A multi-step cognitive behaviour therapy for eating disorders.

Authors: Grave, Riccardo Dalle Source: European Eating Disorders Review, Nov2005, Vol. 13 Issue 6, p373-382; , 10p, 3 Diagrams, 1 Chart Document Type: Article Subject Terms: ANOREXIA nervosa EATING disorders BULIMIA APPETITE disorders BEHAVIOR modification Abstract: This paper describes a novel model of cognitive behaviour therapy (CBT) for eating disorders called CBT-Multi-Step (CBT-MS). The treatment, derived from the transdiagnostic cognitive behaviour theory of eating disorders described by Fairburn, Cooper and Shafran, expands the range of applicability of standard CBT. It is designed to be applicable to different levels of care (outpatient, intensive outpatient, day-hospital, inpatient and post-inpatient), and to eating disorder patients of all diagnostic categories, ages and BMI. Distinguishing CBT-MS is the adoption of a multi-step approach conducted by a multidisciplinary (but non eclectic) team, the inclusion of a CBT family module for patients < 18 years, and the use of meal planning and mechanical eating at all the levels of care. Copyright 2005 John Wiley & Sons, Ltd and Eating Disorders Association. [ABSTRACT FROM AUTHOR]

Copyright of European Eating Disorders Review is the property of John Wiley & Sons, Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) ISSN: 1072-4133 DOI:

10.1002/erv.671 Accession Number: 19001222

Suspect an eating disorder? Suggest CBT. Authors: Schumann, Sarah-Anne Source: Journal of Family Practice, May2009, Vol. 58 Issue 5, p265-266; , 2p Document Type: Article Subject Terms: COGNITIVE therapy EATING disorders -- Treatment BULIMIA -- Treatment ANOREXIA nervosa -- Treatment SEROTONIN uptake inhibitors BEHAVIOR therapy PSYCHOTHERAPY PSYCHIATRY -- Research Geographic Terms: GREAT Britain Abstract: The article focuses on the use of cognitive behavioral therapy (CBT) for the treatment of patients with eating disorder not otherwise specified (NOS). The therapy, which has been used for bulimia and anorexia nervosa treatment, is considered effective for patients with NOS. It cites the similarity of selective serotonin reuptake inhibitors (SSRIs) and CBT in effectively treating eating disorders. It also indicates the effectiveness of CBT for the treatment of binge-eating disorder. The results of a study in Great Britain of the treatment of eating disorders with CBT are also discussed.

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CognitivMedication and psychotherapy in the treatment of bulimia nervosa

Walsh, B Timothy ; Wilson, G Terence ; Loeb, Katharine L ; Devlin, Michael J ; et al. The American Journal of Psychiatry 154. 4 (Apr 1997): 523-31. Turn on hit highlighting for speaking browsers Turn off hit highlighting

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Two treatments for bulimia nervosa have emerged as having established efficacy: cognitivebehavioral therapy and antidepressant medication. This study sought to address 1) how the efficacy of a psychodynamically oriented supportive psychotherapy compared
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Objective: Two treatments for bulimianervosa have emerged as having established efficacy: cognitive-behavioral therapyand antidepressant medication. This study sought to address 1) how the efficacy of a psychodynamically oriented supportive psychotherapy compared to that of cognitive-behavioral therapy; 2) whether a two-stage medication intervention, in which a second antidepressant (fluoxetine) was employed if the first (desipramine) was either ineffective or poorly tolerated, added to the benefit of psychological treatment; and 3) if the combination of medication and psychological treatment was superior to a course of medication alone. Method: A total of 120 women with bulimianervosa participated in a randomized, placebo-controlled trial. Results: Cognitive-behavioral therapywas superior to supportive psychotherapy in reducing behavioralsymptoms of bulimianervosa (binge eating and vomiting). Patients receiving medication in combination with psychological treatment experienced greater improvement in binge eating and depression than did patients receiving placebo and psychological treatment. In addition, cognitive-behavioral therapyplus medication was superior to medication alone, but supportive psychotherapy plus medication was not. Conclusions: At present, cognitive-behavioral therapyis the psychological treatment of choice for bulimianervosa. A two-stage medication intervention using fluoxetine adds modestly to the benefit of psychological treatment. (Am J Psychiatry 1997; 154:523-531) When bulimianervosa was first identified, it was viewed as "extremely difficult to treat" (1). Since that time, a variety of treatment approaches have been explored, and two interventions have emerged as having established efficacy. One is cognitive-behavioral therapy, which was originally developed by Fairburn (2). The outcome of patients treated with cognitivebehavioral therapyhas been clearly shown to be superior to that of patients assigned to a waiting list or a delayed treatment condition, and it appears that the benefits of cognitivebehavioral therapyare often well maintained at followup (3). Cognitive-behavioral therapyhas been shown to be superior to alternative forms of psychological treatment in some but not all controlled trials (4-7). The other major intervention currently employed in the treatment of bulimianervosa is antidepressant medication. Since 1979, over 15 placebo-controlled studies have documented that the short-term outcome of patients receiving antidepressant medication is superior to that of patients receiving placebo (8). However, the utility of antidepressants as the sole treatment for bulimianervosa has been questioned because of the frequency of side effects of some agents and concerns about long-term outcome (9,10). Not surprisingly, the emergence of cognitive-behavioral therapyand of antidepressant medication as leading treatments for bulimianervosa has raised questions about their comparative efficacy and about the advantages of combining them. The results of some studies examining these issues indicate that cognitive-behavioral therapyalone is generally superior to a trial of a single antidepressant agent and suggest that there may be some advantage to combining cognitive-behavioral therapywith antidepressant medication (9, 1113). However, several important clinical questions were not completely resolved by the available data. One is how the efficacy of more traditional, psychodynamically oriented, supportive psychotherapy compares to that of cognitive-behavioral therapy. Second, does a more sophisticated two-stage medication intervention, in which a second antidepressant is employed if the first is either ineffective or poorly tolerated, add to the benefits of

psychological treatment? And third, is the combination of psychotherapy and medication superior to a course of medication alone? This article describes the short-term results of a randomized, placebo-controlled study of 120 women with bulimianervosa that was designed to address these questions. METHOD Patient Selection To participate in this study, patients were required to meet DSMIII-R criteria for bulimianervosa for at least 1 year. Only patients who used self-induced vomiting as a primary method of compensating for binge eating were included. Patients were also required to be women between the ages of 18 and 45 years whose weights were between 80% and 120% of ideal. Patients were excluded if they were medically ill, had evidence of cardiac conduction disease, were pregnant, had abused drugs or alcohol within the past year, were judged to be acutely suicidal, or had previously had an adverse reaction to either desipramine or fluoxetine. Patients were recruited through adver tisements in local media. Individuals who seemed eligible for the study on the basis of a telephone screening were invited to an evaluation appointment, in which a research assistant assessed the eating disorder through use of the Eating Disorder Examination (14) and other axis I psychiatric disorders through use of the Structured Clinical Interview for DSM-III-R (15). Candidates who appeared to meet the entry criteria returned 1 week later to meet with a psychiatrist who confirmed the diagnoses, obtained a medical history, and conducted a physical examination. A complete blood count, serum chemistries, and an ECG were also obtained. After providing written informed consent, eligible patients entered a single-blind placebo washout phase lasting 7-10 days. Following this phase, individuals who continued to meet the study entry criteria were randomly assigned to one of five treatment groups (table 1). A total of 209 patients were seen for the initial evaluation; 149 returned for the second assessment. One hundred twenty individuals were eventually randomly assigned to treatment. The most common reason for attrition during the evaluation phase was failure to return for the subsequent appointment; other reasons included failure to meet diagnostic criteria for bulimianervosa and improvement during the single-blind placebo washout. This study was reviewed and approved by the New York State Psychiatric Institute/Columbia University Institutional Review Board. Treatment In four of the five treatment groups, patients received a psychological treatment (cognitivebehavioral therapyor supportive psychotherapy). Approximately half of the patients receiving psychological treatment were assigned to medication and half to placebo; in these four groups, medication assignment was unknown to both patients and staff (double-blind). Patients assigned to the fifth group received medication but no formal psychological treatment and were informed that they were receiving medication. Thus, the study included a 2x2 factorial design to compare cognitive-behavioral therapywith supportive psychotherapy and to examine the benefit of medication versus placebo among patients receiving psychological treatment. In addition, by comparing the outcome of patients receiving medication only to that of patients receiving cognitive-behavioral therapyor supportive

psychotherapy and medication, we planned to determine the benefit of adding each of these forms of psychological treatment to a course of medication. Cognitive-behavioral therapy. This treatment was based on a manual (G.T. Wilson, 1989) derived from the treatment approach of Fairburn et al. (4). Stage 1 (sessions 1-8) consists of the following components: an overview and explanation of the philosophy and goals of the treatment program; the use of daily self-monitoring homework to identify high-risk situations that trigger binge eating and purging; introduction of cognitiverestructuring strategies in which patients learn to identify and challenge dysfunctional cognitions related to their disorder; instruction and guidance in learning to normalize eating patterns (e.g., eat three meals a day); and an emphasis on alternative, more constructive strategies for coping with high-risk situations for binge eating. Patients are given information about weight regulation and about how dieting is linked to the development and maintenance of binge eating. Stage 2 (sessions 9-16) emphasizes problem-solving strategies for coping with high-risk situations for binge eating and purging. Cognitiverestructuring is focused on specific concerns about body weight and shape. Flexible eating habits are emphasized, and patients are helped to incorporate previously avoided foods into their diet. Stage 3 (sessions 17-20) continues to emphasize the strategies acquired in stage 2. The major focus of treatment is on the maintenance of improvement and on relapse prevention. Supportive psychotherapy. This treatment was a manual-based, modified version of the shortterm psychotherapy used in the Fairburn et al. study (4). Our treatment differed from that of Fairburn et al. in at least two important respects: 1) we eliminated elements that overlap with the putative active therapeutic ingredients of cognitivebehavioral therapy, such as patient self-monitoring of eating and the conditions that trigger binge eating, as well as instruction and implicit advice on necessary changes in diet and eating patterns; and 2) supportive psychotherapy was less directive and focal in nature. In stage 1 (sessions 1-8), therapists obtained a comprehensive description of the eating problem and its development, as well as a detailed personal and family history, and helped patients identify underlying problems that might be responsible for the eating disorder. Stage 2 (sessions 9-16) had the following aims: to encourage patients to explore underlying emotional problems, to facilitate self-disclosure and expression of feelings, and to foster independence and raise the issue of termination of treatment. Stage 3 (sessions 17-20) continued the exploration of underlying issues and how they might affect future adjustment. Termination of therapywas also addressed. Supportive psychotherapy in the present study was designed to control for nonspecific therapeutic influences inherent in cognitive-behavioral therapy. In contrast to cognitivebehavioral therapy, supportive psychotherapy was nondirective and emphasized patient selfexploration and understanding. It was intended to represent the type of treatment that outpatients might typically receive from psychodynamically oriented psychotherapists providing short-term supportive therapy. Therapist background and orientation. Cognitive-behavioral therapyand supportive psychotherapy were provided by three therapists (one psychiatrist, one doctoral-level psychologist, and one master's-level psychologist obtaining a doctoral degree). Each therapist provided both cognitive-behavioral therapyand supportive psychotherapy. All three therapists considered themselves eclectic in orientation and were trained to implement the manualbased treatments employed in this study. Therapists received biweekly group supervision in cognitive-behavioral therapyand supportive psychotherapy that was provided, respectively, by an expert in cognitive-behavioral therapyfor eating disorders (G.T.W.) and by a

psychoanalyst with extensive experience in the treatment of patients with eating disorders (S.P.R.). Medication. Patients randomly assigned to receive medication first received desipramine for 8 weeks. If binge frequency had not declined by at least 75% or if intolerable side effects occurred, the desipramine was tapered and discontinued over the succeeding 2 weeks, and patients then received fluoxetine. Patients randomly assigned to placebo first received desipramine placebo and, following the same criteria, were then given fluoxetine placebo. Patients met weekly with a psychiatrist. During these brief visits, the psychiatrist collected binge/purge diaries and assessed medication response and side effects. The psychiatrist inquired briefly about developments since the previous session, provided basic education concerning medical aspects of eating disorders, and supported whatever attempts the patient was making to improve without specifically endorsing any particular approach. During the first week after randomization, the dose of desipramine was raised to 200 mg/day, and, if tolerated, this dose was continued for the next 3 weeks. The dose could then be raised to 300 mg/day if improvement was not satisfactory. Fluoxetine was initiated at 60 mg/day. The dose of medication could be lowered to minimize side effects. Assessment Throughout the study, patients were asked to record the number of daily binge eating and vomiting episodes in a diary, which was collected by the psychiatrist weekly. Patients were asked to complete the following self-report questionnaires during the initiation phase, at specified intervals during the study, and at termination: the Body Shape Questionnaire (16), the Eating Attitudes Test (17), the Beck Depression Inventory (18), the SCL-90 (19), the Three-Factor Eating Questionnaire (20), and a visual analogue scale to rate the treatment's logic and relevance. At termination of treatment, the patient's status was assessed by an interviewer who was unaware of the patient's treatment assignment, through use of the Eating Disorders Examination. All treatment sessions were audiotaped, and randomly selected tapes were rated by an advanced doctoral candidate in clinical psychology. Statistical Analysis Data from all 120 patients randomized were included in the analyses. Response to treatment was evaluated by using termination data; for patients who discontinued treatment prematurely, data from the last visit were carried forward, with the exception of one patient who attended only the first session. For continuous variables, the difference between postand pretreatment levels was calculated and used as the dependent variable. Logarithmic transformations were used to reduce excessive skewness in the following variables: binge and vomiting frequencies; Beck inventory; Eating Disorders Examination eating concern subscale; SCL-90 obsessive-compulsive, interpersonal sensitivity, anxiety, anger-hostility, and paranoid ideation subscales; and the body mass index. Effects of treatments were estimated by using analysis of variance (ANOVA) for continuous variables and logistic regression for categorical variables. Odds ratio values were tested with likelihood chi-square tests, with 1 degree of freedom. Other comparisons were analyzed by using ANOVA or the chi-square statistic.

The primary outcome measures were the frequencies of binge eating and of vomiting recorded in patient diaries at the end of treatment. Data from other, secondary measures are presented to provide a more complete description of patient outcome; except when noted, significance levels are reported without correction for multiple comparisons, and, because of the number of secondary measures examined, these results should be interpreted with caution. RESULTS Pretreatment Characteristics The clinical characteristics of the patients treated in this study are presented in tables 2 and 3. On average, patients were 26.1 years old, were of normal body weight (mean body mass index=21.9 kg/m2), and had had bulimianervosa for 7.91 years. Of the 120 patients, 100 (83%) were white, seven (6%) were black, seven (6%) were Hispanic, and six (5%) were Asian. Twentyone percent were currently in an episode of major depression, and 29% had a history of anorexia nervosa. Twenty-one patients ( 18 % ) had previously taken fluoxetine, and four (3%) had previously taken desipramine. The five treatment groups did not differ significantly on any of these characteristics. Description of Treatments Both cognitive-behavioral therapyand supportive psychotherapy were designed to be administered in 20 sessions over 16 weeks; the average number of psychotherapy visits attended was 17.2 (SD=4.8) over an average of 17.0 weeks (SD=6.2). Neither the number of visits nor the duration of treatment differed between the two forms of psychological treatment. Patients assigned to receive only medication were expected to attend a total of 16 sessions over 16 weeks; the average number of visits attended was 11.5 (SD=4.5) over 12.5 weeks (SD=5.6). Both the number of visits and the duration of treatment for patients assigned to medication only were significantly less than those for patients receiving psychological treatment (number of visits: F=30.9, df=1, 118, p=0.0001; duration: F=11.8, df=1, 118, p=0.0008). This reflects the planned length of the treatments, the slightly higher rate of dropout in the medication only condition, and the fact that for patients receiving medication only, premature discontinuation of medication because of side effects shortened the overall length of treatment. For patients who were also receiving psychological treatment, the full course of cognitive-behavioral therapyor supportive psychotherapy was offered regardless of changes in medication status. Patients were asked to rate the degree to which their treatment assignment was logical and relevant to their problems. There was a significant difference across the three therapyassignments (cognitive-behavioral therapy, supportive psychotherapy, and medication only) in ratings after the first session (logical: F=4.28, df=2, 94, p=0.02; relevant: F=4.68, df=2, 94, p=0.01). Patients assigned to medication only rated their treatment as less logical than did patients assigned to cognitive-behavioral therapyor supportive psychotherapy and less relevant than did those assigned to supportive psychotherapy (p< 0.OS by Tukey's honestly significant difference). There were no significant differences between ratings of cognitive-behavioral therapyand supportive psychotherapy. At the end of treatment, there were no significant differences in ratings across therapyassignment. A total of 227 audiotaped therapysessions were assessed by an independent rater. There was a difference between treatments in the degree of understanding conveyed and in interpersonal

effectiveness. On both measures, cognitive-behavioral therapyand supportive psychotherapy were similar to each other but superior to medication alone (understanding: F=51.1, df=2, 224, p= 0.0001, p<0.05 by Tukey's honestly significant difference; interpersonal effectiveness: F=9.01, df=2, 223, p=0.0002, p<0.05 by Tukey's honestly significant difference). The proportion of patients terminating treatment prematurely was 34% overall and did not differ significantly across groups (X^sup2^= 1.91, df=4, p>0.70); the rate of premature termination was highest in the medication only group (43%), but this was not significantly greater than the rate of premature termination among patients receiving psychological treatment (32%) (X^sup^2= 12, df=1, p>0.20). One hundred of the 120 patients remained in treatment long enough to have the opportunity to have their medication changed from desipramine (or desipramine placebo) to fluoxetine (or fluoxetine placebo). Overall, this change was made with 74% of the eligible patients. The frequency of changing medication was lower among patients receiving cognitive-behavioral therapythan among those receiving supportive psychotherapy (7% versus 84%) (y2=6.7, df=1, p<0.01). This difference appears to reflect the greater improvement in binge eating attained by those receiving cognitive-behavioral therapy(see later discussion). Among patients receiving psychological treatment, there was no difference in the frequency of changing medication between those assigned to placebo and those assigned to medication (64% versus 76%) (X2=1.5, df=1, p>0.20). Among patients receiving medication, the average maximum dose of desipramine was 188 mg/day (SD=89), and the average maximum dose of fluoxetine was 55 mg/day (SD=15). The maximum desipramine dose differed across therapyconditions: for cognitive-behavioral therapy,143 mg/day (SD=92); for supportive psychotherapy, 220 mg/day (SD=80); and for medication only, 198 mg/day (SD=83) (p<0.01; supportive psychotherapy and cognitivebehavioral therapydiffered by Tukey's honestly significant difference). The fluoxetine dose did not differ significantly across therapyconditions. Response to Treatment At baseline, the five treatment groups did not differ on any outcome measure. In all treatment groups, the end-of-treatment frequencies of binge eating and vomiting and most measures of psychopathology were statistically significantly lower than the frequencies before treatment (table 3). Thus, there was significant clinical improvement in all groups. Comparison of Patients Receiving Psychological Treatment With Medication or Placebo. The comparison of cognitive-behavioral therapywith supportive psychotherapy and of the combination of psychological treatment and antidepressant medication versus psychological treatment and placebo was conducted by using a 2x2 factorial design; data from the medicationonly group were not used in these comparisons. There were no statistically significant interactions between type of psychological treatment (cognitive-behavioral therapyversus supportive psychotherapy) and medication (active versus placebo) on any outcome measure. Cognitive-Behavioral TherapyVersus Supportive Psychotherapy. The frequencies of binge eating and of vomiting per week were calculated from the last 2 weeks of patient diaries and from the Eating Disorders Examination interview, which focused on the preceding month.

Data from both sources indicated that cognitive-behavioral therapyhad a much greater impact than supportive psychotherapy in reducing binge eating and vomiting (table 3). Examination of the rates of cessation of binge eating and vomiting also favored cognitive-behavioral therapyover supportive psychotherapy (table 4). There were few other indications of significant differences in outcome between cognitivebehavioral therapyand supportive psychotherapy. Cognitive-behavioral therapywas associated with a greater reduction in the score of the Eating Attitudes Test, a self-rating instrument that assesses both behavioraland attitudinal symptoms of eating disorders (table 3). However, there were no differences between cognitive-behavioral therapyand supportive psychotherapy in improvement in mood, assessed by both the Beck inventory and the SCL90. There was a significant difference between cognitivebehavioral therapyand supportive psychotherapy in change in weight during treatment; cognitive-behavioral therapywas associated with a weight gain of 1.13 lb., compared with a weight loss of 1.29 lb. for supportive psychotherapy. Medication Versus Placebo. On several measures, there was evidence that patients receiving medication in combination with psychological treatment experienced greater improvement than did patients receiving placebo with psychological treatment. On the basis of patient diaries, medication affected binge eating more than placebo did. Reductions in Eating Attitudes Test scores were significantly greater in the patients receiving medication, as was improvement in scores on the Beck inventory and the depression subscale of the SCL-90 (table 3). Patients receiving medication and psychological treatment lost an average of 1.54 lb., compared to a weight gain of 1.49 lb. with placebo and psychological treatment. This difference was statistically significant. Comparison of Patients Receiving Medication Alone With Patients Receiving Psychological Treatment With Medication. We also assessed the benefits of combining medication and psychological treatment by comparing the outcome of patients treated exclusively with medication to the outcome of patients treated with either medication and cognitive-behavioral therapyor with medication and supportive psychotherapy. Because data from the medicationonly cell were used in both comparisons, a Bonferroni correction was applied, and only comparisons with a p value of 0.025 or less were accepted as significant. Cognitive-Behavioral TherapyPlus Medication Versus Medication Alone. The combination of cognitivebehavioral therapyand medication was superior to medication alone in reducing vomiting frequency, as assessed by patient diary, and the total Eating Attitudes Test score (table 3). Patients receiving medication alone lost significantly more weight than did patients receiving cognitive-behavioral therapyand medication (-3.50 lb., SD=5.9, versus -0.01 Ib., SD=3.7). Supportive Psychotherapy Plus Medication Versus Medication Alone. The only indications of statistically significant differences between the group receiving supportive psychotherapy with medication and that receiving medication alone were found on the basis of the Eating Disorders Examination. Surprisingly, the combination of supportive psychotherapy and medication was significantly inferior to medication alone in reducing frequency of binge

eating (table 3). It should be noted that Eating Disorders Examination data on binge eating and vomiting were available from only 37 of the SO patients relevant to this analysis. On the basis of patient diary information, which was available for all 50 patients, there were no statistically significant differences between patients receiving supportive psychotherapy plus medication and patients receiving medication alone. Supportive psychotherapy significantly added to medication alone in reducing the importance of shape and weight as assessed by the Eating Disorders Examination. Results From Patients Who Completed Treatment. Additional analyses were conducted to examine behavioralchanges (binge eating and vomiting as recorded in patient diaries) among the 79 patients who completed an entire course of treatment. The results were consistent with the intent-to-treat analyses, with two minor exceptions. First, there was a significant difference in reduction in binge eating, but not vomiting, between supportive psychotherapy plus medication and medication alone (F=5.54, df=1, 30, p=0.03). This finding is similar to the results of the intent-to-treat analysis of the Eating Disorders Examination data described in the preceding paragraph. Second, in the 2x2 analyses, there were trends toward an interaction between type of psychological treatment and type of medication, suggesting that the difference between medication and placebo was smaller among patients receiving supportive psychotherapy (binge eating: F=3.85, df=1, 59, p=0.06; vomiting: F=2.92, df=1, 59, p=0.09). DISCUSSION Cognitive-behavioral therapyis widely viewed as the preferred treatment for bulimianervosa (21). Our findings are consistent with previous studies in showing that cognitive-behavioral therapyis significantly more effective than supportive psychotherapy (22, 23). Both psychological treatments were associated with clinically important improvement. Cognitivebehavioral therapy, however, was clearly superior in reducing the frequencies of binge eating and vomiting and in producing improvement on the Eating Attitudes Test, a self-report measure of behavioraland attitudinal features of eating disorders. There was also a trend favoring cognitive-behavioral therapyin reducing some measures of dietary restraint and of abnormal concerns with shape and weight. Additional evidence of the efficacy of cognitivebehavioral therapywas found in the comparisons showing that combining cognitivebehavioral therapywith antidepressant medication was superior to medication alone, while combining supportive psychotherapy with medication was not. Supportive psychotherapy was designed to provide a credible comparison treatment resembling that employed by practitioners and equating for nonspecific factors such as patient expectations and the therapist-patient relationship. This was accomplished. Patients' ratings of the treatment's logic and relevance were similar for cognitive-behavioral therapyand supportive psychotherapy, and, as judged by an independent rater, there were no significant differences between the treatments in the therapists' ability to convey understanding and engage the patient. Therefore, the superiority of cognitive-behavioral therapyover supportive psychotherapy can be attributed to specific therapeutic elements of cognitive-behavioral therapy. Comparative studies of cognitive-behavioral therapyand other psychotherapies have yielded less clear-cut findings. Cognitive-behavioral therapywas generally more effective than a brief psychodynamic psychotherapy (7) and, in the shortterm, than interpersonal psychotherapy (24). However, after 1 year, the outcomes of cognitive-behavioral therapyand interpersonal psychotherapy were similar. Hence, while cognitive-behavioral therapyis currently the best established treatment for bulimianervosa,

additional research on the effects of other forms of psychological treatment is of theoretical and clinical interest. In the current study, the use of antidepressant medication, when combined with psychological treatment, was modestly but significantly superior to placebo in reducing the frequency of binge eating and in improving mood. There were also trends favoring medication over placebo in the reduction of vomiting frequency and on several additional measures of psychopathology. Few other studies have examined advantages of combining medication and psychological treatment for outpatients with bulimianervosa. In the only other placebocontrolled trial of which we are aware, Mitchell et al. (9) found that imipramine, when combined with an intensive form of group psychotherapy, was associated with greater reductions in depression and anxiety than was placebo. However, there was no evidence that antidepressant treatment added to the impressive reduction in binge eating and vomiting produced by group psychotherapy and placebo. Although they did not employ a placebo condition, Agras et al. (11) compared individual cognitive-behavioral therapyalone to the combination of cognitive-behavioral therapyand a modest dose of desipramine for either 16 or 24 weeks. The improvement in binge eating and vomiting of patients receiving both medication and cognitive-behavioral therapywas not significantly greater than that of patients receiving cognitive-behavioral therapyalone. The combination of cognitive-behavioral therapyand 24 weeks of desipramine was superior to cognitive-behavioral therapyalone on only a single measure of dietary restraint. The current study extends these results in finding that on several behavioraland psychological measures, the combination of antidepressant medication and psychological treatment was significantly superior to that of placebo and psychological treatment. It is possible that the benefit of medication was detectable in part because the effect of psychological treatment was somewhat less impressive than that observed in other studies (9, 11), thereby allowing more opportunity for the effect of medication to be observed. It is also likely that the twostage intervention we employed enhanced the benefit. Twothirds of the patients who were assigned to medication eventually received fluoxetine, either because desipramine caused intolerable side effects or because of inadequate improvement. Thus, the second stage of the medication intervention was used by a majority of patients. In a previous placebo-controlled study conducted in the same center with a similar patient population, we examined the effect of a single course of desipramine without psychological treatment (10). The average reduction in binge frequency was 47% among the patients receiving desipramine, and 13% had ceased binge eating at the end of treatment. In the present study, the average reduction in binge frequency among patients receiving medication only was 69%, and 29% ceased binge eating. These results suggest that the two-stage medication intervention was substantially more effective than a single course of a tricyclic antidepressant, the intervention employed in previous studies of medication and psychological treatment for bulimianervosa. At the time this study was conceived, two other groups had reported that psychological treatment of bulimianervosa was superior to medication alone (9, 11 ). The current study was therefore not designed to address this issue and did not include a group that received psychological treatment alone (25). The post hoc finding that the benefit of medication alone was indistinguishable from that of cognitive-behavioral therapyplus placebo was surprising and suggests that the use of a two-stage medication intervention or of fluoxetine or both may improve the efficacy of medication alone treatment relative to that of cognitivebehavioral therapy.

The effects of cognitive-behavioral therapyand of medication on weight are of note. Compared with supportive psychotherapy, cognitive-behavioral therapywas associated with a small but statistically significant weight gain, while, compared to placebo, medication was associated with a small weight loss. Similar findings have been reported in previous studies. Cognitivebehavioral therapyhas been associated with a small amount of weight gain (4, 26). Weight loss associated with fluoxetine is well documented (27, 28), and treatment of bulimianervosa with tricyclic antidepressants has also been found to produce slight weight loss (9, 10, 29). These data suggest that the mechanisms by which cognitive-behavioral therapyand antidepressant medication affect eating behavior in patients with bulimianervosa are different. One specific aim of cognitive-behavioral therapyis to encourage patients to avoid dieting and to consume foods that have been viewed as forbidden. The mechanisms by which antidepressant medications lead to a reduction in binge frequency remain unclear but may include a subtle reduction in appetite. Agras et al. (30) previously presented information suggesting that antidepressant medication led to an increase in dietary restraint among patients with bulimianervosa. In the current study, there was no indication of a medication effect on restraint, while cognitive-behavioral therapytended to reduce restraint as measured by the Eating Disorders Examination. In closing, we note several limitations of the current study. First, our design did not include a psychotherapy-only group. Therefore, the conclusion that medication adds to psychological treatment rests on the assumption, which has been questioned (25), that psychotherapy plus placebo is equivalent to psychotherapy alone. Second, while medication was provided in double-blind fashion for four of the five treatment groups, the presence of side effects may sometimes have compromised this methodological precaution. Similarly, neither clinician nor patient was blind to the type of psychological treatment administered. Third, while a twostage medication intervention more fully reflects the range of possible pharmacological interventions than does a trial using only a single agent, additional medications and more complex strategies are available and might be even more effective. Fourth, the current report is based only on data available at the end of treatment; data on outcome during the succeeding year have not yet been analyzed. Despite these limitations, we believe that the current study has implications for clinical practice. Although studies of other forms of psychotherapy, such as interpersonal psychotherapy, are warranted, our results support the view that at present, cognitivebehavioral therapyis the psychological treatment of choice for bulimianervosa. Our data also suggest that a two-stage medication intervention using fluoxetine adds significantly to the benefits of psychological treatment. However, the modest gains of adding medication to psychotherapy must be weighed against the risk of side effects and the costs of medication and monitoring. Conversely, the modest gains of adding psychological treatment to medication must be examined in the context of the cost and limited availability of cognitivebehavioral therapyfor eating disorders. Such decisions would be greatly aided by knowledge of factors that would allow the clinician to identify those patients most likely to benefit from medication, psychological treatment, or their combination and by information on the most advantageous way of sequencing treatments.
References

Presented at the 148th annual meeting of the American Psychiatric Association, Miami, May 20-25, 1995, and at the Seventh International Conference on Eating Disorders, New York, April 26-28, 1996. Received April 9, 1996; revision received Aug. 14, 1996; accepted Nov.

22, 1996. From the Department of Psychiatry, College of Physicians and Surgeons, Columbia University, and the New York State Psychiatric Institute. Address reprint requests to Dr. Walsh, New York State Psychiatric Institute, Unit 98, 722 West 168th St., New York, NY 10032. Supported in part by NIMH grant MH-38355. Marion Merrell Dow and Eli Lilly and Company provided medication and placebo. The authors acknowledge the assistance of the following individuals in the planning, execution, and analysis of this work: Juli Goldfein, Colleen Hadigan, Tracey Strasser, Sara Rivelli, Kathryn Bleiberg, Pamela Raizman, and Eva Petrova.
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REFERENCES
References

1. Russell G: Bulimianervosa: an ominous variant of anorexia nervosa. Psychol Med 1979; 9:429-448 2. Fairburn CG: A cognitive behaviouralapproach to the treatment of bulimia. Psychol Med 1981;11:707-711 3. Fairburn CG, Norman PA, Welch SL, O'Connor ME, Doll HA, Peveler RC: A prospective study of outcome in bulimianervosa and the long-term effects of three psychological treatments. Arch Gen Psychiatry 1995; 52:304-312 4. Fairburn CG, Kirk J, O'Connor M, Cooper PJ: A comparison of two psychological treatments for bulimianervosa. Behav Res Ther 1986; 24:629-643 5. Freeman CPL, Barry F, Dunkeld-Turnbull J, Henderson A: Controlled trial of psychotherapy for bulimianervosa. BMJ 1988; 296:521-525 6. Fairburn CG, Jones R, Peveler RC, O'Connor ME, Hope RA: Three psychological treatments for bulimianervosa: a comparative trial. Arch Gen Psychiatry 1991; 48:463-469 7. Garner DM, Rockert W, Davis R, Garner MV, Olmsted MP, Eagle M: A comparison of cognitive-behavioraland supportiveexpressive therapyfor bulimianervosa. Am J Psychiatry 1993; 150:3746 8. Walsh BT, Devlin MJ: Psychopharmacology of anorexia netvosa, bulimianervosa, and binge eating, in Psychopharmacology: The Fourth Generation of Progress. Edited by Bloom FE, Kupfer DJ. New York, Raven Press, 1995, pp 1581-1589 9. Mitchell JE, Pyle RL, Eckert ED, Hatsukami D, Pomeroy C, Zimmerman R: A comparison study of antidepressants and structured group psychotherapy in the treatment of bulimianervosa. Arch Gen Psychiatry 1990; 47:149-157

References

10. Walsh BT, Hadigan CM, Devlin MJ, Gladis M, Roose SP: Longterm outcome of antidepressant treatment for bulimianervosa. Am J Psychiatry 1991; 148:1206-1212 11. Agras WS, Rossiter EM, Arnow B, Schneider JA, Telch CF, Raeburn SD, Bruce B, Perl M, Koran LM: Pharmacologic and cognitive-behavioraltreatment for bulimianervosa: a controlled comparison. Am J Psychiatry 1992; 149:82-87 12. Leitenberg H, Rosen JC, Wolf J, Vara LS, Detzer MJ, Srebnik D: Comparison of cognitive-behavior therapyand desipramine in the treatment of bulimianervosa. Behav Res Ther 1994; 32:37-45 13. Fichter MM, Leibl K, Rief W, Brunner E, Schmidt-Auberger S, Engel RR: Fluoxetine versus placebo: a double-blind study with bulimic inpatients undergoing intensive psychotherapy. Pharmacopsychiatry 1991; 24:1-7 14. Cooper Z, Fairburn CG: The Eating Disorder Examination: a semi-structured interview for the assessment of the specific psychopathology of eating disorders. Int J Eating Disorders 1987; 6:1-8 15. Spitzer RL, Williams JBW, Gibbon M: Structured Clinical Interview for DSM-III-R (SCID). New York, New York State Psychiatric Institute, Biometrics Research, 1987 16. Cooper PJ, Taylor MJ, Cooper Z, Fairburn CG: The development and validation of the Body Shape Questionnaire. Int J Eating Disorders 1987; 6:485-494 17. Garner DM, Olmsted MP, Bohr Y, Garfinkel P: The Eating Attitudes Test: psychometric features and clinical correlates. Psychol Med 1982; 12:871-878 18. Beck AT, Ward CH, Mendelson M, Mock J, Erbaugh J: An inventory for measuring depression. Arch Gen Psychiatry 1961; 4:561-571 19. Peveler RC, Fairburn CG: Measurement of neurotic symptoms by self-report questionnaire: validity of the SCL-90R. Psychol Med 1990; 20:873-879 20. Stunkard AJ, Messick S: The three-factor eating questionnaire to measure dietary restraint, disinhibition and hunger. J Psychosom Res 1985; 29:71-83 21. Fairburn CG, Agras WS, Wilson GT: The research on the treat
References

ment of bulimianervosa: practical and theoretical implications, in The Biology of Feast and Famine: Relevance to Eating Disorders. Edited by Anderson GH, Kennedy SH. New York, Academic Press,1992, pp 317-340 22. Agras WS, Schneider JA, Arnow B, Raeburn SD, Telch CF: Cognitive-behavioraland response-prevention treatments for bulimianervosa. J Consult Clin Psychol 1989; 57:215-221

23. Kirkley BG, Schneider JA, Agras WS, Bachman JA: Comparison of two group treatments for bulimia. J Consult Clin Psychol 1985; 53:43-48 24. Fairburn CG, Jones R, Peveler RC, Hope RA, O'Connor M: Psychotherapy and bulimianervosa: longer-term effects of interpersonal psychotherapy, behavior therapy, and cognitivebehavior therapy. Arch Gen Psychiatry 1993; 50:419-428 25. Telch MJ, Lucas RA: Combined pharmacological and psychological treatment of panic disorder: current status and future directions, in Treatment of Panic Disorder: A Consensus Development Conference. Edited by Wolfe BE, Maser JD. Washington, DC, American Psychiatric Press,1994, pp 177-197 26. Fairburn CG, Jones R, Peveler RC: Three psychological treatments for bulimianervosa: a comparative trial. Arch Gen Psychiatry 1991; 48:463-469 27. Levine LR, Rosenblatt S, Bosomworth J: Use of a serotonin reuptake inhibitor, fluoxetine, in the treatment of obesity. Int J Obes 1987; 11(suppl 3):185-190 28. Marcus MD, Wing RR, Ewing L, Kern E, McDermott M, Gooding W: A double-blind, placebo-controlled trial of fluoxetine plus behavior modification in the treatment of obese binge-eaters and non-binge-eaters. Am J Psychiatry 1990; 147:876-881 29. Mitchell JE, Groat R: A placebo-controlled, double-blind trial of amitriptyline in bulimia. J Clin Psychopharmacol 1984; 4:186193 30. Agras WS, Rossiter EM, Arnow B, Telch CF, Raeburn SD, Bruce B, Koran LM: Oneyear follow-up of psychosocial and pharmacologic treatments for bulimianervosa. J Clin Psychiatry 1994; 55:179-18

e Behavior Therapy For Adolescents With Bulimia Nervosa: Results Of Case Series
Lock, James . American Journal of Psychotherapy 59. 3 (2005): 267-81. Turn on hit highlighting for speaking browsers Turn off hit highlighting

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This article reviews the types of adjustments needed to an adult protocol of cognitivebehavioral therapy (CBT) for bulimia nervosa (BN) to make it more acceptable to an adolescent population. Employing developmental principles as well as clinical experience
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This article reviews the types of adjustments needed to an adult protocol of cognitivebehavioral therapy(CBT) for bulimianervosa (BN) to make it more acceptable to an adolescent population. Employing developmental principles as well as clinical experience as guidelines, these modifications include the involvement of parents, recognition of the interaction of treatment with normal adolescent developmental tasks, and allowances for typical cognitiveand emotional immaturity on treatment procedures. Outcomes from a series of adolescents with BN who were treated with this modified-CBT approach show results similar to those expected in adult populations treated using CBT. INTRODUCTION Psychological interventions with youth work best when they mesh with normal developmental processes (Holmbeck et al., 2000; Kendall, 1993). However, in a recent review of treatment studies of adolescents, Holmbeck et al. found that relatively few (26%) even mentioned adolescent development and identified only one study that examined age as a moderator of treatment effects (Holmbeck et al., 2000). Cognitive-Behavioral Therapy(CBT) has been modified for use with younger patients with depression and anxiety disorders and appears to be effective for these conditions with patients in this age group (Brent et al., 1997; Kendall, 1994). However, there is no systematic research and no comprehensive descriptions of how best to adjust CBT for adolescents with bulimianervosa (BN), even though substantial evidence supports the efficacy of this form of therapyfor BN in adults (Agras, Walsh, Fairburn, Wilson, & Kraemer, 2000; C. G. Fairburn et al., 1991). The purpose of this article is to describe how to adjust CBT for adolescents with BN. General principles and illustrations of specific modifications are provided. BACKGROUND Both clinical and research data suggest that adolescents differ from adults in a number of ways that might have an impact on the acceptability and efficacy of psychotherapy (Feldman & Elliott, 1990). Because of developmental differences between adults and adolescents, treatments need to be adjusted to better match the needs of younger patients (Shirk, 1999; Kendall, Learner, & Craighead, 1984). Adolescence is a transitional developmental period between childhood and adulthood that is characterized by more biological, psychological, and social role changes than any other stage of life except infancy (Feldman & Elliott, 1990). The three main changes of adolescence are physiologic maturity (puberty), increased cognitivecapacity (abstract thinking), and increased social maturity through role redefinition. Compared with adults, adolescents have more limited abstracting abilities and poorer executive functioning, goal-setting, and planning abilities (Sternberg, 1977; Sternberg &

Nigro, 1980). This limits their perspectives on the hazards of their behaviors and decreases motivation to seek and participate in treatment. As a result of these differences adolescents may have a more limited capacity to utilize therapiesthat depend on insight, emotional processing, self-evaluation and goal-setting (Izard & Harris, 1995). In addition, autonomy struggles, as well as the high value placed on peer relationships, can compromise treatment collaboration, treatment adherence, and ultimately treatment effectiveness (Savin-Williams & Bernt, 1990; Trickett & Schmid, 1993). Adolescents may generalize autonomy struggles from parents to other adults, including therapists, thus compromising the development of a productive therapeutic collaboration. In addition, autonomy struggles (which are often severe enough to require therapeutic attention) with parents and other authority figures make focused psychological treatments for BN difficult to maintain. Similarly, adolescents with difficulties in peer relationships (e.g. dating or other problems with social performance and role) can derail a focused treatment by forcing therapeutic attention to these problems at the expense of time spent focused on the eating disorder. Because of these types of predictable developmental differences, adolescents are likely to be difficult to engage, motivate, and keep focused in psychotherapy. Nonetheless, there are ways that psychotherapeutic strategies can be adapted to be more suitable for adolescents, thereby increasing the likelihood that these treatments will be acceptable and effective. Key to the application of any psychological treatment to a younger cohort is developmental expertise in the area of adolescence. The following are key components of such a knowledge and experiential base: 1) an understanding of the biological/pubertal changes; psychological/cognitivechanges; changes in emotional awareness and processing; 2) an appreciation of the changes in and importance of interpersonal relationships, including family relationships, peer relationships and the school; 3) an understanding of the developmental tasks of adolescence including the need for increased autonomy, development of individual identity, and an increased capacity and need for interpersonal intimacy outside the family. On the other hand, one of the major differences between adolescents and adults is their continued involvement with and dependence on their families in both an emotional and practical sense. Treatment studies for adolescent AN suggest that family involvement may be beneficial. One small case series of adolescents with BN treated with family therapyalso supported this view (Dodge, Hodes, Eisler, & Dare, 1995; Eisler et al., 2000; Le Grange, Eisler, Dare, & Russell, 1992; Le Grange, Lock, & Dymek, 2003; Lock, 2002; Russell, Szmukler, Dare, & Eisler, 1987). An appreciation of these important developmental considerations serves as the foundation upon which therapists decide how best to adjust psychotherapy so that it is appropriate and acceptable for a particular adolescent's developmental needs and current trajectory. METHODS SAMPLE We conducted a pilot program of CBT adjusted as described below with a series of 34 adolescents with BN over an 18-month period. All were female. These patients ranged in age from 12 to 18 years (mean 15.8 years). Approximately 55% were from divorced families. Approximately 32% were from minority groups (8% Asian, 10% Hispanic, 4% AfricanAmerican, and 10% multi-racial). Comorbid psychiatric illnesses were common in the group (depressive disorders = 25%; anxiety disorders = 7%). Antidepressants (selective serotonin reuptake inhibitors) were used to treat these co-morbid conditions in 20% of subjects. Dose

levels of these antidepressants were not titrated up to dosages known to be effective for bulimia. ASSESSMENT PROCEDURE Patients were diagnosed using DSM-IV criteria by the author of this report using a standard clinical interview of a patients and parents. Within treatment and at end of treatment, rates of binge eating and purging were gathered via self-report to therapists providing CBT. Patients were followed by pediatricians with specialized training in adolescence during treatment to ensure that the patients were medically safe for outpatient treatment (Lock, 1999). CBT MODIFIED FOR ADOLESCENTS WITH BN CBT for adults with BN, as conceived by Fairburn et al. (1993), is a three-stage treatment program consisting of about 20 sessions over a period lasting approximately six months (Fairburn, 1981; Fairburn & Hay, 1992; Fairburn, Marcus, & Wilson, 1993). The first stage is focused primarily on normalizing patterns of eating. The second stage is directed principally at correcting distorted thoughts and beliefs. The third stage is a short one, aimed at preventing relapse by anticipatory problem solving. The manualized version of CBT for adolescents follows a similar overall course with identical aims. The main differences are described and illustrated below. Stage 1: The first stage of CBT for BN, which usually consists of about 10 sessions, is modified for adolescents, mainly to address problems related to motivation for treatment, collaboration in treatment, and understanding of the therapeutic process. Development of rapport and collaboration with adolescents often requires special efforts on the part of therapists. Therapists should anticipate that adolescents are slower than adults when accepting therapists as helping figures and at collaborating in treatment. To promote this working alliance, therapists should express overt interest in the adolescents' experience, perspective on their problems, treatment, and social and family context. Therapists also need to develop the ability to tolerate occasional adolescent lack of focus and need for attention to other aspects of life (e.g. friends, school) while keeping within the CBT model. Therapists often find it useful to have frequent contact with adolescent patients at the start of treatment, so brief telephone conversations and sessions scheduled close together can be used to support therapeutic engagement. Therapists tend to need to spend additional time on educating adolescents about the purpose and process of therapy. In order to illustrate how psychotherapy (whatever the type) is supposed to work, therapists may employ diagrams, other illustrations, and an array of concrete examples. When presenting these models, therapists must carefully sequence information and frequently stop to check with patients to make sure that they are following. Additionally, therapists must choose interventions that respect the adolescents' ability to take perspective on themselves or situations, by frequently assessing their understanding. To support these efforts at being clear, therapists will often use less abstract language and employ age-relevant examples. Teaching adolescents about the physical and psychological problems of BN as well as the model of treatment used in CBT for BN is a cornerstone of the initial treatment phase. We have found that adolescents often have difficulty acknowledging BN is a problem because they have not personally experienced any significant problems with their behaviors. In their efforts at educating adolescents therapists need to provide examples

of problems that the youngsters can relate to. Some examples of information particularly relevant to adolescents include: If friends or romantic partners discover you have BN, you might be embarrassed and humiliated; BN often makes it difficult to participate in many social gatherings (because they involve eating); Chronic purging can lead to swollen salivary glands and punctate lesions in the eyes, which are unattractive, Chronic binge eating leads to weight gain (which is the opposite of the adolescent's goal). On a practical level, therapists working with adolescents should expect that psycho-education about BN will require reiteration during treatment. Although this is also true with older patients, it is particularly likely that educational efforts at the start of treatment with adolescents will require reinforcement throughout the first two stages of treatment. CBT FOR BN Self-monitoring of eating and compensatory behaviors (purging, binge eating, etc.) through keeping food and weight records is a key component of CBT for BN. It is sometimes challenging for adolescents to keep logs because this involves both the ability to self-observe, as well as the effort involved in writing down these observations. Therapists should expect that adolescents will be less skilled at self-monitoring than adults, and thus, therapists will need to spend extra time focusing on the importance of keeping food records and on helping adolescents in completing samples. In the beginning of treatment, therapists working with adolescents with BN have sometimes found it necessary to complete the teens' food records for them during the sessions. Although this strategy ultimately is not ideal-the most accurate records are those completed at the time of eating, binge eating, or purging-completing records during sessions helps get the process started or maintains the process if records were not completed between sessions. How to help adolescents with food logs can be illustrated through work with Delia, a 14-yearold patient with BN. Delia refused to keep food records. She said she was embarrassed to have them in her purse and that she didn't have time (or could not remember) to write them up until it was too late. Her therapist patiently asked Delia to complete a food record based on her eating behaviors from the previous day during sessions. Delia was willing to do this. After carefully going over the food record, Delia was slightly more open to food record keeping, but did not keep a record for the next session. This pattern continued, with the therapist patiently persisting in explaining the importance of keeping these records and illustrating to Delia what could be learned from them. Over a period of several weeks, Delia occasionally completed a food record, a task for which she was praised highly. Throughout this negotiation, the therapist avoided criticizing Delia, instead emphasizing the need for records. Parental involvement may be needed to keep adolescents motivated for treatment. In addition, parents need to know something of what occurs in therapy(within the bounds of confidentiality) in order to support it. We found that many (though not all) adolescents

respond well to having their parents involved in meal planning and after-meal monitoring as a way to assist them in decreasing binge-eating and purging episodes. Some parents are asked to make sure their child comes to therapyand to provide regularly schedules meals (three meals and two snacks), which helps prevent binge eating by limiting access to trigger foods. These parents are asked to stay with the patient for a period of time after the mean to prevent purging by the adolescent. How parental support can make a difference in CBT for BN in adolescents is seen in Tonya's case. As typical of many patients with BN, Tonya's pattern was to limit her food intake all morning and through the early afternoon. However, when she got home from school, she would begin to snack; this usually escalated into a binge-eating episode and subsequent purging. The importance of changing this eating pattern was emphasized to Tonya, and various methods to support this change were discussed. Ultimately, Tonya decided it would help her reestablish a healthy eating pattern if her mother to ate breakfast with her and was at home with her after school. Although this meant that Tonya's mother needed to take a leave from work, her presence helped change Tonya's eating patterns; reducing episodes of binge eating and purging. Over the next two months, Tonya was helped to be more independent in these areas and her mother returned to her usual routines. Problems in school settings and academic performance difficulties may also complicate treatment. Therapists working with adolescents need to familiarize themselves with the school context (structure, eating schedules, and social activities) so that they can better understand how school influences eating attitudes and behaviors. On a practical level, therapists often need to provide excuses for their adolescent patients who need to miss class for psychological or medical treatments. For example, 17-year-old Rhoda's schedule at school changed daily, and on several days a week her lunch period was scheduled for after 2:00 P.M. Rhoda's food logs suggested that this long delay between breakfast and lunch supported the development of binge eating later in the afternoon. The therapist worked with Rhoda's parents and the school to change Rhoda's schedule so that she could eat at regular intervals and to ensure that she ate lunch at midday. Adolescents, like adults, have other problems besides BN. For adolescents, though, these other problems may be more difficult to defer. This makes maintaining a strict therapeutic focus on BN more challenging. Therapists working with adolescents should expect to be more flexible overall and more tolerant of these diversions, while still maintaining a therapeutic focus on CBT for BN. To do this, therapists must set the therapeutic agenda at the beginning of each session. They may set aside a prescribed amount of time for attention to other problems the adolescent needs to discuss. Usually, these set-aside times last no more than 10 minutes, scheduled at the beginning or end of the treatment session. However, some of these common problems can be perceived incorrectly by the patient, as the following vignette illustrates: Rachel believed her boyfriend broke up with her because she was overweight. The therapist asked Rachel if she knew of other couples who had broken up. Rachel said she did. The therapist then asked Rachel if she could remember why these couples dissolved. Rachel came up with a list of reasons, none of which included weight. As they further examined the implication of this, Rachel struggled with seeing herself in the same category as other girls. She said she was fat, they weren't. She had difficulty identifying other possibilities for the break up with her boyfriend. Again, the therapist asked Rachel to envision each of her friends. The therapist helped her to see that her friends' weights varied considerably, some

were heavier than Rachel, and some were thinner. And in no case was the girl's weight the reason for the break up. Related to the problem of maintaining a therapeutic focus, is the potential for crises to disrupt treatment. Such crises must be addressed through an assessment of their impact on the appropriateness and practicality of maintaining CBT for BN as the treatment. For example, if an adolescent reports being sexually abused by a parent, it is likely that CBT treatment for BN will need to be interrupted until after this crisis is addressed. On the other hand, crises related to peer relationships, usual family struggles, or school performance may briefly require the therapist's attention, but once addressed, CBT with a focus on BN can resume. Stage 2: The second stage of CBT treatment usually spans seven or eight sessions. One aim of the second stage of treatment is to continue to monitor, progress toward, or maintenance of a regular pattern of eating. The next goal is to help the patient delineate the nature of feared and avoided foods, and to gradually reintroduce-with the help of parents-some of these foods into the diet. In addition, this stage introduces cognitiverestructuring and problem-solving techniques to address common triggers for binge eating. Food records and self-monitoring in Stage 2 are focused on the thoughts, emotional responses, and beliefs that commonly are distorted among bulimic patients. A common problem for the therapist during this stage is finding ways to help adolescents refine their self-observations, especially as these observations now focus on the emotional and social context as they relate to eating, binge eating, and purging behaviors and thoughts. Adolescents sometimes struggle with identifying, labeling, and processing their emotional states. Again, this is true for older patients as well, but with adolescents, therapists will likely need to facilitate this process more. For example, it is not uncommon for adolescents to say they "don't know" what they felt just before binge eating. Therapists sometimes find it necessary to "coach" teen-aged patients by presenting options to them and helping them to elaborate on the context. The kinds of questions therapists might ask are: "What were you doing just before you started to binge?" " Who was with you?" "Do you remember feeling angry, sad, or bored earlier in the day? " "What are you like when you feel sad, angry, or bored?" "Were you feeling like that before you binge ate?" These questions are designed to help youngsters develop self-observation skills and to promote better understanding of emotional states. With increased awareness and understanding, adolescents are more likely to make the connection needed for accurate emotional self-monitoring. Principle targets of Stage 2 are distorted thoughts and beliefs about the body and eating. Many adolescents (like some adults) are unable to use formal cognitive-restructuring techniques without a lot of therapist assistance. This is the case because cognitiverestructuring requires perspective taking, generation of a range of alternatives, and the use of judgment about each option's viability and value. When using cognitiverestructuring techniques with adolescents, the burden of helping adolescents to use perspective, develop alternatives, and assess alternatives falls to the therapist. Therapists experienced with adolescent patients recognize that the need to do the groundwork on such efforts, especially at first. Therapists need to avoid "taking over" but will be very active in these cognitiverestructuring processes. Problem solving is commonly used when formal cognitiverestructuring strategies are too difficult for or are rejected by patients. Problem solving is more direct, appeals to the immediate needs of the adolescents, requires less in the way of judgment, and is practical. CBT therapists working with adolescents have found that

problem solving is more likely to be employed with this age group than formal cognitiverestructuring. An example of this approach is with Rachel, a 13 year old with BN. When Rachel broke up with her boyfriend, who was the only person outside her family who know about her eating disorder, she felt she had no where to turn. She isolated herself from both her friends and family and increased binge eating and purging behaviors. In session she reported she had no other supports-she was angry with her mother and her brother, both of whom she felt tried to control her. She did not want any of tell any friends who were potential supports because of the shame she felt about bulimia. In examining the problem of how Rachel could find emotional support, the therapist worked with her to identify which of the options she considered to be least objectionable and why. In reviewing her need for support. Rachel felt that her mother would be the person who was most available and who was most willing to help her. This meant Rachel had to identify for her mother the ways she could be helpful as well as ways she could potentially make matters worse by being too intrusive. In a meeting with Rachel and her mother, the therapist helped Rachel explain her need for support now that her she had broken up with her boyfriend, but more important Rachel explained to her mother how she could help without making Rachel resentful and angry. Behavioralexperiments are employed in CBT to help patients extend their mastery over food, eating, and temptations to binge eat and purge. Often these behavioralexperiments involve patients putting themselves in situations that are challenging (e.g. buffet meals, bakeries, eating with friends or romantic partners). Adolescents sometimes have difficulty carrying out behavioralexperiments because they are practically and psychologically less independent. That is, adolescents often do not control their time and situations to the same degree as adults. For example, adolescents have meal times are set by parents or school authorities and food choices often are limited to those made available at the school and or by adults in the home setting. In addition, many adolescents (as is expected developmentally) are inexperienced with taking on independent challenges and need support in doing so. Therefore, therapists working with adolescents often need to take a more gradual approach to recommending such experiments. That is, therapists must start slow and proceed with small steps. Therapists might also consider being a part of the experiments, for example by asking patients to bring feared food to sessions, supporting adolescents as they eat the foods, and assisting the patient in making self-observations afterwards. Therapists have also found it helpful to ask parents to assist their adolescents in behavioralexperiments. In these cases, therapists, patients, and parents decide together how this support is best structured. It may be as simple as informing the parent about the planned experiment and having the parent ask their son or daughter how it's going. Alternatively, it may be that the parents are asked to be present during the experiment and to actively support the teenager during an experiment. For example, after the son or daughter tries a feared food, the parent can volunteer to take the patient shopping, provide some other type of distraction, or to sit with the patient to support him or her as he or she tries to manage feelings of anxiety. Parents also can be helpful in these experimental activities by contributing their own observations of patient behaviors. Although the parents are not involved in the specific activities of problem solving, they provide insight and assistance in in a family context. Therapists need to educate parents about these thought processes so they can assist their children at home. Stage 3: The third stage is primarily concerned with maintaining the change following treatment. Progress is reviewed, and realistic expectations are established. Relapse prevention

strategies are taught to patients to prepare for future setbacks. In general, adolescents have had less experience with chronic BN, therefore, the possibility of relapse (which generally is well known to adults with BN) is less experientially appreciated by adolescents. Therapists should expect adolescents to minimize the potential for relapse. Therefore, therapists should focus on potential relapse in ways relevant to the adolescent, particularly through an assessment of how adolescents' developmental challenges and tasks may threaten progress in controlling BN. This attitude is exemplified by Lucinda. Lucinda had done well in CBT and had reported no problems with binge eating or purging for several months. Her focus on weight and body shape , as a source of her self-esteem also diminished. However, she remained dissatisfied with her weight and intermittently restricted food intake for six to eight hours each day. Lucinda was unconcerned about possible relapse"I'm over that. It's too stupid. I've learned how to control it." However, the therapist gently but firmly reminded Lucinda of how she had felt she could control it before and that her current dieting still put her at risk for relapse. The therapist encouraged Lucinda to change her episodic severe dieting, but not to feel that all was lost if she should binge eat and purge. Lucinda continued to maintain that relapse was unlikely, but was open to understanding that the possibility existed. The therapist also discussed relapse with Lucinda's worried parents. The therapist reassured them that even if Lucinda had an episode of bulimic behavior in the future, this did not necessarily mean that she would again become bulimic. They were encouraged to support Lucinda by keeping a watchful eye on her and if problems arose, to encourage her to use what she had learned to stop the behaviors from becoming reentrenched. A special focus of CBT for adolescents with BN is the review of progress on adolescent issues and how BN and treatment affect these. Therapists need to focus on assessing which developmental tasks of adolescence patients have accomplished, and then help patients and parents identify problem areas that they may wish to focus on, particularly as they relate to prevention of a BN relapse. For example, 18-year-old Tomi was preparing to attend college at some distance from home. Her parents were worried about a recurrence of BN at college since they had read that BN was an "epidemic" on college campuses. The therapist helped to assure both Tomi and her parents that she was prepared to leave home and that the BN was well controlled. The therapist informed Tomi and her parents that most patients treated with CBT continue to do well, but advised Tomi to contact the student health center at her college to identify resources available to her should she have renewed symptoms. Termination issues with adolescents may be somewhat more complex than with adults. The treatment relationship usually entails the family, especially the parents. In addition, adolescents can develop especially strong emotional connections to their therapists, so therapists working with this age group should be prepared to address these stronger attachments. On the other hand, many adolescents are prepared to move onto other aspects of their lives, such a college, a dating relationship, etc., so that the loss of a therapist seems of little consequence. Therefore, therapists working with adolescents should expect a range of responses to ending treatment. However, because parents (and sometimes other family members) have been involved, some time should be devoted to terminating with them as well. It is likely that adolescents who have benefited from CBT for BN will have developed a strong attachment to their therapists and therefore, therapists should expect that even after formal termination, patients may contact them from time to time. RESULTS

At baseline, the rate of binge eating and purging ranged from two to 21 episodes per week with a mean of 15.8 episodes per week. At end of treatment, the abstinence rate was 56% and mean episodes had been reduced to 3.4 episodes per week (range 0-21). Only 6 patients (15%) did not complete a minimum of 10 weeks or 6 sessions of therapy(18%). Data were obtained at end of treatment. See Table I. DISCUSSION These data suggest that CBT for BN adjusted for adolescents is acceptable and suggests that response rates are similar to those in adults (i.e. decreases in the rate of binge eating and purging and the abstinence rates are very similar to that found in adults treated with CBT). In applying CBT for adolescent BN, it is of central importance that therapists have both knowledge of and experience with adolescents. For therapists to engage adolescents effectively throughout the treatment process, it is vital that therapists understand the developmental challenges of adolescence and their implications. Modifications applied to CBT for BN in adolescents include the following: 1) increased intensity of contact early in treatment to build the treat ment alliance; 2) education and involvement of parents and other significant friends or partners when indicated; 3) simplification of language and communication style; 4) flexibility in the use of homework and food logs, especially early in treatment; 5) flexibility in the use of treatment time to examine other important, but less directly relevant issues (e.g. crises with friends, parents, and other predictable developmental problems). None of these changes alters the fundamental features of CBT as designed for adults, but it is likely they increase the chance that treatment will be taken up, adhered to, and completed. Attention to the external context of the adolescent's life (family and school) is an important aspect of working with most teenagers. Therapists working with adolescents often find it necessary to educate and involve (to various degrees) parents and other family members in therapyto support motivation and to enhance the milieu for therapeutic change. Therapists working with adolescents, regardless of the specific focus of therapy, should expect to devote some attention to peers and school environments because these arenas are important concerns for adolescents. In addition, some focus on the relationship of therapeutic progress to the mastery of adolescent tasks (autonomy, identity development, and work and education activities) should be expected. Therapists should expect that work on these issues will relate to other focused therapystrategies. For example, autonomy concerns may interfere with treatment acceptance and limit family support unless the therapist is able to separate these issues. Anxiety or problems related to sexual development and experimentation are also common problems. Educational goals, such as attending college, can also become a paramount issue for some older adolescents and may require attention by therapists. Therapists should be comfortable

with these developmental issues and support a circumscribed examination of them in the context of more focused therapy(i.e. CBT). There are a number of important limitations to our current report. The sample used was a convenient clinical sample to our center, which is a tertiary treatment center for adolescents with eating disorders. In addition, it is a small case series and outcomes are limited to specific behavioralmeasures and do not include measures of psychological preoccupations around eating, weight, and shape which would be desirable. Therapists who provided treatment were all trained in CBT and supervised by the author of this report, which may also limit generalizabiliy of the findings. Finally, enhanced versions of CBT have been developed that include treatment modules related to self-esteem, perfectionism, and social problems that might be particularly relevant for adolescents with BN, but the treatment program used in this study did not incorporate these additional treatments.(C. G. Fairburn, Cooper, & Safran, 2002) In sum, although CBT is the treatment of choice for adults with BN, it has not been studied among adolescents with BN. This article describes a way to adjust CBT for BN so that it is more acceptable to adolescents and their families. The principles described here are also likely to be useful in making adjustments to other types of therapy, though the particulars would vary based on the specific strategies of the approach. An approach that is developmentally appropriate and manualized will make it possible to conduct clinical trials to test empirically the usefulness of CBT for adolescents with BN. Currently no such studies have been published, though they are much needed to help guide clinicians in their work with adolescents with BN.

Headnote This article reviews the types of adjustments needed to an adult protocol of cognitivebehavioral therapy(CBT) for bulimianervosa (BN) to make it more acceptable to an adolescent population. Employing developmental principles as well as clinical experience as guidelines, these modifications include the involvement of parents, recognition of the interaction of treatment with normal adolescent developmental tasks, and allowances for typical cognitiveand emotional immaturity on treatment procedures. Outcomes from a series of adolescents with BN who were treated with this modified-CBT approach show results similar to those expected in adult populations treated using CBT. INTRODUCTION Psychological interventions with youth work best when they mesh with normal developmental processes (Holmbeck et al., 2000; Kendall, 1993). However, in a recent review of treatment studies of adolescents, Holmbeck et al. found that relatively few (26%) even mentioned adolescent development and identified only one study that examined age as a moderator of treatment effects (Holmbeck et al., 2000). Cognitive-Behavioral Therapy(CBT) has been modified for use with younger patients with depression and anxiety disorders and appears to be effective for these conditions with patients in this age group (Brent et al., 1997; Kendall, 1994). However, there is no systematic research and no comprehensive descriptions of how best to adjust CBT for adolescents with bulimianervosa (BN), even though substantial

evidence supports the efficacy of this form of therapyfor BN in adults (Agras, Walsh, Fairburn, Wilson, & Kraemer, 2000; C. G. Fairburn et al., 1991). The purpose of this article is to describe how to adjust CBT for adolescents with BN. General principles and illustrations of specific modifications are provided. BACKGROUND Both clinical and research data suggest that adolescents differ from adults in a number of ways that might have an impact on the acceptability and efficacy of psychotherapy (Feldman & Elliott, 1990). Because of developmental differences between adults and adolescents, treatments need to be adjusted to better match the needs of younger patients (Shirk, 1999; Kendall, Learner, & Craighead, 1984). Adolescence is a transitional developmental period between childhood and adulthood that is characterized by more biological, psychological, and social role changes than any other stage of life except infancy (Feldman & Elliott, 1990). The three main changes of adolescence are physiologic maturity (puberty), increased cognitivecapacity (abstract thinking), and increased social maturity through role redefinition. Compared with adults, adolescents have more limited abstracting abilities and poorer executive functioning, goal-setting, and planning abilities (Sternberg, 1977; Sternberg & Nigro, 1980). This limits their perspectives on the hazards of their behaviors and decreases motivation to seek and participate in treatment. As a result of these differences adolescents may have a more limited capacity to utilize therapiesthat depend on insight, emotional processing, self-evaluation and goal-setting (Izard & Harris, 1995). In addition, autonomy struggles, as well as the high value placed on peer relationships, can compromise treatment collaboration, treatment adherence, and ultimately treatment effectiveness (Savin-Williams & Bernt, 1990; Trickett & Schmid, 1993). Adolescents may generalize autonomy struggles from parents to other adults, including therapists, thus compromising the development of a productive therapeutic collaboration. In addition, autonomy struggles (which are often severe enough to require therapeutic attention) with parents and other authority figures make focused psychological treatments for BN difficult to maintain. Similarly, adolescents with difficulties in peer relationships (e.g. dating or other problems with social performance and role) can derail a focused treatment by forcing therapeutic attention to these problems at the expense of time spent focused on the eating disorder. Because of these types of predictable developmental differences, adolescents are likely to be difficult to engage, motivate, and keep focused in psychotherapy. Nonetheless, there are ways that psychotherapeutic strategies can be adapted to be more suitable for adolescents, thereby increasing the likelihood that these treatments will be acceptable and effective. Key to the application of any psychological treatment to a younger cohort is developmental expertise in the area of adolescence. The following are key components of such a knowledge and experiential base: 1) an understanding of the biological/pubertal changes; psychological/cognitivechanges; changes in emotional awareness and processing; 2) an appreciation of the changes in and importance of interpersonal relationships, including family relationships, peer relationships and the school; 3) an understanding of the developmental tasks of adolescence including the need for increased autonomy, development of individual identity, and an increased capacity and need for interpersonal intimacy outside the family. On the other hand, one of the major differences between adolescents and adults is their continued involvement with and dependence on their families in both an emotional and practical sense. Treatment studies for adolescent AN suggest that family involvement may be beneficial. One small case series of adolescents with BN treated with family therapyalso supported this view (Dodge, Hodes, Eisler, & Dare, 1995; Eisler et al., 2000; Le Grange, Eisler, Dare, & Russell,

1992; Le Grange, Lock, & Dymek, 2003; Lock, 2002; Russell, Szmukler, Dare, & Eisler, 1987). An appreciation of these important developmental considerations serves as the foundation upon which therapists decide how best to adjust psychotherapy so that it is appropriate and acceptable for a particular adolescent's developmental needs and current trajectory. METHODS SAMPLE We conducted a pilot program of CBT adjusted as described below with a series of 34 adolescents with BN over an 18-month period. All were female. These patients ranged in age from 12 to 18 years (mean 15.8 years). Approximately 55% were from divorced families. Approximately 32% were from minority groups (8% Asian, 10% Hispanic, 4% AfricanAmerican, and 10% multi-racial). Comorbid psychiatric illnesses were common in the group (depressive disorders = 25%; anxiety disorders = 7%). Antidepressants (selective serotonin reuptake inhibitors) were used to treat these co-morbid conditions in 20% of subjects. Dose levels of these antidepressants were not titrated up to dosages known to be effective for bulimia. ASSESSMENT PROCEDURE Patients were diagnosed using DSM-IV criteria by the author of this report using a standard clinical interview of a patients and parents. Within treatment and at end of treatment, rates of binge eating and purging were gathered via self-report to therapists providing CBT. Patients were followed by pediatricians with specialized training in adolescence during treatment to ensure that the patients were medically safe for outpatient treatment (Lock, 1999). CBT MODIFIED FOR ADOLESCENTS WITH BN CBT for adults with BN, as conceived by Fairburn et al. (1993), is a three-stage treatment program consisting of about 20 sessions over a period lasting approximately six months (Fairburn, 1981; Fairburn & Hay, 1992; Fairburn, Marcus, & Wilson, 1993). The first stage is focused primarily on normalizing patterns of eating. The second stage is directed principally at correcting distorted thoughts and beliefs. The third stage is a short one, aimed at preventing relapse by anticipatory problem solving. The manualized version of CBT for adolescents follows a similar overall course with identical aims. The main differences are described and illustrated below. Stage 1: The first stage of CBT for BN, which usually consists of about 10 sessions, is modified for adolescents, mainly to address problems related to motivation for treatment, collaboration in treatment, and understanding of the therapeutic process. Development of rapport and collaboration with adolescents often requires special efforts on the part of therapists. Therapists should anticipate that adolescents are slower than adults when accepting therapists as helping figures and at collaborating in treatment. To promote this working alliance, therapists should express overt interest in the adolescents' experience, perspective on their problems, treatment, and social and family context. Therapists also need to develop the ability to tolerate occasional adolescent lack of focus and need for attention to other aspects of life (e.g. friends, school) while keeping within the CBT model. Therapists often find it useful to have frequent contact with adolescent patients at the start of treatment,

so brief telephone conversations and sessions scheduled close together can be used to support therapeutic engagement. Therapists tend to need to spend additional time on educating adolescents about the purpose and process of therapy. In order to illustrate how psychotherapy (whatever the type) is supposed to work, therapists may employ diagrams, other illustrations, and an array of concrete examples. When presenting these models, therapists must carefully sequence information and frequently stop to check with patients to make sure that they are following. Additionally, therapists must choose interventions that respect the adolescents' ability to take perspective on themselves or situations, by frequently assessing their understanding. To support these efforts at being clear, therapists will often use less abstract language and employ age-relevant examples. Teaching adolescents about the physical and psychological problems of BN as well as the model of treatment used in CBT for BN is a cornerstone of the initial treatment phase. We have found that adolescents often have difficulty acknowledging BN is a problem because they have not personally experienced any significant problems with their behaviors. In their efforts at educating adolescents therapists need to provide examples of problems that the youngsters can relate to. Some examples of information particularly relevant to adolescents include: If friends or romantic partners discover you have BN, you might be embarrassed and humiliated; BN often makes it difficult to participate in many social gatherings (because they involve eating); Chronic purging can lead to swollen salivary glands and punctate lesions in the eyes, which are unattractive, Chronic binge eating leads to weight gain (which is the opposite of the adolescent's goal). On a practical level, therapists working with adolescents should expect that psycho-education about BN will require reiteration during treatment. Although this is also true with older patients, it is particularly likely that educational efforts at the start of treatment with adolescents will require reinforcement throughout the first two stages of treatment. CBT FOR BN Self-monitoring of eating and compensatory behaviors (purging, binge eating, etc.) through keeping food and weight records is a key component of CBT for BN. It is sometimes challenging for adolescents to keep logs because this involves both the ability to self-observe, as well as the effort involved in writing down these observations. Therapists should expect that adolescents will be less skilled at self-monitoring than adults, and thus, therapists will need to spend extra time focusing on the importance of keeping food records and on helping adolescents in completing samples. In the beginning of treatment, therapists working with adolescents with BN have sometimes found it necessary to complete the teens' food records for them during the sessions. Although this strategy ultimately is not ideal-the most accurate records are those completed at the time of eating, binge eating, or purging-completing records during sessions helps get the process started or maintains the process if records were not completed between sessions.

How to help adolescents with food logs can be illustrated through work with Delia, a 14-yearold patient with BN. Delia refused to keep food records. She said she was embarrassed to have them in her purse and that she didn't have time (or could not remember) to write them up until it was too late. Her therapist patiently asked Delia to complete a food record based on her eating behaviors from the previous day during sessions. Delia was willing to do this. After carefully going over the food record, Delia was slightly more open to food record keeping, but did not keep a record for the next session. This pattern continued, with the therapist patiently persisting in explaining the importance of keeping these records and illustrating to Delia what could be learned from them. Over a period of several weeks, Delia occasionally completed a food record, a task for which she was praised highly. Throughout this negotiation, the therapist avoided criticizing Delia, instead emphasizing the need for records. Parental involvement may be needed to keep adolescents motivated for treatment. In addition, parents need to know something of what occurs in therapy(within the bounds of confidentiality) in order to support it. We found that many (though not all) adolescents respond well to having their parents involved in meal planning and after-meal monitoring as a way to assist them in decreasing binge-eating and purging episodes. Some parents are asked to make sure their child comes to therapyand to provide regularly schedules meals (three meals and two snacks), which helps prevent binge eating by limiting access to trigger foods. These parents are asked to stay with the patient for a period of time after the mean to prevent purging by the adolescent. How parental support can make a difference in CBT for BN in adolescents is seen in Tonya's case. As typical of many patients with BN, Tonya's pattern was to limit her food intake all morning and through the early afternoon. However, when she got home from school, she would begin to snack; this usually escalated into a binge-eating episode and subsequent purging. The importance of changing this eating pattern was emphasized to Tonya, and various methods to support this change were discussed. Ultimately, Tonya decided it would help her reestablish a healthy eating pattern if her mother to ate breakfast with her and was at home with her after school. Although this meant that Tonya's mother needed to take a leave from work, her presence helped change Tonya's eating patterns; reducing episodes of binge eating and purging. Over the next two months, Tonya was helped to be more independent in these areas and her mother returned to her usual routines. Problems in school settings and academic performance difficulties may also complicate treatment. Therapists working with adolescents need to familiarize themselves with the school context (structure, eating schedules, and social activities) so that they can better understand how school influences eating attitudes and behaviors. On a practical level, therapists often need to provide excuses for their adolescent patients who need to miss class for psychological or medical treatments. For example, 17-year-old Rhoda's schedule at school changed daily, and on several days a week her lunch period was scheduled for after 2:00 P.M. Rhoda's food logs suggested that this long delay between breakfast and lunch supported the development of binge eating later in the afternoon. The therapist worked with Rhoda's parents and the school to change Rhoda's schedule so that she could eat at regular intervals and to ensure that she ate lunch at midday. Adolescents, like adults, have other problems besides BN. For adolescents, though, these other problems may be more difficult to defer. This makes maintaining a strict therapeutic focus on BN more challenging. Therapists working with adolescents should expect to be

more flexible overall and more tolerant of these diversions, while still maintaining a therapeutic focus on CBT for BN. To do this, therapists must set the therapeutic agenda at the beginning of each session. They may set aside a prescribed amount of time for attention to other problems the adolescent needs to discuss. Usually, these set-aside times last no more than 10 minutes, scheduled at the beginning or end of the treatment session. However, some of these common problems can be perceived incorrectly by the patient, as the following vignette illustrates: Rachel believed her boyfriend broke up with her because she was overweight. The therapist asked Rachel if she knew of other couples who had broken up. Rachel said she did. The therapist then asked Rachel if she could remember why these couples dissolved. Rachel came up with a list of reasons, none of which included weight. As they further examined the implication of this, Rachel struggled with seeing herself in the same category as other girls. She said she was fat, they weren't. She had difficulty identifying other possibilities for the break up with her boyfriend. Again, the therapist asked Rachel to envision each of her friends. The therapist helped her to see that her friends' weights varied considerably, some were heavier than Rachel, and some were thinner. And in no case was the girl's weight the reason for the break up. Related to the problem of maintaining a therapeutic focus, is the potential for crises to disrupt treatment. Such crises must be addressed through an assessment of their impact on the appropriateness and practicality of maintaining CBT for BN as the treatment. For example, if an adolescent reports being sexually abused by a parent, it is likely that CBT treatment for BN will need to be interrupted until after this crisis is addressed. On the other hand, crises related to peer relationships, usual family struggles, or school performance may briefly require the therapist's attention, but once addressed, CBT with a focus on BN can resume. Stage 2: The second stage of CBT treatment usually spans seven or eight sessions. One aim of the second stage of treatment is to continue to monitor, progress toward, or maintenance of a regular pattern of eating. The next goal is to help the patient delineate the nature of feared and avoided foods, and to gradually reintroduce-with the help of parents-some of these foods into the diet. In addition, this stage introduces cognitiverestructuring and problem-solving techniques to address common triggers for binge eating. Food records and self-monitoring in Stage 2 are focused on the thoughts, emotional responses, and beliefs that commonly are distorted among bulimic patients. A common problem for the therapist during this stage is finding ways to help adolescents refine their self-observations, especially as these observations now focus on the emotional and social context as they relate to eating, binge eating, and purging behaviors and thoughts. Adolescents sometimes struggle with identifying, labeling, and processing their emotional states. Again, this is true for older patients as well, but with adolescents, therapists will likely need to facilitate this process more. For example, it is not uncommon for adolescents to say they "don't know" what they felt just before binge eating. Therapists sometimes find it necessary to "coach" teen-aged patients by presenting options to them and helping them to elaborate on the context. The kinds of questions therapists might ask are: "What were you doing just before you started to binge?" " Who was with you?" "Do you remember feeling angry, sad, or bored earlier in the day? " "What are you like when you feel sad, angry, or bored?" "Were you feeling like that before you binge ate?" These questions are designed to help youngsters develop self-observation skills and to promote better understanding of

emotional states. With increased awareness and understanding, adolescents are more likely to make the connection needed for accurate emotional self-monitoring. Principle targets of Stage 2 are distorted thoughts and beliefs about the body and eating. Many adolescents (like some adults) are unable to use formal cognitive-restructuring techniques without a lot of therapist assistance. This is the case because cognitiverestructuring requires perspective taking, generation of a range of alternatives, and the use of judgment about each option's viability and value. When using cognitiverestructuring techniques with adolescents, the burden of helping adolescents to use perspective, develop alternatives, and assess alternatives falls to the therapist. Therapists experienced with adolescent patients recognize that the need to do the groundwork on such efforts, especially at first. Therapists need to avoid "taking over" but will be very active in these cognitiverestructuring processes. Problem solving is commonly used when formal cognitiverestructuring strategies are too difficult for or are rejected by patients. Problem solving is more direct, appeals to the immediate needs of the adolescents, requires less in the way of judgment, and is practical. CBT therapists working with adolescents have found that problem solving is more likely to be employed with this age group than formal cognitiverestructuring. An example of this approach is with Rachel, a 13 year old with BN. When Rachel broke up with her boyfriend, who was the only person outside her family who know about her eating disorder, she felt she had no where to turn. She isolated herself from both her friends and family and increased binge eating and purging behaviors. In session she reported she had no other supports-she was angry with her mother and her brother, both of whom she felt tried to control her. She did not want any of tell any friends who were potential supports because of the shame she felt about bulimia. In examining the problem of how Rachel could find emotional support, the therapist worked with her to identify which of the options she considered to be least objectionable and why. In reviewing her need for support. Rachel felt that her mother would be the person who was most available and who was most willing to help her. This meant Rachel had to identify for her mother the ways she could be helpful as well as ways she could potentially make matters worse by being too intrusive. In a meeting with Rachel and her mother, the therapist helped Rachel explain her need for support now that her she had broken up with her boyfriend, but more important Rachel explained to her mother how she could help without making Rachel resentful and angry. Behavioralexperiments are employed in CBT to help patients extend their mastery over food, eating, and temptations to binge eat and purge. Often these behavioralexperiments involve patients putting themselves in situations that are challenging (e.g. buffet meals, bakeries, eating with friends or romantic partners). Adolescents sometimes have difficulty carrying out behavioralexperiments because they are practically and psychologically less independent. That is, adolescents often do not control their time and situations to the same degree as adults. For example, adolescents have meal times are set by parents or school authorities and food choices often are limited to those made available at the school and or by adults in the home setting. In addition, many adolescents (as is expected developmentally) are inexperienced with taking on independent challenges and need support in doing so. Therefore, therapists working with adolescents often need to take a more gradual approach to recommending such experiments. That is, therapists must start slow and proceed with small steps. Therapists might also consider being a part of the experiments, for example by asking patients to bring feared food to sessions, supporting adolescents as they eat the foods, and assisting the patient in making self-observations afterwards.

Therapists have also found it helpful to ask parents to assist their adolescents in behavioralexperiments. In these cases, therapists, patients, and parents decide together how this support is best structured. It may be as simple as informing the parent about the planned experiment and having the parent ask their son or daughter how it's going. Alternatively, it may be that the parents are asked to be present during the experiment and to actively support the teenager during an experiment. For example, after the son or daughter tries a feared food, the parent can volunteer to take the patient shopping, provide some other type of distraction, or to sit with the patient to support him or her as he or she tries to manage feelings of anxiety. Parents also can be helpful in these experimental activities by contributing their own observations of patient behaviors. Although the parents are not involved in the specific activities of problem solving, they provide insight and assistance in in a family context. Therapists need to educate parents about these thought processes so they can assist their children at home. Stage 3: The third stage is primarily concerned with maintaining the change following treatment. Progress is reviewed, and realistic expectations are established. Relapse prevention strategies are taught to patients to prepare for future setbacks. In general, adolescents have had less experience with chronic BN, therefore, the possibility of relapse (which generally is well known to adults with BN) is less experientially appreciated by adolescents. Therapists should expect adolescents to minimize the potential for relapse. Therefore, therapists should focus on potential relapse in ways relevant to the adolescent, particularly through an assessment of how adolescents' developmental challenges and tasks may threaten progress in controlling BN. This attitude is exemplified by Lucinda. Lucinda had done well in CBT and had reported no problems with binge eating or purging for several months. Her focus on weight and body shape , as a source of her self-esteem also diminished. However, she remained dissatisfied with her weight and intermittently restricted food intake for six to eight hours each day. Lucinda was unconcerned about possible relapse"I'm over that. It's too stupid. I've learned how to control it." However, the therapist gently but firmly reminded Lucinda of how she had felt she could control it before and that her current dieting still put her at risk for relapse. The therapist encouraged Lucinda to change her episodic severe dieting, but not to feel that all was lost if she should binge eat and purge. Lucinda continued to maintain that relapse was unlikely, but was open to understanding that the possibility existed. The therapist also discussed relapse with Lucinda's worried parents. The therapist reassured them that even if Lucinda had an episode of bulimic behavior in the future, this did not necessarily mean that she would again become bulimic. They were encouraged to support Lucinda by keeping a watchful eye on her and if problems arose, to encourage her to use what she had learned to stop the behaviors from becoming reentrenched. A special focus of CBT for adolescents with BN is the review of progress on adolescent issues and how BN and treatment affect these. Therapists need to focus on assessing which developmental tasks of adolescence patients have accomplished, and then help patients and parents identify problem areas that they may wish to focus on, particularly as they relate to prevention of a BN relapse. For example, 18-year-old Tomi was preparing to attend college at some distance from home. Her parents were worried about a recurrence of BN at college since they had read that BN was an "epidemic" on college campuses. The therapist helped to assure both Tomi and her parents that she was prepared to leave home and that the BN was well controlled. The therapist informed Tomi and her parents that most patients treated with

CBT continue to do well, but advised Tomi to contact the student health center at her college to identify resources available to her should she have renewed symptoms. Termination issues with adolescents may be somewhat more complex than with adults. The treatment relationship usually entails the family, especially the parents. In addition, adolescents can develop especially strong emotional connections to their therapists, so therapists working with this age group should be prepared to address these stronger attachments. On the other hand, many adolescents are prepared to move onto other aspects of their lives, such a college, a dating relationship, etc., so that the loss of a therapist seems of little consequence. Therefore, therapists working with adolescents should expect a range of responses to ending treatment. However, because parents (and sometimes other family members) have been involved, some time should be devoted to terminating with them as well. It is likely that adolescents who have benefited from CBT for BN will have developed a strong attachment to their therapists and therefore, therapists should expect that even after formal termination, patients may contact them from time to time. RESULTS At baseline, the rate of binge eating and purging ranged from two to 21 episodes per week with a mean of 15.8 episodes per week. At end of treatment, the abstinence rate was 56% and mean episodes had been reduced to 3.4 episodes per week (range 0-21). Only 6 patients (15%) did not complete a minimum of 10 weeks or 6 sessions of therapy(18%). Data were obtained at end of treatment. See Table I. DISCUSSION These data suggest that CBT for BN adjusted for adolescents is acceptable and suggests that response rates are similar to those in adults (i.e. decreases in the rate of binge eating and purging and the abstinence rates are very similar to that found in adults treated with CBT). In applying CBT for adolescent BN, it is of central importance that therapists have both knowledge of and experience with adolescents. For therapists to engage adolescents effectively throughout the treatment process, it is vital that therapists understand the developmental challenges of adolescence and their implications. Modifications applied to CBT for BN in adolescents include the following: 1) increased intensity of contact early in treatment to build the treat ment alliance; 2) education and involvement of parents and other significant friends or partners when indicated; 3) simplification of language and communication style; 4) flexibility in the use of homework and food logs, especially early in treatment; 5) flexibility in the use of treatment time to examine other important, but less directly relevant issues (e.g. crises with friends, parents, and other predictable developmental problems).

None of these changes alters the fundamental features of CBT as designed for adults, but it is likely they increase the chance that treatment will be taken up, adhered to, and completed. Attention to the external context of the adolescent's life (family and school) is an important aspect of working with most teenagers. Therapists working with adolescents often find it necessary to educate and involve (to various degrees) parents and other family members in therapyto support motivation and to enhance the milieu for therapeutic change. Therapists working with adolescents, regardless of the specific focus of therapy, should expect to devote some attention to peers and school environments because these arenas are important concerns for adolescents. In addition, some focus on the relationship of therapeutic progress to the mastery of adolescent tasks (autonomy, identity development, and work and education activities) should be expected. Therapists should expect that work on these issues will relate to other focused therapystrategies. For example, autonomy concerns may interfere with treatment acceptance and limit family support unless the therapist is able to separate these issues. Anxiety or problems related to sexual development and experimentation are also common problems. Educational goals, such as attending college, can also become a paramount issue for some older adolescents and may require attention by therapists. Therapists should be comfortable with these developmental issues and support a circumscribed examination of them in the context of more focused therapy(i.e. CBT). There are a number of important limitations to our current report. The sample used was a convenient clinical sample to our center, which is a tertiary treatment center for adolescents with eating disorders. In addition, it is a small case series and outcomes are limited to specific behavioralmeasures and do not include measures of psychological preoccupations around eating, weight, and shape which would be desirable. Therapists who provided treatment were all trained in CBT and supervised by the author of this report, which may also limit generalizabiliy of the findings. Finally, enhanced versions of CBT have been developed that include treatment modules related to self-esteem, perfectionism, and social problems that might be particularly relevant for adolescents with BN, but the treatment program used in this study did not incorporate these additional treatments.(C. G. Fairburn, Cooper, & Safran, 2002) In sum, although CBT is the treatment of choice for adults with BN, it has not been studied among adolescents with BN. This article describes a way to adjust CBT for BN so that it is more acceptable to adolescents and their families. The principles described here are also likely to be useful in making adjustments to other types of therapy, though the particulars would vary based on the specific strategies of the approach. An approach that is developmentally appropriate and manualized will make it possible to conduct clinical trials to test empirically the usefulness of CBT for adolescents with BN. Currently no such studies have been published, though they are much needed to help guide clinicians in their work with adolescents with BN.

Newest Look at Bulimia Nervosa Says Cognitive Behavioral Therapy Most Effective Treatment: [1]

Targeted News Service [Washington, D.C] 01 Feb 2011.

The ECRI Institute issued the following news release: A new evidence report by ECRI Institute comparing the effectiveness of various Bulimia Guide treatments for bulimia nervosa indicates that cognitive behavioral therapy is more effective than antidepressant medications and supportive therapies in improving eating disorder symptoms. ECRI Institute, an independent nonprofit organization that researches the best approaches to improving patient care, published the comprehensive report and other updated resources at www.bulimiaguide.org for free access by patients, healthcare professionals, and concerned families and friends. The Bulimia Nervosa Resource Guide website provides in-depth information about the disorder, risk factors, diagnosis, treatment options and costs, tips for family and friends on how to be supportive to the patient, and much more. "This expanded assessment delves deeper into establishing which of the available treatments is most effective," says Stacey Uhl, M.S.S., Senior Research Analyst, ECRI Institute. A few key findings from the current systematic review indicate that: Cognitive behavioral therapy is more effective than antidepressant medications in reducing the average number of binge eating episodes for some individuals. Patients who receive cognitive behavioral therapy are more likely to go into remission from purging and demonstrate improvements in associated eating disorder pathology than patients treated with supportive therapies. (Supportive therapies focus on management and resolution of personal difficulties and life decisions using the patient's strengths.) Cognitive behavioral therapy is more effective than behavioral therapy in reducing the average number of purging episodes for some individuals. The complete evidence report, Bulimia Nervosa: Comparative Efficacy of Available Psychological and Pharmacological Treatments, technical and non-technical summaries of the report, and other patient-focused resources are available for free at www.bulimiaguide.org.
Cite Title Newest Look at Bulimia Nervosa Says Cognitive Behavioral Therapy Most Effective Treatment: [1] Publication title Targeted News Service Publication year 2011 Publication Date

Feb 1, 2011 Year 2011 Dateline PLYMOUTH MEETING, Pa. Publisher Targeted News Service Place of Publication Washington, D.C. Country of publication United States Journal Subjects Public Administration Source type Newspapers Language of Publication English Document type WIRE FEED ProQuest Document ID 851503356 Document URL http://search.proquest.com/docview/851503356?accountid=38885

A randomized controlled trial of internet-based cognitivebehavioural therapy for bulimia nervosa or related disorders in a student population

Snchez-Ortiz, V C ; Munro, C; Stahl, D; House, J; Startup, H ; Treasure, J; Williams, C; Schmidt, U; et al. Psychological Medicine 41. 2 (Feb 2011): 407-417. Turn on hit highlighting for speaking browsers Turn off hit highlighting

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Background: Bulimic eating disorders are common among female students, yet the majority do not access effective treatment. Internet-based cognitive-behavioural therapy (iCBT) may be able to bridge this gap.

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(ProQuest: ... denotes non-US-ASCII text omitted.) [dagger] These authors contributed equally to this work. Introduction The transition from school to higher education is associated with a steep rise in the incidence of mental health problems, and these are seriously disruptive to students' education and emotional development (The Royal College of Psychiatrists, 2003). Female students are at high risk of eating disorders (EDs), particularly bulimia nervosa (BN) (Sell & Robson, 1998). This distressing condition causes significant impairment (Simon et al. 2005). Cognitivebehavioural therapy (CBT) is the treatment of choice (NICE, 2004) and early intervention improves outcome (Reas et al. 2000). However, most young people with EDs do not access effective treatment (Hoek & van Hoeken, 2003). In many areas, the availability of CBT is limited. Usually, young people prefer self-help to conventional health care for mental health problems (Oliver et al. 2005). In BN, shame commonly acts as a barrier to help-seeking.

Moreover, student mobility between term-time and holiday addresses disrupts treatment (Treasure et al. 2005). To overcome these barriers and engage young people with BN in effective treatment without delay or disruption, new ways of service delivery need to be identified. Computerized CBT may be able to bridge this gap. CBT delivered by interactive CD-ROMs or the internet is effective in the prevention of EDs in student and community populations (Taylor et al. 2006; Jacobi et al. 2007; Paxton et al. 2007) and has shown promise in the treatment of BN, binge eating disorder (BED) and partial syndromes (Carrard et al. 2006; Shapiro et al. 2007 b; Schmidt et al. 2008). E-mail has been used to support manual-based self-help for BN or BED (Ljotsson et al. 2007). As yet there has been no randomized controlled trial (RCT) of internet-based CBT (iCBT) in the treatment of BN. The main aim of this study was to evaluate the efficacy of iCBT (Williams et al. 1998), supplemented with e-mail support, among students with BN or eating disorder not otherwise specified (EDNOS) against a waiting list control. The main hypothesis was that iCBT would be superior to waiting list on eating disorders and other outcomes. The subsidiary aim of the study was to evaluate the effectiveness of immediate delivery of iCBT compared with delayed treatment, mimicking the experience of patients in the National Health Service (NHS). Previous work suggests that waiting for treatment leads to poor engagement and treatment retention (Schmidt et al. 2008). The subsidiary hypotheses therefore were that the group that received delayed iCBT would have poorer up-take of treatment, use fewer iCBT sessions and would not 'catch up' with the 'immediate' iCBT group in terms of improvement. Method Participants Participants were recruited from six higher education institutions (HEIs) in London between December 2005 and January 2007. Ethical approval for the study was obtained from the joint research ethics committee of the Institute of Psychiatry and the South London and Maudsley NHS Foundation Trust and the ethics committees of participating HEIs. Potential participants were drawn from a pool of approximately 68 380 students (see Fig. 1). Based on information from four of the six institutions we estimated that approximately two-thirds of all students ( n=45 000) were female across all six institutions. Recruitment was through university e-mail addresses, supplemented with posters and pamphlets, and in one institution (the Laban Centre) by letters sent to the students' university mail boxes. It is uncertain what proportion of students who received the recruitment e-mail/letter read it, making it difficult to estimate the number of people who constituted our pool for recruitment. Fig. 1. Participants flow through study of internet-based cognitive behaviour therapy (iCBT) for bulimia nervosa (BN). Respondents were sent an information sheet and on further contact offered telephone assessment. All potential participants, following assessment and prior to randomization, were offered a meeting to introduce them to the iCBT treatment and to obtain informed consent. Participants who preferred not to meet face-to-face were introduced to iCBT over the telephone and the consent form was sent by post.

Students who met DSM-IV criteria for BN or EDNOS were eligible for participation. EDNOS was defined as recurrent episodes of binge eating and/or compensatory behaviours that occurred less than 24 times during the previous 3 months or an ED where the abstinence period between episodes was greater than 2 weeks. This included cases with purging disorder (Keel, 2007). We did not specify any minimum number of binge or purge episodes as an inclusion criterion. However, where these behaviours occurred less than once a week, a clinician reviewed all the person's ED symptoms (e.g. including other compensatory behaviours such as food restriction and exercise and cognitive symptoms such as weight/shape concerns) to decide whether this was a clinically significant case warranting inclusion. There were only two such cases in the study. Exclusion criteria were: insufficient English to use the treatment, a diagnosis of BED (because of concerns that this group has a high placebo response; Jacobs-Pilipski et al. 2007), a body mass index (BMI)<18.5 kg/m2, currently receiving CBT, major mental disorders requiring different intervention (e.g. psychosis), pregnancy, serious physical illness or ED-related high medical risk (e.g. severe hypokalaemia). Antidepressant medication was not an exclusion criterion, provided the dose was stable. Intervention and study groups iCBT Overcoming Bulimia Online (Williams et al. 1998) is a cognitive-behavioural interactive multimedia treatment program. It consists of eight sessions, combining cognitivebehavioural, motivational and educational strategies. The content of the eight sessions has been described in detail elsewhere (Schmidt et al. 2008). Each session requires about 45 min at the computer. Sessions have to be worked through in sequence. Workbooks and 'homework' accompany each session. Anxiety management exercises are provided on CD and as downloads. Embedded self-assessment tools provide patients with feedback on their progress. Participants accessed the program over the internet at any time using a personal password. They were supported in their use of the online package by e-mails by two cognitive-behavioural therapists with ED experience. Their remit was to support and encourage participants to use the package. Therapists sent e-mails once every 1-2 weeks and responded to any e-mails received. iCBT group Participants in this group started treatment immediately after randomization. They were encouraged to complete the program over 8-12 weeks, but they continued to have access to the online sessions for 24 weeks. Therapist support focused on the first 3 months and tailed off during follow-up. Waiting List/Delayed Treatment Control Group (WL/DTC) Participants in this group waited 3 months providing a control for the iCBT group, to allow testing of our main efficacy hypothesis. Participants in this group received iCBT after 3 months, thus becoming a DTC group, mimicking the experience of assessment and then waiting list, inherent to many specialist ED services, and allowing testing of our subsidiary hypotheses. Assessments and measures

Assessments were conducted by telephone interview (Rohde et al. 1997) and questionnaires (completed online) at three time points: baseline, 3 months and 6 months. Interview-based measures The Structured Clinical Interview for DSM-IV (SCID) was given at baseline to determine comorbidity. Version 12 of the Eating Disorder Examination (EDE; Fairburn & Cooper, 1993) was completed at all three time points. The EDE is a widely used, standardized, semistructured interview that assesses ED psychopathology and has good psychometric properties when used with adult populations. It can generate ED diagnoses based on DSM-IV criteria. Assessors received training in the EDE and the SCID to ensure reliable use. Self-report measures The Hospital Anxiety and Depression Scale (HADS; Zigmond & Snaith, 1983) and the World Health Organization Quality of Life scale brief version (WHOQOL-BREF; The WHOQOL Group, 1998) are widely used and well-validated self-report questionnaires. Primary and secondary outcomes The primary outcomes were the EDE-Global (EDE-G) score and frequencies of the two key bulimic symptoms, bingeing and vomiting at 3 and 6 months. The secondary outcomes were the EDE subscale scores, the proportion of patients in remission from bingeing, vomiting and purging, and the HADS and the WHOQOL-BREF scores. Proposed sample size When the trial commenced there were no pilot data using the EDE as an outcome measure after iCBT. Therefore, the power calculation was based on remission rates from self-induced vomiting assessed by questionnaire in a pilot study of a CD-ROM version of the iCBT programme used here (Bara-Carril et al. 2004). Remission from vomiting rather than bingeing was chosen as the basis for the power calculation, as the present study includes participants who do not binge. It was assumed that 67% in the iCBT group (as in the pilot study) and 29.8% in the waiting list group would be in remission from vomiting at 3 months. To detect such an effect with a power of 80%, a sample size of 26 patients per group would be required using a two-sided [chi] 2 test at a significance level of 5%. Applying an attrition correction factor of 1/(1-a), where the attrition to follow-up rate is a=0.20, a total of 62 participants would be needed. Randomization, blinding and protection against bias An independent statistician in the Clinical Trials Unit (CTU) at the Institute of Psychiatry generated the randomization codes. Randomization was stratified by diagnosis and recruitment site. Treatment assignment codes were contained in a computerized randomization database held in the CTU, which concealed the sequence until groups were assigned. The unique identification code for each participant was provided to the statistician and a random group allocation then returned by e-mail. Outcome assessments were conducted by an assessor who was blind to treatment allocation. Participants were reminded at the beginning of each assessment not to reveal their treatment allocation to the assessor. To test the successfulness of the blinding, assessors were asked to guess the treatment group of

the participant after the 3 months assessment. Treatment allocation was guessed correctly in 69% of cases; that is, blinding was not completely successful. Statistical analysis The trial was analysed using general linear mixed models (GLMMs; Brown & Prescott, 2006) to assess changes in the outcome scores over time (baseline, 3 and 6 months) between the two treatment groups (iCBT and WL/DTC). For each variable a GLMM was used, with time and group as fixed factors and an unstructured covariance matrix. A mixed model with an unstructured covariance structure allows unequal variances and covariances (correlations) between repeated measures. Unlike repeated-measurement ANOVA, a GLMM model allows the analysis of all data in the presence of missing values. The main interest of this study was the change in differences between the iCBT and WL/DTC groups, between baseline and 3 months, because the WL/DTC group received treatment after 3 months. For this reason a planned contrast was tested for each outcome score to assess the change in the mean difference between the two groups between baseline and 3 months' time points. A contrast of this type is equivalent to a test for an interaction between group and time for the baseline and 3 months' measurements. A greater improvement in the iCBT group in comparison with the control group would result in a significant negative b regression coefficient (=decrease in the change score) for all variables except for quality of life subscales, where a positive b coefficient means greater improvement. Following a significant effect of time, post-hoc pairwise comparisons were made for the primary outcome variables to explore the nature of the differences. Positively skewed data were log-transformed (e.g. bingeing, vomiting and purge episodes) to achieve an approximate normal distribution of the residuals. To account for the multiple testing of 14 contrasts, a Simes' improved Bonferroni method was applied (Simes, 1986). To assess the changes between two observations of binary outcome variables, a McNemar test was used (Siegel & Castellan, 1988). Exact non-parametric statistics were used to test these binary variables because of the small sample size and often low prevalence of events. All analyses were based on the intention-to-treat principle and carried out using SPSS for windows version 15.0 (SPSS Inc., USA). Results Patient flow Fig. 1 is the CONSORT diagram describing the flow of participants through the study. Baseline characteristics There were no imbalances between the two groups at baseline on any of the sociodemographic or clinical characteristics (see Table 1). Only one participant was male. Just over half of the sample met full DSM-IV criteria for BN, the remainder had EDNOS. Five of the EDNOS participants reported only purging behaviours and no objective bingeeating episodes at baseline. Half of the sample had not been diagnosed with an ED prior to entering the study. Seventy-two per cent had not previously received any form of psychological treatment. Co-morbidity was high, most commonly with generalized anxiety disorder.

Table 1. Baseline demographics and clinical characteristics of the sample iCBT, Internet-based cognitive-behavioural therapy; WL/DTC, waiting list/delayed treatment control; BN, bulimia nervosa; EDNOS, eating disorder not otherwise specified; BMI, body mass index; EDE-G, Eating Disorder Examination Global; s.d., standard deviation. a Number of binges, vomit and purge episodes in the previous month. Treatment outcomes Table 2 shows the results of the linear mixed model analysis for different EDE variables and other outcomes. There were significant interactions between randomization group and time for the EDE-G score and the EDE subscales of weight and shape concern and dietary restraint and a similar trend for bingeing and the EDE subscale of eating concern. This indicates that the group differences differed significantly between the different time points. Likewise, there were significant overall groupxtime interactions for HADS depression and anxiety and for three out of four subscales of the WHOQOL-BREF. (A completer analysis, of those who had completed four or more computer sessions, yielded similar results. Details can be obtained from the authors.) Table 2. Means, standard deviations and results of the linear mixed effects analysis EDE-G, Eating Disorder Examination Global; iCBT, internet-based cognitive-behavioural therapy; WL/DTC, waiting list/delayed treatment control; HADS, Hospital Anxiety and Depression Scale; WHOQOL, World Health Organization Quality of Life scale; df, degrees of freedom; s.d., standard deviation. Main hypothesis outcomes Table 3 shows the results of the planned contrast analysis and Cohen's (Cohen, 1988) effect sizes for the change in all the outcomes from baseline to 3 months for each group. Planned contrast analysis showed that differences between the iCBT and the WL/DTC groups increased significantly from baseline to 3 months on two of the three primary outcome variables (i.e. the EDE-G score and binge eating) and on the secondary outcome variables of EDE subscale scores, HADS anxiety and depression and three out of four WHOQOL-BREF subscales. On all of these variables the iCBT group showed a greater improvement than the WL/DTC group at 3 months, that is after the treatment period in the iCBT group and the waiting period in the WL/DTC group. All significant contrasts remained significant after Simes' improved Bonferroni correction for multiple testing. Table 3.

Results of planned contrasts analysis and effect sizes (Cohen's d) of the change scores from baseline to 3 months. The planned contrasts assess the changes in difference between the two groups from baseline to 3 months EDE-G, Eating Disorder Examination Global; iCBT, internet-based cognitive-behavioural therapy; WL/DTC, waiting list/delayed treatment control; HADS, Hospital Anxiety and Depression Scale; WHOQOL, World Health Organization Quality of Life scale; df, degrees of freedom; CI, confidence interval. Pairwise comparisons are reported for the primary outcome variables only. On the EDE-G score, there were significant improvements in both groups at 3 months (iCBT p<0.001; WL/DTC p<0.001). On episodes of binge eating, pairwise comparisons showed that there was a significant improvement in both groups at 3 months (iCBT p<0.001; WL/DTC p=0.011). On episodes of vomiting, pairwise comparisons showed that there was a significant improvement in the number of vomit episodes in both groups at 3 months (iCBT p<0.001; WL/DTC p=0.010). Subsidiary hypothesis outcomes Pairwise comparisons showed that on the EDE-G scores, between 3 and 6 months there was a significant improvement for the WL/DTC group (p=0.003), who by then had had iCBT, but not for the immediate iCBT group (p=0.161), who by then were in follow-up. However, the iCBT group showed a significantly larger improvement at 6 months than the WL/DTC group (p=0.006). On episodes of binge eating, pairwise comparisons showed that there was significant improvement between 3 and 6 months for both groups (immediate iCBT p=0.035; WL/DTC p=0.007). At 6 months there was still some evidence of a larger improvement in the immediate iCBT group than in the WL/DTC group (p=0.072). On vomiting episodes, pairwise comparisons showed that there was a significant improvement between 3 and 6 months in the WL/DTC group (p=0.007) and the iCBT group had a similar trend (p=0.065). There were no significant differences at 6 months between the two groups (p=0.419). Abstinence rates, change in diagnoses and clinically significant change Table 4 shows the proportions of participants in each group who are abstinent, subclinical or clinical from bingeing, vomiting and laxative use combined at the different time points and also the proportions in the diagnostic categories of BN, EDNOS or no diagnosis for an ED using DSM-IV criteria. For these analyses, clinical and subclinical categories were grouped into one and also BN and EDNOS. Pairwise comparisons using a McNemar test revealed a significant improvement on abstinence rates in the iCBT group at 3 months ( p=0.039) and this was maintained at 6 months. There was a similar trend in the DCT group at 3 months (p=0.063) that was maintained at 6 months. In terms of diagnosis, iCBT had a significant improvement at 3 months (p=0.016) and the change was maintained at 6 months. WL/DCT did not have a significant improvement at 3 months (p=1.000) but the improvement became significant at 6 months, after treatment (p=0.016). All the analyses were not significant after correction for multiple testing. Table 4.

Abstinence rates and eating disorder diagnoses over the course of the study iCBT, Internet-based cognitive-behavioural therapy; WL/DTC, waiting list/delayed treatment control; BN, bulimia nervosa; EDNOS, eating disorder not otherwise specified. Values given as n (%). Definitions for categories are as follows: Clinical: episodes of bingeing and vomiting or laxative use occurred, on average, twice a week in the past month. Subclinical: episodes of bingeing, vomiting and/or laxative use occurred, on average, less than twice a week. Abstinent: No objective binges, episodes of vomiting and laxative use in the past month. a This patient used other compensatory methods (such as extreme food restriction, fasting and overexercise). Treatment uptake, adherence and use of e-mail support In the immediate iCBT group, 78.9% started treatment compared to 65.8% in the WL/DTC group, a non-significant difference. In participants who completed at least one session, the mean number of sessions completed in both groups was very similar [iCBT: 5.5 (s.d.=2.5) and 5.3 (s.d.=2.5)]. The mean time spent by the therapists on providing e-mail support, per participant, was 45 (s.d.=33.2) min. This includes time checking online symptom scores and maintaining a record of contact. Adverse events were assessed directly through participants' e-mail responses and through a feedback questionnaire at the end of treatment. No significant adverse events were reported. Discussion The main hypothesis was confirmed: supported iCBT produced significantly greater reductions compared to 3 months waiting list in two out of three primary outcomes (EDE-G score and binge eating episodes), in all other ED variables, affective symptoms and quality of life. These gains were maintained or continued to improve during the follow-up period. At 3 months, the WL/DTC group showed some changes on the ED outcomes. This contrasts with previous studies, which found no change in BN patients waiting for treatment (Treasure et al. 1994). The process of diagnosis or confirmation of an ED by entering the study may have motivated some participants to change their eating-related behaviours while waiting for iCBT. However, their lack of improvement or deterioration on the affective and quality of life outcomes at 3 months suggested that these initial changes in ED symptoms were unlikely to be sustainable. This contrasts with the changes in the group that received iCBT immediately, where improvements in ED symptoms took place simultaneously with improvements in affective symptoms and quality of life. The subsidiary hypotheses were also broadly confirmed. Uptake of iCBT was (nonsignificantly) poorer in the WL/DTC group. At 6 months, significant differences between the group that received immediate iCBT and the WL/DTC group persisted on two out of three primary outcomes, with poorer outcomes for delayed iCBT at this point. The WL/DTC group mimicked the usual clinical process of assessment followed by a waiting list before treatment.

The poorer outcomes in this group highlight the benefit of iCBT in providing immediate access to effective treatment. The abstinence rates from bulimic behaviours of those who completed the assessments were 25.8% at the end of iCBT and 39.1% at follow-up. Over half of the 6-month assessment completers in the iCBT group (52.2%) no longer met diagnostic criteria for an ED. However, it should be noted that the absolute numbers were small. These figures compare well with those found in studies of manual-based guided CBT selfhelp (20% to 40% at end of treatment and follow-up respectively) and most studies of faceto-face CBT of bulimic-type ED (30% to 50%) (NICE, 2004; Perkins et al. 2006; Shapiro et al. 2007 a; Wilson et al. 2007; Snchez-Ortiz & Schmidt, 2010), although a recent large study of extended CBT for all ED individuals who were not markedly underweight had even better outcomes (Fairburn et al. 2009). Abstinence rates and other outcomes in the present study were much better than in an earlier RCT by our group testing a CD-ROM based version of Overcoming Bulimia without therapist guidance in BN and EDNOS patients referred to a specialist ED service (Schmidt et al. 2008). The reasons for this are likely to include a more optimal delivery of the intervention in the present study, although differences in study populations cannot be ruled out. A recent non-randomized study of supported iCBT for BN found that 22.6% of participants were abstinent from bingeing and vomiting at post-treatment assessment (Fernandez-Aranda et al. 2008). These rates are broadly comparable to those found in our study, although our abstinence criterion was more stringent. Qualitative feedback obtained from participants through face-to-face interviews indicated that they liked iCBT because of its flexibility (Snchez-Ortiz et al. 2007). Participants completed a mean of just over five online sessions. This compares well with adherence in other studies of self-help treatments in BN (Schmidt et al. 2008). Much of the information was also in the accompanying workbooks and some participants used these instead of some online sessions. Furthermore, the ongoing improvement following iCBT suggests that participants continued to work on their difficulties even if they no longer used the online sessions. This is the first RCT of computer-based CBT treatment for bulimic disorders with guidance by a clinician. The idea that clinician guidance improves the outcomes of iCBT is supported by studies of manual-based self-care in BN (Perkins et al. 2006) and depression (Gellatly et al. 2007). Like people with depression, those with BN often suffer from poor motivation and therapist guidance may help to reduce this. Of note, clinician guidance in the present study was provided by specialists with expertise in both ED and CBT. Clinician guidance was provided by e-mail, amounting to less than one hour on average of clinician time per participant. The study fits with existing evidence that computerized CBT interventions can be efficacious with minimal support (Marks et al. 2004; Carlbring et al. 2007; Proudfoot et al. 2004). A report from the UK ED charity beat (beating eating disorders) found that only 15% of patients felt their general practitioner (GP) understood their ED, or knew how to help them (beat, 2009). GPs themselves often have a sense of 'not doing a good job' for their eating disordered patients because of lack of training and lack of suitable interventions available to them (Currin, 2006). Thus, alternative routes of delivering care for EDs, such as BN and

related disorders, should be considered. Offering iCBT through reputable self-help organizations such as beat would allow people with bulimia and related disorders to access effective treatment and bypass primary care. However, primary care health professionals, including those working in student health services, should be empowered to deliver an efficacious low-cost treatment at the first point of access, avoiding the need to refer to specialist services, as has been suggested for other common mental disorders (Centre for Economic Performance, 2006). Our findings suggest that immediate access improves outcomes, probably harnessing the initial motivation to change. Moreover, the study suggests that students and possibly other high-risk groups for EDs (e.g. athletes), many of whom are not currently presenting through traditional health service channels, can be engaged in efficacious treatment over the internet. This raises the potential for outreach work to deliver effective secondary prevention. The study has significant strengths and some limitations. This is the first RCT of iCBT for EDs. Participants were able to access treatment rapidly, largely anonymously, and use it with a degree of flexibility that other interventions do not offer. A novel means of recruitment was used that attracted a population, the majority of whom had not received psychological help for their ED. The study used reliable and valid interview measures for assessment and also used blind assessments. The number of participants retained in treatment was acceptable. A larger sample size would have been desirable; however, the study was adequately powered to address the primary outcomes. Maintaining blinding would have been ideal but proved impossible. The inclusion of an internet-based attention placebo control condition would have been desirable but was beyond the budget of this study. The results may not generalize to all bulimic-type ED patients as students may be more willing and able to use an internet-based intervention. However, the results may be generalizable to the many people with BN or EDNOS who do not seek treatment through conventional routes (Fairburn et al. 1996). Further research should address the efficacy and effectiveness of iCBT in different populations (e.g. including those with BED) and different settings of care (e.g. primary or specialist), in comparison to face-to-face CBT for bulimic disorders and with a longer followup. iCBT has the potential to provide an accessible and cost-effective intervention in nonspecialist settings as part of a stepped care model for BN and EDNOS. Acknowledgements This project was supported by a grant from the South London and Maudsley NHS Foundation Trust's Research and Development Fund. V. Snchez-Ortiz was supported by a Mexican Government Ph.D. scholarship from CONACyT (Consejo Nacional de Ciencia y Tecnologa) and by a grant from the National Institute for Health Research Biomedical Research Centre (Institute of Psychiatry, King's College London). We thank the students who took part in the study and the counselling services in participating HEIs. We also thank Dr M. Yoshioka for help with data collection. Declaration of Interest C. Williams is one of the developers of the treatment package Overcoming Bulimia Online used in this trial and receives royalties for this (Trial Registration: ISRCTN07388346). 3

Department of Biostatistics, Institute of Psychiatry, King's College London, UK 4 Section of Family Therapy, Institute of Psychiatry, King's College London, UK 5 Division of Community Based Sciences, Faculty of Medicine, University of Glasgow, UK Copyright Cambridge University Press 2010
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Cite Subjects Eating disorders, Bulimia, Clinical trials, Clinical outcomes, College students, Cognitive therapy, Internet Title A randomized controlled trial of internet-based cognitive-behavioural therapy for bulimia nervosa or related disorders in a student population Authors Snchez-Ortiz, V C; Munro, C; Stahl, D; House, J; Startup, H; Treasure, J; Williams, C; Schmidt, U Publication title Psychological Medicine Volume 41 Issue 2 Pages 407-417 Number of pages

11 Publication year 2011 Publication Date Feb 2011 Year 2011 Publisher Cambridge University Press Place of Publication Cambridge Country of publication United Kingdom Journal Subjects Medical Sciences--Psychiatry And Neurology, Psychology ISSN 00332917 CODEN PSMDCO Source type Scholarly Journals Language of Publication English Document type Feature Document Features References

Subfile Eating disorders, Bulimia, Clinical trials, Clinical outcomes, College students, Cognitive therapy, Internet DOI 10.1017/S0033291710000711 ProQuest Document ID 822660691 Document URL http://search.proquest.com/docview/822660691?accountid=38885 Copyright Copyright Cambridge University Press 2010 Last updated 2011-06-22 Database ProQuest Research Library

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Relapse predictors of patients with bulimia nervosa who achieved abstinence through cognitive behavioral therapy
Halmi, Katherine A ; W Stewart Agras ; Mitchell, James ; Wilson, G Terence; et al. Archives of General Psychiatry 59. 12 (Dec 2002): 1105-9. Turn on hit highlighting for speaking browsers Turn off hit highlighting

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BACKGROUND: Little information exists on relapse in patients with bulimia nervosa who responded with complete abstinence from binge eating and purging to cognitive behavioral therapy. Identification of relapse predictors may be useful to design effective early intervention strategies for relapse of susceptible patients with bulimia nervosa. METHODS: This multisite study examined relapse in 48 patients with bulimia nervosa who had responded to cognitive behavioral therapy with complete abstinence from binge eating and purging. Structured interviews and questionnaires were used to assess patients before and after treatment and at 4 months after treatment. RESULTS: Four months after treatment, 44% of the patients had relapsed. Those who relapsed had a higher level of preoccupation and ritualization of eating and less motivation for change, and had maintained abstinence for a

shorter time during the treatment period. CONCLUSIONS: The predictors of relapse found in this study can be readily determined by clinicians. The effectiveness of early additional treatment interventions needs to be determined with well-designed studies of large samples. Show less

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Five-year outcome of cognitive behavioral therapy and exposure with response prevention for bulimia nervosa
McIntosh, V V W ; Carter, F A; Bulik, C M ; Frampton, C M A ; Joyce, P R . Psychological Medicine 41. 5 (May 2011): 1061-1071.

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Background: Few data exist examining the longer-term outcome of bulimia nervosa (BN) following treatment with cognitive behavioral therapy (CBT) and exposure with response prevention (ERP). Method: One hundred and thirty-five women with purging BN received

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Introduction Outcome of bulimia nervosa

Cognitive behavioral therapy (CBT) is widely regarded as the treatment of choice for bulimia nervosa (BN), and there is considerable evidence from review and meta-analysis of clinical trials that CBT is effective in reducing both behavioral and psychological features of BN (Thompson-Brenner et al. 2003; Shapiro et al. 2007). The long-term outcome of CBT treatment has not been reported (Fairburn et al. 1995), but has been identified as a key area for further research (Shapiro et al. 2007). CBT is a multi-component treatment including diverse elements: normalizing eating, psychoeducation, identifying and challenging overvalued cognitions about food, eating, weight and shape, identifying cues for bulimic behaviors and use of strategies such as stimulus control to manage cues, exposure with response prevention (ERP), and relapse prevention (Fairburn et al. 1993). Little is known about which of these many components are necessary for effective treatment, although dismantling studies suggest that the cognitive component is crucial to therapeutic outcome (Fairburn et al. 1991). Consensus is lacking as to what should constitute criteria for the outcome of treatment for BN. It is proposed that abstinence from bulimic behaviors rather than reduced behavior frequency is a key outcome (Kordy et al. 2002; Shapiro et al. 2007), yet few studies report this. Method Participants Participants for the study were women aged 17-45 years with a current primary DSM-III-R diagnosis of BN (APA, 1987). Exclusion criteria were current anorexia nervosa, current body mass index (BMI) [= or >, slanted]30 kg/m2, current severe major depression with severe suicidal intent or requiring treatment with antidepressants, current severe medical illness or severe medical complications of BN, and current use of psycho-active medication and unwillingness to undergo a supervised drug wash-out period. Procedure Assessment Baseline assessment The presence of Axis I and II disorders was determined with the Structured Clinical Interview for DSM-III-R (I and II) (Spitzer et al. 1987, 1990) conducted by one of the investigators. The status of core bulimic symptoms was assessed by a structured clinical interview with the patient, and prospective self-monitoring data were available for corroboration. Subsequent assessments Assessments occurred at the point of randomization (between CBT and ERP or relaxation training) and at the end of treatment. Participants were contacted to complete a face-to-face assessment at 6 months, 1, 2, 3, 4 and 5 years post-treatment. Follow-up results to 3 years post-treatment have been reported previously (Bulik et al. 1998a, b; Carter et al. 2003). Outcome measures

Primary, secondary and tertiary outcome measures were determined a priori. Primary outcome measures were core behavioral features of BN, the number of episodes of objective binging, self-induced vomiting, and purging (vomiting plus laxative use) over the previous 2 weeks. Data were obtained by using the same clinician-administered interview as at baseline. The weekly frequency of binging and purging over the period since the previous assessment was also determined during the clinical interview. Retrospective recall was aided by a life events inventory assessing occurrence of bulimic behaviors in conjunction with salient life events. Secondary outcome measures were cognitive aspects of BN, body dissatisfaction, eating restraint and food restriction. These were dietary restriction and body dissatisfaction over the previous fortnight as assessed by structured clinical interview and subscales of the Eating Disorders Inventory (EDI; Garner et al. 1983a, b), drive for thinness, bulimia and body dissatisfaction. Tertiary outcome measures were mood symptoms on the Hamilton Depression Rating Scale (HAMD; Hamilton, 1960) and the global assessment of functioning, Axis V of DSM-III-R (GAF; APA, 1987). Treatments Treatments in the study have been described elsewhere (Bulik et al. 1998a). All treatments were manual based. Therapists were clinical psychologists who delivered all three experimental conditions. Patients had one therapist for the complete treatment protocol. To reduce the occurrence of exposure-based interventions within CBT, treatment departed from standard CBT for BN (Fairburn et al. 1993) in an important way: normal eating was not prescribed and homework did not include incorporating avoided foods into daily eating. Instead, modifications that individuals commonly made with eating were through identifying and challenging cognitions related to restriction of food intake or identifying restrictive or erratic eating as cues for subsequent binge eating. Phase II: Experimental treatments At the completion of eight CBT sessions, participants were randomized to a BT: B-ERP, PERP, or relaxation training. ERP involved individualized assessment of cues for binging and purging respectively in the B-ERP and P-ERP conditions. Treatment involved therapistassisted exposure to individualized high-risk cues, with prevention of the targeted response (binging in B-ERP, purging in P-ERP). In P-ERP, participants ate foods that were strong cues for purging (typically binge foods) while also being exposed to other cues (such as having laxatives available, being in a restaurant rest room or their home bathroom, and focusing on feelings of fullness or thoughts of weight gain), until the urge to purge was elicited, but were asked to refrain from purging. Participants in B-ERP did not eat during ERP, but were exposed to high-risk cues that elicited the urge to binge, and refrained from binging. Cues for binging included seeing and smelling (but not eating) binge foods along with non-food cues, activities, memories or affect associated with binging. Combinations of food and non-food cues from individualized assessments were used in each ERP session to approximate real antecedents for bulimic episodes. Exposure sessions continued until individuals had habituated to the urge to binge or purge. Sessions occurred both at and away from the clinic.

Relaxation training consisted of breathing techniques, imagery and progressive deep muscle relaxation, without a focus on food, eating, weight or shape. Sessions provided therapist contact without further cognitive or exposure techniques. Structured self-guided exposure or relaxation was assigned as homework during BT. Data analyses Data analyses involved three series of analyses. The first examined the effect of the experimental treatments at 5 years. The second examined the impact of treatment completion on outcome. The third involved comparison of response rates for the sample as a whole, according to different definitions of outcome. For the first series, for continuously distributed outcome variables (frequency of binge eating and purging, clinician-rated body dissatisfaction and food restriction, EDI subscales, HAMD and GAF), change from point-of-randomization scores were calculated. Scores were inspected for normality using normal probability plots. Analysis of variance (ANOVA) was used to compare outcome at 5 years among the three treatment groups for normally distributed change from point-of-randomization variables. For non-normally distributed variables, the non-parametric Kruskal-Wallis statistic compared median values. Given the high proportion of participants with no bulimic behaviors at 5 years, primary outcome measures were recoded as dichotomous variables (abstinence: yes/no). Logistic regression models were fitted with abstinence (from binging, purging and combined binging+purging) at 5 years as the dependent variables, main effects of experimental condition, and abstinence at point of randomization as covariates. Two linear mixed effects regression models were used to model the frequency of binge eating and purging (combined vomiting and laxative use) over all assessment times. Baseline binge frequency and three variables found to have distinguished among the three treatment groups at earlier assessments, change in food restriction and body dissatisfaction from baseline to point of randomization, and anxiety during the cue reactivity assessment (area under the curve), were used as covariates in the models. Subject was incorporated as a random effect and assessment time as a fixed effect. All available data were used, and no imputation of missing data was performed. For the second series of analyses participants were categorized into three groups: no treatment completed; CBT treatment only completed; both treatments (CBT and BT) completed. For continuous primary, secondary and tertiary outcome variables, change-frombaseline scores were calculated. Scores were inspected for normality using normal probability plots. ANOVA was used to compare outcome among the three groups according to treatment completion status for change-from-baseline outcome variables. Primary outcome variables, binging and purging behaviors, were recoded as dichotomous variables (abstinence: yes/no). Logistic regression models were fitted with abstinence (from binging, vomiting, purging and combined binging+purging) at 5 years as the dependent variables and main effects of treatment completion status. All analyses were performed using SPSS version 17 (SPSS Inc., USA). Significance was determined using the criterion p<0.05.

Results One hundred and thirty-five women met all inclusion and no exclusion criteria and began treatment. Fig. 1 shows participant flow during treatment and follow-up. Nineteen individuals (14.1%) did not complete the first phase of therapy, with drop-out occurring across the course of CBT. The remaining 116 individuals were randomized to an experimental condition (BERP n=39, P-ERP n=38, RELAX n=39). There were no differences in co-morbidity among the three treatment groups. One hundred and six women completed five or more sessions of the experimental treatment (B-ERP n=35, P-ERP n=33, RELAX n=38). Ten individuals did not complete the experimental treatment, with completion defined as attending five or more of the eight sessions. Thus, less than 9% of those randomized to BT dropped out. The proportion completing treatment was similar across the three treatment groups ( p=0.23). Overall, 29 of the 135 participants (21.5%) failed to complete therapy, the majority dropping out from the first phase of treatment. The proportion of the total sample attending for followup assessment at 5 years was 81% of the original sample of 135 ( n=109), 94% completed at least one assessment, and over half completed all follow-up assessments. Eighty per cent were followed up within 2 months of the planned 5-year assessment (range 56-74 months). Fig. 1. Overview of study design and patient flow at assessment points. ERP, Exposure with response prevention; B-ERP, exposure to pre-binge cues; P-ERP, exposure to pre-purge cues; RELAX, relaxation training. Effects of randomization Table 1 presents means and standard errors, or percentage abstinence rates, and statistical analyses of effects of the experimental treatments. Data are primary, secondary and tertiary outcome variables for participants randomized to B-ERP, P-ERP and relaxation at point of randomization and 5 years. Change from point-of-randomization values for primary, secondary and tertiary outcome variables were normally distributed. Table 1. Statistical summary of the effects of the experimental treatments for primary, secondary and tertiary outcome variables for participants randomized to B-ERP, P-ERP and RELAX at point of randomization and 5 years ERP, Exposure with response prevention; B-ERP, exposure to pre-binge cues; P-ERP, exposure to pre-purge cues; RELAX, relaxation training; EDI, Eating Disorder Inventory; HAMD, Hamilton Depression Rating Scale; GAF, global assessment of functioning; LR, logistic regression; df, degrees of freedom. Values given as mean (standard error) or percentage abstinent. For primary outcome variables, no differences were found among groups in change from point-of-randomization to 5-year frequencies of binging, vomiting, purging or combined binging+purging, using ANOVA on change scores. Logistic regression models with abstinence at 5 years as the dependent variable and relevant measures at the point of randomization as covariates revealed significant differences among the groups in abstinence

rates from binging, with 93.8% of those randomized to B-ERP, 88.2% of those randomized to P-ERP, and 63.3% of those randomized to relaxation abstinent from binging at the 5-year follow-up, from 51.3, 34.2 and 35.9% at the point of randomization for B-ERP, P-ERP and relaxation respectively. The two exposure treatments were associated with significantly greater reductions in binging abstinence rates (42.5% and 54% for B-ERP and P-ERP respectively) than the relaxation condition (27.4%), with no difference between B-ERP and P-ERP. No significant effects of treatment type were found for abstinence from purging or combined binging+purging. For all secondary and tertiary outcome variables, no differences were found among groups in change from the point of randomization to 5 years, using ANOVA on change scores. For the mixed effects regression model for binge frequency, over 5 years there were significant effects of baseline binge frequency (p=0.001), change in body dissatisfaction from baseline to point of randomization (p<0.004), and an interaction of assessment time by treatment group (p=0.004); however, the main effect of treatment was not significant (p=0.547) (see Fig. 2). Fig. 2. Binge frequency for the three treatment groups for all assessment times over 5 years. ERP, Exposure with response prevention; B-ERP, exposure to pre-binge cues; P-ERP, exposure to pre-purge cues; RELAX, relaxation training. For the mixed effects regression model for purge frequency (vomiting and laxative use), over 5 years there were significant effects of baseline purge frequency (p<0.001), change in body dissatisfaction (p<0.001) and dietary restriction (p<0.001) from baseline to point of randomization, a main effect of treatment (p<0.001) and an interaction of assessment time by treatment group (p=0.024) (see Fig. 3). Pairwise comparisons among treatments indicated significantly lower purge frequencies for the two exposure treatment groups than the relaxation training group (p<0.001). Fig. 3. Purge frequency for the three treatment groups for all assessment times over 5 years. ERP, Exposure with response prevention; B-ERP, exposure to pre-binge cues; P-ERP, exposure to pre-purge cues; RELAX, relaxation training. To compare outcome for exposure-based versus non-exposure-based treatment at 5 years, we combined B-ERP and P-ERP conditions. No differences were found in the frequencies of binging (F=2.28, df=1, p=0.14), vomiting (F=0.05, df=1, p=0.82), purging (F=0.37, df=1, p=0.54), or combined binging+purging (F=0.01, df=1, p=0.93) between the combined exposures group and the relaxation training group. Binge-eating abstinence rates were significantly different between the exposure and relaxation groups (Wald=8.60, df=1, p=0.003), and there were non-significant trends towards differences between the groups on abstinence rates for purging (Wald=3.38, df=1, p=0.06) and combined binging+purging (Wald=3.01, df=1, p=0.08). Effects of treatment completion status

Table 2 presents statistical analyses of the effects of treatment completion status for primary, secondary and tertiary outcome variables, with participants classified according to whether they completed neither CBT nor BT, only CBT, or both CBT and BT. Data are means and standard errors, percentage abstinence, or medians at baseline and at 5 years. Change from baseline values for primary, secondary and tertiary outcome variables were normally distributed. Table 2. Statistical summary of the effects of treatment completion status for primary, secondary and tertiary outcome variables CBT, Cognitive-behavioral therapy; BT, behavioral treatment (exposure treatment or relaxation training); EDI, Eating Disorder Inventory; HAMD, Hamilton Depression Rating Scale; GAF, global assessment of functioning; LR, logistic regression; df, degrees of freedom. Values given as mean (standard error), percentage abstinent or median (interquartile range). No differences were found among treatment completion groups in the change from baseline to 5-year frequencies or medians for primary, secondary or tertiary outcome variables or in abstinence rates for bulimic behaviors. Outcome for the total sample In addition to a priori definitions of outcome for the study (number of binge and purge episodes over the previous 2 weeks), percentage abstinence from binging and purging for the interval since the previous assessment (6 or 12 months) was calculated. Percentage abstinence from binging and purging and percentage with no diagnosis of BN or any eating disorder were calculated over the course of the study for the total sample. Fig. 4 presents the outcome for the total sample from baseline to 5 years using these different definitions of outcome. The 'strictest' definition of outcome in the present study is the absence of any bulimic behaviors (i.e. binging or purging) over the previous 12 months. The percentage of the total sample meeting this definition of recovery was 13% at 1 year posttreatment and rose steadily over the 5-year period to 36% at 5 years post-treatment. Rates of the most 'lenient' definition of outcome, no longer meeting diagnostic criteria for BN, rose to 76% after 6 months of treatment and remained high across the 5 years of follow-up. Fig. 4. Outcome for the total sample from baseline to 5-year follow-up assessment for different definitions of outcome. Rates of recovery at 5 years according to other definitions of outcome were 40% (absence of purging in the past year), 54% (absence of binging in the past year), 65% (no current eating disorder diagnosis), and 68% (absence of binging and purging in the past 2 weeks). With the exception of the diagnosis of BN, the rates for all definitions of outcome continued to increase over the 5 years post-treatment.

Discussion The current study examined the long-term outcome of individuals with BN treated with CBT plus either relaxation training or one of two forms of exposure with response prevention: either exposure to pre-binge cues or exposure to pre-purge cues. Modest effects at the end of treatment of superior outcome of B-ERP, but not P-ERP, with reduced anxiety on cue reactivity assessment (exposure to high-risk foods), food restriction, body dissatisfaction and depression, and at 12 months with lower food restriction and better global functioning, had disappeared at the 3-year follow-up. At 5 years no differences were found among the three treatment groups on measures of food restriction, body dissatisfaction or depression, but differences were found in rates of abstinence from binge eating, and over the entire 5 years of the study the two exposure treatments have lower rates of purging behaviors than the relaxation training condition. The pattern of results requires cautious interpretation, and discussion of the implications of the study remains speculative. The absence of differences among the three groups at the end of treatment, at 12 months and 3 years, may suggest that the observed differences in binge abstinence rates at 5 years and in purging frequency overall represent chance occurrences. Alternatively, it is possible that the skills and/or conditioning experiences associated with exposure treatment may inoculate individuals in such a way as to protect against the more long-term continuation or re-emergence of symptoms. In contrast to the two other RCTs in which CBT was compared with ERP (Leitenberg et al. 1988) and a waiting list control was compared with CBT with or without ERP (Agras et al. 1989b), the present study used an additive design in which ERP was added to a core of eight sessions of CBT. CBT was administered without the prescription of normal eating to avoid introducing exposure within CBT. In addition, CBT involved fewer sessions than in standard CBT. However, despite these departures from standard treatment, CBT was highly effective in reducing binge and purge behaviors, with over 40% of those completing CBT abstinent from binging and 28% abstinent from both binging and purging in the 2 weeks prior to randomization. It is possible that the substantial improvement that occurred during the eight sessions of CBT obscured the potential effects of ERP. Martinez-Malln et al. (2007) reported significant reductions in binge eating after exposure treatment for individuals who had failed to respond to combined CBT plus SSRI treatment. It is possible that the effects of ERP may be most marked in individuals who do not respond, or respond only partially, to standard treatments. Neither of the other RCTs of ERP for BN have examined long-term outcome of treatment.
Subjects Bulimia, Cognitive therapy, Behavior modification Title Five-year outcome of cognitive behavioral therapy and exposure with response prevention for bulimia nervosa Authors McIntosh, V V W; Carter, F A; Bulik, C M; Frampton, C M A; Joyce, P R

Publication title Psychological Medicine Volume 41 Issue 5 Pages 1061-1071 Number of pages 11 Publication year 2011 Publication Date May 2011 Year 2011 Publisher Cambridge University Press Place of Publication Cambridge Country of publication United Kingdom Journal Subjects Medical Sciences--Psychiatry And Neurology, Psychology ISSN 00332917 CODEN

PSMDCO Source type Scholarly Journals Language of Publication English Document type Feature Subfile Bulimia, Cognitive therapy, Behavior modification DOI 10.1017/S0033291710001583 ProQuest Document ID 858857171 Document URL http://search.proquest.com/docview/858857171?accountid=38885 Copyright Copyright Cambridge University Press 2010 Last updated 2011-04-19 Database ProQuest Research Library

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CHRIST UNIVERSITY

Transdiagnostic Cognitive-Behavioral Therapy for Patients With Eating Disorders: A Two-Site Trial With 60-Week Follow-Up
; Hawker, Deborah M, PhD, DClinPsy; Wales, Jackie A, BA; Palmer, Robert L, FRCPsych; et al. The American Journal of Psychiatry 166. 3 (Mar 2009): 311-9.

The aim of this study was to compare two cognitive-behavioral treatments for outpatients with eating disorders, one focusing solely on eating disorder features and the other a more complex treatment that also addresses mood intolerance, clinical perfectionism,
Headnote

Objective: The aim of this study was to compare two cognitive-behavioral treatments for outpatients with eating disorders, one focusing solely on eating disorder features and the

other a more complex treatment that also addresses mood intolerance, clinical perfectionism, low self-esteem, or interpersonal difficulties. Method: A total of154 patients who had a DSM-IV eating disorder but were not markedly underweight (body mass index over 17.5), were enrolled in a two-site randomized controlled trial involving 20 weeks oftreatment and a 60-week closed period offollow-up. The control condition was an 8-week waiting list period preceding treatment. Outcomes were measured by independent assessors who were blind totreatment condition. Results: Patients in the waiting list control condition exhibited little change in symptom severity, whereas those in the two treatment conditions exhibited substantial and equivalent change, which was well maintained during follow-up. At the 60-week follow-up assessment, 51.3% ofthe sample had a level ofeating disorder features less than one standard deviation above the community mean. Treatment outcome did not depend on eating disorder diagnosis. Patients with marked mood intolerance, clinical perfectionism, low self-esteem, or interpersonal difficulties appeared torespond better tothe more complex treatment, with the reverse pattern evident among the remaining patients. Conclusions: These two transdiagnostic treatments appear tobe suitable for the majority ofoutpatients with an eating disorder. The simpler treatment may best be viewed as the default version, with the more complex treatment reserved for patients with marked additional psychopathology ofthe type targeted by the treatment. (Am J Psychiatry 2009; 166:311-319) DSM-IV recognizes two specific eating disorders, anorexia nervosa and bulimianervosa, together with a residual diagnostic category termed "eating disorder not otherwise specified" (1). In outpatient settings, the most common eating disorder diagnosis is eating disorder not otherwise specified, followed by bulimianervosa and then anorexia nervosa (2-5). Despite its prevalence, there have been no studies ofthe treatment ofeating disorder not otherwise specified. Some treatment studies have included subthreshold cases ofanorexia nervosa or bulimianervosa (6, 7), and there has been interest in binge eating disorder (8), a subtype ofeating disorder not otherwise specified, but such cases constitute less than half those with eating disorder not otherwise specified (5). The majority have a mixed clinical picture in which the features ofanorexia nervosa and bulimianervosa are combined in various ways (5). The treatment ofthese patients has not been studied. Given that the clinical features of bulimianervosa and eating disorder not otherwise specified are very similar, it has been postulated that treatments that have beneficial effects on bulimianervosa should also benefit patients with eating disorder not otherwise specified (9). Were this tobe the case, such treatments would be ofgreat clinical value as they could be used with about 80% ofoutpatients with an eating disorder. The leading treatment for bulimianervosa is a specific form ofcognitive-behavioral therapy (CBT) (10, 11). Recently this treatment has been reformulated so that rather than being a treatment for bulimianervosa in particular, it is now a treatment for eating disorder psychopathology whatever the DSM-IV diagnosis (12). There are two forms ofthis "enhanced" treatment (CBT-E): a focused form (CBT-Ef) that targets eating disorder psychopathology exclusively, and a more complex broad form (CBT-Eb) that also addresses certain additional problems - mood intolerance, clinical perfectionism, low self-esteem, and

interpersonal difficulties - that commonly appear tomaintain eating disorders or complicate treatment (12). In this study we compared these two treatments in outpatients with any form ofeating disorder provided that their body mass index (BMI) was over 17.5. Thus the patients in the study met DSM-TV diagnostic criteria for bulimianervosa or eating disorder not otherwise specified, but patients in the anorexia nervosa weight range were excluded by the BMI cutoff. The first aim ofthe study was tocompare the two treatments with a waiting list control condition. This was essential because nothing is known about the spontaneous remission rate among patients with eating disorder not otherwise specified. The second and main aim was tocompare the effects ofthe treatments at treatment completion and after a 60-week period offollow-up. A substantial period offollow-up was essential because eating disorders are prone torelapse and treatments have been found todiffer in their relative longer-term effects (13, 14). The third aim was todetermine whether DSM-IV eating disorder diagnosis was a moderator oftreatment response, a question ofclinical and nosological significance. The fourth aim was toexplore the relative effects ofthe two treatments in patients with and without mood intolerance, clinical perfectionism, low self-esteem, or marked interpersonal difficulties. Method Design A randomized controlled trial was conducted at two eating disorder centers. Eligible patients underwent randomized assignment tofour treatment conditions: CBT-Ef, CBT-Eb, or an 8week delay in starting treatment followed either by CBT-Ef or CBT-Eb. Patients were assessed before treatment, after 8 weeks oftreatment, at the end oftreatment, and, for those in the control condition, at the end ofthe waiting list period preceding treatment. After treatment, patients were entered into a period offollow-up and reassessed 20, 40, and 60 weeks later. During follow-up, the patients received no further treatment unless it was judged necessary on clinical grounds (i.e., follow-up was closed). The study was approved by the two local human subjects committees. The trial was registered with Current Controlled Trials (ISRCTN no. 15562271. http://controlled-trials.com). Recruitment Participants were recruited from consecutive referrals by family doctors and other clinicians totwo well-established eating disorder clinics in the United Kingdom, one serving central Oxfordshire and the other Leicester city. Figure 1 summarizes participant enrollment and flow through the study. Recruitment was designed tobe broadly inclusive, with few exclusion criteria. Tobe eligible, patients had tohave an eating disorder requiring treatment, as judged both by the referring clinician and subsequently by the senior eating disorder specialist at each site (Z.C., C.G.F., or R.L.R); be 18 to65 years ofage: have a BMl over 17.5; and provide written informed consent after receiving a complete description ofthe study. The exclusion criteria were prior receipt ofa treatment closely resembling C-BT-E or an evidence-based treatment for the same eating disorder (N=12); a coexisting axis I psychiatric disorder that precluded eating disorder-focused treatment (N=22); medical instability or pregnancy (N=O); and not being available for the following 28 weeks (N=39). Patients who were receiving ongoing psychiatric treatment were weaned from it before entering the study (N=4); an

exception was clinically warranted antidepressant medication (N=76), which was kept stable during treatment. Treatment Both forms of CBT-E are designed for adult outpatients with any form ofeating disorder. A detailed treatment manual is available (15, 16). Both treatments comprise twenty 50-minute sessions, preceded by one 90-minute preparatory session and followed by a review session 20 weeks after treatment. The first 4 weeks of CBT-Ef and CBT-Eb are identical and solely address the eating disorder. Thereafter the two treatments diverge, and at this point the therapists in the trial learned which treatment their patients had been assigned toreceive. In (BT-Ef the remainder oftreatment is concerned with addressing the remaining eating disorder features (e.g., the overconcern with shape and weight, extreme dieting, binge eating, purging) (15). whereas in CBT-Eb the remaining sessions also address mood intolerance, clinical perfectionism, low self-esteem, or interpersonal difficulties, as indicated in the individual patient (16). The two treatments are illustrated in the clinical vignettes. (Further information about the treatments can be obtained at www.psychiatry.ox.ac.uk/credo; the web site also provides access free ofcharge tothe materials needed topractice CBT-E.) Five therapists took part; four were psychologists and one was a psychiatric nurse specialist. All had generic clinical experience and experience treating patients with eating disorders, and each received 6 months' initial training. Each therapist conducted both treatments. Weekly supervision meetings were led by Z.C. and CG. F. throughout the study. All sessions were recorded and were regularly audited toensure that the treatments were well implemented. Assessment Eating disorder features. These were assessed using the 16th edition ofthe Eating Disorder Examination interview (EDE) (17) and its self-report version (EDE-Q) (18). The EDE was administered by assessors who were trained and supervised by M.E.O., an expert on the instrument. The assessors were blind tothe patients' treatment condition and had no involvement with treatment. Two primary outcome variables were generated from the EDE ratings: change in the severity ofeating disorder features as measured by the global EDE score, and having a global EDE score less than one standard deviation above the community mean (i.e., below 1.74) (19). Normative comparisons ofthis type are widely used toidentify clinically significant change (19-21). General psychiatric features. These were measured using the Brief Symptom Inventory (BSI) (22), a short version ofthe Symptom Checklist- 90 (23). The Structured Clinical Interview for DSM-IV (24) was used at baseline toidentify the presence ofcoexisting axis I psychiatric disorders. Treatment suitability and expectancy. These were measured after two treatment sessions and after 8 weeks using widely employed visual analogue scales (14). Suitability was measured again at the end oftreatment. Severity ofadditional psychopathology. For the exploratory fourth aim, the therapists rated the severity ofeach patient's mood intolerance, clinical perfectionism, low self-esteem, and interpersonal difficulties after 4 weeks oftreatment. In the absence ofvalidated measures ofthese constructs, their severity was assessed using a 4-point Likert scale; detailed

definitions ofthe four constructs are provided in the CBT-Eb treatment manual (16). These ratings were made before the therapist learned the patient's treatment assignment. Power and Sample Size Sample size calculations were performed a priori in terms ofthe first two aims and outcome variables, on an intent-to-treat basis. With regard tothe second and main aim ofthe study, it was calculated that a sample size of75 patients per treatment condition was required toprovide 80% power at two-sided p<0.05 todetect a difference in global EDE change of0.45 points, assuming a standard deviation ofglobal EDE change scores of1.0 (14) (i.e., a moderate effect size of0.45) and also todetect a difference between the two conditions ofat least 25% in the categorical outcome measure. For the first aim, a larger difference was expected, and a sample size of50 per group would provide 80% power at two-sided p<0.05 todetect a large effect size of0.6. Thus, the patients were allocated tothe four treatment conditions in the ratio 25:25:50:50 (8-week wait then CBT-Ef, 8-week wait then CBTEb, immediate CBT-Ef, immediate CBT-Eb, respectively). The third and fourth aims were not the subject ofpower analyses as the analyses were exploratory. Randomization A computer-based minimization algorithm was used by one ofthe authors (H.A.D., who had no involvement in recruitment) toallocate patients tothe four treatment conditions, balancing gender, eating disorder diagnosis, BMI, and need toremain on psychotropic medication. When groups were evenly balanced, preprepared blocked randomization lists ofvarying size were used toallocate patients tothe four conditions. Statistical Methods The statistical analysis was undertaken by one ofthe authors (H.A.D.) blind totreatment condition. Standard treatment trial data analytic procedures were used. For the first aim, the endpoint was at 8 weeks. This comparison did not include data on the subsequent treatment response ofpatients who had first been in the waiting list control condition as their data would have appeared twice. For the other aims the endpoints were at completion oftreatment and at 60-week follow-up. Change scores were calculated. Data are presented as Ns and percentages for categorical data and means and standard deviations for continuous data; 95% confidence intervals (CIs) are used toindicate the uncertainty around the estimates. For data assessed at any one time point, categorical data were compared using chi-square tests or logistic regression analysis. Continuous data were compared using grouped t tests or Mann-Whitney tests and analysis ofvariance or Kruskal-Wallis tests. Follow-up data were analyzed using both repeatedmeasures analysis ofvariance and mixed models totake into account the correlation between repeated measurements and toexamine main effects and their interaction, adjusting for the baseline score. Results were similar across both methods. Unless otherwise stated, the analyses were by intent-to-treat with the initial data brought forward. Other imputation methods were tested, but as there were few missing data, this made little difference tothe main findings. Results

Sample A total of154 eligible patients were recruited and underwent randomized assignment between March 2002 and July 2005 (Figure 1). Ninety- three (60.4%) were from Oxford, and 61 (39.6%) from Leicester. Five did not attend their initial assessment, all ofwhom had been assigned tothe waiting list condition. Among the remainder (N= 149), 57 (38.3%) had a diagnosis of bulimianervosa and 92 (61.7%) a diagnosis ofeating disorder not otherwise specified. Seven patients (4.7% ofthe full sample) fulfilled the DSM-IV research criteria for binge eating disorder. The characteristics ofthe sample are summarized in Table 1 . Ofthe 154 patients, 53 were assigned toimmediate CBTEf, 50 toimmediate CBT-Eb, and 51 tothe waiting list control condition, after which they received either CBT-Ef (N= 25) or CBTEb (N=26). The study groups were balanced on all baseline factors except that patients assigned toimmediate CBT-Eb were less likely tohave a current major depressive episode or a history ofanorexia nervosa (Table 1). Adjusting for these two factors in the analyses made no difference tothe findings. Suitability, Expectancy, and Attrition The ratings ofsuitability and expectancy were high and did not differ between the two forms of CBT-E. Ofthe 149 patients who started treatment, 33 (22.1%) did not complete treatment or were withdrawn because oflack ofresponse. The noncompletion figures were 14.0% (8/57) for the patients with bulimianervosa and 27.2% (25/92) for those with eating disorder not otherwise specified (chisquare p=0.09). Effects ofImmediate Treatment Versus Delayed Treatment There was little change in patients in the waiting list control condition, whereas there was substantial change in those in the two CBT-E conditions and no significant differences between them (Table 2). There were no significant effects ofsite. The mean changes in global EDE-Q score were -0.09 (95% CI=-0.28 to0.10), -0.94 (95% CI=-1.28 to-0.61) and -1.17 (95% CI=-1.45 to-0.90) in the waiting list, CBT-Ef, and CBT-Eb conditions, respectively. Effects of CBT-Ef and CBTEb at End ofTreatment and at 60-Week Follow-Up There was a substantial response totreatment across all measures (Table 3) and no significant differences between the two treatments; indeed, the mean absolute and change scores were almost identical for the two treatments (e.g., global EDE change: -1.51 |SD=1.351 versus 1.53 [SD=1.281 for CBT-Ef and CBT-Eb, respectively). By the end oftreatment, half the overall sample (N=79; 51.3%) had global EDE scores below 1.74. There were no significant effects ofsite. The changes were greater in the patients who completed treatment; for example, at the end oftreatment two-thirds (N=77/116, 66.4%) had a global EDE score below 1.74, and there was no difference between the two treatments (66. 1% ofthe CBT-Ef group versus 66.7% ofthe CBT-Eb group). Compliance with follow-up was high, with 95.1% (331/ 348) ofthe assessments successfully completed. Ofthe 116 patients who entered follow-up, eight had additional treatment and nine had one tofive brief "booster" sessions. The changes were well maintained across the followup period. At 60-week follow-up, 50.0% ofthe overall sample (N=77) had a global EDE score

below 1 .74. The mean changes in global EDE in the CBT-Ef and CBT-Eb groups were similar at 1.36 (SD= 1.42) and 1.33 (SD= 1.30), respectively. Eating Disorder Diagnosis as a Moderator ofTreatment Response The patients with bulimianervosa and eating disorder not otherwise specified entered the study with very similar psychopathology, as described in a separate report (5). This similarity was also present at 8 weeks (data not shown), and on repeated-measures analysis ofvariance there was no significant main effect ofdiagnosis at this point. There were also no significant differences between the two diagnostic groups at end oftreatment and at 60- week follow-up. At the end oftreatment, 52.7% (30/57) ofthe patients with bulimianervosa and 53.3% (49/92) ofthose with eating disorder not otherwise specified had a global EDE score below 1.74, and at 60-week follow-up these figures were 61.4% (35/57) and 45.7% (42/92), respectively. Additional Psychopathology and the Relative Effects of CBT-Ef and CBT-Eb In this exploratory analysis, the clinicians' ratings oftheir patients' mood intolerance, clinical perfectionism, low selfesteem, and interpersonal difficulties were used toidentify patients with marked additional psychopathology ofthe type that CBT-Eb was designed totarget. Outcomes for these patients were compared with those ofthe remainder in relation tothe form of CBT-E received. A notable pattern offindings emerged. This was clearest when at least two ofthe domains had been rated as moderate or major clinical problems. This applied to54 patients (54/138, 39.1%). This subgroup with "complex" additional psychopathology responded less well in general than the "less complex" subgroup; their mean global EDE score at 60-week follow-up, adjusted for baseline, was 2.09 (95% CI=1.74-2.44), compared with 1 .77 in the less complex subgroup (95% CI= 1 .492.05; overall adjusted ? value on repeated-measures analysis ofcovariance, p=0.041), and 48% (95% CI=35-61) had a global EDE score below 1.74, compared with 60% (95% CI= 49-70) ofthe less complex subgroup. Within the complex subgroup ofpatients, those who received CBT-Eb had consistently lower adjusted global EDE scores than those who received CBT-Ef (Table 4), and they were more likely tohave scores below 1.74 (see Figure 2; e.g., at 60-week follow-up 60% [95% CI=4079] versus 40% |95% CI=22-58]). The reverse pattern offindings was consistentiy present among the less complex patients, with CBT-Ef proving superior to CBT-Eb (see Table 4 and Figure 2). Discussion This study is novel since it focused on the treatment ofpatients with any form ofDSM-IV eating disorder provided that their BMI was over 17.5 (i.e., only patients in the anorexia nervosa weight range were excluded). Two transdiagnostic treatments were compared, one that focused solely on eating disorder features and a more complex treatment that also addressed mood intolerance, clinical perfectionism, low self-esteem, or interpersonal difficulties. The sample was a clinically relevant one, as it was recruited from two catchment area clinics and few exclusion criteria were applied. However, over 40% ofthe potentially eligible patients did not take part, the two main reasons being not being available for the necessary 28 weeks and not wanting toparticipate in research. A low proportion ofthe sample had binge eating disorder, which is consistent with previous findings (2, 3). With regard tooutcome assessment, this is typically measured in terms ofchange in both the severity ofeating disorder features and the proportion ofpatients with certain clinical features that were

universally present at the outset (e.g., binge eating, purging, or being underweight). In this study we were able touse the former criterion (reduction in global EDE score) but the latter could not be employed given the heterogeneous character ofthe sample (e.g., not everyone engaged in binge eating or purging at the outset). Accordingly, we chose as a second (categorical) outcome variable a normative comparison, namely, achieving a level ofeating disorder features less than one standard deviation above the community mean. This is wellestablished practice in other fields (19-21) and has been done before in this area (14). Four findings are ofnote. The first is that it was feasible totreat this broad range ofpatients using one or the other form of CBT-E. The second is that in the waiting list control condition the patients' symptom severity did not change. Absence ofchange in bulimianervosa patients allocated toa waiting list is consistent with previous findings (25), but this is the first time that such data have been reported for patients with eating disorder not otherwise specified. This lack ofchange is not surprising given that these patients generally present with a long, unremitting history. The third finding is that the patients responded well toboth treatments and that their DSM-IV eating disorder diagnosis was not a moderator ofoutcome. At the end of20 weeks, more than half the overall sample (52.7% and 53.3% ofthose with bulimianervosa and eating disorder not otherwise specified, respectively) had a level ofeating disorder features less than one standard deviation above the community mean, and at 60- week follow-up the comparable figures were 61.4% and 45.7%. With regard tothe bulimianervosa response rate, at the end oftreatment 38.6% (22/57) reported no episodes ofbinge eating or purging over the previous 28 days, and at 60-week followup the proportion was 45.6% (26/57). These figures suggest that CBT-E might be more effective than its earlier version (14), especially given the inclusive nature ofthis study's sample, although a direct comparison ofthe two treatments is needed tosubstantiate this conclusion, as response rates vary from study tostudy. The fact that diagnosis did not moderate outcome at any time point suggests that the distinction between bulimianervosa and eating disorder not otherwise specified may be oflimited prognostic significance. The fourth finding is tentative and it concerns the relative effects ofthe two forms of CBT-E. In the full sample, they were no different in their effectiveness. However, the planned exploratory analysis revealed that in patients with substantial additional psychopathology ofthe type targeted in CBT-Eb, this version ofthe treatment appeared tobe more effective than the focused form, whereas in the remaining patients the opposite was the case. While this pattern ofresults was consistent over time (Figure 2), many ofthe individual ? values fell short ofstatistical significance. However, ? values are not central tothe interpretation ofexploratory analyses ofthis type (26). Todetermine the robustness ofthis finding, further comparisons ofthe two treatments are required using designs that directly address this question. In the meantime it would seem reasonable touse the present findings toguide clinical practice. Thus the simpler focused form ofthe treatment, CBT-Ef, should perhaps be viewed as the default form as it is easier tolearn and implement, with the more complex form, CBT-Eb, reserved for patients with marked additional psychopathology ofthe type that it targets.
References

References

1. American Psychiatric Association: Diagnostic and Statistical Manual ofMental Disorders (4th ed). Washington, DC, American Psychiatric Association, 1994 2. Martin CK, Williamson DA, Thaw JM: Criterion validity ofthe multiaxial assessment ofeating disorders symptoms. Int J Eat Disord 2000; 28:303-310 3. Ricca V, Mannucci E, Mezzani B, Di Bernardo M, Zucchi T, Paionni A, Placidi GP, Rotella CM, Faravelli C: Psychopathological and clinical features ofoutpatients with an eating disorder not otherwise specified. Eat Weight Disord 2001; 6:157-165 4. Turner H, Bryant-Waugh R: Eating disorder not otherwise specified (EDNOS): profiles ofclients presenting at a community eating disorder service. Eur Eat Disord Rev 2004; 12:1826 5. Fairburn CG1 Cooper Z, Bohn K, O'Connor ME, Doll HA, Palmer RL: The severity and status ofeating disorder NOS: implications for DSM-V. Behav Res Ther 2007; 45:1705-1715 6. Mcintosh WW, Jordan J, Carter FA, Luty SE, McKenzie JM, Bulik CM, Frampton CMA, Joyce PR: Three psychotherapies for anorexia nervosa: a randomized, controlled trial. Am J Psychiatry 2005; 162:741-747 7. Walsh BT, Fairburn CG, Mickley D, Sysko R, Pandes MK: Treatment of bulimianervosa in a primary care setting. Am J Psychiatry 2004; 161:556-561 8. Mitchell JE, Devlin MJ, de Zwaan M, Crow SJ, Peterson CB: Binge-Eating Disorder. New York, Guilford, 2007 9. Fairburn CG, Cooper Z, Shafran R: Cognitive behaviour therapy for eating disorders: a "transdiagnostic" theory and treatment. Behav Res Ther 2003; 41:509-528 10. National Collaborating Centre for Mental Health: Eating Disorders: Core Interventions in the Treatment and Management ofAnorexia Nervosa, BulimiaNervosa, and Related Eating Disorders. London, British Psychological Society and Royal College ofPsychiatrists, 2004 11. Shapiro JR, Berkman ND, Brownley KA, Sedway JA, Lohr KN, Bulik CM: Bulimianervosa treatment: a systematic review ofrandomized controlled trials. Int J Eat Disord 2007; 40:321-336 12. Fairburn CG, Cooper Z, Shafran R: Enhanced cognitive behavior therapy for eating disorders ("CBT-E"): an overview, in Cognitive Behavior Therapy and Eating Disorders. Edited by Fairburn CG. New York, Guilford, 2008 13. Fairburn CG, Jones R, Peveler RC, Hope RA, O'Connor ME: Psychotherapy and bulimianervosa: longer-term effects ofinterpersonal psychotherapy, behavior therapy, and cognitive-behavior therapy. Arch Gen Psychiatry 1993; 50:419-428 14. Agras WS, Walsh BT. Fairburn CG, Wilson GT, Kraemer HC: A multicenter comparison ofcognitive-behavioral therapy and interpersonal psychotherapy for bulimianervosa. Arch Gen Psychiatry 2000; 57:459-466

15. Fairburn CG, Cooper Z, Shafran R, Bohn K, Hawker DM. Murphy R, Straebler S: Enhanced cognitive behavior therapy for eating disorders: the core protocol, in Cognitive Behavior Therapy and Eating Disorders. Edited by Fairburn CG. New York, Guilford. 2008 16. Fairburn CG, Cooper Z, Shafran R, Bohn K, Hawker DM: Clinical perfectionism, core low self-esteem, and interpersonal problems, in Cognitive Behavior Therapy and Eating Disorders. Edited by Fairburn CG. New York, Guilford, 2008 17. Fairburn CG, Cooper Z, O'Connor ME: Eating Disorder Examination (16.0D), in Cognitive Behavior Therapy and Eating Disorders. Edited by Fairburn CG. New York, Guilford, 2008 18. Fairburn CG, Beglin SJ: Eating Disorder Examination Questionnaire (EDE-Q 6.0), in Cognitive Behavior Therapy and Eating Disorders. Edited by Fairburn CG. New York, Guilford, 2008 19. Kendall PC, Marrs-Garcia A, Nath SR, Sheldrick RC: Normative comparisons for the evaluation ofclinical significance. J Consult Clin Psychol 1999; 67:285-299 20. Ogles BM, Lunnen KM, Bonesteel K: Clinical significance: history, application, and current practice. Clin Psychol Rev 2001 ; 21:421-446 21 . Kazdin AE: Research Design in Clinical Psychology. Boston, Allyn & Bacon, 2003 22. Derogatis LR, Spencer PM: The Brief Symptom Inventory: Administration, Scoring, and Procedures Manual. Baltimore, Clinical Psychometric Research, 1982 23. Derogatis LR: The SCL-90 Manual: Scoring, Administration, and Procedures for the SCL-90. Baltimore, Clinical Psychometric Research, 1977 24. First MB. Spitzer RL, Gibbon M, Williams JBW: Structured Clinical Interview for DSMIV Axis I Disorders (SCID). Washington, DC, American Psychiatric Press, 1995 25. Wilson GT, Fairburn CG: Treatments for eating disorders, in A Guide toTreatments That Work. Edited by Nathan PE, Gorman JM. New York, Oxford University Press, 2007 26. Kraemer HC, Wilson GT, Fairburn CG, Agras WS: Mediators and moderators oftreatment effects in randomized clinical trials. Arch Gen Psychiatry 2002; 59:877-883
The American Journal of Psychiatry Volume 166 Issue 3 Pages

311-9 Number of pages 9 Publication year 2009 Publication Date Mar 2009 Year 2009 Section Article Publisher American Psychiatric Association Place of Publication Washington Country of publication United States Journal Subjects Medical Sciences--Psychiatry And Neurology ISSN 0002953X CODEN AJPSAO Source type Scholarly Journals Language of Publication English

Document type PERIODICAL Document Features Charts;Tables;Graphs;References Subfile Bulimia, Eating disorders, Psychopathology, Clinical trials, Standard deviation, Patients, Human subjects, Design, Diagnostics, Behavior modification Accession number 19074978 ProQuest Document ID 220473166 Document URL http://search.proquest.com/docview/220473166?accountid=38885 Copyright Copyright American Psychiatric Association Mar 2009 Last updated 2011-09-12

Bulimia nervosa
Mehler, Philip S . The New England Journal of Medicine 349. 9 (Aug 28, 2003): 875-881.

Abstract (summary)
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The efficacy of cognitive-behavioral therapy in patients with bulimia nervosa has been convincingly demonstrated in randomized, controlled trials.37 This therapy is designed to educate patients about other ways to cope with the feelings that precipitate a

This Journal Jeature begins with a case vignette highlighting a common clinical problem. Evidence supporting various strategies is then presented, followed by a review offormal guidelines, mhen they exist. The article ends with the author's clinical recommendations. A 20-year-old woman presents with fatigue; laboratory tests reveal a serum potassium level of2.3 mmol per liter and a serum bicarbonate level of36 mmol per liter. She is 163 cm (64 in.) tall and weighs 54 kg (119 lb). The findings on physical examination are normal. On questioning, she admits tobinge eating and vomiting as frequently as five times per day. How should she be treated? THE CLINICAL PROBLEM Bulimianervosa, a disorder characterized by binge eating and purging, generally begins during adolescence, with the peak period ofonset around 18 years ofage.1 The lifetime prevalence is 3 percent,2 and the ratio offemale patients tomale patients ranges from 10:1 to20:1.3 Most patients with bulimiahave a coexisting psychiatric condition, such as an anxiety disorder or depression.4 There is also an association with substance abuse and promiscuity.5 Almost half ofpatients with bulimiahave residual features ofthe eating disorder after six years offollow-up.6 Certain personality disorders (borderline, narcissistic, and antisocial disorders), impulsivity, and depression predict a worse prognosis.7 Bulimianervosa is characterized by recurrent episodes ofbinge eating followed by inappropriate compensatory purging behavior toprevent weight gain (Table 1).8 Although the formal criteria ofthe Diagnostic and Statistical Manual ofMental Disorders, 4th edition (DSM-IV), require that both the binge eating and the compensatory behavior occur, on average, at least twice a week for a period ofthree months, there is wide variability in these types ofbehavior, and some patients purge 5 to10 times or more per day. In contrast toanorexia nervosa, which is characterized by a weight that is less than 85 percent ofthe normal value, most persons with bulimiaare ofnormal weight. The risk ofdeath is much lower among patients with bulimianervosa than among those with anorexia nervosa9 but nevertheless appears tobe greater than that among women ofsimilar age in the general population.10 Bulimiais a disorder ofuncertain cause; there is mounting evidence that genetic factors have an important role.11 Disturbances in the serotonergic systems, which are implicated in the regulation offood intake, and cultural attitudes toward standards ofphysical attractiveness are also believed tocontribute. Routine screening for bulimiais not currently the standard ofcare12 but may be prudent in college-age populations. There are three main modes ofpurging: self-induced vomiting, abuse oflaxatives, and misuse ofdiuretics. Most patients with bulimiainduce vomiting with a finger, but some use ipecac. As the illness progresses, many can vomit reflexively without mechanical stimulation. The

laxatives abused are the stimulant type containing bisacodyl, cascara, or senna. Diuretic preparations and diet pills such as those containing ephedrine are less frequently used.13 The medical complications of bulimianervosa are related tothe mode and frequency ofpurging, whereas in anorexia nervosa, they arise as a result ofstarvation (restricting) and weight loss. MEDICAL COMPLICATIONS Oral Complications Pharyngeal soreness and loss ofenamel on the lingual surface ofthe anterior teeth (perimyolysis) are thought toresult from repeated exposure toacidic gastric contents in the vomitus. Dental caries may be more prevalent,14 and dentists are in a good position torefer patients for treatment.15 Another complication associated with excessive vomiting is sialadenosis, a painless swelling ofthe salivary glands that develops after an intense cycle ofpurging. Gastrointestinal Complications Frequent vomiting may lead togastroesophageal reflux or Mallory-Weiss tears. Dyspepsia is common,16 but esophageal motility is normal.17 Some patients with bulimiaingest up to50 laxative pills per day. Severe constipation with a laxative-dependence syndrome, due todamage tothe myenteric plexus, may result from the abuse ofstimulant laxatives.18 Electrolyte Complications Recurrent purging can result in serious fluid and electrolyte disturbances (Table 2). The most severe cases ofmetabolic alkalosis are almost always due tovomiting. Abuse ofdiuretics also causes hypochloremic metabolic alkalosis. Acute diarrhea associated with laxative use results in hyperchloremic metabolic acidosis. Hypokalemia occurs in approximately 5 percent ofbulimic patients19,20 and may predispose them tocardiac arrhythmias. Given its low sensitivity, screening for hypokalemia cannot be recommended as a means ofdetecting bulimia. However, the finding ofhypokalemia in an otherwise healthy young woman is highly specific for bulimianervosa. Measurement ofurinary potassium levels may be useful; a value ofless than 10 mmol per liter in a "spot" urine specimen usually suggests a gastrointestinal cause ofpotassium loss. The patient with purely restricting anorexia nervosa is not at risk for any metabolic abnormality, acid-base disturbance, or hypokalemia.21 Pseudo-Bartter's syndrome, defined as normotensive, hypokalemic alkalosis, is common among patients who vomit or use diuretics excessively.22 Volume depletion induces hyperaldosteronism.23 Troublesome edema in the legs, caused by persistently high levels ofaldosterone, may occur in patients who purge excessively and then stop abruptly. Idiopathic edema, a condition characterized by irregular episodes offluid retention in the absence ofa recognizable cause, may also be a manifestation of bulimiain women who use diuretics tocontrol cyclical fluid retention.24 Endocrine Complications

In contrast topatients with anorexia nervosa, patients with bulimiararely have endocrine abnormalities. Generally, bone density is normal unless there is a history ofanorexia nervosa, in which case, bone densitometry is warranted.25 Although irregular menses, which affect fertility, are common during episodes ofactive bulimia, the future ability toconceive is not impaired in patients who recover from bulimia.26 The majority ofwomen with bulimiahave improvement in symptoms during pregnancy, but an exacerbation ofsymptoms after delivery is common.27 The prevalence of bulimianervosa may be increased among patients with type 1 diabetes; some patients deliberately avoid taking insulin in order toinduce weight loss.28 An earlier onset ofmicrovascular complications has been reported among these patients.29 Other Complications Repeated abuse ofipecac can cause serious, although usually reversible, toxic effects in the form ofcardiomyopathy and muscle weakness.30 Erosions covering the dorsum ofthe hands (Russell's sign) result from self-induced vomiting. STRATEGIES AND EVIDENCE TREATMENT OFMEDICAL COMPLICATIONS Most ofthe medical complications of bulimianervosa are treatable. In the absence ofclinical trials, suggested therapies for these complications are largely based on clinical experience. Gentle brushing and use ofa fluoride mouth rinse immediately after purging may prevent caries.31 Sialadenosis responds toa combination ofabstinence from vomiting, the application ofheat, and sucking oftart candies. If the sialadenosis has not begun torecede after a few weeks, oral pilocarpine (5 mg three times per day) may decompress the glands.32 Reflux symptoms respond toproton-pump inhibitors. The prokinetic agent metoclopramide may occasionally be worth considering as a means ofdecreasing the frequency ofvomiting; presumably, it acts on the central "emetic center" and by increasing the tone ofthe lower esophageal sphincter. It is difficult totreat laxative dependence. Patients must be counseled about the ineffectiveness ofstimulant laxatives for weight loss. The restoration ofbowel function is the norm after laxative use has been discontinued, but it may take several weeks.33 Ample hydration, a high-fiber diet, and moderate amounts ofexercise should be encouraged, as long as the patient does not have a history ofexcessive exercise as a means ofcontrolling weight. If constipation persists for more than a few days, a glycerin suppository or a nonstimulating osmotic laxative such as lactulose may be useful; stool softeners are oflittle value.34 Leg edema caused by pseudo-Bartter's syndrome is treated with salt restriction (less than 3 g per day), elevation ofthe legs, and patience; loop diuretics will only exacerbate the problem. An aldosterone antagonist, such as spironolactone (25 to50 mg per day), may be given for one totwo weeks, at which point the symptoms will probably have resolved. Such treatment is particularly worth considering if the distress ofhaving edema is thought likely toprecipitate a relapse of bulimia.

Calcium (1200 to1500 mg per day) with vitamin D (400 to800IU per day) should be recommended routinely, particularly in patients with a history ofanorexia nervosa, among whom bone loss is likely. For these patients, treatment with an oral contraceptive is also reasonable, although it may not be sufficient torestore bone density.35 Hypokalemia The treatment ofmarked hypokalemic metabolic alkalosis requires volume repletion (with intravenous normal saline), in order toturn off the reninangiotensin system. Normalization ofvolume status is needed for effective potassium repletion. A general principle is that every decrease of1 mmol per liter in the serum potassium level represents a loss of150 mmol in the total body potassium level. Oral potassium chloride is generally preferred for potassium repletion. Typically, potassium is administered in a split dose of40 to80 mEq per day for a few days. The potassium level should initially be measured daily during replacement therapy, because the required amount cannot be calculated reliably.36 Once euvolemia has been restored, if there is ongoing frequent purging, the electrolytes should be monitored; long-term potassium supplementation may be needed. PSYCHIATRIC TREATMENT Psychotherapy The efficacy ofcognitive-behavioral therapy in patients with bulimianervosa has been convincingly demonstrated in randomized, controlled trials.37 This therapy is designed toeducate patients about other ways tocope with the feelings that precipitate a desire topurge and totry tocorrect maladaptive beliefs regarding body image (e.g., that physical appearance dictates one's value as a person). In a five-month study involving 220 patients who were randomly assigned toeither individual cognitive-behavioral therapy or interpersonal psychotherapy, 30 percent ofthe patients receiving cognitive-behavioral therapy were in remission (defined by a frequency ofpurging ofless than twice per week) at the end oftreatment, as compared with only 6 percent in the psychotherapy group.38 This improvement has been corroborated in a four-month study ofindividual and group cognitivebehavioral therapy involving 60 bulimic patients; the rate ofbinge eating and purging behavior declined by 80 percent with either ofthese approaches.39 A reduction in the frequency ofpurging of70 percent or more by the sixth session ofcognitive-behavioral therapy is predictive ofa good longer-term response tothis therapy.40 Although short-term studies ofcognitive-behavioral therapy have demonstrated benefits, there are sparse data demonstrating that the benefits are maintained over the longer term. A recent study evaluated 101 women (80 percent ofthe original study cohort) long after they had participated in a placebo-controlled trial ofcognitive-behavioral therapy, pharmacotherapy (imipramine), or both; at 10 years, women who had been treated with cognitive-behavioral therapy, imipramine, or both performed better than women in the placebo group on measures ofsocial adjustment at work and in family activities.41 Rates ofabstinence from binge eating and purging after cognitive-behavioral therapy are less impressive, averaging less than 40 percent.42 Other forms ofpsychotherapy, such as interpersonal psychotherapy, which focuses on current interpersonal problems rather than the eating disorder, have also been used, but there is less evidence tosupport their use.

Pharmacotherapy Irrespective ofthe presence or absence ofassociated depressive symptoms, various classes ofantidepressants (tricyclics, selective serotonin-reuptake inhibitors, monoamine oxidase inhibitors, bupropion, and trazodone) have been demonstrated, in short-term (three-month), double-blind, placebo-controlled trials, tobe effective in reducing the severity ofsymptoms of bulimia.43 The available data suggest that each ofthese pharmacologic treatments may decrease the frequency ofbulimic behavior by 50 to60 percent within six toeight weeks. Fluoxetine is the only medication for bulimianervosa that has been approved by the Food and Drug Administration (FDA) todate. It received FDA approval on the basis ofits demonstrated efficacy in two 8-week double-blind trials and in one 16-week double-blind trial. The latter was a multicenter study involving 400 outpatients that demonstrated significantly greater decreases in the number ofweekly binge-purge episodes among patients treated with fluoxetine (60 mg per day) than among patients in the placebo group (a 50 percent reduction vs. a 21 percent reduction).44 A study involving 387 women with bulimiawho were randomly assigned toreceive fluoxetine, at a dose of20 mg per day or 60 mg per day, or placebo for eight weeks showed that the 60-mg dose was significantly more effective.45 Side effects included tremor, insomnia, and nausea but were not dose-related, and the rate ofdiscontinuation ofstudy treatment because ofan adverse event among women receiving the higher dose offluoxetine was similar tothe rate in the placebo group. Like cognitive-behavioral therapy, pharmacotherapy alone results in complete suppression ofbinge eating and purging in only 30 to40 percent ofpatients.46 Approximately one third ofpatients who initially have improvement with medication will have a resurgence oftheir bulimic behavior; the risk ofresurgence is highest during the first year after recovery.10 A recent study demonstrated that fluoxetine treatment reduced the risk ofa relapse of bulimiaover a 52-week treatment period, as compared with placebo (19 percent vs. 37 percent).47 A combination ofantidepressants and cognitive-behavioral therapy appears tobe more effective in reducing the frequency ofhinging and purging than either treatment alone. A review using data from seven trials involving a total of600 patients toassess the effect ofantidepressants (desipramine, imipramine, or fluoxetine) plus cognitive-behavioral therapy as compared with the effect ofone ofthese therapies alone reported average remission rates of42 to49 percent with a combination oftherapies and average rates of23 to36 percent with any single therapy.48 As a single therapy, cognitive-behavioral therapy was more effective than drug therapy. Patients in whom this therapy fails may have a response toan alternative therapy, but available data suggest that the response rate is relatively low in this situation. In a study ofpatients in whom cognitive-behavioral therapy had failed, the rate ofresponse tointerpersonal therapy was 16 percent, and the rate ofresponse topharmacotherapy (fluoxetine or desipramine) was 10 percent.49 AREAS OFUNCERTAINTY Most patients with bulimianervosa may reasonably be treated as outpatients. Factors that suggest a need for hospitalization include severe depression, disabling symptoms, purging that is rapidly worsening and has proved refractory tooutpatient treatment, severe hypokalemia (plasma potassium level, <2.0 to3.0 mmol per liter), and major orthostatic changes in blood pressure (>30 mm Hg) and pulse (>30 beats per minute). Data are lacking on how these factors affect the ultimate outcome.50 Although some experts advocate

hospitalization for any patient with a potassium level below 3.0 mmol per liter, in practice it is not uncommon for patients with lower potassium levels tobe cared for on an outpatient basis. Most studies ofcognitive-behavioral therapy and medication have not included adolescent subjects (those younger than 18 years ofage); thus, it is uncertain what the preferred therapy for such patients is. Other medications that are not discussed above may be effective in treating bulimia. Limited data from three short-term clinical trials, only one ofwhich was randomized, double-blind, and placebo-controlled, suggest that the antiemetic agent ondansetron may be effective in patients with bulimianervosa.51 Anecdotal data indicate that the novel anticonvulsant agent topiramate may also be effective.52 However, more data are needed. The effects ofdietary counseling on the development and course of bulimiahave not been well studied. It is also uncertain which patients can be effectively treated by a generalist rather than a psychiatrist; the involvement ofboth is generally recommended. It remains unknown whether bulimiamay be prevented by programs that teach assertiveness toyoung girls and help them tobe critical ofmedia claims promoting the value ofthinness. GUIDELINES The American Psychiatric Association has issued comprehensive guidelines for the management of bulimia(http://www.psych.org/clin_res/guide. bk42301.cfm).53 These offer guidance regarding the site oftreatment (whether it occurs in the hospital, is partially accomplished during hospitalization, is provided on an intensive outpatient basis, or is officebased) and the type oftreatment, including cognitive-behavioral therapy and medications. Although definitive data are lacking, the American Dietetic Association has published a position paper regarding nutritional counseling for patients with bulimianervosa,54 which recommends the involvement ofa dietitian in order todevelop a plan for normalizing eating patterns, minimizing restrictions on the types offood consumed, and correcting misconceptions about dieting. CONCLUSIONS Bulimianervosa should be considered in patients with unexplained hypokalemia and metabolic alkalosis and is particularly common in late adolescence. The primary objectives oftreatment are tointerrupt the binge-purge cycles with the use ofpharmacotherapy, cognitivebehavioral therapy, or both and totreat associated medical complications. All patients should be educated about the medical complications of bulimiaand about the benefits ofrestoring a regular pattern ofeating. On the basis ofthe degree ofhypokalemia in the woman described in the vignette, I would recommend a short stay in the hospital torestore a normal volume status with intravenous saline at 75 ml per hour and would aim toreplenish her potassium orally by providing 60 to80 mEq per day in a split dose, with daily monitoring ofelectrolytes until the levels returned tonormal. Subsequently, the electrolyte levels should be monitored intermittently; although there are no clear guidelines, I would do so at least every few months initially toscreen for evidence ofsurreptitious purging and torule out potentially dangerous potassium levels.

With the goal ofreducing the frequency ofbinging and purging, if not completely eliminating this behavior, I would refer the patient for cognitive-behavioral therapy with a mental health specialist who had expertise in eating disorders, and I would also treat her with medication. Fluoxetine would be my first choice, because ofits proven efficacy and tolerability. Given data showing the superiority ofa 60-mg dose over a 20-mg dose, I would aim toincrease the dose to60 mg over the course ofseveral days. Although data on the effects ofnutritional counseling are lacking, seeing a dietitian may also be helpful for some patients, particularly those who have extensive lists of"forbidden" foods or whose bulimiahas been active for years. I am indebted toAdriana Padgett for her assistance in the preparation ofthe manuscript.

References

REFERENCES 1. Lewinsohn PM, Striegel-Moore RH, Seeley JR. Epidemiology and natural course ofeating disorders in young women from adolescence toyoung adulthood. J Am Acad Child Adolesc Psychiatry 2000;39:1284-92. 2. Kreipe RE, Birndorf SA. Eating disorders in adolescents and young adults. Med Clin North Am 2000;84:1027-49. 3. Woodside DB, Garfinkel PE, Lin E, et al. Comparisons ofmen with full or partial eating disorders, men without eating disorders, and women with eating disorders in the community. Am J Psychiatry 2001;158:570-4. 4. O'Brien KM, Vincent NK. Psychiatric comorbidity in anorexia and bulimianervosa: nature, prevalence, and causal relationships. Clin Psychol Rev 2003;23:57-74. 5. Neumark-Sztainer D, Story M, French SA. Covariations ofunhealthy weight loss behaviors and other high-risk behaviors among adolescents. Arch Pediatr Adolesc Med 1996;150:3048. 6. Fairburn CG, Norman PA, Welch SL, O'Connor ME, Doll HA. Peveler RC. A prospective study ofoutcome in bulimianervosa and the long-term effects ofthree psychological treatments. Arch Gen Psychiatry 1995;52:304-12. 7. Vaz FJ. Outcome of bulimianervosa: prognostic indicators. J Psychosom Res 1998;45:391400. 8. Pryor T. Diagnostic criteria for eating disorders: DSM-IV revisions. Psychiatr Ann 1995;25:40-5. 9. Steinhausen HC. Eating disorders. In: Steinhausen HC, Verhulst FC, eds. Risks and outcomes in developmental psychopathology. Oxford, England: Oxford University Press, 1999:210-30.

10. Keel PK, Mitchell JE. Outcome in bulimianervosa. Am J Psychiatry 1997;154:313-21. 11. Bulik CM, Devlin B, Bacanu SA, et al. Significant linkage on chromosome 1Op in families with bulimianervosa. Am J Hum Genet 2003;72:200-7. 12. Cotton MA, Ball C, Robinson P. Four simple questions can help screen for eating disorders. J Gen Intern Med 2003;18:53-6. 13. Roerig JL, Mitchell JE, De Zwaan M, et al. The eating disorders medicine cabinet revisited: a clinician's guide toappetite suppressants and diuretics. Int J Eat Disord 2003:33:443-57. 14. Little JW. Eating disorders: dental implications. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;93:138-43. 15. Woodmansey KF. Recognition of bulimianervosa in dental patients: implications for dental care providers. Gen Dent 2000;48:48-52. 16. Mendell DA, Logemann JA. Bulimiaand swallowing: cause for concern. Int J Eat Disord 2001;30:252-8. 17. Nickl NJ, Brazer SR, Rockwell K, Smith JW. Patterns ofesophageal motility in patients with stable bulimia. Am J Gastroenterol 1996;91:2544-7. 18. Mehler P. Constipation: diagnosis and treatment in eating disorders. Eat Disord J Treat Prev 1997:5:41-6. 19. Wolfe BE, Metzger ED, Levine JM, Jimerson DC. Laboratory screening for electrolyte abnormalities and anemia in bulimianervosa: a controlled study, Int J Eat Disord 2001;30:288-93. 20. Greenfeld D, Mickley D, Quinlan DM, Roloff P. Hypokalemia in outpatients with eating disorders. Am J Psychiatry 1995;152:60-3. 21. Mehler PS. Diagnosis and care ofpatients with anorexia nervosa in primary care settings. Ann Intern Med 2001:134:1048-59. 22. Schulte M, Mehler PS. Metabolic abnormalities in eating disorders. In: Mehler PS, Andersen AE, eds. Eating disorders: a guide tomedical care and complications. Baltimore: Johns Hopkins University Press, 1999:76-85. 23. Jamison RL, Ross JC, Kempson RL, Sufit CR, Parker TE. Surreptitious diuretic ingestion and pseudo-Bartter's syndrome. Am J Med 1982;73:142-7. 24. Bihun JA, McSherry J, Marciano D. Idiopathic edema and eating disorders: evidence for an association. Int J Eat Disord 1993;14:197-201. 25. Zipfel S, Seibel MJ, Lowe B, Beumont PJ, Kasperk C, Herzog W. Osteoporosis in eating disorders: a follow-up study ofpatients with anorexia and bulimianervosa. J Clin Endocrinol Metab 2001;86:5227-33.

26. Crow SJ, Thuras P, Keel PK, Mitchell JE. Long-term menstrual and reproductive function in patients with bulimianervosa. Am J Psychiatry 2002:159:1048-50. 27. Conrad R, Schablewski J, Schilling G, Liedtke R. Worsening ofsymptoms of bulimianervosa during pregnancy. Psychosomatics 2003;44:76-8. 28. Takii M, Uchigata Y, Nozaki T, et al. Classification oftype 1 diabetic females with bulimianervosa into subgroups according topurging behavior. Diabetes Care 2002;25:1571-5. 29. Rydall AC, Rodin GM, Olmsted MP, Devenyi RG, Daneman D. Disordered eating behavior and microvascular complications in young women with insulin-dependent diabetes mellitus. N Engl J Med 1997;336:1849-54. 30. Ho PC, Dweik R, Cohen MC. Rapidly reversible cardiomyopathy associated with chronic ipecac ingestion. Clin Cardiol 1998;21:780-3. 31. Milosevic A, Brodie DA, Slade PD. Dental erosion, oral hygiene, and nutrition in eating disorders. Int J Eat Disord 1997;21:195-9. 32. Mehler PS, Wallace JA. Sialadenosis in bulimia: a new treatment. Arch Otolaryngol Head Neck Surg 1993;119:787-8. 33. Colton P, Woodside DB, Kaplan AS. Laxative withdrawal in eating disorders: treatment protocol and 3 to20-month followup. Int J Eat Disord 1999;25:311-7. 34. Tramonte SM, Brand MB, Mulrow CD, Amato MG, O'Keefe ME, Ramirez G. The treatment ofchronic constipation in adults: a systematic review. J Gen Intern Med 1997;12:15-24. 35. Grinspoon S, Thomas E, Pitts S, et al. Prevalence and predictive factors for regional osteopenia in women with anorexia nervosa. Ann Intern Med 2000;133:790-4. 36. Gennari FJ. Hypokalemia. N Engl J Med 1998;339:451-8. 37. Hay PJ, Bacaltchuk J. Extracts from "Clinical evidence": bulimianervosa. BMJ 2001:323:33-7. 38. Agras WS, Walsh T, Fairburn CG, Wilson GT, Kraemer HC. A multicenter comparison ofcognitive-behavioral therapy and interpersonal psychotherapy for bulimianervosa. Arch Gen Psychiatry 2000;57:459-66. 39. Chen E, Touyz SW, Beumont PJV, et al. Comparison ofgroup and individual cognitivebehavioral therapy for patients with bulimianervosa. Int J Eat Disord 2003;33:241-54. 40. Agras WS, Crow SJ, Halmi KA, Mitchell JE, Wilson GT, Kraemer HC. Outcome predictors for the cognitive behavior treatment of bulimianervosa: data from a multisite study. Am J Psychiatry 2000;157:1302-8. 41. Keel PK, Mithcell JE, Davis TL, Crow SJ. Long-term impact oftreatment in women diagnosed with bulimianervosa. Int J Eat Disord 2002;31:151-8.

42. Peterson CB, Mitchell JE. Psychosocial and pharmacological treatment ofeating disorders: a review ofresearch findings. J Clin Psychol 1999;55:685-97. 43. Jimerson DC, Wolfe BE, Brotman AW, Metzger ED. Medications in the treatment ofeating disorders. Psychiatr Clin North Am 1996:19:739-54. 44. Goldstein DJ, Wilson MG, Thompson VL, Potvin JH, Rampey AH Jr. Long-term fluoxetine treatment of bulimianervosa. Br J Psychiatry 1995;166:660-6. 45. Fluoxetine BulimiaNervosa Collaborative Study Group. Fluoxetine in the treatment of bulimianervosa: a multicenter, placebo-controlled, double-blind trial. Arch Gen Psychiatry 1992;49:139-47. 46. Bacaltchuk J, Hay P, Mari JJ. Antidepressants versus placebo for the treatment of bulimianervosa: a systematic review. Aust N Z J Psychiatry 2000;34:310-7. 47. Romano SJ, Halmi KA, Sarkar NP, Koke SC, Lee JS. A placebo-controlled study offluoxetine in continued treatment of bulimianervosa after successful acute fluoxetine treatment. Am J Psychiatry 2002;159:96-102. 48. Bacaltchuk J, Trefiglio RP, Oliveira IR, Hay P, Lima MS, Mari JJ. Combination ofantidepressants and psychological treatments for bulimianervosa: a systematic review. Acta Psychiatr Scand 2000;101:256-64. 49. Mitchell JE, Halmi K, Wilson GT, Agras WS, Kraemer H, Crow S. A randomized secondary treatment study ofwomen with bulimianervosa who fail torespond to CBT. lnt J Eat Disord 2002;32:271-81. 50. Woodside DB. Inpatient treatment and medical management ofanorexia nervosa and bulimianervosa. In: Earing disorders and obesity: a comprehensive handbook. 2nd ed. Fairburn CG, Brownell KD, eds. New York: Guilford Press, 2002:335-9. 51. Paris PL, Kim SW, Melier WH, et al. Effect ofdecreasing afferent vagal activity with ondansetron on symptoms of bulimianervosa: a randomised, double-blind trial. Lancet 2000;355:792-7. 52. Felstrom A, Blackshaw S. Topiramate for bulimianervosa with bipolar II disorder. Am J Psychiatry 2002;159:1246-7. 53. Practice guideline for the treatment ofpatients with eating disorders (revision). Am J Psychiatry 2000;157:Suppl:1-39. 54. Position ofthe American Dietetic Association: nutrition intervention in the treatment ofanorexia nervosa, bulimianervosa, and eating disorders not otherwise specified (EDNOS). J Am Diet Assoc 2001;101:810-9.
AuthorAffiliation

Philip S. Mehler, M.D.

AuthorAffiliation

From Internal Medicine and Community Health Services, Denver Health, and the University ofColorado Health Sciences Center - both in Denver. Address reprint requests toDr. Mehler at Denver Health, 660 Bannock St., MC1914, Denver, CO 80204, or at pmehler@dhha.org.

Indexing (details)
Cite Subjects Bulimia, Vomiting, Mental depression, Medical treatment, Psychiatry Title Bulimia nervosa Authors Mehler, Philip S Publication title The New England Journal of Medicine Volume 349 Issue 9 Pages 875-881 Publication year 2003 Publication Date Aug 28, 2003 Year 2003 Section Clinical practice

Publisher Massachusetts Medical Society Place of Publication Boston Country of publication United States Journal Subjects Medical Sciences ISSN 00284793 CODEN NEJMAG Source type Scholarly Journals Language of Publication English Document type Commentary Subfile Bulimia, Vomiting, Mental depression, Medical treatment, Psychiatry ProQuest Document ID 223930250 Document URL http://search.proquest.com/docview/223930250?accountid=38885 Copyright Copyright Massachusetts Medical Society, Publishing Division Aug 28, 2003 Last updated

2010-06-09 Database ProQuest Research Library

Practice guideline for the treatment of patients with eating disorders (revision)
American Psychiatric Association. The American Journal of Psychiatry, suppl. Practice Guideline for the Treatment of Patients With.. 157. 1 (Jan 2000): 1-39.

Abstract (summary)

A practice guideline from the American Psychiatric Association is presented for psychiatrists treating patients with eating disorders, focusing on the clinical factors that need to be considered when treating a patient with anorexia nervosa or bulimia nervosa. American Psychiatric Association I. EXECUTIVE SUMMARY A. CODING SYSTEM Each recommendation is identified as falling into one ofthree categories ofendorsement, indicated by a bracketed Roman numeral following the statement. The three categories represent varying levels ofclinical confidence regarding the recommendations: [I] recommended with substantial clinical confidence. [II] recommended with moderate clinical confidence. [III] may be recommended on the basis ofindividual circumstances. B. GENERAL CONSIDERATIONS Patients with eating disorders display a broad range ofsymptoms that frequently occur along a continuum between those ofanorexia nervosa and bulimianervosa. The care ofpatients with eating disorders involves a comprehensive array ofapproaches. These guidelines contain the

clinical factors that need tobe considered when treating a patient with anorexia nervosa or bulimianervosa. 1. Choosing a site oftreatment Pretreatment evaluation ofthe patient with an eating disorder is essential for determining the appropriate setting oftreatment. The most important physical parameters that affect this decision are weight and cardiac and metabolic status [I]. Patients should be psychiatrically hospitalized before they become medically unstable (i.e., display abnormal vital signs) [I]. The decision tohospitalize should be based on psychiatric, behavioral, and general medical factors [I]. These inelude rapid or persistent decline in oral intake and decline in weight despite outpatient or partial hospitalization interventions, the presence ofadditional stressors that interfere with the patient's ability toeat (e.g., intercurrent viral illnesses), prior knowledge ofweight at which instability is likely tooccur, or comorbid psychiatric problems that merit hospitalization. Most patients with uncomplicated bulimianervosa do not require hospitalization. However, the indications for hospitalization for these patients can include severe disabling symptoms that have not responded tooutpatient treatment, serious concurrent general medical problems (e.g., metabolic abnormalities, hematemesis, vital sign changes, and the appearance ofuncontrolled vomiting), suicidality, psychiatric disturbances that warrant hospitalization independent ofthe eating disorders diagnosis, or severe concurrent alcohol or drug abuse. Decisions tohospitalize on a psychiatric versus a general medical or adolescent/pediatric unit depend on the patient's general medical status, the skills and abilities oflocal psychiatric and general medical staffs, and the availability ofsuitable intensive outpatient, partial and day hospitalization, and aftercare programs tocare for the patient's general medical and psychiatric problems. 2. Psychiatric management Psychiatric management forms the foundation oftreatment for patients with eating disorders and should be instituted for all patients in combination with other specific treatment modalities. Important components ofpsychiatric management for patients with eating disorders are as follows: establish and maintain a therapeutic alliance; coordinate care and collaborate with other clinicians; assess and monitor eating disorder symptoms and behaviors; assess and monitor the patient's general medical condition; assess and monitor the patient's psychiatric status and safety; and provide family assessment and treatment [I]. 3. Choice ofspecific treatments for anorexia nervosa The aims oftreatment for patients with anorexia nervosa are to1) restore patients tohealthy weight (at which menses and normal ovulation in females, normal sexual drive and hormone levels in males, and normal physical and sexual growth and development in children and adolescents are restored); 2) treat physical complications; 3) enhance patients' motivations tocooperate in the restoration ofhealthy eating patterns and toparticipate in treatment; 4) provide education regarding healthy nutrition and eating patterns; 5) correct core maladaptive thoughts, attitudes, and feelings related tothe eating disorder; 6) treat associated psychiatric conditions, including defects in mood regulation, self-esteem, and behavior; 7) enlist family support and provide family counseling and therapy where appropriate; and 8) prevent relapse.

a. Nutritional rehabilitation A program ofnutritional rehabilitation should be established for all patients who are significantly underweight [I]. Nutritional rehabilitation programs should establish healthy target weights and have expected rates ofcontrolled weight gain (e.g., 2-3 lb/week for most inpatient and 0.5-1 lb/week for most outpatient programs). Intake levels should usually start at 30-40 kcal/kg per day (approximately 1000-1600 kcal/day) and should be advanced progressively. During the weight gain phase, this may be increased toas high as 70-100 kcal/kg per day. During weight maintenance and for ongoing growth and development in children and adolescents, intake levels should be 40-60 kcal/kg per day. Patients who require higher caloric intakes may be discarding food, vomiting, or exercising frequently or have more nonexercise motor activity (e.g., fidgeting); others may have a truly higher metabolic rate. Patients also benefit from vitamin and mineral supplements (and in particular may require phosphorus before serum hypophosphatemia occurs). Medical monitoring during refeeding is essential [I]. It should include assessment ofvital signs as well as food and fluid intake and output; monitoring ofelectrolytes (including phosphorus); and observation for edema, rapid weight gain (associated primarily with fluid overload), congestive heart failure, and gastrointestinal symptoms, particularly constipation and bloating. For children and adolescents who are severely malnourished (weight <70% ofthe standard body weight), cardiac monitoring may be useful, especially at night. Physical activity should be adapted tothe food intake and energy expenditure ofthe patient. Nutritional rehabilitation programs should also include helping patients deal with their concerns about weight gain and body image changes, educating them about the risks oftheir eating disorder, and providing ongoing support topatients and their families [I]. b. Psychosocial interventions The establishment and maintenance ofa psychotherapeutically informed relationship is beneficial [II]. Once weight gain has started, formal psychotherapy may be very helpful. There is no clear evidence that any specific form ofpsychotherapy is superior for all patients. Psychosocial interventions need tobe informed by understanding psychodynamic conflicts, cognitive development, psychological defenses, and complexity offamily relationships as well as the presence ofother psychiatric disorders. Psychotherapy alone is generally not sufficient totreat severely malnourished patients with anorexia nervosa. Ongoing treatment with individual psychotherapeutic interventions is usually required for at least a year and may take 5-6 years because ofthe enduring nature ofmany ofthe psychopathologic features ofanorexia nervosa and the need for support during recovery. Family therapy and couples psychotherapy are frequently useful for the alleviation ofboth the symptoms ofthe eating disorder and the problems in familial relationships that may be contributing tothe maintenance ofthese disorders [II]. Group psychotherapy is sometimes used as an adjunctive treatment for anorexia nervosa, but caution must be taken that patients do not compete tobe the thinnest or sickest patient or become excessively demoralized through bearing witness tothe difficult, ongoing struggles ofother patients in the group. c. Medications

Psychotropic medications should not be used as the sole or primary treatment for anorexia nervosa [I]. The role for antidepressants is usually best assessed following weight gain, when the psychological effects ofmalnutrition are resolving. These medications should be considered for the prevention ofrelapse among weight-restored patients or totreat associated features ofanorexia nervosa, such as depression or obsessivecompulsive problems [II]. 4. Choice ofspecific treatments for bulimianervosa a. Nutritional rehabilitation/counseling Nutritional counseling as an adjunct toother treatment modalities may be useful for reducing behaviors related tothe eating disorder, minimizing food restriction, increasing the variety offoods eaten, and encouraging healthy but not excessive exercise patterns [I]. b. Psychosocial interventions Psychosocial interventions should be chosen on the basis ofa comprehensive evaluation ofthe individual patient, considering cognitive and psychological development, psychodynamic issues, cognitive style, comorbid psychopathology, patient preferences, and family situation [I]. Cognitive behavioral psychotherapy is the psychosocial treatment for which the most evidence for efficacy currently exists, but controlled trials have also shown interpersonal psychotherapy tobe very useful. Behavioral techniques (e.g., planned meals, selfmonitoring) may also be helpful. Clinical reports have indicated that psychodynamic and psychoanalytic approaches in individual or group format may be useful once bingeing and purging are improving. Patients with concurrent anorexia nervosa or severe personality disorders may benefit from extended psychotherapy. Family therapy should be considered whenever possible, especially for adolescents still living with parents or older patients with ongoing conflicted interactions with parents [II]. c. Medications Antidepressants are effective as one component ofan initial treatment program for most patients [I]. Selective serotonin reuptake inhibitors (SSRIs) are currently considered tobe the safest antidepressants and may be especially helpful for patients with significant symptoms ofdepression, anxiety, obsessions, or certain impulse disorder symptoms or for those patients who have had a suboptimal response toprevious attempts at appropriate psychosocial therapy. Other antidepressant medications from a variety ofclasses can reduce the symptoms ofbinge eating and purging and may help prevent relapse among patients in remission. While tricyclic and monoamine oxidase inhibitor (MAOI) antidepressants can be used totreat bulimianervosa, tricyclics should be used with caution for patients who may be at high risk for suicide attempts, and MAOIs should be avoided for patients with chaotic binge eating and purging. Emerging evidence has shown that a combination ofpsychotherapeutic interventions and medication resuits in higher remission rates and therefore should be considered when initiating treatment for patients with bulimianervosa [II]. II. DISEASE DEFINITION, EPIDEMIOLOGY, AND NATURAL HISTORY

A. CLINICAL FEATURES The DSM-IV criteria for establishing the diagnosis ofanorexia nervosa or bulimianervosa appear in table 1 and table 2, respectively. Although DSM-IV criteria allow clinicians todiagnose patients with a specific eating disorder, the symptoms frequently occur along a continuum between those ofanorexia nervosa and those of bulimianervosa. Weight preoccupation and excessive self-evaluation ofweight and shape are primary symptoms in both anorexia nervosa and bulimianervosa, and many patients demonstrate a mixture ofboth anorexic and bulimic behaviors. For example, up to50% ofpatients with anorexia nervosa develop bulimic symptoms, and some patients who are initially bulimic develop anorexic symptoms (1). Atypical patients-who deny fear ofweight gain, appraise their bodies as malnourished, and deny distorted perceptions oftheir bodies-are not uncommon among Asian patients (2). In one U.S. series (3), these atypical features were seen in about one-fifth ofthe patients admitted toa specialty eating disorder program. Anorexia nervosa appears in two subtypes: restricting and binge-eating/purging; classification into subtypes is based on the presence ofbulimic symptoms. Patients with anorexia nervosa can alternate between bulimic and restricting subtypes at different periods oftheir illness (4-9). Among the binge-eating/purging subtype ofpatients with anorexia nervosa, further distinctions can be made between those who both binge and purge and those who purge but do not objectively binge. Patients with bulimianervosa can be subclassified into the purging subtype and the nonpurging subtype. Many patients, particularly in younger age groups, have combinations ofeating disorder symptoms that cannot be strictly categorized as either anorexia nervosa or bulimianervosa and are technically diagnosed as "eating disorder not otherwise specified" (10). Patients with anorexia nervosa and bulimianervosa often experience other associated psychiatric symptoms and behaviors. Individuals with anorexia nervosa often demonstrate social isolation. Depressive, anxious, and obsessional symptoms, perfectionistic traits, and rigid cognitive styles as well as sexual disinterest are often present among restricting anorexic patients (11). Early in the course ofillness, patients with anorexia nervosa often have limited recognition oftheir disorder and experience their symptoms as ego-syntonic; this is sometimes accompanied by corresponding limited recognition by the family. Depressive, anxious, and impulsive symptoms as well as sexual conflicts and disturbances with intimacy are often associated with bulimianervosa. Although patients with bulimianervosa are likely torecognize their disorder, shame frequently prevents them from seeking treatment at an early stage (12-15). Patients with anorexia nervosa ofthe binge-eating/ purging subtype are sometimes suicidal and self-harming. In one subgroup ofpatients with bulimianervosa (the 11 multi-impulsive" bulimic patients), significant degrees ofimpulsivity (manifested as stealing, self-harm behaviors, suicidality, substance abuse, and sexual promiscuity) have been observed (16). Some ofthe clinical features associated with eating disorders may result from malnutrition or semistarvation ( 17, 18). Studies ofvolunteers who have submitted tosemistarvation and semistarved prisoners ofwar report the development offood preoccupation, food hoarding, abnormal taste preferences, binge eating, and other disturbances ofappetite regulation as well as symptoms ofdepression, obsessionality, apathy, irritability, and other personality changes. In patients with anorexia nervosa, some ofthese starvation-related state phenomena, such as

abnormal taste preference, may completely reverse with refeeding, although it may take considerable time after weight restoration for them toabate completely (19). However, some ofthese symptoms may reflect both preexisting and enduring traits, such as obsessivecompulsiveness, which are then further exacerbated by semistarvation and, therefore, may only be partially reversed with nutritional rehabilitation (20). Complete psychological assessments may not be possible until some degree ofweight normalization is achieved (21). Although patients with bulimianervosa may appear tobe physically within the standards ofhealthy weight, they may also show psychological and biological correlates ofsemistarvation-such as depression, irritability, and obsessionality-and may be below a biologically determined setpoint even at a weight considered tobe "normal" according topopulation norms (22, 23). Common physical complications ofanorexia nervosa are listed in table 3. Amenorrhea ofeven a few months may be associated with osteopenia, which may progress topotentially irreversible osteoporosis and a correspondingly higher rate ofpathological fractures (24-26). Pains in the extremities may signal stress fractures that may not be evident from examination ofplain X-rays but whose presence may be signaled by abnormal bone scan results. Patients with anorexia nervosa who develop hypoestrogenemic amenorrhea in their teenage years that persists into young adulthood are at greatest risk for osteoporosis, since they not only lose bone mass but also fail toform bone at a critical phase ofdevelopment. As a result, prepubertal and early pubertal patients are also at risk ofpermanent growth stunting (27). The areas most vulnerable toosteoporosis are the lumbar spine and hip. Acute complications ofanorexia nervosa include dehydration, electrolyte disturbances (with purging), cardiac compromise with various arrhythmias (including conduction defects and ventricular arrhythmias), gastrointestinal motility disturbances, renal problems, infertility, premature births, other perinatal complications, hypothermia, and other evidence ofhypometabolism (28). Death from anorexia nervosa is often proximally due tocardiac arrest secondary toarrhythmias. Common physical complications ofbulimic behaviors are listed in table 4. The most serious physical complications occur in patients with chronic and severe patterns ofbinge eating and purging and are most concerning in very-low-weight patients (29). Laboratory abnormalities in anorexia nervosa may include neutropenia with relative lymphocytosis, abnormal liver function, hypoglycemia, hypercortisolemia, hypercholesterolemia, hypercarotenemia, low serum zinc levels, electrolyte disturbances, and widespread disturbances in endocrine function. Thyroid abnormalities may include low T^sub 3^ and T^sub 4^ levels, which are reversible with weight restoration and generally should not be treated with replacement therapy (30-33). Normal serum phosphorus values may be misleading, since they do not reflect total body phosphorus depletion (which is usually reflected in serum phosphorus only after refeeding has begun). In very severe cases ofmalnutrition, elevated serum levels ofmuscle enzymes associated with catabolism may be seen in more than one-half ofthe patients with anorexia nervosa (34). MRI abnormalities reflect changes in the brain. White matter and cerebrospinal fluid volumes appear toreturn tothe normal range following weight restoration. However, gray matter volume deficits, which correlate with the patient's lowest recorded body mass indices, may persist even after weight restoration (35-39). Some patients show persistent deficits in their

neuropsychological testing results, which has been shown tobe associated with poorer outcomes (40). It is important toconsider that laboratory findings in anorexia nervosa may be normal in spite ofprofound malnutrition. For example, patients may have low total body potassium levels even when serum electrolytes are normal and thus may be prone tounpredictable cardiac arrhythmias (41). Laboratory abnormalities in bulimianervosa may include electrolyte imbalances such as hypokalemia, hypochloremic alkalosis, mild elevations ofserum amylase, and hypomagnesemia and hypophosphatemia, especially in laxative abusers (30, 42). B. NATURAL HISTORY AND COURSE 1. Anorexia nervosa The percentage ofindividuals with anorexia nervosa who fully recover is modest. Although some patients improve symptomatically over time, a substantial proportion continue tohave disturbances with body image, disordered eating, and other psychiatric difficulties (43). A review ofa large number ofcarefully done follow-up studies conducted with hospitalized or tertiary referral populations at least 4 years after onset ofillness show that the outcomes ofabout 44% ofthe patients could be rated as good (weight restored towithin 15% ofrecommended weight for height; regular menstruation established), about 24% were poor (weight never reached within 15% ofrecommended weight for height; menstruation absent or at best sporadic), and about 28% ofthe outcomes fell between those ofthe good and poor groups; approximately 5% ofthe patients had died (early mortality). Overall, about twothirds ofpatients continue tohave enduring morbid food and weight preoccupation, and up to40% have bulimic symptoms. Even among those who have good outcomes as defined by restoration ofweight and menses, many have other persistent psychiatric symptoms, including dysthymia, social phobia, obsessivecompulsive symptoms, and substance abuse (44). In a carefully done 10-15-year follow-up study ofadolescent patients hospitalized for anorexia nervosa-76% ofwhom met criteria for full recovery-time torecovery was quite protracted, ranging from 57 to79 months depending on the definition ofrecovery (3, 45). Anorexic patients with atypical features, such as denying either a fear ofgaining weight or a distorted perception oftheir bodies, had a somewhat better course (3). Mortality, which primarily resulted from cardiac arrest or suicide, has been found toincrease with length offollow-up, reaching up to20% among patients followed for more than 20 years (46). A 1995 metaanalysis suggests a 5.6% mortality rate per decade (47). However, in the aforementioned 1015-year follow-up study ofadolescents, in which patients received intensive treatment, no deaths were reported (45). Some studies estimate that death rates ofyoung women with anorexia nervosa are up to12 times those ofagematched women in the community and up totwice those ofwomen with any other psychiatric disorders. However, these studies have involved clinical populations, and it is not clear what the corresponding community rates would be (47). Nevertheless, recent data suggest that ofall psychiatric disorders, the greatest excess ofpatient mortality due tonatural and unnatural causes is associated with eating disorders and substance abuse (48). Poorer prognosis has been associated with initial lower minimum weight, the presence ofvomiting, failure torespond toprevious treatment, disturbed family relationships before illness onset, and marital status (being married) (49, 50). Patients with anorexia nervosa who

purge are at much greater risk for developing serious general medical complications (51). In general, adolescents have better outcomes than adults, and younger adolescents have better outcomes than older adolescents (52-54). However, many ofthese prognostic indicators have not been consistently replicated and may be sturdier predictors ofshort-term but not longterm outcomes. 2. Bulimianervosa Very little is known about the long-term prognosis ofpatients with untreated bulimianervosa. Over a 1- to2-year period, a community sample reported modest degrees ofspontaneous improvement, with roughly 25%-30% reductions in binge eating, purging, and laxative abuse (55, 56). The overall short-term success rate for patients receiving psychosocial treatment or medication has been reported tobe 50%-70% (43). Relapse rates between 30% and 50% have been reported for successfully treated patients after 6 months to6 years offollow-up, and some data suggest that slow improvement continues as the period offollowup extends to10-15 years (57-60). In a large study ofthe long-term course of bulimianervosa patients 6 years after successful treatment in an intensive program (61), outcomes of60% ofthe patients were rated as good, 29% were ofintermediate success, and 10% were poor, with 1 % deceased. Patients who function well and have milder symptoms at the start oftreatment, and who are therefore more likely tobe treated as outpatients, often have a better prognosis than those who function poorly and whose disordered eating symptoms are ofsufficient severity tomerit hospitalization (62). Some studies suggest that higher frequency ofpretreatment vomiting is associated with poor outcomes (63, 64). The importance ofworking on patients' motivation as a preliminary measure before starting other treatments has gained recent attention and has been found toimpact the rapidity ofresponse tocare (65). C. EPIDEMIOLOGY Estimates ofthe incidence or prevalence ofeating disorders vary depending on the sampling and assessment methods. The reported lifetime prevalence ofanorexia nervosa among women has ranged from 0.5% for narrowly defined to3.7% for more broadly defined anorexia nervosa (66, 67). With regard to bulimianervosa, estimates ofthe lifetime prevalence among women have ranged from 1.1% to4.2% (68, 69). Some studies suggest that the prevalence of bulimianervosa in the United States may have decreased slightly in recent years (70). Eating disorders are more commonly seen among female subjects, with estimates ofthe male-female prevalence ratio ranging from 1:6 to1:10 (although 19%-30% ofthe younger patient populations with anorexia nervosa are male) (71-73). The prevalence ofanorexia nervosa and bulimianervosa in children and younger adolescents is unknown. In many other countries, there appears tobe an overall increase in eating disorders, even in cultures in which the disorder is rare (74). Japan appears tobe the only non-Western country that has had a substantial and continuing increase in eating disorders, with figures that are comparable toor above those found in the United States (75, 76). In addition, eating disorder concerns and symptoms appear tobe increasing among Chinese women exposed toculture clashes and modernization in cities such as Hong Kong (77, 78). The prevalence ofeating disorders appears tobe increasing rapidly in other non-English-speaking countries such as Spain, Argentina, and Fiji (79-82).

In the United States, eating disorders appear tobe about as common in young Hispanic women as in Caucasians, more common among Native Americans, and less common among blacks and Asians (83). However, several studies in the Southeastern United States (84, 85) have shown that many eating disorder behaviors are even more common among African American women than others. Black women are more likely todevelop bulimianervosa than anorexia nervosa and are more likely topurge with laxatives than by vomiting (86). It has recently been suggested that in some patients, excessive exercise may precipitate the eating disorder (87, 88). Female athletes in certain sports such as distance running and gymnastics are especially vulnerable. Male bodybuilders are also at risk although the symptom picture often differs, since the bodybuilder may emphasize a wish to"get bigger" and may also abuse anabolic steroids. First-degree female relatives ofpatients with anorexia nervosa have higher rates ofanorexia nervosa (89) and bulimianervosa (67, 90). Identical twin siblings ofpatients with anorexia nervosa or bulimianervosa also have higher rates ofthese disorders, with monozygotic twins having higher concordance than dizygotic twins. The evidence regarding rates of bulimianervosa in other first-degree female relatives remains unclear; some studies report a higher rate among first-degree female relatives while others do not (69). Families ofpatients with bulimianervosa have been found tohave higher rates ofsubstance abuse (particularly alcoholism) (91, 92), but transmission ofsubstance abuse in these families may be independent oftransmission of bulimianervosa (93). In addition, families ofpatients with bulimianervosa have higher rates ofaffective disorders (91, 94) and obesity (95). In the psychodynamic literature, patients with anorexia nervosa have been described as having difficulties with separation and autonomy (often manifested as enmeshed relationships with parents), affect regulation (including the direct expression ofanger and aggression), and negotiating psychosexual development. These deficits may make women who are predisposed toanorexia nervosa more vulnerable tocultural pressures for achieving a stereotypic body image (96-100). Patients with bulimianervosa have been described as having difficulties with impulse regulation resulting from a dearth ofparental (usually maternal) involvement. Bulimianervosa has also been described as a dissociated self-state, as resulting from deficits in selfregulation, and as representing resentful, angry attacks on one's own body out ofmasochistic/sadistic needs (13, 14). High rates ofcomorbid psychiatric illness are found in patients seeking treatment at tertiary psychiatric treatment centers. Comorbid major depression or dysthymia has been reported in 50%-75% ofpatients with anorexia nervosa (44) and bulimianervosa (44, 101, 102). Estimates ofthe prevalence ofbipolar disorder among patients with anorexia nervosa or bulimianervosa are usually around 4%-6% but have been reported tobe as high as 13% (103). The lifetime prevalence ofobsessive-compulsive disorder (OCD) among anorexia nervosa cases has been as high as 25% (44, 104, 105), and obsessive-compulsive symptoms have been found in a large majority ofweight-restored patients with anorexia nervosa treated in tertiary care centers (20). OCD is also common among patients with bulimianervosa (101). Comorbid anxiety disorders, particularly social phobia, are common among patients with anorexia nervosa and patients with bulimianervosa (44, 101, 102). Substance abuse has been found in as many as 30%-37% ofpatients with bulimianervosa; among patients with anorexia nervosa, estimates

ofthose with substance abuse have ranged from 12% to18%, with this problem occurring primarily among those with the binge/purge subtype (44, 102). Comorbid personality disorders are frequently found among patients with eating disorders, with estimates ranging from 42% to75%. Associations between bulimianervosa and cluster B and C disorders (particularly borderline personality disorder and avoidant personality disorder) and between anorexia nervosa and cluster C disorders (particularly avoidant personality disorder and obsessive-compulsive personality disorder) have been reported (106). Eating disorder patients with personality disorders are more likely than those without personality disorders toalso have concurrent mood or substance abuse disorders (101). Comorbid personality disorders are significantly more common among patients with the binge/purge subtype ofanorexia nervosa than the restricting subtype or normal weight patients with bulimianervosa (107). Sexual abuse has been reported in 20%-50% ofpatients with bulimianervosa (108) and those with anorexia nervosa (109, 110), although sexual abuse may be more common in patients with bulimianervosa than in those with the restricting subtype ofanorexia nervosa (111-113). Childhood sexual abuse histories are reported more often in women with eating disorders than in women from the general population. Women who have eating disorders in the context ofsexual abuse appear tohave higher rates ofcomorbid psychiatric conditions than other women with eating disorders (113, 114). III. TREATMENT PRINCIPLES AND ALTERNATIVES In the following sections, the available data on the efficacy oftreatments for eating disorders are reviewed. Most studies have consisted of6-12-week trials designed toevaluate the shortterm efficacy oftreatments. Unfortunately, there is a scarce amount ofdata on the long-term effects oftreatment for patients with eating disorders, who often have a chronic course and variable long-term prognosis. Many studies also inadequately characterize the phase ofillness when patients were first treated, e.g., early or late, which may have an impact on outcomes. In addition, most studies have examined the efficacy oftreatments only on eating disorder symptoms; few have examined the effectiveness oftreatments on associated features and comorbid conditions such as the persistent mood, anxiety, and personality disorders that are common among "real world" populations. A variety ofoutcome measures are employed in trials for patients with eating disorders. Outcome measures in studies ofpatients with anorexia nervosa primarily are the amount ofweight gained within specified time intervals or the proportion ofpatients achieving a specified percentage ofideal body weight, as well as the return ofmenses in those with secondary amenorrhea. Measures ofthe severity or frequency ofeating disorder behaviors have also been reported. In studies of bulimianervosa, outcome measures include reductions in the frequency or severity ofeating disorder behaviors and the proportion ofpatients achieving elimination ofor a specific reduction in eating disorder behaviors. When interpreting the results ofstudies, particularly for psychosocial interventions that may consist ofmultiple elements, it may be difficult toidentify the elements) responsible for treatment effects. It is also important tokeep in mind when comparing the effects ofpsychosocial treatments between studies that there may be important variations in the nature ofthe treatments delivered topatients.

A. TREATMENT OFANOREXIA NERVOSA Anorexia nervosa is a complex, serious, and often chronic condition that may require a variety oftreatment modalities at different stages ofillness and recovery. Specific treatments include nutritional rehabilitation, psychosocial interventions, and medications; all may be used tocorrect malnutrition, culturally mediated distortions, and psychological, behavioral, and social deficits. 1. Nutritional rehabilitation a. Goals The goals ofnutritional rehabilitation for seriously underweight patients are torestore weight, normalize eating patterns, achieve normal perceptions ofhunger and satiety; and correct biological and psychological sequelae ofmalnutrition (115). In general, a healthy goal weight is the weight at which normal menstruation and ovulation are restored. For women who had healthy menses and ovulation in the past, one can estimate that healthy weight will be restored at approximately the same weight at which full physical and psychological vigor were present. Assuming that the patient was not obese tostart with, restored healthy weight is unlikely toever be much lower than that. Since some patients continue tomenstruate even at low weight (66), and some others never regain menses, a minimum goal weight is often estimated as 90%, ofideal weight for height according tostandard ta tiles. At that weight, 86% ofpatients resume menstruating (although not necessarily ovulating) within 6 months (116). Sonic studies have relied on pelvic sonography todemonstrate the return ofa dominant follicle, which indicates that ovulation has returned (117). Others use anthropomorphic measures toestimate the percentage ofbody fat (approximately 20%-25%0) usually needed for normal fertility (118). In premenarchal girls, a health) goal weight is the weight at which normal physical and sexual development resumes. It is important touse pediatric growth charts toestimate what height and weight the patient might be expected toachieve. b. Efficacy Measures ofnutritional status include several different standards ofideal body weight, which can he quite variable (119, 120). Some studies calculate the body mass index, a measure that has become standard in studies ofobesity and increasingly in eating disorders research as well. This index is calculated with the formula (weight [in kg]/height lin meters]^sup 2^). Individuals with body mass indexes <18.5 are considered tobe underweight, and body mass indexes <=17.5, in the presence ofthe other diagnostic criteria, indicate anorexia nervosa. Body mass indexes are increasingly used in research studies, particularly tocompare groups according topercentiles ofthe body mass index, which take into account height, sex, and age in their calculations (121). However, most clinicians still use standard tables todetermine healthy body weights in relation toheights. In children and adolescents, growth curves should be followed and are most useful when longitudinal data are available, since extrapolations from crosssectional data at one point in time can be misleading. Therefore, for most clinical work, it is reasonable tosimply weigh the patient and gauge how far she is from her individually estimated healthy body weight (122). The efficacy with which weight restoration can be achieved varies with treatment setting. For most severely underweight patients, e.g., patients whose weight is 25%-30% below healthy body weight at the start oftreatment, little weight gain will be achieved with outpatient

treatment. However, most inpatient weight restoration programs can achieve a weight gain of2-3 lb/week without compromising the patient's safety. Weight at discharge in relation tothe healthy target weight may vary depending on the patient's ability tofeed herself, the patient's motivation and ability toparticipate in aftercare programs, and the adequacy ofaftercare, including partial hospitalization. The closer the patient is toideal body weight before discharge, the less the risk ofrelapse. Most outpatient programs find weight gain goals of0.5-1 lb/week tobe realistic, although gains ofup to2 lb/week have been reported in a partial hospital program in which patients are scheduled for 12 hours a day, 7 days a week (123). The latter is solely a step-down program, in which patients had been treated previously as inpatients. The clinicians running the program do not believe that it would work as effectively as a "step-up" program for never-hospitalized patients. Considerable evidence suggests that with nutritional rehabilitation, other eating disorder symptoms diminish as weight is restored, although not necessarily tothe point ofdisappearing. Clinical experience suggests that with weight restoration, food choices increase, food hoarding decreases, and obsessions about food decrease in frequency and intensity. However, it is by no means certain that abnormal eating habits will improve simply as a function ofweight gain (50). There is general agreement that distorted attitudes about weight and shape are least likely tochange and that excessive exercise may be one ofthe last ofthe behaviors associated with the eating disorder toabate. Regular structured diets may also enable some patients with anorexia nervosa with associated binge-eating and purging behaviors toimprove. For some patients, however, giving up severe dietary restrictions and restraints appears toincrease binge-eating behavior, which is often accompanied by compensatory purging. As weight is regained, changes in associated mood and anxiety symptoms can be expected. Initially, the apathy and lethargy associated with malnourishment may abate. As patients start torecover and feel their bodies getting larger, especially as they approach frightening magical numbers on the scale, they may experience a resurgence ofanxious and depressive symptoms, irritability, and sometimes suicidal thoughts. These mood symptoms, non-food-related obsessional thoughts, and compulsive behaviors, while often not eradicated, usually decrease with sustained weight gain. c. Side effects and toxicity Although weight gain results in improvement in most ofthe physiological complications ofsemistarvation, including improvement in electrolytes, heart and kidney function, and attention and concentration, many adverse physiological and psychological symptoms may appear during weight restoration. Initial refeeding may be associated with mild transient fluid retention. However, patients who abruptly stop taking laxatives or diuretics may experience marked rebound fluid retention for several weeks, presumably from salt and water retention due tothe elevated aldosterone levels associated with chronic dehydration. Refeeding edema and bloating are frequent occurrences. In rare instances, congestive heart failure may also develop (124). Patients may experience abdominal pain and bloating with meals from the delayed gastric emptying that accompanies malnutrition. Excessively rapid refeeding and nasogastric or parenteral feeding may be particularly dangerous due tothe potential ofinducing severe fluid retention, cardiac arrhythmias, cardiac failure, delirium, or seizures, especially in those with

the lowest weights (125, 126). Hypophosphatemia, which can be life threatening, can emerge during refeeding when reserves are depleted (127). Constipation can occur, which can progress toobstipation and acute bowel obstruction. As weight gain progresses, many patients also develop acne and breast tenderness. Many patients become unhappy and demoralized about resulting changes in body shape. Management strategies for dealing with these side effects include careful refeeding (toresult in not more than 2-3 lb/week ofweight gain aside from simple rehydration); frequent physical examinations; monitoring ofserum electrolytes (including sodium, potassium, chloride, bicarbonate, calcium, phosphorus, and magnesium) in patients developing refeeding edema; and forewarning patients about refeeding edema. When nasogastric feeding is necessary, continuous feeding (i.e., over 24 hours) may be less likely than three tofour bolus feedings a day toresult in metabolic abnormalities or subjective discomfort and may be better tolerated by patients. d. Implementation Healthy target weights and expected rates ofcontrolled weight gain should be established (e.g., 2-3 lb/ week on inpatient units). Refeeding programs should be implemented in nurturing emotional contexts. Staff should convey topatients their intentions totake care ofthem and not let them die even when the illness prevents the patients from taking care ofthemselves. Staff should clearly communicate that they are not seeking toengage in control battles and are not trying topunish patients with aversive techniques. Some positive and negative reinforcements should be built into the program (e.g., required bed rest, exercise restrictions, or restrictions ofoff-unit privileges; these restrictions are reduced or terminated as target weights and other goals are achieved). Intake levels should usually start at 30-40 kcal/kg per day (approximately 1000-1600 kcal/day). Intake may have tobe increased toas high as 70-100 kcal/kg per day for some patients during the weight gain phase. Intake levels during weight maintenance and as needed in children and adolescents for further growth and maturation should be set at 40-60 kcal/kg per day. Kaye and colleagues (128) found that weight-restored patients with anorexia nervosa often require 200-400 calories more than gender-, age-, weight-, and height-matched control subjects tomaintain weight. Some ofthis difference may be due tohigher rates offidgeting and other non-exercise-related energy expenditure in these patients (129). Some patients who require higher caloric intakes are exercising frequently, vomiting, or discarding food, while others may have truly higher metabolic rates or other forms ofenergy expenditure, e.g., fidgeting. Dietitians can help patients choose their own meals and provide a structured food plan that ensures nutritional adequacy and makes certain that none ofthe major food groups are avoided. Some patients are extremely unable torecognize their illness, accept the need for treatment, or tolerate the guilt that would accompany eating, even when performed tosustain their lives. On these rare occasions staff has totake over the responsibilities for providing life-preserving care. Nasogastric feedings are preferable tointravenous feedings and may be experienced positively by some patients-particularly younger patients-who may feel relieved toknow that they are being cared for and who, while they cannot bring themselves toeat, are willing toallow physicians tofeed them. Total parenteral feeding is required only very rarely and in life-threatening situations. Forced nasogastric or parenteral feeding can be accompanied by substantial dangers (e.g., severe fluid retention and cardiac failure from rapid refeeding), so these interventions should not be used routinely. In situations where involuntary forced feeding is considered, careful thought should be given toclinical circumstances, family opinion, and relevant legal and ethical dimensions ofthe patient's treatment.

General medical monitoring during refeeding should include assessment ofvital signs, food and fluid intake, and output, if indicated, as well as observation for edema, rapid weight gain (associated primarily with fluid overload), congestive heart failure, and gastrointestinal symptoms. Minerals and electrolytes should also be closely monitored since hypophosphatemia and clinically significant electrolyte imbalances can be life-threatening. Serum potassium levels should be regularly monitored in patients who are persistent vomiters. Hypokalemia should be treated with oral potassium supplementation and rehydration. Serum phosphorus levels may drop precipitously during refeeding from the utilization ofphosphorus during anabolism in the face oftotal body depletion. In such cases phosphorus supplementation will be necessary (125). Patients suspected ofartificially increasing their weight should be weighed in the morning after voiding, wearing only a gown; their fluid intake also should be carefully monitored. Assessment ofurine specimens obtained at the time ofweigh-in for specific gravity may help ascertain the extent towhich the measured weight reflects excessive water intake. Physical activity should be adapted tothe food intake and energy expenditure ofthe patient, taking into account bone mineral density and cardiac function. For the severely underweight, patient exercise should be restricted and always carefully supervised and monitored. Once a safe weight is achieved, the focus ofan exercise program should be on physical fitness as opposed toexpending calories. The focus on fitness should be balanced with restoring patients' positive relationships with their bodies-helping them totake back control and get pleasure from physical activities rather than being self-critically, even masochistically, enslaved tothem. Staff should help patients deal with their concerns about weight gain and body image changes, since these are particularly difficult adjustments for patients tomake. Research that addresses the optimal length ofhospitalization is sparse. Two studies have reported that hospitalized patients who are discharged at lower than their target weight subsequently relapse and are rehospitalized at higher rates than those who achieve their target weight. Often, these low-weight discharges were associated with brief lengths ofstay. The closer the patient is toideal weight at the time ofdischarge from the hospital, the lower the risk ofrelapse (130, 131). There is no available evidence toshow that brief stays for anorexia nervosa are associated with good long-term outcomes. 2. Psychosocial treatments a. Goals The goals ofpsychosocial treatments are tohelp patients 1) understand and cooperate with their nutritional and physical rehabilitation, 2) understand and change the behaviors and dysfunctional attitudes related totheir eating disorder, 3) improve their interpersonal and social functioning, and 4) address comorbid psychopathology and psychological conflicts that reinforce or maintain eating disorder behaviors. Achieving these goals often requires an initial enhancement ofpatients' motivation tochange along with ongoing efforts tosustain this motivation. b. Efficacy Few systematic trials ofpsychosocial therapies have been completed, and a few others are under way. Most evidence for the efficacy ofpsychosocial therapies comes from case reports or case series (21). Additional evidence comes from the considerable clinical experience that

suggests a well-conducted regimen ofpsychotherapy plays an important role in both ameliorating the symptoms ofanorexia nervosa and preventing relapse. Structured inpatient and partial hospitalization programs. Most inpatient programs employ one ofa variety ofbehaviorally formulated interventions. These behavioral programs commonly provide a combination ofnonpunitive reinforcers (e.g., empathic praise, exerciserelated limits and rewards, bed rest and privileges linked toachieving weight goals and desired behaviors). Behavioral programs have been shown toproduce good short-term therapeutic effects (132). One meta-analysis that compared behavioral psychotherapy programs totreatment with medications alone found that behavior therapy resulted in more consistent weight gain among patients with anorexia nervosa as well as shorter hospital stays (132). Some studies (133, 134) have shown that "lenient" behavioral programs, which utilize initial bed rest and the threat ofreturning the patient tobed if weight gain does not continue, may be as effective and perhaps in some situations more efficient than "strict" programs, in which meal-by-meal caloric intake or daily weight is tied precisely toa schedule ofprivileges (e.g., time out ofbed, time off the unit, permission toexercise or receive visitors). The use ofvarious modalities considered coercive by patients with anorexia nervosa, for whom control is ofsuch importance, is an issue tobe carefully considered. The setting oflimits is developmentally appropriate in the management ofadolescents and may help shape the patient's behavior in a healthy direction. It is essential for caregivers tobe clear about their own intentions and empathic regarding the patients' impressions ofbeing coerced. Caregivers should be seen as using techniques that are not meant as coercive measures but rather are components ofa general medical treatment required for the patient's health and survival. Individual psychotherapy. During the acute phase oftreatment, the efficacy ofspecific psychotherapeutic interventions for facilitating weight gain remains uncertain. Clinical consensus suggests that during acute refeeding and while weight gain is occurring, it is virtually always beneficial toprovide patients with individual psychotherapeutic management that is psychodynamically sensitive and informed and that provides empathic understanding, explanations, praise for posifive efforts, coaching, support, encouragement, and other positive behavioral reinforcement. During the acute phase oftreatment, as well as later on, seeing patients' families is also helpful. For patients who initially lack motivation, psychotherapeutic encounters that employ techniques based on motivational enhancement may help patients increase their awareness and desire for recovery. On the other hand, attempts toconduct formal psychotherapy with starving patients-who are often negativistic, obsessional, or mildly cognitively impaired-- may often be ineffective. Clinical consensus suggests that psychotherapy alone is generally not sufficient totreat severely malnourished patients with anorexia nervosa. While the value ofestablishing and maintaining a psychotherapeutically informed relationship is clearly beneficial, and psychotherapeutic sessions toenhance motivation and tofurther weight gain are likely tobe helpful, the value offormal psychotherapy during the acute refeeding stage is uncertain (135). As yet, no controlled studies have reported whether cognitive behavior psychotherapy or other specific psychotherapeutic interventions are effective for nutritional recovery. Some practitioners have used various modalities ofgroup psychotherapy programs adjunctively in the treatment ofanorexia nervosa (136-138). However, practitioners have also found that group psychotherapy programs conducted during the acute phase among malnourished patients with anorexia nervosa may be ineffective and can sometimes have negative therapeutic effects (e.g., patients may compete for who can be thinnest or exchange countertherapeutic techniques on simulating weight gain or hiding food) (139).

However, once malnutrition has been corrected and weight gain has started, considerable agreement exists that psychotherapy can be very helpful for patients with anorexia nervosa. Although there has been little formal study ofits effectiveness, psychotherapy is generally thought tobe helpful for patients tounderstand 1) what they have been through; 2) developmental, family, and cultural antecedents oftheir illness; 3) how their illness may have been a maladaptive attempt tocope and emotionally self-regulate; 4) how toavoid or minimize risks ofrelapse; and 5) how tobetter deal with salient developmental and other important life issues in the future. At present there is no absolute weight or percentage ofbody fat that indicates when a patient is actually ready tobegin formal psychotherapy. However, clinical experience shows that patients often display improved mood, enhanced cognitive functioning, and clear thought processes even before there is substantial weight gain. Many clinicians favor cognitive behavior psychotherapy for maintaining healthy eating behaviors and cognitive or interpersonal psychotherapy for inducing cognitive restructuring and promoting more effective coping (140, 141). Many clinicians also employ psychodynamically oriented individual or group psychotherapy after acute weight restoration toaddress underlying personality disorders that may contribute tothe illness ahd tofoster psychological insight and maturation (15, 97, 98, 100, 142). Thus, verbal or experiential psychotherapeutic interventions can begin as soon as the patient is no longer in a medically compromised state. In a minority ofpatients whose refractory anorexia nervosa continues despite notable trials ofnutritional rehabilitation, medications, and hospitalizations, more extensive psychotherapeutic measures may be undertaken in further efforts toengage and help motivate them, or, failing that, as compassionate care. This "difficult totreat" subgroup may represent an as yet poorly understood group ofpatients with malignant, chronic anorexia nervosa. Efforts made tounderstand and toengage the unique plight ofsuch a patient may sometimes result in engagement in the therapeutic alliance such that the nutritional protocol may begin (97-99, 143). For patients who have difficulty talking about their problems, clinicians have also tried a variety ofnonverbal therapeutic methods, such as creative arts and movement therapy programs, and have reported them tobe useful (144). At various stages ofrecovery, occupational therapy programs may also enhance deficits in self-concept and self-efficacy (145, 146). Family psychotherapy. Family therapy and couples psychotherapy are frequently useful for both symptom reduction and dealing with family relational problems that may contribute tomaintaining the disorder. In one controlled study ofpatients with anorexia nervosa with onset at or before age 18 and a duration offewer than 3 years, those treated with family therapy showed greater improvement 1 year after discharge from the hospital than those treated with individual psychotherapy. The 5-year follow-up study showed, quite remarkably, a continuing effect offamily therapy (147, 148). The study also points out that family therapy may have more impact for adolescents with eating disorders than for adults. One limitation ofthis study was that patients were not assigned toreceive both family and individual treatment, a combination frequently used in practice. Particular help should be offered topatients with eating disorders who are themselves mothers. Attention should be paid totheir mothering skills and totheir offspring tominimize the risk oftransmission ofeating disorders (149-151). Psychosocial interventions based on addiction models. Some clinicians consider that eating disorders may be usefully treated through addiction models, but no data from short- or longterm outcome studies that used these methods have been reported. Some concerns about

addiction-oriented programs for eating disorders result from zealous and narrow application ofthe 12-step philosophy. Clinicians have reported encountering patients who, while attempting toresolve anorexia nervosa by means of12-step programs alone, could have been greatly helped by adding conventional treatment approaches tothe 12-step model, such as medications, nutritional counseling, and psychodynamic or cognitive behavior approaches. By limiting their attempts torecover to12 steps alone, such patients not only deprive themselves ofthe potential benefits ofconventional treatments but also may expose themselves tomisinformation about nutrition and eating disorders offered by well-intentioned nonprofessionals encountered in these groups. It is important for programs that employ these models tobe equipped tocare for patients with the substantial psychiatric and general medical problems that are often associated with eating disorders. Some programs attempt toblend features ofaddiction models, such as the 12 steps, with medical model programs that employ cognitive behavior approaches (152). However, no systematic data exist regarding the effectiveness ofthese approaches for any patients with anorexia nervosa. Support groups. Support groups led by professionals or by advocacy organizations are available and provide patients and their families with mutual support, advice, and education about eating disorders. These groups may be ofadjunctive benefit in combination with other treatment modalities. Patients and their families are increasingly using on-line web sites, news groups, and chat rooms as resources. While a substantial amount ofworthwhile information and support are available in this fashion, lack ofprofessional supervision may sometimes lead tomisinformation and unhealthy dynamics among users. Clinicians should inquire about the use ofelectronic support and other alternative and complementary approaches and be prepared todiscuss information and ideas that patients and their families have gathered from these sources. c. Implementation Although a variety ofdifferent management models are used for patients with anorexia nervosa, there are no data available on their efficacies. When competent todo so, the psychiatrist should manage both the general medical and psychiatric needs ofthe patient. Some programs routinely arrange for interdisciplinary team management (sometimes called split management) models oftreatment, wherein a psychiatrist writes orders, handles administrative and general medical requirements, and prescribes behavioral techniques intended tochange the disturbed eating and weight patterns. Other clinicians then provide the psychotherapeutic intervention (in the form ofcognitive behavior psychotherapy, psychodynamic psychotherapy, or family therapy) with the patient alone or in a group. For this management model towork effectively, all personnel must work closely together, maintaining open communication and mutual respect toavoid reinforcing some patients' tendencies toplay staff off each other, i.e., tosplit the staff. An alternative interdisciplinary management approach has general medical care providers (e.g., specialists in internal medicine, pediatrics, adolescent medicine, and nutrition) manage general medical issues, such as nutrition, weight gain, exercise, and eating patterns, while the psychiatrist addresses the psychiatric issues. In adolescence, the biopsychosocial nature ofanorexia nervosa and bulimianervosa especially indicates the need for interdisciplinary treatment. Each aspect ofcare must be developmentally tailored tothe treatment ofadolescents (153).

3. Medications a. Goals Medications are used most frequently after weight has been restored tomaintain weight and normal eating behaviors as well as treat psychiatric symptoms associated with anorexia nervosa. b. Efficacy Antidepressants. Studies ofantidepressants for restoration ofweight are limited, and these medications are not routinely used in the acute phase oftreatment for severely malnourished patients. One recent controlled study (154) showed no advantage for adding fluoxetine tonutritional and psychosocial interventions in the treatment ofhospitalized, malnourished patients with anorexia nervosa with respect toeither the amount or the speed ofweight recovery. Results from an uncontrolled trial (155) suggest that fluoxetine may help some treatment-resistant patients with weight restoration, but many patients will not be helped. Antidepressants may be considered after weight gain when the psychological effects ofmalnutrition are resolving, since these medications have been shown tobe helpful with weight maintenance (128). In one controlled trial, weight-restored patients with anorexia nervosa who took fluoxetine (average 40 mg/day) after hospital discharge had less weight loss, depression, and fewer rehospitalizations for anorexia nervosa during the subsequent year than those who received placebo. Few other controlled studies ofantidepressant treatment ofanorexia nervosa have been published. In an open outpatient study (156), those treated with psychotherapy plus citalopram did worse (losing several kilograms) than underweight anorexia nervosa patients treated with psychotherapy alone (whose weights dropped about 0.2 kg during the period ofobservation), which suggests that this SSRI medication was counterproductive for this population. In one study (157), lower-weight patients with the restricting subtype ofanorexia who were receiving intensive inpatient treatment seemed tobenefit, albeit toa small degree, from a combination ofamitriptyline and cyproheptadine. In another study (158), no significant beneficial effect was observed from adding clomipramine tothe usual treatment (although doses ofonly 50 mg/day were used). SSRIs are commonly considered for patients with anorexia nervosa whose depressive, obsessive, or compulsive symptoms persist in spite ofor in the absence ofweight gain. Other medications. Few controlled studies have been published on the use ofother psychotropic medications for the treatment ofanorexia nervosa. In one study (159), lithium carbonate resulted in no substantial benefit. Another study suggested no significant benefit for pimozide (160). Other psychotropic medications are most often used totreat psychiatric symptoms that may be associated with anorexia nervosa. Examples include low doses ofneuroleptics for marked obsessionality, anxiety, and psychotic-like thinking and antianxiety agents used selectively before meals toreduce anticipatory anxiety concerning eating (31, 161). Although there are no controlled studies tosupport effectiveness, eating disorders clinicians are increasingly using low doses ofnewer novel antipsychotic medications together with SSRIs or other new antidepressants in treating highly obsessional and compulsive patients with anorexia nervosa. Other somatic treatments, ranging from vitamin and hormone treatments toelectroconvulsive therapy, have been tried in uncontrolled studies. None has been shown tohave specific value

in the treatment ofanorexia nervosa symptoms (162). Although estrogen replacement is sometimes used in anorexia nervosa patients with chronic amenorrhea toreduce calcium loss and thereby reduce the risks ofosteoporosis (25), existing evidence in support ofhormone replacement therapy for the treatment or prevention ofosteopenia in women with anorexia nervosa is marginal at best. Estrogen replacement has not been evaluated in children or adolescents. Seeman and colleagues (163) reported that the lumbar bone mineral density ofwomen with anorexia nervosa who were taking oral contraceptives was significantly higher than that ofpatients not supplemented with estrogen, although the bone mineral density in both groups remained below normal for age. In preliminary studies (164, 165), hormone replacement therapy did not effectively improve bone mass density. The only controlled trial todate that looked at the effects ofestrogen administration on women with anorexia nervosa showed that estrogen-- treated patients had no significant change in bone mass density compared tocontrol subjects. However, a subgroup ofthe estrogen-treated patients whose initial body weight was less than 70% oftheir ideal weight had a 4.0% increase in mean bone density, whereas subjects ofcomparable body weight not treated with estrogen had a further 20.1% decrease in bone density. This finding suggests that hormone replacement therapy may help a subset oflow-weight women with anorexia nervosa (27). At the same time, artificially inducing menses carries the risk ofsupporting or reinforcing a patient's denial that she does not need togain weight. On the other hand, weight rehabilitation has been shown tobe an effective means ofincreasing bone mineral density (24, 166). Tosummarize, estrogen alone does not generally appear toreverse osteoporosis or osteopenia, and unless there is weight gain, it does not prevent further bone loss. Before offering estrogen, many clinicians stress that efforts should first be made toincrease weight and achieve resumption ofnormal menses 167). Furthermore, at the present time there is no evidence that any ofthe new treatments for postmenopausal osteoporosis, such as biphosphonates, are effective for treating osteoporosis in patients with anorexia nervosa (168). However, studies concerning these medications, bone growth factors, and other investigative treatments are now under way. If fracture risk is substantial, patients should be cautioned toavoid high-impact exercises. Pro-motility agents such as metoclopramide are commonly offered for the bloating and abdominal pains due togastroparesis and premature satiety seen in the some patients. c. Side effects and toxicity Many clinicians report that malnourished depressed patients are more prone toside effects and less responsive tothe beneficial effects oftricyclics, SSRIs, and other novel antidepressant medications than depressed patients ofnormal weight. For example, the use oftricyclics may be associated with greater risks ofhypotension, increased cardiac conduction times, and arrhythmia, particularly in purging patients whose hydration may be inadequate and whose cardiac status may be nutritionally compromised. Although fluoxetine has been found toimpair appetite and cause weight loss in normal weight and obese patients at higher doses, this effect has not been reported in anorexia nervosa patients treated with lower doses. Citalopram has been associated with additional weight loss in anorexia nervosa (156). Because ofthe reported higher seizure risk associated with bupropion in purging patients, this medication should not be used in such patients (169, 170). Strategies tomanage side effects include limiting the use ofmedications topatients with persistent depression, anxiety, or obsessive-compulsive symptoms; using low initial doses in

underweight patients; and being very vigilant about side effects. Given other alternatives, tricyclic antidepressants should be avoided in underweight patients and in patients who are at risk for suicide. In patients for whom there is a concern regarding potential cardiovascular effects ofmedication, cardiovascular consultation toevaluate status and toadvise on the use ofmedication may be helpful. d. Implementation Because anorexia nervosa symptoms and associated features such as depression may remit with weight gain, decisions concerning the use ofmedications should often be deferred until weight has been restored. Antidepressants can be considered for weight maintenance. The decision touse medications and which medications tochoose will be determined by the remaining symptom picture (e.g., antidepressants are usually considered for those with persistent depression, anxiety, or obsessive-compulsive symptoms). B. TREATMENT OF BULIMIANERVOSA Strategies for the treatment of bulimianervosa include nutritional counseling and rehabilitation; psychosocial interventions (including cognitive behavior, interpersonal, behavioral, psychodynamic, and psychoanalytic approaches) in individual or group format; family interventions; and medications. 1. Nutritional rehabilitation Reducing binge eating and purging are primary goals in treating bulimianervosa. Because most patients described in the bulimianervosa psychotherapy treatment literature have been ofnormal weight, weight restoration is usually not a focus oftherapy as it is with patients with anorexia nervosa. Even if they are within statistically normal ranges, many patients with bulimianervosa weigh less than their appropriate biologically determined set points (or set ranges) and may -have togain some weight toachieve physiological and emotional stability. These patients require the establishment ofa pattern ofregular, non-binge meals, with attention paid toincreasing their caloric intake and expanding macronutrient selection. Although many patients with bulimianervosa report irregular menses, improvement in menstrual function has not been systematically assessed in the available outcome studies. Even among patients ofnormal weight, nutritional counseling can be used toaccomplish a variety ofgoals, such as reducing behaviors related tothe eating disorder, minimizing food restriction, correcting nutritional deficiencies, increasing the variety offoods eaten, and encouraging healthy but not excessive exercise patterns. There is some evidence that treatment programs that include dietary counseling and management as part ofthe program are more effective than those that do not (171). 2. Psychosocial treatments a. Goals The goals ofpsychosocial interventions vary and can include the following: reduction in, or elimination of, binge-eating and purging behaviors; improvement in attitudes related tothe eating disorder; minimization offood restriction; increasing the variety offoods eaten; encouragement ofhealthy but not excessive exercise patterns; treatment ofcomorbid

conditions and clinical features associated with eating disorders; and addressing themes that may underlie eating disorder behaviors such as developmental issues, identity formation, body image concerns, self-esteem in areas outside ofthose related toweight and shape, sexual and aggressive difficulties, affect regulation, gender role expectations, family dysfunction, coping styles, and problem solving. b. Efficacy Individual psychotherapy. Cognitive behavioral psychotherapy, specifically directed at the eating disorder symptoms and underlying cognitions in patients with bulimianervosa, is the psychosocial intervention that has been most intensively studied and for which there is the most evidence ofefficacy (16, 171-188). Significant decrements in binge eating, vomiting, and laxative abuse have been documented among some patients receiving cognitive behavior therapy; however, the percentage ofpatients who achieve full abstinence from binge/purge behavior is variable and often includes only a minority ofpatients (16, 172, 174-- 178, 180, 181, 183, 185). Among studies with control arms, cognitive behavior therapy has been shown tobe superior towaiting list (16, 174, 177, 181), minimal intervention (185), or nondirective control (180) conditions. In most ofthe published cognitive behavior therapy trials, significant improvements in either self-reported (177, 189) or clinician-rated (179) mood have been reported. In practice, many other types ofindividual psychotherapy are employed in the treatment of bulimianervosa, such as interpersonal, psychodynamically oriented, or psychoanalytic approaches. Clinical experience also suggests that these approaches can help in the treatment ofthe comorbid mood, anxiety, personality, interpersonal, and trauma- or abuse-related disorders that frequently accompany bulimianervosa (190). Evidence for the efficacy ofthese treatments for bulimianervosa comes mainly from case reports and case series. Some modes oftherapy, including the interpersonal and psychodynamic approaches, have also been studied in randomized trials as comparison treatments for cognitive behavior therapy or in separate trials (175, 178, 191). In general, these and other studies have shown interpersonal psychotherapy tobe helpful. The specific forms offocused psychodynamic psychotherapy that have been studied in direct comparison tocognitive behavior therapy have generally not been as effective as cognitive behavior therapy in short-term trials (192, 193). Behavioral therapy, which consists ofprocedures ofexposure (e.g., tobinge eating food) plus response prevention (e.g., inhibiting vomiting after eating), has also been considered as treatment for bulimianervosa. However, the evidence regarding the efficacy ofthis approach is conflicting, as studies have reported enhanced (194), not significantly altered (195), and reduced (172) responses tocognitive behavior therapy when behavioral therapy was used as an adjunct. On the basis ofresults from a large clinical trial, and given its logistical complexity, exposure treatment does not appear tohave additive benefits over a solid core ofcognitive behavior therapy (90). Very few studies have directly compared the effectiveness ofvarious types ofindividual psychotherapy for treatment of bulimianervosa. One study by Fairburn and colleagues that compared cognitive behavior therapy, interpersonal psychotherapy, and behavior therapy showed that all three treatments were effective in reducing binge-eating symptoms by the end oftreatment, but cognitive behavior therapy was most effective in improving disturbed attitudes toward shape and weight and restrictive dieting (175, 176, 192, 193, 196, 197). However, at long-term follow-up (mean= ..8 years), the study found equal efficacy for

interpersonal psychotherapy and cognitive behavior therapy on eating variables, attitudes about shape and weight, and restrictive dieting (197), which suggests that interpersonal psychotherapy patients had "caught up" in terms ofbenefits over time. An ongoing multicenter study ( 12) has basically replicated these findings. Group psychotherapy. Group psychotherapy approaches have also been used totreat bulimianervosa. A meta-analysis of40 group treatment studies suggested moderate efficacy, with those studies that reported 1-year follow-up data reporting that improvement was typically maintained (184). There is some evidence -that group treatment programs that include dietary counseling and management as part ofthe program are more effective than those that do not (171), and that frequent visits early in treatment (e.g., sessions several times a week initially) result in improved outcome (175, 176, 183). Many clinicians favor a combination ofindividual and group psychotherapy. Psychodynamic and cognitive behavior approaches may be combined. Group therapy may help patients tomore effectively deal with the shame surrounding their disease as well as provide additional peer-based feedback and support. Family and marital therapy. Family therapy has been reported tobe helpful in the treatment of bulimianervosa in a large case series, but more systematic studies are not available (186). Family therapy should be considered whenever possible, especially for adolescents who still live with their parents, older patients with ongoing conflicted interactions with parents, or patients with marital discord. For women with eating disorders who are mothers, parenting help and interventions aimed at assessing and, if necessary, aiding their children should be included (149-151). Support groups/12-step programs. Considerable controversy exists regarding the role of12step programs as the sole intervention in the treatment ofeating disorders, primarily because these programs do not address nutritional considerations or the complex psychological/behavioral deficits ofpatients with eating disorders. Twelve-step programs or other approaches that exclusively focus on the need for abstinence without attending tonutritional considerations or behavioral deficits are not recommended as the sole initial treatment approach for bulimianervosa. Some patients have found Overeaters Anonymous and similar groups tobe helpful as adjuncts toinitial treatments or for preventing subsequent relapses (182, 198), but no data from shortor long-term outcome studies ofthese programs have been reported. Because ofthe great variability ofknowledge, attitudes, beliefs, and practices from chapter tochapter and from sponsor tosponsor regarding eating disorders and their general medical and psychotherapeutic treatment, and because ofthe great variability ofpatients' personality structures, clinical conditions, and susceptibility topotential countertherapeutic practices, clinicians should carefully monitor patients' experiences with these programs. c. Side effects and toxicity Patients occasionally have difficulty with certain elements ofpsychotherapy. For example, among patients receiving cognitive behavior therapy, some are quite resistant toselfmonitoring while others have difficulty mastering cognitive restructuring. Many patients are initially resistant tochanging their eating behaviors, particularly when it comes toincreasing their caloric intake or reducing exercise. However, complete lack ofacceptance ofthe approach appears tobe rare, although this has not been systematically studied.

Management strategies todeal with potential negative effects ofpsychotherapeutic interventions include 1) careful pretreatment evaluation, during which time the therapist must assess and enhance the patient's level ofmotivation for change and identify appropriate candidates for a given approach and format (e.g., individual versus group); 2) being alert toa patient's reactions toand attitudes about the proposed treatment and listening toand discussing the patient's concerns in a supportive fashion; 3) ongoing monitoring ofthe quality ofthe therapeutic relationship; and 4) identification ofpatients for whom another treatment should be coadministered or given before psychotherapy begins (e.g., chemical dependency treatment for those actively abusing alcohol or other drugs, antidepressant treatment for patients whose depression makes them unable tobecome actively involved, more intensive psychotherapy for those with severe personality disorders, and group therapy for those not previously participating). Alternative strategies may be necessary tomove the therapeutic process forward and toprevent abrupt termination oftherapy. d. Implementation A review ofthe literature shows that the way in which psychotherapy has been implemented varies, in some cases considerably. For cognitive behavior therapy, several controlled trials used fairly short-term, time-limited interventions, such as 20 individual psychotherapy sessions over 16 weeks, with two scheduled visits per week for the first 4 weeks (172, 175, 176, 192, 193, 196, 197, 199-201). Some investigators have examined whether more than one visit per week is needed, particularly early in treatment. In one study ofgroup cognitive behavior psychotherapy (183), additional visits early in treatment or twice weekly visits throughout treatment were both superior regimens toone psychotherapy session per week. A growing literature has suggested that cognitive behavior therapy can be administered successfully through self-help or guided self-help manuals, at times in association with pharmacotherapy (202-206). While such techniques are not yet sufficiently developed torecommend their acceptance as a primary treatment strategy, developments in this area may prove ofgreat importance in providing treatment topatients who otherwise might not have access toadequate care. Clinicians unfamiliar with the cognitive behavior therapy approach may benefit from acquainting themselves with these treatment manuals and obtaining specialized training in cognitive behavior therapy tofurther help their bulimianervosa patients by using such manuals in treatment (192, 207-212). This section has presented the results ofcognitive behavior therapy and other short-term treatments, since these treatments have been the subject ofthe preponderance ofstudies. However, the field is in great need ofwell-conducted studies that examine other treatment approaches, particularly psychodynamically informed therapies. In addition, most available studies report relatively short-term results. Better studies are needed ofthe long-term effectiveness ofthese as well as other psychotherapeutic approaches, particularly for the complex presentations with multiple comorbid conditions that are usually seen in psychiatric practice. 3. Medications a. Goals Medications, primarily antidepressants, are used toreduce the frequency ofdisturbed eating behaviors such as binge eating and vomiting. In addition, pharmacotherapy is employed

toalleviate symptoms that may accompany disordered eating behaviors, such as depression, anxiety, obsessions, or certain impulse disorder symptoms. b. Antidepressants Efficacy. The observation that some patients with bulimianervosa were clinically depressed led tothe first uses ofantidepressants in the acute phase oftreatment (213). However, later randomized trials demonstrated that nondepressed patients also responded tothese medications and that baseline presence ofdepression was not a predictor ofmedication response (214-- 216). Although wide variability exists across studies, reductions in hinge eating and vomiting rates in the range of50%-75% have been achieved with active medication (170, 217-231). The available studies also suggest that antidepressants improve associated comorbid disorders and complaints such as mood and anxiety symptoms. Some studies show improved interpersonal functioning with medication as well. Specific antidepressant agents that have demonstrated efficacy among patients with bulimianervosa in double-blind, placebo-controlled studies include tricyclic compounds such as imipramine (213, 232), desipramine (214, 233-235), and amitriptyline (for mood but not eating variables) (215); the SSRI fluoxetine (221-223); several MAOIs, including phenelzine (216), isocarboxazide (236), and brofaramine (for vomiting but not binge eating) (237); and several other antidepressants, including mianserin (231), bupropion (170), and trazodone (229). (Bupropion, however, was associated with seizures in purging bulimic patients, so its use is not recommended.) One study (230) suggests that patients with atypical depression and bulimianervosa may preferentially respond tophenelzine in comparison with imipramine. However, since MAOIs are potentially dangerous in patients with chaotic eating and purging, great caution should be exercised in their use for bulimianervosa. Todate, the only medication approved by the Food and Drug Administration for bulimianervosa is fluoxetine. Two trials have examined the utility ofantidepressant maintenance therapy. One trial with fluvoxamine (219) demonstrated an attenuated relapse rate versus placebo in patients with bulimianervosa who were on a maintenance regimen ofthe medication after leaving an inpatient treatment program; however, in the continuation arm ofa clinical trial with desipramine (235), 29% ofthe patients entering that phase experienced a relapse within 4 months. Trials using fluoxetine for relapse prevention are currently under way. Side effects and toxicity. Side effects vary widely across studies depending on the type ofantidepressant medication used. For the tricyclic antidepressants, common side effects include sedation, constipation, dry mouth, and, with amitriptyline, weight gain (213215, 232234). The toxicity oftricyclic antidepressants in overdose, up toand including death, also dictates caution in patients who are at risk for suicide. In the first multicenter fluoxetine trial (221), the most common side effects at 60 mg/day were insomnia (30%), nausea (28%), and asthenia (23%). In the second multicenter study (223), the most common side effects were insomnia (35%), nausea (30%), and asthenia (21%). Sexual side effects are also common in patients receiving SSRIs. Studies using various other medications have reported substantial dropout rates, although attrition rates across clinical trials have varied dramatically, and the degree towhich medication side effects are the cause ofhigh dropout rates has not been defined. Other common contributors todropping out ofclinical trials may involve subtle interpersonal and psychodynamic factors in the physician-patient relationships, which if left unaddressed will also contribute totreatment resistance. The quality ofcollaboration between patient and clinician is key tosuccess in medication trials (238).

For patients with bulimianervosa who require mood stabilizers, lithium carbonate is problematic, since lithium levels may shift markedly with rapid volume changes. Both lithium carbonate and valproic acid frequently lead toundesirable weight gains. Selection ofa mood stabilizer that avoids these problems may result in better compliance and effectiveness. No clear risk factors for the development ofside effects among patients with bulimianervosa have been identified. As in most clinical situations, careful preparation ofthe patient regarding possible side effects and their symptomatic management if they develop should be employed (e.g., stool softeners for constipation). Implementation. Often, several different antidepressant medications may have tobe tried sequentially toachieve the optimum effect. Doses oftricyclic and MAOI antidepressants for treating patients with bulimianervosa parallel those used totreat patients with depression, although fluoxetine at doses higher than those used for depression may be more effective for bulimic symptoms (e.g., 60-80 mg/day). The first multicenter fluoxetine study (221) demonstrated that 60 mg was clearly superior to20 mg on most variables, and in the second study (223) all subjects receiving active medication started with 60 mg. The medication was surprisingly well tolerated at this dose, and-many clinicians initiate treatment for bulimianervosa with fluoxetine at the higher dose, titrating downward if necessary due toside effects. In cases where symptoms do not respond tomedication, it is important toassess whether the patient has taken the medication shortly before vomiting. Serum levels ofmedication may be obtained todetermine whether presumably effective levels have actually been achieved. One study (214) suggested that desipramine serum levels similar tothose targeted in depression studies are most therapeutic in patients with bulimianervosa, but in general serum level/response data have not been presented. There are few reports on the use ofantidepressant medications in the maintenance phase. Available data suggest high rates ofrelapse while taking medication and possibly higher rates when medications are withdrawn (235). In the absence ofmore systematic data, most clinicians recommend continuing antidepressant therapy for a minimum of6 months and probably for a year in most patients with bulimianervosa. c. Other medications A number ofother medications have been used experimentally for bulimianervosa without evidence ofefficacy, including fenfluramine (218) and lithium carbonate (224). Fenfluramine has now been taken off the market because ofassociations between its use (mainly in combination with phentermine) and cardiac valvular abnormalities. Lithium continues tobe used occasionally as an adjunct for the treatment ofcomorbid conditions. The opiate antagonist naltrexone has been studied in three ra j vials at doses used for narcotic addiction and for relapse prevention in alcohol abuse (50-120 mg/day). The results consistently show that the medication is not superior toplacebo in the reduction ofbulimic symptoms (217, 225, 228). In a small, double-blind crossover study involving higher doses (e.g., 200-300 mg/day), naltrexone did appear tohave some efficacy. Further studies using these dose ranges are needed. However, there have been mixed reports concerning the risk ofhepatotoxicity with the use ofhigh doses (226, 227, 239). 4. Combinations ofpsychosocial and medication treatment

Six studies have examined the relative efficacy ofpsychotherapy, medication, or both in the treatment of bulimianervosa. In the first study (240), intensive group cognitive psychotherapy (45 hours oftherapy over 10 weeks) was superior toimipramine alone in reducing symptoms ofbinge eating and purging and symptoms ofdepression. Imipramine plus intensive group cognitive behavior therapy did not improve the outcome on eating variables but did improve depression and anxiety variables. In the second study (241), patients in group cognitive behavior therapy improved more than those receiving desipramine alone. Some advantage was also seen for combination therapy on some variables, such as dietary restraint. The third study (242), which compared fluoxetine treatment, cognitive behavior therapy, and combination therapy, favored cognitive behavior therapy alone and suggested little benefit for combination therapy. Results ofthis study are difficult tointerpret because ofa high attrition rate (50% by the 1-month follow-up). In the fourth study (243), cognitive behavior therapy was superior tosupportive psychotherapy; active medication (consisting ofdesipramine, followed by fluoxetine if abstinence from binge eating and purging was not achieved) was superior toplacebo in reducing eating disorder behaviors. The combination ofcognitive behavior therapy and active medication resulted in the highest abstinence rates. The use ofsequential medication in this study addressed a limitation ofearlier studies in that typically when one antidepressant fails, a clinician tries other agents, which often result in better antidepressant efficacy than seen with the first medication alone. In the fifth study (220), no advantage was found for the use offluoxetine over placebo in an inpatient setting, although both groups improved significantly. In the sixth study (244), combination treatment with desipramine and cognitive behavior therapy was terminated prematurely because ofa high dropout rate. In conclusion, the studies suggest that target symptoms such as binge eating and purging and attitudes related tothe eating disorder generally respond better tocognitive behavior therapy than pharmacotherapy (240-242), with at least two studies (241, 243) showing that the combination ofcognitive behavior therapy and medication is superior toeither alone. Two ofthe studies suggest a greater improvement in mood and anxiety variables when antidepressant therapy is added tocognitive behavior therapy (240, 243). Ofnote, many experienced clinicians do not find cognitive behavior therapy tobe as useful as described by researchers. This may be due toseveral factors, including clinician inexperience or discomfort with the methods or differences between patients seen in the community and those who have participated as research subjects in these studies. IV. DEVELOPING A TREATMENT PLAN FOR THE INDIVIDUAL PATIENT The following are recommendations for developing a treatment plan for individual patients with eating disorders. A number offactors should be considered when developing the treatment plan. Table 5 provides guidance for these clinical dimensions (245). A. CHOOSING A SITE OFTREATMENT The services available for the treatment ofeating disorders can range from intensive inpatient settings (in which subspecialty general medical consultation is readily available), through partial hospital and residential programs, tovarying levels ofoutpatient care (from which the patient can receive general medical treatment, nutritional counseling, and/or individual, group, and family psychotherapy). Pretreatment evaluation ofthe patient is essential for determining the appropriate setting oftreatment (246). Weight and cardiac and metabolic status are the most important physical parameters for determining choice ofsetting. Generally,

patients who weigh less than approximately 85% oftheir individually estimated healthy weights have considerable difficulty gaining weight in the absence ofa highly structured program. Those weighing less than about 75% oftheir individually estimated healthy weights are likely torequire a 24-hour hospital program. Once weight loss is severe enough tocause the indications for immediate medical hospitalization, treatment may be less effective, refeeding may entail greater risks, and prognosis may be more problematic than when intervention is provided earlier. Knowledge about gray matter deficits that result from malnutrition and persist following refeeding also point tothe need for earlier rather than later effective interventions. Therefore, hospitalization should occur before the onset ofmedical instability as manifested by abnormal vital signs. The decision tohospitalize should be based on psychiatric and behavioral grounds, including rapid or persistent decline in oral intake; decline in weight despite maximally intensive outpatient or partial hospitalization interventions; the presence ofadditional stressors-such as intercurrent viral illnesses-- that may additionally interfere with the patient's ability toeat; prior knowledge ofweight at which instability is likely tooccur; and comorbid psychiatric problems that merit hospitalization. Indications for immediate medical hospitalization include marked orthostatic hypotension with an increase in pulse of>20 bpm or a drop in blood pressure of>20 mm Hg/minute standing, bradycardia below 40 bpm, tachycardia over 110 bpm, or inability tosustain body core temperature (e.g., temperatures below 97.0 deg F). Most severely underweight patients, those with physiological instability, and many children and adolescents whose weight loss, while rapid, has not been as severe as in adult patients nonetheless require inpatient medical management and comprehensive treatment for support ofweight gain. Guidelines for treatment settings are provided in table 5. Although most patients with uncomplicated bulimianervosa do not require hospitalization, indications for hospitalization can include severe disabling symptoms that have not responded toadequate trials ofcompetent outpatient treatment, serious concurrent general medical problems (e.g., metabolic abnormalities, hematemesis, vital sign changes, or the appearance ofuncontrolled vomiting), suicidality, psychiatric disturbances that would warrant the patient's hospitalization independent ofthe eating disorders diagnosis, or severe concurrent alcohol or drug abuse. Legal interventions, including involuntary hospitalization and legal guardianship, may be necessary toensure the safety oftreatment-reluctant patients whose general medical conditions are life-threatening (247). Decisions tohospitalize on a psychiatric versus general medical or adolescent/pediatric unit depend on the patient's general medical status, the skills and abilities oflocal psychiatric and general medical staffs, and the availability ofsuitable programs tocare for the patient's general medical and psychiatric problems (248). Some evidence suggests that patients treated in eating disorders inpatient specialty units have better outcomes than patients treated in general inpatient settings that lack expertise and experience in treating patients with eating disorders (65). Partial hospitalization and day hospital programs are being increasingly used in attempts todecrease the length ofsome inpatient hospitalizations; for milder cases, these programs are being increasingly used in place ofhospitalization. However, such programs may not be appropriate for patients with lower initial weights (e.g., those who are 575% ofaverage weight for height). In clinical practice, failure ofoutpatient treatment is one ofthe most frequent indications for more intensive treatment, either day/partial hospital or inpatient. In deciding whether totreat in a partial hospitalization program, the patient's level ofmotivation

toparticipate in treatment and ability towork in a group setting should be considered (93, 249). Patients with high motivation tocomply with treatment, cooperative families, brief symptom duration, and who are less than 20% below healthy body weight may benefit from treatment in outpatient settings, but only if they are carefully monitored and if they and their families understand that a more restrictive setting may be necessary if persistent progress is not evident in a few weeks (250-252). Careful monitoring includes at least weekly (and often two tothree times a week) postvoiding gowned weighings, which may also include measurement ofurine specific gravity together with orthostatic vital signs and temperatures. While patients treated in the outpatient setting can remain with their families and continue toattend school or work, these advantages must be balanced against the risks offailure toprogress in recovery. B. PSYCHIATRIC MANAGEMENT Psychiatric management includes a broad range oftasks that are performed by the psychiatrist or that the psychiatrist should ensure are provided tothe patient with an eating disorder. These should be instituted for all patients with eating disorders in combination with other specific treatment modalities. 1. Establish and maintain a therapeutic alliance At the very outset, clinicians should attempt tobuild trust, establish mutual respect, and develop a therapeutic relationship with the patient that will serve as the basis for ongoing exploration and treatment ofthe problems associated with the eating disorder. Eating disorders are frequently long-term illnesses that can manifest themselves in different ways at different points during their course; treating them often requires the psychiatrist toadapt and modify therapeutic strategies over time. During the course oftreatment, patients with eating disorders may resist looking beyond immediate eating disorder symptoms tocomorbid psychopathology and underlying psychodynamics. Psychiatrists should be mindful ofthe fact that the interventions they prescribe for individuals with anorexia nervosa create extreme anxieties in the patients. Encouraging them togain weight asks for them todo the very thing ofwhich they are most frightened. Recognizing and acknowledging topatients one's awareness ofthese effects can assist in building the therapeutic alliance and decrease the patients' perceptions that the psychiatrist just wants tomake them fat and does not understand or empathize with their underlying emotions. Addressing these resistances may be important in allowing treatment toproceed through impasses as well as helping toameliorate factors that serve toaggravate and maintain eating disorders (253). Patients with eating disorders also present treating physicians with extraordinary challenges in understanding and working with countertransference reactions. Because these illnesses are often difficult toameliorate with short-term interventions, they often evoke the feeling in treating clinicians that they have not done enough tochange or alleviate the patient's plight. A frequent range ofcountertransference feelings include beleaguerment, demoralization, and excessive needs tochange the patient with a chronic eating disorder. Some authorities have observed that the gender ofthe therapist plays a role in the particular kind ofcountertransference reactions that come into play (254-256). Concerns about choice ofgender ofthe therapist may be tied topatient concerns about boundary violations and should be attended toin selecting health care providers (257, 258). In addition togender differences, cultural differences between patients and therapists and between patients and other aspects

ofthe care system may also influence the course and conduct oftreatment and require mindful attention. Most authorities believe ongoing processing ofone's countertransference reactions, sometimes with the help ofa supervisor or consultant, can be useful in helping the therapist persevere and reconcile intense, troublesome countertransference reactions. Regardless ofthe theoretical base the clinician uses, countertransference reactions have been described by a wide variety oftherapists who used differing clinical approaches (96-98, 255, 256, 259-261). Patients who have been sexually abused or who have otherwise been the victims ofboundary violations are prone tostir a profound need torescue the patient, which can occasionally result in a loosening ofthe therapeutic structure, loss oftherapeutic boundary keeping, and a sexualized countertransference reaction. In some cases, these countertransference responses have led toovert sexual acting out and unethical treatment on the part ofthe therapist, which may not only compromise treatment but also severely harm the patient (262). Clear boundaries are critical in the treatment ofall patients with eating disorders, not only those who have been sexually abused but also those who may have experienced other types ofboundary intrusions regarding their bodies, eating behaviors, and other aspects ofthe self by family members and others. 2. Coordinate care and collaborate with other clinicians An important task for the psychiatrist is tocoordinate and, depending on expertise, oversee the care ofpatients with eating disorders. A variety ofprofessionals may collaborate in the care and provide such services as nutritional counseling, working with the family, and establishing various individual and group psychotherapeutic, cognitive behavior, or behavior programs. Other physician specialists and dentists should be consulted when necessary for management ofgeneral medical (e.g., cardiac dysfunction) and dental complications. Particularly in treatment settings where the staff does not have training or experience dealing with patients with eating disorders, the provision ofeducation and supervision by the psychiatrist can be crucial tothe success oftreatment (263). 3. Assess and monitor eating disorder symptoms and behaviors The psychiatrist should make a careful assessment ofthe patient's eating disorder symptoms and behaviors (264). Obtaining a detailed report ofa single day or using a calendar as a prompt may help elicit specific information, particularly regarding perceived intake. Having a meal together or observing a meal may provide useful information, permitting the clinician toobserve difficulties patients may have in eating particular foods, anxieties that erupt in the course ofa meal, and rituals concerning food (such as cutting, separating, or mashing) that they may feel compelled toperform. The patient's understanding ofhow the illness developed and the effects ofany interpersonal problems on the onset ofthe eating disorder should be explored. Family history should be obtained regarding eating disorders and other psychiatric disorders, obesity, family interactions in relation tothe patient's disorder, and attitudes toward eating, exercise, and appearance. It is essential not toarticulate theory in order toblame or permit family members toblame one another or themselves. Rather, the point is toidentify stressors whose amelioration may facilitate recovery. In the assessment ofyoung patients, it may be helpful toinvolve parents, school personnel, and health professionals who routinely work with children. The complete assessment usually requires at least several hours, and often patients and their families may not initially reveal pertinent information about sensitive issues, even when directly questioned. Some important information may be uncovered only

after a trusting relationship has been established and the patient is better able toaccurately identify inner emotional states. Formal measures are also available for the assessment ofeating disorders, including selfreport questionnaires and semistructured interviews. Representative examples are listed in table 6. 4. Assess and monitor the patient's general medical condition A full physical examination should be performed by a physician familiar with common findings in patients with eating disorders, with particular attention tovital signs; physical and sexual growth and development (including height and weight); the cardiovascular system; and evidence ofdehydration, acrocyanosis, lanugo, salivary gland enlargement, and scarring on the dorsum ofthe hands (Russell's sign). A dental examination should also be performed. It is generally useful toassess growth, sexual development, and general physical development in younger patients. The use ofa pediatric growth chart may permit identification ofpatients who have failed togain weight and who have growth retardation (265). The need for laboratory analyses should be determined on an individual basis depending on the patient's condition or when necessary for making treatment decisions. Some laboratory assessments indicated for patients with eating disorders and for specific clinical features appear in table 7. 5. Asses and monitor the patient's psychiatric status and safety Attention should be paid tocomorbid psychiatric disturbances, especially affective and anxiety disorders, suicidality, substance abuse, obsessive and compulsive symptoms, and personality disturbances. Shoplifting, stealing food, and self-mutilatory behaviors should be noted. A developmental history should attend totemperament, psychological, sexual and physical abuse, and sexual history. Psychological testing, particularly after nutritional rehabilitation, may clarify personality and neuropsychological disturbances. In addition toassessing behavioral and formal psychopathological aspects ofthe case, it is always useful toinvestigate psychodynamic and interpersonal conflicts that may be relevant tounderstanding and treating the patient's eating disorder. 6. Provide family assessment and treatment Eating disorders impose substantial burdens on the families ofpatients. Parents often avoid recognizing that the child or adolescent is ill and may have difficulties in accepting the seriousness ofthe illness. Parents then often struggle with the belief that they have themselves caused the illness and need help overcoming their guilt so that they can face their children's needs. The feelings ofguilt are exacerbated by the rejection oftheir parenting that is implicit in the child's refusal ofnurturance in the form offood. Parents also have difficulties in accepting the need for treatment or requiring that their child accept treatment, since the child's protest that treatment is noxious only increases the parent's guilt. Parents typically become angry at their child's secretive purging, exercising, and other efforts toavoid food or burn off calories and may come toview the children as "manipulative" rather than desperate. Parents may increasingly avoid their responsibilities ofproviding meals within specific contexts that bind family relationships. They are often riddled with anxieties that their child will die and, depending on the family and gravity ofthe case, may go on todevelop anger,

exhaustion, and despair. The patient's and family's preoccupations, social concerns, and rituals may begin toorient and focus around the illness, particularly family interactions involving meals. Decisions concerning food may impact family get-togethers, social visits, vacations, and even vocational choices. Assessment ofthe family is important whenever possible, particularly for patients living at home or those who are enmeshed with their families. Family assessment may be extremely useful for some patients in order tounderstand interactions that may contribute toongoing illness or that may potentially facilitate recovery. Comprehensive treatment ofthe patient should include an assessment ofthe burden ofthe illness on the family, with support and education given tothe family as part ofthe overall treatment. C. CHOICE OFSPECIFIC TREATMENTS FOR ANOREXIA NERVOSA The aims oftreatment are to1) restore patients tohealthy weight (at which menses and normal ovulation in females, normal sexual drive and hormone levels in males, and normal physical and sexual growth and development in children and adolescents are restored); 2) treat physical complications; 3) enhance patients' motivations tocooperate in the restoration ofhealthy eating patterns and toparticipate in treatment; 4) provide education regarding healthy nutrition and eating patterns; 5) correct core dysfunctional thoughts, attitudes, and feelings related tothe eating disorder; 6) treat associated psychiatric conditions, including defects in mood regulation, self-esteem, and behavior; 7) enlist family support and provide family counseling and therapy where appropriate; and 8) prevent relapse. 1. Nutritional rehabilitation For patients who are markedly underweight, a program ofnutritional rehabilitation should be established. Hospital-based programs should be considered, particularly for the most nutritionally compromised patients (e.g., those whose weight is less than 75% ofthe recommended weight for their height or for children and adolescents whose weight loss may not be as severe but who are losing weight at a rapid ratel. Nutritional rehabilitation programs should establish healthy target weights and have expected rates ofcontrolled weight gain (e.g., 2-3 lb/week for inpatient units and 0.5-1 lb/ week for outpatient programs). Intake levels should usually start at 30-40 kcal/kg per day (approximately 1000-1600 kcal/day) and should be advanced progressively. During the weight gain phase, intake may be increased toas high as 70-100 kcal/kg per day for some patients. During weight maintenance and for ongoing growth and development in children and adolescents, intake levels should be 40-60 kcal/kg per day. Patients who require higher caloric intakes may be discarding food, vomiting, or exercising frequently or have more nonexercise motor activity such as fidgeting; others may have a truly elevated metabolic rate. In addition tocalories, patients benefit from vitamin and mineral supplements (and in particular may require phosphorus before serum hypophosphatemia occurs). Medical monitoring during refeeding is essential and should include assessment ofvital signs as well as food and fluid intake and output; monitoring ofelectrolytes (including phosphorus); and observation for edema, rapid weight gain associated primarily with fluid overload, congestive heart failure, and gastrointestinal symptoms, particularly constipation and bloating. For children and adolescents who are severely malnourished (weight <70% standard body weight) cardiac monitoring, especially at night, may be desirable. Physical activity should be adapted tothe food intake and energy expenditure ofthe patient.

Other treatment options for nutritional rehabilitation include temporary supplementation or replacement ofregular food with liquid food supplements. On occasion, nasogastric feedings may be required. In lifethreatening or very unusual circumstances, parenteral feedings for brief periods may be considered; however, infection is always a risk with parenteral feedings in emaciated and potentially immunocompromised patients with anorexia nervosa. These forceful interventions should be considered only when patients are unwilling tocooperate with oral feedings; when the patient's health, physical safety, and recovery are being threatened; and after appropriate legal and ethical considerations have been taken into account. Additional goals ofnutritional rehabilitation programs include education, ongoing support, and helping patients deal with their concerns about weight gain and body image changes. 2. Psychosocial interventions It is essential that psychosocial interventions incorporate an understanding ofpsychodynamic conflicts, cognitive development, psychological defenses, and the complexity offamily relationships as well as the presence ofother psychiatric disorders. Although research studies regarding psychotherapy treat different interventions as distinctly separate treatments, in practice there is frequent overlap. Most nutritional rehabilitation programs employ a milieu incorporating emotional nurturance and one ofa variety ofbehavioral interventions (which involve a combination ofreinforcers that link exercise, bed rest, and privileges totarget weights, desired behaviors, and informational feedback). Other forms ofindividual psychotherapy are also used in the treatment ofanorexia nervosa, initiated as the patient is gaining weight. However, there has been little formal study ofthe optimal role for either individual or group psychotherapy in treating anorexia nervosa. Because ofthe enduring nature ofmany ofthe psychopathologic features ofanorexia nervosa and the need for support during recovery, ongoing treatment with individual psychotherapeutic interventions is frequently required for at least a year and may take 5-6 years (45). Family therapy and couples psychotherapy are frequently useful for both symptom alleviation and alleviation ofproblems in familial relationships that may be contributing tothe maintenance ofthe disorders. Some practitioners use group psychotherapy as an adjunctive treatment for anorexia nervosa, but caution must be taken that patients do not compete tobe the thinnest or sickest patient or become excessively demoralized through hearing witness tothe difficult, ongoing struggles ofother patients in the group. Programs that focus exclusively on the need for abstinence (e.g., 12-step programs) without attending tonutritional considerations or cognitive and behavioral deficits are not recommended as the sole initial treatment approach for anorexia nervosa; interventions based on addiction models blended with features ofother psychotherapeutic approaches can be considered. Support groups led by professionals or advocacy organizations may be beneficial as adjuncts toother psychosocial treatment modalities. 3. Medications Psychotropic medications should not be used as the sole or primary treatment for anorexia nervosa. In addition, medication therapy should not be used routinely during the weight restoration period. The role for antidepressants is usually best assessed following weight gain, when the psychological effects ofmalnutrition are resolving. However, these medications

should be considered toprevent relapse among weight-- restored patients or totreat associated features ofanorexia nervosa, such as depression or obsessive-compulsive problems. D. CHOICE OFSPECIFIC TREATMENTS FOR BULIMIANERVOSA 1. Nutritional rehabilitation/counseling A primary focus for nutritional rehabilitation concerns monitoring the patient's patterns ofbinge eating and purging. Most patients with bulimianervosa are ofnormal weight, so nutritional restoration will not be a central focus oftreatment. However, even among patients ofnormal weight, nutritional counseling as an adjunct toother treatment modalities may be useful for reducing behaviors related tothe eating disorder, minimizing food restriction, increasing the variety offoods eaten, and encouraging healthy but not excessive exercise patterns. 2. Psychosocial interventions Psychosocial interventions should be chosen on the basis ofa comprehensive evaluation ofthe individual patient, considering cognitive and psychological development, psychodynamic issues, cognitive style, comorbid psychopathology, patient preferences, and family situation. With respect toshort-term interventions for treating acute episodes of bulimianervosa, cognitive behavioral psychotherapy is the psychosocial treatment for which the most evidence for efficacy currently exists. However, controlled trials have also shown interpersonal psychotherapy tobe very useful for this disorder. Behavioral techniques, such as planned meals and self-monitoring, may also be helpful for initial symptom management and interrupting the binge-- purge behaviors. There are clinical reports indicating that psychodynamic and psychoanalytic approaches in individual or group format are useful once bingeing and purging are improving. These approaches address developmental issues, identity formation, body image concerns, sexual and aggressive difficulties, affect regulation, gender role expectations, interpersonal conflicts, family dysfunction, coping styles, and problem solving. Some patients, such as those with concurrent anorexia nervosa or concurrent severe personality disorders, may benefit from extended psychotherapy. Family therapy should be considered whenever possible, especially for adolescents still living with parents or older patients with ongoing conflicted interactions with parents. Patients with marital discord may benefit from couples therapy. Support groups and 12-step programs such as Overeaters Anonymous may be helpful as adjuncts toinitial treatment of bulimianervosa and for subsequent relapse prevention but are not recommended as the sole initial treatment approach for bulimianervosa. 3. Medications Antidepressants are effective as one component ofan initial treatment program for most patients. Although antidepressant medications from a variety ofclasses can reduce symptoms ofbinge eating and purging and may help prevent relapse among patients in remission, SSRIs are safest. They may be especially helpful for patients with substantial symptoms ofdepression, anxiety, obsessions, or certain impulse disorder symptoms, or for patients who have failed or had a suboptimal response toprevious attempts at appropriate psychosocial therapy. Dose levels oftricyclic and MAOI antidepressants for treating bulimianervosa are

similar tothose used totreat depression; practitioners should try toavoid prescribing tricyclics topatients who may be suicidal and MAOIs topatients with chaotic binge eating and purging. 4. Combinations ofpsychosocial interventions and medications In some research, the combination ofantidepressant therapy and cognitive behavioral therapy results in the highest remission rates. Therefore, clinicians should consider a combination ofpsychotherapeutic interventions and medication when initiating treatment. V. CLINICAL AND ENVIRONMENTAL FEATURES INFLUENCING TREATMENT A. OTHER IMPORTANT CLINICAL FEATURES OFEATING DISORDERS 1. Eating disorder not otherwise specified Eating disorder not otherwise specified is a commonly used diagnosis, given tonearly 50% ofpatients with eating disorders who present totertiary care eating disorders programs. Eating disorder not otherwise specified appears tobe particularly common among adolescents. This heterogeneous group ofpatients largely consists ofsubsyndromal cases ofanorexia nervosa or bulimianervosa (e.g., those who fail tomeet one criterion, such as not having 3 months ofamenorrhea or having fewer binge eating episodes per week than required for strictly defined diagnosis). One variant ofeating disorder not otherwise specified consists ofabusers ofweight reduction medications who are trying tolose excessive amounts ofweight for cosmetic reasons. In general, the nature and intensity oftreatment depends on the symptom profile and severity ofimpairment, not the DSM-IV diagnosis. One diagnosis within the eating disorder not otherwise specified category is binge-eating disorder. Although it is not an approved DSM-IV diagnosis at this time, there are research criteria listed in DSM-IV, which consist ofdisturbances in one or more ofthe following spheres: behavioral (e.g., binge eating), somatic (e.g., obesity is common although not required), and psychological (e.g., body image dissatisfaction, low self-esteem, depression) (250). Although binge-eating disorder appears tobe relatively rare in community cohorts (2% prevalence), it is common among patients seeking treatment for obesity at hospital-affiliated weight programs (30% prevalence) (266). About onethird ofthese patients are male. Bingeeating disorder occurs much more frequently in adults than in adolescents. Strategies for the treatment ofbinge-eating disorder include nutritional counseling and dietary management; individual or group behavioral, cognitive behavior, interpersonal, or psychodynamic psychotherapy; and medications. a. Nutritional rehabilitation and counseling; effect ofdiet programs on weight Very-low-calorie diets in patients with binge-eating disorder have been associated with substantial initial weight losses, with over one-third ofthese patients maintaining their weight loss I year after treatment (267-270). Very-low-calorie diets employed together with group behavioral weight control have been effective in reducing binge eating during the period offasting but may be less effective during or following refeeding (267, 268, 270). However, since such dieting may disinhibit eating and lead tocompensatory overeating and binge eating (271), and since chronic calorie restriction can also increase symptoms ofdepression, anxiety, and irritability (19), new alternative therapies that use a nondiet approach by focusing on selfacceptance, improving body image, better nutrition and health, and increased physical

movement and not on weight loss have been developed (272274). Studies that compared traditional behavioral weight loss programs with nondieting programs have found similar rates ofmaintained weight loss, with the nondiet programs also producing significant reductions in symptoms related tobinge eating, depression, anxiety, bulimia, drive for thinness, and body dissatisfaction (275, 276). Patients with histories ofrepeated weight loss attempts followed by weight gain (so-called "yo-yo" dieting) or patients with an early onset ofbinge eating might benefit from following programs that focus on decreasing binge eating rather than weight loss (277, 278). b. Psychosocial treatments Cognitive behavior therapy, behavior therapy, and interpersonal therapy have all been associated with binge frequency reduction rates oftwo-thirds or more and significant abstinence rates during active treatment. However, deterioration during the follow-up period has been observed with all three forms ofpsychotherapy. Behavior therapy, but not cognitive behavior therapy, has generally been associated with a significant initial weight loss that is then partially regained during the first year following treatment (279-287). This pattern ofweight regain after initial weight loss is common in all general medical and psychological treatments for obesity, not only for obesity associated with binge-eating disorder. One 6-year study (288) that followed intensively treated patients with binge-- eating disorder found that approximately 57% had good outcomes, 35% intermediate outcomes, and 6% had poor outcomes; 1% had died. Self-help programs using self-guided professionally designed manuals have been effective in reducing the symptoms ofbinge-eating disorder in the short run for some patients and may sometimes have long-term benefit (289). Addictionbased 12step approaches, self-help organizations, or treatment programs based on the Alcoholics Anonymous model have been tried, but no systematic outcome studies ofthese programs are available. c. Medications It must be pointed out that medication treatment studies ofbinge-eating disorder have generally reported very high placebo response rates (around 70%) (217, 290). These high placebo response rates suggest that great caution is needed in evaluating claims ofeffective treatments, particularly in studies that use only a waiting list control condition. Medications, primarily antidepressants, have been used in the treatment ofbinge-eating disorder and related syndromes. Tricyclic antidepressants and fluvoxamine have been associated with reductions of63%90% in binge frequency during 2-3 months oftreatment (217, 291-293). Naltrexone has been-associated with a decrease in binge frequency on the same order (73%), although this rate did not differ from the response toplacebo (217). Patients tend torelapse after medication is discontinued (290, 293). Although the appetite suppressant medications fenfluramine and dexfenfluramine have also been found tosignificantly reduce binge frequency (290), their use has been associated with serious adverse events, including,a 23-fold increase in the risk ofdeveloping primary pulmonary hypertension when used for longer than 3 months (294). Very recent studies suggest that patients taking the combination offenfluramine and phentermine may be at greater risk ofheart valve deformation and pulmonary hypertension; as a result, fenfluramine has been withdrawn from the market (294-297). Studies in animals indicate that fenfluramine and dexfenfluramine may be associated with persistent serotonergic neurotoxicity (298, 299).

d. Combined psychosocial and medication treatment strategies In most studies, the co-administration ofmedication with psychotherapy has been found tobe associated with significantly more weight loss than with psychotherapy alone (280, 300). 2. Chronicity ofeating disorders Many patients who have a chronic course ofanorexia nervosa, extending for a decade or more, are unable tomaintain a healthy weight and suffer from chronic depression, obsessionality, and social withdrawal. Individualized treatment planning and careful case management are necessary for such chronic patients. Treatment may require consultation with other specialists, repeated hospitalizations, partial hospitalizations, residential care, individual or group therapy, other social therapies, trials ofvarious medications as indicated, and, occasionally, ECT in patients who are seriously depressed. Communication among professionals is especially important throughout the outpabent care ofsuch patients. With chronic patients, small progressive gains and fewer relapses may be the goals ofpsychological interventions. More frequent outpatient contact and other supports may sometimes help prevent further hospitalizations. Expectations for weight gain with hospitalization may be more modest for chronic patients. Achieving a safe weight compatible with life rather than a healthy weight may be all that is possible. Focusing on quality-of-life issues, rather than change in weight or normalization ofeating, and providing compassionate care may be all one can realistically achieve (260, 301). B. OTHER PSYCHIATRIC FACTORS 1. Substance abuse/dependence Substance abuse/dependence is common among women with eating disorders (93). Among individuals with bulimianervosa, 22.9% have been observed tomeet criteria for alcohol abuse (302). Substance abuse appears tobe less common among restricting patients with anorexia nervosa than among those having the binge-eating/purge type (102, 303, 304). For example, one recent prospective, longitudinal study (305) found bulimic anorectic women tobe seven times more likely todevelop substance abuse problems than restricting anorectic patients. Patients with comorbid substance abuse and eating disorders appear tohave more severe problems with impulsivity in general, including greater risks ofshoplifting, suicide gestures, and laxative abuse (114, 304, 306). Available studies indicate that eating disorder patients with a history ofprior but currently inactive substance abuse respond tostandard therapies in the same manner as those without such a history (307-309) and do not appear toexperience exacerbations oftheir substance abuse disorders after successful treatment (308). However, the presence ofa currently active comorbid substance abuse problem does have implications for treatment. A study of70 patients with comorbid eating disorders and substance abuse found that the associated axis III medical disorders reflected complications ofboth eating disorders and substance abuse disorders. Patients with comorbid eating and substance abuse disorders required longer inpatient stays and were less compliant with treatment following hospitalization than those with substance abuse disorders alone (310). Where treatment staff are competent totreat both disorders, concurrent treatment should be attempted. 2. Mood and anxiety disorders

A very high percentage oftreatment-seeking patients with eating disorders report a lifetime history ofunipolar depression (103, 311, 312). Nutritional insufficiency and weight loss often predispose patients tosymptoms ofdepression (19). Depressed individuals with an eating disorder experience greater levels ofanxiety, guilt, and obsessionality, but less social withdrawal and lack ofinterest, than depressed individuals without eating disorders (313). Several studies suggest that the presence ofcomorbid depression at initial presentation has minimal or no predictive value for treatment outcome (58). However, the experience ofmany clinicians suggests that severe depression can impair a patient's ability tobecome meaningfully involved in psychotherapy and may dictate the need for medication treatment for the mood symptoms from the beginning oftreatment. Lifetime prevalence rates for anxiety disorders also appear tobe higher for patients with both anorexia nervosa and bulimianervosa, but rates for specific anxiety disorders vary (101). In patients with anorexia nervosa, social phobia and OCD are the anxiety disorders most commonly described. For those with bulimianervosa, comorbid presentations ofsocial phobia, OCD, or simple phobia are most often described. Overanxious disorders ofchildhood are also common in both anorexia nervosa and bulimianervosa and precede the onset ofthese eating disorders (314). Although there is no clear evidence that comorbid anxiety disorders impact significantly on eating disorder treatment outcome, such comorbid problems should be addressed in treatment planning. 3. Personality disorders The reported prevalence ofpersonality disorders has varied widely across eating disorders and across studies. Individuals with anorexia nervosa tend tohave higher rates ofcluster C personality disorders, while normal weight patients with bulimianervosa are more likely todisplay features ofcluster B disorders, particularly impulsive, affective, and narcissistic trait disturbances (107, 315-320). The presence ofborderline personality disorder seems tobe associated with a greater disturbance in eating attitudes, a history ofmore frequent hospitalizations, and the presence ofother problems such as suicide gestures and selfmutilation (316, 320). The presence ofborderline personality disorder is also associated with poorer treatment outcome and higher levels ofpsychopathology at follow up (321, 322). Although it has not yet been systematically studied, clinical consensus strongly suggests that the presence ofa comorbid personality disorder, particularly borderline personality disorder, dictates the need for longer-term therapy that focuses on the underlying personality structure and dealing with interpersonal relationships in addition tothe symptoms ofthe eating disorder. 4. Posttraumatic stress disorder (PTSD) Available data on the extent ofPTSD among patients with eating disorders are still limited. According toone national survey (323), the lifetime rate ofPTSD was nearly 37% among women with bulimianervosa, much higher than the rate ofPTSD seen in community cohorts. There are higher rates ofabuse history in patients with bulimianervosa. Histories oftrauma and PTSD are likely tobe important in therapy and should be taken into consideration. C. CONCURRENT GENERAL MEDICAL CONDITIONS 1. Type 1 diabetes mellitus

Eating disorder symptoms appear tobe more common among females with diabetes mellitus than in the general population. Thus, a high index ofsuspicion for these disorders is warranted for those working with young female diabetic patients. The presentation ofeating disorders in the context ofdiabetes mellitus may be substantially more complex than that seen with eating disorders alone, may require more interaction with general medical specialists, and may present as numerous general medical crises before the presence ofthe eating disorder is diagnosed and treated. There is good evidence that when bulimianervosa or eating disorder not otherwise specified co-occur with diabetes mellitus, rates ofdiabetic complications are higher. Diabetics with eating disorders often underdose their insulin in order tolose weight. Out-of-control diabetics with bulimianervosa may require a period ofinpatient treatment for stabilization ofboth the diabetes mellitus and the disturbed eating (324, 325). Parenthetically, poor compliance or underdosing with weight-inducing medications such as steroids, anticonvulsants, lithium, and other psychotropic medications necessary for the treatment ofother conditions occurs often in patients with eating disorders and even in those with subclinical weight concerns. 2. Pregnancy Eating disorders may begin de novo during pregnancy, but many patients get pregnant even while they are actively symptomatic with an eating disorder. The behaviors associated with eating disorders including inadequate nutritional intake, binge eating, purging by various means, and the use or abuse ofsome teratogenic medications (e.g., tovarying degrees lithium, benzodiazepines, or divalproex) can all result in fetal or maternal complications (326). The care ofa pregnant patient with an eating disorder is difficult and usually requires the collaboration ofa psychiatrist and an obstetrician who specializes in high-risk pregnancies (327-330). Although some patients may be able toeat normally and decrease binge eating and purging during their pregnancy, it is best for the eating disorder tobe treated before the pregnancy if possible. Among patients whose symptoms abate during pregnancy, there is some evidence that the eating disorder symptoms often recur after delivery (331). Although women with lifetime histories ofanorexia nervosa may not have reduced fertility, they do appear tobe at risk ofa greater number ofbirth complications than comparison subjects and ofgiving birth tobabies oflower birth weight (304). This is true both for women who are actively anorectic at the time ofpregnancy as well as for women with a prior history ofanorexia nervosa. Mothers with eating disorders may have more difficulties than others in feeding their babies and young children than other mothers and may need additional guidance, assistance, and monitoring oftheir mothering (149-151). D. DEMOGRAPHIC VARIABLES 1. Male gender Especially in bulimiasubgroups, males with eating disorders who present totertiary care centers may have more comorbid substance use disorders and more antisocial personality disorders than females. Like females, they are prone toosteoporosis (332). Although gender does not appear toinfluence the outcome oftreatment, some aspects oftreatment may need tobe modified on the basis ofgender. Open-- blind studies suggest that normalizing testosterone in males during nutritional rehabilitation for anorexia nervosa may be helpful in increasing lean muscle mass, but definitive studies are not completed. Although studies in clinical samples have suggested that there might be a higher incidence ofhomosexuality

among males with eating disorders (333, 334), this has not yet been confirmed epidemiologically. Nevertheless, since issues concerning sexual orientation are not uncommon among males with eating disorders seen in clinical settings, these issues should be considered in treatment (333). Where possible, therapy groups for males alone may address some ofthe specific needs ofthese patients and help them deal with the occasional stigmatization ofmales by females in treatment. Males with anorexia nervosa may require higher energy intakes (up to4,000-4,500 kcal/day), since they normally have higher lean body mass and lower fat mass compared tofemales. And, since they are larger tobegin with, males with anorexia nervosa often require much larger weight gains toget back tonormal weight (335). Ofnote, epidemiological prevalence studies ofanorexia nervosa and bulimianervosa indicate that in North America there are probably more males with bulimianervosa than females with anorexia nervosa. Although eating disorders are much more prevalent in women, males with eating disorders are not rare and case series ofmales often report on hundreds ofpatients (333, 335). The stereotype that eating disorders are female illnesses may limit a full understanding ofthe scope and nature ofproblems faced by male patients with eating disorders. 2. Age Although most eating disorders start while patients are in their teens and 20s, earlier and later onsets are encountered as well. In some patients with early onsets (i.e., between ages 7 and 12), obsessional behavior and depression are common. Children often present with physical symptoms such as nausea, abdominal pain, feeling full, or being unable toswallow; their weight loss can be rapid and dramatic. Children with early-onset anorexia nervosa may suffer from delayed growth (153, 336-340) and may be especially prone toosteopenia and osteoporosis (24, 25). In a few cases, exacerbations ofanorexia nervosa and OCD-like symptoms have been associated with pediatric infection-triggered autoimmune neuropsychiatric disorders (341, 342). Bulimianervosa under the age of12 is rare. Anorexia nervosa has been reported in elderly patients in their 70s and 80s, in whom the illness has generally been present for 40 or 50 years. In many cases the illness started after age 25 (so-called anorexia tardive). In some case reports, adverse life events such as deaths, marital crisis, or divorce have been found totrigger these older-onset syndromes. Fear ofaging has also been described as a major precipitating factor in some patients (98, 343). Rates ofcomorbid depression have been reported tobe higher among these patients in some studies but not in others (344). 3. Cultural factors Specific pressures and values concerning weight and shape vary among different cultures. Strivings for beauty and acceptance according tothe stereotypes they perceive in global-cast media are leading increasing numbers ofwomen around the world todevelop attitudes and eating behaviors associated with eating disorders (80, 345). Clinicians should engage these women in informed and sensitive discussions regarding their struggles and personal experiences about what it means tobe feminine and what it means tobe "perfeet" in the modern world (346). Clinicians should be sensitive toand inquire as tohow weight and shape concerns are experienced by patients, especially those who are minorities, from non-Western or other cultural backgrounds, or are transitioning and assimilating into Western societies.

4. Eating disorders in athletes Eating disorders are more common among competitive athletes than the general age-matched population (347, 348). Female athletes are especially at risk in sports that emphasize a thin body or appearance, such as gymnastics, ballet, figure skating, and distance running. Males in sports such as bodybuilding and wrestling are also at greater risk. Certain antecedent factors such as cultural preoccupation with thinness, performance anxiety, and athlete self-appraisal may predispose a female athlete tobody dissatisfaction, which often mediates the development ofeating disorder symptoms (349). Parents and coaches ofyoung athletes may support distorted shape and eating attitudes in the service ofguiding the athlete tobe more competitive. Physicians working with adolescent and young adult athletes, particularly those athletes participating in the at-risk sports, must be alert toearly symptoms ofeating disorders. Simple screening questions about weight, possible dissatisfaction with appearance, amenorrhea, and nutritional intake on the day before evaluation may help identify an athlete who is developing an eating disorder. Early general medical and psychiatric intervention is key toprompt recovery. Extreme exercise appears tobe a risk factor for developing anorexia nervosa, especially when combined with dieting (87). A "female athlete triad" has been identified, consisting ofdisordered eating, amenorrhea, and osteoporosis (350). Similarly, an "overtraining syndrome" has been described: a state ofexhaustion, depression, and irritability in which athletes continue totrain but their performance diminishes (351). Both have been linked tothe syndrome of"activity anorexia," which has been observed in animal models (352). 5. Eating disorders in high schools and colleges Eating disorders are common among female high school and college students, and psychiatrists and other health and mental health professionals may' be involved in their care in various ways. From a primary prevention perspective, health professionals may be called upon toprovide information and education about eating disorders in classrooms, athletic programs, and assorted other extracurricular venues. The efficacy ofsuch programs for the reduction ofeating disorders is still uncertain (353, 354). Helping in early intervention, health professionals may serve as trainers, coordinators, and professional supports for peer counseling efforts conducted at school, in dormitories, and through other campus institutions. Through student health and student psychological services, they may serve as initial screeners and diagnosticians and help manage students with varying levels ofseverity ofeating disorders (355). On occasion psychiatrists may be called upon as clinicians and as agents ofthe school administration tooffer guidance in the management ofimpaired students with serious eating disorders. In such situations the suggested guidelines for levels ofcare described in table 5 should be followed. Accordingly, tostay in school students must be treatable as outpatients. It is advisable that students be required totake a leave ofabsence if they are severely ill (355, 356). The student should be directed toinpatient hospital care if weight is 30%, or more below an expected healthy weight, or if any ofthe other indications for hospitalization listed in table 5 are present.

For students with serious eating disorders who remain in school, the psychiatrist and other health providers should work with the school's administration toward developing policies and programs that make student attendance contingent upon participation in a suitable treatment program. For the severely ill student, the clinical team must include a general medical clinician who can gauge safety and monitor weight, vital signs, and laboratory indicators. For the student tobe permitted tocontinue in school, these clinicians may require a minimum weight and other physical, behavioral, or laboratory target measures toensure basic medical safety. An explicit policy should be developed specifying that clinicians have the final say regarding the student's participation in physically demanding activities such as organized athletics. Restrictions must be based on actual medical concerns. Procedures should be in compliance with the school's policies regarding management ofstudents with psychiatric disabilities and the Americans with Disabilities Act (356). VI. RESEARCH DIRECTIONS Further studies ofeating disorders are needed that address issues surrounding the epidemiology, causes, and course ofillness. Areas ofspecific concern include: 1. Genetic and other biological, gender-related, psychological, familial, social, and cultural risk factors that contribute tothe development ofspecific eating disorders, greater morbidity and higher mortality, treatment resistance, and risk ofrelapse. 2. Structure-function relationships associated with predisposing vulnerabilities, nutritional changes associated with the disorders, and changes in recovery examined through imaging studies. 3. The differential presentation ofeating disorders across various developmental periods from early childhood through late adulthood. 4. Linkages between physiological and psychological processes ofpuberty and the onset oftypical eating disorders. 5. The impact ofvarious comorbid conditions (including mood, anxiety, substance abuse, obsessivecompulsive symptoms, personality disorders, PTSD, cognitive impairments, and other commonly encountered concurrent disorders) on course and treatment response. 6. The effect ofexercise, including the role ofextreme exercise, and food restriction in precipitating and maintaining eating disorders. Conversely, the possible protective effect ofcontemporary women's athletics on girls' eating and weight attitudes. 7. Further delineation and definition ofeating disorder not otherwise specified and bingeeating disorder, with clarification ofrisk factors, morbidity, treatments, and prognosis. 8. Family studies on factors associated with onset and maintenance ofeating disorders, as well as concerning the impact ofeating disorders on other family members. 9. Culturally flexible diagnostic criteria toallow for the identification and treatment ofthe many "atypical" cases, which may represent a large number ofeating disorders patients in non-Western societies.

Additional studies and assessments ofnew interventions are also needed, specifically with regard to 1. Primary prevention programs in schools and through the media. 2. Targeted prevention through screenings and riskfactor early intervention programs. 3. Improved guidelines for choice oftreatment setting and selection ofspecific treatments on the basis ofmore refined clinical indicators and a better understanding ofthe stages ofthese disorders (including follow-up issues for short-term and long-term treatment studies). , 4. Development and testing ofnewer biological agents affecting hunger, satiety, and energy expenditure as well as commonly associated psychiatric symptoms and conditions. 5. Development and testing ofvarious individually administered and "bundled" individual and group psychotherapies including cognitive behavior, interpersonal, psychodynamic, psychoanalytic, and family therapies as well as nutritional therapies and other psychosocial therapies (creative arts, 12-step models, and professional or layperson-led support groups and selfhelp groups for patients and families). 6. Treatment outcome studies related tovarious systems or settings ofcare, including HMO versus fee for service; limitations ofhospital or other intensive treatment resources due tomanaged care and other resource limitations; treatment in eating disorder specialty units versus general psychiatry treatment units; and impact ofstaff composition, professional background ofproviders, system or setting characteristics, and roles ofprimary care versus mental health providers in the treatment ofeating disorders. 7. Further development and testing ofprofessionally designed self-administered treatments by manuals and computer-based treatment programs. 8. Modifications oftreatment required because ofvarious comorbid conditions. 9. The impact ofcommonly used "alternative" and "complementary" therapies on the course ofillness. 10. New methods for assessing and treating osteopenia, osteoporosis, and other long-term medical sequelae. 11. Further delineation ofproper education and training for psychiatrists and other healthcare providers todeal with patients with eating disorders.
References

VIII. REFERENCES
References

The following coding system is used toindicate the nature ofthe supporting evidence in the references:

[A] Randomized clinical trial. A study ofan intervention in which subjects are prospectively followed over time; there are treatment and control groups; subjects are randomly assigned tothe two groups; both the subjects and the investigators are blind tothe assignments.
References

[B] Clinical trial. A prospective study in which an intervention is made and the results ofthat intervention are tracked longitudinally; study does not meet standards for a randomized clinical trial. [C] Cohort or longitudinal study. A study in which subjects are prospectively followed over time without any specific intervention. [D] Case-control study. A study in which a group ofpatients and a group ofcontrol subjects are identified in the present and information about them is pursued retrospectively or backward in time. [E] Review with secondary analysis. A structured analytic review ofexisting data, e.g., a meta-analysis or a decision analysis.
References

[F] Review. A qualitative review and discussion ofpreviously published literature without a quantitative synthesis ofthe data. [G] Other. Textbooks, expert opinion, case reports, and other reports not included above.
References

1. Bulik C, Sullivan PF, Fear J, Pickering A: Predictors ofthe development of bulimianervosa in women with anorexia nervosa. J New Ment Dis 1997; 185:704-707 [GI 2. Lee S, Ho TP, Hsu LKG: Fat phobic and non-fat phobic anorexia nervosa-a comparative study of70 Chinese patients in Hong Kong. Psychol Med 1993; 23:999-1004 fD]
References

3. Strober VI, Freeman R, Morrell NXT: Atypical anorexia nervosa: separation from typical cases in course and outcome in a longterm prospective study. Int J Eat Disord 1999; 25:135142 [C] 4. Beumont PJ, George GC, Smart DE: Dieters and vomiters and purgers in anorexia nervosa. Psychol Med 1976; 6:617-622 ICJ
References

5. Casper RC, Eckert ED, Halmi KA, Goldberg SC, Davis JM: Bulimia: its incidence and clinical importance in patients with anorexia nervosa. Arch Gen Psychiatry 1980; 37:10301035 [C]

6. Garfinkel PE, Moldofsky H, Garner DM: The heterogeneity ofanorexia nervosa: bulimiaas a distinct group. Arch Gen Psychiatry 1980; 37:1036-1040 [Cl Kassett JA, Gwirtsman HE, Kaye WH, Brandt HA, Jimerson DC: Pattern ofonset ofbulimic symptoms in anorexia nervosa. Am Psychiatry 1988; 145:1287-1288 [CJ
References

8. Wilson CP, Hogan CC, Mintz IL: Fear ofBeing Fat: The Treatment OfAnorexia Nervosa and Bulimia, 2nd ed. Northvale, NJ, Jason Aronson, 1985 [Fl 9. Wilson CP, Hogan CC, Mintz IL: Psychodynamic Technique in the Treatment ofEating Disorders. Northvale, NJ, Jason Aronson, 1992 IF]
References

10. Bunnell DDi%, Shenker IR, Nussbaum MP, Jacobson MS, Cooper P, Phil D: Subclinical versus formal eating disorders: differentiating psychological features. Int J Eat Disord 1990; 9:357362 [D] 11. Zerbe KJ: The emerging sexual self ofthe patient with an eating disorder: implications for treatment. Eating Disorders: J Treatment and Prevention 1995; 3:197-215 fB]
References

12. Favazza AR, DeRosear L, Conterio K: Self-mutilation and eating disorders. Suicide Life Threat Behav 1989; 19:352-361 [GI 13. Johnson C, Connors ME: The Etiology and Treatment of BulimiaNervosa. New York, Basic Books, 1987 [11 14. Rizzuto A: Transference, language, and affect in the treatment ofbulimarexia. Int J Psychoanal 1988; 69:369-387 [GI 15. Schwartz HJ: Bulimia: Psychoanalytic Treatment and Theory, 2nd ed. Madison, Conn, International Universities Press, 1990 [I]
References

16. Lacey H: Bulimianervosa, binge-eating, and psychogenic vomiting: a controlled treatment study and long-term outcome. Br Med J 1983; 2:1609-1613 [Al 17. Casper RC, Davis JM: On the course ofanorexia nervosa. Am J Psychiatry 1977; 134:974-978 IC] 18. Garfinkel PE, Kaplan AS: Starvation based perpetuating mechanisms in anorexia nervosa and bulimia. Int J Eat Disord 1985; 4:651-655 [El

19. Keys A, Brozek J, Henschel A, Mickelsen 0, Taylor HL: The Biology ofHuman Starvation. Minneapolis, University ofMinnesota Press, 1950 [BI 20. Srinivasagam NM, Kaye WH, Plotnicov KH, Greeno C, Weltzin TE, Rao R: Persistent perfectionism, symmetry, and exactness after long-term recovery from anorexia nervosa. Amj Psychiatry 1995; 152:1630-1634 [C] 21. Garner DM, Garfinkel PE (eds): Handbook ofPsychotherapy for Anorexia Nervosa and Bulimia. New York, Guilford Press, 1985 JG)
References

22. Fichter MM: Starvation-related endocrine changes, in Psychobiology and Treatment ofAnorexia Nervosa and BulimiaNervosa. Edited by Halmi KA. Washington, DC, American Psychopathological Association, 1992, pp 193-210 IGI 23. Fichter MM, Pirke KM, Pollinger J, Wolfram G, Brunner E: Disturbances in the hypothalamo-pituitary-adrenal and other neuroendocrine axes in bulimia. Biol Psychiatry 1990; 27: 1021-1037 tDI
References

24. Bachrach LK, Guido D, Katzman DK, Litt IF, Marcus RN: Decreased bone density in adolescent girls with anorexia nervosa. Pediatrics 1990; 86:440-447 JC[ 25. Bachrach LK, Katzman DK, Litt IF, Guido D, Marcus RN: Recovery from osteopenia in adolescent girls with anorexia nervosa. J Clin Endocrinol Metab 1991; 72:602-606 [B] 26. Rigotti NA, Neer RM, Skates SJ, Herzog DB, Nussbaum SR: The clinical course ofosteoporosis in anorexia nervosa: a longitudinal study ofcortical bone mass. JAMA 1991; 265:11331138 [B] 27. Klibanski A, Biller BM, Schoenfeld DA, Herzog DB, Saxe VC: The effects ofestrogen administration on trabecular bone loss in young women with anorexia nervosa. J Clin Endocrinol Metab 1995; 80:898-904 [B] 28. Stewart DE, Robinson E, Goldbloom DS, Wright C: Infertility and eating disorders. Am J Obstet Gynecol 1990; 163:17 961199 ICi
References

29. Beumont PJV, Kopec-Schrader EM, Lennerts W: Eating disorder patients at a NSW teaching hospital: a comparison with state-wide data. Aust NZ J Psychiatry 1995; 29:96-103 IGI 30. de Zwaan IM, Mitchell JE: Medical complications ofanorexia nervosa and bulimianervosa, in Medical Issues and the Eating Disorders: The Interface. Edited by Kaplan AS, Garfinkel I'E. New York, Brunner/Mazel, 1993, pp 60-100 [Gi

31. Garfinkel PE, Garner DM: The Role ofDrug Treatments for Eating Disorders. New York, Brunner/Mazel, 1987 111 32. Halmi KA: Anorexia nervosa and bulimia. Annu Rev \led 1987; 38:373-380 IFI 33. Herzog DB, Copeland PM: Eating disorders. N Engl J Med 1985; 313:295-303 [FI 34. Krieg JC, Pirke KM, Lauer C, Backmund H: Endocrine, metabolic, and cranial computed tomographic findings in anorexia nervosa. Biol Psychiatry 1988; 23:377-387 [Cry
References

35. Golden NH, Ashtari M, Kohn MR, Patel M, Jacobson MS, Fletcher A, Shenker IR: Reversibility ofcerebral ventricular enlargement in anorexia nervosa demonstrated by quantitative magnetic resonance imaging. ] Pediatr 1996; 128:296-301 [B]
References

36. Katzman DK, Lambe EK, Mikulis DJ, Ridgley JN, Goldbloom DS, Zipursky RB: Cerebral gray matter and white matter volume deficits in adolescent girls with anorexia nervosa. J Pediatr 1996; 129:794-803 IDI 37. Kingston K, Szmukler G, Andrewes D, Tress B, Desmond P: Neuropsychological and structural brain changes in anorexia nervosa before and after refeeding. Psychol Med 1996; 26:1528 IC]
References

38. Lambe EK, Katzman DK, Mikulis DJ, Kennedy S, Zipursky RB: Cerebral gray matter volume deficits after weight recovery from anorexia nervosa. Arch Gen Psychiatry 1997; 54:537542 [CI
References

39. Swayze VW II, Andersen A, Arndt S, Rajarethinam R, Fleming F, Sato Y, Andreasen NC: Reversibility ofbrain tissue loss in anorexia nervosa assessed with a computerized Talairach 3-D proportional grid. Psychol Med 1996; 26:381-390 ICI 40. Hamsher K, Halmi KA, Benton Al.: Prediction ofoutcome in anorexia nervosa from neuropsychological status. Psychiatry Res 1981; 4:79-88 [C] 41. Powers PS, Tyson IB, Stevens BA, Heal AV: Total body potassium and serum potassium among eating disorder patients. Int J Eat Disord 1995; 18:269-276 IGI 42. Mitchell JE, Pyle RL, Eckert ED, Hatsukami D, Lentz R: Electrolyte and other physiological abnormalities in patients with bulimia. Psychol Med 1983; 13:273-278 [GI 43. Herzog. DR, Nussbaum KM, Marmor AK: Comorbidity and outcome in eating disorders. Psychiatr Clin North Am 1996; 19:843-859 IF]

References

44. Hahi KA, Eckert E, Marchi P, Sampugnaro V, Apple R, Cohen J: Comorbidity ofpsychiatric diagnoses in anorexia nervosa. Arch Gen Psychiatry 1991; 48:712-718 IC] 45. Strober NI, Freeman R, Morrell W: The long-term course ofsevere anorexia nervosa in adolescents: survival analysis ofrecovery, relapse, and outcome predictors over 10-15 years in a prospective study. hit Eat Disord 1997; 22:339-360 JC 46. Theander S: Outcome and prognosis in anorexia nervosa and bulimia: some results ofprevious investigations compared with those ofa Swedish long term study. J Psychiatr Res 1985; 19: 493-508 ICI
References

47. Sullivan PF: Mortality in anorexia nervosa. Am J Psychiatry 1995; 152:1073-1074 [E] 48. Harris EC, Barraclough B: Excess mortality ofmental disorder. Br J Psychiatry 1998; 173:11-53 IF] 49. Hsu LKG: Outcome and treatment effects, in Handbook ofEating Disorders. Edited by Beaumont PJV, Burrows BD, Casper RC. Amsterdam, Elsevier, 1987, pp 371-377 II] 50. Hsu KG: Eating Disorders. New York, Guilford Press, 1990 [II]
References

51. Russell G: Bulimianervosa: an ominous variant ofanorexia nervosa. Psychol Med 1979; 9:429-488 IE) 52. Kreipe RE, Churchill BH, Strauss J: Long-term outcome ofadolescents with anorexia nervosa. Am J Dis Child 1989; 43: 1322-1327 ICI 53. Nussbaum MP, Shenker IR, Baird D, Saravay S: Follow up investigation ofpatients with anorexia nervosa. J Pediatr 1985; 106:835-840 JC]
References

54. Steiner H, Mazer C, Litt IF: Compliance and outcome in anorexia nervosa. West j Med 1990; 153:133-139 [C] 55. Drewnowski A, Yee DK, Krahn DD: Dieting and Bulimia: A Continuum ofBehaviors. Washington, DC, American Psychiatric Press, 1989 [GJ 56. Yager J, Landsverk J, Edelstein CK: A 20-month follow-up study of628 women with eating disorders, 1: course and severity. Am J Psychiatry 1987; 144:1172-1177 [B1 57. Hsu LK, Sobkiewicz TA: Bulimianervosa: a four tosix year follow up. Psychol Med 1989; 19:1035-1038 [BI

58. Keel PK, Mitchell JE: Outcome in bulimianervosa. Am J Psychiatry 1997; 154:313-321 [Fl 59. Keel PK, Mitchell JE, Miller KB, Davis TL, Crow Aj: Long-term outcome of bulimianervosa. Arch Gen Psychiatry 1998; 56: 63-69 [El
References

60. Luka LP, Agras WS, Schneider JA: Thirty month follow up ofcognitive behavioral group therapy for bulimia(letter). Br J Psychiatry 1986; 148:614-615 [B] 61. Fichter MM, Quadflieg N: Six-year course of bulimianervosa. Int J Eat Disord 1997; 22:361-384 [C] 62. Swift WJ, Ritholz M, Kalin NH, Kaslow N: A follow-up study ofthirty hospitalized bulimics. Psychosom Med 1987; 49:4555 [B] 63. Agras WS, Walsh T, Wilson G: A multisite comparison ofcognitive behavior therapy (CBT) and interpersonal therapy (IPT) in the treatment of bulimianervosa. Fourth London International Conference on Eating Disorders, April 20-22, 1999, p 61 [GI 64. Olmsted MP, Kaplan AS, Rockert W: Rate and prediction ofrelapse in bulimianervosa. Am J Psychiatry 1994; 151:738-743 [CJ
References

65. Treasure J, Palmer RL: Providing specialized services for anorexia nervosa. Br J Psychiatry (in press) [D] 66. Garfinkel PE, Lin E, Goering P, Spegg C, Goldbloom D, Kennedy S, Kaplan AS, Woodside DB: Should amenorrhoea be necessary for the diagnosis ofanorexia nervosa. Br J Psychiatry 1996; 168:500-506 IGI 67. Walters EE, Kendler KS: Anorexia nervosa and anorexic-like syndromes in a populationbased female twin sample. Am J Psychiatry 1995; 152:64-71 [DI 68. Garfinkel PE, Lin E, Goering P, Spegg C, Goldbloom DS, Kennedy S, Kaplan AS, Woodside DB: Bulimianervosa in a Canadian community sample: prevalence and comparison ofsubgroups. Am J Psychiatry 1995; 152:1052-1058 [C] 69. Kendler KS, MacLean C, Neale M, Kessler R, Heath A, Eaves L: The genetic epidemiology of bulimianervosa. Am J Psychiatry 1991; 148:1627-1637 [HI 70. Heatherton TF, Nichols P, Mahamedi F, Keel P: Body weight, dieting, and eating disorder symptoms among college students, 1982 to1992. Am J Psychiatry 1995; 152:16231629 [Dl 71. Fosson A, Knibbs J, Bryant-Waugh R, Lask B: Early onset ofanorexia nervosa. Arch Dis Childhood 1987; 62:114-118 [Fl 72. Hawley RM: The outcome ofanorexia nervosa in younger subjects. Br J Psychiatry 1985; 146:657-660 [C]

73. Higgs JF, Goodyer IN, Birch J: Anorexia nervosa and food avoidance emotional disorder. Arch Dis Childhood 1989; 64: 346-351 [DI 74. Pate JE, Pumariega AJ, Hester C, Garner DM: Cross cultural patterns in eating disorders: a review. Am J Child Adolesc Psychiatry 1992; 31:802-809 [El 75. Kiriike N, Nagata T, Tanaka M, Nishiwaki S, Takeuchi N, Kawakita Y: Prevalence ofbinge-eating and bulimiaamong adolescent women in Japan. Psychiatry Res 1988; 26:163169 [D]
References

76. Nadaoka T, Oiji A, Takahashi S, Morioka Y, Kashiwakura IVI, Totsuka S: An epidemiological study ofeating disorders in a northern area ofJapan. Acta Psychiatr Scand 1996; 93:305310 [D] 77. Davis C, Katzman MA: Chinese men and women in the USA and Hong Kong: body and self-esteem ratings as a prelude todieting and exercise. Int J Eat Disord 1998; 23:99-102 11)] 78. Davis C, Katzman MA: Perfection as acculturation: psychological correlates ofeating problems in Chinese male and female students living in the United States. Int J Eat Disord 1999; 25: 65-70 [D] 79. Becker AE: Acculturation and Disordered Eating in Fiji. Washington, DC, American Psychiatric Press, 1999 [GI 80. Nasser MI: Culture and Weight Consciousness. New York, Routledge, 1997 [GI 81. Toro J, Cervera M, Perez P: Body shape, publicity and anorexia nervosa. Social Psychiatry Psychiatr Epidemiol 1988; 23:132136 [El 82. Toro J, Nicolau R, Cervera M, Castro J, Blecua MJ, Zaragoza M, Toro A: A clinical and phenomenological study of185 Spanish adolescents with anorexia nervosa. Eur Child Adolesc Psychiatry 1995; 4:165-174 [El
References

83. Crago M, Shisslak CM, Estes LS: Eating disturbances among American minority groups: a review. Int J Eat Disord 1996; 19: 239-248 IF] 84. Langer L, Warheit G, Zimmerman R: Epidemiological study ofproblem eating behaviors and related attitudes in the general population. Addict Behav 1992; 16:167-173 ID] 85. Warheit G, Langer L, Zimmerman R, Biafora F: Prevalence ofbulimic behaviors and bulimiaamong a sample ofthe general population. Am J Epidemiol 1993; 137:569-576 [DJ 86. Pumariega AJ, Gustavson CR, Gustavson JC: Eating attitudes in African-American women: the essence. Eating Disorders: J Treatment and Prevention 1994; 2:5-16 ID]

87. Davis C, Kennedy SH, Ravelski E, Dionne M: The role ofphysical activity in the development and maintenance ofeating disorders. Psychol Med 1994; 24:957-967 IB] 88. Garner DM, Rosen LW, Barry D: Eating disorders among athletes: research and recommendations. Child Adolesc Psychiatr Clin North Am 1998; 7:839-857 ITI
References

89. Strober M, Lampert C, Morrell W, Burroughs J, Jacobs C: a controlled family study ofanorexia nervosa: evidence offamilial aggregation and lack ofshared transmission with affective disorders. Int J Eat Disord 1990; 9:239-253 [Bl 90. Bulik C, Sullivan P, Carter FA, McIntosh VV, Joyce PR: The role ofexposure with response prevention in the cognitive behavioral therapy for bulimianervosa. Psychol Med 1998; 28: 611-623 lB] 91. Lilenfeld L, Kaye W, Greeno C, Merikangas KR, Plotnicov KH, Pollice C, Radhika R, Strober M, Bulik C, Nagy L: Psychiatric disorders in women with bulimianervosa and their first-degree relatives: effects ofcomorbid substance dependence. Int J Eat Disord 1997; 22:253-264 [D] 92. Mitchell JE, Hatsukami D, Pyle R, Eckert E: Bulimiawith and without a family history ofdrug use. Addict Behav 1988; 13: 245-251 [C]
References

93. Kaye W, Kaplan AS, Zucker ML: Treating eating disorders in a managed care environment. Psychiatr Clin North Am 1996; 19:793-810 [F] 94. Hudson JI, Pope HG Jr, Yurgelun-Todd D, Jonas JM, Frankenburg FR: A controlled study oflifetime prevalence ofaffective and other psychiatric disorders in bulimic outpatients. Am J Psychiatry 1987; 144:1283-1287 [C] 95. Pyle RL, Mitchell JE, Eckert ED: Bulimia: a report of34 cases. J Clin Psychiatry 1981; 42:60-64 [G] 96. Bloom C, Gitter A, Gutwill S: Eating Problems: A Feminist Psychoanalytic Treatment Model. New York, Basic Books, 1994 [GI 97. Zerbe KJ: The Body Betrayed: Women, Eating Disorders, and Treatment. Washington, DC, American Psychiatric Press, 1993 [G]
References

98. Zerbe KJ: Whose body is it anyway? understanding and treating psychosomatic aspects ofeating disorders. Bull Menninger Clin 1993; 57:161-177 IF] 99. Zerbe KJ: Feminist psychodynamic psychotherapy ofeating disorders: theoretic integration informing clinical practice. Psychiatr Clin North Am 1996; 19:811-827 IF]

100. Zerbe KJ, March S, Coyne L: Comorbidity in an inpatient eating disorders population: clinical characteristics and treatment implications. Psychiatr Hospital 1993; 24:3-8 [D] 101. Braun DL, Sunday SR, Halmi KA: Psychiatric comorbidity in patients with eating disorders. Psychol Med 1994; 24:859-867 ICI
References

102. Herzog DB, Keller MB, Sacks NR, Yeh CJ, Lavori PW: Psychiatric comorbidity in treatment-seeking anorexics and bulimics. J Am Acad Child Adolesc Psychiatry 1992; 31:810-818 ID] 103. Hudson JI, Pope HG, Jonas JM, Yurgelun-Todd D: Phenomenologic relationship ofeating disorders tomajor affective disorder. Psychiatry Res 1983; 9:345-354 [D] 104. Hecht H, Fichter MM, Postpeschil Ft Obsessive-compulsive neuroses and anorexia nervosa. Int J Eat Disord 1983; 2:69-77 [DI t 105, Kasvikis YG, Tsakiris F, Marks IM, Basogul M, Noshirvani HF: Past history ofanorexia nervosa in women with obsessive compulsive disorder. Int Eat Disord 1986; 5:1069-1076 [C]
References

106. Skodol AE, Oldham JM, Hyler SE, Kellman HD, Doidge N, Davies M: Comorbidity ofDSM-111-R eating disorders and personality disorders. Int J Eat Disord 1993; 14:403-416 [D] 107. Herzog DB, Keller MB, Lavori PW, Kenny GM, Sacks NR: The prevalence ofpersonality disorders in 210 women with eating disorders. J Clin Psychiatry 1992; 53:147152 [GI 108. Bulik CM, Sullivan PF, Rorty M: Childhood sexual abuse in women with bulimia. J Clin Psychiatry 1989; 50:460-464 [Cj 109. Schmidt U, Tiller J, Treasure J: Self-treatment of bulimianer vosa: a pilot study. Int J Eat Disord 1993; 13:273-277 [B] 110. Vize CM, Cooper PJ: Sexual abuse in patients with eating disorder patients with depression and normal controls: a comparative study. Br J Psychiatry 1995; 167:80-85 [D] 111. Pope HG Jr, Hudson JI: Is childhood sexual abuse a risk factor for bulimianervosa? Am J Psychiatry 1992; 149:455-463 [El 112. Rorty M, Yager J, Rossotto E: Childhood sexual physical and psychological abuse and their relationship tocomorbid psychopathology in bulimianervosa. Int J Eat Disord 1994; 16:317334 [Cl
References

113. Wonderlich SA, Brewerton TD, Jocic Z, Dansky BS, Abbott DW: Relationship ofchildhood sexual abuse and eating disorders. J Am Acad Child Adolesc Psychiatry 1997; 36:11071115 [Fl 114. Wonderlich SA, Mitchell JE: Eating disorders and comorbidity: empirical, conceptual and clinical implications. Psychopharmacol Bull 1997; 33:381-390 fF) 115. Kaye WH, Gwirtsman H, Obarzanek E, George DT: Relative importance ofcalorie intake needed togain weight and level ofphysical activity in anorexia nervosa. Am J Clin Nutr 1988; 47: 989-994 [C] 116. Golden NH, Jacobson MS, Schebendach J, Solanto MV, Hertz SM, Shenker IR: Resumption ofmenses in anorexia nervosa. Arch Pediatr Adolesc Med 1997; 151:16-21 [C] 117. Treasure JL, Wheeler M, King EA, Gordon PA, Russell GF: Weight gain and reproductive function: ultra sonographic and endocrine features in anorexia nervosa. Clin Endocrinol 1988; 29:607-616 [C 118. Frisch RE: Fatness and fertility. Sci Am 1988; 258:88-95 IF] 119. Metropolitan Life Insurance Company: 1983 Metropolitan height and weight tables. Stat Bull Metrop Life Found 1983; 64:3-9 [El
References

120. Hamill PV, Johnston FE, Lemeshow S: Height and weight ofyouths 12-17 years, United States. Vital Health Star 1 1973: 11:1-81 IC] 121. Hebebrand J, Himmelmann GW, Heseker H, Schafer H, Remschmidt H: Use ofpercentiles for the body mass index in anorexia nervosa: diagnostic, epidemiological and therapeutic considerations. Intj Eat Disord 1996; 19:359-369 [D] 122. Reiff DW, Reiff KKL: Set point, in Eating Disorders: Nutrition Therapy in the Recovery Process. Gaithersburg, Md, Aspen, 1992, pp 104-105 [G] 123. Guarda AS, Heinberg LJ: Effective weight-gain in step down partial hospitalization program for eating disorders. Annual Meeting ofAcademy for Eating Disorders, San Diego, 1999 [GI 124. Powers PS: Heart failure during treatment ofanorexia nervosa. Am J Psychiatry 1982; 139:1167-1170 [GI 125. Kohn MR, Golden NH, Shenker IR: Cardiac arrest and delirium: presentations ofthe refeeding syndrome in severely malnourished adolescents with anorexia nervosa. J Adolesc Health 1998; 22:239-243 [GI
References

126. Scott M, Solomon, Kriby DF: The refeeding syndrome: a review. JPEN Parenter Enteral Nutr 1990; 14:90-97 [F]

127. Treasure J, Todd G, Szmukler G: The inpatient treatment ofanorexia nervosa, in Handbook ofEating Disorders. Edited by Szmukler G, Dare C, Treasure J. Chichester, UK, John Wiley Sons, 1995, pp 275-291 [G] 128. Kaye WH, Weltzin TE, Hsu LK, Bulik CM: An open trial offluoxetine in patients with anorexia nervosa. J Clin Psychiatry 1991; 52:464-471 [G] 129. Levine JA, Eberhardt NL, Jensen MD: Role ofnonexercise activity thermogenesis in resistance tofat gain in humans. Science 1999; 283:212-214 [B]
References

130. Baran SA, Weltzin TE, Kaye WH: Low discharge weight and outcome in anorexia nervosa. Am J Psychiatry 1995; 152: 1070-1072 [CI 131. Halmi KA, Licinio-Paixao J: Outcome: hospital program for eating disorders, in 1989 Annual Meeting Syllabus and Proceedings Summary. Washington, DC, American Psychiatric Association, 1989, p 314 [GI 132. Agras WS: Eating Disorders: Management ofObesity, Bulimiaand Anorexia Nervosa. Oxford, UK, Pergamon Press, 1987 [I] 133. Nusbaum JG, Drever E: Inpatient survey ofnursing care mea sures for treatment ofpatients with anorexia nervosa. Issues Ment Health Nuts 1990; 11:175184 [GI 134. Touyz SW, Beumont PJ, Glaun D, Phillips T, Cowie I: A comparison oflenient and strict operant conditioning programmes in refeeding patients with anorexia nervosa. Br J Psychiatry 1984; 144:517-520 IF] 135. Danziger Y, Carel CA, Tyano S, Mimouni M: Is psychotherapy mandatory during the actual refeeding period in the treatment ofanorexia nervosa. J Adolesc Health Care 1989; 10:328-331 fBI
References

136. Duncan J, Kennedy SH: Inpatient group treatment, in Group Psychotherapy for Eating Disorders. Edited by Harper-Giuffre H, MacKenzie KR. Washington, DC, American Psychiatric Press, 1992, pp 149-160 [GI 137. Maxmen JS: Helping patients survive theories: the practice ofan educative model. Intj Group Psychother 1984; 34:355-368 [GI 138. Yellowlees P: Group psychotherapy in anorexia nervosa. Int J Eat Disord 1988; 7:649655 [GI 139. Maher M:. Group therapy for anorexia nervosa, in Current Treatment ofAnorexia Nervosa and Bulimia. Edited by Powers PS, Fernandez RC. Basel, Switzerland, Karger, 1980, pp 265276 [G]

References

140. Garner DM: Individual psychotherapy for anorexia nervosa. J Psychiatr Res 1985; 19:423-433 [F] 11 141. Hall A, Crisp AH: Brief psychotherapy in the treatment ofanorexia nervosa: outcome at one year. BrJ Psychiatry 1987; 151: 185-191 [A] 142. Wilson CP, Mintz IL (eds): Psychosomatic Symptoms: Psychoanalytic Treatment ofthe Underlying Personality Disorder. Northvale, NJ, Jason Aronson, 1989 [F] 143. Dare C: The starting and the greedy. J Child Psychotherapy 1993; 19:3-22 [F] 144. Hornyak LM, Baker EK: Experiential Therapies for Eating Disorders. New York, Guilford Press, 1989 [G] 145. Breden AK: Occupational therapy and the treatment ofeating disorders. Occupational Therapy in Health Care 1992; 8:4968 IGI
References

146. Lim PY: Occupational therapy with eating disorders: a study on treatment approaches. Br J Occupational Therapy 1994; 57: 309-314 [GI 147. Eisler I, Dare C, Russell G, Szmukler G, leGrange D, Dodge E: Family and individual therapy in anorexia nervosa: a 5-year follow-up. Arch Gen Psychiatry 1997; 54:1025-1030 [BI 148. Russell GF, Szmukler GI, Dare C, Eisler I: An evaluation offamily therapy in anorexia nervosa and bulimianervosa. Arch Gen Psychiatry 1987; 44:1047-1056 [Al 149. Agras WS, Hammer LD, McNicholas F: A prospective study ofthe influence ofeatingdisordered mothers on their children. Int J Eat Disord 1999; 25:253-262 [C] 150. Russell GF, Treasure J, Eisler I: Mothers with anorexia nervosa who underfeed their children: their recognition and management. Psychol Med 1998; 28:93-108 [D] 151. Stein A, Woolley H, Cooper SD, Fairburn CG: An observational study ofmothers with eating disorders and their infants. J Child Psychol Psychiatry 1994; 35:733-748 tC] 152. Johnson CL, Taylor C: Working with difficult totreat eating disorders using an integration oftwelve-step and traditional psychotherapies. Psychiatr Clin North Am 1996; 19:829-941 [Fl ' 153. Fisher M, Golden NH, Katzman DK, Kreipe RE, Rees J, Schebendach J, Sigman G, Ammerman S, Hoberman HM: Eating
References

disorders in adolescents: a background paper. J Adolesc Health 1995; 16:420-437 IF] 154, Attia fi, Haiman C, Walsh BT, Flater SR: Does fluoxetine augment the inpatient treatment ofanorexia nervosa? Am J Psychiatry 1998; 155:548-551 [Al 155. Gwirtsman HE, Guze BH, Yager J, Gainsley B: Fluoxetine treatment ofanorexia nervosa: an open clinical trial. j Clin Psychiatry 1990; 51:378-382 [GI 156. Bergh C, Eriksson M, Lindberg G, Sodersten P: Selective serotonin reuptake inhibitors in anorexia. Lancet 1996; 348:14591460 [B]
References

157. Halmi KA, Eckert E, LaDu 'T), Cohen J: Anorexia nervosa: treatment efficacy ofcyproheptadine and amitriptyline. Arch Gen Psychiatry 1986; 43:177-181 [Al 158. Lacey JH, Crisp AH: Hunger, food intake and weight: the impact ofclomipramine on a refeeding anorexia nervosa population. Postgrad Med J 1980; 56(suppl 1):79-85 JAI 159. Gross HA, Ebert MH, Faden VB: A double-blind controlled study oflithium carbonate in primary anorexia nervosa. ("[in Psychopharmacol 1981; 1:376-381 JAI 160. Vandereycken )XI, Pierloot R: Pimozide combined with behavior therapy in the shortterm treatment ofanorexia nervosa: a double blind placebo-controlled cross-over study. Acta Psychiatr Scand 1982, 66:445-450 IA I 161. Wells LA, Logan KM: Pharmacologic treatment ofeating disorders: a review ofselected literature and recommendations. Psychosomatics 1987; 28:470-479 IF 162. Garfinkel PE, Garner DM: Anorexia Nervosa: A Multidimensional Perspective. New York, Brunner/Mazel, 1982 [I] 163. Seeman E, Szmukler G, Formica C, Tsalamandris C, Mestrovic R: Osteoporosis in anorexia nervosa: the influence ofpeak bone density, bone loss, oral contraceptive use and exercise. J Bone Miner Res 1992; 7:1467-1474 [CI 164. Hegenroeder AC: Bone mineralization, hypothalamic amenorrhea, and sex steroid therapy in female adolescents and voting adults.,) Pediatr 1995; 126:683-689 [FJ 165. Kreipe RE, Hicks DG, Rosier RN, Puzas JE: Preliminary findings on the effects ofsex hormones on bone metabolism in anorexia nervosa. J Adolesc Health 1993; 14:319-324 [BI
References

166. Treasure JL, Russell GF, Fogelman I, Murby Bi Reversible bone loss in anorexia nervosa. Br Med J (Clin Res Ed) 1987; 295: 474-475 [DI 167. Emans SJ, Goldstein DP: Pediatric and Adolescent Gynecology, 3rd ed. Boston, Little, Brown, 1990 [CGI

168. Grinspoon S, Baum H, Lee K, Anderson E, Herzog 1), Klibanski A: Effects ofshort-term recombinant human insulin-like growth factor I administration on bone turnover in osteopenic women with anorexia nervosa. J Clin Endocrinol Metab 1996; 81:3864-3870 [13 169. Phvsicians' Desk Reference, 46th ed. Montvale, NJ, Medical Economics, 1992 [GI 170. Horne RI,, Ferguson JM, Pope Hj, Hudson JI, Lineberry CG, Ascher J, Cato A: Treatment of bulimiawith bupropion: a multicenter controlled trial. J Clin Psychiatry 1988; 49:262-266 [Al
References

171. Laessle KCi, Zoettle C, Pirke KM: Meta-analysis oftreatment studies for bulimia. Int J Eat Disord 1987; 6:647-654 [El 172. Agras WS, Schneider JA, Arnow B, Raeburn SD, Telch CF: Cognitive-behavioral and response prevention treatments for bulimianervosa., J Consult Clin Psychol 1989; 57:215-221 JAI 173. Beck AT, Ward CH, Mendelson M, Mock J, Erbaugh J: An inventory for measuring depression. Arch Gen Psychiatry 1961; 4:561-571 [GI 174. Connors ME, Johnson Cl- Stuckey MK: Treatment of bulimiawith brief psychoeducational group therapy. Am J Psychiatry 1984; 141:1512-1516 [BI 175. Fairburn CG, Jones R, Peveler RC, Hope RA, O'Connor NI: Psychotherapy and bulimianervosa: longer-term effects ofinterpersonal psychotherapy, behavior therapy, and cognitive behavioral therapy. Arch Gen Psychiatry 1993; 50:419-428 [A] 176. Fairburn CG, Marcus MD, Wilson (Th: Cognitive-behavioral therapy for binge eating and bulimianervosa: a comprehensive
References

treatment manual, in Binge Eating: Nature, Assessment, and Treatment. Edited by Fairburn CG, Wilson GT. New York, Guilford Press, 1993, pp 361-404 [GI 177. Freeman CP, Barry F, Dunkeld-Turn bull J, Henderson A: Controlled trial ofpsychotherapy for bulimianervosa. Br Med J (Clin Res Ed) 1988; 296:521-525 [B] 178. Garner DM, Rockert W, Davis R, Garner MV, Olmsted MP, Eagle M: A comparison ofcognitive-behavioral and supportive-expressive therapy for bulimianervosa. Am j Psychiatry 1993; 150:37-46 [B] 179. Hamilton M: A rating scale for depression. J Neurol Neurosurg Psychiatry 1960; 23:5662 [DI 180. Kirkley BG, Schneider JA, Agras WS, Bachman JA: Comparison oftwo group treatments for bulimia. J Consult Clin Psychol 1985; 53:43-48 [Al

181. Lee NF, Rush AJ: Cognitive-behavioral group therapy for bulimia. Int J Eat Disord 1986; 5:599-615 [Al 182. Malenbaum R, Herzog D, Eisenthal S, Wyshak G: Overeaters anonymous. Int J Eat Disord 1988; 7:139-144 [GI 183. Mitchell JE, Pyle RL, Pomeroy C, Zollman M, Crosby R, Sein H, Eckert ED, Zimmerman R: Cognitive-behavioral group psychotherapy of bulimianervosa: importance oflogistical variables. Int.) Eat Disord 1993; 14:277-287 [B], 184. Oesterheld JR, McKenna MS, Gould NB: Group psychotherapy of bulimia: a critical review. hit J Group Psychother 1987; 37:163-184 IF]
References

185. Ordman AM, Kirschenbaum DS: Cognitive-behavioral therapy for bulimia: an initial outcome study. J Consult Clin Psychol 1985; 53:305-313 [B] 186. Schwartz RC, Barest MJ, Saba G: Family therapy for bulimia, in Handbook ofPsychotherapy for Anorexia Nervosa and Bulimia. Edited by Garner DM, Garfinkel PE. New York, Guilford Press, 1985, pp 280-307 [GI 187. Vandereycken W: The addiction model in eating disorders: some critical remarks and a selected bibliography. IntJ Eat Disord 1990; 9:95-102 [GI 188. Yager J, Landsverk J, Edelstein CK: Help seeking and satisfaction with care in 641 women with eating disorders I: patterns ofutilization attributed change and perceived efficacy oftreatment. J New Ment Dis 1989; 177:632-637 [GJ 189. Beck AT, Steer RA, Garbin MG: Psychometric properties ofthe BDI: twenty-five years ofevaluation. Clin Psychol Rev 1988; 8: 77-100 IGI
References

190. Root MPP: Persistent, disordered eating as a gender-specific, post-traumatic stress response tosexual assault. Psychotherapy 1991; 28:96-102 [GJ 191. Laessle RG, Tuschl RJ, Kotthaus BC, Pirke ,JM: A comparison ofthe validity ofthree scales for the assessment ofdietary restraint. J Abnorm Psychol 1989; 98:504-507 JEJ 192. Fairburn CG: Cognitive behavioral treatment for bulimia, in Handbook ofPsychotherapy for Anorexia Nervosa and Bulimia. Edited by Garner DM, Garfinkel PE. New York, Guilford Press, 1985, pp 160-192 [GI 193. Fairburn CG, Kirk J, O'Connor M, Cooper PJ: A comparison oftwo psychological treatments for bulimianervosa. Behav Res Ther 1985; 24:629-643 [B] 194. Leitenberg H, Rosen J, Gross J, Nudelman S, Vara LS: Exposure plus responseprevention treatment of bulimianervosa. J Consult Clin Psychol 1988; 56:535-541 IA]

195. Johnson C: Diagnostic survey for eating disorders in initial consultation for patients with bulimiaand anorexia nervosa, in Handbook ofPsychotherapy for Anorexia Nervosa and Bulimia. Edited by Garner DM, Garfinkel PE. New York, Guilford Press, 1985, pp 19-51 IGC 196. Fairborn CG: A cognitive behavioral approach tothe treatment of bulimia. Psychol Med 1981; 11:707-711 lB[ 197. Fairburn CG, Norman PA, Welch SL, O'Conner ME, Doll HA, Paveler RC: A prospective study ofoutcome in bulimianervosa and the long-term effects ofthree psychological treatments. Arch Gen Psychiatry 1995; 52:304-312 IA] 198. Rorty Ni, Yager J: Why and how do women recover from bulimianervosa? Int J Eat Disord 1993; 14:249-260 [DI
References

199. Fairburn CG, Jones R, Peveler RC: Three psychological treatments for bulimianervosa. Arch Gen Psychiatry 1991; 48:453469 [Al
References

200. Wilson GT, Eldredge KL, Smith D: Cognitive behavioral treatment with and without response prevention for bulimia. Behav Res Ther 1991; 29:575-583 [A] 201. Wilson GT, Rossiter E, Kleifield El, Lindholm L: Cognitive-behavioral treatment of bulimianervosa: a controlled evaluation. Behav Res Ther 1986; 24:277-288 [B] 202. Cooper PJ, Coker S, Fleming C: Self-help for bulimianervosa: a preliminary report. IntJ Eat Disord 1994; 16:401-404 lB] 203. Cooper PJ, Coker S, Fleming C: An evaluation ofthe efficacy of supervised cognitive behavioral self-help for bulimianervosa. J Psychosom Res 1996; 40:281-287 [B] 204. Thiels C, Schmidt U, Treasure J, Garthe R, Troop N: Guided self-change for bulimianervosa incorporating use ofa self-care manual. Am J Psychiatry 1998; 155:947-953 [B] 205. Treasure J, Schmidt U, Troop N, Tiller J, Todd G, Keilen M, Dodge E: First step in managing bulimianervosa: controlled trial oftherapeutic manual. Br Med J 1994; 308:686689 [BI 206. Treasure J, Schmidt U, Troop N, Tiller J, Todd G, Turnbull S: Sequential treatment for bulimianervosa incorporating a selfcare manual. Br J Psychiatry 1995; 167:1-5 IBI 207. Agras WS: Cognitive Behavior Therapy Treatment Manual for BulimiaNervosa. Stanford, Calif, Stanford University School ofMedicine, Department ofPsychiatry and Behavioral Sciences, 1991 [F]

References

208. Agras WS, Apple R: Overcoming Eating Disorders-Therapist's Guide. San Antonio, Tex, Psychological Corp (Harcourt), 1998 [GI 209. Apple R, Agras WS: Overcoming Eating Disorders-Client Workbook. San Antonio, Tex, Psychological Corp (Harcourt), 1998 [GI 210. Boutacoff LI, Zollman M, Mitchell JE: Healthy Eating: A Meal Planning System-Group Treatment Manual. Minneapolis, University ofMinnesota Hospital and Clinic, Department ofPsychiatry, 1989 [GI 211. Mitchell JE, Eating Disorders Program Staff: BulimiaNervosa: Individual Treatment Manual. Minneapolis, University ofMinnesota Hospital and Clinic, Department ofPsychiatry, 1989 [F] 212. Mitchell JE, Eating Disorders Program Staff: BulimiaNervosa: Group Treatment Manual. Minneapolis, University ofMinnesota Hospital and Clinic, Department ofPsychiatry, 1991 [Fl 213. Pope HG Jr, Hudson JI, Jonas JM, Yurgelun-Todd D: Bulimiatreated with imipramine: a placebo-controlled, double-blind study. Am J Psychiatry 1983; 140:554-558 [Al 214. Hughes PL, Wells LA, Cunningham CJ, Ilstrup DM: Treating bulimiawith desipramine: a double-blind placebo-controlled study. Arch Gen Psychiatry 1986; 43:182-186 [Al 215. Mitchell JE, Groat R: A placebo-controlled double-blind trial ofamitriptyline in bulimia. J Clin Psychopharmacol 1984; 4: 186-193 [Al
References

216. Walsh BT, Stewart JW, Roose SP, Gladis M, Glassman AH: Treatment of bulimiawith phenelzine: a double-blind placebo controlled study. Arch Gen Psychiatry 1984; 41:11051109 [A]
References

217. Alger SA, Schwalberg MD, Bigaoutte JM, Michalek AV, Howard Li: Effects ofa tricyclic antidepressant and opiate antagonists on binge-eating behavior in normal weight bulimic and obese binge-eating subjects. J Clin Nutr 1991; 53:865-871 JAI 218. Fahy TA, Eisler I, Russell GFM: A placebo-controlled trial ofd-- fenfluramine in bulimianervosa. Br J Psychiatry 1993; 162: 597-603 [BI 219. Fichter MM, Kruger R, Rief W, Holland R, Dohne J: Fluvoxamine in prevention ofrelapse in bulimianervosa: effects on eating-specific psychopathology. J Clin Psychopharmacol 1996; 16:9-18 [A]

220. Fichter MM, Leibl K, Rief VC; Brunner E, Schmidt-Auberger S, Engel RR: Fluoxetine versus placebo: a double-blind study with bulimic inpatients undergoing intensive psychotherapy. Pharmacopsychiatry 1991; 24:1-7 [A]
References

221. Fluoxetine BulimiaNervosa Collaborative Study Group: Fluoxetine in the treatment of bulimianervosa. Arch Gen Psychiatry 1992; 49:139-147 tA] 222. Freeman CP, Morris JE, Cheshire KE, Davies F, Hamson M: A double-blind controlled trial offluoxetine versus placebo for bulimianervosa. Proceedings ofthe Third International Conference on Eating Disorders, New York, 1988 [Al 223. Goldstein DJ, Wilson MG, Thompson VL, Potvin JH, Rampey AH Jr (Fluoxetine BulimiaNervosa Research Group): Longterm fluoxetine treatment of bulimianervosa. Br J Psychiatry 1995; 166:660-666 [A] 224. Hsu LKG, Clement L, Santhouse R, Ju ESY: Treatment of bulimianervosa with lithium carbonate: a controlled study. J New Ment Dis 1991; 179:351-355 [Al 225. Igoin-Apfelbaum L, Apfelbaum M: Naltrexone and bulimic symptoms (letter). Lancet 1987; 2:1087-1088 [Al 226. Jonas JM, Gold MS: Naltrexone reverses bulimic symptoms (letter). Lancet 1986; 1:807 [G] 227. Jonas JM, Gold MS: Treatment ofantidepressant-resistant bulimiawith naltrexone. Int J Psychiatry Med 1986; 16:306-309 [BI
References

228. Mitchell JE, Christenson G, Jennings J, Huber M, Thomas B, Pomeroy C, Morley J: A place bo-controlled double-blind crossover study ofnaltrexone hydrochloride in outpatients with normal weight bulimia. J Clin Psychopharmacol 1989; 9:94-97 [Al 229. Pope HG Jr, Keck PE Jr, McElroy SL, Hudson JI: A placebocontrolled study oftrazodone in bulimianervosa. J Clin Psychopharmacol 1989; 9:254-259 [A) 230. Rothschild R, Quitkin HM, Quitkin FM, Stewart JW, Ocepek-- Welikson K, McGrath PJ, Tricamo E: A double-blind placebocontrolled comparison ofphenelzine and imipramine in the treatment of bulimiain atypical depressives. Int J Eat Disord 1994; 15:1-9 [Al 231. Sabine EJ, Yonace A, Farrington AJ, Barratt KH, Wakeling A: Bulimianervosa: a placebo-controlled double-blind therapeutic trial ofmianserin. Br J Clin Pharmacol 1983; 15:1955-2025 [Al
References

232. Agras WS, Dorian B, Kirkley BG, Arnow B, Bachman J: Imipramine in the treatment of bulimia: a double-blind controlled study. Int J Eat Disord 1987; 6:29-38 [Al

233. Barlow J, Blouin J, Blouin A, Perez E: Treatment of bulimiawith desipramine: a double blind crossover study. Can J Psychiatry 1988; 33:129-133 [A] 234. Blouin AG, Blouin JH, Perez EL, Bushnik T, Zuro C, Mulder E: Treatment of bulimiawith fenfluramine and desipramine. J Clin Psychopharmacol 1988; 8:261-269 [Al 235. Walsh BT, Hadigan CM, Devlin MJ, Gladis M, Roose SP: Long-term outcome ofantidepressant treatment for bulimianervosa. Am J Psychiatry 1991; 148:1206-1212 [Al 236. Kennedy SH, Piran N, Warsh JJ, Prendergast P, Mainprize E, Whynot C, Garfinkel PE: A trial ofisocarboxacid in the treatment of bulimianervosa. J Clin Psychopharmacol 1988; 8: 391-396; correction, 1989; 9:3 [A] 237. Kennedy SH, Goldbloom DS, Ralevski E, Davis C, D'Souza JD, Lofchy J: Is there a role for selective monoamine oxidase inhibitor therapy in bulimianervosa? a placebo-controlled trial ofbrofaromine. J Clin Psychopharmacol 1993; 13:415-422 [Al 238. Raymond NC, Mitchell JE, Fallon P, Katzman MA: A collaborative approach tothe use ofmedication, in Feminist Perspectives on Eating Disorders. Edited by Fallon P, Katzman MA, Wooley SC. New York, Guilford Press, 1994, pp 231-250 fG] 239. Marrazzi MA, Wroblewski JM, Kinzie J, Luby ED: High dose naltrexone in eating disorders-liver function data. Am J Addict 1997; 6:621-629 [BI
References

240. Mitchell JE, Pyle RL, Eckert ED, Hatsukami D, Zimmerman R, Pomeroy C: A comparison study ofantidepressants and structured intensive group psychotherapy in the treatment of bulimianervosa. Arch Gen Psychiatry 1990; 47:149-157 [A] 241. Agras WS, Rossiter EM, Arnow B, Schneider IA, Telch CF, Raeburn SD, Bruce B, Perl M, Koran LM: Pharmacologic and cognitive-behavioral treatment for bulimianervosa: a controlled comparison. Am J Psychiatry 1992; 149:82-87 [A]
References

242. Goldbloom DS, Olmsted NI, Davis R, Clewes J, Heinmaa M, Rockert W, Shaw B: A randomized controlled trial offluoxetine and cognitive behavioral therapy for bulimianervosa: short-term outcome. Behav Res Ther 1997; 35:803-811 [Al 243. Walsh BT, Wilson GT, Loeb KL, Devlin MJ, Pike KM, Roose SP, Fleiss J, Waternaux C: Medication and psychotherapy in the treatment of bulimianervosa. Am j Psychiatry 1997; 154:523531 [GI 244. Leitenberg H, Rosen JC, Wolf J, Vara LS, Detzer MJ, Srebnik D: Comparison ofcognitive-behavior therapy and desipramine in the treatment of bulimianervosa. Behav Res Ther 1994; 32: 37-45 [A]
References

245. LaVia M, Kaye WH, Andersen A, Bowers W, Brandt HA, Brewerton TD, Costin C, Hill L, Lilenfeld L, McGilley B, Powers PS, Pryor T, Yager J, Zucker ML: Anorexia nervosa: criteria for levels ofcare. Eating Disorders Research Society Annual Meeting, Boston, 1998 IGI 246. Crisp AH, Callender JS, Halek C, Hsu LK: Long-term mortality in anorexia nervosa: a 20-year follow-up ofthe St George's and Aberdeen cohorts. Br J Psychiatry 1992; 161:104107 JC] 247. Appelbaum PS, Rumpf T. Civil commitment ofthe anorexic patient. Gen Hosp Psychiatry 1998; 20:225-230 [GI 248. Maxmen JS, Silberfarb PM, Ferrell RB: Anorexia nervosa: practical initial management in a general hospital. JAMA 1974; 229:801-803 [GI 249. Kaplan AS, Olmsted MP: Partial hospitalization, in Handbook ofTreatment for Eating Disorders, 2nd ed. Edited by Garner DM, Garfinkel PE. New York, Guilford Press, 1997, pp 354360 IGI
References

250. American Psychiatric Association: Practice guideline for eating disorders. Am J Psychiatry 1993; 150:212-228 [IT 251. Andersen AE: Practical Comprehensive Treatment ofAnorexia Nervosa and Bulimia. Baltimore, Md, Johns Hopkins University Press, 1985 [11 252. Owen W, Halmi KA: Medical evaluation and management ofanorexia nervosa, in Treatments ofPsychiatric Disorders: A Task Force Report ofthe American Psychiatric Association, vol 1. Washington, DC, APA, 1989, pp 17-519 [II 253. Kaplan AS, Garfinkel P: Difficulties in treating patients with eating disorders: a review ofpatient and clinician variables. Can J Psychiatry 1999 (in press) [GI 254. Wooley SC: Uses ofcountertransference in the treatment ofcating disorders: a gender perspective, in Psychodynamic Treatment ofAnorexia Nervosa and Bulimia. Edited by Johnson CL. New York, Guilford Press, 1991, pp 245-294 [GJ 255. Zerbe KJ: Knowable secrets: transference and countertransference manifestations in eating disordered patients, in Treating Eating Disorders: Ethical, Legal, and Personal Issues. Edited by Vandereycken W Beumont PJV. New York, New York University Press, 1998, pp 30-55 [G 256. Zunino N, Agoos E, Davis WN: The impact oftherapist gender on the treatment ofbulimic women. Int J Eat Disord 1991; 10: 253-263 [E]
References

257. Katzman VIA, Walter G: Implications oftherapist gender in the treatment ofeating disorders: daring toask the questions. in The Burden ofthe Therapist. Edited by Vandereycken W. London, Athelone Press. 1998, pp 56-79 [(5[ 258. Walter G, Katzman MA: Female or male therapists for women with eating disorders? a pilot study ofexpert opinions. Int J Eat Disord 1997; 22:111-114 [ 259. Werne J: Treating Eating Disorders. San Francisco, Jossey-Bass, 1996 [Gj 260. Yager J: Patients with chronic, recalcitrant eating disorders, in Special Problems in Managing Eating Disorders. Edited by Yager J, Gwirtsman HE, Edelstein CK. Washington, DC:, American Psychiatric Press, 1992, pp 205-231 [G]
References

261. Zerbe Kj: Integrating feminist and psychodynamic principles in the treatment ofan eating disorder patient: implications for using countertransference responses. Bull Menninger Clin 1995; 59:160-176 IG) 262. Kaplan AS, Fallon P: Therapeutic boundaries in the treatment ofpatients with eating disorders. Fourth London International Conference on Eating Disorders, April 20-22, 1999, p 30 1GI
References

263. Andersen AE: Hospital Treatment ofAnorexia Nervosa. Washington, DC, American Psychiatric Press, 1989 II] 264. Kaplan AS: Medical and nutritional assessment, in Medical Issues and the Eating Disorders: The Interface. Edited by Kaplan AS, Garfinkel PE. New York, Brunner/Mazel, 1993, pp 1-16 IGI
References

265 Powers PS: Initial assessment and early treatment options for anorexia nervosa and bulimianervosa. Psychiatr Clin North Am 1996; 19:639-655 IF] 266. Spitzer RL, Devlin MJ, Walsh BT, Hasin D: Binge eating disorder: a multisite field trial ofthe diagnostic criteria. Int J Eat Disord 1992; 11:191-203 ID] 267. de Zwaan NI, Biener D, Bach M, Wiesnagrotzki S, Stacher G: Pain sensitivity, alexithymia, and depression in patients with eating disorders: are they related? J Psychosom Res 1996; 41: 65-70 [DI
References

268. Telch CF, Agras WS: The effects ofa very low calorie diet on binge eating. Behavior Therapy 1993; 24:177-193 [BI

269. Wadden TA, Foster GD, Letizia KA: Response ofobese binge eaters totreatment by behavior therapy combined with very low calorie diet. J Consult Clin Psychol 1992; 60:808811 [Al 270. Yanovski SZ, Gormally JF, Leser MS, Gwirtsman HE, Yanovski JA: Binge eating disorder affects outcome ofcomprehensive very-low-calorie diet treatment. Obesity Res 1994; 2: 205-212 IRI 271. Policy .J, Herman CP: Dieting and hinging: a casual analysis. Am Psychol 1985; 40:193-201 [Fl 272. Carrier KM, Steinhardt MA, Bowman S: Rethinking traditional weight management programs: a 3-year follow-up evaluation ofa new approach. J Psychol 1993; 128:517-535 [D] 273. Ciliska D: Beyond Dieting: Psychoeducational Interventions for Chronically Obese Women. New York, Brunner/Mazel, 1990 IGI
References

274. Kaplan AS, Ciliska D: The relationship between eating disorders and obesity: psychopathologic and treatment considerations. Psychiatr Annals 1999; 29:197-202 IBI 275. Goodrick GK, Poston WS 11, Kimball KT, Reeves RS, Foreyt JP: Nondieting versus dieting treatment ofoverweight binge-eating women. J Consult Clin Psychol 1998; 66:363368 lB] 276. Tanco S, Linden W, Earle T: Well-being and morbid obesity in women: a controlled therapy evaluation. Int J Eat Disord 1998; 23:32--339 [B] 277. Grilo CM: Treatment ofobesity: an integrative model, in Body Image, Eating Disorders, and Obesity. Edited by Thompson JK. Washington, DC, American Psychological Association, 1996, pp 389-423 (GI
References

278. Marcus MD: Obese patients with binge-eating disorder, in The Management ofEating Disorders and Obesity. Edited by Goldstein DJ. Totowa, NJ, Humana Press, 1999, pp 125138 [GJ 279. Agras WS, Telch CF, Arnow B, Eldredge K, Detzer MNJ, Henderson J, Marnell M: Does interpersonal therapy help patients with binge-eating disorder who fail torespond tocognitive-behavioral therapy? J Consult Clin Psychol 1995; 63:356-360 lB] 280. Agras WS, Telch CF, Arnow B, Eldredge K, Wilfley DE, Raeburn SD, Henderson S, Marnell M: Weight loss cognitive-behavioral and desipramine treatments in binge-eating disorder: an addictive design. Behavior Therapy 1994; 25:225-238 JAI 281. Carter FA, Bulik CM, Lawson RH, Sullivan PF, Wilson JS: Effect ofmood and food cues on body image in women with bulimiaand controls. Int j Eat Disord 1996; 20:65-76 [BI

282. Eldredge KI., Agras WS, Arnow B, Telch CF, Bell S, Castonguay L, Marnell M: The effects ofextending cognitive-behavioral therapy for binge eating disorder among initial treatment nonresponders. Int j Eat Disord 1999; 21:347-352 [BI 283. Marcus MD, Wing RR: Cognitive treatment ofbinge eating, V: behavioral weight control in the treatment ofbinge eating disorder (letter). Ann Behav Med 1995; 17:5090 [Al 284. Peterson C, Mitchell JM, Engbloorn S, Nugent S, t4ussell MP, Miller JP: Group cognitive-behavioral treatment ofbinge eating disorder: a comparison oftherapist-led versus self-help formats. hit J Eat Disord 1998; 24:125-136 [B]
References

285. Smith DE, Marcus MD, Kaye W Cognitive-behavioral treatment ofobese binge eaters. Int J Eat Disord 1992; 12:257-262 [B]
References

286. Telch CF, Agras WS, Rossiter EM, Wilfey D, Kenardy J: Group cognitive-behavioral treatment for the nonpurging bulimic: an initial evaluation. J Consult Clin Psychol 1990; 58:629-635 lB) 287. Wilfey DE, Agras WS, Telch CF, Rossiter EM, Schneider JA, Cole AG, Sifford LA, Raeburn SD: Group cognitive-behavioral therapy and group interpersonal psychotherapy for the nonpurging bulimic individual: a controlled comparison. J Consult Clin Psychol 1993; 61:296-305 [Al 288. Fichter MM, Quadflieg N, Gnutmann A: Binge-eating disorder: treatment outcome over a 6-year course. J Psychosom Res 1998; 44:385-405 [E] 289. Carter JC, Fairburn CG: Cognitive-behavioral self-help for binge eating disorder: a controlled effectiveness study. J Consuit Clin Psychol 1998; 66:616-623 [B] 290. Stunkard A, Berkowitz R, Tanrikut C, Reiss E, Young L: d-Fenfluramine treatment ofbinge eating disorder. Am J Psychiatry 1996; 153:1455-1459 [Al 291. Gardiner HM, Freeman CP, Jesinger DK, Collins SA: Fluvoxamine: an open pilot study in moderately obese female patients suffering from atypical eating disorders and episodes ofbingeing. Int J Obes Relat Metab Disord 1993; 17:301-305 [B] 292. Hudson JI, McElroy SL, Raymond NC, Crow S, Keck PE Jr, Carter WP, Mitchell JE, Strakowski SM, Pope HG Jr, Coleman BS, Jonas JM: Fluvoxamine in the treatment ofbingeeating disorder: a multicenter placebo-controlled, double-blind trial. Am J Psychiatry 1998; 155:1756-1762 [Al 293. McCann UD, Agras WS: Successful treatment ofnonpurging bulimianervosa with desipramine: a double-blind, placebocontrolled study. Am J Psychiatry 1990; 147:1509-15 13 [A]

294. Abenhaim L, Moride Y, Brenot F, Rich S, Benichou J, Kurz X, Higenbottam T, Oakley C, Wouters E, Aubier M, Simonneau G, Beguad B: Appetite-suppressant drugs and the risk ofprimary pulmonary hypertension. N Engl Med 1996; 335:609616 [D]
References

295. Connolly H, Crary J, McGoon M, Hensrud D, Edwards B, Edwards W, Schaff H: Valvular heart disease associated with fenfluramine-phentermine. N Engl J Med 1997; 337:581-588 [C] 296. Graham DJ, Green L: Further cases ofvalvular heart disease associated with fenfluramine-phentermine (letter). N Engl J Med 1997; 337:635 IG] 297. Mark EJ, Patalas ED, Chang HT, Evans RJ, Kessler SC: Fatal pulmonary hypertension associated with short-term use offenfluramine and phentermine. N Engl J Med 1997; 337:602-606 [GI
References

298. McCann U, Hatzidimitriou G, Ridenour A, Fischer C, Yuan J, Katz J, Ricaurte G: Dexfenfluramine and serotonin neurotoxicity: further preclinical evidence that clinical caution is indicated. J Pharmacol Exp Ther 1994; 269:792-798 [GI 299. Ricaurte GA, Martello MB, Wilson MA, Molliver ME, Katz JL, Martello AL: Dexfenfluramine neurotoxicity in brains ofnon-human primates. Lancet 1991; 338:1487-1488 [GI 300. Marcus MD, Wing RR, Ewing L, Kern E, McDermott M, Gooding W: A double-blind, placebo-controlled trial offluoxetine plus behavior modification in the treatment ofobese binge-eaters and non-binge-eaters. Am J Psychiatry 1990; 147: 876-881 JAI 301. Kerr A, Leszcz M, Kaplan AS: Continuing care groups for chronic anorexia nervosa, in Group Psychotherapy for Eating Disorders. Edited by Harper-Giuffre H, MacKenzie KR. Washington, DC, American Psychiatric Press, 1992, pp 261-272 [G 302. Holderness C, Brooks-Gunn J, Warren M: Comorbidity ofeating disorders and substance abuse: review ofthe literature. Int J Eat Disord 1994; 16:1-35 [FJ 303. Bulik C, Sullivan P, Epstein L, McKee M, Kaye W, Dahl R, Weltzin T: Drug use in women with anorexia and bulimianervosa. lnt J Eat Disord 1992; 11:214-225 [Di 304. Bulik C, Sullivan P, Fear J, Pickering A, Dawn A, McCullin M: Fertility and reproduction in women with anorexia nervosa: a controlled study. J Clin Psychiatry 1999; 60:130-135 tB]
References

305. Strober M, Freeman R, Bower S, Rigali J: Binge-eating in anorexia nervosa predicts later onset ofsubstance use disorder: a ten-year prospective, longitudinal follow-up of95 adolescents. J Youth and Adolescence 1997; 25:519-532 [CI

306. Hatsukami D), Mitchell JE, Eckert E, Pyle R: Characteristics ofpatients with bulimiaonly, bulimiawith affective disorder and bulimiawith substance abuse problems. Addict Behav 1986; 11:399-406 IDI 307. Collings S, King M: Ten year follow-up of50 patients with bulimianervosa. Br J Psychiatry 1994; 165:80-87 ICI 308. Mitchell JE, Pyle RL, Eckert ED, Hatsukami D: The influence ofprior alcohol and drug abuse problems on bulimianervosa treatment outcome. Addict Behav 1990; 15:169-173 ID] 309. Strasser T, Pike K, Walsh B: The impact ofprior substance abuse on treatment outcome for bulimianervosa. Addict Behav 1992; 17:387-395 [C] 310. Westermeyer J, Specker S: Social resources and social function in comorbid eating and substance disorder: a matched-pairs study. Am J Addict (in press) IA]
References

311. Cooper PJ: Eating disorders and their relationship tomood and anxiety disorders, in Eating Disorders and Obesity: A Comprehensive Handbook. Edited by Brownell KD, Fairborn CG. New York, Guilford Press, 199.5, pp 159-164 [GJ , 312. Edelstein CK, Yager J: Eating disorders and affective disorders, in Special Problems in Managing Eating Disorders. Edited by Yager J, Gwirtsman HE, Edelstein CK. Washington, DC, American Psychiatric Press. 1992, pp 15-50 IG] 313. Cooper P 11, Fairburn GG: The depressive symptoms of bulimianervosa. Br J Psychiatry 1986; 148:268-274 [GI 314, Bulik Sullivan P, Fear J, Joyce PR: Eating disorders and antecedent anxiety disorders: a controlled study. Acta Psychiatr Stand 1997; 92:101-107 IBI 315. Bulik CM, Sullivan PE Joyce PR, Carter FA: Temperament, character, personality disorder in bulimianervosa. J New Ment Dis 1995; 183:593-598 [B] 316. Johnson C, Tobin 1), Enright A: Prevalence and clinical characteristics ofborderline patients in an eating disordered population. ,/ Clin Psychiatry 1989; 50:9-15 [D] 317. Vitousek K, Manke F: Personality variables and disorders in anorexia nervosa and bulimianervosa. J Abnorm Psychol 1994; 103:137-147 [GI 318. Wonderlich SA: Personality and eating disorders, in Eating Disorders and Obesity: A Comprehensive Textbook. Edited by Brownell KD, Fairburn C. New York, Guilford Press, 1996, pp 171-176 IG]
References

319. Wonderlich SA, Mitchell JE: Eating disorders and personality disorders, in Special Problems in Managing Eating Disorders. Edited by Yager J, Gwirtsman HE, Edelstein CK. Washington, DC, American Psychiatric Press, 1992, pp 51-86 [GI

320. Wonderlich SA, Swift WJ: Borderline versus other personality disorders in the eating disorders: clinical description. Int J Eat Disord 1990; 9:629-638 IGI 321. Ames-Frankel J, Devlin Mi, Walsh TJ, Strasser (, Satick JM, Oldham JIM, Roose SP: Personality disorder diagnoses in patients with bulimianervosa: clinical correlates and changes with treatment. J Clin Psychiatry 1992; 53:90-96 [CI 322. Johnson oC, Tobin DL, Dennis A: Differences in treatment outcome between borderline and non-borderline bulimics at oneyear follow-up. Int J Eat Disord 1990; 9:617-627 [BI 323. Dansky BS, Brewerton TD, Kilpatrick DG, O'Neil PM: The National Women's Study: relationship ofvictimization and posttraumatic stress disorder to bulimiaJIM OSA. Int j Eat Disord 1997; 21:213-228 IDI
References

324. Rodin Ci, Daneman DI De(root J: The interaction ofchronic medical illness and eating disorders, in Medical Issues and the Eating Disorders: The Interface. Edited by Kaplan AS, (Garfinkel PE. New York, Brunner/Mazel, 1993, pp 179-181 325. eager J, Young RI: Eating disorders and diabetes mellitus, in Special Problems in Managing Eating Disorders. Edited bv Yager 1, Gwirtsman FIE, Edelstein CK. Washington, DC, American Psychiatric Press, 1992, pp 185-203 JGJ
References

326. Powers PS: Management ofpatients with comorbid medical conditions, in Handbook ofTreatment for Eating Disorders, 2nd ed. Edited by Garner DMl, Garfinkel PE. New York, Guilford Press, 1997, pp 424-436 JGJ 327. Brinch M, [sageer T, Tolstrup K: Anorexia nervosa and motherhood: reproduction pattern and mothering behavior of50 women. Acta Psychiatr Stand 1988; 77:61 71 [CI
References

328. Rand CSW, Willis DC, Kuldau JM: Pregnancy after anorexia nervosa. Int J Eat Disord 1987; 6:671-674 IGI 329. Stewart DE, Raskin J, Garfinkel PE, MacDonald OL, Robinson GE: Anorexia nervosa, bulimiaand pregnancy. Am J Obstet Gynecol 1987; 157:1194-1198 ICI 330. Treasure JL, Russell GF: Intrauterine growth and neonatal weight gain in babies ofwomen with anorexia nervosa. Br Med J 1988; 296:1038-1039 [BI 331. Lacey H, Smith G: Bulimianervosa: the impact ofpregnancy on mother and baby. Br J Psychiatry 1987; 150:777-781 IDI 332. Powers PS, Spratt EG: Males and females with eating disorders. Eating Disorders: J Treatment and Prevention 1994; 2:197-214 (Dl
References

333. Carlat DJ, Camargo CA Jr, Herzog DB: Eating disorders in males: a report on 135 patients. Am J Psychiatry 1997; 154: 1127-1132 IG] 334. Fichter MM, Daser CC: Symptomatology, psychosexual development, and gender identity in 42 anorexic males. Psychol Med 1987; 17:409-418 [GI 335. Andersen AE: Males With Eating Disorders. New York, Brunner/Mazel, 1990 [GI
References

336. Golden NH, Kreitzer P, Jacobson MS, Chasalow FI, Schebendach J, Freedman SIM, Shenker IR: Disturbances in growth hormone secretion and action in adolescents with anorexia nervosa. J Pediatr 1994; 125:655-660 DJ 337. Katzman DK, Zipursky RB: Adolescents with anorexia nervosa: the impact ofthe disorder on bones and brains. Ann NY Acad Sci 1997; 817:127-137 [FI 338. Katzman DK, Zipursky RB, Lambe EK, Mikulis DJ: A longitudinal magnetic resonance imaging study ofbrain changes in adolescents with anorexia nervosa. Arch Pediatr Adolesc Med 1997; 151:793-79- ICII
References

339. Nussbaum MP, Baird D, Sonnenblick NI, Cowan K, Shenker IR: Short stature in anorexia nervosa patients. J Adolesc Health Care 1985; 6:453-455 ID] 340. Pfeiffer RJ, Lucas AR, Ilstrup DM: Effects ofanorexia nervosa on linear growth. Clin Pediatr (Phila) 1986; 25:7-12 (Gi 341. Henry MC, Perlmutter SJ, Swedo SE: Anorexia, OCD, and streptococcus. J Am Acad Child Adolesc Psychiatry 1999; 38: 228-229 [GI 342. Sokol MS, Gray NS: Case study: an infection triggered, autoimmune subtype ofanorexia nervosa. J Am Acad Child Adolesc Psychiatry 1997; 36:1128-1133 IG
References

343. Gupta MA: Concerns about aging and a drive for thinness: a factor in the biopsychosocial model ofeating disorders? Int J Eat Disord 1995; 18:351-357 [BJ 344. Boast N, Coker E, Wakeling A: Anorexia nervosa oflate onset. Br J Psychiatry 1992; 160:257-260 [G] 345. Davis C, Yager J: Transcultural aspects ofeating disorders: a critical literature review. Cult Med Psychiatry 1992; 16:377382 [G]
References

346. Katzman MA, Lee S: Beyond body image: the integration offeminist and transcultural theories in the understanding ofself-- starvation. Int J Eat Disord 1997; 22:385-394 [FI 347. Powers PS, Johnson C: Small victories: prevention ofeating disorders among athletes. Eating Disorders: J Treatment and Prevention 1997; 4:364-377 ID] 348. Thompson RA, Sherman RT: Helping Athletes With Eating Disorders. Champaign, III, Human Kinetics, 1993 IGI 349. Williamson DA, Netemeyer RG, Jackman LP, Anderson DA, Funsch CL, Rabalais JY: Structural equation modeling for risk factors for the development ofeating disorder symptoms in female athletes. Int J Eat Disord 1995; 17:387-393 JE 350. Nattiv A, Agostini R, Drinkwater B, Yeager KK: The female athlete triad: the interrelatedness ofdisordered eating, amenorrhea, and osteoporosis. Clin Sports Med 1994; 13:405-418 I(II
References

351. Yates A: Athletes, eating disorders and the overtraining syndrome, in Activity Anorexia: Theory, Research and Treatment. Edited by Epling W, Pierce W Hillsdale, NJ, Lawrence Erlbaum Associates, 1996, pp 179-188 [GI 352. Epling W, Pierce W: Activity Anorexia: Theory, Research, Treatment. Hillsdale, NJ, Lawrence Erlbaum Associates, 1996 fGI
References

353. Mann nf Nolen-Hoesksema S, Huang K, Burgard D, Wright A, Hanson K: Are two interventions worse than none? joint primary and secondary prevention ofeating disorders in college females. Health Psychol 1997; 16:215-225 [B] 354. Shisslak CM, Crago M, Estes LS, Gray N: Content and method ofdevelopmentally appropriate prevention programs, in The Developmental Psychopathology ofEating Disorders: Implications for Research, Prevention, and Treatment. Edited by Smolak L, Levine MP, Striegel-Moore RH. Mahwah, NJ, Lawrence Erlbaum Associates, 1996, pp 341363 [E] 355. Glenn AA, Pollard 1W, Denovcheck JA, Smith AF: Eating disorders on campus: a procedure for community intervention. J Counseling & Development 1986; 65:163-165 [G] 356. Coll KM: Mandatory psychiatric withdrawal from public colleges and universities: a review ofpotential legal violations and appropriate use. J College Student Psychotherapy 1991; 5:9198 [E]

Issues related to combining risk factor reduction and clinical treatment for eating disorders in defined populations
C Barr Taylor ; Cameron, Rebecca P ; Newman, Michelle G ; Junge, Juliane. The Journal of Behavioral Health Services & Research 29. 1 (Feb 2002): 81-90. Turn on hit highlighting for speaking browsers Turn off hit highlighting

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Population-based psychotherapy considers the provision of services to a population at risk for or already affected with a disease or disorder. Using existing data on prevalence, incidence, risk factors, and interventions (both preventive and clinical)for Abstract
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Population-based psychotherapy considers the provision ofservices toa population at risk for or already affected with a disease or disorder. Using existing data on prevalence, incidence, risk factors, and interventions (both preventive and clinical)for eating disorders (anorexia excluded), this article examines issues related tointegrating and providing risk reduction and treatment toa population offemale college students. Population-based psychotherapy models have important implications for the provision ofservices and for future directions in research on eating and other types ofmental health disorders, but the assumptions need tobe carefully

examined. Studies that provide data combining population-based risk factor reduction and clinical treatment are needed toadvance this field. Introduction Population-based psychotherapy considers the provision ofservices toa population at risk for or already affected with a disease or disorder.' Thus, it incorporates elements ofprevention, case identification, and treatment. Population-based psychotherapy uses data from epidemiology, risk factor identification and modification, and clinical treatment outcome research todetermine preventive/treatment approaches for the targeted population. In this article, the links among risk factors, subclinical and clinical disorders, screening, stepped care, and costs are considered. A model is proposed-for heuristic purposes-for considering how a prevention/clinical eating disorders intervention might be provided toa defined population such as an insured group or a college population and how different assumptions might affect different cost-benefit models. Application toa College Population Ideally, in developing a population-based psychotherapy intervention for a particular disorder, the prevalence, incidence, and risk factors ofthat disorder would be well known. Also, there would be evidence that the risk factors can be modified, that modification ofrisk factors leads toa reduction in the incidence ofthe disorder, and that effective treatments are available for individuals with the disorder. The development ofthe model also requires reliable diagnoses and measurable outcomes. These and other features ofpopulation-based psychotherapy are summarized in Table 1. The extensive research literature on eating disorders, including treatment studies and recent work on identification ofrisk factors, allows us tomodel a population-based approach tothese problems. Incidence and prevalence Extensive epidemiologic work has found that approximately 1% to3% ofthe young adult, female population suffers from "full-syndrome eating disorders"; that is, they meet the Diagnostic and Statistical Manual, revised third (DSM-III-R) or fourth edition (DSM-IV) diagnostic criteria 2 for an eating disorder.3,4 However, many more young women suffer from "partial syndrome" or subclinical eating disorders; that is, they meet many but not all ofthe criteria for a full-syndrome eating disorder. For the purposes ofthis discussion, individuals meeting DSM-IV criteria for partial, subclinical and full-syndrome eating disorders will be considered clinical cases. Risk factors In recent years, a number ofstudies using cross-sectional samples and clinical populations have identified various cultural, familial, and personal factors that are associated with eating disorders.5 More important, several longitudinal studies have shown that in adolescents excessive weight and shape concerns, as well as the drive for thinness, predict the onset ofsubclinical and clinical eating disorders.67

By combining risk factor, prevalence, and incidence data from older adolescents and college students, it is possible tostratify a college-age female population by both risk and prevalence. For instance, Drewnowski et a14 (see Table 2) undertook a longitudinal survey of557 college women whom he categorized as no risk (18%), low risk (44%), high risk (25%), subclinical (10%), and clinical (1%-2%). At follow-up, students generally moved from a lesser toa greater symptomatic or risk category. Evidence That Risk Factors Can Be Modified Once potential risk factors have been identified, it becomes important toexamine interventions that can modify them. As prospective studies identifying potential risk factors for eating disorders have only been completed recently, it is not surprising that there is relatively little research on reducing risk factors. Nonetheless, cognitive-behavioral and psychoeducational interventions focused on subclinical populations have been shown toreduce eating disorder symptoms and improve attitudes.8 Interventions toimprove body image also have been effective in controlled studies.9-11 Several recent studies have demonstrated that a relatively low-cost, multimedia intervention can significantly reduce body shape concerns in college students at risk for eating disorders. Students who used a computer-delivered psychoeducational eating disorder prevention program (called Student Bodies, Stanford University) were able toimprove their body image, as well as adopt healthier eating attitudes and behaviors.","3 In one study,14 14 of26 women in the intervention group had Body Shape Questionnaire (BSQ) scores at baseline that would put them at risk for an eating disorder (BSQ > 110). At posttreatment, 10 ofthe 14 students had BSQ scores below 110, 3 reported lower scores but not below 110, and 1 score did not change. It is important tonote that the overall effect size ofthe changes in the intervention actually exceeded those generally reported for controlled studies using face-to-face therapy. Multimedia interventions are certainly not the only approach for reducing risk factors for eating disorders, but they have the advantage ofbeing relatively inexpensive todeliver tolarge populations (at least those populations with computer access). Student Bodies was recently provided toa group of110 high school students at a cost ofabout $25 per student. For purposes ofthis discussion, it is assumed that Student Bodies could be provided toa group ofhigh-risk students for this amount per student. (Actual delivery costs would depend on a number offactors including the cost ofthe moderator's time, availability/cost ofhardware, Internet connections, and servers.) Effective interventions Effective psychological therapies for bulimiahave been standardized and manualized, permitting widespread dissemination. For instance, a number ofcontrolled trials have found cognitive-behavioral therapy tobe effective in reducing symptoms of bulimia.11 Stepped care approaches Recent work 15-17 has focused on stepped care models for eating disorders. For example, Theils et al 16 compared 3 weeks ofa self-help manual followed by eight sessions ofcognitive behavior therapy (CBT) for patients still symptomatic with 16 sessions ofindividual CBTonly. The two groups had similar outcomes (40% and 41 % were symptom-free at 18 months), with the stepped care approach being considerably less expensive. Agras 15 outlined one such approach for bulimia. Drawing on several studies oftreatment effectiveness

and cost, he suggested that a cognitive-behavioral self-help manual plus periodic clinical supervision might be offered first, which could result in approximately 25% ofpatients showing clinically significant improvement. Second, antidepressant medications could be added, starting with a tricyclic (TCA) such as desipramine and followed up with a serotonin reuptake inhibitor (SRI), such as fluoxetine, in the event offailure ofthe TCA. This might result in improvement among 40% ofthis group (approximately 30% ofthe original group). A final approach for those who have not responded tothe medications) would be touse CBT, which might result in a 50% improvement (or about 22% ofthe original group). Thus, 75% to80% ofpatients would be treated successfully. He suggested that the optimal treatment, if cost were not a factor, might be CBTwith the option ofadding medication if progress is unsatisfactory, which would be a less cost-effective approach toachieving a similar (approximately 78%) rate ofimprovement. This model combined data from separate investigations, so rates ofimprovement may not reflect fully the impact oftreatment-refractory patients. In the following discussion, this model is extended torisk factor reduction and intervention. Implementation ofthe Model with a College Population Step 1 In providing a population-based intervention toa college student population, all female students would take a short screen (eg, the weight concerns instrument developed by Killen et al7) todetermine if they are at high risk for an eating disorder or have an eating disorder. (Toincrease efficiency and hence reduce cost, the screen would focus on female students only, given the relatively low rate ofeating disorders in males.) Students identified as being at high risk could then receive a relatively inexpensive intervention like Student Bodies and those with subclinical/clinical eating disorders could receive a stepped care intervention (except for students with anorexia who would be referred toindividual assessment and treatment as needed). The cost-effectiveness ofscreening varies depending on the prevalence ofthe disorder and the sensitivity and specificity ofthe screen. Traditionally, screens are used toidentify potential cases; in this model the screen is used toidentify a student at risk. Because there is no immediate gold standard as towhen a student is at risk (this only becomes evident over time), the use oftraditional sensitivity and specificity measures is not entirely applicable. In screening a population for students at risk, one also identifies cases. There are no data in the literature examining the sensitivities and specificities ofscreens used tostratify a population by risk and caseness at the same time, for instance, todetermine in a sample of100 students that 10 were at risk (needing prevention) and 2 were cases (needing referral and treatment). However, each individual who screened positive would need tobe further evaluated and categorized. Table 3 presents the different screening costs/100 identified high-risk students based on different levels ofprevalence ofhigh-risk individuals and assuming that the sensitivity and specificity estimates apply tohigh-risk individuals. "False positives" are those individuals who, on further evaluation, would be considered not at risk or not a case. An on-line or optically scanned screen can be processed very inexpensively ($1.00/screen), and further evaluation could be done cheaply with a paper-and-pencil instrument (such as the Eating Disorder Examination Self-Report Questionnairel8) for an estimated cost of$10. The cost ofthe overall screening jumps dramatically, related tothe prevalence ofthe disorder and

the number offalse positives that need tobe excluded. For instance, it would require $10,125 toidentify 100 high-risk cases if the prevalence ofhigh-risk cases in the population was 4% and the screening instrument was 80% specific and sensitive (Table 3). Much ofthis cost is driven by the suboptimal positive predictive value ofonly 14%. If the cost ofevaluating screen-positive individuals required a clinical interview, which could cost as much as $300 (2 hours ofa clinical psychologist's time), then the costs would soar. It is anticipated that the prevalence ofhigh-risk individuals would be about 10% and the instrument would be 90% sensitive and specific. At $10 for a screen, the cost ofidentifying 100 cases is only $3,111. But if all screen-positive individuals required a $300 clinical interview, then, for Example 4 in the table, the costs for reviewing "false positives" would jump from about $1,000 to$30,000, and the cost ofreviewing all screen positive cases would be twice that. Computerassisted screening procedures that derive from signal-detection-type analyses might make this process more efficient (eg, Smith et a19). Also note that the initial screen costs might very well exceed $1.00 in many settings. Step 2 Individuals identified as being at high risk (and not being cases) would then be given the Student Bodies 13 multimedia intervention (or some other low-cost psychoeducational program proven tobe equally effective and safe). The cost-benefit (cost per case prevented) ofproviding the intervention would depend on prevalence, incidence, and efficacy ofthe intervention. As shown in Table 4, these parameters strongly affect the cost-benefit. Under optimistic assumptions (Example 5), the intervention would require $449 per case prevented. However, if the intervention were only 25% effective, a more realistic assumption, the cost would be $898. For low prevalence conditions (eg, 4%) with a relatively low probability ofbecoming a case (eg, 10%), even a very effective intervention is expensive: $1,790 per case prevented (see Example 11 in Table 4). Step 3 The students who failed this intervention might benefit from simply being monitored, with more active interventions applied when and if they reached a subclinical level ofthe disorder. On the other hand, they might then be entered into a more aggressive stepped care approach. The stepped care and intervention numbers presented in Figure 1 are derived from Agras. 15 The 25% ofpatients not improving with stepped care might require partial day hospital care, inpatient hospitalization, more complicated psychopharmacology, or innovative treatment approaches. Agras 15 estimates that the cost oftreating a case in this model is approximately $4,000. In actual practice, many ofthe high-risk individuals who went on todevelop clinical syndromes would neither want nor receive treatment or might be treated in less expensive ways (eg, with group therapy). In addition, changes in any ofthe parameters listed in Table 4 or the development ofnew approaches could dramatically change treatment costs. For instance, 12 sessions of CBT/interpersonal group therapy or another group approach 20,21 may be as effective as Steps 2 and 3 in the above model. All ofthe examples provided in Table 4 suggest that the prevention cost would be lower than the treatment cost. However, in these models, case identification and referral increase the number ofstudents in a population receiving treatment. An individual is prevented from becoming a case and needing treatment, but that individual may not have actually received treatment had she not been identified through population-based screening. For example, in Table 4, Example 6, the cost ofpreventing six cases is about $5,610 that would cost $24,000

totreat. But how many ofthese six individuals would actually seek treatment? If only one ofthe six cases actually would have wanted/sought treatment without screening/referral, then the cost ofprevention is greater than the cost oftreatment tothe payer ofthese services. For lower prevalence rates ofindividuals at high risk for eating disorders, with lower 1-year incidence rates for those high-risk interventions, and with less effective interventions, the cost-benefit ofprevention becomes marginal. For instance, in Example 12, in Table 4, the cost ofpreventing two cases was almost $7,000, not much less than the cost oftreating them. It is worth noting that prevention may confer many benefits tothose individuals who would not have sought treatment. For instance, participation in the kind ofprevention activities described here for high-risk individuals might improve self-image, school, and even work performance that might confer direct personal and perhaps indirect financial benefit. There are many other ways toreduce costs ofthe preventive intervention. For instance, another approach would be toprovide the high-risk intervention only tostudents who demonstrated that their risk factor profile worsened (a watchful waiting approach) and then provide them a high-risk intervention. An ecologic intervention, designed toreduce the normative acceptance ofrisk behaviors (eg, bingeing and/or purging among students in the dorm or in sororities, for instance), might also be a cost-effective preventive measure. There are additional costs-benefits tobe considered in deciding how tobalance prevention and intervention. For instance, step 2, the use ofmedication, might reduce symptoms but impair sexual function in a high percentage ofstudents. In contrast, high-risk interventions might confer general benefits on students (eg, improving confidence and health) in addition topotentially reducing incidence ofeating disorders, although such treatments also might have downsides, such as leading tolabeling and stigmatization.22 Implications for Behavioral Health Services Population-based psychotherapy offers an approach tointegrating clinical treatments and high-risk interventions in order tooffer services toprevent/treat eating disorders within a defined population. This model, presented mostly for heuristic purposes, is based on a number ofuntested assumptions and focuses on a relatively straightforward problem (subclinical/clinical eating disorders, anorexia excluded). The information necessary todetermine how tobest treat a population is quite different from the information necessary totreat an individual. The elegant research strategies that have evolved toexamine treatment outcome efficacy among individuals in narrowly defined populations oftreatment volunteers are only partly relevant tothe effectiveness ofthese interventions as applied topopulations with the goal ofreducing incidence and/or ofproviding cost-effective care toeveryone in the population who may benefit from it. Furthermore, from the standpoint oflinking prevention and intervention, psychopathology often exists on a continuum ofdisorder not only from clinical tosubclinical populations, but also from high-risk tosubclinical/clinical groups. The applicationand monitoring ofeffects ofstandardized interventions on defined populations would help elucidate these continua. For instance, are there characteristics ofcertain individuals with subclinical disorders that predispose them todevelop more serious psychopathology? Do successfully treated individuals have higher risk rates than high-risk individuals who have never been cases? The application ofstandardized and stepped care interventions across populations might be a better way toidentify nonresponsive subpopulations ofpatients requiring different or new treatments and ofexamining the ecologic validity ofnarrowly defined population studies.

However, stepped care approaches may lead todecreased credibility or increased dropout rates ofthose who do not benefit from preliminary interventions. Thus, it also might be important for future research tobegin toempirically identify individual predictors ofnonresponsiveness toparticular types oftreatment interventions (eg, risk factors for failure ofpsychoeducation or self-help interventions). Such predictors could be used toidentify individuals who would benefit from the immediate application ofmore costly interventions. The population-based approach offers advantages toresearchers interested in the effectiveness or generalizability oftheir interventions and prevention strategies, or tothose interested in understanding the role ofeconomics in whether their research has real-world clinical utility. The cost-benefit models presented in Tables 3 and 4 show that different assumptions about incidence and prevalence, screening and treatment costs, and efficacy, dramatically alter costbenefit numbers. The model presented focused on treating individuals within a population. Population-based psychotherapy interventions also should consider environmental/ecologic/community/system factors that might positively reduce risk. While primary prevention interventions are much more likely tobe effective if they include "environmental or community" interventions, the same also may be true ofselected and indicated interventions. For instance, consider a female undergraduate with a body mass index (BMI) >27, who is struggling with poor body image and who attends a fraternity party in which the members are encouraged tocarry a stuffed pig around if they date someone in her weight range. An individually directed intervention might help her cope with this humiliating message, but peer pressure on fraternities todiscontinue such practices might be a more effective approach. How can the model shown in Figure 1 be used toinform research strategies? Assuming that the end result ofa program ofresearch is todevelop population-based therapy, then, for any disorder, data on the factors listed in Table 1 need tobe considered programmatically. Researchers interested in issues ofidentifying an at-risk or impaired population might want toconsider the cost implications oftheir measures 22; individuals studying treatment might examine whether treated individuals remain at high risk or fall into some other category (ie, movement back and forth between categories over time can be examined tohelp guide the judicious use ofinterventions). Work on moderators and mediators might provide important data on the movement from high-risk tosubclinical/clinical cases. Acknowledgments This research was partially funded by a grant from the National Institute ofMental Health (NIH 2801 MH60453-OlAI).
References

References
References

1. Katon W, Von Korff M, Lin E, et al. Population-based care ofdepression: effective disease management strategies todecrease prevalence. General Hospital Psychiatry. 1997; 19:169178.

2. American Psychiatric Association. Diagnostic and Statistical Manual ofMental Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994. 3. Fairburn CG, Beglin SJ. Studies ofthe epidemiology of bulimianervosa. American Journal ofPsychiatry. 1990;147:401-408. 4. Drewnowski A, Yee DK, Kurth CL, Krahn DD. Eating pathology and DSM-III-R bulimianervosa: a continuum ofbehavior. American Journal ofPsychiatry. 1994;151:12171219. 5. Striegel-Moore RG, Silberstein LR, Rodin J. Toward an understanding ofrisk factors for bulimia. Journal ofthe American Psychological Association. 1986;41:246-263.
References

6. Killen JD, Hayward C, Taylor CB, et al. Factors associated with symptoms of bulimianervosa in a community sample of6th and 7th grade girls. International Journal ofEating Disorders. 1994; 15(4):357-367. 7. Killen JD, Taylor CB, Hayward CH, et al. Weight concerns influence the development ofeating disorders: a four-year prospective study. Journal ofConsulting and Clinical Psychology. 1996;64:936-940. 8. Carter JC, Fairburn CG. Cognitive-behavioral self-help for binge eating disorder: a controlled effectiveness study. Journal ofConsulting and Clinical Psychology. 1998;66(4):616-623. 9. Cash TE Body-Image Therapy: A Program for Self-Directed Change. New York: The Guilford Press; 1991. 10. Rosen JC. Body image assessment and treatment in controlled studies ofeating disorders. International Journal ofEating Disorders. 1996:20:331-343. It, Lewandowski LM, Gebing TA, Anthony IL, O'Brien WH. Meta-analysis ofcognitivebehavioral treatment studies or bulimia. Clinical Psychology Review. 1997;17(7):703-718.
References

12. Winzelberg AJ, Taylor CB, Altman TM, Eldredge KL, Dev P, Constantinou PS. Evaluation ofa computer-mediated eating disorder intervention program. International Journal ofEating Disorders. 1998;24:339-349. 13. Celio AA, Winzelberg AJ, Wilfley DE, et al. Reducing risk factors for eating disorders: comparison ofan Internet- and a classroom-delivered psychoeducation program. Journal ofClinical and Consulting Psychology. 2000;68(4):650-657. 14. Winzelberg AJ, Eppstein D, Eldredge KL, et al. Effectiveness ofan Internet-based program for reducing risk factors for eating disorders. Journal ofConsulting and Clinical Psychology. 2000;68:346-350.

15. Agras WS. The treatment of bulimianervosa. Drugs ofToday. 1997;33(6):405-411. 16. Wilson GT, Vitousek KM, Loeb KL. Stepped care treatment for eating disorders. Journal ofConsulting and Clinical Psychology. 2000;68(4):564-572.
References

17. Thiels C, Schmidt U, Treasure J, Garthe R, Troop N. Guided self-change for bulimianervosa incorporating use ofa self-care manual. American Journal ofPsychiatry. 1998; 155(7):947-953. 18. Luce KH, Crowther JH. The reliability ofthe Eating Disorder Examination-Self-Report Questionnaire Version (EDE-Q). International Journal ofEating Disorders. 1999:25:349-351. 19. Smith PM, Kraemer HC, Miller NH, DeBusk RF, Taylor CB. In-hospital smoking cessation programs: who responds, who doesn't. Journal ofConsulting and Clinical Psychology. 1999;67:19-27. 20. McKisack C, Waller G. Factors influencing the outcome ofgroup psychotherapy for bulimianervosa. International Journal ofEating Disorders. 1997;22:1-13. 21. Mitchell JE, Pyle RL, Pomeroy C, et al. Cognitive-behavioral group psychotherapy of bulimianervosa: importance oflogistical variables. International Journal ofEating Disorders. 1993;14:277-287. 22. Offord D, Kraemer HC, Kazdin AE, Jensen PS, Harrington R. Lowering the burden ofsuffering from child psychiatric disorder: trade-offs among clinical, targeted, and universal interventions. Journal ofthe American Academy ofChild andAdolescent Psychiatry. 1998;37(7):686694.
AuthorAffiliation

C. Barr Taylor, MD Rebecca P. Cameron, PhD Michelle G. Newman, PhD Juliane Junge, Dipl-Psych
AuthorAffiliation

Address correspondence toC. Barr Taylor, MD, Professor, Department ofPsychiatry and Behavioral Sciences, Stanford University School ofMedicine, Stanford, CA 94305-5722; email: btaylor@stanford.edu. Rebecca P. Cameron, PhD, is an Assistant Professor, Department ofPsychology, California State University, Sacramento.

Michelle G. Newman, PhD, is an Assistant Professor, Department ofPsychology, Pennsylvania State University. Juliane Junge, Dipl-Psych, is a Research Associate, Department ofClinical Psychology and Psychotherapy, Dresden University ofTechnology.

Indexing (details)
Cite Subjects Statistical analysis, Studies, Mental health, Health services, College students, Women, Eating disorders MeSH Adolescent, Adult, Cost-Benefit Analysis, Eating Disorders -- diagnosis, Eating Disorders -epidemiology, Evidence-Based Medicine, Female, Humans, Models, Psychological, Prevalence, Risk Assessment, Risk Factors, Students -- psychology, Universities, Community Health Planning (major), Community Health Planning (major) -- economics, Eating Disorders -- prevention & control (major), Psychotherapy (major), Psychotherapy (major) -- economics Locations United States, US Classification 9190: United States, 8320: Health care industry, 9130: Experimental/theoretical Title Issues related to combining risk factor reduction and clinical treatment for eating disorders in defined populations Authors Cameron, Rebecca P; Newman, Michelle G; Junge, Juliane Publication title The Journal of Behavioral Health Services & Research Volume 29 Issue 1

Pages 81-90 Number of pages 10 Publication year 2002 Publication Date Feb 2002 Year 2002 Publisher Springer Science & Business Media Place of Publication Gaithersburg Country of publication Netherlands Journal Subjects Public Health And Safety, Health Facilities And Administration, Social Services And Welfare ISSN 10943412 Source type Scholarly Journals Language of Publication English Document type PERIODICAL Subfile

Statistical analysis, Studies, Mental health, Health services, College students, Women, Eating disorders Accession number 11840907 ProQuest Document ID 205218686 Document URL http://search.proquest.com/docview/205218686?accountid=38885 Copyright Copyright Aspen Publishers, Inc. Feb 2002 Last updated 2011-04-29 Database ProQuest Research Library

American Psychiatric Association Title Practice guideline for the treatment of patients with eating disorders (revision) Authors American Psychiatric Association Publication title The American Journal of Psychiatry Volume 157 Issue 1 Supplement Practice Guideline for the Treatment of Patients With... Pages 1-39 Number of pages 39 Publication year 2000 Publication Date Jan 2000 Year 2000

Publisher American Psychiatric Association Place of Publication Washington Country of publication United States Journal Subjects Medical Sciences--Psychiatry And Neurology ISSN 0002953X CODEN AJPSAO Source type Scholarly Journals Language of Publication English Document type PERIODICAL Subfile Psychiatry, Therapy, Anorexia, Bulimia, Guidelines Accession number 10642782, 20107394 ProQuest Document ID 220459510 Document URL http://search.proquest.com/docview/220459510?accountid=38885 Copyright Copyright American Psychiatric Association Jan 2000 Last updated 2011-09-06 Database ProQuest Research Library

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Cognitive behaviour therapy--clinical applications: BMJ

Enright, Simon J. British Medical Journal 314. 7097 (Jun 21, 1997): 1811-6. Turn on hit highlighting for speaking browsers Turn off hit highlighting

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The clinical applications of cognitive behavior therapy are examined.

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Aaron Beck developed an insight-focused therapy that emphasizes recognizing and changing negative thoughts and maladaptive beliefs known as Cognitive therapy. Although there are many variants of cognitive behaviour therapy, these are unified by the proposition that psychological problems arise as a direct consequence of faulty patterns of thinking and behaviour. Patients tend to misinterpret situations or symptoms in ways that undermine their coping. Their abnormal behavioural patterns exacerbate and consolidate these problems. The critical factor lies in how patients assess specific situations or problems-as summarised by Epictetus, a first century Greek philosopher: "Men are disturbed not by things, but the views they take of them." Clinical applications of cognitive behaviour therapy Cognitive therapy initially gained recognition as an approach to treating depression, but extensive research has also devoted to the study and treatment of panic disorder and agoraphobia, post-traumatic stress disorder, generalised anxiety disorder, social phobia, obsessive-compulsive disorder, hypochondriasis, psychosis and schizophrenia, Personality disorders, offenders, eating disorders.

Methods This review of cognitive behaviour therapyis based on a literature search ofall papers, books, and chapters related toits applicationin mental health and general medicine. In thesearch I used thefollowing key words-cognitive, behaviour, behavioural, theory, therapy, treatmentand searched thefollowing databases on theEmbase CD ROM from September 1985 toSeptember 1996-Healthplan, Psych-Lit, Excerpta Medica (psychiatry, drugs, pharmacology), Cinahl, Medline, and Social Science Citation Index. This review covers themajor clinical applications of cognitive behaviour therapy, focusing on those aspects ofpsychology, psychiatry, and medicine where theresearch data are most substantial. Cognitive behaviourtheory Thelink between psychological problems and faulty patterns ofthinking and behaviourcan be illustrated Beck's original model ofdepression.2 He proposed that negative thinking in depression has its origins in attitudes and assumptions arising from experiences early in life.

Such assumptions can be positive and motivating, but they can also be too extreme, held too rigidly, and be highly resistant torevision. Problems arise when critical incidents occur that contradict a person's goals and beliefs. For example, theassumption "My worth is dependent on my success" might cause a person tobe vulnerable toan event like failing toget a job at interview. Once activated by thecritical incident, thecore assumption leads to theproduction ofspontaneous negative automatic thoughts such as "I am a worthless failure." Such thoughts lower mood and increase thelikelihood of Summary points Cognitive behaviour therapyascribes a central role toconscious thought, beliefs, and behaviourin theperpetuation ofdisability The therapyis a brief, problem oriented approach that aims tohelp patients toidentify and modify dysfunctional thoughts, assumptions, and patterns of behaviour It is now thetreatment ofchoice for many mental health disorders and has extensive application togeneral medicine, supported by increasing numbers ofclinical research studies There are relatively few qualified cognitive behaviourtherapists: if thetreatment is toachieve its clinical potential there must be substantial and rapid expansion oftraining opportunities More research is needed in all areas of cognitive behaviour therapy torefine theory and therapyfurther negative automatic thoughts since research has shown that specific types ofaffect will automatically increase theaccessibility ofthoughts congruent with that mood" Once a person is depressed a set of cognitivedistortions known as the cognitivetriad (negative view ofoneself, current experience, and thefuture) exert a general influence over theperson's day today functioning, and negative automatic thoughts become increasingly pervasive. Other biases in information processing also act toconsolidate thedepression, whereby patients exaggerate and overgeneralise fi-om minor problems and selectively attend toevents that confirm their negative view ofthemselves. Behavioural factors will also serve toexacerbate thedepression. Sufferers' activity levels begin toreduce. Reduced exercise may also be associated with a lowering ofmood. Depressed people go out less and gradually withdraw from life, thereby experiencing less stimulation and reduced opportunity for positive experiences. Cognitive behaviourtheory does not claim that negative thinking and abnormal behaviourcause depression but rather that these factors exacerbate and maintain theemotional disturbance. Cognitive behaviour therapy The cognitive behaviourtherapist and patient work together toidentify specific patterns ofthinking and behaviourthat underpin thepatient's difficulties. Treatment continues between sessions with homework assignments both tomonitor and challenge specific thinking patterns and toimplement behavioural change.

The cognitivemethods in therapyinclude: Detailed explanation and discussion of the cognitivemodel Keeping a diary monitoring situations, thoughts, and feelings todevelop awareness about these * Identifying connections between thoughts, affect, and behaviour * Examining evidence "for" and "against" thethoughts * Coaching patients in challenging negative thoughts by question and rationalising techniques * Learning toidentify dysfunctional assumptions underpinning distortions * Cognitiverehearsal ofcoping with difficult situations or use ofimagery Thebehavioural elements in therapymay include: * Setting up behavioural experiments totest irrational thoughts against reality * Graded exposure tofeared situations in reality or theimagination * Target setting and activity scheduling * A programme ofreinforcement and reward * Teaching specific skills such as relaxation * Role playing, behavioural rehearsal, therapist modelling coping behaviours Growth of cognitive behaviour therapy Though cognitive behaviour therapywas initially developed for treating depression, in thepast 25 years thesubject has rapidly expanded. This expansion is based on thepremise that cognitiveand behavioural factors are relevant toall human experience. It is therefore logical toassert that there is no psychological or physical problem that cannot be potentially assisted by a cognitivebehavioural approach. It is easy tosee theappeal of the cognitive behaviour therapybandwagon. Its methods are well documented and readily accessible. It focuses on well defined targets that can be quantified and researched. Treatment is brief, highly structured, problem oriented, and prescriptive. Patients are seen as active collaborators who can readily understand and apply thetheory and techniques. Clinical applications of cognitive behaviour therapy

The efficacy of cognitive therapy in treating depression, panic disorder and agoraphobia, post-traumatic stress disorder, generalised anxiety disorder, social phobia, obsessive-

compulsive disorder, hypochondriasis, psychosis and schizophrenia, Personality disorders, offenders, eating disorders well documented.

depression is. Cognitive behaviour therapyfor patients who experience panic attacks is based on identifying and modifying catastrophic misinterpretations of theinitial physical symptoms of theanxiety. Specific exercises that enable exposure tofeared bodily sensations and actual exposure tofear cues are central to thetreatment. Controlled studies attest to theefficacy of cognitive behaviour therapyin treating panic and agoraphobia and its superiority over supportive therapy, relaxation, and drugs. Thelong term effects of cognitive behaviour therapyseem tobe superior toother techniques.

Perceived unpredictability and uncontrollability have a pivotal role in thedevelopment ofposttraumatic stress disorder. In addition, cognitive behaviour therapyfocuses on active exposure to theexperience of thetrauma through repeated activation of thefear memoties and eliminating imaginal and behavioural avoidance.11 Behaviour therapyand cognitive behaviour therapyhave been reviewed by Hacker-Hughes and Thompson in treating post-traumatic stress disorder.'2 They report encouraging results but highlight theneed for more empirical support for thespecific cognitivecomponents of thetreatment Worry lies at thecore ofgeneralised anxiety disorder. Sufferers overestimate thelikelihood and severity ofthings going wrong and underestimate both their internal and external coping resources. A review of11 studies using cognitive behaviour therapy totreat generalised anxiety disorder indicated that these methods were at least as effective as anxiolytic drugs and superior toplacebo or tono treatment.5 Theresults of thetreatment in studies oflong term follow up are also encouraging." Social phobics interpret social situations as threatening; their attention is self focused, leading toa belief that others are evaluating them negatively; and they exhibit a greater awareness oftheir own bodily symptoms. Despite having poorer memories ofrecent social interactions than control subjects, social phobics tend toconduct long post mortems after social encounters typified by negative self evaluation. This process leads ultimately tobehavioural avoidance. Combined exposure and cognitiverestructuring has proved beneficial." However, cognitive behaviour therapyhas been shown tobring greater benefit topatients with circumscribed social phobia rather than those with generalised social phobia.'5

Behavioural treatments involving exposure ofpatients totheir fears while preventing obsessive ritualising have proved highly successful in treating many obsessive-compulsive disorders. However, those who fail torespond to behaviour therapytend tohave "overvalued ideas" concerned with exaggerated personal responsibility, perfectionism, and fear ofpunishment or catastrophic outcomes." These beliefs are thefocus for cognitiveinterventions with obsessivecompulsive patients. A recent review of15 studies of cognitive behaviour therapyin obsessive-compulsive disorder concluded that, because ofmethodological problems, claims for theadded benefit of cognitivetechniques toexisting behavioural methods were encouraging but as yet unproved." Eating disorders In anorexia thecentral dysfunctional assumption is thestatement "I must be thin." Thedevelopmental distresses ofadolescence are allayed through thepursuit ofthinness, and feelings ofself doubt and deficiency are overridden by maintaining a figure perceived tobe theenvy ofall others.'9 Despite thecentral role ascribed tocognition in theaetiology ofthis disorder, anorexia has remained remarkably resistant to cognitive behaviour therapy. Outcome studies are limited and offer only marginal support of cognitive behaviour therapycompared with other types ofintervention .19 Fairburn and Cooper are credited with themost comprehensive model of bulimianervosa with regard to cognitive behaviour therapy. They emphasise a preoccupation with weight and shape, leading toexcessive and inflexible dietary rules. Sufferers fail toadhere totheir regimen and view this failure catastrophically, leading toabandonment of therules and bingeing behaviour. Self esteem becomes solely associated with weight or shape, increasing theperceived value ofdieting. Bingeing and purging behavioursreinforce low self esteem tocomplete thevicious cycle. Thespecificity of cognitive behaviour therapyin treating bulimiais still a matter for debate. In most outcome studies, important therapeutic effects are reported in about half ofthose treated by cognitive behaviour therapy.

Cognitive behaviour therapyfocuses on patients' enduring tendency tomisinterpret innocuous physical symptoms as evidence ofserious illness. The ensuing anxiety leads torepeated reassurance seeking, hypervigilance toinformation about illness, increased bodily focus, and avoidance.

Cognitive behaviour therapyfor patients with psychoses is based on theidea that first rank symptoms occur as a result ofnormal attempts tomake sense ofabnormal perceptual experiences. Treatment helps patients distract themselves from their symptoms and alter their beliefs about thenature oftheir experiences. Beck and colleagues have suggested that each of thesubcategories ofpersonality disorder reflect specific dysfunctional beliefs and an associated maladaptive behavioural strategy that is harmful to theindividual or tosociety. As yet there are few controlled trials tovalidate

treatment ofpersonality disorder with cognitive behaviour therapy. Treatment can last for more than two years, and most research is based on single case studies. Much more evidence ofefficacy is needed.28 Numerous studies attest to theefficacy of cognitive behaviour therapyin modifying behaviourand reducing recidivism. Themain areas ofstudy relate tosex offenders, violence, juvenile crime, and mentally disordered offenders

Caveats, criticisms, and future directions For many diagnostic groups, controlled trials indicate that, at best, only about half ofpatients exhibit clinically important improvement after cognitive behaviour therapy. Many ofthese studies have been conducted by theoriginal theorists, and there is evidence ofallegiance effects whereby less expert practitioners or those from another theoretical base often fail toreplicate such positive results from treatment.35 36 Some applications of cognitive behaviour therapyremain highly experimental and require considerably more research and more sophisticated theoretical models. Without this increased understanding ofwhat works for whom, and why, we should remain cautious ofoverenthusiastic claims for efficacy and of theclumsy application ofgeneric cognitivebehavioural theory being made tofit increasingly diverse disorders. A considerable increase in thenumber oftrained practitioners of cognitive behaviour therapyis needed tomeet increasing demands. Without this investment thepotential benefits of cognitive behaviour therapywill never be fully realised. Funding: None. Conflict ofinterest: None. Footnote 1Meichenbaum D. Cognitive-behaviourmodification Morristown, NJ: General Learning Press, 1974. Beck AT Cognitive therapyand theemotional disorders. New York: International Universities Press, 1976. Teasdale JD. Cognitivevulnerability topersistent depression. Cogn Emotion 1988;2:247-74. Beck AT, Rush AJ, Shaw BF, Emery G. Cognitive therapy ofdepression: a treatment manual New York: Guilford Press, 1979. Blackburn I-M, Twaddle V Cognitive therapyin action London: Souvenir Press, 1996. Miller IW, Norman WH, Keitner GI. Cognitive-behavioural treatment ofdepressed inpatients: six and twelve month follow-up. Am J Psychiatry 1989; 145:1274-9. Evans MD, Hollon SD, DeRubeis RJ, Paisecki JM, Grove WM. Garvey MJ, et al. Differential relapse following cognitive therapyand pharmacotherapy for depression Arch

Gen Psychiatry 1992;49:802-8. Fava GA, Grandi S, Zielezny M, Rafanelli C, Canestrari R. Fo

Assessment and treatment of bulimia nervosa

McGilley, Beth M; Pryor, Tamara L. American Family Physician 57. 11 (Jun 1998): 27432750. Turn on hit highlighting for speaking browsers Turn off hit highlighting

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Bulimia nervosa is characterized by binge eating and inappropriate compensatory behaviors, such as vomiting, fasting, excessive exercise and the misuse of diuretics, laxatives or enemas. Although the etiology of this disorder is unknown, genetic and neurochemical Show all

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Headnote Bulimia nervosa is characterized by binge eating and inappropriate compensatory behaviors, such as vomiting, fasting, excessive exercise and the misuse of diuretics, laxatives or enemas. Although the etiology of this disorder is unknown, genetic and neurochemical factors have been implicated. Bulimia nervosa is 10 times more common in females than in males and affects up to 3 percent of young women. The condition usually becomes symptomatic between the ages of 13 and 20 years, and it has a chronic, sometimes episodic course. The

long-term outcome has not been clarified. Other psychiatric conditions, including substance abuse, are frequently associated with bulimia nervosa and may compromise its diagnosis and treatment. Serious medical complications of bulimia nervosa are uncommon, but patients may suffer from dental erosion, swollen salivary glands, oral and hand trauma, gastrointestinal irritation and electrolyte imbalances (especially of potassium, calcium, sodium and hydrogen chloride). Treatment strategies are based on medication, psychotherapy or a combination of these modalities. Bulimia nervosa is a psychiatric syndrome with potentially serious consequences.lz Relatively effective treatments for this disorder have been developed, and early intervention is more likely to facilitate eventual recovery.2 Unfortunately, few health care professionals receive training in the assessment of bulimia nervosa. Therefore, they may be unable to identify and treat patients with the disorder. Historically, patients with bulimia nervosa often were hospitalized until the most disruptive symptoms ceased. In today's health care environment, hospitalization for bulimia nervosa is infrequent and tends to take the form of brief admissions focused on crisis management.3 Specialists in the field of eating disorders have responded to the present cost-containment measures by developing a combination of treatment modalities, including medication and individual and group psychotherapy, that can be used in the outpatient care of patients with bulimia nervosa. This article discusses the assessment and treatment of bulimia nervosa and considers how this disorder can best be handled in a managed care environment. Definitions and Etiology Bulimia nervosa is a multifaceted disorder with psychologic, physiologic, developmental and cultural components.1,2; There may be a genetic predisposition for the disorder. Other predisposing factors include psychologic and personality factors, such as perfectionism, impaired self-concept, affective instability, poor impulse control and an absence of adaptive functioning to maturational tasks and developmental stressors (e.g., puberty, peer and parental relationships, sexuality, marriage and pregnancy). Biologic researchers suggest that abnormalities of central nervous system neurotransmitters may also play a role in bulimia nervosa.4 Furthermore, several familial factors may increase the risk of developing this disorder. For example, researchers have discovered that first- and second-degree relatives of individuals with bulimia nervosa have an increased incidence of depression and manic-depressive illnesses, eating disorders, and alcohol and substance abuse problems.5-7 Regardless of the cause, once bulimia nervosa is present, the physiologic effects of disordered eating appear to maintain the core features of the disorder, resulting in a selfperpetuating cycle. Diagnostic Criteria The diagnostic criteria for bulimia nervosa (Table I) now include subtypes to distinguish patients who compensate for binge eating by purging (vomiting and/or the abuse of laxatives and diuretics) from those who use nonpurging behaviors (e.g., fasting or excessive exercising).1 A binge eating/purging subtype of anorexia nervosa also exists. Low body weight is the major factor that differentiates bulimia nervosa from this subtype of anorexia nervosa. Thus, according to the established diagnostic criteria,1 patients who are 15 percent below natural body weight and binge eat or purge are considered to have anorexia nervosa. Patients can,

and frequently do, move between diagnostic categories as their symptom pattern and weight change over the course of the illness. Some patients do not meet the full criteria for bulimia nervosa or anorexia nervosa. These patients may be classified as having an eating disorder "not otherwise specified" (Table 2).' Prevalence and Prognosis Bulimia nervosa appears to have become more prevalent during the past 30 years. The disorder is 10 times more common in females than in males and affects 1 to 3 percent of female adolescents and young adults.6 Both anorexia nervosa and bulimia nervosa have a peak onset between the ages of 13 and 20 years. The disorder appears to have a chronic, sometimes episodic course in which periods of remission alternate with recurrences of binge/purge cycles. Some patients have bulimia nervosa that persists for 30 years or more.8 Recent data suggest that patients with subsyndromal bulimia nervosa may show morbidity comparable to that in patients with the full syndrome. The long-term outcome of bulimia nervosa is not known. Available research indicates that 30 percent of patients with bulimia nervosa rapidly relapse and up to 40 percent remain chronically symptomatic.9 Psychiatric Comorbidity Clinical and research reports" 13 emphasize a frequent association between bulimia nervosa and other psychiatric conditions. Comorbid major depression is commonly noted (Table 3), although it is not clear if the mood disturbance is a function of bulimia nervosa or a separate phenomenon.11 Information concerning the comorbidity rates of bipolar disorders (e.g., manic depression, rapid cycling mood disorder) and bulimia nervosa is somewhat limited. However, recent epidemiologic data indicate an increased incidence of rapid cycling mood disorders in patients with more severe, chronic bulimia nervosa.13 The association between bulimia nervosa and other anxiety and substance-related disorders has been well documented.7 For example, substance abuse or dependence, particularly involving alcohol and stimulants, occurs in one third of patients with bulimia nervosa. Thus, a comorbid substance-related disorder must be addressed before effective treatment for bulimia nervosa can be initiated. Significant research has been devoted to the high frequency of personality disturbances in patients with bulimia nervosa. Overall, between 2 and 50 percent of women with bulimia nervosa have some type of personality disorder, most commonly borderline, antisocial, histrionic or narcissistic personality disorder10,14-16 To ensure that the treatment approach is properly designed and effective, the physician must look carefully for symptoms of comorbid psychiatric illness in patients with bulimia nervosa. Although further research is needed to determine the extent to which comorbid conditions influence the course of bulimia nervosa, the presence of these additional problems clearly complicates the treatment process. Medical Complications

The medical complications of bulimia nervosa range from fairly benign, transient symptoms, such as fatigue, bloating and constipation, to chronic or life-threatening conditions, including hypokalemia, cathartic colon, impaired renal function and cardiac arrest"ls (Table 4). Binge Eating Binge eating alone rarely causes significant medical complications. Gastric rupture, the most serious complication, is uncommon.17 More often, patients describe nausea, abdominal pain and distention, prolonged digestion and weight gain. The combination of heightened anxiety, physical discomfort and intense guilt provokes the drive to purge the food by self-induced vomiting, excessive exercise or the misuse of ipecac, laxatives or diuretics. These purgative methods are associated with the more serious complications of bulimia nervosa. Self-Induced Vomiting Self-induced vomiting, the most common means of purging, is used by more than 75 percent of patients with bulimia nervosa.19 Most patients vomit immediately or soon after a binge. During the binge, they commonly drink excessive fluids to "float the food" and facilitate regurgitation. Vomiting is induced by stimulation of the pharynx using a finger or a narrow object such as a toothbrush. Some patients describe the learned ability to vomit by pressure or contraction of the abdominal muscles. A minority of patients develop reflux following the consumption of virtually any amount of food or fluid. Treatment of this reflux is difficult and requires that the patient practice relaxation during food ingestion. Self-induced vomiting can lead to a number of serious medical complications. Dental Erosion. Gastric acids may cause deterioration of tooth enamel (perimolysis), particularly involving the occlusal surfaces of molars and the posterior surfaces of maxillary incisors. Since these effects are irreversible, patients with this complication need to have regular dental care. Enlarged Salivary Glands. Frequent vomiting has been reported to cause swelling of the salivary glands in approximately 8 percent of patients with bulimia nervosa.20 The exact etiology is unknown. The glandular enlargement is typically painless and may occur within several days of excessive vomiting. It appears to be a cosmetically distressing but medically benign condition. Other than cessation of vomiting, no specific treatment has been identified. Oral and Hand Trauma. The induction of vomiting with a finger or an object can cause lacerations of the mouth and throat. Bleeding lacerations can also occur on the knuckles because of repeated contact with the front teeth. Some patients with bulimia nervosa develop a calloused, scarred area distal to their knuckles. Oral or hand trauma can provide evidence of vomiting even when patients deny bulimic symptoms. Esophageal and Pharyngeal Complications. Because of repeated contact with gastric acids, the esophagus or pharynx may become irritated. Heartburn and sore throats may occur and are best treated with antacids and throat lozenges, respectively.l7 Blood in the vomitus is an indication of upper gastrointestinal tears, which are a more serious complication of purging. Most tears heal well with cessation of vomiting. Perforation of the

upper digestive tract, esophagus or stomach is an extremely rare but potentially lethal complication. Patients with gastric pain and excessive blood in their vomitus should be evaluated on an urgent basis.17 Electrolyte Imbalances. Serious depletions of hydrogen chloride, potassium, sodium and magnesium can occur because of the excessive loss of fluids during vomiting. Hypokalemia represents a potential medical emergency, and serum electrolyte levels should be measured as part of the initial evaluation in all new patients. Patients who complain of fatigue, muscle spasms or heart palpitations may be experiencing transient episodes of electrolyte disturbance. Paresthesias, tetany, seizures or cardiac arrhythmias are potential metabolic complications that require acute care.l7 Chemistry profiles should be obtained regularly in patients who continue to vomit or abuse purgatives on a regular basis. Patient Evaluation Physical Features Since bulimia nervosa has numerous medical complications, a complete physical examination is imperative in patients with this disorder. The examination should include vital signs and an evaluation of height and weight relative to age. The physician should also look for general hair loss, lanugo, abdominal tenderness, acrocyanosis (cyanosis of the extremities), jaundice, edema, parotid gland tenderness or enlargement, and scars on the dorsum of the hand. Routine laboratory tests in patients with bulimia nervosa include a complete blood count with differential, serum chemistry and thyroid profiles, and urine chemistry microscopy testing. Depending on the results of the physical examination, additional laboratory tests, such as a chest radiograph and an electrocardiogram, may be indicated. Finally, patients who engage in self-induced vomiting should be referred for a complete dental examination. Psychiatric Assessment Because of the multifaceted nature of bulimia nervosa, a comprehensive psychiatric assessment is essential to developing the most appropriate treatment strategy. Patients should be referred to a mental health professional with specific expertise in this area. Frequently, student health programs or university medical centers have personnel who are experienced in the evaluation and treatment of eating disorders. Referral lists can also be obtained from the organizations listed in Table 5. The most appropriate course of treatment can usually be determined on the basis of a thorough evaluation of the patient's medical condition, associated eating behaviors and attitudes, body image, personality, developmental history and interpersonal relationships. In the present managed care environment, hospitalization for patients with bulimia nervosa is no longer readily available. It has become especially important to determine a treatment approach that. will be effective as quickly as possible.3 The physician needs to know when inpatient treatment is or is not indicated. A comprehensive evaluation provides the rationale for this judgment and includes the following: 1. Standardized testing to document the patient's general personality features, characterologic disturbance and attitudes about eating, body size and weight. 2. A complete history of the patient's body weight, eating patterns and attempts at weight loss, including typical daily food intake, methods of purging and perceived ideal weight.

3. An investigation of the patient's interpersonal history and functioning, including family dynamics, peer relationships, and present or past physical, sexual or emotional abuse. 4. An evaluation of medical and psychiatric comorbidity, as well as documentation of previous attempts at treatment. Treatment Considerable research has been devoted to identifying the most effective pharmacologic and psychologic treatments for bulimia nervosa, including the effects of different medications (e.g., tricyclic antidepressants and selective serotonin reuptake inhibitors) and the benefits of different psychotherapy approaches (e.g., behavioral treatment versus cognitive-behavioral therapy and individual versus group therapies). In addition, a few studies have compared the efficacies of different combinations of medications and psychotherapy. Pharmacologic Interventions Tricyclic Antidepressants. A number of placebo-controlled, double-blind studies2l-27 have examined the effectiveness of tricyclic antidepressants in patients with bulimia nervosa. Several of these studies 23,5-27 found that desipramine, 150 to 300 mg per day, was clearly superior to placebo. Two parallel studies 2l,24 reported that imipramine, 176 to 300 mg per day, was also more beneficial than placebo. Amitriptyline, 150 mg per day, was shown to be more effective than placebo in reducing binge eating (72 percent versus 52 percent) and vomiting (78 percent versus 53 percent).22 Overall, short-term placebo-controlled trials in patients with bulimia nervosa have reported that tricyclic antidepressants reduce binge eating by 47 to 91 percent and vomiting by 45 to 78 percent. Monoamine Oxidase Inhibitors. Phenelzine, 60 to 80 mg per day, has been found to be more effective than placebo in reducing binge eating (64 percent versus 5 percent).28 Isocarboxazid, 60 mg per day, has also been superior to placebo in controlling binge eating.29 However, the monoamine oxidase inhibitors have considerable side effects and therefore are not recommended as initial pharmacologic therapy for bulimia nervosa. Other Antidepressants. Several atypical antidepressants have been investigated in placebocontrolled double-blind studies. Bupropion, 25 to 450 mg per day, can effectively diminish the frequency of binge eating, but an increased rate of seizures discourages the use of this medication in patients with bulimia.3 Binge eating has been reduced by 31 percent in patients treated with trazodone, 400 to 650 mg per day.31 Selective Serotonin Reuptake Inhibitors. The most promising results have been reported in studies investigating the use of fluoxetine in the treatment of bulimia nervosa.3233 In the most comprehensive drug trial to date,33 382 patients were evaluated in a multicenter study comparing 20- and 60-mg dosage of fluoxetine with placebo. At the 20-mg dosage, fluoxetine therapy resulted in a 45 percent reduction in binge eating, compared with a 33 percent reduction with placebo. Vomiting was reduced by 29 percent in patients treated with fluoxetine and by 5 percent in those who received placebo. Notably, the patients who received fluoxetine in a dosage of 60 mg per day showed the best treatment response, demonstrating a 67 percent reduction in binge eating and a 56 percent reduction in vomiting.33 A smaller study32 replicated these findings, reporting a 51 percent

reduction of binge eating in patients treated with fluoxetine at 60 mg per day, compared with a 17 percent reduction in those who were given placebo. The U.S. Food and Drug Administration has recently approved the use of fluoxetine for the treatment of bulimia nervosa. Other Medications. In one placebo-controlled crossover study,34 no improvement in bulimic symptoms was noted in patients treated with naltrexone, 50 mg per day. Likewise, a brief placebo-controlled trial of lithium 35 resulted in no significant differences between groups in the reduction of binge eating frequency. Psychotherapy Despite differences in the application of techniques, the skill level of clinicians and the duration of the illness, controlled studies have clearly established the superiority of cognitivebehavioral therapy for the treatment of bulimia nervosa. Based on comparative studies, this therapy used alone or in combination with another technique has resulted in the most significant reductions of binge eating and/or purging. Cognitive-behavioral therapy principally involves a systematic series of interventions aimed at addressing the cognitive aspects of bulimia nervosa, such as the preoccupation with body, weight and food, perfectionism, dichotomous thinking and low self-esteem. This therapy also addresses the behavioral components of the illness, such as disturbed eating habits, binge eating, purging, dieting and ritualistic exercise. The initial goal of cognitive-behavioral therapy is to restore control over dietary intake. Caloric restriction and dieting efforts that set patients up to binge are avoided. Patients typically record their food intake and feelings. They then receive extensive feedback concerning their meal plan, symptom triggers, caloric intake and nutritional balance. Patients are also instructed in cognitive methods for challenging rigid thought patterns, methods for improving self-esteem, assertiveness training, and the identification and appropriate expression of feelings. A thorough explanation of cognitive-behavioral therapy for the treatment of bulimia nervosa is available elsewhere.36 The relative benefits of medications and cognitive-behavioral therapy have been assessed and compared. Study results indicate that cognitive-behavioral therapy is superior to medication alone and that the combination of cognitive-behavioral therapy and medication is more effective than the use of medication alone.37 Similarly, the durable effects of cognitivebehavioral therapy have been well documented. In contrast, there has been only one study of the long-term effectiveness of pharmacologic treatment. In that study, six months of desipramine therapy produced lasting improvement, even after the medication was withdrawn.38 Although cognitive-behavioral therapy is the first-line treatment of choice for bulimia nervosa, its effectiveness is limited. Approximately 50 percent of patients who receive this therapy stop binge eating and purging. The remaining patients show partial improvement, but a small number do not benefit at all.37 A comorbid personality disorder is associated with a poorer response not only to cognitive-behavioral therapy but also to alternative therapies.

The approach to take when cognitivebehavioral therapy is not effective remains unclear. Some patients may not respond to additional pharmacologic or psychologic therapy. However, the hope is that some treatment is better than no treatment at all. Thus, no patient should be dismissed as "chronic and untreatable." References REFERENCES References 1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, D.C.: American Psychiatric Association, 1994:539-50. 2. American Psychiatric Association. Practice guidelines for eating disorders. Am J Psychiatry 1993; 150:212-28. References 3. Kaye W. Can we manage managed care? Eating Disord Rev 1995;6(1):1-4. 4. Kaye WH. Neuropeptide abnormalities. In: Halmi KA, ed. Psychobiology and treatment of anorexia nervosa and bulimia nervosa. Washington, D.C.: American Psychiatric Press, 1992. 5. Lilenfeld LR, Strober M, Kaye WH. Genetics and family studies of anorexia nervosa and bulimia nervosa. In: Kaye WH, Jimerson DC, eds. Eating disorders. London: Balliere's Tindal (In press). References Herzog D, Agras WS, Marcus MD, Mitchell J, Walsh BT. Eating disorders: recent advances. Symposium of the American Psychiatric Association, May 20, 1995. Holderness CC, Brooks-Gunn J, Warren MP Co-morbidity of eating disorders and substance abuse: review of the literature. Int J Eating Disord 1994;16:1-34. 8. Agras WS. Disorders of eating: anorexia nervosa, bulimia nervosa and binge eating disorder. In: Shader RI, ed. Manual of psychiatric therapeutics. 2d ed. Boston: Little, Brown, 1994. 9. Ferbe KJ, Marsh SR, Coyne L. Comorbidity in an inpatient eating disordered population: clinical characteristics and treatment implications. Psychiatr Hosp 1993;24(1/2):3-8. References 10. Gartner AF, Marcus RN, Halmi K, Loranger AW. DSM-III-R personality disorders in patients with eating disorders. Am J Psychiatry 1989;146:1585-91. 11. Strober M, Katz JL. Depression in the eating disorders: a review and analysis of descriptive, family, and biological findings. In: Garner DM, Garfinkel PE, eds. Diagnostic issues in anorexia nervosa. New York: Brunner/Mazel, 1988. 12. Yeary JR, Heck CL. Dual diagnosis: eating disorders and psychoactive substance dependence. J Psychoactive Drugs 1989;21:239-49. 13. Mury M, Verdoux H, Bourgeois M.

Comorbidity of bipolar and eating disorders. Epidemiologic and therapeutic aspects [French]. Encephale 1995;21: 545-53. References 14. Ames-Frankel J, Devlin MJ, Walsh BT, Strasser TJ, Sadik C, Oldham JM, et al. Personality disorder diagnoses in patients with bulimia nervosa: clinical correlates and changes with treatment. J Clin Psychiatry 1992;53:90-6. 15. Herzog DB, Keller MB, Lavori PW, Kenny GM, Sacks NR. The prevalence of personality disorders in 210 women with eating disorders. J Clin Psychiatry 1992;53:147-52. 16. Wonderlich SA, Swift WJ, Slotnick HB, Goodman S. DSM-III-R personality disorders in eating disorder subtypes. Int J Eating Disord 1990;9:607-16. 17. Sansone RA, Sansone LA. Bulimia nervosa: medical complications. In: Alexander-Mott L, Lumsden DB, eds. Understanding eating disorders: anorexia nervosa, bulimia nervosa, and obesity. Washington, D.C.: Taylor & Francis, 1994:181-201. 18. Kaplan AS, Garfinkel PE, eds. Medical issues and the eating disorders: the interface. New York: Brunner/Mazel,1993. References 19. Fairburn CG. Overcoming binge eating. New York: Guilford, 1995. 20. Jacobs MB, Schneider JA. Medical complications of bulimia: a prospective evaluation. Q J Med 1985; 54:177-82. 21. Pope HG Jr, Hudson JI, Jonas JM, Yurgelun-Todd D. Bulimia treated with imipramine: a placebo-controlled, double-blind study. Am J Psychiatry 1983; 140:554-8. 22. Mitchell JE, Groat R. A placebo-controlled, doubleblind trial of amitriptyline in bulimia. J Clin Psychopharmacol 1984;4:186-93. References 23. Hughes PL, Wells LA, Cunningham CJ, Ilstrup DM. Treating bulimia with desipramine. A doubleblind, placebo-controlled study. Arch Gen Psychiatry 1986;43:182-6. 24. Agras W, Dorian B, Kirkely B, Arnow B, Bachman J. Imipramine in the treatment of bulimia: a double-blind controlled study. Int J Eating Disord 1987; 6:29-38. 25. Barlow J, Blouin J, Blouin A, Perez E. Treatment of bulimia with desipramine: a doubleblind crossover study. Can J Psychiatry 1988;33:129-33. 26. Blouin AG, Blouin JH, Perez EL, Bushnik T, Zuro C, Mulder E. Treatment of bulimia with fenfluramine and desipramine. J Clin Psychopharmacol 1988;8: 261-9. References 27. Walsh BT, Hadigan CM, Devlin MJ, Gladis M, Roose SP Long-term outcome of antidepressant treatment for bulimia nervosa. Am J Psychiatry 1991;148:1206-12.

28. Walsh BT, Gladis M, Roose SP, Stewart JW, Stetner F, Glassman AH. Phenelzine vs placebo in 50 patients with bulimia. Arch Gen Psychiatry 1988; 45:471-5. 29. Kennedy SH, Piran N, Warsh JJ, Prendergast P, Mainprize E, Whynot C, et al. A trial of isocarboxazid in the treatment of bulimia nervosa. J Clin Psychopharmacol 1988;8:391-6 [Published erratum appears in J Clin Psychopharmacol 1989;9:3]. 30. Horne RL, Ferguson JM, Pope HG Jr, Hudson Jl, Lineberry CG, Ascher J, et al. Treatment of bulimia with bupropion: a multicenter controlled trial. J Clin Psychiatry 1988;49:262-6. 31. Pope HG Jr, Keck PE Jr, McElroy SL, Hudson JI. A placebo-controlled study of trazodone in bulimia nervosa. J Clin Psychopharmacol 1989;9:254-9. References 32. Goldstein DJ, Wilson MG, Thompson VL, Potvin JH, Rampey AH Jr. Long-term fluoxetine treatment of bulimia nervosa. Br J Psychiatry 1995;166:660-6. 33. Fluoxetine Bulimia Nervosa Collaborative Study Group. Fluoxetine in the treatment of bulimia nervosa. A multicenter, placebo-controlled, doubleblind trial. Arch Gen Psychiatry 1992;49:139-47. 34. Mitchell JE, Christenson G, Jennings J, Huber M, Thomas B, Pomeroy C, et al. A placebo-controlled, double-blind crossover study of naltrexone hydrochloride in outpatients with normal weight bulimia. J Clin Psychopharmacol 1989;9:94-7. References 35. Hsu LK, Clement L, Santhouse R, Ju ES. Treatment of bulimia nervosa with lithium carbonate. A controlled study. J Nerv Ment Dis 1991;179:351-5. 36. Fairburn C, Marcus M, Wilson G. Cognitive behavior therapy for binge eating and bulimia nervosa: a treatment manual. In: Fairburn CG, Wilson GT, eds. Binge eating: nature, assessment, and treatment. New York: Guilford, 1993. 37. Wilson GT. Treatment of bulimia nervosa: when CBT fails. Behav Res Ther 1996;34:197-212. 38. Agras WS, Telch CF, Arnow B, Eldredge K, Wilfley D, Raeburn SD, et al. Weight loss, cognitive-behavioral, and desipramine treatments in binge eating disorder: an additive design. Behav Ther 1994; 25:225-38. AuthorAffiliation BETH M. MCGILLEY, PH.D., and TAMARA L. PRYOR, PH.D. University of Kansas School of Medicine-Wichita, Wichita, Kansas AuthorAffiliation The Authors AuthorAffiliation BETH M. MCGILLEY, PH.D., is a nationally recognized specialist in eating disorders and maintains a private practice. She codirects the eating disorders clinic at the University of Kansas School of Medicine-Wichita, where she is a volunteer faculty member. Dr. McGilley is a member of the Managed Care Task Force of the Academy of Eating Disorders.

AuthorAffiliation TAMARA L. PRYOR, PH.D., is clinical associate professor in the Department of Psychiatry and Behavioral Sciences at the University of Kansas School of Medicine-Wichita, where she founded and currently codirects the eating disorders clinic. Dr. Pryor also developed one of the few postdoctoral internship and fellowship programs in eating disorders accredited by the American Psychological Association. She is a member of the Managed Care Task Force of the Academy of Eating Disorders. AuthorAffiliation Address correspondence to Tamara L. Pryor, Ph.D., University of Kansas School of Medicine-Wichita, Department of Psychiatry and Behavioral Sciences, Eating Disorders Clinic, 1010 N. Kansas, Wichita, KS 67214-3199. Reprints are not available from the authors. Copyright American Academy of Family Physicians Jun 1998 Word count: 4008 Show less

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Cite Subjects Bulimia, Health care Title Assessment and treatment of bulimia nervosa Authors McGilley, Beth M; Pryor, Tamara L Publication title American Family Physician Volume 57 Issue 11 Pages 2743-2750 Publication year 1998 Publication Date Jun 1998 Year 1998 Publisher American Academy of Family Physicians Place of Publication Leawood Country of publication

United States Journal Subjects Medical Sciences ISSN 0002838X CODEN AFPYBF Source type Scholarly Journals Language of Publication English Document type Feature Subfile Bulimia, Health care Accession number 03800241 ProQuest Document ID 234320523 Document URL http://search.proquest.com/docview/234320523?accountid=38885 Copyright Copyright American Academy of Family Physicians Jun 1998 Last updated 2010-06-11 Database ProQuest Research Library

Comorbidity of Bulimia Nervosa and Substance Abuse: Etiologies, Treatment Issues, and Treatment Approaches
Carbaugh, Rebecca J; Sias, Shari M . Journal of Mental Health Counseling 32. 2 (Apr 2010): 125-138. Turn on hit highlighting for speaking browsers Turn off hit highlighting

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Recently the comorbidity of substance abuse and eating disorders has become a concern. Treating these disorders is particularly important for bulimia nervosa, which is characterized by "binge eating and inappropriate compensatory methods to prevent weight Show all

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Headnote Recently the comorbidity of substance abuse and eating disorders has become a concern. Treating these disorders is particularly important for bulimia nervosa, which is characterized by "binge eating and inappropriate compensatory methods to prevent weight gain" (American Psychiatric Association, 2000, p. 589). In this article we explore common pathways to the development of bulimia nervosa and substance abuse, how treatment is begun, and treatment options (cognitive behavioral therapy/coping skills training and dialectical behavioral therapy). A case study shows the application of coping skills training and dialectical behavioral therapy in clinical practice. An important area of concern for mental health counselors is effective treatment of substance abuse in the presence of co-occurring conditions like personality, mood, and thought disorders (Accordino, Keat, & Guerney, 2003; Catn et al, 2006; Holdcraft, Iacono, & McGue, 1998; Linton, 2005). Recently the comorbidity of substance abuse and eating disorders has become a particular concern. Substance abuse and eating disorders have the highest mortality risks of all mental disorders (Harris & Barraclough, 1998), and half of all clients with eating disorders abuse alcohol or illicit drugs (Center on Addiction and Substance Abuse [CASA], 2004). Given the rate of co-occurrence of these two potentially deadly conditions, effective treatment is essential. Characterized by "binge eating and inappropriate compensatory methods to prevent weight gain" (American Psychiatric Association, 1994, p. 589), bulimia nervosa co-occurs with alcohol use disorders in 1 8%-50% of those affected (Bulik & Sullivan, 1993; Daniels, Masheb, Berman, Mickely, & Grilo, 1998). Because these disorders co-occur so often (Herzog, Franko, Dorer, Keel, Jackson, & Marnzo, 2006; Holderness, Brooks-Gunn, & Warren, 1994), identifying the reasons for their comorbidity could be beneficial in exploring treatment options. Common Etiologies of the Disorders

According to the literature, psychological, environmental, and biological mechanisms are all factors in the linkage of bulimia and substance abuse (Holderness et al, 1994). For example, those affected might be more impulsive or more easily able to develop an addiction, or might live in family environments conducive to the development of both disorders. While the literature does not provide a clear explanation for the relation between bulimia and substance abuse, there are several hypotheses, which Wolfe and Maisto (2000) categorized as hypotheses of either shared etiology or causal etiology. Each contains indicators, such as family history or self-medication tendencies, that may help clarify how the disorders are connected. Shared Etiologies Shared etiology hypotheses view the relation between the disorders as the result of a common predisposition (i.e., risk factors common to the development of both bulimia and substance abuse). Such shared etiological factors include specific personality type, common family history, similar developmental issues, and specific biological vulnerability (Baker, Mazzeo, & Kendler, 2007). Specific personality type is key to the shared etiology hypothesis because both diagnoses share addiction traits that may be related to personality (Baker et al, 2007). For example, personality traits common to persons with bulimia and substance abuse are lack of control, craving, and denial (Pearlstein, 2002). In research that has identified eating disorder personality subtypes, one subtype, behaviorally dysregulated, was found to have a tendency to abuse substances (Thompson-Brenner, Eddy, Franko, Dorer, Vashchenko, & Herzog, 2008). The behaviorally dysregulated subtype displays social anxiety and hypersensitivity; shows impulsivity or unpredictability in at least two areas that are self-damaging; has a desire for affection and acceptance; engages in physically self-damaging acts; is prone to suicidal threats, gestures, or attempts; and displays antisocial behavior. Such an individual might be more prone to bulimia and substance abuse because these disorders involve behaviors that are both impulsive and self-damaging. Further, bulimia and substance abuse might provide the affection and acceptance these individuals desire by allowing them to fit in with peers or achieve a culturally ideal body shape (Thompson-Brenner et al.). A second factor in the predisposition to bulimia and substance abuse is family history (Baker et al., 2007). Bulik and Sullivan (1993) found that "76.5% of 17 bulimic women with comorbid alcohol abuse or dependence reported one or more relatives with an alcohol disorder" (p. 50). Holderness and colleagues (1994) also noted that extensive research linked family drug abuse and eating disorders. This research points to the biological similarities of the two disorders. In addition to the commonality of family drug abuse and alcoholism in those diagnosed with bulimia and substance abuse, specific parental traits seem to contribute to the development of both disorders. Bulik and Sullivan (1993) found similar characteristics in fathers and mothers of females with bulimia and alcoholism. Paternal characteristics included lacking enjoyment as a father, having inappropriate seductive boundaries with daughters, and inhibiting the development of independence in daughters. Mothers of these women focused primarily on their daughters' weight and appearance (Bulik & Sullivan). These parental characteristics may play a part in the development of the eating disorder, and substance abuse may be an attempt to cope with parental styles.

A third factor important to the shared etiology hypothesis is that bulimia and substance abuse derive from similar developmental issues. For example, there are Western cultural pressures for females to be thin, and some women are more likely than others to succumb to these pressures. Their susceptibility to pressure may transfer to drug experimentation during the teenage years (Baker et al., 2007). Individuals who easily succumb to societal pressures to achieve a certain ideal or to fit in with others may be more likely to demonstrate both eating disorder and substance abuse behaviors to meet these demands. Further, substance abuse may help individuals to achieve a thinness ideal. Herzog and colleagues (2006) found that cocaine and amphetamines were most often abused by women with eating disorders because of their appetite suppressant effects. For example, "Kathy," a college student in Maryland, started using cocaine recreationally on Friday nights with friends and found that it reduced her appetite and she began to lose weight. As Kathy discovered this secondary effect of cocaine, she continued using, lowering her weight to 95 pounds (ABC 7 News, 2005). As Kathy's case illustrates, individuals may begin using drugs to fit in with friends, find that these drugs aid in weight loss, and continue using them to control appetite and get thinner. Individuals like Kathy who are susceptible to both peer pressure to fit in and cultural pressure to be thin support the shared etiology hypothesis. A final predisposing factor in this comorbid diagnosis is biological vulnerability to the addictions of substance abuse or bulimia. This vulnerability is related not only to the genetic component of familial drug abuse history but also to brain chemistry. When comparing the brain chemistry of individuals with and without bulimia and substance abuse issues, differences in opioid peptide activity were found (Grilo, Sinha, & O'Malley, 2002). These peptides affect both alcohol and food consumption (Mercer & Holder, 1997). Studies have also shown that endogenous peptides may influence control of eating behavior and development of alcoholism (Grilo et al.). However, while brain chemistry and other findings support the view that bulimia and substance abuse have similar origins, this is not the only hypothesis about how the two are linked. Causal Etiologies "Causal etiology hypotheses suggest that having one disorder may put an individual at risk for developing another disorder" (Baker et al, 2007, pp. 673-674). Risk factors include variables that lead to substance abuse in individuals who have bulimia or of bulimia in those with substance abuse issues. These causal factors include self-medication and the effects of food deprivation (Baker et al.). Self-medication seems to be part of the etiology of both disorders because both create guilt and life consequences for the user. For example, individuals with eating disorders have been found to begin using substances as a means of coping with the anxiety caused by treating the eating disorder (Flood, 1989; Zweben, 1987). Those with bulimia may medicate themselves against the anxiety and guilt of the disorder, and those with both these disorders may be selfmedicating an underlying depression or family dysfunction (Holderness et al.). Depression is associated with both eating disorders and substance abuse, and some individuals with bulimia are successfully treated with antidepressants (Holderness et al.). In addition to the hypothesis that comorbid bulimia and substance abuse problems originate from the need to self-medicate against problems caused by one of the disorders or another underlying issue, there is the hypothesis that food deprivation can lead to substance abuse in an individual with bulimia. Animal research has found that food deprivation increases

animals' self-administration of alcohol and other drugs (Grilo et al, 2002). The implication of this for humans with bulimia is that "food deprivation might cause alterations in the central nervous system's reward pathways, thus increasing the consumption of reinforcing substances (e.g., alcohol)" (Grilo et al, p. 154). Thus, the effects of bulimia could lead to substance abuse. In summary, while there is no definitive explanation of the relation between bulimia and substance abuse and dependence, it appears that the disorders can originate together based on similar risk factors, such as an addictive personality type, a family history of drug abuse, parental characteristics, common developmental issues, and biological vulnerability as evidenced by atypical endogenous peptides (Baker et al, 2007; Bulik & Sullivan, 1993; Grilo et al, 2002; Holderness et al, 1994). There is also evidence that bulimia and substance abuse may be causal factors for each another; individuals with bulimia may be self-medicating their concerns about the disorder with alcohol and other drugs, or their food-deprived brains may be triggered to substance use (Grilo et al.; Holderness et al.). No matter how the conditions are linked, the central point is their connection, which implies that treatment needs to address both disorders. How to Begin Treatment Before delving into treatment approaches recommended for this dual diagnosis, it is important to assess how treatment should be conducted: for instance, whether the conditions should be treated together or separately, and if separately, which condition should be treated first (Daniels et al, 1998; Grilo et al, 2002). Given different opinions and inconclusive research, it is best to assess the client's individual needs and situation. Some individuals are thought to be unable to progress in substance abuse treatment until their eating disorder is managed. Starvation and unstable eating patterns have significant effects on thoughts and feelings (Woodside & Staab, 2006), and these distortions are not conducive to positive change. However, some clients may have more problems related to substance abuse than to bulimia nervosa. In these situations, the most severe condition should be treated first (Varner, 1999). When the bulimia and substance abuse diagnoses are equally severe, concurrent treatment is recommended (Varner, 1999) because the two disorders are so similar. As noted, eating disorders and substance abuse can both be conceptualized as manifestations of a predisposition to addiction (Varner). Bulimia includes such addictive behaviors as craving, loss of control, and risk of relapse (Vandereycken, 1990), not unlike an addiction to alcohol or other drugs. In addition, treatment goals for bulimia can be likened to the abstinence goal of many substance abuse treatment techniques, with the individual abstaining from inappropriate weight control methods, such as vomiting, laxative abuse, and excessive exercise (Vandereycken). Further, if both are not treated concurrently, one of the conditions could increase in severity. That is, if the two behaviors constitute methods of coping and one is taken away, this loss of a coping mechanism has to be replaced, possibly by exacerbation of the other coping mechanism. For example, Grilo and colleagues (2002) found that quitting alcohol or other drugs could lead to recurrence of eating disorder symptoms. More research is needed in this area, however, because Daniels et al. (1999) suggested that bulimic symptoms might decrease with cessation of alcohol use. The authors linked alcohol abuse to treatment resistance for individuals with bulimia. When alcohol use ceased, these individuals became more open to

treatment, thus reducing their symptoms. In either case, however, concurrent treatment seems to be important (Varner, 1999). All treatment options for comorbid bulimia and substance abuse have strengths and limitations, especially considering that research on treating this comorbidity is insufficient (Daniels et al., 1999; Pearlstein, 2002). When one disorder is treated at a time, the client is not overwhelmed with too much behavior change. For example, a client with co-occurring bulimia and substance dependence would need to change binging behaviors for food and alcohol/drugs while also changing weight control/reduction methods, such as self-induced vomiting and laxative abuse. Adjusting one of those behaviors is a challenge; adjusting several at once might set a client up for failure. Focusing on one behavior change at a time enables clients to recover at their own pace. However, limitations in treating the disorders separately include possibly overlooking one of them. To illustrate, a client with bulimia and dextromethorphan dependence resumed purging behaviors before being discharged from an inpatient substance abuse treatment program. The purging continued because the substance abuse facility did not have the staff or expertise to monitor eating, bathroom, and exercise behaviors (Marsh, Key, & Spratt, 1997). Thus, failure to take a holistic approach can lead to only partial rehabilitation of the client. The holistic approach is the greatest strength of concurrent treatment. By looking at the whole picture of a client who has bulimia and substance abuse issues, common themes and life patterns can be defined. This information can then lead to collaboration on treatment goals to alleviate the underlying factors related to these disorders. For example, both substance abuse and eating disorders are more likely among those with self-esteem issues, anxiety, depression, and a history of physical or sexual abuse (CASA, 2004). However, while a holistic approach can be a useful element in the treatment of these comorbid disorders, many treatment professionals are not equipped to provide this kind of care. Few programs effectively treat both conditions concurrently (CASA, 2003; 2004). Most treatment facilities specialize in either substance abuse or eating disorder treatment, and most mental health counselors working in these facilities are specialists in only one area. This lack of comprehensive knowledge and skills interferes with the treatment process (Marsh et al., 1997). In summary, more research is needed on the most effective way to begin treatment for comorbid bulimia and substance abuse, and continued assessment of the strengths and limitations of differing approaches is warranted. Nevertheless, concurrent treatment of both seems the best option (Grilo et al., 2002; Varner, 1999), and professionals in both fields need more training about the possible co-occurrence of these conditions (Marsh et al., 1997). Simultaneous treatment is important because it emphasizes the whole person; thus, professionals specializing in eating disorders should have knowledge about substance abuse and vice versa (Marsh et al). Specific Treatment Options Just as knowledge of both bulimia and substance abuse is important to treatment, knowledge of specific treatment options is crucial. If concurrent treatment is chosen, two types of therapies have been identified: cognitive behavioral therapy (CBT), especially coping skills training, and dialectical behavioral therapy (DBT). According to the literature, both are

considered top treatment approaches for either substance abuse or bulimia (Grilo et al, 2002; Hester & Miller, 2003; Corey, 2008). Cognitive behavioral therapy is used to treat a number of issues, including depression, anxiety, marital problems, stress management, substance abuse, lack of assertiveness, and eating disorders. The focus of CBT is on modifying cognitions to bring about desired emotional and behavioral change (Corey, 2008). By changing thoughts related to substance abuse and bulimia, behavior can be affected. To change these thoughts, counselors using CBT incorporate techniques such as disputing irrational beliefs and changing one's language (Corey). Cognitive behavioral therapy is well supported in eating disorder treatment (Grilo et al, 2002), and coping skills training is used by 64% of eating disorder practitioners (Tobin, Banker, Weisberg, & Bowers, 2007). Grilo and colleagues also found that CBT-based treatment taught new coping skills to clients with alcoholism and had a beneficial effect on client eating disorders. Coping skills training focuses on "the underlying conceptualization that the client lacks important coping skills for daily living" (Hester & Miller, 2003, p. 213). Often coping skills are lacking in the areas of mood regulation, socialinterpersonal situations, and personenvironment interactions. With training, individuals can learn coping skills that help them to build better relationships, regulate their moods, and better handle interactions with their environment (Hester & Miller). Training educates clients on effective stress management techniques and helps them explore options other than substance abuse and trigger situations for eating disorder behaviors. A trigger for bulimia would be anything that prompts or maintains binge eating and purging (Wasson, 2003); a substance abuse trigger is any situation that increases the urge to use a substance (Hester & Miller). According to a study of the relapse experiences of women with bulimia nervosa, triggers can fall into two broad categories: internal emotional states (feeling lonely or anxious) or interpersonal relationships (coping with anger at another individual) (Wasson, 2003). This is similar to drinking triggers. Cognitive behavioral therapy, specifically coping skills training, can be applied in holistic treatment of both disorders because eating disorder behaviors and substance abuse are often seen as coping mechanisms that have become destructive. If an individual is abusing substances and binging and purging to relieve anxiety or cope with other feelings, teaching new ways of coping could help these behaviors subside (Grilo et al, 2002). While the time required for individuals to develop adequate coping skills might be a short-term drawback, the long-term value to clients is difficult to dispute (Grilo et al.). An alternative to CBT and coping skills training for comorbid diagnoses of substance abuse and bulimia is DBT (Linehan, 1993). Dialectical behavioral therapy "focuses on awareness of problems and choices, mood regulation techniques, and coping skills" (Grilo et al, 2002, p. 157). It is effective in treating bulimia and substance abuse simultaneously because it focuses on the unique needs of the client, which may include addressing the commonly co-occurring borderline personality disorder for which DBT was originally formulated (Grilo et al.; Linehan). Dialectical behavioral therapy posits that client difficulties result from both emotional vulnerability and an invalidating environment (Barlow, 2008). Emotional vulnerability is characterized by a "susceptibility to emotion dysregulation" (Barlow, p. 371). Examples are engaging in behaviors depending on one's moods, allowing mood states to determine goals, not allowing oneself to experience emotions, or creating an extreme secondary emotion to mask the real emotion being experienced (Barlow).

Whether or not borderline personality disorder is present, those with bulimia and substance abuse can be conceptualized as having this emotional vulnerability. For example, those with bulimia may engage in binge eating to combat such mood states as depression. Also, after guilt and shame feelings arise from binge eating, they may purge to avoid experiencing those emotions. This is not unlike substance abuse, in which individuals may use drugs or alcohol to alleviate a negative mood, or sacrifice other priorities to drug use when they need drugs to feel better. An invalidating environment may also play a role in dysfunction. An invalidating environment is "defined by its tendency to negate, punish, and/or respond erratically and inappropriately to private experiences independent of the validity of the actual behavior" (Barlow, 2008, p. 373). In an invalidating environment family and friends may reject the expression of an individual's experiences (Barlow; Linehan, 1993). For example, individuals with bulimia and substance abuse may constantly have their hunger or their need for pleasure and fun discounted. Through living in environments that invalidate their expression of boredom, individuals learn to use the disorders to mask boredom, and they feel guilt or shame when experiencing this emotion. In addition, in an invalidating environment emotional displays are frowned upon except when escalated to the extreme (Barlow, 2008; Linehan, 1993). For example, individuals with bulimia and substance abuse who are depressed about a recent failure might have their feelings discounted until they engage in extreme behavior, such as self-injury or a suicide attempt (Barlow). Thus, individuals with bulimia and substance abuse may begin and continue these patterns of behavior not only to help cope with their emotions but to secure attention to the depth of what they are experiencing. Finally, in an invalidating environment family members may overestimate an individual's ability to solve problems and meet goals (Barlow, 2008; Linehan, 1993). There is the assumption that the individual has the resources and ability to cope when that is not the case. For example, a young girl who is having demands placed upon her by her family, friends, and school may be having a hard time balancing all these demands appropriately. However, because she seems well adjusted and to be "holding everything together," others may discount her stress. Living in this type of invalidating environment could promote the development of bulimia or substance abuse as coping methods for problems or goals that an individual seems unable to solve or meet (Barlow). In DBT, treatment aims to increase healthy behavioral skills, improve motivation to change dysfunctional behaviors, help translate newly learned behaviors from counseling into life, help the mental health counselor enhance the client's capabilities for treatment, and reinforce effective behaviors (Barlow, 2008; Linehan, 1993). Treatment strategies include the use of diary cards, playing the devil's advocate, and making lemonade out of lemons (Barlow; Linehan). Diary cards are index cards the client fills out during the week and shares with the counselor at weekly sessions. They record the dysfunctional behaviors and behavioral changes that are being targeted (Barlow, 2008; Linehan, 1993). For example, a card could contain a record of daily binge-purge episodes; of the quantity, frequency, and intensity of substance use during the week; or of any kind of suicidal or self-harming behavior. Diary cards help the counselor to measure the client's progress toward specific behavior changes. They also help the

clinician process with the client the events surrounding binge-purge behavior or drug use, and identify alternative behaviors or coping skills that could be used (Barlow; Linehan). Playing the devil's advocate is a cognitive restructuring process in which the clinician presents an extreme version of a client's dysfunctional belief and helps the client to counter this belief. For example, if a client believed she was better off dead if she did not weigh 90 pounds, a mental health counselor of 140 pounds might counter this statement by noting that the client must think the counselor too would be better off dead (Barlow, 2008; Linehan, 1993). Using this extreme example, the counselor could help the client examine the validity of this belief. Finally, making lemonade out of lemons, turning negatives into positives, helps clients to find the positive in specific situations. This allows them to use life problems as an opportunity to practice new coping skills and find strengths in their weaknesses (Barlow, 2008; Linehan, 1993). These DBT techniques provide individuals with skills to operate in invalidating environments and to regulate emotional states. The focus on coping skills and mood regulation, two major factors in substance abuse and bulimic behaviors, suggests DBT's benefits for treating both disorders. CONCLUSION Bulimia and substance abuse are both extremely complex and risky conditions. A dual diagnosis makes treatment more difficult. However, successful outcomes can be increased through proper diagnosis and early intervention (Marsh et al., 1997). For this early recognition to occur, however, substance abuse treatment facilities need to have effective screening for eating disorders, and eating disorder treatment facilities need to have effective screening for substance abuse. Further, mental health professionals need training in both areas and in CBT and DBT methods for use with this dually diagnosed population. Work in this area will lead to better recognition of these two dangerous disorders and, most important, better treatment outcomes for clients. The following case study is an example of CBT-based treatment (coping skills training and DBT) with a client diagnosed with both substance dependence and bulimia nervosa. CASE STUDY Her college advisor referred "Susan," a 20-year-old single Caucasian female, for counseling at the beginning of her junior year of college after she was issued a one-semester suspension for underage drinking and possession of cocaine. At the time of her referral, Susan said, "I have to complete counseling in order to get back in school next semester." During the clinical assessment interview Susan reported first using alcohol at age 14 with her first "real" boyfriend, who was three years her senior. She continued to drink "on and off' with friends, "mostly on weekends," until going to college. At the beginning of her freshman year, Susan said, her boyfriend broke up with her in order to "see other people while I was away at college." "Devastated" by the break-up, Susan began going out more with friends to cope with her feelings of sadness. Before being suspended from school, she reported "drinking like most of my friends," which included five or six drinks at a time Thursday through Saturday. She admitted to having experienced blackouts, increased tolerance, and

occasionally drinking in the morning to "get rid of hangovers." She also reported "snorting cocaine once or twice a month, socially at parties" for the last four months, and admitted to trying marijuana a few times in high school but not liking the way it made her feel. She reported a family history of addiction; her father now had 1 9 years of sobriety from alcohol but her paternal grandfather had died of alcohol-related liver failure. Susan denied current or past suicidal ideations, medical history, legal charges, or history of mental health or substance abuse counseling. Based on the information she provided and supported by her parents, Susan was diagnosed with alcohol dependence and cocaine abuse (American Psychiatric Association, 2000). Since Susan was able to avoid using alcohol and cocaine most weekdays, had a supportive living environment with her parents and two brothers (ages 1 5 and 1 7), and had reliable transportation to treatment, she was referred to the Intensive Outpatient Program (IOP). The theoretical underpinning for IOP was CBT At the time of the clinical assessment, Susan did not disclose any symptoms related to bulimia nervosa, which went undiagnosed until she had been in treatment for substance use. TREATMENT The IOP included group counseling three days a week, three hours a day, for ten weeks. The first hour focused on identifying personal barriers to treatment and recovery (motivation, stressors, and triggers and cues related to use, such as negative self-talk and faulty thinking); the second on learning about the addiction and recovery process (signs, symptoms, consequences of addiction), and the third on creating a sober support system (attending 12step groups or church activities, community involvement) and learning to live drug-free (planning leisure time, improving communication with family and friends). Susan also attended individual sessions every two weeks, and her family participated in the Family Program, which included weekly psychoeducational groups for 10 weeks and family counseling sessions as needed. During the second individual counseling session, Susan disclosed that she was binge eating and purging two or three times a week, usually in response to stressors like arguments with her parents about getting a job or questions from her family about "staying sober." Upon further discussion, it became clear that Susan met the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, Text Revision (DSM-IV-TR; American Psychiatric Association, 2000) criteria for bulimia nervosa (purging type). Additional symptoms were feeling a loss of control to stop binging once it began, skipping four to seven meals a week, and exercising excessively (up to 10 times a week) in response to binging episodes. Although Susan's weight was within the normal range for her age, frame, and height (5 '2", 110 lbs), she was not happy with her shape or size. Asked when the binging and purging began, she reported, "I guess I started dieting like this when I was 1 5 after my boyfriend told me I was getting a little chunky." Susan also disclosed that her cocaine use was a means of weight control. To address Susan's bulimia and substance disorders concurrently, her individual appointments were increased to weekly, the medical director did a medication evaluation, and she continued to attend the IOP. Following the appointment with the medical director, Susan began taking fluoxetine 60 mg daily. The first few individual sessions focused on increasing Susan's motivation for treatment by providing educational information (nutrition, the effects of food restriction, common myths

about dieting) and examining the pros and cons of behavior change. Similar techniques were used to address her chemical addiction in IOP groups (educational information concerning chemical addiction, pros and cons of remaining drug-free). As the sessions progressed, the focus turned to making and maintaining behavior change. To help Susan monitor targeted behavior change (stopping all substance use and inappropriate weight control methods), diary cards were used to record urges to binge eat, purge, over-exercise, or use alcohol/drugs, and the related emotional states (anger, fear, sadness). The diary cards were discussed during individual sessions, which focused on what was occurring before and after the targeted behavior and on identifying positive solutions for change. To address the need for emotional regulation skills, Susan began to identify and understand the function of her emotions through journal writing and individual and group counseling discussions. She also decreased her reactivity to negative emotions by practicing distraction (reading) or self-soothing (breathing exercises). In later sessions Susan began to use the information she was acquiring to address not only her chemical addiction but also her eating disorder. She was able to identify commonalities in both issues, including related triggers and associated negative self-talk. She realized that her low self-esteem was related to her negative evaluation of her body size and shape, which was related to her need to hold to a strict diet regimen, which led to binging/purging or alcohol/cocaine use, which led to feeling like a failure and to negative self-talk, such as "I'm no good. I'll never be able to stop this [binging and alcohol use] so what's the use," which started the cycle anew. In addition to issues with self-esteem, Susan continued to struggle with familial conflicts, which led to a relapse, first in binge eating and purging and then in drinking alcohol. Coping skills training for Susan focused on identifying high-risk situations (familial conflicts, feelings of anger, negative self-talk): teaching coping skills (i.e., improving communication skills by using "I" instead of "you" statements; calling someone when angry, writing about it, or going to an AA meeting): and increasing her self-esteem (developing positive affirmations, identifying successes). Family counseling focused on family dynamics, specifically improving communication between family members. Psychoeducationally, the family learned about chemical addiction, eating disorders, and ways to respond productively to a lapse/relapse in either disorder. For example, Susan and her parents were encouraged to focus on positive changes that Susan had made and to see a return to over-exercising as a lapse rather than a full-blown relapse, the latter of which would constitute a return to her pretreatment level of alcohol use and eating disorder-related behaviors. OUTCOME SUMMARY Susan's counseling continued for one year, during which she postponed returning to school, chose to obtain full-time employment, and moved out of her parents' home. While in counseling she experienced one lapse on alcohol and two binge eating and purging episodes. When asked what was most helpful in counseling, Susan said, "Learning to stop and think about what I'm doing and not just reacting." Susan, a woman with comorbid bulimia and substance abuse, received concurrent treatment for both disorders. Through the use of CBT techniques to change Susan's negative self-talk, coping skills training to help her find other ways to cope with her emotions, and DBT to help her monitor her eating disorder and substance abuse behavior and identify triggers for it, her

mental health counselor was able to help her reduce her symptoms. With concurrent treatment Susan learned positive coping strategies rather than relying on substance use or eating disorder symptoms to help her cope. References REFERENCES ABC 7 News. (2005, April 29). Some young women use cocaine as weight-loss aid. ABC 7 News. Retrieved October 14, 2008, from http://www.thedenverchannel.com/health/4430360/ detail.html Accordino, M. P., Keat II, D. B., & Guerney, Jr., B. G. (2003). Using relationship enhancement counseling with an adolescent with serious mental illness and substance dependence. Journal of Mental Health Counseling, 25, 152-164. American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed.), text revision. Washington, DC: Author. Baker, J. H., Mazzero, S. E., & Kendler, K. S. (2007). Association between broadly defined bulimia nervosa and drug use disorders: Common genetic and environmental influences. International Journal of Eating Disorders, 40, 673-678. Barlow, D. H. (Ed.). (2008). Clinical handbook of psychological disorders: A step-by-step treatment manual. (4th ed.). New York: The Guilford Press. Bulik, C. M., & Sullivan, P. F. (1993). Comorbidity of bulimia and substance abuse: Perceptions of family of origin. International Journal of Eating Disorders, 13, 49-56. Caton, C. L., Hasin, D. S., Shrout, P. E., Drake, R. E., Domnguez, B., Samet, S., & Schanzer, B. (2006). Predictors of psychosis remission in psychotic disorders that co-occur with substance use. Schizophrenia Bulletin, 32, 618-625. Center on Addiction and Substance Abuse (CASA) at Columbia University. (2003/ Food for thought: Substance abuse and eating disorders. New York: National Center on Addiction and Substance Abuse. Center on Addiction and Substance Abuse (CASA) at Columbia University. (2004). People with eating disorders likely to abuse alcohol, drugs. Alcoholism and Drug Abuse Weekly, 16, 3-5. Corey, G. (2008). Theory and practice of counseling and psychotherapy (8th ed.). Belmont, CA: Brooks/Cole. Daniels, E. S., Masheb, R. M., Berman, R. M., Mickely, D., & Grilo, C. M. (1999). Bulimia nervosa and alcohol dependence: A case report of a patient enrolled in a randomized controlled clinical trial. Journal of Substance Abuse Treatment, 17, 163-166. Flood, M. (1989). Addictive eating disorders. Nursing Interventions for Addicted Patients, 24, 45-53.

Grilo, C. M., Sinha, R., & O'Malley, S. S. (2002). Research update: Eating disorders and alcohol use disorders. Alcohol Research and Health, 26, 151-160. Harris, E. C, & Barraclough, B. (1998). Excess mortality of mental disorder. British Journal of Psychiatry, 173, 11-53. Herzog, D. B., Franko, D. L., Dorer, D. J., Keel, P. K., Jackson, S., & Manzo, M. P. (2006). Drug abuse in women with eating disorders. International Journal of Eating Disorders, 39, 364-368. Hester, R., & Miller, W. (2003). Handbook of alcoholism treatment approaches: Effective alternatives (3rd ed.). Boston: Pearson Education Inc. Holdcraft, L. C, Iacono, W. G., & McGue, M. K. (1998). Antisocial personality disorder and depression in relation to alcoholism: A community-based sample. Journal of Studies on Alcohol, 59, 222-226. Holderness, C C, Brooks-Gunn, J., & Warren, M. P. (1994). Co-morbidity of eating disorders and substance abuse: Review of the literature. International Journal of Eating Disorders, 16, 1-34. Linehan, M. M. (1993). Cognitive behavioural treatment of borderline personality disorder. New York: The Gilford Press. Linton, J. M. (2005). Mental health counselors and substance abuse treatment: Advantages, difficulties, and practical issues to solution-focused interventions. Journal of Mental Health Counseling, 27,297-310. Marsh, L. D., Key, J. D., & Spratt, E. (1997). Bulimia and dextromethorphan abuse: A case study. Journal of Substance Abuse Treatment, 14, 373-376. Mercer, M. E., & Holder, M. D. (1997). Food cravings, endogenous opioid peptides, and food intake: A review. Appetite, 29, 325-352. Pearlstein, T. (2002). Eating disorders and co-morbidity. Archives of Women s Mental Health, 4, 67-78 Thompson-Brenner, H., Eddy, K. T., Franko, D. L., Dorer, D., Vashchenko, M., & Herzog, D. B. (2008). Personality pathology and substance abuse in eating disorders: A longitudinal study. International Journal of Eating Disorders, 41, 203-208. Tobin, D. L., Banker, J. D., Weisberg, L., & Bowers, W. (2007). I know what you did last summer (and it was not CBT): A factor analytic model of international psychotherapeutic practice in eating disorders. International Journal of Eating Disorders, 40, 754-757. Vandereycken, W. (1990). The addiction model in eating disorders: Some critical remarks and a selected bibliography. International Journal of Eating Disorders, 9, 95-101. Varner, L. M. (1999). When an eating disorder "isn't just" an eating disorder. Topics in Clinical Nutrition, 14, 4-13.

Wasson, D. H. (2003). A qualitative investigation of the relapse experiences of women with bulimia nervosa. Eating Disorders, 11, 73-88. Wolfe, W. L. & Maisto, S. A. (2000). The relationship between eating disorders and substance use: Moving beyond co-prevalence research. Clinical Psychology Review. 20, 617631. Woodside, B. D., & Staab, R. (2006). Management of psychiatric comorbidity in anorexia nervosa and bulimia nervosa. CNS Drugs, 20, 655-663. Zweben, J. E. (1987). Eating disorders and substance abuse. Journal of Psychoactive Drugs, 19, 181-192. AuthorAffiliation Rebecca J. Carbaugh and Shari M. Sias are affiliated with East Carolina University. Correspondence concerning this article should be addressed to Rebecca J. Carbaugh, M.S., College of Health Sciences, Department of Rehabilitation Studies, East Carolina University, Greenville. North Carolina 27858. E-mail: rjcl015@ecu.edu. Copyright American Mental Health Counselors Association Apr 2010 Word count: 6099 Show less

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Cite Subjects Eating disorders, Bulimia, Substance abuse treatment, Addictive behaviors, Addictions, Self esteem, Behavior Title Comorbidity of Bulimia Nervosa and Substance Abuse: Etiologies, Treatment Issues, and Treatment Approaches Authors Carbaugh, Rebecca J; Sias, Shari M Publication title Journal of Mental Health Counseling Volume 32 Issue 2 Pages 125-138 Number of pages 14 Publication year 2010 Publication Date

Apr 2010 Year 2010 Section PRACTICE Publisher American Mental Health Counselors Association Place of Publication Alexandria Country of publication United States Journal Subjects Education, Psychology ISSN 01931830 Source type Scholarly Journals Language of Publication English Document type Feature Document Features References Subfile Eating disorders, Bulimia, Substance abuse treatment, Addictive behaviors, Addictions, Self esteem, Behavior ProQuest Document ID 198682604 Document URL http://search.proquest.com/docview/198682604?accountid=38885 Copyright Copyright American Mental Health Counselors Association Apr 2010 Last updated 2010-07-16 Database ProQuest Research Library

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A Multidimensional Meta-Analysis of Psychotherapy for Bulimia Nervosa

Thompson-Brenner, Heather ; Glass, Samantha ; Westen, Drew . Clinical Psychology: Science and Practice 10. 3 (Aug 2003): 269. Turn on hit highlighting for speaking browsers Turn off hit highlighting

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We report a multidimensional meta-analysis of psychotherapy trials for bulimia nervosa published between 1980 and 2000, including multiple variables in addition to effect size such as inclusion and exclusion, recovery, and sustained recovery rates. The data point to four conclusions. First, psychotherapy leads to large improvements from baseline. Approximately 40% of patients who complete treatment recover completely, although 60% maintain clinically significant posttreatment symptoms. Second, individual therapy shows substantially better effects than group therapy for the therapies tested. Third, additional approaches or treatment parameters (e.g., number of sessions) need to be tested for the substantial number of patients who enter treatment and do not recover. Finally, the utility of meta-analyses can

be augmented by including a wider range of outcome metrics, such as recovery rates and posttreatment symptom levels. Show less

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Cite Title A Multidimensional Meta-Analysis of Psychotherapy for Bulimia Nervosa Authors Thompson-Brenner, Heather; Glass, Samantha; Westen, Drew Publication title Clinical Psychology: Science and Practice Volume 10 Issue 3 Pages 269 Publication year 2003 Publication Date Aug 2003 Year 2003 Publisher Oxford Publishing Limited(England) Place of Publication New York Country of publication United Kingdom Journal Subjects Psychology ISSN 09695893 Source type Scholarly Journals Language of Publication English Document type PERIODICAL ProQuest Document ID 236399998 Document URL http://search.proquest.com/docview/236399998?accountid=38885 Copyright Copyright Oxford University Press(England) Aug 2003 Last updated 2010-06-11

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Outcome predictors for the cognitive behavior treatment of bulimia nervosa: Data from a multisite study
W Stewart Agras ; Crow, Scott J ; Halmi, Katherine A ; Mitchell, James E; et al. The American Journal of Psychiatry 157. 8 (Aug 2000): 1302-8. Turn on hit highlighting for speaking browsers Turn off hit highlighting

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The aim of this study was to discover clinically useful predictors of attrition and outcome in the treatment of bulimia nervosa with cognitive behavior therapy.

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Headnote Objective: Theaim ofthis study was todiscover clinically useful predictors ofattrition and outcome in thetreatment of bulimianervosa with cognitive behavior therapy.

Method: Pretreatment, course oftreatment, and outcome data were gathered on 194 women meeting theDSM-III-R criteria for bulimianervosa who were treated with 18 sessions ofmanual-based cognitive behavior therapyin a three-site study. Differences between dropouts and nondropouts and between recovered and nonrecovered participants were first examined descriptively, and signal detection analyses were then used todetermine clinically significant cutoff points predicting attrition and abstinence. Results: Thedropouts were characterized by more severe bulimic cognitions Headnote and greater impulsivity, but it was not possible toidentify clinically useful predictors. Theparticipants with treatment failures were characterized by poor social adjustment and a lower body mass index, presumably indicating greater dietary restriction. However, early progress in therapybest predicted outcome. Signal detection analyses revealed that poor outcome was predicted by a reduction in purging ofless than 70% by treatment session 6, allowing identification ofa substantial proportion ofprospective failures. Conclusions: A cutoff point based on reduction ofpurging by session 6 usefully differentiates patients who will and will not respond to cognitive behavior therapyfor bulimianervosa, potentially allowing early use ofa second therapy. Thedelineation ofpatient chtics at useFully predict theoutcome oftreatment is a long-sought but somewhat elusive goal in psychotherapy research. One goal in theidentification ofsuch predictors is toaid in theselection ofpatients who will or will not respond totreatment. This distinction, if made with sufficient accuracy, may reduce thecost ofa treatment, by offering it only tothose with a high probability ofsuccess, and may allow for early identification ofnonresponders toone treatment who may respond toanother treatment. Theidentification ofvariables associated with poor outcome may also lead tohypotheses concerning thereasons for failure ofa particular treatment, possibly leading toimprovements in thetreatment being studied. At present, cognitive behavior therapyis recognized as being themost effective treatment for bulimianervosa, having been demonstrated superior tomost other psychotherapies and also toa single trial ofantidepressant medication (1). Unfortunately, even with cognitive behavior therapyonly some 50% ofbulimic patients recover. Hence, it is important toidentify thecharacteristics ofthose who will and will not respond to cognitive behavior therapy, so that more effective treatment strategies can be developed. Such characteristics have been identified in previous studies. Among thepretreatment variables associated with poor outcome in some studies are low self-esteem (2-4), low weight or previous anorexia nervosa (5, 6), a higher frequency or severity ofbinge eating (2, 7-11), comorbid personality disorder (9, 12-14) or depression (7, 8, 15), attitudes toward weight and shape (4) (themost severely disturbed patients show greater improvement), and a history ofobesity (8). A further predictor ofoutcome may be early response totreatment. In a recent study (11), rapid responders to cognitive behavior therapywere significantly more likely todo well in treatment than slow responders. On average, 20% ofparticipants in controlled trials of cognitive behavior therapyfor bulimianervosa drop out, with a range from 0% to35% (16). Hence, dropouts make a considerable contribution to therapyfailure rates. Todate, findings from some studies have

suggested that thefollowing factors characterize dropouts, as compared with those who complete treatment: more severe depression (16), more severe bulimic symptoms (14, 17), interpersonal difficulties as reflected by comorbid personality disorder (4, 14, 18, 19), and impulsivity (20). Different studies have found different sets ofpredictors both for treatment outcome and for attrition. In many cases, predictors identified as statistically significant in one study were not found significant in others. Several factors may contribute tothese discordant findings. First, thetype of therapy, themode ofdelivery (i.e., individual or group format, outpatient or inpatient treatment), and thepopulation ofbulimic subjects have varied among studies. Second, many studies have had too few subjects toreliably identify outcome predictors. Third, thedefinition oftreatment success has varied; some studies have used abstinence from binge eating and purging, and others have used thecriterion ofno longer meeting theDSM-IIIR diagnostic criteria. Fourth, both pretreatment variables and themethods ofassessing treatment outcome have varied among studies. In addition, these studies offer only general guidance to theclinician as towhich patient will not do well in therapy. Thepresent study addresses some ofthese problems-- first, by entering a relatively large number ofparticipants (N=194) meeting theDSM-III-R criteria for bulimianervosa into thestudy; second, by treating theparticipants with a widely used manual-based form of cognitive behavior therapy(21); third, by paying careful attention to theintegrity of the therapydelivered; and fourth, by using signal detection analyses todetermine if optimal cutoff points could be established todifferentiate between patients for whom treatment is likely tobe a success and those for whom it will fail. Thestudy involved three treatment sites-Cornell University, University ofMinnesota, and Rutgers University-and a data and monitoring center at Stanford University Thedata presented here are derived from thefirst phase ofa controlled study of theefficacy ofpharmacological and psychotherapeutic treatments for nonresponders to cognitive behavior therapy Method Patient Selection A total of194 women meeting theDSM-III-R criteria for bulimianervosa entered thestudy and were treated with cognitive behavior therapyParticipants were recruited from advertisements in thelocal media and from eating disorders clinics. Potential participants were first screened by telephone toascertain their eligibility for thestudy. Of851 individuals calling thethree treatment centers, 592 were screened out; themajor reasons were not meeting thebinge-eating or purging frequency criteria for bulimianervosa, having been treated with an adequate trial ofan antidepressant medication, or not being interested in thestudy Hence, 259 individuals were offered appointments for further screening, 39 ofwhom did not keep their appointments. At theinterview, thestudy procedures were described in detail and thepotential participants then gave their written consent toparticipate. A further 26 individuals were screened out at this interview; theprincipal reason was theabsence ofone or more criteria for thediagnosis of bulimianervosa. Therefore, thefinal number ofsubjects was 194. Other exclusion factors were current anorexia nervosa, current alcohol or drug abuse, associated severe physical or psychiatric illness (e.g., psychosis, significant suicidal risk, cancer), use ofany medication known toaffect weight, current psychiatric or psychotherapeutic treatment, or an adequate trial ofan antidepressant medication or cognitive behavior therapyDuring thetreatment phase

of thestudy, six participants were withdrawn: one became pregnant, four developed major depression requiring antidepressant medication, and one developed a manic episode. Themean age of theparticipants was 28.1 years (SD=7.9); of the188 remaining participants, 88% were white (N=166), 5% were African American (N=10), 3% were Hispanic (N=6), and 3% were Asian (N=6). Two-thirds (66%, N=124) had never married, 24% were currently married (N=45), and 10% were divorced (N=19). Theparticipants reported that their bulimic symptoms had begun an average of10.2 years (SD=7.6) before thestudy Their median rate ofbinge eating was 21.0 episodes during a 4-week period, and their median rate ofpurging was 34.0 episodes over 4 weeks. Nearly one-quarter of theparticipants (22%, N=42) reported a previous episode ofanorexia nervosa, 59%a had a past history ofmajor depression (N=110), and 23% had a current major depression (N=43). Personality disorders were diagnosed in 43%o of theparticipants (N=81); ofthese disorders, about one-half were in cluster B. Treatment Cognitive behavior therapy, which was manual based and had been used in previous treatment research (21), was carried out by doctorate-level psychologists experienced in thetreatment ofeating disorders. Treatment consisted of18 individual 50-minute outpatient sessions over 16 weeks. Sessions were held twice weekly for thefirst 2 weeks and then weekly. None of thepatients received any other psychotherapy or pharmacotherapy during this period. Tostandardize thetherapeutic procedures within and across sites, a training and monitoring process was instituted. This process was aimed at diminishing thelikelihood ofsite-by-- treatment interactions, ensuring therapist compliance with thetherapeutic procedures, and allowing replication by others. Thetherapists were trained in theprocedures at a workshop, and each therapist practiced thetreatment with two patients with weekly on-site supervision. A second workshop was held 6 months later, just before entry of thefirst participant, toreview thetherapeutic procedures and address common problems. These workshops continued at 6-month intervals during this phase of thestudy In addition, a randomly selected sample ofaudiotapes was reviewed, and feedback on theaccuracy of therapywas provided to thetherapist by fax and at times by telephone. On-site supervision of therapycontinued at weekly intervals. Assessments Thepatients were assessed before treatment through both structured interviews and questionnaires. Weight and height were measured in order tocalculate body mass index. Psychopathology was assessed by using theStructured Clinical Interview for DSM-III-R (22). Specific eating-related pathology was assessed before and after treatment by using theEating Disorder Examination ratings for frequencies ofbinge eating and purging, dietary restraint, and concern about weight, shape, and eating (23). During treatment thenumber ofpurging episodes during theprevious week was recorded at 2-week intervals by means ofa computerized questionnaire assessment. Administration ofquestionnaires was aimed at further assessing I) specific eating-related pathology, 2) aspects ofgeneral psychopathology particularly pertinent to bulimianervosa, and 3) interpersonal functioning. In thefirst category thequestionnaire used was theBulimic Thoughts Questionnaire, a measure ofbulimic cognitions (24) and self-efficacy in terms ofovercoming binge eating and purging (25). In thesecond category were theBeck Depression Inventory (26), theRosenberg Self-Esteem Scale (27), and theimpulsivity scale of

theMultidimensional Personality Questionnaire (28). In thethird category were theInventory ofInterpersonal Problems (29), a measure ofinterpersonal relationships, and thequestionnaire form of theSocial Adjustment Scale (30). Posttreatment status was derived from Eating Disorder Examination interviews, allowing classification of theparticipants as responders (no binge eating or purging during thepast 4 weeks) or nonresponders. Thereliability ofthis measure was determined for 20 participants. With theexception ofsubjective binges, which were not used in this study, agreement on all measures exceeded r=0.90. Statistical Analysis Theanalytic approach used here was descriptive and hypothesis generating, rather than hypothesis testing. In thefirst phase of theanalysis, thepretreatment characteristics of thedropouts were compared with those of thepatients who completed treatment, and thetreatment responders were compared with thenonresponders. For continuous outcome measures, Cohen's d (thestandardized mean difference between thegroups) was used as an effect size. For binary outcome measures, thenatural logarithm of theodds ratio comparing theresponse rates of thetwo groups was used. While there are no absolute standards ofwhat constitutes small, medium, and large effect sizes, generally 0.2 (odds ratio=1.2) is considered small, 0.5 (odds ratio=1.6) is considered moderate, and 0.8 (odds ratio=2.2) is considered large. Because adequate prediction ofsuccess and failure often requires use ofcombinations of, rather than individual, variables, thenext step was based on use ofsignal detection. This method was used todetermine themost sensitive and specific algorithm to, first, identify treatment dropouts and, second, identify treatment nonresponders (31). Signal detection is a well-established procedure, in many ways ideally suited toclinical decision making but not as familiar in this context as are standard parametric methods, such as multiple logistic regression analysis or multiple linear discriminant analysis. However, signal detection has major advantages over these methods: 1. Signal detection is nonparametric and distribution free, whereas multiple logistic regression analysis involves linearity assumptions and multiple linear discriminant analysis, in addition, assumes multivariate normal distributions. 2. Signal detection leads toan "and/or" rule that identifies which patients require attention and which not, a rule that clinicians find easy toapply in practice. In contrast, multiple logistic regression analysis and multiple linear discriminant analysis result in weighted averages ofpredictors, which are cumbersome for clinicians tocompute for individual patients and which, at best, order patients in terms oftheir need for attention. These are typically useful in research applicationsbut often are difficult for clinicians toapply toindividual patients. 3. Signal detection explicitly requires an evaluation of therelative clinical importance offalse positives and false negatives. Multiple logistic regression analysis and multiple linear discriminant analysis, by their nature, place equal importance on both, whatever theclinical situation. 4. Signal detection is highly sensitive tointeractive effects ofpredictors. Multiple logistic regression analysis and multiple linear discriminant analysis, like other linear models, require

inclusion ofall "main effects" before interactions can be considered. As a result, they have relatively low power todetect even strong interactions. 5. Signal detection can identify different subgroups ofsubjects who have similar probabilities of theoutcome but for different reasons. Multiple logistic regression analysis and multiple linear discriminant analysis would merely identify these subjects as having similar probabilities. As a result, theclinician is not alerted to thefact that thetype ofattention needed might differ among these subgroups. 6. Signal detection can take thecosts ofevaluations into consideration, although this capacity was not used here. Multiple logistic regression analysis and multiple linear discriminant analysis cannot take costs into consideration. 7. Signal detection, multiple logistic regression analysis, and multiple linear discriminant analysis, when used stepwise, as done here, all are hypothesis-generating, not hypothesistesting, methods. This limitation is often overlooked in consideration of theresults ofmultiple logistic regression analysis and multiple linear discriminant analysis, but it is hard tooverlook in theuse ofsignal detection methods. Briefly, at thefirst step, signal detection considers each possible predictor (including a range ofdifferent cutoff points for any ordinal predictor). For each, it computes thesensitivity and specificity ofthat "test" against theoutcome. Using theselected weighting of therelative clinical importance offalse positives and false negatives, it finds theoptimal predictor (and optimal cutoff point for an ordinal predictor). This is then used tosplit theinitial population into two subsets, theone positive on thefirst "test" and theone that is negative. Theprocess is repeated on each ofthese two subsets. At this stage thesame "test" may be found for both subsets (which would then act like a "main effect" in a linear model) or two different "tests" (like an "interaction"). Theprocess is then repeated on each of theresulting four subsets, then on theresulting eight subsets, etc., ultimately creating a decision tree. Theprocess stops when there are no more "tests," when thesample size in some subset is too small, or when theoptimal test does not achieve some preset criterion (often a statistically significant two-bytwo chi-square test at the5% level, here used as a stopping rule, not as a testing procedure for an a priori hypothesis). Results Treatment Outcome One-fourth of theparticipants (26%, N=48) dropped out oftreatment at an average of4.6 weeks, and 29% ofthese (N=14) dropped out by thesecond week. Of thedropouts, 21% (N=10) cited moving or lack oftime as thereason for dropping out, 21% (N=10) did not feel that thetreatment was suitable, and theremainder dropped out for unknown reasons. According tosubject recall for thepreceding week, nine of thedropouts had ceased tovomit; however, this is probably an overestimate of thenumber who can be regarded as recovered because binge eating and other purging methods were not assessed, and a 1-week recall is not a reliable indicator ofrecovery Hence, we decided toinclude all thedropouts in theanalyses. Of the140 participants who completed treatment, 58 (41%) had stopped binge eating and purging according toscores on theEating Disorder Examination for a 28-day period. Differences Between Dropouts and Completers

Thepretreatment characteristics ofthose who dropped out oftreatment (N=48) were compared with those of thepatients who completed treatment (N=140) (Table 1). Themagnitude of theeffect sizes indicates that thedropouts tended tohave higher levels ofbulimic cognitions (effect size=0.61), greater concern about shape (effect size=0.58), and greater impulsivity (effect size---0.53). A signal detection analysis using thevariables listed in Table 1 revealed that thebest combination ofpredictors ofdropping out oftreatment was a score on theBulimic Thoughts Questionnaire higher than 75 plus a score on theimpulsivity scale of theMultidimensional Personality Questionnaire lower than 6, indicating greater impulsivity (chi^sup 2^=29.5, df=3, p=0.0001). This test has a sensitivity of71% and a specificity of77%. From a clinical viewpoint, if a different treatment were designed for likely dropouts, this test would correctly assign 69% of thegroup either to thenew treatment or to cognitive behavior therapy. However, 32% of theindividuals who would not drop out would be incorrectly assigned to thenew treatment, hence depriving them of cognitive behavior therapyor treating them unnecessarily with an additional treatment if thenew therapywas combined with cognitive behavior therapyIn an attempt tomore precisely select dropouts, a test with thehighest specificity was performed. This test identified only six dropouts and misclassified three individuals who would not drop out. Baseline Differences Between Recovered and Nonrecovered Patients Thepretreatment variables were compared for those who stopped binge eating and purging (N=581, denoted here as recovered, and those who did not (N=82) minus those who dropped out before completing treatment. Thenonrecovered patients, as shown in Table 2, were more likely tohave reported current depression (effect size=-0.57), a low body mass index (effect size=-0.41) (probably indicating severe dietary restriction), and poor social adjustment (effect size=0.46). A signal detection analysis showed that thebest indicator ofpoor response totreatment was a score on theSocial Adjustment Scale higher than 2.0 (indicating poor social adjustment) combined with a body mass index less than 25 (chi^sup 2^=16.6, df=2, p=0.001). This test has a sensitivity of77% and a specificity of56%. Put another way, if this test was used toselect persons who were not going torespond to cognitive behavior therapyand give them a second treatment, 63% would get thecorrect treatment, 7% would respond to cognitive behavior therapybut would be given thesecond treatment unnecessarily, and 30% would get cognitive behavior therapybut would not respond tothat treatment. Differences in Early Performance Between Recovered and Nonrecovered Patients Because early performance in treatment may predict outcome more successfully than pretreatment variables alone, thepurging data at weeks 2, 4, 6, and 8 oftreatment were added to thepretreatment variables used in thepreceding analysis. Theonly significant variable chosen as a cutoff point in this signal detection analysis was thepercentage change in purging after 4 weeks (six sessions) oftreatment (chi^sup 2^=42.5, df=1, p<0.001); those who reduced purging less than 70% were more likely tobe treatment nonresponders. Thesensitivity ofthis test was 86%, and thespecificity was 69%. If we used these criteria toselect patients likely not torespond to cognitive behavior therapyand added a second treatment, 74% would get thecorrect treatment, 4% ofthose who would have recovered with cognitive behavior

therapywould get thesecond treatment unnecessarily and 22% who were assigned to cognitive behavior therapywould not respond tothat treatment. In order tomodel thepredictive value ofthis test in a more clinical manner, thecutoff point was tested on patients who had not dropped out by session 6 (N=162), i.e., thecohort that would be available to theclinician at session 6. For this signal detection analysis, 70% of thegroup would get thecorrect treatment, 6% would get thesecond treatment unnecessarily, and 24% who were assigned to cognitive behavior therapywould not respond tothat treatment-results similar tothose just reported. Discussion Overall, thepreviously reported predictors ofoutcome for cognitive behavior therapywere confirmed in this study. Theprincipal exceptions were high frequencies ofbinge eating and purging; although previously noted tobe associated with both dropping out (13, 16) and poor treatment response (2, 7-11), in this study they were not associated either with thetendency todrop out oftreatment or with treatment response. In thepresent study thedropouts had significantly more frequent bulimic thoughts and exhibited greater impulsivity than did subjects who completed treatment. Moderate effect sizes suggested that thedropouts were more likely tohave a past history ofanorexia nervosa, a past history ofmajor depression, and poorer social adjustment than thecompleters. Patients who did not respond totreatment were significantly more likely tohave poor social adjustment and a lower body mass index than were responders; thelow body mass index probably indicates a history ofsevere dietary restraint. Do these findings provide useful insight into modifications of cognitive behavior therapyeither for dropouts or for treatment completers? In thecase ofdropouts, it is possible that cognitive behavior therapydoes not deal with intense bulimic cognitions rapidly enough toprevent themore impulsive individual from dropping out oftreatment. This is likely because theinitial focus of cognitive behavior therapyis on increasing meal regularity and reducing dietary restraint (21). This focus, including regular weighing, may increase concerns about shape and intensify bulimic cognitions, because patients fear that they will gain weight if they eat more regularly. It is possible that reducing theemphasis on regular eating and dealing with bulimic cognitions early in treatment might reduce theprobability ofdropping out. Alternatively, a treatment approach that does not focus on eating behaviordirectly, such as interpersonal therapy, which has been shown in one study tobe as effective as cognitive behavior therapyalthough slower in achieving maximal effectiveness (32), might be valuable for these individuals. Thecomparison oftreatment responders and nonresponders provides less guidance concerning potential changes in treatment strategies. It is possible that those with a lower body mass index, indicating a long history ofdietary restriction, may be more resistant totreatment or require longer treatment. In addition, poor social adjustment may interfere with thetherapeutic relationship. However, although such associations may provide some guidance in choosing more effective treatment strategies, they can provide theclinician with only broad and imprecise indications as towhich patient will drop out or not respond totreatment. Signal detection analysis can be used toestablish cutoff points for a variable or set ofvariables that provide maximal efficiency in distinguishing between two mutually exclusive groups; in this case, thefirst distinction is between dropouts and nondropouts, and thesecond is between

responders and nonresponders to cognitive behavior therapy. In thefirst case, pretreatment characteristics, while statistically significant, were not clinically useful in identifying who would or would not drop out oftreatment, because too high a proportion ofnondropouts (32%) would be considered dropouts. However, thereason for dropping out of thestudy was unknown for 68% of thedropouts, posing a significant limitation for this analysis. In thesecond case, thebest predictor ofresponse totreatment was thereduction in purging at session 6, providing a better prediction than any pretreatment variable. Modeling this cutoff point indicated that 70% of thebulimic patients would be identified and correctly treated, at a cost ofonly 6% of thepatients who would have recovered with cognitive behavior therapybut who would be assigned to thesecond treatment. Theremaining patients, who would not respond to cognitive behavior therapy, could be given thealternative treatment at theend of cognitive behavior therapy. Assigning themajority ofpatients toa second treatment early in thecourse of therapyshould decrease thecost of therapyThis is an important issue in theera ofmanaged care. Such triage would allow treatment providers tobetter manage thelimited mental health care benefits available totheir patients. Moreover, more rapidly abandoning an ineffective treatment may lessen patient frustration and lower thedropout rate. Theidentification ofcutoff points that provide useful guidance for judging who will or will not improve early in treatment is important for thedevelopment oftreatment algorithms. When tested in outcome studies, such algorithms can guide clinicians as towhen tochange a treatment and which treatment tothen offer totheir patients. These results require replication in another large group ofpatients with bulimianervosa treated with cognitive behavior therapyHowever, in theinterim theresults suggest that clinicians using cognitive behavior therapymight consider adding a second treatment, for example, an antidepressant, if six treatment sessions do not lead thepatient toreduce purging by at least 70%. Received April 16, 1999; revisions received Aug. 24 and Nov. 30, 1999; accepted Jan. 6, 2000. From theDepartment ofPsychiatry, Stanford University; theDepartment ofPsychiatry, University ofMinnesota, Minneapolis; theDepartment ofPsychiatry, Cornell University, New York; theDepartment ofNeuroscience, University ofNorth Dakota, and Neuropsychiatric Research Institute, Grand Forks, N.D.; and theDepartment ofPsychology, Rutgers University, Piscataway, N.J. Address reprint requests toDr. Agras, Department ofPsychiatry, Stanford University, 401 Quarry Rd., Stanford, CA 94305-5722. Supported in part by grants from theMcKnight Foundation toCornell University, theUniversity ofMinnesota, Rutgers University, and Stanford University. References References References 1.Wilson GT, Fairburn CG, Agras WS: Cognitive-behavioral therapyfor bulimianervosa, in Handbook ofTreatment for Eating Disorders. Edited by Garner DM, Garfinkel PE. New York, Guilford, 1997, pp 67-93

2. Baell WK, Wertheim EH: Predictors ofoutcome in thetreatment of bulimianervosa. Br J Clin Psycho) 1992; 31:330-332 3. Fairburn CG, Kirk J, O'Connor M, Anastasiades P, Cooper PJ: Prognostic factors in bulimianervosa. Br J Clin Psycho) 1987; 26:223-224 4. Fairburn CG, Peveler RC, Jones R, Hope RA, Doll HA: Predictors of12-month outcome in bulimianervosa and theinfluence ofattitudes toshape and weight. J Consult Clin Psycho) 1993; 61: 696-698 5. Lacey JH: Bulimianervosa, binge eating and psychogenic vomiting: controlled treatment and long-term outcome. Br Med J 1983;286:1609-1613 6. Wilson GT, Rossiter E, Kleifield RI, Lindholm L: Cognitive-behavioral treatment of bulimianervosa: a controlled evaluation, Behav Res Ther 1986; 24:277-288 7. Bossert S, Schmeolz U, Wiegand M, Junker M, Krieg JC: Predictors ofshort-term treatment outcome in bulimianervosa inpatients. Behav Res Ther 1992; 30:193-199 8. Bulik CM, Sullivan PF, Joyce PR, Carter FA, McIntosh VV: Predictors of1-year treatment outcome in bulimianervosa, Compr Psychiatry 1998; 39:206-214 9. Garner DM, Olmsted MP, Davis R, Rockert W, Goldbloom D, Eagle M: Theassociation between bulimic symptoms and reported psychopathology. Int J Eat Disord 1990; 9:1-15 10. Turnbull Sj, Schmidt U, Troop NA, Tiller J, Todd G, Treasure JL: Predictors ofoutcome for two treatments of bulimianervosa: short and long-term. Int J Eat Disord 1997; 21:17-22 11. Wilson GT, Loeb KL, Walsh BT, Labouvie E, Petkova E, Liu X, Waternaux C: Psychological versus pharmacological treatments of bulimianervosa: predictors and processes ofchange. J Consult Clin Psychol 1999; 67:451-459 12. Rossiter EM, Agras WS, Teich CF, Schneider JA: Cluster B personality disorder characteristics predict outcome in thetreatment of bulimianervosa. Int] Eat Disord 1993; 13:349-357 References 13. Stieger H, Leung F, Thibaudeau J, Houle L: Prognostic utility ofsubcomponents of the"borderline personality construct" in bulimianervosa. BrJ Clin Psychol 1993; 32:187-197 14. Walter G: Dropout and failure toengage in individual outpatient cognitive-behavior therapyfor bulimic disorders. Int J Eat Disord 1997; 22:35-41 15. Davis R, Olmsted MP, Rockert W: Brief group psychoeducation for bulimianervosa, 11: prediction ofclinical outcome. Int J Eat Disord 1992; 11:205-211 16. Mitchell J: A review ofcontrolled trials ofpsychotherapy for bulimianervosa. J Psychosom Res 1991; 35(suppl 1):23-31

17. Lee NF, Rush AJ: Cognitive-behavioral group therapyfor bulimia. Int J Eat Disord 1986; 5:599-615 18. Blouin J, Schnarre K, Carter J, Blouin A, Tener L, Zuro C, Barlow J: Factors affecting dropout rate from cognitive-behavioral group treatment for bulimianervosa. Int ) Eat Disord 1995; 17: 323-329 19. Olmsted MP, Davis R, Rockert W, Irvine MJ, Eagle M, Garner DM: Efficacy ofa brief psychoeducational intervention for bulimianervosa. Behav Res Ther 1991; 29:71-8 3 20. Kirkley B, Schneider J, Agras WS, Bachman J: Comparison oftwo group treatments for bulimia. J Consult Clin Psychol 1985; 53:43-48 21. Fairburn CG, Marcus MD, Wilson GT: Cognitive-behavioral therapyfor binge eating and bulimianervosa: a comprehensive treatment manual, in Binge Eating: Nature, Assessment, and Treatment. Edited by Fairburn CG, Wilson GT. New York, Guilford, 1993, pp 361-404 22. Spitzer RL, Williams JBW, Gibbon M: Structured Clinical Interview for DSM-III-R (SCID). New York, New York State Psychiatric Institute, Biometrics Research, 1987 References 23. Cooper Z, Fairburn CG: TheEating Disorder Examination: a semi-structured interview for theassessment of thespecific psychopathology ofeating disorders. Int J Eat Disorders 1987; 6:1-8 24. Phelan PW: Correlates of bulimia: theBulimic Thoughts Questionnaire. Int J Eat Disord 1987; 6:593-608 25. Schneider JA, O'Leary A, Agras WS: Therole ofperceived self-efficacy in recovery from bulimia: a preliminary examination. Behav Res Ther 1987; 25:429-432 26. Beck AT, Ward CH, Mendelson M, Mock ), Erbaugh J: An inventory for measuring depression. Arch Gen Psychiatry 1961; 4: 561-571 27. Rosenberg M: Conceiving theSelf. New York, Basic Books, 1979 28. Tellegen A, Waller N: Exploring personality through test construction: development of theMultidimensional Personality Questionnaire, in Personality Measures: Development and Evaluation, vol 1. Edited by Briggs SR, Cheek JM. Greenwich, Conn, JAI Press, 1994, pp 172-208 29. Horowitz LM, Rosenberg SE, Baer BA, Ureno G, Villasenor VS: Inventory ofInterpersonal Problems: psychometric properties and clinical applications. J Consult Clin Psychol 1988; 56:885892 30. Weissman MM, Bothwell S: Assessment ofsocial adjustment by patient self-report. Arch Gen Psychiatry 1976; 33:1111-1115

31. Kraemer HC: Assessment of2 x 2 association: generalization ofsignal detection methods. Am Statistician 1988; 42:37-49 32. Fairburn CG, Kirk J, O'Connor M: A comparison oftwo psychological treatments for bulimianervosa. Behav Res Ther 1986; 24:629-643

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Cite Subjects Bulimia, Cognition & reasoning, Behavior modification, Therapy, Psychiatry MeSH Adult, Bulimia -- psychology, Educational Status, Female, Humans, Patient Dropouts, Patient Selection, Probability, Regression Analysis, Treatment Outcome, Bulimia -- therapy (major), Cognitive Therapy (major) Title Outcome predictors for the cognitive behavior treatment of bulimia nervosa: Data from a multisite study Authors Crow, Scott J; Halmi, Katherine A; Mitchell, James E Publication title The American Journal of Psychiatry Volume 157 Issue 8 Pages 1302-8 Number of pages 7 Publication year 2000 Publication Date Aug 2000 Year 2000 Publisher American Psychiatric Association Place of Publication Washington Country of publication United States Journal Subjects Medical Sciences--Psychiatry And Neurology ISSN 0002953X CODEN AJPSAO Source type Scholarly Journals

Language of Publication English Document type PERIODICAL Subfile Bulimia, Cognition & reasoning, Behavior modification, Therapy, Psychiatry Accession number 10910795, 20372383 ProQuest Document ID 220478684 Document URL http://search.proquest.com/docview/220478684?accountid=38885 Copyright Copyright American Psychiatric Association Aug 2000 Last updated 2011-09-06 Database ProQuest Research Library

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Bulimia nervosa
Mehler, Philip S . The New England Journal of Medicine 349. 9 (Aug 28, 2003): 875-881. Turn on hit highlighting for speaking browsers Turn off hit highlighting

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The efficacy of cognitive-behavioral therapy in patients with bulimia nervosa has been convincingly demonstrated in randomized, controlled trials.37 This therapy is designed to educate patients about other ways to cope with the feelings that precipitate a Show all

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This Journal Jeature begins with a case vignette highlighting a common clinical problem. Evidence supporting various strategies is then presented, followed by a review offormal guidelines, mhen they exist. Thearticle ends with theauthor's clinical recommendations. A 20-year-old woman presents with fatigue; laboratory tests reveal a serum potassium level of2.3 mmol per liter and a serum bicarbonate level of36 mmol per liter. She is 163 cm (64 in.) tall and weighs 54 kg (119 lb). Thefindings on physical examination are normal. On questioning, she admits tobinge eating and vomiting as frequently as five times per day. How should she be treated? THECLINICAL PROBLEM Bulimianervosa, a disorder characterized by binge eating and purging, generally begins during adolescence, with thepeak period ofonset around 18 years ofage.1 Thelifetime prevalence is 3 percent,2 and theratio offemale patients tomale patients ranges from 10:1 to20:1.3 Most patients with bulimiahave a coexisting psychiatric condition, such as an anxiety disorder or depression.4 There is also an association with substance abuse and promiscuity.5 Almost half ofpatients with bulimiahave residual features of theeating disorder after six years offollow-up.6 Certain personality disorders (borderline, narcissistic, and antisocial disorders), impulsivity, and depression predict a worse prognosis.7 Bulimianervosa is characterized by recurrent episodes ofbinge eating followed by inappropriate compensatory purging behavior toprevent weight gain (Table 1).8 Although theformal criteria of theDiagnostic and Statistical Manual ofMental Disorders, 4th edition (DSM-IV), require that both thebinge eating and thecompensatory behavioroccur, on average, at least twice a week for a period ofthree months, there is wide variability in these types of behavior, and some patients purge 5 to10 times or more per day. In contrast toanorexia nervosa, which is characterized by a weight that is less than 85 percent of thenormal value, most persons with bulimiaare ofnormal weight. Therisk ofdeath is much lower among patients with bulimianervosa than among those with anorexia nervosa9 but nevertheless appears tobe greater than that among women ofsimilar age in thegeneral population.10 Bulimiais a disorder ofuncertain cause; there is mounting evidence that genetic factors have an important role.11 Disturbances in theserotonergic systems, which are implicated in theregulation offood intake, and cultural attitudes toward standards ofphysical attractiveness are also believed tocontribute. Routine screening for bulimiais not currently thestandard ofcare12 but may be prudent in college-age populations. There are three main modes ofpurging: self-induced vomiting, abuse oflaxatives, and misuse ofdiuretics. Most patients with bulimiainduce vomiting with a finger, but some use ipecac. As theillness progresses, many can vomit reflexively without mechanical stimulation. Thelaxatives abused are thestimulant type containing bisacodyl, cascara, or senna. Diuretic preparations and diet pills such as those containing ephedrine are less frequently used.13 Themedical complications of bulimianervosa are related to themode and frequency ofpurging, whereas in anorexia nervosa, they arise as a result ofstarvation (restricting) and weight loss. MEDICAL COMPLICATIONS

Oral Complications Pharyngeal soreness and loss ofenamel on thelingual surface of theanterior teeth (perimyolysis) are thought toresult from repeated exposure toacidic gastric contents in thevomitus. Dental caries may be more prevalent,14 and dentists are in a good position torefer patients for treatment.15 Another complication associated with excessive vomiting is sialadenosis, a painless swelling of thesalivary glands that develops after an intense cycle ofpurging. Gastrointestinal Complications Frequent vomiting may lead togastroesophageal reflux or Mallory-Weiss tears. Dyspepsia is common,16 but esophageal motility is normal.17 Some patients with bulimiaingest up to50 laxative pills per day. Severe constipation with a laxative-dependence syndrome, due todamage to themyenteric plexus, may result from theabuse ofstimulant laxatives.18 Electrolyte Complications Recurrent purging can result in serious fluid and electrolyte disturbances (Table 2). Themost severe cases ofmetabolic alkalosis are almost always due tovomiting. Abuse ofdiuretics also causes hypochloremic metabolic alkalosis. Acute diarrhea associated with laxative use results in hyperchloremic metabolic acidosis. Hypokalemia occurs in approximately 5 percent ofbulimic patients19,20 and may predispose them tocardiac arrhythmias. Given its low sensitivity, screening for hypokalemia cannot be recommended as a means ofdetecting bulimia. However, thefinding ofhypokalemia in an otherwise healthy young woman is highly specific for bulimianervosa. Measurement ofurinary potassium levels may be useful; a value ofless than 10 mmol per liter in a "spot" urine specimen usually suggests a gastrointestinal cause ofpotassium loss. Thepatient with purely restricting anorexia nervosa is not at risk for any metabolic abnormality, acid-base disturbance, or hypokalemia.21 Pseudo-Bartter's syndrome, defined as normotensive, hypokalemic alkalosis, is common among patients who vomit or use diuretics excessively.22 Volume depletion induces hyperaldosteronism.23 Troublesome edema in thelegs, caused by persistently high levels ofaldosterone, may occur in patients who purge excessively and then stop abruptly. Idiopathic edema, a condition characterized by irregular episodes offluid retention in theabsence ofa recognizable cause, may also be a manifestation of bulimiain women who use diuretics tocontrol cyclical fluid retention.24 Endocrine Complications In contrast topatients with anorexia nervosa, patients with bulimiararely have endocrine abnormalities. Generally, bone density is normal unless there is a history ofanorexia nervosa, in which case, bone densitometry is warranted.25 Although irregular menses, which affect fertility, are common during episodes ofactive bulimia, thefuture ability toconceive is not impaired in patients who recover from bulimia.26 Themajority ofwomen with bulimiahave improvement in symptoms during pregnancy, but an exacerbation ofsymptoms after delivery is common.27

Theprevalence of bulimianervosa may be increased among patients with type 1 diabetes; some patients deliberately avoid taking insulin in order toinduce weight loss.28 An earlier onset ofmicrovascular complications has been reported among these patients.29 Other Complications Repeated abuse ofipecac can cause serious, although usually reversible, toxic effects in theform ofcardiomyopathy and muscle weakness.30 Erosions covering thedorsum of thehands (Russell's sign) result from self-induced vomiting. STRATEGIES AND EVIDENCE TREATMENT OFMEDICAL COMPLICATIONS Most of themedical complications of bulimianervosa are treatable. In theabsence ofclinical trials, suggested therapiesfor these complications are largely based on clinical experience. Gentle brushing and use ofa fluoride mouth rinse immediately after purging may prevent caries.31 Sialadenosis responds toa combination ofabstinence from vomiting, the application ofheat, and sucking oftart candies. If thesialadenosis has not begun torecede after a few weeks, oral pilocarpine (5 mg three times per day) may decompress theglands.32 Reflux symptoms respond toproton-pump inhibitors. Theprokinetic agent metoclopramide may occasionally be worth considering as a means ofdecreasing thefrequency ofvomiting; presumably, it acts on thecentral "emetic center" and by increasing thetone of thelower esophageal sphincter. It is difficult totreat laxative dependence. Patients must be counseled about theineffectiveness ofstimulant laxatives for weight loss. Therestoration ofbowel function is thenorm after laxative use has been discontinued, but it may take several weeks.33 Ample hydration, a high-fiber diet, and moderate amounts ofexercise should be encouraged, as long as thepatient does not have a history ofexcessive exercise as a means ofcontrolling weight. If constipation persists for more than a few days, a glycerin suppository or a nonstimulating osmotic laxative such as lactulose may be useful; stool softeners are oflittle value.34 Leg edema caused by pseudo-Bartter's syndrome is treated with salt restriction (less than 3 g per day), elevation of thelegs, and patience; loop diuretics will only exacerbate theproblem. An aldosterone antagonist, such as spironolactone (25 to50 mg per day), may be given for one totwo weeks, at which point thesymptoms will probably have resolved. Such treatment is particularly worth considering if thedistress ofhaving edema is thought likely toprecipitate a relapse of bulimia. Calcium (1200 to1500 mg per day) with vitamin D (400 to800IU per day) should be recommended routinely, particularly in patients with a history ofanorexia nervosa, among whom bone loss is likely. For these patients, treatment with an oral contraceptive is also reasonable, although it may not be sufficient torestore bone density.35 Hypokalemia Thetreatment ofmarked hypokalemic metabolic alkalosis requires volume repletion (with intravenous normal saline), in order toturn off thereninangiotensin system. Normalization ofvolume status is needed for effective potassium repletion. A general principle is that every

decrease of1 mmol per liter in theserum potassium level represents a loss of150 mmol in thetotal body potassium level. Oral potassium chloride is generally preferred for potassium repletion. Typically, potassium is administered in a split dose of40 to80 mEq per day for a few days. Thepotassium level should initially be measured daily during replacement therapy, because therequired amount cannot be calculated reliably.36 Once euvolemia has been restored, if there is ongoing frequent purging, theelectrolytes should be monitored; long-term potassium supplementation may be needed. PSYCHIATRIC TREATMENT Psychotherapy Theefficacy of cognitive-behavioral therapyin patients with bulimianervosa has been convincingly demonstrated in randomized, controlled trials.37 This therapyis designed toeducate patients about other ways tocope with thefeelings that precipitate a desire topurge and totry tocorrect maladaptive beliefs regarding body image (e.g., that physical appearance dictates one's value as a person). In a five-month study involving 220 patients who were randomly assigned toeither individual cognitive-behavioral therapyor interpersonal psychotherapy, 30 percent of thepatients receiving cognitive-behavioral therapywere in remission (defined by a frequency ofpurging ofless than twice per week) at theend oftreatment, as compared with only 6 percent in thepsychotherapy group.38 This improvement has been corroborated in a four-month study ofindividual and group cognitivebehavioral therapyinvolving 60 bulimic patients; therate ofbinge eating and purging behaviordeclined by 80 percent with either ofthese approaches.39 A reduction in thefrequency ofpurging of70 percent or more by thesixth session of cognitive-behavioral therapyis predictive ofa good longer-term response tothis therapy.40 Although short-term studies of cognitive-behavioral therapyhave demonstrated benefits, there are sparse data demonstrating that thebenefits are maintained over thelonger term. A recent study evaluated 101 women (80 percent of theoriginal study cohort) long after they had participated in a placebo-controlled trial of cognitive-behavioral therapy, pharmacotherapy (imipramine), or both; at 10 years, women who had been treated with cognitive-behavioral therapy, imipramine, or both performed better than women in theplacebo group on measures ofsocial adjustment at work and in family activities.41 Rates ofabstinence from binge eating and purging after cognitive-behavioral therapyare less impressive, averaging less than 40 percent.42 Other forms ofpsychotherapy, such as interpersonal psychotherapy, which focuses on current interpersonal problems rather than theeating disorder, have also been used, but there is less evidence tosupport their use. Pharmacotherapy Irrespective of thepresence or absence ofassociated depressive symptoms, various classes ofantidepressants (tricyclics, selective serotonin-reuptake inhibitors, monoamine oxidase inhibitors, bupropion, and trazodone) have been demonstrated, in short-term (three-month), double-blind, placebo-controlled trials, tobe effective in reducing theseverity ofsymptoms of bulimia.43 Theavailable data suggest that each ofthese pharmacologic treatments may decrease thefrequency ofbulimic behaviorby 50 to60 percent within six toeight weeks. Fluoxetine is theonly medication for bulimianervosa that has been approved by theFood and Drug Administration (FDA) todate. It received FDA approval on thebasis ofits demonstrated

efficacy in two 8-week double-blind trials and in one 16-week double-blind trial. Thelatter was a multicenter study involving 400 outpatients that demonstrated significantly greater decreases in thenumber ofweekly binge-purge episodes among patients treated with fluoxetine (60 mg per day) than among patients in theplacebo group (a 50 percent reduction vs. a 21 percent reduction).44 A study involving 387 women with bulimiawho were randomly assigned toreceive fluoxetine, at a dose of20 mg per day or 60 mg per day, or placebo for eight weeks showed that the60-mg dose was significantly more effective.45 Side effects included tremor, insomnia, and nausea but were not dose-related, and therate ofdiscontinuation ofstudy treatment because ofan adverse event among women receiving thehigher dose offluoxetine was similar to therate in theplacebo group. Like cognitive-behavioral therapy, pharmacotherapy alone results in complete suppression ofbinge eating and purging in only 30 to40 percent ofpatients.46 Approximately one third ofpatients who initially have improvement with medication will have a resurgence oftheir bulimic behavior; therisk ofresurgence is highest during thefirst year after recovery.10 A recent study demonstrated that fluoxetine treatment reduced therisk ofa relapse of bulimiaover a 52-week treatment period, as compared with placebo (19 percent vs. 37 percent).47 A combination ofantidepressants and cognitive-behavioral therapyappears tobe more effective in reducing thefrequency ofhinging and purging than either treatment alone. A review using data from seven trials involving a total of600 patients toassess theeffect ofantidepressants (desipramine, imipramine, or fluoxetine) plus cognitive-behavioral therapyas compared with theeffect ofone ofthese therapiesalone reported average remission rates of42 to49 percent with a combination of therapiesand average rates of23 to36 percent with any single therapy.48 As a single therapy, cognitive-behavioral therapywas more effective than drug therapy. Patients in whom this therapyfails may have a response toan alternative therapy, but available data suggest that theresponse rate is relatively low in this situation. In a study ofpatients in whom cognitive-behavioral therapyhad failed, therate ofresponse tointerpersonal therapywas 16 percent, and therate ofresponse topharmacotherapy (fluoxetine or desipramine) was 10 percent.49 AREAS OFUNCERTAINTY Most patients with bulimianervosa may reasonably be treated as outpatients. Factors that suggest a need for hospitalization include severe depression, disabling symptoms, purging that is rapidly worsening and has proved refractory tooutpatient treatment, severe hypokalemia (plasma potassium level, <2.0 to3.0 mmol per liter), and major orthostatic changes in blood pressure (>30 mm Hg) and pulse (>30 beats per minute). Data are lacking on how these factors affect theultimate outcome.50 Although some experts advocate hospitalization for any patient with a potassium level below 3.0 mmol per liter, in practice it is not uncommon for patients with lower potassium levels tobe cared for on an outpatient basis. Most studies of cognitive-behavioral therapyand medication have not included adolescent subjects (those younger than 18 years ofage); thus, it is uncertain what thepreferred therapyfor such patients is. Other medications that are not discussed above may be effective in treating bulimia. Limited data from three short-term clinical trials, only one ofwhich was randomized, double-blind, and placebo-controlled, suggest that theantiemetic agent ondansetron may be effective in patients with bulimianervosa.51 Anecdotal data indicate that

thenovel anticonvulsant agent topiramate may also be effective.52 However, more data are needed. Theeffects ofdietary counseling on thedevelopment and course of bulimiahave not been well studied. It is also uncertain which patients can be effectively treated by a generalist rather than a psychiatrist; theinvolvement ofboth is generally recommended. It remains unknown whether bulimiamay be prevented by programs that teach assertiveness toyoung girls and help them tobe critical ofmedia claims promoting thevalue ofthinness. GUIDELINES TheAmerican Psychiatric Association has issued comprehensive guidelines for themanagement of bulimia(http://www.psych.org/clin_res/guide. bk42301.cfm).53 These offer guidance regarding thesite oftreatment (whether it occurs in thehospital, is partially accomplished during hospitalization, is provided on an intensive outpatient basis, or is officebased) and thetype oftreatment, including cognitive-behavioral therapyand medications. Although definitive data are lacking, theAmerican Dietetic Association has published a position paper regarding nutritional counseling for patients with bulimianervosa,54 which recommends theinvolvement ofa dietitian in order todevelop a plan for normalizing eating patterns, minimizing restrictions on thetypes offood consumed, and correcting misconceptions about dieting. CONCLUSIONS Bulimianervosa should be considered in patients with unexplained hypokalemia and metabolic alkalosis and is particularly common in late adolescence. Theprimary objectives oftreatment are tointerrupt thebinge-purge cycles with theuse ofpharmacotherapy, cognitivebehavioral therapy, or both and totreat associated medical complications. All patients should be educated about themedical complications of bulimiaand about thebenefits ofrestoring a regular pattern ofeating. On thebasis of thedegree ofhypokalemia in thewoman described in thevignette, I would recommend a short stay in thehospital torestore a normal volume status with intravenous saline at 75 ml per hour and would aim toreplenish her potassium orally by providing 60 to80 mEq per day in a split dose, with daily monitoring ofelectrolytes until thelevels returned tonormal. Subsequently, theelectrolyte levels should be monitored intermittently; although there are no clear guidelines, I would do so at least every few months initially toscreen for evidence ofsurreptitious purging and torule out potentially dangerous potassium levels. With thegoal ofreducing thefrequency ofbinging and purging, if not completely eliminating this behavior, I would refer thepatient for cognitive-behavioral therapywith a mental health specialist who had expertise in eating disorders, and I would also treat her with medication. Fluoxetine would be my first choice, because ofits proven efficacy and tolerability. Given data showing thesuperiority ofa 60-mg dose over a 20-mg dose, I would aim toincrease thedose to60 mg over thecourse ofseveral days. Although data on theeffects ofnutritional counseling are lacking, seeing a dietitian may also be helpful for some patients, particularly those who have extensive lists of"forbidden" foods or whose bulimiahas been active for years. I am indebted toAdriana Padgett for her assistance in thepreparation of themanuscript.

Sidebar N Engl J Med 2003;349:875-81. Copyright (C) 2003 Massachusetts Medical Society. Sidebar Copyright (C) 2003 Massachusetts Medical Society. Sidebar ELECTRONIC ACCESS TO THEJOURNAL'S CUMULATIVE INDEX At theJournal's site on theWorld Wide Web (http://www.nejm.org) you can search an index ofall articles published since January 1975 (abstracts 1975-1992, full-text 1993-present). You can search by author, key word, tide, type ofarticle, and date. Theresults will include thecitations for thearticles plus links to theabstracts ofarticles published since 1993. For nonsubscribers, time-limited access tosingle articles and 24-hour site access can also be ordered for a fee through theInternet (http://www.nejm.org). References REFERENCES 1. Lewinsohn PM, Striegel-Moore RH, Seeley JR. Epidemiology and natural course ofeating disorders in young women from adolescence toyoung adulthood. J Am Acad Child Adolesc Psychiatry 2000;39:1284-92. 2. Kreipe RE, Birndorf SA. Eating disorders in adolescents and young adults. Med Clin North Am 2000;84:1027-49. 3. Woodside DB, Garfinkel PE, Lin E, et al. Comparisons ofmen with full or partial eating disorders, men without eating disorders, and women with eating disorders in thecommunity. Am J Psychiatry 2001;158:570-4. 4. O'Brien KM, Vincent NK. Psychiatric comorbidity in anorexia and bulimianervosa: nature, prevalence, and causal relationships. Clin Psychol Rev 2003;23:57-74. 5. Neumark-Sztainer D, Story M, French SA. Covariations ofunhealthy weight loss behaviorsand other high-risk behaviorsamong adolescents. Arch Pediatr Adolesc Med 1996;150:304-8. 6. Fairburn CG, Norman PA, Welch SL, O'Connor ME, Doll HA. Peveler RC. A prospective study ofoutcome in bulimianervosa and thelong-term effects ofthree psychological treatments. Arch Gen Psychiatry 1995;52:304-12. 7. Vaz FJ. Outcome of bulimianervosa: prognostic indicators. J Psychosom Res 1998;45:391400.

8. Pryor T. Diagnostic criteria for eating disorders: DSM-IV revisions. Psychiatr Ann 1995;25:40-5. 9. Steinhausen HC. Eating disorders. In: Steinhausen HC, Verhulst FC, eds. Risks and outcomes in developmental psychopathology. Oxford, England: Oxford University Press, 1999:210-30. 10. Keel PK, Mitchell JE. Outcome in bulimianervosa. Am J Psychiatry 1997;154:313-21. 11. Bulik CM, Devlin B, Bacanu SA, et al. Significant linkage on chromosome 1Op in families with bulimianervosa. Am J Hum Genet 2003;72:200-7. 12. Cotton MA, Ball C, Robinson P. Four simple questions can help screen for eating disorders. J Gen Intern Med 2003;18:53-6. 13. Roerig JL, Mitchell JE, De Zwaan M, et al. Theeating disorders medicine cabinet revisited: a clinician's guide toappetite suppressants and diuretics. Int J Eat Disord 2003:33:443-57. 14. Little JW. Eating disorders: dental implications. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;93:138-43. 15. Woodmansey KF. Recognition of bulimianervosa in dental patients: implications for dental care providers. Gen Dent 2000;48:48-52. 16. Mendell DA, Logemann JA. Bulimiaand swallowing: cause for concern. Int J Eat Disord 2001;30:252-8. 17. Nickl NJ, Brazer SR, Rockwell K, Smith JW. Patterns ofesophageal motility in patients with stable bulimia. Am J Gastroenterol 1996;91:2544-7. 18. Mehler P. Constipation: diagnosis and treatment in eating disorders. Eat Disord J Treat Prev 1997:5:41-6. 19. Wolfe BE, Metzger ED, Levine JM, Jimerson DC. Laboratory screening for electrolyte abnormalities and anemia in bulimianervosa: a controlled study, Int J Eat Disord 2001;30:288-93. 20. Greenfeld D, Mickley D, Quinlan DM, Roloff P. Hypokalemia in outpatients with eating disorders. Am J Psychiatry 1995;152:60-3. 21. Mehler PS. Diagnosis and care ofpatients with anorexia nervosa in primary care settings. Ann Intern Med 2001:134:1048-59. 22. Schulte M, Mehler PS. Metabolic abnormalities in eating disorders. In: Mehler PS, Andersen AE, eds. Eating disorders: a guide tomedical care and complications. Baltimore: Johns Hopkins University Press, 1999:76-85. 23. Jamison RL, Ross JC, Kempson RL, Sufit CR, Parker TE. Surreptitious diuretic ingestion and pseudo-Bartter's syndrome. Am J Med 1982;73:142-7.

24. Bihun JA, McSherry J, Marciano D. Idiopathic edema and eating disorders: evidence for an association. Int J Eat Disord 1993;14:197-201. 25. Zipfel S, Seibel MJ, Lowe B, Beumont PJ, Kasperk C, Herzog W. Osteoporosis in eating disorders: a follow-up study ofpatients with anorexia and bulimianervosa. J Clin Endocrinol Metab 2001;86:5227-33. 26. Crow SJ, Thuras P, Keel PK, Mitchell JE. Long-term menstrual and reproductive function in patients with bulimianervosa. Am J Psychiatry 2002:159:1048-50. 27. Conrad R, Schablewski J, Schilling G, Liedtke R. Worsening ofsymptoms of bulimianervosa during pregnancy. Psychosomatics 2003;44:76-8. 28. Takii M, Uchigata Y, Nozaki T, et al. Classification oftype 1 diabetic females with bulimianervosa into subgroups according topurging behavior. Diabetes Care 2002;25:1571-5. 29. Rydall AC, Rodin GM, Olmsted MP, Devenyi RG, Daneman D. Disordered eating behaviorand microvascular complications in young women with insulin-dependent diabetes mellitus. N Engl J Med 1997;336:1849-54. 30. Ho PC, Dweik R, Cohen MC. Rapidly reversible cardiomyopathy associated with chronic ipecac ingestion. Clin Cardiol 1998;21:780-3. 31. Milosevic A, Brodie DA, Slade PD. Dental erosion, oral hygiene, and nutrition in eating disorders. Int J Eat Disord 1997;21:195-9. 32. Mehler PS, Wallace JA. Sialadenosis in bulimia: a new treatment. Arch Otolaryngol Head Neck Surg 1993;119:787-8. 33. Colton P, Woodside DB, Kaplan AS. Laxative withdrawal in eating disorders: treatment protocol and 3 to20-month followup. Int J Eat Disord 1999;25:311-7. 34. Tramonte SM, Brand MB, Mulrow CD, Amato MG, O'Keefe ME, Ramirez G. Thetreatment ofchronic constipation in adults: a systematic review. J Gen Intern Med 1997;12:15-24. 35. Grinspoon S, Thomas E, Pitts S, et al. Prevalence and predictive factors for regional osteopenia in women with anorexia nervosa. Ann Intern Med 2000;133:790-4. 36. Gennari FJ. Hypokalemia. N Engl J Med 1998;339:451-8. 37. Hay PJ, Bacaltchuk J. Extracts from "Clinical evidence": bulimianervosa. BMJ 2001:323:33-7. 38. Agras WS, Walsh T, Fairburn CG, Wilson GT, Kraemer HC. A multicenter comparison of cognitive-behavioral therapyand interpersonal psychotherapy for bulimianervosa. Arch Gen Psychiatry 2000;57:459-66. 39. Chen E, Touyz SW, Beumont PJV, et al. Comparison ofgroup and individual cognitivebehavioral therapyfor patients with bulimianervosa. Int J Eat Disord 2003;33:241-54.

40. Agras WS, Crow SJ, Halmi KA, Mitchell JE, Wilson GT, Kraemer HC. Outcome predictors for the cognitive behaviortreatment of bulimianervosa: data from a multisite study. Am J Psychiatry 2000;157:1302-8. 41. Keel PK, Mithcell JE, Davis TL, Crow SJ. Long-term impact oftreatment in women diagnosed with bulimianervosa. Int J Eat Disord 2002;31:151-8. 42. Peterson CB, Mitchell JE. Psychosocial and pharmacological treatment ofeating disorders: a review ofresearch findings. J Clin Psychol 1999;55:685-97. 43. Jimerson DC, Wolfe BE, Brotman AW, Metzger ED. Medications in thetreatment ofeating disorders. Psychiatr Clin North Am 1996:19:739-54. 44. Goldstein DJ, Wilson MG, Thompson VL, Potvin JH, Rampey AH Jr. Long-term fluoxetine treatment of bulimianervosa. Br J Psychiatry 1995;166:660-6. 45. Fluoxetine BulimiaNervosa Collaborative Study Group. Fluoxetine in thetreatment of bulimianervosa: a multicenter, placebo-controlled, double-blind trial. Arch Gen Psychiatry 1992;49:139-47. 46. Bacaltchuk J, Hay P, Mari JJ. Antidepressants versus placebo for thetreatment of bulimianervosa: a systematic review. Aust N Z J Psychiatry 2000;34:310-7. 47. Romano SJ, Halmi KA, Sarkar NP, Koke SC, Lee JS. A placebo-controlled study offluoxetine in continued treatment of bulimianervosa after successful acute fluoxetine treatment. Am J Psychiatry 2002;159:96-102. 48. Bacaltchuk J, Trefiglio RP, Oliveira IR, Hay P, Lima MS, Mari JJ. Combination ofantidepressants and psychological treatments for bulimianervosa: a systematic review. Acta Psychiatr Scand 2000;101:256-64. 49. Mitchell JE, Halmi K, Wilson GT, Agras WS, Kraemer H, Crow S. A randomized secondary treatment study ofwomen with bulimianervosa who fail torespond toCBT. lnt J Eat Disord 2002;32:271-81. 50. Woodside DB. Inpatient treatment and medical management ofanorexia nervosa and bulimianervosa. In: Earing disorders and obesity: a comprehensive handbook. 2nd ed. Fairburn CG, Brownell KD, eds. New York: Guilford Press, 2002:335-9. 51. Paris PL, Kim SW, Melier WH, et al. Effect ofdecreasing afferent vagal activity with ondansetron on symptoms of bulimianervosa: a randomised, double-blind trial. Lancet 2000;355:792-7. 52. Felstrom A, Blackshaw S. Topiramate for bulimianervosa with bipolar II disorder. Am J Psychiatry 2002;159:1246-7. 53. Practice guideline for thetreatment ofpatients with eating disorders (revision). Am J Psychiatry 2000;157:Suppl:1-39.

54. Position of theAmerican Dietetic Association: nutrition intervention in thetreatment ofanorexia nervosa, bulimianervosa, and eating disorders not otherwise specified (EDNOS). J Am Diet Assoc 2001;101:810-9. AuthorAffiliation Philip S. Mehler, M.D. AuthorAffiliation From Internal Medicine and Community Health Services, Denver Health, and theUniversity ofColorado Health Sciences Center - both in Denver. Address reprint requests toDr. Mehler at Denver Health, 660 Bannock St., MC1914, Denver, CO 80204, or at pmehler@dhha.org.

Indexing (details)
Cite Subjects Bulimia, Vomiting, Mental depression, Medical treatment, Psychiatry Title Bulimia nervosa Authors Mehler, Philip S Publication title The New England Journal of Medicine Volume 349 Issue 9 Pages 875-881 Publication year 2003 Publication Date Aug 28, 2003 Year 2003 Section Clinical practice Publisher Massachusetts Medical Society Place of Publication Boston Country of publication United States Journal Subjects Medical Sciences ISSN 00284793 CODEN

NEJMAG Source type Scholarly Journals Language of Publication English Document type Commentary Subfile Bulimia, Vomiting, Mental depression, Medical treatment, Psychiatry ProQuest Document ID 223930250 Document URL http://search.proquest.com/docview/223930250?accountid=38885