Eating disorders refer to anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED).1, 2 The Diagnostic and Statistical Manual for Mental Disorders (DSM) lists AN and BN separately, while categorizing BED under eating disorders not otherwise specified (EDNOS).1 Although BED has emerged as a clinically significant eating disorder, its independent classification awaits further investigation before its inclusion in the DSM.1 AN, BN, and BED share many common features, including a distorted sense of body image, fear of weight gain, fear of losing control, and feelings of distress and guilt.1 AN and BN also share common weight control strategies such as fasting, excessive exercise, diuretic use, and purging (self-induced vomiting, laxative use, and enemas).1 AN is distinguished by chronic food restriction and extreme, unhealthy weight loss, while BN and BED are associated with frequent binging and consequent mild to significant weight gain.1 BED can be associated with severe weight gain, either without purging or with occasional purging behavior.1, 3 The etiology of eating disorders is complex and may involve a combination of genetic, biological, behavioral, and psychosocial factors.1, 2 Eating disorders often co-occur with depression, insomnia, social withdrawal, or substance abuse, and they are associated with the subsequent onset of serious medical problems such as osteoporosis, infertility, severe dehydration, heart problems, and even death.1, 2 From approximately 2001 to 2004, lifetime prevalence estimates of eating disorders in the United States ranged from 4.5 percent among adults to 5.1 percent among adolescents.3, 4
Search Strategy and Criteria
An extensive search was conducted for systematic reviews published between January 1, 2000, and June 1, 2012. The search was limited to the online catalog of the U.S. Government’s National Library of Medicine PubMed (http://www.pubmed.gov) to ensure free access to abstracts and in some cases full-text articles. Systematic reviews reported in the context of guidelines, consensus statements, or studies were not the target of the search.
The strategy to conduct the search was as follows: “Eating Disorders”[MeSH] AND (systematic[sb] OR Meta-Analysis[pt]) AND English[lang] AND "Humans"[MeSH Terms] AND "2000/01/01"[PDAT] : "2012/06/01"[PDAT]
Each part of the strategy is described below:
- Topics: The medical subject heading “eating disorders” used in the search is defined by PubMed as “a group of disorders characterized by physiological and psychological disturbances in appetite or food intake.”
- Additional limits: Limits were used restricting the search to systematic reviews (with a separate designation for those containing meta-analyses) and articles published in English, focusing on humans, and published no earlier than 2000. The search was further narrowed by hand to those reviews focused on the efficacy of psychosocial interventions for the prevention or treatment of eating disorders.
The literature search yielded a total of 15 systematic reviews. Of these, nine included a meta-analysis (Reviews 2, 5–7, 9, 11, 12, 14, 15). The average number of studies included in the systematic reviews was 26 (range = 5–66; median = 22) and published between 1985 and 2011. The studies were conducted in the United States and internationally. Although not all studies reported settings, some reported outpatient and inpatient, school, university, primary care, and community-based sites. The goal of the studies was to assess the efficacy of eating disorder prevention programs or the efficacy of interventions for AN, BN, BED, or EDNOS. Intervention efficacy was measured by the incidence of symptomatology associated with AN, BN, and BED and measures of depression, anxiety, and other psychiatric outcomes. Biomarkers associated with changes in weight such as body mass index, weight gain or loss, and resumption of menses were also included as measures of intervention efficacy. Five reviews focused on eating disorder prevention (Reviews 2, 5, 9, 11, 14); three focused only on treatment for AN (Reviews 4, 6, 8 ); one focused only on treatment for BN (Review 13); three focused only on treatment for BED (Reviews 3, 12, 15 ); two focused on treatment for BN, BED, and EDNOS (Reviews 7, 10); and one focused on treatment for AN, BN, BED, and EDNOS (Review 1). Most reviews examined psychosocial interventions, but five looked at pharmacological interventions, either independent of or in combination with other types of treatment (Reviews 1, 4, 10, 12, 15).
Eating Disorder Prevention Programs
Prevention programs targeted adolescents and young adults, specifically females (Reviews 2, 9) in school or university settings. Prevention programs were categorized as universal (the intervention was intended for a community sample of adolescents and young adults), selective (the intervention targeted groups that may have a higher than average risk of developing an eating disorder, such as female athletes, gymnasts, college students, dancers, or indicated (the intervention targeted individuals who display minimal signs of an eating disorder, such as heightened preoccupation about body image). Prevention programs employed cognitive-behavioral, psychoeducational, and stress and coping models. StudentBodies (Reviews 2, 6, 14) was the most evaluated eating disorder prevention program. It shows promising effects in improving knowledge about eating disorders and reducing associated eating disorder behaviors such as negative self-body image and the desire to be thin among female adolescents and young adults. Programs showing the largest effects in reducing risk factors in the prevention of eating disorders tended to be selective interventions, interventions solely offered to females, interventions targeting youth aged 15 and older, those delivered by trained interventionists, and those incorporating body acceptance and dissonance-induction rather than psychoeducational content (Review 14).
Eating Disorder Interventions for AN, BN, and BED
Evidence for the treatment of AN is weak, given that evaluations of educational, psychosocial, and pharmacological interventions provide limited effects on treatment efficacy (Review 4). Some evidence supports the use of cognitive behavioral therapy in reducing relapse risk in adults with AN after weight restoration. Family therapy may help young nonchronic AN patients improve weight gain, but these effects do not transfer to adult patients (Review 6). Family therapy may be better than treatment as usual on rates of remission from AN in the short term; however, there are no significant advantages of family therapy over any other educational or psychosocial intervention on relapse rates, weight measures, cognitive distortions, and attrition rates. There is no strong evidence of pharmacological interventions having a significant impact in the treatment of AN.
Evidence suggests that bulimic symptoms may be reduced by interventions that employ cognitive behavioral approaches or pharmacological treatment (Review 13). Modifications of cognitive behavioral therapy for BN are successful in producing higher rates of abstinence and reducing depression (Review 7). Self-help approaches, dialectical behavioral therapy, and guided imagery showed promising results in reducing bingeing episodes, and interpersonal psychotherapy was effective over the long term for BN symptoms. Pharmacological treatments with fluoxetine produced favorable treatment responses in patients with BN.
Medications such as selective serotonin reuptake inhibitors (SSRIs) reduce target eating, psychiatric, and weight symptoms in patients with BED; however, side effects often lead patients to discontinue treatment (Review 3). Pharmacological treatments have clinical significance for short-term remission from binge eating and weight loss. The impact is greater when it is combined with cognitive behavioral or behavioral weight loss therapy (Review 12). Cognitive behavioral therapy and structured self-help promote abstinence from binge behaviors but do not improve depression symptoms. Weight loss treatment provides the most significant effect in weight reduction among patients with BED.
It is important to focus eating disorder research on the mediators that produce strong treatment effects in prevention and treatment interventions to identify factors resulting in greater gains for at-risk populations and those who are battling these disorders.
Read the PDF for the descriptive information for each of the 15 systematic reviews.
- Review 1: Allen & Dalton, 2011 (PDF, 147KB)
- Review 2: Beitner, Jacobi, & Taylor, 2011 (PDF, 119KB)
- Review 3: Brownley, Berkman, Sedway, Lohr, & Bulik, 2007 (PDF, 125KB)
- Review 4: Bulik, Berkman, Brownley, Sedway, & Lohr, 2007 (PDF, 121KB)
- Review 5: Cororve Fingeret, Warren, Cepeda Benito, & Gleaves, 2006 (PDF, 124KB)
- Review 6: Fisher, Hetrick, & Rushford, 2010 (PDF, 119KB)
- Review 7: Hay, Bacaltchuk, Stefano, & Kashyap, 2009 (PDF, 123KB)
- Review 8: Hay, Bacaltchuk, Byrnes, Claudino, Ekmejian, & Yong, 2003 (PDF, 118KB)
- Review 9: Newton & Ciliska, 2006 (PDF, 117KB)
- Review 10: Perkins, Murphy, Schmidt, & Williams, 2006 (PDF, 123KB)
- Review 11: Pratt & Woolfenden, 2002 (PDF, 125KB)
- Review 12: Reas & Grilo, 2008 (PDF, 116KB)
- Review 13: Shapiro, Berkman, Brownley, Sedway, Lohr, & Bulik, 2007 (PDF, 100KB)
- Review 14: Stice, Shaw, & Marti, 2007 (PDF, 118KB)
- Review 15: Vocks, Tuschen-Caffier, Pietrowsky, Rustenbach, Kersting, & Herpetz, 2010 (PDF, 123KB)
1American Psychiatric Association. (2000). Diagnostic
and statistical manual of mental disorders (DSM-IV-TR). 4th ed., revised.
Arlington, VA: American Psychiatric Association.
2National Institute of Mental Health. (2011). Eating disorders. NIH Publication No. 11-4901. Retrieved from http://www.nimh.nih.gov/health/publications/eating-disorders/complete-index.shtml
3Hudson, J. I., Hiripi, E., Pope, H. G., & Kessler, R. C. (2007). The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biological Psychiatry, 61, 348–358.
3Kessler, R. C., Avenevoli, S., McLaughlin., K. A., Greif Green, J., Lakoma, M. D., Petukhova, . . . Merikangas, K. R. (2012).Lifetime co-morbidity of DSM-IV disorders in the U.S. National Comorbidity Survey Replication Adolescent Supplement (NCS-A). Psychological Medicine, 1 of 14. Cambridge University Press.