, 204, 206– 7, 214, 304, 306; long term effects of 232 confiding 10; felt need for 221 conflict over speaking out rating 27, 37–8, 280 confounding 238 Connolly, J. 281 consensus panel meetings 33–4, 266 context 32, 34, 75, 126, 151; boundaries of 171, 309–10 control, high, i.e. discipline/supervision 196, 202–4, 206 controllability, of life events 163 conveyor belt 19 Conway, S. 283 Cooper, J. xv

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Index 321 Copeland, J. xv, 25 coping 16, 84, 86, 116, 151, 154, 234; problem-focussed versus emotional 154 coronary care units, trial of 66 Coryell, W. 231 Costello, C. 114, costs, of research 171 couples, study of 21, 112, 219; therapy 104 Coyne, J. 299 Cragg, D. 140 Craig, T. 27, 215, 219, 277, 278, 280, 281, 282, 283, 301 Creed, F. 27, 263, 276, 284 criterion contamination 127, 133, 140 criticism, 132; critical comments 5, 35; frequency of 99 Cronkite, R. 111 CSC (Chronic Subclinical Symptoms or low grade symptomatology) 163, 212, 308 cycling, rapid 266 Cyranowski, J. 301 danger, rating of 13, 154; and onsets of anxiety 249; of depression 303 Darwin, C. 59, 249 data, collection 3; presentation 42 Davies, E. 89, 90, 91, 309 Day, R. 174 defeat 252; see also failure delogjamming, events 154 Delongis, A. 111 denial 16, 84, 86, 113, 116, 234 depression (MDD or Major Depressive Disorder) chronicity of 128, 215; history of 234; initial onset versus subsequent course 227, 229–34, 299; maternal, impact of on daughters 22, 214; mediating onset of physical illness 278–280; onset before age 20, 231; onset date versus admission date 263; onset of xv, 9ff, 127, 173, 183–4; onset of within bipolar disorder 263; preonset period and season of year 270; pre-onset period 8 vs 20 weeks 270; remission from 20–1, 159–60; social origins of 227; unaware of onset date of 266 design 38–40, 171; see also case-control design deviant, partners 305; peers 131, 214 Devins, G. 114 diabetes 285 Diagnostic Interview Schedule (DIS) 231 diagnostic subgroups 297

dictionaries, of rating examples 8 diet 285 discharge, from hospital 3, 97 discord, parents’ marital 131, 213; family and conduct disorder 206, 213 discrete time survival methods 178, 231 dissatisfaction, rating of 5 distal versus proximal effects 172 Dobash, R. 309 Dohrenwend, B.P. 111, 113, 171, 175, 217 Dohrenwend, B.S. 111, 113, 175, 217 domain specificity of motivational systems 251; and depression 253 dominance, interpersonal versus position, vis-à-vis group 250 dose-response relationships 143 DSV (Dynamic Stress-Vulnerability) model 151–62 Duncan-Jones, P. 15, 57, 152 Dunham, H. 61 Durkheim, E. 23, 61, 62, 292 dyspepsia 279–80 dysphonia 27, 280 eating disorders 28 Eales, M. 44–5, 57, 228, 236, 248, 251, 254, 298 Edwards, A. 21, 113, 219, 221, 248, 301, 307 Ehlers, C. 264, 265, 269 Eisenberg, N. 246, 247 Ekman, P. 99 Elder, G. 172 elderly 157, 162–3; role of severe health events for 159 emotional reactivity 156 empathy 106; sympathy versus nurturant warmth 256 Endicott, J. 231 Ensel, W. 111, 172 entrapment 12, 76, 126, 215, 219, 250–1, 302 EPIC (European Prospective Investigation into Cancer and Nutrition) 173, 180, 190 Epidemiological Catchment Area (ECA) Studies 298 Equal environment assumption 138 ESRC (Economic and Social Science Research Council) xiv, 9 Essen-Moeller, E. 61 Esterson, A. 6 evidence-based approach 56, 91 evolved core motivational systems 245ff explanation versus understanding 72–3, 76 exposure, to risk 129 expressed emotion (EE) 2–4, 31, 67, 93,

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322 Index 97–107, 124, 292, 310, 311; and bipolar disorder, 103; and eating disorder 103 externalising disorders 22, 215 facial expression 246 failure 252; see also defeat, humiliationentrapment Fairburn, C. 143 Family History Research Diagnostic Criteria method 234 family negativity 124, 138 family therapy 104 Faravelli, C. 22, 228 Faris, R. 61 Fava, E. 160 Fava, G. 22 favouritism, of other 201, 205, 206 Fergusson, D. 157, 160, 213, 299 fertility, clinics 112; events 113 Fillion, L. 115 Finlay-Jones, R. 12–13, 248, 249, 298 Flint, J. 156 focal stressor 115 Folkman, S. 111, 152 Fontana, A. 30 formative effect 43–4 Fortuna, goddess 19 Frank, E. 26, 158, 176, 264, 301 Frankenhauser, M. 113 freedom to act 152, 154 Freud, S. 72–3, 246 fresh start, rating of 20; divorce as 237; impact of 143, 154 Frey, J. 30 Frijda, N. 33 Fuller, J. 28, 285 gain, as a dimension of life events 161 Galilean approach 71, 117 Gaminde, I. 24 Garety, P. 77 Garmexy, N. 232 Gatehouse, N. xiv gender 21–2, 113, 160–1, 186–7, 211–22; and attachment style 216–7; and caring role 218; and coping strategies 218; and creating events for others 305; and female excess depression, accounting for 217; and humiliation-entrapment events 305; and loss 183–4 gene-environment correlations 131–2, 135 gene-environment interaction 135 general practice 312 genetic vulnerability 162 Geyer, S. 28, 284

Giel, R. 22; 159 Gilbert, P. 13, 246, 249, 250 glandular fever 280 Glaser, B. 29, 88 Glassner, B. 263 glycaemic control 285 goal frustration, rating of 27, 280 goals, see plans and purposes 153 Goffman, I. 56 Goldberg, D. 57, 151 Goldstein, M. 310 Goodyer, I. 26, 229 Gotlib, I. 216, 229, 234 Grant, I. 28, 283 grief 17, 247 Groningen research 151–162; primary care study 155, 160; well-being study 156 grounded theory 29, 30 group homes 106 Guerrero, D. 91 guilt 218, 247 Guthrie, E. 278 Haan, N. 16 Hagnell, O. 61 Hamilton rating scale for depression (HRS-D) 265, 266, 269 Hammen, C. 111, 133, 253, 263 Hardy, G. 253 harmonious marriage 142 Harre, R. 75 Harrington, R. 229 Hayhurst, H. 102 Hazan, C. 245 health, perceptions of 115, 310; changes in 171 Heard, D. 245, 246, 250 Hebrides, survey in 23, 248, 302 helicobacter pylori 281 helplessness, ratings of 18, 252; powerlessness 206; sense of 113 Henderson, S. 15 Hepworth, C. 13, 22, 57, 206, 250, 251, 255, 256, 298, 299, 305 Herbert, J. 26 heritability 59, 133 Hill, J. 207 Hinde, R. 249 Hinkle, L. 66 Hirschfield, R. 156 HLEQ (Health and Life Experiences Questionnaires) 174 Hobfol, S. 111 Hodson, S. 219 Hoffman, M. 247

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Index 323 Hollingshead, A. 62 Holmes, T. 57, 62, 75, 111 homelessness 218 Hooley, J. 99, 102 hope 90 hopelessness, generalisation of 10–11 Hopkins, A. 91, 94 hormonal, aetiology of depression 211, 301 Horwood, L. 157, 160, 299 hostility 5, 20, 99, 132 House, A. 27, 28, 282 HPA (Hypohalamic-pituitary-adrenal) axis 161 humiliation 12, 76, 126, 212, 219, 250–1; H-E and onset of depression 302–4; possible result of favouritism of other 206 Hunt, N. 263 Hurry, J. 217 Huxley, P. 59 IBS (Irritable Bowel Syndrome) 277, 280 identity-relevant stressor 218 ideographic approach 74–5 idiosyncracies, of perception 112; of reporting 112 illness behaviour 66 illness-relatedness/illness dependence, of life events 263, 266, 267 incident 32, 267 inconsistencies, challenge of for development of models 297 independence of life events 6, 36, 37, 126, 266–7, 304 indifference, parental 196, 202–4, 207, 213 infection 279 Institute of Psychiatry 1, 7, 61 institutionalisation 3, 56, 59 institutional/statutory care 214 intercultural rating 24, 98–9, 199, 200 internal working models, of attachment 252 internalising disorders 215 interpersonal and Social Rhythm disruption therapy (IPSRT) 264, 266, 271 interpersonal sensitivity 156 Interpersonal Therapy (IPT) 269 intervention smorgasbord of 312; studies 20–1, 102, 311–2; targets 238 interviewing 31; ethics of 87; flexibility of 82–3; gratitude of interviewee 89; intensive 310; intercultural, 198; intervention effects of 88–9; joint 88 intimacy rating 42 inventory or checklist 57, 75, 309, 310

investigator 33; approach based on 8, 32, 310 IQ 214 Isle of Wight study 129, 304 Islington survey 12, 13, 15, 16, 17, 21, 302 ISSI (Interview Schedule for Social Interaction) 15 Jaspers, K. 72–3 Jeffreys, M. 7 job loss 154, see unemployment Joffe, R. 263 Joiner, T. 232, 233 Kanner, A. 111 Kaplan-Meier life table method 270 Katschnig, H. 22 Kedward, H. 159 Keller, M. 231 Kendler, K. 131, 133, 135, 139, 140, 141, 142, 156, 157, 158, 235 Kennedy, S. 263 Kessler, R. 28, 113, 127, 129, 176, 178, 184, 217, 218, 231, 232, 234, 235, 299, 300, 311 Kevlin, M-L. 12 kindling 141, 299 Klein, M. 142, 298 Klerman, G. 269 Kraemer, H. 230 Kuhn, N. 59 Kunce, L. 246 Kuipers, E. 101, 102, 124, 140, 143 Kupfer, D. 269 lack of care 196 lack of supervision 196 Laing, R. 6, 65 Lake, B. 245, 246, 250 Lam, D. 102 Lazarus, R. 111, 152, 154 LEDS 6, 75, 112–117, 124, 130–1, 139, 155, 175, 263, 264, 266; covering ten years, 311; time needed to administer 171; uniquely allows constant expansion 271 Leenstra, A. 159 Leff, J. 4, 6, 101, 124, 143, 263, 311 Leibenluft, E. 264 Leighton, A. 23, 61 Lemyre, L. 20, 45, 306, 310 Letchford, L. xvi Leventhal, H. 33 Lewin, K. 111 Lewinsohn, P. 229, 248 Lewis, A. 2, 65, 97 life events 6, 130–1, 139, 155; atypical

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324 Index 251; controllability of 163; ‘domestic’ events 220; event decay 173; gender and, women ‘yoked’ to men’s lives; 217; interplay with chronic adversities 13, 140; ‘joint’ for couples 21, 112; ‘matching’ specific domains 13, 34, 218, 220, 254; mild 159; origins of 19, 302; scores 35, 125 Life History Calendar 172 life stage 9–10, 186 lifespan perspective 298 Lin, N. 111, 172 Lloyd, C. 285 locus of control, external-internal 154 Lora, A. 22 Loss, rating of 13, 76, 154, 173, 181–3, 247–249, 303; and gender 183–4; as failure 161; of parent 16–18; of reward 248 MacArthur Foundation 22, 26 McCall, G. 10 McDougall, W. 245, 247, 250 McGuffin, P. 157 McKinney, W. 117 Maclean, U. 23 McPherson, H. 263 macro-context 154, 302; importance of for origins of life events 306 Magana, A. 124, 140, 310 Magee, W. 231, 232 Malkoff-Schwartz, S. 267, 269 manic depression, 263 Margolin, G. 309 Markov Chain Montecarlo Techniques 189 Marlborough Family Service 104–5 Marmot, M. 27, 281, 311 marriage, quality of 19, 104, 217; violence in 305, 309 Masten, A. 232 mastery 11, 162; perceived 113 Maudsley Hospital 2, 9, 21, 38, 65 Maughan, B. 232 Mayo, J. 263 Mayol, A. 111 meaning 8, 32, 58, 71, 92, 153, 307; politics of 64–5; role-based versus specific purpose 308; versus causality 72–3; versus memory-linked 308 measurement 32; and design 308–11; continuous 45; random error 138 measures, shortened 28, 92, 140 Mechanic, D. 66, 114, 311, 291, 298 mediation/mediator effects 18–20, 157, 232 medical model 61

medically unexplained symptoms 275 medication; antidepresssants 104; antipsychotic drugs 97 memory-linked emotional schema 307 menorrhagia 280 Metalsky, G. 232, 233 Meyer, A. 57 Meyer, J. 139 Midtown Manhattan Study 61 Mill, J. 75 Miller, P. 12 miscarriage 284 mobility, social 18 Moffit, T. 306, 309 Monck, E. 3, 4, 140 Monroe, S. 111, 151, 159 Montreal sample of adolescents 204; harsh punishment linked with indifference 206 Moore, E. 124, 140 Moos, R. 111 Moran, P. 14, 18, 102, 159, 160, 195, 304, 308 MRC (Medical Research Council) xiv, 1, 56; Social Psychiatry Research Unit 1, 7, 32, 55, 62, 97, 124 Mullen, P. 227, 228 multifactorial causation 276 multiple informants 8, 128, 140 multiple motions, theory of in physics 111 multiple sclerosis 282, 283 multiple systems versus primary disturbance 255 Murphy, E. 27, 159, 281 Murphy, H. 195 Mutale, T. 284 myocardial infarction 27, 281–2 Nairobi, Kenya 22 narrative 75, 93, 312 National Comorbidity Survey (NCS) 234, 239; size of 240 Nazroo, J. 21, 113, 161, 219, 221, 248, 301, 307, 309 Ndetei, D. 22 needs 154 Neeleman, J. 154 negative elements in core relationships, NECR 233 negative thinking (automatic thoughts) 251 neglect 215 see also indifference NES (negative evaluation of self) 12 neuro-imaging 161 neuroticism 142, 151–62, 279, 308 neutralisation of threat 154 Ni Brolchain, M. 9, 25, 57

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Index 325 Nielsen, E. 27, 281, 282, 311 nomothetic approach 74 nonexperimental studies 238 Norris, V. 2 Nova Scotia 23, 61 novelty-seeking 214, 306 nurses, community psychiatric 56 Oakley-Browne, M. 227, 228 Oatley, K. 159, 221 objective versus subjective 61, 63–4, 154 observation 57 O’Connor, P. 12 O’Connor, T. 133–4 O’Hare, T. 284 Ohman, A. 249, 292 Okasha, A. 102 Oldehinkel, A. 160, 161–3 Ormel, H. 22, 151, 152, 161, 162, 163, 308 Osoba, D. 92 overanxiety, diagnosis of 201 overinvolvement 4, 5, 98, 99 PACE (psychosocial assessment of children’s experiences) 140 palliative care 87, 91 parental behaviour, contradictions in 206 parental negativity 133–4, 135, 137 parental separation/divorce, effects on child 213, 237–8; increase in since WWII 237 parents 4, 5; mentally ill 132; substance abuse 213 Park, G. 292 Parker, G. 159, 229, 235, 301 Parkes, C. 3, 246 Parsons, T. 29 Pathare, S. 215 pathoplastic phenomena 255 Pawlby, S. 131 Paykel, E. 7, 26, 125, 129, 154, 248 Pearlin, L. 116, 172, 218 peer group, deviant 131, 214 Penrose, R. 282 perceived impact 112 perceived uncertainty 113 peripheral stressor 113 Perlman, D. 245 Personal Life Chart (PLC) 175 personality 142, 151; borderline PD 266; disorder 132, 298, 305 person–environment formula 111 Peto, J. 44, 56 phenothiazine medication 5 phobia 154, 203, 204, 207 physical abuse 196, 202–4, 205, 213

physical illness, chronic 172 Pike, A. 137, 138 Pittsburgh, perhaps an area with low rates of severe events 271 pity 247, 256 planning, capacity 131, 162, 214 plans, and purposes, see goals 34, 145 Plomin, R. 131, 138, 157 Popper, K. 57, 72, 74, 75 positive appraisal 86 positive life events 154, 306; can also be severely threatening 310; PLC 159–60, 163 Post, F. 26, 140, 299 post-partum depression 211 post-traumatic stress disorder (PTSD) 153, 154, 161; and EE 103; and physical illness 106 Power, M. 312 pregnancy, premarital, 19, 212, 214; as a humiliating life event 219; as an exclusion criterion 266 Price, J. 13, 250 Prince, M. 158 prospective longitudinal studies 38; one danger with in missing intervening changes 14; strength of 140 Protheroe, D. 27, 284 provoking agent 11 proximal versus distal effects 172, 302 Prudo, R. 23, 28, 57, 248, 254 PSE (Present State examination) 9, 45, 62 psychoanalysis 72; versus psychiatry 65 psychosis, cognitive approach to 298 psychosomatic research 275–285 pudicity, rating of 28, 37 quality of life 81, 93; versus length of life 90 quantitative versus qualitative research 1, 67, 91, 123–4 Quebec Health of Children Survey 201 questionnaires, compared with interviews 92, 309 Quinton, D. 124, 129, 130, 131, 132, 136, 207, 214, 221 radiotherapy 82, 90 Rahe, R. 57, 62, 75, 111 Ramirez, A. 28, 284, randomised controlled trial (RCT) 20, 40, 65, 102, 312 Raskin, A. 265 ratings, development of scales 34–5, 84; examples of 36–8 Raune, D. 77 readmissions 3, 4

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326 Index Redlich, E. 62 refugees 195–207 refutability 72 Regier, D. 298 reliability, inter-rater 33, 57, 62, 84 reluctance in reporting 297 remission, from depression 20, 159 replication 11, 38 resilience 161–2, 214 retrospective work 40; importance of inserted in prospective studies 310 revolving door 55 Richardson, S. 31 Robins, C. 253, 255 Robins, L. 127, 130, 231, 298, 306 Robinson, N. 285 Robinson, R. 20, 311 Rodgers, B. 151, 227, 228 role(s) 8, 34, 93; as carer 218; axiomatic 308; involvement in 220; overvalued 218 role-identity 10, 218 role responsibility 218, 220 role reversal 200 role strain 217 Romans, S. 227, 228 Rutter, M. 5, 12, 63, 98, 129, 132, 134, 136, 138, 139, 142, 161, 206, 228, 229, 231, 232, 234, 295, 296, 302, 304, 305, 308–11 Rycroft, C. 72 SADS-L (Schedule for Affective Disorders – Lifetime version) 265, 269 St Thomas’ Hospital 7 Salander, P. 91, 93 samples, limitations of selected for data interpretation 38–9, 233; attrition of in longitudinal studies 311 Sandberg, S. 124, 125, 128, 129, 136 Sarason, I. 111 Savoie, J. 115 scapegoating 201, 202–4, 206 Scarr, S. 136 Scheff, T. 250, 309, 310 schizophrenia 2–7, 56, 100ff, 266 Schmidt, U. 28, 37 schools 125 Schutz, A. 8 SCID-IV (Structured Clinical Interview for DSM-IV Axis-1 Disorder) 215, 265, 269 scientific method 61, 71–7, 117 Sclare, P. 263 self-blame 16, 220 self-efficacy 162, 232

self-esteem 10–12, 142, 162, 206, 233, 308; followed up after 8 years 307 self harm 277 Selye, H. 62 sensitivity to death 23 SEPRATE (Structured Event Rating System) 175 SES (socio-economic status, social class) 9, 19, 58, 153 SESS (self evaluation and social support schedule) 12, 81 sexual abuse 196, 205, 213 sexually transmitted disease (STD) 302 shame 13, 218, 249 shame spectrum emotions 250 shared versus unshared environment, effects of 138; unclear distinction 139 Shaver, P. 245, 246 Shepherd, M. 65 shift work 264, 267 siblings 22; as controls 277; studies of pairs of 216 Silberg, J. 128, 133, 134, 137 Simmons, J. 10 Simons, A. 151 sleep disruption 271; sleep/wake cycle 269 smiling, 100 Smith, D. 302 smoking 142, 154, 282, 284 Sneew, K. 92 social comparison 251 social power 250 Social Production Function, theory, 162 Social Rhythm Disruption (SRD) 263, 267; rating of 264; reliability of 267 social support 14, 85, 162, 214; helpfulness of 15; in a crisis 18, 21, 39– 40; less protective against anxiety 248; natural versus professional 312 sociology 61, 65, 123 sociotropy, dependency 253, 254, sons, of Islington Mothers Study, 21 species-typical core motivational systems 245ff specification error 229, 299 speech sample, 5-minute for EE rating 124 specific versus general 125; hopelessness 11 Spitzer, R. 265 SPlus 184 Srole, L. 61 Sroufe, A. 234 SSRC see ESRC statistics 43; modelling 171–90; statistical interaction 44–5, 135

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Index 327 steeling 161–2 Steverink, N. 162 stigmatising 154 Straus, M. 235 Strauss, A. 29, 88 stress, 62; chronic interpersonal 232; see also difficulties, priming low-level physiological responses 256 stroke 28, 282 subarachnoid haemorrhage 282 subjective versus contextual 61, 81, 117, 153; see also self-report 181–3 subjectivism, sin of 90–1 submissive displays 252 substance misuse 130; and males 214 Suomi, S. 245 survival analysis 176 susceptibility 134, 142 Surtees, P. 156, 173, 176, 180, 181 surveys, traditional large scale 61, 309 survival analysis, backward 270 Sweet, L. 115 systems therapy 104 tape-recording of interviews 87 Tarrier, N. 103 Tausig, M. 111 Taylor, S. 111 teacher questionnaire 130 Teasdale, J. 134, 141, 312 tender emotion 247 Tennant, C. 129, 159, 217 Thapar, A. 131, 133 theory of mind 74, 76 therapy, marital 311; therapeutic implications 143, 311–12 Thoits, P. 113, 221 Thorn training 56 threat (threatfulness or unpleasantness) of an event 8, 36–8, 25 time dependent covariate effects 176, 189 time order 39, 57, 93, 126, 140, 171, 184–5, 188 tissue damage 276 Torgersen, S. 298 transmeridian flight 264, 267 trauma 161 Treasure, J. 37 treatment, non-specific effects of 307 treatment-seeking 281 triangulation 112 triggering effect 43–4 Truchon, M. 114

Turner, R. 171 type-A behaviour 28, 282 ulcer, peptic 275, 276, 277, 280; duodenal 281 uncontrollability 153 unemployment 10, 154, 251 unexpectedness, of event 153 unoccupied time 3 unshared versus shared environment 138; unclear distinction 139 US National Comorbidity Survey (NCS) 234 validity 40; respondent-relative agreement 88–9, 140 Vaillant, G. 16 van Os, J. 143 Vaughn, C. 4, 101, 124, 143, 311 Verstehen 8 victimisation 305 Virginia Twin Study 133, 134, 135–6, 137, 139 visiting 2, 55 voice, expressiveness of 31, 98 von Wright, G. 71 vulnerability 10, 126, 134, 232; instrumental 152–3; model 38, 115–162; psychological (NES or CSC, qv) 212 Wainwright, N. 173, 180 Walthamstow, study of loss of parent 16–18 warmth 17; nurturant versus empathy/sympathy 256 Waters, E. 245 Weber, K. 73 Wehr, T. 264, 269 Weissman, M. 232 Wethington, E. 28, 171 Wheaton, B. 171 WHO 173, 275; field trials of CIDI (qv) by 235 Wilhelm, K. 301 Winch, P. 72 Wing, J. xv, 3, 9, 56, 62, 64, 74 Wittchen, H. 159, 235 Wolff, H. 62, 66 Worcester, J. 44 work stress 282 working models 252 WPIC (Western Psychiatric Institute and Clinic, Pittsburgh) 266 Zeitgebers and Zeitstorers 264, 269, 271 Zimbabwe, Harare 24, 302 Zimmerman, M. 111 Zocolillo, M. 131

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