The Loss Of Sadness (2007) Horwitz

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The Loss of Sadness This page intentionally left blank The Loss of Sadness How Psychiatry Transformed Normal Sorrow Into Depressive Disorder Allan V. Horwitz and Jerome C. Wakefield  Oxord University Press, Inc., publishes works that urther Oxord University’s objective o excellence in research, scholarship, and education. Oxord New York Auckland Cape Town Dar es Salaam Hong Kong Karachi Kuala Lumpur Madrid Melbourne Mexico City Nairobi New Delhi Shanghai Taipei Toronto With ofces in Argentina Austria Brazil Chile Czech Republic France Greece Guatemala Hungary Italy Japan Poland Portugal Singapore South Korea Switzerland Thailand Turkey Ukraine Vietnam Copyright © 2007 by Allan V. Horwitz and Jerome C. Wakefield Published by Oxord University Press, Inc. 198 Madison Avenue, New York, New York 10016 www.oup.com Oxord is a registered trademark o Oxord University Press All rights reserved. No part o this publication may be reproduced, stored in a retrieval system, or transmitted, in any orm or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission o Oxord University Press. Library o Congress Cataloging-in-Publication Data Horwitz, Allan V. The loss o sadness : how psychiatry transormed normal sorrow into depressive disorder / Allan V. Horwitz and Jerome C. Wakefield. p. ; cm. Includes bibliographical reerences and index. ISBN 978-0-19-531304-8 1. Psychiatry Miscellanea. 2. Depression, Mental Miscellanea. 3. Mental illness Miscellanea. I. Wakefield, Jerome C. II. Title. [DNLM: 1. Diagnostic and statistical manual o mental disorders. 2. Depression. 3. Depressive Disorder. WM 171 H824L 2007] RC480.5.H667 2007 616.89 dc22 2006032581 9 8 7 6 5 4 3 2 1 Printed in the United States o America on acid-ree paper To David Mechanic —AVH To my parents, Helen and Ted Sherman —JCW This page intentionally left blank Foreword T he book you are about to read is a brilliant tour de orce o scholarship and analysis rom two o our leading thinkers about psychiatric diagnosis and the nature o mental disorders. Allan Horwitz and Jerome Wakefield’s The Loss of Sadness represents the most cogent and compelling “inside” challenge to date to the diagnostic revolution that began almost 30 years ago in the field o psychiatry. The authors begin by arguing or the existence o a universal intuitive understanding that to be human means to naturally react with eelings o sadness to negative events in one’s lie. In contrast, when the symptoms o sadness (e.g., sad eelings, dif culty sleeping, inability to concentrate, reduced appetite) have no apparent cause or are grossly disproportionate to the apparent cause, the intuitive understanding is that something important in human unctioning has gone wrong, indicating the presence o a depressive disorder. Horwitz and Wakefield then persuasively argue, as the book’s central thesis, that contemporary psychiatry conuses normal sadness with depressive mental disorder because it ignores the relationship o symptoms to the context in which they emerge. The psychiatric diagnosis o Major Depression is based on the assumption that symptoms alone can indicate that there is a disorder; this assumption allows normal responses to stressors to be mischaracterized as symptoms o disorder. The authors demonstrate that this conusion has important implications not only or psychiatry and its patients but also or society in general. The book’s thesis is o special interest to me, because I was the head o the American Psychiatric Association’s task orce that in 1980 created the DSM-III (i.e., the third edition o the Diagnostic and Statistical Manual of Mental Disorders, the Association’s of cial listing o recognized mental disorders and the criteria by which they are diagnosed). This was the first edition o the Manual to oer explicit symptomatic criteria or the diagnosis o each mental disorder. Now in its ourth edition, the DSM is generally considered to have revolutionized viii FOREWORD the psychiatric proession. It serves to define how researchers collect their samples, what conditions insurance companies will reimburse, what conditions courts and social agencies treat as illnesses, and how individuals themselves interpret their emotional experiences. The DSM’s standardization o psychiatric diagnosis by using explicit rules or making a diagnosis has been critical to the explosion o research and knowledge in the mental health field. It has allowed clinicians and researchers with diferent theoretical perspectives, and thus dierent languages, to communicate with each other. It has also addressed doubts about psychiatry’s scientific status, such as concerns about the reliability o its diagnoses. Yet the very success o the DSM and its descriptive criteria at a practical level has allowed the field o psychiatry to ignore some basic conceptual issues that have been lurking at the oundation o the DSM enterprise, especially the question o how to distinguish disorder rom normal sufering. This book will bring increased attention to these conceptual problems. My involvement in an earlier debate over whether to remove homosexuality rom DSM-II in 1973 led me to grapple with the question o how to define mental disorder. I ormulated the definitions o mental disorder in the introductions to the DSM-III, the DSM-III-R (the DSM’s third edition revised), and the DSM-IV, which aim to explain the reasons that certain conditions were included in and other types o problems excluded rom the Manual. Since then, Dr. Wakefield has critiqued my eforts in ways that I have largely become convinced are valid. His evolution-based “harmul dysunction” analysis o the concept o mental disorder raises subtle, nuanced questions about mental disorder that challenge one’s thinking, no matter where one alls on the issues. It is easily the most widely cited and provocative analysis o the concept o mental disorder that exists today, simultaneously deending the concept as legitimate and providing a ramework or this book’s critique o current diagnostic standards as too broad. Moreover, Horwitz and Wakefield point out that theDSM is not consistent even in applying its own definition o mental disorder to the diagnostic criteria sets or specific disorders. Whereas the DSM definition o mental disorder, like the harmul-dysunction approach, clearly specifies that a disorder involves a dysunction in the individual and is not an expectable response to a stressor, the ormulation o the DSM’s diagnostic criteria sets rarely took this into account. In other words, its criteria specified the symptoms that must be present to justiy a given diagnosis but ignored any reerence to the context in which they developed. In so doing, they allowed normal responses to stressors to be characterized as symptoms o disorder. Many critiques o the DSM have come rom the “outside” in that they have been suspicious o the very notion o a mental disorder and thus rejected the idea o a psychiatric diagnostic manual as inappropriately medicalizing social problems. In contrast, Horwitz and Wakefield recognize the DSM’s contributions FOREWORD ix and accept its assumption that there are genuine mental disorders in the strict medical sense. Ironically, it is by taking seriously the DSM’s claim to be a manual o mental disorders (and thus to all within the scope o medicine) that the authors are able to mount a devastating critique o the way the DSM operationalizes the diagnosis o depression (and by implication, other diagnostic categories as well) with inadequate attention to context. Because their analysis is anchored in psychiatry’s own assumptions, it will be hard or those now constructing the DSM-V (expected publication in 2011) to ignore. Horwitz and Wakefield trace the history o the diagnosis o depression, beginning with Hippocrates and working through to the present, and show with impressive and persuasive scholarship just how consistently their view—rather than the DSM’s approach in which symptoms alone can indicate disorder—is reflected in the historical traditions o medicine and psychiatry, even including the work o Emil Kraepelin, the psychiatrist oten considered the inspiration or the DSM-III. It should be noted that at the time the diagnostic criteria or depression were srcinally developed, they were intended or research samples in which it was a reasonable assumption that the patients were disordered. The authors argue that, when those same diagnostic criteria that contain no reerence to context are used in community epidemiological studies and screening o the general population, large numbers o people who are having normal human responses to various stressors are mistakenly diagnosed as disordered. The researchers who have conducted the major epidemiological studies over the past two decades have totally ignored this problem. The result has been semiofcial prevalence rates that many find unbelievable. The authors’ analysis o disorder itsel does not state exactly where the line between dysunction and normality is to be drawn and allows that the boundary is uzzy. I have to admit that I would be inclined to draw the boundary so as to include more under “disorder” than they do. Frankly, I remain cautious about the possibility o incorporating context into diagnostic criteria and about the unreliability and alse negatives that might result. But it has yet to be tried in a serious way. This book will place this issue on psychiatry’s agenda and make it one o the major topics that should be considered in the upcoming revisions that will yield the DSM-V. However the problem is resolved, because o this book the question will have to be posed; it can no longer be ignored. Relentless in its logic, Horwitz and Wakefield’s book orces one to conront basic issues that cut to the heart o psychiatry. It has caused me to rethink my own position and to consider how the authors’ concerns might best be handled. It will shape uture discussion and research on depression, and it will be an in- dispensable guide to those who are rethinking psychiatric diagnostic criteria in preparation or the DSM-V. It would be interesting to look back 100 years rom now and see whether context is as crucial to diagnostic criteria as the authors believe it to be or whether the stricter symptom-based approach can somehow x FOREWORD rebound from their critique. But either way, psychiatry will rest on firmer logical foundations as a result of their critique, and this book will stand as a watershed in the conceptual development of the field. Robert L. Spitzer, MD Professor of Psychiatry New York State Psychiatric Institute Preface T his book is the result o an unusually cooperative efort. The order o authors is alphabetical; we are both ully and equally responsible or the intellectual content throughout the book, which has resulted rom a tireless and stimulating mutual process o eedback, incremental improvement, and debate at every stage. Our coauthorship, nevertheless, occurred serendipitously. We were each independently planning books about depression, with essentially the same overall message. When we discovered this in discussion one day, weideas decided to join orces. ways by which we each came to our srcinal o writing such a However, book werethe quite diferent. Jerome Wakefield, having written extensively about the concept o mental disorder, was scheduled to publish an invited journal article critiquing psychologist Neil Jacobson’s behaviorist attack on the medical model o depression. The theme o the article was that neither those who believe in the “disorder” approach to depression expressed in the Diagnostic and Statistical Manual of Mental Disorders (DSM) nor those, like Jacobson, who deny that depression is a medical disorder are correct. Instead, they are talking past each other about diferent kinds o cases. Wakefield intended to argue that instead o trying to decide between these rival views, psychiatry should instead be drawing a distinction between the genuinely disordered and those with normal responses to misortune whom the DSM has misclassified. Following Jacobson’s untimely death, the journal decided not to proceed with the article given that he would be unable to reply to it. Meanwhile, Wakefield realized that the topic was ar broader than first conceived and that a balanced consideration o both the disordered and nondisordered orms o depression and sadness called or book-length treatment. The issue itsel seemed urgent be- cause, i mental health proessionals were talking past each other about it rather than recognizing its complexity, then they would inevitably be talking past some o their patients, as well. We hope that this book will indeed encourage these xii PREFACE diferent actions to talk to each other and to realize the distinctions to be made between those who are depressed and those who are normally sad. Allan Horwitz had recently completed a book about the new paradigm o “diagnostic psychiatry” introduced in the DSM-III in 1980. By then the DSM had grown to several hundred diagnoses, with depression becoming the signature diagnosis o contemporary psychiatry. Careul study o this condition in particular thus promised to illuminate broader issues that aced the field. Horwitz’s work in the sociology o stress had convinced him that many o the conditions that sociologists studied were similar to those that psychiatry classified as Major Depression yet that they were not disordered but were normal human responses to stressul social circumstances. Like Wakefield, he was also convinced that there were depressive conditions that were truly disordered. A book on depression seemed to him to be a way at once to examine the successes and limitations o psychiatry’s new paradigm and to identiy conceptual problems in the sociology o medicine, all through the lens o a detailed analysis o this one pivotal diagnostic category. It also seemed that joining orces with Wakefield might help navigate between the Scylla o social constructionism and the Charybdis o biological essentialism and produce an analysis that grounds the distinction between normality and disorder in biological actors while at the same time maintaining an important role or social actors in making this distinction. We hope that the result o our collaboration is a book that does indeed manage to wend a balanced path between the biological and the social and between normal sufering and mental disorder. All books are products not just o authors but also o the environments in which they are written. It has been our good ortune to have written this book in exceptionally fine circumstances. For Horwitz, the Institute or Health, Health Care Policy, and Aging Research and the Sociology Department at Rutgers have provided intellectual stimulation, extraordinary colleagues, and ideal working conditions. In particular, David Mechanic, the director o the Health Institute, has been a constant source o inspiration, wisdom, and encouragement. Deborah Carr, Gerald Grob, Ellen Idler, Sarah Rosenfield, and Eviatar Zerubavel have been both careul readers and special riends. For Wakefield, these ideas germinated at the Rutgers Health Institute as well but were pursued or publication in his current home at New York University School o Social Work. The school and its dean, Suzanne England, and stimulating new colleagues, as well as NYU’s amazing intellectual energy under the leadership o John Sexton and David McLaughlin, have ofered exceptional support, opportunity, and inspiration. We are also grateul to Peter Conrad, Randolph Nesse, Sharon Schwartz, and Robert Spitzer or their comments on particular chapters o this manuscript. In an ideal world, all authors would have editors with the extraordinary talent and critical skills o Marion Osmun at Oxord University Press. We have been extremely lucky to have her as the editor o this book; we and the book have benefited enormously rom her support and wisdom. PREFACE xiii Finally, personal indebtedness is owed most of all to our families. Wakefield’s wife, Lisa, provided not only consistent support but also a thoughtful and challenging sounding board; his children, Joshua and Zachary, provided a joyful reprieve from work. His parents, Helen and Ted Sherman, provided a background of enduring love and support. Horwitz’s father, who died just after the manuscript was completed, was a lifelong model of scientific creativity and achievement. His daughters, Rebecca, Jessica, and Stephanie, provided welcome and delightful diversions during the writing of this book. This page intentionally left blank Contents Foreword, by Robert L. Spitzer vii 1. The Concept of Depression 3 2. The Anatomy of Normal Sadness 27 3. Sadness With and Without Cause: Depression From Ancient Times Through the Nineteenth Century 53 4. Depression in the Twentieth Century 5. Depression in the DSM-IV 72 104 6. Importing Pathology Into the Community 7. The Surveillance of Sadness 123 144 8. The DSM and Biological Research About Depression 9. The Rise of Antidepressant Drug Treatments 179 10. The Failure of the Social Sciences to Distinguish Sadness From Depressive Disorder 194 11. Conclusion Notes 227 References Index 281 249 212 165 This page intentionally left blank The Loss of Sadness This page intentionally left blank 1 The Concept of Depression he poet W. H. Auden amously deemed the period ater World War II the “age o anxiety.”1 For Auden, the intense anxiety o that era was a normal human response to extraordinary circumstances, such as the devastation o modern wa rare, the horrors o the concentration cam ps, the development o nuclear weapons, and the tensions o the cold war between the United States and the Soviet Union. Were Auden still alive, he might conclude that the era around the turn o the twenty-first century is the “age o depression.”2 There would, however, be a crucial diference between the two characterizations: whereas the age o anxiety was viewed as a natural response T to social circumstances that required collective and political solutions, ours is viewed as an age o sadness that is abnormal—an age o depressive psychiatric disorder that requires proessional treatment. Consider Willy Loman, the lead character in Arthur Miller’s classic play Death of a Salesman and possibly the fictional character most representative o American lie during the decades ollowing World War II. 3 As he enters his 60s, despite his ervent belie in the American dream that hard work will lead to success, Willy Loman has never accomplished very much. He has heavy debts, his health is ailing, he is barely able to continue working at his job as a traveling salesman, and his sons despise him. When he is finally fired rom his job, he is orced to admit to himsel that he is a ailure. He kills himsel in an automobile accident in the hope o getting his amily some money rom an insurance settlement. The tremendous popularity o Death of a Salesman on its introduction on Broadway in 1949 stemmed rom Willy Loman’s embodiment o the Everyman in American lie who embraced the goal o achieving great wealth but ound himsel destroyed by it. Death of a Salesman received a very diferent response during its revival 50 years later.4 According to a piece in The New York Timestitled “Get That Man Some Prozac,” the director o the revived version sent the script to two psychiatrists, who diagnosed Loman as having a depressive disorder. 5 The playwright, Arthur Miller, objected to this characterization, protesting: “Willy Loman is not 3 4 THE LOSS OF SADNESS a depressive. . . . He is weighed down by lie. There are social reasons or why he is where he is.” The response o the psychiatrists is as exemplary o our time as Loman was o his. What our culture once viewed as a reaction to ailed hopes and aspirations it now regards as a psychiatric illness. The transormation o Willy Loman rom a social to a psychiatric casualty represents a undamental change in the way we view the nature o sadness. The Ubiquity of Depression The ascendancy o depressive disorder is a major social trend maniested in a variety o ways: Amount of depression in the community. Many researchers claim that substantial and growing proportions o the population sufer rom depressiv e disorder. Estimates rom epidemiological studies indicate that Major Depression aicts about 10% o adults in the United States each year and nearly a fith o the population at some point in their lives. 6 Rates among women are even higher, about twice as high as in men. 7 Depending on the definition employed, depression can a ict as many as hal o the members o some groups, such as emale adolescents and the elderly. 8 Moreover, these numbers seem to be steadily growing. For the past several decades, each successive birth cohort has reported more depressive disorders than previous generations showed. 9 Although these rising rates are more likely to be an ar tiact o the way community surveys measure this condition than to reflect an actual increase, 10 there is a widespread perception that depressive disorder is growing at an alarming pace. Number of patients in treatment for depression. The number o persons treated or depression in the United States has grown explosively in recent years. Most depressed people are treated in outpatient settings, where treatment o depression increased by 300% between 1987 and 1997. 11 By 1997, ully 40% o all psychotherapy patients, double the percentage o a decade beore, had diagnoses o a mood disorder, the larger category that comprises mainly depression.12 The overall percentage o the population in treatment or depression in a particular year grew rom 2.1% in the early 1980s to 3.7% in the early 2000s, an increase o 76% in just 20 years. 13 Some groups experienced a much greater increase; or example, in just the period between 1992 and 1998, health care providers diagnosed 107% more elderly persons with depression.14 Prescription of antidepressant medication. Although medication has been a common treatment or lie problems since the 1950s, its use has undergone a staggering growth in recent years. Antidepressant medications, such as Prozac, Paxil, Zolot, and Efexor, are now among the largest selling prescription drugs o any sort.15 Their use among adults nearly tripled between 1988 and 2000.16 In any given month, 10% o women and 4% o men now use these drugs.17 During THE CONCEPT OF DEPRESSION 5 the 1990s, spending for antidepressants increased by 600% in the United States, exceeding $7 billion annually by the year 2000.18 Estimates of the social cost of depression. Depression is believed to be the source of huge social costs. The World Health Organization (WHO), the leading international body that deals with health, projects that by 2020 depression will become the second leading cause of worldwide disability, behind only heart disease. The WHO estimates that depression is already the leading cause of disability for 15- to 44-year-olds.19 In the United States, economists estimate that depression is responsible for $43 billion in costs every year.20 Scientific publications on depression. Research on depression has become a major industry.21 In 1966, 703 articles containing the worddepression in their titles were published in medical journals. In 1980, the year in which the American Psychiatric Association (APA) published its landmark third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) with new definitions of depressive disorder, 2,754 articles on depression were published. This number steadily increased over the following 15 years, and then exploded in the mid-1990s. By 2005, there were 8,677 articles about depression published, more than 12 times the number in 1966. The number of articles concerned with depression is now far higher than any other psychiatric diagnosisand has grown far more rapidly than the general growth in psychiatric research publications. Media attention to depression. Depression has become a central concern in the culture more generally. Popular television shows, best-selling books, and major articles in national magazines often feature this illness. Many memoirs about personal experiences of depression, including William Styron’s Darkness Visible, Kay Jamison’s An Unquiet Mind, Elizabeth Wurtzel’s Prozac Nation, and Andrew Solomon’s The Noonday Demon, have reached the best-seller list. A look at the new books in the psychology sections of bookstores reveals a virtual tidal wave of books on how to prevent or cope with depression of all sorts. The acclaimed television series, The Sopranos, features as its central character a Mafia boss who has—among other psychiatric conditions—depression and whose consumption of antidepressant medications is a major theme of the show. A number of prominent public personalities, including Tipper Gore, Mike Wallace, and Brooke Shields, have received massive publicity after disclosing their depressive conditions. Normal Versus Disordered Sadness Although the belief that depression is a widespread phenomenon is new, the symptoms we now associate with it, including intense sadness and the many other emotional experiences and physical symptoms that often accompany sadness, have been noted since the beginning of recorded medical history.22 Yet, in attempting to understand the recent upsurge in diagnosed depressive disorder, 6 THE LOSS OF SADNESS it is important to recognize that until recently, two broad types o conditions that maniest these same symptoms were sharply distinguished rom each other. One, normal sadness, or sadness “with cause,” was associated with experiences o loss or other painul circumstances that seemed to be the obvious causes o distress. The response to such normal reactions was to ofer support, to help the individual cope and move on despite the loss, and to avoid conusing the person’s sadness with illness. The other kind o condition, traditionally known as melancholia, or depression “without cause,” was a medical disorder distinguished rom normal sadness by the act that the patient’s symptoms occurred despite there being no appropriate reason or them in the patient’s circumstances. These conditions were relatively rare but tended to be long lasting and recurrent. Because they were not proportional reactions to actual events, such conditions were assumed to stem rom some sort o internal deect or dysunction that required proessional attention. Yet these pathological conditions involve the same sorts o symptoms— such as sadness, insomnia, social withdrawal, loss o appetite, lack o interest in usual activities, and so on—associated with intense normal sadness. This separation o normal sadness and depressive disorder is a sensible and legitimate, indeed a crucial, one. It is consistent not only with the general distinction between normality and disorder used in medicine and traditional psychiatry but also with common sense, and it has both clinical and scientific importance. Yet contemporary psychiatry has come to largely ignore this distinction. We argue that the recent explosion o putative depressive disorder, in act, does not stem primarily rom a realrise in this condition. Instead, it is largely a product o conflating the two conceptually distinct categories o normal sadness and depressive disorder and thus classiying many instances onormal sadness as mental disorders. The current “epidemic,” although the result o many social actors, has been made possible by a changed psychiatric definition o depressive disorder that oten allows the classification o sadness as disease, even when it is not. The “Age o Depression” Results From a Faulty Defnition o Depressive Disorder Unlike Auden’s “age o anxiety,” which resulted rom identifiable social conditions, there are no obvious circumstances that would explain a recent upsurge in depressive disorder. The most commonly heard suggestions—such as that modern lie is less socially anchored and involves more alienation or that media constantly expose us to extremes o wealth and beauty that cause us to eel inadequate by comparison—would tend to explain only normal sadness reactions (analogous to the normal anxiety responses to which Auden pointed), not the massive growth o a mental disorder. No environmental pathogen that might THE CONCEPT OF DEPRESSION 7 have resulted in a real increase in physiologically, psychologically, or socially induced brain malunctions has been identified or even theorized. Certainly, progress in efectively treating depressive disorder with psychotropic medication has resulted in increased treatment o a condition about which physicians believe they can at least do some good, and perhaps it has motivated diagnosis o ormerly ambiguous cases as depression in the hope o ofering efective treatment. But that does not by itsel explain the vast growth in the numbers o people who seemingly have and are treated or this disorder; better treatments do not usually lead to a substantial increase in disease prevalence. Nor would improved treatments explain the results o epidemiological studies that bypass patients and directly interview community members not in treatment. Thus the seeming explosion o cases o depressive disorder is puzzling. What has happened to create the appearance o this epidemic? What has happened, we argue, is largely diagnostic inflation based on a relatively new definition o depressive disorder that is flawed and that, combined with other developments in society, has dramatically expanded the domain o presumed disorder. To understand how this phenomenon has occurred, it is useul to place current psychiatric practices in historical context and to consider how odd current diagnostic definitions o depressive disorder are by historical standards. One must also conront the esoterica o modern psychiatric classification presented in successive editions o the American Psychiatric Association’s DSM. Oten called the “bible o psychiatry,” the DSM provides diagnostic definitions or all mental disorders. But how can something as simple and limited as a definition have substantial consequences or such a field as psychiatry and thus or the media that popularize its claims and findings and or the thinking o society at large that relies on its expertise? In response to criticisms during the 1960s and 1970s that diferent psychiatrists would not diagnose the same person with the same symptoms in the same way (this problem was known as the “unreliability” o diagnosis), in 1980 the DSM began to use lists o symptoms to establish clear definitions or each disorder.23 Almost all mental health proessionals across avariety o settings, rom hospital clinics to private practices, now use these ormal definitions or clinical diagnosis. Moreover, these definitions have percolated out o the mental health clinical arena and are used in epidemiological studies o disorder in the community, in research studies o treatment outcomes, in marketing o antidepressant medications, in preventive eforts in schools, in screening in general medical practice, in court proceedings, and in many other settings. In efect, theseDSM definitions have become the authoritative arbiter o what is and is not considered mental disorder throughout our society. What might seem like abstract, distant, technical issues concerning thesedefinitions in act have important consequences or individuals and how their sufering is understood andaddressed. The act that these symptom-based definitions are the oundation o the entire mental health research and treatment enterprise makes their validity critically 8 THE LOSS OF SADNESS important. Psychiatric research and treatment are like an upside-down pyramid, and the DSM definitions o mental disorders that determine who is counted as disordered are the one small point on which the soundness o the entire pyramid rests. Even the best clinical history taking and diagnostic interviewing or the best research sample selection, experimental design, and statistical analysis o data will not produce meaningul results i they use an invalid definition o disorder that mixes normal and abnormal eatures. Archimedes amously boasted, “Give me a lever long enough, and a pivot on which to rest it, and I will move the earth.” In modern psychiatry, definitions move the treatment and research firmament, and modern clinicians with an invalidly broad definition can move diagnosed disorder to virtually whatever level they desire, especially when they deal with a disorder such as depression that eatures such symptoms as sadness, insomnia, and atigue, which are widespread among nondisordered people. Thus the recent ocus in psychiatry on reliability o diagnosis based on symptoms has been pursued at some cost to validity—that is, whether the diagnosis represents a correct attribution o disorder.24 The DSM’s criteria or Major Depressive Disorder are one instance in which increased reliability has had the inadvertent side eect o creating substantial new validity problems. The DSM’s Defnition o Major Depression The current ofcial psychiatric definition o depressive disorder that is the basis or clinical diagnosis and research studies is ound in the most recent edition (4th ed., text revision) o the DSM.25 The DSM definition o Major Depressive Disorder (MDD), the category under which most depressive disorders all, is lengthy and has several qualifiers and exceptions. We deer ull analysis and critique o the DSM’s approach to depressive disorder until chapter 5. Forpurposes o this initial discussion, we consider the most important eatures o the definition, which consists o symptom and duration requirements and a bereavement exclusion. DSM diagnosis o MDD requires that fiv e symptoms out o the ollowing nine be present during a 2-week period (the five must include either depressed mood or diminished interest or pleasure): (1) depressed mood; (2) diminished interest or pleasure in activities; (3) weight gain or loss or change in appetite; (4) insomnia or hypersomnia (excessive sleep); (5) psychomotor agitation or retardation (slowing down); (6) atigue or loss oenergy; (7) eelings oworthlessness or excessive or inappropriate guilt; (8) diminished ability to think or concentrate or indecisiveness; 26 and (9) recurrent thoughts odeath or suicidal ideation or uicide s attempt. These symptom criteria orm the heart o the definition o MDD, but there is one urther important clause in the definition: “The symptoms are not better accounted or by Bereavement, i.e., ater the loss o a loved one, the symptoms persist or longer than 2 months or are characterized by marked unctional impairment, morbid preoccupation with worthlessness, suicidal ideation,psychotic symptoms, THE CONCEPT OF DEPRESSION 9 27 or psychomotor retardation.” In other words, patients are exempt rom diagnosis i their symptoms are due to what the DSM defines as a normal period o bereavement ater the death o a loved one, lasting no more than 2 months and not including especially serious symptoms, such as psychosis or thoughts about suicide. This limited “bereavement exclusion” is the definition’s only acknowledgment that some instances o normal intense sadness might satisy the symptom- atic criteria. The DSM definition o depressive disorder is reasonable in many wa ys. Its criteria might give rise to disagreements about particular symptoms, but each is widely and consensually believed to be an indicator o depressive disorder, and pre-DSM psychiatry recognized them as such. One might also debate the exact number o symptoms needed or diagnosis; some w ould argue or laxer requirements with ewer symptoms, others or more stringent symptom requirements to ensure that disorder exists, and still others would insist that there should be no sharp cuto but rather a dimensional continuum o severity.28 One might also dispute w hether the required duratio n o 2 weeks is suficient, but it is sometimes clear within 2 w eeks o onset that someone has a depressive disorder, and clinicians should not be kept rom diagnosing such cases even i the typical duration o depressive disorders is much longer. Likewise, it seems reasonable to exclude people who are recently bereaved. The criteria are also airly clear and, in most cases, not more dif cult to measure than typical psychiatric symptoms in other disorders. The reasonableness, clarity, and eficiency o its use help account or the nearly universal adoption o the DSM definition o MDD. What, then, is the problem with this definition? The essence o the definition is that, aside rom a ew exceptions, the presence o a particular group o symptoms is sufcient to diagnose the presence o the disorder. Yet symptoms such as depressed mood, loss o interest in usual activities, insomnia, lessened appetite, inability to concentrate, and so on might naturally occur or a period o2 weeks in the absence o any disorder ater any o a wide range o negative events, such as betrayal by romantic partners, being passed over or an anticipated promotion, ailing a major test that has serious implications or one’s career, discovering a lie-threatening illness in onesel or a loved one, or enduring the humiliation that ollows revelations o disgraceul behavior. Such reactions, even when quite intense due to the severity o the experience, are surely part o normal human nature. Just as it is obvious why theDSM excludes bereavement rom diagnosis, by parity o reasoning it seems obvious that it should also exclude these other sorts o reactions to negative circumstances. The diagnosis, how ever, does not exclude such nongrie responses. Because o the symptom-based nature o the criteria, any sadness response involving enough o the specified symptoms or at least 2 weeks will be misclassified as a disorder, along with genuine psychiatric disturbances. In attempting to characterize the kinds o symptoms suered in depressive disorders without reerence to the context in which the symptomsoccur, 10 THE LOSS OF SADNESS contemporary psychiatry has also inadvertently characterized intense normal suering as disease. Consider, or example, the ollowing cases: Case 1: Ending of a Passionate Romantic Relationship A 35-year-old single emale proessor has sought psychiatric consultation to obtain medicine or insomnia. She must present a paper as part o a job interview and is araid that she is not able to unction adequately enough to do so. She reports that or the past 3 weeks she has experienced depressed mood and extreme eelings o sadness and emptiness, as well as lack o interest in her usual activities (in act, she has spent much o her time lying in bed or watching television). Her appetite has diminished, and she lies awake long into the night unable to all asleep due to the pain o her sadness. She is atigued and lacking in energy during the day and cannot concentrate on her work. Because her painul eelings distract her during work, she is barely able to meet minimal occupational obligations (e.g., she shows up at her classes poorly prepared, has not attended aculty meetings, and has difculty concentrating on her research). She has also avoided social obligations. When asked about what might have precipitated these distressing eelings, she reports that about a month beore, a married man with whom she had had a passionate 5-year love aair decided he could not leave his wie and ended the aair. The woman had perceived this relationship as a unique, once-in-a-lietime romance that had an extraordinary combination o emotional and intellectual intimacy. The woman agrees to check in with the psychiatrist periodi cally. Subsequently, as weeks go by, her sense o loss subsides gradually and is replaced by a eeling o loneliness and the need to get on with her lie and find a partner. Eventually, she starts dating again, and ater several more months the woman meets a new love interest, and any residual symptoms disappear. Case 2: Loss of a Valued Job A 64-year-old married man has developed eelings o sadness and emptiness, lack o pleasure in activities, insomnia, atigue and lack o energy, and eelings o worthlessness. He is not interested in seeing riends and seems unable to concentrate on anything. He yells at his wie when she attempts to console him and rejects her eorts to comort him. The eelings were triggered 2 weeks beore when the company the man worked or unexpectedly fired him aspart o a corporate downsizing. The firing came just 6 months beore he would have qualified or the company’s retirement plan. One o the major reasons the man chose to work or the THE CONCEPT OF DEPRESSION 11 company and then spend two decades with it had been the prospect ogenerous retirement benefits. The loss o these benefits means that he and his wie have very little retirement income other than Social Security to look orward to. Subsequently, the couple is orced to sell their house and move to a small apartment. The man finds part-time work that, along with Social Security, provides barely enough resources to sustain him and his wie. He remains bitter about how he was treated, but his symptoms gradually subside over time. Case 3: Reaction to a Life-Threatening Medical Diagnosis in a Loved One A 60-year-old divorced woman who is visiting a medical center distant rom her home asks a physician at the center or medication to help her sleep. The woman’s daughter, an attorney and her only child, to whom she is very close and who is the pride o her lie, was diagnosed just 3 weeks beore with a rare and potentially atal blood disease. Ater receiving the news o her daughter’s diagnosis, the mother was devastated by eelings o sadness and despair and was unable to unction at work or socially. Although she kept up a brave ront or her daughter and was able to help her child with the arrangements or the medical consultation, the mother has been in a state o great distress since the diagnosis; she cries intermittently, is unable to sleep, lacks the ability to concentrate, and eels atigued and uninterested in her usual activities as she attempts to come to terms with the news o her daughter’s condition. These symptoms gradually abate over a number o months during her daughter’s treatment and struggle with the illness, which eventually stabilizes but remains a threat. The woman continues to periodically eel sad about her daughter’s situation, but her other symptoms subside as she adjusts to the new circumstances and limits o her daughter’s lie. Each o these people easily meets the symptomatic requirements or MDD and the DSM would thus classiy them as psychiatrically disordered. Their symptoms persist beyond the 2-week duration criterion, they are experiencing significant role impairment or distress, and the bereavement exclusion does not apply to them. Yet these reactions seem to all within the normal range or persons who have sufered rom the sudden end o a passionate romantic relationship, theloss o a valued job, or the diagnosis o a serious illness in a beloved child. The symp- toms that these people report are neither abnormal nor inappropriate in light o their particular situations. What characteristics tend to suggest that these conditions are not disorders? In each case, symptoms emerge only ater the occurrence o a discrete lie event involving great loss. Further, the severity o these loss responses, although very 12 THE LOSS OF SADNESS intense, is reasonably proportional to the nature o the losses that have been experienced. Finally, the symptoms either end when circumstances change or the better, endure because the stressul situation persists, or eventually go away with the passage o time. We do not believe that most thoughtul clinicians today, i making an independent judgment outside the sway o the DSM, would classiy such reactions as disorders, any more than their predecessors did. Stating that the DSM’s definition o depressive disorder mistakenly encompasses some normal emotional reactions in no way implies that there are not genuine depressive disorders. Such disorders do exist, they can be devastating, and the DSM’s definition does encompass them. However, they look very dierent rom the kinds o normal reactions described here. Popular portrayals o depression uniormly present a picture o proound, immense, and immobilizing suering that is bewilderingly disengaged rom actual lie circumstances, and this sort o experience does imply genuine disorder. For example, consider the case o Deanna Cole-Benjamin, eatured in a New York Times Magazine story about a new treatment or depression: Her youth contained no traumas; her adult lie, as she describes it, was blessed. At 22 she joined Gary Benjamin, a career financial of cer in the Canadian Army, in a marriage that brought her happiness and, in the 1990’s, three children. They lived in a comortable house in Kingston, a pleasant university town on Lake Ontario’s north shore, and Deanna, a public-health nurse, loved her work. But in the last months o 2000, apropos o nothing—no lie changes, no losses—she slid into a depression o extraordinary depth and duration. “It began with a eeling o not really eeling as connected to things as usual,” she told me one evening at the amily’s dining-room table. “Then it was like this wall ell around me. I elt sadder and sadder and then just numb.” Her doctor prescribed progressively stronger antidepressants, but they scarcely touched her. A couple o weeks beore Christmas, she stopped going to work. The simplest acts—deciding what to wear, making breakast—required immense will. Then one day, alone in the house ater Gary had taken the kids to school and gone to work, she elt so desperate to escape her pain that she drove to her doctor’s ofce and told him she didn’t think she could go on anymore. “He took one look,” she told me later, “and said that he wanted me to stay right there in the ofce. Then he called Gary, and Gary came to the o29 fice, and he told us he wanted Gary to take me straight to the hospital.” Aside rom the extraordinary severity and duration o the symptoms, it is noteworthy that the seriousness o this depressive condition has no relation to any events that normally might be expected to trigger such episodes. THE CONCEPT OF DEPRESSION 13 Or consider Andrew Solomon’s powerul depiction o his depressive illness: [My depression] had a lie o its own that bit by bit asphyxiated all o my lie out o me. At the worst stage o major depression, I had moods that I knew were not my moods: they belongedto the depression . . . I elt mysel sagging under what was much stronger than I; first I could not use my ankles, and then I could not control my knees, and then my waist began to break under the strain, and then my shoulders turned in, and in the end I was compacted and etal, depleted by this thing that was crushing me without holding me. Its tendrils threatened to pulverize my mind and my courage and my stomach, and crack my bones and desiccate my body. It went on glutting itsel on me when there seemed nothing let to eed it.30 Again, Solomon’s proound depression has “a lie o its own,” in the sense that its seriousness is not related to specific losses or other negative events that might normally lead to such eelings. In perhaps the most eleg ant description o depression, Darkness Visible, William Styron describes his reaction to learning that he had won a prestigious literary prize: The pain persisted during my museum tour and reached a crescendo in the next ew hours when, back at the hotel, I ell onto the bed and lay gazing at the ceiling, nearly immobilized and in a trance o supreme discomort. Rational thought was usually absent rom my mind at such times, hence trance. I can think o no more apposite word or this state o being, a condition o helpless stupor in which cognition is replaced by that “positive and active anguish.” Styron’s condition persists independentl y o any social contex t: “In depression . . . the pain is unrelenting, and w hat makes the condition intoler able is the oreknowledge that no remedy will come—not in a day, an hour, a month, or a minute. I there is mild relie, one kno ws that it is only temporary; more pain wil l ollow.” 31 Styron’s debilitating symptoms did not emerge ater any stressul experience but actually arose ater what would ordinarily be a cause or celebration. The sociologist David Karp’sSpeaking of Sadness ofers another typical depiction: By any objective standard I should have been eeling pretty good. I had a solid academic job at Boston College, had just signed my first book contract, and I had a great wie, beautiul son, and a new baby daughter at home. . . . Each sleepless night my head was filled with disturbing ruminations and during the day I elt a sense o intolerable grie as though somebody close to me had died. I was agitated and sensed a melancholy 14 THE LOSS OF SADNESS qualitatively dierent rom anything in the past. . . . I thought or sure that my depression was rooted in these situational demands and that once I got tenure it would go away. I was promoted in 1977 and ound that the depression actually deepened.32 Just as Styron’s depression developed ater a positive experience, Karp’s dangerously severe condition was isolated rom the actual circumstances o his lie. As these examples illustrate, the cases that both popular media and psychiatric texts typically depict are clearly genuine disorders. Yet these descriptions also illustrate that symptoms in themselves do not distinguish depressive disorders rom normal sadness; the symptoms are not qualitatively dierent rom what an individual might naturally experience ater a devastating loss, as in our earlier case illustrations o normal reactions to major lie disruptions. Instead, it is the absence o an appropriate context or symptoms that indicates a disorder. These cases either emerged in the absence o any loss event or developed ater the occurrence o a positive event, such as winning a prestigious award or obtaining tenure. Their severity was o grossly disproportionate intensity to the suerer’s actual circumstances. Finally, symptoms persisted independently o any stressul contexts, took on a lie o their own, and were immune to changes in external conditions. The act that the literature emphasizes such examples can mislead us into overlooking the act that the DSM diagnostic criteria themselves are not limited to such conditions and invalidly encompass a great range o intense normal reactions. The basic flaw, then, o the DSM definition o MDD, as well as o all eorts that rely on it, is simply that it fails to take into account the context of the symptoms and thus fails to exclude from the disorder category intense sadness, other than in reaction to the death of a loved one, that arises from the way human beings naturally respond to major losses. The resultant lumping o nondisordered with dysunction-caused symptoms o depression, and the classification o both as disorders, is a undamental problem or current research, treatment, and social policy regarding depression. Moreover, as we show, the problem has been getting much worse in recent years, with growing pressure to use a lower number o symptoms, sometimes as  ew as two, as suf cient criteria or diagnosing a disorder. The potential or alse-positive diagnoses—that is, people who meet the DSM ’s diagnostic criteria but do not in act have a mental disorder— increases exponentially as the number o symptoms required or a diagnosis decreases. The DSM’s overinclusive criteria or depressive disorder ultimately compro- mise psychiatry’s own goals and concepts. The DSM aims to identiy psychological conditions that can be considered genuine medical disorders and to distinguish them rom problematic but nondisordered conditions.33 Thus the error we are pointing to in disorder categories such as MDD is an error in terms o the DSM’s own stated aspirations. THE CONCEPT OF DEPRESSION 15 The Distinction Between Normality and Disorder Our core argument about the DSM’s definition o depressive disorder depends on the assumption that normal sadness can be intense; can be accompanied by sleeplessness, lack o concentration, changed appetite, and so on; can be impairing or distressul; and can last or 2 weeks, as the criteria demand. But what is the implicit understanding o normality and disorder by which one can distinguish painul sadness that is normal rom that which is disordered? Normal unctioning is not mere statistical commonality. Some disorders can be statistically “normal” in a population, as are gum disease and atherosclerosis in ours, yet they are disorders nonetheless; and some normal variations can be quite rare. We must also distinguish disorder rom social desirability and social values. Even the DSM acknowledges that an individual who is socially deviant or whose nature is in conflict with the values o society is not thereby necessarily disordered.34 Adequate accounts must not only distinguish disorder rom social values but also explain in what ways disorders are real medical ailments that represent, at least in part, some objective problem in individual unctioning. The most plausible demarcation point between human normality and disorder in the medical sense is, we believe, that between biologically “designed” unctioning (i.e., the result o natural selection) andthe ailure o such unctioning, that is, dysfunction.35 This view comports well with commonsense intuitions and is probably the most widely accepted and deensible viewamong those who are concerned with the conceptual oundationso psychiatry, as well as medicine more generally.36 For example, the criterion or normal unctioning o bodily organs is what they are biologically designed to do and how they are designed to do it. Thus the heart serves to pump blood, the kidneys to eliminate waste, and the lungs to enable us to breathe, and i these unctions are accomplished by the structures designed to accomplish them, unctioningis normal. Disorder exists when the organ is unable to accomplish the unction or which itis biologically designed. Similarly, psychological processes that w ere selected as part o human nature have natural unctions, that is, the efects or which they were naturally selected. Considerable neurobiological and psychological research suggests that the mind is made up o many specific modules or mechanisms that are designed to respond 37 to specific environmental challenges. Thus contextualityis an inherent aspect o many psychological mechanisms; they are designed to activate in particular contexts and not to activate in others. Fear responses, or example, are biologically designed to arise in dangerous situations but not in sae situations. Likewise, innate mechanisms that regulate reactions osadness, despair, and withdrawal naturally come into play ater humans sufer particular kinds o losses.38 Conversely, dysunctions in which sadness mechanisms do not operate as designed constitute disorders. The implication is that only in the light osome account, however provisional or sketchy, o how loss response mechanisms are designed to work and thus 16 THE LOSS OF SADNESS o their normal unctioning do we have grounds or calling some responses to loss disordered. As with all human traits, there is much variation among individuals in the sensitivity with which they respond to loss with sadness. Culture also influences designed tendencies in various ways, so evaluating whether a response fits within the naturally selected range is sometimes no easy task. Nevertheless, under appropriate conditions, virtually all humans have the capacity to develop nondisordered sadness as a biologically selected adaptation to handling loss. In principle, this biological capacity provides a baseline or judging some cases as clear examples o normality and disorder. An important caveat: because o our primitive state o knowledge about mental unctioning, our understanding o how normal emotions, including sadness, are designed to work remains speculative and open to revision. Yet some undamental principles, at least in a broad provisional orm, seem overwhelmingly plausible and oer a sufcient basis or critically examining the validity o criteria or depressive disorder. These principles allow us to make some general distinctions between cases that clearly seem to indicate normal sadness and cases o depressive disorders, while acknowledging a large domain o borderline, ambiguous, and uzzy cases. We emphasize three essential eatures o nondisordered loss in chapter 2: they emerge because o specific kinds o environmental triggers, especially loss; they are roughly proportionate in intensity to the provoking loss; and they end about when the loss situation ends or gradually cease as natural coping mechanisms allow an individual to adjust to the new circumstances and return to psychological and social equilibrium. Important questions arise because we do not yet know precisely which internal mechanisms produce loss responses or what these mechanisms are actually like. I the mechanisms are inerred to exist but their specific nature is unknown, how can one tell that normal loss responses are indeed part o our biological heritage? And, without knowing the mechanisms, how can we tell what is normal and what is disordered? The act is that, although the distinction cannot yet be determined precisely, in the history o medicine and biology scientists have routinely drawn such inerences about normal and disordered unctioning rom circumstantial evidence without knowing the underlying mechanisms. So, or example, Hippocrates knew that blindness and paralysis are disorders and that there are mechanisms that are designed to allow human beings to see via their eyes and move via muscular eort, but he knew little o the mechanisms themselves and thus little o the specific causes o most cases o blindness and paralysis (other than gross injury). It took thousands o years to figure out those mechanisms, but during that time it was universally understood rom circumstantial evidence that sight and movement are parts o human biological design. It is no dierent in principle with human mental capacities that are part o our biological nature, such as basic emotions. THE CONCEPT OF DEPRESSION 17 Another concern might be that, because we do not understand the loss response mechanisms, we cannot with confidence state the function of the loss response and cannot therefore know what is normal and abnormal. Indeed, unlike the functions of the eyes and muscles, the functions of loss responses are not apparent and are subject to dispute.39 Fortunately, it is often possible from available evidence to infer roughly what responses of a mechanism are normal, even without knowing the reason for the responses. For example, everyone agrees that sleep is an elaborately designed response and that some sleep conditions are normal whereas others are sleep disorders, but there is little scientific consensus on the functions that explain why we sleep. Without an adequate understanding of the function of loss responses to guide us, we too must engage in such admittedly presumptive but, we believe, still plausible inferences. By depressive disorders, then, we mean sadness that is caused by a harmful dysfunction (HD) of loss response mechanisms.40 According to the HD definition, a collection of symptoms indicates a mental disorder only when it meets both of two criteria. The first is dysfunction: something has gone wrong with some internal mechanism’s ability to perform one of its biologically designed functions. Second, the dysfunction must be harmful. Cultural values inevitably play the primary role in defining what sorts of dysfunctions are considered harmful. In sum, a mental disorder exists when the failure of a person’s internal mechanisms to perform their functions as designed by nature impinges harmfully on the person’s well-being as defined by social values and meanings. The HD analysis of disorder does not attempt to yield aprecise conceptual boundary because the concepts ofnormality and disorder, like most concepts, do not themselves have precise boundariesand are subject to indeterminacy, ambiguity, fuzziness, and vagueness and so yield many unclear cases. Despite such fuzzy boundaries, the HD concept ofdisorder is useful and coherent because it enables us to adequately distinguish arange of clear normal cases from a rang e of clear disorders. Analogously, there are real distinctions between red and blue, childand adult, and life and death, although there areno sharp boundaries between these pairs. By contrast, current diagnostic criteria for depressive disorder, we argue, substantially fail to distinguish even man y clear cases of normal sadness from disorder . Mechanisms that are biologically designed to generate loss responses may fail to perform their functions in the appropriate contexts in variety a of ways.41 Loss responses can emerge in situations for which they are not designed, they can be of disproportionate intensity and duration to the situations that evoke them, and in extreme cases they can occur spontaneously, with no trigger at all. For example, depressions such as William Styron’s,which arose after the reception ofa presti- gious award, or David Karp’s, which emerged after a successful tenure decision, indicate that loss response mechanisms have one g awry. Dysfunctions of loss responses may also involve distorted cognitive perceptions ofthe self, the world, and 42 the future that trigger inappropriate sadness. Such distortions may yield inappropriately sensitive mechanisms that magnify the meanings ofminor losses beyond 18 THE LOSS OF SADNESS the normal range o culturally appropriate stimuli. Someone w ho becomes deeply depressed ater the death oa pet goldfish or a minor perceived slight, orxample, e displays such overly sensitive, disproportionate loss response mechanisms, unless special circumstances make the loss o much greater importance than is usual. Yet it is not just the emergence o depression in the absence o appropriate causes that defines a dysunction. Disorders might arise ater an initially normallevel response to actual losses, but the response might then become disengaged rom the circumstances o the loss and persist with disproportionate intensity long ater the initial provoking conditions have ended. Or, among susceptible individuals, the experience o loss events can sometimes produce biochemical and anatomical vulnerabilities that make recurrences o depressive episodes more likely with less and less provocation.43 Even i they begin as normal responses, emotional reactions that become detached rom a specific time, place, and circumstance indicate dysunctional loss response mechanisms. Finally, dysunctions in loss responses can sometimes cause symptoms that are so extreme that they indicate dysunction in themselves. Depressiv e reactions that eature prolonged complete immobilization or loss o contact with reality, such as hallucinations, delusions, and the like, would not stem rom appropriately unctioning loss mechanisms and have always been recognized as disorders. Such inappropriate and excessive responses are analogous to dangerously high evers or uncontrolled vomiting, which are design ailures o otherwise adaptive responses. Note that our distinction between sadness due to internal dysunction versus sadness that is a biologically designed response to external events difers in important respects rom the traditional distinction within psychiatry between depressions that are endogenous (i.e., spontaneously caused by internal processes, having no external trigger) and reactive (i.e., triggered by some external event).44 Endogenous depressions by definition arise in the absence o real loss, and so are almost always due to internal dysunctions. In contrast, many reactive depressions are proportionate to environmental events and so are normal responses. However, not all reactive depressions are normal. External events can so deeply afect individuals that they trigger internal dysunctions. For example, environmental traumas such as the sudden death o a loved one, orced relocation rom one’s home, or being the victim o a violent crime can cause designed loss response mechanisms to break down and an enduring disorder to occur.45 As noted, emotional reactions can be so disproportionate to their triggering events as to suggest dysunction, or the symptoms can take on a lie o their own and ail to extinguish when the stressor ends. Thus, among reactive depres- sions to losses, some are disorders and some are not. The presence o an internal dysunction, not the cause o this dysunction (which may be endogenous or reactive), defines depressive disorders. Consequently, there is no simple one-to-one relationship between the traditional endogenous-reactive distinction and our distinction between internal dysunction and biologically designed response. THE CONCEPT OF DEPRESSION 19 To address a final point o possible conusion: the evolutionary design approach to distinguishing normal rom disordered conditions does not imply that all depressive disorders have physiological causes or that there is always a brain problem when there is a depressive disorder. Although physiological causes do oten produce disorders, psychological or social actors can also lead to dysunctions. Biological design includes the design ovarious mental mechanisms (e.g., belie, desire, emotion, perception) that work via meanings humans assign to represent reality, and physiological descriptions may not capture how such meanings operate. There mightbe mental disorders that cannot be described as malun ctions in the underlying physiological machinery but as malunctions at the mental level o meanings. This is not as mysterious as it might sound; think o the act that computer sotware can malunction in hardware that tsel i is working properly . The processing o meanings that recent cognitivescience envisions as analog ous to the “sotware” o the mind can perhaps similarly go awry without any underl ying physiological malunction. Our discussion is neutral on such issues oetiology, although we generally believe that there can be an array o biological, psychological, and social causes oboth normal sadness and depressivedisorder; research that resolves the clash o theories about the causes o depression must decide this issue. One great advantage o our critique based on the HD approach is that it acknowledges that depressive disorders do exist and provides deensible groundsor improving psychiatry’s diagnostic criteria. Thereare other, more radical, critiques o psychiatric diagnosis that dismiss diagnosis in general and that leav e no room or constructive engagement with psychiatry. For example, psychiatrist Thomas Szasz’s argument that there are no mental disorders because disorders require physical lesions; sociologist Thomas Schef’s labeling theory thatreduces diagnosis to social control; behaviorist claims that allbehavior is the outcome o learning processes and thereore that nomental disorder can exist; or anthropologists’ assertions that distinctions between normal and abnormalunctioning are purely cultural and thereore arbitrary all deny the possibility o making a conceptually coherent diagnostic distinction between depressive disorders and normal intense sadness responses.46 They thus understate the real and distinct problems that genuine depressive disorders pose while at the same time they preclude the prospecto efectively critiquing overexpansive psychiatric definitions o disorder. The Advantages of Distinguishing Normal Sadness From Depressive Disorder Even i the DSM criteria are flawed in a way that allows the creation o an inflated amount o depressive disorder, why is correcting this error so important? There are some considerable advantages to doing so: Pathologization of normal conditions may cause harm, and avoidance of such pathologization may decrease such harm. Not only may patients be misled to consider 20 THE LOSS OF SADNESS themselves disordered and undertake unnecessary treatment, but also the social responses to nondisordered and to dysunctional conditions usually dier. Social networks typically respond with social support and sympathy to sadness that appears ater stressul lie events.47 Dysunctional depressions, in contrast, typically elicit hostility, stigma, and rejection and lead to the loss osocial support.48 To subject those with normal sadness to the social prejudice aced by those with mental illness does not serve to combat that prejudice. It remains true, however, that or those who do have a genuine mental disorder, the disadvantages o diagnostic stigma must be balanced against the act that diagnosis o their abnormal conditions with an ofcial label that oers access to services may come as a welcome relie. The distinction between disordered and normal sadness should improve assessments of prognosis. An essential purpose o diagnosis is prognosis: predicting the uture course o a disorder.49 The prognoses or people whose symptoms stem rom nondisordered sadness usually dier rom those or people with disorders. Symptoms o nondisordered conditions are likely to abate over time without intervention, to disappear i precipitating circumstances change, and to be responsive to generic social support. In contrast, symptoms that stem rom internal dysunctions are likely to be chronic and recurrent and to persist independently o stressul lie circumstances. 50 An adequate distinction between disorder and nondisorder should provide better prognostic predictions. Accurate diagnoses point to appropriate treatments. Although medication or therapy can help ease the pain that arises rom both normal sadness and de- pressive disorder, they are oten unnecessary in cases o nondisordered sadness, which do not involve internal dysunctions. In some cases, such as bereavement, treating normal loss responses as diseases can even be counterproductive because it may exacerbate and prolong symptoms.51 Conversely, the treatment o depressive disorders oten involves pharmacotherapies, cognitive and other psychotherapies, or a combination o modalities to overcome dysunctional conditions. An adequate conceptual distinction between dysunctions and normal responses may enable us better to speciy what sorts o responses can work most eectively or symptomatically similar, but actually distinct, conditions. Separating normal sadness from depressive disorders can help in recognizing the relationship of sadness to adverse social conditions and thus in identifying appropriate social interventions. Psychiatry now tends to view depression as a major cause o many social problems, including welare dependence, drug addiction, and poverty.52 The first course o action would be to treat the illness and then to help depressed individuals to overcome their other challenges. Normal sadness, how- ever, is much more likely to be the result rather than the cause o social problems. Recognizing the impact o social problems on normal human emotions would suggest that correcting these problems would be an appropriate initial response. The separation of depressive disorder from normal intense sadness should provide a basis for more accur ate epidemiologica l estimates of the prevalence of depressive THE CONCEPT OF DEPRESSION 21 disorders and the cost of treating it. The ailure to distinguish normal rom disor- dered sadness results in large overestimates o people who have mental disorders, misleading policy makers into ormulating poor public policy. Prevalence estimates count as diseased all people who have sufciently intense symptoms, whether disordered or not.53 They direct the atte ntion o policy makers and mental health proessionals toward conditions that may not need intensive expert attention and away rom problems that can most benefit rom proessional help. Conflating normal sadness with depressive disorder also results in greatly overinflated estimates o the economic costs o depression. 54 These overstatements, in turn, have potentially negative policy implications in that they increase the reluctance o elected of cials, insurance companies, and other policy makers to develop cost-eective responses to depression. Although no one who is suering should be denied access to services, separating nondisordered rom dysunctio nal conditions can ocus the expertise o mental health proessionals on true mental disorders and lead to a more ef cient use o mental health resources. Distinguishing disorder from normal sadness allows for a better estimate of unmet need for mental health services. Because they ail to distinguish normal sadness rom depressive disorder, and because nondisordered individuals are less likely to seek treatment, population surveys make it seem as i only a minority o disordered people are treated or their conditions. This has led social policies to ocus on the presumed vast amount o unmet need or treatment.55 These policies now emphasize widespread screening or depression among people who have not voluntarily sought treatment. Screening instruments likely uncover more normal sadness than depressive disorder but treat both conditions as i they were disorders. The reduction o such overdiagnosis could reduce the needless and potentially harmul overprescription o medication. Drawing a more careful distinction between disorder and normal sadness allows researchers to select samples that more accurately reflect true disorders. Meaningul research into the causes o depressive disorder and into the best treatments or either depressive disorder or intense normal sadness requires that the groups studied be reasonably homogeneous in nature so that the results can be appropriately understood and generalized. The causes o depressive symptoms that arise rom dysunction are generally dierent rom the causes o normal sadness, so the entire field o depression research remains problematic until the appropriate distinction is made. Distinguishing nondisordered from dysfunctional loss responses avoids medicalizing our thinking about normal sadness and thus maintains the conceptual integrity of psychiatry. Aside rom any other advantages, the long-term credibility o psychiatry and psychiatric diagnosis depends on getting the disorder-nondisorder distinction right by labeling only genuine psychiatric conditions as disorders. The ailure to adequately separate naturally designed sadness responses rom internal dysunctions misconstrues as a mental disorder a basic and universal 22 THE LOSS OF SADNESS aspect o the human condition and thus inappropriately pathologizes a tremendous range o human behavior, undermining the credibility o psychiatry. Understanding how psychiatry has blurred a crucial distinction and tends to misclassiy intense sadness as a disorder is also useul to the ordinary person. Every time people enter physicians’ ofces or their children take routine screening instruments in school, the conceptual muddles we identiy in this book could lead to unwarranted diagnoses and treatment. To be an eective consumer o medical services, prepared patients should understand both how proessionals arrive at the diagnoses to which they are subject and what questions to ask about the problems these diagnoses may entail. Finally, it should be kept in mind that the truth about whether someone is disordered or normally sad oten matters in a practical way because diagnoses o mental disorders influence many consequential decisions. For example, such diagnoses can make it more difcult to obtain lie or health insurance or increase the cost o such insurance; they can be negative considerations in divorce proceedings that consider custody o children; and they requently disqualiy individuals rom participating in clinical trials or new medications or severe conditions such as cancer. Because o the role that diagnosis has in so many areas o our lives and the assumption that a diagnosis represents a genuine medical condition, conusing depressive disorder with normal sadness should not be taken lightly. Some Caveats: What About the Disadvantages of Such a Distinction? Some might object that drawing a distinction between normal and disordered sadness, whatever its intellectual merits, is potentially harmul or various reasons. We can’t address all the potential concerns, but it is worth briefly considering a ew. Are we somehow dismissing the suering o those with normal sadness? By calling certain responses “normal,” we in no way intend to minimize, let alone demean, the level o suering involved; indeed, the extreme pain o normal sadness can oten match that o depressive disorder. But just as you would want to distinguish a normal intense pain that results rom, say, childbirth or a broken bone (which you would want to manage and treat) rom an equally intense pain that results rom a pain disorder in which the pain is not a normal response to a bodily lesion (which would have important implications or treatment), these intense orms o sadness need to be distinguished so that they can be understood and optimally managed and treated. Could our analysis result in insurance barriers that would deny treatment to people who seek it even though they are not truly disordered? Yes, that is possible, but unlikely. The reality is that clinicians always have ound and always will find THE CONCEPT OF DEPRESSION 23 ways o responding to patient needs and o classiying these needs consistent with diagnostic definitions so that they receive reimbursement or treatment. Moreover, as in other medical domains, a strong argument can be made or reimbursement o treatment or nondisordered intense emotional responses because o the disabling eects they can have and as a preventive measure. An accepted distinction between normal and disordered intense sadness might even acilitate a discussion o such changes in the reimbursement system. Are we moralists who think that people should not generally rely on treatment, and specifically on medication, but should somehow be orced to muddle through their difculties? We are not arguing or or against using medication to treat normal eelings o sadness. That is a matter or individuals and their physicians to decide. Rather, we are arguing that conceptually illegitimate diagnoses o normal responses to events as disorders could prejudice such decisions by making it seem as though there is an internal malunction or which medication is the optimal treatment when evidence suggests that other interventions may oer equal or better relie and avoid the possible negative side eects o medication. We are simply saying that such treatment decisions should be based on a correct understanding o the condition. Indeed, once an adequate conceptual distinction is made, clearer research on optimal treatment o intense normal sadness might move orward more eectively. Doesn’t diagnosis with a medical disorder reduce blame, and aren’t we thereore encouraging the blaming o sad individuals or being emotionally weak? For example, i intense sadness is not diagnosed as a disorder, won’t it then be assumed that experiencing such eelings is a character flaw, and won’t people be urged to “shape up” and be strong rather than indulging such eelings? There is in act scant scientific evidence on whether diagnosis does lead to beneficial relie rom personal blame, in contrast to the vast evidence that it leads to harmul stigma. But it must be acknowledged that diagnosing individuals with a medical disorder, even i unjustified, may sometimes protect them rom misplaced blame by amily members and others or weakness o character. We argue, however, that there are ways to respond to such misplaced blame other than the extreme misuse o medical categories. In particular, our analysis emphasizes that intense sadness is a natural human capacity and not a character weakness; indeed, normal sadness probably has healing and reparative unctions that are still not understood.56 Oddly enough, many cultures actually blame individuals i they are inadequately sad when loss occurs (such as displaying too ew or too briefly the signs o mourning ater the death o a relative) because it seems to show lack o commitment or caring. The act that intense sadness may be related characterologically to depth o eeling and may thus be more important or coping with loss in some individuals than in others is hardly a weakness. Our analysis suggests that blaming can easily be addressed without labeling the individual as disordered. It should also be recognized that diagnosis with a disorder is no redoubt against personal contempt and blame. 24 THE LOSS OF SADNESS Isn’t it cold-blooded that we ocus on conceptual issues and don’t spend much time exploring the painul experience o depression itsel? There are rats o books detailing the great impact o depression and vividly documenting the experience o it. Our ocus is diferent because our goal is diferent, namely, to provide an understanding and critical perspective on how that experience is conceptualized, how it has come to be exploited by a variety o groups, and how its classification has changed in questionable ways over time. A Note on Terminology A ew terminological clarifications at this point might prevent needless conusion later on. First, although we use sadness to describe both the normal human emotion and the experiences described in depressive disorders, the normal responses we consider in act go beyond sadness and include certain episodes o emotional emptiness, shame, humiliation, and related responses to losses o various kinds, such as loss o sel-esteem or loss o standing in a group. So we sometimes use broader, more abstract language such as loss responses to reer to such experiences. Even when we do use the wordsadness, it should be understood that this is shorthand or a broader domain. Second, when we write o “normal” sadness, we do not mean that everything is statistically normal, or normal in the sense o “okay.” Rather, we mean that the sadness is unctionally normal or nondisordered, that is, it is the result o the relevant mental processes working as they were biologically designed to work in response to loss. Such “normal” responses can be “abnormal” in a variety o ways: they may be much more intense in some people than in others due to human variation in temperament or diferent cultural meaning systems; they may be statistically highly unusual because they are responses to a highly unusual environmental circumstance (e.g., someone experiencing extreme grie due to the deaths o several amily members within a short time); and they may be abnormal in the sense that they constitute a severe deviation rom the individual’s usual unctioning. None o these orms o statistical abnormality implies disorder. Third, many o the same kinds o psychological (e.g., blue mood) and physical (e.g., atigue) phenomena occur in disordered and nondisordered sadness responses. There is no convenient neutral term to describe these phenomena, so we accept the general convention and reer to them as symptoms. But it should be kept in mind that this is potentially misleading because o the association o “symptoms” with a medical diagnosis o disorder. The use o the word symptom here is intended to be neutral as to whether the phenomenon is a maniestation o disorder or a normal response. Fourth, as a convenient way to reer to whatever as yet unknown structures in the mind are designed to produce loss responses, we use the phrase loss response THE CONCEPT OF DEPRESSION 25 mechanisms. The term mechanism is common in evolutionary discussions and should not be construed as implying anything reductionistic or literally “mechanistic” about the mind. We assume, or example, that complex individual and cultural meanings enter into loss responses. The term mechanism simply indicates that, given that loss responses are part o our biological heritage, there are some structures in the person that are biologically designed to produce such responses at appropriate times. Finally, because we oten reer to similar phenomena when we discuss disorders and normal responses, we use several conventions to try to remain clear about what is under discussion at a given time. When we discuss a specific DSM category o disorder (which may, according to our argument, actually mistakenly include some normal as well as disordered conditions), we adopt the DSM convention o capitalizing a category, and so write, or example , o Major Depressive Disorder or, more simply, Major Depression. In addition, because the term “depression” is ambiguous as to normal or disordered conditions, we specifically use the term disorder when discussing depressive pathology— reerring to it usually as “depressive disorder .” We do not capitaliz e this phrase because we are not reerring to a DSM category—which, we argue, conuses disorder and normality—but to just those conditions that are genuine disorders. (We rerain rom using the common phrase clinical depression to reer specifically to disorders because many instances o normal sadness are now seen in clinics.) When we want to reer to all sadness c onditions, whether normal or disordered, we use generic phrases such as “depressive condition” or, simply, “depression.” What We Hope to Accomplish Depression has gained an iconic status in both the contemporary mental health proessions and the culture at large. Many experts claim it is a dire public health problem that a icts a large proportion o the population. The seeming massiveness o the problem simultaneously calls or urgent policy responses and yet paralyzes the will to respond. While recognizing the reality o depressive disorder and the enormous suering it causes, this book strives to bring perspective into discussions o depression. It shows how an inadequate conceptual distinction between disorder and nondisorder is a crucial weakness in the entire clinical and research industry devoted to this condition and demonstrates that the problems ampliy as the erroneous definition echoes through various social institutions. In particular, virtually all discussions o this condition ignore the critical question o when depressive symptoms indicate a mental disorder and when they are nondisordered responses to loss. Answers to this question would afect our understanding o how many people have mental disorders, to what degree we can prevent 26 THE LOSS OF SADNESS depression, whom we should treat for this condition, and what sort of policies we should develop. Exploring the current misdefinition of depression is a way of showing how seemingly esoteric technical issues can inadvertently influence broader social movements and how various constituencies are motivated to exploit and perpetuate conceptual errors once they are made. 2 The Anatomy of Normal Sadness adness traditionally has been viewed as humanity’s natural re- S sponse to deaths of intimates, losses in love, reversals of fortune, and the like. It arises, as Shelley says, because “the world’s wrong!”1 And, when the losses and strains that evoke the sadness are profound, the resulting emotions can also be severe, seeming to defy expression. In Samuel Coleridge’s words: A grief without a pang, void, dark, and drear, A stifled, drowsy, unimpassioned grief, Which finds no natural outlet, no relief, 2 In word, or sigh, or tear. The potential intensity of what appears to be normal sadness poses some difficult questions for psychiatric diagnosis. How is it possible to separate experiences of normal sadness from depressive disorders? How, after all, do we know that intense sadness is within the bounds of human nature and therefore can be psychiatrically normal, as common experience, as well as literature, would suggest? How can the known variations in the expression of sadness across cultures be consistent with a biologically designed and universal human capacity for sadness? And, if sadness is indeed a normal part of human nature, what is it for, that is, for what function could this painful and often debilitating emotion possibly have been naturally selected? To lay a foundation for the argument that modern psychiatry confuses sadness with depressive disorder, this chapter considers the characteristics and evolutionary enigma of normal sadness and presents evidence that it is a designed aspect of human nature. Components of Normal Sadness Normal sadness, or nondisordered responses to loss, has three essential components important to our argument: it is context-specific; it is of roughly 27 28 THE LOSS OF SADNESS proportionate intensity to the provoking loss; and it tends to end about when the loss situation ends, or else it gradually ceases as coping mechanisms adjust individuals to new circumstances and bring them back into psychological and social equilibrium. First, loss responses are inherently context specific in the sense that they respond to a specific range o the “right” stimuli and do not respond outside that range to the “wrong” stimuli. 3 Nevertheless, the kinds o losses that all within the range that can trigger normal sadness vary considerably. Some are losses o valued intimate attachments involving closeness, love, and riendship. Others derive rom the hierarchical aspects o social relationships, such as losses o power, status, resources, respect, or prestige. A third kind o loss relates to the ailure to achieve valued goals and ideals that provide coherence and purpose to 4 lie. Any o these types o losses that are unexpected, humiliating, threatening to long-term well-being, and seemingly without remedy and in which the lost object cannot easily be replaced are especially likely to evoke intense sadness responses.5 Although many sadness responses emerge ater distinct losses, others stem rom persistent and chronically stressul social situations, such as long-standing economic hardships that seem unjustified, enduring conflicts within interpersonal relationships, or continuing inability to achieve important goals.6 As hopes or change wane, these persistent strains can produce long-standing states o sadness that may disappear only when the chronic stressors are over or when people are able to change their evaluative criteria. The act that sadness ollows acute losses or is simultaneous with chronic strains, however, does not in itsel mean that its symptoms are normal. Environmental stresses may trigger depressive disorders in people who are predisposed to depressio n, or the stresses may be o such unusual severity as to produce a breakdown o normal loss response mechanism s in those not predisposed. For example, many combat pilots develop symptoms that suggest disorder i they engage in enough wartime sorties. 7 In other cases, the presence o a disorder precedes and itsel provokes the stressul event that might mistakenly be thought to be its cause, as when preexisting depressions lead people to be fired rom jobs or rejected by romantic partners. 8 Emergence under appropriate circumstances is a necessary but not a sufcient condition or the presence o normal sadness. The second component o nondisordered sa dness is that it is o roughly proportionate intensity to the magnitude and permanency o the loss itsel, which involves two actor s. The first is cognitive: nondisorde red loss responses accurate involve r easonably than gross distortions. 9 perceptions o the negativ e circumstances, rather For examp le, the belie that one’s spouse has been sexually unaithul may cause intense sadness proportional to the perceived loss, bu t i the belie is delusional to begin with, then the sadness is THE ANATOMY OF NORMAL SADNESS 29 not normal. The normality o  such percep tions o the magnitud e o the loss must be judg ed in the context o the lie, values, and meaning system o the individual. The other actor in proportionality is afective: the emotional and symptomatic sev erity o the response should be o roughly proportionate intensity to the seriousness o the loss that has been expe rienced. Minor setbacks should generally be minimally disturbing, leading to relatively mild reactions in which people are disappointed, discouraged, downcast, or dispirited. Moderate loss events should generally trigger relatively medium-intensity reactions o dismay, resignation, and gloominess. Serious and highly threatening situations sho uld generally evoke reactions o greater severity, including intense states o deep sor row, despondency, anguish, pain, numbness, and 10 dejection. It bears emphasis that under the proportionality requirement designed responses to severe losses can also be quite severe—indeed, as severe as some depressive disorders—and can potentially satisy DSM diagnostic criteria or Major Depressive Disorder despite not being disordered. Individual diferences in temperament as well as cultural diferences in expressiveness may also influence responses to be more or less intense. However, evolutionary processes should provid e some limits to the severi ty o depressed moods ater a loss, because responses o disproportionatel y high intensity and long duration would not allow people to disengage rom inhibited states and return to more productive activities. Nondisordered loss responses cannot encompass gross breakdowns in basic psychological systems, such as delusional and psychotic symptoms, i the individual is to be able to adapt to the new circumstances. The third and final component o nondisordered loss responses is that they not only emerge but also persist in accordance with external contexts and internal coping processes. Normal sadness remits when the context changes or the better or as people adapt to their losses. Some loss events, such as the death o an intimate, are irreversible, and the duration o normal sadness ater these losses is highly variable but gradually desists over time. Other loss events, such as breakups o important romantic relationships or losses o valued jobs, naturally lead to sadness that is time limited and that quickly improves ater the emergence o positive changes, such as entering a new relationship ater a marriage dissolves or finding a new job ater a period o unemployment.11 The sensitivity o designed sadness responses to external contexts does not necessarily mean that they will be transient. As long as stressul environments persist, symptoms can also be long-standing. Sadness endures in contexts such as troubled marriages, oppressive jobs, persistent poverty, or chronic illness because the stressul circumstances that produced it remain unchanged. Ordinary sadness, thereore, is not necessarily o shorter duration than dysunctional depression. 30 THE LOSS OF SADNESS Examples of Normal Sadness Grief as a Prototype of Normal Sadness As long as emotions have been recorded, experiences o grie have been central to portrayals o basic human nature. Few depictions match the intensity o Achilles’ reaction on hearing o the death o his riend Patroclus: A black cloud o grie came shrouding over Achilles. oth hands clawing the ground or soot and filth, He poured it over his head, ouled his handsome ace And black ashes settled into his resh clean war-shirt. Overpowered in all his power, sprawled in the dust, Achilles lay there, allen Tearing his hair, defiling it with his own hands.12 Such descriptions are common across cultures and historical epochs. The oldest literary depiction o grie occurs in the epic poem s about the king Gilgamesh, initially composed in abylonia in the third millennium B.C., almost 1500 years beore Homer’s Iliad and in an alien culture. Yet the severe grie o the king Gilgamesh over the death o his close riend Enkidu is portray ed in terms strikingly similar to that o Achilles over his riend Patroclus: Hear me, O Elders o Uruk, hear me, O men! I mourn or Enkidu, my riend, I shriek in anguish like a mourner. . . . And ater you (died) I let a filthy mat o hair grow over my body, and donned the skin o a lion and roamed the wilderness. . . . Like a lioness deprived o her cubs he keeps pacing to and ro. He shears of his curls and heaps them onto the ground, ripping of his finery and casting it away as an abomination. Gilgamesh experiences enormous sadness, cries bitterly, is possessed by restless agitation, and sufers rom a sense o worthlessness leads him to cast aside finery and cover himsel with filth. Unable to bear his ordinary social activities, he wanders alone in the desert. In his travels mourning Enkidu and seeking immortality (thoughts about one’s own death are another common symptom o grie), Gilgamesh comes upon a tavern to which he wishes entry. He boasts o his achievements to establish his identity, but the tavern-keeper notices most the dramatic symptoms o grie, and he challenges Gilgamesh. In a moving descrip- tion o grie ’s expectable efects, Gilgamesh answers: Tavern-keeper, should not my cheeks be emaciated? Should my heart not be wretched, my eatures not haggard? Should there not be sadness THE ANATOMY OF NORMAL SADNESS 31 deep within me! Should I not look like one who has been traveling a long distance, and should ice and heat not have seared my ace!. . . . Should I not roam the wilderness? My riend, Enkidu, the wild ass who chased the wild donkey, panther o the wilderness, we joined together, and went up into the mountain. We grappled with and killed the Bull o Heaven, we destroyed Humbaba who lived in the Cedar Forest, we slew lions in the mountain passes! My riend, Enkidu, whom I love deeply, who went through every hardship with me, the ate o mankind has overtaken him. Six days and seven nights I mourned over him and would not allow him to be buried until a maggot ell out o his nose.13 Such grie ater the death o an intimate provides a model or the way that sadness responses are designed to work. It arises in circumstances o loss, its intensity is proportionate to the importance and centrality to one’s lie o the lost individual, and it persists or some time and then gradually subsides as one adapts to the changed circumstances. The DSM definition o Major Depressive Disorder (MDD) excludes conditions that arise rom bereavement because these normal responses oten meet its symptomatic criteria and could be incorrectly diagnosed as disorders. Bereaved people commonly develop symptoms, including depressed mood, inability to eel pleasure, loss o appetite, inability to concentrate, insomnia, and so orth, which can be identical to those o depressive disorders.14 Although normal bereaved individuals in our culture rarely show some o the common symptoms o depressive disorder, such as lowered sel-esteem, they nevertheless oten report enough depressive symptoms to meet DSM criteria or MDD, and nearly all individuals report at least some symptoms. Over three-quarters o the bereaved report crying, sleep disturbance, and low mood, and over hal also indicate loss o appetite in the month ollowing the loss.15 Without the bereavement exclusion, between one-third and one-hal o bereaved people could be classified as having a depressive disorder during the first month ater the death. 16 Among people who have lost spouses, most studies find that between 20 and 40%—and some find that more than hal—experience symptoms comparable in severity to MDD criteria over the first ew months.17 Rates o depressive symptoms in parents’ reactions to the deaths o their children 18 or o adolescents’ reactions to the deaths o their parents19 are even higher, more intense, and longer lasting than those that ollow the deaths o spouses.20 The intensity o grie generally varies in a roughly proportionate manner with the context and the circumstances that determine the magnitude o the loss, and it also varies greatly rom individual to individual according to temperament. Despite the high proportions o bereaved people who develop symptoms comparable to those o depressive disorder, most do not develop such symptoms, and a substantial number experience no distress at all ater their losses.21 Although individual diferences in sensitivity to loss certainly play a 32 THE LOSS OF SADNESS role, the nature and context o the loss also shape the intensity o the response. For example, expected deaths that occur ater chronic illnesses produce ewer depression-like symptoms than sudden and traumatic or otherwise unexpected deaths.22 Because people who become bereaved at younger ages are more likely to experience one or more o these circumstances, they report more symptoms than older people do.23 The quality o the relationship with the lost intimate also strongly afects the intensity o the subsequent bereavement. Losses o long-standing, close, and intense relationships produce more distress than losses o more distant ties.24 This is the reason that spouses who report good relationships beore the deaths o their husbands or wives report more depressive symptoms.25 Conversely, spouses who had more negative and ambivalent eelings toward their partners beore the death experience ewer depressive symptoms ater it than people with more positive eelings do.26 Likewise, bereaved elderly people with high levels o caregiving strain prior to the deaths o their partners report declining levels o distress ollowing the deaths.27 Indeed, death can bring relie and escape rom stressul situations among those who had elt trapped in bad marriages with seriously ill spouses.28 The persistence, as well as the intensity, o the loss response also depends on the enduring circumstances that ollow the loss. Whether grie persists or not is a unction o the degree o social and economic upheaval the loss produces and o the resources available to cope with these upheavals.29 In the long run, economic deprivation that ollows the death o a husband is more stronglyassociated with the intensity o sadness than is widowhood in itsel.30 The presence or absence o social support that provides resources to cope with the loss is also a good predictor o the duration o sadness.31 Longer duration o the loss response, thereore, need not indicate the presence o a disorder, but it can mark the persistence o the stressul situation that accompanies the loss and thus the correspondingly greater negative meaning o the loss. Normal grie also appears naturally designed to desist with the passage o time. Relatively ew bereaved individuals show serious symptoms or long periods, and most gradually adapt to their losses and recover their preloss levels o unctioning.32 In one major study, 42% o the bereaved met criteria or depressive disorder ater 1 month, but only 16% remained in this state ater a year.33 Other studies confirm that about 10–20% o bereaved persons ulfill DSM diagnostic criteria or depressive disorder a year ater the death, and even or many o these, psychological unctioning returns to preloss levels by 2 years.34 The evidence thus supports the conclusion that, although large numbers o grie DSM reactions satisy symptomatic and duration diagnostic criteria or depressive disorder, the vast majority are transient normal responses to loss, with only a small proportion becoming chronic conditions that are likely disorders. However, grie can sometimes trigger mental dysunction o a more severe or persistent nature than is consistent with a normal response. When grie involves THE ANATOMY OF NORMAL SADNESS 33 extreme immobilization, pronounced psychotic ideation, or severe symptoms that persist despite the passage o time and changing circumstances, then it can be presumed that an individual’s reaction to the death o an intimate has caused a breakdown in his or her psychological unctioning. In general, about 10% o the bereaved come to sufer rom chronic depressive conditions that may well be disorders.35 For some in this group, the death o an intimate intensifies to a pathological level depressive symptoms that existed prior to the death.36 For others, the reaction to the death itsel triggers a ailure in normal coping unctions. Such pathological states constitute Complicated Grie, which the DSM correctly recognizes as a orm o depressive disorder, and such transormations o grie into enduring depressive disorder have been recognized since antiquity.37 For most people, however, bereavement is a normal eature o human experience that will naturally dissipate with the passage o time, not a mental disorder, as the DSM recognizes. Mistakenly labeling such normal responses as depressive disorders can have a variety o negative consequences. Interventions such as grie counseling and eforts that orce people to acknowledge their grie have not been shown to be very efective and can be harmul. 38 Indeed, an alarmingly high number o grieving people worsen ater receiving treatment.39 The problem is that the DSM contains no comparable recognition o the many circumstances other than bereavement that can lead to intense, but normal, sadness. Yet, with respect to these other circumstances o loss, the same sort o evidence exists that sadness responses are as normal as most cases o bereavement. Loss Responses to Profound Threats in Relationships Although th e permanency o the loss associa ted with grie distinguishes it rom most other losses, grie need be no diferent in principle rom intense sadness that arises, or example, ater the unsought end o a love afair, the news that one’s spouse has been unaithul, the dissolution o a marriage, the ailure to achieve one’s cherish ed lie goals , the loss o financial resources, the loss o social supports and relatio nships, or the dia gnosis o a serious illness in onesel or a loved one. 40 Even the death o beloved pets or celebrities w hom one does not personally kno w can create periods o low mood, low initiativ e, and pessimism as normal reactions to loss. 41 The DSM ’s own general definition o mental disorder pro vided in its introduction excl udes all “expectable and culturally sanctioned response(s) to a particular event, for example, the death o a loved one” rom its definit ion o mental disorder , using grie as the prototypical excluded category. 42 Yet, emotionally painul responses to other particular loss events such as marital, romantic, health, or financial reversals plainly can be just as “expectable and culturally sanctioned” responses as those o bereavement and should thereore all under the definition’s 34 THE LOSS OF SADNESS exclusion as well. The criteria or MDD, however, do not ollow out this logic, and they contain no exclusions or other loss respons es comparable to the one or bereavement. Marital dissolution is perhaps the most common trigger o intense normal sadness that can be severe enough to meet DSM symptomatic criteria or depressive disorder.43 The intense sadness that ollows the loss o romantic attachments has long been a central literary theme. The double suicides o Romeo and Juliet, or example, do not result rom mental disorder but rom a tragic misunderstanding ater the perceived loss o a lover. Other literary suicides, such as Emma Bovary’s or Anna Karenina’s, stem rom realizations that the consequences o stigmatized romantic entanglements are inescapable. Current research supports the intuition that severe losses o intimate attachments naturally lead to sadness responses: in many studies marital dissolution is more consistently and powerully associated with depression than any other variable.44 Indeed, rates o depressive episodes that meet DSM criteria are comparable or persons who experience marital dissolution and those who experience bereavement.45 People who undergo marital dissolution are ar more likely to develop first onsets o MDD over a 1-year period than people who do not.46 “Adjusting or age, sex, and baseline history o other psychiatric disorders,” writes sociologist Martha Bruce, “the efect o marital separation and divorce on first-onset major depression is very large (Odds ratio) 18.1.”47 Studies indicate ϭ that rom 30 to 50% o people undergoing the process o marital dissolution experience symptoms comparable in intensity to those o depressive disorder.48 Given that as many as 60% o marriages are expected to end in divorce or separation, a huge proportion o the population should experience nondisordered sadness with symptoms comparable to those o MDD at some point in their lives rom this cause alone. As with bereavement, whether or not people develop symptoms o intense sadness during periods o marital dissolution largely varies as a unction o the social context beore and ater the separation. At one extreme, symptoms can decline when marital stress was high beore the period o dissolution.49 In some cases, marital dissolutions can even lead to better mental states when they involve leaving unwanted marriages and entering new partnerships. At the other extreme, marital dissolutions that are unwanted or that involve eatures that are degrading, shameul, threatening to uture well-being, entrapping, or devaluing o the person who is experiencing the loss are especially prone to produce intense depressive symptoms.50 For example, wives who have sufered humiliation due to the unexpected infidelity o their husbands have three times more depressive symptoms than those who have sufered losses that do not involve such humiliation.51 Just as the intensity o normal sadness ater marital dissolutions varies as a unction o social circumstances, its persistence also depends on the stressulness o the context. In contrast to the highly stressul period o marital separation, the THE ANATOMY OF NORMAL SADNESS 35 divorce itsel oten indicates the resolution o a stressul situation.52 By 2 years ollowing the divorce, divorced people have comparable rates o depression to married people.53 The huge rates o nondisordered sadness that arise during periods o marital dissolution are associated with severe symptoms that rarely persist ar beyond the divorce.54 In addition to the loss o an intimate partner, marital dissolutions oten negatively afect many aspects o lie, including social status, personal identity, financial resources, riendship networks, living situations, and relationships with children, in ways that can intensiy the associated loss response. People undergoing marital dissolution w ho ace the secondary stressors o alling standards o living, weakening o support networks, downw ard residential mobility, and problems in dealing with children all report more symptoms o 55 distress than those who do not ace these additional stressors. Conversely, sadness ater marital dissolution is particularly likely to remit in response to positive environmental changes or “resh start” events such as remarriage or orming new relationships. 56 In a minority o cases, a depressive disorder might have preceded and been one cause o the marital dissolution.57 In another small group o people, the experience o marital dissolution is severe enough to lead to breakdowns o loss response mechanisms that are pathologically immobilizing or that persist long ater the period o the breakup. The preceding evidence suggests, however, that most people who develop symptoms comparable to those o depressive disorder during periods o marital dissolution do not have mental disorders. They are responding to situations that naturally lead people to be intensely sad. Other Examples: Job or Status Loss, Chronic Stress, Disasters In addition to losses o intimate attachments, losses o status and resources oten evoke normal sadness. The loss o a valued job is one common situation that produces high rates o intense sadness. Such losses, as well as financial strain, underemployment, demotions, and ailures to achieve promotions, are associated with declining status, prestige, and resources and consequent sadness that cannot be explained by depressive states that existed beore the economic adversity.58 Becoming unemployed has a particularly strong relationship with elevated levels o depression-like symptoms; indeed, about a quarter o people who become unemployed develop symptoms severe enough to resemble DSM clinical criteria.59 But any serious loss o financial resources or a continu60 ing state o economic strain can yield such experiences. For example, about a third o the people who sufered severe loss o retirement savings as a result o a bank raud developed symptoms comparable to those o MDD.61 The context in which the job loss occurs, and thus its meaning to the individual, predicts which unemployed persons are likely to develop symptoms 36 THE LOSS OF SADNESS equivalent to those o DSM depressive disorder. People who lose valued and rewarding jobs are especially likely to become symptomatic, whereas those who previously held highly stressul jobs are less likely to become sad.62 Also, sadness is more likely to emerge when people unexpectedly lose jobs than when the loss was anticipated.63 Job loss is particularly likely to lead to normal sadness when it is associated with many secondary stressors such as economic and interpersonal strains.64 Just as distress rom loss o intimate attachments ends when new attachments orm, studies indicate that levels o distress become elevated shortly beore or immediately ater becoming unemployed but dramatically decline ater reemployment, a sign o a normally unctioning loss response.65 This is the reason that workers who lose jobs during prosperous periods when opportunities or 66 reemployment are plentiul are not likely to become distressed. Especially humiliating status losses can sometimes be intense enough to produce outcomes as extreme as suicide among individuals who were normal in all respects beore the loss. Examples include executives who are responsible or proound business ailures or persons indicted in corruption scandals.67 Consider the case o Hajimu Asada and his wie Chisako: “The chairman o a Japanese poultry company blamed or ailing to alert the authorities about an outbreak o avian influenza committed suicide with his wie, as the disease showed signs o spreading in Japan.”68 Failures to uphold social norms, especially in intensely collectivist social settings, can lead to shame o enough intensity to provoke suicide.69 For example, suicide rates were extraordinarily high during the Chinese Cultural Revolution, especially among persons accused o being landlords, wealthy peasants, intellectuals, and dissidents.70 Other losses that lead to nondisordered sadness arise when large discrepancies exist between the goals to which people aspire and their actual accomplishments. 71 Undergraduates who are denied admittance to long-desired proessional schools or graduate students who cannot find jobs in their academic fields understandably oten show signs o sadness. 72 Indeed, the ailure to achieve valued goals is the most powerul predictor o low mood among undergraduates. 73 Likewise, adults who do not attain goals they set or themselves earlier in lie report more distress than people whose attainments more closely match their ormer aspirations. 74 Similarly, women who strongly desire to bear children but who are inertile oten experience intense distress. 75 Such symptoms disappear when the discrepancy between aspirations and accomplishments narrows: or example, the depressiv e symptoms o women who have sufered miscar riages do not per sist when they subsequently become 76 pregnant and give birth. Enormous proportions o populations who experience disasters that entail massive losses develop depressive eelings. For example, rom 40 to 70% o civilian reugees displaced rom their homes by mass violence display symptoms o Major Depression. 77 In most cases, however, symptoms do not endure. THE ANATOMY OF NORMAL SADNESS 37 For example, 5 weeks ater the terrorist attack o September 11, 2001, one o every five residents o New York City reported enough symptoms to qualiy or a diagnosis o MDD. During this period, about three-quarters o New York City residents cried, over 60% elt very nervous or tense, about 60% had trouble getting to sleep, and nearly hal elt more tired than usual and didn’t eel like eating. Very ew people who experienced such understandable depressive symptoms immediately ater the attack, however, remained depressed 6 months later, although not many were treated or their conditions. 78 Likewise, immediately ater natural disasters such as earthquakes, tornadoes, or floods nearly all aected individuals report some distress, which quickly dissipates as living conditions normalize.79 Some o the most consistent associations between social context and sadness do not stem rom such acute situations o loss but instead rom chronic social stressors such as long-term joblessness, persistent debt, living in unsae and threatening neighborhoods, chronic physical illnesses, troubled marriages, or oppressive work conditions. Unlike a typical episode o designed sadness that remits when the conditions that gave rise to it end, ongoing stressors can lead to persistent states o sadness that nonetheless are normal reactions to chronically problematic circumstances. Such chronic and persistent strains can be even more strongly related than the number o time-limited stressul lie events to depressive symptoms.80 The relationship between long-term financial and social disadvantage and experiences o sadness is strong enough that persons in the lowest socioeconomic quintile are up to seven times more likely than those in the highest quintile to satisy symptomatic criteria or MDD. 81 Some have claimed that such individuals have depressive disorders that caused them to sink into the conditions they are in, but many careul studies have established that disadvantageous social conditions are ar more likely to precede the development o symptoms o depression than they are to result rom preexisting depressive conditions.82 Supporting the idea that much o this sufering is normal sadness, some evidence shows that when people move rom chronic impoverished conditions to relatively more prosperous ones their levels o distress all. In the course o one large study o rural children, a casino opened, providing the quarter o the sample who were American Indian with substantial income supplements. Depression-like symptoms o children whose amilies rose out o poverty ell about 30% over the 4-year period beore and ater the casino opened, whereas symptom levels o the persistently poor remained stable.83 Rates o symptoms among the group that experienced improved financial conditions were no di- erent rom those among participants who were never poor. Other studies find that rising incomes lead to declining numbers o depressive conditions among impoverished people.84 These findings suggest that a large proportion o apparent depressive disorders among indigent people are not internal dysunctions and would not persist i conditions o deprivation improved. 38 THE LOSS OF SADNESS We are reminded here o an anecdote that a colleague told us. An eminent researcher presented a paper on women who he claimed were suering rom chronic depressive disorder. One woman with children had been abandoned by her husband and was acing an enormous and chronic challenge in dealing with her impoverished circumstances. Her symptoms o sadness, worry, sleeplessness, and so on were indeed severe. Then, the woman won a lottery, yielding her a considerable amount o money. Strikingly, her chronic symptoms disappeared, leading our colleague to doubt that she had ever had a genuine disorder but instead had been understandably distressed by the overwhelming challenges that aced her. We conclude that grie reactions are indeed a model or responses to numerous kinds o loss situations. A airly high proportion o people develop symptoms in response to various losses, including symptoms sufcient in kind, number, severity, and duration to satisyDSM criteria or MDD; these symptoms are proportionate in severity to the meaning o the situation that evoked them; and their persistence stems rom the persistence o the srcinal stressor or rom additional stressors that ollow the initial loss. Leaving aside the death o a loved one, the kinds o acute and chronic losses that lead to intense sadness among some nondisordered people—romantic breakups, losses o jobs or ailure to gain anticipated promotions, disasters, illness, and so orth—are common. When these losses are serious, people who suer them unsurprisingly report the experience o sadness-related depressive symptoms. Neither traditional psychiatry (as we show in chapters 3 and 4) nor common sense considered such reactions to be psychiatric disorders, and they do seem to qualiy as normal or all the very same reasons that intense grie is considered normal. Given the number o people who experience the described kinds o losses, we expect that substantial numbers o people with normal sadness would satisy DSM criteria or depressive disorder at some point in their lives, thus yielding a potentially significant number o alse-positive diagnoses. Evidence That Sadness Is a Normal, Designed Response How do we know that the kind o sadness described in this chapter is indeed normal, that is, a result o human species-typical biological design? Although it may seem obvious that negative emotions such as sadness, anger, and ear in response to certain situations are results o natural selection, some social scien- tists believe instead that such emotional responses reflect learned, socially constructed scripts.85 We consider three lines o evidence relevant to the question o whether the emotion o sadness and its attendant symptoms substantially result rom innate mechanisms or rom cultural scripts: loss responses among human and nonhuman primates, human inant loss responses that occur THE ANATOMY OF NORMAL SADNESS 39 developmentally prior to socialization into a culture’s emotional scripts, and the cross-cultural universality o loss responses. Continuities Across Species Nonhuman primates show a clear resemblance to humans in the way they respond to loss—that is, in their observable eatures o expression, behavior, and brain unctioning. As Darwin noted, apes and humans show similar acial expressions in situations that are associated with sadness, including elevated eyebrows, drooping eyelids, horizontal wrinkles across the orehead, and outward extension and drawing down o the lips.86 In addition, displays o sadness among apes, like human responses, include decreased locomotor activity, agitation, slouched or etal-like posture, cessation o play behavior, and social withdrawal.87 Most important, the loss situations that commonly lead to depressive responses are similar in primates and in humans. Nonhuman primates react to separations rom intimates—or example, an inant monkey separating rom its mother—with physiological responses similar to those that correlate with sadness in humans, including elevated levels o cortisol and ACTH hormones and impairments o the hypothalamic-pituitary-adrenal (HPA) axis. 88 Adult nonhuman primates that are separated rom sexual partners or peers show similar reactions.89 Primate studies also show that symptoms o depression that develop ater separations rapidly disappear when the situation o loss is resolved, such as when an inant monkey is reunited with its mother.90 Also, primates in environments that eature readily available mother substitutes rarely exhibit severe or enduring reactions in response to maternal separations. 91 Such transient sadness responses to separation are part o innate coping mechanisms among many species.92 However, prolonged separations and separations marked by proound isolation can produce neuroanatomical changes that permanently afect nonhuman primate brain unctioning, analogous to the triggering o genuine depressive disorder in humans.93 Nonhuman primates also share with humans social hierarchies with high and low status positions and situations o chronic social subordination that lead to behavioral and brain reactions similar to the normal depressive responses in their human counterparts.94 Subordinate nonhuman primates have higher levels than dominants o stress hormones and lower levels o blood serotonin, the neurochemical linked to depression among humans.95 The loss o rank in nonhuman primate social hierarchies also triggers the production o the neuro96 chemical correlates o depression. Experimental studies o nonhuman primates show how normal depressive symptoms can be a unction o social situations. Psychiatrist Michael McGuire and his colleagues studied vervet monkeys, who possess strong and enduring hierarchical status relationships with one dominant male in each group. 97 40 THE LOSS OF SADNESS The highest ranking males have serotonin levels that are twice as high as those of other males in the group. When experimenters withdrew the dominant males from the group, their serotonin levels fell, and they refused food, showed diminished activity, and appeared to human observers to be depressed. Conversely, the serotonin levels of previously dependent monkeys who gained high status after the removal of the previously dominant male rose to values that characterized dominant males. Similar results have been obtained with female monkeys.98 Studies of nonhuman primates in natural settings confirm the findings of laboratory research.99 Neuroendocrinologist Robert Sapolsky’s studies of wild baboons living freely in East Africa show that chronic social subordination is associated with high stress hormones consistent with depressive symptoms in humans and that when rank in status hierarchies changes, these physiologi100 cal profiles change as well. Moreover, they depend on the social context: the behavioral and neurochemical advantages of high rank are found only in stable dominance hierarchies, whereas in unstable hierarchies in which the position of the dominant is precarious, hi gh rank is not associated with few er stress hormones. 101 Thus humans appear to have inherited from their primate ancestors a natural tendenc y to become sad in particular contex ts of status and relationship loss. Loss Responses in Presocialized Infants The human tendency to become sad in certain contexts appears early—in infancy. Indeed, it appears before the infant has even learned culturally appropriate ways of expressing sadness. The British child psychiatrist John Bowlby has conducted the most influential studies demonstrating how attachment losses lead to depressive reactions among infants. 102 Bowlby persuasively argued that human infants are designed to need strong attachments and that they develop certain types of sadness responses as a coping mechanism when they are separated from their primary caregivers. He observed that healthy infants who were separated from their mothers initially reacted by crying and displaying other expressions of despair. They protested the separation and searched for their mothers. These responses usually evoked sympathy from the mothers, who responded by attending to their infants’ needs. When separations were prolonged, however, the infants withdrew and became inactive and apathetic, similar to the symptoms of an intense adult loss response. Prolong ed separations resulted in a state of detachment in which young children ceased to respond to parental figures even after they were restored to their lives. Bowlby’s work indicates that sadness naturally arises in presocialized infants after the loss of close attachments. The liability to experience separation anxiety and grief results from involvement in intense, loving relationships. Sadness that develops after losses of these relationships seems to be an aspect of normal, presocialized human nature. When these losses are prolonged and without THE ANATOMY OF NORMAL SADNESS 41 compensating remedies, however, they can lead to responses that go beyond normal sadness to become depressive disorders.103 Cross-Cultural Uniformity The capacity or intense sadness in response to loss appears to be a universal eature ound in all human groups. Loss responses with the characteristics we have described are ound not only throughout Western history (see chapter 3) but also in non-Western societies. Charles Darwin was perhaps the first to comment on the universality o sadness responses: “The expression o grie due to the contraction o the grie-muscles, is by no means confined to Europeans, but appears to be common to all the races o mankind.”104 Darwin provided a description o grie among the Australian absrcines that was comparable to the expression o this emotion among Europeans: Ater prolonged sufering the eyes become dull and lack expression, and are oten slightly sufused with tears. The eyebrows not rarely are rendered oblique, which is due to their inner ends being raised. This produces peculiarly-ormed wrinkles on the orehead which are very diferent rom those o a simple rown; though in some cases a rown alone may be present. The corners o the mouth are drawn downwards, which is so universally recognized as a sign o being out o spirits, that it is almost proverbial.105 Considerable subsequent research confirms Darwin’s observations that such expressions, especially the contraction o the muscles at the corners o the mouth, are recognized across cultures as representing grie. The most important studies stem rom psychologist Paul Ekman’s research on basic human emotions, including sadness. In particular, to test the universality o emotions, Ekman studies acial expressions because they are less susceptible to cultural influences than are verbal reports o emotions. In one type o study, Ekman asked people to show how their aces would look i they elt sad “because y our child died.” 106 The resulting acial expressions were photographed. Expressions o sadness in these pictures were marked by eyes that are downcast with drooping or tense upper lids, eyebrows that are drawn together, jaws that are closed or slightly open, and lower lips that are drawn down. The photographs were then shown to people in diferent cultures, and they were asked to select rom among several choices o narratives about the situation that triggered the pictured emotion (the loss o a child is used or sad- ness). Ekman’s results indicate overwhelming agreement among persons in dierent countries about the emotion each photograph expresses. Very high rates o concurrence, ranging rom 73 to 90%, existed across five diferent cultures (Japan, Brazil, Chile, Argentina, and the United States); the concurrence was even higher within each particular culture in ratings o sadness photographs.107 42 THE LOSS OF SADNESS Another study o 10 cultures (Estonia, Germany, Greece, Hong Kong, Italy, Japan, Scotland, Sumatra, Turkey, and the United States) indicated between 76 and 92% agreement on acial expressions o sadness.108 In response to objections that his findings actually demonstrate the impact o common learning experiences because o the influence o worldwide media, Ekman studied the Fore culture in Papua, New Guinea, which had not been exposed to any kind o media or had contact with outside cultures.109 He showed Fore participants photographs o three aces that expressed three diferent emotions— sadness, anger, and surprise. He then told a story involving only one o these emotions and asked which o the photographs best matched the story. For example, he asked his participants which picture best depicted a man whose child had died.He ound that 79% o the Fore—a preliterate, isolated people—agreedwith members o literate cultures on the ace that most corresponded to sadness in the story that was read to them. Because Ekman’s research in this culture did not rely on the use o Western words, it is immune to critiques that Western preconceptions account or the findings. Ekman and his colleague Wallace Friesen also asked the Fore to show the acial expressions they would have i they were the persons described in the emotion stories (e.g., i their children had died). American college students could accurately judge what emotions videotaped responses o the New Guineans represented. In addition, Ekman’s voluminous filming o this culture, as well as o others in Papua New Guinea, showed the same expressions o sadness that were ound elsewhere in the world. Ekman’s findings indicate that some innate eatures o the expression o sadness are present in all cultures, presumably because they stem rom the evolution o humans as a species. Cultural Variation and Normal Sadness The findings that emerge rom studies o primates and very young children and across cultures all indicate that sadness responses are biologically based and not due to social scripts alone. In particular, humans appear biologically designed to become sad in certain kinds o situations, especially those involving losses o close attachments, social status, or meaning systems. However, the biological roots o normal sadness in no way preclude important social influences on when or how sadness is expressed. Given that meanings mediate sadness responses and that cultures shape meanings, normal sadness is inherently a joint product o biology and culture (as well as individual variation and learning). Cultural Meanings and Biological Mechanisms as Complementary Culture and biological design are not always antithetical to each other; when it comes to emotions, they are complemen tary. Culture itsel is an evolved human THE ANATOMY OF NORMAL SADNESS 43 capacity; humans are designed to be capable o a degree o socialization and internalization o social values, meanings, and rules. As the sociologist Jonathan Turner has emphasized, people are hardwired to pay attention to cultural symbols, 110 social roles, and interactional needs. Some evolved mechanisms, such as emotions, involve responses to such meanings. Thus cultural meaning plays an essential and perhaps even designed role in shaping the finalxpression e o emotion. Indeed, many mental eatures are biologically selected to be capable o cultural variation. For example, the capacity or language appears to be a designed human trait, but the details o grammar and o course the specific sounds that comprise the words o a language, as well as the way those sounds are associated with concepts, vary rom culture to culture. Similarly, sexual jealousy is a universal biologically selected emotion that occurs in all human societies, but the specific targets o jealousy vary widely. In some monogamous cultures, anyone who attempts to have sex with another’s spouse is a target o such eeling; in some cultures, certain honored strangers are exempt; and in other cultures, a substantial proportion o the community is not subject to jealousy. Language 111 and sexual jealousy, however, are naturally selected capacities. As linguists suggest, the mechanisms that underlie such eatures may be designed to allow or “parameter setting,” in which culture establishes the specific orm that the expression o the general, evolved structure will take. Culture and Definitions of Loss The categories that trigger sadness—losses o attachment, status, and meaning—are common across all societies.112 “Sickness o liver,” a metaphor or sadness among the Malay, is illustrative: “A Malay loses something he values; he has a bad night in the gambling houses; some o his property is wantonly damaged; he has a quarrel with one whom he loves; his ather dies; or his mistress proves unaithul; any one o these things causes him ‘sickness o liver.’”113 Nonetheless, culture influences evolutionarily shaped loss responses in a variety o ways. First, cultural meanings influence which particular events count as losses. These meanings also influence contextual actors, such as humiliation and entrapment, which determine the severity o loss. For example, in most social groups within the United States, the ailure o a woman to give birth to a male child would not be a reason or intense sadness. But in Zimbabwe, the meaning o such ailure includes a serious decline in social status, undesirability as a marriage partner, and potential divorce. Consequently, ailure to have a male child is a source o serious depressive reactions in Zimbabwean women.114 Or, in India, among the leading causes o suicide in 1990 were quarrels with in-laws and dowry disputes, which represent major losses in India but would not necessarily bring about such extreme responses in other societies. 115 The act that such cultural meanings afect to what extent an event alls under a naturally given category does not in the least conflict with the act that the basic 44 THE LOSS OF SADNESS categories themselves are given biologically. Nature supplies the template or triggers o loss responses, but culture provides the content or this template. Cultural Shaping of Loss Responses Cultural values also set the parameters or what are considered proportionate responses to loss. They set the scale o intensity and duration o appropriate responses, shape how emotionally expressive people are, and influence which aspects o the response public expressions o the emotion emphasize. Emotional experiences themselves are to some degree malleable; some cultures socialize their members to be highly emotional, whereas others encourage suppression and minimalization o emotion. All cultures have display norms or “scripts” that guide the overt expression o emotion. Many non-Western cultures encourage the expression o sadness in public ceremonies and organized rituals that shape the nature o the display. For example, among the Kaluli o New Guinea, losses result not in sel-blame or guilt but in anger that is turned outward into eelings that one is owed compensation or the loss.116 Public ceremonies allow or the expression o these eelings in weeping, songs, and the payment o compensation. Other cultures, such as the Navaho, strongly discourage displays o extreme sadness.117 Cultural norms also afect what is viewed as the appropriate duration o loss responses. Among the Navaho, outward expressions o grie are limited to 4 days.118 The bereaved person is not expected to show grie or reer to the dead person beyond this short period. Conversely, Mediterranean societies traditionally dictated long periods o mourning or bereaved widows that could last or many years.119 It is, however, important to separate cultural norms or expressing emotions rom the experienced emotions themselves. For example, among Iranians: “I someone in your amily dies, you have to really act like you are sorry, to wail and kick, otherwise you’ll be accused o having ill eelings toward that person, regardless o what your inner eelings are, especially i you stand to inherit something.”120 At the extreme, cultural norms can even transorm expressions o grie into cheerulness. The Balinese, or example, respond to bereavement with laughter.121 The Irish wake is another, well-known example. But even when cultural norms dictate expressive responses incompatible with sadness, they recognize sadness as the characteristic underlying eeling; thus the Balinese believe that sadness is the natural response to loss but that its expression should be combated because it is detrimental to health and leads others to be sad. 122 Anthropologists routinely contrast the psychological expression o depres123 sion in the West with its somatic presentation in non-Western cultures. For example, Chinese populations tend to ocus, aterloss, on bodily eelings o distress that oten go along with intense sadness, such as back pain, stomachaches, headaches, and the like.124 Despite the diferent outward maniestations, however, THE ANATOMY OF NORMAL SADNESS 45 common underlying emotions appear to be universal. Chinese patients are aware o the psychological aspects o their eelings, but social norms mandate that they 125 express their problems in somatic terms when they seek help rom physicians. Members o these cultures express intense sadness acially andbehaviorally as do Westerners, and when specifically asked, they report the same psychological and emotional experiences. Moreover, their symptoms are responsive to the same 126 medications that are prescribed or depression in Western societies. The highly varying cultural expressions o sadness are consistent with the existence o a common underlying emotional state. Indeed, the study o cultural variation in depression cannot even proceed without some underlying notion o what is universal, because it is incoherent to claim that some cultures express depression through physiological symptoms and others through psychological symptoms without having some underlying conception o depression that transcends its cultural symptomatic expression. Culture and Rates of Depression Some writers suggest that i depressive symptoms are a result o biological design, then there should not be the substantial amount o social variation that exists in rates o depressive symptoms.127 This argument mistakenly sees sadness as occurring independently o actual triggering events and their interpretations. But cultural contexts influence the requency with which people are exposed to the kinds o losses that can trigger sadness, the availability o social support, and the interpretation o those losses; consequently, cultures also difer in rates o normal sadness. 128 British sociologist George Brown’s cross-cultural studies, in which rates o depressive responses vary tenold across societies, show how this variation is in large part due to varying exposure to the kinds o loss events that naturally cause depression, such as the loss o intimate attachments due to death or separation, the occurrence o chronic stressors, and the inability to achieve goals central to the culture’s meaning system. There is a nearly perect correlation between the number o severe loss events that beall members o diferent societies and resulting rates o depressive symptoms.129 At the lowest rate, only 3% o women in a Basque-speaking rural area o Spain eel depressed; these women experience almost no serious events over the course o a year.130 At the highest rate, over 30% o women in an urban township in Zimbabwe report eeling depressed; women in this area requently sufer severe loss events.131 Also, social reactions to those who experience loss influence rates o sadness. Strong interpersonal ties and networks o social support, as well as powerul collective religious rituals and belie systems, help make people less vulnerable to loss.132 The Kaluli, or example, eature ritualized group ceremonies ater definable loss events, which might account or the apparent rarity o chronic sadness in this society.133 Some societies mandate the replacement o deceased spouses 46 THE LOSS OF SADNESS with a new partner, oten a relative—the Bible, or example, reers to the Hebrew practice o widows marrying their dead husbands’ brothers—and grie seems to be relatively short-lived in such societies. 134 Cultural Relativity of the Threshold Between Normality and Disorder Some also argue that, because culture determines the proportionality o a sadness response, it also determines the threshold between normal and disordered sadness, and thus there is no objective transcultural biological distinction between normality and dysunction.135 They claim that the same response may be normal in one culture and disordered in another, implying the cultural relativity o normality. It is true that such thresholds will vary, but the reason is not that cultures directly or arbitrarily define normality and disorder. Rather, through socialization, cultures shape how normal sadness responses will occur in their members by setting the parameters o the loss response. That is, dierent thresholds or diagnosis o disorder exist in dierent cultures because dierent cultures induce dierent intensities and durations o response to specific triggers o sadness. In judging whether or not an individual is responding normally, such varying meanings must be taken into account. For example, a modern American woman who becomes depressed because she has had no urther contact with a man she has recently met and with whom she has held hands has not suered a sufcient loss to explain these symptoms. Cultural values neither define this situation as humiliating nor lead to urther social stigmatization, and so the woman’s depressive response in the absence o any special personal meanings might be seen as pathological. In contrast, in many Islamic cultures, a young woman who has physical contact with a man whom she does not marry can ace social stigmatization and degradation; any touching, however innocuous by Western standards, can lead to serious social consequences.136 In this case, the woman’s sadness response might be seen as normal. Thereore, it is not simply that what might represent a dysunction in the case o the Western woman can indicate the normal working o loss response mechanisms in the Muslim woman. Rather, this dierence in cultural judgments about normality is based on the proportionality o response to severity o loss; the dierence in diagnosis arises precisely because local meanings imply that a given response is likely a result o normal, designed mechanisms in one case and o dysunction in another. Cultural norms are part o the basis or inerring whether the best explanation or a response is in terms o design or dysunction. Culture and biology are not two opposing explanations but complementary parts o one explanation; each requires the other or comprehensive and coherent explanations o depressive responses. THE ANATOMY OF NORMAL SADNESS 47 Adaptive Functions of Nondisordered Loss Responses The preceding evidence suggests that sadness ater loss is a designed eature o human nature and answers the most common objections to that thesis. But the deepest and most puzzling question about sadness has not been touched: Why does sadness exist? What sort o survival value did this painul and debilitating emotion provide that caused it to be naturally selected? This topic remains controversial, and there is no easy or generally accepted answer at present to the question o the biological unction o sadness. In some cases, a mechanism’s biological unction is immediately obvious; or example, it cannot be accidental that the eyes see, the hands grasp, the eet walk, or the teeth chew, and it is clear that these beneficial efects explain the existence via natural selection o the respective mechanisms. However, in other cases, although it is obvious that a eature is biologically designed, we have little conclusive knowledge o its unction. For example, beore physician William Harvey’s amous experiments in the 1620s demonstrated circulation o the blood, no one ully understood the unction o the heart, even though everyone assumed it was designed or something. Even today, we have little understanding o the unction o sleep, although sleep clearly is a designed part o human unctioning. Sadness is somewhat like sleep in this respect; the unction is not obvious, yet the designed nature is. However, some plausible hypotheses about the unctions o sadness do exist, and they suggest how, despite its painul nature, sadness can have a designed biological role. The puzzle is that depressive experiences seem on their ace to be harmul to reproductive fitness. Intensely sad people experience decreased initiative, findless pleasure in lie to motivate them, and tend to withdraw rom everyday activities. Positive mood, in contrast, encourages activities required to obtain sexual partners, ood, shelter, and other resources that increase survival and reproduction. Thus, under ordinary circumstances, consistent levels o negative mood should be selectively disadvantageous. For intense sadness responses to have been naturally selected, there must have been some special circumstances in which the benefits o temporarily experiencing such symptoms outweighed theobvious costs. In those particular contexts, and only in those contexts, states o low mood must have increased fitness preciselybecause they made people less active, less motivated, and so on.137 The best analogy is to acute pain rom an injury, which stops activity but is adaptive because it helps people avoid urther damage to tissue. In contrast, chronic pain unrelated to any underlying physiological damage 138 would be harmul in the way that depressive disorder is certainly harmul. In considering the unction o sadness, it is important to keep in mind that the unction o a biological mechanism need not be beneficial in the current environment, although it oten is. It must have been beneficial in the past, however, and must thus explain why the underlying mechanism was selected and 48 THE LOSS OF SADNESS now exists. What evolutionary psychologists John Tooby and Leda Cosmides call the environment o evolutionary adaptation (EEA), probably occurring at the time when humans lived in hunter-gatherer societies on the Arican plains beore or during the Pleistocene era between 2 million to 10,000 years ago, was responsible or shaping many o the genetic traits that humans up to the present still hold.139 Sadness is designed to cope with contexts that arose in these ancestral conditions but that may be less apparent in current environments. Analogously, human cravings or sweets, salt, and ats may seem puzzling now, when there are plentiul sources o calories and those cravings can lead to obesity and disease, but they were biologically designed when human environments were marked by scarcity o calories. Consequently, it is now part o normal human nature to enjoy these tastes, whatever else wise nutrition may dictate. Keeping these cautionary points in mind, we can ask: When compared with alternative responses to loss, what benefits might depressive symptoms have conerred that led to their natural selection over the course o human evolution? Attraction of Social Support One explanation o the adaptive unction o depressive eelings ocuses on how emotional behavior communicates inner states to other people so that depressed people attract social support ater attachment losses. The Australian psychiatrist Aubrey Lewis was the first to propose that depressive reactions could unction as a “cry or help” that calls attention to needy states and elicits social support. 140 The withdrawal, inhibition, and vegetative aspects o depression mimic illness and signal others to draw the suering individual back into the group.141 States o social isolation would have been especially threatening in the tightly knit, interdependent human social groups that existed during the EEA, making a positive social response likely. Similarly, some recent evidence indicates that postpartum depression, or example, arises under circumstances, such as poor inant health and a lack o social support, in which it might unction as a signal that mothers will reduce their child care eorts until they receive more support rom others.142 Some reject the idea that depression was designed to attract social support because o empirical evidence that people typically avoid and reject, rather than support, depressed people.143 Perhaps, instead, only nondisordered sadness that arises in appropriate situations attracts social support. Indeed, intense mobilization o ritual expressions o sympathy universally emerges ater bereavements and other serious losses.144 In contrast, dysunctional depressions involving se- vere and sustained states o despondency without sufcient situational cause tend to alienate or anger other people and diminish social support, leading to isolation and rejection o the aicted people and to fitness disadvantages. In addition to the attraction-o-support hypothesis, which makes particular sense in understanding sadness ater loss o intimate attachments, other THE ANATOMY OF NORMAL SADNESS 49 theories about the unctions o sadness have been advanced. One is that depressive symptoms o despair may have served to protect inants in the immediate atermath o parental loss. The despair o inants that succeed s the protest at their mother’s departure activates an inhibitory, quiet state that, during precivilization, might have prevented the abandoned ofspring rom drawing the attention o predators to itsel. 145 But another theory emphasizes the initial period o loud protest, lead ing to a very diferent conclusion; Darwin, or example, explained inant reactions to separation—that is, their screaming—in terms o their attention-getting aspects. 146 Presumably both strategies have their purpose at diferent times ater separation. John Bowlby proposed another influential account o the adaptive nature o depression ater attachment losses.147 For Bowlby, the prospect o the pain o depressive eelings ollowing attachment loss motivates people to vigorously seek reunion with the lost loved one and not to give up the lost tie. Grie at thoughts o loss allowed social bonds to persist during the requent, temporary absences o one party in the EEA and thus promoted the maintenance o social relationships. From this viewpoint, grie ater the death o a loved one was a by-product o adaptive responses to attachment losses that were not permanent, an explanation that has been widely adopted.148 Protection From Aggression After Status Losses Ethological studies indicate that the capacity to become depressed, as indicated by lowered testosterone, elevated cortisol, and retardation in behavior, is deeply rooted in the reptilian brain and is present in most vertebrates and all mammals.149 Such depressive responses might have arisen widely as signals o acceptance o deeat in status contests that are ubiquitous in the animal world. The British psychiatrist John Price and his colleagues have developed the most elaborate explanation o this sort o adaptive unction. They theorize that negative behavior, mood, and thought arose as adaptive responses to circumstances o deeat and subordination.150 Indeed, Price views depression as part o an involuntary subordinate strategy (ISS), which reers to a state o inhibited action marked by withdrawal, lack o sel-assertion, nervousness, and anxiety (in other works, Price calls the ISS ritual agonistic behavior).151 Price connects ISS responses to primeval brain algorithms that assess relative strengths, weaknesses, power, and rank o organisms and adjust actions accordingly to produce responses o flight, fight, or submission in conrontations with other animals. Depressive eeling is one way that behavior is regulated as a consequence o such assessments. Animals develop ISS responses when they judge themselves to be weaker than their competitors. They cease competing with the dominant animal, accept their deeated status, and signal their submission to the winning party. The inhibited aspects o depressive reactions are adaptive responses to subordinate positions rom which there is no possibility o escape.152 50 THE LOSS OF SADNESS The deeated party who has ailed to deend territory or lost a status contest could respond with renewed anger and aggression rather than concede to the winner. However, the open expressiono aggressive emotions and behaviors can lead to the serious injury or death o the deeated party. Many o the symptoms o the ISS involve behaviors that communicate that the loser will not conront the winner, will not attempt to gain dominance, and will give up the struggle. Submissive responses protect the loser rom urther aggression by showing the dominant animal it is sae rom additional challenges and thus need not eel threatened by the continued presence o the loser. Subordinates that make submissive responses are more likely to survive and reproduce than those who respondmore aggressively. The ISS theory explains several aspects o depressive responses. First, it explains the situation-specific qualities o depressive responses; they are adaptive only when acing potential deeat by stronger adversaries. Thus the inhibition o sel-assertion that is at the core o ISS would be naturally selected to occur in those contexts. It is also compatible with the widespread finding that depression is more common among people and other animals at the bottom o status hierarchies and explains the persistence o depressive eelings among those who are in enduring states o subordination. Almost universally, women are more likely than men to be in such subordinate positions, which could partially explain their higher rates o depression.153 Finally, the theory is consistent with the studies reported earlier that show sadness in response to reductions in status. Promotion of Disengagement From Nonproductive Activities Another common situation that produces sadness arises when people cannot obtain a crucial resource that is important to them.154 Depressive experiences also might be adaptive when they disengage people rom their investments in unproductive eorts, in unreachable goals, or in goals with low probability o success. They thus help to make possible the eventual reengagement with new, more productive activities.155 The suspension o current activity, accompanied by the intense ruminative activity that is characteristic o depression, may acilitate the difcult shit o energy to new projects or attachments. 156 Sadness responses are especially likely to emerge ater lie crises, when people are orced to reevaluate their utures, and in this context they may be adaptive in helping individuals to avoid rash decisions, to take all possible dangers into account, and not to overestimate the chances o success in new activities. “In this situation,” according to psychiatrist Randolph Nesse, “pessimism, lack o energy, and earulness can prevent calamity even when they perpetuate misery.”157 The transient nature o most normal sadness allows the individual to emerge properly motivated by newly selected goals. In contrast, depressive disorders involve such severe loss o motivation that eorts cannot be channeled toward new pursuits. THE ANATOMY OF NORMAL SADNESS 51 Depressive responses that arise ater losses o attachment, deeats in status contests, or the collapse o meaning systems or goal strivings thus could have a variety o unctions that would explain why such responses were naturally selected. The communication o low afect ater losses o attachment can attract support and sympathy rom others, and its anticipation can sustain relationships. The submission o depressed people in subordinate positions can prevent punishment rom dominants and promote survival. Lowered motivation and physiological slowness can disengage people rom unproductive orms o activity and allow them to reengage in more productive endeavors. Some recent evidence indicates that diferent situations produce particular types o symptoms: social losses are ollowed by crying and emotional pain, whereas ailure to achieve goals is associated with pessimism, atigue, and anhedonia. 158 Thereore, the explanations considered here are not mutually exclusive; diferent types o situations can tend to produce distinct reactions that meet specific adaptive challenges. Although none o these explanations is proven, the existence o plausible reasons or the adaptive unctions o sadness supports the thesis that contextually proportionate sadness responses are a designed aspect o human nature. Conclusion In contrast to the otherwise universal recognition that it is natural or people to become sad ater a great variety o losses, the DSM diagnoses all loss responses that meet its symptomatic criteria as disorders, with bereavement as the only acknowledged instance o normal intense sadness. However, a wealth o evidence supports the commonsense judgment that many people who develop symptoms o depression ater a loss, even when they meet DSM criteria or a disorder, are not disordered but are experiencing a biologically designed response. Sadness ater loss is ound in all societies, among inants, and in our closest primate cousins; it is clearly biologically rooted and not merely a creation o social scripts. The diferences between the possible advantages o depressive responses in the EEA versus those experiences today deserve special emphasis. Loss response mechanisms would have been ormed within environments that eatured interaction within small, tightly knit groups, strong rituals o social support ater loss, clear social hierarchies, and well-defined goals. In contrast, humans now conront novel environments that pose challenges that inherited loss responses were not designed to meet.159 Modern societies eature many shiting and changeable interactions that are oten being lost, multiple status hierarchies that constantly test one’s worth, mobility away rom close kin who are less able to provide social support ater losses, and ew common rituals o solidarity to deal with loss. In addition, ideologies that emphasize personal responsibility rather than ate, a deity, or collective liability enhance the chances that people will blame themselves or 52 THE LOSS OF SADNESS their failures. Exposure to the mass media allows status comparisons not just within well-defined local groups but also with innumerable others, many of whom will always seem to be of higher status than oneself.160 This exposure also can motivate the pursuit of goals that are unreachable because few people have the means to achieve the ideals of beauty, wealth, fame, and success that are promoted to much of the public on a daily basis.161 In such cases, loss response mechanisms might be functioning appropriately within environments that natural selection did not anticipate. Although therapy may help people cope with such feelings, there is nothing medically wrong with individuals who become transiently sad in these situations. In contrast to normal sadness, depression that is truly disordered was not naturally selected but instead indicates that something has gone wrong with mechanisms that were designed to respond to loss. Such dysfunction-caused conditions tend to be recurrent, chronic, and not proportionately related to real losses rather than context specific and time limited. Such conditions were never adaptive in the past and certainly are not useful in the present. The distinction between normal sadness and depressive disorder has been part of Western literature and science since the earliest recorded documents. Only in recent times has the distinction been greatly eroded and in danger of being substantially lost. The following chapters trace this transformation and explore the steps by which large domains of intense normal sadness came to be incorporated within depressive disorder in contemporary psychiatric diagnosis. 3 Sadness With and Without Cause Depression From Ancient Times Through the Nineteenth Century D epression has been an omnipresent phenomenon over several millennia o human history. For virtually all o that time, rom the earliest writings o the ancient Greek physicians to the late twentieth century, Western diagnosticians routinely distinguished depressive disorders, as a orm o madness, rom symptomatically similar but nondisordered, normal sadness responses to a wide range o painul circumstances. Then, in 1980, seeking a more scientific oundation or diagnosis by ocusing on decontextualized criteria based on symptoms, the DSM-III inadvertently abandoned this critical traditional distinction, which is now essentially lost in current thinking about depression. This chapter and the next trace the history leading up to this momentous and, we argue, ultimately detrimental conceptual shit. Why is reviewing this history important? Current diagnostic practices may seem obviously right and sensible just because they are accepted, and they are all that many o us have ever known. To understand the problems with the current diagnostic approach to depressive disorder and to recognize the choices it represents, it helps to place it in historical context. This history reveals that the way we think about depressive disorder now is quite new—and radically diverges rom what has traditionally been considered appropriate. But the importance o history is more than simply providing context and contrast. It is easy to assume that current practices, i they are diferent, must have emerged rom a process in which the traditional alternatives were ound to be flawed and were superseded by a superior approach. The history o thinking about depression specifically in regard to the role ocontext in diagnosing disorder dispels such belies and reveals instead the contingency and even arbitrariness o some aspects o current diagnostic practices. It shows that the reasons or the recent divergence rom the traditional approach, although well intentioned and shaped by admirable scientific aspirations, are anchored neither in evidence nor 53 54 THE LOSS OF SADNESS in logic, which in act support the older tradition. Despite the many virtues o the new approach, it is in certain important respects weaker than those it replaced. Depressive disorder,unlike many otherdisorders, hasan identifiableand lengthy history. Indeed, depression is probably the psychological disorder that is most easily recognizable throughout history; similar symptomatic descriptions occur over a 2,500-year span, representing what historian Stanley Jackson calls a “remark1 able consistency.” From the earliest medical texts in ancient Greece to the present DSM, deep sadness and its variants—hopelessness, sorrow, dejection, despondency, emptiness, despair, discouragement—were oten menti oned as core eatures o depressive disorder, along with related symptoms such as aversion to ood, eepsl lessness, irritability, restlessness, eelings ohopelessness or worthlessness, suicidal ideation and attempts, ear odeath, repetitive ocus on a ew neg ative ideas, lack o pleasure or lacko interest in usual activities, atigue, and social detachment. Yet traditional diagnostic treatises also agreed in distinguishing depression as a disorder rom a nondisordered type o deep sadness or ear that could have many o the same symptoms but that was a normal, proportionate reaction to serious losses. Such losses included the death o intimates, reversals in ortune, disappointments in attaining valued lie goals, romantic disappointments, and the like. In addition, it was traditionally acknowledged that variations in temperament predispose some people to more readily or intensely experience sadness or ear but that these variations could be within a normal range o reasonably proportionate responses that did not represent a disorder. Depressive disorders difered rom these normal reactions, according to tradition, because they either arose in the absence o situations that would normally produce sadness or were o disproportionate magnitude or duration relative to their provoking causes. Such conditions indicated that something was wrong in the individual, not in the environment. In essence, then, traditional psychiatry took a contextual approach to the diagnosis o depressive disorder; whether a condition was diagnosed as disordered depended not just on the symptoms, which might be similar in normal sadness, and not just on the condition’s severity, or normal sadness can be severe and disordered sadness moderate, but on the degree to which the symptoms were an understandable response to circumstances. In this and the ollowing chapters, we elaborate the history o this contextual approach to depression and how the DSM-III, overturning thousands o years o thinking, replaced it with relatively precise and communicable symptomatic criteria that largely ignored the complexities o context, with detrimental side efects or psychiatric diagnosis. Preliminary Caveats From ancient Greek medical writings until the early twentieth century, what is now termed depressive disorder was generally reerred to as melancholia, which SADNESS WITH AND WITHOUT CAUSE 55 literally means “black bile disorder.” Although the name stuck into modern times, it srcinally reflected the ancient belie that health and disease depend on the balance or imbalance between our bodily fluids, or “humors,” and that an excess o black bile—a humor oten thought to be produced in the spleen—was responsible or depressive symptoms. Ancient physicians thought that black bile had a natural unction in regulating mood and that melancholia represented a ailure o this natural unctioning. As belie in black bile’s role in mental lie waned, depression eventually arose as the dominant term in the nineteenth and twentieth centuries. In recognizing the strikingly similar clinical descriptions o depressive disorder across the millennia, several cautions are necessary. First, one must consider the context o each discussion to tell whether a disorder is being described at all. Like today’s conusingly overused term depression, the terms melancholy and melancholia also tended to do double duty in reerring both to a disorder and to normal emotions, moods, and temperaments. Second, classic texts were written beore most o today’s refined distinctions among mental disorders were recognized, and thus the category o melancholia oten encompassed what in hindsight can be seen to be quite diferent disorders. These included psychotic disorders that ranged rom schizophrenia to paranoid and other delusional states. For example, what may initially appear to be a description o the cycling o mania and depression in what we would now recognize as bipolar disorder may, on closer inspection, turn out to be more likely a description o the alternating agitation and withdrawal o a schizophrenic patient who was mistakenly classified as melancholic.2 Because psychotically depressed individuals sometimes have mood-congruent delusions that provide the content or their sadness, early psychiatrists sometimes extended the category o melancholia to others with circumscribed delusions that caused negative emotions. Also, the withdrawal associated with such current diagnoses as avoidant personality disorder and social phobia appears to sometimes have been mistaken or the withdrawal associated with melancholia. However, the predominant picture o those classified as melancholics clearly indicates depressive disorder as we know it. Third, because melancholia was an etiological description that classified conditions based on their believed cause in excess black bile, older descriptions oten placed other conditions that were considered to have a similar etiology in blackbile imbalance together with depressive disorders as “melancholic disorders” in a broad sense, even i they had nothing to do with depression. In ancient times, these “melancholic disorders” included, or example, epilepsy and boils. Melancholia itsel as a disorder was just one distinct instance o this broader category. Fourth, classic descriptions generally, though not always, ocused on what we would now callpsychotic depression, which includes delusions or hallucinations. Indeed, these descriptions oten defined melancholy as a orm o “delirium 56 THE LOSS OF SADNESS without a ever” to distinguish melancholic delusions and hallucinations rom those that occurred during a high ever caused by various physical diseases. Melancholia o this kind distinctively involved fixed ideas on specific topics linked to depressive aect, which distinguished melancholia rom general cognitive malunction or psychosis. Nonpsychotic depressive disorders were recognized as well but were not emphasized as constituting the bulk o cases until recent times. Fith, there is an ambiguity about the reerent o melancholia that continues to exist in our own time and that can sometimes cause conusion. The exact extent o the meaning o melancholia has varied, sometimes reerring to an overall disease, sometimes to sadness as a specific symptom, and sometimes to a syndromal set o coexisting symptoms, o which sadness is just one.3 Sixth, contrary to current practice, ancient and many subsequent texts routinely grouped sadness and ear together as symptoms o melancholia. Despondency was thought to be related to ear because melancholics were generally worried or morose not only about actual events but also about negative possibilities in the uture that caused apprehension. Contemporary criteria emphasize sadness as an exclusive dominant aect, yet recent studies confirm that anxiety and sadness tend to go together in depression and that it is difcult to distinguish these states, just as tradition would have it.4 But it is also clear rom clinical descriptions that, then as now, sadness alone could be sufcient or melancholia. A final caveat about our methodology: It is important to look past many dierences and conusions in the history o depression to find an underlying coherence and similarity to current judgments. In particular, what are now considered genuine depressive disorders were clearly included within traditional melancholia and were distinguished rom normal sadness. No doubt an alternative, postmodernist history o depression might emphasize the social construction o depression, including variations in definitions and in ranges o behavior that were pathologized and the social control correlates o these variations. Although the history o depression certainly contains such elements, the historical record also recognized a common core condition that has been o concern or several millennia. Indeed, rom the earliest times, this record displays what might be considered an “essentialist” view o the classification o melancholia—that is, it involves an inerence, common to dierent writers who may have disagreed in their specific theories, that in melancholia something is going wrong with the internal unctioning o mechanisms usually responsible or normal sadness in a way that leads to certain standard symptoms. This view is not an artiact o changing social responses to madness but a considered and plausible judgment. Moreover, it is impossible to analyze responsibly the ways groups have exploited the concept o depression or purposes o social power until one understands the logic o the concept o depression itsel. It is the history o this common concept, and especially attempts to distinguish disordered sadness rom normal sadness, that we attempt to understand. SADNESS WITH AND WITHOUT CAUSE 57 The Ancients Writing in the fith century B.C., Hippocrates (460–377 B.C.) provided the first known definition o melancholia as a distinct disorder: “I ear or sadness last or a long time it is melancholia.”5 Although theories o depressive disorder have changed, the symptoms that indicate the disorder have not. In addition to ear and sadness, Hippocrates mentioned as possible symptoms “aversion to ood, despondency, sleeplessness, irritability, restlessness,” much like today’s criteria.6 ut Hippocrates’ definition indicated that it is not such symptoms alone but symptoms o unexpected duration that indicate disorder. Hippocrates’ insistence that the sadness or ear must be prolonged is a first attempt to capture the notion that disproportion to circumstances is an essential aspect o depressive disorder. Indeed, an ancient, possibly apocryphal, story about Hippocrates illustrates the distinction between disordered sadness without cause and normal sadness with cause.7 He was asked to diagnose the problem o Perdiccas II, King o Macedonia rom 454 to 413 B.C., who had allen into a morbid condition and displayed a total lack o concern or matters o state. Hippocrates learned that the king’s condition stemmed rom his secret love or a concubine o his recently deceased ather’s. He suggested that the king acknowledge his love or the concubine and secure her love in return. In essence, Hippocrates recognized that the king sufered not rom a melancholic disease that warranted medical treatment but rom a problem stemming rom romantic longing. A century ater Hippocrates, Aristotle (384–322 B.C.; or one o his students) in the Problemata elaborated the distinction between a variety o normal mood states o sadness on the one hand and pathological disease states on the other. Aristotle clearly expressed the idea that disordered sadness is disproportionate to events. He noted that, i the black bile “be cold beyond due measure, it produces groundless despondency.”8 Here “beyond due measure” reers to what is disproportionate to the circumstances, making the resultant sadness “groundless.” Such despondency, or example, “accounts or the prevalence o suicide by hanging amongst the young and sometimes amongst older men too.”9 Aristotle, the master typologist, suggested several distinctions among types o melancholy. One distinction was between melancholic temperament and melancholic disorder. In this regard, Aristotle inaugurated the tradition that has lasted to our own day o associating depressive temperament with exceptional artistic and intellectual ability: “Why is it that all men who have become outstanding in philosophy, statesmanship, poetry or the arts are melancholic, and some to such an extent that they are inected by the diseases arising 10 rom black bile. . . . They are all, as has been said, naturally o this character.” Aristotle recognized not only melancholic temperament as a normal variant but also an abnormal degree o melancholy that gited individuals may possess—and may be possessed by. He did not consider this abnormal degree to be disordered 58 THE LOSS OF SADNESS because it contributed to their creativity, although it did leave them vulnerable to melancholic disorder. “We are often,” Aristotle noted, “in the condition of feeling grief without being able to ascribe any cause to it; such feelings occur to a slight degree in everyone, but those who are thoroughly possessed by them acquire them as a permanent part of their nature.”11 In Aristotle’s view, such extreme melancholic temperaments were generally disorders except in the rare instances in which they were an integral part of a gifted individual’s creativity. As in Aristotle’s passage, the key distinction in ancient definitions of melancholia was between states of sadness without cause and those with similar symptoms that arose from actual losses; only the former were mental disorders. But “without cause” did not mean uncaused, for throughout history depression has been attributed to postulated physical or psychological causes such as excessive black bile, disturbances in the circulation of blood, or depletion of energy. Rather, “without cause” meant that the symptoms of depression were not proportional to environmental events that wouldappropriately lead to sadness, such 12 as bereavement, rejection in love, economic failure, and the like. Conversely, ancient Greek and Roman physicians didnot consider symptoms of depression that occurred “with cause” as signs of a mental disorder because they were normal reactions within their contexts. Aristotle also grappled with the basic problem of how to define “proportionate” sadness. Thepuzzle he confronted is this: Ifthe level of sadness or fear varies due to circumstances and has no constant “se t point” at which health is defined, how can we define health? Aristotle’s answer was that there can be relational definitions of health in which the appropriate amount of sadness varies at any given time in proportion to the circumstances that surround it. That is, Aristotle had the insight to recognize that the relational property ofthe proportionality between sadness and circumstances can remain present even as the actual amoun t of sadness and the circumstances vary: “It ispossible that even a varying statemay be well attempered, and in a sense be a good condition, . . . since the condition may be warmer when necessary and then cold again, or conversely.” With such proportionate variation as the baseline, Aristotle w ent on to conceptualize his notion of the abnormally melancholic—but not strictly disordered—temperament or personality as the tendency of such variation to be extreme on the hig h end and thus to some degree to overshoot the markemotionally: “owing to the presence ofexcess, all melancholic 13 persons are abnormal, not owing to disease but by nature.” A similar test would reveal disordered statesnot due to temperament, as well. In sum, Aristotle distinguished (1) a melancholic component in all people that gives rise to normal sadness reactions and varying normal moods;(2) a nor- mal-range melancholic temperament inpeople with a preponderance of black bile and thus an inherent inclination to sadness; (3) anextreme variant of such temperament that often occurs in the gifted and may be considered at least statistically abnormal but is not yet a disease, especially when it is a handmaiden to creativity; and (4) a pathological, harmful, disordered state of disproportionate SADNESS WITH AND WITHOUT CAUSE 59 sadness or sadness without adequate cause that is without a redemptive part in a creative process. Several o these distinctions can be discerned, or example, in the ollowing passage, which also interestingly anticipates the modern notion that in bipolar disorder melancholic despondency and manic over-confidence can be etiologically linked: Those who have a small share o this temperament are normal, but those who have much are unlike the majority. I the characteristic is very intense, such men are very melancholic, and i the mixture is o a certain kind, they are abnormal. But i they neglect it, they incline towards melancholic diseases, diferent people in diferent parts o the body; with some the symptoms are epileptic, with others apoplectic, others again are given 14 to deep despondency or to ear, others are over-confident. ncient Roman physicians ollowed their Greek predecessors in distinguishing melancholic states that arose with and without cause, associating only the latter with disease. Thus, or example, the Roman physician Celsus (ca. A.D. 30) ech oed Hippocrates in defining melancholia as “prolonged despondency and prolonged ear and sleeplessness”15 that “consists in depression which seems caused by black bile.”16 He advised that, as part o the treatment, the patient’s “depression should be gently reproved as being withoutcause.”17 Soranus o Ephesus, writing in the late first or early second century A.D., described the melancholic as “downcast and prone to anger and . . . practically never cheerul and relaxed,” with “the signs o melancholy . . . as ollows: mental anguish and distress, dejection, silence, animosity toward members o the household, sometimes a desire to live and at other times a longing or death, suspicion on the part o the patient that a plot is being hatched against him, weeping without reason, meaningless muttering, and, again, occasional joviality,” as well as various, mostly gastrointestinal, symptoms.18 The reerence to “weeping without reason” makes explicit the notion that the emotions o intense sadness are to some extent without cause. retaeus o Cappadocia (ca. A.D. 150–200) made the “without cause” criterion more explicit, noting that melancholic “patients are dull or stern, dejected or unreasonably torpid, without any maniest cause; such is the commencement o melancholy. nd they also become peevish, dispirited, sleepless, and start up rom a disturbed sleep. Unreasonable ear also seizes them.” 19 To urther distinguish the disordered rom the normal who experience, as retaeus put it, “mere anger and grie, and sad dejection o mind,”20 he presented a case (clearly modeled ater the story told o Hippocrates) o extreme but normal sad- ness that eatured symptoms identical to those occurring in melancholia and that, consequently, was mistaken or a disorder:  story is told, that a certain person, incurably afected, ell in love with a girl; and when the physician could bring him no relie, love cured him. But 60 THE LOSS OF SADNESS I think that he was srcinally in love, and that he was dejected and spiritless rom being unsuccessul with the girl, and appeared to the common people to be melancholic. He then did not know that it was love; but when he imparted the love to the girl, he ceased rom his dejection, and dispelled his passion and sorrow; and with joyhe awoke rom his lowness o spirits, and 21 he became restored to understanding, love being his physician. retaeus thus illustrated how the “without cause” criterion diferentiates normal sadness rom melancholic disorder, and he pointed to the possibility that normal conditions can be misdiagnosed i symptoms alone are considered. Like other writers beore him, retaeus emphasized the delusions o what we would term psychotic depression: “a lowness o spirits rom a single phantasy, without ever . . . the understanding is turned . . . in the melancholics to sorrow and despondency only. . . . Those afected with melancholy are not every one o them afected accordin g to one particular orm; but they are either suspicious o poisoning, or flee to the desert rom misanthropy, or tur n superstitious, or contract a ha tred o lie.” 22 Clearly, such delusions, which the literature through to the twentieth century emphasized, provide an alternative to disproportionality as a way o recognizing disorder due to clear cognitiv e dysunction. In the late second century A.D. , Claudius Galenus (131–201), known as Galen, like retaeus a Greek physician living in Rome, unified and synthesized the psychiatric knowledge that had accumulated over the previous 600 years. Galen simply repeated the Hippocratic definition o melancholia: “Fear or a depressive mood (dysthamia) which lasts or a long time.” 23 His description again emphasiz ed psychotic phenomena but also described well the basic symptoms: Fear generally bealls the melancholic patients, but the same type o abnormal sensory images do not always present themselves. s or instance, one patient believes he has been turned into a kind o snail and thereore runs away rom everyone he meets lest [its shell] should get crushed. . . . gain, another patient is araid that tlas who supports the world will become tired and will throw it away and we all will be crushed and pushed together. nd there are a thousand other imaginary ideas. . . . lthough each melancholic patient acts quite diferently than the others, all o them exhibit ear or despondency. They find ault with lie and hate people; but not all want to die. For some the ear o death is o principal concern dur- ing melancholy. Others again will appear to you24quite bizarre because they dread death and desire to die at the same time. In an implicit acknowledgment o the “without cause” criterion, Galen presented a vivid analogy in which he used the color o black bile to characterize the SADNESS WITH AND WITHOUT CAUSE 61 fear that the melancholic was generating from his or her own brain, a fear that would normally be generated from external circumstances: Because of this despondency patients hate everyone whom they see, are constantly sullen and appear terrified, like children or adults in deepest darkness. As external darkness renders almost all persons fearful, with the exception of a few naturally audacious ones or those who were specially trained, thus the color of the black humor induces fear when its darkness throws a shadow over the area of thought [in the brain].25 The doctrine that emerged in the period between Hippocrates and Galen, distinguishing melancholic states that stemmed from internal dysfunctions in which emotion is “without cause” from those that were proportional reactions to external circumstances, persisted for thousands of years.26 Explicit sources regarding melancholia are, however, sparse in the following period. Alexander of Tralles (525–605) included “sadness without reason” among the symptoms of melancholia and recommended that, especially in nonchronic cases, the ideas underlying “groundless sadness” should be addressed. 27 The early tenthcentury Arabic physician Ishaq ibn Imran reiterated the “without cause” notion when he defined melancholia partly as “irrational, constant sadness and dejection”; yet he also recognized that real losses could trigger true disorder: “The loss of a beloved child or an irreplaceable library can release such sadness and dejection that melancholy is the result.”28 Similarly, Constantinus Africanus (1020?– 1087) defined melancholia partly as “fear of things that were not frightening” and noted that the loss of a loved one or of specially beloved possessions, such as a scholar’s loss of his books, could trigger melancholia.29 Avicenna (980–1037) emphasized “fear without cause,” including “the appearance of fear of things which do or do not exist; and a greatness of fear of things which are not customarily feared.”30 Often, the “without cause” requirement was implicit in the explanation that an internal process caused the sadness, as in Hildegard of Bingen’s (ca. 1151–1158) description: “Melancholy as a Disease. Bile is black, bitter, and releases every evil, sometimes even a brain sickness. It causes the veins in the heart to overflow; it causes depression and doubt in every consolation so that the person can find no joy in heavenly life and no consolation in his earthly existence.”31 Not until the Renaissance, however, did melancholia return to the central place it had had in ancient Greek and Roman psychiatric medicine. Depression From the Renaissance to the Nineteenth Century In the late sixteenth and early seventeenth centuries, authors placed even greater emphasis on the “without cause” criterion for disorder. The French 62 THE LOSS OF SADNESS physician Andre Du Laurens (1560–1609), known widely as “Laurentius,” wrote Discourse de la melancholie, which became known throughout Europe and which heavily influenced later thought. Du Laurens summarized the approach o his time as the “without cause” approach: “A kinde o dotage without any ever, having or his ordinarie companions, eare and sadnes, without any apparent occasion.”32 On the English side o the Channel, Timothie Bright (1550–1615), a Cambridge-trained doctor o medicine contemporary with Du Laurens, was also much concerned with religious guilt. In hisTreatise of Melancholy (1568), Bright developed at length the distinction between sorrow with and without cause to allow dierential diagnosis between true melancholic disorder and nondisordered states o intense sadness and despair due to the belie that one had sinned and would be the object o God’s wrath. He noted that melancholic sadness is such “whereo no occasion was at any time beore, nor like to be giv en hereater”33 and argued that “the aiction o soule through conscience o sinne” is “quite another thing than melancholy.”34 Consciousness o sin was “a sorrow and eare upon cause, & that the greatest cause that worketh misery unto man” because o ear o God’s wrath, whereas melancholy was “a meere ancy & hath no ground o true and just object.” Bright explained in lucid detail how the “Particular dierence betwixt melancholy, & the distressed conscience in the same person” which is “the soules proper anguish” could be distinguished based on a contextual understanding o whether the sadnesshad adequate environmental reasons: Whatsoever molestation riseth directly as a proper object o the mind, that in that respect is not melancholicke, but hath a arther ground than ancie, and riseth rom conscience, condemning the guylty soule o those ingraven lawes o nature, which no man is voyde o, be he never so barbarous. . . . On the contrarie part, when any conceite troubleth you that hath no suf cient ground o reason, but riseth onely upon the rame o your brayne, which is subject (as hath bene beore shewed) unto the humour, that is right melancholicke and so to be accounted o you. These are alse points o reason deceaved by the melancholie brayne. . . . Thus I conclude this point o dierence, & marke betwixt melancholy and the soules proper anguish. . . . [T]he sense o those that are under this crosse eele an anguish ar beyond all aiction o naturall passion, coupled with that organicall eare and heavinesse o heart. The melancholie disposeth to eare, doubt, distrust and heavines, but all either without cause, or where there is cause above it inorceth the passion. Bright goes on to vividly characterize what the phrase “without cause” means, firmly anchoring the notion in an understanding o the context o the eelings: We do see by experience certaine persons which enjoy all the comortes o this lie whatsoever wealth can procure, and whatsoever riendship SADNESS WITH AND WITHOUT CAUSE 63 oereth o kindnes, and whatsoever security may assure them: yetto be overwhelmed with heavines, and dismaide with such eare, as they can neither receive consolation, nor hope o assurance, notwithstanding ther be neither matter o eare, or discontentment, nor yet cause o daunger, but contrarily o great comort, and gratulation. This passion being not moved 35 by any adversity present or imminent, is attributed to melancholie. Bright’s assumption, which ormed the background or the literature rom ancient to modern times, was that there exists a “natural passion” or emotion o sadness that was designed to operate a certain way but that had gone wrong in disorder. Subsequent works ollowed suit. For example, Felix Platter (1536–1614) in Praxeos Medicae (1602) defined melancholy as a state in which “imagination and judgment are so perverted that without any cause the victims become very sad and earul. For they cannot adduce any certain cause o grie or ear except a trivial one or a alse opinion which they have conceived as a result o disturbed apprehension.”36 Like other authors, Platter encompassed within the “without cause” category both cases lacking any actual situational cause (in cases o delusion or endogenous depression) and cases without proportionate cause (in which the cause exists but is too trivial to justiy the reaction). Robert Burton’s classic work, The Anatomy of Melancholy, published in 1621, is the most renowned o all Renaissance discussions on the topic. It is ounded squarely on the “without cause” tradition. Burton described three major components o depression—mood, cognition, and physical symptoms—that are still viewed as the distinguishing eatures o the condition. However, he insisted that melancholic symptoms are not in themselves sufcient evidence o disorder; only symptoms that are without cause provided such evidence, as he explained in this codicil to his definition: “without a cause is lastly inserted, to speciy it rom all other ordinary passions o Fear and Sorrow.” And, he noted, “signs in the mind” o melancholia included “Sorrow . . . without any evident cause; grieving still, but why they cannot tell.”37 Burton emphasized that a propensity to melancholy was present in all men, and was a normal and ubiquitous aspect o the human condition: Melancholy . . . is either in disposition or habit. In disposition, it is that transitory melancholy which goes and comes upon every small occasion o sorrow, need, sickness, trouble, ear, grie, passion, or perturbation o the mind, any manner o care, discontent, or thought, which causeth an- guish, dullness, heaviness, and vexation o spirit. . . . And rom these melancholy dispositions, no man living is ree, no Stoic, none so wise, none so happy, none so patient, so generous, so godly, so divine, that can vindicate himsel; so well composed, but more or less, some time or other, he eels the smart o it. Melancholy, in this sense is the character o mortality.38 64 THE LOSS OF SADNESS In contrast to normal melancholy that arises naturally in people who have sufered loss and disappointment and that is part o the “character o mortality,” Burton held that melancholic aictions are “contrary to nature.”39 This latter condition, the disorder o melancholy, he defined (ollowing Du Laurens) as “a kind o dotage without a ever, having or his ordinary companions ear and sadness, without any apparent occasion.”40 Burton was sensitive to the wide individual variation in the nature o loss responses, and he allowed a quite broad range o temperamental reactions to loss to be considered nondisordered as long as they did not become chronic and sel-perpetuating: For that which is but a flea-biting to one, causeth insuferable torment to another, & which one by his singular moderation, & well composed carriage can happily overcome, a second is no whit able to sustaine, but upon every small occasion o misconceived abuse, injurie, griee, disgrace, losse, crosse, rumor, &c. (i solitary, or idle) yields so arre to passion, that his complexion is altered, his digestion hindred, his sleepe gone, his spirits obscured, and his heart heavy, his Hypocondries misafected . . . and he himsele over come with Melancholy. . . . But all these Melancholy fits . . . are but improperly so called, because they continue not; but come & goe, as by some objects they are moved.41 It is only when such normal reactions to specific events become established as an ongoing condition independent o events that Burton sees disorder: (I)t alleth out otentimes that these Dispositions become Habits, and . . . make a disease. Even as one Distillation, not yet growne to custome, makes a cough; but continuall and inveterate causeth a consumption o the lungs: so doe these our Melancholy provocations. . . . This Melancholy o which we are to treat . . . a Chronicke or continuate disease, setled humor . . . not errant but fixed . . . growne to an habit, it will hardly be removed.42 In addition to noting normal variation in temperament, Burton was an astute observer o the extremes to which normal reactions to loss could go. He noted that the most extremely painul losses included separation rom riends and bereavement ollowing loss o a loved one (“in this Labyrinth o accidental causes [o melancholy] . . . loss and death o riends may challenge first place”43) and compellingly described the extremes that nondisordered grie can reach: I parting o riends, absence alone, can work such violent efects, what shall death do, when they must eternally be separated, never in this world to meet again? This is so grievous a torment or the time, that it takes SADNESS WITH AND WITHOUT CAUSE 65 away their appetite, desire o lie, extinguisheth all delights, it causeth deep sighs and groans, tears, exclamations . . . howling, roaring, many bitter pangs, and by requent mediation extends so ar sometimes, they think they see their dead riends continually in their eyes. . . . Still, still, still, that good ather, that good son, that good wie, that dear riend runs in their minds; a single thought fills all their mind all year long. . . . They that are most staid and patient are so uriously carried headlong by the passion o sorrow in this case, that brave discreet men otherwise oten44 times orget themselves, and weep like children many months together. It was not only renowned writers such as Burton but also ordinary medical practitioners who distinguished between melancholic states that arose without cause and those that were proportionate in intensity to their provoking causes. The work o Richard Napier (1559–1634), a physician in rural England whose notebooks have been closely analyzed by the historian Michael MacDonald, illustrates how general physicians o the period classified depressive conditions into three general sorts. The first stemmed rom universal experiences o sorrow and grie, rejection in love, loss o ortune, severe illness, and conflicts with spouses, lovers, or parents. Napier explicitly separated these sorts o ubiquitous adverse states rom melancholic diseases so that “not every gloomy person suered rom the disease o melancholy.”45 Two kinds o melancholic states were considered disorders. First, Napier used the term “baseless sorrow” or some o his disordered patients.46 This reerred to cases that were unprovoked or delusional, thus wholly unexplained by external circumstances. The second type o disordered conditions stemmed rom sources such as “legitimate occasions in the death o loved ones and were revealed to be the sign o melancholy delusion by their unusual intensity and duration.”47 As MacDonald notes, “Contemporaries believed that the eelings experienced by melancholy and troubled people were exaggerations o normal states o mind. The sheer intensity o their moods was abnormal.”48 Napier’s records clearly show that melancholia oten arose without situational provocations but sometimes stemmed rom a disproportionate response to actual losses. Many diagnoses o melancholia, or example, resulted rom bereavement, usually ater the loss o a spouse or a child, 49 in which the sadness was o such intensity and duration that it led to states o madness. Judgments o disease consequently required the physician to obtain knowledge o the relationship o the symptoms to the context o the situations in which they arose and persisted. Writers who ollowed Burton continued to separate depressions that were with and without cause. For example, toward the end o the seventeenth century, Timothy Rogers (1658–1728) considered the diference between bereavement as normal response to loss and as a triggering cause o depressive disorder. He observed that many people can have a melancholic disorder triggered “by the loss o Children, by some sudden and unlooked or disappointment that 66 THE LOSS OF SADNESS ruines all their ormer Projects and Designs.”50 But Rogers made it clear that such horrible losses do not usually lead to melancholic disorder. He specifically contrasts such a disordered reaction with that o one Lady Mary Lane, to whom his book is dedicated, who experienced intense but normal grie and sorrow at the loss o her ather, mother, and several children.51 In the eighteenth century the explicit use o the “without cause” criterion became less common, perhaps because writers in this period ocused on psychotic orms o depression in which this description seemed unnecessary.52 Nevertheless, during this period, madness, according to historian Stanley Jackson, “still usually involved a state o dejection and earulness without an apparent cause, and some particular circumscribed delusion was still a common eature. Sleeplessness, irritability, restlessness, and constipation continued to be usual 53 elements.” Samuel Johnson’s amous dictionary, or example, contained three meanings or melancholia; two reer to mental disorders and one to common, normal emotions.54 Incidentally, Johnson was partially responsible or beginning the trend to gradually replace the term melancholia with depression. Subsequent medical definitions continued to explicitly use the ancient, contextual definition o melancholia. Friedrich Homann (1660–1742) characterized melancholy as “associated with sadness and ear not having any maniest cause.”55 William Cullen (1710–1790), the preeminent authority on melancholy during the latter part o the eighteenth century, noted that melancholy is “always attended with some seemingly groundless, but very anxious, ear.”56 And in the United States, the amed clergyman Cotton Mather (1663–1728) emphasized the lack o sufcient external justification or sadness in melancholic disorder: “These Melancholicks, do sufciently Afict themselves, and are Enough their own Tormentors. As i this present Evil World, would not Really aord Sad Things Enough, they create a World o Imaginary Ones, and by Mediating Terror,they make themselves as Miserable, as they could be rom the most Real Miseries.”57 Even the philosopher Immanuel Kant (1724–1804) broadly defined melancholia as “unjustified . . . grie” and careully distinguished a variety o nondisordered conditions, such as individuals who ashionably immerse themselves in melancholic eelings or the supposed “melancholy mathematician” who in act is merely introverted and thoughtul, rom true mental disorder.58 The Nineteenth Century At the beginning o the nineteenth century, the eminent psychiatrist Philippe Pinel (1745–1826) continued to maintain the undamental separation between melancholic disorders and the consequences o real misortunes. In his 1801 book on mental disorder, Traite Medico-Philosophique Sur ’Alienation l Mentale, Pinel noted that melancholia aicted “some men otherwise in good health, and requently in prosperous circumstances. Nothing, however, can be more hideous SADNESS WITH AND WITHOUT CAUSE 67 than the figure o a melancholic, brooding over his imaginary misortunes.”59 Pinel also provided a particularly important application o the proportionality thesis when he distinguished possible nondisordered rom disordered causes o suicide. Observing that the French philosopher Montesquieu, in a sophisticated cross-Channel putdown, distinguished nondisordered culturally shaped Roman suicides (“the efect o education; it depended upon their customs and manner o thinking”) rom disordered English sel-destruction (“The English requently destroy themselves without any apparent cause to determine them to such an act, and even in the midst o prosperity”), Pinel endorses Montesquieu’s distinction. He elaborates bysaying that normal triggers or sui cide might include severe social humiliation or financial reversal, and he perorms an act o medical diplomacy regarding disordered sources o suicide by asserting that this is not just an English disease: “The propensity to this horrid deed as existing independent o the ordinary powerul motives to it, such as the loss o honour or ortune is by no means a disease peculiar to England: it is ar rom being o rare occurrence in France.”60 A notable student o Pinel’s, Jean-Etienne-Dominique Esquirol (1772– 1840), continued to embrace the contextual tradition, noting that the disparity between reality and the intensity o sadness may be apparent even to the suerer: “Some . . . possess a knowledge o their condition, have a consciousness o its alsity, and o the absurdity o the ears in which they are tormented. They perceive clearly that they are irrational, and oten coness it, with grie and even despair.”61 Benjamin Rush (1745–1813), known as “the ather o American psychiatry,” similarly allowed or melancholia to be characterized by alse belies or disproportionate responses to belies: Partial derangement consists in error in opinion, and conduct, upon some one subject only, with soundness o mind upon all, or nearly all other subjects. The error in this case is two-old. It is directly contrary to truth, or it is disproportioned in its efects, or expected consequences, to the causes which induce them.62 The prominent British psychiatrist, Henry Maudsley (1835–1918), also noted the misdirection o the melancholic’s response in that “impressions which should be agreeable or indiferent are painul.” 63 He ofered some extreme examples o disproportion: In some cases it is striking how disproportionate the delusion is to the extreme mental anguish, the patient assigning some most ridiculously inad- equate cause or his gloom: one man under my care, whose sufering was very great, said that it was because he had drunk a glass o beer which he ought not to have done, and another man was, as he thought, lost or ever because he had muttered a curse when he ought to have uttered a prayer.64 68 THE LOSS OF SADNESS Maudsley insisted that any delusional ideas are a result, not a cause, o the aective intensification that comes with the disorder. The influential German psychiatrist Wilhelm Griesinger (1817–1868) also used the disproportionality o melancholic symptoms to their context to define when they indicated a disorder: The melancholia which precedes insanity sometimes appears externally as the direct continuation o some painul emotion dependent upon some objective cause . . . e.g., grie, jealousy; and it is distinguished rom the mental pain experienced by healthy persons by its excessive degree, by its more than ordinary protraction, by its becoming more and more independent o external influences, and by the other accessory aections which accompany it. In other cases the melancholia srcinates without any moral cause.65 Greisinger called melancholia “a state o proound emotional perversion, o a depressing and sorrowul character”;66 the intended notion o “perversion” is the turning away o a eeling rom the objects at which it would be naturally and proportionately aimed. He noted that melancholia involves the same eelings as in nondisordered responses such as grie and jealousy but that it is distinguished by excessive intensity, duration, and, most o all, its “objective groundlessness” in relation to actual external events. 67 But he acknowledged that “the boundary betwixt the physiological state o emotion and insanity is oten dif cult to trace” because the disorder “may appear as the immediate continuation o a physiological state o the established emotion.” He asserts that “the essential dierence” between the disorder o melancholia and a nondisordered “gloomy disposition” is that “in the ormer the patient cannot withdraw himsel rom his ill-humour.”68 Simultaneously with the urther elaboration and acceptance o the contextual understanding o depressive disorder, another momentous development was occurring in medical thought. As physicians branched out o the asylum and began to see more patients in private practice, they conronted a much larger proportion o patients coming in or help with intense sadness who had no delusions or other psychotic symptoms. Such orms o melancholia had been recognized since antiquity, but the emphasis had always been on the delusional cases (“dotage without a ever”). But now the orm without delusion became singled out as “simple” melancholia, the orerunner o today’s nonpsychotic unipolar major depression. For example, the British psychiatrist D. Hack Tuke (1827–1895) explicitly rejected the idea that melancholia must involve delusion and identified the “simple” orm that is purely a matter o symptoms o sadness without cognitive impairment, embracing a category o “melancholia, without delusion” along with a melancholic orm o “delusional insanity.”69 He insisted that in simple SADNESS WITH AND WITHOUT CAUSE 69 melancholia there is “no disorder o the intellect . . . no delusion or hallucination.”70 But nonetheless he detected “a cerebral malady . . . sustained by a passion o a sad, debilitiating, or oppressive character.”71 Such definitions became broadly accepted and anticipated the contemporary ocus on the kind o depressive disorder that is easiest to conuse with normal emotional responses. The greater attention to simple melancholia implied an even more exclusive ocus on contextual criteria in the general definition o melancholia. For example, psychiatrist John Charles Bucknill (1817–1897), the author o the chapter on diagnosing insanity in a well-known manual, separated normal rom disordered symptoms using the “without cause” criterion but with no reerence to delusion: The symptoms o melancholia are sorrow, despondency, ear, and despair, existing in a degree ar beyond the intensity in which these emotions usually afect the sane mind, even under circumstances most capable o producing them; and in numerous instances existing without any commen72 surate moral cause, and oten without any moral cause whatever. Due to the nervous system’s responses, “proportioned excitement o unction disappears.”73 Bucknill also held that symptoms o “uncomplicated melancholia . . . vary in degree, but not in kind, rom that normal and healthy grie and sorrow, o which all men have their share in this chequered existence.”74 As to precipitating causes, he noted: “it is occasioned by all the moral causes o mental disease; especially by gries, disappointments, reverses, and anxieties o every kind. It is also caused by long-continued ill-health.”75 However, Bucknill insisted that disorder that was triggered by normal grie generally required a hereditary disposition as well.76 Likewise, psychiatrist Charles Mercier (1852–1918), in his entry on melancholia in Tuke’s influential Dictionary of Psychological Medicine, relied exclusively on proportionality to actual events in defining melancholia as “a disorder characterized by a eeling o misery which is in excess o what is justified by the circumstances in which the individual is placed.” 77 He noted the possible gradual onset until an excessive, disproportionate level o symptoms is reached and the possible interaction between stress and heredity: “At length the degree o misery and the other symptoms reach such a grade at which the limits o the normal are unmistakably exceeded, and it becomes maniest that the patient is sufering rom a morbid depression.”78 Mercier recognized that the causes o normal intense sadness could be risk actors or the development o disorder: Untoward circumstances, the loss o riends, or o ortune, or o character; any circumstance which is calculated to produce sorrow, grie, uneasiness, anxiety, in an ordinarily constituted person, may, i it acts upon a person o less than ordinary stamina, produce melancholia. . . . The 70 THE LOSS OF SADNESS more severe the stress, the greater, naturally, is the chance o melancholia occurring.79 French physician Maurice de Fleury (1860–1931), in Medicine and the Mind, characterized the illness simply as “causeless melancholy.”80 He also oered an explanation o how normal grie over time may transorm into disorder, analogous to what is these days known as the “kindling hypothesis”: “Grie is a special, lower pitch o brain activity. The mind, i it stays there or a certain time, will orm the habit, and henceorward everything will appear to it in a painul, melancholy, pessimistic light.”81 Another psychiatrist, George H. Savage (1842–1921), emphasized the internal causes o melancholic states that were disordered. He defined melancholia as “a state o mental depression, in which the misery is unreasonable either in relation to its apparent cause, or in the peculiar orm it assumes, the mental pain depending on physical and bodily changes, and not directly on the environment.”82 Like most other writers, he accepted the category o simple melancholia: “Simple melancholia, i.e., those in whom the misery and its expression are simply slight exaggerations o natural states, those cases in whom there is no real delusion, no fiction such as that they are ruined or damned . . . requently, the misery gives rise to the delusion.”83 The most popular psychiatric text o the late nineteenth century, Richard von Krat-Ebing’s (1840–1902) Text-Book of Insanity, continued to define melancholia in terms o proportionality o response: “The undamental phenomenon in melancholia consists o the painul emotional depression, which has no external, or an insufcient external, cause, and general inhibition o the mental activities, which may be entirely arrested.”84 For Krat-Ebing: A painul, depressed state o eeling . . . that has arisen spontaneously and exists independently, is the undamental phenomenon in the melancholic states o insanity. . . . Even objects which under other conditions would give rise to pleasant impressions seem now, in the mirror o his abnormally changed sense o sel, to be worthy o aversion.85 Krat-Ebing observed the challenge o distinguishing normal rom abnormal depressive states, especially in cases o simple melancholia: The content o the melancholic consciousness is psychic pain, distress, and depression. . . . This painul depression in its content does not dier rom the painul depression due to efcient causes. . . . The content o melancholic delusions is extremely varied, or they include all varieties o human trouble, care, and ear. . . . The common character o all melancholic delusions is that o suering. . . . Simple melancholia is decidedly SADNESS WITH AND WITHOUT CAUSE 71 the most requent orm o mental disease . . . only exceptionally observed in institutions or the insane, but it is extremely requent in private practice (with) innumerable slight cases that do not reach the hospital. 86 Conclusion What is striking about this brie overview o conceptualizations o depressive disorder rom Hippocrates to Kraft-Ebing is, first, the remarkable consistency o the symptoms that are mentioned—by and large the same kinds o symptoms that current diagnostic manuals emphasize. And, second, there is a remarkably solid and well-elaborated tradition o distinguishing disorder rom normal emotion via various versions o the “with cause” versus “without cause” criterion that goes back to ancient times. The entire 2,500-year record indicates an understanding that pathological depression is an exaggerated orm o a normal human emotional response and thus that the first step in diagnostic logic must be to use the relation to triggering causes to distinguish the normal rom the disordered. A third point is the recent move toward greater ocus on “simple melancholia” without delusion, yielding even more reliance on the contextual “without cause” criterion in defining the distinction between normal-range and disordered sadness and presaging our contemporary ocus on nonpsychotic unipolar disorder. The power, consistency, and rationale o the “without cause” medical understanding o depressive disorder orm the backdrop or the next century’s radical departures in diagnostic approach. The ollowing chapter traces the ate o this tradition during the twentieth century. 4 Depression in the Twentieth Century ntil the end o the nineteenth century, psychiatry generally used the relationship o symptoms to their pro voking causes as an essential part o definitions o melancholic disorder. Although some kinds o cases, such as psychotic depressions, almost always displayed symptoms that implied disorder, diagnosticians understood that they had to consider context, because depressive disorder could oten be symptomatically indistinguishable rom proound normal sadness. In the late 1800s, the traditional contextual approach to diagnosis o depressive disorder began to divide into two distinct schools. On one side, Sigmund Freud and his ollowers emphasized the U psychological etiology o all mental disorders, including depression, and their continuity with normal unctioning. Adheren ts o this school studied and interpreted the patient’ s reported thoughts to surmise the existence o underlying unconscious pathogenic meanings and wishes. On the other side, Emil Kraepelin applied a classical medical model that examined the symptoms, course, and progno sis o depression and other disorders to define distinct ph ysical pathologies. Kraepelin’s approach inspired a cadre o researchers to translate it into a research program that oten used statistical techniques to iner discrete disorders rom maniest symptoms. Many psychiatrists viewed the publication o the DSM-III in 1980 as finally resolving the struggle between the Freudian and Kraepelinian schools or the domination o psychiatric nosology largely in avor o Kraepelin’s approach.1 We will see, however, that such a judgment is overly simplistic in many ways. Specifically with respect to depressive disorder, the DSM-III criteria in act represented a rejection o key assumptions underlying both Freud’s and Kraepelin’s systems and an afrmation o a quite dierent research tradition that ignored the prior emphasis on contextual criteria. 72 DEPRESSION IN THE TWENTIETH CENTURY 73 Continuation of the “With” and “Without” Cause Tradition in the Twentieth Century Psychodynamic Approaches to Disordered and Normal Sadness At the beginning o the twentieth century, the Austrian neurologist-turnedpsychoanalyst Sigmund Freud (1856–1939) and his disciples developed a revolutionary approach to the study o mental disorders. The heart o this approach was the efort to understand pathological symptoms in terms o unconscious mental processes, rather than in terms o biological predispositions and organic etiologies. Although he acknowledged that the intensity o specific desires involved in pathogenesis could be indirectly due to constitution, Freud ocused on postulating immediate causes that were oten purely psychogenic, such as repressed desires, psychological conflicts, or the transormation o repressed motivational energy into anxiety, all o which had little to do with hereditary or other direct physical causes. Psychoanalysts paid relatively little direct attention to treating symptoms themselves and ocused instead on identiying the underlying, and presumably unconscious, dynamics o mental disorders, which they thought maintained the symptoms. In addition, given the sorts o conflicts and other psychological processes they postulated as etiologies, psychoanalysts viewed the psychodynamics that underlie mental disorders as generally continuous with, not discrete rom, the psychodynamics present in normality, thus blurring the boundary between normality and disorder. For psychoanalysts, depression was one major mechanism underlying symptom ormation that, to some degree, was present in nearly every neurosis. They postulated a continuum between ordinary states o sadness, neurotic states o depression, and psychotic states o melancholia. Analysts, or example, considered manic depression an extremely exaggerated expression o the same psychological processes that underlie the universal heightening and reduction o sel-esteem that all people experience.2 Analytic attempts to explain depression were based on traditional assumptions about the diferences between depressive conditions that arose with and without expectable environmental causes. Karl Abraham (1877–1925), a disciple o Freud’s, provided the first psychoanalytic explanation o depression, grounding his theory in the distinction between normal grie and depression.3 Abraham considered outwardly similar states, such as grie and depression, as in act distinct because they involved diferent underlying etiological dynamics. The mourner’s grie, Abraham explained, stemmed rom a conscious preoccupation with the lost person. In contrast, the depressed person was preoccupied with guilt and low sel-esteem. Moreover, symptoms o depression resulted rom the depressed person’s unconscious turning inward o hostility toward another person; hence the common psychoanalytic description o depression as “anger 74 THE LOSS OF SADNESS turned inward” and resultant therapeutic strategies aimed at having the patient express the repressed anger. Freud elaborated on Abraham’s distinction between normal grie and depression in his central article on depression, “Mourning and Melancholia.” Freud began his essay by noting the diferences between normal grie and melancholia and explaining that Although grie involves grave departures rom the normal attitude to lie, it never occurs to us to regard it as a morbid condition and hand the mourner over to medical treatment. We rest assured that ater a lapse o time it will be overcome, and we look upon any intererence with it as inadvisable or even harmul.4 Freud distingu ished between the normality o grie and the disorde r o melancholia. He asserted that symptoms associated with mourning are intense and are “grave departures rom the normal,” in the sense that grie is greatly diferent rom usual unctioning. Nevertheless, grie is not a “morbid” condition; that is, it is not a medical disorder that represents the breakdown o a biologically normal response. Thus it does not require medical treatment; indeed, Freud emphasized that it would “never occur to us” to provide medical treatment to the bereaved. In addition, he stressed that grie is naturally sel-healing, so that with time the mourner would return to a normal psychological state. Medical intervention, he suggested, could actually harm the grieving person through interering with this natural process. While noting that mourners did not sufer rom the same unwarranted decline in sel-esteem that characterized melancholics, Freud emphasize d that their symptoms were otherwise similar. Both mourning and melancholia eatured proound dejection, loss o interest in the outside w orld, an inability to eel pleasure, and an inhibition o activity. The distinction between mourning and melancholia lay not so much in their symptoms but in the act that the ormer state was a normal reaction to loss, whereas the latter state was pathological. Freud’s version o the distinction between depressions with cause (mourning) and without cause (melancholia) allowed him to elucidate the diferent psychodynamics that underlay the two conditions. For mourners, the world came to eel empty and without meaning due to conscious losses, whereas melancholics experienced the ego as impoverished due to unconscious losses. The sel-reproaches o melancholics pathologically redirected their internalized hostility rom earlier love objects onto the sel. Therapy, thereore, should teach them to express their inward anger toward the objects that are its actual targets. In contrast, people who experience normal sadness are going through a natural and necessary process that it was “inadvisable or even harmul” to disrupt with medical treatment. DEPRESSION IN THE TWENTIETH CENTURY 75 Freud rejected the 2,500-year tradition that postulated physiological causes o pathological depression and adopted a psychogenic theory o causation. Nonetheless, Freud and other psychoanalysts largely accepted as sel-evident the traditional distinction between normal intense sadness resulting rom loss and symptomatically quite similar pathological depression disproportionate to loss. Kraepelin and Depressive Disorder Emil Kraepelin (1856–1926), a German psychiatrist and a contemporary o Freud, attempted to place psychiatry within a strictly biomedical ramework that considered mental disorders as maniestations o physical brain pathologies. He used the symptoms and course o disorders to create categories that, he claimed, represented distinct underlying pathological conditions, which he hoped would eventually be confirmed by the identification o anatomical lesions. He built on earlier work that attempted to separate asylum patients into those who might be restored to the community versus those likely to deteriorate. Kraepelin amously used prognosis to distinguish between manic-depressive insanity (now bipolar disorder), which tended to occur in episodes and remit, and dementia praecox (now schizophrenia), which tended to have a deteriorating course, as two undamental orms o psychotic disorder. Kraepelin’s contributions to psychiatric diagnosis, especially his eforts at categorization based on careul attention to symptoms, are now generally seen as the orerunner o the later DSM-III transormation o psychiatric diagnosis. Indeed, the recent DSMs are now oten reerred to as “neo-Kraepelinian.”5 Some prominent historians o medicine, prompted by his perceived relationship to the DSM-III approach, see Kraepelin as the major figure in modern psychiatry, surpassing even Freud: “It is Kraepelin,” asserts Edward Shorter, “not Freud, who is the central figure in the history o psychiatry.”6 Because Kraepelin’s diagnostic approach has become linked to that o the DSM, it is pertinent to consider his views at some length. Kraepelin began his career as a physician in a Munich asylum and maintained his almost exclusive interest in psychotic disorders as a proessor at Heidelberg and as the director o the Psychiatric Clinic at Munich.7 He developed his classification system using descriptions o inpatient cases. Inpatient mental institutions had become a common setting or treating the seriously mentally ill during the nineteenth century.8 Beore this time, most depressed patients, such as those o Richard Napier, would have visited community-based physicians who treated a great variety o severe and less severe conditions. Persons whose sadness stemmed rom lie problems would have typically handled the problem themselves, sought help rom riends and amily, or consulted general physicians or clergy.9 The efect o the mental hospital was to concentrate the most seriously disturbed, and only this group, within a single location. Those who entered asylums 76 THE LOSS OF SADNESS would typically have had such severe conditions that the issue o whether or not their current symptoms were proportionate responses to their circumstances would not have arisen. The pressing question or Kraepelin, thereore, was not whether asylum patients had disorders or normal unhappiness but rather what particular types o disorders they had. Kraepelin conronted a field in intellectual chaos, with no consensual diagnostic system. Everyone since Greek times had used symptoms to individuate disorders. But without any commonly shared principle or how to divide up the varied symptomatic presentations that physicians and psychiatrists saw, the use o symptoms allowed or many diferent classification schemes. At one extreme were those who classified virtually any symptom presentation asa separate disorder, leading to disorder prolieration that could reach hundreds ocategories. At the other extreme were those who, ocusing10on psychosis, considered all mental disorders to be variants o a single disorder. For example, the first U.S. census survey to ask about mental disorder in 1840 reflected the latter approach and contained just one category o mental disorder, “insanity.”11 Kraepelin’s careul attention to symptoms and their course in inerring distinct pathological states that caused the symptoms ollowed a tradition in physical medicine started by the eighteenth-century English physician Thomas Sydenham and developed by the nineteenth-century German pathologist Rudolph Virchow. This approach had been highly successul in helping to distinguish physical diseases, especially as knowledge o inectious agents and physical pathology rapidly grew.12 Kraepelin was no doubt also greatly influenced by the growing realization that one o the most dreadul men tal disorders o his time, general paresis (about which he wrote a book), resulted rom the syphilitic inection o the nervous system. This startling discovery seemed to impart two lessons. First, mental disorders, like physical disorders, could be due to underlying physical pathology o some kind and thus fit directly within traditional diagnostic theory. Second, diagnosticians identified general paresis as a specific syndrome based on its symptoms and its horrific and rapid course and poor prognosis; like syphilis itsel, the symptoms changed over time and could difer markedly at diferent stages o the disease, yet the same underlying disorder was present and simply unolding. The moral seemed clear; it is not just symptoms at any particular time but sympt oms over the course o an illness that served to identiy the illness. Kraepelin’s descriptions o the depressive symptoms that occur in the course o various afective or mood disorders—which included psychic symptoms, such as slowness o thinking, sense o hopelessness, inner torment, inhibited activity, and inability to eel pleasure, as well as physical symptoms, such as sleep and appetite disorders and atigue—remain the basis o current diagnostic classifications o depressive disorders. A cornerstone o Kraepelin’s thinking was that a great variety o symptomatic presentations o afective disorders in act DEPRESSION IN THE TWENTIETH CENTURY 77 represented one underlying pathology. Based on this hypothetical underlying unity o various symptom presentations, he classified even individuals who were only depressed and had no manic symptoms as having manic-depressive disorder. “In the course o the years,” Kraepelin emphasized, “I have become more and more convinced that all (melancholic) states only represent maniestations o a single morbid process.”13 Kraepelin’s belie that unipolar depressive states represented variations o the same underlying illness condition as did manicdepressive states was based on the evidence o their overlapping symptoms and the requent appearance o manic symptoms during recurrences later in the course o disorders that initially displayed only depressive symptoms. Over time, many aective patients had depressive states, manic states, and mixed states. Kraepelin also included within the manic-depressive category even “slight” mood disorders that pass “without sharp boundary into the domain o personal predisposition,” under the assumption that these mild conditions were rudiments o and oten developed into more severe disorders.14 Kraepelin also maintained that most aective disorders stemmed rom hereditary predispositions; consequently, “attacks o manic-depressive insanity may be to an astonishing degree independent of external influences.”15 Even many cases that seemed to arise normally rom external influences such as deaths, quarrels, unrequited love, infidelity, or financial difculties actually were maniestations o disorders that stemmed rom innate dispositions. “The real cause,” Kraepelin wrote, “o the malady must be sought in permanent internal changes, which at least very oten, perhaps always, are innate.”16 These conditions could be distinguished rom normality by telltale evidence such as manic symptoms, inexplicable recurrence, psychotic ideation, or duration well beyond the cessation o the trigger. The relationship between Kraepelin’s work and the DSM-III revolution is complex and less clear than is oten maintained. The major developer o the DSM-III, psychiatrist Robert Spitzer, denies being a “neo-Kraepelinian” on the grounds that he assumes neither that there must be distinct categorical pathologies that underlie dierent syndromes nor that mental disorders are largely due to physical brain diseases, both basic tenets o Kraepelin’s approach.17 Most undamentally, Kraepelin rejected the use o any rigid system o symptoms as necessary and sufcient indicators o disorder. Instead, he used all the available evidence, including the prognosis o symptoms, to iner whether various conditions were likely due to the same pathology. He was, contrary to common belie, against the sole use o symptomatic criteria to iner which disorder was present. O course, diagnosticians have to use symptoms as their main resource, but Kraepelin did this in a way that was intended to transcend symptoms and get at underlying pathology, an approach in tension with the DSM-III’s heavy reliance on operational definitions solely via symptom syndromes. Kraepelin’s approach to diagnosing distinct pathologies obviously depended on the prior identification o conditions as pathologies, distinct rom 78 THE LOSS OF SADNESS nonpathological states that do not involve any underlying pathological etiology. How, then, did Kraepelin deal with the distinction between normal sadness and disorder? Kraepelin and Normal Sadness Previous commentators have not examined Kraepelin’s approach to distinguishing normal sadness rom disorder. Admittedly, his works contain little explicitly about this distinction. As noted, the asylum context in which he worked tended to make this distinction irrelevant, as all his patients likely had disorders. Moreover, Kraepelin, like many psychiatrists, was more worried about alse negatives and the harm that missing a true case could do than about alse positives that mislabel a normal person as disordered. Nonetheless, Kraepelin required such a distinction, and he embraced the same doctrine as had the medical tradition that preceded him, namely, that nondisordered intense sadness occurs in response to a variety o losses and can symptomatically resemble depressive disorder. Kraepelin thus accepted the traditional principle that the way to distinguish pathological depressive disorder rom normal sadness was to determine whether the sadness was without cause (or without proportional cause). Although he did not explicitly state the “without cause” principle directly in his diagnostic criteria, he did make his position on normal sadness clear in scattered remarks: Morbid emotions are distinguished rom healthy emotions chiefly through the lack o a sufcient cause, as well as by their intensity and persistence. . . . Even in normal lie moods come and go in an unaccountable way, but we are always able to control and dispel them, while morbid moods dey all attempts at control. Again, morbid emotions sometimes attach themselves to some certain external occasions, but they do not vanish with the cause like normal eelings, and they acquire a certain independence.18 Here, Kraepelin emphasized that either morbid states were without “suf cient cause” in circumstances or, when they initially seem to be with cause, they became independent o circumstances and continued even ater circumstances changed. Such cases include conditions that were initially disorders, as well as conditions that began as normal responses but subsequently became morbid. Kraepelin addressed the issue o dierentiating between disorder and normal sadness in some o his case presentations, such as the ollowing: I will first place beore you a armer, aged fity-nine, who was admitted to the hospital a year ago. . . . On being questioned about his illness, he breaks into lamentations, saying that he did not tell the whole truth on his DEPRESSION IN THE TWENTIETH CENTURY 79 admission, but concealed the act that he had allen into sin in his youth and practiced uncleanness with himsel; everything he did was wrong. “I am so apprehensive, so wretched; I cannot lie still or anxiety. O God, i I had only not transgressed so grievously!” . . . The illness began gradually seven or eight months beore his admission, without any assignable cause. Loss o appetite and dyspepsia appeared first, and then ideas o sin. . . . The most striking eature o this clinical picture is the apprehensive depression. At first sight, it resembles the anxieties o a healthy person, and the patient says that he was always rather apprehensive, and has only grown worse. But there is not the least external cause or the apprehension, and yet it has lasted or months, with increasing severity. This is the diagnostic sign o its morbidity.19 Kraepelin noted that even the extreme emotional and physiological symptoms o this patient were consistent with intense normal sadness, especially in a person with a dispositional tendency toward the melancholic side. But, he observed, the patient’s symptoms started “without any assignable cause.” Moreover, in addition to the act that “there is not the least external cause or the apprehension,” the condition had lasted months (and thus has a prolonged and seemingly inordinate duration) and had not, as normal sadness episodes do, displayed a trajectory o decreasing symptoms; ar rom it, it has shown “increasing severity” over time even though nothing new occurred in the circumstances to warrant such changes. This disconnection o the patient’s condition rom external events, and especially the lack o a trajectory showing normal coping and mastery, “is the diagnostic sign o its morbidity.” Kraepelin diagnosed this patient as depressively disordered, and the patient would surely also qualiy or the DSM diagnosis o Major Depressive Disorder on the basis o the duration and symptoms o the depressive episode, including sleep problems, appetite problems, depressive mood, and intense unjustified guilt and sel-reproach. But Kraepelin’s comments on diferential diagnosis o this depressive disorder rom normal sadness imply a divergence rom the DSM, not in the case o this patient but in the cases o normal responses that might resemble this patient’s in maniest symptomatology. What is critical in Kraepelin’s discussion is that, ater reciting the duration and the symptoms, he noted that “at first sight, it resembles the anxieties o a healthy person,” especially one with somewhat melancholic (but normal range) temperament. (Indeed, the patient’s lamentations and guilt remind one o Timothie Bright’s descriptions, reviewed in the last chapter, o cases o intense normal guilt due to believing one has sinned against God’s law.) That is, Kraepelin recognized that symptoms o this duration and severity can be a normal response to events. It is, according to Kraepelin, not the duration or symptoms in themselves but their lack o proportional relation to any plausible external cause that allowed him to see that this condition was a disorder. In contrast, based on its symptom and 2-week duration 80 THE LOSS OF SADNESS criteria, the DSM would automatically diagnose such an individual as depressively disordered without the kind o assessment Kraepelin perormed. From the DSM’s perspective, Kraepelin’s painstaking discussion is pointless because the possibility o normal response does not exist given the symptoms, so there is no dierential diagnosis to be made. In another passage in which he reiterated the “without cause” criterion as central to diagnosis, Kraepelin made it clear that, even in his day when more severe cases were the rule among psychiatric patients, there was a real possibility o misclassiying a normal person as disordered because the symptoms could be identical: Under certain circumstances it may become very difcult to distinguish an attack o manic-depressive insanity rom a psychogenic state o depression. Several times patients have been brought to me, whose deep dejection, poverty o expression, and anxious tension tempt to the assumption o a circular depression, while it came out aterwards, that they were cases o moodiness, which had or their cause serious delinquencies and threatened legal proceedings. As the slighter depressions o manic-depressive insanity, as ar as we are able to make a survey, may wholly resemble the well-ounded moodiness o health, with the essential dierence that they arise without occasion, it will sometimes not be possible straightway to arrive at a correct interpretation without knowledge o the previous history in cases o the kind mentioned. 20 Although Kraepelin recognized some psychogenic depressions (i.e., those caused by strictly psychological actors that do not include whatever biological pathology underlies manic-depressive conditions) as disorders, he also used the term psychogenic to reer to normal sadness states with sufcient external cause. The crucial point, which Kraepelin derived rom his experience, is that “the slighter depressions o manic-depressive insanity, as ar as we are able to make a survey, may wholly resemble the well-ounded moodiness o health, with the essential dierence that they arise without occasion.” Kraepelin acknowledged that he initially believed that the patients in question were disordered, noting that the acts about the context that reversed his judgment only “came out aterwards.” This confirms that Kraepelin understood that the symptomatic presentation o normal and disordered cases could be the same, and it explains why he emphasized that the causal context was the essential dierentiating criterion. It is also worth noting that none o the normal cases he reported encountering involved bereavement, the one contextual consideration the DSM allows, but rather “had or their cause serious delinquencies and threatened legal proceedings.” Thus, as we shall see, the DSM would likely classiy as disordered these cases that Kraepelin diagnosed as normal because it ignores the “essential dierence” o context. DEPRESSION IN THE TWENTIETH CENTURY 81 Consider another o Kraepelin’s cases that raises the issue o the distinction between disorder and normality: I will now show you a widow, aged fity-our, who has made very serious eforts to take her own lie. This patient has no insane history. She married at the age o thirty, and has our healthy children. She says that her husband died two years ago, and since then she has slept badly. Being obliged to sell her home at that time, because the inheritance was to be divided, she grew apprehensive, and thought that she would come to want, although, on quiet consideration, she saw that her ears were groundless. . . . This patient, too, is quite clear as to her surroundings, and gives connected inormation about her condition. She has no real delusions, apart rom ear that she will never be well again. Indeed, we find that the real meaning o the whole picture o disease is only permanent apprehensive depression, with the same accompaniments as we see in mental agitation in the sane—i.e., loss o sleep and appetite, and ailure o the general nutrition. The resemblance to anxiety in the sane person is all the greater because the depression has ollowed a painul external cause. But we can easily see that the severity, and more especially the duration, o the emotional depression have gone beyond the limits o what is normal. The patient hersel sees clearly enough that her apprehension is not justified by her real position in lie, and that there is absolutely no reason why she should wish to die.21 This patient was experiencing her one and only episode o depressive symptoms; there was “no insane history.” In addition to maniesting depressed mood, the patient was suicidal and had insomnia, loss o appetite, and lack o energy (“ailure o the general nutrition”) and so would qualiy or a DSM diagnosis o MDD. Although the depressive symptoms began soon ater her husband’s death, the immediate trigger seems to have been not that but the subsequent need to sell their home and attendant ears o poverty; as we saw in chapter 2, the financial and social consequences o loss can influence the severity o a normal reaction. Once again, the symptoms—including even suicidality, which can occur in nondisordered people who are highly distraught—consist o “the same accompaniments as we see in mental agitation in the sane.” Indeed, “the resemblance to anxiety in the sane person is all the greater because the depression has ollowed a painul external cause.” How, then, did Kraepelin know that this woman was disordered? Although there was a trigger, the reaction, which had lasted about 2 years and included serious suicide attempts, went beyond any possible proportional relationship to the trigger: “the severity, and more especially the duration, o the emotional depression have gone beyond the limits o what is normal.” In efect, this meant that the eelings were without cause. This was apparent even to the patient 82 THE LOSS OF SADNESS hersel: “On quiet consideration, she saw that her ears were groundless. . . . The patient hersel sees clearly enough that her apprehension is not justified by her real position in lie, and that there is absolutely no reason why she should wish to die.” Indeed, the patient had every reason to live, including our healthy children. The case illustrates that when the severity and duration o symptoms are disproportionate to the trigger, they are in eect symptoms “without cause” because the context interacting with normal human nature does not ully explain them. As Kraepelin elsewhere emphasized, “The dejection which in normal lie accompanies sad experiences gradually wanes, but in disease even a cheerul environment ails to mitigate sadness, indeed, it may even intensiy it.”22 In sum, Kraepelin maintained the traditional distinction between depressive conditions that were “with” or “without cause.” Not symptoms in themselves, but symptoms that became detached rom their contexts and took on a lie o their own, indicated disorder. Kraepelin oered symptoms as evidence to iner a diagnosis but, in contrast to the DSM, he never attempted to define disorders solely in terms o necessary and suf cient symptoms. He clearly recognized normal depressive episodes “with cause” that were proportionate to their triggers and that subsided ater the stressor subsided, and he actively grappled with how to distinguish normal sadness rom disorder given their possible symptomatic similarity. Adolf Meyer on Normal and Disordered Reaction Types Adol Meyer (1866–1950), a Swiss-born psychiatrist who held the Chair in Psychiatry at Johns Hopkins University, is generally considered the leadingAmerican psychiatrist in the first hal o the twentieth century. Both the Kraepelinian physiological and Freudian psychological traditions influenced Meyer, and he was known early on or bringing Kraepelinian ideas to American psychiatry, but he was not a ull-fledged partisan o either school. By the 1920s, he developedhis own distinctive approach that ocused more on lie course, personality, and patients’ capacity or responding to adaptive challenges and less on the particular diseases they might have. Indeed, he reconceptualized psychiatric disorders as impairments in the ability to respond to such everyday problems. Meyer’s approach heavily influenced the descriptions o disorders in the first two editions o the DSM that preceded the pivotal third edition. Like psychoanalysts, Meyer emphasized a contextual approach to depression. He thought that the symptoms, causes, and prognoses o depressive illnesses were ar too heterogeneous to be encompassed within a single disease condition. Instead, he developed a “biopsychosocial” approach, which stressed how each individual’s unique predispositions, environmental circumstances, and specific experiences over the lie course produced their conditions. For Meyer, psychiatric disorders, including depression, were maladaptive reactions that DEPRESSION IN THE TWENTIETH CENTURY 83 arose on the basis o constitutional and psychological predispositions, individual upbringing, and social conditions, as well as rom the interaction o individual organisms and their environments. In a definition that accorded with the “without cause” tradition, Meyer defined simple melancholia as “an excessive and altogether unjustified depression” and simple depression as “more or less, excesses o normal depression.”23 In response to Kraepelin’s ocus on classification as involving inerence to underlying physical pathologies analogous to diagnosis o physical diseases, Meyer included a constitutional (biological) component to stress reactions. Conceiving o mental pathologies as malunctions in the individual’s overall capacity to react adaptively to stressul situations, he developed a general ramework or thinking about all disorders that was summarized in the schema, “situation, 24 reaction, and final adjustment.” Meyer argued that “the conditions we meet in psychopathology are more or less abnormal reaction types.” 25 In talking o reactions and adjustments, Meyer did not include normal sadness in response to loss in his conception o pathology. Rather, conceiving o episodes o disorder as malunctioning responses to events, he was essentially urging psychiatrists to understand disordered individuals as reacting dysunctionally to their environmental contexts. In principle, Meyer and his ollowers held to a clear, coherent, and traditional distinction between normal reactions that were proportionate and disordered reactions that were excessive and disproportionate. They also clearly discerned that the distinction between normal and disordered depression lies not in symptoms but in the relation to events. Wendell Muncie’s Meyerian textbook, Psychobiology and Psychiatry (1939), with a oreword by Meyer, defined depressive disorder as a reaction that is diferentiated rom the universal experience o normal sadness via its disproportionality: Depression is a sweeping reaction in which a dominant and fixed mood o sadness or its equivalent appears as the central issue determining a syndrome. . . . The mood may be rather difuse as sadness, blueness, melancholy, or more topically pointed as worry, or earul or anxious depression. The reaction presents general slowing and reduction o useul activity, loss o initiative . . . slowness in thinking . . . ideas o unworthiness, and sel-depreciation, etc. Pathological depression is to be diferentiated rom normal depression by its greater fixity, depth, and by the disproportion to the causative actors. Depression is the major reaction most easily appreciated since depression o normal proportions is a universal experience.26 Note that Muncie implicitly assumed that the symptoms o normal depression, although proportionate to causes, were similar to those o some pathological depressions. Indeed, he waited until ater his symptom description was complete to add criteria or distinguishing the two kinds o depression via 84 THE LOSS OF SADNESS the familiar, classic criteria: greater duration (“fixity”), unusual severity of symptoms (“depth”), and disproportion to the cause. Both Meyer and psychoanalysts focused their concern more on understanding personalities and life circumstances than on distinguishing distinct disease conditions. Their greatest classificatory impact was on the diagnostic manuals that preceded the DSM-III, the DSM-I and DSM-II, which adopted Meyer’s “reaction” vocabulary and psychoanalytic ideas about anxiety and defense in some of their definitions, including the definition of depressive disorder. Initial Psychiatric Classifications Psychiatric nomenclature in the United States during the first half of the twentieth century did not reflect an intense interest in classification. Instead, the administrative need to keep track of statistics regarding disorders in groups such as hospitalized patients drove the development of diagnostic manuals.27 Diagnoses focused on the conditions of people found within institutional contexts, the predominant form of treatment of mental disorder at the time, and reflected the fact that most psychiatrists practiced in mental hospitals. Thus diagnostic systems tended to gloss over the less severe neurotic conditions that analysts typically saw in outpatient settings. For example, the first standardized classification system in the United States, the Statistical Manual for the Use of Hospitals for Mental Diseases, issued in 1918, divided mental disorders into 22 principal groups, only one of which represented all psychoneuroses.28 The Statistical Manual contains two categories that covered depressive conditions. First, one of the 2 groups was for non-neurotic disorders of psychogenic srcin without clearly defined hereditary or constitutional causes. Manicdepressive psychoses fell into this category (in sharp distinction to Kraepelin’s biological view and more akin to psychodynamic approaches). Second, under the general group of psychoneurosis, was the category of depression under the label reactive depression, in a Meyerian spirit. Its definition of reactive depression is: Here are to be classified those cases which show depression in reaction to obvious external causes which might naturally produce sadness, such as bereavement, sickness and financial and other worries. The reaction, of a more marked degree and of longer duration than normal sadness, may be looked upon as pathological. The deep depression, with motor and mental retardation, shown in the manic-depressive depression is not present, but these reactions may be more closely related in fact to the manic-depressive 29 reactions than to the psychoneuroses. This definition recognized that depressive disorder is to be distinguished from sadness that arises proportionally “with cause” from external circumstances, which is produced “naturally” (i.e., in accord with human nature) and DEPRESSION IN THE TWENTIETH CENTURY 85 thus is normal and not pathological. The definition also ollowed tradition in recognizing that a broad range o negative circumstances can trigger normal sadness, ofering a clearly nonexhaustive list o examples, including grie, medical illness, and financial reversals, in contrast to recent definitions that no longer recognize the range o potential triggers o intense normal sadness. The Statistical Manual’s distinction between normal and pathological depression, not so diferent rom that o Hippocrates, ofered no symptomatic distinction but required pathological depressions to be more severe and o longer duration (“o a more marked degree and o longer duration than normal sadness”). They were not o the depth and severity o manic-depressive illness, yet they were still disorders. An examination o symptoms alone, thereore, could not determine pathology, which was recognized to exist only when symptoms were o disproportionate intensity to their context. The Manual, in a tip o the hat to Kraepelin, speculated that pathological depressive reactions may share an underlying etiological actor with manic-depressive depressions, thus explaining their unwarranted intensity and disproportion. Indeed, this definition mirrored the same three kinds o conditions—depressions with cause, without cause, and o disproportionate severity and duration to a provoking cause—that Robert Burton delineated in Anatomy of Melancholy; like Burton’s definition, it recognized that only the latter two conditions indicated mental disorder. The Statistical Manual guided psychiatric classification rom its 1st edition in 1918 through its 10th edition in 1942. By the early 1950s, the center o gravity in American psychiatry had shited rom state hospitals, which ocused on psychotic cases, to psychodynamic outpatient therapy o less severe pathology. The classifications o psychotic disorders that dominated the Statistical Manual were thus no longer relevant to the vast majority o patients. In 1952, the American Psychiatric Association newly codified mental disorders and produced the first edition o a new manual, the Diagnostic and Statistical Manual of Mental Disorders (DSM-I),30 that better reflected the nature o the psychiatric proession’s changing patient population. A combination o psychodynamic and Meyerian approaches dominated the characterization o depression in the DSM-I, which generally downplayed biological aspects o disorders and ocused on unconscious psychological mechanisms.31 It contained one category o psychotic afective reactions that, in turn, were divided into manic-depressive reactions and psychotic-depressive reactions. Both o these conditions showed severe symptoms that involved “maniest evidence o gross misinterpretation o reality, including, at times, delusions and hallucinations.”32 The ormer also eatured severe mood swings that were sub- ject to remission and recurrence, whereas the latter did not encompass mood swings but requently eatured environmental precipitating actors. The manual characterized psychoneurotic depressive disorders, like all psychoneuroses, as stemming rom unconscious attempts to deal with anxiety, a basically psychoanalytic perspective. Again in a Meyerian ashion, as 86 THE LOSS OF SADNESS a variation o the earlier Statistical Manual ’s “reactive depressions,” DSM-I labeled these conditions Depressive reactions, which it defined as ollows: The anxiety in this reaction is allayed, and hence partially relieved, by depression and sel-depreciation. The reaction is precipitated by a current situation, requently by some loss sustained by the patient, and is oten associated with a eeling o guilt or past ailures or deeds. The degree o the reaction in such cases is dependent upon the intensity o the patient’s ambivalent eeling toward his loss (love, possession) as well as upon the realistic circumstances o the loss. The term is synonymous with “reactive depression” and is to be diferentiated rom the corresponding psychotic reaction. In this diferentiation, points to be considered are (1) lie history o patient, with special reerence to mood swings (suggestive o psychotic reaction), to the personality structure (neurotic or cyclothymic) and to precipitating environmental actors and (2) absence o malignant symptoms (hypochondriacal preoccupation, agitation, delusions, particularly somatic, hallucinations, severe guilt eelings, intractable insomnia, suicidal ruminations, severe psychomotor retardation, proound retardation o thought, stupor).33 This definition o depressive reactions relied heavily on psychodynamic speculations about etiology to define depressive neuroses. The DSM-I not only conceived o depressive conditions as ways that people attempt to deend against underlying states o anxiety but also inused the definition o depression with dynamic assumptions that guilt and eelings o ambivalence were central components o the condition. Aside rom such etiological defining criteria, much o the definition was taken up with distinguishing psychoneurotic-depressive disorders rom psychotic-depressive disorders. The DSM-I’s definition o depressive reaction might appear tobe a historical anomaly in that it did not say a word about the distinction between disordered psychoneurotic-depressive reactions and normal reactions to circumstances. This lapse was more apparent than real, however, because the distinction was implicit, based in the DSM-I’s underlying psychodynamic etiological assumptions. Spelling out the distinction between normal and disordered depressive responses was superfluous precisely because the DSM-I relied on a theory o etiology to identiy disorders and to distinguish them, by implication, rom normal conditions in which the etiology is absent. The definition, in efect, specified the dysunctions o psychological mechanisms that caused the intensity o the sadness, including unwarranted guilt and sel-deprecation, intense ambivalence about the lost object, and the use o deense mechanisms (including depressive eelings) to avoid the natural anxieties that arise rom loss situations. These processes combined to lead to a depressive response that was not merely sadness that was proportional to any actual loss itsel (although the “current situation” and the DEPRESSION IN THE TWENTIETH CENTURY 87 “realistic circumstances o the loss” influenced the response’s intensity) butthat was, rather, an inflated, disproportionate “degree o reaction” due to the action o these internal psychological dysunctions. Note that the examples o the triggers o loss responses that might benormal—or, i there were ambivalence about the loss, disordered—are loss o love and o possessions, not bereavement. The DSM-I was the ofcial manual o the APA between 1952 and 1968. Its successor, the DSM-II, provides a much more succinct definition o “depressive neurosis,” as ollows: This disorder is maniested by an excessive reaction o depression due to an internal conflict or to an identifiable event such as the loss o a love object or cherished possession. It is to be distinguished rom Involutional melancholia and Manic-depressive illness. Reactive depressions or depressive reactions are to be classified here.34 The DSM-II implicitly recognized the distinction between depressions that were proportionateresponses to loss andthose that were “excessiv e” and thus disproportionate. The definition assumedhat t psychiatrists knew what symptomsconstituted depression and attemptedneither to speciy them nor to suggest that one could use symptoms to distinguish disorder rom nondisorder. Again, the definition relied on etiology, in the orm o internal conflict, to suggest internal dysunction, but the definition also recognized that losses may trigger a disproportionate, disordered reaction even inthe absence o internal conflict. The definition also noted normal triggers beyond the loss o a loved one, such as loss o a cherished possession. To some extent, theDSM-II definition was a return to the classic tradition osimply speciying disordered depression as a disproportionate, “excessive” response. In sum, 2,500 years o psychiatry held that normal human n ature included a propensity to potentially intense sadness ater certain kinds o losses. Disorder can be judged to exist, it was widely agreed, only when explanations in terms o triggering eventsail to establish a normal cause or the intensity or duration o symptoms. The major influences on psychiatric classification in the first hal o the twentieth century—Freud, Kraepelin, and Meyer and the early diagnostic manuals, such asDSM-I and II, that they influenced—disagreed on many things, but all explicitly or implicitly embracedthis understanding o depressive disorder. The Breakdown of the “With” and “Without” Cause Tradition The Post-Kraepelinians During the hal-century between about 1920 and 1970, the dominance o the psychodynamic views o Freud and the context-based views o Meyer ensured 88 THE LOSS OF SADNESS the general neglect o Kraepelin’s system o categorization, which assumed underlying physical etiologies. However, Kraepelin’s approach inspired some researchers, especially in the United Kingdom, to pursue an extensive agenda o research into classification o types o depression. Numerous empirical studies examined symptom patterns in an attempt to discover whether depression consisted o one or more distinct disorders. The work o the psychiatrist Aubrey Lewis was especially influential. In 1934 Lewis published a study o 61 patients treated at the Maudsley Hospital in London.35 He argued that the distinction between endogenous and reactive depressions was untenable because most supposedly endogenous depressions had external precipitating actors; also, a lietime o dispositions to depression preceded most reactive depressions. Lewis’s research seemed to confirm Kraepelin’s claim that almost all depression is one disorder, varying along a continuum o severity rom mild to severe but not diering by endogenous or reactive causes. A ew researchers, confirming Lewis’s contentions, ound that depressive symptoms were continuous, and they could not discern patterns that were sufciently robust to suggest diering underlying etiologies. This group, like Kraepelin, concluded that a rigid division between endogenous and reactive or neurotic and psychotic depressions was unjustified.36 Most researchers, however, rejected the notion that all orms o depression ell on a single continuum. Instead, they ound that endogenous or psychotic depression appeared to be a distinct type. The symptoms o psychotic depressions, which oten eatured hallucinations and delusions, did not correlate with the symptoms o other types o depressions and showed distinct responses to treatment;37 psychotic depressions seemed more responsive to both electroconvulsive treatment and the antidepressant drug imipramine and less responsive to placebo treatments than other depressed states.38 Eorts to distinguish psychotic depressions by their lack o environmental precipitants, however, were usually not successul.39 Instead, stressul lie events usually preceded the emergence o all sorts o depressions. Given the paucity o nontriggered depressions that were truly “without cause,” the term endogenous gradually came to reer to a phenomenological pattern o symptoms, not to a particular cause o symptoms. Psychotic or severe more accurately characterized the nature o this condition. Although researchers in this period generally came to agree that psychotic (or endogenous) depressions constituted one distinct type o depression, they could not agree on the nature o nonpsychotic depressions. Gradually, the use o neurotic prevailed over reactive because precipitating events in the environment provoked the great majority o all types o depression. Some concluded that 40 depression was binary, eaturing a neurotic type, as well as a psychotic one. Others elt that three or more distinct types o neurotic depressions existed, although they diered on both the number and the nature o these states.41 In contrast to the relatively homogenous symptoms ound in psychotic depressions, neurotic symptoms were heterogeneous and diuse across studies.42 Depending DEPRESSION IN THE TWENTIETH CENTURY 89 on the study, neurotic depression eatured some combination o symptoms that reflected helplessness, low sel-esteem, dysphoria, demoralization, anger, hostility, irritation, and disappointment reactions that resisted precise diagnostic schemes. For our purposes o understanding the roots o current diagnosis, the detailed content and substantive results o this post-Kraepelinian research program are not as significant as its methodology. Although no consensus emerged about the nature o depression rom empirical research regarding symptom patterns between 1920 and 1970, the studies did help pave the way or the subsequent revolution in psychiatric diagnoses because o the general approach they took to identiying depressive disorder. These researchers claimed to emulate Kraepelin, but their approach in act sharply diverged rom his. Empirical studies during this period relied on measuring only symptom presentations at a single point in time. Researchers largely set aside issues o course, duration, and, especially, the situational context o symptoms. In contrast, as we saw, Kraepelin rejected using symptoms in themselves to distinguish varying types o depression and emphasized instead the need to examine the course and prognosis o conditions as well as the importance o distinguishing between normal and disordered sadness on the basis o context. The symptom-based emphasis reflected the way researchers had exploited newly developed statistical methods, especially actor analysis, to analyze whether depression was a single illness or had multiple types. 43 Factor analysis attempts to distinguish various symptom clusters by examining the extent to which individual symptoms tend to occur together with other symptoms. There is no inherent, in-principle conflict between such statistical methods and the consider ation o the proportion ality o symptoms or the reasonableness o emotional reactions as part o what is statistically analyzed. In actual practice, however, the complexity that such judgments introduced led researchers to deviate rom the clinical tradition and rely on symptom patterns alone, without regard to either their context or course, to distinguish diferent types o depression. Based on the act that the clinical populations they studied were oten hospitalized and in any event generally clearly disordered and had already been diagnosed, researchers who relied on statistical techniques to isolate symptom patterns simply assumed, quite reasonably, that all the symptoms they entered into their models were maniestations o disorder in the sampled populations. But, as w e shall see, the kinds o clinical criteria that eventually emerged rom these symptom-based analyses came to be applied ar beyond the clearly disordered populations rom which they were derived to progressively broader groups in which the same symptoms might not mean the same thing. Lewis’s finding that most depressions ollowed some kind o triggering event made the decision to ocus on symptoms easier, because it suggested that perhaps context in the orm o “with cause” versus “without cause” was not so 90 THE LOSS OF SADNESS important ater all.44 However, Lewis’s research never explored the notion o the disproportionality o a response to the nature o the reported trigger, which was at the heart o the classic tradition. Moreover, Lewis’s study was o an inpatient, clearly disordered, sample, so it could not reveal diferences between the disordered and the nondisordered. The replacement o the “with cause” or “without cause” distinctio n by categories based on types o symptoms had especia lly dire consequences or misdiagnosis o normal individuals because o a major change in the nat ure o those treated or depression that was occurring at this time. Whereas Lewis’s inpatient sample reflected the standard clinical population o depressive patients early in the twentieth century, gradually over the course o the century outpatient psychiatric clinics became the most common settings or treatment or depression. Outpatients, however, presented a ar wider range o problems, including substant ial numbers o normal sadness states, than the more homogeneous groups o severely disordered inpatients that Kraepelin and Lewis studied. 45 “Psychiatrists today,” summarized psychiatrist Hagop Akiskal shortly beore the publication o the DSM-III in 1980, “are aced with a large number o individuals who are seeking help or poorl y defined states o psychic malaise and dysphoria that seem to dey urther characterization. . . . Hence the growing vagueness o neurotic depression is parallele d by its increasing clinical visibility.”46 Extending symptom-based diagnostic methods rom inpatient settings to ar more heterogeneous outpatient clinics, without the simple contextual distinctions used in the past to distinguish the normal rom the disordered, created the potential or unprecedented numbers o alse-positive diagnoses o depressive disorder. By the 1970s, a “hodgepodge o competing and overlapping systems” that contrasted psychotic and neurotic, endogenous and reactive, bipolar and unipolar, and many other types characterized the literature on depression. 47 Aside rom a consensus that psychotic (or endogenous) depressions were distinct rom neurotic states, there was virtually no agreement on the nature o nonpsychotic depressions. Researchers did not agree on whether nonpsychotic depressions were continuous or discontinuous with psychotic orms, on the one hand, or with normality, on the other. They disputed how many orms neurotic conditions took and even whether they had any distinct orms at all. Nor was it known whether some milder orms o depression were early indicators o eventual psychotic orms. In addition, little consensus existed about the particular symptoms that were essential to definitions o nonpsychotic orms o depression. Summarizing the situation in the United States and Great Britain in the mid- to late 1970s, physicians Christopher Callahan and German Berrios noted that “psychiatric diagnostic categories are at best subjective and probably irrelevant.”48 In 1980, responding to this period o conused debate characterized by the highly unsettled state o empirical findings and lack o definitive theory about the nature o non-psychotic depression, psychiatry would nonetheless DEPRESSION IN THE TWENTIETH CENTURY 91 adopt a definitive set o symptomatic criteria or depression that have remained stable until the present. Paving the Road to the DSM-III: The Feighner Criteria The proximate srcins o the DSM-III criteria lie in the work o a group o research psychiatrists at Washington University in St. Louis who elt that as long as the system o classification remained without precise definitions, there was no hope or psychiatry to become a scientific discipline. Led by two prominent psychiatrists—Eli Robins and Samuel Guze—the group was inspired by the neo-Kraepelinian research tradition o analyzing symptoms statistically, and they wanted to remedy the conusing and divergent definitions o disorders by diferent researchers. The St. Louis group emphasized the scientific importance o having agreed-on criteria that primarily used symptomatic presentations as the basis or research studies and diagnostic decisions. In 1972, based on discussions among the aculty regarding how to improve the diagnostic criteria that might be used in their research, a resident at Washington University, John Feighner, codified and published diagnostic criteria or 15 mental disorders, including primary and secondary afective disorders, in what came to be called the Feighner criteria.49 The Feighner criteria were not explicitly ormulated or everyday clinicaluse. Rather, they were an attempt to relieve researchers o the multiplicity o diferent imprecise definitions then in use and thus to make possible more cumulative, comparable, and reproducible research. The stated goal was a “common ground or diferent research groups. . . . The use o ormal diagnostic criteria by a number o groups . . . will result in a resolution o the problem o whether patients described by diferent groups are comparable. This 50 first and crucial taxonomic step should expedite psychiatric investigation.” The Feighner criteria divided primary afective disorders into two categories, depression and mania; we consider only the “depression” category. Diagnosis o depression required satisaction o three criteria. First, the patient must have dysphoric mood marked by symptoms such as being depressed, sad, despondent, or hopeless. Second, at least five additional symptoms must be present (i.e., a total o six or definitive diagnosis; our additional symptoms, or a total o five or probable diagnosis) rom among a list including loss o appetite, sleep dificulty, loss o energy, agitation, loss o interest in usual activities, guilt eelings, slow thinking, and recurrent suicidal thoughts. Finally, the condition must have lasted at least 1 month and not be due to another preexisting mental disorder. O people who met these symptomatic criteria, only those who had liethreatening or incapacitating medical illnesses were excluded rom the diagnosis o primary depressive disorder. One might have thought that this exclusion was based on the act that being intensely sad is oten a normal response to such illnesses. However, it turns out that these patients’ symptoms simply warranted 92 THE LOSS OF SADNESS a diferent diagnosis: that o secondary afective disorder. This category encompassed all conditions that met the same symptomatic criteria as primary disorders but that occurred with a preexisting nonafective psychiatric illness or a lie-threatening or incapacitating medical illness. Thus there were, in act, no exclusions rom disorder whatever or those who satisfied symptomatic criteria. The Feighner criteria or afective disorders difered in significant ways rom the criteria in prior empirical research on depression and, in some ways, were in tension with that research. First, all depressive conditions that did not have manic eatures and that were not preceded by other psychiatric or medical conditions were grouped into a single category. This system conormed to Kraepelin’s theory that depression was a unitary disorder but ignored the vast majority o empirical studies that suggested possible distinctions in depressive symptomatic profiles between psychotic unipolar (i.e., not involving mania) depressions and neurotic depressions. However, we have seen that the research was not conclusive and that no consensus existed about possible distinctions between types o depressive disorder. Where the Feighner criteria most unjustifiably deviated rom considered psychiatric judgment was in making no room at all or depressive reactions o more than 1 month in duration that stemmed rom normal loss responses, even including bereavement. The criteria did not allow or the possibility that some depressive symptoms were proportionate to their provoking causes even i they lasted a month, whereas others stemmed rom dysunctions. This set a crucial precedent or subsequent criteria sets that built on the Feighner work. Why the Feighner group ignored the obvious problem o normal sadness in their criteria remains unclear. One possibility is that, to ensure that researchers would widely use the criteria, they ervently strove to avoid any inerence about causation in their definitions; they might have concluded that the distinction between normality and disorder implied a particular etiological approach to classification.51 Another is that they developed the criteria with research samples whose members clearly had some disorder and assumed the criteria would generally be used with similar samples. Or perhaps they simply were ollowing the research tradition that immediately preceded them, which relied on statistical analysis o symptoms without regard to context. A urther possibility is that the Feighner group implicitly recognized the disordered—nondisordered-sadness distinction but assumed that intense sadness o more than 1 month’s duration is “prolonged” in Hippocrates’ sense and, i it involves the specified number o symptoms, is inherently disproportionate to any possible stressor and thus almost certainly disordered. I so, previous clin- ical observers did not accept this assumption, and it seems to conflict with the trajectory o normal response to major losses documented in chapter 2; even the DSM-III was to allow 2 months o normal symptomatic response to loss o a loved one. In any event, we will see that the DSM-III lowered this duration threshold to the much less plausible criterion o 2 weeks. In sum, unlike Kraepelin, Feighner DEPRESSION IN THE TWENTIETH CENTURY 93 and colleagues provide no background understanding o how to distinguish disorder rom nondisorder, nor do they state the need to evaluate whether those satisying depressive symptom criteria are indeed disordered. How did the Feighner group develop their influential criteria or depression? One o the ironies o psychiatric history is that the later justification or using the Feighner criteria’s symptom-based diagnostic categories as the model or the DSM-III was their claimed grounding in empirical research rather than in theoretical speculation.52 Yet, judging by the citations the article provides, the criteria or depressive disorder, at least, had little empirical support in the prior literature. The article reerences only our published articles as sources or the depression criteria. (A fith reerence cites an unpublished paper by Robins and Guze rom a workshop at the National Institute o Mental Health. In addition, the work gives six citations to publications on mania, which we do not consider here.) One reerenced article asserts that there is no evidence that the particular condition o involutional (i.e., postmenopausal) depressive syndrome is symptomatically distinguishable rom other depressive disorders (a question on which Kraepelin had vacillated), and it concludes with a challenge to the general adequacy o symptomatic criteria: “Attempting to group psychiatric patients into clinical entities by symptom pictures has been rustrating as it has never been clear where the dividing lines belong. This is a serious problem in psychiatry.”53 Two other reerences, coming out o a single research project, indicated that there was some tentative evidence or an endogenous actor that represented the core o depressive symptoms but that the symptoms o reactive depression were most likely to be “phenomenological maniestations o psychiatric disorders other than depression which ‘contaminate’ the depression syndrome.”54 The findings rom these studies, i anything, actually contradicted the Feighner criteria’s lumping o endogenous and reactive conditions. The final reerence explicitly rejected the use o purely symptom-based definitions o depression that do not embody considerations about the causes o symptoms and their normal versus pathological status: In classiying depressive states the first distinction to be made is between normal and pathological reactions. Mourning and grie reactions in general are normal reactions to the loss o a love object—this may be another person, money, the depressed individual’s prestige, his cherished hopes, his health—and it is not always possible to distinguish such normal grie reactions rom pathological depression on phenomenological grounds alone. A depression is judged to be pathological i there is insufcient spe- cific cause or it in the patient’s immediate past, i it lasts too long, or i its symptoms are too severe.55 o the citations that the Feighner article reerences or depression supports the assumption that purely symptom-based criteria can define depressive None 94 THE LOSS OF SADNESS disorders. These sources neither justiy nor even address the validity o the specific definition o aective disorders in the criteria. Soon ater the publication o the Feighner criteria, the Washington University psychiatrists Robert Woodru, Donald Goodwin, and Samuel Guze expanded their discussion o their new diagnostic criteria and their general approach to diagnosis in the first symptom-based psychiatric textbook, Psychiatric Diagnosis.56 The chapter on diagnosis o aective disorders emphasized the importance o observing and measuring symptoms without any etiological inerences because o the poor state o knowledge about the causes o depression. This principle perhaps partly explains why the Feighner criteria did not allow even bereavement to be excluded rom a diagnosis o depressive disorder. In a section on dierential diagnosis in the aective disorders, the text notes the ollowing reg arding bereavement (there is no discussion o other stressors): Making the distinction between grie and primary aective disorder can be difcult. However, grie usually does not last as long as an episode o primary aective disorder. . . . The majority o bereaved persons experience ewer symptoms than do patients with primary aective disorder. Furthermore, some symptoms common in primary aective disorder are relatively rare among persons experiencing bereavement, notably ear o losing one’s mind and thoughts o sel-harm.57 Supporting their points about the dierences between bereavement and depressive disorder, Woodru and colleagues cite several articles by psychiatrist Paula Clayton and her colleagues that document the type and duration o depressive symptoms occurring in bereavement.58 In act, Clayton ound that ater 1 month, which was the Feighner duration threshold or diagnosis o a disorder, about 40% o bereaved individuals display ull DSM-level symptoms. Yet there is little plausibility and no scientific evidence that such a large percentage o the bereaved become disordered. Given the enormous number o individuals who experience bereavement over time, the notion that a “majority” do not experience as many symptoms as the Feighner criteria require o the disordered at the 1-month mark, and the notion that “usually” bereavement at that intense level does not last as long as the Feighner’s 1-month requirement, there is no greatly reassuring evidence o its validity. Indeed, it seems to leave the door open to large numbers o alse positive diagnoses o the normally bereaved, an issue that goes unaddressed. The authors’ apparent assumption that a 1-month duration and fivesymptom threshold or “probable” disorder (six or “definite” diagnosis) was sufcient to discriminate disorder rom normal bereavement is unwarranted on the basis o the very studies that they themselves cite. In any event, the text oers no substantive new empirical support or the proposed criteria DEPRESSION IN THE TWENTIETH CENTURY 95 or depressive disorder, leaving the validity o the new criteria as empirically challengeable as beore. This text, now in its fith edition, was highly influential in shaping the subsequent DSM-III.59 Meanwhile, the Feighner criteria clearly served a need in the research community; by 1989, the article in which they appeared was the single most cited article in the history o psychiatry.60 Their widely influential definition o depressive disorder set the stage or psychiatry’s use o purely symptom-based diagnoses, despite the act that by nature this approach was incapable o distinguishing intense normal rom disordered responses. The Research Diagnostic Criteria Robert Spitzer was the major translator o the Feighner research criteria into what were to become the clinical diagnostic criteria o the DSM-III. The Research Diagnostic Criteria (RDC), which Spitzer created in collaboration with Eli Robins o the Washington University group and published in 1978, was the bridge between these two landmark achievements. 61 In conjunction with the RDC, Spitzer also developed one o the first structured interviews to measure depression, the Schedule or Afective Disorders and Schizophrenia (SADS), an early step toward the development o structured questionnaires that would later be used in epidemiologic studies that applied the new diagnostic approach beyond the clinic to community samples (see chapter 6).62 At the behest o the Nation al Institut e o Mental Hea lth (NIMH), Spi tzer and his colleagues developed the RDC to overcome concerns about the low reliability o psychiatric diagnoses and to create a more sophisticated typology o depression diagnoses. Like the Feighner criteria, the RDC were explicitl y aimed at acilitating research, but their clinical application was not hard to see. Building on the Feighner symptom-based approach, they expanded the 15 diagnoses o the Feighner criteria to 25 major types and many more subtypes o disorder. 63 The symptom criteria or Major Depressive Disorder in the RDC required an episode lasting at least 2 weeks, the presence o a prominent and persistent dysphoric mood or pervasive loss o interest or pleasure, five out o eight additional symptoms (our or a probable diagnosis), help seeking or impaired unctioning because o the disorder, and the absence o eatures that suggest schizophrenia. The major changes in the RDC rom the Feighner criteria were stipulations that pervasive loss o interest or pleasure could be substituted or dysphoric mood as a necessary condition (reflecting a growing view that loss o capacity or plea- sure is central to depression); that symptoms need only be present or 2 weeks instead o 1 month (an unexplained substantial reduction in required duration that potentially allowed or many more alse positive diagnoses o normal individuals but was to find its way into the DSM-III); and that the patient had to have either sought help rom someone or have impaired social unctioning 96 THE LOSS OF SADNESS (essentially an early orm o the later clinical significance criterion). A number o exclusion criteria that eliminated those with schizophrenia rom a depression diagnosis were also added, as were 11 subtypes o MDD. (The nonmutually exclusive subtypes o MDD, the srcinal motivation or NIMH’s interest, were primary, secondary, recurrent unipolar, psychotic, incapacitating, endogenous, agitated, retarded, situational, simple, and predominant mood.) Despite the lowering o both the duration and symptom thresholds rom the Feighner criteria to levels that would later be incorporated into the DSM-III, the RDC’s criteria or MDD contained no exclusions or bereavement or any other normal reaction, although they did require researchers to ascertain during their interviews with patients whether bereavement was present. 64 For reasons we consider in the next section, a major concern in constructing the RDC was reliability o diagnosis, that is, whether diferent diagnosticians would come to the same diagnosis based on the same inormation. Studies using the RDC indicated great overall success in achieving reliability. For Major Depressive Illness, the initial reports indicated the remarkable reliability o .97.65 Other reports indicated reliabilities o about .90.66 Many considered the apparent improvement o reliability to be a great advance, as the remarks o the noted diagnostician Alvin Feinstein indicate: The production o operational identifications has been a pioneering, unique advance in nosology. . . . In the field o diagnostic nosology, the establishment o operational criteria represents a breakthrough that is as obvious, necessary, undamental, and important as the corresponding breakthrough in obstetrics and surgery when Semmelweis, Oliver Wendell Holmes, and, later on, Lord Lister, demanded that obstetricians and sur67 geons wash their hands beore operating on the human body. We will see that Feinstein’s enthusiasm or Spitzer’s accomplishments reflects what was to become Spitzer’s greatest achievement, his shepherding o the creation o an entirely newpsychiatric clinical diagnostic classification system using the same principles as the RDC to ensure reliability. However, we sound a preliminary caution in anticipation o the discussion o the DSM-III: It is true that when symptoms alone are the basis or diagnoses, people can be trained to apply the criteria according to rules and thus to agree, and the reliability o diagnoses may well increase. But are the agreed judgments correct in identiying disorders (i.e., valid)? These studies did not assess thevalidity o the diagnosis in predicting course, response to therapies, or etiology odepressive conditions. Moreover, the RDC and the Feighner criteria did not involve any systematic attempt to distinguish normal intense sadness rom depressive disorder, casting urther doubt on the validity o these approaches. Introducing judgments about normal versus disordered reactions to circumstances into diagnostic criteria is challenging to do and would likely lessen reliability, but even so it might substantially enhance DEPRESSION IN THE TWENTIETH CENTURY 97 validity. To this day, we shall see, psychiatry has not adequately addressed this challenge. The DSM-III as a Response to the Challenges Confronting Psychiatry The publication o the DSM-III in 1980 is justifiably viewed as a watershed in the history o psychiatric diagnosis.68 Yet the revision o the DSM-II was not seen beorehand as particularly important, and there was no political jockeying rom advocates o dierent theoretical perspectives to be in control o the process. Spitzer’s work on the committee charged with revising the DSM-II, his prominent role in brokering the removal o homosexuality rom that manual, and his development o the RDC criteria led to his appointment as chair o the DSM-III task orce. Spitzer used the opportunity to create a new kind o diagnostic system that reflected previous decades o thought about how to make psychiatry more scientific.69 The DSM-III revolution directly incorporated many o the eatures o the Feighner criteria and RDC into the ofcial psychiatric nosology and specifically embraced symptom-based diagnostic criteria. Spitzer himsel recognized that the translation o research criteria into a manual or clinical use required that the diagnostic criteria must reflect “clinical wisdom” as well as evidence rom research.70 His role required not only the skills o a knowledgeable researcher but also those o a master politician attempting to molliy and to find compromise among various clinical constituencies that elt that the new symptom-based system threatened their traditional diagnostic practices. But what motivated Spitzer to borrow so heavily rom the RDC-style symptom-based definitional approach to diagnosis in revising the DSM? And why did clinicians, who are concerned with treating individuals and have little interest in reliable classification systems or research, accept the symptom-based classification system that had emerged rom the Feighner criteria and RDC? It turns out that the new system addressed several major problems that clinicians, as well as researchers, aced at the time. By the 1970s, psychoanalytic influence had waned. The psychiatric proession was divided into numerous theoretical schools, and dierent clinicians shared ew assumptions about the undamental nature, causes, and treatments o mental disorders. The new diagnostic manual, thereore, had to be serviceable or clinicians o many varying perspectives. The lists o explicit symptoms in the DSM-III not only improved reliability but also were theory neutral in the sense that they did not presuppose any particular theory o the cause o psychopathology, psychoanalytic or otherwise. The new criteria were descriptive rather than etiological and purged reerences to postulated psychodynamic causes o a disorder (e.g., internal conflict, deense against anxiety). Defining disorders on the basis o symptoms, regardless o etiology, turned out to be a useul tool in gaining the acceptance o clinicians 98 THE LOSS OF SADNESS o varying allegiances who could at least eel that all actions were on a level playing field in using the theory-neutral definitions. Moreover, psychiatric diagnoses were under attack rom a variety o sources. Behaviorists claimed that all behavior, including psychopathology, is the result o normal learning processes and thus that no mental disorders in the medical sense really exist.71 The “antipsychiatry” movement, inspired by writers such as psychiatrist Thomas Szasz and sociologist Thomas Schef, portrayed psychiatric diagnosis as a matter o using medical terminology to apply social control to undesirable but not truly medically disordered behavior.72 In addition, by 1980 private and public third parties were financing most medical treatment.73 The murky unconscious entities o the DSM-II and the erosion o psychiatry’s medical legitimacy did not provide a solid basis or insurance reimbursement. Although no evidence indicates that insurers influenced the development o the symptom-based disorders o the manual, the new diagnoses provided a better fit with the goal o third parties to reimburse the treatment o only specific diseases. On reflection, clinicians may not have agreed with some eatures in the new manual, such as the abandonment o contextual criteria, but they realized that the new system had many benefits or them. Most pressing o all was an erosion o the credibility o psychiatry due to attacks on the meaningulness o diagnosis. Although he had psychoanalytic training, Spitzer, like the St. Louis group, saw unverified theory and resistance to empirical testing as the major obstacles to psychiatry’s attaining scientific status.74 The central element in Spitzer’s vision o psychiatry, pursued in his prodigious research eforts in the 1960s and 1970s and culminating in the DSM-III in 1980, was the development o a reliable system o classification in which dierent diagnosticians would generally arrive at the same diagnosis based on the same clinical inormation.75 Because the DSM-II did not provide specific symptoms that determined psychiatric diagnoses, psychiatrists were orced to use their own clinical judgments in assessing how well each patient fit a particular diagnosis. This led to great disparities in the application o diagnostic labels. For example, the well-known U.S.-U.K. Diagnostic Project, the results o which were published in 1972, studied the ways that psychiatrists in these two countries diagnosed mental disorders. The study demonstrated an alarming lack o agreement between American and British psychiatrists and among psychiatrists within each group. For example, more than five times as many British as American psychiatrists made diagnoses o depressive disorders.76 In addition to the U.S.-U.K. study, a great number o studies generally showed remarkable lack o diagnostic agreement in cases in which psychiatrists received the same inormation (e.g., a videotaped clinical interview).77 These studies challenged the reliability not only o distinguishing closely related diagnostic categories, such as one afective disorder rom another, but also o distinguishing between larger categories, such as afective versus anxiety disorders, and DEPRESSION IN THE TWENTIETH CENTURY 99 between overall types o disorder, such as psychosis versus neurosis or even psychosis versus normality. Perhaps the most dramatic and influential such study, now seen as a landmark in the critique o psychiatric diagnosis, directly challenged the ability o psychiatrists to distinguish normality rom psychosis. In 1973, psychologist David Rosenhan published a study in the prestigious journal Science in which eight normal individuals presented themselves at hospitals and reported only auditory hallucinatory symptoms (they claimed to hear a voice saying things like “thud,” “dull,” and “empty”), otherwise acting and speaking normally. All o these pseudo-patients were admitted and classified as psychotic (almost all as schizophrenic), and they remained so classified or various periods o time, even though they immediately reverted to normal behavior. Hospital residents, however, did identiy several pseudo-patients as likely normals. To get the flavor o the views prominent at the time, consider a ew o sentences in the introduction to Rosenhan’s article: Normality and abnormality, sanity and insanity, and the diagnoses that flow rom them may be less substantive than many believe them to be. . . . Based in part on theoretical and anthropological considerations, but also on philosophical, legal, and therapeutic ones, the view has grown that psychological categorization o mental illness is useless at best and downright harmul, misleading, and pejorative at worst. Psychiatric diagnoses, in this view, are in the minds o observers and are not valid summaries o characteristics displayed by the observed.78 Based on his results, Rosenhan concluded: “It is clear that we cannot distinguish the sane rom the insane in psychiatric hospitals.” The threat o such gross invalidity and, by implication, unreliability (or surely Rosenhan’s participants would, under other circu mstances, have been judged normal) was not only an acute embarrassment to clinical expertise but also a challenge to the scientific status o psychiatry. Spitzer himsel wrote a scathing critique o 79 the methodological flaws in Rosenhan’s study. However, such a critique could show only that Rosenhan had not proved his claim that psychiatric diagnosis is by its nature flawed; it could not demonstrate that psychiatric diagnosis, in act, had an adequately reliable diagnostic system. Much o Spitzer’s subsequent efort was to be devoted to the project o creating and nurturing such a system. Although acknowledging that a reliable system is not necessarily valid, Spitzer emphasized that validity requires reliability. A valid diagnostic system would categorize diferent syndromes accurately and thereby ought to predict course and response to treatment.80 But i diferent diagnosticians could not even agree on the diagnosis, then clearly many o their diagnoses must be inaccurate, and there must be low overall diagnostic validity. Moreover, without reliability o diagnoses across settings, cumulative research could not proceed 100 THE LOSS OF SADNESS efectively. Thereore, the primary goal o the psychiatric proession had to be the development o a clear system o diagnostic rules that specified inclusion and exclusion criteria or each diagnosis and promoted a high degree o interjudge agreement. Even i lacking in validity, such a reliable system could provide a scientifically adequate starting place rom which researchers could bootstrap themselves to a more valid system. However, as many concerned critics pointed out, just creating a reliable system that has clear rules that everybody can ollow does not ensure even an approximation o validity; unless the rules are accurate, the reliability might just represent everybody together getting the same wrong answer!81 For example, i symptoms o intense sadness are used to indicate depressive disorder, such symptoms might be identified reliably, but the vast majority o conditions so recognized might not, in act, be disorders. The field trials conducted beore the publication o the DSM-III, in which hundreds o psychiatrists had tested the empirical adequacy o the diagnoses, did not compare the efectiveness o symptom-based criteria sets with other alternative ways o conceptualizing depression.82 They tested only whether diferent psychiatrists could use the criteria in the same way but did not establish whether they were valid indicators o disorder. As one o Spitzer’s collaborators notes: “pathologic conditions (were) redefined before empiric investigation (was) conducted.”83 And it is ar rom certain that such a system, i seriously invalid to begin with, would automatically evolve into a valid system. The implication is that considerations o validity cannot be entirely placed on the back burner while issues o reliability are resolved; both must be pursued together, and the two must inorm each other in order to approach more reliable judgments that are also valid. Between psychiatry’s theoretical ragmentation, its diagnostic unreliability, and the antipsychiatry critique, not only psychiatry’s claim to scientific status but even its legitimacy as a medical field seemed in jeopardy. The specific criteria o the DSM-III appeared to meet these challenges and place the field on a more sound scientific ooting. In one ell swoop, Spitzer’s incorporation o symptombased operational definitions o disorders into the DSM managed to conront a range o challenges to psychiatry and to acilitate an about-ace in psychiatry’s status and ortunes, especially coinciding as it did with the advent o new medications that were also bolstering the status o the psychiatric proession. But even a justified revolution has some unwarranted casualties. Having considered the nature and reasons or the DSM-III revolution in general, we now turn to the DSM-III criteria or depressive disorder. DSM-III The ’s Approach to Depressive Disorder The DSM-III criteria or depression almost completely mirrored the approaches o the Feighner and RDC criteria (the next chapter discusses in detail the similar DEPRESSION IN THE TWENTIETH CENTURY 101 DSM-IV criteria). They used symptoms to speciy depressive disorder and aban- doned or demoted etiological concepts, as well as traditional distinctions such as neurotic versus psychotic and endogenous versus reactive as a basis or dierent categories o diagnosis. Like the Feighner criteria and RDC, as well as earlier DSMs, the DSM-III rejected Kraepelin’s unification o manic-depressive insanity and depression, instead distinguishing unipolar depressive disorder, or “major depression,” rom “bipolar” disorders. Although this remains an active area o controversy, amily studies, clinical observations, and distinct patterns o medication responses had all served to thoroughly undermine Kraepelin’s grand unification o afective disorders long beore the DSM-III. Moreover, although MDD covered psychotic depression, it was understood that such conditions comprised only a small minority o those alling under the criteria; “simple depression” had come to be the predominant orm o depression o concern in the manual. Likewise, the DSM-III abandoned the DSM-II distinction between “excessive” versus proportionate reactions to an “identifiable event such as the loss o a love object or cherished possession.” This is surprising given that many other categories o disorder in the DSM-III, such as some anxiety disorders, use qualifiers such as “excessive” or “unreasonable” to separate disorders rom normal responses. Yet the DSM-III distinguishes depressive disorders solely on the basis o symptoms regardless o their relationship to circumstances, with the single exception o the bereavement exclusion. The logic behind the bereavement exclusion, which represents a major improvement over the Feighner criteria and RDC, is that states o grie that otherwise meet symptomatic criteria are not disorders because they represent normal and transient responses to loss. The exclusion seems to have resulted rom the work o Paula Clayton, a prominent member o the Washington University group and o the DSM-III Task Force on Afective Disorders. Her work had shown that depressive-like symptoms commonly arose during periods o bereavement but that they usually remitted ater a airly short time. 84 As we noted earlier, Woodruf, Goodwin, and Guze mentioned Clayton’s work but did not incorporate it into their diagnostic criteria or depression. The DSM-III did incorporate Clayton’s findings in developing the bereavement exclusion , but did not apply the exclusio n to the reactions to any other types o loss that may have the same eatures as bereavement, such as reactions to marital dissolution, ill health, or financial reversal. So ar as we can ascertain, reactions to other stressors simply never came up or discussion by the DSM-III afective disorders work group as a possible basis or exclusions. 85 The lack o such exclu- sions seems to have be en a by-product o deriving the DSM-III criteria rom the exclusionless Feighner and RDC criteria and the symptom-oriented diagnostic spirit o the DSM-III efort. Various reasons have been cited to justiy the DSM’s ailure to allow exclusions rom major depression or normal situations other than bereavement. For 102 THE LOSS OF SADNESS one thing, such exclusions could pose a serious challenge to reliability; other stressors oten lack the relatively clear-cut nature o bereavement, and it would be more difcult to measure their magnitude and to judge their proportionality to the resulting response. However, as we have noted, it makes no sense or reliability to trump validity in constructing diagnostic criteria. In any event, the ramers o the DSM-III, in creating criteria or “complicated” bereavement, discussed in the next chapter, showed that it is possible to reflect such subtle distinctions within a given stressor type. Similar eorts could have been made to provide guidelines or when reactions to other major stressors represent normal versus disordered reactions. The question o whether sadness is a proportionate response to real loss is sometimes argued to be an etiological issue that has no place in a theory-neutral 86 manual. But this objection is based on conusion about the nature and point o theory neutrality. The distinction between normal, proportional responses to events and disorders in which sadness derives rom an internal dysunction is not really a theory-laden distinction in the sense relevant to the DSM-III’s need or theory neutrality. Dierent theories oer dierent accounts—whether biological, psychodynamic, behavioral, cognitive, or social—o the nature and etiology o the dysunction that underlies depressive disorder, and a theory-neutral manual must not accept one theory over another as part o the definition o the disorder. It can, however, acknowledge that all etiological theories share the notion o normal, proportional responses versus dysunction-based responses. Ater all, medical thinkers rom Aristotle to Kraepelin understood this notion in more or less the same way, and it identifies the common target that rival theories attempt to explain. This distinction is not an etiological hypothesis o the kind that a theory-neutral manual needs to exclude. Another objection to considering the broader contexts o depressive responses in the DSM-III might have stemmed rom the impression that psychotropic medication worked on all unipolar depressions, irrespective o the relation to triggering events, so that the “with cause” versus “without cause” distinction was irrelevant to treatment decisions, at least among hospitalized depressives.87 However, even i medication sometimes works with normal reactions, the normality-versus-disorder distinction can have important prognostic implications or how aggressively to treat a condition and or deciding what kinds o treatments or changes in circumstances might help. Analogously, the act that, say, Ritalin works on normal and disordered individuals alike to make them more ocused, or that growth hormone makes both normal and disordered short children taller, does not imply that diagnosis can justifiably ignore the distinc- tion between normality and disorder. Finally, theDSM-III’s ignoring o normal states o intense sadness might have reflected a ear o misdiagnosing the truly disordered as normal, especially giv en that depressed patients are subject to suicide risk. Yet no eort was made to balance the risks o alse negatives with the costs o alse positives that arise rom DEPRESSION IN THE TWENTIETH CENTURY 103 labeling normal people as disordered, acost that is clearer today with the growing apprehension about the possible negative side efects o antidepressive medication and o other treatments or normal sadness, including potentia l increased suicide 88 risk in some populations. Major psychiatric theoreticians prior to theDSM-III elt that it was important to identiy normal cases o sadness and to distinguish them rom depressive disorders, orgood reason. Rather than entirely and unnecessarily ignoring a distinction, it ismore prudent to simply use it when helpul but exercise caution so as to err on the side o saety in applying the distinction. Conclusion DSM-III The ’s largely decontextualized, symptom-based criteria stemmed rom eforts to enhance reliability, to develop a common language or psychiatrists with a variety o theoretical persuasions, and to bolster the scientific credentials o the proession. But in the urgent quest or reliability, the criteria or the most part inadvertently rejected the previous 2,500 years o clinical diagnostic tradition that explored the context and meaning o symptoms in deciding whether someone is sufering rom intense normal sadness or a depressive disorder. The unwitting result o this efort, especially as psychiatry turned rom the serious conditions o inpatients to the ar more heterogeneous conditions o outpatients and community members, was to be a massive pathologization o normal sadness that, ironically, can be argued to have made depressive diagnosis less rather than more scientifically valid. 5 Depression in the DSM-IV e claimed in chapter 1 that a flawed definition may be acilitating the recent surge in reported depressive disorder and may even lie at its very heart. To justiy our claim, we now turn to a detailed examination o the DSM criteria or depressive and related disorders. Although the history o depression presented in the preceding chapter logi cally takes us up to the DSM-III, in order to ensure that our discussion applies to current diagnostic practices, we address the criteria presented in the latest edition—the ourth, text-revised edition DSM-IV-TR (2000). This does not represent much o a conceptual leap because the current criteria are almost identical to those W in the DSM-III. DSM-IV Afective Disorders We start by placing theDSM criteria or Major Depressive Disorder (MDD) in the context o the DSM’s approach to afective disorders, also known as mood disorders, the larger category under which depressive disorders all. The ollowing distinctions are useul to keep in mind: Unipolar Versus Bipolar Mood Disorders MDD is “unipolar” depression, which means that the individual has only depressive symptoms rather than oscillating back and orth between depressive and manic symptoms such as elevated mood and grandiosity. Mood disorders that include manic episodes are known as Bipolar Disorders (ormerly manicdepressive disorders), which are relatively rare compared with the claimed rates o unipolar depressive disorder. Bipolar I Disorder is oten quite severe; milder orms include Bipolar II Disorder and Cyclothymic Personality Disorder. None o these orms o bipolar disorder is the ocus here. 104 DEPRESSION IN THE DSM-IV 105 Major Depressive Disorder Versus Dysthymia MDD generally occurs over time in a series o quasi-discrete symptomatically intense episodes separated by intervals without symptoms or with ewer symptoms. Another, less common orm o depressive disorder is Dysthymia, which occurs more or less continuously or long periods o time at a less intense level and which is discussed later in this chapter. Major Depressive Disorder Versus Major Depressive Episode The DSM defines various subtypes o MDD (e.g., single episode, recurrent) based on the pattern o occurrences o what it calls Major Depressive Episodes (MDE) plus some additional criteria. In act, it is in the criteria or MDE that most o the diagnostic “action” occurs; the criteria or MDD itsel are brie and not very inormative: Criteria for Major Depressive Disorder A. Presence o a Major Depressive Episode. B. The Major Depressive Episode is not better accounted or by Schizoafective Disorder and is not superimposed on Schizophrenia, Schizophreniorm Disorder, Delusional Disorder, or Psychotic Disorder Not Otherwise Specified. C. There has never been a Manic Episode, a Mixed Episode, or a Hypomanic Episode.1 In other words, the criteria or MDD simply require that the patient experience at least one Major Depressive Episode, and that the episode is not part o some other psychotic disorder (note that psychotic symptoms can be part o the depression as long as they cannot be better explained as indicating some other psychotic disorder) and is not part o another kind o mood disorder containing manic elements. However, almost all depressive episodes are indicative o MDD and are not part o some other disorder. Thus, in the vast majority o cases, the criteria or MDD essentially come down to the criteria or MDE. We thus examine the much more inormative definition o MDE at some length. DSM-IV Criteria for Major Depressive Episode A. Five (or more) o the ollowing symptoms have been present during the same 2-week period and represent a change rom previous unctioning; at least one o the symptoms is either (1) depressed mood or (2) loss o interest or pleasure. 106 THE LOSS OF SADNESS 1. Depressed mood most o the day, nearly every day, as indicated by either subjective report (e.g., eels sad or empty) or observation made by others (e.g. appears tearul). Note: In children and adolescents, can be irritable mood. 2. Markedly diminished interest or pleasure in all, or almost all, activities most o the day, nearly every day (as indicated by either subjective account or observation made by others). 3. Significant weight loss when not dieting or weight gain (e.g., a change o more than 5% o body weight in a month), or decrease or increase in appetite nearly every day. Note: In children, consider ailure to make expected weight gain. 4. Insomnia or hypersomnia nearly every day. 5. Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective eelings o restlessness or being slowed down). 6. Fatigue or loss o energy nearly every day. 7. Feelings o worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely sel-reproach or guilt about being sick). 8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others). 9. Recurrent thoughts o death (not just ear o dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan or committing suicide. B. The symptoms do not meet criteria or a Mixed Episode. C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas o unctioning. D. The symptoms are not due to the direct physiological efects o a substance (e.g., a drug o abuse, a medication) or a general medical condition (e.g., hypothyroidism). E. The symptoms are not better accounted or by Bereavement, i.e., ater the loss o a loved one, the symptoms persist or longer than 2 months or are characterized by marked unctional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.2 Anyone reporting at least five o the nine symptoms in criterion A, including at least one o depressed mood or loss o interest or pleasure, or a 2-week period is considered to have Major Depressive Episode and thus, generally, MDD. Note that even or those satisying the symptom criteria, there are the our exclusions in Criteria B through E, eliminating the ollowing rom diagnosis: (1) conditions that also include manic symptoms, which are classified under bipolar disorders; (2) conditions that do not cause clinically significant role impairment or DEPRESSION IN THE DSM-IV 107 distress; (3) conditions that are the direct result of a general medical condition or use of either an illegal substance or prescribed medication; these are diagnosed as Mood Disorder Due to General Medical Condition or Substance-Induced Mood Disorder; or (4) conditions that stem from bereavement, unless the grief has lasted longer than 2 months or involves certain particularly severe symptoms; this is considered a case of “complicated bereavement.” How the DSM Criteria for Major Depression Address the Distinction Between Disorder and Normal Sadness Symptom and Duration Criteria The DSM-IV tries to exclude normal depressive conditions from diagnosis as disorders via the various features of its symptom criteria: (1) its five-symptom threshold for the diagnosis sets a higher threshold than many normal periods of sadness would meet; (2) the specific nature of some of the individual symptoms might inherently suggest pathology , as in feelings of worthlessness, psychomotor retardation, or recurrent thoughts of death; (3) the required duration of 2 weeks, during which five symptoms must cluster together, eliminates shorter periods or sporadic individual symptoms experienced discontinuously over time; and (4) the required severity, intensity, and frequency of the symptoms during at least the 2-week minimal duration—for example, that they must occur “nearly every day” during a 2-week period, be “marked” or “significant,” or featureother benchmarks such as a percentage weight loss—also eliminates many milder forms of normal sadness. There is no question that these features of the symptom criteria do eliminate many episodes of normal sadness from being mistakenly classified as disorders. However, such strategies for distinguishing disordered from normal responses have two disadvantages. First, increases in the symptomatic threshold for diagnosis in order to eliminate false positives can often inadvertently increase false negatives, by which genuine disorders go unrecognized. The disordered status of a condition is not a matter of the number of symptoms because mild disorders with a limited number of symptoms can exist. Second, although the occurrence of a greater number of symptoms is generally more harmful, it is not always the case that more symptoms, more severe symptoms, or more prolonged symptoms imply dysfunction and disorder. As chapter 2 documented, unusually harsh environmental stressors often produce many intense symptoms in otherwise normal individuals, and the depressive symptoms that occur during normal periods of sadness are generally similar to the depressive symptoms listed in the DSM criteria that occur during depressive disorders. Moreover, some people are temperamentally more sensitive and have more severe normal responses to stress than others. 108 THE LOSS OF SADNESS Thus setting high symptom thresholds in terms o number, intensity, or continuity over a 2-week period does not eectively address the dysunction problem—that is, the problem o distinguishing whether the symptoms are part o a normal sadness reaction or are the result o a dysunction o sadnessgenerating mechanisms. Intense normal sadness in response to a variety o major losses can easily include the five symptoms the DSM requires, such as low mood, lack o pleasure in usual activities, sleeplessness, lack o appetite, and difculty concentrating on usual tasks. Nor is the required severity o the DSM symptoms, specified in some cases by qualifiers such as “recurrent,” “marked,” or “diminished,” generally o such a distinctive level that it would characterize disordered rather than intense normal sadness responses. Likewise, the 2-week duration does not adequately distinguish potentially normal-range intense reactions to serious losses, such as the end o a marriage or a potentially terminal medical diagnosis, rom depressive disorders. Normal reactions to major losses can easily last more than 2 weeks. Certainly, the severity o the symptoms themselves, having five o them, and experiencing them almost every day during a 2-week period does oer a stark contrast to usual unctioning and thus may seem on first glance to impart validity. But when the contrast is between depressive disorder and periods o intense normal sadness in response to major losses, normal sadness can easily meet these requirements. Moreover, many o the symptoms, such as difculty sleeping and atigue, have very high base rates in the general population in response to a variety o stresses and are not at all distinctive o depression, normal or disordered, or even o disorder in general. Thus individuals without a depressive disorder might accidentally reach the threshold due to the presence o unrelated symptoms during a period o normal low mood. It is true that some symptoms, such as complete immobilization, a morbid and unjustified preoccupation with one’s worthlessness, hallucinations, and delusions, do not significantly overlap with normal unctioning. These symptoms might generally indicate dysunctions rather than designed sadness, especially i persistent. However, the diagnosis o MDD does not require the presence o such especially severe symptoms. Exclusion for Bereavement One way in which the DSM attempts to make up or any weaknesses in the symptom criteria’s ability to distinguish disorder rom nondisorder is through the exclusion clauses. This is the main purpose o the bereavement exclusion. However, like every other mental or physical unction, grie can “go wrong” and become disordered. For this reason, the bereavement exclusion has its own exclusion-tothe-exclusion that allows depressive symptoms associated with grie sometimes to be classified as true disorders ater all. This occurs when grie responses persist or longer than 2 months, cause marked unctional impairment, or include DEPRESSION IN THE DSM-IV 109 especially severe symptoms, such as morbid preoccupation with worthless3 ness, suicidal ideation, psychomotor retardation, or psychotic symptoms. (It is also worth noting that during bereavement transienthallucinations o a lost loved one’s presence are not uncommon, and they are not generally considered pathological.) One might dispute the 2-month limit on normal bereavement, and one might argue that normal bereavement may sometimes include one o the “complicated” symptoms that the DSM says are sufcient or disorder. However, by ar the major flaw in this exclusion criterion is its ailure to take into account normal sadness responses to any losses other than the death o a loved one. It would have been easy to generalize the bereavement exclusion clause (and its accompanying exclusion-to-the-exclusion criteria) to cover all severe losses, but this opportunity was oregone, or reasons explored earlier. Consequently, this constructive attempt to validly delineate the normally sad rom the disordered is too limited to adequately address the glaring weaknesses in the symptomatic criteria. Exclusion for General Medical and Substance-Use-Induced Depressions The exclusion rom MDD diagnosis o depressive conditions that directly result rom the physiological eects o medical conditions or substance use simply shits such cases into alternative disorder categories o Mood Disorder Due to General Medical Condition or Substance-Induced Mood Disorder. These categories, although not our ocus here, are subject to their own potential conusions. For example, such disorders are sometimes conused with normal sadness responses to having a medical condition or with sadness in response to the problems that result rom using or being addicted to a substance. This is an instance o the complex challenges practitioners ace in separating symptoms that indicate depression rom similar symptoms that are not disordered or that are the result o dierent disorders. The Clinical-Significance Requirement Perhaps the most important attempt in theDSM’s exclusion clauses to distinguish disordered rom normal sadness responses is the “clinical significance” criterion, which requires that “the symptomscause clinically significant distress orimpairment in social, occupational, or other important areas ounctioning.” This clause implicitly acknowledges that even nonbereaved cases that satisy theduration and symptom criteria might still not involve disorder. However, the clause does not address the basic validity problems o the MDD criteria. It was meant to ensure that the negative consequences o a condition exceed a threshold o significance i the condition is to be clinically relevant and thus potentially classifiable asa disorder, 110 THE LOSS OF SADNESS and it does this successully. But it does not recognize some crucial distinctions. First, periods o sadness in general,whether normal or disordered, inherently entail negative emotions that involve distress. Indeed, it is hard to imagine having five o the specified symptoms without experiencing distress. Second, intense normal loss responses almost always involve impairment and diminished interest and ability in various areas o unctioning; the very prototype o these responses involves social withdrawal and wanting to be let alone (e.g., one does not eel like seeing riends or going to work). Indeed, intense normal loss responses may be designed to cause distress and social withdrawal to enable one to avoid threats and reconsider one’s lie and goal structure (see chapter 2).4 Thus the clinical-significance exclusion might eliminate rom the disorder category a ew conditions whose eeble symptoms occasion no harm. But it is likely to be used quite rarely because the listed symptoms themselves already involve obvious orms o distress and impairment, rendering the requirement o distress or impairment virtually redundant 5 The clinical-significance criterion ails to resolve the problem o distinguishing normal rom disordered conditions that satisy DSM criteria because, like the symptom and duration criteria, it potentially applies to both kinds o conditions and ails to address the question o dysunction. Nor is the addition o the qualifier “clinically significant” helpul in making the distinction clearer because the qualifier is let undefined. Thus the phrase can mean only “significant enough to . indicate a clinical—that is, disordered—condition,” making the criterion circular with respect to distinguishing normal rom disordered conditions. Implications of the DSM’s Own Definition of Mental Disorder Interestingly, our claim that there is a flaw in theDSM’s definition o Major Depressive Disorder with respect to distinguishing disordered rom normal sadness appears to be implicit in the text o the DSM itsel. The DSM’s preace contains a brie general definition o mental disorder that is supposed to be used to determine which conditions are allowed into the manual in the first place. The DSM-IV’s definition o mental disorder reads as ollows: In DSM-IV, each o the mental disorders is conceptualized as a clinically significant behavioral or psychological syndrome or pattern that occurs in an individual and that typically is associated with present distress (e.g., a painul symptom) or disability (i.e., impairment in one or more impor- tant areas o unctioning) or with a significantly increased risk o sufering death, pain, disability, or an important loss o reedom. In addition, this syndrome or pattern must not be merely an expectable and culturally sanctioned response to a particular event, or example, the death o a loved one. Whatever its srcinal cause, it must currently be considered a DEPRESSION IN THE DSM-IV 111 manifestation of a behavioral, psychological, or biological dysfunction in the individual. Neither deviant behavior (e.g., political, religious, or sexual) nor conflicts that are primarily between the individual and society are mental disorders unless the deviance or conflict is a symptom of a dysfunction in the individual, as described above.6 This definition commendably distinguishes disordered from nondisordered conditions in terms of the presence of internal dysfunction, albeit in a cursory way, without attempting to explain the concept of dysfunction. Given that this is a general definition of the concept of disorder that should apply to each of the manual’s categories, it follows that the sets of diagnostic criteria for particular disorders presumably should meet the general rule that only dysfunctioncaused symptoms should count as disorders. However, neither theDSM-III nor later editions of the manual ever made a systematic attempt to rectify the diagnostic criteria with the general definition of mental disorders. This is unfortunate because it appears that in many instances the definition is more valid than the specific diagnostic criteria sets are. The definition of mental disorder, which relies on the distinction between symptoms that emerge because of a dysfunction in the individual rather than because of socially expectable or undesirable conditions, is quite similar in some important respects to the “harmful dysfunction” account of disorder that forms the background for our discussion.7 In particular, the DSM definition seems to indicate that even conditions that manifest certain symptoms may not be disorders, because the presence of a disorder depends on whether the symptoms result from a dysfunction. The definition also usefully asserts that a condition cannot be considered a disorder sheerly on the basis of its personal or social undesirability, even if there is distress or impairment or other harmful symptoms. Rather, the condition is a disorder only if a dysfunction in the person causes the symptoms. But, according to this definition, it would seem that a person reacting to external stressful events in the way we naturally react, namely, with certain emotional and other reactions of the kind the DSM’s symptom list for depressive disorder partly describes, does not have a dysfunction and thus does not have a disorder. Consequently, the DSM’s own definition of disorder, combined with the most plausible account of “dysfunction” as failure of natural function, implies that the criteria for MDD are invalid because they misclassify intense but naturally selected loss responses as disorders. The Precedent of Conduct Disorder It may seem impossible that the expert diagnosticians who formulated the diagnostic criteria in the DSM could arrive at criteria that are not only invalid but also inconsistent with DSM’s own stated definition of disorder. However, 112 THE LOSS OF SADNESS clinical diagnosis is a quite dierent task rom conceptual analysis o the defining criteria that separate disorder rom normality. The two require dierent skills (just as, or example, recognizing chairs when you see them is very dierent rom ormulating a principled definition o the concept “chair” that picks out all and only chairs), and it is thus possible or such errors to enter into the manual. Consider an acknowledged precedent: the DSM-IV text itsel states that the criteria or an important disorder o childhood and adolescence, Conduct Disorder (i.e., a disorder o antisocial behavior, diagnosed by three or more out o a list o behaviors such as thet, running away, etc.), are invalid and encompass some conditions that should not be diagnosed as disorders despite their satisying the diagnostic criteria. The problem, the DSM-IV inorms us, is that the symptomatic antisocial behaviors used to diagnose Conduct Disorder may occur in some conditions that are not due to a psychological dysunction but only to a normal reaction to difcult environmental circumstances. Here is what the DSM-IV has to say about its own Conduct Disorder criteria: Concerns have been raised that the Conduct Disorder diagnosis may at times be misapplied to individuals in settings where patterns o undesirable behavior are sometimes viewed as protective (e.g., threatening, impoverished, high-crime). Consistent with the DSM-IV definition o mental disorder, the Conduct Disorder diagnosis should be applied only when the behavior in question is symptomatic o an underlying dysunction within the individual and not simply a reaction to the immediate social context. Moreover, immigrant youth rom war-ravaged countries who have a history o aggressive behaviors that may have been necessary or their survival in that context would not necessarily warrant a diagnosis o Conduct Disorder. It may be helpul or the clinician to consider the social and economic context in which the undesirable behaviors have occurred.8 This passage says that the DSM criteria or Conduct Disorder are not valid when applied to symptoms that could occur as a normal response to circumstances, as, or example, when psychiatrically normal youths join gangs or selprotection in a threatening neighborhood and engage in antisocial behavior as part o required gang activities. Thus the Conduct Disorder criteria do not always pick out dysunctions. We are making exactly the same point about the criteria or MDD. The symptomatic criteria do sometimes pick out dysunctions and thus disorders, but they also pick out a potentially large range o normal responses to problematic environments. As in Conduct Disorder, the problem is not particularly hard to see once one considers obvious examples. Yet it is a proound problem that throws into doubt the meaning o much recent research on depression, as we show in later chapters. In addition, the criteria or Conduct Disorder contain the same kind o “clinical significance” requirement that appears in the MDD criteria. But the textual DEPRESSION IN THE DSM-IV 113 comment just quoted implies that the Conduct Disorder criteria are incapable o adequately distinguishing normal rom disordered conditions even with the addition o the clinical-significance clause. This clause certainly addresses whether there is sufcient harm or a disorder diagnosis, but it does not address whether a dysunction causes the harm. In the case o Conduct Disorder, even though the clinical-significance criterion eliminates conditions with symptoms too mild to constitute a disorder, the DSM-IV recognizes that a separate question remains about whether or not there is a dysunction causing the symptoms and thus about whether the symptoms represent a disorder or a normal reaction to circumstances. Precisely the same issue remains in the case o MDD despite the inclusion o the clinical-significance criterion. How the DSM Attempts to Address Contextual Triggers of Sadness Even i the MDD criteria taken in isolation have the problems we have identified, some would answer our criticisms by suggesting that theDSM must be looked at as a whole. They could say that our objections to the criteria are dealt with via other complementary categories or other eatures o the manual that somehow address the issue o normal loss responses. So, in this part, we consider various other categories and eatures that theDSM uses to handle depressive symptoms. We argue that, ar rom compensating or the weaknesses in the MDD criteria, these complementary categories and eatures either do not address the problem at all or in some cases actually make things considerably worse by urther broadening the scope o normal sadness responses that can be labeled as pathological. Textual Mention of Normal Sadness Textual commentary that accompanies the criteria or MDD and the other Mood Disorders does indeed mention the challenge o distinguishing normal sadness rom depressive disorder. However, the way it addresses the issue simply reinorces the problems noted earlier. Under a section on “dierential diagnosis,” ater a lengthy discussion that suggests how depressive disorder can be discriminated rom various other mental disorders and rom bereavement (here, the text simply repeats the requirements stated in the MDD criteria’s bereavement exclusion clause), the DSM-IV-TR says the ollowing: Finally, periods o sadness are inherent aspects o the human experience. These periods should not be diagnosed as a Major Depressive Episode unless criteria are met or severity (i.e., five out o nine symptoms), duration (i.e., most o the day, nearly every day or at least 2 weeks), and clinically significant distress or impairment.9 114 THE LOSS OF SADNESS This passage just reiterates the diagnostic criteria or MDD and reasserts that they are sufcient or disorder. The clear implication is that normal periods o sadness never satisy the criteria. But, as demonstrated earlier in this book, this is not so. Part o the range o normal variation in sadness, especially in response to severe losses and threats, can easily meet DSM criteria. Thus, in stark contrast to the textual comment that accompanies the criteria or Conduct Disorder, the MDD comment seems a hal-hearted gesture toward acknowledging the problem o distinguishing depressive disorder rom normal sadness; however, it only repeats the srcinal error in the criteria. Multiaxial System A second way in which theDSM tries to addressthe issue o development o symptoms in response to stressors is via its multiaxial system odiagnosis. This system rates patients on five distinct dimensions that go beyond the diagnostic criteria. Diagnoses o MDD (and all other mental disorders) are recorded on Axis I, per sonality disorders on Axis II, general medical conditions onAxis III, psychosocial and environmental problems on Axis IV,and global assessment o unctioning on Axis V. The various axes are intended to give the clinician a more comprehensive picture o the context o the patient’s problem than the diagnostic criteria alone provide. In particular, Axis IV involves reporting psychosocial and environmental problems that aect the diagnosis, treatment, andprognosis o mental disorders and would include stressors that trigger a lossresponse. The problem is that the Axis IV grouping o psychosocial stressors simply places them on a completely separate dimension rom the diagnoses o disorders. Symptoms that meet criteria or MDD would have already been defined as disordered beore Axis IV would come into play. This added inormation, valuable as it may be, does not in any way address the normal-versus-disordered relation between existing stressors and symptomatic responses, and so it ails to address the problem o whether the condition is a psychological dysunction or a nondisordered response to a stressor. This axis provides a way or clinicians to take stressors into account in case descriptions, not a means o separating disordered rom nondisordered conditions that meet symptomatic criteria. V Codes for Nondisordered Conditions Third, the DSM contains a short section called “Additional Conditions That May Be a Focus o Clinical Attention,” which includes nondisordered conditions or which patients oten consult proessionals. These categories are oten called “V codes” ater the letter that precedes their numerical diagnostic codes in the DSM-III. Among the V codes is Bereavement, under which it is noted that “As part o their reaction to the loss, some grieving individuals present with symptoms characteristic o a Major Depressive Episode. . . . The diagnosis o Major DEPRESSION IN THE DSM-IV 115 Depressive Episode is generally not given unless the symptoms are still present 2 months ater the loss.”10 The category o Bereavement thus explicitly recognizes that a condition can satisy the ull set o symptomatic criteria or a Major Depressive Episode and yet not be a mental disorder. But this category is limited to grie ater loss o a loved one, and consequently, insoar as recognition o nondisordered conditions goes, it just repeats what the bereavement exclusion clause in the MDD criteria already contains. Among the other V codes are separate categories or academic, occupational, identity, spiritual, acculturation, and phase-o-lie problems. The V codes do not provide any symptom criteria or such nondisordered problems; in each case, they state only that a condition can be classified under the category i it is “not due to a mental disorder.” Thus the DSM-IV does recognize that many problems in living are not mental disorders. However, it gives no criteria or distinguishing symptoms o mental disorders rom those that are nondisordered problems in living. In particular, it makes no provision or overriding the criteria or MDD to classiy a condition that satisfies those criteria as a normal response. When the DSM states that to qualiy as a V code the condition must be “not due to a mental disorder,” it in efect means that the condition cannot satisy DSM criteria or a mental disorder, including MDD. Consequently, conditions that meet symptomatic criteria or MDD must be given a specific diagnosis as a disorder and not a V code. Only residual conditions that do not satisy disorder criteria may be placed under a V code. Thereore, the V codes do not address the problem o normal loss responses that satisy the DSM criteria or MDD. In act, the V-codes section is exactly where many potential diagnoses o MDD likely belong. Adjustment Disorder The main way the DSM-IV addresses the issue o sadness responses to stressors is via the diagnostic category o Adjustment Disorder With Depressed Mood. This category in efect attempts to define what the DSM-I and DSM-II used to call “reactive” depressions that occur in response to circumstances. The challenge in ormulating such a definition is that most normal sadness is also “reactive” to circumstances, so the criteria must somehow distinguish disordered rom normal reactions. The criteria or Adjustment Disorder With Depressed Mood, however, ail to surmount this challenge and thus inadvertently manage to pathologize (i.e., incorrectly treat as disorder) a vast range o additional normal loss responses beyond those that would all under the criteria or MDD. Intended to distinguish pathological overreactions to stress rom normal re- actions, the overall category o Adjustment Disorder encompasses a set o subcategories, each o which involves a specific kind o symptomatic reaction to a stressor, including depressed mood, anxiety, antisocial conduct, mixed symptoms, and a catchall “unspecified” category or physical complaints, social withdrawal, work inhibitions, and other problematic reactions to stress. Adjustment 116 THE LOSS OF SADNESS disorder is a residual “category that should not be used if the disturbance meets 11 the criteria for another specific Axis I disorder,” such as MDD. To qualify specifically as Adjustment Disorder “With Depressed Mood,” the condition must meet the general criteria for Adjustment Disorder (discussed next) and, in addition, fulfill the following symptomatic criterion: “This subtype should be used when the predominant manifestations are symptoms such as depressed mood, tearfulness, or feelings of hopelessness.”12 The requirement that any of these symptoms be present is so weak that virtually any normal sadness response would satisfy it. Indeed, in principle, the vague depressive symptom criterion allows diagnosis with just one common sadness-response symptom, such as depressed mood or crying. However, diagnosis also requires satisfying the general Adjustment Disorder criteria, and the validity of Adjustment Disorder With Depressed Mood thus hangs on these general criteria, which are as follows: A. The development of emotional or behavioral symptoms in response to an identifiable stressor(s) occurring within 3 months of the onset of the stressor(s). B. These symptoms or behaviors are clinically significant as evidenced by either of the following: 1. Marked distress that is in excess of what would be expected from exposure to the stressor 2. Significant impairment in social or occupational (academic) functioning C. The stress-related disturbance does not meet the criteria for another specific Axis I or II disorder. D. The symptoms do not represent Bereavement. E. Once the stressor (or its consequences) has terminated, the symptoms do not persist for more than an additional 6 months.13 Adjustment Disorder, unlike MDD, is specifically limited to conditions that are reactions to triggering events. Clause C formalizes the “residual” character of the diagnosis and implies that Adjustment Disorder With Depressed Mood can be diagnosed only if the individual does not satisfy criteria for MDD. As in the criteria for MDD, the only exemption from disorder status is bereavement; reactions to any other losses that satisfy the criteria are considered disordered. It is certainly true that the process of adjusting to stressors, or “coping,” can go awry and become pathological. The critical issue is whether the criteria for Adjustment Disorder succeed in their intended purpose of distinguishing such disordered reactions from normal-range but intense coping responses that can accompany stressful events. The criteria require that the symptom(s) must occur within 3months of the stressor and must end within 6 months ofthe termination of the stressor. These DEPRESSION IN THE DSM-IV 117 timing criteria are designed to ensure that the symptoms are indeed a reaction to a stressor and not independent of it. The problem is that thevast majority of normal loss responses are characterized by a close temporal relationship to the stressor that triggers them; they tend to start soon after the occurrence of the stressor and to subside soon after the stressor abates. Thus the timing requirements potentially encompass the vast majority of episodes of normal sadness and do not distinguish disordered from nondisordered reactions to loss. The requirement that the reaction cease within 6 months of termination of the stressor (or its consequences) is of particular concern because one of the best indicators that a reaction might be considered pathological is that it doesnot gradually subside after the stressor ceases but takes on a life of its own independent of events. The temporal requirements aside, the distinction that the DSM Adjustment Disorder criteria make between normal and disordered coping comes down entirely to whether the condition satisfies at least one of the two specified “clinical significance” criteria under criterion B. To be classified as a disorder, the reaction must include either “marked distress that is in excess of what would be expected from exposure to the stressor” or “significant impairment in social or occupational (academic) functioning.” Regarding the “excess distress” criterion, even normal reactions to stressors are inherently prone to be distressing, and when the stressor is a marked one, normal responses are (by the principle of proportionality) prone to be, or at least capable of being, marked. So this criterion’s ability to distinguish normal from disordered reactions comes down to itsrequirement that the distress in disordered conditions is “in excess of what would be expected” for that stressor. The problem is how to construe this criterion. It cannot be understood as requiring that the symptoms are “in excess of what is expectable in a normal reaction,” because that raises the question of how these criteria are supposed to distinguish normality from disorder. One obvious alternative is to construe“in excess of what is expectable” as a statistical requirement. However, the statistical interpretation would allow the top half or third (say) of the distribution of normal responders to be classified as disordered. But having greater than the typical or expected level of reaction does not necessarily imply that one’s reaction is due to a disorder. For example: (1) the individual’s meaning system and values may make a stressor much more problematic or threatening than it isfor most people; (2) the individual may exist within a problematic environment in which the stressor is more serious or more enduring than usual; (3) the individual may come from a more expressive cultural background or family than other individuals do;or (4) the individual may temperamentally respond more intensely than most people do to life events. A more charitable interpretation is that, by an “expectable” response, the DSM means whatever is a “proportionate” response when all the factors, includ- ing the nature and context of the stressor itself, as well as the subjective and cultural meanings of the stressor, are taken into account. We argued earlier that rough proportionality is one of the earmarks of a nondisordered loss response. 118 THE LOSS OF SADNESS I the first component o criterion B is interpreted as speciying that a reaction “in excess” is outside the range o proportional responses, then, taken by itsel, it is potentially a valid indicator o dysunction and does correctly place some disorders into the Adjustment Disorder category and avoid obvious alse positives. But then there is the problem o criterion B’s second component, impairment in social or occupational unctioning. This, by itsel, is oered as a sufcient alternative or classiying a condition as disordered. Unortunately, it ails to exclude great numbers o normal loss response conditions. Whenever major stressors occur, it is likely that people will suer impairment in their social, occupational, or academic unctioning. Just the time and concentration it takes to deal with the stressor, the emotional eelings that make it difcult to ocus on routine tasks, and the real-lie changes that people must make can easily lead them to resist usual tasks and roles. Moreover, the issues and challenges that major stressors trigger may make some role unctioning seem temporarily insignificant by comparison, causing a loss o motivation and interest. Virtually any low mood might have such consequences. Thus, even i the “marked distress” criterion is charitably interpreted, the flaws in the alternative impairment criterion ensure that a vast number o normal loss responses can be diagnosed as Adjustment Disorders. We conclude that the criteria or Adjustment Disorder and or its subtype Adjustment Disorder With Depressed Mood potentially classiy as disordered an enormous number o normal responses that are triggered by stressors and that subside ater the stressor ends, just as such responses are designed to do. And they do so on the basis o as little as one symptom that reduces role unctioning. Indeed, any normal loss response o any consequence that does not all under the DSM criteria or MDD is almost sure to all under the criteria or Adjustment Disorder With Depressed Mood. The flaws in the Adjustment Disorder category are so apparent that researchers and epidemiologists have largely ignored it. They have clearly “voted with their eet” that Adjustment Disorder is not o interest, judging rom the very low numbers o research studies on it and the lack o growth in those numbers, which stand in stark contrast to the growth o research on other DSM categories in general and on MDD in particular. In 1980, 80 medical articles contained “adjustment disorder” in their titles, a number that actually declined to 55 articles in 2005.14 By the latter year, nearly 158 articles appeared with “depression” in their titles or each article about adjustment disorder. In short, MDD, not Adjustment Disorder With Depressed Mood, has become the operative category or the field when it comes to studying depressive states. This neglect o Adjustment Disorder by researchers appears to be justified. The diagnosis suers rom such glaring problems in distinguishing normal rom disordered conditions that it has collapsed as a serious target o research under the weight o its own invalidities. However, within the clinical realm, the diagnosis o Adjustment Disorder may nonetheless sometimes still be useul as a way o providing a potentially DEPRESSION IN THE DSM-IV 119 reimbursable label or reactions to stressul circumstances that may or may not be genuine disorders but that oten deserve and need clinical attention. Other Depression-Related Categories and Features of the DSM-IV Subthreshold Diagnoses I: Minor Depression Conditions that ail to meet theull symptomatic or duration criteria orMDD but that include some symptoms mentioned in the criteria are called “subthreshold” conditions. TheDSM-IV placed a new category, Minor Depressive Disorder, which would subsume such conditions in an appendix on “Criteria Sets and Axes Provided or Further Study.” It would require only two, instead o five, symptoms rom the nine criteria or MDD, as long as one symptom is eitherdepressed mood or diminished interest or pleasure. In other respects,such as the duration requirement 15 and various exclusions, it is essentially the same as Major Depressive Disorder. As we shall see in the next chapter, various arguments in the recent literature propose that subthreshold conditions should be defined as genuine disorders. None o these recommendations seriously addresses the problem that allowing subthreshold conditions opens the floodgates to diagnosing as disorders normal sadness responses that are not even particularly intense or enduring. Indeed, such a category could encompassvirtually all significant loss responses or periods o sadness. Thus ar, however , the DSM has not adopted minor depression as an ofcial category. Subthreshold Diagnoses II: Mood Disorder Not Otherwise Specified Nevertheless, the DSM does already speciy that mental health proessionals at their discretion can classiy as depressive disorders subthreshold conditions that do not meet the DSM criteria or MDD. This is due to the act that, as it does or many other kinds o categories, the manual includes an additional “wastebasket” category o Mood Disorder Not Otherwise Specified (NOS). One o the main purposes o this category is to diagnose “disorders with mood symptoms 16 that do not meet the criteria or any specific mood disorder.” The manual’s introduction includes a section titled “Use o Not Otherwise Specified Categories” that identifies the situations in which an NOS diagnosis may be appropriate. The first applies to conditions or which there is Enough inormation available to indicate the class o disorder that is present, but urther specification is not possible, either because there is not sufcient inormation to make a more specific diagnosis or because the clinical eatures o the disorder do not meet the criteria or any o the specific categories in that class.17 120 THE LOSS OF SADNESS The intention here was no doubt the legitimate one o giving clinicians the flexibility to diagnose occasionally clear disorders that do not quite meet the ofcial threshold or a more specifically named condition in a class. Butapplying the NOS category to depressive disorder, with no precautions about distinguishing it rom normal reactions, could allow clinicians to diagnose as disorders many normal responses that are not intense enough to meet the five-symptom, 2-week threshold. The second situation the manual specifies as one in which the NOS category can be used is when “the presentation conorms to a symptom pattern that has not been included in the DSM classification but that causes clinically significant distress or impairment.”18 This is equally problematic because both normal and disordered sadness can easily possess significant distress and role impairment. So, when it comes to loss responses, the Mood Disorder NOS category in eect gives clinicians carte blanche to classiy normal reactions as disorders. Dysthymic Disorder A second category o depressive disorders in the DSM-IV is Dysthymic Disorder. Conceived in part as a concession to psychodynamic clinicians, this disorder was substituted or the traditional category o neurotic depression (and actually appeared under the title “Dysthymic Disorder (or Depressive Neurosis)” in the DSM-III).19 Its criteria are quite dierent, however, rom those or traditional neurotic depressions, which included excessive but oten time-limited reactions to specific stressors. Diagnosis o Dysthymic Disorder requires a disturbance o mood and only two additional symptoms, but it also requires that the symptoms must have lasted or at least 2 years (1 year or children and adolescents) and during that time must have been present or most o the day on most days. Like MDD, Dysthymic Disorder is diagnosed solely on the basis o symptoms, without reerence to such actors as chronic stressors (e.g., the gradual decline and death o an ill child) that might distinguish normal rom disordered states o chronic depressive symptoms. Nor do the symptomatic criteria allow a distinction between depressive disorder and normal-range melancholic personality or temperament, the latter identified since the time o Aristotle. These problems present major challenges or the validity o the Dysthymic Disorder category itsel, and certainly its inclusion as a category o milder but chronic depressive conditions does nothing to fix the problems that stem rom the lack o adequate distinction between normality and disorder in the MDD criteria. Melancholic Major Depressive Disorder DSM For some persons who meet the MDD criteria, the specifies a “With Melancholic Features” subcategory. This classifies an individual who either has lost pleasure in all or almost all activities or who does not react to usually pleasurable stimuli and who displays three additional symptoms rom a list that includes a distinct quality o the depressed mood in contrast to usual sadness, DEPRESSION IN THE DSM-IV 121 greater severity in the morning, early-morning awakening, marked psychomotor retardation, weight loss, and excessive guilt. The subcategory o melancholia was intended to correspond to traditional cases o endogenous depression, which were considered to be particularly clear instances o depressive disorder.20 However, the DSM does not actually use the term endogenous because, by tradition, that term connotes certain types o “vegetative” or seemingly physiologically based symptoms and a lack o any external triggering circumstances, all o which do indeed suggest disorder but involve an etiological assumption. Instead, the DSM uses symptoms alone to diagnose the melancholic subcategory. Consequently, many conditions that theDSM’s symptomatic criteria classiy as melancholic do have associated precipitating stresses and would not traditionally be considered “endogenous.” It is possible that, due to their special symptomatic requirements, DSM melancholic depressions may, on average, be actual disorders more oten than other types o depression. But melancholic depressions make up only a small raction o DSM Major Depressive Disorders. Thus the distinction between melancholic and other depressive conditions cannot yield any solution to the validity problems o the overall MDD criteria.21 Would it have helped to resolve the problem o distinguishing normal rom disordered sadness i the DSM had ormulated the criteria or melancholic depression to reflect the traditional notion o “endogenous” in contrast to “reactive” depressions? As we argued in chapter 1, theendogenous-reactive distinction does not adequately distinguish disorder rom nondisorder because, although endogenous depressions are generally disorders, so are many reactive depressions by virtue o a disproportionate symptomatic response to the magnitude o the triggering loss. TheDSM justly abandoned this distinction but, unortunately, did not find an adequate replacement or it. Conclusion The symptom-based diagnoses in the DSM-III and DSM-IV in many ways improved previous eforts to classiy depression. They overcame the cursory and ambiguous definitions o depression ound in previous manuals. Explicit criterion sets enhanced communication among researchers and clinicians about the meaning o depression. Researchers could create more homogeneous populations o participants, and clinical diagnoses had greater chances o reerring to the same types o conditions. These undoubted advances, however, also had costs. The main cost was that the symptom-based diagnoses did not validly distinguish depressions that indicate the presence o disorder rom expectable reactions to situational contexts. The many eatures o the DSM that deal with responses to stressors ail to resolve this problem. The manual’s own definition o mental disorders, combined with 122 THE LOSS OF SADNESS the empirical data cited in chapter 2, suggests that its criteria for depressive disorder are not valid. The multiaxial system does not help because it uses the relevant axis of psychosocial stressors only to supplement, not to modify, a diagnosis of disorder. The category of Adjustment Disorder merely compounds the problem because it pathologizes even those normal reactions that display fewer than the usual symptoms and that go away when the stressor ceases. Nor does the inclusion of V codes overcome the fundamental problem that all conditions that meet diagnostic criteria must be diagnosed as disorders. It would have been easy enough for the definition of MDD to have included a more extensive set of exclusion criteria comparable to the exclusion for bereavement, but this was not attempted. The result is a major invalidity that leads to the pathologization of intense normal sadness. Kraepelin conceptually embraced the “with cause” versus “without cause” distinction, although it was not an important practical consideration in classifying his inpatient populations. By the time the DSM-III was published in 1980, outpatient therapy was much more common, and, consequently, the range of the problems people brought to psychiatrists had enormously expanded. Just when it would have been most useful to further develop the “with cause” versus “without cause” distinction so as to avoid false positive diagnoses, the DSM-III abandoned the distinction and thus inadvertently reclassified as mental disorders many conditions that were problems of living. The resulting problems went unremedied in subsequent editions of the manual. But the problem of pathologizing normal sadness does not end there. The next step in transforming normal unhappiness into mental disorder came when the symptom-based logic behind the DSM-III and DSM-IV went beyond the clinic and formed the basis for studies of depression among untreated individuals in the community. 6 Importing Pathology Into the Community he transormation o intense normal sadness into depressive disorder occurred in several stages. The development o influential symptom-based research criteria or afective disorders in the Feighner criteria and RDC provided an initial step. Such criteria lacked the contextual assessment that had traditionally protected diagnosis rom misclassiying intense sadness as disorder and thus created the potential or alse positives. Research on depression was, however, primarily concerned with hospitalized patients and quite severely aicted community members who were clearly disordered. Within this context, the symptom-based criteria worked well to distinguish afective disor- T ders rom other serious disorders, and the potential or alse positives was not immediately realized. The second step occurred when the DSM-III applied the symptom-based logic to clinical practice in general, including burgeoning outpatient practices and community clinics in which therapists might see all orms o mental distress. Applying decontextualized criteria to this heterogeneous group o outpatients made it more likely that these diagnoses would be applied to those sufering rom normal sadness. However, several actors work to minimize the overapplication o the DSM’s criteria to normal sadness in outpatient clinical settings. Patients tend to selselect, so although many individuals do seek help or normal sadness, more oten they seek treatment only ater they attribute their symptoms to internal problems and not to stressul situations. 1 Moreover, clinicians themselves, in spite o enticements by insurance reimbursement to see depressive disorder wherever possible, can still use their commonsense judgments to correct or flaws in the DSM criteria and to recognize when a patient is not disordered but perhaps just in need o reassurance and support to alleviate painul but normal and likely transient eelings. It is not, then, in the clinical context that the conusion between what is normal and abnormal is most in danger o occurring. Instead, the most radical transormation o ordinary sadness into pathology happened when the DSM’s criteria, developed primarily or treated cases, were lited out o the 123 124 THE LOSS OF SADNESS clinical context with its special constraints and applied to studies o depression in the community among people who had not sought proessional help or their conditions. The field o psychiatric epidemiology viewed the symptom-based logic o the DSM criteria as an opportunity to achieve its long-pursued goal o assessing prevalence o mental illness in the general population through the use o relatively simple, lay-administered checklist questionnaires. Such checklists eliminated the need or mental health proessionals to diagnose large populations and made the cost and logistics o such studies much more achievable. By using the DSM criteria, epidemiological instruments were supposed to uncover the same disordered conditions in the community that were presumed to exist among treated patients. But, as we shall see, in the change o context rom the DSM clinic to the community, the alse-positives problem latent in the criteria emerged with a vengeance; in act, the new epidemiological instruments equally identified both pathological depression and widespread intense normal sadness that exists in community members, and thus they grossly overestimated the number o depressive disorders in untreated populations. Community Studies Prior to DSM-III To understand the enormous impact o DSM depression criteria on epidemiological studies o how many people in the community have depressive disorders, it is useul to step back and consider the history o psychiatric epidemiology. At a certain historical moment, the goals o epidemiology and those o the DSM converged, and the DSM criteria ofered epidemiologists both improved criteria and a seeming solution to problems that conronted their field. In the early days o psychiatric epidemiology during the first ha l o the twentieth century, estimates o rates o mental disorder were based on surveys o various treatment settings and relied on the diagnoses contained in medical charts.2 However, it soon became apparent that surveys o treated patients provided a poor indicator o the degree o mental disorder in a community. Not everyone who has a disorder seeks treatment—or reasons having to do with stigma, cost, or the ailure to recognize that the problem is a disorder—and many who might seek treatment do not have proessional services readily available. Moreover, many o those who do seek treatment or various problems are not disordered. Thus, in order to guide mental health policy and estimate the need or services, as well as to gain a better understanding o the etiology and prevalence o mental illness, epidemiological studies attempted to surmount these problems by directly surveying the community at large. Community studies try to determine the amount o mental illness among people who are not in clinical treatment but whose conditions are presumed to be diagnosable in a way comparable to the conditions o people who are being IMPORTING PATHOLOGY INTO THE COMMUNITY 125 treated. To accomplish this aim, researchers must develop measures that can assess psychiatric symptoms among individuals who oten neither consider themselves to be mentally ill nor seek mental health treatment and so have never been proessionally diagnosed. Because some disorders aect a small number o people, surveys must study quite large numbers to obtain accurate estimates o the amount o specific kinds o mental disorder in a population. Since the beginning o psychiatric epidemiology, ormulating valid indicators o disorder to use in such surveys has represented a major challenge to the ingenuity o researchers. 3 The major impetus or attempts to measure the amount o depression and other common mental disorders in community populations lay in the experiences o World War II military psychiatrists who had treated and studied what they labeled combat neuroses, a combination o depressive, anxious, and psychophysiological symptoms that resulted rom battlefield experiences. Similar war neuroses had been amiliar to psychiatrists rom earlier wars—or example, Freud occasionally used them as a model or his thinking about trauma—but they did not take on central theoretical importance in the psychiatric proession until World War II. In that war, very high proportions o previously normal soldiers who were exposed to highly stressul combat conditions were ound to develop psychological problems. Overall, nearly 1 million American soldiers suered neuropsychiatric breakdowns: in combat divisions, admission rates to hospitals or psychiatric conditions numbered 250 per 1,000 soldiers. 4 Moreover, up to 70% o soldiers exposed to long stretches o combat suered mental breakdowns. One report in 1946 estimated that the average soldier would have a psychiatric breakdown ater 88 days o continuous combat. Not considering any other sources o casualties, the report also estimated that 95% o soldiers would break down ater 260 combat days. “Practically all men in rifle battalions who were not otherwise disabled,” the report added, “ultimately became psychiatric casualties.”5 Furthermore, no preexisting psychological characteristics predicted which soldiers would break down and which would not.6 Instead, it was the intensity and duration o combat experiences that led to the development o combat neuroses. When aced with sufcient stressors rom the environment, all individuals could become seriously disturbed. “It would seem,” military psychiatrists Grinker and Spiegel asserted in 1945, “to be a more rational question to ask why the soldier does not succumb to anxiety, rather than why he does.”7 Their wartime experiences turned the attention o psychiatrists away rom the qualities o individuals toward the qualities o stressul environments. The typical response to psychiatric casualties during World War II was to provide these soldiers with hot ood, rest and sleep, showers, and reassurance. Such responses, “which basically consisted o resting the soldier and indicating to him that he would soon rejoin his unit,” did not require extensive psychiatric training.8 The most careul postwar study indicated that over hal o psychiatric 126 THE LOSS OF SADNESS casualties returned to duty with virtually no treatment and that over two-thirds o those given rest and sedation returned to their units within 48 hours ater treatment.9 Surely, many o these individuals whose conditions endured had developed mental disorders. One might ponder, however, whether the majority who recovered quickly and spontaneously without any real treatment had extreme normal stress responses in reaction to truly abnormal circumstances.10 But what is important historically or the development o psychiatric epidemiology is that psychiatrists came to view all such psychological consequences o combat as mental disorders.11 Ater the war, socially oriented psychiatrists saw combat stress disorders as a useul model or the mental disorders o civilian lie and equated the ex12 traordinary stressors o war with the ordinary stressors o postwar lie. The theme that “every person has his breaking point” was transerred rom soldiers to ordinary citizens. The combat neuroses thus provided a new paradigm or the mental health field or the next several decades that remains influential to the present.13 Failing to recognize that most soldiers who sufered breakdowns recovered with minimal or no treatment, postwar psychiatrists came to emphasize the point that any stressul experience among normal people could precipitate serious, enduring breakdowns i not subject to early intervention. They turned their attention to creating theories and measures to study numerous environmental stressors in everyday lie that they presumed would lead to psychiatric disorders.14 This erosion o the distinction between normal distress and disorder was urthered by another basic theme o researchers rom the 1940s throug h the 1970s that derived rom the psychodynamic tenets o Freud and Meyer: mental health and illness were not categorically distinct but lay on a continuum o symptom severity, rom mild to severe.15 Only rare individuals who were entirely symptom ree were considered to be entirely mentally healthy. 16 All other points o the continuum were viewed as disordered or, at least, as less than ully healthy. An important aspect o the continuum concept was that i placed under stress persons who had symptoms at the mild end were at risk o developing more severe conditions in the absence o proessional interv ention. A consequent article o aith among community-o riented psychiatrists at the time was that early treatment o mild disorders in community settings could prevent the development o more serious conditions. 17 It became a major goal o psychiatry to develop instruments that could identiy indi viduals most at risk or becoming mentally ill and to treat them beore their conditions became more severe. The continuum notion, coupled with the assumption that sociocultural stresses caused mental disorder in the normal and caused the mildly symptomatic to become severely disordered, meant that virtually the entire population could be conceived as ill to some degree and at risk or becoming more seriously mentally ill. IMPORTING PATHOLOGY INTO THE COMMUNITY 127 Thus the evolving philosoph y o community psychiatry made it imperative to study actors that determine the risk o presumed pathology among untreated populations. In the 1950s and 196 0s, teams o dynamically oriented psychiatrists and social scientists jointly ocused on studying how sociocultural actors caused many distressing conditions in the genera l population. To study the symptoms o modern urban populations, the psychiatrist Th omas A. C. Rennie and sociologists Leo Srole and Thomas Langner developed the Midtown Manhattan project, which surveyed more than 1,600 residents o Manhattan. 18 A second major project, the Stirling County study, was another collaboration between psychiatrists and social scientists that correlated types o stressors with the distribution o psychological symptoms among the population o a rural area o the Canadian province o Nova Scotia. 19 The two major purposes o these initial postwar community studies were, first, to ascertain the magnitude o mental health problems in the population and, second, to test the hypothesis that sociocultural actors caused mental disorders.20 Beore they could answer these questions, these studies had to address the problem o how to define a psychiatric case among untreated individuals. The ofcial psychiatric manual at the time, the DSM-I, did not provide any explicit criteria to measure specific types o mental illness. Clinicians used general and vague standards that were heavily dependent on their idiosyncratic judgments. Community studies could not rely on these judgments because they would produce ar too much variance in outcome rom interviewer to interviewer when used to establish rates o mental illness in untreated populations. Such studies also aced a significant practical problem: relying on mental health proessionals to conduct large numbers o interviews was ar too expensive to be an efcient option in community studies. For both practical and substantive reasons, these studies had to develop standardized measures that lay interviewers could administer. Decontextualized, symptom-based measures o mental illness have tremendous practical appeal or surveys o mental illness. They provide standardized outcomes that do not vary rom interviewer to interviewer. Because they do not require (or even permit) probes about the personal meaning o responses, interviewers do not need any clinical training or experience. This considerably lowers the cost o administering surveys, an especially important consideration in large epidemiological research. Studies developed questions that lay interviewers could ask in standardized ormats, which could then be used to categorize respondents as disordered or not. The decision o these studies to use decontextualized measures o symptoms stemmed rom considerations o practicality 21 and cost, not rom tests showing that these methods were accurate. The definition o depression in the DSM-I posed an additional obstacle or these community studies that strove to determine the influence o sociocultural actors on rates o distress. The DSM-I defined neurotic depression as “psychoneurotic depressive reaction,” stating that “this reaction is precipitated by a 128 THE LOSS OF SADNESS current situation, requently by some loss sustained by the patient. . . .”22 When situational causes by definition precipitate nonpsychotic depressions, it is impossible to separate the influence o social rom other, intraindividual, causes because the ormer must be implicated in all cases.23 Epidemiological studies tried to solve this problem in the DSM-I by first removing etiology rom the definition o depression and then assuming that all symptoms were pathological. Situational actors were not taken into account in the definition o what counted as a disorder in the first place but, instead, were viewed as one type o cause o the symptoms. This decision meant that symptoms that were reactive to losses and other contextual actors, as well as those that were not, all counted as disordered. This solution allowed epidemiologists to achieve their goal o showing the relative influence o social and nonsocial actors in causing symptoms. At the same time, it created the problem o making disordered and nondisordered symptoms indistinguishable. Isolating symptoms rom their context and assuming that they indicated disorders abandoned the historical recognition that only “excessive” or “disproportionate” symptoms were signs o disorders. The result was that sadness, by definition, could not be a normal response to a stressul situation but must indicate a disordered condition. Thus the problem o decontextualization and consequent muddying o the distinction between depressive disorder and normal sadness that was to occur later in the clinical arena with the advent o the DSM-III actually occurred or independent reasons within the discipline o psychiatric epidemiology even beore the DSM-III. Indeed, the problem was worse in these community studies because they did not account or the degree o severity, duration, and other requirements—that is, the extended criteria sets—that the DSM-III took pains to identiy. Instead, individual symptoms themselves were taken as sufcient indicators o disorder, a situation that soon led to what were widely acknowledged to be absurd estimates o levels o pathology. The earliest community studies did not measure specific types o mental illness (such measures were not yet available) but instead developed broad, continuous, and nonspecific measures o psychological distress interpreted to indicate levels o disorder.24 They used scales containing general symptoms o depression, anxiety, and psychophysiological problems to develop global measures that they arrayed on a continuum rom mild tosevere.25 Many o these items, such as “trouble getting tosleep,” “in low or very low spirits,” “can’t get going,” or “wonder i anything isworthwhile,” can oten be signs onormal distress. Because these studies defined all symptoms, including everyday unhappiness, as signs o pathology, they unsurprisingly ound massive rates o disorder. In the Midtown Manhattan study, only 18.5% o respondents were “well,” that is, reported no symptoms.26 In contrast, 23.4% o respondents were “impaired,” an additional 21.8% displayed “moderate” symptom ormation, and the remaining 36.3% were “mildly” impaired. The Stirling County Study reported even higher rates, IMPORTING PATHOLOGY INTO THE COMMUNITY 129 asserting that 57% o the sample was likely to be comparable to psychiatric cases.27 Both the Midtown Manhattan and Stirling County studies ound strong correlations between low socioeconomic status and poor social conditions and high rates o presumed mental illness. These studies justified their findings o such high rates o disorder by the act that control groups o treated psychiatric patients also reported large numbers o similar symptoms, presumably providing criterion validation or the symptom measures. Yet had these studies used as their control groups untreated community members who were not disordered but who had sufered recent lie events such as bereavement, romantic breakups, or unemployment, they would also have ound highly elevated rates o symptoms. They could have easily concluded that they measured ordinary unhappiness rather than mental disorder. The high rates o putative disorders in community studies in the 1950s and 1960s generated conside rable skepticism at the time. “I all persons who cough,” noted the renowned epidemiologist Rema Lapouse, “are counted as cases o tuberculosis, both incidence and prevalence rates will skyrocket. Fortunately, the laboratory provides a saeguard against that kind o diagnostic extravagance. Psychiatric diagnosis as yet has no such saeguards.” 28 Even Stanley Michael, a psychiatrist associated with the Midtown study, questioned its results: The uncovering o mental and emotional symptoms in our-fiths o the sample representing an urban population suggests that either a degree o psychopathology is the norm in the statistical sense o the population average or that mental mechanisms which by psychodynamic derivation can be considered pathological may be a mode o normal adjustment.29 The assumption that normal people would be symptom-ree regardless o their lie circumstances indicated a thoroughgoing conusion about normality and disorder. The atal error o community studies was to define all symptoms as pathological without considering the context in which they arose and persisted. Despite the problems inherent in the use o decontextualized symptom measures, subsequent community studies quickly adopted them and treated mental disorder as a continuum rom less to more severe conditions. They regarded all points along the continuum as indicating pathology. Critiques o these studies, instead o trying to distinguish symptoms that indicated a disorder rom those that were appropriate responses to stressors, ocused on the nonspecific nature o the symptom scales. They claimed that the scales were so broad and unspecific that it was not clear how they were related to specific psychiatric conditions.30 It was this particular flaw—the vagueness o the symptom measures with regard to actual diagnoses—that set the stage or a shit to DSM-style criteria sets or specific disorders. 130 THE LOSS OF SADNESS Diagnoses Enter Community Studies Using continuous distributions o highly generalized symptoms was incommensurate with the radically new paradigm o criteria sets or specific categories o mental disorder that the DSM-III implemented in 1980. But earlier community studies already shared the new manual’s underlying assumptions that decontextualized symptoms must be the basis or diagnosis. The congruence o the symptom-based approach epidemiologists used and the DSM-III’s symptombased measures perhaps accounts or the act that epidemiologists quickly adopted DSM criteria in the new wave o community studies that emerged in the 1980s.31 The comparatively seamless transition rom the dynamically oriented yet symptom-based community studies in the 1950s and 1960sto the symptombased community studies o the 1980s was likely due to the act that, unlike their psychodynamic counterparts in the clinical community, community psychiatrists had already adopted a model that equated decontextualized symptoms with the presence o some degree o pathology. In contrast, the DSM-III emerged only ater a protracted battle between the neo-Kraepelinians, who purged etiological assumptions rom the manual, and the dynamic psychiatrists, who resisted their eforts.32 Because the DSM-III required that conditions satisy an extended criteria set beore being classified as a specific disorder, psychiatric epidemiologists expected DSM diagnoses to provide not only category-specific diagnoses but also more real istic estim ates o the amount o mental diso rder in the community. For example, the fiv e symptoms necessar y or diagnoses o Major Depressive Disorder seemingly set ar more stringent standards than the one symptom that characterized a “mild” condition in the Midtown Manhattan study. Indeed, because the DSM criteria were generall y accepted as authoritative and reasonably valid, psychiatric epidemiologists could base their questionnaires on these criteria without having to do elaborate validity studies o their own and without m uch independent assessment o whether the criteria in act yielded valid results in the community context, with its great diferences rom clinical contexts. The categorical system o the DSM-III was thus the basis o all large American community studies o psychiatric disorders that have been implemented since the late 1970s. Simultaneously with the development o the DSM-III, the National Institute o Mental Health decided to launch the first study that would measure the prevalence o particular types o mental disorder in the community.33 Researchers rom Washington University—the same institution that produced the Feighner criteria that underlay theDSM-III—constructed the Diagnostic Interview Schedule (DIS) that the new epidemiological studies used. This instrument measured specific diagnostic conditions in community populations that were supposed to be comparable to the major clinical entities ound in theDSM-III, including Major Depression and Dysthymia. IMPORTING PATHOLOGY INTO THE COMMUNITY 131 Because DSM-III diagnoses were based entirely on symptoms, epidemiologists could, with little change, simply translate criteria developed or diagnosis o clinical patient populations into questions or surveys o the general population, using a symptom checklist approach similar to that o earlier studies but with more complex algorithms or making a diagnosis. Their core assumption was that a structured diagnostic interview would allow researchers “to obtain psychiatric diagnoses comparable to those a psychiatrist would obtain.”34 The results would presumably provide good estimates o how much untreated mental disorder existed. These estimates, in turn, would provide policy makers with knowledge o how much unmet need existed or psychiatric services. The DIS, ounded on the same symptom-based logic o the DSM-III, uses closed-ormat questions that trained lay interviewers can administer to gather inormation about symptoms. Identical questions are asked in precisely the same way: “The interviewer reads specific questions and ollows positive responses with additional prescribed questions. Each step in the sequence o identiying a psychiatric symptom is ully specified and does not depend upon the judgment o the interviewers.”35 This standardization is necessary because even minor variations in question wording, interviewer probes, or instructions can lead to major dierences in results. The DIS was the basis o the first national study o the prevalence o specific mental illnesses in the community—the Epidemiologic Catchment Area (ECA) study launched in the early 1980s.36 The ECA surveyed more than 18,000 adults in the community and 2,500 persons in institutions in five sites (New Haven, Durham, Baltimore, St. Louis, and Los Angeles). It used estimates o the amount o disorder in these five sampled sites plus sophisticated statistical analyses to generate national estimates o prevalence. The second major community study o the prevalence o specific psychiatric disorders was the National Comorbidity Survey (NCS), which the NIMH fielded in 1991 with a 10-year ollow-up begun in 2001.37 The NCS, a sample o about 8,100 persons meant to represent the population o the United States, used the Composite International Diagnostic Interview (CIDI), an instrument similar to the DIS. Its age range o 15–54 years was somewhat dierent rom the 18–65 age range that the ECA sampled. The NCS illustrates how these DSM-based community surveys measure depression. It uses two steps to obtain diagnoses o depression based on DSM-III-R criteria.38 In the first, respondents must afrm at least one stem question that appears at the beginning o the interview. These questions ask: “In your lietime, have you ever had 2 weeks or more when nearly every day you elt sad, blue, or depressed?” “Have you ever had 2 weeks or more when nearly every day you elt down in the dumps, low, or gloomy?” “Has there ever been 2 weeks or more when you lost interest in most things like work, hobbies, or things you usually liked to do?” and “Have you ever had 2 weeks or more during which you elt sad, blue, depressed or where you lost all interest and pleasure in things that you usually cared about or enjoyed?” Given the broad nature o these questions and the act 132 THE LOSS OF SADNESS that they have no exclusion criteria or the circumstances in which they arose, it is not surprising that 56% o the population reported at least one “yes” response to them.39 Later, in the second step o the interview, this group is asked questions about symptoms o appetite and sleep disturbances, atigue, and eelings o sadness, worthlessness, hopelessness, and the like, which are comparable to the symptoms in the DSM criteria or Major Depression. A computer program then determines whether respondents meet the criteria or a diagnosis o depression. The NCS estimates that about 5% o participants had a current (30-day) episode o Major Depression, that about 10% had experienced this disorder in the previous year, that about 17% had had an episode over their lietimes, and that about 24% reported enough symptoms or a lietime diagnosis o either Major Depression or Dysthymia.40 Likewise, a study in New Haven that was a precur41 sor to the ECA ound lietime rates o 20% or Major Depression. Rates rom the ECA were lower, with 6.5% o respondents reporting Major Depression over the preceding year and about 11%, either Major Depression or Dysthymia over their lietimes.42 The findings rom the ECA and the NCS are the basis or the estimates regarding the prevalence o mental disorder that the scientific, policy, and popular literatures now widely cite. The Myth of the Equivalence of Community and Clinical Diagnoses Are the many cases o putative Major Depression that post-DSM-III community studies uncover equivalent to treated clinical cases? I so, do they present an accurate picture o the total amount o mental disorder, as epidemiologists assume? Even some o those who design and execute such studies have started to worry that the reported symptoms may oten represent transient normal responses to stress.43 Such concerns are well justified because current epidemiological instruments inherit and greatly magniy the problems in distinguishing disorder rom nondisorder that aict the DSM criteria on which they are based and because diagnoses arrived at in such studies have none o the mitigating circumstances that exist in clinical diagnosis to reduce the practical eects o such invalidity. As mentioned beore, people who seek help rom clinicians are by definition sel-selected, and they use all sorts o contextual inormation to decide or themselves whether their conditions exceed ordinary and temporary responses to stressors. Sociologist David Karp, or example, ound that depressed people seek help rom psychiatrists only ater they attribute their symptoms to internal psychological problems and not to stressul situations: Once it becomes undeniable that something is really wrong, that one’s difculties are too extreme to be pushed aside aseither temporary or reasonable, IMPORTING PATHOLOGY INTO THE COMMUNITY 133 eorts begin in earnest to solve the problem. Now choices to relieve pain are made with a conscious and urgent deliberation. The shit in thinking oten occurs when the presumed cause o pain is removed, but the difculty persists. Tenure is received, you finally get out o an oppressive home environment, a destructive relationship is finally ended, and so on, but the depression persists. Such events destroy theories about theimmediate situational sources o depression and orce the unwelcome interpretation that the problem might be permanent and have an internal locus. One has to consider that it might be a problem o the sel rather than the situation.44 Patients who enter treatment thus have already decided that their problems go beyond normal reactions to social stressors. In addition to patient sel-selection, in clinical practice contextual probes are usual, and all o the DSM manuals assume, with varying levels o explicitness, that clinicians will use their commonsense judgments in applying diagnostic criteria. Clinicians can, or example, reassure highly distressed people whose marriages are unraveling that their problems are mainly situational rather than internal. In treatment settings, the symptom-based logic o diagnoses need not be rotely applied. In contrast, symptom-based diagnoses in community studies consider all persons who report enough symptoms as having the mental disorder o depression and thus cannot separate intense expectable responses rom disorders. The context in which the symptoms developed (aside rom bereavement), their duration (beyond a 2-week period), or their remission ater a stressor has ended are irrelevant to a decision about whether or not a disorder exists. The computer scoring o the participant’s symptoms o depression in surv ey research lacks any discretionary checks over whether symptoms indicate a mental disorder. Interviewers can neither exercise clinical judgment nor use flexible probes about responses. Indeed, they are orbidden to make any judgments about the validity o respondent answers. Even i the respondent seems to have misunderstood the question, the interviewer is instructed to repeat the question verbatim.45 The rigid standardization o structured interviews has the advantage o improving the consistency o symptom assessment across interviewers and research sites and the consequent reliability o diagnostic decisions.46 However, the standardized questions and scoring procedures in community studies preclude the possibility o using discretion and thus treat all symptoms, regardless o their context, as signs o pathology. The sorts o experiences that produce normal sadness responses—breakups o romantic relationships and marriages, job losses, severe physical illness, disappointed career goals, and the like—are rampant in community populations. Many, perhaps most, community members have experienced major losses at some point in their lives that produce nondisordered episodes o sadness, some severe enough to qualiy or a diagnosis 134 THE LOSS OF SADNESS o Major Depression and thereore to contribute to the seemingly high rate o depressive disorders in community populations.47 In short, the inflexibility o symptom ascertainment and criteria application greatly increases the chances o alse-positive diagnoses. Not surprisingly, agreement between clinical diagnoses and diagnoses o depression that use standardized measures is generally weak.48 Standardization may produce more reporting o depressive symptoms, but many o them may be normal sadness responses. A respondent might recall symptoms such as depressed mood, insomnia, loss o appetite, or diminished pleasure in usual activities that lasted or longer than 2 weeks ater the breakup o a romantic relationship, the diagnosis o a serious illness in an intimate, or the unexpected loss o a job. Although these symptoms might have dissipated as soon as a new relationship developed, the intimate recovered, or another job was ound, this individual would join the many millions o people who sufer rom the presumed disorder o depression each year. Because the kinds o symptoms that presumably indicate depressive disorders are oten common products o ordinary stressors, the number o people who do not have mental disorders but who are diagnosed as depressed must be assumed to be quite high until proven otherwise and might even exceed the number o people who are accurately classified as depressed.49 Diagnostically oriented community studies did not demonstrably uncover high rates o depressive disorders so much as plausibly demons trate that the natural results o stressul social exper iences could be distressing enoug h to meet symptom criteria or a disorder. Yet, without adequate consideration o the nature o the reported conditions, th e high untreated rates o depression are used to argue that depression is a public heal th problem o epidemic proportions, that relatively ew people who are depressed seek appropriate treatment, that untreated depression creates vast economic costs, that the amount o mental health services is inadequate, and that many people ought to tak e prescription medications to overcome their depression. 50 Back to the 1960s: Eliminating DSM Symptom Thresholds in Community Studies Whatever its shortcomings, theDSM does make a good-aith efort to construct diagnostic criteria that indicate disorders as distinct rom transient unhappiness, using a symptom threshold as its major tool. Indeed, theDSM criteria are genuinely more stringent than the earlier epidemiological single-symptom approach. The groundwork, however, is currently being laid or an erosion o even this progress and or a much more radical expansion o the symptom-based approach to diagnosing depressive disorder in the community. The argument or this new approach—which is not really so new at all but is, in act, a throwback to IMPORTING PATHOLOGY INTO THE COMMUNITY 135 the single-symptom measures o the 1950s—is unolding currently in research journals, in psychiatric conerences, and in programs that screen or the presence o depressive disorders. It is, above all, based on epidemiological findings that start rom symptom-based criteria and that argue or including as disorders conditions with even ewer symptoms than the number required byDSM criteria or MDD. This approach would largely abandon the constraints o the DSM’s symptom thresholds and would classiy below-threshold conditions as disorders. The community studies o psychiatric conditions in the 1950s and 1960s had ramed mental illness as a continuum rom mild to severe depending on the number o reported symptoms rather than as a set o discrete disorders that were categorically distinct rom ordinary distress. In contrast, the major community studies since the 1980s have reported their results as categories that DSM corresponded to definitions. Cases o Major Depression required five or more symptoms, which meant that persons with ewer than five symptoms were not considered disordered. Epidemiologists expected that this change would eliminate the obvious inflation o disorder estimates that the continuum approach produced. However, the symptom threshold that is at the heart o the DSM’s approach to depression diagnosis is now itsel seen as a problem. Even the most avid proponents o the DSM’s categorical diagnosis o MDD recognize that the particular number o symptoms required or distinguishing disorders rom nondisorders is somewhat arbitrary and largely a matter o diagnostic convention.51 In clinical practice, speciying an objective cutof point is convenient in order to generate diagnoses, decide on treatments, and receive reimbursements. But there is no compelling scientific reason or why that point or MDD is set at five rather than, or example, at our or six symptoms. Indeed, even the DSM implicitly recognizes that conditions with ewer than the required five may be depressive disorders and allows them to be diagnosed under the “Afective Disorders Not Otherwise Specified” category.52 The arbitrariness o a symptom cutof or diagnosis o depressive disorder is less problematic in clinical settings than in community studies, because clinicians can use their judgment as to the pathological or nonpathological nature o a case, and, at least prior to recent use o aggressive screening and casefinding methods, people with mild cases with very ew symptoms were unlikely to enter proessional treatment in the first place. Most (though by no means all) treated patients with depression have tended to show long-standing symptoms, chronic courses, and requent relapses and thus have been less likely to be alsepositive cases—people who meet diagnostic criteria but who do not have mental 53 disorders. In contrast, symptoms among untreated community members lie on a continuous distribution that ranges rom mild to severe and rom ew to many, with the number who report a small number o symptoms ar exceeding those who report many symptoms.54 For example, 8.7% o ECA respondents reported 136 THE LOSS OF SADNESS one depressive symptom over the previous month compared with the 2.3% o respondents who met the ull criteria or major depression.55 Likewise, although the average duration o symptoms among treated outpatients is between 6 and 9 months, diagnostic standards in community studies require only a 2-week duration.56 The continuous distribution o symptoms in the general population, along with the act that the preponderance o conditions all toward the mild end, poses a challenge or the categorical classification o depression or two reasons. First, the smoothness o the curve o symptom distribution itsel, with no particular discontinuity, makes it difcult to justiy a categorical symptom cuto because the symptoms themselves do not naturally suggest the break between categories. Second, and central to recent analyses, the harm associated with dierent levels o symptoms, such as degree o social, occupational, and health disabilities, also appears to increase smoothly and proportionately as symptom number rises.57 When there is no clear demarcation point in the distribution o impairments at dierent symptom levels, it seems hard to justiy a categorical concept based on the number o symptoms. Milder cases, it is argued, just represent milder disorders, not normality.58 The use o impairment as a validating criterion inevitably leads to pressures to measure depression as a continuous rather than a categorical disorder. Consequently, a flood o studies since the mid-1990s have argued or expanding the notion o depressive disorder by lowering the symptom threshold or diagnosis. In essence, these new studies have reinvented the notion rom the community research in the 1950s that depression is a symptomatic continuum rom ew symptoms (well below the current five-symptom threshold) to many. The proximate srcin o this movement lies in studies that showed that people in primary medical care who have depressive symptoms, but not depressive disorders, have much unctional impairment.59 Indeed, the degree o disability associated with depressive symptoms without disorder exceeded that o eight common, chronic medical conditions such as hypertension or diabetes. The DSM criteria or Major Depression, however, excluded this large and seemingly very impaired group o people rom the ranks o persons who were considered to have disorders. Such findings generated suspicion that the arbitrary boundaries o categorical criteria could raise the number o alse negatives: people who have disorders but who are not counted as disordered because they report ewer than five symptoms.60 Thus a ear that the categorical criteria o epidemiological studies actually underestimate the number o depressive disorders underlies the consider- able body o depression resear ch that has now accumula ted. The first theme o this new research is that depressiv e disorders vary along a continuum that ranges rom minor to major. “To accept depression as disease,” psychiatrist Peter Kramer concludes, “is to see pathology or risk in minor versions.” 61 Minor or subthreshold depression includes persons who report between two and IMPORTING PATHOLOGY INTO THE COMMUNITY 137 our symptoms o depression but who do not meet the ull criteria or MDD or Dysthymia.62 Other studies extend the categ ory o minor depression ev en urther, counting persons with one or more symptoms o depression, includin g mood disturbance, as impaired.63 At the extreme, reporting a single depressive symptom o any type qualifies one as having a disorder.64 The basic argument is that  ewer symptoms represent milder versions o depressive disorder along a diagnostic continuum that contains no sharp boundary between disorder and nondisorder. Applying Kraepelin’s argument or his inpatient samples to untreated community samples, some researchers assert that “depressive symptoms at the major, mild, Dysthymic and subthreshold levels are all part o the long term clinical structure o major depression.” 65 Any sign o sadness is an aspect o a unitary depressive disorder.66 As a second theme, the new research emphasizes that all points along the continuum are disorders because they are associated with increasingly higher rates o disability. The justification or lower cutting points or depressive disorder stems rom the gradations in impairment that ollow rom increasing numbers o symptoms.67 Studies indicate that subthreshold conditions are associated with significantly higher levels o household strain, social irritability, and financial difculties, as well as limitations in physical and job unctioning, restricted activity, and poor health status.68 Likewise, the NCS data show a gradient o increasing impairment among persons with 2–4 symptoms, 5–6 symptoms, and 7–9 symptoms, as indicated by the intererence o these symptoms with lie activities and by whether or not the patients had seen a physician or some other mental health proessional or were taking medication.69 “The act that the correlates o mD (minor depression) and MD (Major Depression) are similar,” assert one group o researchers, “means that mD cannot be dismissed as simply a normal reaction to environmental stress while MD is seen as something quite dierent.”70 Impairments such as social and occupational disabilities, physical disorders, and uture hospitalizations increase continuously as the number o symptoms increases.71 Even one symptom o depression, compared with no symptoms, is associated with more adverse outcomes on most measures o disability.72 Thereore, attention must be paid to the ull range o depressive conditions, not just to conditions that meet the DSM criteria or MDD. A third aspect o the new wave o community studies is their ocus on mild conditions as risk actors or uture disorders o greater severity and their lowering o the threshold o disorder because o these risks. For example, in the ECA, people who reported two or more lietime symptoms were ar more likely to develop Major Depression during the ollowing year than those who reported 73 ewer symptoms. In this study, more than 50% o cases o first-onset Major Depression were associated with prior depressive symptoms. “Our findings,” the authors conclude, “tentatively suggest that i depressive symptoms could be identified and treated beore major depression first develops, many cases o firstonset major depression could potentially be prevented.”74 The NCS data, as well, 138 THE LOSS OF SADNESS indicate that mild cases o disorder at the first period predict more serious cases at the ollow-up period.75 The “development o early interventions to prevent progression along a given severity continuum might reduce the prevalence o serious cases.”76 Not surprisingly, lowering the criteria or depression greatly increases prevalence rates. In a 1-month period, nearly a quarter o the population (22.6%) in the ECA study report at least one putative symptom o depression.77 At some point in their lives, about one in every our people in the ECA who do not meet criteria or MDD or Dysthymia report enough symptoms to qualiy or a diagnosis o subsyndromal depression.78 Likewise, when the disorder o “mild depression” is defined as the display o two to our symptoms, the lietime prevalence o depression increases dramatically rom 15.8% to 25.8%.79 In some populations, especially among the elderly, rates o minor depression exceed 50%.80 The high prevalence o mild depression, coupled with the accompanying adverse outcomes, the increased risk or ull-fledged mood disorders, and the increased social disability that accompanies it, leads to arguments that this condition is “a truly hidden, unrecognized public health problem that has an enormous 1-year prevalence in the society” that should be a ocus o research and preventive eforts.81 These major themes o psychiatric epidemiology in the early twenty-first century almost precisely echo those o the initial postwar community studies in the 1950s and 1960s, except that what was then tended to be construed as a disorder caused by environmental stress now tends to be viewed as a disorder caused by biological malunction. To sum up these common themes: (1) mental disorder is continuous, and all points along this continuum should be viewed as problematic; (2) mild conditions at one time are likely to become major conditions at another; (3) even a single symptom o depression is worrisome because it is associated with uture disability and can be a risk actor or major depression; (4) because o its extremely high prevalence, social policies should ocus on preventing depression rom developing in the general population. Psychiatric epidemiology has come ull circle, returning to its concern with even the mildest presumed conditions o depression. Fallacies Behind the “Minor Depression” Movement What is right and what is wrong in the proposed expa nsion o disorder to inDSM clude “minor depression” that has ewer symptoms than the requires? What is right about it is, first, that we do need to be alert to subthreshold conditions in some circumstances in which they can help predict uture problems. But the act that a condition is a risk  actor or uture problems does not mak e it a disorder, a point to which we return subsequently. IMPORTING PATHOLOGY INTO THE COMMUNITY 139 Second, and most important, the DSM cuto is somewhat arbitrary and is not a magic dividing line between pathology and normality. No doubt some subthreshold conditions deserve to be diagnosed as disorders; also, DSM criteria or depressive disorder likely do yield some alse negatives, in addition to the alse positives we have emphasized. More generally, viewing depression as continuous rather than categorical has a number o theoretical advantages.82 Many disorders, such as depression, might naturally be based on underlying, continuous dimensional processes rather than on dichotomies, and so continua might be more likely than diagnoses to “carve nature at its joints” and yield ruitul research and theory. However, the assertion that, because there is a linear relationship between number o symptoms and impairment, each point along the continuum theredisorder ore represents a is highly problematic. When all symptoms are counted as disordered, ordinary sadness is hopelessly conounded with genuine dysunction, and prevalence rates reach even more untenable levels than they do now. For example, in the ECA study, the most common symptoms are “trouble alling asleep, staying asleep, or waking up early” (33.7%), being “tired out all the time” (22.8%), and “thought a lot about death” (22.6%). 83 College students during exam periods (particularly those studying existential philosophy), people who must work overtime, those who are worrying about an important upcoming event, or respondents who take a survey around the time o the death o a amous person would all naturally experience some o these symptoms. Symptoms that neither respondents nor clinicians would ever consider as reasons or entering mental health treatment nevertheless can indicate disorder in community surveys. Moreover, the duration criteria require that the symptom last or only a 2-week period, ensuring that many transient and sel-correcting symptoms are counted as disordered. Given the common nature and brie persistence o many putative symptoms o depression, it is difcult to imagine that there are many people who have not experienced episodes o mild or subthreshold depression at some point in their lives, although there certainly are some people with temperaments that seem to virtually preclude intense sadness. Indeed, the very high rates o depression ound when cutting points are lowered almost certainly underestimate the number o people who experience putative symptoms o depression. One reason or undercounts is that respondents do not recall all symptoms that have occurred at some point in their lietimes. One group o researchers, or example, ound that most respondents who reported episodes o lietime depression at the baseline interview in the ECA ailed to report any lietime episodes at the 12-year ollow-up 84 period. The majority o respondents simply orgot previous depressive states. I respondents accurately recalled all episodes o depression, lietime prevalence rates o depressive disorder would exceed 50% in the ECA data. A second reason or the undercount o symptom prevalence is that respondents disregard the instructions o surveys, apply their own contextual criteria or symptoms, and 140 THE LOSS OF SADNESS fail to report symptoms that they attribute to life crises or medical conditions.85 Epidemiologist Rema Lapouse’s critique of the postwar community studies—“If all persons who cough are counted as cases of tuberculosis, both incidence and prevalence rates will skyrocket”—holds as well for contemporary psychiatric epidemiology’s continuous concept of depressive disorder in which no provision is made for distinguishing normal sadness from mild disorders. 86 The major justification for treating all symptoms as disordered is that they are associated with current or future disability. This assumes that any psychological condition that is related to a problematic outcome must be a mental disorder. Yet it is entirely possible, for example, that a temperament prone to somewhat more sadness, and thus to normal-range depressive symptoms in response to life’s vicissitudes, may also be somewhat more vulnerable to the development of depressive disorder; but that does not make temperamental variation a disorder. Moreover, this conclusion would be warranted only if symptoms of normal sadness are not impairing. Yet both disordered and nondisordered depression can vary continuously on a number of dimensions, including severity, duration, and impairment, and can certainly cause social role disabilities. One need only consider grief as an example, but surely more moderate forms of normal sadness also incline people to withdraw from social interaction, to become less capable of concentrating on routine role performances, and to develop other impairments.87 Such interference with role functioning and productivity does not make sadness a disorder. Aside from associated disability and impairment, epidemiological studies justify their decision to treat subthreshold symptoms as disorders with the argument that mild conditions at one point are likely to become more serious conditions that reach the DSM threshold for disorder in the future; they argue that the milder condition is therefore part of a larger disease process and that early detection of and intervention with mild conditions can make it possible to stop disorders from developing.88 Perhaps this is sometimes true. However, a basic problem with this as a general argument about minor depression is that, especially given the potential invalidity of MDD diagnoses themselves, even when a subthreshold condition does precede a full-syndrome condition, it is unclear whether either condition is an actual disorder or not, much less what the relationship of one condition is to the other. For example, a person might feel bad as a troubling situation at work, a marital conflict, or a physical illness in a loved one develops, might report two or three symptoms, and then, when the trouble gels into a loss, might have a more intense response. Both the initial sadness and the later, more intense reaction might be perfectly normal, and yet an epidemi- ologist might interpret the sequence as one in which a minor depressive disorder led to a major depressive disorder. The fact that a few sadness symptoms are later followed by more intense sadness symptoms tells us little by itself about whether the earlier, milder condition or the later, more severe condition or both or neither are disorders. Valid criteria in either case must go beyond symptoms. IMPORTING PATHOLOGY INTO THE COMMUNITY Moreover, subthreshold symptoms do not necessarily predict DSM 141 Major Depression diagnosis at a later time; in act, evidence or the prediction o later major depression is quite weak. Many, or even most, symptoms uncovered in community studies will be transient and limited in duration to the context o the stressul si tuations that gave rise to them. In the ECA study, one-hal o people wi th mild depression became asymptom atic during the ollowing year.89 In this study, only 10% o persons with minor depression with mood disturbance and only 2% with minor depression without mood disturbance developed Major Depression in the 1-year ollow-up, and because o the ECA’s DSM symptom-based criteria, we do not know ho w many o those were truly disordered. Conversely , over one-third o the group with Majo r Depression became asymptomatic, and nearly 40% ell into the group with 90 minor depression. These findings indicate that more serious conditions are more likely to become less serious conditions than the conv erse. Because o the extraordinary instability o “caseness,” with people slipping in and out o varying states o severity, there are no reliable ways o identiying which conditions will get worse and which will not. Although persons with mild depression might be more likely than those without symptoms to develop uture cases o Major Depression, the vast majority o people with a small number o depressive symptoms will not develop Major Depression in the uture. Indeed, studies indicate that, in the absence o any intervention, up to two-thirds o depressive symptoms naturally remit.91 For example, in the ECA study mentioned earlier, 97 o 114 participants diagnosed as depressed in the initial interview recovered during the ollow-up period.92 Symptoms that result rom lie problems typically go away when these problems are over, even though they might initially meet clinical criteria. It is dif cult to understand the logic o the argument that because some subthreshold conditions might be disorders rather than normal sadness, all should be classified as disorders. The explanation seems to be that the minor-depression movement rejects DSM symptom thresholds but tenaciously clings to the DSM’s basic assumption that context-ree, symptom-based criteria can best diagnose depressive disorder. Consequently, the extension o depressive disorder to subthreshold conditions, which may eliminate some alse negatives, comes at the price o a much greater likely expansion in alse-positive diagnoses o nondisordered sadness as disorder. Yet those who advocate diagnosing minor depression have notably disregarded the problem o how to avoid misdiagnosis o normal sadness as disorder. Only i a more valid approach to the disorder-nondisorder distinction is first put in place will it be justifiable to encompass low-symptom conditions within the disorder category. Because o these weaknesses in the current approach to minor depression, the policy implications that stem rom the use o the continuous concept o depressive disorder are questionable. The highest priority o good public policy 142 THE LOSS OF SADNESS ought to be to provide mental health services to persons who are most in need o them. When the concept o a continuum o mental health problems was applied in the 1960s, the result was the pathologization o a large proportion o the population, the extension o services to many people with problems o living, and a consequent diminution in services provided to the seriously mentally ill.93 The minor-depression movement could be laying the groundwork or the same mistake again. Advocates or the men tally ill, the NIMH, and psychiatric researchers have been receptive to findings o high rates o Major Depression in community sur veys because they think these findings will help to decrease the stigma associated with labels o mental disorder and to obtain public and legislativ e support or unding mental health programs. 94 Yet extending definitional thresholds or depressive disorder downward in community studies so that even more people are counted as depressively disordered might, like the already high prevalence rates rom DSM-based epidemiological studies o Major Depression, have the opposite efect o undermining the political will to deal with the problem due to ears among public and private unders about the huge costs o providing services to such a large population. 95 As psychologist James Coyne emphasizes, “improving the outcomes o known cases o depression should take precedence over increasing the detection o depression,” and this is all the more true when what is being detected is likely not depressive disorder at all. 96 We should heed the warning o Rema Lapouse, writing in the srcinal era o the continuous concept: Rates which include a large proportion o equivocal or mild cases, or actually nonsick individuals, may even have the deleterious efect o encouraging the deployment o the limited mental health orces or the treatment o those who are least sick and have the best prognosis.97 Conclusion There is nothing wrong per se with the use o symptom continua in research and theory on depression. However, such continua are not in themselves a substitute or the distinction between disorder and nondisorder. The problem o alse positives has its root in the ailure to connect symptoms and associated disabilities to the context in which they arise, an issue that suraces at all points on the symptom severity continuum. The problem o alse positives becomes progressively worse, however, as ewer and ewer symptoms are used to define disorders. Indeed, i consideration o context is abandoned, all normal sadness responses potentially can be seen as a sign o pathology; the very possibility o normal sadness is lost. IMPORTING PATHOLOGY INTO THE COMMUNITY 143 We have thus far considered the unintended consequences when the DSM’s decontextualized symptom-based criteria were applied to untreated samples in the community, with the resulting great expansion of the group labeled as having pathological depression. But the consequent inflated epidemiological prevalence estimates have not remained mere scientific abstractions. Instead, they have become the basis for sweeping and intrusive new social policies toward depression, to which we now turn. 7 The Surveillance of Sadness  you are a typical resident o New York City, the chances are that you’ll visit your primary care physician at some point over the next year. I your doctor ollows the advice o the New York City Commissioner o Mental Health, he or she will ask you to fill out a questionnaire that asks: “Over the past 2 weeks, how oten have you been bothered by any o the ollowing problems?”1 Each o nine symptoms are rated as 0 (not at all), 1 (several days), 2 (more than half the days ), or 3 (nearly every day). Here are the nine symptoms: I 1. Little interest or pleasure in doing things. 2. 3. 4. 5. Feeling down, depressed, or hopeless. Trouble alling or staying asleep, or sleeping too much. Feeling tired or having too little energy. Poor appetite or overeating. 6. Feeling bad about yoursel, or that you are a ailure or have let yoursel or your amily down. 7. Trouble concentrating on things, such as reading the newspaper or watching TV. 8. Moving or speaking so slowly that other people could have noticed; or the opposite, being so fidgety or restless that you have been moving around a lot more than usual. 9. Thoughts that you would be better of dead, or hurting yoursel in some way. The instrument is scored as ollows: i five or more o the nine symptoms, including one o the first two, score 2 or 3 (a total score o at least 10), then you would receive a diagnosis o Major Depressive Disorder; you would be diagnosed with minor depressive disorder i at least two questions, including one o the first two, all in the 2 or 3 range (a total score o at least 4). For example, i you elt down and tired most days or the past 2 weeks (i.e., or 8 days or more), you would qualiy or a diagnosis o minor depressive disorder; i on most days or 144 THE SURVEILLANCE OF SADNESS 145 the past 2 weeks you elt down and tired and bad about yoursel and also had trouble alling asleep and trouble concentrating on things, you would qualiy or Major Depressive Disorder. The city claims that individuals whose scores are high enough to indicate likely disorder will be reerred or a clinical assessment. However, because these symptoms are so common, it is hard to see how enough resources would be available to assess the potentially enormous number o reerrals. Moreover, most people who report having the specified symptoms likely are experiencing them because o some immediate loss or problem that is preoccupying them and causing them to be sad, distracted, and so on. Yet physicians could be easily tempted to prescribe medication even to those with minor depression, a diagnosis that a substantial proportion o primary care patients would warrant. Thus the tentative labeling o the individual as depressed without taking into account that individual’s circumstances can set in motion a clinical response that is based on inadequate substantive inormation. New York City’s program is part o a national movement toward screening adults and children or depression that a Presidential Commission report supports. 2 In this chapter we explore the depression-screening movement and some o the problems that result because o its use o decontextualized, symptombased criteria or identiying depressed individuals. The Depression-Screening Movement Epidemiologists, as we saw in chapter 6, ailed to adequately distinguish normal sadness rom depressive disorder in community studies. As a result, they presented mental health policy makers with surprisingly high estimates o the number o people who have untreated depressive disorders. Fearing that there was an enormous unmet need or mental health services among people who might not even recognize that they were sufering rom a disorder, these policy makers in turn placed a high priority on finding ways to identiy people with untreated disorders in the community and to bring them into treatment. And it was decided that i people would not come in or diagnosis, then diagnosis must go to the people. The result has been a set o screening programs that, in principle, aim to diagnostically evaluate every single person in America or the presence o depressive disorder. Several assumptions underlie the attempt to identiy and treat previously unrecognized cases o depression. One is that, unless brought into treatment, peo- ple who meet symptomatic criteria in community studies may develop chronic, recurrent, and deteriorating conditions.3 Another is that individuals with unrecognized cases o depressive disorder are sufering needlessly and can benefit rom available medications and therapies.4 A concern that untreated depressive disorders could have very negative outcomes such as suicide also drives the 146 THE LOSS OF SADNESS urgency or treatment. Moreover, untreated depression has significant hidden economic costs: patients with undiagnosed depression overutilize the health care system, have many unnecessary medical evaluations, and drive up the costs o medical services. 5 The major question acing initiatives that deal with unmet need or treat ment is how best to identiy and make contact with untreated cases o depression. Eforts that target entire populations, such as public service announcements, educational campaigns, and direct-to-consumer advertisements, are one way to reach such cases. Pharmaceutical companies and other concerned organizations were quick to take this approach and to plant in the public’s mind a quite broad notion, based on common DSM symptoms, o the possibility that, even unbeknownst to onesel, one might have a depressive disorder and ought to consult one’s physician. Such appeals encourage people to monitor themselves and their amilies and associates or signs o sadness and to interpret these common signs according to the worrisome meanings derived rom expansive definitions o depressive disorder. No doubt such initiatives do encourage some individuals with depressive disorder to beneficially entertreatment. They likelyhave contributed to increased rates o treated depression and prescriptions or antidepressant medication over the past two decades.6 However, in the end, such eforts are o limited efectiveness because they depend on individuals themselves to recognize that they might be depressed enough to warrant medical treatment. The screening movement, thereore, has ocused on extending medical authority beyond the usual response to spontaneous help seeking. This is a critical goal o the movement because current diagnostic criteria do not correspond to what most laypeople believe is disorder.7 Thus many people whom the DSM would classiy as disordered do not themselves believe that they have signs o mental disorder, do not raise such questions with their physicians, do not seek help, and thus do not present themselves as targets o treatment. Because o this, assessment must go out into the community, somehow be externally imposed, and proceed on the patient’s behal. We turn now to how this new surveillance via screening is conducted and how specific screening programs help to redefine the experience o intense sadness as disorder or the lay population. Beore proceeding to examine how such screening works, we need to mention one important caveat regarding the limits o our argument. Our analysis specifically concerns the redefinition o the experience o normal sadness as a disorder that results rom using current DSM criteria, including subthreshold criteria, in community screening programs. Our analysis could easily be mistaken or a critique o depression screening in and o itsel. However, the desirability o screening is a separate issue that depends on whether screening, either in its current orm or in some uture orm, can be shown to yield benefits in preventing or alleviating sufering that demonstrably outweighs its costs. At present, such empirical support does not exist; there is simply no evidence that mass screening or depression is efective in achieving THE SURVEILLANCE OF SADNESS 147 any major mental health goal. This chapter thus addresses not the pros and cons o screening per se but the problem o the pathologization o normal sadness that results rom screening solely with symptom-based criteria. Prescreening and Diagnostic Screening for Depressive Disorder The goal o depression screening is to reveal those persons in the community who either do not recognize that they have depressive disorders or or some other reason have not acted to get help or their disorders. Having mental health proessionals clinically diagnose each and every person in the community would be ar too expensive and time-consuming to be practical. Thus brieer tests, or screening instruments, must be used to decide whether someone has a higher than usual probability o having a disorder, and only those people who test positive are then ully diagnosed. Screening is an ambiguous term that can reer to two distinct processes (although we will see later that these two processes oten collapse into one). First, it can mean giving community members a test that is suf cient by itsel to provide a likely diagnosis o a target disorder. For example, various businesses have health-screening days when employees can get their blood pressure checked and their blood cholesterol level measured, with tests that diagnose high blood pressure and hypercholesteremia more or less accurately. Similarly, tuberculosis screening can involve teams o physicians who, equipped with mobile X-ray machines and other necessary equipment, go into the community to provide underserved populations with medical tests that establish a likely diagnosis o tuberculosis i it is present. We reer to such screening as diagnostic screening. One important eature o diagnostic screens is that a positive result is taken to indicate pathology and thus is sufcient to justiy treatment. But screening also commonly reers to mass testing that provides only some initial indication o whether there might be a problem and thus whether an individual requires a reerral to a proessional or urther diagnosis. Such screening does not provide a likely or presumptive diagnosis by itsel and oten generates a large number o positive results that are ultimately not confirmed in later diagnostic testing. For example, positive results on patch tests or tuberculosis only provide some indication that a disorder may be present; they are not diagnoses. Further ollow-up diagnostic assessments are required to establish the presence o a disease, and many people who show positive on the patch test end up testing negative or tuberculosis. Similarly, mammograms that detect lumps in the breast indicate the need or urther evaluation, but a large proportion o detected lumps are benign, so diagnosis must await a urther test, such as a biopsy. We reer to such nondiagnostic screening that serves as a stage prior to actual 148 THE LOSS OF SADNESS diagnosis as prescreening. Only the second-stage evaluation, not the prescreen itsel, justifies reerral or treatment. Prescreening instruments can be better or worse at correctly detecting the likely presence o disorder. There is a complex trade-of in the design o prescreens. On the one hand, it is desirable to eliminate as many normal people as possible rom the pool o those who require urther diagnostic screening. The costs and sometimes the risks o diagnostic testing are such that one wants to minimize the number o alse positives on the prescreen—that is, those who test positive on the prescreen and are sent on or diagnostic screening but are not ultimately ound to be disordered. On the other hand, one wants to avoid missing any disordered individuals; ideally, one wants to send all such individuals on or diagnostic screening. O these two goals, prescreening instruments or depressive disorder have emphasized the goal o not missing any cases o disorder. Consequently, they have been designed to use the ewest possible screening questions to detect any possibility o depressive disorder. The unintended result, as we will see, is an immense number o individuals who test positive on the prescreen and who thus require urther diagnostic evaluation but who have no disorder (alse positives). Unlike screening tests or most physical disorders, which provide inormation that respondents would not otherwise know, typical questions in depression prescreening instruments ask people variants o the question, “Are you depressed?” For example, in the first major study o screening, the three (o eight) items in a first-stage prescreen that were most highly correlated with receiving a secondstage diagnosis o depression according to DSM criteria were: “I elt depressed”; “In the past year, have you had 2 weeks or more during which you elt sad, blue, or depressed . . .”; and “Have you had 2 years or more in your lie when you elt depressed or sad most days. . . .” 8 Because almost anyone who has a true depressive disorder has symptoms o this type, such questions ensure that truly depressed people will prescreen positively. The flip side o this inclusiveness is that the great majority o individuals who score positively on the prescreen and who thus must be clinically evaluated do not end up receiving a diagnosis o depressive disorder when diagnostically screened. This is to be expected given the ubiquity o sadness. Unlike many screening programs or physical disorders, there is no “gold standard,” such as a biological test, that can show when symptoms o sadness indicate depressive disorder and thus can ensure that normal people are not prescreened or ultimately diagnosed as disordered. For example, an early study that used an eight-item prescreen or depressive disorder in primary medical care settings ound that a second-stage diagnostic assessment using DSM criteria confirmed only 29% o those identified as possibly having Major Depression and only 25% o those possibly having Dysthymia as actually having these disorders.9 In other words, over 70% o the cases that the prescreen indicated as possibly disordered were not ultimately diagnosed THE SURVEILLANCE OF SADNESS 149 with a disorder, despite the act that potentially overly inclusiveDSM criteria were used in the second-stage assessment. Further studies o screening confirm such findings. An overview o screening studies in primary care settings concludes that, under the assumption o a 5% prevalence rate o depression, 31 o every 100 patients will prescreen positively or depression but that second-stage interviews will diagnose only 4 patients in this group with Major Depression. 10 Expectedly, the number o MDD alse positives is especially high when prescreening involves a very small number o questions. A recent study that used two prescreening questions about experiencing 2 weeks or more o sadness during the preceding year or o losing interest in things that are normally enjoyed shows in ollow-up that about 73–82% o those who prescreen positively do not have MDD.11 The act that so many normal individuals may be sent on or a second stage o clinical evaluation is itsel a massive intervention that may have unanticipated side efects. Studies find wide variability in the proportion o patients who prescreen positively or depression, ranging rom 15 to 50%. For example, one large study that compared three diferent screening instruments ound that 20, 25, and 36%, respectively, o primary care patients prescreened positively or depressive disorder.12 Some studies that used just two questions report that nearly hal o patients have positive prescreens.13 The implication or the broader question o misdiagnosis is that the prescreen stage, whatever it accomplishes, does not eliminate anyone who might constitute a DSM alse positive. Prescreening is o interest within our broader argument or three reasons. First, prescreening itsel constitutes a minipathologization o normal emotional experiences that can lead to labeling, stigma, or sel-doubts and other concerns. Because prescreens are oten based on a small number o questions about common symptoms o sadness, they identiy virtually all intense sadness as a potential red flag. The efect is to at least raise the question o possible disorder and thus make every individual who experiences normal intense sadness a potential candidate or diagnosis. Even those who screen positively and then do not later qualiy or a DSM diagnosis may have some concerns about what made proessionals suspicious enough about their mental health to warrant a diagnostic interview. The prescreening process itsel creates a space o pathological possibilities that did not previously exist. No research is available that assesses the potential negative efects o such interventions. Second, prescreening in mass venues, such as the primary care and school settings we discuss later, sends on or second-stage DSM diagnosis all those in the community with intense sadness responses, whether or not they themselves eel disordered. Consequently, the second-stage diagnostic screening applies the DSM diagnostic criteria to virtually every individual in those settings who might qualiy or diagnosis. This means that the flaws in the DSM criteria can no longer be dismissed as merely theoretical anomalies, challenges to research validity, or loopholes o limited clinical impact that are useul or getting reimbursement 150 THE LOSS OF SADNESS or those wanting treatment. Rather, the aggressive use o minimal-symptom prescreening in efect transorms what might have remained a relatively esoteric conceptual conusion into a tool o emotional surveillance and potential misdiagnosis or each and every one o us. Third, the pressures o time and money have led to what amounts to a baitand-switch tactic in which instruments initially presented as prescreens are actually used as the ull diagnostic screens. Discussions about possible screening programs to be launched in a community initially claim that all those who prescreen positively will be clinically evaluated or disorder and thus not summarily diagnosed. However, once such programs are inaugurated, the trend is or the costly second-stage diagnostic screens to be eliminated or reduced and or the minimal prescreen itsel to become the basis or diagnosis and treatment decisions. The ollowing sections illustrate how prescreening and diagnostic screening have been pursued within two community venues, primary medical care and school settings, and how prescreening instruments oten become ull diagnostic instruments in these settings. Screening for Depression Among Medical Patients Depression in Primary Care Settings Primary medical care settings have been the major locus o screening programs to identiy and treat depression. These settings seem ideally suited or such eorts. General physicians are in a particularly strategic position to detect and treat previously unrecognized depressive disorder in large segments o the population because most people make a primary care visit over the course o any given year.14 Moreover, people with depressive symptoms are especially likely to make such visits: studies show that they are between two to three times as likely as others to visit primary care settings. 15 Thus many experts believe that there are many unidentified primary care patients who do indeed have depressive disorders; various studies claim that rom 10 to 35% o primary care patients have these disorders, a rate that jumps to about hal among those who visit general physicians most oten.16 Primary care settings are also a good locus or ollow-up interventions ater individuals are diagnosed with disorders, because many people with presumptive depressive disorder receive their only treatment in the general medical sector.17 General physicians are the sole treatment providers or one-quarter to one-hal o the people whom community surveys identiy as depressively disordered.18 Primary care settings are seen as especially good places in which to implement preventive eforts or persons with little income and education, or ethnic and racial minorities, and or the elderly, because these groups are relatively unlikely THE SURVEILLANCE OF SADNESS 151 to seek treatment rom mental health proessionals but are more likely to seek help rom their general physicians. However, despite the large proportion o primary care patients who are presumably depressed and the seemingly ideal nature o the general physician’s ofce or depression intervention, the ability to recognize and treat depression 19 in general medical settings is generally regarded as poor. Studies repeatedly report that general practitioners recognize only rom one-third to one-hal o their patients who are depressed.20 One reason or this could stem rom patient reluctance to present emotional symptoms and greater willingness to express physical complaints. Another is that physicians’ medical training naturally leads them to ocus and place higher priority on treating somatic complaints. Their busy ofce schedules also do not allow them the time to sort out psychological rom physiological illnesses, so they naturally concentrate on the physical complaints. Studies urther emphasize the inadequate treatment that primary care physicians provide to patients whom they do recognize and diagnose as depressed. Less than hal o these patients receive antidepressant medications or other standard types o depression-specific care, and even those who are medicated oten receive the wrong types or inadequate doses o medication.21 The concern about unmet need or services, combined with the deficiencies o general physicians’ responses to depression, has led to many initiatives that try to improve the recognition and treatment o depression in primary care settings.22 All such diagnostic screening eorts depend on the development and use o instruments that allow physicians to identiy cases o depressive disorder in primary care settings that would otherwise remain undetected. Because o the many time pressures in typical ofce practices, these screening instruments, i they are to be useul, must be short, easy to administer, and take little physician or patient time.23 Typically, they attempt to perorm what essentially amounts to a brie version o a DSM diagnosis using a reduced set o sel-administered questions about common symptoms o depression that are assumed to be roughly equivalent to the ull DSM criteria. Developers o screening initiatives in primary care ace two major decisions. First, how broad a population should receive them? That is, should they be applied to as many primary care patients as possible, or only to patients who are viewed as being at special risk or having unrecognized disorders? Second, what level o criteria should yield positive screens at the prescreening and diagnostic stages? The trend has increasingly been both to broaden the population that is subject to screening and to use more liberal criteria or positive screens. Beginning with the NIMH-sponsored Depression Awareness, Recognition, and Treatment (DART) campaign in 1987, a number o initiatives have tried to ocus attention o patients and providers on the underrecognition and undertreatment o depression in primary care settings.24 The initial eorts were notable or their cautious attitude toward screening, and none recommended widespread screening in primary care. 25 “The conclusion to be drawn,” the 152 THE LOSS OF SADNESS summary o the first volume devoted to this issue indicates, “is that depression questionnaires should not be routinely administered to ambulatory medical patients. There is merit, however, to such assessment practice in selected circumstances and with well-defined populations.”26 These early eforts were just as concerned with the problems created when too many people were wrongly diagnosed with depression as they were with accurately identiying people who were actually depressed. 27 To this end, these programs recommended using cutof points or depression that were higher than those used in community populations. 28 One study concluded: In sum, it does not appear, at least rom the data produced by this study, that enough o an advantageous balance o sensitivity and positive misclassification rates o these screens can be achieved at this time to enthusiastically recommend them or use in screening or afective disorders in primary care populations.29 Screening initiatives during the 1990s, however, ignored these warnings and urged the routine use o screening among as broad a group as possible.30 The World Health Organization (WHO), or example, urges that every patient who visits primary care be screened or depression.31 At the same time, the criteria used in these more recent screening eforts have become more liberal. Many initiatives came to use criteria or detecting cases o possible disorder in untreated groups that were well below DSM standards, in efect encompassing almost anyone who experienced intense sadness or a couple o weeks. The U.S. Preventive Services Task Force, or example, recommends that physicians ask patients just two questions to prescreen or possible cases o depression: “During the past 2 weeks, have you elt down, depressed, or hopeless?” and “During the past 2 weeks, have you elt little interest or pleasure in doing things?”32 Likewise, the WHO suggests that all primary care patients should be asked whether they had experienced 2 weeks or more during the preceding year when they elt sad, empty, or depressed or lost interest in things they normally enjoyed and whether these symptoms had occurred or 1 week or longer during the preceding month.33 Such minimal prescreens, when positive, are supposed to be ollowed by a ull diagnostic assessment. Diagnostic interviews that use DSM criteria to validate positive prescreens typically find that about 10–20% o primary care patients meet ull criteria or MDD. 34 The trend toward expanding prescreens to encompass subthreshold diagnoses with only two or more symptoms, however, has greatly increased the number o positive second-stage diagnoses, so that about one-quarter o primary care patients are ound to have some sort o depressive disorder. For example, the Michigan Depression Study, which usedDSM-III criteria, ound that 13.5% o amily practice patients had MDD and that 23% had some kind o depressive disorder.35 THE SURVEILLANCE OF SADNESS 153 As a practical matter, however, using two stages o screening has not proven to be a easible method o detecting cases o depressive disorder in primary care. In actual medical settings (as opposed to research studies), it is prohibitively expensive to subject the one-quarter to one-third o all patients who screen positively or depression to a second-stage screening instrument. General physicians, who see our or five patients in an hour, do not have time to interpret the results o prescreenings or to conduct ull ollow-up diagnostic interviews, and most practices do not have specialized mental health personnel available to conduct such interviews.36 Thereore, the trend has been toward collapsing screening and diagnosis into a single stage using very brie instruments. Robert Spitzer’s PRIME-MD (Primary Care Evaluation o Mental Disorders), one o the first screening instruments designed specifically to be used in primary care settings and still one o the most popular o such instruments, was the initial eort to encompass within one instrument a two-stage process that first perorms a prescreen and then, i the prescreen is positive, yields ull diagnoses o mental disorders, roughly according to DSM criteria.37 It asks patients to respond to a one-page, sel-administered questionnaire that contains 26 yes-or-no questions about common psychiatric symptoms they have experienced over the preceding month. Two o the questions prescreen or the presence o depression. They ask whether patients have oten been bothered in the past month by having “little interest or pleasure in doing things” and by “eeling down, depressed, or hopeless.” Positive responses to either o these questions trigger a clinician-administered depression module that yields diagnoses o major depression, dysthymia, or subthreshold conditions. Reflecting DSM criteria, there is no allowance or the context in which the prescreen symptoms developed, so that their presence in themselves is enough to trigger the use o the diagnostic interview. The clinician instrument takes only about 8 minutes to administer, so it appears to be a very efcient way or busy physicians to screen or possible psychiatric disorders. The overall PRIME-MD prescreening scale detects symptoms that occur so commonly that 81% o 1,000 primary care patients in the developmental trials screened positively or some disorder; only 19% were not given the second diagnostic stage. In eect, physicians would almost always administer the entire two-stage process. Results at the second stage show that about 25% o primary care patients, ranging rom 19 to 35% across dierent sites, receive diagnoses o Major Depression, Dysthymia, or both. 38 Even the 8-minute PRIME-MD interview, however, was too lengthy or routine use in regular medical settings, in which entire appointments average just 15 minutes. Spitzer subsequently developed the Patient Health Questionnaire (PHQ), which contains a nine-item depression module based on DSM criteria that does not involve a two-stage screening procedure but that directly ascertains sel-reported symptoms o MDD and subthreshold depressive conditions.39 The nine particular symptoms are ound in the example at the beginning o 154 THE LOSS OF SADNESS this chapter. As noted, the PHQ diagnoses Major Depression when at least five symptoms, including depressed mood or anhedonia, are present and diagnoses “other depression” when only two or more symptoms exist, again as long as one is depressed mood or anhedonia. In validation studies, the PHQ provides somewhat lower estimates o all depressive conditions than the PRIME-MD, averaging 16% across eight sites with a range o rom 11 to 28%. The use o such singlestage interviews is now becoming common practice in primary care settings. This compression o the process, which immediately makes a final diagnosis based only on the PHQ, leaves even less opportunity to evaluate the possibility that a nondisordered patient might receive a alse-positive diagnosis. In addition, the transormation o DSM criteria into a screening instrument that is as brie and easy to administer and score as possible can unintentionally weaken the criteria. For example, theDSM requires that most symptoms occur “nearly every day” within the preceding 2 weeks, whereas the PHQ allows a symptom to support diagnosis i it occurs on “most days.” In some instances, the DSM includes severity modifiers such as “marked,” which the PHQ does not include; and, although the PHQ presents a clinical-significance question analogous to the DSM’s clinical-significance criterion, it does not use this question in scoring. In addition, the PHQ’s two-symptom threshold or diagnosis o “other depressive disorder” illustrates the growing acceptance o the use o subthreshold symptomatology as sufcient in and o itsel or diagnosis. This trend toward using ewer criteria to identiy depressive disorders has remarkable implications when the recommendation to screen all primary care patients is taken into account. In 2001, about 84% o the U.S. population made at least one visit to a doctor’s ofce or an emergency room or had a home visit by a physician.40 I current policy recommendations to screen all primary care patients at least once a year were actually ollowed,41 roughly 60 million people would screen positively or either MDD or a subthreshold depressive disorder in a single year! Moreover, the more oten patients are screened or depression, the higher the probability is that they will receive a alse diagnosis o depression based on transient normal symptoms.42 Indeed, it seems likely that, with repeated screening, a large proportion o the population will be alsely considered to be depressively disordered at one time or another and possibly treated or a disorder that they do not in act have. The Problem of False-Positive Diagnoses in Primary Care Screening There are good reasons to expect that many primary care patients will have symptoms that meet DSM criteria or depressive disorder yet that do not truly indicate major or minor depressive disorders. Stressul lie events, which can produce high levels o intense normal sadness, precede many entries into primary THE SURVEILLANCE OF SADNESS 155 care. Although rates o help seeking rom mental health proessionals have grown exponentially in recent decades, many people still regard their primary care physicians as the first line o help when problems o living arise.43 Severe lie events such as bereavement, marital disruption, and job loss are more likely to precede the onset o symptoms among amily practice patients than among psychiatric patients, suggesting that cases o normal sadness are ound more in medical than in psychiatric settings.44 And, o course, depressive symptoms oten arise as reactions to the stresses o having medical conditions. Because normal sadness oten maniests the same symptoms as depressive disorders, including not only symptoms such as eeling depressed and losing interest in doing things but also a variety o somatic complaints such as atigue and problems with sleeping and appetite, many people who have experienced recent stressul DSM lie events will be likely to consult their physicians and may meet diagnostic criteria or Major Depression despite not having a disorder. (Note that when the symptoms do result directly rom a medical condition or substance, neither MDD nor minor depression should be diagnosed; rather, the appropriate diagnosis is depressive disorder due to a general medical condition or to substance use, a challenging discrimination or the physician to make quite independently o any issues with screening but one that screening or depressive symptoms may bring to the ore.) The problem is not just the alse-positive diagnoses that result rom primary care screening or depressive disorderbut also the skewing o the resulting decisionmaking process regarding treatment or those who are thus diagnosed. About 40% o individuals who visit primary care settings are now screened or depression and 45 other behavioral problems. In everyday medical practice, less than a quarter o 46 persons diagnosed with depressive disorders receive reerrals to specialty care. Primary care physicians, who are ar more comortable using medication than any other modality totreat depression, themselves treat thegreat majority o diagnosed patients.47 The typical result o a depression diagnosis is thereore likel y to be a prescription or antidepressant medication. Consequently, individuals treated or depression were 4.5 times more likely to receive a psychotropic medication in 1997 than in 1987.48 Many o these people who receive medications maynot have depressive disorders but may be acing serious lie challenges. It could, o course, be argued that peoplewho report normal sadness, as well as those who sufer rom depressive disorders, can benefit rom and will not be harmed by treatment. The evidence does indicate that the benefits o treatment exceed those o placebo or persons with serious cases odepression. However, depression among many patients in primary care isin the less severe range, and in this range 49 there is no demonstrated advantage or treatment over placebo. Wayne Katon, an expert on screening or depression in primarycare, summarizes: Research suggests that hal the patients initiating antidepressant in primary care have minor depression. In these patients, active treatments 156 THE LOSS OF SADNESS have not been shown to be more efective than placebo and disease management programs have not been shown to be more efective than usual care.50 Moreover, in recent years, those who have been prescribed medication by general physicians are tending to get less personal contact, with many never seeing their physicians or seeing them only one or a ew times. 51 Thus patients sufering rom normal sadness who are on medication may ail to get the accompanying counseling and support that their circumstances oten warrant. In any event, the decision to take medication is best made with as accurate an understanding o the nature and prognosis o the condition as possible and with all reasonable options or treatment considered. Diagnosis o a depressive disorder tends to quickly oreclose such discussions in the direction o medication as the most appropriate response, when normal sadness may require more flexible responses or optimal treatment. Even or those primary care patients whose depressive symptoms are severe enough to satisy ull DSM criteria, the act that they are not actively seeking treatment o their depressive conditions is a potentially important consideration. Studies o the efectiveness o therapy generally use persons who voluntarily seek treatment, and patients’ attitudes toward treatment can influence treatment efectiveness. In particular, patients with negative attitudes toward antidepressants actually have worse outcomes in intervention programs than those who get no treatment at all, suggesting that efective medication therapies require motivated participants.52 In actual practice, hal o patients have such negative attitudes.53 I many patients in primary care settings submit to physician-recommended treatment but are not spontaneously motivated to receive treatment or their unrecognized depression, therapy could be inefective. It is possible that treating normal sadness as i it were depressive disorder can not only be wasteul but also have costs or patients that must be balanced against any benefits. Screening and identiying otherwise unrecognized cases o depression may undermine normal recovery by intensiying a person’s eelings o distress and disrupting normal coping processes and use o inormal support networks.54 Providing results that indicate that people are depressively disordered can alarm and stigmatize them, especially i they themselves do not experience their eelings as disorders. It is thus perhaps not surprising that many people who screen positively resist being treated or depression. 55 Others might start taking medications but then discontinue treatment ater a short period o time.56 Such “noncompliance,” although certainly o concern in some cases, in other instances might result rom an accurate recognition o conditions that result rom ordinary lie stressors and a choice to approach the problem in an alternative way. The primary care depression screening movement is a well-intentioned efort to develop and deploy psychological instruments that enable us to prevent THE SURVEILLANCE OF SADNESS 157 potentially harmul outcomes o unrecognized, untreated depressive disorder in the general population. Despite the limitations and concerns raised here, the enormous eorts invested into the development and dissemination o screening instruments may have an increasing payo as the instruments are refined. In particular, screening in primary care may well be made more worthwhile in the uture i contextual indicators o normal reactions can be built into instruments so as to allow better identification o likely cases o disorder. Aside rom context, it may be presumed that i symptoms are chronic, recurrent, or unusually severe, the condition is more likely to stem rom a depressive disorder. Focusing resources on preventing recurrence in cases with multiple prior episodes, or example, may be a more efcient policy goal than screening all primary care patients or depression.57 Pending the development o better screening instruments and considering scarce resources, eorts to improve the treatment o selpresenting cases o depressive disorder should take priority over mass screening programs.58 Most important, when physicians screen or depression, and contrary to the current advice to attend only to symptom scores, they should be cautioned to attend also to the context o the reported symptoms and urged to use their diagnostic common sense and a policy o “watchul waiting” rather than blindly ollowing DSM criteria-based results and reflexively prescribing medication. Screening for Adolescent Depression Schools are a second major target or screening o depressive disorder. Adolescents provide a particularly attractive ocus or screening and preventive eorts because they appear to have high rates o depressive disorder, yet at the same time they are rarely treated or their conditions.59 Suicide among adolescents provides another rationale or depression screening. About 4,000 American children and adolescents commit suicide each year, making it the thirdleading cause o death among 15- to 24-year-olds and the ourth among 10- to 14-year-olds; over hal a million adolescents attempt suicide with sufcient seriousness to require medical attention.60 Moreover, enormous publicity is accorded to rare but shocking school shootings by adolescents who in some instances have been depressed, imparting an additional urgency to arguments or preventive screening eorts. The belie that, in addition to these immediate problems, untreated adolescent depressive disorder is also likely to persist into adulthood and become chronic motivates screening eorts, as well.61 Early identification and treatment are claimed to stop the downward spiral o increasingly worsening problems. Finally, all adolescents are mandated to attend school, and everyone is an adolescent at some time, so the schools provide a readily available opportunity to screen a population that over time will include virtually all individuals. Consequently, it is claimed, “prevention o the entire spectrum o depressive problems experienced by adolescents 158 THE LOSS OF SADNESS is o paramount importance i the needs o the largest number o adolescents are to be met.”62 Concern about teenage depression in general and suicide in particular has led to major policy initiatives. The 2003 President’s New Freedom Commission Report recommends that every adolescent in the entire country ought to “have the opportunity or early and appropriate mental health screening, assessment, and reerral to treatment.” Already several state legislatures have adopted measures with the goal that “every child should be screened or mental illness once in their youth in order to identiy mental illness and prevent suicide among youth.”63 In 2004 President George W. Bush signed a bill authorizing $82 million to und such screening programs beginning in sixth grade, with the goal o preventing suicide among young people.64 Our concerns about these well-intentioned eforts to help adolescents are similar to those that arise with respect to primary care screening. These eforts tend to ignore the distinction between disorders and conditions that are normal reactions to real losses. They thus ocus clinical resources on many who are in transient normal states and they trigger interventions that tend to emphasize medication rather than addressing possible real problems in the adolescent’s circumstances that might be causing intense distress. Moreover, the decontextualized instruments used to prescreen youths or depressive disorder or suicidal potential cast such a broad net that they identiy much o the adolescent population as potentially at risk and as in need o urther evaluation, conusing normal emotions with likely mental disturbance. A second-stage diagnostic screening may eliminate many o these errors but also applies symptom-based DSM criteria to adolescents’ labile emotions, possibly still yielding substantial alse-positive identifications o depressive disorder and suicide risk. Nor thus ar is there scientific evidence that provides support or the efectiveness o teen screening. Pathologizing Adolescent Distress The primary justification or screening and preventive eforts in schools lies in the high perceived prevalence o depression among adolescents. A review o 52 studies rom more than 20 countries indicates that about 20% o adolescents have depressive disorders according to DSM criteria.65 Studies undertaken ater 1990 showed even higher mean prevalence rates o 26% or some depressive disorders. Some researchers estimate that up to a third o adolescents will experience episodes o MDD by age 20.66 Nearly hal o one large sample o ado67 lescents report having either a subthreshold or ull diagnosis o depression. For most researchers, these data support an obvious conclusion: “It is clear that 68 depression is a major, pervasive, and perhaps increasing problem or youth.” However, as in primary medical care, the nature o the screening and diagnostic instruments used or adolescents ensures that they are ar more likely to THE SURVEILLANCE OF SADNESS 159 uncover transitory and self-limiting cases of normal sadness than depressive disorders. These instruments do not inquire about the context in which symptoms develop. Thus, they cannot distinguish disorder from normal distress that arises from common adolescent stressors, such as arguments with parents, perceived betrayals by friends, or not being chosen for a valued activity, club, or athletic team. For example, many adolescents who have recently broken up with a boyfriend or girlfriend surely do not have depressive disorders, but nevertheless they may report enough symptoms in the ensuing period of time that screening and diagnostic instruments count them as depressively disordered.69 Indeed, the potentially misleading nature of the statistics on adolescent depressive disorder is strikingly illustrated by the fact that the recent breakup of romantic attachments is the strongest predictor of depression in a large, national sample.70 Unlike typical cases of disorder, symptoms of adolescent depressio n are extremely unstable. Studies commonly find that most high scorers on selfreport measures change their status when retested soon after. a third of adolescents remain depres sed after only 1 month. 71 72 Only about The relative emotional lability of adolescents, w hich would naturally lead to higher rates of transient neg ative emotions than in other g roups, compounds the problem of using measurements that do not tak e context into account. The instability of symptoms among adolescents sugges ts that they are more likely to be transient respon ses to stressful life circum stances than the results of internal dysfunctions. Research also fails to support claims that mild symptoms at one point in time are likely to become more severe at later periods. Most adolescents who initially report mild symptoms of depression report a year later that their symptoms are minimal or mild—that is, that their symptoms have decreased or remained the same; conversely, most adolescents who initially report severe symptoms report after a year that their symptoms have decreased rather than remained severe.73 Nonetheless, a minority of adolescents with mild symptoms does get worse, and a minority with severe symptoms remains severe after a year. We might surmise that this minority of cases tends to include the truly disordered. The focus in screening research should be on developing more fruitful strategies for identifying and targeting this minority for intervention. Columbia University TeenScreen One major motivation for widespread screening of adolescents is to prevent suicide, and recently screening instruments have been developed that are spe- cifically designed to detect suicidality and related mental disorder in teens. The President’s New Freedom Commission cites the Columbia University Teen Screen program as a model and urges its use in every school in the country. We therefore take a closer look at TeenScreen as an example of the current state of the art in adolescent screening. 160 THE LOSS OF SADNESS The TeenScreen program has developed two scales for use in prescreening adolescents. Both are derived from questions on a child diagnostic survey, the DISC (Diagnostic Interview Schedule for Children), and both require administration of the DISC as a second-stage diagnostic screening for those who test positive on initial evaluation. One, the DISC Predictive Scale (DPS), diagnoses eight mental disorders. With respect to depression diagnosis, it is very similar to the prescreening instruments we considered in the previous section on primary care. It asks very general questions at the beginning of the instrument, such as “In the past six months, were there times when you were very sad?” or “In the past six months, has there been a time when you weren’t interested in anything and felt bored or just sat around most of the time?”74 Any “yes” answer to these questions leads to several further questions about specific symptoms, such as having “a time when nothing was fun for you, even things you used to like” or being “so down that it was hard for you to do your schoolwork” or “grouchy or irritable . . . so that even little things would make you mad.” Although designed as a prescreen instrument, the DPS has come to be seen as a potential stand-alone diagnostic instrument. The executive director of TeenScreen, Laurie Flynn, in testimony before a congressional committee, stated: “In 2003, we were able to screen approximately 14,200 teens . . . ; among those students, we were able to identify approximately 3,500 youth with mental health problems and link them with treatment.”75 Flynn here equates a positive prescreen with having “mental health problems,” yielding about a 25% rate of such problems among a general student population. Yet studies show that the DPS yields four to five false-positive diagnoses for every DISC-confirmed diagnosis. Moreover, the DISC itself is simply an application to children and adolescents of DSM-style symptom-based criteria, and we have seen the questionable validity of these “confirming” criteria. If the DPS is widely used as either a prescreening or diagnostic instrument, the result is likely to be a massive pathologization of normal adolescent sadness and distress. The other major TeenScreen instrument, the Columbia Suicide Screen (CSS), a brief 11-item (or sometime s 8-item; the number varies with the version) prescreening instrument self-administered by students, is designed to prescreen for risk factors that specifically increase suicide risk, including depressive disorder. To avoid making it obvious that the instrument is about suicide, the operati ve question s are embedded with in a broader set of health questions and the instr ument itself is labeled a “health sur vey.” The CSS asks whether the individual has ever attempted suicide, has thought about suicide with in the past 3 months , has exper ienced an y of a short list of depres- sive symptoms (e.g., “unhappy or sad,” “withdrawn”), anxiety symptoms, or substance use symptoms within the past 3 months, or feels a need to talk to a professional . Any student who answers “yes” to any one of the questions about suicide attempt, suicidal ideation, or need for help or “yes” to three of the questions about sympto ms of depression, anxie ty, or substance use is THE SURVEILLANCE OF SADNESS 161 “positive” and is referred to a professional for further diagnosis and possible treatment. How well does the CSS accomplish its goal of identifying those students with significant risk of suicide? If the numbers are any indicator, the answer is “not very well.” In a major test of the CSS by its srcinators, 28% of 9th- to 12th-grade students tested positive on prescreening for risk of suicide, with the rate approaching half of all students (44%) in one school.76 Seventeen percent of students report either thinking about suicide in the preceding 3 months or attempting suicide sometime in the past. The fact that nearly one in five adolescents reports either suicide attempts or suicidal ideation and that over 10% report thinking about suicide in the previous 3 months alone is either truly alarming or, more likely, indicative that the questions are not assessing what they are trying to assess and instead are tapping thoughts and feelings that many adolescents who are not truly at risk occasionally experience. A further problem for both the CSS and the confirming DISC is the surprisingly low reliability in the answers to the relevant DISC questions. When the same questions about suicidal potential are asked at 8-day intervals, only about half of students who provide positive answers at one time also score positively just a week later! Given the extraordinarily unstable nature of the responses about suicidal ideation on the TeenScreen instrument, even the designers of TeenScreen admit that: “Poor test-retest reliability could be related to the ephemeral nature of suicidal ideation and depressive feelings among teens.”77 The low reliability means that we cannot be sure howseriously to take either the CSS or the follow-up DISC results. And we have seen that the DISC’sDSM-style decontextualized criteria, especially when applied to emotionally reactive and labile teens, are of questionable validity in ferreting out the disorders among all those who are transiently distressed for a variety of normal reasons. Even though the DISC does reduce the percentage of positive diagnoses to 4% of the student population, it is impossible to have confidence that they are the right 4% who are really at risk or disordered. One way to check the validity of the DISC is to compare its results with clinicians’ diagnoses. Disturbingly, despite the fact that clinician diagnoses themselves are generally based on DSM criteria, studies indicate extremely low levels of agreement between DISC and clinician diagnoses, further eroding confidence in the validity of even the two-stage TeenScreen procedure.78 TeenScreen researchers, aware of many of these problems, suggest at one point that perhaps even the enormous number of false positives generated by the CSS without DISC verification is not such a bad thing after all: “It is impor- tant not to lose sight of the fact that many of these so-called false-positive cases may be experiencing painful depressive symptoms with social and academic impairment and are likely to benefit from treatment.”79 This passage suggests that even if the CSS were used as a stand-alone suicide screen without a second DISC stage, teens who are not disordered may nonetheless benefit from treatment, 162 THE LOSS OF SADNESS and the same argument could be applied to DISC alse positives. But the treatment o alse positives may not be so innocuous. Recall that the goal o screening programs, now being enacted into law, is to screen “every child in America” or depression and suicide potential. 80 Once TeenScreen identifies cases o putative depression and suicidal tendencies, the most common next step would be to treat with antidepressant medication, and this does seem to be TeenScreen’s goal: “For antidepressant medication to be used efectively, cases o depression need to be identified, adding to the importance o screens o the type described here.” 81 Although many normal but troubled youths can benefit rom talking with a counselor, the possibility o treating nondisordered adolescents in large numbers with antidepressant medication or normal situational reactions that are likely transient and that might be dealt with in other ways raises special issues and concerns. There are real questions as to whether antidepressant medication works efectively in teenagers. 82 Most studies o this issue show no greater benefits o antidepressant medications compared with placebo.83 Those studies that do find that medication benefits depressed adolescents are limited to voluntary samples with diagnoses o MDD that are stable over time. And even here the diferences between treated and placebo groups tend to be minimal.84 Moreover, as we saw with respect to primary care screening, the screened-positive populations may be diferent rom, and may react to treatment diferently than, sel-reerred clinical populations. Indeed, the U.S. Preventive Services Task Force does not recommend screening children or adolescents or depression or suicide.85 Evidence is also beginning to emerge that the risks o drug treatments may be greater or children than or adults.86 Although clinical trials o medications have not yet reported any actual suicides, they do appear to show higher rates o suicidal ideation and other adverse events among groups taking antidepressant medication compared with placebo.87 In some cases, such as school shootings, which are sometimes used to justiy the need or screening, perpetrators were already using SSRIs that at least a ew experts believe might even have contributed to the murderous state o mind o those particular teens. 88 I millions o adolescents were diagnosed as depressed and then medicated, the possibility that a number o teens would newly develop suicidal thoughts would have to be balanced against the number whose suicidal thoughts drugs would efectively control. The alarm generated by these findings has led regulatory agencies in Great Britain to warn physicians not to prescribe most antidepressant medications or persons younger than 18. Likewise, in the United States, the FDA now requires warnings on every bottle o pills about the possible adverse efects o antidepressants on younger persons. This whole area remains highly controversial, but the possibility o vast increases in the number o teens taking such medication due to invalid screening raises these concerns with a vengeance. At the least, the questionable or minimal efectiveness o antidepressant medications or children and adolescents, coupled with the possible efects o these THE SURVEILLANCE OF SADNESS 163 medications on increasing adverse events and the as-yet-unknown eects o imposing long-term medication regimens on large numbers o still-developing teenagers who may not be disordered, are reasons or pursuing cautious rather than sweeping screening programs until more inormation is available. These considerations also argue or prudence in the treatment recommendations those programs may be used to support. With regard to our ocal issue o the overdiagnosis o depressive disorder, anyone who reports a ew depressive symptoms on the CSS, even without suicidal behaviors or thoughts, is sent on or a DISC. In eect, the CSS is a way, motivated by the urgency o the desire to prevent suicide, o screening vast numbers o teens or depressive disorder with the associated alse-positive problems we have identified. Yet unlike in epidemiologic research, the result o a TeenScreen “alse positive” is not merely theoretical or statistical. The result is the personal identification o a specific young person as having a major mental disorder and perhaps as being in danger o urther deterioration or suicide. This in turn can suggest a reconceptualization o the nature o that youth to him- or hersel, his or her parents, and school ofcials; can alert parents, as well as school personnel, to the individual’s presumed disorder; and possibly (i treatment is not reused) can lead to treating the individual with medication or psychotherapy that has unknown impact on a normally developing youth. As the news media’s sensational stories remind us, there is a very small but real possibility that undetected mental disorder in one’s own children or in their classmates could lead to some horrific outcome such as suicide or homicide. The desire to do something to make our children saer rom such threats is understandable. The problem is that the science does not yet exist to allow us to predict and intervene in ways that are known to prevent such tragedies. Moreover, screening programs that are justified by assurances that the results will be careully evaluated clinically to eliminate alse positives tend over time to be reinterpreted as conclusive diagnostic instruments and used as triggers or treatment in their own right. Yet none o the currently available instruments or screening young people takes the context o distressing eelings into account. Thus none can discriminate normal adolescent emotionality rom mental disorder. The result is a potential or a proound intrusion into our children’s emotional lives using diagnostic labeling that is o questionable validity. Conclusion Routine screening or depression in the general population at locations such as schools and doctors’ ofces is now viewed as a major policy goal and an almost unqualified good. Given that such initiatives can influence the lives o millions o people, it is important to consider their possible costs and to critically scrutinize 164 THE LOSS OF SADNESS their underlying assumptions. Screening programs have repeated the mistake made in epidemiology o ailing to seriously reassess validity when transporting the DSM’s criteria to the new context o community screening. They monitor the nuances o changing emotional reactions in us and our children in response to lie’s vicissitudes and label a considerable number o them as pathological without adequate contextual constraints. As these programs become part o our lives, they potentially influence our sel-concepts and our judgments o others and oer a new orm o social penetration o our private emotions. This orm o influence is hard to quantiy but real nonetheless. The ultimate eect could be to reconstitute our view o the normality o distressing eelings and to expand psychiatry’s power to monitor, classiy, and perhaps control our emotions in order to prevent even transient role impairment. Screening initiatives might be beneficial or they might not be; at present, we just do not know. Remarkably, there currently exists no controlled scientific study that shows that these massive screening and treatment programs improve overall outcomes o depressive disorder or suicide. Nor does evidence exist that the benefits o such programs outweigh the costs o the inappropriate diagnosis and treatment they may initiate. This should especially trigger alarm bells when it comes to teen screening. I one looks or historical analogies, this new surveillance o sadness is arguably comparable in its magnitude, its penetration o our intimate lives, and its encouragement o both proessional and amily hypervigilance o ordinary lie to the much-discussed surveillance and medical pathologization o childhood masturbation that typified the sexual ears o the Victorian era. Just as that misconceived sexual control distorted children’s natural sexual development even as it claimed to prevent or cure disorder, current campaigns to screen or depression, although they sometimes identiy true disorder, have the potential to distort reactions to the natural experience o sadness in normal individuals and to disrupt any constructive eatures o normal sadness. The challenge in eectively targeting preventive eorts via screening is to create instruments that are sufciently sensitive to context so that they are able to distinguish the truly disordered rom the normally distressed within the population o individuals who do not spontaneously present themselves or treatment. Policy eorts should promote pilot projects to develop scales that will be sensitive to the context and duration o symptoms and that will distinguish depressive disorders rom normal sadness, thus better identiying those individuals who truly need proessional help. 8 The DSM and Biological Research About Depression R esearch into the biological causes o depressive disorder, such as its grounding in neurochemicals, receptors, genes, and the structure and unction o the brain, holds great promise o contributing to our growing understanding o behavior, as well as o leading to new and more efective treatments. Such studies include, or example, those that use magnetic resonance imaging (MRI) to explore brain activity in depressed patients, examinations o neurotransmitters and their role in depression (bolstered by the success o medications in influencing the level o neurotransmitters), and research on the genetic influences on depressive disorder. Around the same time as the publication o the DSM-III in 1980, biologically grounded models o depression began to dominate psychiatric theory and practice, and the influence o psychosocial models began to wane.1 Moreover, a number o leading figures in the construction o the DSM were also leading biologically oriented psychiatrists. It is thus tempting to see the two as conceptually linked. Yet, as we have seen, the DSM definition was not in act intended to imply any particular cause o depression. Instead, it was designed to be theory-neutral and compatible with social and psychological, as well as biological, causes o symptoms. Nonetheless, the DSM criteria have played a prominent role in research studies on the biology o depression. The presence o agreed-on, theory-neutral criteria that could orm a basis or communication among researchers has certainly been beneficial to biological research, as to all psychiatric research. However, on the other side o the ledger, we argue that the conflation o normal sadness and depressive disorder in DSM criteria has handicapped biological research and created conusion that can potentially lead researchers to draw misleading con- clusions rom their data. The basic problem is simply that biological processes underlie nondisordered, as well as disordered, human traits. No doubt disordered sadness reactions 165 166 THE LOSS OF SADNESS oten are due to underlying biological malunctions. But the same symptoms o sadness are present in both normal and disordered conditions. The biological processes that are specific to disorder must be distinguished rom the biological processes that underlie normal sadness. For example, studies show that many normal emotions and attitudes, such as introversion, religiosity, and even political belies, have a genetic component. 2 Genetic influences also explain to some 3 extent why people naturally grieve when a beloved intimate dies. The act that there is a genetic basis or grie does not show that grie is a disorder—rather, bereavement is biologically grounded in normal, not in deective, genetic processes. Thus research that shows a biological or genetic correlate o a sadness condition says nothing in itsel about whether or not that condition is a disorder. Similarly, brain scans used in studies that induce states o sadness in normal participants indicate biological changes comparable to those ound among persons with depressive disorders.4 Thus the MRI o a normal individual who has sufered a severe loss resembles the MRI o a depressively disordered individual, most likely because o their similar subjective experiences.5 The pattern o brain activity associated with symptoms consequently cannot be used as a basis to iner disorder, unless the context o the brain images is taken into account. The same point applies to studies o neurotransmitter levels; changes in neurotransmitter levels may occur during periods o normal intense sadness, as well as o depressive disorder, and some more complex underlying processes that involve neurotransmitters that are not properly responsive to environmental circumstances are liable to be present in disorders. I scientists consider only the correlation between biological markers and DSM criteria without taking into account the context in which they occur, they could wrongly conclude that a marker indicates disorder rather some phenomenon common to normal sadness and disorder. This chapter considers some o the most common ways that biological psychiatry has attempted to show how depression is grounded in abnormalities o brain unctioning. These include studies o twins and adoptees, o neurochemical deficiencies, o genetic deects, and o anatomical lesions. We argue that an adequate context-based distinction between normal sadness and depressive disorder would enhance each o these styles o research. Twin and Adoption Studies For most o the twentieth century, biological research ocused on using twin and adoption studies in attempts to show the genetic basis o depression. The central goal o these studies was to separate the impact o genetic and environmental actors in the illness. Twin studies capitalize on the act that there are two kinds o twins that have known, but diferent, degrees o genetic similarity. Dizygotic THE DSM AND BIOLOGICAL RESEARCH ABOUT DEPRESSION 167 (DZ) twins, like regular siblings, share 50% of their genes, whereas monozygotic (MZ) twins are genetically identical. Both types of twins presumably share the same family environment. To the extent that genetic factors influence depression, MZ twins ought to have twice the concordance rate as DZ twins. Conversely, if environmental factors are predominant causes, both types of twins should exhibit comparable levels of depression. The logic of adoption studies derives from the fact that the parents who transmit genes to their children are not the same parents who raise these children. Therefore, findings that show high rates of depression among children born to depressed mothers but raised by nondepressed adoptive parents would indicate that depression has a genetic component. In contrast, rates of depression among adopted children that more closely resemble those among their adoptive than among their natural parents would indicate that environmental factors have a stronger influence than genetic ones. The voluminous literature on twin and adoption studies regarding the genetic contribution to depression yields ambiguous findings. Some twin studies show strong genetic but weak environmental influences, others show the reverse, and many show only a slightly higher concordance among MZ than among DZ twins.6 Likewise, some adoption studies indicate a higher concordance in rates of depression among adopted children and their natural parents than among those children and their adoptive parents,7 whereas others indicate just the reverse.8 But overall, it appears reasonable to conclude that the heritability of depressive disorder can lie in the range of about 30–40%. 9 Even if it were possible to draw definitive conclusions from these studies, we would still not know whether what is geneticallyor environmentally transmitted is a depressive disorder or normal sadness. No evidence demonstrates that depres sive disorders have a higher probability of inheritance than tendencies to become sad. Indeed, it appears that people inherit predispositions to be on the high or low range in the distribution ofsadness responses or to have depressiv e disorder to about the same degree. Twin studies indicate that personality traits related to sadness, such as introversion, haveheritabilities of about 40–50%, quite similar tothose of depressive disorder.10 Therefore, showing that some trait a hs a high probability ofbeing inherited says little about whether that trait is a disorder or a normally distributed personality characteristic. Before researchers can legitimately conclude that their biological findings reflect the egnetic basis of conditions that aredisorders, they must first use a definition of depression that adequately separatestheir research groups into those with depressive disorder and those with normal sadness. Depression Stems From a Chemical Imbalance Current biological research has the potential to be more informative than twin and adoption studies about the specific causes of depression because it directly 168 THE LOSS OF SADNESS examines genes and brains, rather than inerring genetic contributions rom the degree o relatedness among individuals. Nevertheless, it sufers rom the same conceptual problems as these studies. One typical kind o study searches or neurochemical levels that are related to depressive disorders. 11 But in order to reach appropriate conclusions, we must understand the context in which various levels o chemicals arise. Showing an association between some brain state and depressive symptoms cannot in itsel answer the question o whether the symptoms are normal responses to stressul environments or indicators o a disorder. The findings o current studies o neurochemicals and depression are oten uninterpretable because they do not adequately make this distinction. One o the most popular theories posits that a chemical imbalance in the brain, specifically deficient amounts o the neurochemical serotonin, causes depression. It ollows, then, that drug treatments targeting serotonin, the selective serotonin reuptake inhibitors (SSRIs), which presumably correct this chemical imbalance, are the appropriate response to depressive disorders. This theory is relentlessly promoted in many ways: pharmaceutical advertisements emphasize how correctable chemical imbalances cause depressive disorders, public service messages stress that depression stems rom flaws in brain chemistry rather than in character, and mental health advocacy groups advance the message that depression is a physical, brain-based illness, just like diabetes or asthma.12 These ubiquitous messages have led to the widespread impression that research has actually shown that chemical deficiencies are the cause o depressive disorders and that drugs work because they correct these impairments in the neurotransmission system. Thereore, it might seem that one way to separate depressive disorders rom normal sadness would be to examine levels o serotonin in the brain. The chemical deficiency theory o depression srcinated with psychiatrist Joseph Schildkraut’s hypothesis, published in 1965, that low levels o amines were associated with the development o depressive disorders. His paper is still one o the most requently cited articles in the history o psychiatry.13 Interestingly, Schildkraut thought that norepinephrine, not serotonin, was the neurochemical implicated in depressive disorder: The “catecholamine hypothesis o afective disorders,” proposes that some, i not all depressions are associated with an absolute or relative deficiency o catecholamines, particularly norepinephrine at unctionally important adrenergic receptor sites in the brain. Elation conversely may be associated with an excess o such amines.14 The major source o evidence or the chemical deficiency hypothesis stems rom the success o drug treatments, which raise levels o amines, in alleviating depressive symptoms. Schildkraut himsel recognized that “even i the drugs are efective in treating the disorders, that does not necessarily imply that their mode THE DSM AND BIOLOGICAL RESEARCH ABOUT DEPRESSION 169 o action involves correction o the underlying abnormality.”15 Nevertheless, many subsequent arguments relating to serotonin rely on the premise that i enhancing its transmission improves depression, then a deficiency in the serotonin system may be responsible or the initial emergence o the condition. Many problems beset such theories. One is that the SSRIs cause immediate changes in levels o serotonin, but the resulting eects on depression typically take several weeks to transpire. The impact o the drugs on depression, thereore, might not result rom the change in neurotransmitter levels that they create but instead rom a number o other processes associated with the change in amine activity. Another is that some drugs that do not aect either serotonin or norepinephrine, the major amines involved in the catecholamine hypothesis, also can alleviate depression.16 Indeed, some antidepressant drugs developed ater the SSRIs influence dopamine and other amines, but not serotonin. A third difculty is that the drugs used to treat depression work with at least equal eectiveness on other disorders, including those o anxiety, eating, attention deficit, substance abuse, personality, and a host o other conditions that may or may not be comorbid with depression. This suggests that the drugs are not correcting a specific neurochemical abnormality that underlies depression but are instead acting on very general brain unctions that influence many emotional and behavioral systems. No theory explains how such a single abnormality in brain chemistry could be related to such a wide range o resulting problems. In addition, measures typically show that only about 25% o depressed patients actually have low levels o norepinephrine or serotonin. 17 Even i the deficiency hypothesis is proven to be correct, it would explain only a portion o depressed cases, as Schildkraut himsel recognized in his srcinal article. 18 Another undamental problem is that the hypothesized deficiencies o serotonin or other brain chemicals quite possibly may be the consequences, rather than the causes, o depression. No evidence thus ar has demonstrated that chemical imbalances actually precede and cause depressive disorders. 19 Instead, depression itsel, as well as the drugs used to treat it, could be responsible or the inerred deficiencies that exist in patients with depression. Because most research participants have long histories o medication treatment, it is impossible to know what their unmedicated brains looked like beore they began using antidepressant drugs. The most serious conceptual problem with the neurochemical deficiency hypothesis, rom our perspective, is that no adequate contextually grounded standard exists or normal versus disordered levels o serotonin or other amines. High or low levels o any neurochemical are not abnormal in themselves, but only in relation to a particular set o circumstances and to the way the brain is biologically designed to respond to those kinds o circumstances. The mechanisms that underlie levels o serotonin (and other neurochemicals) likely are biologically designed to be quite responsive to their contexts: the brains o normal people who are experiencing serious losses would expectably show depleted 170 THE LOSS OF SADNESS states o serotonin. The normality o amine levels can be established only relative to the environmental context in which they occur. For example, as the studies considered in chapter 2 show, serotonin levels among primates vary substantially as a unction o social situations: gains and losses o social status are associated with rising and alling levels o serotonin, respectively.20 Thus low levels o serotonin in humans also could reflect the emotions that normally accompany a recent change in social status rather than a depressive disorder. Likewise, baboons living in the wild show highly elevated levels o glucocorticoids (stress hormones) ater experiencing bereavement, loss o social rank, or other stressul events.21 These levels return to normal ater the afected animals resume grooming behaviors with members o their social networks. In these cases, extreme levels o neurochemicals do not indicate disorders but show instead the way that normal brains respond to stressul situations. Conversely, disordered states are associated not with extreme levels o neurochemicals alone but also with extreme levels that are inappropriate responses to environmental contexts. The sorts o changes in the brain that result rom depressive disorders are similar to responses to acutely stressul situations.22 Indeed, an extreme amount o serotonin or other amine in response to a stressor can be adaptive in the situation in which it occurs. 23 The diference between normal and abnormal levels o neurochemicals lies not in the level o the neurotransmitter per se but rather in the act that the neurotransmitter level has escaped rom usual restraints and become more chronic and removed rom environmental circumstances. Statements that depression is a “flaw in chemistry” or a “physical disease” are premature; cognitive, psychodynamic, social, or other actors that enduringly disrupt biologically designed sadness reactions but that may or may not correlate with brain abnormality may well cause at least some depressive disorders. “The truth is,” notes psychologist Eliot Valenstein, “that it is really not known how drugs alleviate the symptoms o mental disorders, and it should not be assumed that they do so by correcting an endogenous chemical deficiency.”24 But or uture research to have a better chance o confirming or disconfirming that some deficiency in neurotransmitter systems is causally related to cases o depressive disorder, researchers will have to use criteria that can separate cases in which various levels o neurochemicals result rom normal brains operating in stressul environments rom those in which some abnormality leads to inappropriate brain unctioning. The Genetic Basis of Depression Studies o the genetics o depression have entered a new era. Major breakthroughs in genetic research during the 1990s have allowed researchers to directly map specific genes and examine their connection to the development THE DSM AND BIOLOGICAL RESEARCH ABOUT DEPRESSION 171 of symptoms. 25 Yet, despite these advances, current research on the genetics of depression remains handicapped by its failure to distinguish under which circumstances genetic factors lead to biologically selected responses to loss or to mental disorders. Current DSM symptom-based definitions of depression do not adequately distinguish intense normal sadness from disorder, yet much important genetics research relies on population-based samples that are likely to be composed of predominantly normal individuals. Thus researchers are in jeopardy of mistakenly identifying findings about the roots of normal sadness as discoveries about the causes of depressive disorder. To illustrate how this error might occur, we focus on a single article, “Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene” by psychologist Avshalom Caspi and colleagues.26 This article’s influence on the general scientific community may be greater than that of any genetic study of any mental illness that has been conducted to date. Science magazine named it, along with two other articles on the genetics of mental illness, the second most important scientific breakthrough of 2003 (after only an article about newfound insights into the nature of the cosmos). The National Institute of Mental Health’s (NIMH) Web site cites the study as one of the great accomplishments of the agency’s focus on the biological basis of mental illness. Thomas Insel, the director of the NIMH, claims that: “What they have done is going to change the paradigm for how we think about genes and psychiatric disorders.”27 Another NIMH psychiatrist calls the study “the biggest fish yet netted for psychiatry.”28 The study’s findings were broadly disseminated and featured in both U.S. and worldwide media.29 The research stems from a longitudinal study of a cohort of 847 Caucasians in New Zealand born in the early 1970s and followed from birth into young adulthood. The researchers’ central concern was to examine the association between stressful life events, depression, and the 5-HTT gene when cohort members were 26 years old. The 5-HTT gene was chosen for study because it controls the way that serotonin, itself the focus of much genetic research on depression, passes messages through brain cells. Previous research suggested that the gene is associated with reactions to stressful stimuli in mice, monkeys, and people undergoing brain imaging, although no prior studies had found a direct link between the gene and depression. The 5-HTT gene has three genotypes: in the New Zealand sample, 17% of respondents had two copies of the short allele; 31%, two copies of the long allele; and 51%, one short and one long allele. The study measured stress through an additive index of 14 life events, including employment, financial, housing, health, and relationship stressors that participants experienced between ages 21 and 26. It also used the Diagnostic Interview Schedule (DIS), designed to perform DSM diagnoses, to determine whether or not participants had experienced an episode of Major Depression over the preceding year. The study also reported on number of depressive symptoms, on suicidal ideation, and on informant 172 THE LOSS OF SADNESS reports o depression. Its central hypothesis was that people who have one or two o the short versions o the 5-HTT allele might be especially vulnerable to highly stressul environments, whereas those with genes containing the long version might be more resistant to adverse environmental stressors. The study ound that 17% o this population sample o 26-year-olds reported episodes o depression severe enough to meet MDD criteria over the preceding year. It showed no association between the 5-HTT gene and those who became depressed. There was, in other words, no direct genetic efect on depression: people with two short alleles, two long alleles, or one o each allele had equivalent chances o becoming depressed . The study also ound no relationship between the 5-HTT genotype groups and the number o stressul lie events that participants experienced, so the genotype should not account or diferential exposure to stressors. That is, it was unlikely that possessing a given genotype was the cause o the number o stressul lie events that respondents reported. The study did find a strong positive relationship between experiencing more stressul lie events and developing depression. As the number o lie stressors increased rom zero to our or more, rates o MDD increased rom 10% to 13, 15, 20, and 33%, respectively. Put another way, people who experienced our or more stressul lie events were about three and a hal times more likely to develop depression than those who experienced no stressul events. The study’s major finding, and the one that generated much attention, was a significant gene-by-environment interaction. Among the 15% o the sample who experienced our or more stressul lie events ater their 21st and beore their 26th birthdays, those with one or two copies o the short allele on the 5-HTT gene were significantly more likely to have MDD, as well as sel- and inormantreported depressive symptoms, than those with two copies o the long allele. In the group that aced our or more stressul lie events, 43% o individuals with two short alleles and 33% with one short allele became depressed compared with 17% o those with two long alleles who did. In summary, the study did not find a direct efect o the 5-HTT gene on depression. It did find a airly strong relationship o stressul lie events with depression, so that people who experienced more stressul events had a greater chance o becoming depressed. And it ound that the 5-HTT gene interacts with the number o lie events to predict depression; at high levels o stressul events, possession o the short gene leads to more depression. The authors viewed their finding as confirmation o the “diathesis-stress theory o depression,” which predicts that experiences o higher levels o stress will elevate the vulnerability o depression much more among people who are at high genetic risk than among those at low genetic risk.30 The short allele on the 5-HTT gene presumably makes people more sensitive to stress, whereas the long allele protects them rom the impact o stress. Thereore, the short allele is the stress-sensitive genotype associated with depression. THE DSM AND BIOLOGICAL RESEARCH ABOUT DEPRESSION 173 But this interpretation o the short allele is open to question, at least or the most classic case o depressive disorder, endogenous depression. The study ound that about 10% o the 263 people who had experienced no negative lie events over the preceding 5 years developed depression. This 10% was the group who most clearly had depressive disorders as opposed to normal intense sadness, yet there was no impact o the 5-HTT genotype on this group’s response to stress. I there is a genetic cause o endogenous depression, it does not seem to show up here, so this particular type o depressive disorder appears unrelated to the 5-HTT gene or, at least, to the widespread variants o it that Caspi et al. studied. There is a much more undamental problem with Caspi et al.’s interpretation o their findings: it is not clear that the identified gene has much to do with depressive disorder at all. The study used DSM criteria or depression, which contain no systematic distinction between normal sadness and depressive disorder. The extraordinarily high rate o depression among the young people in this study—17% o the entire community sample o 26-year-olds met DSM criteria or MDD—itsel suggests that many o these cases actually reflected normal intense sadness, not depressive disorders. Nor was there some unusual situation that might explain high rates o depressive disorder: the research took place in a modern and prosperous country during a period o tranquility when there were no wars, major economic downturns, or cultural upheavals,31 and it excluded the Maori, a deprived ethnic minority that would be expected to have high rates o depression. The undamental question o whether the measure o disorder was valid and thus whether the observed interaction reflected normal variation or disorder remains entirely unaddressed and unanswerable based on the existing data. Concluding that the short allele is a genotype or depressive disorders is especially premature because o the particular kinds o stressul lie events the Caspi et al. study measured. Most o the 14 stressul lie events that the study measured were associated with inadequate financial resources, such as problems with debt, not having money or ood and household expenses, lacking money or medical expenses, and difculty paying bills. Consequently, many o these events might be co-occurring results o a single stressor, such as unemployment or long-term poverty. In many cases, reports o our or more stressors would indicate not an additive increase in stressul lie events but the experience o a particular kind o financial stressor connected with many o the measures the study uses. The short allele’s impact, thereore, might not be associated so much with experiencing more stressors as it is with experiencing particular kinds o stressors that are linked to financial problems that are especially likely to be related to normal sadness. Although this study does not report the association o social class with these lie events, other studies o similar age groups find strong relationships between low socioeconomic status and the number o major lie events that young adults experience.32 The Caspi et al. study may actually mainly show how people with 174 THE LOSS OF SADNESS limited economic resources are exposed to the kinds o stressors—financial debt, social inequality, and poverty—that might naturally lead people to report symptoms o normal sadness. I correct, this inte rpretation has important implications or prevention or treatment eforts, because over two-thirds o the population has at least one short allele. The Caspi et al. article ocuses on the possibility o medication, noting that “more knowledge about the unctional properties o the 5-HTT gene may lead to better pharmacological treatments or those already depressed.”33 But i the 5-HTT gene is largely responsible or normal sadness that emerges because o social inequality rather than depressive disorders, preventive eforts, at least, would best address social conditions and not exclusively ocus on medicating a presumed internal genetic deect. In any event, the meaning o the Caspi et al. findings remains ambiguous. Whether the studied genes interact with certain types o stressors or stressors in general rather than revealing the genetic underpinnings o depressive disorder, the findings could be interpreted equally well as revealing normal genetic variations in the tendency or people to become sad when they are under intense stress. The study’s data are entirely consistent with the possibility that the short and long alleles represent two roughly equal, fitness-enhancing variations on the pattern o sensitivity in normal loss responses. Subsequent attempts to replicate the study’s findings display serious discrepancies both among themselves and in relation to the srcinal study, yielding a conusing rather than scientifically congealing picture.34 The resulting ambiguities may stem rom the act that all this research ailed to separate natural rom dysunctional conditions and thus likely encompassed some heterogeneous mix o normal and disordered sadness with varying genetic determinants. The use o measures that separate normal sadness rom disordered depression could help clariy this problematic situation. Anatomical Brain Abnormalities as the Basis for Depressive Disorder A final type o biological research looks or anatomical abnormalities in various brain regions, in particular the prerontal cortex, the hippocampus, and the amygdala, to demonstrate the biological basis o depressive disorders. The prerontal cortex helps regulate evaluations o rewards and punishments, ear states, and changes in mood, including those that occur when people display normal states o sadness. 35 Thereore, abnormalities in this area should afect processes that are integrally involved in depressive disorders. The hippocampus has a central role in learning and memory, which could help explain the cognitive deficits that oten accompany major depression. 36 Finally, the amygdala has an especially important role in processing negative afect, which should obviously have a critical role in sadness and depression. 37 THE DSM AND BIOLOGICAL RESEARCH ABOUT DEPRESSION 175 As early as the nineteenth century, studies o brain anatomy had already indicated the major localized regions associated with diferent brain unctions.38 More recently, brain images rom MRIs that are able to pinpoint the brain circuitry associated with depressive eelings are coming to dominate articles in psychiatric journals. Studies that use MRIs and other imaging techniques can use computer analysis to visualize living brains at the level o subcellular molecules, neurons, and genetic material. An extensive body o research suggests that particular lesions might be the primary sites o aberrant mood regulation among people with depression.39 We saw in our examination o the Caspi et al. research that genetics researchers who rely on DSM criteria are in jeopardy o interpreting eatures o normal sadness as characteristics o depressive disorder.40 There is a second kind o error that can also derive rom reliance on the DSM criteria or depressive disorder in biological research: i results o research on brain lesions that are confirmed or a clearly disordered clinical population are mistakenly generalized to all those who satisy the DSM criteria and are thus presumptively disordered, then the lesion may be mistakenly attributed to many who are experiencing normal sadness. We examine a heralded study o brain circuitry by anatomist Grazyna Rajkowska and colleagues, “Morphometric Evidence or Neuronal and Glial Prerontal Cell Pathology in Major Depression,” to illustrate the possibility o this second kind o error. Rajkowska’s study was published in 1999 as a special “priority communication” in the journal Biological Psychiatry. Peter Kramer, in his book Against Depression, cites it as the most important work yet done on depression because it “changed the way doctors view their patients.”41 Rajkowska et al. compared brain tissue rom 12 chronically depressed patients who died suddenly with brain tissue rom 12 normal controls who also died suddenly. They ound that the depressed group had distinct pathological characteristics associated with brain abnormalities. In particular, these patients had abnormal levels o glial cells, which help mediate between neurons and their environment, in the prerontal cortex. These deficits can contribute to a variety o pathological changes in this brain region. Elevated levels o glucocorticoids, in turn, can cause damage to the hippocampus, so that patients who are depressed have significantly smaller volume in the hippocampus than control participants.42 Other research finds that the reduction o glial cell density and neuronal size is especially acute in patients with MDD compared with patients with bipolar disorder and schizophrenia, as well as with normal control participants, suggest43 ing the specific kind o lesion that might indicate a particular disorder. Moreover, modifications o the brain associated with MDD are present even when the symptoms o the illness no longer are. Studies have observed brain changes in individuals with MDD when the illness is in remission, suggesting that the disorder has caused permanent damage to particular regions o the brain.44 Some 176 THE LOSS OF SADNESS research also shows that participants with depression have enlarged amygdalas, which might be related to hippocampal volume loss. 45 Major Depression, such evidence suggests, is a disruption in a defined circuit in specific regions o the brain.46 The evidence that depression is related to a brain lesion, however, has ambiguous implications or the causes o depressive disorders. Many researchers assume that the demonstrated morphological changes are more likely to be the consequences, rather than the causes, o depression, although this issue remains unsettled.47 As Rajkowska emphasizes, no evidence shows that anatomical abnormalities precede and predispose people to depression; it only suggests that brain damage is associated with depression. 48 In addition, because the patients in such studies are generally being seen by clinicians, it is possible that the abnormal brain reorganization observed among people with depression could be the result o exposure to long-term treatment with antidepressant medications rather than the consequence o depressive disease.49 We simply do not know what the brains o depressed people looked like beore they started extensive regimens o medications. But, these doubts aside, i the findings that a neuroanatomical substrate is associated with, or causes, depressive disorder are confirmed in the population Rajkowska studied, what would be the range o their applicability? Kramer’s discussion o Rajkowska’s work simply assumes that because Rajkowska studied MDD patients, the results likely have wide applicability to virtually all patients who all under the diagnosis o MDD, even subthreshold conditions. This interpretation supports Kramer’s view o the deeply pathological nature o all depressive states. Depression at every point in the spectrum, according to Kramer, is “debilitating, progressive and relentless in its downhill course” across the entire range o presentations.50 All criteria, including the number o symptoms, their severity, and their duration, all on continua that are assumed to indicate some degree o pathology at each level.51 Moreover, while many minor states are dangerous on their own, whereas others are likely to degenerate into major states, every point on the continuum represents a state o high risk o developing the kinds o lesions that the Rajkowska study demonstrated in extremely severe cases. “To accept depression as disease,” asserts Kramer, “is to see pathology or risk in minor versions.”52 In assessing such claims, it is important to consider the nature o those individuals in the Rajkowska sample whose brains showed pathology. These were patients in long-term treatment or chronic conditions. Despite treatment, 7 o the 12 who were depressed died as a result o suicide. Three o the five individuals who were not suicides were taking antipsychotic medications at the time o their deaths. Only two members o the depressed sample were neither suicides nor presumably sufering rom psychosis. The group was thus almost entirely composed o extremely severe cases o what were very likely true depressive disorders. THE DSM AND BIOLOGICAL RESEARCH ABOUT DEPRESSION 177 So how ar can the results o these studies be generalized? Given the heterogeneous mix o not only mild and severe cases but also normal and disordered sadness that currently alls under the MDD diagnostic criteria, it is unlikely that the Rajkowska results apply to the entire category o MDD cases, not to mention subthreshold conditions. Ther e is no evidence that the demonstrated brain abnormalitie s afect more than a small minority o those who satisy the DSM criteria and who are the most clearly disordered. No one has ever shown, or example, that most people who experience symptoms o depression that satisy these criteria have lost glial cells; one would expect this theory to ail to generalize to those who meet DSM criteria but are in act experiencing intense normal sadness. 53 Nor, regarding Kramer’s remark about risk, has any study ever shown that people with normal states o sadness are more likely than others to develop later anatomical pathologies. Kramer’s claims go well beyond the evidence in a way that could lead to precarious clinical assumptions about those experiencing intense sadness. Although brain research has not as yet demonstrated that most cases o depressive disorder have an anatomical grounding, it does have some interesting implications or the anatomical basis o normal sadness. One important study asked volunteer participants with no history o depression to prepare scripts describing recent personal experiences o sadness.54 They then gave positron emission tomography (PET) scans to the participants while they used these scripts to provoke a sad mood state. Participants who experienced provoked states o normal sadness showed increases in blood flow in limbic-paralimbic regions o the brain and diminished blood flow in prerontal regions that are comparable to those ound in studies o patients with clinical depression.55 This result suggests that these regions are related to both normal sad moods and pathological depression. States o normal sadness that can be provoked in laboratory settings are likely a pale reflection o sadness that arises in natural situations o actual major loss. The preceding findings thus imply that normal participants who are given a biological diagnostic or screening test or depression while they are exposed to sadness stimuli would likely score high on these measures because they show the bio- logical markers that underlie the symptoms o normal sadness and pathological depression alike. Conclusion We have argued that i brain researchers ail to consider the context in which sadness develops, they are in danger o misdiagnosing the normally sad as having depressive disorders and o muddling their samples with a heterogeneous mix o disordered and normal participants. Normal sadness, no less than depressive disorder, has correlates with brain states and can include intense sadness 178 THE LOSS OF SADNESS symptoms; people experiencing sadness may have some o the same biological markers as the truly depressively disordered. Thus showing a biological substrate to a condition o intense sadness symptoms that satisy DSM criteria is not enough to indicate whether that particular substrate or the condition itsel is normal or disordered. Understanding the context in which brain activity occurs is an essential precondition or knowing whether brains are unctioning in normal or abnormal ways. An enhanced understanding o how normal brains respond to situations that involve loss would provide an essential benchmark to compare with the possible brain dysunctions that are connected to depressive disorders. Better defined research on the brain thus has the potential to more efectively distinguish and illuminate both abnormal and normal responses to loss. 9 The Rise of Antidepressant Drug Treatments he DSM-III’s neutral stance toward the etiology of mental disorders meant that advocates of all treatment orientations were supposed to find equal value in its symptom-based classification system. In practice, however, pharmaceutical companies were best able to capitalize on the DSM’s focus on symptoms, which allowed them to broadly construe states of intense sadness as depressive disorder and thus to vastly increase the potential market for antidepressant medication. Several other developments helped propel an explosive growth in the use of these drugs, including the emergence of the selective serotonin reuptake inhibitors (SSRIs) in the late 1980s, the spread of managed T care throughout the U.S. health care system in the 1990s, and the approval of direct-to-consumer (DTC) advertisements in 1997. This chapter considers the relationship between the DSM revolution and the roughly contemporaneous exponential growth of drug treatments for depression. A Brief History of Drug Treatments for Sadness and Depression The First Tranquilizers For thousands of years, physicians have used medications to treat depression. Beginning with the ancient Greeks and Romans, doctors commonly prescribed purgative and laxative medicines that induced vomiting and evacuation of the bowels.1 Richard Napier, the seventeenth-century physician mentioned in chapter 3, typically used sedatives and analgesics, as well as laxatives and purging concoctions, in his practice.2 He prescribed opium for about 10% of his melancholic patients. By the nineteenth century opium, morphine, and other alkaloids had become common treatments for depression, joined by the barbiturate sedatives during the early twentieth century.3 179 180 THE LOSS OF SADNESS During the 1950s specific drugs to treat distress over lie problems emerged, beginning with the tranquilizer meprobamate (Miltown). The sedative and muscle relaxant qualities o Miltown made it efective or everyday tension and anxiety. It was immediately successul, and the demand or it and closely related drugs was, according to historian Edward Shorter, “greater than or any drug ever marketed in the United States.” 4 Despite the misgivings o the American Psychiatric Association that these drugs were widely misused to alleviate “the routine tensions o everyday living,” by 1956 1 in 20 Americans were taking some sort o tranquilizer.5 In the early 1960s, the benzodiazepines Librium and Valium were developed, quickly supplanting Miltown as the most successul drugs ever introduced in pharmaceutical history. Their efects were qualitatively similar to, but more potent than, Miltown. By 1969, Valium was the most prescribed medication in the United States. Surveys at the time indicated that between 15 and 25% o the population had ever used one o the tranquilizing drugs. 6 Research also showed that only about a third o the prescriptions or these drugs were written or people with diagnosed mental disorders, whereas most medications were given to those experiencing psychic distress, lie crises, and psychosocial problems. 7 Prescription drug use then, as it is now, was gender imbalanced, with women receiving about two o every three prescriptions.8 Even the colloquial term or these medications, made amous by the Rolling Stones’ hit song, “Mother’s Little Helper,” indicates their association with the normal misery o housewives, suggesting that “though she’s not really ill” the pills help a mother to calm down, deal with her busy day, meet her husband’s demands, and thus “minimize your plight.”9 Popular women’s magazines, in particular, viewed these drugs as helpul in dealing with common problems such as sexual unresponsiveness, infidelity, troublesome children, or inability to attract a man.10 Ater their explosive growth in the 1950s and 1960s, a counterreaction to the antianxiety drugs set in. Some critics cited how these drugs numbed people’s reactions to social problems and, in particular, how women used them to avoid conronting oppressive interpersonal situations.11 Others worried about the use o these drugs to cope with daily lie: “It is only now,” wrote one psychiatrist, “that we are aced with the possible utilization o psychoactive drugs by a major portion o the population in what might be considered problems o daily living.”12 Likewise, Stanley Yolles, the director o the NIMH, expressed unease about whether “the chemical deadening o anxiety” was harmul and about whether “Western culture (would) be altered by widespread use o tranquiliz13 ers.” Still others expressed serious concerns about the addicting qualities, adverse side efects, and overdose potential o these drugs. Numerous Congressional hearings at the time ocused on the dangers and misuse o psychotropic medications, begi nning with the well-kno wn Keauver hearings in 1960 and continuing through the 1970s. The use o THE RISE OF ANTIDEPRESSANT DRUG TREATMENTS 181 the benzodiazepines or treating common problem s o living was a specific concern. For example, during a hearing in 1971 Senator Gaylord Nelson asked the commissioner o the FDA: “Isn’t there a very undamental distinction between prescribing a drug to help the patient manage a serious problem o depression and tension and prescribing a drug to help the patient meet the ordinary . . . rustration o daily living?” 14 The commissioner o the FDA, Charles Edwards, responded by expr essing the “growing concern” o his agency that “advertisements have also promoted their use in the treatment o symptoms arising rom the stresses o everyday living, which cannot properly be defined as pathological.”15 During the 1960s and 1970s the FDA took action against pharmaceutical companies’ claims to treat problems o living. For example, in 1971, it requested that advertisers o psychotropic drugs rerain rom promoting their use in coping with everyday lie strains. This action evidently had some efect, and such general appeals disappeared rom these ads or the rest o the decade.16 The FDA also placed both meprobamate and the benzodiazepines on its list o “schedule IV” drugs in 1975, which meant restricting refills and initiating “special reporting requirements” or their use.17 In 1980, FDA regulations specifically noted that “anxiety or tension associated with the stress o everyday lie usually does not require treatment with an anxiolytic.”18 The attitude o the popular press also sharply changed, rom its initially avorable reception o these drugs when they were introduced toward a decidedly critical view. The proportion o articles in lay periodicals that took unavorable attitudes toward tranquilizers more than doubled, rom about a third in the 1950s to over two-thirds in the 1970s.19 The climate had clearly turned against the widespread use o the benzodiazepines, and the craze or antianxiety drugs was tapering of by the time the DSM-III was published in 1980. Valium was still the largest selling prescription drug o any sort, but tranquilizer and benzodiazepine use had declined dramatically, rom a peak o over 100 million prescriptions written in 1975 to slightly over 70 million in 1980, and it continued to decrease during the 1980s.20 The Rise of Antidepressants The initial tranquilizing drugs were called anxiolytics because they targeted anxiety rather than depression. Drugs that were specifically targeted at depression also emerged in the 1950s, including monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants, such as imipramine (Toranil) and amitriptyline (Elavil). Although by 1980 nearly 30 million prescriptions were being written or antidepressants, this was ar ewer than the number or the anxiolytics. 21 At the time, depression was not viewed as a widespread problem, and conditions o normal misery were lik ely to be seen as problems o tension and anxiety. 22 Moreover, the tricyclics and especially the MAOIs 182 THE LOSS OF SADNESS had substantial side efects that limited their useulness. Thus antidepressant drugs had a airly small market niche, a situation that would quickly change over the next decade. The SSRIs There is no evidence that pharmaceutical companies had a role in developing DSM-III diagnostic criteria. Yet, serendipitously, the new diagnostic model was ideally suited to promoting the pharmaceutical treatment o the conditions it delineated. Since 1962, the FDA had required manuacturers to market drugs only or the relie o specific diseases rather than or more general purposes such as reduction o tension or distress stemming rom problems in living (although, as noted earlier, advertisements sometimes violated these regulations). But because all o the diagnoses in the DSM-III were ormulated as categorical disease entities, they provided many diferent targets or the products o pharmaceutical companies to treat.23 The diagnosis o Major Depression, which used common symptoms such as sadness, lack o energy, or sleeplessness as indicators, was particularly well suited or expanding the market or psychotropic drugs because it inevitably encompassed many patients who ormerly might have been thought to be sufering rom problems o living. It would not take long or pharmaceutical companies to capitalize on this elicitous aspect o the DSM-III. The DSM-III also unintentionally provided drug companies with a way out o the dilemma they aced in marketing their antianxiety medications. As noted, or many years anxiety, rather than depression, was viewed as the most common psychic problem resulting rom the stresses o daily lie. Drug companies typically marketed their products as treatments or anxiety disorders, and their products were generally viewed as antianxiety agents. In act, there is a huge overlap between symptoms o anxiety and those o depression.24 Indeed, as we saw in chapter 3, clinical theorists traditionally saw anxiety as an integral part o depressive conditions, but the DSM-III attempted to identiy a pure depressive syndrome independent o anxiety. Which condition is emphasized largely depends on diagnostic ashions, the interests o various proessional and advocacy groups, and economic costs and benefits.25 By 1980, the balance o these actors was shiting away rom anxiety because o the backlash against the anxiolytics. In this climate, the DSM diagnosis o MDD was more suitable than any o the various anxiety disorders or capturing the distress o persons seeking help rom general physicians and outpatient psychiatrists. Subsequently, MDD gradually replaced anxiety as the diagnosis o choice in these venues.26 During the 1980s, this transormation accelerated when research on new drug treatments began to ocus on the serotonin system and on the development o SSRIs to increase the amount o serotonin in the brain.27 These new medications had ewer negative side efects and were saer than the earlier anxiolytics and antidepressants, so they required less monitoring through blood testing. The THE RISE OF ANTIDEPRESSANT DRUG TREATMENTS 183 SSRIs do not target a specific illness but instead act on a general neurochemical 28 system that influences many brain unctions in healthy, as well as ill, patients. They are used to treat a variety o problems, including anxiety, panic, obsessivecompulsive disorder, eating problems, substance abuse, and attention-deficit disorder,as well as depression and general distress in nondisordered people. Moreover, although this issue remainscontroversial, they appear to influence temperament, unhappiness, and demoralization as well as depressive symptoms.29 Given that the FDA requires that a drug must be efcacious against a particular disease beore it can be put on the market, the SSRIs could not be called “psychic energizers,” “personality boosters,” or “distress inhibitors,” however accurate these terms might be in describing their eects. They could have easily been marketed as “antianxiety” medications, but when they were approved in the late 1980s they were marketed instead as “antidepressants” 30because o the negative associations that had developed around the anxiolytics. By 2001, about two and a hal times more people were using SSRIs than antianxiety medications, and their use was growing nearly five times as quickly as that o the anxiolytics.31 The “antidepressant” label provided tremendous impetus or making depression, rather than anxiety, the primary target o pharmaceutical promotions. In 1993, Peter Kramer’s Listening to Prozac: A Psychiatrist Explores Antidepressant Drugs and the Remaking of the Self galvanized the ormulation o lie problems as problems o depression and their treatment with “antidepressant” medications. Kramer himsel observed that the SSRIs work across a variety o conditions. “The same medications,” he concludes, “are eective against panic anxiety, and they could as appropriately have been called anxiolytics. The term ‘antidepressant’ encourages us to attend arbitrarily to one use to which these drugs can be put.”32 Nevertheless, his use o the term antidepressants to characterize the SSRIs and his book’s ocus on depression helped associate both the drugs and the condition that they treat specifically with depression. Kramer’s book also helped create a mythic status or Prozac (his generic term or the SSRIs) by asserting that it not only alleviated particular symptoms but also influenced normal as well as disordered eelings and thus made people “better than well.” For Kramer, the SSRIs had distinctly dierent eects rom the earlier drugs such as Miltown, Valium, and Librium that were used to deal with lie problems. Whereas these drugs relaxed and tranquilized people, drugs such as Prozac energized them and boosted their sel-esteem. They did not so much blunt negative emotional responses to the world as act as agents o personality enhancement. Formerly depressed people became more energetic, outgoing, ex- troverted, and flexible. Prozac, or Kramer, seemed to transorm personal identity more than to treat a disease. What ollowed Kramer’s wildly successul book was, in the historian Edward Shorter’s words, “a media psychocircus o suggestion, as Prozac and its competitors were extended to the world public as a panacea or coping with lie’s 184 THE LOSS OF SADNESS problems even in the absence o psychiatric illness.”33 Reflecting the initial enthusiasm or Miltown and, then, Librium and Valium, the new drugs were regarded uncritically and were overvalued. The use o antidepressant drugs, specifically the SSRIs, soared while that o the antianxiety drugs plunged.34 By 1994, Prozac had become the second best-selling drug in the world, ollowed closely by its siblings Paxil and Zolot. Although Kramer and many others asserted that people took Prozac and related drugs to enhance their lives, only anecdotal support indicates that these drugs make people “better than well.” 35 Actually, the great preponderance o evidence indicates that they are no more eective than older antidepressants; they are simply better tolerated, their side eects are more benign, and they lack the addictive nature and potential lethality o the antianxiety medications.36 Moreover, the evidence remains uncertain regarding the degree to which they influence normal sadness. Whatever their true efcacy, the SSRIs entered the culture as the newest “wonder drugs” and were promoted with the promise not only o alleviating depression and attendant ills but also o enhancing the lives o their many potential users. The Impact of Managed Care The earlier antianxiety drugs were rarely promoted as stand-alone treatments but instead as adjuncts to psychotherapy and counseling.37 The SSRIs, however, entered a very dierent organizational environment. By the 1990s, managed care rose to become a dominant mode o providing mental health treatment in both general medicine and psychiatry, and it is now a powerul social orce promoting the use o medications to treat depression and other mental conditions. Managed care approaches, although diverse, generally rely on strategies that reduce health care expenditures by underwriting the least expensive possible treatments.38 Managed care also encourages the use o general physicians, who almost always prescribe medication, instead o mental health specialists who may be more likely to use alternatives. As a result, general physicians have increasingly supplanted psychiatrists as the primary source o prescriptions or antidepressant drugs.39 Because medication therapy takes considerably less practitioner and patient time than most psychotherapy, it is more amenable to the cost / benefit logic o managed care organizations.40 Most managed care plans, thereore, provide more generous benefits or pharmaceutical than or psychotherapeutic treatments and usually place no barriers on SSRI use.41 Conversely, these plans usually place severe limits on payment or psychotherapies, which they view as less necessary and more wasteul than medication. Medication thus involves lower out-o-pocket costs or patients than psychotherapy does, which also influences patients themselves to preer drug treatments.42 Under the pressures o managed care, “visits in ofce-based psychiatry became shorter, less oten included psychotherapy, and more oten included a medication THE RISE OF ANTIDEPRESSANT DRUG TREATMENTS 185 prescription. The proportion o visits that were 10 minutes or less in length increased.”43 Indeed, unlike earlier drugs, the SSRIs are more rarely used in conjunction with other, more expensive orms o therapy and are likely to be the sole source o treatment. At the same timeas the number o people treated or depression with medication is growing explosively, the proportion who get psychother44 apy is gradually declining. For example, by 1998 two-thirds o elderly persons treated or depression received only an antidepressant, whereas a little more than 45 10% obtained only psychotherapy. Payment or long-term psychotherapy has almost disappeared.46 In sum, managed care organizations have increasingly become the arbiters o appropriate and inappropriate treatments, reinorcing the ascendancy o medication as a response to emotional difculties.47 The Impact of Direct-to-Consumer Advertisements A urther step in the expanding use o SSRIs came in 1997 when the FDA approved the use o direct-to-consumer (DTC) drug advertisements in popular media. DTC ads undamentally changed patterns o inormation flow about drugs. In the past, pharmaceutical companies marketed their products directly to physicians, through advertisements that appeared only in medical and psychiatric journals. These ads asked their target audience o physicians and psychiatrists to identiy problems in their patients, whereas DTC ads appeal directly to consumers themselves to sel-identiy symptoms o a given condition and “ask their doctors” about taking antidepressants and other medications. “By the end othe twentieth century,” Edward Shorter notes, “these drugs had acquired such currency that, much as in the eighteenth century, patients began to view physicians as mere con duits to abled new products rather than as counselors capable ousing the doctor-patient relationship itsel therapeutically.”48 By 2000, the pharmaceutical industry was spending over $2 billion annually onDTC advertisements.49 Given regulations restricting the marketing o drugs to the treatment o diseases rather than o everyday lie problems and the consequent need to present simple but inclusive descriptions o disease entities to the general public, the DSM definition o MDD could hardly have been better suited or the purposes o DTC advertisements. Pharmaceuticalcompanies could legitimately claim that theyare conorming to the FDA regulations when they alert thepublic to the act that “sadness,” “atigue,” “sleeplessness,” and the like are potential symptoms o a disease. DTC ads, in act, exploit the DSM’s lack o contextual constraints by typically portraying people who have DSM symptoms yet who appear to be suering not necessarily rom mental disorders but rom symptoms commonly associated with problems in relating to intimates, with difculties in the workplace, or with challenges in accomplishing valued goals. For example, an ad or Paxil eatures a woman on one side and her husband and son on the other side, with a list o symptoms drawn rom the MDD diagnosis separating the two sides. The ad 186 THE LOSS OF SADNESS implies that symptoms of depression are the cause, rather than the result, of the family’s problems. Other ads portray people who are already taking antidepressants and have fulfilling interactions with families, friends, and workmates as a result. Moreover, they present generic models of attractive women (and, occasionally, men) that are designed to appeal to the broadest possible audience. The images of the DTC ads unambiguously, although implicitly, show how drugs are used to regulate normality, as well as disease. DTC ads, therefore, capitalize on the symptom-based definition ofdepression to thoroughly blur the boundary between normal sadness and depressive disorder. Pharmaceutical companies can hardly be faulted for trying toells their products to the greatest possible number ofpeople. The DSM definition of depression supplies them with the perfect vehicle for creatinga large demand for theSSRIs. The formulation of common symptoms as illnesses provides both legitimate a way for people to obtain prescriptions and a legal way for companies to advertise their products. DTC advertisements have the additional consequence of circumventing the psychiatric profession. They urge consumers to “consult your doctor,” not explicitly a mental health professional. As a result, the major growth in prescriptions for antidepressants has occurred within the primary medical care sector, not in the specialty mental health care sector.50 The percentage of emotional disorders treated in the general medical sector grew from about one-third in 1990–1992 to about one-half in 2001–2003, an absolute increase of more than 150%.51 “The increased rate of treatment,” according to epidemiologist Ronald Kessler and colleagues, “may have been due to aggressive, direct-to-consumer marketing of new psychotropic medications.”52 General medicine, not specialty mental health services, is now the major arena for the treatment of emotional distress. Three-quarters of the visits to ambulatory care for mental health or substance abuse problems now result in a prescription, usually for an SSRI, and often without any other type of treatment. Some evidence indicates that DTC ads are responsible for part of this increased use of antidepressants: rising rates of prescriptions for antidepressants follow periods of increased spending on DTC ads.53 Moreover, research confirms that when patients mention to their doctors specific drugs they have seen advertised, the doctor is much more likely to prescribe that medication.54 It is not clear whether people actually define and experience their emotions of sadness as depressive disorders or are simply taking advantage of the opportunity to obtain legal medications to regulate their emotions. There is no question, however, that DTC advertisements have become a major conduit by which pharmaceutical companies use the DSM criteria to reshape the way that many people frame and interpret their emotions of sadness. The Triumph of Big Pharma The result of the emergence of the SSRIs, of their use within the context of managed care, of their promotion via DTC ads, and of their greater safety wit h THE RISE OF ANTIDEPRESSANT DRUG TREATMENTS 187 respect to overdosing and lesser side eects is their exponential growth in use since their initial marketing in the late 1980s. Persons treated or depression were our and a hal times more likely to have received a psychotropic medication in 1997 than in 1987. 55 This trend substantially expanded during the mid-1990s. The number o people using SSRIs and other newer antidepressants almost doubled, rom 7.9 million in 1996 to 15.4 million in 2001. 56 Especially notable is their rising use or children, adolescents, and the elderly, or whom prescription rates increased by between 200 and 300% during the 1990s. 57 Between 1996 and 2001, overall spending on antidepressants rose rom $3.4 billion to $7.9 billion. 58 By 2000, Prozac, Zolot, and Paxil were all among the eight most prescribed drugs o any sort, and the antidepress ants were the best-selling category o drugs in the United States. 59 Nevertheless, it is worth noting that a considerable segment o the public still resists using drugs or lie problems; 64% o respondents in a national survey in 1998 said they were unlikely to take psychiatric medication in response to troubles in personal lie, and even when the question was ramed in terms o treating specific symptoms that result rom lie problems (“eeling depressed, tired, having trouble sleeping and concentrati ng, and eelings o worthlessness”), 45% still said they were unlikely to take medication.60 That said, the influence o the pharmaceutical industry is considerable and now extends well beyond the specific promotion o drugs. It donates substantial amounts o money to patient and amily advocacy groups that promote the view that depression is a chemical deficiency to be remedied through the use o drugs. These companies also sponsor widespread educational campaigns, such as National Depression Awareness Day, which oer ree screening or depression in universities and hospitals. In addition, they provide 800 numbers and Internet screening sites that allow responders to make sel-diagnoses o depression and that urge them to consult their physicians to obtain prescriptions or the companies’ products. Drug companies also und the screening eorts in primary medical care and schools that were the subject o chapter 6. Moreover, the pharmaceutical industry sponsors a considerable proportion o clinical research on depression; the discipline o psychiatry itsel is now thoroughly enmeshed with the corporate culture o this industry.61 Industry-academic collaborations are becoming increasing sources o unding or universities, academic medical centers, and hospitals.62 The DSM’s easily applied symptom-based definition acilitates these eorts, and they, in turn, reinorce the validity o the definition. The use o pharmaceuticals to deal with everyday lie problems preceded the DSM-III. In many ways, the legal drug culture surrounding the SSRIs continues the craze or Miltown in the 1950s and or Valium and Librium in the 1960s and 1970s.Yet never beore has this culture been so heavily promoted through the mass media, embedded in central institutions, and embraced by policy makers. Previously, establishment psychiatrists and government ofcials were oten openly critical o the overprescribing o these medications and, in particular, o 188 THE LOSS OF SADNESS their use or coping with problems o living. Now, however, the legitimacy that the DSM concept o depression accords to the widespread treatment o common symptoms o normal malaise has become so entrenched that these groups have come to accept a definition o depressive disorder that encompasses much normal sadness and to endorse the use o antidepressant medications to deal with such conditions. As happened with the antianxiety medications in the 1970s, a backlash is now developing against the expanding use o antidepressants, especially or children and adolescents.63 Drug companies now ace stier requirements to disclose potentially harmul side eects and possible risks o suicidality rom their products. Moreover, as during the 1970s, the media have grown more skeptical o the claims o limited risks and vast benefits rom antidepressant medications. What impact this more critical climate will have on the actual use o these drugs remains to be seen. Antidepressants and the Treatment of Normal Sadness The relationship between DSM diagnosis and medication is complicated by the act that antidepressant medications, and the SSRIs in particular, aect general aspects o brain unctioning and, as noted, may be capable o having similar eects on both normal sadness and depressive disorder. The ew studies that compare the changes that SSRIs produce in presumably healthy people with the changes experienced by those diagnosed with a depressive disorder find that the SSRIs work on the disordered and nondisordered alike.64 Thus the psychic relie that results rom medication does not necessarily indicate that what has been relieved is a disease condition. For example, grieving people who are not disordered report ewer symptoms ater treatment with antidepressants.65 Few would argue that medication has no role in the response to depressive disorders; medications can dramatically alleviate the hopelessness that accompanies MDD, and they helped to acilitate the process o deinstitutionalization in the mental health system that allows many people to avoid extended periods o hospitalization. A more controversial question regards the use o medication or painul but normal emotions. The SSRIs raise serotonin levels in the synapses, so it is plausible that unhappiness and mood disorder alike oten respond to them. “We are entering,” as Peter Kramer claims, “an era in which medication can be used to enhance the unctioning o the normal mind.”66 Assuming that the findings that SSRIs can influence normal emotions are confirmed, should these drugs be prescribed or people who experience normal misery, as well as or those with MDD? Legitimate arguments exist on both sides o this issue. One position, embodied in ofcial treatment guidelines, evidence-based medicine, and government position papers, regards medication treatment in THE RISE OF ANTIDEPRESSANT DRUG TREATMENTS 189 unambiguously positive terms. The Surgeon General’s Report on Mental Health, or example, claims that “antidepressant medications are efective across the ull range o severity o major depressive episodes in major depressive disorder and bipolar disorder.”67 Moreover, a vast majority o U.S. psychiatrists avor using SSRIs as the first-line treatment or depression.68 In this view, drug treatment has proven efectiveness or the relie o depressive symptoms, albeit with small risks o negative side efects and other undesirable consequences. Moreover, the monetary benefits o such treatment are viewed as ar exceeding its costs.69 In addition, drugs are viewed as capable o preventing mild conditions rom becoming more severe. Mild disorders thus ought to be treated as vigorously as more severe ones, it is claimed, not just to prevent a substantial proportion o uture serious cases but also to limit uture outcomes such as hospitalization, 70 work disability, and suicide attempts. Advocates o medications worry about the underuse o the antidepressants and try to find ways to motivate people to seek and use them. They want to encourage people to recognize that they have treatable illnesses, to seek medical care or their conditions, and to overcome the perceived stigma about taking medication.71 Moreover, they are concerned that not only the public but also general physicians underrecognize depression and, thereore, underprescribe antidepressant medications.72 For advocates, increasing awareness o and education about the benefits o psychotropic drugs can optimize the treatment o depression. Opposition to using medication reflects, in psychiatrist Gerald Klerman’s term, “pharmacological Calvinism” that considers any drug that makes people eel good as something bad: Psychotherapeutically, the world is divided into the first class citizens, the saints who can achieve their cure or salvation by willpower, insight, psychoanalysis or by behavior modification, and the rest o the people, who are weak in their moral fiber and need a crutch, whether it is Thorazine, Miltown, or Compoz.73 What Klerman calls the “Calvinist” view o psychotropic medication leads a substantial proportion o the public to resist taking drugs because they associate their use with a moral weakness, despite the benefits they might receive rom taking them. Most advocates, ollowing the DSM, simply assume that the conditions that drugs treat are depressive disorders and not normal sadness. Their position regarding the use o medication to treat normal sadness is, thereore, not explicit. Some advocates, however, are quite clear that drugs should be used to treat any orm o sufering.74 The pain arising rom, or instance, the death o an intimate, the breakup o a romantic relationship, or the loss o a job is just as real as that stemming rom a depressive disorder. The position o these advocates is that there is simply no good reason why people should tolerate the psychic pain rom 190 THE LOSS OF SADNESS normal sadness as long as sae and efective means are available to palliate it. Ater all, ew people would not want women to be able to use anesthesia to numb the normal pain that stems rom childbirth. Advocates argue that i people think that SSRIs can brighten their lives, provide greater control over their emotions, and increase their sel-esteem, as well as relieve the inevitable pain that arises rom human existence, they should be able to use them, even in the absence o any disorder. The relie o sufering, in this view, is a greater value than any costs that might accrue rom medicating normal sadness. Challenges to this pro-medication position generally come rom outside o the psychiatric proession, the clinical research community, and government agencies. One argument against medicating normal sadness is that it treats as pathological what is actually an inherent and valuable part o the human condition. For thousands o years, people have used religion, spirituality, and philosophy to understand how their unhappiness is tied into larger questions about lie.75 Such questioning allows people to comprehend how their emotions are related to basic aspects o human existence and to gain a deeper appreciation o their eelings than palliation through medication can provide. “At least part o the nagging worry about Prozac and its ilk,” philosopher Carl Elliott laments, “is that or all the good they do, the ills that they treat are part and parcel o the lonely, orgetul, unbearably sad place where we live.”76 Using pills represents an escape rom truly conronting lie’s problems. Quite aside rom philosophical issues, there may be psychological benefits o normal sadness that treatment would nulliy. We do not as yet ully understand why we are biologically designed to experience sadness in response to loss, and, until we do, it is possible that there are benefits o withdrawing into a sad state ater a major loss that are not immediately apparent but that are nonetheless real and important to long-term psychological unctioning. Another argument, echoing criticisms made in the 1950s and 1960s, emphasizes that widespread antidepressant use leads people to accept, rather than resist, oppressive situations. From this perspective, psychotropic drug use promotes a view o the world that erroneously misconstrues social problems as personal problems. Prescribing a pill communicates that public issues— inegalitarian marriages, deplorable working conditions, inadequate finances, and the like— are private concerns o the individual to be treated with medication.77 “Diseasing” normal sadness that arises over these concerns implies that medication is the appropriate way to deal with them, at the cost o ignoring other possible remedies. This process deflects attention away rom developing policies that might change the conditions that give rise to sadness.78 Indeed, in 1958, the Surgeon General, L. 79 E. Burney, warned that “problems o daily living” cannot be “solved with a pill,” a ar cry rom the attitude o recent surgeon generals. Others raise the issue o whether normal emotions o sadness are a legitimate subject or public concern or, instead, a personal matter. The promotion o antidepressants sets orth a view o the sel that is eeble and ragile and that THE RISE OF ANTIDEPRESSANT DRUG TREATMENTS 191 requires the continuous intervention and protection o proessional experts.80 Private selves become increasingly available or public scrutiny and regulation through screening and subsequent medication. The detection o emotions and eelings is inevitably ar more intrusive and coercive than is the detection o physical diseases that usually do require expert help. Other critics do not question the political and cultural implications o antidepressant drugs so much as their efectiveness and saety. They contest the benign nature o the antidepressants and contend that the side efects o these medications, such as loss o sexual desire, nausea, diarrhea, and headaches, are more common and malignant than their advocates claim. 81 They also cite the heightened potential or suicidality, especially or young people during the initial stages o taking these drugs, although evidence or this claim is not well estab82 lished. Finally, they point to the potential or adverse efects rom the long-term use o these medications. Although there is little doubt that the newer antidepressants are saer than their predecessors, there is still reason or concern over their widespread use. Moreover, critics claim that advocates have grossly overinflated the efectiveness o these medications. Current guidelines promote the SSRIs as the first-line medications or moderate to severe depression.83 The evidence, however, that antidepressant medications are more efective than placebo, as judged by randomized, double-blind placebo trials, is mixed. “Although many trials,” one research team summarizes, “do find antidepressants are superior to placebo, many do not, including some o the largest and most well known landmark trials such as the Medical Research Council trial and the early National Institute or Mental Health trial.”84 A comprehensive review by the National Institute or Health and Clinical Excellence (NICE) in England suggests that SSRIs do not have clinically meaningul advantages over placebos across the entire range o severity o conditions. A report on this study concludes: “Given doubts about their benefits and concern about their risks, current recommendations or prescribing antidepressants should be reconsidered.”85 The evidence lends little support to the enthusiasm or prescribing medications. Still less evidence exists or the efectiveness o antidepressants in treating nonpsychotic conditions that are not especially intense (sometimes called “mild” depression), many o which are undoubtedly cases o normal sadness. Even the ervor or antidepressant medication in the Surgeon General’s report is somewhat mitigated or these cases. “With mild depressive episodes,” the report concludes, “the overall response rate is about 70 percent, including a placebo rate o about 60 percent.”86 The efectiveness o antidepressants or mild conditions, in other words, exceeds that o placebos by only 10%. Indeed, rom hal to twothirds o patients with mild depression improve with placebo alone. This might indicate that what was treated in the first place was not a disorder but normal sadness that naturally remits over time or through such ordinary interventions as interacting with and receiving the emotional support o others. Even some 192 THE LOSS OF SADNESS o the most vigorous advocates or treating mild cases o depression conclude: “Controlled treatment trials have provided no evidence that pharmacotherapy significantly improves mild disorders.”87 When compared with control groups who receive active placebos that mimic some o the side eects rom antidepressants, no dierences between antidepressants and placebos emerge.88 The evidence regarding the eectiveness o antidepressant medications, especially or mild depression, is thus ambiguous. Still, given their popularity, it is dif cult to believe that the eectiveness o antidepressants is as limited and their negative side eects are as great as the critics claim. Many people find that antidepressants provide legal and generally sae ways to regulate their distressing emotions. Moreover, the results o clinical trials can be misleading. In practice, consumers and their physicians oten try out several dierent drugs beore 89 one finally works. In contrast, clinical trials might minimize the overall rate o eectiveness because they deal with one particular type o medication, which might not be eective or particular individuals in the trial although another, untested type might be. Indeed, recent multidrug trials designed to address this issue do seem to achieve higher rates o improvement.90 So the act that medication has little more eectiveness than placebos is perhaps less o a decisive criticism than is oten believed. It is, however, difcult to find any compelling reasons why public policy ought to encourage the use o drugs to treat mild conditions, many o which are likely to be cases o normal sadness. It is not easy to sort out the competing claims regarding antidepressant use. All o the considerations on both sides o the debate seem to have some merit, and there is no one general answer to the question o whether psychotropic medication should be prescribed or normal, negative emotions. Ultimately, consumers themselves have to integrate all these considerations and be the judges o whether they ought to use antidepressant medications to regulate their moods. Over the past ew decades, the public’s judgment has certainly swung in the direction o medication; tolerance or normal but painul emotions has declined, and many people in the modern world have come to value medication as a way to control their eelings.91 I they find that their lives seem brighter when they are medicated, a belie in autonomy and ree choice dictates that people should not be prevented rom seeking that relie rom a responsible physician. It should also not be orgotten that DTC ads do get many truly depressed people to seek help and to receive useul medications rom their physicians.92 The issue to keep in mind, we have argued, is that diagnosis should not be invalidly shaped to indicate disorder so as to bias such decisions. Conclusion Given how many issues regarding the appropriate role o antidepressant medication remain unresolved, the wisest course would involve caution and the THE RISE OF ANTIDEPRESSANT DRUG TREATMENTS 193 avoidance o sweeping statements advocating or condemning their use. In the past, governmental ofcials were concerned about the possible dangers and overuse o psychotropic medications, as well as with the pharmaceutical industry’s eorts at encouraging ever-wider segments o the population to take them. Numerous congressional hearings questioned the promotion o pharmaceuticals, especially or problems in living. In a vast turnabout, symptom-based diagnostic criteria now easily reconceptualize the “stresses o everyday living” as indications o disease. Surely, there is a sensible middle course. What, or example, might the consequences be or DTC advertising i the criteria or Major Depression in theDSM were changed to more adequately distinguish normal sadness and depressive disorder? By way o comparison, in the 1960s the pharmaceutical company Sandoz marketed a new tranquilizer, Serentil, using an ad that explicitly promoted its use or general problems oliving: “The newcomer in town whocan’t make riends. The organization man whocan’t adjust to altered status within his company. The woman who can’t get along with her new daughter-in-law. The executive whocan’t accept retirement.” The FDA orced Sandoz to withdraw the ad and publish a correction stating that it did not intend that Serentil be used or “everyday anxiety situations encountered in the normal course o living” but only or “certain disease states.”93 I the DSM were to create more restrictive standards orMDD, DTC advertisements or antidepressants would have to ollow these criteria. Theresult would be to at least marginally lessen the appeal o drug use or normal lie problems, i in act that is a desirable goal. But the sorts o debates that took place beore 1980 regarding the wisdom o medicating normal distress have largely disappeared rom psychiatry, although similar discussions continue in general medicine (e.g., whether normally short individuals should be administered growth hormones).94 Instead, discussions more narrowly ocus on issues o eectiveness, side eects, or whether alternative therapies to medication would be more desirable. This lack o discussion seems to be due to the act that, when conditions are predefined as diseases, the consideration o what treatment is most appropriate is already skewed by the assumption that something is wrong within the individual. The question o whether interering with normal mechanisms should be subject to a higher threshold than correcting dysunctional mechanisms is defined out o existence, and medical thinking becomes correspondingly less nuanced. Our analysis suggests the need or greater conceptual clarity by the diagnosing proessional and or more ully inormed consent by the patient. A undamental part o inormed consent is receiving an accurate diagnosis to the degree possible, and there is no more basic diagnostic distinction than that between a disorder and a normal emotional state in response to lie circumstances that is likely to remit over time without intervention. Prognosis and decisions about the appropriateness o possible treatments depend on this distinction, and it is important or the proessional to share this inormation with the patient in deciding on an inormed course o action. 10 The Failure of the Social Sciences to Distinguish Sadness From Depressive Disorder T he field o psychiatry does not exist in a v acuum; it depends on other disciplines or much o the intellectual underpinnin gs o its clinical theory. One might thus expect that disciplines such as anthropology and sociology should be in good positions to help correct the conusion in psychiatric nosology about the distinction between depressive disorder and normal intense sadness. Anthropologists could identiy universal emotional mechanisms that are part o human nature and elaborate the cultur al variations in their expression, and they could pinpoint when these normal variations lead to mistaken labeling o disorder. Sociologists could demonstrate how stressul social arrangements oten produce nondisordered sadness, which can sometimes be severe enough to meet DSM criteria, and could distinguish between the study o normal emotional response s to social stress and the study o mental disorder. In act, however, rather than ofering the grounds or a critique o psychiatry’s conflation o normal sadness and disorder, these disciplines have unctioned as “enablers” o psychiatry’s overinclusive definitions o disorder by themselves ailing to draw the appropriate distinctions within their disciplinary domains. Anthropologists ocus on the presumed cultural relativity o definitions o sadness and disorder, claiming that no definitions o these conditions are possible outside o each culture’s particular value system. Sociolo gists interchangeably use concepts o distress and disorder without separa ting the two. This chapter examines how the ailure o these disciplines to adequately distinguish ordinary sadness rom depressive disorder has not only abandoned psychiatry to its conceptual challenges but has also caused these disciplines to descend into conusion in their own research. 194 THE FAILURE OF THE SOCIAL SCIENCES 195 Anthropology The Role of Universal Concepts As chapter 2 argued, both cultural values and the universal functional design of loss response mechanisms must enter into good definitions of normal sadness and depressive disorders. General experiences of loss, such as humiliating declines in social status, loss of valued attachments, and inability to achieve social goals, are universal. And the emotion of sadness and some of its associated symptoms, although subject to variation in their expressions, are also universal across cultures. But loss response mechanisms are programmed to react according to culturally defined ideas of status, valued attachments, or worthy goals, so distinctions between normal and disordered loss responses must take into account cultural systems of meaning. Culture also influences how people learn to express sadness and depression in appropriate ways. Anthropologists are well positioned to study which aspects of loss responses are culturally influenced and which belong to the domain of human speciestypical functioning. But instead they have helped perpetuate psychiatry’s confusion by denying that a cogent distinction between normal and dysfunctional loss responses rooted in natural selection is even possible. This denial is to some extent an expression of an enduring resistance in anthropology to the very notion that there is a “human nature,” because Eurocentric notions of normality have been used for oppressive purposes in the past to classify non-Western societies as inferior. But it is also an expression of a confused postmodernist perspective that regards more or less everything human as thoroughly culturally determined. Anthropologists who study depression generally claim that the distinction between normality and disorder depends entirely on the value systems of particular cultural groups. Ruth Benedict’s classic article, “Anthropology and the Abnormal,” set the agenda for anthropological research about depression and other mental disorders, emphasizing that all definitions of normality and pathology derive from local concepts that cannot be generalized across cultures. 1 What some cultures view as disordered depression, Benedict argued, others view as normal sadness. For example, the Zuni of Arizona regard states of extreme passivity and fatalism, which Western psychiatrists might diagnose as Major Depression, as normal and even admirable expressions of a culturally defined personality style. For Benedict, all universal concepts of disorder and normality stem from ethnocentric Western norms that do not accurately reflect the indigenous behaviors to which they are applied. Instead, she claimed, local cultural definitions constitute what is normal or pathological in each society. There are several weaknesses in Benedict’s argument. It seems plain that the Zuni conditions she describes are indeed largely normal conditions that are rooted in philosophical attitudes and personality tendencies that the culture’s meaning system shapes. Western psychiatrists who diagnosed these conditions as 196 THE LOSS OF SADNESS mentally disordered would be wrong. But Benedict did not careully distinguish these salient conditions rom other, less culturally explainable conditions that the Zuni themselves would consider to be true disorders. It is entirely possible or a condition in one culture to be considered normal but or a superficially similar condition in another culture to be considered disordered. This can occur i, in the first case, the condition arises rom normal cultural shaping o meaning and expressive systems, whereas, in the other case, it is a product o a dysunction in loss response mechanisms. For example, the appearance o extreme and chronic lack o pleasure that could be normal among the Zuni because o their cultural socialization could well indicate a depressive disorder in members o modern Western cultural groups that have experienced diferent socialization that would not normally lead to such eelings. But the act that cultural norms must be taken into account in determining the normality-disorder distinction does not mean that such norms ully constitute this distinction because they are only one actor that shapes normal variation. Benedict’s assumptions persist as the central tenets o the new cross-cultural psychiatry that has dominated anthropological studies o mental illness since the 1970s. Centered around the work o Harvard anthropologist and psychiatrist Arthur Kleinman, this school has produced a great deal o insightul and detailed research about the culturally-specific aspects o depression, and it has developed cogent critiques o psychiatry’s tendency to exaggerate the universal nature o depression. In particular, Kleinman’s own careul cross-cultural scholarship, with its eloquent and illuminating rendering o the social and personal meanings behind patients’ behaviors, has reshaped the understanding and study o cross-cultural psychiatry. Yet, in reacting against ethnocentrism, anthropologists working within Kleinman’s paradigm have gone too ar in the other direction by emphasizing cultural variability to the excessive exclusion o common, worldwide eatures o depression. This has consequently raised challenging conceptual questions about their entire approach. Many anthropologists reuse to use any distinction that is grounded in biological unctioning, which is constant across cultures, to explain the huge diferences in definitions and maniestations o depression in diferent societies.2 Psychological unctions such as thought, language, perception, and mood, they claim, stem much more rom culture than rom biology. Psychological systems, according to anthropologist Laurence Kirmayer, “are so malleable that they can be or almost anything. . . . Beyond a ew relatively simple physiological unctions, it is impossible to identiy what psychological systems or unctions are or in any universal sense.”3 Anthropologists o depression thus emphasize cultural uniqueness. Culture reers to customs, symbols, belies, values, and norms that individuals within a group share but that are diferent among individuals in diferent groups. For anthropologists, such varying cultural rulesconstitute concepts o normality and pathology, making a universal definition o normal sadness or depressive disorder THE FAILURE OF THE SOCIAL SCIENCES 197 that is anchored in human nature impossible. Disorder, according to this view, just consists o whatever a culture defines as deviant or negative behavior. Assertions o common human standards o psychological unctioning actually impose ethnocentric Western categories about appropriate or inappropriate behavior onto other cultures.4 Claims about the naturalunctioning o sadness as an emotion and as a loss response mechanism, or example, involve taking cultural categories that Western psychiatrists and Western culture create and superimposing them on the products o another culture’s definitions, rules, and expressions in 5 which the Western categories do not apply. The anthropologist Gananeth Obeyesekere, or example, claims that Buddhists in Sri Lanka view symptoms o hopelessness, meaninglessness, and sorrow as part o a culturally recognized philosophy o lie, not as an illness.6 He asserts that Buddhists respond to loss by generalizing their despair rom themselves to the world at large so that sadness takes on nonpathological meaning rom Buddhist worldviews. Such extreme cultural variability in definitions o depression indicates, according to Obeyesekere, that it cannot be a universal disease category. What is considered to be depression must be described and analyzed within the terms o each particular cultural group. The Sri Lankan Buddhists whom Obeyesekere describes certainly do not have depressive disorders, although they might meet DSM criteria or Major Depression. He is clearly talking about normal sadness, because the symptoms he describes develop and persist only as a unction o the situation o loss and o philosophical views o lie. Obeyesekere does not discuss cases o chronic deep sadness that arise or no philosophical or loss-event reason, which might properly be classified as a disorder. He ofers no evidence that Sri Lankans themselves would not consider such conditions as disordered. Indeed, the history o Western accounts o depressive disorder is filled with disclaimers, similar to Obeyesekere’s, that there are orms o philosophical depression, much like those the Sri Lankans cherish, that are not true disorders. The problem that Obeyesekere detects in trying to impose DSM criteria on Buddhist culture is not the imposition o invalid Western categories on a culture to which they do not apply. Rather, he detects the act that the DSM definition o depressive disorder is invalid according to both Western and Buddhist views and that there is general agreement that proportionate reactions to loss or philosophical dispositions should not be labeled as depressive disorders. Western and Sri Lankan conceptualizations only seem to difer because o errors in the DSM’s ormulation o the Western view. Instead o examining his data through the lens o a proper distinction be- tween disorder and nondisorder, Obeyesekere uses the Sri Lankan example to deny the possibility o making any universal statements about the nature o mental disorder: “The conception o the disease (i.e., illness) is the disease. Or to 7 put it diferently, there are only illnesses and no diseases.” Here, illness is supposed to reer to culturally bound definitions o who is placed in the sick role, 198 THE LOSS OF SADNESS whereas disease is the notion o an objective pathology and the claim is that disease is nothing more than illness. But Obeyesekere’s data show nothing o the sort; rather, they show that diferent cultures correctly recognize that sadness responses are normal, the DSM’s problems notwithstanding. Catherine Lutz’s work among the Ialuk o Micronesia is another well-known anthropological study o depression. Lutz regards the concept o depression as a “specifically Western cultural category” and contrasts Ialuk responses to loss with those ound in Western medicine. She finds that Ialuk whose intimates die or leave the island develop sadness that involves “excessive thinking/eeling about the missed person, loss o the desire to eat or engage in conversation or other activities, and sleepiness.”8 Lutz goes on to contrast Ialuk symptoms with the presumably intrapsychic conditions that Western psychiatry eatures: These various interpretations or situations o loss all point to people as the primary object to which one can be attached and rom which one can be separated. Unocused or objectless loss responses are not spoken o, as ar as I know. All [these] emotions are considered normal states. 9 She concludes, “the cross-cultural investigation o depression might be replaced by the examination o indigenous definitions o situations o loss and the blocking o goals, and the social organization o responses to them.”10 Lutz provides an excellent description o normal sadness among the Ialuk. Her critique ought to ocus on the overexpansive definitions o depressive disorder in Western psychiatry, which might mistakenly classiy these responses as dysunctions. Instead, like Obeyesekere, she uses her work to critique the possibility o using universal definitions and to advocate the study o purely local concepts. In act, her analysis shows how the Ialuk make the same sorts o distinctions between normal sadness and depressive disorder that people in many times and places typically do. She then uses the act that the DSM has mistakenly abandoned such standards in its symptom-based emphasis to argue that Western medicine classifies as disorders conditions that the Ialuk would not. But it is likely that i the same ethnographic methods were used in Western cultures to compare the opinions o ordinary people across cultures, Westerners would agree that the conditions Lutz describes are not disorders. Lutz’s work shows not that universally applicable distinctions are impossible but that the relationship between loss and normal sadness has a universal element that current Western psychiatric definitions do not adequately capture. Arthur Kleinman himsel has conducted the best-known and most path- breaking studies o cultural diferences in the expression o depression. At times, Kleinman adopts the extreme position that depression “is a cultural category constructed by psychiatrists in the West to yield a homogeneous group o patients.” 11 In some o his writings he regards W estern psychiatric categories as examples o a category allacy that mistak es culture-bound diagnoses THE FAILURE OF THE SOCIAL SCIENCES 199 or universal eatures o illness. In act, Kleinman asserts that there are no culture-ree entities but onl y culturally specific modes o explanation. 12 More commonly, however, Kleinman makes a distinction between disease and illness.13 For him, disease reers to abnormal physiological states that are aspects o the natural world. Illness reers to the actual lived experience o disease and encompasses the perceptions, interpretations, coping responses, and presentations that people give to various disease states. Diseases are universal somatic sensations; in contrast, cultural norms and meanings undamentally shape illness, and so it varies widely in dierent social groups. Through extensive observation and interviews in China, Kleinman concludes that the physiological symptoms that Chinese use to express depression are undamentally dierent rom the psychological presentations that Westerners make. Among Chinese patients, the major eature o depression lies in its physiological emphasis and corresponding lack o psychological symptoms. They present somatic complaints but, unlike Westerners, usually do not report eeling depressed. Furthermore, Chinese patients view their illnesses as physiological and reject the idea that they have any sort o mental disorder. Kleinman links the ocus on physical symptoms and the denial o psychological symptoms to the values o Chinese culture. Chinese norms discourage verbal expression o intimate personal emotions and emphasize the ulfillment o social roles and interpersonal relationships. Expressions o eelings such as loneliness and sadness lead to stigma and embarrassment and indicate excessive sel-absorption. In contrast, Chinese culture encourages expressions o physical complaints. Kleinman’s studies lead him to assert that the central anthropological ocus must be on illness rather than on disease: Depression experienced entirely as low back pain and depression experienced entirely as guilt-ridden existential despair are such substantially dierent orms o illness behaviour with dierent symptoms, patterns o help-seeking, course and treatment responses that though the disease in each instance may be the same, the illness rather than the disease is the determinant actor.14 In principle, we agree with Kleinman’s distinction between disease as a universal underlying dysunction and illness as the culturally shaped expression o a given dysunction. The difculties with his argument arise because he places almost exclusive emphasis on the “illness” aspect o disorder. There are several problems with such a ocus. First, i there are indeed underlying com- mon dysunctions, then treatment presumably depends in large part on the science o identiying and intervening in such dysunctions irrespective o their cultural presentation. Second, Kleinman labels various conditions as “depression” in China even as he claims that these conditions have little in common with Western-defined depression . This raises the question o what he sees across 200 THE LOSS OF SADNESS cultures that is the same and that thus makes all these conditions instances o the same disorder—depression. It would seem that either the context, such as loss, or some other shared characteristic must be at work to constitute such a concept and to lead Kleinman and others to iner a shared underlying dysunction, but that assumption already suggests that there is something misleading in his antiuniversalist argument. In act, every culture recognizes depression in orms that Westerners would recognize. Third, however one identifies depressive states in general, Kleinman never takes seriousl y the question o how various cultures distinguish normal rom disordered depressive conditions, because this would involve exploring how individuals iner underlying dysunction that does not solely involve negative cultural presentations. He uses illness in a very broad way or unpleasant, subjective, culturally recognized experiences and then defines disease as whatever physiological state underlies an illness. This runs together normal negative emotions and disorder, thus obscuring distinctions that every culture makes. Fourth, oddly or an anthropologist, Kleinman does not clearly distinguish what people are willing to say because it is socially desirable to say it rom what people really eel or believe. Some cultural tendencies to publicly hide eelings suggest the possibility that observed diferences are only superficial and hide the emotions that people actually experience. 15 This lack o refined distinctions between underlying experiences and their culturally shaped expression leads to the final problem. Kleinman’s central and signature point—that Chinese people experience psychosomatic symptoms o depression and not Western-style emotional symptoms—is questionable. A careul examination o his own data shows that, although his Chinese sample did not spontaneously characterize their depressive experiences by ocusing on the same symptoms as Westerners, they in act reported high rates o DSM-style symptoms when they were specifically asked about them. Moreover, subsequent empirical work shows that Chinese and Western samples generally experience much more similar symptoms than Kleinman claimed.16 Thus his classic finding that Asian populations express their depression through an “idiom o distress” that ocuses on somatic complaints rather than on mental DSM symptoms seems to be more a finding about how people tend to socially present themselves than about what people actually experience.17 To the degree that there remain diferences in expression, the somatization o depression may occur because some cultures may not have linguistic terms to describe internal, emotional states, or they may have social norms against perceiving or talking about inner eelings. Moreover, whether or not the expression o depression difers across cultures, this research ails to address the undamental question o whether diferent expressions o emotions are variants o normal sadness or o depressive disorders. THE FAILURE OF THE SOCIAL SCIENCES 201 The Need to Balance Universal and Cultural Factors The study o cross-cultural variation in normal and disordered depressive conditions is a ertile field that yields surprising insights into the power o cultural meaning systems to shape human experience. Yet the contemporary ocus in medical anthropology on such variation to the exclusion o underlying universal structures that are constraints on such experiences has had problematic consequences. Anthropologists who study depression have generally embraced a relativistic view according to which there is no way to apply a concept o disorder or normality beyond local cultural practices. Consequently, they oten take the DSM symptom checklist itsel as representative o the Western conception o depressive disorder, enabling them to easily demonstrate that other cultures’ conception o normality includes conditions that we would place under the category o disorder and thus supporting a position o cultural relativity. Intellectually dominated by relativistic doctrines and ear o cultural ethnocentrism, anthropologists cannot step back and critique the DSM’s implicit assumptions about human nature rom a perspective that is not itsel culturally relative. It is true that reality can be divided up in many diferent ways and that categories rom one culture must not be imperialistically imposed on another. But it is equally true thatno sensible cross-cultural understanding odisorder categories can ignore universals ohuman nature due to our common evolutionary heritage and the role these universals play in identiying normal and disordered conditions. Even i concepts are socially deployed structures, w hat the concepts reer to in the world need not be socially constructed. The review inchapter 2 showed the universality o sadness as an emotion and o some o the elements that determine how it is triggered; where universal emotion-generating mechanisms exist, one would also expect that there are some universal kinds othings that could go wrongwith those mechanisms. Although culture shapes the particular ways that people express intense and even disordered sadness,what is being shaped is a more universal state. Great cultural variance in symptoms is compatible with a universal base around which symptomatic presentationsdiverge. Moreover, the study o variation in depression cannot adequately proceed without some notion o what is universal. For example, the claim that some cultures express depression through physiological symptoms and others through psychological symptoms depends on some underlying conception o depression that transcendsits symptomatic expression. The reusal to explore universal concepts o disorder and normality also prevents anthropologists rom ormulating compelling critiques o Western psychi- atry. The view that all definitions o normality and pathology are culturally relative means that anthropologists have no definition o normality that transcends any particular diagnostic system and that would show the inadequacy o psychiatric diagnoses within that system. Until anthropologists recognize that proper specifications o what is culturally relative depend on notions o what is 202 THE LOSS OF SADNESS universal, they will not be able to develop strong concepts o either normality or disorder or strong theories o the actors that determine cultural expressions o depressive conditions. They thus severely limit their ability to derive substantive lessons rom their studies or Western psychiatry or to provide a corrective to the excesses o Western diagnosis. Further development o the notion o “dysunction” and study o how dysunction interacts with cultural meanings could ofer a welcome realization o the powerul insights rom the “new cross-cultural anthropology” or making constructive critiques o psychiatric diagnosis. Sociology The Sociology of Stress Sociologists should be in an excellent position to critique the overly inclusive DSM definition o mental disorder and t o show the distinc tiveness o sadness and depressive disorder . The major goal o the dominant socio logical paradigm o mental hea lth, the sociolog y o stress, is to assess the psy chological consequences o stressul social arrang ements. 18 To this end, sociologists examine how exposure to stressors, such as acute lie events or chronic and persisting negative social conditions, afects health outcomes. The kinds o stressors that sociolog ists usually study—ailing mar riages, lost jobs, blocked social mobility, conflicts between work and amily obligations, inequitable living conditions, and the lik e—lead to just the kind o distressed responses that nondisordered people should be expected to have to their social circumstances, although such stressors also can sometimes trigger disorder. Likewise, the natural thrust o sociologi cal work points toward social conditions, rather than individual patholo gies, as being the source o symptoms, w hich should provide a corrective to the psychiatric proession’s pervasive medicalization o social pro blems. Numerous sociological studies indicate that stressul social arrangements typically lead to distress that both emerges and fluctuates in accordance with social conditions.19 Indeed, the three major general processes that predict high rates o distress correspond to the low positions in status hierarchies, losses o valued attachments, and the inability to achieve valued goals that chapter 2 indicated are the major sources o normal sadness.20 Sociological research demonstrates the distressing mental health consequences not only o socioeconomic stratification but also o subordinate positions in amilial and interpersonal 21 hierarchies. Low positions in status hierarchies expose people to the kinds o circumstances, such as inadequate financial resources, oppressive work and amily conditions, and severe health problems in onesel and others that naturally produce distress. Moreover, research shows that such inerior statuses are ar more likely to be the cause than the consequence o normal sadness.22 THE FAILURE OF THE SOCIAL SCIENCES 203 The second major source o distress stems rom the loss o intimate attachments. Indeed, the three lie events considered most stressul in samples o ordinary Americans are the death o a spouse, divorce, and marital separation.23 Losses o valued attachments are powerul enough to produce intense distress among huge proportions—generally between one-third and one-hal—o people who experience them.24 Finally, the inability to achieve valued social goals is also associated with elevated levels o distress. Situations in which people cannot disengage rom unreachable goals or eel their lives have not turned out in ways that they desire commonly produce nondisordered sadness. Examples are graduate students who cannot find jobs in their academic fields or aculty members who ail to get tenure.25 Likewise, adults who do not attain goals they set or themselves in earlier stages o lie report more distress than those whose attain26 ments match their srcinal aspirations. Women who intensely desire to bear children but who are inertile also experience very high rates o distress.27 Studies rom the sociology o stress do not just show how inequality, attachment loss, and ailure to achieve goals commonly trigger distress; they also indicate that the severity and duration o the loss response are related to the degree o stressulness ound in the conditions o people’s lives. The severity o symptoms is a direct unction o the number and intensity o the chronic stressors and acute lie events that people experience.28 Likewise, distress persists as a unction o the duration o economic and interpersonal stressors.29 The conclusion is inescapable that the great majority o distress-inducing conditions that sociologists study appear to involve normal distress that arises because o social circumstances and endures roughly as long as those circumstances persist. One might think that this body o research would sound an alarm about the potential medicalizing o what are really socially induced conditions o normal distress. To the contrary, sociologists have themselves accepted aDSM-like symptom-based approach that classifies a broad range o negative emotional reactions as disorders. They have thus supported and even extended the conusions o the DSM rather than drawn the necessary distinctions that would possibly correct the situation. Most prevalence estimates in sociological studies stem rom the Center or Epidemiological Studies measure o depression (CES-D), a scale developed during the 1970s to assess depression in community populations.30 The CES-D contains a series o 20 standardized questions that ask how oten a symptom occurred during the previous week. Responses are scored rom 0 to 3 on the basis o their requency over this time rame, and answers are summarized into a total number. The particular questions are: 1. I was bothered by things that usually don’t bother me. 2. I did not eel like eating; my appetite was poor. 3. I elt that I could not shake of the blues even with help rom my amily or riends. 204 THE LOSS OF SADNESS 4. 5. 6. 7. 8. 9. I elt that I was just as good as other people (reverse scored). I had trouble keeping my mind on what I was doing. I elt depressed. I elt that everything I did was an efort. I elt hopeul about the uture (reverse scored). I thought my lie had been a ailure. 10. 11. 12. 13. 14. 15. I elt earul. My sleep was restless. I was happy (reverse scored). I talked less than usual. I elt lonely. People were unriendly. 16. 17. 18. 19. 20. I enjoyed lie (reverse scored). I had crying spells. I elt sad. I elt that people disliked me. I could not get “going.” Total scores are considered to lie on a continuum o pathology that ranges rom mild to severe. Especially high scores, usually those o 16 and above, are considered to be probably comparable to treated cases o depression. The CES-D, like the DSM, does not consider the context in which symptoms develop. In other respects, it is ar easier to make a diagnosis o depression with the CES-D than with the DSM. Whereas the DSM requires either the presence o depressed mood or the inability to experience pleasure, the CES-D has no necessary symptom o depression. This means that a score o 16 can be reached in numerous ways, even when people do not have the cardinal markers o a depressed state. More important, the CES-D has ar less stringent duration requirements than the DSM. The DSM requires that all symptoms persist or at least a 2-week period. In contrast, the CES-D gives some positive score when a symptom is present or even a single day over the preceding week. Given its nature, it is not surprising that the CES-D uncovers enormous prevalence rates. For example, more than hal o bereaved participants, hal o those who had undergone marital separations, and a third who became unemployed have CES-D scores that are considered to be comparable to treated cases o clinical depression.31 In addition, about one-third to two-thirds o adolescents report scores that are generallyviewed as comparable to cases oclinical depression on the CES-D.32 Four studies undertaken as part o the OregonAdolescent Depression Project in the late 1980s ound that between 39 and 60%33 o boys and 56 and 63% o girls met CES-D caseness criteria or clinical depression. Another large study that used measures at two diferent points in time ound that only about a third o adolescents werenot 34 depressed at either assessment. Even studies that significantly raise CES-D criteria 35 to 24 or higher still find that about 10% oall adolescents are depressed. THE FAILURE OF THE SOCIAL SCIENCES 205 The minimal duration requirement means that the CES-D is extraordinarily sensitive to such transitory yet commonly occurring phenomena as ailing a test, losing a crucial game in sports, or discovering that a boyriend or girlriend is going out with someone else.36 Indeed, the best predictor o high CES-D scores among adolescents is the breaking up o a romantic relationship, a nearly ubiquitous phenomenon in this age group. People who say they were bothered by things, had trouble concentrating, elt depressed, had restless sleep, were not happy, did not enjoy lie, elt sad, and could not shake of the blues would be considered possible “cases” o depressive disorder even i symptoms disappeared a ew days ater such events took place. Yet sociologists persistently ail to distinguish whether high scores on symptom scales stem rom persons with chronic and recurrent conditions that fluctuate independently o social conditions or rom those with transitory and situationally induced distress. Typical sociological articles interchangeably use terms such as depression, distress, lack of well-being, mental illness, or mental disorder. Common psychological consequences o stressul social arrangements are sometimes called distress and at other times (oten in the same paragraph o the same article) depression or mental disorder. Instead o separating nondisordered distress that fluctuates as a unction o external situations and is proportionate to these situations rom depressive disorders that indicate the presence o an internal psychological dysunction, sociologists have only perpetuated the conusion between these two conditions. Consequently, lacking any delineation o disorder and distress, sociologists have ailed to appreciate that current studies in the sociology o stress conflate two diferent domains o research. The first domain has nothing at all to do with mental disorder and instead concerns the consequences or normal distress o various stressors and positions within the social system. The second domain concerns the sociological determinants o genuine mental disorder to the degree that severe social stressors can cause or trigger such disorder. Traumatic external conditions can lead wartime combatants, victims o violent crimes, or Holocaust survivors, or example, to develop psychological dysunctions.37 Not just extreme conditions o trauma but also longstanding social stressors can produce lasting internal dysunctions. Chronic poverty without prospects o redress, or example, can lead people to develop internalized and pervasive senses o hopelessness and helplessness, which oten do not change even i their social circumstances do change or the better.38 However, the typical outcomes o the sorts o stressul social arrangements that sociologists usually study are not internal psychological dysunctions but instead are natural responses that nondisordered people have to stressul conditions. They are the kinds o “expectable and culturally sanctioned response(s) to a particular event, or example the death o a loved one,” that even the DSM specifically excludes rom its definition o mental disorder.39 They arise in exactly the types o situations—low and declining positions in status hierarchies, 206 THE LOSS OF SADNESS losses o attachments, and the ailure to achieve desirable goals—that normally unctioning loss response mechanisms were designed to deal with.40 The ailure o sociology to recognize these acts renders potentially conusing and ambiguous much o the research in the sociology o stress. George Brown’s Studies of Depression George Brown, a British sociologist, is possibly the world’s preeminent researcher on depression. His work has had more influence on psychiatry, especially in Great Britain, than that o any other social scientist. The sophisticated social model o depression that Brown has developed amply justifies his influence. His comprehensive approach includes an unusual combination o attention to subtle subjective meanings that influence emotional states and to methodologically sophisticated strategies o both qualitative and quantitative measurement. Brown’s work exemplifies an all-too-rare kind o sociological research that combines exploration o human meaning with careul methodology and penetrating theory. That said, we ocus here on one area we consider to be a limitation o Brown’s work, namely, its ambiguity about the distinction between disorder and nondisorder. Indeed, it is unclear exactly what set o conditions his model explains or is intended to explain. Most o the cases that Brown considers to be depressive disorders actually seem to be cases o normal sadness, although others are probably genuine disorders. In ailing to adequately distinguish cases o normal sadness rom disordered depression, Brown unnecessarily limits the useulness o his very valuable model o depression and inadvertently contributes to the conusion pervading current approaches to the diagnosis o depressive disorder. Brown’s great achievement has been to develop a strong methodology or measuring the social causes o loss responses. Most research on the relationship between stressul lie events and depressive symptoms relies on respondent reports o what stressul lie events they have sufered and how stressul they were. Such respondent-based methods inherently conound the subjective mental states o individuals with the properties o the stressul events that they experience. Thus it is not surprising that such studies find relationships between the stressulness o lie events (as reported by the respondent) and the intensity o symptoms (as reported by the respondent); the respondent will be likely to recall events as highly stressul i he or she recalls them as leading to intense symptoms. Brown’s system, in contrast, uses objective independent ratings o observers (which can be done blindly, without knowledge o the respondent’s subsequent symptoms) about how much distress a particular individual would be expected to sufer, given the nature and context o the lie events that he or she experiences, including their various likely meanings (e.g., humiliation or entrapment). The resulting system provides ratings o the stressulness o lie events that are not dependent on respondents’ psychological condition or THE FAILURE OF THE SOCIAL SCIENCES 207 assessment. Brown, thereore, clearly separates the measurement o stressul lie events rom the resulting outcome measures while at the same time building a variety o subtle biographical and contextual variables into the objective assessment o the lie events. This kind o methodological care and attention to the subtleties o meaning associated with various lie events is unprecedented in depression research. Brown’s system could be especially valuable rom our perspective because it can allow researchers to compare the proportionality o resulting sadness responses with the independent ratings o the severity o the stressors that triggered the responses. Such measures are precisely what is needed to begin to get at the notion o a “proportional” response and thus to examine the distinction between normal and disordered depressive conditions. This, however, is not the direction in which Brown’s work evolved, and he does not draw such a distinction. Rather, Brown presents his work as a study o depressive disorder in the community. His measure o depression is the Present State Exam (PSE), a structured clinical interview developed in the early 1970s. The PSE yields diagnoses o depression that are very similar to those that stem rom DSM criteria, requiring the presence o depressed mood over the preceding month, as well as at least our o the ollowing symptoms: hopelessness, suicidal ideas or actions, weight loss, early waking, delayed sleep, poor concentration, brooding, loss o interest, sel-depreciation, and anergia (the ailure to respond to a toxin). Brown sometimes uses the lowered criteria o depressed mood and at least one other symptom o the PSE to measure what he calls borderline cases o depression that are analogous to subthreshold or minor depression.41 The major diference between the PSE and structured interviews based on DSM criteria is that the PSE does not ascertain lietime histories o depression; Brown examines preceding-year episodes o depression exclusively. Brown’s studies uncover rates o depression in community samples that are even higher than in U.S. studies. For example, about 15% o working-class women in London have what Brown callsclinical depression over a 12-month period.42 When he adds rates o borderline symptoms o depression and anxiety to cases that meet ull criteria, he considers that about hal o the community populations he studies have disorders. 43 Using the same methodology translated cross-culturally, Brown finds that rates o depression over the previous year fluctuate widely across societies, ranging (as noted in chapter 2) rom a high o 30% in urban areas o Zimbabwe to a low o about 3% in rural Basque-speaking areas o Spain.44 This great variation in rates across societies leads Brown to conclude that psychosocial, rather than biological, actors account or most cases o clinical depression. Brown’s initial research ocused on the connection between loss events and the subsequent development o depression among urban working-class women. He ound that severe lie events among women who had lost mothers in 208 THE LOSS OF SADNESS childhood, who had three or more children living at home, who had no intimate, confiding relationships with husbands or boyriends, and who were not employed accounted or the association between social class and depression.45 This research indicated that severely threatening lie events occurred shortly beore depressive onsets in between 67 and 90% o cases.46 Most o these events involved interpersonal difculties, such as a woman’s husband calling her an unfit mother, a boyriend deciding he did not want an exclusive relationship, or a child leaving the mother’s home to live with other relatives.47 Brown’s subsequent work ocused on the particular nature o losses. Those that involve core roles, important and consequential plans, or cherished ideas about onesel or an intimate are especially likely to lead to depression.48 Two qualities, in particular, are related to subsequent depression among people who 49 have suered those types o losses. First, humiliating losses that devalue people, undermine their sel-esteem, and result in subordination lead to depression. Second, losses that are entrapping and so do not allow people to escape rom the loss situation are depressing. Brown ound that nearly 50% o women who had experienced events considered both humiliating and entrapping had depressive responses; such women were three times more likely to develop depression than those who solely suered some loss event.50 Qualities o lie events account not only or which women develop depression but also or which ones recover rom it. What Brown calls “resh start” events, such as finding a new boyriend, obtaining a better job, or moving to better housing, aect the chronicity o depressive episodes.51 Reducing the stressulness o environments or experiencing positive events accounts or recovery or improvement. The course o depression is thus the mirror imag e o its onset: certain kinds o lie events predict both the emergence and the length o depression. Brown’s approach to the majority o depressive reactions he describes is seemingly very compatible with the conceptualization o normal sadness that this book presents. He views depression as rooted in a common human nature, reflecting the act that the human brain has evolved to deal with stressul lie events.52 Thereore, the capacity to develop depressive responses is universal. 53 He also stresses the role o particular kinds o losses as provoking most depressed conditions. Likewise, he regards cognitions associated with depressive states, such as helplessness and hopelessness, as ully understandable in the context o adverse social conditions, not as inappropriate.54 As well, he indicates that “we humans have an uncanny tendency to adapt to adversity and deprivation” and stresses that many loss responses end when environmental conditions change.55 Brown’s emphasis on the findings that particular kinds o losses precede the onset o depression and that particular kinds o positive social changes predict recovery rom it seems to indicate that he is studying normal sadness and not depressive disorder. Brown’s characterization o the conditions he studies, however, makes it clear that he considers them to be depressive disorders and not normal sadness. THE FAILURE OF THE SOCIAL SCIENCES 209 He does distinguish a small minority o largely endogenous cases rom the majority o depressive conditions that he studies: “Melancholic/psy chotic depressive conditions as a whole are unlikely to orm more than one-tenth o the total range o clinically relevant depression. ” 56 But Brown reers to the remaining 90% o conditions as depressive disorders, clinically relevant depression, or neurotic depression, irrespective o their urther properties. He consistentl y says that his community samples sufer rom psychiatric disorders that are the same as those ound in patient populations and emphasizes that the conditions o the community members he has studied are compa rable to those o treated psychiatric patients.57 His justification or this claim is that his studies comparing community populations with treated patients find that provoking events precede the vast majority o cases in both settings. 58 Likewise, he finds that, or the most part, community members and patients share common symptoms. Granted that the two populations are similar in these respects, we have seen that this similarity alone does not ensure that both groups are equally disordered. Normal and disordered responses to stress can maniest similar symptoms, and some responses to severe stresses can be proportional and related to the ongoing presence o the stressor, while others may be disproportionate or continue despite changing circumstances. Moreover, it is entirely possible that the psychiatrically treated outpatient group contains a considerable number o nondisordered individuals reacting normally to extreme losses. The problem is that that Brown does not urther pursue the question o which members o either group have disorders and which do not. In one article, Brown does explicitly consider whether the conditions he studies are instances o distress or disease, and one might hope to find here some illumination o the disorder-versus-nondisorder distinction.59 He finds that cases in the community that meet PSE criteria are comparable to cases ound in clinical treatment. Except or the 10% o cases that are “melancholic/ psychotic,” particular types o losses usually precede depression in both community members and psychiatric outpatients, and both groups have symptoms o comparable severity and duration. Brown thereore rejects the notion that community members sufer rom distress, whereas psychiatric outpatients have diseases, and he concludes instead that in both groups, “depression (is) basically a distress response.”60 But these assertions do not address the disorder status o the conditions because neither o Brown’s terms corresponds to disorder or nondisorder. By disease, Brown means endogenous or biological conditions that have no social triggers, which presumably are disorders. By distress, he means all reactions with social triggers. However, as we have seen, a stressor can trig- ger a disordered reaction or a reaction that is initially normal but that eventually develops into a malunction involving disproportionate duration or intensity in depressive response, so that what Brown calls “distress” encompasses both disordered and normal reactions to loss. Brown’s demonstration that most cases in both community and clinical samples are distress, not disease, thus ails to 210 THE LOSS OF SADNESS address the distinction between nondisordered and dysfunctional responses. In fact, Brown himself considers his comparison to be between two kinds of depressive disorder (roughly corresponding to the traditional categories of “endogenous” and “reactive” depression); he calls cases of either kind that meet PSE criteria psychiatric disorders. Brown’s study thus illustrates the kinds of challenging terminological obstacles to interpreting current literature that does not start with a cogent distinction between disorder and nondisorder built into the methodology. The evidence in fact suggests that Brown’s studies mix together disordered and nondisordered individuals with depressive symptoms and that it is likely that most of his cases reflect normal sadness. Most not only arise in response to certain kinds of loss events but also persist with proportionate intensity to social circumstances and end when these circumstances change. A minority of cases in Brown’s studies, however, endure beyond the circumstances that brought them about and are not responsive to positive environmental changes. About a third of the people in his community samples who experience major improvements in their living situations remain depressed.61 Although Brown’s work commendably focuses on conditions triggered by carefully specified social situations, it neglects depressive conditions that become disengaged from environmental contexts and appear to be maintained by some internal dysfunction and thus are likely to be disordered. We thus believe that Brown’s greatest achievement has been to accurately measure and characterize the nature and causes of intense, mostly normal sadness, even if he does not call it that. Further, he has developed the most nuanced theory of the particular qualities of losses—severity, humiliation, and entrapment—that most powerfully produce normal sadness and has documented how such conditions persist only as long as environmental stressors remain. Although Brown presents his research as a study of depressive disorder, it seems instead to be primarily a landmark contribution to the study of normal sadness in extremely adverse and often unjust social circumstances. Brown’s superb work illustrates how even the best social scientific studies have tended to accept and support rather than challenge the growing confusion within psychiatry about the distinction between disorder and normal negative emotion. Conclusion Anthropological and sociological studies have helped perpetuate the conflation of normal sadness and depressive disorder. Because they reject the possibility of developing any concepts of depression that transcend local understandings, anthropologists lack any grounds for saying that the definitions of Western psychiatry could be improved. Sociologists use terms such as distress and depression interchangeably, implying that all sadness responses are variants of mental THE FAILURE OF THE SOCIAL SCIENCES 211 disorders, and so they too are unable to challenge psychiatry’s overexpansive definition of depressive disorder. George Brown has built a sophisticated theory of the circumstances under which sadness arises, yet he does not distinguish depressive conditions that arise from dysfunctions from those that are normal reactions. Part of the reason that an adequate distinction between normality and disorder eludes us is the failure of the social scientific disciplines that study depression to take an independent critical stance and to challenge the diagnostic criteria. DSM 11 Conclusion n this final chapter, we tie up several loose ends o our argument. First, we consider the question: I the flaws in current diagnostic criteria are as compellingly clear as we argue that they are, then why haven’t they been changed, or why can’t they easily be changed? In addressing this question, we shit rom the logic o diagnosis to the logic o powerul constituencies and vested interests that come into existence once a definition o disorder is in place. Second, we return to the evolutionary perspective on disorder that we presented in the first two chapters and that serves as the ramework or much o our argument. The scholarly literature has posed many objections to this view. We review I some o the most interesting objections and briefly explain why we think none o them places the evolutionary understanding o normal human unctioning in doubt. Finally, this book is mainly an analysis and critique. However, many readers will be wondering what the solution to the problems we identiy might be. So we ofer some initial thoughts on strategies by which the approach to diagnosis o MDD might be changed to be more valid. The Constituencies for Depressive Disorder We have argued that there is an obvious logical problem with the current DSM definition o Major Depressive Disorder. We have documented how this problem has radiated throughout the mental health treatment and research establishment, as well as into the realm o public policy, to expand the domain o depressive disorder. Yet the definition is resilient; it has survived three revisions o the DSM, and there are ew signs to suggest that changes in the MDD criteria are a high priority or the next revision, DSM-V. Assuming that our argument has merit, it seems reasonable to ask: What stands in the way o simply changing this definition and correcting a logical gap? All else being equal, there are legitimate reasons or being conservative about changing diagnostic criteria. Perhaps the major one is that studies that use 212 CONCLUSION 213 dierent criteria or sample selection cannot easily be scientifically compared and cannot yield cumulative knowledge, thus undermining the very point o having reliable, scientifically respectable standards in the first place. It is also true that many proposals exist to change criteria in the direction avored by one group or another, but these proposals are almost never based on an accumulation o valid research evidence that would scientifically warrant the change. Thus transorming criteria can become a matter o politics rather than science. However, all else is not equal when it comes to the problem we have outlined; there is a compelling, clear, and major violation o validity that can be identified on general conceptual and theoretical grounds, and it should be fixed. It makes little sense to deend diagnostic continuity or research purposes when what is being preserved is known to be invalid and thus inadequate or scientific research to begin with. So i the standard reasons or resistance to change do not apply in this case, why aren’t the criteria being changed? Addressing this question moves us rom the sphere o definitional concepts into the realm o power relations within society and among its institutions. The exploitation o a concept or purposes o power can be judged only against an understanding o how the concept could legitimately be deployed. Thus an understanding o the concept’s logical structure, on which we have ocused, is required. But it is social actors, more than purely logical issues that determine how a concept is actually exploited and deployed, even allaciously at times, to serve broader interests.1 For example, the concept o depression, as we have analyzed it, picks out clear instances o normal sadness and o depressive disorder. But this concept also contains a high degree o indeterminacy, ambiguity, and vagueness around its boundaries, allowing dierent groups to exploit it in ways that suit their own interests. In particular, a number o constituencies have ound a symptom-based concept o depression that generates high rates o pathology to be advantageous. The proession o medicine more broadly and o psychiatry in particular has been a major promoter and beneficiary o a definition that allows it to label and treat previously nonmedical problems as disorders. All proessions strive to broaden the realm o phenomena subject to their control, and whenever the label o disease is attached to a condition, the medical proession has the primary claim to jurisdiction over it.2 Symptom-based conceptions o mental disorder thus expand the range o conditions that can be the legitimate objects o psychiatric management.3 Piggybacked on justifiable exercises o psychiatric power aimed at mental disorder, normal human emotions, once they have been classified as disorders, are generally subjected to technologies such as psycho- tropic medications or psychotherapy. These technologies have spread rom the mental hospital or psychiatric clinic to the doctor’s ofce, the school classroom, and the Internet sel-help site. For mental health clinicians, symptom-based measures o depression justiy reimbursement rom third-party insurers or the treatment o a broad range 214 THE LOSS OF SADNESS o patients who might not otherwise qualiy, because insurers will pay to treat disorders but not problems o living. Individual clinicians are aced every day with patients seeking help or conditions that appear to be intense normal sadness but that satisy the DSM’s criteria or disorder. Many clinicians will readily admit that a sizable proportion o their “depression” caseload consists o individuals who are psychiatrically normal but experiencing stressul lie events. The result is a strange case o two “wrongs” seemingly making a “right”: The DSM provides flawed criteria that do not adequately distinguish disorder rom nondisorder; the clinician, who cannot be aulted or applying ofcially sanctioned DSM diagnostic criteria, knowingly or unknowingly misclassifies some normal individuals as disordered; and these two errors lead to the patient receiving desired treatment or which the therapist is reimbursed. Symptom-based diagnoses allow clinicians to rationalize such decisions when the alternative is reusal o treatment to those who are suering. Researchers, too, have much to gain rom symptom-based diagnoses. The conflation o mental disorder and ordinary sadness legitimizes a broad interpretation o the mandated domain o the National Institute o Mental Health (NIMH), the major sponsor o research on mental illness. An expansive definition allows it to argue more persuasively or increased unding on the basis that depression is rampant in the population. In addition, in contrast to the 1960s, when the NIMH was concerned about the psychological consequences o social problems such as poverty, racism, and discrimination, in today’s political climate support is ar more likely to accrue to an agency that is devoted to preventing and curing a widespread disease than to one that conronts controversial social problems.4 Mental health researchers also have much to lose i criteria or depression should change. Symptom-based criteria are relatively easy to use. They reduce the cost and complexity o research studies and allow or higher research productivity. Enhanced reliability also coners enhanced scientific respectability. Moreover, theDSM’s criteria are used in virtually all o the thousands o recent depression studies on which researchers’ careers are built, and any major reconceptualization o diagnostic criteria would cast into doubt the value o that past research. Adequately distinguishing normal sadness rom depressive disorder could also possibly narrow opportunities or research unding, especially i the NIMH chose to ocus its eorts on true disorder. Nevertheless, researchers certainly appreciate that reaching the goal o understanding the etiology and appropriate treatment o depressive disorder ultimately depends on using a valid definition o disorder as the basis or sample selection in their studies. Symptom-based definitions are also useul or constructing estimates o the apparently huge social and economic costs o depression, which in turn can justiy providing more resources or treating and preventing depression. The World Health Organization (WHO) is the major group responsible or disseminating DSM definitions o depression rom the United States to a worldwide audience. CONCLUSION 215 Its signature concern has been to publicize the immense costs o depression. Most literature about depression cites WHO projections that by 2020 depression will become the second leading cause o worldwide disability, behind only heart disease, and that depression is already the single leading cause o disability or people in midlie and or women o all ages.5 This massive amount o disability lends a sense o urgency to policy eforts designed to respond to depressive illness. Peter Kramer, reviewing the WHO study, proclaims: “The most disabling illness! The costliest!” According to Kramer, “depression is the major scourge o humankind.”6 In act, the claimed enormity o this burden and its useul rhetorical qualities result rom the ailure to distinguish depressive disorders rom normal sadness. The WHO calculations o disease burden are extremely complex but arise rom two basic components: the number o people who sufer rom a condition and the amount o disability and premature death the condition causes. The first component o burden, the requency o the condition, derives rom symptombased definitions that estimate that 9.5% o women and 5.8% o men sufer rom depression in a 1-year period. The second component, disability, is ordered into seven classes o increasing severity, stemming rom the amount o time lived with a disease, weighted by the severity o the disease. The severity scores come rom consensual judgments o health workers rom around the world that are applied to all cases o the disease. Depression is placed in the second most severe category o illness, behind only extremely disabling and unremitting conditions such as active psychosis, dementia, and quadriplegia, and is considered comparable to the conditions o paraplegia and blindness. It is viewed as more severe than, or example, Down syndrome, deaness, below-the-knee amputation, and angina. This extreme degree o severity assumes that all cases o depression share the depth, chronicity, and recurrence that are characteristic o the conditions that health workers see in their practices. Yet, in contrast to the severity o the treated conditions that oten comprise proessional caseloads, a high proportion o individuals who meet symptom-based criteria in the community populations that provide the requency estimates or depression have acute episodes with little impairment that remit ater short periods.7 The WHO severity ratings thus ignore the great heterogeneity o impairment in cases o depression and apply the most serious rating to all cases. The conflation o normal sadness and depressive disorder leads to overestimates o both the severity and the prevalence components o disability ratings, accounting or the widely quoted WHO figures. Advocates, in turn, use this apparently scientific evidence that depression is a massive public health prob- lem to argue or committing ar more resources to combating such a disabling condition. Family advocacy organizations, such as the National Alliance on Mental Illness (NAMI), which became an influential political movement during the 1980s, are another powerul orce upholding symptom-based definitions o 216 THE LOSS OF SADNESS depression. They have at the top o their agenda the destigmatization o mental illness and the achievement o insurance reimbursement parity or mental disorder. Symptom-based diagnoses expand the notion o mental illness to such an extent that they encompass a large proportion o the population. This lowers the boundary between normality and abnormality and seemingly can help achieve a greater acceptability o mental illness in the broader society. In addition, advocacy groups argue that mental disorders, including depression, are biological disorders, just like physical disorders, and deserve to be treated equally with respect to reimbursement. Admitting that current DSM criteria ail to distinguish true depressive disorders rom normal sadness reactions would certainly muddy this argument and appears to go against these groups’ agendas. Pharmaceutical companies, which earn enormous profits rom the transormation o sadness into depressive disorder, are perhaps the most visible beneficiaries o the DSM’s symptom-based diagnoses. Consequently, these companies are now major sponsors o the activities o both the psychiatric proession and advocacy groups, who in turn emphasize the benefits o using medication as the rontline treatment or depression.8 Ubiquitous advertisements or antidepressant medication, using DSM criteria, emphasize that individuals who experience such common symptoms as sadness, atigue, sleep or appetite difculties, and the like should consult their physicians to see whether they might have a depressive disorder, and such campaigns have been enormously successul.9 Like clinicians, drug companies can legitimately explain that they are only using the criteria ofcially sanctioned by the psychiatric proession, even as their ads tend to urther conuse the public about the boundary between normality and disorder. Finally, perhaps the most important constituency or medicalized definitions o distress is aicted individuals themselves, who find that recognizing their symptoms as those o treatable illnesses enables them to get medical help more easily and thus to regulate their painul emotions. Advertisements and other media messages reinorce an image o consumers enjoying desirable liestyles because they use psychotropic drugs, reducing the gap between actual suering and desired normality. Such individuals may genuinely benefit rom medication or other treatment, and embracing a sel-definition as the victim o an illness provides a socially acceptable account o one’s problems and some release rom responsibility or those problems. Many constituencies, including proessional groups, researchers, mental health advocates, and pharmaceutical companies, as well as many individuals who want control over their emotional pain, thus have an interest in keeping the current diagnostic standards or depression, making it difcult to change these criteria. In the long run, however, it is difcult to imagine that any enterprise that claims to be based on scientific principles can continue to be grounded in obviously invalid criteria such as those that presently exist or MDD. By mixing together normal and disordered individuals in research samples, such conused CONCLUSION 217 criteria also hinder scientific progress in understanding the etiology o disorder and how it might best be treated. Unreasonably broad definitions o psychological disorder also have the potential costs o stigmatizing the disadvantaged as mentally ill, replacing social policies with unwarranted medical treatment, and creating a one-dimensional public discourse that can undermine the capacity or making moral and political distinctions. The very magnitude o the figures on the prevalence o depressive disorder, despite their rhetorical useulness, can paralyze the will to respond to a problem o such seeming enormity. At present, some critics argue against reimbursement parity or mental health care because, by allowing every instance o normal unhappiness to qualiy or treatment, it would break the health care bank. A more honest discussion o normal versus abnormal conditions and their appropriate rights to reimbursement might help to address some o these objections. As well, the advantages o treating the normally sad as having depressive disorders might be ofset by the liabilities o creating in such people a sense o victimhood, a diminished sense o personal responsibility, and a view o themselves as passive suferers o biochemical deficiency.10 Ultimately, the transormation o sadness into depressive disorder has the questionable efect o shrinking the range o normal emotions and expanding pathology to ever-widening realms o human experience. Objections to Our Position Much o our argument rests on distinguishing disorder rom normal human unctioning according to evolutionary criteria or how human beings are biologically designed to behave. The resulting approach reflects the dominant tradition in the history o psychiatry, as we documented in chapter 3. But is it possible that our distinction between depressive disorder and normal sadness is nonetheless simply wrong? Indeed, a number o objections have been posed to various aspects o our position. Debates over the concept o disorder are common across many disciplines, so our consideration o such objections is not at all meant to be complete. One set o objections asserts that disorder is inherently just a value-laden term denoting undesirable mental or behavioral conditions, with no actual component that might have a real reerent in human nature. Objective distinctions 11 between disorder and nondisorder, in this view, are impossible to make. We do agree that “disorder” is, in part, a value-laden concept; a condition that does no harm cannot be considered a disorder, and the notion o harm has an intrinsic value component. In addition, as we have seen, diferent groups manipulate this concept to suit their own interests. However, although it might seem attractive to equate disorder with whatever is negative, disorders are just one kind o negative condition. The claim that “disorder” is solely a value concept, although 218 THE LOSS OF SADNESS common, makes no sense simply because there are many negatively evaluated mental states that no one considers to be disorders, rom ignorance and lack o talent to lust or extramarital partners and male aggressiveness to a taste or atty and sugary oods that may be harmul in our current environment. Thus there must be something beyond the value judgment, specifically some actual criterion, that distinguishes disorders rom the myriad other negative mental and behavioral conditions that are negatively evaluated but are not considered disorders. That criterion seems to be whether the individual’s biologically designed mechanisms are unctioning in the ways they were naturally selected or; i the condition is within human nature in this sense, then even i the condition is currently harmul, it is not a disorder. A related objection is that whether we call any given condition a mental disorder must be capricious and ultimately vacuous because no sharp natural boundary exists between disordered and normal conditions. 12 Instead, normality and abnormality are arrayed on a continuum. It ollows, it is argued, that attempts to divide conditions into those that are dysunctional and those that are normal are arbitrary and must rest on social values.13 It is a misconception to think that a scientific concept o disorder must set such precise boundaries. What is essential is that the concept and its oppos ite can be clearly applied to a range o important cases; vagueness along the boundary is not critical and indeed is to be expected because the defining eatures themselves have vague boundaries. Continuous distributions in nature are completely compatible with objective concepts, although it istrue that the uzziness o the concept means that fixing an exact boundary or practical purposes will indeed be more likely to depend on social values and conventions than on objective acts. For example, there are real diferences, rooted in biological acts, between children and adults, between being asleep and being awake, between normal and high blood pressure, and between the colors black and white, yet in every one o these cases intermediate cases exist that create a uzziness or a continuum. Another common critique is that definitions o disorder must be rooted exclusively in the actual social practices o some community. This objection holds that concepts o disorder are relative to particular times and places and cannot be universally valid. For example, anthropologists Laurence Kirmayer and Alan Young argue that: Inappropriateness has much more to do with socially defined norms and circumstances than with evolutionarily defined ones. The inappropriateness that distinguishes disordered or dysunctional responses rom nor- mal ones is recognized and defined in terms o social context; deciding what is inappropriate is a social judgment. 14 As we have seen, there is some truth in the cultural view o depression. Local cultural values and practices do help define the meanings o situations and thus CONCLUSION 219 which circumstances will be perceived as alling within one o the categories that trigger sadness. Yet this cultural relativity is quite consistent with the act that universal biological processes underlie sadness responses and shape their sensitivity to certain kinds o meanings. The central flaw in this argument is that the concept o inappropriate circumstances, which is critical to distinctions between disordered and normal responses, is not a purely socially shaped judgment but is itsel partly an evolutionarily grounded concept. Loss responses are evolutionarily selected to respond to a specific range o stimuli and not to respond outside that range; they are as much designed to not respond to the wrong stimuli as they are to respond to the right stimuli. Cultural values do enter into definitions o what particular losses are defined as inside or outside the appropriate range o loss stimuli and can suggest standards or how intense an expression o a sadness response is socially acceptable. Yet the categories that trigger sadness responses—losses o intimate attachments, low or declining social status, or the ailure to achieve desired goals—are universal. Moreover, when concepts o disorder are equated with whatever conditions are called disorders in a particular group, the possibility o scientifically evaluating and critiquing these concepts is lost. Also lost is the commonsense understanding that a culture could be wrong in its judgments about disorder. For example, the Victorians were wrong in believing that masturbation and emale orgasm were disorders, and some ante-bellum Southerners were wrong in holding that runaway slaves were sufering rom a mental disorder. But i disorders are just culturally relative conditions, then we cannot explain why these judgments were wrong, because those diagnoses did indeed express the values o their times. The reason why they could be wrong is that there is an additional, actual claim being made when one asserts that a condition is a disorder, namely, a claim that the condition involves a ailure o human biological design (e.g., women are designed not to experience orgasmic pleasure or slaves are designed to be subservient), and this actual claim turns out to be just plain alse. That is, the diagnostic claims were based on incorrect theories about human nature. In placing issues o diagnostic judgment outside the scope o science, the cultural view leaves no grounds or claiming that any definition o depression is any better or worse than any other. It is thus not just wrong but counterproductive, because it undermines the ability to constructively critique and improve psychiatric diagnosis. Our approach, in contrast, aims to help the psychiatric proession develop more useul definitions that do not define every undesirable consequence o sadness as a disorder. Another set o objections rejects the particular evolutionary standard that we use to ascertain disorder status. One o these types o objections accepts a biological approach in using the fitness o a behavior to establish whether it is healthy but objects that current fitness, not what the mechanism was selected 220 THE LOSS OF SADNESS or in the past, determines disorder status. 15 According to this view, maladaptive conditions in the present environment, not standards taken rom evolutionary unctioning, should provide the criteria or disordered conditions. Yet the past is relevant because it explains how we came to be the way we are and thus determines which o our eatures were biologically selected and thus part o human nature. The question o whether a mechanism’s efect is adaptive at present is distinct rom the question o whether the efect is part o the mechanism’s design. Problematic mismatches between human nature and current social desirability such as adulterous longings, male aggressiveness, or becoming sad ater losses are not in themselves disordered. For example, it may be fitness enhancing in our culture not to have tastes or at and sugar, but that does not mean that people who have such tastes are disordered; that is how we were designed to be, due to conditions that existed when we were evolving. The explanatory role o the concept o disorder is such that dysunctions o psychological mechanisms are properly defined against evolutionary, rather than contemporary, standards. However, sometimes environmental conditions that are too diferent rom what is evolutionarily expected can produce real depressive disorders because people were not naturally selected to unction in such settings. Modern warare, or example, leads many soldiers to develop mental disorders that persist ar beyond the immediate combat situation because the human brain was not developed to unction under such conditions. More commonly, however, problematic loss responses in a new environment are not disorders at all; rather, the relevant mechanisms are acting in designed ways in response to novel types o losses.16 A diferent objection is that depression serves no evolutionary unction at all but instead is, in Steven Jay Gould’s terms, a spandrel or exaptation.17 The term spandrel stems rom the triangular spaces below the domes o Gothic cathedrals that were not planned but that necessarily result rom the way that the dome is mounted on surrounding arches. Spandrels are evolutionary accidents that are not themselves selected but are unintended consequences that have no evolutionary advantages. When spandrels are put to a later use, as when designers o cathedrals painted images o the apostles on them, they become exaptations that put the accidental structure to some purposive use. Depression, according to this thesis, is a spandrel that has never held any overt nor hidden benefits either in the past or at present.18 The objection that depression was never selected or its evolutionary benefits sufers rom several conusions. First, we do not believe that depressive disorders were ever adaptive. They are dysunctions o loss response mechanisms and so were never selected over the course o evolution as either adaptations or exaptations. The argument that symptoms must have been selected or their adaptive qualities at some point in evolutionary history applies only to normal sadness, not to depressive disorder. Second, any adaptive unctions that intense sadness ater losses might have had in evolutionary history need not be salient at CONCLUSION 221 present. Arguments that depression-like symptoms are not currently adaptive are irrelevant to whether they were selected to arise in appropriate circumstances at some point in the distant past. As we argued in chapter 2, at least some orms o sadness in response to certain triggers were naturally selected, as seems evident rom the cross-cultural universality and inant and nonhuman primate expression o such emotions. But, admittedly, universality by itsel does not argue or the specific biological design o a particular response, or the simple reason that spandrels can be universal i they are invariable by-products o universal designed eatures. To take a biological example, pain during childbirth may be a universal eature that is a side efect o selection or optimal skull size o inants and may have no unction. Philosopher Dominick Murphy and psychologist Robert Woololk, citing the presumed universal spandrel o the chin, argue that mental spandrels could exist and cause pathology without ailure o unction: The human chin is a amous spandrel. It has no unction itsel but is simply a by-product o the engineering requirements o speech, chewing, and respiration. I mental spandrels exist, then there are mental mechanisms that are the by-products o evolution but have themselves never possessed adaptive unctions (in Wakefield’s evolutionary sense) and, thereore, could not malunction. Such mechanisms, however, could produce pathological behavior.19 Perhaps the most common argument about depression in this regard is that intense sadness responses were selected specifically or the attachment relationship in inancy, and all other such responses are a spandrel-like side efect having no unction.20 In act, there is evidence that sadness responses are not all alike and that they are fitted to the specific kind o loss, thus suggesting natural selection rather than an accidental by-product.21 For example, pessimism, atigue, and anhedonia are associated with the ailure to achieve valued goals, whereas crying and emotional pain are related to attachment losses. Moreover, it seems inexplicable that the sorts o sadness responses commonly seen in humans and other primates to attachment and status losses, respectively, would come about as a spandrel, because the triggers are just too unalike. Until a morepersuasive orm o the spandrel account is provided, the ubiquity o sadness ater specific kinds o losses is prima acie evidence that it is perorming some naturally selected unction, even though we can only speculate about what that unction might have been. A final type o objection to our position is that it has negative implications or treatment. Many people ear that using evolutionarily derived criteria or psychological disorders would lead to unnecessarily strict standards or entitlement to treatment that would deny needed proessional help to many suferers. “Such a definitional criterion or disorder,” according to psychiatrist 222 THE LOSS OF SADNESS John Sadler, “would be used bureaucratically to exclude people rom care who otherwise might have a credible need.” 22 Such ears stem rom a belie that there is a one-to-one mapping between dysunctions and treatable conditions so that only dysunctions would be reimbursable conditions.23 Issues o who should be treated, however, are not reducible to which conditions are disorders. Physicians oten treat conditions and provide procedures that have nothing to do with disorders (e.g., childbirth, contraception). This is in part a political issue regarding mandated reimbursement or services and in part an empirical issue having to do with what can help people. It is true that our analysis does encourage reocusing policies away rom eforts that attempt to reach unrecognized and untreated cases o sadness toward treating recognized disorders. It also leads us to be skeptical about the benefits o widespread screening programs or direct-to-consumer advertising campaigns that encourage people with common symptoms to enter treatment, because their symptoms are more likely to indicate normal sadness than depressive disorder. Yet it is also true that nondisordered sadness can cause enormous sufering and that medication or counseling can relieve many cases o painul, but normal, sadness, although the general transience and sel-correcting nature o normal reactions complicates the judgment o whether or not to treat. When people desire proessional help or such acute emotional pain, they deserve clinical attention as a matter o justice and compassion. However, just as administering painkillers during childbirth does not make this process a disorder, medicating or counseling people with normal sadness should not be conused with treating a disorder. Some Directions for Solving the Problem This book has ocused on critiquing current overexpansive definitions o depression. We have tried to clariy the conceptually conused situation in which psychiatry and the social sciences find themselves in the study o depression. Once this situation is acknowledged, these fields can proceed to develop the methods necessary to make distinctions between normal and abnormal conditions. Although it is beyond the scope o this book to develop such detailed methods, it is worth outlining some promising ways to proceed. In this section we provide some preliminary suggestions regarding how criteria could be improved in ways that would distinguish depressive disorders rom normal sadness. Each suggestion depends on using contextual criteria, as well as the presence o symptoms, to make diagnostic decisions. The particular ways that these criteria are incorporated will depend on the settings in which diagnoses are made, such as in clinical practice, in screening programs, or in community studies. The DSM definition o Major Depressive Disorder is primarily designed or use in clinical practice. The bereavement exclusion ound in the current manual, CONCLUSION 223 which states, “the symptoms are not better accounted or by Bereavement,” provides one model or valid criteria in clinical settings. 24 There is no reason why a clause could not be added to this exclusion that would either expand it into a more general condition, such as “Bereavement or some other major lie stressor,” or provide urther specific examples, such as “Bereavement, marital dissolution, the loss o a valued job, etc.” An expanded exclusion clause o this nature would keep the clinician as the ultimate judge o whether a patient presents with normal sadness or depressive disorder. Because current clinical diagnoses are made or patients who have already judged themselves as needing mental health treatment, expansions in the exclusion clause will probably not have a major efect on diagnostic decisions. Nevertheless, such changes would enhance the validity and integrity o DSM diagnoses. In addition, the “V codes,” discussed in chapter 5, could be expanded to contain conditions excluded rom diagnoses o MDD that are “nondisordered but treatable” conditions. Screening instruments or depression in general medical practice are applied in settings with intense time pressures and must be very brie. Incorporating contextual criteria into these instruments thus involves a challenge. On the one hand, many patients in general medical settings are likely tohave normal sadness stemming rom stressul events such as physical illness. On the other hand, screening instruments that use contextual criteria will consume more time, and they might be less reliable than current instruments and so might not be practical. Contextual criteria could be incorporated into such instruments at two levels: in the questions used in the sel-administered instruments and in the instructions or physicians interpreting the results o these instruments. The addition o a simple instruction on a sel-administered depression screen—or instance, “Did these symptoms emerge ater particularly stressul events such as . . .”—could provide the appropriate cues to respondents that symptoms o normal sadness need not indicate a depressive disorder. Indeed, early community studies used questions such as whether heart palpitations arise “when you are not exercising or working hard” that contextualized responses or particular symptoms.25 In addition, instructions to physicians about how to interpret the results o checklists could explicitly mention the need to attend to the context o reported symptoms and judge whether symptoms reflect a physical condition or the impact o medication or o stressul lie events instead o a depressive disorder. Physicians should also be explicitly cautioned to use their diagnostic common sense rather than to unquestioningly ollow DSM-style symptom scales. The physician could also be encouraged in appropriate cases to respond to positive screens that involve contextual triggers with “watchul waiting” rather than immediate medication. Using contextual criteria in these ways could lower the number o alse-positive screens without adding much time to the clinical encounter. Given the particular dangers o overmedicating adolescents, screening instruments in schools must be especially sensitive to the contextual nature o 224 THE LOSS OF SADNESS many adolescent symptoms. Screening in these settings does not involve the intense time pressures o a physician’s ofce. Using media presentations o cases with normal problems o adjustment, as well as o depressive disorders, beore the administration o scales could help provide a context or adolescents to use in raming their answers. Such techniques could help minimize the number o alse positives in school settings, where they can potentially have the most harmul results. Incorporating contextual criteria into community studies involves a dierent set o issues than in clinical practice, primary care, or schools. Unlike clinicians, who can use their judgment to distinguish culturally expectable symptoms rom internal dysunctions, epidemiologists and sociologists must use standardized scales in their research. Using clinical judgments to distinguish expectable and proportionate responses rom disordered, disproportionate ones is not practical and would damage the reliability o judgments across interviewers that are necessary to obtain valid estimates o rates o disorders in community populations. It should, however, be possible to develop standardized, yet contextual, scales that relate the degree o stressulness in people’s lives to the consequent number o symptoms they report. The key to adequately distinguishing whether symptoms indicate distress or disorder in survey research is to examine their proportionality to the severity and duration o stressulness in people’s actual lives. As noted, George Brown has developed objective measures o stressulness that use the context and meaning o events to determine how much distress a typical person is likely to experience in given circumstances.26 Recently, researchers have drawn on Brown’s approach to develop standardized scales or use in survey research that assign quantitative scores to the content, severity, and threat level o stressul events that people experience.27 These scores can be used to predict the likely amount o distress that an average respondent should display in a given situation. Those with disproportionately higher symptom levels than expected, given the degree o stressulness o their situations, can be assumed to be the most likely group to have mental disorders. Although contextual criteria would be used in a dierent way in survey research than or diagnostic purposes, in each case they should result in ewer alse-positive diagnoses and more valid estimates o the amount o depressive disorder. Despite the challenges, a serious trial-and-error process o developing contextual criteria or clinical and research diagnoses o MDD should, in all likelihood, eventually yield criteria o satisactory reliability and validity. However it is accomplished, resolving this challenge is critical or the uture o depression research. Based on the data presented in chapter 2 and other circumstantial arguments, it is clear that the “alse positives” problem or MDD diagnosis is sizable. But no one can say exactly how sizable it is, simply because none o the diagnostic instruments clinicians and researchers now use adequately discriminates disordered rom nondisordered sadness, and thereore no research CONCLUSION 225 studies address the issue.28 Only when valid diagnostic criteria are devised and corresponding research instruments are developed will the magnitude and implications o the current alse positives problem become known. Depression research, including treatment research, will then enter a new era in which questions and answers about both depressive disorder and normal sadness can be asked and answered in a more refined way than they are today. Conclusion Psychiatry has made immense strides in recent decades and now has many powerul techniques at its disposal to uncover the causes o depressive disorders. In addition, available treatments or depression are ar better than at any time in human history. Yet eforts at identiying disorders, speciying their causes, and providing efective treatments or them are all handicapped by the absence o a valid definition o depressive disorder. When the DSM-III was written, the challenge was to justiy that psychiatry could be a legitimate part o medicine at all and not merely an instrument o social control. But times have changed. It is now generally accepted that there are genuine medical disorders o the mind; the problem is to understand the limits o the concept o disorder so that it does not engul all the problems that lie poses. Developing adequate criteria that distinguish disorders rom normal sadness should be one o the major priorities or students o depression. Sadness is an inherent part o the human condition, not a mental disorder. Thus to conront psychiatry’s invalid definition o depressive disorder is also to consider a painul but important part o our humanity that we have tended to shunt aside in the modern medicalization o human problems. As science allows us to gain more control over our emotional states, we will inevitably conront the question o whether normal intense sadness has any redeeming eatures or should be banished rom our lives. Such a momentous scientific and moral issue should not be spuriously resolved by using a semantic conusion in the DSM that mistakenly places states o intense sadness under the medical category o disorder. We can only adequately conront the complex and important concerns involved i we clearly diferentiate normal sadness rom mental disorder. We hope that by examining the consequences o the current ailure to adequately draw such a distinction, this book may encourage mental health proessionals to embrace the needed distinction and to start talking to each other and to their patients in a more nuanced way that yields improved understanding and treatment. This page intentionally left blank Notes Chapter 1 1. Auden, 1947/1994. 2. Klerman, 1988; Blazer, 2005. 3. Miller, 1949/1996. 4. Dohrenwend, 2000. 5. McKinley, 1999. 6. Blazer, Kessler, McGonagle, & Swartz, 1994; Kessler,Berglund, Demler, Jin, Koretz, Merikangas, et al., 2003. 7. Kessler, Berglund, et al., 2003. 8. Roberts, Andrews, Lewinsohn, & Hops, 1990; Lavretsky & Kumar, 2002; Lewinsohn, Shankman, Gau, & Klein, 2004. 9. Klerman, 1988; Klerman & Weissman, 1989; Hagnell, Lanke, Rorsman, & Ojesjo, 1982. 10. Murphy, Laird, Monson, Sobel, & Leighton, 2000; Kessler et al., 2005; Blazer, 2005, pp, 114 115. 11. Olfson, Marcus, Druss, Elinson, Tanielian, & Pincus, 2002. 12. Olfson, Marcus, Druss, & Pincus, 2002. 13. Kessler, Berglund, et al., 2003. 14. Crystal, Sambamoorthi, Walkup, & Akincigil, 2003. 15. Horwitz, 2002, p. 4. 16. Pear, 2004. 17. Pear, 2004. 18. Croghan, 2001. 19. Murray & Lopez, 1996. 20. Greenberg, Stiglin, Finkelstein, & Berndt, 1993. 21. See also Blazer, 2005, pp, 28 29; McPherson & Armstrong, 2006. Citation counts stem from Medline searches. 22. Jackson, 1986. 23. 24. 25. 26. Kirk & Kutchins, 1992; Horwitz, 2002. Regier et al., 1998; Narrow, Rae, Robins, & Regier, 2002. American Psychiatric Association (APA), 2000. APA, 2000, p. 356. 227 228 NOTES TO PAGES 9–29 27. 28. 29. 30. APA, 2000, p. 356. Watson, 2006. Dobbs, 2006, pp. 51 52. Solomon, 2001, p. 18. 31. 32. 33. 34. 35. 36. 37. 38. 39. Styron, 1990, pp. 17 18; p. 62. Karp, 1996, pp. 3 6. APA, 2000, p. xxxi. APA, 2000, p. xxxi. Wakefield, 1992. E.g., Klein, 1978; Spitzer, 1999. E.g. Fodor, 1983; Buss, 1999; Pinker, 1997. Keller & Nesse, 2005. Young, 2003. 40. Wakefield, 1992. 41. Buss, 1999. 42. Beck, 1967. 43. Post, 1992. 44. E.g. Jackson, 1986, Ch. 9; Mendels & Cochrane, 1968; Kendell, 1968. 45. Dohrenwend, 2000; Kirkpatrick et al., 2003; Marshall, Schell, Elliott, Berthold, & Chun, 2005. 46. Szasz, 1961; Schef, 1966; Kirmayer & Young, 1999. 47. Archer, 1999. 48. Klerman, 1974; Coyne, 1976; Gilbert, 1992 49. Goodwin & Guze, 1996. 50. Post, 1992. 51. Coyne et al., 2000; Nesse, 2005. 52. Kramer, 2005. 53. Horwitz & Wakefield, 2006. 54. Murray & Lopez, 1996. 55. U.S. Department o Health & Human Services (USDHHS), 2001; World Health Organization (WHO), 2004. 56. Nesse, 2000. Chapter 2 1. 2. 3. 4. 5. 6. Shelley, 1824/1986. Coleridge, 1805/1986. Keller & Nesse, 2006. Nesse, 2006. Brown, 2002; Dohrenwend, 2000. E.g., Turner, Wheaton, & Lloyd, 1995; Wheaton, 1999. 7. Grinker & Spiegel, 1945. 8. Kendler, Karkowski, & Prescott, 1999. 9. E.g., Coyne, 1992; Oatley & Bolton, 1985; Gilbert, 1992. 10. Turner, 2000. NOTES TO PAGES 29–35 11. 12. 13. 14. 229 Brown, 1993. 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Aneshensel, 1992; McLeod & Nonnemaker, 1999; Mirowsky & Ross, 2003; Turner & Lloyd, 1999; Turner, Wheaton & Lloyd, 1995. 22. E.g., Dohrenwend et al., 1992; Ritsher,Warner, Johnson, & Dohrenwend, 2001; Johnson, Cohen, Dohrenwend, Link, & Brook, 1999; Lorant et al., 2003. 23. Holmes & Rahe, 1967. 24. Radlof, 1977. 25. Nesse, 2000. 26. 27. 28. 29. Carr, 1997. McEwan, Costello, &Taylor, 1987. Turner & Lloyd, 1999; Turner, 2003; Turner & Avison, 2003. Pearlin, 1999. 246 NOTES TO PAGES 203–215 30. Radlof, 1977; Radlof & Locke, 1986. 31. Radlof, 1977. 32. Roberts, Andrews, Lewinsohn, & Hops, 1990; Roberts, Lewinsohn, & Seeley, 1991; Roberts, Roberts, & Chen, 1997. 33. Roberts et al., 1990. 34. Roberts et al., 1990. 35. Rushton et al., 2002. 36. Coyne, 1994. 37. E.g., Mollica, Poole, & Tor, 1998; Mollica et al., 1999; Marshall et al., 2005; Dohrenwend, 2000; Schwartz, Dohrenwend, & Levav, 1994. 38. Seligman, 1975; Sapolsky, 1998. 39. APA, 1994, p. xxi. 40. Price, Sloman, Gardner, Gilbert, & Rohde, 1994; Bowlby, 1980; Nesse, 2000. 41. 42. 43. 44. 45. 46. 47. 48. 49. Brown, 1993. Brown, 2002. Brown, Craig & Harris, 1985, p. 616. Brown, 2002. Brown & Harris, 1978. Brown, Biulco & Harris, 1987; Brown, 1998. Brown, Harris & Hepworth, 1995. Brown, 2002. Brown et al., 1987, p. 34. 50. 51. 52. 53. 54. 55. 56. 57. 58. Brown et al., 1995. Brown, Adler, & Biulco, 1988. Brown, 1998, p. 368. Brown, 2002. Brown, 1998, p. 367. Brown, 1998, p. 366. Brown, 1998, p. 361. Brown, Harris, Hepworth, & Robinson, 1994. Brown et al., 1995. 59. Brown et al., 1985. 60. Brown et al., 1985, p. 620. 61. Brown et al., 1988, p. 492. Chapter 11 1. Foucault, 1965, 1979. 2. Friedson, 1970; Abbott, 1988; Conrad, 2004. 3. 4. 5. 6. Horwitz, 2002. Kirk, 1999. Murray & Lopez, 1996. Kramer, 2005, p. 155, p. 153. NOTES TO PAGES 215–225 247 7. Blazer, 2005, p. 31; Spijker, deGraaf, Bijl, Beekman, Ormel, & Nolen, 2003. 8. Valenstein, 1998. 9. Donohue et al., 2004. 10. 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This page intentionally left blank Index Abraham, Karl, 73 74 sadness treatment debate, 188 192 Achilles, 30 adaptive unctions, normal sadness, 47 51, 190, 220 221 Adjustment Disorder, 115 119 adolescents antidepressant prescriptions, 187 depressive disorder statistics, 4 screening processes, 157 163, 223 224 sociology study, 204 205 adoption and twin studies, 166 167 advertising, drug, 181, 185 186, 216 tranquilizer precedent, 179 182 anxiolytics, 180 181, 182, 183 Aretaeus o Cappadocia, 59 60 Aristotle, 57 59 attachment losses in evolutionary unction argument, 221 inants, 40 41, 49 monkeys, 39 as stress source, 203 See also relationship losses attraction-o-support hypothesis, normal advocacy groups, as special interest constituency, 215 216 afective disorders, generally DSM-IV, 104 105 Feighner criteria, 91 95 Against Depression (Kramer), 175 age o anxiety, 3 age-related statistics, 4, 185, 187 Akiskal, Hagop, 90 Alexander o Tralles, 61 amine level hypothesis, 168 170 amygdala, 174, 176 The Anatomy of Melancholy (Burton), 63 65, 85 anthropological perspectives, 41 46, 194 202, 218 219 “Anthropology and the Abnormal” (Benedict), 195 antianxiety drugs, 180 181, 182, 183 antidepressants overview, 179, 192 193 and adolescent screening, 162 163 advertising impact, 185 186 sadness, 48 Auden, W. H., 3 Australian absrcinal culture, loss responses, 41 Avicenna, 61 Axis system, in DSM-IV, 114 baboon studies, 40, 170 Balinese culture, loss responses, 44 Basque culture, loss responses, 45 Benedict, Ruth, 195 196 benzodiazepines, 180 181 bereavement exclusion, 8 9, 31, 101, 106, 108 109, 114 115, 222 223 Berrios, German, 90 biological evidence, normal sadness, 38 42, 219 220 biological research, depressive disorders overview, 165 166, 177 178 brain abnormalities, 174 177 chemical balances, 167 170, 188 genetics, 170 174 twin and adoption studies, 166 167 and chemical deficiency hypothesis, 168 170 development o, 182 184 growth o, 4 5, 184, 185 186 and managed care, 184 185 biopsychosocial approach, Meyer’s, 82 84 bipolar mood disorders, in DSM-IV, 104 black bile disorder, 55, 57, 60 61 See also melancholia blame argument, about redefined criteria, 23 281 282 INDEX Bowlby, John, 40 41, 49 brain abnormalities, 174 177 Bright, Timothie, 62 63 Britain, depression studies, 98, 206 209 Brown, George, 45, 206 210, 224 Bruce, Martha, 34 Bucknill, John Charles, 69 Buddhists, Sri Lanka, 197 198 Burney, L. E., 190 Burton, Robert, 63 65, 85 Bush, George W., 158 Callahan, Christopher, 90 Caspi, Avshalom, 171 174 catecholamine hypothesis, 168 169 Celus, 59 See also community studies; historical perspectives continuum concept and community studies, 126 127, 135 141 and screening movement, 145 Cosmides, Leda, 48 costs antidepressants, 184, 185, 187 depressive disorder trend, 5, 21, 102 103 screening programs, 158 untreated depression, 146 See also public policy implications cross-cultural psychiatry, 196 cross-cultural studies, 41 46, 207 CSS (Columbia Suicide Screen), 160 161, CES-D scale, 203 205 chemical deficiency hypothesis, 167 170 Chinese culture, loss responses, 44 45, 199 200 chronic social stressors, 28, 37 38 CIDI (Composite International Diagnostic Interview), 131 Clayton, Paula, 94, 101 clinical-significance criteria, in DSM-IV, 109 110, 112 113, 117 118 Cole-Benjamin, Deanna, 12 163 Cullen, William, 66 cultural comparisons, 41 46, 194 202, 218 219 Coleridge, Samuel, 27 Columbia Suicide Screen (CSS), 160 161, 163 Columbia University, 158 163 combat neuroses, 28, 125 126 community studies, psychiatric continuum concept efects, 126 127, 135 141 definition problem, 127 128 DSM criteria adoption, 123 124, 130 132 equivalence myth, 132 134 impetus or, 124 126 measures in, 128 129 proposed changes, 224 public policy implications, 141 142, 145 146 symptom threshold elimination, 134 138 Complicated Grie, 33 Composite International Diagnostic Interview (CIDI), 131 Conduct Disorder, 111 114 Constaninus Aricanus, 61 151 152 depression category, in Feighner criteria, 91 92 depression criteria, DSM-III, 100 103 depressive disorder trend, 4 8 depressive neurosis, in DSM-II, 87 depressive reaction, in DSM-I, 86 87, 127 128 Diagnostic and Statistical Manual of Mental Disorders. See DSM entries Diagnostic Interview Schedule (DIS), 130 131 diagnostic manuals, early development, 84 87, 91 97 See also DSM entries Diagnostic Project, U.S.-U.K., 98 diagnostic screening vs. prescreening, 147 150 diathesis-stress theory, 172 direct-to-consumer advertisements, 185 186 DISC (Diagnostic Interview Schedule or Children), 160, 161 162 Darkness Visible (Styron), 13 DART campaign, 151 152 Darwin, Charles, 41, 49 Death of a Salesman (Miller), 3 4 Depression Awareness, Recognition, and Treatment (DART campaign), context/contexuality in DSM-IV criteria, 14, 113 119 in normality vs. disorder, 15 19 as normal sadness component, 27 28 proposed inclusion o, 223 225 DISC Predictive Scale (DPS), 160 DIS (Diagnostic Interview Schedule), 130 131 disease vs. distress, Brown’s studies, 209 210 INDEX 283 disease vs. illness, in anthropological studies, 197 198, 199 200 disengagement unction, normal sadness, 50 51 disorder, defined, 25 See also normality vs. disorder, generally divorce, 34 35 drug treatments. See antidepressants DSM criteria, generally in adolescent screening tools, 158 159, 160 161 in antidepressant advertising, 185 186, 188 in brain abnormality studies, 175 context problem, 14 influence generally, 7 8 endogenous depression, 18, 88, 121 Enkidu, 30 31 epidemiological advantage, with redefined criteria, 20 21 See also community studies, psychiatric Epidemiologic Catchment Area (ECA), 131, 132, 135 136, 137 138, 139, 141 equivalence myth, community studies, 132 134 Esquirol, Jean-Etienne-Dominique, 67 evolutionary unction argument, about redefined criteria, 219 221 excess distress criterion, in Adjustment Disorder, 117 118 and loss examples, 10 14 in New Zealand study, 173 in primary care screening tools, 151, 152, 153 154 recommendations or change process, 222 225 redefinition advantages, 19 24 in social science studies, 197 198, 201, 203 205 special interest constituencies, 213 216 DSM-I, 85 87, 127 128 actor analysis, 89 FDA regulations, 181, 182, 185, 188, 193 Feighner, John, 90 Feighner criteria, 91 95, 97 Feinstein, Alvin, 96 financial losses, responses, 35 38 5-HTT gene, New Zealand study, 171 174 Fleury, Maurice de, 70 Flynn, Laurie, 160 Fore culture, loss responses, 42 Freud, Sigmund, 72 73, 74 75 DSM-II, 87, 97 DSM-III Friesen, Walter, 42 unction distinction, normality vs. disorder, 15 19 in community studies, 130 132 depression criteria, 100 103 Feighner criteria oundation, 91 95 incentives or symptom-based approach, 97 100 and Research Diagnostic Criteria, 95 97 DSM-IV-TR depression-related categories, 119 121 limitations summarized, 121 122 DSM-IV-TR, Major Depressive Disorder (MDD) within afective disorder category, 104 105 Conduct Disorder compared, 111 113 contextual trigger discussions, 113 119 criteria or, 8 10, 14, 105 111 Du Laurens, Andre, 62 dysunction distinction, generally, 15 19 Dysthymia Disorder, inDSM-IV,105, 120 acial expressions, grie, 39, 41 42 Galen, 60 61 gender-related statistics, 4, 180 genetic studies, 170 174 Gilgamesh, 30 31 glial cells, 175 goal losses, responses, 28, 36, 203, 221 Goodwin, Donald, 94 95 Gould, Stephen Jay, 220 Great Britain, depression studies, 98, 206 209 Greek perspectives, 57 59, 179 grie acial expressions, 41 42 and Feighner criteria, 92 94 as normal sadness, 30 38 in Research Diagnostic Criteria, 96 See also bereavement exclusion; historical perspectives Griesinger, Wilhelm, 68 ECA (Epidemiologic Catchment Area), 131, 132, 135 136, 137 138, 139, 141 Edwards, Charles, 181 Ekman, Paul, 41 42 Elliott, Carl, 190 Grinker, R. R., 125 Guze, Samuel, 90, 91, 94 95 HD (harmul dysunction) distinction, 17 19 Hildegard o Bingen, 61 284 INDEX hippocampus, 174, 175, 176 Hippocrates, 57 historical perspectives overview, 53 56, 71 72, 87, 103 diagnostic manual beginnings, 84 87 DSM-III publication, 97 103 Feighner criteria development, 91 95 Freud’s psychological model, 73 75 Greek approaches, 57 59, 179 Kraepelin’s medical model, 75 82 Meyer’s biopsychosocial approach, 82 84 post-Krapelian research, 87 91 Research Diagnostic Criteria development, 95 97 Roman approaches, 59 61, 179 Kraft-Ebbing, Richard von, 70 71 Kramer, Peter, 136, 175, 176, 177, 183 184, 188, 215 sedatives and tranquilizers, 61 66, 179 180 sixteenth through nineteenth centuries, 61 71, 179 Hofmann, Friedrich, 66 5-HTT gene, New Zealand study, 171 174 loss responses, defined, 24 Lutz, Catherine, 198 ibn Imran, Ishaq, 61 Ialuk culture, loss responses, 198 impairment criterion, in Adjustment Disorder, 117, 118 India, loss responses, 43 inant responses, 40 41, 49 “Influences o Lie Stress on Depression” (Caspi), 171 174 Insel, Thomas, 171 insurance argument, about redefined criteria, 22 23 insurance industry, 98, 184 185, 214 involuntary subordinate strategy (ISS), 49 50 Iranian culture, loss responses, 44 ISS (involuntary subordinate strategy), 49 50 Jackson, Stanley, 54, 66 job loss, responses, 10 11, 35 36 Johnson, Samuel, 66 journal articles, statistics, 5 Kaluli culture, loss responses, 44, 45 Kant, Immanuel, 66 Karp, David, 13 14, 132 133 Katon, Wayne, 155 156 Langner, Thomas, 127 language, biology-culture interactions, 43 Lapuse, Rema, 129 lesion-based studies, 174 177 Lewis, Aubrey, 48, 88 90 Librium, 180 Listening to Prozac (Kramer), 183 184 Loman, Willie, 3 4 loss response mechanisms defined, 24 25 in normality vs. disorder distinction, 15 17 MacDonald, Michael, 65 Major Depressive Disorder (MDD), statistics, 4 See also DSM-IV-TR, Major Depressive Disorder (MDD) Major Depressive Episode, in DSM-IV, 105 107 Malay culture, sadness metaphor, 43 managed care plans, 184 185 See also primary care settings Manhattan study. See Midtown Manhattan study MAOIs, 181 182 marital dissolution, 34 35 Mather, Cotton, 66 Maudsley, Henry, 67 68 McGuire, Michael, 39 40 MDD (Major Depressiv e Disorder), statistics, 4 See also DSM-IV-TR, Major Depressive Disorder (MDD) MDE (Major Depressive Episode), in DSM-IV, 105 107 mechanism, defined, 25 medical exclusion, Major Depressive Disorder, 106, 109 medical model, Kraepelin’s, 72, 75 82 medical proession, as special interest constituency, 213 See also primary care settings Medicine and the Mind (Fleury), 70 Keauver hearings, 180 181 Kessler, Ronald, 186 Kirmayer, Laurence, 196 Kleinman, Arthur, 196, 198 200 Klerman, Gerald, 189 Kraepelin, Emil, 72, 75 82 Mediterranean societies, loss responses, 44 melancholia Freud’s explanation, 73 75 Greek writings, 57 59 as historical term, 54 56 Roman writings, 59 61 INDEX sixteenth through nineteenth century explanations, 61 71 Melancholic Major Depressive Disorder, in DSM-IV,120 121 mental disorder generally, inDSM-IV, 110 111 mental health proession, as special interest constituency, 213 mental institutions, Kraepelin’s research, 72, 75 82 meprobamate, 180, 181 Mercier, Charles, 69 70 Meyer, Adol, 82 84 Michael, Stanley, 129 Michigan Depression Study, 152 Midtown Manhattan study, 127, 128 129 Miller, Arthur, 3 4 Miltown, 180 Minor Depressive Disorder, inDSM-IV,119 monkey studies, 38 40 monoamine oxidase inhibitors (MAOIs), 181 182 Mood Disorder Not Otherwise Specified, in DSM-IV,119 120 “Morphometric Evidence or ... Major Depression” (Rajkowska), 175 177 “Mother’s Little Helper” (song), 180 MRI studies, 165, 166 multiaxial diagnostic system, in DSM-IV, 114 Muncie, Wendell, 83 84 Murphy, Dominick, 221 Napier, Richard, 65, 179 National Alliance on Mental Illness (NAMI), 215 216 National Comorbidity Study (NCS), 131 132, 137 138 National Institute or Health and Clinical Excellence (NICE), 191 National Institute o Mental Health (NIMH), 95, 130 131, 171, 214 Navaho culture, loss responses, 44 NCS (National Comorbidity Study), 131 132, 137 138 Nelson, Gaylord, 181 neo-Kraepelinian approach. See DSM entries Nesse, Randolph, 50 neurochemical deficiency hypothesis, 167 170 285 New Zealand study, 171 174 NICE (National Institute or Health and Clinical Excellence), 191 NIMH (National Institute o Mental Health), 95, 130 131, 171, 214 norepinephrine hypothesis, 168 169 normality vs. disorder, generally advantages o distinguishing, 19 24 unction distinction, 15 19 normal sadness overview, 51 52 adaptive unctions, 47 51, 190, 220 221 biological evidence or, 38 42 components, 16, 27 29 cultural influences, 42 46 defined, 24 examples, 30 38 traditional understanding, 5 6 See also specific topics, e.g., antidepressants; historical perspectives; screening movement Obeyesekere, Gananeth, 197 198 opium, 179 Oregon Adolescent Depression Project, 204 Papua, New Guinea, 42 Patient Health Questionnaire, 153 154 Patroclus, 30 Paxil, 184 185, 187 Perdiccas II, King, 57 pharmaceutical industry, 179, 187, 216 See also antidepressants Pinel, Philippe, 66 67 Platter, Felix, 63 policy implications, public, 20 21, 141 142, 145 146, 190 191, 214 216 poverty, loss responses, 28, 37 Praxeos Medicae (Platter), 63 prerontal cortex, 174, 175 prescreening processes, 147 150 prescription statistics, 4 5, 187 Present State Exam (PSE), 207 Preventive Services Task Force, U.S., 152 Price, John, 49 Primary Care Evaluation o Mental Disorders, 153 154 primary care settings antidepressant prescriptions, 184 185 neurotic depression, in post-Krapelian research, 88 89 New Freedom Commission Report, 158 New Guinea culture, loss responses, 44 New York City, depression screening, 144 145 prescreening efects, 148 149 screening processes, 150 157 primate studies, nonhuman, 38 40, 170 PRIME-MD, 153 154 prognosis advantage, with redefined criteria, 20 286 INDEX proportionate responses in Adjustment Disorder, 117 118 in Brown’s studies, 206 207 and cultural argument, 219 cultural influences, 44, 46 in loss examples, 10 14, 38 in normality vs. disorder distinction, 18 19 in normal sadness, 28 29 in proposed changes, 224 See also historical perspectives Prozac, 183 184, 187 PSE (Present State Exam), 207 Psychiatric Diagnosis (Woodruf, et al.), 94 95 psychiatric epidemiology.See community Sadler, John, 222 sadness, defined, 24 See also normal sadness SADS (Schedule or Afective Disorders and Schizophrenia), 95 Sandoz, 193 Sapolsky, Robert, 40 Savage, George H., 70 Schedule or Afective Disorders and Schizophrenia (SADS), 95 Schef, Thomas, 19, 98 Schildkraut, Joseph, 168 169 school settings, screening processes, 157 163 screening, definitions, 147 148 screening movement studies, psychiatric Psychobiology and Psychiatry (Muncie), 83 psychogenic depression, in Kraepelin’s work, 80 psychological model, Freud’s, 72 75 psychotic depression, 55 56, 88 public policy implications, 20 21, 141 142, 145 146, 190 191, 214 216 Rajkowska, Grazyna, 175 177 reactive depression, defined, 18, 84 85 overview, 163 164 adolescent-oriented, 157 163 assumptions/incentives, 145 146 New York City example, 144 145 pharmaceutical industry support, 187 prescreening efects, 147 150 primary care settings, 150 157 proposed changes, 223 224 scripted sadness studies, 177 sedative/tranquilizer precedent, 179 182, 183 redefined criteria, obstacles arguments summarized, 217 222 recommendations or overcoming, 222 225 special interest constituencies, 212 217 relationship losses examples, 10, 33 35 and normal sadness, 28, 29 as stress source, 203 See also grie reliability actor, inDSM-III development, 98 100 See also validity problem Rennie, Thomas A. C., 127 research advantage, with redefined criteria, 21 Research Diagnostic Criteria (RDC), 95 97 researchers, depression as growth industry, 5 pharmaceutical sponsorship, 187 as special interest constituency, 214 215 Robins, Eli, 90, 91, 95 selective serotonin reuptake inhibitors (SSRIs). See antidepressants sel-selection actor, 132 133, 156 September 11 attacks, 37 Serentil, 193 serotonin levels, 39 40, 168 170, 171 See also antidepressants sexual jealousy, biology-culture interactions, 43 Shorter, Edward, 75, 180, 183 184, 185 sleep unctions, 17 social costs statistics, 5 social intervention advantage, with redefined criteria, 20 social practices argument, about redefined criteria, 190, 218 219 See also cultural comparisons social sciences contributions overview, 194, 210 211 anthropological perspectives, 194 202 sociological perspectives, 202 210 social stressors, chronic, 28, 37 38 social support unction, normal sadness, Rogers, Timothy, 65 66 Rolling Stones, 180 Roman perspectives, 59 61, 179 Rosenhan, David, 99 Rush, Benjamin, 67 47 48 sociological perspectives, 194, 202 210 Solomon, Andrew, 13 Soranus o Ephesus, 59 Spain, 45 INDEX 287 spandrels, 220 221 Speaking of Sadness (Karp), 13 14 special interest constituencies, 212 217 spending statistics. See costs Spiegel, J. P., 125 Spitzer, Robert, 77, 95, 97 100, 153 Sri Lanka Buddhists, 197 198 Srole, Leo, 127 SSRIs (selective serotonin reuptake inhibitors). See antidepressants Statistical Manual for the Use of Hospitals for Mental Diseases, 84 85 status losses, responses, 28, 35, 36, 39 40, 202 Stirling County study, 127, 128 129 stress See also community studies, psychiatric; screening movement Tooby, John, 48 Traite Medico-Philosophiuqe . . . Mentale (Pinel), 66 67 tranquilizer/sedative precedent, 179 182, 183 Treatise of Melancholy (Bright), 62 treatment advantage/exclusion argument, with redefined criteria, 19 20, 22 23, 221 222 tricyclic antidepressants, 181 182 Tuke, D. Hack, 68 69 Turner, Jonathan, 43 twin and adoption studies, 166 167 in Brown’s studies, 206 210 New Zealand study, 171 174 sociology o, 202 206 Styron, William, 13 subordination unction, normal sadness, 49 50 substance use exclusion, Major Depressive Disorder, 106, 109 subthreshold condition, 119, 136 137, 138 141 sufering argument, about redefined criteria, undercount problem, community studies, 139 140 United Kingdom, depression studies, 98, 206 209 universal concepts, anthropological perspectives, 194 202 See also cultural comparisons 22 23 suicide, 36, 43, 57, 157, 162 Surgeon General’s Report on Mental Health, 189, 191 192 Sydenham, Thomas, 76 symptom criteria, generally, 8 14, 17 See also specific topics, e.g., community studies; historical perspectives; screening movement symptoms, defined, 24 Szasz, Thomas, 19, 98 proposed changes, 224 225 Valium, 180, 181 value judgment argument, about redefined criteria, 217 219 See also anthropological perspectives V codes, 114 115, 223 Virchow, Rudolph, 76 TeenScreen, Columbia University, 158 163 Text-Book of Insanity (Kraft-Ebing), 70 71 time actor CES-D scale, 204 205 in DSM-IV criteria, 8 10, 106 109, 116 117, 120 in loss examples, 10 12, 32, 35, 37 in normal sadness, 28, 29 Valenstein, Eliot, 170 validity problem in DSM-III development, 8, 99 100 with/without cause. See proportionate responses Woodruf, Robert, 94 95 Woololk, Robert, 221 World Health Organization (WHO) , 5, 152, 214 215 World War II, 125 126 Yolles, Stanley, 180 Zimbabwe, 43, 44, 45, 207 208 Zolot, 184, 186 Zuni culture, 195 196