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When ‘eating healthy’ becomes disordered, you can return patients to genuine health
Orthorexia nervosa, from the Greek orthos (straight, proper) and orexia (appetite), is a disorder in which a person demonstrates a pathological obsession not with weight loss but with a “pure” or healthy diet, which can contribute to significant dietary restriction and food-related obsessions. Although the disorder is not a formal diagnosis in DSM 5,1 it is increasingly reported on college campuses and in medical practices, and has been the focus of media attention.
How common is orthorexia?
The precise prevalence of orthorexia nervosa is unknown; some authors have reported estimates as high as 21% of the general population2 and 43.6% of medical students.3 The higher prevalence among medical students might be attributable to the increased focus on factors that can contribute to illnesses (eg, food and diet), and thus underscores the importance of screening for orthorexia symptoms among this population.
How do you identify the disorder?
Orthorexia nervosa was first described by Bratman,4 who observed that a subset of his eating disorder patients were overly obsessed with maintaining an extreme “healthy diet.” Although diagnostic criteria for orthorexia nervosa have not been established, Bratman proposed the following as symptoms indicative of the disorder:
- spending >3 hours a day thinking about a healthy diet
- worrying more about the perceived nutritional quality or “purity” of one’s food than the pleasure of eating it
- feeling guilty about straying from dietary beliefs
- having eating habits that isolate the affected person from others.
Given the focus on this disorder in the media and its presence in medical practice, it is important that you become familiar with the symptoms associated with orthorexia nervosa so you can provide necessary treatment. A patient’s answers to the following questions will aid the savvy clinician in identifying symptoms that suggest orthorexia nervosa5:
- Do you turn to healthy food as a primary source of happiness and meaning, even more so than spirituality?
- Does your diet make you feel superior to other people?
- Does your diet interfere with your personal relationships (family, friends), or with your work?
- Do you use pure foods as a “sword and shield” to ward off anxiety, not just about health problems but about everything that makes you feel insecure?
- Do foods help you feel in control more than really makes sense?
- Do you have to carry your diet to further and further extremes to provide the same “kick”?
- If you stray even minimally from your chosen diet, do you feel a compulsive need to cleanse?
- Has your interest in healthy food expanded past reasonable boundaries to become a kind of brain parasite, so to speak, controlling your life rather than furthering your goals?
No single item is indicative of orthorexia nervosa; however, this list represents a potential clinical picture of how the disorder presents.
Overlap with anorexia nervosa. Although overlap in symptom presentation between these 2 disorders can be significant (eg, diet rigidity can lead to malnutrition, even death), each has important distinguishing features. A low weight status or significant weight loss, or both, is a hallmark characteristic of anorexia nervosa; however, weight loss is not the primary goal in orthorexia nervosa (although extreme dietary restriction in orthorexia could contribute to weight loss). Additionally, a person with anorexia nervosa tends to be preoccupied with weight or shape; a person with orthorexia nervosa is obsessed with food quality and purity. Finally, people with orthorexia have an obsessive preoccupation with health, whereas those with anorexia are more consumed with a fear of fat or weight gain.
Multimodal treatment is indicated
Treating orthorexia typically includes a combination of interventions common to other eating disorders. These include cognitive-behavioral therapy, dietary and nutritional counseling, and medical management of any physical sequelae that result from extreme dietary restriction and malnutrition. Refer patients in whom you suspect orthorexia nervosa to a trained therapist and a dietician who have expertise in managing eating disorders.
It is encouraging to note that, with careful diagnosis and appropriate treatment, recovery from orthorexia is possible,6 and patients can achieve an improved quality of life.
1. Diagnostic and statistical manual of mental disorders. 5th ed. Washington, DC: American Psychiatric Association; 2013.
2. Ramacciotti CE, Perrone P, Coli E, et al. Orthorexia nervosa in the general population: a preliminary screening using a self-administered questionnaire (ORTO-15). Eat Weight Disord. 2011;16(2):e127-e130.
3. Fidan T, Ertekin V, Isikay S, et al. Prevalence of orthorexia among medical students in Erzurum, Turkey. Compr Psychiatry. 2010;51(1):49-54.
4. Bratman S, Knight D. Health food junkies: orthorexia nervosa: overcoming the obsession with healthful eating. New York, NY: Broadway Books; 2000.
5. Bratman S. What is orthorexia? http://www.orthorexia.com. Published January 23, 2014. Accessed March 3, 2016.
6. Fairburn CG, Bohn K. Eating disorder NOS (EDNOS): an example of the troublesome “not otherwise specified” (NOS) category in DSM-IV. Behav Res Ther. 2005;43(6):691-702.
Orthorexia nervosa, from the Greek orthos (straight, proper) and orexia (appetite), is a disorder in which a person demonstrates a pathological obsession not with weight loss but with a “pure” or healthy diet, which can contribute to significant dietary restriction and food-related obsessions. Although the disorder is not a formal diagnosis in DSM 5,1 it is increasingly reported on college campuses and in medical practices, and has been the focus of media attention.
How common is orthorexia?
The precise prevalence of orthorexia nervosa is unknown; some authors have reported estimates as high as 21% of the general population2 and 43.6% of medical students.3 The higher prevalence among medical students might be attributable to the increased focus on factors that can contribute to illnesses (eg, food and diet), and thus underscores the importance of screening for orthorexia symptoms among this population.
How do you identify the disorder?
Orthorexia nervosa was first described by Bratman,4 who observed that a subset of his eating disorder patients were overly obsessed with maintaining an extreme “healthy diet.” Although diagnostic criteria for orthorexia nervosa have not been established, Bratman proposed the following as symptoms indicative of the disorder:
- spending >3 hours a day thinking about a healthy diet
- worrying more about the perceived nutritional quality or “purity” of one’s food than the pleasure of eating it
- feeling guilty about straying from dietary beliefs
- having eating habits that isolate the affected person from others.
Given the focus on this disorder in the media and its presence in medical practice, it is important that you become familiar with the symptoms associated with orthorexia nervosa so you can provide necessary treatment. A patient’s answers to the following questions will aid the savvy clinician in identifying symptoms that suggest orthorexia nervosa5:
- Do you turn to healthy food as a primary source of happiness and meaning, even more so than spirituality?
- Does your diet make you feel superior to other people?
- Does your diet interfere with your personal relationships (family, friends), or with your work?
- Do you use pure foods as a “sword and shield” to ward off anxiety, not just about health problems but about everything that makes you feel insecure?
- Do foods help you feel in control more than really makes sense?
- Do you have to carry your diet to further and further extremes to provide the same “kick”?
- If you stray even minimally from your chosen diet, do you feel a compulsive need to cleanse?
- Has your interest in healthy food expanded past reasonable boundaries to become a kind of brain parasite, so to speak, controlling your life rather than furthering your goals?
No single item is indicative of orthorexia nervosa; however, this list represents a potential clinical picture of how the disorder presents.
Overlap with anorexia nervosa. Although overlap in symptom presentation between these 2 disorders can be significant (eg, diet rigidity can lead to malnutrition, even death), each has important distinguishing features. A low weight status or significant weight loss, or both, is a hallmark characteristic of anorexia nervosa; however, weight loss is not the primary goal in orthorexia nervosa (although extreme dietary restriction in orthorexia could contribute to weight loss). Additionally, a person with anorexia nervosa tends to be preoccupied with weight or shape; a person with orthorexia nervosa is obsessed with food quality and purity. Finally, people with orthorexia have an obsessive preoccupation with health, whereas those with anorexia are more consumed with a fear of fat or weight gain.
Multimodal treatment is indicated
Treating orthorexia typically includes a combination of interventions common to other eating disorders. These include cognitive-behavioral therapy, dietary and nutritional counseling, and medical management of any physical sequelae that result from extreme dietary restriction and malnutrition. Refer patients in whom you suspect orthorexia nervosa to a trained therapist and a dietician who have expertise in managing eating disorders.
It is encouraging to note that, with careful diagnosis and appropriate treatment, recovery from orthorexia is possible,6 and patients can achieve an improved quality of life.
Orthorexia nervosa, from the Greek orthos (straight, proper) and orexia (appetite), is a disorder in which a person demonstrates a pathological obsession not with weight loss but with a “pure” or healthy diet, which can contribute to significant dietary restriction and food-related obsessions. Although the disorder is not a formal diagnosis in DSM 5,1 it is increasingly reported on college campuses and in medical practices, and has been the focus of media attention.
How common is orthorexia?
The precise prevalence of orthorexia nervosa is unknown; some authors have reported estimates as high as 21% of the general population2 and 43.6% of medical students.3 The higher prevalence among medical students might be attributable to the increased focus on factors that can contribute to illnesses (eg, food and diet), and thus underscores the importance of screening for orthorexia symptoms among this population.
How do you identify the disorder?
Orthorexia nervosa was first described by Bratman,4 who observed that a subset of his eating disorder patients were overly obsessed with maintaining an extreme “healthy diet.” Although diagnostic criteria for orthorexia nervosa have not been established, Bratman proposed the following as symptoms indicative of the disorder:
- spending >3 hours a day thinking about a healthy diet
- worrying more about the perceived nutritional quality or “purity” of one’s food than the pleasure of eating it
- feeling guilty about straying from dietary beliefs
- having eating habits that isolate the affected person from others.
Given the focus on this disorder in the media and its presence in medical practice, it is important that you become familiar with the symptoms associated with orthorexia nervosa so you can provide necessary treatment. A patient’s answers to the following questions will aid the savvy clinician in identifying symptoms that suggest orthorexia nervosa5:
- Do you turn to healthy food as a primary source of happiness and meaning, even more so than spirituality?
- Does your diet make you feel superior to other people?
- Does your diet interfere with your personal relationships (family, friends), or with your work?
- Do you use pure foods as a “sword and shield” to ward off anxiety, not just about health problems but about everything that makes you feel insecure?
- Do foods help you feel in control more than really makes sense?
- Do you have to carry your diet to further and further extremes to provide the same “kick”?
- If you stray even minimally from your chosen diet, do you feel a compulsive need to cleanse?
- Has your interest in healthy food expanded past reasonable boundaries to become a kind of brain parasite, so to speak, controlling your life rather than furthering your goals?
No single item is indicative of orthorexia nervosa; however, this list represents a potential clinical picture of how the disorder presents.
Overlap with anorexia nervosa. Although overlap in symptom presentation between these 2 disorders can be significant (eg, diet rigidity can lead to malnutrition, even death), each has important distinguishing features. A low weight status or significant weight loss, or both, is a hallmark characteristic of anorexia nervosa; however, weight loss is not the primary goal in orthorexia nervosa (although extreme dietary restriction in orthorexia could contribute to weight loss). Additionally, a person with anorexia nervosa tends to be preoccupied with weight or shape; a person with orthorexia nervosa is obsessed with food quality and purity. Finally, people with orthorexia have an obsessive preoccupation with health, whereas those with anorexia are more consumed with a fear of fat or weight gain.
Multimodal treatment is indicated
Treating orthorexia typically includes a combination of interventions common to other eating disorders. These include cognitive-behavioral therapy, dietary and nutritional counseling, and medical management of any physical sequelae that result from extreme dietary restriction and malnutrition. Refer patients in whom you suspect orthorexia nervosa to a trained therapist and a dietician who have expertise in managing eating disorders.
It is encouraging to note that, with careful diagnosis and appropriate treatment, recovery from orthorexia is possible,6 and patients can achieve an improved quality of life.
1. Diagnostic and statistical manual of mental disorders. 5th ed. Washington, DC: American Psychiatric Association; 2013.
2. Ramacciotti CE, Perrone P, Coli E, et al. Orthorexia nervosa in the general population: a preliminary screening using a self-administered questionnaire (ORTO-15). Eat Weight Disord. 2011;16(2):e127-e130.
3. Fidan T, Ertekin V, Isikay S, et al. Prevalence of orthorexia among medical students in Erzurum, Turkey. Compr Psychiatry. 2010;51(1):49-54.
4. Bratman S, Knight D. Health food junkies: orthorexia nervosa: overcoming the obsession with healthful eating. New York, NY: Broadway Books; 2000.
5. Bratman S. What is orthorexia? http://www.orthorexia.com. Published January 23, 2014. Accessed March 3, 2016.
6. Fairburn CG, Bohn K. Eating disorder NOS (EDNOS): an example of the troublesome “not otherwise specified” (NOS) category in DSM-IV. Behav Res Ther. 2005;43(6):691-702.
1. Diagnostic and statistical manual of mental disorders. 5th ed. Washington, DC: American Psychiatric Association; 2013.
2. Ramacciotti CE, Perrone P, Coli E, et al. Orthorexia nervosa in the general population: a preliminary screening using a self-administered questionnaire (ORTO-15). Eat Weight Disord. 2011;16(2):e127-e130.
3. Fidan T, Ertekin V, Isikay S, et al. Prevalence of orthorexia among medical students in Erzurum, Turkey. Compr Psychiatry. 2010;51(1):49-54.
4. Bratman S, Knight D. Health food junkies: orthorexia nervosa: overcoming the obsession with healthful eating. New York, NY: Broadway Books; 2000.
5. Bratman S. What is orthorexia? http://www.orthorexia.com. Published January 23, 2014. Accessed March 3, 2016.
6. Fairburn CG, Bohn K. Eating disorder NOS (EDNOS): an example of the troublesome “not otherwise specified” (NOS) category in DSM-IV. Behav Res Ther. 2005;43(6):691-702.
Binge eating disorder: Evidence-based treatments
Binge eating is consumption of an unusually large amount of food coupled with a feeling of loss of control over eating. Binge eating disorder (BED) is characterized by recurrent episodes of binge eating without inappropriate compensatory behaviors (eg, self-induced vomiting, misuse of laxatives, diuretics, or other agents, excessive exercise).1 It is the most common eating disorder in the United States, with a lifetime prevalence of approximately 3.5% in women and 2% in men.2 The diagnosis falls within the DSM-IV-TR category of eating disorders not otherwise specified,1 but clinicians often view it as a distinct clinical phenomenon. In DSM-IV-TR, an individual would meet criteria for BED if he or she engages in regular binge eating behavior in the absence of recurrent compensatory behaviors ≥2 days per week over 6 months.1 Proposed changes for DSM-5 recognize a distinct BED diagnosis, reduce the frequency criterion to once per week and the duration criterion to the past 3 months, and shift the focus from binge days to binge episodes (Table 1).3
Table 1
Proposed DSM-5 criteria for binge eating disorder
|
Source:Reference 3 |
BED can occur in individuals of all body mass indices (BMI), but is common among individuals who are overweight or obese as well as those with depression or type 2 diabetes; BED can complicate treatment of these conditions.2,4,5 Primary treatment goals are:
- abstinence from binge eating
- improved psychological functioning
- appropriate weight regulation in overweight patients.
We report on 3 approaches to BED treatment: medication only, behavioral intervention only, and medication plus behavioral intervention. This article provides insights about emerging changes in diagnostic criteria for BED as well as evidence-informed treatment options and recommendations.
The evidence base
We conducted a review of 23 BED studies: 7 medication only, 5 medication plus behavioral, and 11 behavioral only. We focused on studies conducted since September 2005 that included binge frequency, weight, and depression as primary outcomes (see Berkman et al6 for a review of BED treatment studies before 2005). The studies included 2,527 participants (2,216 women and 311 men). Although the sex distribution of BED in the general population tends to slightly favor women,2 the proportion of women presenting for treatment generally is considerably higher than that of men. In studies that reported on race and/or ethnicity, 1,639 participants were identified as white, 191 as African American, 25 as Hispanic, 2 as Asian, 1 as Native American, and 25 as “other.” Ages ranged from 18 to 77.
Several medications are effective
In placebo-controlled studies, a high-dose selective serotonin reuptake inhibitor (escitalopram7), 2 anticonvulsants (zonisamide8 and topiramate9), a selective norepinephrine reuptake inhibitor (atomoxetine10), and an appetite suppressant (sibutramine11) were associated with significant decreases in binge eating frequency, weight, and BMI in overweight/obese patients diagnosed with BED (Table 2). In an open-label trial, memantine—a N-methyl-D-aspartate receptor antagonist often used to treat symptoms of Alzheimer’s disease—was associated with a significant reduction in binge eating but no change in weight.12 Lamotrigine was not significantly different from placebo in reducing binge eating or weight, but showed promise in reducing metabolic parameters such as glucose and triglyceride levels commonly associated with obesity and type 2 diabetes.13 Because BED often is comorbid with obesity and type 2 diabetes, lamotrigine augmentation when treating obese individuals with BED warrants further investigation. As with any pharmacologic agent, carefully consider potential side effects and interactions with other drugs before prescribing medications for BED. Informing patients of potential side effects is crucial for patient safety and accuracy of the data collected in well-controlled treatment studies.
Table 2
Pharmacotherapy for binge eating disorder
Study | Drug/dosage | Comments |
---|---|---|
Guerdjikova et al, 20087 | Escitalopram, 10 to 30 mg/d, vs placebo for 12 weeks | Escitalopram was significantly better than placebo in reducing weight, BMI, and illness severity |
McElroy et al, 20068 | Zonisamide, 100 to 600 mg/d, vs placebo for 16 weeks | Zonisamide was significantly better than placebo in reducing BE, weight, BMI, and various aspects of unhealthy eating behavior |
McElroy et al, 20079 | Topiramate, 25 to 400 mg/d, vs placebo for 16 weeks | Topiramate was significantly better than placebo in reducing BE, weight, BMI, and related psychological features of BE |
McElroy et al, 200710 | Atomoxetine, 40 to 120 mg/d, vs placebo for 10 weeks | Atomoxetine was significantly better than placebo in reducing BE, weight, BMI, and obsessive-compulsive features of BE, and in achieving remission |
Wilfley et al, 200811 | Sibutramine, 15 mg/d, vs placebo for 24 weeks | Sibutramine was significantly better than placebo in reducing BE, weight, BMI, and related psychological features of BE |
Brennan et al, 200812 | Open-label memantine, 5 to 20 mg/d, for 12 weeks | Memantine was associated with decreased binge frequency and related psychological features of BE |
Guerdjikova et al, 200913 | Lamotrigine, 50 to 400 mg/d, vs placebo for 16 weeks | Lamotrigine was not significantly different from placebo |
BE: binge eating; BMI: body mass index |
CBT vs other behavioral approaches
Cognitive-behavioral therapy (CBT), which focuses on identifying and modifying unhealthy thoughts that maintain disordered eating behaviors, is the most widely studied behavioral intervention for BED. Other studied treatments include interpersonal psychotherapy (IPT), motivational interviewing (MI), and structured behavioral weight loss (BWL) (Table 3).14-24 IPT is a psychodynamically based, time-limited treatment that focuses on the interpersonal context of the disorder and on building interpersonal skills. MI emphasizes exploring and resolving ambivalence about treatment, and works to facilitate change through motivational processes. BWL is centered on making dietary and physical activity changes to achieve weight loss. Behavioral treatments have been delivered in various formats, such as an individual or group setting, by electronic interface, and via self-help approaches. Most studies compared active treatment to a control group, but some compared active treatments head-to-head.
Table 3
CBT and other behavioral interventions for BED
Study | Intervention | Comments |
---|---|---|
Annunziato et al, 200914 | 2 groups received CBT and hypocaloric diet for 8 weeks followed by 14 weeks of enhanced nutritional program (ie, reduced consumption of high energy density foods and once-daily liquid meal replacement) or control (normal diet) | Enhanced nutritional program was not significantly different from the control in reducing weight, BE, or psychological features of BE; variability in adherence to the enhanced nutritional program was identified as a significant effect modifier |
Ashton et al, 200915 | 4 sessions of group CBT in an open trial | CBT was associated with significant reductions in BE and psychological features of BE in post-bariatric surgery patients |
Dingemans et al, 200716 | CBT vs wait-list control | CBT significantly better than the wait-list control in reducing BE and psychological features of BE, and in achieving abstinence from BE |
Friederich et al, 200717 | 15-session CBT blended with elements of interpersonal therapy (IPT), nutritional counseling, and supervised walking program; no control group | Treatment significantly reduced weight, BE, and related psychological features of BE in patients meeting sub-threshold and full criteria for BED |
Grilo et al, 200518 | Guided self-help CBT (CBTgsh) vs guided self-help behavioral weight loss (BWLgsh) vs non-specific attention control for 12 weeks | CBTgsh significantly better than BWLgsh and control in BE remission; CBTgsh significantly better than BWLgsh, which was significantly better than control in reducing cognitive restraint; CBTgsh significantly better than control in reducing depression and eating-related psychopathology; no differences between groups in BMI change |
Ricca et al, 201019 | Individual (I-CBT) vs group CBT (G-CBT) for 24 weeks in patients meeting subthreshold and full criteria for BED | BE and BMI were significantly reduced in both groups at 24 weeks and 3-year follow-up. I-CBT was not better than G-CBT in reducing BE or weight at 24 weeks or 3-year follow-up; I-CBT was significantly better than G-CBT in reducing eating-related psychopathology at 24 weeks and 3-year follow-up; I-CBT was significantly better than G-CBT in recovery (ie, no longer meeting full BED criteria) at 24 weeks but not at 3-year follow-up |
Schlup et al, 200920 | 8 weekly sessions of group CBT vs wait-list control | CBT was significantly better than wait-list control in reducing BE and eating concerns and in achieving abstinence at end of treatment; CBT was not different than control in reducing BMI; treatment-related reductions in BE and eating concerns were maintained at 12-month follow-up |
Shapiro et al, 200721 | 10 weekly sessions of group CBT (G-CBT) vs CD-ROM delivered CBT (CD-CBT) vs wait-list control | G-CBT and CD-CBT were not different from each other but both were significantly better than wait-list control in reducing BE |
Tasca et al, 200622 | Group CBT (G-CBT) vs group psychodynamic interpersonal therapy (G-IPT) vs wait-list control for 16 weeks | G-CBT and G-IPT were not different from each other; G-CBT and G-IPT were significantly better than wait list in reducing BE and interpersonal problems (but not BMI) and increasing cognitive restraint post-treatment; depression was reduced in both groups at 6 months but only in G-IPT at 12 months; reductions in BE maintained at 12 months |
Wilson et al, 201023 | 10 sessions of guided self-help CBT (CBTgsh) vs 19 sessions of IPT vs 20 sessions of behavioral weight loss (BWL) over 6 months | BWL was significantly better than IPT and CBTgsh in reducing BMI and in the number of patients achieving 5% weight loss at post-treatment but effects were not sustained over time; BWL was significantly better than CBTgsh in increasing dietary restraint |
Cassin et al, 200824 | Self-help book + motivational interviewing (SH-MI) vs self-help book alone (SH) for 16 weeks | SH-MI was significantly better than SH in reducing BE and depression |
BE: binge eating; BED: binge eating disorder; BMI: body mass index; CBT: cognitive-behavioral therapy |
Studies found that CBT and IPT are effective in reducing the frequency of binge eating, whether measured by the number of binge eating episodes or days a patient reports having engaged in binge eating.14-23 However, some studies suggested that CBT can help a substantial number of patients achieve abstinence from binge eating.16,20 Adding MI to a self-help approach may improve binge eating outcomes,24 and binge eating can be successfully reduced using individual, group, and CD-ROM delivery formats.21 In direct comparisons, individual CBT outperformed group CBT in helping patients recover from BED (ie, no longer meeting diagnostic criteria),19 and CBT delivered via guided self-help outperformed BWL in helping patients achieve remission.18
Psychological features of BED typically include low levels of cognitive restraint and high levels of disinhibition, hunger, and shape and weight concerns. Improvements in these psychological measures were observed with CBT,15-20,22 IPT,22 and MI.24 In direct comparisons, self-help CBT demonstrated greater reductions in perceived hunger and disinhibition than self-help BWL,18 and individual CBT outperformed group CBT in reducing shape and weight concerns.19 Isolated studies reported improvements in depression after self-help CBT18 and MI,24 and sustained improvements22 after group CBT (6 months) and group IPT (12 months). Additional research is needed to determine whether CBT crafted specifically for BED improves self-rated depression or if enhancements targeting depressive symptoms are required.
The impact of behavioral interventions on weight in overweight patients has been mixed. Although some CBT studies reported a substantial decrease in weight,17,19 others suggested that weight loss among patients treated with CBT is not superior to those in a wait-list control group16 or is not significant over the course of treatment.20,21 The impact of BWL on weight outcomes in BED also has been unimpressive: after 12 weeks, self-help BWL was no better than self-help CBT in reducing BMI18; after 16 weeks, BWL was better than CBT and IPT in achieving clinically significant (≥5%) weight loss, but this advantage was not sustained at 1- and 2-year follow-up.23 It is difficult to determine why successfully treated BED patients fail to lose weight because one would expect decreases in binge eating to lead to weight loss. It is possible that calories previously consumed during binge eating episodes are distributed over non-binge meals or that patients label binges and non-binge meals differently as a result of treatment.
Combining treatments
BED patients often are treated with a combination of psychotherapy and pharmacotherapy (Table 4).25-29 When added to CBT, topiramate was associated with improvements in weight and some psychological outcomes,25,26 but fluoxetine was not.27,28 Direct comparisons also showed that CBT, alone or combined with fluoxetine, was better than fluoxetine alone in reducing binge eating.27 When combined with an individualized hypocaloric diet, the anti-obesity medication orlistat reduced weight in obese BED patients but had no appreciable effect on binge eating.29 Collectively, the studies we reviewed suggested that combining medication and CBT may improve binge eating and weight loss outcomes; however, additional trials are necessary to determine more definitively which medications combined with CBT are best at producing sustained weight loss while reducing binge eating frequency.
Table 4
Combining medication with behavioral interventions for BED
Study | Drug/dosage | Comments |
---|---|---|
Brambilla et al, 200925 | 3 groups treated for 6 months: Group 1: CBT + setraline (50 to 150 mg/d) + topiramate (25 to 150 mg/d) + reduced calorie diet Group 2: CBT + sertraline (50 to 150 mg/d) + reduced calorie diet Group 3: CBT + nutritional counseling | Weight, BMI, and psychological features of BE reduced significantly only in group 1 |
Claudino et al, 200726 | Group 1: CBT + topiramate (25 to 300 mg/d) Group 2: CBT + placebo 19 sessions over 21 weeks | Significant reductions in BE and depression in both groups; topiramate significantly better than placebo in reducing weight and in achieving BE remission |
Devlin et al, 200527 | 4 groups, all received behavioral weight control intervention for 5 months (20 weeks) plus either: Group 1: CBT + fluoxetine Group 2: CBT + placebo Group 3: fluoxetineGroup 4 placebo (fluoxetine dose, 20 to 60 mg/d) | CBT groups (1 and 2) significantly better than non-CBT groups (3 and 4) in reducing BE and achieving abstinence from BE; fluoxetine significantly better than placebo in reducing depression |
Molinari et al, 200528 | 3 groups, all received nutritional and diet counseling for 54 weeks (4 were inpatient) plus: Group 1: CBT Group 2: fluoxetine (20 to 60 mg/d) Group 3: CBT + fluoxetine | At 12 months, CBT (groups 1 and 3) associated with lower BE frequency and greater percentage of weight loss than fluoxetine |
Golay et al, 200529 | Hypocaloric diet + orlistat (120 mg/d) vs hypocaloric diet + placebo for 24 weeks | Orlistat not different from placebo in reducing the number of patients classified with BED; orlistat significantly better than placebo in reducing weight and body fat |
BE: binge eating; BED: binge eating disorder; BMI: body mass index; CBT: cognitive-behavioral therapy |
Recommendations
Evidence suggests that pharmacotherapy and CBT—alone or in combination—are effective in reducing binge eating, and pharmacotherapy is effective in reducing weight in overweight individuals with BED. More research is needed for IPT and MI. It is unclear which medications provide the greatest benefit in terms of binge eating remission; however, pharmacotherapy has a clear advantage in facilitating short-term weight loss. Also, all BED patients should receive medical management to address possible complications such as hypertension or type 2 diabetes. In addition to reducing binge eating, CBT can improve related psychological comorbidities (eg, eating-related psychopathology and depression) and may have additional benefit when combined with pharmacotherapy.
In light of these findings, we recommend augmenting psychotherapeutic care with pharmacotherapy and medical management to address all relevant psychological and medical domains. Future investigations should address the benefits of coordinated psychological and medical care and evaluate how to maintain treatment gains.
Related Resources
- Binge Eating Disorder Association. www.bedaonline.com.
- Brownley KA, Berkman ND, Sedway JA, et al. Binge eating disorder treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007;40(4):337-348.
Drug Brand Names
- Atomoxetine • Strattera
- Escitalopram • Lexapro
- Fluoxetine • Prozac
- Lamotrigine • Lamictal
- Memantine • Namenda
- Orlistat • Alli, Xenical
- Sertraline • Zoloft
- Sibutramine • Meridia
- Topiramate • Topamax, Topiragen
- Zonisamide • Zonegram
Disclosures
Dr. Peat receives a post-doctoral trainee grant from the National Institutes of Health.
Drs. Brownley, Berkman, and Bulik report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington DC: American Psychiatric Association; 2000.
2. Hudson JI, Hiripi E, Pope HG, et al. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry. 2007;61(3):348-358.
3. American Psychiatric Association. Proposed revision to DSM-5: K-05 Feeding and eating disorders. http://www.dsm5.org/ProposedRevision/Pages/proposedrevision.aspx?rid=372. Updated January 31 2011. Accessed March 26, 2012.
4. Grucza RA, Pryzbeck TR, Cloninger CR. Prevalence and correlates of binge eating disorder in a community sample. Compr Psychiatry. 2007;48(2):124-131.
5. Meneghini LF, Spadola J, Florez H. Prevalence and associations of binge eating disorder in a multiethnic population with type 2 diabetes. Diabetes Care. 2006;29(12):2760.-
6. Berkman ND, Bulik CM, Brownley KA, et al. Management of eating disorders. Evidence report/technology assessment No. 135. Rockville, MD: Agency for Healthcare Research and Quality; 2006. AHRQ Publication No. 06-E010.
7. Guerdjikova AI, McElroy SL, Kotwal R, et al. High-dose escitalopram in the treatment of binge-eating disorder with obesity: a placebo-controlled monotherapy trial. Hum Psychopharmacol. 2008;23(1):1-11.
8. McElroy SL, Kotwal R, Guerdjikova AL, et al. Zonisamide in the treatment of binge eating disorder with obesity: a randomized controlled trial. J Clin Psychiatry. 2006;67(12):1897-1906.
9. McElroy SL, Hudson JI, Capece JA, et al. Topiramate for the treatment of binge eating disorder associated with obesity: a placebo-controlled study. Biol Psychiatry. 2007;61(9):1039-1048.
10. McElroy SL, Guerdjikova A, Kotwal R, et al. Atomoxetine in the treatment of binge-eating disorder: a randomized placebo-controlled trial. J Clin Psychiatry. 2007;68(3):390-398.
11. Wilfley DE, Crow SJ, Hudson JI, et al. Efficacy of sibutramine for the treatment of binge eating disorder: a randomized multicenter placebo-controlled double-blind study. Am J Psychiatry. 2008;165(1):51-58.
12. Brennan BP, Roberts JL, Fogarty KV, et al. Memantine in the treatment of binge eating disorder: an open-label, prospective trial. Int J Eat Disord. 2008;41(6):520-526.
13. Guerdjikova AI, McElroy SL, Welge JA, et al. Lamotrigine in the treatment of binge-eating disorder with obesity: a randomized, placebo-controlled monotherapy trial. Int Clin Psychopharmacol. 2009;24(3):150-158.
14. Annunziato RA, Timko CA, Crerand CE, et al. A randomized trial examining differential meal replacement adherence in a weight loss maintenance program after one-year follow-up. Eat Behav. 2009;10(3):176-183.
15. Ashton K, Drerup M, Windover A, et al. Brief, four-session group CBT reduces binge eating behaviors among bariatric surgery candidates. Surg Obes Relat Dis. 2009;5(2):257-262.
16. Dingemans AE, Spinhoven P, van Furth EF. Predictors and mediators of treatment outcome in patients with binge eating disorder. Behav Res Ther. 2007;45(11):2551-2562.
17. Friederich HC, Schild S, Wild B, et al. Treatment outcome in people with subthreshold compared with full-syndrome binge eating disorder. Obesity. 2007;15(2):283-287.
18. Grilo CM, Masheb RM. A randomized controlled comparison of guided self-help cognitive behavioral therapy and behavioral weight loss for binge eating disorder. Behav Res Ther. 2005;43(11):1509-1525.
19. Ricca V, Castellini G, Mannucci E, et al. Comparison of individual and group cognitive behavioral therapy for binge eating disorder. A randomized, three-year follow-up study. Appetite. 2010;55(3):656-665.
20. Schlup B, Munsch S, Meyer AH, et al. The efficacy of a short version of a cognitive-behavioral treatment followed by booster sessions for binge eating disorder. Behav Res Ther. 2009;47(7):628-635.
21. Shapiro JR, Reba-Harrelson L, Dymek-Valentine M, et al. Feasibility and acceptability of CD-ROM-based cognitive-behavioral treatment for binge-eating disorder. Eur Eat Disord Rev. 2007;15(3):175-184.
22. Tasca GA, Ritchie K, Conrad G, et al. Attachment scales predict outcome in a randomized controlled trial of two group therapies for binge eating disorder: an aptitude by treatment interaction. Psychother Res. 2006;16(1):106-121.
23. Wilson GT, Wilfley DE, Agras WS, et al. Psychological treatments of binge eating disorder. Arch Gen Psychiatry. 2010;67(1):94-101.
24. Cassin SE, von Ranson KM, Heng K, et al. Adapted motivational interviewing for women with binge eating disorder: a randomized controlled trial. Psychol Addict Behav. 2008;22(3):417-425.
25. Brambilla F, Samek L, Company M, et al. Multivariate therapeutic approach to binge-eating disorder: combined nutritional, psychological and pharmacological treatment. Int Clin Psychopharmacol. 2009;24(6):312-317.
26. Claudino AM, de Oliveira IR, Appolinario JC, et al. Double-blind, randomized, placebo-controlled trial of topiramate plus cognitive-behavior therapy in binge-eating disorder. J Clin Psychiatry. 2007;68(9):1324-1332.
27. Devlin MJ, Goldfein JA, Petkova E, et al. Cognitive behavioral therapy and fluoxetine as adjuncts to group behavioral therapy for binge eating disorder. Obes Res. 2005;13(6):1077-1088.
28. Molinari E, Baruffi M, Croci M, et al. Binge eating disorder in obesity: comparison of different therapeutic strategies. Eat Weight Disord. 2005;10(3):154-161.
29. Golay A, Laurent-Jaccard A, Habicht F, et al. Effect of orlistat in obese patients with binge eating disorder. Obes Res. 2005;13(10):1701-1708.
Binge eating is consumption of an unusually large amount of food coupled with a feeling of loss of control over eating. Binge eating disorder (BED) is characterized by recurrent episodes of binge eating without inappropriate compensatory behaviors (eg, self-induced vomiting, misuse of laxatives, diuretics, or other agents, excessive exercise).1 It is the most common eating disorder in the United States, with a lifetime prevalence of approximately 3.5% in women and 2% in men.2 The diagnosis falls within the DSM-IV-TR category of eating disorders not otherwise specified,1 but clinicians often view it as a distinct clinical phenomenon. In DSM-IV-TR, an individual would meet criteria for BED if he or she engages in regular binge eating behavior in the absence of recurrent compensatory behaviors ≥2 days per week over 6 months.1 Proposed changes for DSM-5 recognize a distinct BED diagnosis, reduce the frequency criterion to once per week and the duration criterion to the past 3 months, and shift the focus from binge days to binge episodes (Table 1).3
Table 1
Proposed DSM-5 criteria for binge eating disorder
|
Source:Reference 3 |
BED can occur in individuals of all body mass indices (BMI), but is common among individuals who are overweight or obese as well as those with depression or type 2 diabetes; BED can complicate treatment of these conditions.2,4,5 Primary treatment goals are:
- abstinence from binge eating
- improved psychological functioning
- appropriate weight regulation in overweight patients.
We report on 3 approaches to BED treatment: medication only, behavioral intervention only, and medication plus behavioral intervention. This article provides insights about emerging changes in diagnostic criteria for BED as well as evidence-informed treatment options and recommendations.
The evidence base
We conducted a review of 23 BED studies: 7 medication only, 5 medication plus behavioral, and 11 behavioral only. We focused on studies conducted since September 2005 that included binge frequency, weight, and depression as primary outcomes (see Berkman et al6 for a review of BED treatment studies before 2005). The studies included 2,527 participants (2,216 women and 311 men). Although the sex distribution of BED in the general population tends to slightly favor women,2 the proportion of women presenting for treatment generally is considerably higher than that of men. In studies that reported on race and/or ethnicity, 1,639 participants were identified as white, 191 as African American, 25 as Hispanic, 2 as Asian, 1 as Native American, and 25 as “other.” Ages ranged from 18 to 77.
Several medications are effective
In placebo-controlled studies, a high-dose selective serotonin reuptake inhibitor (escitalopram7), 2 anticonvulsants (zonisamide8 and topiramate9), a selective norepinephrine reuptake inhibitor (atomoxetine10), and an appetite suppressant (sibutramine11) were associated with significant decreases in binge eating frequency, weight, and BMI in overweight/obese patients diagnosed with BED (Table 2). In an open-label trial, memantine—a N-methyl-D-aspartate receptor antagonist often used to treat symptoms of Alzheimer’s disease—was associated with a significant reduction in binge eating but no change in weight.12 Lamotrigine was not significantly different from placebo in reducing binge eating or weight, but showed promise in reducing metabolic parameters such as glucose and triglyceride levels commonly associated with obesity and type 2 diabetes.13 Because BED often is comorbid with obesity and type 2 diabetes, lamotrigine augmentation when treating obese individuals with BED warrants further investigation. As with any pharmacologic agent, carefully consider potential side effects and interactions with other drugs before prescribing medications for BED. Informing patients of potential side effects is crucial for patient safety and accuracy of the data collected in well-controlled treatment studies.
Table 2
Pharmacotherapy for binge eating disorder
Study | Drug/dosage | Comments |
---|---|---|
Guerdjikova et al, 20087 | Escitalopram, 10 to 30 mg/d, vs placebo for 12 weeks | Escitalopram was significantly better than placebo in reducing weight, BMI, and illness severity |
McElroy et al, 20068 | Zonisamide, 100 to 600 mg/d, vs placebo for 16 weeks | Zonisamide was significantly better than placebo in reducing BE, weight, BMI, and various aspects of unhealthy eating behavior |
McElroy et al, 20079 | Topiramate, 25 to 400 mg/d, vs placebo for 16 weeks | Topiramate was significantly better than placebo in reducing BE, weight, BMI, and related psychological features of BE |
McElroy et al, 200710 | Atomoxetine, 40 to 120 mg/d, vs placebo for 10 weeks | Atomoxetine was significantly better than placebo in reducing BE, weight, BMI, and obsessive-compulsive features of BE, and in achieving remission |
Wilfley et al, 200811 | Sibutramine, 15 mg/d, vs placebo for 24 weeks | Sibutramine was significantly better than placebo in reducing BE, weight, BMI, and related psychological features of BE |
Brennan et al, 200812 | Open-label memantine, 5 to 20 mg/d, for 12 weeks | Memantine was associated with decreased binge frequency and related psychological features of BE |
Guerdjikova et al, 200913 | Lamotrigine, 50 to 400 mg/d, vs placebo for 16 weeks | Lamotrigine was not significantly different from placebo |
BE: binge eating; BMI: body mass index |
CBT vs other behavioral approaches
Cognitive-behavioral therapy (CBT), which focuses on identifying and modifying unhealthy thoughts that maintain disordered eating behaviors, is the most widely studied behavioral intervention for BED. Other studied treatments include interpersonal psychotherapy (IPT), motivational interviewing (MI), and structured behavioral weight loss (BWL) (Table 3).14-24 IPT is a psychodynamically based, time-limited treatment that focuses on the interpersonal context of the disorder and on building interpersonal skills. MI emphasizes exploring and resolving ambivalence about treatment, and works to facilitate change through motivational processes. BWL is centered on making dietary and physical activity changes to achieve weight loss. Behavioral treatments have been delivered in various formats, such as an individual or group setting, by electronic interface, and via self-help approaches. Most studies compared active treatment to a control group, but some compared active treatments head-to-head.
Table 3
CBT and other behavioral interventions for BED
Study | Intervention | Comments |
---|---|---|
Annunziato et al, 200914 | 2 groups received CBT and hypocaloric diet for 8 weeks followed by 14 weeks of enhanced nutritional program (ie, reduced consumption of high energy density foods and once-daily liquid meal replacement) or control (normal diet) | Enhanced nutritional program was not significantly different from the control in reducing weight, BE, or psychological features of BE; variability in adherence to the enhanced nutritional program was identified as a significant effect modifier |
Ashton et al, 200915 | 4 sessions of group CBT in an open trial | CBT was associated with significant reductions in BE and psychological features of BE in post-bariatric surgery patients |
Dingemans et al, 200716 | CBT vs wait-list control | CBT significantly better than the wait-list control in reducing BE and psychological features of BE, and in achieving abstinence from BE |
Friederich et al, 200717 | 15-session CBT blended with elements of interpersonal therapy (IPT), nutritional counseling, and supervised walking program; no control group | Treatment significantly reduced weight, BE, and related psychological features of BE in patients meeting sub-threshold and full criteria for BED |
Grilo et al, 200518 | Guided self-help CBT (CBTgsh) vs guided self-help behavioral weight loss (BWLgsh) vs non-specific attention control for 12 weeks | CBTgsh significantly better than BWLgsh and control in BE remission; CBTgsh significantly better than BWLgsh, which was significantly better than control in reducing cognitive restraint; CBTgsh significantly better than control in reducing depression and eating-related psychopathology; no differences between groups in BMI change |
Ricca et al, 201019 | Individual (I-CBT) vs group CBT (G-CBT) for 24 weeks in patients meeting subthreshold and full criteria for BED | BE and BMI were significantly reduced in both groups at 24 weeks and 3-year follow-up. I-CBT was not better than G-CBT in reducing BE or weight at 24 weeks or 3-year follow-up; I-CBT was significantly better than G-CBT in reducing eating-related psychopathology at 24 weeks and 3-year follow-up; I-CBT was significantly better than G-CBT in recovery (ie, no longer meeting full BED criteria) at 24 weeks but not at 3-year follow-up |
Schlup et al, 200920 | 8 weekly sessions of group CBT vs wait-list control | CBT was significantly better than wait-list control in reducing BE and eating concerns and in achieving abstinence at end of treatment; CBT was not different than control in reducing BMI; treatment-related reductions in BE and eating concerns were maintained at 12-month follow-up |
Shapiro et al, 200721 | 10 weekly sessions of group CBT (G-CBT) vs CD-ROM delivered CBT (CD-CBT) vs wait-list control | G-CBT and CD-CBT were not different from each other but both were significantly better than wait-list control in reducing BE |
Tasca et al, 200622 | Group CBT (G-CBT) vs group psychodynamic interpersonal therapy (G-IPT) vs wait-list control for 16 weeks | G-CBT and G-IPT were not different from each other; G-CBT and G-IPT were significantly better than wait list in reducing BE and interpersonal problems (but not BMI) and increasing cognitive restraint post-treatment; depression was reduced in both groups at 6 months but only in G-IPT at 12 months; reductions in BE maintained at 12 months |
Wilson et al, 201023 | 10 sessions of guided self-help CBT (CBTgsh) vs 19 sessions of IPT vs 20 sessions of behavioral weight loss (BWL) over 6 months | BWL was significantly better than IPT and CBTgsh in reducing BMI and in the number of patients achieving 5% weight loss at post-treatment but effects were not sustained over time; BWL was significantly better than CBTgsh in increasing dietary restraint |
Cassin et al, 200824 | Self-help book + motivational interviewing (SH-MI) vs self-help book alone (SH) for 16 weeks | SH-MI was significantly better than SH in reducing BE and depression |
BE: binge eating; BED: binge eating disorder; BMI: body mass index; CBT: cognitive-behavioral therapy |
Studies found that CBT and IPT are effective in reducing the frequency of binge eating, whether measured by the number of binge eating episodes or days a patient reports having engaged in binge eating.14-23 However, some studies suggested that CBT can help a substantial number of patients achieve abstinence from binge eating.16,20 Adding MI to a self-help approach may improve binge eating outcomes,24 and binge eating can be successfully reduced using individual, group, and CD-ROM delivery formats.21 In direct comparisons, individual CBT outperformed group CBT in helping patients recover from BED (ie, no longer meeting diagnostic criteria),19 and CBT delivered via guided self-help outperformed BWL in helping patients achieve remission.18
Psychological features of BED typically include low levels of cognitive restraint and high levels of disinhibition, hunger, and shape and weight concerns. Improvements in these psychological measures were observed with CBT,15-20,22 IPT,22 and MI.24 In direct comparisons, self-help CBT demonstrated greater reductions in perceived hunger and disinhibition than self-help BWL,18 and individual CBT outperformed group CBT in reducing shape and weight concerns.19 Isolated studies reported improvements in depression after self-help CBT18 and MI,24 and sustained improvements22 after group CBT (6 months) and group IPT (12 months). Additional research is needed to determine whether CBT crafted specifically for BED improves self-rated depression or if enhancements targeting depressive symptoms are required.
The impact of behavioral interventions on weight in overweight patients has been mixed. Although some CBT studies reported a substantial decrease in weight,17,19 others suggested that weight loss among patients treated with CBT is not superior to those in a wait-list control group16 or is not significant over the course of treatment.20,21 The impact of BWL on weight outcomes in BED also has been unimpressive: after 12 weeks, self-help BWL was no better than self-help CBT in reducing BMI18; after 16 weeks, BWL was better than CBT and IPT in achieving clinically significant (≥5%) weight loss, but this advantage was not sustained at 1- and 2-year follow-up.23 It is difficult to determine why successfully treated BED patients fail to lose weight because one would expect decreases in binge eating to lead to weight loss. It is possible that calories previously consumed during binge eating episodes are distributed over non-binge meals or that patients label binges and non-binge meals differently as a result of treatment.
Combining treatments
BED patients often are treated with a combination of psychotherapy and pharmacotherapy (Table 4).25-29 When added to CBT, topiramate was associated with improvements in weight and some psychological outcomes,25,26 but fluoxetine was not.27,28 Direct comparisons also showed that CBT, alone or combined with fluoxetine, was better than fluoxetine alone in reducing binge eating.27 When combined with an individualized hypocaloric diet, the anti-obesity medication orlistat reduced weight in obese BED patients but had no appreciable effect on binge eating.29 Collectively, the studies we reviewed suggested that combining medication and CBT may improve binge eating and weight loss outcomes; however, additional trials are necessary to determine more definitively which medications combined with CBT are best at producing sustained weight loss while reducing binge eating frequency.
Table 4
Combining medication with behavioral interventions for BED
Study | Drug/dosage | Comments |
---|---|---|
Brambilla et al, 200925 | 3 groups treated for 6 months: Group 1: CBT + setraline (50 to 150 mg/d) + topiramate (25 to 150 mg/d) + reduced calorie diet Group 2: CBT + sertraline (50 to 150 mg/d) + reduced calorie diet Group 3: CBT + nutritional counseling | Weight, BMI, and psychological features of BE reduced significantly only in group 1 |
Claudino et al, 200726 | Group 1: CBT + topiramate (25 to 300 mg/d) Group 2: CBT + placebo 19 sessions over 21 weeks | Significant reductions in BE and depression in both groups; topiramate significantly better than placebo in reducing weight and in achieving BE remission |
Devlin et al, 200527 | 4 groups, all received behavioral weight control intervention for 5 months (20 weeks) plus either: Group 1: CBT + fluoxetine Group 2: CBT + placebo Group 3: fluoxetineGroup 4 placebo (fluoxetine dose, 20 to 60 mg/d) | CBT groups (1 and 2) significantly better than non-CBT groups (3 and 4) in reducing BE and achieving abstinence from BE; fluoxetine significantly better than placebo in reducing depression |
Molinari et al, 200528 | 3 groups, all received nutritional and diet counseling for 54 weeks (4 were inpatient) plus: Group 1: CBT Group 2: fluoxetine (20 to 60 mg/d) Group 3: CBT + fluoxetine | At 12 months, CBT (groups 1 and 3) associated with lower BE frequency and greater percentage of weight loss than fluoxetine |
Golay et al, 200529 | Hypocaloric diet + orlistat (120 mg/d) vs hypocaloric diet + placebo for 24 weeks | Orlistat not different from placebo in reducing the number of patients classified with BED; orlistat significantly better than placebo in reducing weight and body fat |
BE: binge eating; BED: binge eating disorder; BMI: body mass index; CBT: cognitive-behavioral therapy |
Recommendations
Evidence suggests that pharmacotherapy and CBT—alone or in combination—are effective in reducing binge eating, and pharmacotherapy is effective in reducing weight in overweight individuals with BED. More research is needed for IPT and MI. It is unclear which medications provide the greatest benefit in terms of binge eating remission; however, pharmacotherapy has a clear advantage in facilitating short-term weight loss. Also, all BED patients should receive medical management to address possible complications such as hypertension or type 2 diabetes. In addition to reducing binge eating, CBT can improve related psychological comorbidities (eg, eating-related psychopathology and depression) and may have additional benefit when combined with pharmacotherapy.
In light of these findings, we recommend augmenting psychotherapeutic care with pharmacotherapy and medical management to address all relevant psychological and medical domains. Future investigations should address the benefits of coordinated psychological and medical care and evaluate how to maintain treatment gains.
Related Resources
- Binge Eating Disorder Association. www.bedaonline.com.
- Brownley KA, Berkman ND, Sedway JA, et al. Binge eating disorder treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007;40(4):337-348.
Drug Brand Names
- Atomoxetine • Strattera
- Escitalopram • Lexapro
- Fluoxetine • Prozac
- Lamotrigine • Lamictal
- Memantine • Namenda
- Orlistat • Alli, Xenical
- Sertraline • Zoloft
- Sibutramine • Meridia
- Topiramate • Topamax, Topiragen
- Zonisamide • Zonegram
Disclosures
Dr. Peat receives a post-doctoral trainee grant from the National Institutes of Health.
Drs. Brownley, Berkman, and Bulik report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Binge eating is consumption of an unusually large amount of food coupled with a feeling of loss of control over eating. Binge eating disorder (BED) is characterized by recurrent episodes of binge eating without inappropriate compensatory behaviors (eg, self-induced vomiting, misuse of laxatives, diuretics, or other agents, excessive exercise).1 It is the most common eating disorder in the United States, with a lifetime prevalence of approximately 3.5% in women and 2% in men.2 The diagnosis falls within the DSM-IV-TR category of eating disorders not otherwise specified,1 but clinicians often view it as a distinct clinical phenomenon. In DSM-IV-TR, an individual would meet criteria for BED if he or she engages in regular binge eating behavior in the absence of recurrent compensatory behaviors ≥2 days per week over 6 months.1 Proposed changes for DSM-5 recognize a distinct BED diagnosis, reduce the frequency criterion to once per week and the duration criterion to the past 3 months, and shift the focus from binge days to binge episodes (Table 1).3
Table 1
Proposed DSM-5 criteria for binge eating disorder
|
Source:Reference 3 |
BED can occur in individuals of all body mass indices (BMI), but is common among individuals who are overweight or obese as well as those with depression or type 2 diabetes; BED can complicate treatment of these conditions.2,4,5 Primary treatment goals are:
- abstinence from binge eating
- improved psychological functioning
- appropriate weight regulation in overweight patients.
We report on 3 approaches to BED treatment: medication only, behavioral intervention only, and medication plus behavioral intervention. This article provides insights about emerging changes in diagnostic criteria for BED as well as evidence-informed treatment options and recommendations.
The evidence base
We conducted a review of 23 BED studies: 7 medication only, 5 medication plus behavioral, and 11 behavioral only. We focused on studies conducted since September 2005 that included binge frequency, weight, and depression as primary outcomes (see Berkman et al6 for a review of BED treatment studies before 2005). The studies included 2,527 participants (2,216 women and 311 men). Although the sex distribution of BED in the general population tends to slightly favor women,2 the proportion of women presenting for treatment generally is considerably higher than that of men. In studies that reported on race and/or ethnicity, 1,639 participants were identified as white, 191 as African American, 25 as Hispanic, 2 as Asian, 1 as Native American, and 25 as “other.” Ages ranged from 18 to 77.
Several medications are effective
In placebo-controlled studies, a high-dose selective serotonin reuptake inhibitor (escitalopram7), 2 anticonvulsants (zonisamide8 and topiramate9), a selective norepinephrine reuptake inhibitor (atomoxetine10), and an appetite suppressant (sibutramine11) were associated with significant decreases in binge eating frequency, weight, and BMI in overweight/obese patients diagnosed with BED (Table 2). In an open-label trial, memantine—a N-methyl-D-aspartate receptor antagonist often used to treat symptoms of Alzheimer’s disease—was associated with a significant reduction in binge eating but no change in weight.12 Lamotrigine was not significantly different from placebo in reducing binge eating or weight, but showed promise in reducing metabolic parameters such as glucose and triglyceride levels commonly associated with obesity and type 2 diabetes.13 Because BED often is comorbid with obesity and type 2 diabetes, lamotrigine augmentation when treating obese individuals with BED warrants further investigation. As with any pharmacologic agent, carefully consider potential side effects and interactions with other drugs before prescribing medications for BED. Informing patients of potential side effects is crucial for patient safety and accuracy of the data collected in well-controlled treatment studies.
Table 2
Pharmacotherapy for binge eating disorder
Study | Drug/dosage | Comments |
---|---|---|
Guerdjikova et al, 20087 | Escitalopram, 10 to 30 mg/d, vs placebo for 12 weeks | Escitalopram was significantly better than placebo in reducing weight, BMI, and illness severity |
McElroy et al, 20068 | Zonisamide, 100 to 600 mg/d, vs placebo for 16 weeks | Zonisamide was significantly better than placebo in reducing BE, weight, BMI, and various aspects of unhealthy eating behavior |
McElroy et al, 20079 | Topiramate, 25 to 400 mg/d, vs placebo for 16 weeks | Topiramate was significantly better than placebo in reducing BE, weight, BMI, and related psychological features of BE |
McElroy et al, 200710 | Atomoxetine, 40 to 120 mg/d, vs placebo for 10 weeks | Atomoxetine was significantly better than placebo in reducing BE, weight, BMI, and obsessive-compulsive features of BE, and in achieving remission |
Wilfley et al, 200811 | Sibutramine, 15 mg/d, vs placebo for 24 weeks | Sibutramine was significantly better than placebo in reducing BE, weight, BMI, and related psychological features of BE |
Brennan et al, 200812 | Open-label memantine, 5 to 20 mg/d, for 12 weeks | Memantine was associated with decreased binge frequency and related psychological features of BE |
Guerdjikova et al, 200913 | Lamotrigine, 50 to 400 mg/d, vs placebo for 16 weeks | Lamotrigine was not significantly different from placebo |
BE: binge eating; BMI: body mass index |
CBT vs other behavioral approaches
Cognitive-behavioral therapy (CBT), which focuses on identifying and modifying unhealthy thoughts that maintain disordered eating behaviors, is the most widely studied behavioral intervention for BED. Other studied treatments include interpersonal psychotherapy (IPT), motivational interviewing (MI), and structured behavioral weight loss (BWL) (Table 3).14-24 IPT is a psychodynamically based, time-limited treatment that focuses on the interpersonal context of the disorder and on building interpersonal skills. MI emphasizes exploring and resolving ambivalence about treatment, and works to facilitate change through motivational processes. BWL is centered on making dietary and physical activity changes to achieve weight loss. Behavioral treatments have been delivered in various formats, such as an individual or group setting, by electronic interface, and via self-help approaches. Most studies compared active treatment to a control group, but some compared active treatments head-to-head.
Table 3
CBT and other behavioral interventions for BED
Study | Intervention | Comments |
---|---|---|
Annunziato et al, 200914 | 2 groups received CBT and hypocaloric diet for 8 weeks followed by 14 weeks of enhanced nutritional program (ie, reduced consumption of high energy density foods and once-daily liquid meal replacement) or control (normal diet) | Enhanced nutritional program was not significantly different from the control in reducing weight, BE, or psychological features of BE; variability in adherence to the enhanced nutritional program was identified as a significant effect modifier |
Ashton et al, 200915 | 4 sessions of group CBT in an open trial | CBT was associated with significant reductions in BE and psychological features of BE in post-bariatric surgery patients |
Dingemans et al, 200716 | CBT vs wait-list control | CBT significantly better than the wait-list control in reducing BE and psychological features of BE, and in achieving abstinence from BE |
Friederich et al, 200717 | 15-session CBT blended with elements of interpersonal therapy (IPT), nutritional counseling, and supervised walking program; no control group | Treatment significantly reduced weight, BE, and related psychological features of BE in patients meeting sub-threshold and full criteria for BED |
Grilo et al, 200518 | Guided self-help CBT (CBTgsh) vs guided self-help behavioral weight loss (BWLgsh) vs non-specific attention control for 12 weeks | CBTgsh significantly better than BWLgsh and control in BE remission; CBTgsh significantly better than BWLgsh, which was significantly better than control in reducing cognitive restraint; CBTgsh significantly better than control in reducing depression and eating-related psychopathology; no differences between groups in BMI change |
Ricca et al, 201019 | Individual (I-CBT) vs group CBT (G-CBT) for 24 weeks in patients meeting subthreshold and full criteria for BED | BE and BMI were significantly reduced in both groups at 24 weeks and 3-year follow-up. I-CBT was not better than G-CBT in reducing BE or weight at 24 weeks or 3-year follow-up; I-CBT was significantly better than G-CBT in reducing eating-related psychopathology at 24 weeks and 3-year follow-up; I-CBT was significantly better than G-CBT in recovery (ie, no longer meeting full BED criteria) at 24 weeks but not at 3-year follow-up |
Schlup et al, 200920 | 8 weekly sessions of group CBT vs wait-list control | CBT was significantly better than wait-list control in reducing BE and eating concerns and in achieving abstinence at end of treatment; CBT was not different than control in reducing BMI; treatment-related reductions in BE and eating concerns were maintained at 12-month follow-up |
Shapiro et al, 200721 | 10 weekly sessions of group CBT (G-CBT) vs CD-ROM delivered CBT (CD-CBT) vs wait-list control | G-CBT and CD-CBT were not different from each other but both were significantly better than wait-list control in reducing BE |
Tasca et al, 200622 | Group CBT (G-CBT) vs group psychodynamic interpersonal therapy (G-IPT) vs wait-list control for 16 weeks | G-CBT and G-IPT were not different from each other; G-CBT and G-IPT were significantly better than wait list in reducing BE and interpersonal problems (but not BMI) and increasing cognitive restraint post-treatment; depression was reduced in both groups at 6 months but only in G-IPT at 12 months; reductions in BE maintained at 12 months |
Wilson et al, 201023 | 10 sessions of guided self-help CBT (CBTgsh) vs 19 sessions of IPT vs 20 sessions of behavioral weight loss (BWL) over 6 months | BWL was significantly better than IPT and CBTgsh in reducing BMI and in the number of patients achieving 5% weight loss at post-treatment but effects were not sustained over time; BWL was significantly better than CBTgsh in increasing dietary restraint |
Cassin et al, 200824 | Self-help book + motivational interviewing (SH-MI) vs self-help book alone (SH) for 16 weeks | SH-MI was significantly better than SH in reducing BE and depression |
BE: binge eating; BED: binge eating disorder; BMI: body mass index; CBT: cognitive-behavioral therapy |
Studies found that CBT and IPT are effective in reducing the frequency of binge eating, whether measured by the number of binge eating episodes or days a patient reports having engaged in binge eating.14-23 However, some studies suggested that CBT can help a substantial number of patients achieve abstinence from binge eating.16,20 Adding MI to a self-help approach may improve binge eating outcomes,24 and binge eating can be successfully reduced using individual, group, and CD-ROM delivery formats.21 In direct comparisons, individual CBT outperformed group CBT in helping patients recover from BED (ie, no longer meeting diagnostic criteria),19 and CBT delivered via guided self-help outperformed BWL in helping patients achieve remission.18
Psychological features of BED typically include low levels of cognitive restraint and high levels of disinhibition, hunger, and shape and weight concerns. Improvements in these psychological measures were observed with CBT,15-20,22 IPT,22 and MI.24 In direct comparisons, self-help CBT demonstrated greater reductions in perceived hunger and disinhibition than self-help BWL,18 and individual CBT outperformed group CBT in reducing shape and weight concerns.19 Isolated studies reported improvements in depression after self-help CBT18 and MI,24 and sustained improvements22 after group CBT (6 months) and group IPT (12 months). Additional research is needed to determine whether CBT crafted specifically for BED improves self-rated depression or if enhancements targeting depressive symptoms are required.
The impact of behavioral interventions on weight in overweight patients has been mixed. Although some CBT studies reported a substantial decrease in weight,17,19 others suggested that weight loss among patients treated with CBT is not superior to those in a wait-list control group16 or is not significant over the course of treatment.20,21 The impact of BWL on weight outcomes in BED also has been unimpressive: after 12 weeks, self-help BWL was no better than self-help CBT in reducing BMI18; after 16 weeks, BWL was better than CBT and IPT in achieving clinically significant (≥5%) weight loss, but this advantage was not sustained at 1- and 2-year follow-up.23 It is difficult to determine why successfully treated BED patients fail to lose weight because one would expect decreases in binge eating to lead to weight loss. It is possible that calories previously consumed during binge eating episodes are distributed over non-binge meals or that patients label binges and non-binge meals differently as a result of treatment.
Combining treatments
BED patients often are treated with a combination of psychotherapy and pharmacotherapy (Table 4).25-29 When added to CBT, topiramate was associated with improvements in weight and some psychological outcomes,25,26 but fluoxetine was not.27,28 Direct comparisons also showed that CBT, alone or combined with fluoxetine, was better than fluoxetine alone in reducing binge eating.27 When combined with an individualized hypocaloric diet, the anti-obesity medication orlistat reduced weight in obese BED patients but had no appreciable effect on binge eating.29 Collectively, the studies we reviewed suggested that combining medication and CBT may improve binge eating and weight loss outcomes; however, additional trials are necessary to determine more definitively which medications combined with CBT are best at producing sustained weight loss while reducing binge eating frequency.
Table 4
Combining medication with behavioral interventions for BED
Study | Drug/dosage | Comments |
---|---|---|
Brambilla et al, 200925 | 3 groups treated for 6 months: Group 1: CBT + setraline (50 to 150 mg/d) + topiramate (25 to 150 mg/d) + reduced calorie diet Group 2: CBT + sertraline (50 to 150 mg/d) + reduced calorie diet Group 3: CBT + nutritional counseling | Weight, BMI, and psychological features of BE reduced significantly only in group 1 |
Claudino et al, 200726 | Group 1: CBT + topiramate (25 to 300 mg/d) Group 2: CBT + placebo 19 sessions over 21 weeks | Significant reductions in BE and depression in both groups; topiramate significantly better than placebo in reducing weight and in achieving BE remission |
Devlin et al, 200527 | 4 groups, all received behavioral weight control intervention for 5 months (20 weeks) plus either: Group 1: CBT + fluoxetine Group 2: CBT + placebo Group 3: fluoxetineGroup 4 placebo (fluoxetine dose, 20 to 60 mg/d) | CBT groups (1 and 2) significantly better than non-CBT groups (3 and 4) in reducing BE and achieving abstinence from BE; fluoxetine significantly better than placebo in reducing depression |
Molinari et al, 200528 | 3 groups, all received nutritional and diet counseling for 54 weeks (4 were inpatient) plus: Group 1: CBT Group 2: fluoxetine (20 to 60 mg/d) Group 3: CBT + fluoxetine | At 12 months, CBT (groups 1 and 3) associated with lower BE frequency and greater percentage of weight loss than fluoxetine |
Golay et al, 200529 | Hypocaloric diet + orlistat (120 mg/d) vs hypocaloric diet + placebo for 24 weeks | Orlistat not different from placebo in reducing the number of patients classified with BED; orlistat significantly better than placebo in reducing weight and body fat |
BE: binge eating; BED: binge eating disorder; BMI: body mass index; CBT: cognitive-behavioral therapy |
Recommendations
Evidence suggests that pharmacotherapy and CBT—alone or in combination—are effective in reducing binge eating, and pharmacotherapy is effective in reducing weight in overweight individuals with BED. More research is needed for IPT and MI. It is unclear which medications provide the greatest benefit in terms of binge eating remission; however, pharmacotherapy has a clear advantage in facilitating short-term weight loss. Also, all BED patients should receive medical management to address possible complications such as hypertension or type 2 diabetes. In addition to reducing binge eating, CBT can improve related psychological comorbidities (eg, eating-related psychopathology and depression) and may have additional benefit when combined with pharmacotherapy.
In light of these findings, we recommend augmenting psychotherapeutic care with pharmacotherapy and medical management to address all relevant psychological and medical domains. Future investigations should address the benefits of coordinated psychological and medical care and evaluate how to maintain treatment gains.
Related Resources
- Binge Eating Disorder Association. www.bedaonline.com.
- Brownley KA, Berkman ND, Sedway JA, et al. Binge eating disorder treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007;40(4):337-348.
Drug Brand Names
- Atomoxetine • Strattera
- Escitalopram • Lexapro
- Fluoxetine • Prozac
- Lamotrigine • Lamictal
- Memantine • Namenda
- Orlistat • Alli, Xenical
- Sertraline • Zoloft
- Sibutramine • Meridia
- Topiramate • Topamax, Topiragen
- Zonisamide • Zonegram
Disclosures
Dr. Peat receives a post-doctoral trainee grant from the National Institutes of Health.
Drs. Brownley, Berkman, and Bulik report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington DC: American Psychiatric Association; 2000.
2. Hudson JI, Hiripi E, Pope HG, et al. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry. 2007;61(3):348-358.
3. American Psychiatric Association. Proposed revision to DSM-5: K-05 Feeding and eating disorders. http://www.dsm5.org/ProposedRevision/Pages/proposedrevision.aspx?rid=372. Updated January 31 2011. Accessed March 26, 2012.
4. Grucza RA, Pryzbeck TR, Cloninger CR. Prevalence and correlates of binge eating disorder in a community sample. Compr Psychiatry. 2007;48(2):124-131.
5. Meneghini LF, Spadola J, Florez H. Prevalence and associations of binge eating disorder in a multiethnic population with type 2 diabetes. Diabetes Care. 2006;29(12):2760.-
6. Berkman ND, Bulik CM, Brownley KA, et al. Management of eating disorders. Evidence report/technology assessment No. 135. Rockville, MD: Agency for Healthcare Research and Quality; 2006. AHRQ Publication No. 06-E010.
7. Guerdjikova AI, McElroy SL, Kotwal R, et al. High-dose escitalopram in the treatment of binge-eating disorder with obesity: a placebo-controlled monotherapy trial. Hum Psychopharmacol. 2008;23(1):1-11.
8. McElroy SL, Kotwal R, Guerdjikova AL, et al. Zonisamide in the treatment of binge eating disorder with obesity: a randomized controlled trial. J Clin Psychiatry. 2006;67(12):1897-1906.
9. McElroy SL, Hudson JI, Capece JA, et al. Topiramate for the treatment of binge eating disorder associated with obesity: a placebo-controlled study. Biol Psychiatry. 2007;61(9):1039-1048.
10. McElroy SL, Guerdjikova A, Kotwal R, et al. Atomoxetine in the treatment of binge-eating disorder: a randomized placebo-controlled trial. J Clin Psychiatry. 2007;68(3):390-398.
11. Wilfley DE, Crow SJ, Hudson JI, et al. Efficacy of sibutramine for the treatment of binge eating disorder: a randomized multicenter placebo-controlled double-blind study. Am J Psychiatry. 2008;165(1):51-58.
12. Brennan BP, Roberts JL, Fogarty KV, et al. Memantine in the treatment of binge eating disorder: an open-label, prospective trial. Int J Eat Disord. 2008;41(6):520-526.
13. Guerdjikova AI, McElroy SL, Welge JA, et al. Lamotrigine in the treatment of binge-eating disorder with obesity: a randomized, placebo-controlled monotherapy trial. Int Clin Psychopharmacol. 2009;24(3):150-158.
14. Annunziato RA, Timko CA, Crerand CE, et al. A randomized trial examining differential meal replacement adherence in a weight loss maintenance program after one-year follow-up. Eat Behav. 2009;10(3):176-183.
15. Ashton K, Drerup M, Windover A, et al. Brief, four-session group CBT reduces binge eating behaviors among bariatric surgery candidates. Surg Obes Relat Dis. 2009;5(2):257-262.
16. Dingemans AE, Spinhoven P, van Furth EF. Predictors and mediators of treatment outcome in patients with binge eating disorder. Behav Res Ther. 2007;45(11):2551-2562.
17. Friederich HC, Schild S, Wild B, et al. Treatment outcome in people with subthreshold compared with full-syndrome binge eating disorder. Obesity. 2007;15(2):283-287.
18. Grilo CM, Masheb RM. A randomized controlled comparison of guided self-help cognitive behavioral therapy and behavioral weight loss for binge eating disorder. Behav Res Ther. 2005;43(11):1509-1525.
19. Ricca V, Castellini G, Mannucci E, et al. Comparison of individual and group cognitive behavioral therapy for binge eating disorder. A randomized, three-year follow-up study. Appetite. 2010;55(3):656-665.
20. Schlup B, Munsch S, Meyer AH, et al. The efficacy of a short version of a cognitive-behavioral treatment followed by booster sessions for binge eating disorder. Behav Res Ther. 2009;47(7):628-635.
21. Shapiro JR, Reba-Harrelson L, Dymek-Valentine M, et al. Feasibility and acceptability of CD-ROM-based cognitive-behavioral treatment for binge-eating disorder. Eur Eat Disord Rev. 2007;15(3):175-184.
22. Tasca GA, Ritchie K, Conrad G, et al. Attachment scales predict outcome in a randomized controlled trial of two group therapies for binge eating disorder: an aptitude by treatment interaction. Psychother Res. 2006;16(1):106-121.
23. Wilson GT, Wilfley DE, Agras WS, et al. Psychological treatments of binge eating disorder. Arch Gen Psychiatry. 2010;67(1):94-101.
24. Cassin SE, von Ranson KM, Heng K, et al. Adapted motivational interviewing for women with binge eating disorder: a randomized controlled trial. Psychol Addict Behav. 2008;22(3):417-425.
25. Brambilla F, Samek L, Company M, et al. Multivariate therapeutic approach to binge-eating disorder: combined nutritional, psychological and pharmacological treatment. Int Clin Psychopharmacol. 2009;24(6):312-317.
26. Claudino AM, de Oliveira IR, Appolinario JC, et al. Double-blind, randomized, placebo-controlled trial of topiramate plus cognitive-behavior therapy in binge-eating disorder. J Clin Psychiatry. 2007;68(9):1324-1332.
27. Devlin MJ, Goldfein JA, Petkova E, et al. Cognitive behavioral therapy and fluoxetine as adjuncts to group behavioral therapy for binge eating disorder. Obes Res. 2005;13(6):1077-1088.
28. Molinari E, Baruffi M, Croci M, et al. Binge eating disorder in obesity: comparison of different therapeutic strategies. Eat Weight Disord. 2005;10(3):154-161.
29. Golay A, Laurent-Jaccard A, Habicht F, et al. Effect of orlistat in obese patients with binge eating disorder. Obes Res. 2005;13(10):1701-1708.
1. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington DC: American Psychiatric Association; 2000.
2. Hudson JI, Hiripi E, Pope HG, et al. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry. 2007;61(3):348-358.
3. American Psychiatric Association. Proposed revision to DSM-5: K-05 Feeding and eating disorders. http://www.dsm5.org/ProposedRevision/Pages/proposedrevision.aspx?rid=372. Updated January 31 2011. Accessed March 26, 2012.
4. Grucza RA, Pryzbeck TR, Cloninger CR. Prevalence and correlates of binge eating disorder in a community sample. Compr Psychiatry. 2007;48(2):124-131.
5. Meneghini LF, Spadola J, Florez H. Prevalence and associations of binge eating disorder in a multiethnic population with type 2 diabetes. Diabetes Care. 2006;29(12):2760.-
6. Berkman ND, Bulik CM, Brownley KA, et al. Management of eating disorders. Evidence report/technology assessment No. 135. Rockville, MD: Agency for Healthcare Research and Quality; 2006. AHRQ Publication No. 06-E010.
7. Guerdjikova AI, McElroy SL, Kotwal R, et al. High-dose escitalopram in the treatment of binge-eating disorder with obesity: a placebo-controlled monotherapy trial. Hum Psychopharmacol. 2008;23(1):1-11.
8. McElroy SL, Kotwal R, Guerdjikova AL, et al. Zonisamide in the treatment of binge eating disorder with obesity: a randomized controlled trial. J Clin Psychiatry. 2006;67(12):1897-1906.
9. McElroy SL, Hudson JI, Capece JA, et al. Topiramate for the treatment of binge eating disorder associated with obesity: a placebo-controlled study. Biol Psychiatry. 2007;61(9):1039-1048.
10. McElroy SL, Guerdjikova A, Kotwal R, et al. Atomoxetine in the treatment of binge-eating disorder: a randomized placebo-controlled trial. J Clin Psychiatry. 2007;68(3):390-398.
11. Wilfley DE, Crow SJ, Hudson JI, et al. Efficacy of sibutramine for the treatment of binge eating disorder: a randomized multicenter placebo-controlled double-blind study. Am J Psychiatry. 2008;165(1):51-58.
12. Brennan BP, Roberts JL, Fogarty KV, et al. Memantine in the treatment of binge eating disorder: an open-label, prospective trial. Int J Eat Disord. 2008;41(6):520-526.
13. Guerdjikova AI, McElroy SL, Welge JA, et al. Lamotrigine in the treatment of binge-eating disorder with obesity: a randomized, placebo-controlled monotherapy trial. Int Clin Psychopharmacol. 2009;24(3):150-158.
14. Annunziato RA, Timko CA, Crerand CE, et al. A randomized trial examining differential meal replacement adherence in a weight loss maintenance program after one-year follow-up. Eat Behav. 2009;10(3):176-183.
15. Ashton K, Drerup M, Windover A, et al. Brief, four-session group CBT reduces binge eating behaviors among bariatric surgery candidates. Surg Obes Relat Dis. 2009;5(2):257-262.
16. Dingemans AE, Spinhoven P, van Furth EF. Predictors and mediators of treatment outcome in patients with binge eating disorder. Behav Res Ther. 2007;45(11):2551-2562.
17. Friederich HC, Schild S, Wild B, et al. Treatment outcome in people with subthreshold compared with full-syndrome binge eating disorder. Obesity. 2007;15(2):283-287.
18. Grilo CM, Masheb RM. A randomized controlled comparison of guided self-help cognitive behavioral therapy and behavioral weight loss for binge eating disorder. Behav Res Ther. 2005;43(11):1509-1525.
19. Ricca V, Castellini G, Mannucci E, et al. Comparison of individual and group cognitive behavioral therapy for binge eating disorder. A randomized, three-year follow-up study. Appetite. 2010;55(3):656-665.
20. Schlup B, Munsch S, Meyer AH, et al. The efficacy of a short version of a cognitive-behavioral treatment followed by booster sessions for binge eating disorder. Behav Res Ther. 2009;47(7):628-635.
21. Shapiro JR, Reba-Harrelson L, Dymek-Valentine M, et al. Feasibility and acceptability of CD-ROM-based cognitive-behavioral treatment for binge-eating disorder. Eur Eat Disord Rev. 2007;15(3):175-184.
22. Tasca GA, Ritchie K, Conrad G, et al. Attachment scales predict outcome in a randomized controlled trial of two group therapies for binge eating disorder: an aptitude by treatment interaction. Psychother Res. 2006;16(1):106-121.
23. Wilson GT, Wilfley DE, Agras WS, et al. Psychological treatments of binge eating disorder. Arch Gen Psychiatry. 2010;67(1):94-101.
24. Cassin SE, von Ranson KM, Heng K, et al. Adapted motivational interviewing for women with binge eating disorder: a randomized controlled trial. Psychol Addict Behav. 2008;22(3):417-425.
25. Brambilla F, Samek L, Company M, et al. Multivariate therapeutic approach to binge-eating disorder: combined nutritional, psychological and pharmacological treatment. Int Clin Psychopharmacol. 2009;24(6):312-317.
26. Claudino AM, de Oliveira IR, Appolinario JC, et al. Double-blind, randomized, placebo-controlled trial of topiramate plus cognitive-behavior therapy in binge-eating disorder. J Clin Psychiatry. 2007;68(9):1324-1332.
27. Devlin MJ, Goldfein JA, Petkova E, et al. Cognitive behavioral therapy and fluoxetine as adjuncts to group behavioral therapy for binge eating disorder. Obes Res. 2005;13(6):1077-1088.
28. Molinari E, Baruffi M, Croci M, et al. Binge eating disorder in obesity: comparison of different therapeutic strategies. Eat Weight Disord. 2005;10(3):154-161.
29. Golay A, Laurent-Jaccard A, Habicht F, et al. Effect of orlistat in obese patients with binge eating disorder. Obes Res. 2005;13(10):1701-1708.