Binge eating disorder

Eating disorder characterized by overeating

Medical condition

Binge eating disorder

Periwinkle ribbon for awareness of pulmonary hypertension, eating disorders, and esophageal cancer
Specialty| Psychiatry, Clinical Psychology
Symptoms| Eating much faster than normal, eating until feeling uncomfortably full, eating a large amount when not hungry
Complications| Obesity, tooth decay, diabetes,[1] non-alcoholic fatty liver disease,[2] acid reflux, heartburn,[3] amenorrhea,[4] disruptions in sleep[5]
Causes| Unclear
Risk factors| Low self-esteem, family history of eating disorders, childhood abuse or trauma, anxiety, depression, drug and alcohol use
Diagnostic method| Psychiatry, psychology
Differential diagnosis| Bulimia nervosa
Treatment| Psychiatry, psychology
Medication| Lisdexamfetamine,[6] Selective serotonin reuptake inhibitor[7]

Binge eating disorder (BED) is an eating disorder characterized by frequent and recurrent binge eating episodes with associated negative psychological and social problems, but without the compensatory behaviors common to bulimia nervosa, OSFED, or the binge-purge subtype of anorexia nervosa.

BED is a recently described condition,[8] which was required to distinguish binge eating similar to that seen in bulimia nervosa but without characteristic purging. Individuals who are diagnosed with bulimia nervosa and binge eating disorder exhibit similar patterns of compulsive overeating, neurobiological features of dysfunctional cognitive control and food addiction, and biological and environmental risk factors.[9] Some professionals consider BED to be a milder form of bulimia with the two conditions on the same spectrum.[10]

Binge eating is one of the most prevalent eating disorders among adults,[11] though there tends to be less media coverage and research about the disorder in comparison to anorexia nervosa and bulimia nervosa.

## Signs and symptoms

[edit]

Binge eating is the core symptom of BED; however, not everyone who binge eats has BED.[12] An individual may occasionally binge eat without experiencing many of the negative physical, psychological, or social effects of BED. This may be considered disordered eating rather than a clinical disorder. Precisely defining binge eating can be problematic,[8] however, binge eating episodes in BED are generally described as having the following potential features:

* Eating much faster than normal,[13] perhaps in a short space of time[14]
* Eating until feeling uncomfortably full[13]
* Eating a large amount when not hungry[13]
* Subjective loss of control over how much or what is eaten[15]
* Planning and allocating specific times for binging[13]
* Eating alone or secretly[13]
* Not being able to remember what was eaten after the binge[13]
* Feelings of guilt, shame or disgust following a food binge[13][15]
* Body image disturbance[16]

In contrast to bulimia nervosa, binge eating episodes are not regularly followed by activities intended to compensate for the amount of food consumed,[8] such as self-induced vomiting, laxative or enema misuse, or strenuous exercise.[15] BED is characterized more by overeating than dietary restriction.[17] Those with BED often have poor body image and frequently diet, but are unsuccessful due to the severity of their binge eating.[17]

Obesity is common in persons with BED,[18] as is depression,[8] low self-esteem, stress and boredom.[14] Regarding cognitive abilities, individuals showing severe binge eating symptoms may experience small dysfunctions in executive functions.[19] Those with BED are also at risk of Non-alcoholic fatty liver disease,[20][21] menstrual irregularities such as amenorrhea,[4] and gastrointestinal problems such as acid reflux and heartburn.[3]

## Causes

[edit]

As with other eating disorders, binge eating is an "expressive disorder"—a disorder that is an expression of deeper psychological problems.[9] People who have binge eating disorder have been found to have higher weight bias internalization, which includes low self-esteem, unhealthy eating patterns, and general body dissatisfaction.[22] Binge eating disorder commonly develops as a result or side effect of depression, as it is common for people to turn to comfort foods when they are feeling down.[23]

There was resistance to give binge eating disorder the status of a fully fledged eating disorder because many perceived binge eating disorder to be caused by individual choices.[11] Previous research has focused on the relationship between body image and eating disorders, and concludes that disordered eating might be linked to rigid dieting practices.[24] In the majority of cases of anorexia, extreme and inflexible restriction of dietary intake leads at some point to the development of binge eating, weight regain, bulimia nervosa, or a mixed form of eating disorder not otherwise specified. When under a strict diet that mimics the effects of starvation, the body may be preparing for a new type of behavior pattern, one that consumes a large amount of food in a relatively short period of time.[25][26][27]

Some studies show that BED aggregates in families and could be genetic. However, very few published studies around the genetics exist.[28]

However, other research suggests that binge eating disorder can also be caused by environmental factors and the impact of traumatic events. One study showed that women with binge eating disorder experienced more adverse life events in the year prior to the onset of the development of the disorder, and that binge eating disorder was positively associated with how frequently negative events occur.[29] Additionally, the research found that individuals who had binge eating disorder were more likely to have experienced physical abuse, perceived risk of physical abuse, stress, and body criticism.[29] Other risk factors may include childhood obesity, critical comments about weight, low self-esteem, depression, and physical or sexual abuse in childhood.[30] A systematic review concluded that bulimia nervosa and binge eating disorder are impacted by family separations, a loss in their lives, and negative parent-child interactions[31] A few studies have suggested that there could be a genetic component to binge eating disorder,[11] though other studies have shown more ambiguous results. Studies have shown that binge eating tends to run in families and a twin study by Bulik, Sullivan, and Kendler has shown a, "moderate heritability for binge eating" at 41 percent.[32] Studies have also shown that eating disorders such as anorexia and bulimia reduce coping abilities, which makes it more likely for those suffering to turn to binge eating as a coping strategy.[33]

"In the U.S, it is estimated that 3.5% of young women and 30% to 40% of people who seek weight loss treatments, can be clinically diagnosed with binge eating disorder."[34]

## Diagnosis

[edit]

### International Classification of Diseases

[edit]

The 2017 update to the American version of the ICD-10 includes BED under F50.81.[35] ICD-11 may contain a dedicated entry (6B62), defining BED as frequent, recurrent episodes of binge eating (once a week or more over a period of several months) which are not regularly followed by inappropriate compensatory behaviors aimed at preventing weight gain.[15]

According to the World Health Organization's ICD-11 classification of BED, the severity of the disorder can be classified as mild (1-3 episodes/week), moderate (4-7 episodes/week), severe (8-13 episodes/week) and extreme (>14 episodes/week).[36]

### Diagnostic and Statistical Manual

[edit]

Initially considered a topic for further research exploration, binge eating disorder was first included in the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1994 simply as a feature of eating disorder. In 2013 it gained formal recognition as a psychiatric condition in the DSM-5.[36] Until 2013, binge eating disorder was categorized as an Eating Disorder Not Otherwise Specified, an umbrella category for eating disorders that don't fall under the categories for anorexia nervosa or bulimia nervosa. Prior to DSM-5, Eating Disorder Not Otherwise Specified, which included BED, was diagnosed more often than both anorexia nervosa and bulimia nervosa.[37] Because it was not a recognized psychiatric disorder in the DSM until 2013, it has been difficult to obtain insurance reimbursement for treatments.[38] The disorder now has its own category under DSM-5, which outlines the signs and symptoms that must be present to classify a person's behavior as binge eating disorder. Studies have confirmed the high predictive value of these criteria for diagnosing BED.[39]

One study claims that the method for diagnosing BED is for a clinician to conduct a structured interview using the DSM-5 criteria or taking the Eating Disorder Examination.[36] The Structured Clinical Interview for DSM (SCID-5) takes no more than 75 minutes to complete and has a systematic approach which follows the DSM-5 criteria. The Eating Disorder Examination is a semi-structured interview that identifies the frequency of binges and associated eating disorder features.[36]

The DSM-5 characterizes diagnosis under several categories—mild, moderate, severe, and extreme—each determined by the number of binges the patient exhibits per week. Mild: 1-3 episodes per week, Moderate: 4-7 episodes per week, Severe: 8-13 episodes per week, Extreme: 14 or more episodes per week[40]

Further, the remission states are classified under the following. Partial Remission: Following a previous diagnosis, the average frequency of binge eating episodes decreases to less than one episode per week for a sustained period of time. Full Remission: Following a previous diagnosis, none of the criteria have been met for a sustained period of time.[41]

## Management

[edit]

Counselling and some medication, such as certain stimulants (e.g. lisdexamfetamine), selective serotonin reuptake inhibitors (SSRIs), and GLP-1 receptor agonists, may help those affected by BED.[42] Some recommend a multidisciplinary approach in the treatment of the disorder.[14]

### Medication

[edit]

#### Lisdexamfetamine

[edit]

See also: Lisdexamfetamine § Binge Eating Disorder

As of July 2024, lisdexamfetamine is the only pharmacotherapy approved by the USFDA and TGA for BED[43][44] Evidence indicates that its efficacy in treating BED may be partially attributed to a psychopathological overlap with Attention deficit hyperactivity disorder, a cognitive control disorder that also benefits from treatment with lisdexamfetamine.[45][46]

Medical reviews of randomized controlled trials have established that lisdexamfetamine, administered at doses between 50 and 70 mg, is safe and effective for treating BED.[sources 1] These reviews consistently report significant reductions in the number of binge eating days and episodes per week.[sources 1] Furthermore, a meta-analytic systematic review highlighted a 12-month extension study demonstrating that lisdexamfetamine maintained its effectiveness in reducing binge eating days throughout the study duration.[47] Two reviews have found lisdexamfetamine to be superior to placebo in several secondary outcomes, including persistent binge eating cessation, reduction of obsessive-compulsive binge eating symptoms, body weight, and triglycerides.[46][47]

Lisdexamfetamine is a pharmacologically inert prodrug that confers its therapeutic effects for BED after conversion to its active metabolite, dextroamphetamine, which acts in the central nervous system.[44] Dextroamphetamine increases the activity of dopamine and norepinephrine in prefrontal cortical regions that regulate cognitive control of behavior.[43][44][45] By enhancing the ability to exert cognitive control over behavior, dextroamphetamine helps patients with BED override prepotent feeding responses that precede binge eating episodes.[45][47][49] Lisdexamfetamine, like all pharmaceutical amphetamines, possesses direct appetite suppressant effects, which may be therapeutically beneficial for BED and its associated comorbidities.[46][47] Neuroimaging studies involving BED-diagnosed participants suggest that long-term neuroadaptations in dopaminergic and noradrenergic systems resulting from lisdexamfetamine treatment may play a role in the sustained improvements in eating behavior regulation observed even after discontinuation of the drug.[43][44][47]

#### Off-label medications

[edit]

Three other classes of medications are also used in the treatment of binge eating disorder: antidepressants, anticonvulsants, and anti-obesity medications.[7] Antidepressant medications of the selective serotonin reuptake inhibitor (SSRI) have been found to effectively reduce episodes of binge eating and reduce weight.[7] Similarly, anticonvulsant medications such as topiramate and zonisamide may be able to effectively suppress appetite.[7] The long-term effectiveness of medication for binge eating disorder is currently unknown.[50] For BED patients with manic episodes, risperidone is recommended. If BED patients have bipolar depression, lamotrigine is appropriate to use.[51]

Trials of antidepressants, anticonvulsants, and anti-obesity medications suggest that these medications are superior to placebo in reducing binge eating.[52] Medications are not considered the treatment of choice because psychotherapeutic approaches, such as CBT, are more effective than medications for binge eating disorder. A meta-analysis concluded that using medications did not reduce binge-eating episodes and BMI posttreatment at 6–12 months. This indicates a potential possibility of relapse after withdrawal from the medications.[53] Medications also do not increase the effectiveness of psychotherapy, though some patients may benefit from anticonvulsant and anti-obesity medications, such as phentermine/topiramate, for weight loss.[52]

Blocking opioid receptors leads to less food intake. Additionally, bupropion and naltrexone used together may cause weight loss. Combining these alongside psychotherapies like CBT may lead to better outcomes for BED.[54]

GLP-1 receptor agonist medications such as semaglutide (Ozempic), dulaglutide (Trulicity), and liraglutide (Saxenda) have been used for treating BED in recent years. Often prescribed for lowering appetite and subsequent weight loss in obese and diabetic patients, they can successfully stop or reduce obsessive thoughts about food, binging urges, and other impulsive behaviors.[55][56][57][58] Some users of these drugs have reported a major, sudden improvement in what is colloquially known as "food noise" – constant, unstoppable thoughts about eating despite not being physically hungry – which can be a symptom of BED.[59][60] This is a promising treatment, however more research is needed as of January 2024.[61]

### Counselling

[edit]

Cognitive behavioral therapy (CBT) treatment has been demonstrated as a more effective form of treatment for BED than behavioral weight loss programs. 50% of BED individuals achieve complete remission from binge eating[62] and 68-90% will reduce the amount of binge eating episodes they have.[36] CBT has also been shown to be an effective method to address self-image issues and psychiatric comorbidities (e.g., depression) associated with the disorder.[62] The goal of CBT is to interrupt binge-eating behaviour, learn to create a normal eating schedule, change the perception around weight and shape and develop positive attitudes about one's body.[36] Although this treatment is successful in eliminating binge eating episodes, it does not lead to losing any weight.[63] Recent reviews have concluded that psychological interventions such as psychotherapy and behavioral interventions are more effective than pharmacological interventions for the treatment of binge eating disorder.[50] A meta-analysis concluded that psychotherapy based on CBT not only significantly improved binge-eating symptomatology but also reduced a client's BMI significantly at posttreatment and longer than 6 and 12 months after treatment.[53] Behavioral weight loss treatment has been proven to be effective as a means to achieve weight loss amongst patients.[64]

### Surgery

[edit]

Bariatric surgery has also been proposed as another approach to treat BED and a recent meta-analysis showed that approximately two-thirds of individuals who seek this type of surgery for weight loss purposes have BED. Bariatric surgery recipients who had BED prior to receiving the surgery tend to have poorer weight-loss outcomes and are more likely to continue to exhibit eating behaviors characteristic of BED.[62]

### Lifestyle interventions

[edit]

Other treatments for BED include lifestyle interventions like weight training, peer support groups, and investigation of hormonal abnormalities.

## Prognosis

[edit]

Individuals with BED often have a lower overall quality of life and commonly experience social difficulties.[50] Early behavior change is an accurate prediction of remission of symptoms later.[65]

Individuals who have BED commonly have other comorbidities such as major depressive disorder, personality disorder, bipolar disorder, substance abuse, body dysmorphic disorder, kleptomania, irritable bowel syndrome, fibromyalgia, or an anxiety disorder.[62][7] Individuals may also exhibit varying degrees of panic attacks and a history of attempted suicide.[14]

While people of a normal weight may overeat occasionally, an ongoing habit of consuming large amounts of food in a short period of time may ultimately lead to weight gain and obesity. The main physical health consequences of this type of eating disorder are brought on by the weight gain resulting from calorie-laden bingeing episodes. Mental and emotional consequences of binge eating disorder include social weight stigma and emotional loss of control.[17] Up to 70% of individuals with BED may also be obese,[14] and therefore obesity-associated morbidities such as high blood pressure[14] and coronary artery disease,[14] type 2 diabetes mellitus, gastrointestinal issues (e.g., gallbladder disease), high cholesterol levels, musculoskeletal problems and obstructive sleep apnea[62][50][66] may also be present. One study found a 42% obesity rate in those who have received a BED diagnosis.[37] Additionally, a higher morbid obesity prevalence was observed in this population compared to a population without eating disorders.[37]

## Epidemiology

[edit]

### General

[edit]

The prevalence of BED in the general population is approximately 1-3%.[67]

BED cases usually occur between the ages of 12.4 and 24.7, but prevalence rates increase until the age of 40.[68]

### Age

Binge eating disorder is the most common eating disorder in adults.[50]

The limited amount of research that has been done on BED shows that rates of binge eating disorder are fairly comparable among men and women.[69] The lifetime prevalence of binge eating disorder has been observed in studies to be 2.0 percent for men and 3.5 percent for women, higher than that of the commonly recognized eating disorders anorexia nervosa and bulimia nervosa.[62] However another systematic literature review found the prevalence average to be about 2.3% in women and about 0.3% in men.[36] Lifetime prevalence rates for BED in women can range anywhere from 1.5 to 6 times higher than in men.[68] One literature review found that point prevalence rates for BED vary from 0.1 percent to 24.1 percent depending on the sample.[68] This same review also found that the 12-month prevalence rates vary between 0.1 percent to 8.8 percent.[68] Adolescents also face a notable risk of binge eating behavior. Incidents rates of 10.1 and 6.6 per 10,000 person years have been observed in male and female adolescents in the U.S., respectively.[37]

### Sexuality

[edit]

Recent studies found that eating disorders which included anorexia nervosa, bulimia nervosa and binge-eating disorder are common among sexual and gender minority populations, including gay, lesbian, bisexual and transgender people. This could be due to the stress and discrimination this population experiences.[70] Furthermore, adolescent and young adult sexual minority males binge at higher rates than their heterosexual counterparts.[71]

### Race and ethnicity

[edit]

Due to limited and inconsistent information and research on ethnic and racial differences, prevalence rates are hard to determine for BED.[68] However, the racial makeup of BED distinctly varies from anorexia nervosa and bulimia nervosa.[37] Rates of binge eating disorder have been found to be similar among black women, white women, and white men,[72] while some studies have shown that binge eating disorder is more common among black women than among white women.[11] However, majority of the research done around BED is focused on White women.[73] One literature review found information citing no difference between BED prevalence among Hispanic, African American, and White women while other information found that BED prevalence was highest among Hispanics followed by Black individuals and finally White people.[68] A 2021 study has observed "higher rates of BED as compared to other ethnic groups" for African Americans.[74] The likelihood of reporting eating disorder symptoms is also lower in some groups, including African Americans.[74] Asian-Americans also face decreased reporting of ED symptoms. This can be partly attributed to "significantly higher thin ideal internalization" compared to other ethnic groups.[74]

Migration can also influence BED risk. Mexican-American immigrants have been observed to face a greater risk of BED following migration.[37]

### Socioeconomic status

[edit]

Individuals with low socioeconomic status often face many barriers in the diagnosis and treatment of eating disorders like BED. These barriers include longer clinical waiting times, worse care, and less clinical investigation for individuals that "defy illness stereotypes".[75] The costs associated with specialized mental health care pose another barrier for low socioeconomic status individuals.[75] Furthermore, associated factors such as food insecurity and environmental stress have been shown to contribute to higher rates of eating disorders, such as BED, in these populations.[75] Food security has been found to be a notable predictor of eating disorder behaviors. Low food security has been shown to increase the prevalence and frequency of binge eating.[74] Researchers have been called on to reframe eating-related disorders to better fit low socioeconomic status populations and improve future investigations.[75]

### Worldwide Prevalences

[edit]

Contrary to historical beliefs, BED is not limited to Western societies. Evidence of increasing eating disorder prevalence has been observed in "non-Western countries and among ethnic minorities".[37] Though the research on binge eating disorders tends to be concentrated in North America, the disorder occurs across cultures.[76] Increasing globalization has influenced the prevalence of eating disorders outside of the West.[37] In the US, BED is present in 0.8% of male adults and 1.6% of female adults in a given year.[77]

The prevalence of BED is lower in Nordic countries compared to Europe in a study that included Finland, Sweden, Norway, and Iceland.[78] The point prevalence ranged from 0.4 to 1.5 percent and the lifetime prevalence ranged from 0.7 to 5.8 percent for BED in women.[78]

In a study that included Argentina, Brazil, Chile, Colombia, Mexico, and Venezuela, the point prevalence for BED was 3.53 percent.[79] Therefore, this particular study found that the prevalence for BED is higher in these Latin American countries compared to Western countries.[79]

The prevalence of BED in Europe ranges from <1 to 4 percent.[80]

### Co-morbidities

[edit]

BED is co-morbid with diabetes, hypertension, previous stroke, and heart disease in some individuals.[68]

In people who have obsessive-compulsive disorder or bipolar I or II disorders, BED lifetime prevalence was found to be higher.[68]

Additionally, 30 to 40 percent of individuals seeking treatment for weight-loss can be diagnosed with binge eating disorder.[62]

### Underreporting in men

[edit]

Eating disorders are oftentimes underreported in men.[78] Underreporting could be a result of measurement bias due to how eating disorders are defined.[78] The current definition for eating disorders focuses on thinness.[78] However, eating disorders in men tend to center on muscularity and would therefore warrant a need for a different measurement definition.[78] Overvaluation rates of body weight or shape in adolescent males is significantly lower than their female counterpart (4.9% and 24.2%, respectively). Little is known if this discrepancy is an indicator of later onset of body image distortion in males or a consequence of female-centric diagnostic frameworks for eating disorders.[71]

The lack of representation of men in eating disorder research has been hindered by historical perceptions of eating disorders as a "female phenomenon".[71] Researchers have been called on to address this gap by advancing methods of "identification, assessment, classification, and treatment" for eating disorders in a male-specific context, specifically in young men.[71]

## Frequency

[edit]

BED is the most common eating disorder, with 47% of people with eating disorders have BED, 3% of them have anorexia nervosa and 12% of them have bulimia nervosa.[81] Over 57% of people with BED are female[81] and it often begins in the late teens or early 20s.[82]

## History

[edit]

The disorder was first described in 1959 by psychiatrist and researcher Albert Stunkard as "night eating syndrome" (NES).[83] The term "binge eating" was coined to describe the same bingeing-type eating behavior but without the exclusive nocturnal component.[84]

There is generally less research on binge eating disorder in comparison to anorexia nervosa and bulimia nervosa.[11]

## See also

[edit]

* Prader–Willi syndrome

## Reference notes

[edit]

1. ^ a b [43][44][46][47][48]

## References

[edit]

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42. ^ Brownley KA, Berkman ND, Peat CM, Lohr KN, Cullen KE, Bann CM, Bulik CM (September 2016). "Binge-Eating Disorder in Adults: A Systematic Review and Meta-analysis". Annals of Internal Medicine. 165 (6): 409–20\. doi:10.7326/M15-2455. PMC 5637727. PMID 27367316.409-20&rft.date=2016-09&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5637727#id-name=PMC&rft_id=info:pmid/27367316&rft_id=info:doi/10.7326/M15-2455&rft.aulast=Brownley&rft.aufirst=KA&rft.au=Berkman,+ND&rft.au=Peat,+CM&rft.au=Lohr,+KN&rft.au=Cullen,+KE&rft.au=Bann,+CM&rft.au=Bulik,+CM&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5637727&rfr_id=info:sid/en.wikipedia.org:Binge+eating+disorder" class="Z3988">
43. ^ a b c d Rodan SC, Bryant E, Le A, Maloney D, Touyz S, McGregor IS, Maguire S (July 2023). "Pharmacotherapy, alternative and adjunctive therapies for eating disorders: findings from a rapid review". Journal of Eating Disorders. 11 (1): 112. doi:10.1186/s40337-023-00833-9. PMC 10327007. PMID 37415200. "LDX is commonly used in the treatment of ADHD, and is the only treatment for BED that is currently approved by the Food and Drug Administration (FDA) and the Therapeutic Goods Administration (TGA). LDX, like all amphetamine stimulants, has direct appetite suppressant effects that may be therapeutically useful in BED, although long-term neuroadaptations in dopaminergic and noradrenergic systems caused by LDX may also be relevant, leading to improved regulation of eating behaviours, attentional processes and goal-directed behaviours. ...
Evidently, there is a substantial volume of trials with high-quality evidence supporting the efficacy of LDX in reducing binge eating frequency in treatment of adults with moderate to severe BED at 50–70 mg/day."
44. ^ a b c d e Boswell RG, Potenza MN, Grilo CM (January 2021). "The Neurobiology of Binge-eating Disorder Compared with Obesity: Implications for Differential Therapeutics". Clinical Therapeutics. 43 (1): 50–69\. doi:10.1016/j.clinthera.2020.10.014. PMC 7902428. PMID 33257092. "Stimulant medications may be especially effective for individuals with BED because of dual effects on reward and executive function systems. Indeed, the only FDA-approved pharmacotherapy for BED is LDX, a d-amphetamine prodrug. ...
In humans, RCTs found that LDX reduced binge eating and impulsivity/compulsivity symptoms. Notably, there is a strong correlation between compulsivity symptoms and severity/frequency of binge eating episodes observed in LDX trials. Further, in individuals with BED, changes in prefrontal brain systems associated with LDX treatment were related to treatment outcome."50-69&rft.date=2021-01&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7902428#id-name=PMC&rft_id=info:pmid/33257092&rft_id=info:doi/10.1016/j.clinthera.2020.10.014&rft.aulast=Boswell&rft.aufirst=RG&rft.au=Potenza,+MN&rft.au=Grilo,+CM&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7902428&rfr_id=info:sid/en.wikipedia.org:Binge+eating+disorder" class="Z3988">
45. ^ a b c Heal DJ, Smith SL (June 2022). "Prospects for new drugs to treat binge-eating disorder: Insights from psychopathology and neuropharmacology". Journal of Psychopharmacology. 36 (6): 680–703\. doi:10.1177/02698811211032475. PMC 9150143. PMID 34318734. "BED subjects have substantial decrements in their ventral striatal reward pathways and diminished ability to recruit fronto-cortical impulse-control circuits to implement dietary restraint. ...
There is not only substantial overlap between the psychopathology of BED and ADHD but also a clear association between these two disorders. Lisdexamfetamine's ability to reduce impulsivity and increase cognitive control in ADHD supports the hypothesis that efficacy in BED is dependent on treating its core obsessive, compulsive and impulsive behaviours."680-703&rft.date=2022-06&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9150143#id-name=PMC&rft_id=info:pmid/34318734&rft_id=info:doi/10.1177/02698811211032475&rft.aulast=Heal&rft.aufirst=DJ&rft.au=Smith,+SL&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9150143&rfr_id=info:sid/en.wikipedia.org:Binge+eating+disorder" class="Z3988">
46. ^ a b c d McElroy SL (2017). "Pharmacologic Treatments for Binge-Eating Disorder". The Journal of Clinical Psychiatry. 78 Suppl 1: 14–19\. doi:10.4088/JCP.sh16003su1c.03. PMID 28125174. "Genetic polymorphisms associated with abnormal dopaminergic signaling have been found in individuals who exhibit binge-eating behavior, and the binge-eating episodes,which often involve the consumption of highly palatable food, further stimulate the dopaminergic system. This ongoing stimulation may contribute to progressive impairments in dopamine signaling. Lisdexamfetamine is hypothesized to reduce binge-eating behavior by normalizing dopaminergic activity. ...
After 12 weeks, both studies found significant reductions in the number of binge-eating days per week in the active treatment group compared with placebo (P < .001 for both studies; Figure 1). Lisdexamfetamine was also found to be superior to placebo on a number of secondary outcome measures including global improvement, binge-eating cessation for 4 weeks, and reduction of obsessive-compulsive binge-eating symptoms, body weight, and triglycerides."14-19&rft.date=2017&rft_id=info:doi/10.4088/JCP.sh16003su1c.03&rft_id=info:pmid/28125174&rft.aulast=McElroy&rft.aufirst=SL&rfr_id=info:sid/en.wikipedia.org:Binge+eating+disorder" class="Z3988">
47. ^ a b c d e f Schneider E, Higgs S, Dourish CT (December 2021). "Lisdexamfetamine and binge-eating disorder: A systematic review and meta-analysis of the preclinical and clinical data with a focus on mechanism of drug action in treating the disorder". European Neuropsychopharmacology. 53: 49–78\. doi:10.1016/j.euroneuro.2021.08.001. PMID 34461386. "Our meta-analysis of the four RCT data sets (Guerdjikova et al., 2016; McElroy et al., 2015b; McElroy et al., 2016a) showed an overall significant effect of LDX on binge-eating symptom change. ...
BED has been described as an impulse control disorder since one of the key symptoms of the disorder is a lack of control over eating (American Psychiatric Association, 2013) and it is possible that LDX may be effective in treating BED at least in part by reducing impulsivity, compulsivity, and the repetitive nature of binge eating. There is extensive evidence that loss of impulse control in BED is a causal factor in provoking bingeing symptoms (Colles et al., 2008; Galanti et al., 2007; Giel et al., 2017; McElroy et al., 2016a; Nasser et al., 2004; Schag et al., 2013). More specifically, BED is associated with motor impulsivity and non-planning impulsivity which could initiate and maintain binge eating (Nasser et al., 2004). Neuroimaging studies using the Stroop task to measure impulse control have shown that BED patients have decreased BOLD fMRI activity in brain areas involved in self-regulation and impulse control including VMPFC, inferior frontal gyrus (IFG), and insula during performance of the task compared to lean and obese controls (Balodis et al., 2013b). ...
It is conceivable that in BED patients a low 30 mg dose of LDX could reduce food intake by suppressing appetite or enhancing satiety and higher (50 and 70 mg) doses of the drug may have a dual suppressant effect on food intake and binge-eating frequency."49-78&rft.date=2021-12&rft_id=info:doi/10.1016/j.euroneuro.2021.08.001&rft_id=info:pmid/34461386&rft.aulast=Schneider&rft.aufirst=E&rft.au=Higgs,+S&rft.au=Dourish,+CT&rfr_id=info:sid/en.wikipedia.org:Binge+eating+disorder" class="Z3988">
48. ^ Muratore AF, Attia E (July 2022). "Psychopharmacologic Management of Eating Disorders". Current Psychiatry Reports. 24 (7): 345–351\. doi:10.1007/s11920-022-01340-5. PMC 9233107. PMID 35576089. "An 11-week, double-blind RCT examined the effects of three doses of lisdexamfetamine (30 mg/day, 50 mg/day, 70 mg/day) and placebo on binge eating frequency. Results indicated that 50 mg and 70 mg doses were superior to placebo in reducing binge eating. Two follow-up 12-week RCTs confirmed the superiority of 50 and 70 mg doses to placebo in improving binge eating and secondary outcome measures, including obsessive–compulsive symptoms, body weight, and global improvement. ... Subsequent studies of lisdexamfetamine provided further support for the medication's safety and efficacy and provided additional evidence that continued use may be better than placebo in preventing relapse. While it is considered safe and effective, lisdexamfetamine's side effect profile and risk for misuse may make it inappropriate for certain patients."345-351&rft.date=2022-07&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9233107#id-name=PMC&rft_id=info:pmid/35576089&rft_id=info:doi/10.1007/s11920-022-01340-5&rft.aulast=Muratore&rft.aufirst=AF&rft.au=Attia,+E&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9233107&rfr_id=info:sid/en.wikipedia.org:Binge+eating+disorder" class="Z3988">
49. ^ Malenka RC, Nestler EJ, Hyman SE, Holtzman DM (2015). "Chapter 14: Higher Cognitive Function and Behavioral Control". Molecular neuropharmacology: a foundation for clinical neuroscience (3rd ed.). New York: McGraw-Hill Medical. ISBN 9780071827706. "Because behavioral responses in humans are not rigidly dictated by sensory inputs and drives, behavioral responses can instead be guided in accordance with short- or long-term goals, prior experience, and the environmental context. The response to a delicious-looking dessert is different depending on whether a person is alone staring into his or her refrigerator, is at a formal dinner party attended by his or her punctilious boss, or has just formulated the goal of losing 10 lb. ...
Adaptive responses depend on the ability to inhibit automatic or prepotent responses (eg, to ravenously eat the dessert or run from the snake) given certain social or environmental contexts or chosen goals and, in those circumstances, to select more appropriate responses. In conditions in which prepotent responses tend to dominate behavior, such as in drug addiction, where drug cues can elicit drug seeking (Chapter 16), or inattention deficit hyperactivity disorder (ADHD; described below), significant negative consequences can result."
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### Bibliography

[edit]

* Fairburn CG (1995). Overcoming Binge Eating. New York: Guilford Press. ISBN 0-89862-961-6.
* Grilo CM (1998). "The Assessment and Treatment of Binge Eating Disorder". Journal of Practical Psychiatry and Behavioral Health. 4 (4): 191–201\. doi:10.1097/00131746-199807000-00001.191-201&rft.date=1998&rft_id=info:doi/10.1097/00131746-199807000-00001&rft.aulast=Grilo&rft.aufirst=CM&rft_id=https://doi.org/10.1097%2F00131746-199807000-00001&rfr_id=info:sid/en.wikipedia.org:Binge+eating+disorder" class="Z3988">
* Siegel M, Brisman J, Weinshel M (1988). Surviving an Eating Disorder: New Perspectives and Strategies for Family and Friends. New York: Harper & Row. ISBN 0-06-015859-X.
* Yanovski SZ (July 1993). "Binge eating disorder: current knowledge and future directions". Obesity Research. 1 (4): 306–24\. doi:10.1002/j.1550-8528.1993.tb00626.x. PMID 16350580.306-24&rft.date=1993-07&rft_id=info:doi/10.1002/j.1550-8528.1993.tb00626.x&rft_id=info:pmid/16350580&rft.aulast=Yanovski&rft.aufirst=SZ&rft_id=https://doi.org/10.1002%2Fj.1550-8528.1993.tb00626.x&rfr_id=info:sid/en.wikipedia.org:Binge+eating+disorder" class="Z3988">
* Eating Disorders: Recognition and Treatment. NICE Guideline NG69. NICE. 2017. ISBN 978-1-4731-2508-7.

## External links

[edit]

* Media related to Binge eating disorder at Wikimedia Commons
* Pull, Charles B (January 2004). "Binge eating disorder". Current Opinion in Psychiatry. 17 (1): 43–48\. doi:10.1097/00001504-200401000-00008.43-48&rft.date=2004-01&rft_id=info:doi/10.1097/00001504-200401000-00008&rft.aulast=Pull&rft.aufirst=Charles+B&rfr_id=info:sid/en.wikipedia.org:Binge+eating+disorder" class="Z3988">
* Binge Eating Disorder on National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

Classification|

* ICD-10: F50.81
* ICD-9-CM: 307.59
* MeSH: D056912

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External resources|

* MedlinePlus: 003265

Authority control databases: National |

* Czech Republic

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