Abstract
Introduction
Up to 1% of young women may have bulimia nervosa, characterised by an intense preoccupation with body weight, uncontrolled binge-eating episodes, and use of extreme measures to counteract the feared effects of overeating. People with bulimia nervosa may be of normal weight, making it difficult to diagnose. After 10 years, about half of people with bulimia nervosa will have recovered fully, one third will have made a partial recovery, and 10% to 20% will still have symptoms.
Methods and outcomes
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of treatments for bulimia nervosa in adults? What are the effects of discontinuing treatment in people with bulimia nervosa in remission? We searched: Medline, Embase, The Cochrane Library, and other important databases up to January 2010 (Clinical Evidence reviews are updated periodically, please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
Results
We found 27 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
Conclusions
In this systematic review we present information relating to the effectiveness and safety of the following interventions: cognitive behavioural therapy (CBT; alone or plus exposure/response prevention enhancement), cognitive orientation therapy, dialectical behavioural therapy, discontinuing fluoxetine in people with remission, guided self-help cognitive behavioural therapy, hypnobehavioural therapy, interpersonal psychotherapy, mirtazapine, monoamine oxidase inhibitors (MAOIs), motivational enhancement therapy, pharmacotherapy plus psychotherapy, pure or unguided self-help cognitive behavioural therapy, reboxetine, selective serotonin reuptake inhibitors (SSRIs), topiramate, tricyclic antidepressants (TCAs), and venlafaxine.
Key Points
Up to 1% of young women may have bulimia nervosa, characterised by an intense preoccupation with body weight, uncontrolled binge-eating episodes, and use of extreme measures to counteract the feared effects of overeating.
People with bulimia nervosa may be of normal weight, making it difficult to diagnose.
Obesity has been associated with both an increased risk of bulimia nervosa and a worse prognosis, as have personality disorders and substance misuse.
After 10 years, about half of people with bulimia nervosa will have recovered fully, one third will have made a partial recovery, and 10% to 20% will still have symptoms.
Cognitive behavioural therapy for bulimia nervosa (CBT-BN) may improve clinical problems of bulimia nervosa compared with no treatment, and may be as effective in reducing symptoms as interpersonal psychotherapy at 1 year, or as other psychological treatments, or antidepressants. However, we found no RCTs meeting eligibility criteria comparing the efficacy of interpersonal psychotherapy with waiting list control.
We don't know whether other psychological therapies such as cognitive orientation therapy, hypnobehavioural therapy, dialectical behavioural therapy, or motivational enhancement therapy are more effective than a waiting list control at improving symptoms, as we found only a few trials.
We found insufficient evidence to support enhancing CBT-BN with exposure and response prevention (ERP).
Pure or unguided self-help CBT is likely to be no more effective than waiting list control at reducing binge eating.
The evidence we found for guided self-help CBT is insufficient to judge this intervention because of high attrition in trials.
Some antidepressant drugs (fluoxetine, citalopram, desipramine, and imipramine) may improve symptoms in people with bulimia nervosa compared with placebo.
Monoamine oxidase inhibitors (MAOIs) may increase remission rates compared with placebo, but may not reduce bulimic symptoms or depression scores.
We don't know whether other antidepressants (topiramate, mirtazapine, reboxetine, or venlafaxine) can improve symptoms or remission in people with bulimia nervosa.
We don't know whether continuation of antidepressant treatment may maintain a reduction in vomiting frequency compared with withdrawing treatment in people in remission.
We don't know if combining pharmacotherapy with psychotherapy enhances outcome. Trials that have suggested combinations may enhance outcomes have been limited in power.
About this condition
Definition
Bulimia nervosa is an intense preoccupation with body weight and shape, with regular episodes of uncontrolled overeating (binge eating) associated with extreme measures to counteract the feared effects of the overeating. If a person also meets the diagnostic criteria for anorexia nervosa, then the diagnosis of anorexia nervosa takes precedence. Bulimia nervosa can be difficult to identify because of extreme secrecy about binge eating and purgative behaviour. Weight may be normal, but there is often a history of anorexia nervosa or of restrictive dieting. Some people alternate between anorexia nervosa and bulimia nervosa. Nearly all cases of bulimia nervosa identified in a national community survey featured an additional psychiatric disorder, and common comorbidities were mood, anxiety, impulse control, and substance-misuse disorders. Some RCTs included people with subthreshold bulimia nervosa, or with a related eating disorder, binge-eating disorder. Where possible, only results relevant to bulimia nervosa are reported in this review.
Incidence/ Prevalence
In community-based studies, the prevalence of bulimia nervosa is between 0.5% and 1.0% in young women, with an even social-class distribution. About 90% of people diagnosed with bulimia nervosa are women. The numbers presenting with bulimia nervosa in industrialised countries increased during the decade after its recognition in the late 1970s, although the incidence has plateaued or even fallen since then, with an incidence of new diagnoses at 6.6 per 100,000 in 2000. A "cohort effect", with an increasing incidence, has been reported in community surveys. The prevalence of eating disorders such as bulimia nervosa is lower in non-industrialised populations and varies across ethnic groups. African-American women have a lower rate of restrictive dieting compared with white American women, but they have a similar rate of recurrent binge eating.
Aetiology/ Risk factors
The aetiology of bulimia nervosa is complex, but sociocultural pressures to be thin and the promotion of dieting seem to increase risk. One community-based case-control study compared 102 people with bulimia nervosa versus 204 healthy controls, and found higher rates of obesity, mood disorder, sexual and physical abuse, parental obesity, substance misuse, low self-esteem, perfectionism, disturbed family dynamics, parental weight/shape concern, and early menarche in people with the eating disorder. Heritability is high, ranging from 28% to 83% in one review; although it has been suggested that genotypic variations map onto intermediate phenotypes, such as traits of affective instability and impulsivity, rather than onto a "gross" bulimia nervosa phenotype.
Prognosis
A 10-year follow-up study (50 people with bulimia nervosa from a placebo-controlled trial of mianserin treatment) found that 52% of people receiving placebo had fully recovered, and only 9% continued to experience full symptoms of bulimia nervosa. A larger study (222 people from a trial of antidepressants and structured, intensive group psychotherapy) found that, after a mean follow-up of 11.5 years, 11% still met criteria for bulimia nervosa, whereas 70% were in full or partial remission. Short-term studies found similar results: about 50% of people made a full recovery, 30% made a partial recovery, and 20% continued to be symptomatic. One study (102 women) of the natural course of bulimia nervosa found that 31% continued to have the disorder at 15 months and 15% continued to have the disorder at 5 years. Only 28% received treatment during the follow-up period. A 5-year naturalistic study of 23 people with bulimia nervosa found a 74% remission at 5 years, with a 47% probability of relapse within the 5-year follow-up study in those in remission. There are few consistent predictors of long-term outcome. Good prognosis has been associated with shorter illness duration, a younger age of onset, higher social class, and a family history of alcohol abuse. Poor prognosis has been associated with a history of substance misuse, premorbid and paternal obesity, and, in some studies, a personality disorder. In an evaluation of the response to cognitive behavioural therapy (CBT), outcome was best predicted by early progress (reduction in purging of >70% by session 6). However, a subsequent systematic review of the outcome literature found no consistent evidence to link early intervention with a better prognosis. A systematic review evaluating the cost effectiveness of treatments and prognostic indicators found only 4 consistent pretreatment predictors of poor outcome for treatment of bulimia nervosa: features of borderline personality disorder, concurrent substance misuse, low motivation for change, and a history of obesity. A consistent post-treatment predictor of a better outcome is an early response to treatment. A more recent systematic review (search date 2009, 3 RCTs, 22 retrospective non-controlled studies) also found features of borderline personality disorder to be associated with treatment withdrawal, but this review included studies of eating disorder (not otherwise specified) and anorexia nervosa as well as bulimia nervosa.
Aims of intervention
To reduce symptoms of bulimia nervosa; to improve general psychiatric symptoms; to improve social functioning and quality of life; to minimise the adverse effects of treatment.
Outcomes
Symptom improvement Frequency of binge eating or bingeing, abstinence from binge eating or bingeing, frequency of behaviours to reduce weight and counter the effects of binge eating, severity of extreme weight and shape preoccupation, severity of general psychiatric symptoms, severity of depression, improvement in social and adaptive functioning, remission rates, relapse rates, withdrawal rates, quality of life, and adverse effects.
Methods
Clinical Evidence search and appraisal January 2010. The following databases were used to identify studies for this systematic review: Medline 1966 to January 2010, Embase 1980 to January 2010, and The Cochrane Database of Systematic Reviews 2009, Issue 4 (1966 to date of issue). An additional search within The Cochrane Library was carried out for the Database of Abstracts of Reviews of Effects (DARE) and Health Technology Assessment (HTA). We also searched for retractions of studies included in the review. Abstracts of the studies retrieved from the initial search were assessed by an information specialist. Selected studies were then sent to the contributor for additional assessment, using predetermined criteria to identify relevant studies. Study design criteria for inclusion in this review were: published systematic reviews and RCTs in any language containing >20 individuals of whom >80% were followed up. There was no minimum length of follow-up required to include studies. We included studies described as "open", "open label", or not blinded. We included systematic reviews of RCTs and RCTs where harms of an included intervention were studied applying the same study design criteria for inclusion as we did for benefits. We also searched for systematic reviews and RCTs on the harms of topiramate for eating disorders. In addition, we use a regular surveillance protocol to capture harms alerts from organisations such as the FDA and the MHRA, which are added to the reviews as required. To aid readability of the numerical data in our reviews, we round many percentages to the nearest whole number. Readers should be aware of this when relating percentages to summary statistics such as relative risks (RRs) and odds ratios (ORs). We have performed a GRADE evaluation of the quality of evidence for interventions included in this review (see table). The categorisation of the quality of the evidence (high, moderate, low, or very low) reflects the quality of evidence available for our chosen outcomes in our defined populations of interest. These categorisations are not necessarily a reflection of the overall methodological quality of any individual study, because the Clinical Evidence population and outcome of choice may represent only a small subset of the total outcomes reported, and population included, in any individual trial. For further details of how we perform the GRADE evaluation and the scoring system we use, please see our website (www.clinicalevidence.com).
Table.
GRADE Evaluation of interventions for Bulimia nervosa.
| Important outcomes | Quality of life, Symptom improvement | ||||||||
| Studies (Participants) | Outcome | Comparison | Type of evidence | Quality | Consistency | Directness | Effect size | GRADE | Comment |
| What are the effects of treatments for bulimia nervosa in adults? | |||||||||
| 1 (<77) | Symptom improvement | CBT for bulimia nervosa (CBT-BN) versus waiting list control, no treatment, or placebo | 4 | –3 | 0 | 0 | 0 | Very low | Quality points deducted for sparse data, no intention-to-treat analysis, and incomplete reporting of results |
| 1 (<77) | Symptom improvement | CBT plus exposure/response prevention therapy (CBT-ERP) versus waiting list control | 4 | –3 | 0 | 0 | 0 | Very low | Quality points deducted for sparse data, no intention-to-treat analysis, and incomplete reporting of results |
| 1 (39) | Symptom improvement | CBT-ERP versus CBT-BN | 4 | –3 | 0 | 0 | 0 | Very low | Quality points deducted for sparse data, no intention-to-treat analysis, and incomplete reporting of results |
| 2 (101) | Symptom improvement | Pure or unguided self-help CBT versus waiting list, no treatment, or placebo medication | 4 | –2 | 0 | –1 | 0 | Very low | Quality points deducted for sparse data and baseline differences in purging between groups. Directness point deducted for inclusion of co-intervention (contact with health professionals) |
| 1 (48) | Symptom improvement | Pure or unguided self-help CBT versus fluoxetine | 4 | –1 | 0 | –1 | 0 | Low | Quality point deducted for sparse data. Directness point deducted for inclusion of co-intervention (contact with health professionals) |
| 2 (143) | Symptom improvement | Guided self-help CBT versus CBT for bulimia nervosa (CBT-BN) | 4 | –2 | 0 | 0 | 0 | Low | Quality points deducted for sparse data and incomplete reporting of results |
| 2 (295) | Symptom improvement | IPT versus CBT for bulimia nervosa (CBT-BN) | 4 | –1 | –1 | 0 | 0 | Low | Quality point deducted for incomplete reporting of results. Consistency point deducted for different results for different outcomes |
| 1 (<78) | Symptom improvement | Hypnobehavioural therapy (HBT) versus no treatment, placebo, or waiting list | 4 | –3 | 0 | 0 | 0 | Very low | Quality points deducted for sparse data, incomplete reporting of results, and significant differences between groups at baseline |
| 1 (<78) | Symptom improvement | HBT versus CBT for bulimia nervosa (CBT-BN) | 4 | –3 | 0 | 0 | 0 | Very low | Quality points deducted for sparse data, unbalanced groups at baseline, and incomplete reporting of results |
| 1 (31) | Symptom improvement | Dialectical behavioural therapy versus placebo, no treatment, or waiting list | 4 | –3 | 0 | 0 | 0 | Very low | Quality points deducted for sparse data, incomplete reporting of results, and unclear measurement of outcomes |
| 1 (68) | Symptom improvement | Motivational enhancement therapy versus CBT for bulimia nervosa (CBT-BN) | 4 | –3 | 0 | 0 | 0 | Very low | Quality points deducted for sparse data, short-term follow-up, and no intention-to-treat analysis |
| at least 5 (at least 706) | Symptom improvement | SSRIs versus placebo or no treatment | 4 | –2 | 0 | 0 | 0 | Low | Quality points deducted for incomplete reporting of results and for different results for different outcomes |
| 2 (<111) | Symptom improvement | SSRIs versus CBT for bulimia nervosa (CBT-BN) | 4 | –3 | 0 | 0 | 0 | Very low | Quality points deducted for sparse data, incomplete reporting of results, and no intention-to-treat analysis |
| 4 (156) | Symptom improvement | Monoamine oxidase inhibitors (MAOIs) versus placebo or no treatment | 4 | –2 | –1 | 0 | 0 | Very low | Quality points deducted for sparse data and incomplete reporting of results. Consistency point deducted for different results for different outcomes |
| 3 (132) | Symptom improvement | Tricyclic antidepressants (TCAs) versus placebo | 4 | –2 | –1 | 0 | 0 | Very low | Quality points deducted for sparse data and incomplete reporting of results. Consistency point deducted for different results for different outcomes |
| 2 (<211) | Symptom improvement | TCAs versus CBT for bulimia nervosa (CBT-BN) | 4 | –1 | –1 | –1 | 0 | Very low | Quality point deducted for incomplete reporting of results. Consistency point deducted for conflicting results. Directness point deducted for different regimens between studies |
| 1 (60) | Symptom improvement | Topiramate versus placebo | 4 | –2 | 0 | –1 | 0 | Very low | Quality points deducted for sparse data and short-term follow-up. Directness point deducted for composite outcome |
| 1 (60) | Quality of life | Topiramate versus placebo | 4 | –3 | 0 | 0 | 0 | Very low | Quality points deducted for sparse data, short-term follow-up, and incomplete reporting of results |
| 2 (<242) | Symptom improvement | CBT for bulimia nervosa (CBT-BN) plus tricyclic antidepressants (TCAs) versus TCAs alone | 4 | –2 | 0 | –1 | 0 | Very low | Quality points deducted for incomplete reporting and no statistical test between groups. Directness point deducted for conflicting results |
| 2 (<242) | Symptom improvement | CBT-BN plus TCAs versus CBT-BN alone | 4 | –1 | 0 | 0 | 0 | Moderate | Quality point deducted for incomplete reporting of results |
| 1 (<76) | Symptom improvement | CBT-BN plus fluoxetine versus fluoxetine alone | 4 | –2 | 0 | 0 | 0 | Low | Quality points deducted for sparse data and incomplete reporting of results |
| 1 (<76) | Symptom improvement | CBT-BN plus fluoxetine versus CBT-BN alone | 4 | –2 | 0 | 0 | 0 | Low | Quality points deducted for sparse data and incomplete reporting of results |
| 1 (47) | Symptom improvement | Pure self-help CBT plus fluoxetine versus fluoxetine alone | 4 | –1 | 0 | –1 | 0 | Low | Quality point deducted for sparse data. Directness point deducted for inclusion of co-intervention (contact with health professionals) |
| 1 (43) | Symptom improvement | Pure self-help CBT plus fluoxetine versus self-help CBT alone | 4 | –3 | 0 | 0 | 0 | Very low | Quality points deducted for sparse data, incomplete reporting of results, and inclusion of co-intervention (contact with health professionals) |
We initially allocate 4 points to evidence from RCTs, and 2 points to evidence from observational studies. To attain the final GRADE score for a given comparison, points are deducted or added from this initial score based on preset criteria relating to the categories of quality, directness, consistency, and effect size. Quality: based on issues affecting methodological rigour (e.g., incomplete reporting of results, quasi-randomisation, sparse data [<200 people in the analysis]). Consistency: based on similarity of results across studies. Directness: based on generalisability of population or outcomes. Effect size: based on magnitude of effect as measured by statistics such as relative risk, odds ratio, or hazard ratio.
Glossary
- Beck Depression Inventory
A 21-item ordinal scale of symptoms of depression. Scores less than 10 are normal or minimal depression: 10–18 indicates mild to moderate depression, 19–29 indicates moderate to severe depression, and greater than 30 indicates severe depression. A short version has 13 items; scores above 4 indicate increasing levels of depression.
- Beck Depression Inventory
Standardised scale to assess depression. This instrument consists of 21 items to assess the intensity of depression. Each item is a list of 4 statements (rated 0, 1, 2, or 3), arranged in increasing severity, about a particular symptom of depression. The range of scores possible are 0 = least severe depression to 63 = most severe depression. It is recommended for people aged 13 to 80 years. Scores of more than 12 or 13 indicate the presence of depression.
- Binge eating
Modified from DSM-IV. Eating, in a discrete period (e.g., hours), a large amount of food, accompanied by a lack of control over eating during the episode.
- Bulimia nervosa
The DSM-IV criteria include recurrent episodes of binge eating; recurrent inappropriate compensatory behaviour to prevent weight gain; frequency of binge eating and inappropriate compensatory behaviour, with both occurring, on average, at least twice a week for 3 months; self-evaluation unduly influenced by body shape and weight; and disturbance occurring not exclusively during episodes of anorexia nervosa. Types of bulimia nervosa, modified from DSM-IV, are purging (using self-induced vomiting, laxatives, diuretics, or enemas) and non-purging (fasting, exercise, but not vomiting or other abuse as for the purging type). However, many studies evaluate efficacy for samples that may include people with subthreshold bulimia nervosa or binge eating disorder. Where possible, only data for bulimia nervosa participants are reported in this review.
- Cognitive behavioural therapy
A specific form of cognitive behavioural therapy (CBT) has been developed for bulimia nervosa (CBT-BN), which uses three overlapping phases for 19 sessions over 20 weeks. Phase one aims to educate the person about bulimia nervosa. People are helped to increase the regularity of eating and resist the urge to binge or purge. Phase two introduces procedures to reduce dietary restraint (e.g., broadening food choices). In addition, cognitive procedures supplemented by behavioural experiments are used to identify and correct dysfunctional attitudes, beliefs, and avoidance behaviours. Phase three is the maintenance phase. Relapse-prevention strategies are used to prepare for possible future setbacks. Although many studies have used variants of CBT for bulimia nervosa, for the purposes of this review only those that resemble CBT-BN are cited unless otherwise specified. In this review, CBT-BN refers to all treatments that closely resemble CBT-BN.
- Cognitive orientation therapy
The cognitive orientation theory aims to generate a systematic procedure for exploring the meaning of a behaviour around themes, such as avoiding certain emotions. Therapy for modifying behaviour focuses on systematically changing beliefs related to themes, rather than beliefs referring directly to eating behaviour. No attempt is made to persuade the people that their beliefs are incorrect or maladaptive.
- Dialectical behavioural therapy
A type of behavioural therapy that views emotional dysregulation as the core problem in bulimia nervosa, with binge eating and purging understood as attempts to influence, change, or control painful emotional states. People are taught a repertoire of skills to replace dysfunctional behaviours.
- Exposure therapy
In bulimia nervosa, this is a modification of the exposure and response prevention therapy developed for obsessive compulsive disorder. It involves, for example, exposure to food, and then psychological prevention strategies to control weight behaviour, such as vomiting after eating, until the urge or compulsion to vomit has receded.
- Guided self-help cognitive behavioural therapy
A modified form of cognitive behavioural therapy, in which a treatment manual is provided with support, usually from a non-professional or professional without specialist expertise in eating disorders. A good discussion of the development and types of self-help can be found in Williams (2003).
- Hypnobehavioural psychotherapy
Therapy that uses a combination of behavioural techniques, such as self-monitoring, to change maladaptive eating disorders, and hypnotic techniques to reinforce and encourage behaviour change.
- Interpersonal psychotherapy (IPT)
In bulimia nervosa, this is a three-phase treatment. Phase one analyses in detail the interpersonal context of the eating disorder. This leads to the formulation of an interpersonal problem area, which forms the focus of the second stage; this is aimed at helping the person to make interpersonal changes. Phase three is devoted to the person's progress and an exploration of ways to handle future interpersonal difficulties. At no stage is attention paid to eating habits or body attitudes.
- Low-quality evidence
Further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate.
- Moderate-quality evidence
Further research is likely to have an important impact on our confidence in the estimate of effect and may change the estimate.
- Remission
Sustained abstinence (longer than 1 month) from binge eating.
- Short-Form Health Survey-36 items (SF-36)
A scale that assesses health-related quality of life across eight domains: limitations in physical activities (physical component), limitations in social activities, limitations in usual role activities due to physical problems, pain, psychological distress and wellbeing (mental health component), limitations in usual role activities because of emotional problems, energy and fatigue, and general health perceptions.
- Very low-quality evidence
Any estimate of effect is very uncertain.
Disclaimer
The information contained in this publication is intended for medical professionals. Categories presented in Clinical Evidence indicate a judgement about the strength of the evidence available to our contributors prior to publication and the relevant importance of benefit and harms. We rely on our contributors to confirm the accuracy of the information presented and to adhere to describe accepted practices. Readers should be aware that professionals in the field may have different opinions. Because of this and regular advances in medical research we strongly recommend that readers' independently verify specified treatments and drugs including manufacturers' guidance. Also, the categories do not indicate whether a particular treatment is generally appropriate or whether it is suitable for a particular individual. Ultimately it is the readers' responsibility to make their own professional judgements, so to appropriately advise and treat their patients. To the fullest extent permitted by law, BMJ Publishing Group Limited and its editors are not responsible for any losses, injury or damage caused to any person or property (including under contract, by negligence, products liability or otherwise) whether they be direct or indirect, special, incidental or consequential, resulting from the application of the information in this publication.
Contributor Information
Phillipa J Hay, School of Medicine, Campbelltown Campus, Western Sydney University, Sydney, Australia.
Angélica Medeiros Claudino, Federal University of Sao Paulo, Sao Paulo, Brazil.
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