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

**Authors:** Stefano Di Michele, Chiara Camoglio, Pierluigi Chieppa, Giosuè Giordano Incognito, Alessandro Caiazzo, Alessia Cabras, Federica Picci, Stefano Angioni

PMC · DOI: 10.1007/s00404-026-08325-2 · 2026-01-21

## TL;DR

This paper explores the link between endometriosis and eating disorders, suggesting shared biological and psychological factors that increase vulnerability.

## Contribution

The paper introduces a multidimensional framework linking endometriosis and eating disorders through shared neurobiological and psychosocial mechanisms.

## Key findings

- Women with endometriosis have a threefold higher genetic risk for eating disorders.
- Dysregulated molecules like leptin and dopamine are linked to both endometriosis and disordered eating.
- Psychological factors such as body image issues and emotional dysregulation contribute to eating disorder vulnerability.

## 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.

The online version contains supplementary material available at 10.1007/s00404-026-08325-2.

## Linked entities

- **Proteins:** lepa (leptin a)
- **Chemicals:** dopamine (PubChem CID 681)
- **Diseases:** endometriosis (MONDO:0005133)

## Full-text entities

- **Genes:** DRD2 (dopamine receptor D2) [NCBI Gene 1813] {aka D2DR, D2R}, CNR1 (cannabinoid receptor 1) [NCBI Gene 1268] {aka CANN6, CB-R, CB1, CB1A, CB1K5, CB1R}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}
- **Diseases:** mood or anxiety disorders (MESH:D001008), weight loss (MESH:D015431), overweight (MESH:D050177), cognitive rigidity (MESH:D003072), nutritional deficiencies (MESH:D044342), obsessive-compulsive traits (MESH:D009771), Depression (MESH:D003866), metabolic disturbances (MESH:D024821), chronic illness (MESH:D002908), infertility (MESH:D007246), metabolic (MESH:D008659), mood disorders (MESH:D019964), weight gain (MESH:D015430), Inflammatory (MESH:D007249), impaired (MESH:D060825), processing (MESH:D010335), anxiety (MESH:D001007), BED (MESH:D056912), dysfunctional hunger (MESH:D006331), IBS (MESH:D043183), psychosocial impairment (MESH:D008607), BN (MESH:D052018), ARFID (MESH:D000080146), ovarian endometriomas (MESH:D010049), nutrient deficiencies (MESH:D007153), bone demineralization (MESH:D018488), pica (MESH:D010842), endometriotic lesions (MESH:D009059), obsessive tendencies (MESH:C536965), chronic pelvic pain (MESH:D011472), bradycardia (MESH:D001919), Pain (MESH:D010146), endocrine dysfunction (MESH:D004700), personality disorders (MESH:D010554), Psychiatric (MESH:D001523), dysmenorrhea (MESH:D004412), Eating Disorder (MESH:D001068), vomiting (MESH:D014839), neuroinflammation (MESH:D000090862), binge eating (MESH:D002032), Body image disturbance (MESH:D057215), obstetric complications (MESH:D007744), Endometriosis (MESH:D004715), body dissatisfaction (MESH:D001835), pelvic disease (MESH:D000292), obesity (MESH:D009765), AN (MESH:D000856), pelvic pain (MESH:D017699), syncope (MESH:D013575), rumination disorder (MESH:D000079562), amenorrhea (MESH:D000568), neuroendocrine (MESH:D018358), dietary restriction (MESH:D002313), addiction (MESH:D019966), dyspareunia (MESH:D004414), intermenstrual pain (MESH:D008796), chronic pain (MESH:D059350), image disturbance (MESH:C564543), fatigue (MESH:D005221)
- **Chemicals:** serotonin (MESH:D012701), 2-AG (MESH:C094503), arachidonic acid (MESH:D016718), Endocannabinoid (MESH:D063388), BioRender (-), Dopamine (MESH:D004298), AEA (MESH:C078814)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12823736/full.md

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Source: https://tomesphere.com/paper/PMC12823736