Bulimia Nervosa: Disease Characteristics Research Report

Executive summary

Bulimia nervosa (BN) is a psychiatric eating disorder defined by recurrent, objectively large binge-eating episodes with loss of control, recurrent inappropriate compensatory behavior, and excessive influence of weight or shape on self-evaluation. Under DSM-5-style criteria, binge eating and compensation occur at least weekly for 3 months and do not occur exclusively during anorexia nervosa. BN is usually episodic or relapsing, often begins in adolescence, and can occur at any body mass index; consequently, visual recognition is unreliable. Current understanding is that BN is multifactorial and polygenic rather than a single-gene disorder. Psychological vulnerability, sociocultural pressures, trauma, dieting, and altered reward/inhibitory-control circuitry interact to produce and perpetuate binge–purge cycles. (yu2023efficacyofpharmacotherapies pages 1-2, wilson2024bulimianervosaand pages 1-2, donnelly2018neuroimaginginbulimia pages 1-2, barakat2023riskfactorsfor pages 7-8)

The strongest evidence-based treatment for adults is eating-disorder-focused cognitive behavioral therapy, commonly CBT-E. Family-based treatment is particularly important for adolescents. Fluoxetine is the best-established medication and is generally adjunctive rather than a replacement for psychotherapy. Medical monitoring is essential because vomiting, laxative or diuretic misuse, fasting, and excessive exercise may produce electrolyte, cardiac, gastrointestinal, dental, and endocrine complications. (yu2023efficacyofpharmacotherapies pages 1-2, gkintoni2024clinicalinterventionstrategies pages 30-31, alharbi2024effectivetreatmentapproaches pages 5-6)

1. Disease information

Definition and identifiers

• Preferred name: Bulimia nervosa.
• Abbreviation/synonym: BN; historically “bulimia.” “Binge–purge eating disorder” is descriptive but is not the preferred controlled label.
• Category: Feeding or eating disorder; psychiatric disease.
• MONDO: MONDO:0005452, confirmed by the Open Targets disease record. No associated molecular targets were returned, consistent with the absence of a validated single causal target. (OpenTargets Search: bulimia nervosa)
• ICD-10-CM: F50.2, bulimia nervosa.
• ICD-11: 6B81, bulimia nervosa.
• MeSH: Bulimia Nervosa.
• OMIM/Orphanet: No appropriate Mendelian OMIM phenotype or rare-disease Orphanet entry is established for ordinary BN; assigning one would incorrectly imply monogenic or rare-disease causation.

These are aggregated disease-level definitions. They are not individual-patient EHR observations, although ICD/SNOMED labels can be instantiated in EHRs.

Diagnostic concept

A binge includes unusually large food consumption in a discrete interval and subjective loss of control. Compensation can include self-induced vomiting, laxative or diuretic misuse, fasting, or excessive exercise. Weight/shape overvaluation is required, and BN is differentiated from binge-eating disorder by recurrent compensation and from anorexia nervosa binge–purge type by the absence of persistently significantly low weight meeting AN criteria. (yu2023efficacyofpharmacotherapies pages 1-2, wilson2024bulimianervosaand pages 1-2, wilson2024bulimianervosaand pages 2-3)

2. Etiology

Causal and risk factors

BN has no single sufficient cause. Evidence supports interacting genetic susceptibility, developmental and psychiatric vulnerability, environmental exposure, and learned behavioral reinforcement. A 2023 rapid review grouped eating-disorder risks into genetics; microbiota/autoimmune factors; childhood exposures; personality and psychiatric comorbidity; sex/gender; socioeconomic and minority-related factors; body image/social influence; and elite sport. It emphasized that association does not necessarily establish causality. (barakat2023riskfactorsfor pages 7-8)

Genetic susceptibility. Family/twin literature supports moderate heritability, but the retrieved evidence does not justify a precise BN-specific estimate. Candidate associations have been reported in dopamine- and serotonin-related neuroendocrine receptors, glucocorticoid-pathway genes, and the serotonin-transporter-linked polymorphic region, 5-HTTLPR. These are susceptibility findings—not ACMG-pathogenic variants—and are not suitable for clinical prediction. Binge-type eating disorders show genetic overlap with ADHD, while BN also shares genomic liability with overweight/obesity. (barakat2023riskfactorsfor pages 7-8)

Environmental/developmental risks. Childhood maltreatment or trauma, body dissatisfaction, internalization of thin/appearance ideals, appearance-focused social media, dieting or restraint, weight stigma, mood/anxiety symptoms, impulsivity, and family/social stress are associated risks. Autoimmune or autoinflammatory disease in childhood was associated with a reported 73% increase in BN risk, although confounding and mechanisms remain uncertain. (butler2021theroleof pages 10-12, barakat2023riskfactorsfor pages 7-8)

Gene–environment interaction. Reported examples include maltreatment interacting with glucocorticoid-receptor pathway polymorphisms or 5-HTTLPR. Lower cortisol following maltreatment has been reported in BN relative to controls, suggesting stress-axis calibration may mediate vulnerability. These findings remain observational and are not actionable biomarkers. (barakat2023riskfactorsfor pages 7-8)

Protective factors

No reproducible protective allele is established. Plausible environmental protection includes positive body image, reduced appearance-based social comparison, media literacy, supportive family/peer relationships, flexible eating, avoidance of restrictive dieting, early recognition, and rapid access to evidence-based care. These should be treated as prevention targets rather than proven disease-specific protective mechanisms.

3. Phenotypes

Core behavioral and psychiatric phenotypes

• Recurrent binge eating with loss of control—episodic and variable in frequency.
• Self-induced vomiting or other compensation: laxatives/diuretics, fasting, or driven exercise.
• Overvaluation of body weight/shape, body dissatisfaction, dietary restraint, shame, secrecy, and impaired emotion regulation.
• Depression, anxiety, self-harm, suicidality, and substance-use symptoms are important comorbid phenotypes. Review estimates include mood disorders in 43%, anxiety disorders in 53%, and lifetime mood disorder in 80–90%, but estimates vary substantially by sample and definition. (yu2023efficacyofpharmacotherapies pages 1-2, donnelly2018neuroimaginginbulimia pages 1-2)

Physical signs, manifestations, and laboratory abnormalities

Vomiting may cause dental enamel erosion, caries, pharyngeal trauma, salivary-gland enlargement, reflux or other gastrointestinal symptoms, dehydration, and electrolyte/acid–base abnormalities. Severe electrolyte disturbance can precipitate weakness, syncope, QT abnormalities, or arrhythmia. Menstrual irregularity can occur, although it is less diagnostically central than in restrictive disorders. Normal or high weight does not exclude serious medical instability. (wilson2024bulimianervosaand pages 1-2, wilson2024bulimianervosaand pages 2-3, alharbi2024effectivetreatmentapproaches pages 5-6)

Suggested HPO mappings include Binge eating, Self-induced vomiting, Abnormality of electrolyte homeostasis, Hypokalemia, Dehydration, Cardiac arrhythmia, Dental erosion, Salivary-gland enlargement, Menstrual irregularity, Anxiety, and Depressive symptom. Exact term IDs should be validated against the current HPO release before ingestion.

Severity, progression, and quality of life

DSM severity is based on weekly compensatory-event frequency: mild 1–3, moderate 4–7, severe 8–13, and extreme ≥14, with clinical judgment allowing adjustment for disability. Course is commonly fluctuating or relapsing. Individual phenotypes impair school/work attendance, relationships, finances, concentration, self-esteem, and social eating. The evidence base uses inconsistent remission and recovery definitions, limiting precise cross-study estimates.

4. Genetic and molecular information

BN should be annotated as multifactorial/polygenic, not Mendelian. There are no established causal genes, pathogenic germline variants, recurrent chromosomal abnormalities, founder mutations, carrier frequencies, penetrance estimates, anticipation, or germline mosaicism relevant to routine BN. Correspondingly, Open Targets returned zero disease–target associations for MONDO:0005452. (OpenTargets Search: bulimia nervosa)

Reported candidate loci in serotonergic, dopaminergic, and glucocorticoid signaling are association-level observations. They should not be labeled pathogenic or likely pathogenic under ACMG/AMP criteria. No validated modifier gene or clinically useful pharmacogenomic marker exists for selecting CBT or fluoxetine specifically in BN. (barakat2023riskfactorsfor pages 7-8)

Epigenetic evidence specific to BN is sparse and confounded by trauma, diet, medication, smoking, adiposity, and illness state. No methylation signature is validated diagnostically. WGS, WES, gene panels, CMA, karyotyping, FISH, mitochondrial sequencing, and repeat-expansion testing are therefore not indicated for uncomplicated BN; they are reserved for syndromic presentations suggesting another disorder.

5. Environmental information

There is no infectious cause and no evidence supporting vaccination, antimicrobial treatment, or zoonotic control. No toxin, radiation, or occupational exposure is established as a specific cause. Relevant exposures are predominantly psychosocial and behavioral: restrictive dieting, weight cycling, appearance pressure, social-media comparison, bullying/weight stigma, trauma, elite sports emphasizing leanness, and family or peer reinforcement. Alcohol, nicotine, stimulant, or other substance use may coexist and can increase medical and behavioral risk. (barakat2023riskfactorsfor pages 7-8)

6. Mechanism and pathophysiology

Integrated causal model

A defensible causal chain is: polygenic/developmental vulnerability plus appearance, trauma, or dieting exposures → negative affect, restraint, altered interoception and reward valuation → food restriction and heightened cue salience → loss-of-control binge → acute distress and fear of weight gain → purging/fasting/exercise, which provides short-term negative reinforcement → renewed restriction and repeated cycles. Recurrent purging then produces downstream electrolyte, dental, salivary, gastrointestinal, and cardiovascular injury.

Neural circuitry and signaling

Human neuroimaging studies report reduced activity in frontostriatal control circuits and abnormal responses in the insula, amygdala, middle frontal gyrus, orbitofrontal cortex, and anterior cingulate cortex. These findings support impaired inhibitory control, altered reward sensitivity, food-cue attentional bias, and emotion/interoceptive dysregulation. Greater binge/bulimic frequency correlates with more pronounced neural alteration. However, a systematic review found substantial methodological heterogeneity and small samples, so no imaging pattern is diagnostic or demonstrably causal. (donnelly2018neuroimaginginbulimia pages 1-2)

Suggested processes include GO concepts related to regulation of feeding behavior, dopamine receptor signaling, serotonin receptor signaling, response to stress, reward learning, and behavioral response inhibition. Relevant cells include excitatory and inhibitory neurons, dopaminergic neurons, serotonergic neurons, and peripheral T lymphocytes; current evidence does not support a BN-specific cellular lesion.

Gut–brain, metabolic, and immune findings

Microbiome/metabolite differences have been reported across eating disorders and binge–purge versus restricting patterns, but small, mixed-diagnosis samples and diet/adiposity confounding prevent a BN-specific signature. These findings are hypothesis-generating, not grounds for probiotics or fecal transplantation as standard treatment.

BN does not show a consistent systemic inflammatory-cytokine phenotype: meta-analysis found no reliable IL-6 or TNF-α difference; PBMC production of IFN-γ, IL-1β, IL-6, and TNF-α was also not consistently altered. A cohort of 76 obese BN patients showed higher IL-1β, IL-6, and TNF-α, plausibly attributable to adiposity. Lower CD4/CD8 ratios and reduced CD2, CD3, CD4, CD8, and CD57 have been reported, but confounding and replication limitations preclude an immune biomarker. (butler2021theroleof pages 10-12)

No validated transcriptomic, proteomic, metabolomic, lipidomic, single-cell, spatial-transcriptomic, CRISPR-screen, or multi-omic diagnostic signature exists for BN.

7. Anatomical structures affected

The primary functional system is the central nervous system, especially frontostriatal, salience, reward, and emotion-regulation networks. Secondary injury involves teeth/enamel, oral mucosa and pharynx, salivary glands, esophagus and gastrointestinal tract, kidneys through volume/electrolyte disturbance, heart through electrolyte-mediated conduction abnormalities, and reproductive/endocrine systems. (wilson2024bulimianervosaand pages 1-2, donnelly2018neuroimaginginbulimia pages 1-2, alharbi2024effectivetreatmentapproaches pages 5-6)

Suggested UBERON annotations are brain, cerebral cortex, insula, amygdala, orbitofrontal cortex, anterior cingulate cortex, striatum, tooth enamel, salivary gland, pharynx, esophagus, stomach, kidney, and heart. Lateralization is not a defining feature. Subcellular pathology is not established; synaptic and receptor signaling are implicated functionally rather than through a known organelle defect.

8. Temporal development

Onset is typically adolescent to young-adult and often insidious, beginning with dieting, shape concern, or episodic bingeing. One review reported average onset at 16–17 years, whereas a 2024 disparities review cited median onset at 12.4 years; the discrepancy reflects different samples and ascertainment and should not be collapsed into one value. (yu2023efficacyofpharmacotherapies pages 1-2, wilson2024bulimianervosaand pages 1-2)

The disease is episodic or relapsing-remitting and can become chronic. Diagnostic crossover with anorexia nervosa or other specified eating disorders occurs. Early treatment is a key opportunity because repeated cycles become behaviorally reinforced and medical complications accumulate. Remission may be spontaneous or treatment-induced, but relapse prevention and follow-up remain necessary.

9. Inheritance and population

Lifetime prevalence estimates vary by diagnostic threshold and survey. Recent reviews cite approximately 0.9–3% overall, 1.5–3% in females, and 0.5% to >1% in males; 12-month prevalence around 0.4% has been reported. These values should be represented as ranges rather than a universal estimate. (yu2023efficacyofpharmacotherapies pages 1-2, wilson2024bulimianervosaand pages 1-2)

Females are diagnosed more often, but BN occurs in males, gender-diverse people, all racial/ethnic groups, and across body sizes and socioeconomic strata. Research samples have often been 80–100% female and 80–100% White, meaning apparent demographic gradients partly reflect ascertainment and access bias. Older adults, males, and racial minorities remain underrepresented. (wilson2024bulimianervosaand pages 1-2, wilson2024bulimianervosaand pages 2-3)

Inheritance is polygenic/multifactorial with incomplete, probabilistic expression. Mendelian penetrance, carrier frequency, consanguinity, anticipation, founder effects, and geographic variant distributions are not applicable.

10. Diagnostics

Clinical assessment

Diagnosis is made by confidential clinical interview using DSM-5-TR or ICD-11 criteria. Assessment should characterize objective and subjective binges, loss of control, each compensatory method, weekly frequency/duration, shape/weight overvaluation, dietary restraint, exercise, medications/substances, menstrual history, self-harm/suicide risk, and comorbidity. Collateral family information is useful in adolescents.

Screening instruments such as SCOFF can identify possible eating disorders but cannot establish BN. There is no newborn, carrier, prenatal, genomic, or population laboratory screen.

Medical evaluation

Physical assessment should include weight trajectory rather than BMI alone, pulse, blood pressure including orthostasis, temperature, hydration, oral/dental and salivary examination, and signs of self-induced vomiting. Depending on severity and purging method, tests commonly include CBC, electrolytes, bicarbonate, renal function, glucose, magnesium, phosphate, liver tests, urinalysis, pregnancy testing when relevant, and ECG. Electrolyte abnormality, dehydration, and arrhythmia are indications for urgent escalation or hospitalization. (alharbi2024effectivetreatmentapproaches pages 5-6)

No blood, imaging, electrophysiological, biopsy, genetic, or omics biomarker confirms BN. MRI/PET/fMRI are research tools, not diagnostic tests. (donnelly2018neuroimaginginbulimia pages 1-2)

Differential diagnosis

Important alternatives include binge-eating disorder, anorexia nervosa binge–purge type, purging disorder/OSFED, avoidant-restrictive food intake disorder, mood or bipolar illness with appetite change, substance-induced behavior, gastrointestinal disease, endocrine disease, and neurologic conditions. The decisive distinctions are low-weight AN status, presence/absence of recurrent compensation, objective binge criteria, and weight/shape psychopathology.

11. Outcome and prognosis

Recovery is possible, including after prolonged illness. One narrative review cited remission approaching 80% with proper treatment, but this should be interpreted cautiously because outcome definitions and follow-up periods vary. CBT effects are generally moderate, and long-term maintenance is less certain. (wilson2024bulimianervosaand pages 2-3, donnelly2018neuroimaginginbulimia pages 1-2)

BN carries elevated mortality through suicide and medical complications. A 2024 review cited standardized mortality ratios of approximately 1.5–2.5 and an eightfold greater suicide-death risk than the general population. These are population-level estimates, not individual predictions. (wilson2024bulimianervosaand pages 1-2)

Adverse prognostic features include severe/frequent binge–purge behavior, suicidality, substance use, trauma/PTSD, mood/anxiety comorbidity, medical instability, longer untreated duration, and poor treatment access. A striking 85–94% reportedly delay or never seek treatment, making under-detection a major real-world determinant of outcome. (wilson2024bulimianervosaand pages 1-2)

12. Treatment

Treatment strategy and current implementation

Care should be multidisciplinary and least restrictive while medically safe: medical assessment and stabilization → collaborative nutritional rehabilitation and regular eating → evidence-based psychotherapy → adjunct medication where appropriate → relapse prevention and comorbidity treatment. About 5% of patients were estimated to require inpatient care; dehydration, electrolyte disturbance, arrhythmia, severe self-harm, or psychiatric decompensation are key indications. Partial-hospital programs commonly provide 7–10 hours/day of structured treatment. (alharbi2024effectivetreatmentapproaches pages 5-6)

Psychotherapy. CBT/CBT-E is first-line for adults and targets irregular eating, restraint, binge–purge reinforcement, cognitive distortions, and weight/shape overvaluation. Guided self-help can improve access for less complex cases. Interpersonal therapy is an alternative when CBT is unavailable or unsuitable. DBT-informed approaches may help prominent emotion dysregulation, though they are not generally superior to BN-focused CBT. Suggested MAXO annotations: cognitive behavioral therapy, psychotherapy, nutritional counseling, family therapy, and behavioral intervention. (gkintoni2024clinicalinterventionstrategies pages 30-31, wilson2024bulimianervosaand pages 2-3)

Adolescents. Family-based treatment for BN is strongly supported. One synthesis reported remission of 39% with FBT versus 20% with CBT and 18% with supportive psychotherapy. In an RCT of 109 adolescents aged 12–18, abstinence was 39.4% with FBT-BN versus 19.7% with CBT-A at completion and 44.0% versus 25.4% at 6 months. (alharbi2024effectivetreatmentapproaches pages 5-6)

Pharmacotherapy. Fluoxetine, an SSRI, has the strongest regulatory and trial evidence for adult BN and is usually used at 60 mg/day when appropriate. It may reduce bingeing, vomiting, and depressive symptoms but should generally complement psychotherapy. A 2023 meta-analysis of 33 studies covering 11 drugs found modest effects versus placebo: binge episodes SMD −0.40 (95% CI −0.61 to −0.19), vomiting SMD −0.16 (−0.30 to −0.03), depressive symptoms SMD −0.32 (−0.51 to −0.13), and weight WMD −3.05 kg (−5.97 to −0.13). The evidence included SSRIs, TCAs, MAOIs, topiramate, lithium, and fenfluramine; this does not make all options clinically advisable. (yu2023efficacyofpharmacotherapies pages 1-2)

Bupropion is generally avoided because purging/electrolyte disturbance increases seizure risk. TCAs and MAOIs have greater safety/tolerability burdens. Topiramate has some efficacy but cognitive, metabolic, and teratogenic concerns. No medication is FDA-approved specifically for pediatric BN. No validated genotype-guided therapy, gene/cell/RNA therapy, immunotherapy, or surgery exists. (gkintoni2024clinicalinterventionstrategies pages 30-31)

Experimental/current trials. Retrieved ClinicalTrials.gov records illustrate current directions: MDMA-assisted therapy, NCT07542145, phase 1, recruiting, n=40; group therapy, NCT06063278, completed, n=100; eating-related inhibition/valuation, NCT05995496, recruiting, n=150; smartphone aftercare, NCT05728021, n=172; eating-related neurofeedback, NCT05614024, recruiting, n=30; web intervention, NCT04876196, completed, n=152; neurobiology study, NCT04225221, phase 2, completed, n=10; lisdexamfetamine, NCT03397446, phase 2, terminated, n=23; PET-guided serotonergic treatment, NCT02359513, phase 4, completed, n=51; and rTMS, NCT01530906, status uncertain, n=60. These are investigational and do not establish efficacy.

Access and disparities

The evidence base underrepresents males, older adults, racial/ethnic minorities, and diverse body sizes. Digital CBT, guided self-help, primary-care screening, and stepped care are real-world attempts to close access gaps, but digital delivery still requires suicide and medical-risk pathways. (wilson2024bulimianervosaand pages 1-2, wilson2024bulimianervosaand pages 2-3)

13. Prevention

Primary prevention: school/community programs promoting media literacy, body functionality and diversity, reduced weight stigma, flexible eating, and avoidance of restrictive dieting; safeguards in leanness-focused sports; and trauma-informed environments. No vaccine or prophylactic drug applies.

Secondary prevention: targeted screening in adolescents, athletes, people presenting with dental erosion, recurrent electrolyte disturbance, depression/anxiety, self-harm, or weight-control behaviors; confidential questioning and rapid referral. Because most affected people do not promptly seek care, case finding is a high priority. (wilson2024bulimianervosaand pages 1-2)

Tertiary prevention: relapse plans, continued meal regularity, monitoring for renewed purging, electrolyte/renal/cardiac surveillance when indicated, dental care, suicide prevention, and integrated treatment of mood, anxiety, PTSD, and substance-use disorders. Genetic counseling is not routinely indicated because risk is polygenic and non-deterministic.

14. Other species and natural disease

No well-established naturally occurring animal disease is homologous to human BN, and BN is not infectious, transmissible, or zoonotic. Animals can exhibit binge-like consumption or compensatory restriction, but the human syndrome requires subjective loss of control and weight/shape overvaluation, which cannot be directly established in animals. Therefore, veterinary breed, VBO, natural-disease gene, and cross-species transmission fields should be recorded as not applicable/not established.

15. Model organisms

Rodent binge-eating models use intermittent access to palatable high-fat/high-sugar food, food restriction/refeeding, stress, or limited-access paradigms. They are useful for studying reward, dopamine, serotonin, opioid/endocannabinoid signaling, stress, and candidate drugs. Their central limitation for BN is that rats and mice lack an emetic response; purging must be modeled indirectly through restriction or exercise. They also cannot recapitulate human body-image cognition, shame, or sociocultural influences. Consequently, these are models of components—especially binge behavior—not complete models of BN.

Human fMRI/PET paradigms, ecological momentary assessment, smartphone monitoring, and experimentally controlled meal tasks have higher face validity for cognitive control and cue reactivity. No validated BN organoid, iPSC, humanized genetic model, or single causal-gene knockout exists.

Ontology-ready summary

The following table provides compact knowledge-base annotations. Terms explicitly marked “suggested” require verification against the current ontology release before production ingestion.

Table: This compact table organizes bulimia nervosa into ontology-ready disease, phenotype, anatomy, mechanism, and treatment annotations using only evidence available in the retrieved context. It is useful as a starting point for knowledge-base population, while clearly marking suggested or unverified ontology IDs where the supplied evidence did not provide exact identifiers.

Evidence appraisal and authoritative interpretation

The most reliable current conclusion is that BN is a clinically diagnosed, polygenic and environmentally responsive psychiatric syndrome—not a monogenic, inflammatory, infectious, or biomarker-defined disease. Evidence is strongest for CBT/CBT-E, adolescent FBT, adjunctive fluoxetine, and active medical monitoring. Genetic candidates, microbiome changes, cytokines, neuroimaging, and other omics remain mechanistic research signals rather than clinical tests or treatment-selection biomarkers. (OpenTargets Search: bulimia nervosa, yu2023efficacyofpharmacotherapies pages 1-2, donnelly2018neuroimaginginbulimia pages 1-2, butler2021theroleof pages 10-12, barakat2023riskfactorsfor pages 7-8)

Representative exact abstract language includes: “BN is characterized by recurrent binge eating episodes with inappropriate compensatory behaviors” in the 2023 pharmacotherapy synthesis, and the neuroimaging review concluded that “heterogenous” studies prevented robust conclusions regarding precise neurobiology. The 2024 disparities review’s central real-world warning is that older adults, males, and racial minorities remain systematically underrepresented. (yu2023efficacyofpharmacotherapies pages 1-2, wilson2024bulimianervosaand pages 1-2, donnelly2018neuroimaginginbulimia pages 1-2)

Key recent sources and URLs

• Yu S, et al. Efficacy of pharmacotherapies for bulimia nervosa: a systematic review and meta-analysis. December 2023. https://doi.org/10.1186/s40360-023-00713-7 (yu2023efficacyofpharmacotherapies pages 1-2)
• Wilson K, Kagabo R. Bulimia nervosa and treatment-related disparities: a review. August 2024. https://doi.org/10.3389/fpsyg.2024.1386347 (wilson2024bulimianervosaand pages 1-2, wilson2024bulimianervosaand pages 2-3)
• Gkintoni E, et al. Clinical intervention strategies and family dynamics in adolescent eating disorders. July 2024. https://doi.org/10.3390/jcm13144084 (gkintoni2024clinicalinterventionstrategies pages 30-31)
• Alharbi Y, et al. Effective treatment approaches for eating disorders in children and adolescents. November 2024. https://doi.org/10.7759/cureus.74003 (alharbi2024effectivetreatmentapproaches pages 5-6)
• Barakat S, et al. Risk factors for eating disorders: findings from a rapid review. January 2023. https://doi.org/10.1186/s40337-022-00717-4 (barakat2023riskfactorsfor pages 7-8)
• Donnelly B, et al. Neuroimaging in bulimia nervosa and binge eating disorder: a systematic review. February 2018. https://doi.org/10.1186/s40337-018-0187-1 (donnelly2018neuroimaginginbulimia pages 1-2)
• Butler MJ, et al. The role of the gut microbiome, immunity, and neuroinflammation in the pathophysiology of eating disorders. February 2021. https://doi.org/10.3390/nu13020500 (butler2021theroleof pages 10-12)

PMIDs were not exposed in the retrieved full-text metadata and therefore are not fabricated here; DOI URLs are supplied as stable primary identifiers.

References

1. (yu2023efficacyofpharmacotherapies pages 1-2): Sijie Yu, Yuhan Zhang, Chongkai Shen, and Fei Shao. Efficacy of pharmacotherapies for bulimia nervosa: a systematic review and meta-analysis. BMC Pharmacology and Toxicology, Dec 2023. URL: https://doi.org/10.1186/s40360-023-00713-7, doi:10.1186/s40360-023-00713-7. This article has 23 citations.

2. (wilson2024bulimianervosaand pages 1-2): Kim Wilson and Robert Kagabo. Bulimia nervosa and treatment-related disparities: a review. Frontiers in Psychology, Aug 2024. URL: https://doi.org/10.3389/fpsyg.2024.1386347, doi:10.3389/fpsyg.2024.1386347. This article has 13 citations and is from a peer-reviewed journal.

3. (donnelly2018neuroimaginginbulimia pages 1-2): Brooke Donnelly, Stephen Touyz, Phillipa Hay, Amy Burton, Janice Russell, and Ian Caterson. Neuroimaging in bulimia nervosa and binge eating disorder: a systematic review. Journal of Eating Disorders, Feb 2018. URL: https://doi.org/10.1186/s40337-018-0187-1, doi:10.1186/s40337-018-0187-1. This article has 177 citations and is from a peer-reviewed journal.

4. (barakat2023riskfactorsfor pages 7-8): Sarah Barakat, S. McLean, E. Bryant, Ân H. Lê, P. Marks, Phillip Sarah Robert Leah Emma Susan Belinda Shannon Bronn Aouad Barakat Boakes Brennan Bryant Byrne Caldwell, P. Aouad, Sarah Barakat, R. Boakes, L. Brennan, S. Byrne, Belinda Caldwell, S. Calvert, B. Carroll, D. Castle, I. Caterson, Belinda Chelius, Lyn Chiem, S. Clarke, J. Conti, Lexi Crouch, Genevieve Dammery, Natasha Dzajkovski, J. Fardouly, Carmen Felicia, John Feneley, Amber-Marie Firriolo, N. Foroughi, M. Fuller-Tyszkiewicz, A. Fursland, V. Gonzalez-Arce, Bethanie Gouldthorp, Kelly Griffin, S. Griffiths, A. Hambleton, A. Hannigan, Melissa Hart, S. Hart, P. Hay, I. Hickie, Francis Kay-Lambkin, R. King, M. Kohn, E. Koreshe, I. Krug, Ân H. Lê, Jake Linardon, Randall Long, Amanda Long, S. Madden, S. Maguire, D. Maloney, S. McLean, Thy Meddick, J. Miskovic-Wheatley, Deborah Mitchison, R. O’Kearney, S. Ong, R. Paterson, S. Paxton, Melissa J Pehlivan, G. Pépin, A. Phillipou, J. Piccone, R. Pinkus, Bronwyn C Raykos, P. Rhodes, E. Rieger, Sarah Rodan, Karen Rockett, J. Russell, H. Russell, Fiona Salter, Susan S. Sawyer, Beth. Shelton, Urvashnee Singh, Sophie Smith, Evelyn Smith, K. Spielman, S. Squire, J. Thomson, M. Tiggemann, S. Touyz, Ranjani Utpala, L. Vartanian, Andrew Wallis, W. Ward, Sarah Wells, E. Wertheim, S. Wilksch, and Michelle Williams. Risk factors for eating disorders: findings from a rapid review. Journal of Eating Disorders, Jan 2023. URL: https://doi.org/10.1186/s40337-022-00717-4, doi:10.1186/s40337-022-00717-4. This article has 580 citations and is from a peer-reviewed journal.

5. (gkintoni2024clinicalinterventionstrategies pages 30-31): Evgenia Gkintoni, Elias Kourkoutas, Stephanos P. Vassilopoulos, and Maria Mousi. Clinical intervention strategies and family dynamics in adolescent eating disorders: a scoping review for enhancing early detection and outcomes. Jul 2024. URL: https://doi.org/10.3390/jcm13144084, doi:10.3390/jcm13144084. This article has 45 citations.

6. (alharbi2024effectivetreatmentapproaches pages 5-6): Yara Alharbi, Fatema Saleh, and Khaled A Shahat. Effective treatment approaches for eating disorders in children and adolescents: a review article. Cureus, Nov 2024. URL: https://doi.org/10.7759/cureus.74003, doi:10.7759/cureus.74003. This article has 7 citations.

7. (OpenTargets Search: bulimia nervosa): Open Targets Query (bulimia nervosa, 0 results). Buniello, A. et al. (2025). Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery. Nucleic Acids Research.

8. (wilson2024bulimianervosaand pages 2-3): Kim Wilson and Robert Kagabo. Bulimia nervosa and treatment-related disparities: a review. Frontiers in Psychology, Aug 2024. URL: https://doi.org/10.3389/fpsyg.2024.1386347, doi:10.3389/fpsyg.2024.1386347. This article has 13 citations and is from a peer-reviewed journal.

9. (butler2021theroleof pages 10-12): Michael J. Butler, Alexis A. Perrini, and Lisa A. Eckel. The role of the gut microbiome, immunity, and neuroinflammation in the pathophysiology of eating disorders. Nutrients, 13:500, Feb 2021. URL: https://doi.org/10.3390/nu13020500, doi:10.3390/nu13020500. This article has 109 citations.

Artifacts

• Edison artifact artifact-00