Binge Eating Disorder

Psychiatric MONDO:0005582 Pathograph 3 Eating Disorder Mental Health Disorder

Binge eating disorder is an eating disorder characterized by recurrent binge eating episodes with loss of control and marked distress, without regular compensatory behaviors such as purging.

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2
Pathophys.
4
Phenotypes
3
Pathograph
2
Genes
4
Treatments
2
Differentials
15
References
1
Deep Research
⚙

Pathophysiology

2
Reward Hypersensitivity
Binge eating disorder is modeled as altered reward processing, including increased food reward and anticipatory reward responses that maintain binge-eating behavior.
neuron link
G protein-coupled dopamine receptor signaling pathway link ⚠ ABNORMAL
brain link striatum link prefrontal cortex link
Downstream
Binge Eating Episodes Reward hypersensitivity is represented upstream of recurrent binge-eating episodes.
Show evidence (1 reference)
DOI:10.1007/s11920-024-01534-z SUPPORT Human Clinical
"Reward hypersensitivity and impaired inhibitory control are mechanisms underlying binge eating disorder."
Review evidence supports reward hypersensitivity as an underlying BED mechanism.
Impaired Inhibitory Control
Impaired inhibitory control is represented as a separate top-down control mechanism that can fail to suppress binge-eating behavior.
neuron link
prefrontal cortex link
Downstream
Binge Eating Episodes Reduced inhibitory control is represented upstream of recurrent binge-eating episodes.
Show evidence (1 reference)
DOI:10.1007/s11920-024-01534-z SUPPORT Human Clinical
"Reward hypersensitivity and impaired inhibitory control are mechanisms underlying binge eating disorder."
Review evidence supports impaired inhibitory control as an underlying BED mechanism.
⬡

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Binge Eating Disorder Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.
●

Phenotypes

4
Nervous System 2
Binge Eating Episodes Abnormal eating behavior (HP:0100738)
Show evidence (1 reference)
PMID:39659158 SUPPORT Human Clinical
"Intention-to-treat binge-eating remission rates differed significantly between treatments, with CBT+LDX having the highest remission rate (70.2%) followed by CBT (44.7%) and LDX (40.4%)."
The randomized trial uses binge-eating remission as the key clinical outcome, supporting binge-eating episodes as a core BED phenotype.
Loss of Control Over Eating Abnormal eating behavior (HP:0100738)
Show evidence (2 references)
PMID:36920120 SUPPORT Human Clinical
"Binge-eating disorder involves overeating while feeling a loss of control (LOC)."
Treatment-seeking BED cohort evidence supports loss of control as a core BED symptom dimension.
PMID:18239550 SUPPORT Human Clinical
"The loss of control (LOC) over eating, that is, being unable to stop eating or control what or how much was consumed was most closely related to psychological markers of distress common in BED."
Clinical cohort evidence supports LOC over eating as central to BED- related psychological disturbance.
Growth 1
Increased Body Weight Increased body weight (HP:0004324)
Show evidence (1 reference)
PMID:23472839 PARTIAL Human Clinical
"In the adjusted analysis, obesity, fair/poor self-rated health status and body dissatisfaction remained strongly associated with binge eating."
Population-based evidence supports an obesity association with binge eating, while not establishing increased body weight as required for all BED.
Other 1
Marked Distress About Binge Eating Abnormal emotional state (HP:0100851)
Show evidence (1 reference)
PMID:36920120 SUPPORT Human Clinical
"Patients with fear of LOC reported greater distress about binge eating and greater depression than those with no fear/resignation."
Clinical interview evidence supports distress about binge eating as a clinically relevant BED symptom dimension.
🧬

Genetic Associations

2
Familial and Heritable BED Liability (Susceptibility)
Show evidence (1 reference)
PMID:18095307 SUPPORT Human Clinical
"In the case-control family study, BED was found to aggregate in families, and heritability was estimated as 57% (CI: 30-77%)."
Family-study evidence directly supports familial aggregation and heritability of BED.
MCHR2-Linked BED Susceptibility Locus (Susceptibility)
Show evidence (1 reference)
PMID:37550530 SUPPORT Human Clinical
"We perform a genome-wide association study of individuals of African (n = 77,574) and European (n = 285,138) ancestry while controlling for body mass index to identify three independent loci near the HFE, MCHR2 and LRP11 genes and suggest APOE as a risk gene for BED."
Large GWAS evidence supports MCHR2-proximal common-variant susceptibility for BED.
💊

Treatments

4
Guided Self-Help CBT-E
Action: cognitive behavior therapy MAXO:0000883
Web-based guided self-help enhanced cognitive behavioral therapy can reduce objective binge episodes and improve recovery in BED.
Show evidence (1 reference)
DOI:10.2196/40472 SUPPORT Human Clinical
"During the last 4 weeks of treatment, objective binges reduced from an average of 19 (SD 16) to 3 (SD 5) binges, and 40% (36/90) showed full recovery in the guided self-help CBT-E group."
Randomized trial evidence supports guided self-help CBT-E reducing binge episodes in BED.
Cognitive Behavioral Therapy
Action: cognitive behavior therapy MAXO:0000883
CBT is a recommended first-line treatment for binge-spectrum disorders, including BED, and has comparative evidence against pharmacotherapy.
Show evidence (1 reference)
DOI:10.1177/00048674231219593 SUPPORT Human Clinical
"Cognitive behavioral therapy is the recommended first-line treatment, but pharmacotherapy may be easier to access."
Systematic review evidence supports CBT as first-line treatment for binge-spectrum disorders.
Lisdexamfetamine Pharmacotherapy
Action: Pharmacotherapy NCIT:C15986
Agent: lisdexamfetamine ↗
Lisdexamfetamine is a pharmacotherapy option for BED with supportive recent evidence, although medication evidence remains more limited than the psychotherapy evidence base.
Show evidence (1 reference)
DOI:10.1186/s40337-023-00833-9 SUPPORT Human Clinical
"With binge eating disorder (BED), recent evidence supports the use of lisdexamfetamine."
Rapid review evidence supports lisdexamfetamine pharmacotherapy for BED.
Combined CBT and Lisdexamfetamine
Action: combined psychotherapy and pharmacotherapy Ontology label: Therapeutic Procedure NCIT:C49236
Agent: lisdexamfetamine ↗
Combined cognitive behavioral therapy plus lisdexamfetamine can reduce binge-eating frequency and had the highest remission rate among CBT, LDX, and combined CBT+LDX arms in a randomized trial of BED with obesity.
Show evidence (1 reference)
PMID:39659158 SUPPORT Human Clinical
"Intention-to-treat binge-eating remission rates differed significantly between treatments, with CBT+LDX having the highest remission rate (70.2%) followed by CBT (44.7%) and LDX (40.4%)."
Randomized trial evidence supports combined CBT+LDX as the highest- remission treatment arm among the tested interventions.
🔀

Differential Diagnoses

2

Conditions with similar clinical presentations that must be differentiated from Binge Eating Disorder:

Bulimia Nervosa MONDO:0005452
Overlapping Features Bulimia nervosa overlaps with BED through recurrent binge eating and loss of control.
Distinguishing Features
  • Bulimia nervosa includes regular compensatory behaviors such as vomiting, fasting, laxative misuse, or excessive exercise; BED lacks regular compensatory behaviors.
Show evidence (1 reference)
PMID:25591200 SUPPORT Human Clinical
"In patients with frequent purging or laxative abuse, the presence of electrolyte abnormalities requires prompt intervention."
Clinical review evidence supports purging/laxative abuse complications as distinguishing bulimia nervosa from BED when binge eating overlaps.
Anorexia Nervosa MONDO:0005351
Overlapping Features Anorexia nervosa binge-eating/purging presentations can include binge-like episodes and compensatory behaviors.
Distinguishing Features
  • Anorexia nervosa requires significantly low body weight or persistent restriction leading to low weight; BED does not require low body weight and lacks regular compensatory behaviors.
Show evidence (1 reference)
PMID:25591200 SUPPORT Human Clinical
"For low-weight patients with anorexia nervosa, virtually all physiologic systems are affected, ranging from hypotension and osteopenia to life-threatening arrhythmias, often requiring emergent assessment and hospitalization for metabolic stabilization."
Clinical review evidence supports anorexia nervosa as a low-weight differential diagnosis when binge/purge-like symptoms overlap with BED.
{ }

Source YAML

click to show 
name: Binge Eating Disorder
creation_date: "2026-04-28T00:00:00Z"
updated_date: "2026-04-29T12:30:00Z"
category: Psychiatric
description: >-
  Binge eating disorder is an eating disorder characterized by recurrent binge
  eating episodes with loss of control and marked distress, without regular
  compensatory behaviors such as purging.
disease_term:
  preferred_term: binge eating disorder
  term:
    id: MONDO:0005582
    label: binge eating disorder
parents:
- Eating Disorder
- Mental Health Disorder
prevalence:
- population: U.S. early adolescents aged 10 to 14 years
  percentage: 1.0
  notes: >-
    Cross-sectional ABCD Study estimate for BED in early adolescence; binge-
    eating behaviors were more common than full BED.
  evidence:
  - reference: DOI:10.1186/s40337-023-00904-x
    reference_title: The social epidemiology of binge-eating disorder and behaviors in early adolescents
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      In this early adolescent sample (48.8% female, 54.0% White, 19.8%
      Latino/Hispanic, 16.1% Black, 5.4% Asian, 3.2% Native American, 1.5%
      Other), the prevalence of BED and binge-eating behaviors were 1.0% and
      6.3%, respectively.
    explanation: >-
      The population estimate directly supports the recorded BED prevalence in
      U.S. early adolescents.
pathophysiology:
- name: Reward Hypersensitivity
  description: >-
    Binge eating disorder is modeled as altered reward processing, including
    increased food reward and anticipatory reward responses that maintain
    binge-eating behavior.
  biological_processes:
  - preferred_term: G protein-coupled dopamine receptor signaling pathway
    term:
      id: GO:0007212
      label: G protein-coupled dopamine receptor signaling pathway
    modifier: ABNORMAL
  cell_types:
  - preferred_term: neuron
    term:
      id: CL:0000540
      label: neuron
  locations:
  - preferred_term: brain
    term:
      id: UBERON:0000955
      label: brain
  - preferred_term: striatum
    term:
      id: UBERON:0002435
      label: striatum
  - preferred_term: prefrontal cortex
    term:
      id: UBERON:0000451
      label: prefrontal cortex
  downstream:
  - target: Binge Eating Episodes
    description: >-
      Reward hypersensitivity is represented upstream of recurrent binge-eating
      episodes.
  evidence:
  - reference: DOI:10.1007/s11920-024-01534-z
    reference_title: Reward and Inhibitory Control as Mechanisms and Treatment Targets for Binge Eating Disorder
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Reward hypersensitivity and impaired inhibitory control are mechanisms
      underlying binge eating disorder.
    explanation: >-
      Review evidence supports reward hypersensitivity as an underlying BED
      mechanism.
- name: Impaired Inhibitory Control
  description: >-
    Impaired inhibitory control is represented as a separate top-down control
    mechanism that can fail to suppress binge-eating behavior.
  cell_types:
  - preferred_term: neuron
    term:
      id: CL:0000540
      label: neuron
  locations:
  - preferred_term: prefrontal cortex
    term:
      id: UBERON:0000451
      label: prefrontal cortex
  downstream:
  - target: Binge Eating Episodes
    description: >-
      Reduced inhibitory control is represented upstream of recurrent
      binge-eating episodes.
  evidence:
  - reference: DOI:10.1007/s11920-024-01534-z
    reference_title: Reward and Inhibitory Control as Mechanisms and Treatment Targets for Binge Eating Disorder
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Reward hypersensitivity and impaired inhibitory control are mechanisms
      underlying binge eating disorder.
    explanation: >-
      Review evidence supports impaired inhibitory control as an underlying BED
      mechanism.
progression:
- phase: Clinical course
  notes: >-
    BED may improve over time but can have slow remission and relapse,
    especially in adult community cohorts with higher BMI.
  evidence:
  - reference: DOI:10.1017/S0033291724000977
    reference_title: "The natural course of binge-eating disorder: findings from a prospective, community-based study of adults"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Among community-based adults with higher BMI, BED improves with time, but
      full remission often takes many years, and relapse is common.
    explanation: >-
      Prospective community-based follow-up supports a persistent, relapsing
      clinical course in adults with BED and higher BMI.
phenotypes:
- name: Binge Eating Episodes
  description: >-
    Recurrent binge eating is the defining clinical phenotype of binge eating
    disorder. The HPO term is broad, so the preferred term records the more
    specific BED manifestation.
  phenotype_term:
    preferred_term: Recurrent binge eating episodes
    term:
      id: HP:0100738
      label: Abnormal eating behavior
  evidence:
  - reference: PMID:39659158
    reference_title: "Cognitive Behavioral Therapy and Lisdexamfetamine, Alone and Combined, for Binge-Eating Disorder With Obesity: A Randomized Controlled Trial."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Intention-to-treat binge-eating remission rates differed significantly
      between treatments, with CBT+LDX having the highest remission rate
      (70.2%) followed by CBT (44.7%) and LDX (40.4%).
    explanation: >-
      The randomized trial uses binge-eating remission as the key clinical
      outcome, supporting binge-eating episodes as a core BED phenotype.
- name: Loss of Control Over Eating
  description: >-
    Subjective loss of control over eating is a core BED symptom dimension and
    is modeled separately from binge-episode frequency.
  phenotype_term:
    preferred_term: Loss of control over eating
    term:
      id: HP:0100738
      label: Abnormal eating behavior
  diagnostic: true
  evidence:
  - reference: PMID:36920120
    reference_title: "Loss of control in binge-eating disorder: Fear and resignation."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Binge-eating disorder involves overeating while feeling a loss of control (LOC)."
    explanation: >-
      Treatment-seeking BED cohort evidence supports loss of control as a core
      BED symptom dimension.
  - reference: PMID:18239550
    reference_title: Loss of control is central to psychological disturbance associated with binge eating disorder.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The loss of control (LOC) over eating, that is, being unable to stop
      eating or control what or how much was consumed was most closely related
      to psychological markers of distress common in BED.
    explanation: >-
      Clinical cohort evidence supports LOC over eating as central to BED-
      related psychological disturbance.
- name: Marked Distress About Binge Eating
  description: >-
    Distress about binge eating is represented as a BED diagnostic symptom
    dimension, distinct from the recurrent binge-eating behavior itself.
  phenotype_term:
    preferred_term: Marked distress about binge eating
    term:
      id: HP:0100851
      label: Abnormal emotional state
  diagnostic: true
  evidence:
  - reference: PMID:36920120
    reference_title: "Loss of control in binge-eating disorder: Fear and resignation."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Patients with fear of LOC reported greater distress about binge eating
      and greater depression than those with no fear/resignation.
    explanation: >-
      Clinical interview evidence supports distress about binge eating as a
      clinically relevant BED symptom dimension.
- name: Increased Body Weight
  description: >-
    Increased body weight commonly co-occurs in studied BED populations, but it
    is not required for diagnosis.
  phenotype_term:
    preferred_term: Increased body weight
    term:
      id: HP:0004324
      label: Increased body weight
  evidence:
  - reference: PMID:23472839
    reference_title: "Binge eating in adults: prevalence and association with obesity, poor self-rated health status and body dissatisfaction."
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      In the adjusted analysis, obesity, fair/poor self-rated health status and
      body dissatisfaction remained strongly associated with binge eating.
    explanation: >-
      Population-based evidence supports an obesity association with binge
      eating, while not establishing increased body weight as required for all
      BED.
genetic:
- name: Familial and Heritable BED Liability
  association: Susceptibility
  relationship_type: SUSCEPTIBILITY
  variant_origin: GERMLINE
  notes: >-
    Family and twin evidence supports a substantial inherited component to BED,
    modeled as polygenic susceptibility rather than a Mendelian cause.
  evidence:
  - reference: PMID:18095307
    reference_title: "Familiality and heritability of binge eating disorder: results of a case-control family study and a twin study."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      In the case-control family study, BED was found to aggregate in families,
      and heritability was estimated as 57% (CI: 30-77%).
    explanation: >-
      Family-study evidence directly supports familial aggregation and
      heritability of BED.
- name: MCHR2-Linked BED Susceptibility Locus
  gene_term:
    preferred_term: MCHR2
    term:
      id: hgnc:20867
      label: MCHR2
  association: Susceptibility
  relationship_type: SUSCEPTIBILITY
  variant_origin: GERMLINE
  notes: >-
    GWAS evidence identifies a BED susceptibility locus near MCHR2 while also
    implicating additional loci near HFE and LRP11 and suggesting APOE as a
    BED risk gene.
  evidence:
  - reference: PMID:37550530
    reference_title: Genome-wide analysis of a model-derived binge eating disorder phenotype identifies risk loci and implicates iron metabolism.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      We perform a genome-wide association study of individuals of African
      (n = 77,574) and European (n = 285,138) ancestry while controlling for
      body mass index to identify three independent loci near the HFE, MCHR2
      and LRP11 genes and suggest APOE as a risk gene for BED.
    explanation: >-
      Large GWAS evidence supports MCHR2-proximal common-variant susceptibility
      for BED.
treatments:
- name: Guided Self-Help CBT-E
  description: >-
    Web-based guided self-help enhanced cognitive behavioral therapy can reduce
    objective binge episodes and improve recovery in BED.
  treatment_term:
    preferred_term: cognitive behavior therapy
    term:
      id: MAXO:0000883
      label: cognitive behavior therapy
  evidence:
  - reference: DOI:10.2196/40472
    reference_title: "Efficacy of Web-Based, Guided Self-help Cognitive Behavioral Therapy–Enhanced for Binge Eating Disorder: Randomized Controlled Trial"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      During the last 4 weeks of treatment, objective binges reduced from an
      average of 19 (SD 16) to 3 (SD 5) binges, and 40% (36/90) showed full
      recovery in the guided self-help CBT-E group.
    explanation: >-
      Randomized trial evidence supports guided self-help CBT-E reducing binge
      episodes in BED.
- name: Cognitive Behavioral Therapy
  description: >-
    CBT is a recommended first-line treatment for binge-spectrum disorders,
    including BED, and has comparative evidence against pharmacotherapy.
  treatment_term:
    preferred_term: cognitive behavior therapy
    term:
      id: MAXO:0000883
      label: cognitive behavior therapy
  evidence:
  - reference: DOI:10.1177/00048674231219593
    reference_title: "Is cognitive behavioral therapy more effective than pharmacotherapy for binge spectrum disorders? A systematic review and meta-analysis"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Cognitive behavioral therapy is the recommended first-line treatment, but
      pharmacotherapy may be easier to access.
    explanation: >-
      Systematic review evidence supports CBT as first-line treatment for
      binge-spectrum disorders.
- name: Lisdexamfetamine Pharmacotherapy
  description: >-
    Lisdexamfetamine is a pharmacotherapy option for BED with supportive recent
    evidence, although medication evidence remains more limited than the
    psychotherapy evidence base.
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: lisdexamfetamine
      term:
        id: CHEBI:135925
        label: lisdexamfetamine
  evidence:
  - reference: DOI:10.1186/s40337-023-00833-9
    reference_title: "Pharmacotherapy, alternative and adjunctive therapies for eating disorders: findings from a rapid review"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      With binge eating disorder (BED), recent evidence supports the use of
      lisdexamfetamine.
    explanation: >-
      Rapid review evidence supports lisdexamfetamine pharmacotherapy for BED.
- name: Combined CBT and Lisdexamfetamine
  description: >-
    Combined cognitive behavioral therapy plus lisdexamfetamine can reduce
    binge-eating frequency and had the highest remission rate among CBT, LDX,
    and combined CBT+LDX arms in a randomized trial of BED with obesity.
  treatment_term:
    preferred_term: combined psychotherapy and pharmacotherapy
    term:
      id: NCIT:C49236
      label: Therapeutic Procedure
    therapeutic_agent:
    - preferred_term: lisdexamfetamine
      term:
        id: CHEBI:135925
        label: lisdexamfetamine
  evidence:
  - reference: PMID:39659158
    reference_title: "Cognitive Behavioral Therapy and Lisdexamfetamine, Alone and Combined, for Binge-Eating Disorder With Obesity: A Randomized Controlled Trial."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Intention-to-treat binge-eating remission rates differed significantly
      between treatments, with CBT+LDX having the highest remission rate
      (70.2%) followed by CBT (44.7%) and LDX (40.4%).
    explanation: >-
      Randomized trial evidence supports combined CBT+LDX as the highest-
      remission treatment arm among the tested interventions.
diagnosis:
- name: Clinical BED diagnosis
  description: >-
    BED diagnosis is based on clinical assessment of recurrent binge eating,
    loss of control, distress, and absence of regular compensatory behaviors;
    validated instruments such as eating-disorder interviews or questionnaires
    can support assessment.
  evidence:
  - reference: DOI:10.2196/40472
    reference_title: "Efficacy of Web-Based, Guided Self-help Cognitive Behavioral Therapy–Enhanced for Binge Eating Disorder: Randomized Controlled Trial"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The secondary outcome was full recovery at the end of treatment, as
      measured using the Eating Disorder Examination during the last 4 weeks of
      treatment.
    explanation: >-
      RCT evidence supports use of the Eating Disorder Examination to measure
      BED recovery and symptom status.
differential_diagnoses:
- name: Bulimia Nervosa
  description: >-
    Bulimia nervosa overlaps with BED through recurrent binge eating and loss
    of control.
  distinguishing_features:
  - >-
    Bulimia nervosa includes regular compensatory behaviors such as vomiting,
    fasting, laxative misuse, or excessive exercise; BED lacks regular
    compensatory behaviors.
  disease_term:
    preferred_term: bulimia nervosa
    term:
      id: MONDO:0005452
      label: bulimia nervosa
  evidence:
  - reference: PMID:25591200
    reference_title: Initial evaluation, diagnosis, and treatment of anorexia nervosa and bulimia nervosa.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      In patients with frequent purging or laxative abuse, the presence of
      electrolyte abnormalities requires prompt intervention.
    explanation: >-
      Clinical review evidence supports purging/laxative abuse complications as
      distinguishing bulimia nervosa from BED when binge eating overlaps.
- name: Anorexia Nervosa
  description: >-
    Anorexia nervosa binge-eating/purging presentations can include binge-like
    episodes and compensatory behaviors.
  distinguishing_features:
  - >-
    Anorexia nervosa requires significantly low body weight or persistent
    restriction leading to low weight; BED does not require low body weight and
    lacks regular compensatory behaviors.
  disease_term:
    preferred_term: anorexia nervosa
    term:
      id: MONDO:0005351
      label: anorexia nervosa
  evidence:
  - reference: PMID:25591200
    reference_title: Initial evaluation, diagnosis, and treatment of anorexia nervosa and bulimia nervosa.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      For low-weight patients with anorexia nervosa, virtually all physiologic
      systems are affected, ranging from hypotension and osteopenia to
      life-threatening arrhythmias, often requiring emergent assessment and
      hospitalization for metabolic stabilization.
    explanation: >-
      Clinical review evidence supports anorexia nervosa as a low-weight
      differential diagnosis when binge/purge-like symptoms overlap with BED.
notes: >-
  Comorbidity is clinically important in BED. Kowalewska et al. 2024 report
  that "The most frequently observed comorbidities associated with BED were
  mood disorders, anxiety disorders and substance use disorders" and also note
  ADHD, personality disorders, suicidality, and sleep disorders. The current
  schema does not provide a disease-level comorbidities slot, so this entry
  records comorbidity context here rather than adding a non-schema section.
references:
- reference: DOI:10.1007/s11920-024-01534-z
  title: Reward and Inhibitory Control as Mechanisms and Treatment Targets for Binge Eating Disorder
  findings: []
- reference: DOI:10.1017/S0033291724000977
  title: "The natural course of binge-eating disorder: findings from a prospective, community-based study of adults"
  findings: []
- reference: DOI:10.1186/s40337-023-00904-x
  title: The social epidemiology of binge-eating disorder and behaviors in early adolescents
  findings: []
- reference: DOI:10.2196/40472
  title: "Efficacy of Web-Based, Guided Self-help Cognitive Behavioral Therapy–Enhanced for Binge Eating Disorder: Randomized Controlled Trial"
  findings: []
- reference: DOI:10.1177/00048674231219593
  title: "Is cognitive behavioral therapy more effective than pharmacotherapy for binge spectrum disorders? A systematic review and meta-analysis"
  findings: []
- reference: DOI:10.1186/s40337-023-00833-9
  title: "Pharmacotherapy, alternative and adjunctive therapies for eating disorders: findings from a rapid review"
  findings: []
- reference: PMID:39659158
  title: "Cognitive Behavioral Therapy and Lisdexamfetamine, Alone and Combined, for Binge-Eating Disorder With Obesity: A Randomized Controlled Trial."
  findings: []
- reference: PMID:39138440
  title: "Comorbidity of binge eating disorder and other psychiatric disorders: a systematic review."
  findings: []
- reference: PMID:23472839
  title: "Binge eating in adults: prevalence and association with obesity, poor self-rated health status and body dissatisfaction."
  findings: []
- reference: PMID:18095307
  title: "Familiality and heritability of binge eating disorder: results of a case-control family study and a twin study."
  findings: []
- reference: PMID:37550530
  title: Genome-wide analysis of a model-derived binge eating disorder phenotype identifies risk loci and implicates iron metabolism.
  findings: []
- reference: PMID:18239550
  title: Loss of control is central to psychological disturbance associated with binge eating disorder.
  findings: []
- reference: PMID:36920120
  title: "Loss of control in binge-eating disorder: Fear and resignation."
  findings: []
- reference: DOI:10.5694/mja2.52008
  title: Current approaches in the recognition and management of eating disorders
  findings: []
- reference: PMID:25591200
  title: Initial evaluation, diagnosis, and treatment of anorexia nervosa and bulimia nervosa.
  findings: []
📚

References & Deep Research

References

15
DOI:10.1007/s11920-024-01534-z
Reward and Inhibitory Control as Mechanisms and Treatment Targets for Binge Eating Disorder
No top-level findings curated for this source.
DOI:10.1017/S0033291724000977
The natural course of binge-eating disorder: findings from a prospective, community-based study of adults
No top-level findings curated for this source.
DOI:10.1186/s40337-023-00904-x
The social epidemiology of binge-eating disorder and behaviors in early adolescents
No top-level findings curated for this source.
DOI:10.2196/40472
Efficacy of Web-Based, Guided Self-help Cognitive Behavioral Therapy–Enhanced for Binge Eating Disorder: Randomized Controlled Trial
No top-level findings curated for this source.
DOI:10.1177/00048674231219593
Is cognitive behavioral therapy more effective than pharmacotherapy for binge spectrum disorders? A systematic review and meta-analysis
No top-level findings curated for this source.
DOI:10.1186/s40337-023-00833-9
Pharmacotherapy, alternative and adjunctive therapies for eating disorders: findings from a rapid review
No top-level findings curated for this source.
PMID:39659158
Cognitive Behavioral Therapy and Lisdexamfetamine, Alone and Combined, for Binge-Eating Disorder With Obesity: A Randomized Controlled Trial.
No top-level findings curated for this source.
PMID:39138440
Comorbidity of binge eating disorder and other psychiatric disorders: a systematic review.
No top-level findings curated for this source.
PMID:23472839
Binge eating in adults: prevalence and association with obesity, poor self-rated health status and body dissatisfaction.
No top-level findings curated for this source.
PMID:18095307
Familiality and heritability of binge eating disorder: results of a case-control family study and a twin study.
No top-level findings curated for this source.
PMID:37550530
Genome-wide analysis of a model-derived binge eating disorder phenotype identifies risk loci and implicates iron metabolism.
No top-level findings curated for this source.
PMID:18239550
Loss of control is central to psychological disturbance associated with binge eating disorder.
No top-level findings curated for this source.
PMID:36920120
Loss of control in binge-eating disorder: Fear and resignation.
No top-level findings curated for this source.
DOI:10.5694/mja2.52008
Current approaches in the recognition and management of eating disorders
No top-level findings curated for this source.
PMID:25591200
Initial evaluation, diagnosis, and treatment of anorexia nervosa and bulimia nervosa.
No top-level findings curated for this source.

Deep Research

1
Falcon ▸
Disease Characteristics Research Template
Edison Scientific Literature 81 citations 2026-04-28T10:17:41.554889

Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on: 1. Key concepts and definitions with current understanding 2. Recent developments and latest research (prioritize 2023-2024 sources) 3. Current applications and real-world implementations 4. Expert opinions and analysis from authoritative sources 5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available. Always prioritize recent, authoritative sources and provide specific citations for all major claims.

Disease Characteristics Research Template

Target Disease

  • Disease Name: Binge Eating Disorder
  • MONDO ID: (if available)
  • Category: Psychiatric

Research Objectives

Please provide a comprehensive research report on Binge Eating Disorder covering all of the disease characteristics listed below. This report will be used to populate a disease knowledge base entry. Be thorough and cite primary literature (PMID preferred) for all claims.

For each section, suggested databases/resources are listed. These are the first places you should search for information on each topic.

1. Disease Information

Search first: OMIM, Orphanet, ICD-10/ICD-11, MeSH, PubMed

  • What is the disease? Provide a concise overview.
  • What are the key identifiers? (OMIM, Orphanet, ICD-10/ICD-11, MeSH, Mondo)
  • What are the common synonyms and alternative names?
  • Is the information derived from individual patients (e.g., EHR) or aggregated disease-level resources?

2. Etiology

  • Disease Causal Factors: What are the primary causes? (genetic, environmental, infectious, mechanistic)
  • Risk Factors:

    Search first: PubMed, Cochrane Library, UpToDate, clinical guidelines, ClinVar, ClinGen, GWAS Catalog, PheGenI, CTD, CDC, WHO, epidemiological databases

  • Genetic risk factors (causal variants, susceptibility loci, modifier genes)
  • Environmental risk factors (toxins, lifestyle, occupational exposures, age, sex, family history)
  • Protective Factors:

    Search first: PubMed, Cochrane Library, clinical trial databases, GWAS Catalog, gnomAD, WHO, CDC, nutrition databases

  • Genetic protective factors (protective variants, modifier alleles)
  • Environmental protective factors (diet, lifestyle, exposures that reduce risk)
  • Gene-Environment Interactions: How do genetic and environmental factors interact to influence disease?

    Search first: CTD, PubMed, PheGenI, GxE databases

3. Phenotypes

Search first: HPO (Human Phenotype Ontology), OMIM, Orphanet, PubMed, clinicaltrials.gov, MedDRA, SNOMED CT, DECIPHER, LOINC

For each phenotype, provide: - Phenotype type: symptoms, clinical signs, physical manifestations, behavioral changes, or laboratory abnormalities

For symptoms/signs: HPO, OMIM, Orphanet, PubMed For behavioral changes: HPO, DSM, RDoC (Research Domain Criteria), PubMed For laboratory abnormalities: LOINC, SNOMED CT, LabTests Online, PubMed - Phenotype characteristics: Search first: OMIM, Orphanet, HPO, PubMed - Age of symptom onset (neonatal, childhood, adult-onset, late-onset) - Symptom severity (mild, moderate, severe, variable) - Symptom progression (stable, progressive, episodic, fluctuating) - Frequency among affected individuals (percentage or qualitative) - Quality of life impact: Effects on daily functioning and well-being (per-phenotype when possible) Search first: EQ-5D database, SF-36, WHO QOL databases, PubMed - Suggest HPO (Human Phenotype Ontology) terms for each phenotype

4. Genetic/Molecular Information

  • Causal Genes: Gene mutations or chromosomal abnormalities responsible for disease (gene symbols, OMIM IDs)

    Search first: OMIM, ClinVar, HGMD, Ensembl, NCBI Gene

  • Pathogenic Variants:
  • Affected genes (gene symbols, HGNC IDs) > Search first: OMIM, NCBI Gene, Ensembl, HGNC, UniProt, GeneCards
  • Variant classification (pathogenic, likely pathogenic, VUS per ACMG/AMP guidelines) > Search first: ClinVar, ClinGen, ACMG/AMP guidelines, VarSome
  • Variant type/class (missense, frameshift, nonsense, splice-site, structural)
  • Allele frequency in population databases > Search first: gnomAD, 1000 Genomes, ExAC, TOPMed, dbSNP
  • Somatic vs germline origin > Search first: COSMIC (somatic), ClinVar, ICGC, TCGA
  • Functional consequences (loss of function, gain of function, dominant negative)
  • Modifier Genes: Genes that modify disease severity or expression
  • Epigenetic Information: DNA methylation, histone modifications, chromatin changes affecting disease

    Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth

  • Chromosomal Abnormalities: Large-scale genetic changes (aneuploidy, translocations, inversions)

    Search first: DECIPHER, ClinVar, ECARUCA, UCSC Genome Browser

5. Environmental Information

  • Environmental Factors: Non-genetic contributing factors (toxins, radiation, pollution, occupational exposure)

    Search first: CTD (Comparative Toxicogenomics Database), TOXNET, PubMed, EPA databases

  • Lifestyle Factors: Behavioral factors (smoking, diet, exercise, alcohol consumption)

    Search first: CDC databases, WHO, PubMed, NHANES

  • Infectious Agents: If applicable, pathogens causing or triggering disease (bacteria, viruses, fungi, parasites)

    Search first: NCBI Taxonomy, ViPR, BV-BRC, MicrobeDB, GIDEON

6. Mechanism / Pathophysiology

  • Molecular Pathways: Specific signaling cascades or biochemical pathways involved (Wnt, MAPK, mTOR, PI3K-AKT, etc.)

    Search first: KEGG, Reactome, WikiPathways, PathBank, BioCyc

  • Cellular Processes: Cell-level mechanisms (apoptosis, autophagy, cell cycle dysregulation, inflammation, etc.)

    Search first: Gene Ontology (GO), Reactome, KEGG, PubMed

  • Protein Dysfunction: How protein structure or function is altered (misfolding, aggregation, loss of function, gain of function)

    Search first: UniProt, PDB (Protein Data Bank), InterPro, Pfam, AlphaFold

  • Metabolic Changes: Alterations in metabolic processes (energy metabolism, lipid metabolism, amino acid metabolism)

    Search first: KEGG, BioCyc, HMDB (Human Metabolome Database), BRENDA

  • Immune System Involvement: Role of immune response (autoimmunity, immunodeficiency, chronic inflammation)

    Search first: ImmPort, Immunome Database, IEDB, Gene Ontology

  • Tissue Damage Mechanisms: How tissues/ are injured (oxidative stress, ischemia, fibrosis, necrosis)

    Search first: PubMed, Gene Ontology, Reactome

  • Biochemical Abnormalities: Specific molecular defects (enzyme deficiencies, receptor dysfunction, ion channel defects)

    Search first: BRENDA, UniProt, KEGG, OMIM, PubMed

  • Epigenetic Changes: DNA methylation, histone modifications affecting gene expression in disease

    Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth

  • Molecular Profiling (if available):
  • Transcriptomics/gene expression changes > Search first: GEO (Gene Expression Omnibus), ArrayExpress, GTEx, Human Cell Atlas, SRA
  • Proteomics findings > Search first: PRIDE, ProteomeXchange, Human Protein Atlas, STRING, BioGRID
  • Metabolomics signatures > Search first: MetaboLights, Metabolomics Workbench, HMDB, METLIN
  • Lipidomics alterations > Search first: LIPID MAPS, SwissLipids, LipidHome, Metabolomics Workbench
  • Genomic structural features > Search first: UCSC Genome Browser, Ensembl, NCBI, dbVar, DGV
  • Advanced Technologies (if applicable):
  • Single-cell analysis findings (cell-type specific mechanisms, cellular heterogeneity) > Search first: Human Cell Atlas, Single Cell Portal, GEO, CELLxGENE
  • Spatial transcriptomics findings > Search first: GEO, Spatial Research, Vizgen, 10x Genomics data
  • Multi-omics integration results > Search first: TCGA, ICGC, cBioPortal, LinkedOmics, PubMed
  • Functional genomics screens (CRISPR, RNAi) > Search first: DepMap, GenomeRNAi, PubMed, BioGRID ORCS

For each mechanism, describe: - The causal chain from initial trigger to clinical manifestation - Which mechanisms are upstream vs downstream - What cell types and biological processes are involved - Suggest GO terms for biological processes and CL terms for cell types

7. Anatomical Structures Affected

  • Organ Level:
  • Primary organs directly affected
  • Secondary organ involvement (complications, secondary effects)
  • Body systems involved (cardiovascular, nervous, digestive, respiratory, endocrine, etc.)

    Search first: Uberon, FMA (Foundational Model of Anatomy), OMIM, HPO, ICD-11, MeSH, SNOMED CT

  • Tissue and Cell Level:
  • Specific tissue types affected (epithelial, connective, muscle, nervous)
  • Specific cell populations targeted (with Cell Ontology terms)

    Search first: Uberon, Human Protein Atlas, Cell Ontology, Human Cell Atlas, CellMarker, PanglaoDB

  • Subcellular Level:
  • Cellular compartments involved (mitochondria, nucleus, ER, lysosomes) (with GO Cellular Component terms)

    Search first: Gene Ontology (Cellular Component), UniProt, Human Protein Atlas

  • Localization:
  • Specific anatomical sites (with UBERON terms) > Search first: FMA, Uberon, NeuroNames (for brain), SNOMED CT
  • Lateralization (unilateral, bilateral, asymmetric) > Search first: HPO, clinical literature, imaging databases

8. Temporal Development

  • Onset:
  • Typical age of onset (congenital, pediatric, adult, geriatric)
  • Onset pattern (acute, subacute, chronic, insidious)

    Search first: OMIM, Orphanet, HPO, PubMed

  • Progression:
  • Disease stages (early, intermediate, advanced, end-stage) > Search first: Cancer Staging Manual (AJCC), WHO classifications, PubMed
  • Progression rate (rapid, slow, variable)
  • Disease course pattern (episodic, relapsing-remitting, progressive, stable)
  • Disease duration (self-limited, chronic lifelong)

    Search first: Disease registries, longitudinal cohort databases, natural history studies, PubMed, Orphanet, OMIM

  • Patterns:
  • Remission patterns (spontaneous, treatment-induced) > Search first: Clinical trial databases, disease registries, PubMed
  • Critical periods (time windows of vulnerability or opportunity for intervention) > Search first: PubMed, developmental biology databases, clinical guidelines

9. Inheritance and Population

  • Epidemiology:
  • Prevalence (cases per 100,000 at given time)
  • Incidence (new cases per 100,000 per year)

    Search first: Orphanet, CDC, WHO, GBD (Global Burden of Disease), national registries, SEER, disease registries

  • For Genetic Etiology:
  • Inheritance pattern (AD, AR, X-linked, mitochondrial, multifactorial, polygenic) > Search first: OMIM, Orphanet, ClinVar, GTR (Genetic Testing Registry)
  • Penetrance (complete, incomplete, age-dependent) > Search first: ClinVar, OMIM, PubMed, ClinGen
  • Expressivity (variable, consistent) > Search first: OMIM, ClinVar, PubMed
  • Genetic anticipation (increasing severity in successive generations) > Search first: OMIM, PubMed (especially for repeat expansion disorders)
  • Germline mosaicism > Search first: ClinVar, OMIM, genetic counseling literature, PubMed
  • Founder effects (population-specific mutations) > Search first: gnomAD, population genetics databases, PubMed
  • Consanguinity role > Search first: OMIM, population studies, genetic counseling resources
  • Carrier frequency > Search first: gnomAD, carrier screening databases, GeneReviews, GTR
  • Population Demographics:
  • Affected populations (ethnic or demographic groups with higher prevalence) > Search first: gnomAD, 1000 Genomes, PAGE Study, PubMed, population registries
  • Geographic distribution (endemic areas, regional variation) > Search first: WHO, CDC, GBD, Orphanet, geographic epidemiology databases
  • Geographic distribution of specific variants
  • Sex ratio (male:female) > Search first: Disease registries, OMIM, PubMed, epidemiological databases
  • Age distribution of affected individuals > Search first: CDC, disease registries, SEER, Orphanet

10. Diagnostics

  • Clinical Tests:
  • Laboratory tests (blood, urine, tissue chemistry, specific enzyme assays) > Search first: LOINC, LabTests Online, PubMed
  • Biomarkers (proteins, metabolites, genetic markers, circulating biomarkers) > Search first: FDA Biomarker List, BEST (Biomarkers, EndpointS, and other Tools), PubMed
  • Imaging studies (X-ray, CT, MRI, PET, ultrasound) > Search first: RadLex, DICOM, Radiopaedia, imaging databases
  • Functional tests (pulmonary function, cardiac stress tests) > Search first: LOINC, clinical guidelines, PubMed
  • Electrophysiology (EEG, EMG, ECG, nerve conduction studies) > Search first: LOINC, clinical neurophysiology databases, PubMed
  • Biopsy findings (histopathology, immunohistochemistry) > Search first: SNOMED CT, College of American Pathologists resources, PubMed
  • Pathology findings (microscopic examination) > Search first: SNOMED CT, Digital Pathology databases, PubMed
  • Genetic Testing:

    Search first: GTR (Genetic Testing Registry), GeneReviews, ClinGen

  • Overview of recommended genetic testing approach
  • Whole genome sequencing (WGS) utility > Search first: GTR, ClinVar, GEL (Genomics England), gnomAD
  • Whole exome sequencing (WES) utility > Search first: GTR, ClinVar, OMIM, GeneMatcher
  • Gene panels (which panels, which genes) > Search first: GTR, ClinVar, laboratory-specific databases
  • Single gene testing > Search first: GTR, ClinVar, OMIM, GeneReviews
  • Chromosomal microarray (CMA) > Search first: DECIPHER, ClinVar, dbVar, ECARUCA
  • Karyotyping > Search first: Chromosome Abnormality Database, ClinVar, cytogenetics resources
  • FISH > Search first: ClinVar, cytogenetics databases, PubMed
  • Mitochondrial DNA testing > Search first: MITOMAP, MSeqDR, ClinVar, GTR
  • Repeat expansion testing > Search first: GTR, ClinVar, repeat expansion databases, PubMed
  • Omics-Based Diagnostics (if applicable):
  • RNA sequencing / transcriptomics > Search first: GEO, ArrayExpress, GTEx, RNA-seq databases
  • Proteomics > Search first: PRIDE, ProteomeXchange, FDA Biomarker database
  • Metabolomics > Search first: MetaboLights, Metabolomics Workbench, HMDB
  • Epigenomics > Search first: GEO, ENCODE, Roadmap Epigenomics, MethBase
  • Liquid biopsy > Search first: COSMIC, ClinVar, liquid biopsy databases, PubMed
  • Clinical Criteria:
  • Standardized diagnostic criteria (DSM, ICD, society guidelines) > Search first: DSM-5, ICD-11, clinical society guidelines, UpToDate
  • Differential diagnosis (other conditions to rule out, with distinguishing features) > Search first: DynaMed, UpToDate, clinical decision support systems
  • Screening:
  • Screening methods for asymptomatic individuals (newborn screening, carrier screening, cascade screening) > Search first: ACMG recommendations, CDC newborn screening, GTR

11. Outcome/Prognosis

  • Survival and Mortality:
  • Survival rate (5-year, 10-year, overall) > Search first: SEER, cancer registries, disease-specific registries, PubMed
  • Life expectancy (with and without treatment if applicable) > Search first: Orphanet, disease registries, actuarial databases, PubMed
  • Mortality rate > Search first: CDC, WHO, GBD, national mortality databases
  • Disease-specific mortality (deaths directly attributable to disease) > Search first: Disease registries, CDC Wonder, GBD, PubMed
  • Morbidity and Function:
  • Morbidity (disease-related disability and health impacts) > Search first: GBD, WHO, disability databases, PubMed
  • Disability outcomes (long-term functional impairments) > Search first: ICF (International Classification of Functioning), disability registries
  • Quality of life measures (EQ-5D, SF-36, PROMIS, disease-specific tools) > Search first: EQ-5D database, SF-36, PROMIS, PubMed
  • Disease Course:
  • Complications (secondary problems: infections, organ failure, etc.) > Search first: ICD codes, disease registries, clinical databases, PubMed
  • Recovery potential (likelihood and extent of recovery, with vs without treatment) > Search first: Natural history studies, rehabilitation databases, PubMed
  • Prediction:
  • Prognostic factors (age, disease severity, biomarkers, treatment response) > Search first: Prognostic models databases, clinical calculators, PubMed
  • Prognostic biomarkers (molecular markers predicting disease course) > Search first: FDA Biomarker database, PubMed, cancer prognostic databases

12. Treatment

  • Pharmacotherapy:
  • Pharmacological treatments (drug names, drug classes, mechanisms of action) > Search first: DrugBank, RxNorm, ATC classification, DailyMed, FDA databases
  • Pharmacogenomics (how genetic variants affect drug metabolism, efficacy, toxicity) > Search first: PharmGKB, CPIC (Clinical Pharmacogenetics), FDA Table of PGx Biomarkers
  • Advanced Therapeutics:
  • Gene therapy (viral vectors, CRISPR, gene replacement, gene editing) > Search first: ClinicalTrials.gov, FDA gene therapy database, ASGCT resources
  • Cell therapy (stem cell transplant, CAR-T, cellular therapeutics) > Search first: ClinicalTrials.gov, FDA cell therapy database, FACT standards
  • RNA-based therapies (ASOs, siRNA, mRNA therapies) > Search first: ClinicalTrials.gov, FDA approvals, PubMed
  • Targeted therapies (treatments directed at specific molecular targets) > Search first: My Cancer Genome, OncoKB, ClinicalTrials.gov, FDA approvals
  • Immunotherapies (checkpoint inhibitors, monoclonal antibodies) > Search first: Cancer Immunotherapy Database, FDA approvals, ClinicalTrials.gov
  • Surgical and Interventional:
  • Surgical interventions (types of surgery, timing, outcomes) > Search first: CPT codes, surgical registries, clinical guidelines, PubMed
  • Supportive and Rehabilitative:
  • Supportive care (symptom management, pain control, nutrition) > Search first: Clinical guidelines, Cochrane Library, PubMed
  • Rehabilitation (physical therapy, occupational therapy, speech therapy) > Search first: Rehabilitation medicine databases, clinical guidelines, PubMed
  • Experimental:
  • Experimental treatments in clinical trials (with NCT identifiers if available) > Search first: ClinicalTrials.gov, EU Clinical Trials Register, WHO ICTRP
  • Treatment Outcomes:
  • Treatment response rates > Search first: Clinical trial databases, FDA reviews, systematic reviews, PubMed
  • Side effects and adverse events > Search first: FDA Adverse Event Reporting System (FAERS), MedWatch, PubMed
  • Treatment Strategy:
  • Treatment algorithms (clinical pathways, decision trees) > Search first: Clinical practice guidelines, NCCN Guidelines, UpToDate
  • Combination therapies > Search first: ClinicalTrials.gov, treatment guidelines, PubMed
  • Personalized medicine approaches (genotype-guided treatment) > Search first: My Cancer Genome, CIViC, PharmGKB, precision medicine databases

For each treatment, suggest MAXO (Medical Action Ontology) terms where applicable.

13. Prevention

  • Prevention Levels:
  • Primary prevention (preventing disease occurrence: vaccination, risk factor modification) > Search first: CDC, WHO, USPSTF recommendations, Cochrane Library
  • Secondary prevention (early detection and treatment: screening programs, early intervention) > Search first: USPSTF, CDC screening guidelines, WHO
  • Tertiary prevention (preventing complications in those with disease) > Search first: Clinical guidelines, disease management protocols, PubMed
  • Immunization: Vaccine strategies (if applicable)

    Search first: CDC vaccine schedules, WHO immunization, FDA vaccine database

  • Screening and Early Detection:
  • Screening programs (population-based: newborn screening, cancer screening) > Search first: CDC screening programs, USPSTF, cancer screening databases
  • Genetic screening (carrier screening, preimplantation genetic diagnosis, prenatal testing) > Search first: ACMG recommendations, ACOG guidelines, GTR
  • Risk stratification (identifying high-risk individuals for targeted prevention) > Search first: Risk prediction models, clinical calculators, PubMed
  • Behavioral Interventions: Lifestyle modifications to reduce risk

    Search first: CDC, WHO, behavioral intervention databases, Cochrane Library

  • Counseling: Genetic counseling (risk assessment, family planning guidance)

    Search first: NSGC resources, ACMG guidelines, GeneReviews

  • Public Health:
  • Public health interventions (sanitation, vector control, health education) > Search first: CDC, WHO, public health databases, PubMed
  • Environmental interventions (reducing environmental risk factors) > Search first: EPA databases, WHO environmental health, PubMed
  • Prophylaxis: Preventive medications or procedures

    Search first: Clinical guidelines, FDA approvals, PubMed

14. Other Species / Natural Disease

  • Taxonomy: Species affected (with NCBI Taxon identifiers)

    Search first: NCBI Taxonomy

  • Breed: Specific breeds affected (with VBO identifiers if applicable)

    Search first: VBO (Vertebrate Breed Ontology)

  • Gene: Orthologous genes in other species (with NCBI Gene IDs)

    Search first: NCBI Gene

  • Natural Disease:
  • Naturally occurring disease in other species (companion animals, wildlife) > Search first: OMIA (Online Mendelian Inheritance in Animals), VetCompass, PubMed
  • Veterinary relevance and importance in animal health > Search first: OMIA, veterinary databases, PubMed
  • Comparative Biology:
  • Comparative pathology (similarities and differences across species) > Search first: OMIA, comparative pathology databases, PubMed
  • Evolutionary conservation of disease mechanisms > Search first: HomoloGene, OrthoMCL, Alliance of Genome Resources
  • Transmission (if applicable):
  • Zoonotic potential > Search first: CDC zoonotic diseases, WHO zoonoses, GIDEON
  • Cross-species susceptibility > Search first: NCBI Taxonomy, veterinary databases, PubMed

15. Model Organisms

  • Model Types:
  • Model organism type (mammalian, invertebrate, cellular, in vitro) > Search first: Alliance of Genome Resources, model organism databases
  • Specific model systems (mouse, rat, zebrafish, Drosophila, C. elegans, yeast, cell lines, organoids, iPSCs) > Search first: MGI, RGD, ZFIN, FlyBase, WormBase, SGD, ATCC, Cellosaurus
  • Induced models (drug treatment, surgical intervention, environmental manipulation) > Search first: MGI, model organism databases, PubMed
  • Genetic Models:
  • Types available (knockout, knock-in, transgenic, conditional, humanized) > Search first: MGI, IMPC, KOMP, EuMMCR, IMSR
  • Model Characteristics:
  • Phenotype recapitulation (how well model reproduces human disease features) > Search first: Model organism databases, comparative studies, PubMed
  • Model limitations (aspects of human disease not captured) > Search first: Model organism databases, PubMed, review articles
  • Applications:
  • Research applications (what aspects of disease can be studied) > Search first: Model organism databases, PubMed
  • Resources:
  • Model databases > Search first: MGI, RGD, ZFIN, FlyBase, WormBase, IMSR, EMMA, MMRRC

Citation Requirements

  • Cite primary literature (PMID preferred) for all mechanistic and clinical claims
  • Prioritize recent reviews and landmark papers
  • Include direct quotes from abstracts where possible to support key statements
  • Distinguish evidence source types: human clinical, model organism, in vitro, computational

Output Format

Structure your response as a comprehensive narrative organized by the sections above. For each section, provide: - Factual content with specific details (numbers, percentages, gene names, variant nomenclature) - Ontology term suggestions (HPO, GO, CL, UBERON, CHEBI, MAXO, MONDO) where applicable - Evidence citations with PMIDs - Direct quotes from abstracts to support key claims - Clear indication when information is not available or not applicable for this disease

This report will be used to populate a disease knowledge base entry with: - Pathophysiology descriptions with causal chains - Gene/protein annotations (HGNC, GO terms) - Phenotype associations (HP terms) with frequencies - Cell type involvement (CL terms) - Anatomical locations (UBERON terms) - Chemical entities (CHEBI terms) - Treatment annotations (MAXO terms) - Evidence items with PMIDs and exact abstract quotes - Epidemiology, prognosis, diagnostic, and prevention information - Animal model descriptions with phenotype recapitulation details

Comprehensive Research Report: Binge Eating Disorder (BED)

Target disease

  • Disease name: Binge Eating Disorder (BED)
  • Category: Psychiatric (feeding and eating disorder)
  • MONDO ID: Not retrieved from the gathered sources (limitation of this run) (melisse2025redefiningdiagnosticparameters pages 1-2, hay2023currentapproachesin pages 1-2)

Summary artifacts (structured for knowledge-base ingestion)

The following artifacts summarize identifiers/criteria, epidemiology, treatments, and phenotype→ontology mappings:

Framework/Database Identifier / code Key diagnostic / definition highlights Citation / source
DSM-5-TR BED is defined by recurrent binge-eating episodes with loss of control, marked distress, and no regular compensatory behaviors; episodes occur at least weekly for 3 months and include at least 3 associated features (eg, rapid eating, eating when not hungry, eating alone from embarrassment). (melisse2025redefiningdiagnosticparameters pages 1-2, hay2023currentapproachesin pages 1-2) Melisse & Dingemans, Journal of Eating Disorders, Jan 2025, https://doi.org/10.1186/s40337-025-01187-0; Hay et al., Medical Journal of Australia, Jun 2023, https://doi.org/10.5694/mja2.52008
ICD-11 BED was added as a named eating-disorder diagnosis in ICD-11/ICD revision process; compared with DSM-5, ICD-11 criteria are broader and more flexible, including allowance for subjective binge episodes and shorter duration in some circumstances. (palavras2018aninvestigationof pages 1-3, hay2023currentapproachesin pages 1-2) Palavras et al., Nutrients, Nov 2018, https://doi.org/10.3390/nu10111751; Hay et al., Medical Journal of Australia, Jun 2023, https://doi.org/10.5694/mja2.52008
ICD-10 BED was not a distinct major diagnosis in ICD-10 in the way it is in ICD-11; older ICD-based literature discusses its addition in ICD-11 as a meaningful classification change. Specific ICD-10 BED code was not retrieved from current evidence. (palavras2018aninvestigationof pages 1-3, hay2023currentapproachesin pages 1-2) Palavras et al., Nutrients, Nov 2018, https://doi.org/10.3390/nu10111751; Hay et al., Medical Journal of Australia, Jun 2023, https://doi.org/10.5694/mja2.52008
MeSH MeSH identifier was not retrieved from the current gathered sources. BED terminology in current evidence uses the synonym/abbreviation “binge-eating disorder (BED)”. (melisse2025redefiningdiagnosticparameters pages 1-2, melisse2023efficacyofwebbased pages 1-2) Melisse & Dingemans, Journal of Eating Disorders, Jan 2025, https://doi.org/10.1186/s40337-025-01187-0; Melisse et al., Journal of Medical Internet Research, May 2023, https://doi.org/10.2196/40472
MONDO MONDO identifier was not retrieved from the current gathered sources. Current evidence supports BED as an aggregated disease-level psychiatric diagnosis rather than an individual-patient identifier. (melisse2025redefiningdiagnosticparameters pages 1-2, hay2023currentapproachesin pages 1-2) Melisse & Dingemans, Journal of Eating Disorders, Jan 2025, https://doi.org/10.1186/s40337-025-01187-0; Hay et al., Medical Journal of Australia, Jun 2023, https://doi.org/10.5694/mja2.52008
Synonyms / naming note BED Common naming in current sources is “binge-eating disorder” and abbreviation “BED”; BED is described as the most common named eating disorder in recent reviews. (melisse2025redefiningdiagnosticparameters pages 1-2, melisse2023efficacyofwebbased pages 1-2, kowalewska2024comorbidityofbinge pages 1-2) Melisse & Dingemans, Journal of Eating Disorders, Jan 2025, https://doi.org/10.1186/s40337-025-01187-0; Melisse et al., Journal of Medical Internet Research, May 2023, https://doi.org/10.2196/40472; Kowalewska et al., BMC Psychiatry, Aug 2024, https://doi.org/10.1186/s12888-024-05943-5

Table: This table summarizes the main diagnostic frameworks and identifier status for binge eating disorder based only on gathered evidence. It is useful for anchoring a knowledge-base entry to current diagnostic systems while clearly noting which ontology IDs were not retrieved.

Study (author, year) Population/setting Design Key quantitative findings (prevalence/incidence, odds ratios, remission/relapse) Notable comorbidities/impairments/treatment uptake URL/DOI
Nagata et al., 2023 (nagata2023thesocialepidemiology pages 1-2) U.S. ABCD Study; 10,197 early adolescents aged 10-14 years Cross-sectional analysis BED prevalence 1.0%; binge-eating behaviors 6.3%. Greater odds of BED with gay/bisexual identity vs heterosexual (AOR 2.25, 95% CI 1.01-5.01) and household income <\$75,000 (AOR 2.05, 95% CI 1.21-3.46). Greater odds of binge-eating behaviors in males (AOR 1.28), Native American youth (AOR 1.60), low income (AOR 1.34), and sexual minority responses (~AOR 1.81-1.95). BED linked to later diabetes, metabolic syndrome, cardiovascular disease, suicidality; adolescent binge eating predicts depressive symptoms. Only 11.9% of adolescents with BED seek clinical care. https://doi.org/10.1186/s40337-023-00904-x
Javaras et al., 2024 (javaras2024thenaturalcourse pages 1-2) Community-based adults with DSM-IV BED; baseline n=156, follow-up n=137; mean age 47.2 years, mean BMI 36.1 Prospective natural-history study with 2.5- and 5-year follow-up At 2.5 years: 61.3% full BED, 23.4% subthreshold, 15.3% no BED. At 5 years: 45.7% full BED, 32.6% subthreshold, 21.7% no BED. Median time to remission >60 months; median time to relapse after remission 30 months. No participants developed AN or BN during follow-up. Demonstrates protracted course with frequent relapse; baseline sample predominantly female (78.1%). https://doi.org/10.1017/S0033291724000977
Kowalewska et al., 2024 (kowalewska2024comorbidityofbinge pages 1-2, kowalewska2024comorbidityofbinge pages 2-4) Systematic review of 63 studies on BED and psychiatric comorbidity Systematic review Reported U.S. lifetime incidence 2.8%; global lifetime prevalence ~1.9%. Higher lifetime incidence in women (3.5%) than men (2.0%). Most frequent psychiatric comorbidities: mood, anxiety, and substance use disorders; also ADHD, personality disorders, stress/adjustment disorders, psychotic disorders, sleep disorders, suicidality. Review highlights barriers to treatment uptake including shame, lack of awareness, and clinician knowledge gaps. https://doi.org/10.1186/s12888-024-05943-5
Melisse et al., 2023 (melisse2023efficacyofwebbased pages 1-2) Adults with BED in treatment context; summary epidemiologic framing within RCT report Randomized controlled trial report background Reports BED lifetime prevalence about 2% overall and up to 30% among people with excess weight. Describes BED as the most common eating disorder and emphasizes substantial unmet treatment need due to long waiting periods. https://doi.org/10.2196/40472
Appolinario et al., 2022 (kowalewska2024comorbidityofbinge pages 38-39) Representative metropolitan Rio de Janeiro sample; 2,297 adults aged 18-60 years Cross-sectional population survey BED prevalence 1.4%; recurrent binge eating 6.2%; BN 0.7%. BED associated with depression, anxiety, ADHD, elevated BMI, marked impairment in work/school, social and family life, reduced mental and physical HRQoL; under half had sought treatment. https://doi.org/10.1007/s00127-022-02223-z
Caldiroli et al., 2024 (caldiroli2024clinicalfactorsassociated pages 16-17) ED outpatient sample; subgroup with objective binge-eating episodes (OBEs) Cross-sectional clinical study 29% of subjects with OBEs exhibited a chronic ED course. BN/BED comprised 37.3% of ED diagnoses in the sample. OBE group had longer illness duration, more hospitalizations, more pharmacotherapy exposure; comorbid anxiety disorders, borderline personality disorder, and polysubstance misuse were more common. https://doi.org/10.3390/jpm14060609

Table: This table summarizes recent and closely relevant evidence on binge eating disorder epidemiology, demographic correlates, psychiatric burden, and longitudinal course. It is useful for quickly locating quantitative prevalence, odds ratios, and remission/relapse findings alongside real-world impairment and treatment uptake data.

Intervention (psychotherapy/pharmacotherapy/digital) Evidence type & key study (author year) Key quantitative outcomes (binge frequency/remission/weight/QoL) Safety/limitations Real-world implementation notes Suggested MAXO term(s) (free text) DOI/URL
Guided self-help CBT-E (digital psychotherapy) Randomized controlled trial; Melisse et al. 2023 (melisse2023efficacyofwebbased pages 1-2, melisse2023efficacyofwebbased pages 10-13) Objective binges fell from mean 19 (SD 16) to 3 (SD 5) by end of treatment; full recovery 40% (36/90); between-group effect size for objective binges d=1.0; treatment completion 78.9%; clinical impairment improved faster in treatment arm (melisse2023efficacyofwebbased pages 1-2, melisse2023efficacyofwebbased pages 10-13) Dropout ~21.1%; outcomes after both groups received treatment converged at follow-up; QoL not specifically quantified in gathered text (melisse2023efficacyofwebbased pages 1-2) Addresses long waiting lists and expands access to specialized BED care via web delivery (melisse2023efficacyofwebbased pages 1-2) cognitive behavioral psychotherapy; guided self-help; telehealth/digital psychotherapy https://doi.org/10.2196/40472
CBT vs pharmacotherapy for binge-spectrum disorders Systematic review/meta-analysis; Samara et al. 2024 (samara2024iscognitivebehavioral pages 4-5, samara2024iscognitivebehavioral pages 1-2) CBT superior to antidepressants for remission (pooled RR 2.24, 95% CI 1.03-4.87); superior for binge-frequency reduction (pooled SMD -0.35, 95% CI -0.69 to -0.01); some individual comparisons showed no significant differences vs methylphenidate/sibutramine (samara2024iscognitivebehavioral pages 4-5, samara2024iscognitivebehavioral pages 1-2) Small, underpowered trials; heterogeneity; psychotherapy blinding limitations; no clear superiority for QoL, anxiety, depression, weight, or dropouts overall (samara2024iscognitivebehavioral pages 4-5, samara2024iscognitivebehavioral pages 1-2) Supports guideline positioning of CBT as first-line when available, but access barriers may favor medication use in some settings (samara2024iscognitivebehavioral pages 1-2) cognitive behavioral psychotherapy; evidence-based psychotherapy selection https://doi.org/10.1177/00048674231219593
Digital eating-disorder interventions (mostly CBT-informed) Systematic review/meta-analysis; Thomas et al. 2024 (thomas2024behaviorchangetechniques pages 17-20, thomas2024behaviorchangetechniques pages 20-22, thomas2024behaviorchangetechniques pages 11-14) Pooled EDE-Q improvement vs WL/TAU MD -0.57 (95% CI -0.80 to -0.39); follow-up EDE-Q MD -0.33; 16/17 studies showed efficacy post-intervention; some studies reported ongoing reductions in bingeing/purging (thomas2024behaviorchangetechniques pages 17-20, thomas2024behaviorchangetechniques pages 20-22) High heterogeneity (I2 77% for main analysis); attrition ranged 6.7%-58%; limited BED-specific remission or binge-episode data in gathered text (thomas2024behaviorchangetechniques pages 17-20, thomas2024behaviorchangetechniques pages 11-14) Mostly web-based; therapist involvement ranged none to minimal; useful for scalable, lower-intensity implementation (thomas2024behaviorchangetechniques pages 11-14) digital behavioral intervention; internet-based psychotherapy; self-management support https://doi.org/10.2196/57577
Lisdexamfetamine (LDX) Rapid review and patient-perception synthesis; Rodan et al. 2023, Armanious et al. 2024 (rodan2023pharmacotherapyalternativeand pages 7-8, armanious2024patientperceptionsof pages 1-3) Recent evidence supports LDX use in BED; phase II/III trials collectively showed reduced weekly binge-eating episodes; efficacy strongest at 50-70 mg/day; patient-reported weight loss associated with higher perceived efficacy (rodan2023pharmacotherapyalternativeand pages 7-8, armanious2024patientperceptionsof pages 1-3) About 85% reported at least one treatment-emergent adverse event; common AEs include dry mouth, insomnia/sleep disturbance, jitteriness; abuse liability noted at high non-approved doses (armanious2024patientperceptionsof pages 1-3) Only FDA-approved medication for BED in gathered evidence; real-world perceptions suggest weight change influences acceptability and perceived benefit (armanious2024patientperceptionsof pages 1-3) stimulant medication administration; pharmacotherapy for binge eating https://doi.org/10.1186/s40337-023-00833-9; https://doi.org/10.1016/j.psycom.2024.100195
CBT alone Randomized controlled trial; Grilo et al. 2025 (grilo2025cognitivebehavioraltherapy pages 6-8, grilo2025cognitivebehavioraltherapy pages 1-3) Significant binge-frequency reductions; remission 44.7% (21/47); minimal weight loss effect (0.5% mean reduction; 4.3% achieved ≥5% weight loss) (grilo2025cognitivebehavioraltherapy pages 6-8, grilo2025cognitivebehavioraltherapy pages 8-10) Less weight loss than LDX-containing arms; not clearly superior to LDX alone on primary binge endpoint in this trial (grilo2025cognitivebehavioraltherapy pages 6-8, grilo2025cognitivebehavioraltherapy pages 8-10) Appropriate when psychotherapy access exists and weight loss is not the main treatment target; may be combined with medication for greater effect (grilo2025cognitivebehavioraltherapy pages 6-8) cognitive behavioral psychotherapy https://doi.org/10.1176/appi.ajp.20230982
Lisdexamfetamine alone Randomized controlled trial; Grilo et al. 2025 (grilo2025cognitivebehavioraltherapy pages 6-8, grilo2025cognitivebehavioraltherapy pages 8-10, grilo2025cognitivebehavioraltherapy pages 1-3) Remission 40.4% (19/47); binge-eating reduction ~79.7%; mean weight loss 5.5%; 53.2% achieved ≥5% weight loss; fastest early monthly reduction at month 1 (grilo2025cognitivebehavioraltherapy pages 6-8, grilo2025cognitivebehavioraltherapy pages 8-10) Medically withdrawn participants 21.3%; detailed AE profile not provided in gathered excerpt, but LDX-associated AEs elsewhere include xerostomia/headache/insomnia and common TEAEs (grilo2025cognitivebehavioraltherapy pages 8-10, armanious2024patientperceptionsof pages 1-3) Useful when medication access is easier than psychotherapy and weight loss is clinically relevant; FDA-approved option (grilo2025cognitivebehavioraltherapy pages 1-3, armanious2024patientperceptionsof pages 1-3) stimulant medication administration; pharmacotherapy for binge eating https://doi.org/10.1176/appi.ajp.20230982
Combined CBT + lisdexamfetamine Randomized controlled trial; Grilo et al. 2025 (grilo2025cognitivebehavioraltherapy pages 6-8, grilo2025cognitivebehavioraltherapy pages 8-10, grilo2025cognitivebehavioraltherapy pages 1-3) Highest remission 70.2% (33/47); largest binge-eating reduction (~96.1%); mean weight loss 4.8%; 42.6% achieved ≥5% weight loss; superior overall symptom reduction vs single modalities (grilo2025cognitivebehavioraltherapy pages 6-8, grilo2025cognitivebehavioraltherapy pages 8-10) Medical withdrawal 21.3%; trial lacked placebo/control medication and had limited diversity; AE details not fully reported in gathered text (grilo2025cognitivebehavioraltherapy pages 8-10) Strongest quantitative efficacy in gathered sources; suggests complementary mechanisms of psychotherapy plus stimulant treatment (grilo2025cognitivebehavioraltherapy pages 8-10) combination psychotherapy and pharmacotherapy; cognitive behavioral psychotherapy; stimulant medication administration https://doi.org/10.1176/appi.ajp.20230982
Anti-obesity drugs under investigation (e.g., phentermine/topiramate, naltrexone/bupropion, liraglutide, semaglutide) Narrative/systematic review of trials; Riboldi & Carrà 2024 (rodan2023pharmacotherapyalternativeand pages 7-8) Across 14 clinical trials, most anti-obesity drugs except orlistat may improve both body weight and binge severity/frequency; quantitative pooled estimates not provided in gathered excerpt (rodan2023pharmacotherapyalternativeand pages 7-8) Evidence limited by small samples and methodological variability; misuse risk may potentiate dietary restriction/pathological weight loss (rodan2023pharmacotherapyalternativeand pages 7-8) Emerging off-label/experimental option, especially where obesity comorbidity is prominent; ongoing trials likely to clarify role (rodan2023pharmacotherapyalternativeand pages 7-8) anti-obesity pharmacotherapy; appetite-modulating medication administration https://doi.org/10.5152/alphapsychiatry.2024.241464

Table: This table summarizes evidence-based psychotherapy, digital, and pharmacologic interventions for binge eating disorder using only the gathered sources. It highlights quantitative outcomes, safety considerations, implementation issues, and suggested MAXO-style intervention labels for knowledge-base use.

Clinical feature/phenotype Brief description Typical onset/course notes Example quantitative frequency/data if available from gathered evidence Suggested HPO term(s) (free text) Key citation(s)
Recurrent binge-eating episodes Core BED feature: recurrent episodes of eating accompanied by subjective loss of control Chronic or recurrent; DSM-5-TR requires episodes at least weekly for 3 months DSM-5-TR threshold: at least 1 episode/week for at least 3 months (melisse2025redefiningdiagnosticparameters pages 1-2, kowalewska2024comorbidityofbinge pages 2-4) Binge eating; Abnormal eating behavior; Loss of control over eating (melisse2025redefiningdiagnosticparameters pages 1-2, kowalewska2024comorbidityofbinge pages 2-4)
Loss of control during eating Sense of inability to stop or control what/how much is eaten during episodes Present during binge episodes; central phenomenologic feature across definitions Included as an essential feature in DSM-5-TR and ICD-11-oriented summaries (melisse2025redefiningdiagnosticparameters pages 1-2, palavras2018aninvestigationof pages 1-3, melisse2023efficacyofwebbased pages 1-2) Impaired impulse control; Loss of control over eating (melisse2025redefiningdiagnosticparameters pages 1-2, palavras2018aninvestigationof pages 1-3, melisse2023efficacyofwebbased pages 1-2)
Rapid eating Eating much more rapidly than normal during episodes Episodic, occurring during binges; one of the associated DSM-5-TR descriptors One of the 5 associated DSM-5-TR binge descriptors; ≥3 descriptors required (melisse2025redefiningdiagnosticparameters pages 1-2) Rapid eating (melisse2025redefiningdiagnosticparameters pages 1-2)
Eating until uncomfortably full Continued eating beyond comfortable satiety during episodes Episodic with binge events One of the 5 associated DSM-5-TR binge descriptors (melisse2025redefiningdiagnosticparameters pages 1-2) Early satiety abnormality / Postprandial discomfort; Abnormal satiety behavior (melisse2025redefiningdiagnosticparameters pages 1-2)
Eating when not physically hungry Intake continues despite absence of physiologic hunger cues Episodic with binge events; suggests disrupted satiety/interoception One of the 5 associated DSM-5-TR binge descriptors (melisse2025redefiningdiagnosticparameters pages 1-2) Hyperphagia; Abnormal hunger/satiety behavior (melisse2025redefiningdiagnosticparameters pages 1-2)
Eating alone because of embarrassment Socially avoidant eating driven by shame/embarrassment Episodic; may contribute to concealment and delayed care seeking One of the 5 associated DSM-5-TR binge descriptors (melisse2025redefiningdiagnosticparameters pages 1-2) Social withdrawal during eating; Embarrassment; Avoidant behavior (melisse2025redefiningdiagnosticparameters pages 1-2)
Negative affect after overeating Feelings such as guilt, disgust, or low mood after binges Episodic but can reinforce chronic cycle; linked to impairment and severity Melisse 2023 describes shame, guilt, and disgust as characteristic feelings in BED (melisse2023efficacyofwebbased pages 1-2) Guilt; Shame; Dysphoric mood (melisse2023efficacyofwebbased pages 1-2)
Marked distress about binge eating Clinically significant distress is required for diagnosis Persistent distress often accompanies chronic course and poorer functioning Marked distress identified as an essential feature in diagnostic summaries (palavras2018aninvestigationof pages 1-3, hay2023currentapproachesin pages 1-2) Emotional distress; Psychological distress (palavras2018aninvestigationof pages 1-3, hay2023currentapproachesin pages 1-2)
Absence of regular compensatory behaviors Distinguishes BED from bulimia nervosa; no recurrent purging/compensation after binges Stable diagnostic discriminator across DSM-5/DSM-5-TR descriptions Explicitly noted in Melisse 2023 and Hay 2023 (melisse2023efficacyofwebbased pages 1-2, hay2023currentapproachesin pages 1-2) Binge eating without compensatory behavior (melisse2023efficacyofwebbased pages 1-2, hay2023currentapproachesin pages 1-2)
Functional impairment / reduced quality of life BED is associated with impairment in daily functioning and health-related quality of life Often chronic; persists with ongoing BED and comorbidity In a population survey, BED was associated with marked work/school, social, and family impairment and reduced mental/physical HRQoL; under half sought treatment (kowalewska2024comorbidityofbinge pages 38-39) Reduced quality of life; Impaired social functioning; Occupational impairment (kowalewska2024comorbidityofbinge pages 38-39)
Clinical impairment improves with treatment BED-related impairment is measurable and treatment responsive Improves with psychotherapy; can recur if illness persists/relapses Guided self-help CBT-E showed faster reduction in clinical impairment assessment scores vs delayed treatment (melisse2023efficacyofwebbased pages 10-13) Reduced quality of life; Functional impairment (melisse2023efficacyofwebbased pages 10-13)
Mood, anxiety, and substance-use comorbidity Most frequent psychiatric comorbidities in BED; associated with greater severity Often persistent across illness course and important for prognosis Systematic review identified mood disorders, anxiety disorders, and substance use disorders as the most frequent BED comorbidities (kowalewska2024comorbidityofbinge pages 1-2, kowalewska2024comorbidityofbinge pages 2-4) Anxiety; Depressive episode; Substance abuse (kowalewska2024comorbidityofbinge pages 1-2, kowalewska2024comorbidityofbinge pages 2-4)
Additional psychiatric comorbidity burden BED also co-occurs with ADHD, personality disorders, sleep disorders, suicidality, stress-related and psychotic disorders Contributes to broader morbidity and complexity Broad psychiatric comorbidity profile summarized in 2024 systematic review (kowalewska2024comorbidityofbinge pages 1-2, kowalewska2024comorbidityofbinge pages 11-12) Attention deficit hyperactivity disorder; Sleep disturbance; Suicidal ideation/behavior; Personality dysfunction (kowalewska2024comorbidityofbinge pages 1-2, kowalewska2024comorbidityofbinge pages 11-12)
Adult chronicity / slow remission Natural course in adults is often prolonged rather than brief Chronic, relapsing course common; remission may take years Median time to remission exceeded 60 months in a prospective community cohort (javaras2024thenaturalcourse pages 1-2) Chronic course; Relapsing course (javaras2024thenaturalcourse pages 1-2)
Partial persistence over time Many adults remain full or subthreshold cases over multi-year follow-up Fluctuating between full, subthreshold, and remitted states At 2.5 years: 61.3% full BED, 23.4% subthreshold, 15.3% no BED; at 5 years: 45.7% full, 32.6% subthreshold, 21.7% no BED (javaras2024thenaturalcourse pages 1-2) Relapsing-remitting course; Fluctuating severity (javaras2024thenaturalcourse pages 1-2)
Relapse after remission Remission is often not durable Relapsing course common after initial remission Median time to relapse after remission was 30 months (javaras2024thenaturalcourse pages 1-2) Relapsing course (javaras2024thenaturalcourse pages 1-2)
Female predominance but affects all sexes BED is more common in females, though substantial male burden exists Lifetime risk spans adolescence to adulthood; prevalence peaks later than some other EDs Review reported lifetime incidence 3.5% in women vs 2.0% in men; in a natural-history cohort 78.1% were female (kowalewska2024comorbidityofbinge pages 1-2, javaras2024thenaturalcourse pages 1-2) Abnormal eating behavior in female; Abnormal eating behavior in male (kowalewska2024comorbidityofbinge pages 1-2, javaras2024thenaturalcourse pages 1-2)

Table: This table summarizes the core clinical manifestations, impairment profile, and longitudinal course of binge eating disorder using only gathered evidence. It is useful for mapping BED features into structured phenotype fields and ontology-oriented knowledge base entries.

Visual evidence (diagnostic criteria / treatment pathway)

Hay et al. (2023) includes a visual summary of DSM-5-TR eating-disorder criteria (including BED) and a treatment-pathway indicator box, retrievable as cropped images. These can be used to populate UI-facing knowledge-base views of diagnostic criteria and treatment pathways (hay2023currentapproachesin media 97e600c1, hay2023currentapproachesin media 07cb9dc5).

1. Disease information

1.1 Concise overview (current understanding)

Binge eating disorder (BED) is defined by recurrent binge-eating episodes characterized by a sense of loss of control, accompanied by marked distress, and not followed by compensatory behaviors (distinguishing it from bulimia nervosa). In DSM-5-TR, binge episodes must occur at least once per week for at least 3 months and include ≥3 associated features (e.g., rapid eating, eating until uncomfortably full, eating when not physically hungry, eating alone due to embarrassment, and negative feelings after overeating). (melisse2025redefiningdiagnosticparameters pages 1-2, melisse2023efficacyofwebbased pages 1-2, hay2023currentapproachesin pages 1-2)

1.2 Key identifiers and classification systems

A structured summary of DSM-5-TR vs ICD-11 positioning and identifier availability in the retrieved corpus is provided in Artifact-00. ICD-11 inclusion is supported by clinical-utility work comparing DSM-5 and proposed ICD-11 BED schemes; ICD-11 criteria are described as broader and may include subjective binge episodes and more flexible duration thresholds in certain circumstances. (palavras2018aninvestigationof pages 1-3, hay2023currentapproachesin pages 1-2)

Limitations: This run did not retrieve BED’s MeSH or MONDO identifiers, nor a specific ICD-11 code string for BED from the included texts (melisse2025redefiningdiagnosticparameters pages 1-2, hay2023currentapproachesin pages 1-2).

1.3 Synonyms / alternative names

The common naming in the retrieved sources is “binge-eating disorder” with the abbreviation “BED.” (melisse2025redefiningdiagnosticparameters pages 1-2, melisse2023efficacyofwebbased pages 1-2)

1.4 Evidence provenance (patient-level vs aggregated)

Most evidence in this report is from aggregated disease-level resources: clinical reviews, systematic reviews/meta-analyses, and cohort/RCT data, rather than EHR-only descriptions. Examples include: a national adolescent cohort analysis (ABCD), a community adult natural-history cohort, and randomized trials of psychotherapy delivery. (nagata2023thesocialepidemiology pages 1-2, javaras2024thenaturalcourse pages 1-2, melisse2023efficacyofwebbased pages 1-2)

2. Etiology

2.1 Disease causal factors (multifactorial)

BED is understood as multifactorial, with interacting neurobehavioral mechanisms (reward/inhibitory-control imbalance), psychosocial drivers (stress/negative affect), and polygenic genetic liability, often co-occurring with obesity and cardiometabolic risk but not reducible to obesity alone. (pasquale2024rewardandinhibitory pages 2-4, chen2024neuroimagingstudiesof pages 12-15, burstein2023genomewideanalysisof pages 8-10)

2.2 Risk factors

2.2.1 Genetic risk factors

GWAS/PRS (human): - A 2023 Nature Genetics study performed GWAS on a model-derived BED phenotype and validated at least one locus (e.g., rs17789218 near MCHR2), with additional replication signals; it also found nominal enrichment in neural lineages (limbic neurons, inhibitory/non-excitatory neurons, enteric neurons/glia, astrocytes), supporting a neurobiological substrate. (burstein2023genomewideanalysisof pages 8-10) - Polygenic liability to schizophrenia in a binge-eating genetics cohort (BEGIN) was associated with earlier age at first ED symptom (−0.35 year), higher ED symptom scores (0.16), and greater risk of major depressive disorder (HR 1.18) and substance use disorder (HR 1.36), indicating cross-disorder shared liability relevant to clinical course and comorbidity. (zhang2023theimpactof pages 1-2)

Candidate-gene synthesis (human): A 2024 systematic review of genetic polymorphisms/microbiome work summarized repeated candidate associations involving dopaminergic and appetite/reward genes (e.g., DRD2, COMT, MC4R, BDNF, FTO, OPRM1, SLC6A3, GHRL, CARTPT, MCHR2), but emphasized heterogeneity and limitations typical of candidate-gene designs. (hernandez2024relationshipofgenetic pages 1-2, hernandez2024relationshipofgenetic pages 5-7)

2.2.2 Environmental / social risk factors

In U.S. early adolescents (ABCD cohort), BED odds were higher with: - Gay/bisexual identity vs heterosexual (AOR 2.25, 95% CI 1.01–5.01) - Household income < $75,000 (AOR 2.05, 95% CI 1.21–3.46) Additionally, binge-eating behaviors (broader than BED diagnosis) were associated with male sex, Native American descent, lower income, and sexual minority status responses. (nagata2023thesocialepidemiology pages 1-2)

2.2.3 Protective factors

No robust, specific protective factors (genetic or environmental) were retrieved in the gathered texts; this remains a gap in this run’s evidence set.

2.3 Gene–environment interactions

Direct, quantified GxE interaction studies specific to BED were not retrieved in the gathered texts. However, convergent mechanistic evidence supports that stress/negative affect interacts with reward/inhibitory systems to precipitate binge episodes, and animal work demonstrates sex-specific stress-triggered binge-like eating circuitry. (anversa2023aparaventricularthalamus pages 1-2, dufour2026advancingtranslationalresearch pages 5-8)

3. Phenotypes

3.1 Core clinical phenotypes and ontology suggestions

A structured phenotype table with suggested HPO terms and course features is provided in Artifact-03. Core diagnostic descriptors (DSM-5-TR) are explicitly enumerated in a 2025 BED diagnostic-parameter review and are consistent with clinical summaries. (melisse2025redefiningdiagnosticparameters pages 1-2, hay2023currentapproachesin pages 1-2)

3.2 Age of onset, severity, progression

  • Early adolescence prevalence and sociodemographic risk patterns are described in ABCD data (age 10–14). (nagata2023thesocialepidemiology pages 1-2)
  • In a prospective adult community sample, BED tended to improve but often over years, with substantial subthreshold persistence and relapse. (javaras2024thenaturalcourse pages 1-2)

3.3 Quality of life (QoL) impact

A representative population survey reported BED associated with marked impairments in work/school, social and family life and reduced mental and physical HRQoL, with under half seeking treatment. (kowalewska2024comorbidityofbinge pages 38-39)

4. Genetic / molecular information

4.1 Causal genes

BED is not a monogenic disorder in the retrieved evidence; it is best characterized as polygenic with loci contributing small effects. (burstein2023genomewideanalysisof pages 8-10, zhang2023theimpactof pages 1-2)

4.2 Pathogenic variants

No ClinVar/ACMG-classified pathogenic variants specific to BED were identified in the retrieved evidence.

4.3 Epigenetic information

The retrieved evidence set did not include a BED-specific EWAS. A BED-relevant epigenetic candidate finding in obesity-spectrum males reported sex-specific OXTR DNA methylation differences (lower methylation in males with BED vs obese males without BED), suggesting possible sex-dependent epigenetic vulnerability, though peripheral methylation is not a validated diagnostic biomarker. (hernandez2024relationshipofgenetic pages 1-2)

5. Environmental information

5.1 Lifestyle and social context

BED is frequently associated with obesity and may be embedded in contexts of food availability, stress, and socioeconomic adversity; adolescent data specifically highlight income and sexual minority status associations. (nagata2023thesocialepidemiology pages 1-2)

5.2 Infectious agents

Not applicable based on retrieved evidence.

6. Mechanism / pathophysiology

6.1 Current mechanistic model (reward + inhibitory control imbalance)

A 2024 mechanistic review synthesizes evidence that BED involves reward hypersensitivity and impaired inhibitory control, including an imbalance between anticipatory reward and experienced reward signals and frontostriatal/prefrontal dysfunction. It describes implicated circuitry including reward regions (VTA, ventral striatum/NAc, OFC/PFC) and inhibitory-control nodes (prefrontal cortex, dACC, inferior frontal gyrus, pre-SMA), consistent with addiction-inspired incentive-sensitization frameworks. (pasquale2024rewardandinhibitory pages 2-4, pasquale2024rewardandinhibitory pages 8-9)

6.2 Neuroimaging (rs-fMRI network-level findings)

A 2024 resting-state fMRI review reports BED-associated alterations across large-scale networks (DMN/CEN/salience network) and regionally highlights reduced dACC connectivity in the salience network and increased PCC/mPFC connectivity in the DMN, aligning with impaired salience/inhibitory control and altered self-referential processing. (chen2024neuroimagingstudiesof pages 1-2)

6.3 Stress and negative affect mechanisms

Animal-model evidence indicates a sex-specific “emotional stress-induced binge eating” phenotype and identifies a glutamatergic paraventricular thalamus (PVT) → medial insular cortex projection that gates stress-induced binge eating in females; chemogenetic inhibition suppresses the behavior, supporting a causal circuit mechanism. (anversa2023aparaventricularthalamus pages 1-2)

6.4 Suggested biological annotation terms

GO biological processes (examples): reward processing; dopaminergic synaptic transmission; response to stress; regulation of feeding behavior; inhibitory control/executive function (conceptual mapping) (pasquale2024rewardandinhibitory pages 2-4, chen2024neuroimagingstudiesof pages 12-15).

Cell Ontology (CL) (examples): cortical pyramidal neurons; medium spiny neurons; astrocytes (supported by heritability enrichment in astrocytes and neural lineages) (burstein2023genomewideanalysisof pages 8-10).

UBERON (examples): brain; prefrontal cortex; anterior cingulate cortex; insular cortex; ventral striatum/nucleus accumbens (pasquale2024rewardandinhibitory pages 2-4, chen2024neuroimagingstudiesof pages 1-2, anversa2023aparaventricularthalamus pages 1-2).

7. Anatomical structures affected

Primary involvement is functional dysregulation in brain reward and control circuits (prefrontal cortex, ACC/dACC, insula, striatum/NAc, OFC), with downstream impacts on eating behavior and metabolic health risk. (pasquale2024rewardandinhibitory pages 2-4, chen2024neuroimagingstudiesof pages 1-2)

8. Temporal development

8.1 Onset

Early adolescence can show measurable BED prevalence (1.0% in a 10–14 year-old U.S. cohort). (nagata2023thesocialepidemiology pages 1-2)

8.2 Progression, remission, relapse

In a prospective community-based adult BED cohort: - At 2.5 years: 61.3% full BED, 23.4% subthreshold, 15.3% no BED - At 5 years: 45.7% full BED, 32.6% subthreshold, 21.7% no BED - Median time to remission exceeded 60 months; median time to relapse after remission was 30 months This supports a protracted course with common relapse. (javaras2024thenaturalcourse pages 1-2)

9. Inheritance and population

9.1 Epidemiology

Recent evidence collated in Artifact-01 includes: - Early adolescent BED prevalence 1.0% in ABCD follow-up data (nagata2023thesocialepidemiology pages 1-2) - Systematic-review estimates for global lifetime prevalence ~1.9% and U.S. lifetime incidence 2.8%, with higher lifetime incidence in women than men (3.5% vs 2.0%) (kowalewska2024comorbidityofbinge pages 1-2) - Population-based adult survey prevalence 1.4% in Rio de Janeiro (kowalewska2024comorbidityofbinge pages 38-39)

9.2 Inheritance pattern

Evidence supports polygenic/multifactorial inheritance rather than Mendelian inheritance. (burstein2023genomewideanalysisof pages 8-10, zhang2023theimpactof pages 1-2)

10. Diagnostics

10.1 Clinical criteria

DSM-5-TR diagnostic elements (frequency/duration and associated features) are summarized in recent reviews and are visually represented in Hay et al. (2023) boxes (melisse2025redefiningdiagnosticparameters pages 1-2, hay2023currentapproachesin media 97e600c1).

10.2 Screening and assessment tools (real-world implementation)

  • BEDS-7: a brief 7-item screener with a published scoring algorithm; in an overweight/obesity validation context, the systematic review reports sensitivity and NPV ≥0.83 for BMI >30, though specificity can be modest and depends on BMI range. (herman2016developmentofthe pages 1-2, house2022identifyingeatingdisorders pages 16-16, house2022identifyingeatingdisorders pages 17-17)
  • QEWP-5: in an Italian obesity-treatment sample (n=604) compared to EDE interview, sensitivity 0.49 and specificity 0.93 (PPV 0.34; NPV 0.96; κ 0.35), supporting use as a screening tool but not a stand-alone diagnostic instrument. (calugi2020psychometricproprietiesof pages 1-3)
  • LOCES: a 24-item measure capturing subjective loss of control; in an undergraduate sample (n=261) it showed excellent internal consistency (α≈0.95) and predicted OBE and SBE frequency (e.g., OBE: b=2.40, β=0.41; SBE: b=2.95, β=0.43). (stefano2016lossofcontrol pages 2-3, stefano2016lossofcontrol pages 1-2)
  • EDE/EDE-Q: systematic-review evidence indicates variable sensitivity/specificity depending on population and outcome definition; one bariatric candidate study reported EDE-Q sensitivity 0.59, specificity 0.86 for BED. (house2022identifyingeatingdisorders pages 13-13)

10.3 Biomarkers and imaging

No clinically validated blood biomarker was retrieved. Candidate biomarkers include rs-fMRI connectivity patterns (DMN/salience network; dACC/PCC/mPFC), PFC activation patterns (fNIRS), ERP indices of anticipatory vs consummatory reward, and PET measures of dopamine/opioid signaling, but these remain research-stage with small, heterogeneous samples. (pasquale2024rewardandinhibitory pages 2-4, chen2024neuroimagingstudiesof pages 1-2)

11. Outcome / prognosis

11.1 Morbidity and complications

BED is linked to substantial psychiatric comorbidity (mood, anxiety, substance-use disorders most frequent; also ADHD, sleep disorders, personality disorders, suicidality) and is associated with medical sequelae such as diabetes/metabolic syndrome and cardiovascular risk (particularly in obesity contexts). (kowalewska2024comorbidityofbinge pages 1-2, nagata2023thesocialepidemiology pages 1-2)

11.2 Prognostic factors

In adolescents, socioeconomic and sexual-minority status markers identify higher odds of BED, suggesting target groups for prevention/screening. (nagata2023thesocialepidemiology pages 1-2)

11.3 Mortality

BED-specific mortality rates were not retrieved from the gathered sources; however, eating disorders overall are recognized as severe illnesses with elevated morbidity and mortality. (caldiroli2024clinicalfactorsassociated pages 16-17)

12. Treatment

A structured treatment evidence table with quantitative outcomes, implementation notes, and MAXO-style term suggestions is provided in Artifact-02.

12.1 First-line psychotherapy and digital delivery

A 2023 RCT of web-based guided self-help CBT-E showed large reductions in binge episodes and 40% full recovery in 12 weeks, supporting scalable real-world implementation to address treatment access gaps. (melisse2023efficacyofwebbased pages 1-2)

12.2 Pharmacotherapy

Lisdexamfetamine (LDX) is described as the only FDA-approved medication for BED in the retrieved 2024 patient-perception analysis, with common treatment-emergent adverse events and ~85% reporting at least one AE in trials. (armanious2024patientperceptionsof pages 1-3)

12.3 Combined treatment (psychotherapy + medication)

A randomized controlled trial in adults with BED and obesity reported post-treatment remission rates of 70.2% (CBT+LDX) vs 44.7% (CBT) vs 40.4% (LDX), and greater weight loss in LDX-containing arms (e.g., LDX mean 5.5% weight loss; 53.2% achieving ≥5% weight loss). (grilo2025cognitivebehavioraltherapy pages 6-8, grilo2025cognitivebehavioraltherapy pages 8-10)

12.4 Emerging/adjunct approaches

Anti-obesity drugs (e.g., phentermine/topiramate, naltrexone/bupropion, liraglutide, semaglutide) have been reviewed as potential options to address both binge symptoms and weight outcomes, but evidence is limited and responsible prescribing is emphasized due to misuse risk. (rodan2023pharmacotherapyalternativeand pages 7-8)

13. Prevention

No BED-specific prevention trial outcomes were retrieved in the evidence set; however, adolescent sociodemographic risk patterns suggest targeted screening and early intervention in high-risk groups may be pragmatic. (nagata2023thesocialepidemiology pages 1-2)

14. Other species / natural disease

Not applicable as a naturally occurring veterinary diagnosis in retrieved evidence; however, binge-like intake behaviors are modeled in rodents for mechanistic and therapeutic work. (anversa2023aparaventricularthalamus pages 1-2, awad2024alteredrewardprocessing pages 1-3)

15. Model organisms

15.1 Common rodent models and translational relevance

  • Intermittent access palatable food/sucrose paradigms generate binge-like intake escalation and allow testing reward-related outcomes; sucrose bingeing altered ethanol conditioned place preference without marked emotional changes, with stronger binge escalation in females over prolonged exposure. (awad2024alteredrewardprocessing pages 1-3)
  • Stress-induced binge models: a female-specific emotional stress-induced binge model identifies the PVT→insular cortex pathway as a causal gate. (anversa2023aparaventricularthalamus pages 1-2)
  • A translational review emphasizes that animal models capture behavioral hyperphagia/compulsivity but incompletely model human subjective distress, guilt, stigma, and body-image concerns—key limitations for BED translation. (dufour2026advancingtranslationalresearch pages 5-8)

Direct abstract quotes supporting key claims (selected)

  • “Objective binges reduced from an average of 19 (SD 16) to 3 (SD 5) binges, and 40% (36/90) showed full recovery in the guided self-help CBT-E group.” (Melisse et al., May 2023) (melisse2023efficacyofwebbased pages 1-2)
  • “At 2.5 (and 5) years, 61.3% (45.7%), 23.4% (32.6%), and 15.3% (21.7%) … exhibited full, sub-threshold, and no BED … Median time to remission exceeded 60 months, and median time to relapse … was 30 months.” (Javaras et al., May 2024) (javaras2024thenaturalcourse pages 1-2)
  • “Identifying as gay or bisexual … (AOR: 2.25 …) and having a household income of less than $75,000 (AOR: 2.05 …) were associated with greater odds of BED.” (Nagata et al., Oct 2023) (nagata2023thesocialepidemiology pages 1-2)

Key limitations of this evidence synthesis

  1. Ontology identifiers (MONDO/MeSH) and explicit ICD-11 code for BED were not retrieved from the available texts in this run. (melisse2025redefiningdiagnosticparameters pages 1-2, hay2023currentapproachesin pages 1-2)
  2. Mortality: BED-specific mortality estimates were not retrieved; comorbidity and general ED severity were available but not BED-specific mortality rates. (caldiroli2024clinicalfactorsassociated pages 16-17)
  3. Protective factors and formal GxE: Not well represented in retrieved sources.
  4. Some evidence is from 2025 trials (e.g., CBT+LDX RCT), included because it provides high-quality quantitative effect estimates; 2023–2024 evidence was prioritized where available. (grilo2025cognitivebehavioraltherapy pages 6-8)

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