Growing evidence suggests that women with endometriosis may be particularly vulnerable to disordered eating behaviors (DEBs) and clinically defined eating disorders (EDs). This narrative review aims at integrating and critically analyzing the current evidence regarding the relationship between endometriosis and EDs, as well as highlighting the psychosocial and neurobiological vulnerabilities of women with endometriosis to DEBs. A large-scale genetic study showed a nearly threefold increase in the odds of EDs in women with endometriosis, and a significant genetic correlation. Although the prevalence of formal ED diagnoses appears low in small clinical samples, DEBs such as emotional eating, binge tendencies, and maladaptive dietary restriction, are common and strongly associated with pain intensity, and borderline BMI. Psychological factors, including body image disturbance, heightened self-criticism, emotional dysregulation, and the need for control further contribute to the vulnerability to EDs. At the biological level, the dysregulation of leptin, endocannabinoids, dopamine, brain-derived neurotrophic factor, and inflammatory cytokines, molecules involved in both appetite regulation and some aspects of the pathophysiology of endometriosis, suggests overlapping neuroimmune pathways that may link endometriosis to DEBs and EDs. Clinical management must, therefore, integrate screening for DEBs, supervised and personalized dietary counseling, balanced exercise prescription, and psychological interventions targeting pain coping, emotion regulation, and body image. A multidimensional, biopsychosocial framework is essential to prevent the onset or exacerbation of EDs in women with endometriosis.

Endometriosis and eating disorders: epidemiology, shared neurobiology, and clinical implications

Stefano Di Michele
Primo
;
Chiara Camoglio;Alessandro Caiazzo;Alessia Cabras;Federica Picci;Stefano Angioni
Ultimo
2026-01-01

Abstract

Growing evidence suggests that women with endometriosis may be particularly vulnerable to disordered eating behaviors (DEBs) and clinically defined eating disorders (EDs). This narrative review aims at integrating and critically analyzing the current evidence regarding the relationship between endometriosis and EDs, as well as highlighting the psychosocial and neurobiological vulnerabilities of women with endometriosis to DEBs. A large-scale genetic study showed a nearly threefold increase in the odds of EDs in women with endometriosis, and a significant genetic correlation. Although the prevalence of formal ED diagnoses appears low in small clinical samples, DEBs such as emotional eating, binge tendencies, and maladaptive dietary restriction, are common and strongly associated with pain intensity, and borderline BMI. Psychological factors, including body image disturbance, heightened self-criticism, emotional dysregulation, and the need for control further contribute to the vulnerability to EDs. At the biological level, the dysregulation of leptin, endocannabinoids, dopamine, brain-derived neurotrophic factor, and inflammatory cytokines, molecules involved in both appetite regulation and some aspects of the pathophysiology of endometriosis, suggests overlapping neuroimmune pathways that may link endometriosis to DEBs and EDs. Clinical management must, therefore, integrate screening for DEBs, supervised and personalized dietary counseling, balanced exercise prescription, and psychological interventions targeting pain coping, emotion regulation, and body image. A multidimensional, biopsychosocial framework is essential to prevent the onset or exacerbation of EDs in women with endometriosis.
2026
Endometriosis; Eating disorders; Emotional eating; Binge eating disorder; Diet; Neurobiology
File in questo prodotto:
File Dimensione Formato  
Di Michele Archives.pdf

accesso aperto

Tipologia: versione editoriale (VoR)
Dimensione 1.53 MB
Formato Adobe PDF
1.53 MB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11584/470206
Citazioni
  • ???jsp.display-item.citation.pmc??? 1
  • Scopus 0
  • ???jsp.display-item.citation.isi??? 0
social impact