Binge eating disorder

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Editor(s)-in-Chief: C. Michael Gibson, M.S.,M.D. [1] Phone:617-632-7753; Mark Warren, M.D., M.P.H.; Fellow, Academy of Eating Disorders [2]; Associate Editor(s)-in-Chief:  Kiran Singh, M.D. [3] Sonya Gelfand

Synonyms and keywords: BED

## Overview

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Binge eating disorder (BED) is an eating disorder characterized by binge eating episodes during which one consumes a large amount of food in a brief period of time and feels a loss of control and noticeable distress over their eating habits. Unlike bulimia nervosa, BED does not present subsequent purging episodes. Though BED can occur in normal weight individuals, it often leads to obesity. There may be a genetic inheritance factor involved in BED independent of other obesity risks and there is also a higher incidence of psychiatric comorbidity, with the percentage of individuals with BED and an axis I comorbid psychiatric disorder being 78.9% and 63.6% for those with subclinical BED.[1]

## Historical Perspective

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* In 1959, BED was first described by psychiatrist and researcher Albert Stunkard as "night eating syndrome" (NES), and the term "binge eating disorder" was coined to describe the same binging-type eating behavior without the exclusive nocturnal component.[2]
* In 2013, BED was officially classified in the Diagnostic and Statistic Manual of Mental Disorders as an eating disorder.

## Classification

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* There is no established system for the classification of binge eating disorder.

## Pathophysiology

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* Though the ultimate cause of the development of eating disorders is unknown, they are suggested to be influenced by genetic and environmental factors.

* Possible genetic influences were suggested after family and twin studies of eating disorders revealed that eating disorders run in families and are heritable.[3]
* Environmental influences include:[4][5][6][7][8][9]
* Sociocultural factors such as 'Western' ideals of thin and attractive body image that encourage sexual objectification
* Socioeconomic status
* Personality characteristics
* Anxiety
* Impulsivity
* Perfectionism

## Differential Diagnosis

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* Binge eating disorder shall be differentiated from the following diseases:[10]

* Bipolar and depressive disorders
* Food Addiction (FA)
* Borderline personality disorder
* Bulimia nervosa
* Compulsive overeating
* Obesity

### Bulemia Nervosa

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* Binge eating symptoms are also present in bulimia nervosa.
* The formal diagnosis criteria are similar in that subjects must binge at least twice per week for a minimum period of three months.[11]
* Unlike in bulimia, those with BED do not purge, fast or engage in strenuous exercise after binge eating.
* Additionally, bulimics are typically of normal weight or slightly overweight, whereas those with binge eating disorder are typically overweight or obese.

### Compulsive overeating

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* Binge eating disorder is similar to, but it is distinct from, compulsive overeating.
* Those with BED do not have a compulsion to overeat and do not spend a great deal of time fantasizing about food.
* On the contrary, some people with binge eating disorder have very negative feelings about food.
* As with other eating disorders, binge eating is an "expressive disorder" — a disorder that is an expression of deeper psychological problems.
* Some researchers believe BED is a milder form, or subset of bulimia nervosa, while others argue that it is its own distinct disorder.
* Currently, the DSM-IV categorizes it under eating disorder not otherwise specified (EDNOS), an indication that more research is needed.

## Epidemiology and Demographics

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### Prevalence

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* BED is the most common eating disorder in adults.[12]
* The past year prevalence of binge eating disorder in adults was 1200 per 100,000 individuals (1.2%) of the overall population.[10]
* The lifetime prevalence of binge eating disorder in adults was 2800 per 100,000 individuals (2.8%) of the overall population.[13]

### Gender

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##### 12 Month Prevalence

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The prevalence of binge eating disorder in 2007 according to gender is depicted in the table below:[14]

Disorder  | Male Prevalence  | Female Prevalence

|
|

Binge eating disorder | 0.8% | 1.6%
Subthreshold binge eating | 0.8% | 0.4%
Any binge eating | 1.7% | 2.5%

##### Lifetime Prevalence

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The lifetime prevalence of binge eating disorder according to gender is depicted in the table below:[14]

Disorder  | Male Prevalence  | Female Prevalence

|
|

Binge eating disorder | 2.0% | 3.5%
Subthreshold binge eating | 1.9% | 0.6%
Any binge eating | 4.0% | 4.9%

### Ethnicity

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* BED is found in all ethno-cultural and racial populations.[15]

## Risk Factors

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* It is not known for certain what causes binge eating disorder, however studies have shown a correlation between genetic factors and BED, sociocultural influences and BED, as well as environmental factors and BED.
* Family studies of eating disorders suggest that BED is familial and is significantly influenced by genetic factors that are suggested to contribute to liability to BED. Though there is not one gene for eating disorders such as BED, there are a number of genes that could potentially code for proteins that may create vulnerability to such disorders. [16][17][18][19][20]
* The primary suggested causes of BED are environmental risk factors, including sociocultural influences and gene-environment correlation.
* Sociocultural influences such as unrealistically thin media images have been anticipated to cause factors that lead to BED including body dissatisfaction and disordered eating.[21][14]
* Three types of gene-environment (G-E) correlations have been established as hypothesized causal models for BED:
* Passive G-E correlation occurs due to the fact that (unless the child is adopted) parents that pass down genes to their children also create their family environment, and thus parents that pass down genes that influence liability to eating disorders may also be modeling behaviors associated with eating disorders such as restriction, compulsive exercise, and body dissatisfaction. Therefore, children under these circumstances are at double risk of developing eating disorders such as BED as a result of being under genetic and environmental exposure.[22]
* Evocative G-E correlation refers to the idea that an individual with a genetic predisposition to a certain disorder may repeatedly seek reassurance and appearance-related comments from parents or peers. These comments, regardless of whether positive or negative, reinforce a tendency for the individual to over-value their appearance and create an environment for themselves that is highly appearance focused, thus initiating disordered eating behaviors.[22]
* Active G-E correlations occur when an individual with genetic vulnerability to a particular eating disorder seeks environments that present a high risk of eating disorder development such as gymnastics, ballet, cheerleading, or modeling.[22]

## Natural History, Complications, and Prognosis

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### Natural History

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* The symptoms of BED usually develop in the second or third decade of life, and start with symptoms such as eating unusually large amounts of food within a particular period of time while feeling at a loss of control over your eating, or feeling guilty, depressed, or ashamed about your eating. Without treatment, the patient will develop symptoms that may often lead to the following:[10]

* Cardiovascular disease
* Diabetes
* Insomnia or sleep apnea
* Hypertension
* Gallbladder disease
* Muscle or joint pain
* Gastrointestinal difficulties
* Depression
* Anxiety

### Complications

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* Binge eating can lead to several serious health complications, including:[10]

* Severe obesity
* Diabetes
* Hypertension
* Cardiovascular diseases
* Significant distress

### Prognosis

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* Patients with binge eating disorder often have a lower overall quality of life and commonly experience social impairments.[23]
* Though patients with binge eating disorder are not necessarily overweight, the ongoing habit of excessive eating may ultimately lead to weight gain and obesity, thus creating the risk of obesity-related morbidities such as hypertension, diabetes, and heart diseases.[24][25]
* Despite the fact that BED is associated with significant impairment, the prognosis of BED is good with proper therapeutic intervention which targets prevention of binge eating, excess and modest weight gain, as well as weight and body shape concerns.[12]

## Diagnosis

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### Diagnostic Criteria

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#### DSM-V Diagnostic Criteria for Binge Eating Disorder[10]

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“  |

* Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:

* Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that is definitely larger than what most people would eat in a similar period of time under similar circumstances.
* A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or control what or how much one is eating).

* The binge eating episodes are associated with three (or more) of the following:

* Eating much more rapidly than normal.
* Eating until feeling uncomfortably full.
* Eating large amounts of food when not feeling physically hungry.
* Eating alone because of feeling embarrassed by how much one is eating.
* Feeling disgusted with oneself, depressed, or very guilty afterward.

* Marked distress regarding binge eating is present.
* The binge eating occurs, on average, at least once a week for 3 months.
* The binge eating is not associated with the recurrent use of inappropriate compensatory behaviors (e.g., purging) as in bulimia nervosa and does not occur exclusively during the course of bulimia nervosa or anorexia nervosa.

| ”

|
|

### History and Symptoms

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* Patients with BED often lose control over their eating, and do not subsequently experience purging, fasting, or excessive exercise. As a result, people with binge eating disorder are often overweight or obese. Symptoms of BED include:

* Eating abnormally large amounts of food in a set amount of time
* Eating when one is full or not hungry
* Eating rapidly during binge episodes
* Eating until one feels uncomfortably full
* Eating alone or in secret in order to avoid embarrassment or appearing uncomfortable when eating around others
* Feeling distressed, ashamed, or guilty about one's eating
* Frequently dieting, often without losing any weight
* New practice with food diets (eg., no sugar, no carbs, vegetarianism/veganism)
* Stealing and hoarding food
* Deliberately making time for binge sessions
* Social withdrawal
* Extreme concern with body appearance
* Irregular mealtimes
* Fluctuations in weight
* Difficulty concentrating
* Non-specific gastrointestinal complaints

### Laboratory Findings

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* There are no diagnostic laboratory findings associated with binge eating disorder.

### Imaging

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* Imaging studies are usually not indicated in diagnosis of binge eating disorder.

## Treatment

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* Treatment for BED primarily aims to achieve abstinence and sustainable weight loss, in addition to targeting the increase of motivation to maintain a healthier eating and life style, the modification of abnormal thoughts and habits, the knowledge of how to handle conflicts and negative emotions, and relapse prevention.[26][27][28]
* Treatment programs should promote a controlled reduction of caloric intake as well as healthier habits involving eating and lifestyle. Programs should encourage patients to self-monitor symptoms including mood fluctuations, anxiety, and stress levels. Setting a treatment plan as early as possible is optimal for treatment specificity and stepped-care treatments.
* The beginning of treatment should specifically target binge abstinence as well as weight stabilization, as opposed to weight loss. [29]

### Behavioral Interventions

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* Behavioral treatments (BWL) which focus on diet and lifestyle modification as well as obesity treatment have proven to be especially effective as basic interventions for patients with low associated psychopathology.[29][30]

* Diet therapy is a primary component to the achievement of weight loss, and therefore is an object of attention among patients experiencing high body dissatisfaction. Attention to weight loss influences perceived wellness, mood, self-esteem and consequently lessens binge vulnerability.[31][32][33][34]
* When attempting to moderate eating habits, poor compliance to diet should not be blamed but rather addressed to decrease the risk of further unstable control over eating behaviors.
* Physical activity can be coupled with a balanced diet to take action on fat consumption and maintaining goals reached through dieting. Physical activity also improves mood and overall general health, limiting BED vulnerability. [35]

### Psychoeducational Interventions

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* Psychoeducational treatments for BED focus on informing patients about their disease in order to ensure a deeper comprehension of their condition and therefore, increase the possibility of self-management.[36]
* These treatments revolve around explanations of BED symptoms, teaching patients to self-monitor food intake, informing them about factors that cause binges, and teaching them how to correct their lifestyles.
* Psychoeducational interventions serve as useful baseline therapies for later more complex treatment.

### Medical Therapy

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* Medical therapy in BED focuses on the reduction of eating impulsiveness, binges, and negative feelings.[26][37][38]
* Antidepressants are the most commonly applied medications in BED treatment, showing efficacy on eating impulsiveness, general psychopathology, and anxiety and depressive symptoms.
* It is recommended to use compounds that present side effects on weight and hunger, such as selective serotonin reuptake inhibitors (SSRIs).

### Psychotherapy

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* According to data, reviews, and analysis, psychotherapies are the most effective treatments for BED. There are many psychotherapies used as treatment for BED, including the following:

* Cognitive-Behavioral Therapies (CBT), which focus on the causes of bingeing and its correlation to self-esteem that depends on body shape. Long term effects of CBT approaches include a gradual normalization of eating habits, reduced relapse, improvement of hunger, negative feelings, and perceived global health.[37]
* Dialect-Behavioral Therapy (DBT), which focuses on emotion regulation and stress tolerance through effective binge reduction and lowering concerns about food and body shape.[12]
* Interpersonal Psychotherapy (IPT), which focuses on personal relations and role transitions that may have played a role in EDs to subsequently achieve better social interactions and to be able to cope with interpersonal conflicts. [39][40][12]

### Surgical Interventions

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* For patients with severe obesity, bariatric surgery is a recommended treatment.[41][42]
* Bariatric surgery has been proven useful due to the fact that weight loss is closely linked to improvements in mood, wellness, and quality of life.
* Thus, bariatric surgery often acts as protection against binge vulnerability.

## Future and Investigational Therapies

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* Future investigations outline the hope to study eating disorders in developing countries such as India in order to test the role of culture in the etiology of eating disorders.[43][44]
* Additionally, scientists and researchers hope to investigate "atypical" clinical presentations of eating disorders in India such as those without weight concern in order to determine whether usual models of psychotherapy would be sufficient in treating these particular EDs, or whether other models would be needed to cater to the unique needs of certain populations.

## References

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1. ↑ Kessler RC, Berglund P, Chiu WT, Demler O, Heeringa S, Hiripi E; et al. (2004). "The US National Comorbidity Survey Replication (NCS-R): design and field procedures". Int J Methods Psychiatr Res. 13 (2): 69–92. PMID 15297905.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
2. ↑ STUNKARD AJ (1959). "Eating patterns and obesity". Psychiatr Q. 33: 284–95. PMID 13835451.
3. ↑ Yilmaz Z, Hardaway JA, Bulik CM (2015). "Genetics and Epigenetics of Eating Disorders". Adv Genomics Genet. 5: 131–150. doi:10.2147/AGG.S55776. PMC 4803116. PMID 27013903.CS1 maint: Multiple names: authors list (link)
4. ↑ Kent A, Waller G (2000). "Childhood emotional abuse and eating psychopathology". Clin Psychol Rev. 20 (7): 887–903. PMID 11057376.
5. ↑ Lunner K, Werthem EH, Thompson JK, Paxton SJ, McDonald F, Halvaarson KS (2000). "A cross-cultural examination of weight-related teasing, body image, and eating disturbance in Swedish and Australian samples". Int J Eat Disord. 28 (4): 430–5. PMID 11054790.CS1 maint: Multiple names: authors list (link)
6. ↑ Polivy J, Herman CP (2002). "Causes of eating disorders". Annu Rev Psychol. 53: 187–213. doi:10.1146/annurev.psych.53.100901.135103. PMID 11752484.
7. ↑ Schmidt U, Tiller J, Blanchard M, Andrews B, Treasure J (1997). "Is there a specific trauma precipitating anorexia nervosa?". Psychol Med. 27 (3): 523–30. PMID 9153673.CS1 maint: Multiple names: authors list (link)
8. ↑ Spencer SJ (2013). "Perinatal programming of neuroendocrine mechanisms connecting feeding behavior and stress". Front Neurosci. 7: 109. doi:10.3389/fnins.2013.00109. PMC 3683620. PMID 23785312.
9. ↑ Striegel-Moore RH, Bulik CM (2007). "Risk factors for eating disorders". Am Psychol. 62 (3): 181–98. doi:10.1037/0003-066X.62.3.181. PMID 17469897.
10. ↑ 10.0 10.1 10.2 10.3 10.4 Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.
11. ↑ United States Department of Health and Human Services - Substance Abuse and Mental Health Services Administration (2007-07-10). "Eating Disorders". Retrieved 2007-07-10.
12. ↑ 12.0 12.1 12.2 12.3 Iacovino JM, Gredysa DM, Altman M, Wilfley DE (2012). "Psychological treatments for binge eating disorder". Curr Psychiatry Rep. 14 (4): 432–46. doi:10.1007/s11920-012-0277-8. PMC 3433807. PMID 22707016.CS1 maint: Multiple names: authors list (link)
13. ↑ Kessler RC, Avenevoli S, Costello EJ, Green JG, Gruber MJ, Heeringa S; et al. (2009). "Design and field procedures in the US National Comorbidity Survey Replication Adolescent Supplement (NCS-A)". Int J Methods Psychiatr Res. 18 (2): 69–83. doi:10.1002/mpr.279. PMC 2774712. PMID 19507169.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
14. ↑ 14.0 14.1 14.2 Hudson JI, Hiripi E, Pope HG, Kessler RC (2007). "The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication". Biol Psychiatry. 61 (3): 348–58. doi:10.1016/j.biopsych.2006.03.040. PMC 1892232. PMID 16815322.CS1 maint: Multiple names: authors list (link)
15. ↑ Lee-Winn AE, Reinblatt SP, Mojtabai R, Mendelson T (2016). "Gender and racial/ethnic differences in binge eating symptoms in a nationally representative sample of adolescents in the United States". Eat Behav. 22: 27–33. doi:10.1016/j.eatbeh.2016.03.021. PMC 4983227. PMID 27085166.CS1 maint: Multiple names: authors list (link)
16. ↑ Bulik CM (2005). "Exploring the gene-environment nexus in eating disorders". J Psychiatry Neurosci. 30 (5): 335–9. PMC 1197278. PMID 16151538.
17. ↑ Bulik CM, Sullivan PF, Kendler KS (1998). "Heritability of binge-eating and broadly defined bulimia nervosa". Biol Psychiatry. 44 (12): 1210–8. PMID 9861464.CS1 maint: Multiple names: authors list (link)
18. ↑ Hudson JI, Pope HG, Jonas JM, Yurgelun-Todd D, Frankenburg FR (1987). "A controlled family history study of bulimia". Psychol Med. 17 (4): 883–90. PMID 3432462.CS1 maint: Multiple names: authors list (link)
19. ↑ Lilenfeld LR, Kaye WH, Greeno CG, Merikangas KR, Plotnicov K, Pollice C; et al. (1998). "A controlled family study of anorexia nervosa and bulimia nervosa: psychiatric disorders in first-degree relatives and effects of proband comorbidity". Arch Gen Psychiatry. 55 (7): 603–10. PMID 9672050.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
20. ↑ Strober M, Freeman R, Lampert C, Diamond J, Kaye W (2000). "Controlled family study of anorexia nervosa and bulimia nervosa: evidence of shared liability and transmission of partial syndromes". Am J Psychiatry. 157 (3): 393–401. doi:10.1176/appi.ajp.157.3.393. PMID 10698815.CS1 maint: Multiple names: authors list (link)
21. ↑ Striegel-Moore RH, Silberstein LR, Rodin J (1986). "Toward an understanding of risk factors for bulimia". Am Psychol. 41 (3): 246–63. PMID 3457546.CS1 maint: Multiple names: authors list (link)
22. ↑ 22.0 22.1 22.2 Mazzeo SE, Bulik CM (2009). "Environmental and genetic risk factors for eating disorders: what the clinician needs to know". Child Adolesc Psychiatr Clin N Am. 18 (1): 67–82. doi:10.1016/j.chc.2008.07.003. PMC 2719561. PMID 19014858.
23. ↑ Nazar BP, Gregor LK, Albano G, Marchica A, Coco GL, Cardi V; et al. (2017). "Early Response to treatment in Eating Disorders: A Systematic Review and a Diagnostic Test Accuracy Meta-Analysis". Eur Eat Disord Rev. 25 (2): 67–79. doi:10.1002/erv.2495. PMID 27928853. Check `|pmid=` value (help).CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
24. ↑ Invalid `<ref>` tag; no text was provided for refs named `Westerburg2013`
25. ↑ Marazziti D, Corsi M, Baroni S, Consoli G, Catena-Dell'Osso M (December 2012). "Latest advancements in the pharmacological treatment of binge eating disorder" (PDF). Eur Rev Med Pharmacol Sci. 16 (15): 2102–7. PMID 23280026.
26. ↑ 26.0 26.1 Vocks S, Tuschen-Caffier B, Pietrowsky R, Rustenbach SJ, Kersting A, Herpertz S (2010). "Meta-analysis of the effectiveness of psychological and pharmacological treatments for binge eating disorder". Int J Eat Disord. 43 (3): 205–17. doi:10.1002/eat.20696. PMID 19402028.CS1 maint: Multiple names: authors list (link)
27. ↑ Brambilla F, Samek L, Company M, Lovo F, Cioni L, Mellado C (2009). "Multivariate therapeutic approach to binge-eating disorder: combined nutritional, psychological and pharmacological treatment". Int Clin Psychopharmacol. 24 (6): 312–7. doi:10.1097/YIC.0b013e32832ac828. PMID 19794312.CS1 maint: Multiple names: authors list (link)
28. ↑ Flückiger C, Meyer A, Wampold BE, Gassmann D, Messerli-Bürgy N, Munsch S (2011). "Predicting premature termination within a randomized controlled trial for binge-eating patients". Behav Ther. 42 (4): 716–25. doi:10.1016/j.beth.2011.03.008. PMID 22035999.CS1 maint: Multiple names: authors list (link)
29. ↑ 29.0 29.1 Grilo CM, White MA, Wilson GT, Gueorguieva R, Masheb RM (2012). "Rapid response predicts 12-month post-treatment outcomes in binge-eating disorder: theoretical and clinical implications". Psychol Med. 42 (4): 807–17. doi:10.1017/S0033291711001875. PMC 3288595. PMID 21923964.CS1 maint: Multiple names: authors list (link)
30. ↑ Munsch S, Meyer AH, Biedert E (2012). "Efficacy and predictors of long-term treatment success for Cognitive-Behavioral Treatment and Behavioral Weight-Loss-Treatment in overweight individuals with binge eating disorder". Behav Res Ther. 50 (12): 775–85. doi:10.1016/j.brat.2012.08.009. PMID 23099111.CS1 maint: Multiple names: authors list (link)
31. ↑ Bautista-Díaz ML, Franco-Paredes K, Mancilla-Díaz JM, Alvarez-Rayón G, López-Aguilar X, Ocampo Téllez-Girón T; et al. (2012). "Body dissatisfaction and socio-cultural factors in women with and without BED: their relation with eating psychopathology". Eat Weight Disord. 17 (2): e86–92. doi:10.3275/8243. PMID 22314226.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
32. ↑ Grilo CM, Crosby RD, Masheb RM, White MA, Peterson CB, Wonderlich SA; et al. (2009). "Overvaluation of shape and weight in binge eating disorder, bulimia nervosa, and sub-threshold bulimia nervosa". Behav Res Ther. 47 (8): 692–6. doi:10.1016/j.brat.2009.05.001. PMC 2742994. PMID 19552897.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
33. ↑ Carrard I, Crépin C, Ceschi G, Golay A, Van der Linden M (2012). "Relations between pure dietary and dietary-negative affect subtypes and impulsivity and reinforcement sensitivity in binge eating individuals". Eat Behav. 13 (1): 13–9. doi:10.1016/j.eatbeh.2011.10.004. PMID 22177390.CS1 maint: Multiple names: authors list (link)
34. ↑ Masheb RM, Grilo CM, Rolls BJ (2011). "A randomized controlled trial for obesity and binge eating disorder: low-energy-density dietary counseling and cognitive-behavioral therapy". Behav Res Ther. 49 (12): 821–9. doi:10.1016/j.brat.2011.09.006. PMC 3223390. PMID 22005587.CS1 maint: Multiple names: authors list (link)
35. ↑ Masheb RM, White MA, Grilo CM (2013). "Substantial weight gains are common prior to treatment-seeking in obese patients with binge eating disorder". Compr Psychiatry. 54 (7): 880–4. doi:10.1016/j.comppsych.2013.03.017. PMC 3779527. PMID 23639407.CS1 maint: Multiple names: authors list (link)
36. ↑ Balestrieri M, Isola M, Baiano M, Ciano R (2013). "Psychoeducation in Binge Eating Disorder and EDNOS: a pilot study on the efficacy of a 10-week and a 1-year continuation treatment". Eat Weight Disord. 18 (1): 45–51. doi:10.1007/s40519-013-0014-2. PMID 23757250.CS1 maint: Multiple names: authors list (link)
37. ↑ 37.0 37.1 Reas DL, Grilo CM (2008). "Review and meta-analysis of pharmacotherapy for binge-eating disorder". Obesity (Silver Spring). 16 (9): 2024–38. doi:10.1038/oby.2008.333. PMC 3650491. PMID 19186327.
38. ↑ McElroy SL, Guerdjikova AI, Mori N, O'Melia AM (2012). "Pharmacological management of binge eating disorder: current and emerging treatment options". Ther Clin Risk Manag. 8: 219–41. doi:10.2147/TCRM.S25574. PMC 3363296. PMID 22654518.CS1 maint: Multiple names: authors list (link)
39. ↑ Tasca GA, Balfour L, Presniak MD, Bissada H (2012). "Outcomes of specific interpersonal problems for binge eating disorder: comparing group psychodynamic interpersonal psychotherapy and group cognitive behavioral therapy". Int J Group Psychother. 62 (2): 197–218. doi:10.1521/ijgp.2012.62.2.197. PMID 22468572.CS1 maint: Multiple names: authors list (link)
40. ↑ Wilson GT, Wilfley DE, Agras WS, Bryson SW (2010). "Psychological treatments of binge eating disorder". Arch Gen Psychiatry. 67 (1): 94–101. doi:10.1001/archgenpsychiatry.2009.170. PMC 3757519. PMID 20048227.CS1 maint: Multiple names: authors list (link)
41. ↑ Peterson CB, Miller KB, Crow SJ, Thuras P, Mitchell JE (2005). "Subtypes of binge eating disorder based on psychiatric history". Int J Eat Disord. 38 (3): 273–6. doi:10.1002/eat.20174. PMID 16142786.CS1 maint: Multiple names: authors list (link)
42. ↑ Faulconbridge LF, Wadden TA, Thomas JG, Jones-Corneille LR, Sarwer DB, Fabricatore AN (2013). "Changes in depression and quality of life in obese individuals with binge eating disorder: bariatric surgery versus lifestyle modification". Surg Obes Relat Dis. 9 (5): 790–6. doi:10.1016/j.soard.2012.10.010. PMC 3609883. PMID 23260806.CS1 maint: Multiple names: authors list (link)
43. ↑ Gandhi DH, Appaya MP, Machado T (1991). "Anorexia nervosa in Asian children". Br J Psychiatry. 159: 591–2. PMID 1751884.CS1 maint: Multiple names: authors list (link)
44. ↑ Mammen P, Russell S, Russell PS (2007). "Prevalence of eating disorders and psychiatric comorbidity among children and adolescents". Indian Pediatr. 44 (5): 357–9. PMID 17536137.CS1 maint: Multiple names: authors list (link)

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