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Anorexia Nervosa

1. Disease Information

2026-04-24
Falcon MONDO:0005351 Model: Edison Scientific Literature 39 citations

1. Disease Information

1.1 Concise overview

AN is “an eating disorder characterized by the restriction of energy intake, fear of gaining weight despite low weight, and disturbances in the perception of body weight or shape and the influence of these factors on self-worth.” (wu2024peripheralbiomarkersof pages 1-2)

1.2 Key identifiers (ontology/coding)

  • MONDO: anorexia nervosa = MONDO_0005351 (Open Targets disease entity; used for disease-target aggregation). (voderholzer2025anorexianervosaanupdate. pages 1-2)
  • ICD-11: AN = 6B80. Krawczyk & Święcicki state: “The most extensive category is ‘anorexia nervosa’ (6B80).” (Psychiatria Polska, 2020-02; https://doi.org/10.12740/pp/103876). (krawczyk2020icd11vs.icd10 pages 7-10)
  • ICD-10: commonly coded as F50.0 and F50.1 in administrative datasets (used to identify AN admissions in a national Canadian hospitalization cohort). (patten2024postdischargemortalityin pages 1-2)
  • Orphanet: early-onset/prepubertal anorexia nervosa (EOAN) referenced as ORPHA 525738 (rare early-onset subtype/descriptor). (ayrolles2024earlyonsetanorexianervosa pages 1-2)

Note on DSM-5/DSM-5-TR: Direct DSM-5 text was not retrieved in the accessible full-text set in this run; however, ICD-11 definitional text and multiple peer-reviewed studies provide DSM-aligned core features (restriction → low weight; weight/shape overvaluation and/or fear of weight gain; weight-restoration prevention behaviors). (radden2022capturingtheanorexia pages 1-2, wu2024peripheralbiomarkersof pages 1-2, voderholzer2025anorexianervosaanupdate. pages 1-2)

1.3 Synonyms / alternative names

  • Anorexia nervosa (standard)
  • Jadłowstręt psychiczny (Polish ICD discussion) as the AN descriptor in ICD-11 context. (krawczyk2020icd11vs.icd10 pages 7-10)
  • Early-onset / prepubertal anorexia nervosa (EOAN) (rare early-onset form). (ayrolles2024earlyonsetanorexianervosa pages 1-2)

1.4 Evidence source type

This report integrates: - Aggregated disease-level resources (rapid reviews, meta-analyses) (hay2023epidemiologyofeating pages 1-2, wu2024peripheralbiomarkersof pages 1-2) - Population registries / administrative health data (mortality; cardiovascular outcomes) (patten2024postdischargemortalityin pages 1-2, tseng2024incidenceandrisk pages 4-5) - Human case-control/longitudinal clinical biomarker studies (cytokines) (kaver2024cytokineandmicrobiome pages 1-2) - GWAS summary-statistics analyses (genetic architecture) (bang2023genomewideanalysisof pages 1-2) - ClinicalTrials.gov trial registry entries (ongoing/registered interventions). (NCT05918835 chunk 1, NCT05788042 chunk 1)

2. Etiology

2.1 Disease causal factors (multifactorial model)

Recent clinical synthesis emphasizes that AN has a multifactorial etiology including biological, psychological, and sociocultural contributors. (voderholzer2025anorexianervosaanupdate. pages 1-2)

Genetic causality / susceptibility

  • AN is described as heritable, with twin-based heritability ~50–60%. (bang2023genomewideanalysisof pages 1-2)
  • A 2023 genome-wide cross-trait analysis leveraged genetic overlap with major psychiatric disorders and related traits to identify 58 novel AN loci using conditional FDR methods and found shared loci with schizophrenia, bipolar disorder, major depression, and psychological traits. (bang2023genomewideanalysisof pages 1-2)

Direct abstract quote (genetics, Bang 2023): “Anorexia nervosa (AN) is a heritable eating disorder (50–60%)…” and “Using conditional FDR we identified 58 novel AN loci.” (Translational Psychiatry, 2023-09; https://doi.org/10.1038/s41398-023-02585-1). (bang2023genomewideanalysisof pages 1-2)

Environmental / psychosocial causal factors (risk domains)

A recent update summarized risk domains including: - Sociocultural: unrealistic body ideals, social media/screen time, societal pressure, obesogenic environments. (voderholzer2025anorexianervosaanupdate. pages 1-2) - Psychological traits: perfectionism, low self-esteem, emotional dysregulation, neuroticism, disgust sensitivity; compulsive/impulsive traits. (voderholzer2025anorexianervosaanupdate. pages 1-2) - Stress/trauma: stressful life events (moving, conflicts, bullying, losses, abuse) and vulnerable developmental windows (e.g., puberty). (voderholzer2025anorexianervosaanupdate. pages 2-3) - Comorbid psychiatric and neurodevelopmental conditions: anxiety/depression/PTSD, autism spectrum disorders, ADHD. (voderholzer2025anorexianervosaanupdate. pages 1-2) - Somatic/medical triggers: celiac disease, diabetes mellitus, and post-bariatric surgery states are cited as risk/trigger contexts. (voderholzer2025anorexianervosaanupdate. pages 1-2, voderholzer2025anorexianervosaanupdate. pages 2-3)

2.2 Protective factors

Specific protective factors were not explicitly enumerated in the retrieved full texts in this run. Given the strong evidence base for early identification and treatment being associated with better outcomes in youth, “early detection/treatment” can be considered a pragmatic protective factor against chronicity/complications rather than onset prevention. (voderholzer2025anorexianervosaanupdate. pages 1-2)

2.3 Gene–environment interactions

Direct gene–environment interaction (GxE) analyses were not present in the extracted materials. However, multiple sources highlight epigenetics and environment-mediated pathways as plausible mediators linking risk exposures to biological changes. (kaver2024cytokineandmicrobiome pages 1-2)

3. Phenotypes

3.1 Core clinical phenotypes (symptoms/signs)

Key clinical features include: - Self-induced weight loss via restrictive eating and/or compensatory behaviors (vomiting, laxatives, excessive exercise). (voderholzer2025anorexianervosaanupdate. pages 1-2) - Distorted body image and intense fear of gaining weight (noted as typical associations in ICD-11 framing). (voderholzer2025anorexianervosaanupdate. pages 1-2, radden2022capturingtheanorexia pages 1-2) - Hyperactivity/excessive exercise is frequent and difficult to treat; one inpatient sample reported 52.3% prevalence of compulsive/excessive exercise. (voderholzer2025anorexianervosaanupdate. pages 2-3)

HPO suggestions (labels; IDs not asserted here): low body weight; food restriction; fear of weight gain; body image distortion; hyperactivity/excessive exercise; anxiety. (voderholzer2025anorexianervosaanupdate. pages 1-2, voderholzer2025anorexianervosaanupdate. pages 2-3)

3.2 Medical complications (major systems)

The syndrome is associated with multi-system complications driven by malnutrition and starvation physiology.

Cardiovascular

A large matched cohort study (Taiwanese claims database) reported markedly increased cardiovascular events: - MACE occurred in 4.8% of AN vs 0.8% of controls; incidence rates 9.63 vs 1.65 per 1000 person-years; adjusted HR (AHR) 3.78 (95% CI 2.83–5.05). (tseng2024incidenceandrisk pages 4-5) - Any cardiovascular condition: 6.0% vs 2.3%; incidence rates 12.55 vs 4.60 per 1000 person-years; AHR 1.93 (95% CI 1.54–2.41). (tseng2024incidenceandrisk pages 4-5) - Five-year cumulative incidence in AN: MACE 4.82% (95% CI 3.85–6.02%) and any cardiovascular condition 6.19% (95% CI 5.19–7.53%). (tseng2024incidenceandrisk pages 4-5)

These findings are also reflected in the retrieved Table 2/Figure 1 snippet. (tseng2024incidenceandrisk media 19a1fdc3, tseng2024incidenceandrisk media d468e988)

HPO suggestions: bradycardia; hypotension; cardiac arrhythmia; QT prolongation; congestive heart failure. (tseng2024incidenceandrisk pages 1-2, voderholzer2025anorexianervosaanupdate. pages 3-4)

Electrolyte/renal/bone complications

A clinical update describes complications including electrolyte disturbances (e.g., hypokalemia; magnesium deficiency; hyponatremia in polydipsia contexts), renal impairment up to dialysis dependency, and irreversible bone loss (osteopenia/osteoporosis) with prevention/treatment considerations (calcium, vitamin D, bisphosphonates, transdermal estradiol). (voderholzer2025anorexianervosaanupdate. pages 2-3)

HPO suggestions: hypokalemia; hyponatremia; renal impairment; osteoporosis/osteopenia. (voderholzer2025anorexianervosaanupdate. pages 2-3)

3.3 Age of onset / severity / progression

3.4 Quality-of-life impact

Eating disorders substantially reduce health-related quality of life across diagnoses; a meta-analysis cited in a rapid review found similarly low HRQoL across AN, BN, and BED (with some variation by study). (hay2023epidemiologyofeating pages 37-38)

4. Genetic / Molecular Information

4.1 “Causal genes” vs polygenic risk

AN is not established as a monogenic disorder in the retrieved evidence; current genetics support polygenic inheritance with many loci of small effect and substantial shared genetic architecture with other psychiatric traits. (bang2023genomewideanalysisof pages 1-2)

4.2 GWAS loci and pathways (recent developments)

Ontology suggestions (GO; labels): Hippo signaling; synapse organization; nervous system development/neurogenesis; stress response/immune-response pathways (pathway-level mapping supported by GWAS functional analyses and neuroimaging review themes). (bang2023genomewideanalysisof pages 1-2, chen2024neuroimagingstudiesof pages 1-2)

4.3 Disease-target associations (authoritative aggregation)

Open Targets disease-target aggregation identifies associated targets including (examples): DRD2, ESR1, NCAM1, CACNA1C, TCF4 with PubMed literature links. This should be treated as association evidence rather than proof of causality. (voderholzer2025anorexianervosaanupdate. pages 1-2)

4.4 Epigenetics

Direct epigenetic marks were not extracted from the retrieved full texts; however, adolescent immune/microbiome work explicitly frames AN etiology as involving “genetics, epigenetics, neurobiology, cognition, psychosocial” factors. (kaver2024cytokineandmicrobiome pages 1-2)

5. Environmental Information

5.1 Environmental/lifestyle contributing factors

A clinical update describes multiple environmental/lifestyle factors relevant to onset and maintenance: - exposure to thin-ideal messaging/social media - restrictive diets, excessive physical activity - stressors (bullying, conflicts, life events) - family dynamics and societal reinforcement. (voderholzer2025anorexianervosaanupdate. pages 1-2, voderholzer2025anorexianervosaanupdate. pages 2-3)

5.2 Infectious agents

No infectious etiology is implicated in the retrieved evidence (not applicable).

6. Mechanism / Pathophysiology

6.1 Causal chain (high-level)

A consistent mechanistic framing from recent evidence is: 1) Predisposition (polygenic psychiatric + metabolic liability) (bang2023genomewideanalysisof pages 1-2) 2) Behavioral restriction / compensatory behaviors → negative energy balance (voderholzer2025anorexianervosaanupdate. pages 1-2) 3) Starvation physiology (endocrine/metabolic adaptation) including altered appetite hormones and GH–IGF-1 axis changes (wu2024peripheralbiomarkersof pages 9-11) 4) Systemic complications (electrolyte disturbances; cardiovascular, renal, bone impacts) (voderholzer2025anorexianervosaanupdate. pages 2-3, tseng2024incidenceandrisk pages 1-2) 5) Neurocognitive/neurocircuit features (altered functional connectivity and reward/control circuitry) that may reinforce restrictive behavior (chen2024neuroimagingstudiesof pages 1-2)

6.2 Endocrine/metabolic adaptations (biomarkers)

A 2024 meta-analysis of peripheral biomarkers reported higher ghrelin forms and lower leptin, and discusses “ghrelin resistance” hypotheses and GH resistance (high GH, low IGF-1) as starvation-adaptation patterns in AN. (wu2024peripheralbiomarkersof pages 1-2, wu2024peripheralbiomarkersof pages 9-11)

CHEBI suggestions (labels): ghrelin; leptin; cortisol; glucose; insulin; IGF-1. (wu2024peripheralbiomarkersof pages 1-2)

6.3 Immune involvement (recent human data)

In adolescents, cytokine dysregulation may differ from adult low-grade pro-inflammatory assumptions: - In 63 female adolescents with AN vs 41 controls, IL-1β and IL-6 were lower at admission; IL-1β normalized after weight recovery; IL-15 was elevated at all time points; TNF-α did not differ. (kaver2024cytokineandmicrobiome pages 1-2)

GO suggestions (labels): cytokine-mediated signaling pathway; regulation of interleukin-15 production/signaling; inflammatory response (nuanced). (kaver2024cytokineandmicrobiome pages 1-2)

6.4 Microbiome–gut–brain axis

  • Mendelian randomization suggests potential causal roles of specific gut taxa (e.g., a subset increasing risk and a subset protective), highlighting the plausibility of microbiome-mediated pathways as intervention targets. (kaver2024cytokineandmicrobiome pages 1-2)
  • The adolescent cytokine study links microbiome composition with cytokine alterations and clinical variables. (kaver2024cytokineandmicrobiome pages 1-2)

6.5 Neurobiology / neuroimaging

Resting-state fMRI synthesis reports altered large-scale networks in eating disorders; in AN, findings include altered connectivity patterns involving DMN, salience and executive networks and regions tied to social cognition and sensory/aesthetic processing. (chen2024neuroimagingstudiesof pages 1-2)

UBERON suggestions (labels): brain; hypothalamus; cortex; cerebellum; pituitary. (supported by genetic enrichment and neuroimaging emphasis on brain regions/networks). (chen2024neuroimagingstudiesof pages 1-2, bang2023genomewideanalysisof pages 1-2)

CL suggestions (labels): hypothalamic neuron; cortical neuron; microglia; T cell/lymphocyte populations (as biomarkers include CD3/CD8 and immune discussion). (wu2024peripheralbiomarkersof pages 1-2)

7. Anatomical Structures Affected

Organ/system level

Subcellular / processes

Starvation-associated shifts include metabolic pathway changes and immune signaling alterations; refeeding syndrome risk is linked to intracellular phosphate depletion as a key mechanism described in clinical synthesis. (voderholzer2025anorexianervosaanupdate. pages 3-4)

8. Temporal Development

Onset

Course / remission

  • A cited meta-analytic outcome summary in a clinical update reported: 45% recovery, 24% improvement, 23% chronicity, 32% hospitalization rate, and 0.7% mortality rate (context: meta-analysis summarized in the update). (voderholzer2025anorexianervosaanupdate. pages 2-3)

9. Inheritance and Population

Epidemiology (selected recent quantitative data)

Heritability / inheritance pattern

High-risk/underserved populations (policy-relevant)

In Australia-focused rapid review, LGBTQI+ individuals—particularly males—were reported to have a six-fold increase in prevalence vs the general male population, with limited evidence available for other underserved populations. (hay2023epidemiologyofeating pages 1-2)

10. Diagnostics

10.1 Clinical criteria and ICD-11 definitional specifics

ICD-11 definition details reproduced/analysed by Radden (2022) include: - “Dangerously low body weight” benchmarks: adult BMI <18.5 at age 18; for children/adolescents BMI-for-age below the 5th percentile as a benchmark. (radden2022capturingtheanorexia pages 1-2, radden2022capturingtheanorexia pages 2-3) - Low weight is accompanied by behaviors preventing weight restoration (restriction, purging, excessive exercise) and weight/shape centrality to self-evaluation or misperception of normality/excess. (radden2022capturingtheanorexia pages 1-2) - ICD-11 demotes fear of weight gain from essential to “typically” associated. (radden2022capturingtheanorexia pages 2-3)

A clinical update also emphasizes ICD-11 removal of amenorrhea as a mandatory criterion, facilitating diagnosis in men, prepubertal children, and women on hormonal contraception. (voderholzer2025anorexianervosaanupdate. pages 1-2)

10.2 Biomarkers (not yet established for routine diagnosis)

The 2024 meta-analysis concludes that reliable biomarkers are not yet established but identifies multiple peripheral biomarker differences (e.g., ghrelin ↑, leptin ↓, IGF-1 ↓) that may relate to starvation adaptation and pathophysiology. (wu2024peripheralbiomarkersof pages 1-2)

10.3 Differential diagnosis (example explicitly referenced)

A clinical update highlights differentiation from ARFID (avoidant/restrictive food intake disorder; ICD-11 6B83) as a key diagnostic distinction. (voderholzer2025anorexianervosaanupdate. pages 2-3)

11. Outcome / Prognosis

Mortality

  • A recent clinical update reports standardized mortality ratio (SMR) 5.21 (95% CI 4.10–6.62). (voderholzer2025anorexianervosaanupdate. pages 1-2)
  • Postdischarge mortality study (Canada): after age/sex adjustment, no significant all-cause mortality difference between AN and other psychiatric admissions (HR 1.04; p=0.46), but AN contributed substantially to cause-of-death coding: 25% of AN-group deaths attributed to psychiatric ICD-F conditions; 88% of those had AN as underlying cause (22% of all AN-group deaths). (patten2024postdischargemortalityin pages 1-2)

Morbidity / complications

Cardiovascular morbidity is strongly supported by a 2024 cohort with increased MACE and multiple cardiac diagnoses. (tseng2024incidenceandrisk pages 4-5)

Prognostic factors

The FBT modification review notes predictors of poorer response to standard FBT (e.g., cognitive inflexibility, familial criticism, slow initial weight gain), but detailed prognostic modeling is beyond the extracted evidence. (pedersen2024modificationstoenhance pages 1-2)

12. Treatment

12.1 Core treatment modalities (current practice)

  • Psychotherapy is first-line: clinical update cites CBT (adolescents and adults) and FBT as most extensively studied for children/adolescents; also references FPT and MANTRA. (voderholzer2025anorexianervosaanupdate. pages 3-4)
  • Nutritional rehabilitation / inpatient refeeding reduces acute mortality risk through weight restoration; however, refeeding carries risks including refeeding syndrome and requires careful medical management (phosphate depletion mechanism emphasized). (hambleton2025advancementsinfamilybased pages 1-2, voderholzer2025anorexianervosaanupdate. pages 3-4)
  • Pharmacotherapy: limited robust evidence; olanzapine has “moderate evidence” for weight gain in a clinical update. (voderholzer2025anorexianervosaanupdate. pages 1-2)

12.2 Treatment outcomes and real-world implementation

Family-Based Treatment (FBT) outcomes and modifications (2024 scoping review) - Standard FBT recovery rates depend on definition: 50–70% when recovery defined as maintaining >85% body weight vs 28–50% when both weight restoration and symptom reduction required at end of treatment. (pedersen2024modificationstoenhance pages 1-2) - Virtual FBT evidence: in one comparison, full remission at end of treatment 30% (V-FBT) vs 11% (guided self-help); at 3-month follow-up 20% vs 22.2%. (pedersen2024modificationstoenhance pages 4-6) - Home-treatment modification: significantly higher weight gain by 3 months (medium effect size) and hospitalization 0% vs 13.6% at 3 months (significance not reported). (pedersen2024modificationstoenhance pages 4-6)

Access barriers and telehealth A telehealth-focused review concludes that telehealth-delivered FBT shows preliminary outcomes comparable to in-person care while potentially increasing access in underserved areas. (hambleton2025advancementsinfamilybased pages 1-2)

12.3 Experimental/advanced therapeutics (clinical trials)

Neuromodulation is actively studied: - NCT05918835 (registered 2023; recruiting; n=72): HF-rTMS vs sham for adults with AN, targeting individualized right DLPFC region functionally connected to dorsal striatum. (NCT05918835 chunk 1) - NCT05788042 (registered 2023; recruiting; n=70): tDCS and rTMS (iTBS) vs sham arms, primary outcome EDE-Q change at 8 weeks. (NCT05788042 chunk 1) - Additional rTMS/TBS studies include NCT03984344 and others with varying status (recruiting/terminated/withdrawn). (NCT03984344 chunk 1, NCT04061304 chunk 1)

MAXO suggestions (labels): cognitive behavioral therapy; family-based treatment; nutritional rehabilitation; inpatient hospitalization/medical stabilization; olanzapine therapy; repetitive transcranial magnetic stimulation; transcranial direct current stimulation. (voderholzer2025anorexianervosaanupdate. pages 3-4, NCT05788042 chunk 1)

13. Prevention

Primary/secondary/tertiary prevention (evidence-based framing)

Specific preventive interventions were not detailed in retrieved guideline-level sources. However: - Rapid review emphasizes low help-seeking and under-recognition, supporting secondary prevention via early identification and access to evidence-based care. (hay2023epidemiologyofeating pages 37-38) - Clinical update highlights improved outcomes with earlier detection and treatment, especially in youth. (voderholzer2025anorexianervosaanupdate. pages 1-2)

14. Other Species / Natural Disease

No naturally occurring veterinary anorexia nervosa analogs were identified in the retrieved evidence (not addressed in this run).

15. Model Organisms

In this run, retrieved evidence did not include a primary model-organism paper suitable for detailed mapping. Mechanistic microbiome work in other parts of the retrieved corpus (not fully extracted) suggests germ-free/transfer paradigms are used in the field, but this report does not assert specifics without extracted evidence.

Notes on Evidence Quality and Gaps

  • DSM-5-TR diagnostic criteria, MeSH identifier, and OMIM/Orphanet entries for AN (general) were not directly retrieved as primary documents in the accessible full texts; the report therefore anchors identifiers to ICD-11/ICD-10 and MONDO/OpenTargets plus peer-reviewed definitional text. (krawczyk2020icd11vs.icd10 pages 7-10, patten2024postdischargemortalityin pages 1-2, voderholzer2025anorexianervosaanupdate. pages 1-2)
  • Some mechanistic domains (epigenome-wide methylation studies; transcriptomics/proteomics; single-cell/spatial omics in humans) were not captured in the extracted 2023–2024 evidence set in this run.

Direct Abstract Quotes (for knowledge-base evidence items)

1) Biomarker meta-analysis definition: “an eating disorder characterized by the restriction of energy intake, fear of gaining weight despite low weight, and disturbances in the perception of body weight or shape…” (Wu et al., Nutrients, 2024-06; https://doi.org/10.3390/nu16132095). (wu2024peripheralbiomarkersof pages 1-2) 2) Genetics: “Anorexia nervosa (AN) is a heritable eating disorder (50–60%)…” and “Using conditional FDR we identified 58 novel AN loci.” (Bang et al., Translational Psychiatry, 2023-09; https://doi.org/10.1038/s41398-023-02585-1). (bang2023genomewideanalysisof pages 1-2) 3) ICD-11 code statement: “The most extensive category is ‘anorexia nervosa’ (6B80).” (Krawczyk & Święcicki, Psychiatria Polska, 2020-02; https://doi.org/10.12740/pp/103876). (krawczyk2020icd11vs.icd10 pages 7-10)

Key Figure/Table Evidence (visual)

Tseng et al. (JAMA Network Open, 2024-12-19) Figure 1 and Table 2 (cumulative incidence and adjusted hazard ratios for cardiovascular outcomes in AN vs controls) were retrieved as cropped evidence images. (tseng2024incidenceandrisk media 19a1fdc3, tseng2024incidenceandrisk media d468e988)

References

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  14. (ayrolles2024earlyonsetanorexianervosa pages 1-2): Anaël Ayrolles, Julia Clarke, Nathalie Godart, Céline André-Carletti, Clémentine Barbe, Anne Bargiacchi, Corinne Blanchet, Florence Bergametti, Valérie Bertrand, Emmanuelle Caldagues, Marylene Caquard, Danielle Castellotti, Richard Delorme, Laurence Dreno, Dominique Feneon Landou, Priscille Gerardin, Selim Guessoum, Ludovic Gicquel, Juliane Léger, Stéphanie Legras, Lucile Noel, Anne Fjellestad-Paulsen, Hélène Poncet-Kalifa, Flora Bat-Pitault, and Coline Stordeur. Early-onset anorexia nervosa: a scoping review and management guidelines. Journal of Eating Disorders, Nov 2024. URL: https://doi.org/10.1186/s40337-024-01130-9, doi:10.1186/s40337-024-01130-9. This article has 12 citations and is from a peer-reviewed journal.

  15. (radden2022capturingtheanorexia pages 1-2): Jennifer Radden. Capturing the anorexia nervosa phenotype: conceptual and normative issues in icd-11. Journal of evaluation in clinical practice, 28:807-813, Jun 2022. URL: https://doi.org/10.1111/jep.13586, doi:10.1111/jep.13586. This article has 8 citations and is from a peer-reviewed journal.

  16. (hay2023epidemiologyofeating pages 1-2): Phillipa Hay, Phillip Aouad, Anvi Le, Peta Marks, Danielle Maloney, Sarah Barakat, Robert Boakes, Leah Brennan, Emma Bryant, Susan Byrne, Belinda Caldwell, Shannon Calvert, Bronny Carroll, David Castle, Ian Caterson, Belinda Chelius, Lyn Chiem, Simon Clarke, Janet Conti, Lexi Crouch, Genevieve Dammery, Natasha Dzajkovski, Jasmine Fardouly, John Feneley, Nasim Foroughi, Mathew Fuller-Tyszkiewicz, Anthea Fursland, Veronica Gonzalez-Arce, Bethanie Gouldthorp, Kelly Griffin, Scott Griffiths, Ashlea Hambleton, Amy Hannigan, Mel Hart, Susan Hart, Ian Hickie, Francis Kay-Lambkin, Ross King, Michael Kohn, Eyza Koreshe, Isabel Krug, Jake Linardon, Randall Long, Amanda Long, Sloane Madden, Siân McLean, Thy Meddick, Jane Miskovic-Wheatley, Deborah Mitchison, Richard O’Kearney, Roger Paterson, Susan Paxton, Melissa Pehlivan, Genevieve Pepin, Andrea Phillipou, Judith Piccone, Rebecca Pinkus, Bronwyn Raykos, Paul Rhodes, Elizabeth Rieger, Karen Rockett, Sarah Rodan, Janice Russell, Haley Russell, Fiona Salter, Susan Sawyer, Beth Shelton, Urvashnee Singh, Sophie Smith, Evelyn Smith, Karen Spielman, Sarah Squire, Juliette Thomson, Marika Tiggemann, Ranjani Utpala, Lenny Vartanian, Andrew Wallis, Warren Ward, Sarah Wells, Eleanor Wertheim, Simon Wilksch, Michelle Williams, Stephen Touyz, and Sarah Maguire. Epidemiology of eating disorders: population, prevalence, disease burden and quality of life informing public policy in australia—a rapid review. Journal of Eating Disorders, Feb 2023. URL: https://doi.org/10.1186/s40337-023-00738-7, doi:10.1186/s40337-023-00738-7. This article has 189 citations and is from a peer-reviewed journal.

  17. (NCT05918835 chunk 1): Alexandra F Muratore, PhD. Effects of rTMS on Food Choice in Anorexia Nervosa. New York State Psychiatric Institute. 2023. ClinicalTrials.gov Identifier: NCT05918835

  18. (NCT05788042 chunk 1): Trial of Enhanced Neurostimulation for Anorexia. The George Institute. 2023. ClinicalTrials.gov Identifier: NCT05788042

  19. (voderholzer2025anorexianervosaanupdate. pages 2-3): Ulrich Voderholzer, Silke Naab, Ulrich Cuntz, and Sandra Schlegl. Anorexia nervosa-an update. Der Nervenarzt, May 2025. URL: https://doi.org/10.1007/s00115-025-01820-y, doi:10.1007/s00115-025-01820-y. This article has 5 citations.

  20. (tseng2024incidenceandrisk media 19a1fdc3): Mei-Chih Meg Tseng, Kuan-Rau Chiou, Joni Yu-Hsuan Shao, and Hung-Yi Liu. Incidence and risk of cardiovascular outcomes in patients with anorexia nervosa. JAMA Network Open, 7:e2451094, Dec 2024. URL: https://doi.org/10.1001/jamanetworkopen.2024.51094, doi:10.1001/jamanetworkopen.2024.51094. This article has 13 citations and is from a peer-reviewed journal.

  21. (tseng2024incidenceandrisk media d468e988): Mei-Chih Meg Tseng, Kuan-Rau Chiou, Joni Yu-Hsuan Shao, and Hung-Yi Liu. Incidence and risk of cardiovascular outcomes in patients with anorexia nervosa. JAMA Network Open, 7:e2451094, Dec 2024. URL: https://doi.org/10.1001/jamanetworkopen.2024.51094, doi:10.1001/jamanetworkopen.2024.51094. This article has 13 citations and is from a peer-reviewed journal.

  22. (voderholzer2025anorexianervosaanupdate. pages 3-4): Ulrich Voderholzer, Silke Naab, Ulrich Cuntz, and Sandra Schlegl. Anorexia nervosa-an update. Der Nervenarzt, May 2025. URL: https://doi.org/10.1007/s00115-025-01820-y, doi:10.1007/s00115-025-01820-y. This article has 5 citations.

  23. (hay2023epidemiologyofeating pages 37-38): Phillipa Hay, Phillip Aouad, Anvi Le, Peta Marks, Danielle Maloney, Sarah Barakat, Robert Boakes, Leah Brennan, Emma Bryant, Susan Byrne, Belinda Caldwell, Shannon Calvert, Bronny Carroll, David Castle, Ian Caterson, Belinda Chelius, Lyn Chiem, Simon Clarke, Janet Conti, Lexi Crouch, Genevieve Dammery, Natasha Dzajkovski, Jasmine Fardouly, John Feneley, Nasim Foroughi, Mathew Fuller-Tyszkiewicz, Anthea Fursland, Veronica Gonzalez-Arce, Bethanie Gouldthorp, Kelly Griffin, Scott Griffiths, Ashlea Hambleton, Amy Hannigan, Mel Hart, Susan Hart, Ian Hickie, Francis Kay-Lambkin, Ross King, Michael Kohn, Eyza Koreshe, Isabel Krug, Jake Linardon, Randall Long, Amanda Long, Sloane Madden, Siân McLean, Thy Meddick, Jane Miskovic-Wheatley, Deborah Mitchison, Richard O’Kearney, Roger Paterson, Susan Paxton, Melissa Pehlivan, Genevieve Pepin, Andrea Phillipou, Judith Piccone, Rebecca Pinkus, Bronwyn Raykos, Paul Rhodes, Elizabeth Rieger, Karen Rockett, Sarah Rodan, Janice Russell, Haley Russell, Fiona Salter, Susan Sawyer, Beth Shelton, Urvashnee Singh, Sophie Smith, Evelyn Smith, Karen Spielman, Sarah Squire, Juliette Thomson, Marika Tiggemann, Ranjani Utpala, Lenny Vartanian, Andrew Wallis, Warren Ward, Sarah Wells, Eleanor Wertheim, Simon Wilksch, Michelle Williams, Stephen Touyz, and Sarah Maguire. Epidemiology of eating disorders: population, prevalence, disease burden and quality of life informing public policy in australia—a rapid review. Journal of Eating Disorders, Feb 2023. URL: https://doi.org/10.1186/s40337-023-00738-7, doi:10.1186/s40337-023-00738-7. This article has 189 citations and is from a peer-reviewed journal.

  24. (radden2022capturingtheanorexia pages 2-3): Jennifer Radden. Capturing the anorexia nervosa phenotype: conceptual and normative issues in icd-11. Journal of evaluation in clinical practice, 28:807-813, Jun 2022. URL: https://doi.org/10.1111/jep.13586, doi:10.1111/jep.13586. This article has 8 citations and is from a peer-reviewed journal.

  25. (NCT03984344 chunk 1): Theta Burst Stimulation in Anorexia Nervosa. King's College London. 2020. ClinicalTrials.gov Identifier: NCT03984344

  26. (NCT04061304 chunk 1): A Clinical Trial Into the Efficacy of rTMS Treatment for Treating Anorexia Nervosa and Bulimia Nervosa. University of Manitoba. 2020. ClinicalTrials.gov Identifier: NCT04061304