Bulimia Nervosa and Binge Eating Disorder: Shared and Distinct Features, CBT-E, and Pharmacotherapy

Bulimia nervosa (BN) and binge eating disorder (BED) are the two most prevalent eating disorders characterized by recurrent episodes of binge eating — the consumption of an objectively large amount of food accompanied by a subjective sense of loss of control. Despite sharing this core behavioral feature, they diverge in critical ways: the presence or absence of regular compensatory behaviors, the degree of overvaluation of weight and shape, body composition profiles, comorbidity patterns, and treatment response trajectories. Understanding both their overlap and their distinctiveness is essential for accurate diagnosis, effective treatment planning, and meaningful prognostic assessment.

Historically, BED was not recognized as an independent diagnostic entity until DSM-5 (2013), having existed for two decades in the appendix of DSM-IV as a condition requiring further study. This delayed recognition contributed to underdiagnosis and undertreatment. BN, by contrast, was formally classified in DSM-III in 1980 following Gerald Russell's landmark 1979 description. Both disorders carry substantial medical morbidity, psychosocial impairment, and mortality risk — BN particularly through electrolyte disturbances and esophageal complications from purging, and BED through obesity-related cardiometabolic disease.

This article provides a detailed clinical comparison of BN and BED, examining diagnostic criteria, neurobiological substrates, epidemiology, evidence-based treatments with specific outcome data, prognostic factors, and emerging research directions. The goal is to equip clinicians and advanced learners with the depth of knowledge needed for nuanced clinical decision-making.

DSM-5-TR Criteria for Bulimia Nervosa

According to the DSM-5-TR, BN requires: (A) recurrent episodes of binge eating, defined as eating an amount of food that is definitively larger than what most individuals would eat under similar circumstances, accompanied by a sense of lack of control; (B) recurrent inappropriate compensatory behaviors to prevent weight gain, including self-induced vomiting, misuse of laxatives, diuretics, or other medications, fasting, or excessive exercise; (C) both binge eating and compensatory behaviors occurring, on average, at least once per week for three months; (D) self-evaluation being unduly influenced by body shape and weight; and (E) the disturbance not occurring exclusively during episodes of anorexia nervosa. Severity is graded by frequency of compensatory behaviors: mild (1–3/week), moderate (4–7/week), severe (8–13/week), and extreme (≥14/week).

DSM-5-TR Criteria for Binge Eating Disorder

BED requires: (A) recurrent episodes of binge eating, as defined above; (B) binge-eating episodes associated with three or more of the following: eating much more rapidly than normal, eating until uncomfortably full, eating large amounts when not physically hungry, eating alone due to embarrassment, and feeling disgusted, depressed, or guilty afterward; (C) marked distress regarding binge eating; (D) binge eating occurring on average at least once per week for three months; and (E) binge eating not associated with the recurrent use of inappropriate compensatory behaviors and not occurring exclusively during the course of BN or AN. Severity is graded by binge frequency: mild (1–3/week), moderate (4–7/week), severe (8–13/week), extreme (≥14/week).

Key Diagnostic Distinctions and Pitfalls

The cardinal distinction is compensatory behavior: BN requires it, BED excludes it. However, clinical reality presents challenges. Some individuals with BED engage in occasional compensatory behaviors that do not meet the frequency threshold for BN — the DSM-5-TR describes this as "recurrent" compensatory behavior, though the boundary can be ambiguous. Additionally, self-evaluation unduly influenced by shape and weight is a required criterion for BN but is not part of the BED criteria — yet research consistently demonstrates that a substantial subset (estimated 50–60%) of individuals with BED also show significant overvaluation of weight and shape, which has been proposed as a specifier for future diagnostic iterations.

Differential diagnosis must also consider: (1) Anorexia nervosa, binge-eating/purging type, which is differentiated by significantly low body weight; (2) Other specified feeding or eating disorder (OSFED), particularly subthreshold presentations; (3) Night eating syndrome, where the predominant pattern is evening/nocturnal eating without necessarily meeting binge criteria; and (4) Obesity without BED, as not all individuals with obesity binge eat and not all individuals with BED are obese (approximately 30–40% of individuals with BED have a BMI in the normal or overweight range). ICD-11 criteria are broadly congruent with DSM-5-TR but use a dimensional severity framework and emphasize functional impairment more explicitly.

BED is the most common eating disorder in the United States and globally. Lifetime prevalence estimates from the WHO World Mental Health Surveys and NIMH data indicate a lifetime prevalence of approximately 2.8% for BED in women and 1.0% in men in U.S. samples, with 12-month prevalence around 1.2% for women and 0.4% for men. For BN, lifetime prevalence is approximately 1.0–1.5% in women and 0.1–0.5% in men. BED is notably more equally distributed across sexes than BN or AN, with an approximate female-to-male ratio of 3:2, compared to roughly 10:1 for AN and 5:1 for BN.

Importantly, BED is more prevalent in Black, Latino/a, and Native American populations compared to white populations — unlike AN and BN, which have historically shown higher rates in white samples (though this likely reflects ascertainment bias). BED also shows a later average age of onset (approximately 21–25 years) compared to BN (approximately 18–20 years) and AN (approximately 15–18 years). Both BN and BED are underdiagnosed in men, older adults, and racial/ethnic minorities, and in individuals with higher body weight who may have binge eating normalized or attributed solely to weight status.

Incidence data are more limited, but the incidence of BN in primary care settings has been estimated at approximately 6.1 per 100,000 person-years in women, with evidence suggesting a decline in BN incidence since the 1990s that may partly reflect diagnostic migration to BED following its formal recognition. BED incidence data remain sparse but studies suggest rates of 150–400 per 100,000 person-years in community samples.

Reward and Dopaminergic Systems

Both BN and BED involve dysregulation of reward circuitry, but the specifics differ. Functional neuroimaging studies consistently demonstrate that individuals with BED show heightened activation in the ventral striatum and orbitofrontal cortex (OFC) in response to food cues — a pattern resembling the incentive salience model of addiction, where anticipatory reward is amplified. In contrast, individuals with BN show a more complex pattern: heightened food cue reactivity but blunted consummatory reward, consistent with a model in which the act of binge eating fails to deliver expected satisfaction, potentially perpetuating the cycle. PET studies using [¹¹C]raclopride have demonstrated reduced striatal dopamine D2/D3 receptor binding potential in BED, analogous to findings in substance use disorders.

Serotonergic and Opioidergic Systems

The serotonin (5-HT) system is implicated in both disorders, particularly via the 5-HT_2C and 5-HT_1A receptor subtypes. Reduced central serotonergic function is associated with impulsivity and diminished satiety signaling — both core features of binge eating. The efficacy of SSRIs in both BN and BED provides indirect pharmacological evidence for serotonergic involvement. The endogenous opioid system also contributes: mu-opioid receptor activation in the nucleus accumbens shell enhances the hedonic impact of palatable food ("liking"), and animal models demonstrate that opioid antagonists reduce binge eating, providing the rationale for naltrexone-based strategies.

Prefrontal and Inhibitory Control Circuits

Both disorders show deficits in cognitive control, mediated by the dorsolateral prefrontal cortex (dlPFC) and anterior cingulate cortex (ACC). However, BN appears to involve more pronounced impulsivity across domains (behavioral, cognitive, and motor), likely reflecting broader prefrontal hypofunction. BED, while also associated with impulsivity, may be more specifically characterized by decision-making deficits and attentional biases toward food stimuli, with relatively more preserved general impulse control compared to BN.

Hypothalamic-Pituitary-Adrenal (HPA) Axis and Stress

Stress-induced binge eating is a well-documented phenomenon in both disorders. Cortisol dysregulation — including elevated basal cortisol and blunted cortisol reactivity to acute stress — has been reported in both conditions. Emotional eating in BED may be more closely linked to affect regulation deficits (eating to cope with negative affect), while in BN, the purge component may serve an additional emotion-regulation function.

Genetic and Epigenetic Factors

Twin studies estimate heritability at approximately 55–62% for BN and 41–57% for BED. Genome-wide association studies (GWAS) have identified shared genetic risk loci between BN and metabolic traits (BMI, insulin resistance), and between BED and psychiatric phenotypes (depression, ADHD). Notably, a large GWAS from the Psychiatric Genomics Consortium Eating Disorders Working Group identified a significant locus on chromosome 3 associated with AN that shows cross-disorder signal with BN, suggesting shared transdiagnostic genetic architecture. Candidate gene studies have implicated variants in HTR2A (serotonin 2A receptor), DRD2 (dopamine D2 receptor), BDNF, and OPRD1 (delta opioid receptor), though most single-gene findings await replication in adequately powered samples.

Psychiatric comorbidity is the rule rather than the exception in both BN and BED, and comorbidity profiles differ in important ways that affect treatment planning and prognosis.

Mood Disorders

Major depressive disorder (MDD) co-occurs with BN in approximately 50–70% of cases and with BED in approximately 30–50%. Bipolar spectrum disorders may be more common in BN than BED. The temporal relationship is bidirectional: depression can precede, follow, or co-occur with eating disorder onset. Importantly, persistent depressive comorbidity is a consistent predictor of poorer treatment outcome in both disorders.

Anxiety Disorders

Anxiety disorders co-occur in approximately 50–65% of individuals with BN and 35–55% of those with BED. Social anxiety disorder is particularly common in both, with prevalence estimates of 20–35%. Generalized anxiety disorder, specific phobias, and PTSD are also significantly elevated. In BN, obsessive-compulsive disorder (OCD) shows notable comorbidity (10–15%), reflecting shared compulsive features.

Substance Use Disorders

BN has a significantly elevated rate of substance use disorders (SUDs), estimated at 20–35%, particularly alcohol use disorder. This association is less pronounced in BED (approximately 15–20%), though still elevated relative to the general population. The BN-SUD link may reflect a shared impulsivity-related neurobiological substrate. Multi-impulsive bulimia — a clinical phenotype characterized by co-occurring self-harm, substance misuse, and BN — carries a particularly guarded prognosis.

Attention-Deficit/Hyperactivity Disorder (ADHD)

Emerging evidence links both BN and BED to ADHD, with prevalence estimates of approximately 10–20% in BED and 8–15% in BN. The impulsivity and executive function deficits characteristic of ADHD may represent a shared diathesis for loss-of-control eating. The efficacy of lisdexamfetamine in BED (discussed below) may partly reflect its action on ADHD-related pathways.

Personality Disorders

Cluster B personality disorders, especially borderline personality disorder (BPD), co-occur in approximately 20–30% of BN cases and 10–15% of BED cases. BPD comorbidity is associated with greater severity, higher rates of self-harm, and poorer treatment response. Cluster C traits (avoidant, dependent) are common across both disorders.

Overview of Enhanced Cognitive-Behavioral Therapy

Cognitive-behavioral therapy enhanced (CBT-E), developed by Christopher Fairburn and colleagues at Oxford, is the most extensively studied and empirically supported psychotherapy for both BN and BED. CBT-E is transdiagnostic, built on the theory that eating disorders are maintained by a shared psychopathological mechanism: the overvaluation of eating, shape, and weight and their control. It exists in two forms: a focused form (CBT-Ef) addressing core eating disorder pathology, and a broad form (CBT-Eb) that also addresses external maintaining mechanisms — clinical perfectionism, core low self-esteem, interpersonal difficulties, and mood intolerance. Standard treatment consists of 20 sessions over 20 weeks for patients who are not significantly underweight.

CBT-E proceeds through four stages: Stage 1 (sessions 1–7) establishes engagement, psychoeducation, regular eating, and real-time self-monitoring; Stage 2 (sessions 8–9) is a brief review and formulation refinement; Stage 3 (sessions 10–17) targets core maintaining mechanisms (dietary restraint, overvaluation of shape/weight, event-driven eating); Stage 4 (sessions 18–20) focuses on relapse prevention and maintaining gains.

Outcomes in Bulimia Nervosa

CBT (CBT-BN and later CBT-E) has been the first-line treatment for BN since the landmark 1993 study by Fairburn and colleagues comparing CBT, behavior therapy, and interpersonal therapy (IPT). Meta-analyses consistently demonstrate that CBT-E achieves binge-purge abstinence rates of approximately 40–50% at end of treatment, with sustained remission at 60-week follow-up in approximately 50–60% of treatment completers. The number needed to treat (NNT) for CBT versus waitlist control is approximately 3–4 for achieving binge-purge abstinence. The Fairburn et al. (2009) trial comparing the focused and broad forms of CBT-E in a transdiagnostic eating disorder sample demonstrated comparable outcomes for less complex cases, while the broad form showed advantages in patients with marked clinical perfectionism or interpersonal difficulties.

Outcomes in Binge Eating Disorder

CBT-E shows even higher binge abstinence rates in BED, with end-of-treatment abstinence typically around 50–60% and sometimes exceeding 65% in completer analyses. However, a critical limitation is that CBT-E for BED does not typically produce significant weight loss — a finding that can be disappointing for patients and clinicians who expect binge cessation to resolve obesity. The Grilo et al. (2011) study in BED confirmed that while CBT was superior to behavioral weight loss (BWL) for binge remission, BWL produced more weight loss, and neither intervention produced clinically meaningful long-term weight change.

CBT-E versus Other Psychotherapies: Comparative Data

Interpersonal therapy (IPT) is the principal alternative to CBT-E for both BN and BED. In BN, the landmark Fairburn et al. (1993) and Agras et al. (2000) trials demonstrated that CBT was superior to IPT at end of treatment, though IPT showed a "catch-up" effect by 8–12 months follow-up, approaching equivalent outcomes. For BED, IPT and CBT show broadly comparable outcomes by follow-up, as demonstrated in the Wilfley et al. (2002) trial. Dialectical behavior therapy (DBT) adapted for BED has shown promising results, with binge abstinence rates of approximately 64% in the Telch et al. (2001) randomized trial, though the evidence base is smaller than for CBT-E.

Pharmacotherapy for Bulimia Nervosa

Fluoxetine (60 mg/day) remains the only FDA-approved medication for BN and is the most studied pharmacological agent for this indication. The landmark Fluoxetine Bulimia Nervosa Collaborative Study Group (1992) trial demonstrated a reduction in binge-purge frequency of approximately 50–67% compared to 33% for placebo, with binge abstinence in approximately 20–30% versus 10–15% for placebo. Meta-analyses of SSRIs in BN suggest an NNT for binge remission of approximately 9, highlighting that pharmacotherapy alone has modest efficacy compared to CBT. Higher doses of fluoxetine (60 mg versus 20 mg) are more effective in BN, which is notable because this exceeds the typical antidepressant dose. Other SSRIs (sertraline, fluvoxamine) have shown efficacy in smaller trials but without the same depth of evidence.

Topiramate has demonstrated efficacy in reducing binge-purge frequency and promoting weight loss in BN, but its use is limited by cognitive side effects (word-finding difficulty, concentration impairment) and teratogenicity. Tricyclic antidepressants (desipramine, imipramine) showed early efficacy in BN trials in the 1980s but are now rarely used due to safety concerns. Bupropion is contraindicated in BN due to significantly elevated seizure risk in the context of purging-related electrolyte disturbances.

Pharmacotherapy for Binge Eating Disorder

Lisdexamfetamine dimesylate (Vyvanse) is the only FDA-approved medication for moderate-to-severe BED. Three pivotal Phase III trials (SPD489-343, -344, -345; McElroy et al., 2015, 2016) demonstrated binge-day cessation rates of approximately 36–50% with lisdexamfetamine 50–70 mg/day versus 13–21% for placebo (NNT ≈ 4–5). Effect sizes for binge-day reduction were large (Cohen's d ≈ 0.80–1.00). Importantly, lisdexamfetamine also produced modest weight loss (approximately 5–6 kg over 12 weeks), differentiating it from CBT and SSRIs. However, as an amphetamine prodrug, it carries abuse potential (Schedule II), and it is not recommended for concurrent weight loss indication.

SSRIs have demonstrated moderate efficacy in BED, though none is FDA-approved for this indication. Meta-analytic data suggest SSRIs reduce binge frequency by approximately 50% more than placebo, with binge abstinence rates of approximately 25–35% versus 15–20% for placebo. Topiramate has shown strong efficacy in BED for both binge reduction and weight loss (mean weight loss approximately 4.5–6.0 kg versus placebo), with the McElroy et al. (2007) trial being a key reference, but tolerability limits its use.

Combination Treatment

The question of whether combined CBT + pharmacotherapy outperforms either alone has been addressed in several trials with mixed results. For BN, the Walsh et al. (1997) trial found that CBT + medication was modestly superior to CBT alone, but the added benefit was small. For BED, the Grilo et al. (2005) study found that CBT + fluoxetine did not significantly outperform CBT + placebo. The clinical consensus is that CBT-E should be the primary intervention, with pharmacotherapy considered when CBT is unavailable, insufficient, or when significant comorbidities (e.g., depression, ADHD) warrant additional treatment.

Identifying predictors of treatment response is crucial for clinical decision-making and for personalizing treatment approaches. Research has identified several consistent predictors across both BN and BED.

Favorable Prognostic Indicators

• Early behavioral change: Rapid reduction in binge frequency during the first 4–6 sessions of CBT is one of the most robust predictors of end-of-treatment remission in both BN and BED. The Fairburn et al. (2004) rapid response analysis found that patients who achieved ≥70% binge reduction by session 4 were significantly more likely to be remitted at end of treatment and at 60-week follow-up.
• Shorter duration of illness: Earlier presentation and treatment engagement are associated with better outcomes across eating disorders.
• Lower baseline psychopathology severity: Less severe overvaluation of shape/weight and lower baseline binge frequency predict better outcomes.
• Absence of personality disorder: Particularly the absence of borderline personality disorder or cluster B traits.
• Adequate treatment dose: Completing a full course of CBT-E (all 20 sessions) is strongly associated with better outcomes; dropout rates across trials range from 15–30% and are a significant barrier to effectiveness.

Unfavorable Prognostic Indicators

• Comorbid depression: Persistent, untreated MDD during eating disorder treatment is associated with poorer outcomes in both BN and BED.
• Childhood trauma and PTSD: History of sexual abuse and current PTSD predict higher severity at baseline and reduced treatment response.
• Multi-impulsive presentation: Co-occurring substance use, self-harm, and impulsive behaviors predict poorer response to standard CBT and may require adapted approaches (e.g., DBT-informed treatment).
• High overvaluation of shape and weight in BED: This subgroup of BED patients shows greater severity, more comorbidity, and poorer prognosis, resembling BN more closely.
• Higher BMI in BED: While not consistently predictive of binge outcome, higher baseline BMI is associated with less weight loss and greater medical morbidity.
• Purging type and frequency in BN: More frequent purging (severe/extreme) predicts lower remission rates.

Synthesizing across domains, BN and BED can be compared along several dimensions that clarify their relationship and clinical distinctions.

Psychopathological Architecture

Both disorders share the core feature of binge eating with loss of control, but BN is characterized by a more consistent and pronounced overvaluation of weight and shape that drives compensatory behavior. BED, while often involving body dissatisfaction, does not universally center self-evaluation on weight and shape. This distinction has theoretical importance: in Fairburn's cognitive-behavioral model, the overvaluation of shape and weight is the "core psychopathology" that drives dietary restriction, which in turn triggers binge eating, which in turn triggers purging in BN. In BED, the pathway may be more affect-driven, with negative emotional states and interpersonal triggers playing a proportionally larger role in initiating binges.

Body Weight and Metabolic Consequences

Individuals with BN are typically at a normal or near-normal weight (BMI 18.5–30), as compensatory behaviors partially offset caloric intake from binges. Individuals with BED have higher average BMIs, with approximately 60–70% meeting criteria for obesity (BMI ≥30). However, this is not a diagnostic requirement, and clinicians must avoid the assumption that only obese patients can have BED. The metabolic consequences differ accordingly: BN carries risk of hypokalemia, metabolic alkalosis (from vomiting), dental erosion, parotid enlargement, and esophageal tears (Mallory-Weiss syndrome), while BED carries risk of type 2 diabetes, dyslipidemia, hypertension, and obstructive sleep apnea through obesity-mediated pathways.

Course and Chronicity

Both disorders tend toward chronicity without treatment. Longitudinal data suggest that approximately 45–55% of individuals with BN recover fully within 5–10 years, with 20–30% continuing to meet full criteria and 20–30% showing partial remission with subthreshold symptoms. For BED, recovery rates appear somewhat higher (approximately 50–65% at 5-year follow-up), though recurrence is common. Diagnostic crossover between BN and BED occurs in approximately 10–25% of cases over time, with transitions more commonly from BN to BED than the reverse, particularly when compensatory behaviors decrease but binge eating persists.

Several populations warrant specific clinical attention in the context of BN and BED.

Males

Eating disorders in males are underdiagnosed and undertreated. Males with BN and BED may present with different body image concerns (muscularity-oriented rather than thinness-oriented), may use different compensatory behaviors (excessive exercise more than vomiting), and may be less likely to seek treatment. Prevalence may be underestimated by 50% or more due to gendered diagnostic criteria and clinical biases.

Adolescents

Both BN and BED occur in adolescents, though BED is less commonly diagnosed before age 18 partly due to clinician unfamiliarity. CBT-E has been adapted for adolescents (CBT-Ea) with promising preliminary outcomes. Family-based treatment (FBT), while the gold standard for adolescent AN, has limited evidence in adolescent BN, though one RCT (Le Grange et al., 2007) found FBT comparable to CBT in adolescent BN.

Bariatric Surgery Candidates

BED prevalence in bariatric surgery populations ranges from approximately 15–40% depending on assessment method. Pre-surgical BED does not consistently predict poor surgical outcomes, but loss-of-control eating that persists or re-emerges post-surgery is associated with inferior weight loss and weight regain. Screening for BED should be standard in bariatric assessment, and post-surgical monitoring for recurrence is recommended.

Pregnancy

Both BN and BED carry specific risks during pregnancy, including higher rates of gestational diabetes (particularly in BED), hyperemesis, preterm delivery, and low birth weight (particularly in BN with active purging). Pharmacotherapy decisions require careful risk-benefit analysis, as fluoxetine and lisdexamfetamine have different safety profiles in pregnancy.

Several research frontiers hold promise for improving outcomes in BN and BED.

Neuromodulation

Repetitive transcranial magnetic stimulation (rTMS) targeting the left dorsolateral prefrontal cortex (dlPFC) has shown preliminary efficacy in reducing binge-purge episodes in BN. A sham-controlled trial by Van den Eynde et al. (2010) demonstrated acute reductions in food craving and binge urges after a single session, and subsequent small trials have reported reductions in binge frequency over multi-session protocols. This approach leverages the known dlPFC hypofunction in BN and parallels rTMS applications in substance use disorders and depression. Transcranial direct current stimulation (tDCS) targeting similar regions is also under investigation, with the advantage of lower cost and easier scalability.

Digital and Guided Self-Help Interventions

Internet-delivered CBT and app-based guided self-help programs have shown moderate efficacy for both BN and BED. A meta-analysis by Linardon et al. (2020) found that internet-based CBT produced binge abstinence rates of approximately 25–35%, lower than face-to-face CBT but significantly superior to waitlist. Given the large treatment gap — estimates suggest fewer than 25% of individuals with BED and fewer than 40% with BN receive any eating disorder-specific treatment — scalable interventions represent a critical public health priority.

Pharmacological Horizons

GLP-1 receptor agonists (semaglutide, liraglutide), originally developed for type 2 diabetes and obesity, have shown significant potential for BED. These agents reduce appetite and food reward through both peripheral and central mechanisms, including effects on hypothalamic appetite circuits and mesolimbic dopamine signaling. Case series and early clinical data suggest marked reductions in binge eating and body weight, and several RCTs are currently underway. If efficacy is confirmed, GLP-1 agonists could represent the first pharmacological option to simultaneously address binge eating and obesity in BED — a combination that has eluded existing treatments.

Precision and Personalized Approaches

Research is increasingly moving toward identifying moderators and mediators of treatment response to enable personalized treatment allocation. The concept of "rapid response" — significant symptomatic improvement in the first 4 weeks — is being explored as a clinical decision point: non-rapid responders to CBT may benefit from early augmentation with pharmacotherapy or a switch to an alternative modality. Biomarker research, including neuroimaging-based predictors and genetic risk scores, is in early stages but holds long-term promise for treatment personalization.

Based on the current evidence, the following treatment algorithm reflects best practice for BN and BED:

Bulimia Nervosa

• First-line: CBT-E (20 sessions over 20 weeks). Expected binge-purge abstinence: 40–50%. NNT ≈ 3–4 versus waitlist.
• Augmentation or alternative if CBT unavailable/insufficient: Fluoxetine 60 mg/day. Expected binge-purge reduction: 50–67% versus 33% for placebo. Binge abstinence: 20–30%. NNT ≈ 9.
• Second-line psychotherapy: IPT (20 sessions), which shows equivalent outcomes to CBT by 8–12 month follow-up but slower initial response.
• Complex presentations (BPD, multi-impulsivity, trauma): Consider CBT-Eb (broad form) or DBT-informed approaches.

Binge Eating Disorder

• First-line: CBT-E (20 sessions). Expected binge abstinence: 50–60%. NNT ≈ 3 versus waitlist.
• Pharmacotherapy (moderate-severe, or CBT unavailable/insufficient): Lisdexamfetamine 50–70 mg/day. Expected binge-day cessation: 36–50% versus 13–21% placebo. NNT ≈ 4–5.
• Alternative pharmacotherapy: Topiramate (if tolerated) or SSRIs.
• If weight loss is a concurrent goal: Sequential approach — address binge eating first with CBT-E, then consider behavioral weight management. Concurrent behavioral weight loss programs may address weight but are less effective for binge cessation than CBT.
• Second-line psychotherapy: IPT or DBT adapted for BED.

In both disorders, medical monitoring (electrolytes in BN, metabolic parameters in BED), treatment of comorbidities, and nutritional counseling are important adjuncts to the core psychological and pharmacological interventions. Long-term follow-up is recommended given recurrence rates of 20–40% across both conditions.