The Bipolar Spectrum

THE BIPOLAR SPECTRUM

Diagnosis or Fad?

Joel Paris

http://www.routledgementalhealth.com/9780415891813 First published 2012 by Routledge 711 Third Avenue, New York, NY 10017 Simultaneously published in the UK by Routledge 27 Church Road, Hove, East Sussex BN3 2FA Routledge is an imprint of the Taylor & Francis Group, an informa business © 2012 by Taylor & Francis Group, LLC The right of Joel Paris to be identified as author of this work has been asserted by him in accordance with sections 77 and 78 of the Copyright, Designs and Patents Act 1988. All rights reserved. No part of this book may be reprinted or reproduced or utilised in any form or by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying and recording, or in any information storage or retrieval system, without permission in writing from the publishers. Trademark notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Library of Congress Cataloging in Publication Data Paris, Joel, 1940– The bipolar spectrum : diagnosis or fad? / by Joel Paris. p. ; cm.Includes bibliographical references and index. (hardback : alk. paper) I. Title. [DNLM: 1. Bipolar Disorder—diagnosis. 2. Diagnostic Errors—trends. WM 207] 616.89'5—dc232011043560

ISBN: 978–0–415–89181–3 (hbk) Typeset in Bembo by Swales & Willis Ltd, Exeter, Devon Printed and bound in the United States of America on acid-free paper. Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the Routledge Web site at http://www.routledgementalhealth.com

http://www.routledgementalhealth.com/9780415891813 CONTENTS

Introduction 1

PART I Concepts 9

1 The Bipolar Diagnosis 11

2 “Diagnostic Creep” in the Bipolar Spectrum 23

3 Affective Instability 37

PART II Disorders 45

4 Differential Diagnosis of Unstable Mood 47

5 Bipolarity and Personality Disorders 57

6 Bipolarity and Childhood Behavioral Disorders 65

http://www.routledgementalhealth.com/9780415891813 viii Contents

PART III Implications 73

7 How Psychiatric Fads Develop 75

8 The Impact of Overdiagnosis 85

References 91 Index 105

http://www.routledgementalhealth.com/9780415891813 1 THE BIPOLAR DIAGNOSIS

Emil Kraepelin: The Pioneer It has been recognized since antiquity that some mental illnesses are characterized by dramatic shifts in mood. This clinical picture was known to Hippocrates (Angst & Sellaro, 2000), but descriptions of a specific illness marked by alternating mania and depression only appeared in the nineteenth century (Healy, 2009). For modern psychiatrists, the pioneer and crucial figure in defining this illness was Emil Kraepelin (1856–1926). Serving as a professor at several leading German universities, Kraepelin was the most seminal figure in twentieth-century psychiatry (Shorter, 1997), and his influence continues to be felt today. Before Kraepe- lin’s time, the only meaningful distinction in diagnosis was between psychosis and non-psychosis. Within psychoses, classification was a confusing hodge-podge of overlapping syndromes. Kraepelin, although not a researcher in a contemporary sense, was a hero of systematic observation, and the first person to make sense out of mania. Kraepelin was the first psychiatrist to diagnose mental illness by delineating a specific course rather than diagnosing by symptoms alone. He reorganized the psychoses into two overarching categories. Schizophrenia (then called dementia praecox) had a continuous course that became steadily worse with time. In contrast, manic-depression had a cyclical course in which patients could be normal, or at least near-normal, between episodes (Kraepelin, 1921). While these distinc- tions are not absolute, they remain crucial for classification. Kraepelin died in 1926, but his ideas never lost influence in Europe. In North America, during the period after World War II when psychoanalysis was dominant, Kraepelinian psychiatry went into a temporary eclipse (Shorter, 1997). In the United States, the classification of mental disorders was often seen as a dry

http://www.routledgementalhealth.com/9780415891813 12 The Bipolar Diagnosis and unrewarding subject. This was reflected in a general lack of interest in earlier editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM-I and DSM-II). Psychoanalysts, as well as many other psychiatrists, viewed psychopathology as a reaction to circumstance, not as a biologically determined pattern. Recent decades have been marked by a sea change in the orientation of Amer- ican psychiatry. DSM-III was associated with the triumph of what has been called a “neo-Kraepelinian” school of thought (Klerman, 1986). Psychiatry took a U- turn away from psychoanalysis and rejoined the mainstream of medicine, becom- ing oriented towards neuroscience and psychopharmacology. As drug treatment advanced, it became possible to offer specific treatments for specific diagnoses. That is why classification gained importance. That is also why Kraepelin came back in a big way in the 1970s. Shorter (1997) has described him as the most important psychiatrist of the twentieth century. Under the influence of neo- Kraepelinian ideas, diagnosis became tied to family history, outcome, and the possibility of discovering biological markers of disease. Kraepelin was the first person to suggest the existence of a bipolar spectrum, which he envisaged as a dimension of mood disturbances ranging from psychotic illness to near-normal variants. As we will see later in this book, contemporary psychiatrists have resurrected and greatly expanded this idea. But since Kraepelin’s experience was confined to severely ill patients who were hospitalized, he might have been surprised by claims that 10% or more of the general population suffer from some form of bipolar disorder.

Changing the Name For decades after Kraepelin, the concept of manic-depressive illness underwent little change. But under the influence of another German psychiatrist, Karl Leon- hard (1902–1988), the name was changed. The term “bipolar disorder,” intro- duced in 1957 (Goodwin & Jamison, 2007), was one of many suggestions made by Leonhard (1999) for reclassifying mental disorders, but the only one to be gen- erally adopted. Leonhard separated mood disorders into a unipolar type (depression or mania but not both) and a bipolar type. While unipolar depression is common, unipolar mania is very rare; however, almost all bipolar patients eventually suffer from both depressive and manic episodes. With time, the term “bipolar” came to replace manic-depression entirely. While the older terminology points to the necessity of manic episodes and suggests a severe illness, the newer label is more neutral. The term “bipolar” has made it easier to expand the boundaries of the disorder.

Before and After Lithium Fifty years ago, bipolar disorder could often go unrecognized, particularly in North America. In the 1960s, a “New York–London Study” documented wide

http://www.routledgementalhealth.com/9780415891813 The Bipolar Diagnosis 13 divergences in diagnostic practices between American and British psychiatrists (Cooper, Kendell, & Gurland, 1972). When presented with identical filmed interviews of psychotic patients, the Americans diagnosed most as schizophrenic, while the British diagnosed the same patients as having manic-depression. Ameri- can psychiatrists at the time had a very broad concept of schizophrenia, and almost anybody with psychotic symptoms, especially paranoid delusions, tended to get that diagnosis. Yet a few years later, the Americans came around to see things the British way. The reason was that bipolar disorder now had a specific treatment. Psychiatry had arrived in the age of lithium. Treatment with lithium carbonate was the most important event in the history of bipolar disorder. An Australian psychiatrist, John Cade (1949), was the first to report that this simple salt offered an effective treatment for mania. However his discovery was not followed up, mainly because lithium had been tried for cardiac patients and discarded due to side effects. The Danish psychiatrist Mogens Schou (2001) reintroduced lithium in the late 1960s. The results of this treatment could sometimes be miraculous (see the Introduction to this book). Before lithium, it did not make much difference whether a psychotic patient was diagnosed with mania, schizophrenia, or some other disorder. Either way, treatment, at least since the 1950s, had depended mainly on antipsychotic drugs. But these agents did not prevent recurrences of mania. If bipolar disorder responded specifically to lithium, and if many patients who were lithium-responsive could be maintained without antipsychotic drugs, the clinical advantage was enormous. With a lower threshold for a bipolar diagnosis, some patients who had not been recognized as having manic episodes were rediagnosed and given more appropriate treatment. But patients unlikely to respond to lithium (or other mood stabilizers) were also prescribed these drugs, sometimes for long periods. Most suffered from other psychotic conditions, particularly schizophrenia. If the original diagnosis was correct, these patients would not benefit. The problem was that it was impossible to determine if adding lithium to an antipsychotic regime was making any difference. This was the first indication that enthusiasm for a bipolar spectrum could create trouble.

Variants of Bipolar Disorder Illness is not the same in every patient. That is most certainly true for bipolar disorder. For example, cases that begin early in life tend to have a poorer prog- nosis (Goodwin & Jamison, 2007). Other cases start late and are less severe. Some patients have a strong family history of disorder, while others do not. Sometimes response to treatment can define clinical subgroups. Patients who respond to lithium may have a fundamentally different form of illness than those who do not (Alda, 1999). The most important variant of classic manic-depression is bipolar-II disorder. This category, described in the literature for decades (Dunner, Fleiss, & Fieve,

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1976), was only officially accepted as a diagnosis in the fourth edition of the Diag- nostic and Statistical Manual of Mental Disorders (DSM-IV; American Psychiatric Association–APA, 1994). Essentially, bipolar-II is a milder form of the illness, with hypomanic rather than full manic episodes. It has been suggested that this disorder could have a separate etiology and pathogenesis (Goodwin & Jamison, 2007). As we will see, bipolar-II has boundary problems, mainly relating to the definition of a hypomanic episode. Manic episodes, the defining feature of bipolar-I disorder, are fairly unmis- takable. They are characterized by what has been called a “classical triad” of elevated affect, psychomotor excitement, and racing thoughts, all of which need to last for at least a week. Other characteristic symptoms include grandiose ideas, a decreased need for sleep, distractibility, and a variety of impulsive behaviors (such as overspending). However, since manic episodes are usually associated with psychosis, and with either grandiose or paranoid delusions, they have to be differentiated from schizophrenia. The main twist is that some manic patients present more with irritability than with euphoria (Winokur & Tsuang, 1975), a possibility that DSM-IV later included in its definition. That does not, however, mean that everyone who is highly irritable must be manic. Irritability is also a common symptom in depression, in which it is more related to severity than to latent bipolarity (Perlis et al., 2009). Bipolar-II requires episodes of both major depression and hypomania. As currently defined, it is a heterogeneous construct (Vieta & Suppes, 2008) that is often not diagnosed with great precision. If you have never had hypomania, you cannot have bipolar-II. That makes the definition of a hypomanic episode a crucial issue. In DSM-IV-TR (APA, 2000), the requirement is for “a distinct period of persistently elevated, expansive, or irritable mood, lasting throughout at least four days, that is clearly different from the usual non-depressed mood.” To be classi- fied as hypomanic, patients must then have at least three of the following (four if the mood is irritable and not euphoric): inflated self-esteem or grandiosity, decreased need for sleep, talking more than usual or pressure to keep talking, flight of ideas or the subjective experience that thoughts are racing, distractibility, increase in goal-directed activity (either socially, at work or school, or sexually), psychomotor agitation, and excessive involvement in pleasurable activities that have a potential for painful consequences. A hypomanic episode also must be associated with an unequivocal change in functioning that is uncharacteristic of the person when not symptomatic, and (crucially) is observable by other people. In contrast to full mania, hypomania need not be severe enough to cause marked impairment in social or occupational functioning, or to necessitate hospitalization; and it does not show psychotic features. If all these criteria are met, bipolar-II can be diagnosed. This diagnosis forms a distinct category of illness; every clinician will have seen such cases. But as

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Dunner and Tay (1993) have noted, patients do not always report mental states accurately. For example, patients may remember a period in which mood was unstable as continuous, rather than variable. This makes it crucial to interview relatives or friends to determine whether hypomania has been present. It is also worth noting that patients with both bipolar-I and bipolar-II may spend more time feeling low than high. Since bipolar depression is difficult to treat, it has been the subject of a great deal of recent research (Nivoli et al., 2011). Another bipolar variant is a “mixed state,” defined by DSM-IV-TR as at least a week in which a patient meets criteria for both major depression and mania. This category is problematic. Research is thin, and it is difficult to distinguish a mixed state from agitated depression (Goodwin & Jamison, 2007), or from agitation associated with other mental disorders. The result is that mixed states are diagnosed too readily, placing patients with other forms of psychopathology in the bipolar spectrum. Finally, DSM-IV-TR allows for a diagnosis of bipolar disorder not otherwise specified (NOS). The DSM system has an NOS category in each major grouping to account for patients who have some but not all features of specific diagnostic entities. In this case, the diagnosis describes any disorder with bipolar features that does not meet criteria for any of the above types. One of the examples given in the DSM manual for a bipolar-NOS diagnosis is “rapid cycling of mood over brief durations.” But while the subcategory of rapid-cycling bipolar disorder (defined as more than four episodes in a year) has been much studied (Bauer, Beaulieu, Dunner, Lafer, & Kupka, 2008), there is no reference to shifts over brief durations, and it is doubtful whether the term “rapid cycling” should be used to describe such phenomena. What is actually being described is affective instability, which is not necessarily bipolarity (see Chapter 3). Bipolar-NOS itself has not been well researched. One chart review study (Bader & Dunner, 2007) found that some patients have first-degree relatives with classic bipolar disorder, but many do not. There is a case to be made that subclinical features of bipolarity can be a risk factor for developing the full disorder. How- ever, that does not mean that one can jump from these clinical features to a firm diagnosis. The strength of the relationship depends on how broadly the diagnosis is used. The problem is that the NOS diagnosis as currently defined leaves the door open for clinicians to diagnose bipolarity in almost any patient they wish. These definitions will not change dramatically in DSM-5, except for one likely revision: the four-day rule for hypomania. This time scale has been challenged on the grounds that it is arbitrary. And this criticism is absolutely correct—except that any other length would be equally arbitrary. A two-day instead of a four-day rule may well prevail in the new manual. Yet one would still need to determine whether mood has been consistently abnormal within that time frame. As Chapter 3 shows, patients with symptoms of affective instability rarely remain in the same mood for as long as two full days.

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Redefining hypomania to include even briefer periods of mood change (as short as a day or less), as well as reducing the number of required symptoms, would lead to a radical expansion of bipolar diagnosis. That is already happen- ing—in spite of the definitions provided by DSM-IV. Clinicians do not necessarily pay attention to all these details. Instead of following algorithms, diagnoses tend to be based on features considered to be characteristic of bipolar disorder (especially mood swings of any kind).

Diagnostic Validation How do psychiatrists go about validating the diagnosis of any mental disorder? In modern medicine, diagnosis is initially based on signs and symptoms, but is usually confirmed by laboratory tests, imaging procedures, and pathologi- cal findings. Since the nineteenth century, under the influence of the German pathologist Rudolf Virchow and the Canadian-American internist William Osler, it has been accepted that medical diagnoses should be grounded in objec- tive data. Psychiatrists have not been able to meet that standard. They still depend almost entirely on clinical observation to make diagnoses. In this respect, they are in much the same position as other specialists were 100 years ago. (There are also important syndromes in internal medicine, such as migraine, that are no better understood than mental disorders.) One can quantify the measurement of signs and symptoms with structured interviews or by using clinical rating scales. But such procedures can hardly be considered “gold standards” since they can be no more accurate than the clinical phenomena by which they are validated. While physicians will always continue to assess signs and symptoms, the convergence of a characteristic clinical picture with biological findings provides the data that make diagnoses valid. Over 40 years ago, Eli Robins and Samuel Guze, two psychiatrists at Washing- ton University in St. Louis, who founded the neo-Kraepelinian school, proposed ways to validate diagnoses. Robins and Guze (1970) recommended a combina- tion of disciplined observation, supported by a characteristic course of illness and buttressed by the eventual discovery of laboratory methods. Robins and Guze listed five pathways to validity. The first was precise clinical description. That principle became the basis of the DSM-III system, published 10 years later. The second pathway was laboratory studies to identify biological markers. That idea turned out to be rather futuristic; biological markers did not exist for any categories of mental illness in 1970, and psychiatrists still have none. The third criterion was clear delineation from other disorders. Yet in practice, patients often meet criteria for multiple diagnoses that can lead to a massive degree of “comorbidity.” This term, which implies the presence of more than one disorder in the same patient, is misleading because separate disorders can have overlapping symptoms. The problem is that DSM manuals have no way to

http://www.routledgementalhealth.com/9780415891813 The Bipolar Diagnosis 17 determine what is primary and what is secondary, so that multiple diagnoses are both allowed and encouraged. The fourth pathway is a characteristic outcome in follow-up studies—Kraepelin’s approach. That criterion has been frustrated by heterogeneity in outcome, raising questions about the validity of many categories. The fifth Robins–Guze criterion was a genetic pattern in family history studies, a concept of relevance to bipolar disorder. Identifying bipolar relatives has often been used to delineate the boundaries of the spectrum. However, problems with defining bipolar disorder itself makes its identification even more difficult in a relative than in a proband. Psychiatry is still struggling to achieve validity for most diagnoses. The Robins–Guze criteria represented a noble attempt to offer useful general guide- lines. But until specific and sensitive biological markers are identified, we cannot be sure whether patients do or do not merit any diagnosis. For this reason, the DSM manual should not be followed religiously. It is a provisional classification based on consensus and clinical observation. The signs and symptoms it describes will probably be understood differently a few decades from now.

How Diagnostic Problems Affect Research Since 1950, about 28,000 articles have been published in medical journals on bipolar disorder. The interested reader is advised to consult the massive and com- prehensive text by Goodwin and Jamison (2007). However, all research depends on the validity of diagnosis. When that is uncertain, all else is uncertain. We can see this problem most dramatically in epidemiological studies conducted in the community. A number of problems plague this kind of research. On a purely practical level, studies of the general population are expensive, and cost limits their scope. You need a large and representative sample, and there are just so many questions you can ask each subject. Moreover, survey interviews are not conducted by specialists but by research assistants who receive brief train- ing in diagnosis and have no clinical experience. Thus, even when measures are standardized, these assistants may not reach the same diagnostic conclusions as experienced clinicians or researchers. In some surveys, the reliability of diagnosis has been surprisingly low (Goodwin & Jamison, 2007). For example, in one recent large-scale study (Angst et al., 2010), reliability for bipolar-I was excel- lent (kappa=.88), but only modest reliability (.50) was found for bipolar-II. It is not clear whether experienced clinicians would do better, but diagnosing mental disorder from highly structured assessment tools clearly leaves greater room for uncertainty. If bipolar diagnoses can be questioned on the grounds of reliability and validity, so can the findings of community surveys. Epidemiological findings are no better or no worse than DSM manuals in identifying who has bipolar disorder and who does not. The use of structured interviews limits variability in diagnosis but does not resolve these issues.

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The problem becomes more severe when surveys move beyond the manual and measure subclinical symptoms that place patients in a broader bipolar spectrum. No one knows whether epidemiological studies examining such phenomena measure what they are supposed to measure. Another way in which diagnostic uncertainty affects research is the assessment of family history. We know from twin studies that bipolar disorder is one of the most heritable of the major mental disorders (Goodwin & Jamison, 2007). That is why establishing a family history of the illness in first-degree relatives is so important. But doing so is more difficult than it seems. Most clinicians who assess family history get their information from the patient. That leads to all kinds of self-report biases. Patients may have a strong opinion about their own diagnosis (or that of a parent or sibling). A previous physician may have jumped to conclusions from inadequate information, shaping how everyone views the matter. One patient told me that she had been diagnosed as bipolar largely because her father suffered from life-long irritability. She also had a pattern of long-term insomnia in which she would get up and clean the house, which was interpreted by some of her treating physicians as hypomanic behavior. Did either father or daughter have bipolar disorder? It was impossible to tell. It is not sufficient for a relative to be described as moody and irritable to be determined to be bipolar. It is not even sufficient, in an age when mood stabilizers are so readily prescribed, to use a history of previous treatment to confirm a diagnosis. To qualify for bipolar disorder, a patient must have experienced either hypomania or frank mania. Therefore, I ask whether a relative has been hospitalized, or whether other people said that patients went through periods when they were not behaving like their usual selves. If these features are absent, I tend to doubt any conclusions about bipolarity. Ideally, first-degree relatives should be directly interviewed. Some researchers have done so. Craddock and Jones (1999) reviewed 13 studies in which some (but not all) relatives were contacted, and the data did point to a higher relative risk for the disorder. But that systematic procedure cannot be compared to the common clinical situation in which a patient says, “My father was bipolar, even if he never saw a doctor for it.” In summary, while the presence of definitive bipolar disorder in a first-degree relative should definitely influence diagnosis, one should not leap ahead on limited evidence. Why are these research problems important for clinicians? The reason is that studies of community prevalence and family history are frequently used to support the existence of a bipolar spectrum. The data look scientific, but really are far from empirically sound.

Screening for Bipolarity Clinicians have been primed to fear missing a bipolar diagnosis. One way to man- age the problem could be the use of screening instruments.

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The Mood Disorder Questionnaire (MDQ; Hirschfeld, Williams, & Spitzer, 2000) has been the most popular option, and this screener has been used both in research and practice to identify patients who may be bipolar. It is a simple self- reporting measure consisting of 16 questions, each answered yes or no, covering some of the most common symptoms of hypomania. However, the answers can be interpreted in different ways, and they do not have the same weight. Being so “hyper” that other people comment on it, or not needing sleep for several days, are clinical features that should be fairly sensitive to bipolarity. On the other hand, being more self-confident or irritable than usual from time to time can reflect changes in mood that can happen for other reasons. Based on a sample of patients with a specialized mood disorder, Hirschfeld et al. (2000) recommended that a “yes” answer to only 7 of the 16 questions would be sufficient to suggest a diagnosis. This procedure leads inevitably to false positives. It would be misleading to use this measure in most clinical settings. But it often is. Screeners based on self-report need to be confirmed by diagnosis based on assessment by trained clinicians. Even so, the MDQ has benefited from being “quick and dirty”; it has been used in at least 67 research studies since it was first published. The MDQ is also available on the internet, helping it to become a clinical tool. Patients have told me they were given this instrument, followed by a brief interview, followed by a diagnosis of bipolarity and a prescription of drugs. Finally, scores on the MDQ are not specific to bipolar disorder. Zimmerman et al. (2010a) found that what the MDQ mainly picks up is mood instability, as opposed to distinct episodes of abnormal mood, and that many patients who score positive on the screen meet criteria for borderline personality disorder. As Chapter 5 shows, this is a serious source of confusion, since the drugs that work for bipolar disorder are much less useful in personality disorders. Another screening instrument of dubious validity is the Bipolar Spectrum Diagnostic Scale (BSDS; Ghaemi et al., 2005). Promoted as a clinically useful measure, it is offered free of charge online. The problem is that in spite of impressive internal psychometrics, the BSDS simply assumes that the bipolar spectrum is a valid concept. Using it will lead clinicians to make the diagnosis more often. Another problematic measure is the Bipolarity Index for Bipolar Diagnosis (Sachs, 2004). The problem with this self-report screener is that there are many ways to get a high score that do not require the presence of either manic or hypomanic features. Once again, the basic features of bipolarity are downplayed in favor of spectrum symptoms that are likely to overlap with other mental disorders. The result is a scientific gloss on the practice of making a diagnosis of bipolarity easier, followed by treatment methods that were developed for patients who have mania or hypomania.

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Does Everybody Have Bipolar Disorder? A few years ago the Canadian Journal of Psychiatry, of which I am the editor- in-chief, published a debate about the boundaries of the bipolar diagnosis. My colleague from Calgary, Scott Patten (2006), entitled his side: “Does almost everybody suffer from a bipolar disorder?” That may sound like an exaggeration, but it is not a large one. There is little doubt that the increased recognition of bipolar disorder in clinical practice has brought benefits to patients in whom the diagnosis leads to definitive and effective treatment. On the other hand, this diagnosis (and the treatment that follows) will not be beneficial in patients who do not have bipolar disorder. Only a minority of those currently receiving a diagnosis in the bipolar spectrum will have had manic or hypomanic episodes. This is not to deny that the bipolar diagnosis can sometimes be missed. As Chapter 4 shows, we need to seriously consider bipolarity in patients suffering from severe recurrent depression. However, the diagnosis is often made on the basis of “soft bipolar” symptoms (moodiness, irritability, impulsivity), rather than on clear-cut mania or hypomania. While the exact boundaries of the disorder remain unclear, soft bipolarity describes a population that may be at risk for classic bipolarity but may also suffer from other disorders (or no disorder at all). The main source of the problem derives from diagnosing bipolarity when patients complain of moodiness. Many people in community studies report significant mood swings, particularly adolescents (Spindel, Gabbay, & Coffey, 2008) and menopausal women (Freeman, 2008). The problem of establishing a boundary between normal variation and psychopathology arises for many psychiatric diagnoses. Jerome Wakefield, a New York University researcher, has pointed out the differences between sadness and depression (Horwitz & Wakefield, 2007), between shyness and social anxiety (Wakefield, Horwitz, & Schmitz, 2004), and between childhood misbehavior and conduct disorder (Wakefield, Pottick, & Kirk, 2002). If no one is normal, the very meaning of mental illness falls under question.

Academia, Industry, and Bipolar Disorder Academic physicians like to focus on a disease about which they are expert. Some want to make their favorite diagnosis as often as possible. Allen Frances (2010b) comments that while he has been involved in three versions of the DSM manual, in none of these cases did he ever find experts who wanted to reduce the scope of any diagnosis on which they had carried out research. And every research grant application begins with a statement on how common a disease is—with the clear implication that funding should be provided to study it. Human nature being what it is, we are all biased in this way. Attention deficit hyperactivity disorder specialists see that condition everywhere. That also holds

http://www.routledgementalhealth.com/9780415891813 The Bipolar Diagnosis 21 true for bipolar specialists. (My own research examines personality disorders, but I bend over backwards not to diagnose these conditions in people who are simply troubled or unhappy.) Another player is the pharmaceutical industry. Patients who have psychologi- cal symptoms may or may not benefit from drugs. But once declared to have bipolar disorder, treatments will be prescribed for them. Thus, the industry can make large profits when expanded diagnosis opens up a new market. This helps to explain why pharmaceutical companies have invested so much money in pro- moting the bipolar diagnosis. And much of their advertising to physicians suggests that spectrum symptoms should be treated in the same way as classic bipolarity, that is, with their products. Industry also has been successful in convincing potential patients that they have bipolar disorder. The USA and New Zealand are the only countries in the world that permit direct-to-consumer advertising of pharmaceutical products, and Americans often see these ads in magazines and on television. In recent years, ads in magazines and on television in America have promoted rediagnosis of highly prevalent conditions, most particularly depression, as bipolar disorder. One directs the consumer to a website called “amIreallybipolar.com.” Of course, the rules require each ad to instruct patients to “ask your doctor.” However, when patients ask their doctor for a new diagnosis and are primed to support it, their friendly physicians may well go along with what patients want. The pharmaceutical industry has also promoted the use of screening questionnaires such as the MDQ, which have the potential to inflate the diagnosis of bipolar disorder (Zim- merman, Pasternak, Chelminski, & Solomon, 2004). In this way, companies use financial clout to make it more likely that their products will be prescribed.

Clinical Consequences of Diagnostic Errors If mania and hypomania define bipolarity, then bipolar disorder is being overdiag- nosed. But if a wider variety of clinical phenomena fall within a spectrum, then bipolarity is being underdiagnosed. In the absence of solid evidence that could answer the question and determine the presence or absence of the illness, the issue boils down to a question of utility and cost. Missing bipolar disorder could carry a cost, since patients will not get the right medication. That has happened in the past and could still happen today. Some patients with depression will eventually develop bipolarity. Yet given the much lower clinical threshold for diagnosis being used today, missing bipolar disorder has become less likely. Making the diagnosis in patients who do not fall in the bipolar spectrum also has a cost. Bipolar disorder is a condition that continues for the patient’s whole life, and unlike other mental disorders, does not often remit in old age (Jacoby, 2006). Thus, once treatment is initiated, it may continue for decades. It must be admitted that it can be very difficult to be sure whether or not

http://www.routledgementalhealth.com/9780415891813 22 The Bipolar Diagnosis some patients suffer from bipolar disorder. But clinicians, when faced with doubt, may favor making a diagnosis that leads directly to medical treatment. But even when psychiatric drugs seem to help patients, it is very hard to be sure that they are working. It is well established that antidepressants can be placebos (Kirsch et al., 2008), and the same scenario can apply to almost any intervention. When the consequence of a diagnostic choice is life-long pharmacological therapy, clinical decisions should be made with caution.

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