Binge Eating Disorder (BED)

Binge eating disorder (BED) was first characterized in 1959 by Stunkard as the presence of recurrent episodes of binge eating. BED can also include night eating with resultant weight gain but by definition does not include the use of vomiting or medications such as laxatives, emetics, or diuretics.[4]

Rumination and anxiety typically includes the recurrent thought: "Will I get fat?"[5]

Neural network areas involved show impairments in reward processing, inhibitory control, and emotion regulation, which can respond to psychotherapeutic interventions.[6]

Neuroanatomical studies of neuropeptide Y, a compound in the brain, have shown that it may regulate and control weight. Areas in the brain involved in binge eating include the medial orbitofrontal cortex, insula, and striatum; altered brain circuitry may also be associated with taste pleasantness and reward value. When 6-hydroxydopamine was injected into noradrenergic terminals, a direct cause was loss of normal function of hypothalamic ventral bundle termination areas with resultant hyperphagia, thus confirming that a function of the noradrenergic bundle included suppression of feeding, a function critical to body weight regulation. Without an intact noradrenergic bundle, d-amphetamine–induced loss of appetite was not observed.[7]

The anterior insula integrates sensory reward aspects of taste in the service of nutritional homeostasis as corticolimbic circuits regulate appetite.[8]

Alterations in the left orbitofrontal cortex, as can occur with lesions, result in increased insula volume, a finding that is nonspecific and seen in all eating disorders. Increased gray matter gyrus rectus volume specifically correlates with increased weight gain and an exaggerated response to sucrose pleasantness ratings in general.[8] Reduced white matter in the medial temporal lobe, as well as in the parietal lobe, may also be associated with binge eating disorder (BED).[9]

Overvaluation of body weight and a specific focus that one is overweight can begin in childhood; this may account for the internalization of weight bias and may be a belief that is modeled between caregivers and children and that continues into adolescence and young adulthood.

In a study, 245 treatment-seeking obese individuals with BED were evaluated with diagnostic and semistructured interviews and completed the Weight Bias Internalization Scale (WBIS) and the Rosenberg Self-Esteem Scale (RSE). Correlations and bootstrapping mediation analyses were computed to evaluate the relationships among self-esteem, overvaluation of shape/weight, and weight bias internalization. Significant correlations emerged between WBI, RSE, and overvaluation of shape and weight. Body mass index (BMI) did not correlate with any measure, and binge-eating frequency correlated only with overvaluation. Mediation analyses provided support for the hypothesis that overvaluation of shape and weight mediates the relationship between self-esteem and weight bias internalization.

Binging may acutely relieve negative mood; however, afterward, it generally causes the person’s negative mood to return even more intensely, reinforcing binging via negative reinforcement. Lower self-esteem and overvaluation of shape and weight contribute to weight bias internalization among patients with BED.[10]

A longitudinal study in Australia that monitored 1,383 persons from pregnancy to age 20 years elucidated early childhood factors of female sex and parent-perceived child overweight at age 10 years as being significant multivariate predictors. Later on, eating, weight, and shape concerns of the adolescent at age 14 years were predictive of later-onset binge-eating disorder. Evaluation of family interaction, including observing the binge eater engaging in a meal with his or her family, may reveal pathological family dynamics.[9]

A study by Bauer et al utilized eye tracking technology and found that persons with an eating disorder tend to look more at unattractive areas of their body; this may explain the cognitive distortion involved and the preoccupation and distress over one's body size.[11]

One US study found that the overall lifetime incidence of binge eating disorder (BED) could be as high as 3.5% among adult (>18 years) women and 2% among men, with slightly lower rates among younger persons aged 13–18 years (girls, 2.3%; boys, 0.8%).[10]

In a study of a large cohort of adolescents and young adults (in the Growing Up Today Study of the children of the Nurses’ Health Study II, a cohort study of >116,000 female registered nurses in the Boston, Massachusetts, area), binge eating was more common among females and was associated with incident overweight/obesity and with the onset of high depressive symptoms, as well as with initiation of marijuana use and other drugs, but not binge drinking. The prevalence of overeating or binge eating increased with age and peaked at 3.2% at age 19 years and was more common among females than males, with 2.3%-3.1% of females and 0.3%-1% of males reporting binge eating between ages 16 and 24 years.[12]

Studies have reported significantly elevated relative risk among family members of persons with BED, and data from twin studies indicated a range of heritability estimates ranging from 41%–57%.[13, 14]

Cultural factors may play a role in incidence, as well as access to care for binge eating. Asian Americans are more likely than whites to report binge eating; however, Asian Americans are less likely to receive services for binge eating.[15]

Gay and bisexual men with an eating disorder had a significantly higher prevalence of anxiety and substance-abuse disorders than gay and bisexual men without an eating disorder, similar to results from studies of predominantly heterosexual men with eating disorders in the general population, who were more likely to have anxiety and substance-abuse disorders than men without eating disorders. Lesbians and bisexual women with eating disorders were more likely to have a mood disorder than lesbians and bisexual women who did not have an eating disorder.[16]

Among 1680 individuals (32 blacks, 1648 whites) who received treatment for an eating disorder at a specialized center between 1979 and 1995 and who had completed an eating disorder questionnaire, blacks were more likely to report dissatisfaction with their body; they were also more likely to be obese than the white participants. This study was relatively small in number, as the 32 black participants were matched to 153 white participants; thus, the findings of this study should be interpreted with caution, as they should be replicated with a larger sample size.[17]

Another study examined interventions in African American women and found that technology can be helpful for self-monitoring.[18]

An Australian study by Mulders-Jones, Mitchison, Girosi and Hay in 2017, found no stratification by socioeconomic status for eating disorders, thus highlighting the imporance of considering the possibility of an eating disorder for all persons, including those unemployed or underemployed.[19]

Children, adolescents, and adults may experience a prodromal phase prior to meeting full criteria for binge-eating disorder.[20] Persons with binge eating disorder (BED) may be older than individuals with bulimia or anorexia nervosa who seek treatment. Long-term outcome studies indicate that BED may have a more favorable remission rate than other eating disorders. The severity, persistence, and duration, as well as suicide risk, for BED are comparable.[21]

The following links may be helpful for patients:

• National Eating Disorders Foundation

• Self-help

• Information from the National Institute of Mental Health

A youth or adult at high risk for binge-eating disorder (BED) is likely to binge in response to emotional triggers such as abandonment, loss, or work or school-related stress. The impact of societal pressures should not be ignored; media inputs such as movies, television, and the internet often show eating large portions of ice cream as an accepted method to cope with stress (eg, of a relationship breakup). Genetic factors, such as a family history of obesity or BED, should also be considered.[12]

BED can present in childhood, and the history may reveal that the patient experienced or witnessed disordered eating behavior as they were growing up. A small but well-conducted longitudinal study of adolescent females with early childhood experience of maternal restriction of caloric intake examined the risk of binge-eating disorders over a 13-year period. The study concluded that witnessing or experiencing disordered eating behaviors in childhood correlated with binge eating of snacks; the binging occurred despite eating to satiety.[22]

Thorough history taking should include query regarding suicidal ideation or planning or self-harm.[23] It is critically important to ask about substance misuse because of the frequent comorbidity of substance-use disorders with binge-eating disorder,[24] and questionnaires such as the AUDIT-C can be very helpful.[25]

A childhood history of emotional abuse also is a risk factor for BED.[26]

The use of a screening questionnaire such as the WRAQ (weight-related abuse questionaire) as designed by Salwen and Hymowitz in 2015 appears to be reliable and helpful.[27]

The role of the primary care provider should be to oversee the medical workup and to rule out physical conditions that can cause or contribute to morbidity and prevent mortality in eating disorders.[28]

Referral to a specialized eating disorders center can be helpful, especially a center that can perform certain procedures such as observing the binge eater eating in the context of the family, which is not feasible for a primary care provider to include as part of the evaluation.[29, 30]

Additional roles of the primary care provider include encouraging appropriate treatment of binge eating disorder (BED) and determining if treatment can safely occur on an outpatient basis or if a higher level of care is needed.[28]

The use of questionnaires such as the SCOFF and PHQ-9 can be very helpful to rule in or out comorbid conditions such as mood disorders or eating disorders besides binge-eating disorder and to ensure that an appropriate level of care is recommended.[31, 32]

Research trends include the study of autoantibodies against neuropeptides that are associated with psychological traits in eating disorders.[33] Specific anti-ghrelin immunoglobulins have been found to modulate ghrelin stability and its orexigenic effect and may be helpful in treatment.[34]

Screening for suicidality is especially important in the setting of bariatric surgery. Predictive factors for suicidality found by Adamowicz, Salwen, Hymowitz and Vivian included depressive symptomatology and hopelessness, as well as hopelessness and mood disorder diagnosis.[35]

 

When the physical examination or history suggests specific medical conditions that can cause or may be associated with weight gain, appropriate testing should be performed, such as blood testing for hypothyroidism or genetic testing to rule in or out a deletion or translocation syndrome such as Prader-Willi syndrome (such as on chromosome 15) or a different genetically related cause such as is accompanied by a mitochondrial dysfunction or an intellectual disability as etiologically related to binge eating disorder (BED).[36]

Treatment for binge eating disorder (BED) is generally performed on an outpatient basis. However, if the patient has severe comorbidities such as self-harm, suicidality, or substance misuse or the severity of the binge eating places the person at risk for significant physical illness, residential treatment should be considered.[29, 37] The role of loneliness should not be underestimated, especially when treatment is ineffective.[38]

Consultation/counseling from a nutrition specialist can be very effective in binge eating disorder (BED), especially when provided in combination with cognitive-behavioral therapy (CBT) or other interventions.[39]

Consultation with a psychologist and/or psychiatrist may also be considered.

Medication treatment should not be the first or only treatment for bingeeating disorder because of the efficacy of some nonpharmacologic approaches.

Fluoxetine (Prozac) is the only medication thus far approved by the US Food and Drug Administration for acute and maintenance treatment of binge eating and vomiting behaviors in patients with moderate-to-severe bulimia nervosa. However, other medications such as sertraline (Zoloft), fluvoxamine (Luvox), paroxetine (Paxil), and escitalopram (Lexapro), as well as other selective serotonin/norepinephrine reuptake inhibitors (SNRIs) and antidepressants that are generally FDA approved for depression and obsessive compulsive disorder, can also be useful alternatives when fluoxetine is not tolerated or is ineffective. Nonetheless, antidepressants are associated with weight gain in some cases, which can be a significant barrier to success.[40]

Lisdexamfetamine (Vyvanse) was approved by the FDA in January 2015 to treat moderate-to-severe BED in adults. It is the first FDA-approved medication to treat this condition.[41, 42]

Antiepileptic medications that decrease obsessive and compulsive behavior, such as topiramate, zonisamide, and lamotrigine, as well as other medications that decrease compulsive eating, such as exenatide and liraglutide, may be effective owing to their effect on the regulation of neuropeptide Y that may help to control weight. Antiobesity medications such as phentermine and orlistat are also options for controlling weight.

Older antiobesity medications such as sibutramine and d-fenfluramine have been removed from the worldwide market owing to cardiovascular safety concerns.

Acamprosate appeared to have a favorable side effect profile but may not be consistently effective for BED. Memantine also appeared ineffective. Some other medications that appear to be ineffective or that worsen BED include valproate, phenytoin, and oxcarbazepine.[43]

So far, pilot studies of agomelatine, a medication that increases levels of melatonin, have shown that it may be especially useful in persons that also have night eating syndrome (NES), which is characterized by reduced feeding during the day, evening hyperphagia accompanied by difficulty falling asleep (initial insomnia), and difficulties in sleep maintenance, including frequent nocturnal awakenings that are associated with episodes (while awake) of craving and compulsive ingestion of food and that can be associated with obesity.[39, 44]

Forty-five stable adults (ie, non-rapid cycling, absence of clinically significant hypomanic symptoms) with bipolar I/II disorder and comorbid attention deficit hyperactivity disorder (ADHD) were enrolled in a phase IV, 4-week, flexible-dose, open-label study of adjunctive LDX. All subjects were initiated at 30 mg/day of adjunctive LDX for the first week with flexible dosing (ie, 30-70 mg/day) between weeks 2 and 4. Of 45 subjects enrolled, 40 received adjunctive LDX (mean dose, 60 ± 10 mg/day).

A statistically significant decrease from baseline to endpoint was evident in weight (P  <  0.001), BMI (P  < 0.001), fasting total cholesterol (P  = 0.011), low-density lipoprotein cholesterol (P  = 0.044), and high-density lipoprotein cholesterol (P  = 0.015), but not triglycerides or blood glucose. Significant reductions were also observed in leptin (P  = 0.047), but not in ghrelin, adiponectin, or resistin levels.[45]

Cognitive behavior therapy (CBT) is a treatment of choice in binge eating disorder (BED), especially in the context of high levels of specific eating disorder psychopathology, such as overvaluation of body shape and weight. A randomized placebo-controlled trial found that CBT with placebo was superior to fluoxetine only, and adding fluoxetine to CBT did not enhance findings compared to adding placebo to CBT at 12-month follow-up after treatment completion.[46]

A meta-analysis of 45 studies found only moderate support for the efficacy of CBT and CBT guided self-help, and modest support for interpersonal psychotherapy (IPT), selective serotonin reuptake inhibitors (SSRI), and lisdexamfetamine in the treatment of adults with BED in terms of cessation of or reduction in the frequency of binge eating.[47]

Family therapy should be considered when family dynamics figure prominently as triggers for binging and in children and younger adolescents. Family therapy can be very helpful, but has not been proven superior to other approaches for BED such as interpersonal psychotherapy (IPT) or dialectical behavior therapy (DBT).

Family therapy can be effective to improve communication by decreasing negative emotional expressivity. Improved positive communication between family and friends of the person with BED may play an important role in encouraging persistence with treatment.[30]

IPT is a proven treatment for BED and focuses on identification of interpersonal conflict as triggers for binges.[48]

Guided self-help (GSH) appears to be less effective than CBT or DBT for BET. Although this approach is popular because of its low cost and easy accessibility (eg, as with self-help groups such as Something Fishy), this approach should be viewed carefully, as not all online GSH resources are balanced and supportive.[49, 19]

Integrative response therapy, which has the mnemonic RESPONSES (Reflect, Exercise, Start distracting, Problem Solve, Open communication, get distaNce, Soothe, get cEntered, Social and/or pleasurable activities) appeared to be an effective group-based cognitive restructuring and emotion management technique. Integrative response therapy appeared to show significant reduction in numbers of binge days by providing a structured intervention that provides temporary relief from aversive emotions.[50]

Behavioral weight loss (BWI):Self-monitoring strategies for behavioral weight loss typically include the following (1) A paper diary of diet, physical activity, weight, and obesity-related risk behaviors such as drinking sugary drinks to self-monitor weight maintenance and/or (2) electronic devices such as web-based dietary monitoring, mobile applications with food diaries, and activity trackers can be used with the potential to allow for more proximal reporting and immediate feedback.[18]

Dialectical behavior therapy (DBT) can be helpful to reduce binge eating, as it helps to reduce sudden intense surges of emotion. DBT is a manual-based treatment developed by Dr. Marsha Linehan that helps the person identify interpersonal relationship situations that can trigger cognitions that cause dysphoric emotions, to use their own strengths in collaboration with the therapist to be able to self–soothe, and to accept dysphoric emotions without needing to engage in maladaptive behaviors.[51, 52]

Embodied cognition therapy includes the idea that abnormal eating behaviors are both influenced by and influence how the brain encodes incoming perceptual data about the body such as the person’s perception of their own body image and internal states such as hunger and satiety.[53]

Virtual reality therapy uses technology to help to identify triggers for binge eating and is especially helpful in persons who do not integrate body image with a solid sense of self by reducing shame and improving body image. The idea of autobiographical awareness and memory as an external observation can be integrated in virtual reality.[54]

Mindfulness meditation is a Western form of meditation derived from a very old Buddhist practice called Vipassana or insight meditation, the skill of paying attention to one’s experiences with calm patient acceptance and compassion in a nonjudgmental manner. Mindfulness meditation can be practiced alone or with others; it involves the practice of being fully present in the moment with the breath to help with centering. Mindfulness meditation, when added to other interventions, appeared to be helpful.[55]

Yoga has appeared to provide lasting maintenance of stable BMI in some persons with BED.[56]

Bariatric surgery, although proven to help obese individuals with weight loss, may not be as effective in persons with BED unless they also receive an evidence-based intervention to ensure that the weight loss from the bariatric surgery is maintained.[57]

Functional consequences of binge eating disorder (BED) include social role adjustment problems, impaired health-related quality of life and life satisfaction, increased medical morbidity and mortality, and increased associated health care utilization compared with persons with equivalent BMI who do not have BED.

Being overweight or obese is often associated with BED.

Psychiatric comorbidities such as bipolar disorder, anxiety, and depressive disorders, as well as borderline personality disorder, can potentially confer increased risk of suicide or self-harm; long-term monitoring is important to ensure safety and positive outcomes.

Lower self-esteem has been associated with increased risk of suicidality, especially for males who are candidates for bariatric surgery.[58]

The American Psychiatric Association (APA) published guidelines for the treatment of eating disorders in February 2023.[59, 60] The guidelines recommend that screening for the presence of an eating disorder should be part of an initial psychiatric evaluation. The initial evaluation of a patient with a possible eating disorder should include assessment of multiple factors, including but not limited to, patient’s history of height and weight, eating-related behaviors, food repertoire, weight control behaviors, and family history. The evaluation should also identify co-occurring health conditions and psychiatric disorders.

Patients with binge-eating disorder (BED) should be treated with eating disorder–focused cognitive-behavioral therapy or interpersonal therapy, either individually or in a group. Adults with BED who prefer medication or have not responded to psychotherapy alone should be treated with either an antidepressant medication or lisdexamfetamine.

The goals of pharmacotherapy are to stop or reduce the compulsive behavior, to reduce morbidity, and to prevent complications.

Although nalmefene is an opioid antagonist that is not new, a recent small-size, open-label study found the drug to be well tolerated with no serious adverse effects in patients with comorbid borderline personality disorder (BPD) and alcohol use disorder (AUD). The drug demonstrated potential efficacy in improving self-injurious behavior and binge eating as well as in reducing alcohol consumption.[61]

Class Summary

These agents have been reported to reduce binge eating, vomiting, and depression, and to improve eating habits although their impact on body dissatisfaction remains unclear.

Paroxetine (Paxil, Pexeva)

Alternative DOC. Potent selective inhibitor of neuronal serotonin reuptake. Also has a weak effect on norepinephrine and dopamine neuronal reuptake.

For maintenance dosing, make dosage adjustments to maintain patient on lowest effective dosage, and reassess patient periodically to determine need for continued treatment.

Fluoxetine (Prozac)

Selectively inhibits presynaptic serotonin reuptake with minimal or no effect in the reuptake of norepinephrine or dopamine.

May cause more gastrointestinal adverse effects than other SSRIs now currently available, which is the reason it is not recommended as a first choice. May be given as a liquid and a capsule.

May give as 1 dose or divided doses. Presence of food does not appreciably alter levels of the medication. May take up to 4-6 weeks to achieve steady state levels of the medication as it has longest half-life (72 h).

Long half-life is both an advantage and a drawback. If it works well, an occasional missed dose is not a problem; if problems occur, eliminating all active metabolites takes a long time. The choice depends on adverse effects and drug interactions. Adverse effects of SSRIs seem to be quite idiosyncratic; thus, relatively few reasons exist to prefer one over another at this point if dosing is started at a conservative level and advanced as tolerated.

Indicated for the treatment of binge-eating and self-induced vomiting in patients with moderate-to-severe bulimia nervosa.

The antidepressant, anti–obsessive-compulsive, and antibulimic actions are presumed to be linked to inhibition of CNS neuronal uptake of serotonin.

Sertraline (Zoloft)

Selectively inhibits presynaptic serotonin reuptake.

Fluvoxamine (Luvox CR)

Enhances serotonin activity due to selective reuptake inhibition at neuronal membrane. Does not significantly bind to alpha-adrenergic, histamine, or cholinergic receptors and thus has fewer side effects than tricyclic antidepressants.

Has been shown to reduce repetitive thoughts, maladaptive behaviors, and aggression, and to increase social relatedness and language use.

Escitalopram (Lexapro)

Selective serotonin reuptake inhibitor (SSRI) and S-enantiomer of citalopram. Used for the treatment of depression. Mechanism of action is thought to be potentiation of serotonergic activity in central nervous system resulting from inhibition of CNS neuronal reuptake of serotonin. Onset of depression relief may be obtained after 1-2 wk, which is sooner than other antidepressants.

Class Summary

Agents in this class may be used off-label in some cases to prevent weight gain from binge-eating disorder and has the potential to decrease impulsive eating.

Lisdexamfetamine (Vyvanse)

Inactive prodrug of dextroamphetamine. Elicits CNS stimulant activity. Blocks norepinephrine and dopamine reuptake in presynaptic neurons and increases release of these monoamines in extraneuronal space. It is indicated for treatment of moderate-to-severe binge eating disorder.

Class Summary

These agents may regulate neuropeptide Y, which may help to control weight.

Liraglutide (Saxenda)

Incretin mimetic; analogue of human glucagonlike peptide-1 (GLP-1); acts as GLP-1 receptor agonist to increase insulin secretion in the presence of elevated blood glucose; delays gastric emptying to decrease postprandial glucose; also decreases glucagon secretion. It is indicated as an adjunct to a reduced-calorie diet and increased physical activity for chronic weight management in adults with a body mass index (BMI) of ≥30 (obesity) or adults with a BMI of ≥27 (overweight) who have at least 1 weight-related condition (eg, hypertension, type 2 diabetes, dyslipidemia). It is not specifically indicated for BED.

Exenatide (Bydureon, Byetta)

Incretin mimetic agent that mimics glucose-dependent insulin secretion and several other antihyperglycemic actions of incretins. Improves glycemic control in patients with type 2 diabetes mellitus by enhancing glucose-dependent insulin secretion by pancreatic beta cells, suppresses inappropriately elevated glucagon secretion, and slows gastric emptying. Drug's 39–amino acid sequence partially overlaps that of the human incretin, glucagonlike peptide-1. Indicated as adjunctive therapy to improve glycemic control in patients with type 2 diabetes who are taking metformin or a sulfonylurea but have not achieved glycemic control.

Class Summary

These agents may help to control weight.

Lorcaserin (Belviq)

February 13, 2020: FDA requested lorcaserin be withdrawn from the market owing to a potential risk of cancer

Thought to decrease food consumption and promote satiety by selectively activates 5-HT2C receptors on anorexigenic pro-opiomelanocortin neurons located in the hypothalamus

Phentermine (Adipex-P, Suprenza)

Sympathomimetic amine, increases release and reuptake of norepinephrine and dopamine. Anorexiant effect occurs as result of satiety center stimulation in the hypothalamic and limbic areas of the brain. Pharmacological component of comprehensive weight reduction program (behavioral modification, caloric restriction, exercise) intended for patients with initial BMI 3 30 kg/m2 or 3 27 kg/m2 if other risk factors (eg, diabetes, hyperlipidemia, hypertension) are present.

Class Summary

These agents inhibit absorption of dietary fats.

Orlistat (Alli, Xenical)

Gastrointestinal lipase inhibitor that induces weight loss by inhibiting nutrient absorption. Effectiveness in producing weight loss does not depend on systemic absorption. May reduce absorption of some fat-soluble vitamins (A, D, E, K) and beta-carotene. Administer multivitamin supplement containing fat-soluble vitamins PO qd 2 h ac or 1 h pc or every PM at bedtime. The prescription strength (Xenical) contains 120 mg/cap. The over-the-counter (OTC) strength (Alli) contains 60 mg/cap.

Class Summary

Anticonvulsants that decrease obsessive compulsive behavior may be effective.

Topiramate (Qudexy XR, Topiragen, Trokendy XR, Topamax)

Sulfamate-substituted monosaccharide with broad spectrum of antiepileptic activity that may have state-dependent sodium channel– blocking action. Potentiates inhibitory activity of neurotransmitter GABA. May block glutamate activity.

Zonisamide (Zonegran)

Does not affect GABA activity. Through action at sodium and calcium channels may stabilize neuronal membranes and suppress neuronal hypersynchronization.

Lamotrigine (Lamictal)

Inhibits voltage-sensitive sodium channels and release of glutamate (an excitatory amino acid).