What is the link between endometriosis and adiposity?

Hong J, Juyeon Hong, Kyong Wook Yi, Yi KW
Obstetrics & Gynecology Science · 2022 · vol. 65(3) , pp. 227–233 · doi:10.5468/ogs.21343 · PMID:35081675 · PMC9119730 · W4210416540
article OA: gold CC0 ⤵ 18 in-corpus citations
📄 Open PDF Full text JSON View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

This review examines studies on the association between body size, particularly adiposity, and the risk of endometriosis, discussing the clinical and biological significance of this relationship.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

This paper is a narrative review examining epidemiological and biological studies on how adiposity and anthropometric measures relate to endometriosis risk, severity, and adipose tissue distribution. Across population-based case-control and cohort data, most studies report an inverse association in which higher BMI and obesity correlate with lower odds of endometriosis, including a meta-analysis showing reduced risk with increasing BMI, while the authors note key limitations such as BMI being an indirect marker and possible diagnostic bias (obese women with pelvic pain may be less likely to undergo operative diagnosis). The review also summarizes evidence that lean body habitus and lower adipose tissue—especially adipose located below the waist—may be linked to endometriosis, and that findings regarding disease severity are inconsistent across study cohorts. This paper is centrally about endometriosis — it reviews the literature on the link between endometriosis and adiposity/body size, including potential mechanisms and methodological caveats.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Endometriosis is defined by the presence of extrauterine endometrial tissue and presents with symptoms of dysmenorrhea, chronic pelvic pain, and impaired fertility. This condition often follows a chronic progressive course with favorable recurrence, even after surgical or medical treatment. The etiology or exact pathophysiology of endometriosis remains to be clarified, although it is thought to be a complex and multifactorial disease. Prior epidemiological or population-based studies have reported several risk factors related to endometriosis, such as environmental, menstrual, habitual, and lifestyle factors. Moreover, anthropometry has been found to be significantly associated with the diagnosis of endometriosis, as a lower body mass index is associated with an elevated risk of endometriosis. Here, we review studies that have examined the association between body size and the risk of endometriosis and discuss the clinical and biological significance of the relationship between adiposity and endometriosis.
Full text 16,312 characters · extracted from pmc-nxml · 3 sections · click to expand

Intro

Endometriosis is defined as the ectopic implantation of endometrial cells outside the uterus [ 1 ]. The prevalence of endometriosis is estimated to be approximately 10% in reproductive-aged women, and 30–50% in symptomatic women [ 2 – 5 ]. Endometriosis often presents with symptoms, such as dysmenorrhea, pelvic pain, and infertility, which may result in profuse morbidity in chronic conditions and reduced quality of life. The natural history and exact pathogenesis of endometriosis are not fully understood, but the most cited theory is that endometrial cells in retrograde menstruation into the pelvic cavity are implanted and grown by the complex effects of immune, angiogenic, and growth factors [ 6 , 7 ]. Other pathogenic theories, such as lymphatic, hematogenous, and mechanical spread of endometrial fragments, have been suggested for extrapelvic endometriosis [ 8 , 9 ]. Worldwide epidemiological studies have focused on the risk factors for endometriosis and identified that race, ethnicity, lifestyle, and habitual factors such as diet, exercise, caffeine consumption, and smoking are associated with endometriosis diagnosis. However, some of these associations have shown conflicting results [ 10 – 13 ]. Menstrual and reproductive risk factors have less controversial associations with endometriosis. Moreover, lower parity, earlier age at menarche, shorter menstrual cycle, heavier menstrual volume, and longtime tampon use increase the risk of endometriosis [ 13 – 15 ]. Many studies have addressed the significant association between anthropometric parameters and the incidence of endometriosis. Here, we review the studies that have examined the association between the risk of endometriosis and body size as well as discuss the clinical and biological relevance of the findings and proposed mechanisms involved in adiposity and endometriosis.

Other

Mediating mechanisms that can explain the inverse relationship between obesity and the risk of endometriosis are poorly understood, but several hypotheses and pathways have been suggested in published research areas. One potential pathway suggests that adipose tissue macrophages are differently expressed by body size or fat amount. M2 macrophages have anti-inflammatory properties and promote tissue regeneration in injured tissue, while M1 macrophages promote inflammation and inhibit angiogenesis and tissue remodeling [ 36 , 42 ]. Research has shown that M2 macrophages may be involved in the development of endometriosis, potentially through the actions of M2, including angiogenesis and tissue remodeling [ 43 – 45 ]. Interestingly, leanness is associated with a predominance of M2 macro-phages, whereas being larger is associated with a predominance of M1 macrophages [ 36 , 46 ]. Adipocytokine (or adipokine), a cytokine family mainly secreted from adipocytes, might be one of the biomolecules that can mediate the adiposity and establishment or progression of endometriosis. Adipokines play various biological roles as immune mediators, regulation of cell survival, inflammation, and angiogenesis, which are also critical functions in the establishment or development of endometriosis [ 47 – 51 ]. In addition, many adipokine levels in circulation are known to correlate with adiposity, such as an increase or decrease in those who are overweight or obese. Considering the anatomical proximity of visceral fat to the pelvic organs where endometriosis commonly occurs, there could be certain paracrine effects of adipokines secreted from visceral fat into the pelvic cavity, which may influence the establishment or progression of endometriosis [ 52 ]. Therefore, determining the adipokine levels in the peritoneal cavity with a correlation between an endometriotic condition and visceral fat amount and to study the biological or molecular effects of adipokines on endometriosis would be important to determine the underlying mechanism for biological connections between adiposity and endometriosis. Indeed, some studies have demonstrated aberrant expression of various adipokines in endometriotic peritoneal fluid (PF) and endometriosis lesions [ 53 – 57 ]. We previously reported that resistin concentration is increased in endometriotic PF, and its expression is upregulated in ectopic endometrial tissues compared to that in normal eutopic endometrium [ 52 , 53 ]. Adiponectin is an adipokine with anti-inflammatory and anti-angiogenic properties, and its circulating levels are negatively correlated with obesity [ 49 , 50 , 58 ]. One study found that adiponectin levels in the PF of women with endometriosis were significantly lower than those of controls, suggesting that this molecule may be an anti-endometriotic factor due to its anti-inflammatory and anti-angiogenic properties [ 54 ]. In contrast, our study did not find a significant difference in PF adiponectin levels between the endometriosis and control groups [ 53 ]. Despite the findings of aberrant expression of adipokines in various biosamples in patients with endometriosis, the explanation for the causal effect of adiposity on endometriosis is still limited because most studies did not assess the anthropometric indices or did not measure the amount of total or visceral fat or fat distribution in their study subjects. In addition, the correlation between visceral fat mass and the concentrations of adipokines in the peritoneal cavity is not well understood. An experimental study in mice with induced endometriosis revealed differentially regulated 26 genes in the liver. Among them, six genes were found to be involved in metabolism [ 59 ]. Four of the six genes, Cyp2r1 , Fabp4 , Mrc1 , and Rock2 , were upregulated and were related to weight loss, whereas two genes, Igfbp1 and Mmd2 , were downregulated and linked to obesity. Altered metabolism mediated by the liver contributes to the clinically observed low BMI that is characteristic of women with endometriosis, suggesting the systemic and multiorgan nature of endometriosis [ 59 ].

Conclusions

Obesity and endometriosis are common entities characterized by systemic inflammation [ 32 ]. Thus, the finding of an inverse association between these two conditions is interesting but not yet clear. The direction of studies for elucidating this finding can be approached in terms of genetic traits, immune system, and hormonal factors linked to both conditions. Endometriosis is believed to be inherited as a complex genetic trait by which multiple genes confer disease susceptibility and interact with one another and the environment to produce the phenotype [ 17 , 39 , 60 ]. Therefore, genetic factors involved in endometriosis susceptibility might also be associated with those involved in the physiology of adiposity or obesity [ 17 , 61 ]. Although the etiology of endometriosis remains unclear, endometriosis has historically been regarded as a focal disease primarily within the pelvic and peritoneal cavities [ 62 ]. However, recent evidence highlights the multiple links between endometriosis and systemic diseases with immunologic and metabolic changes and has identified comorbidities associated with endometriosis, such as autoimmune diseases, cancers, and cardiovascular disease [ 63 , 64 ]. The factors that transmit systemic signaling beyond the peritoneal cavity remain unclear; thus, research on extracellular signaling pathways such as exosomes, microRNAs, and stem cell biology in terms of the pathophysiology of endometriosis would provide more information on the systemic nature and complexity of endometriosis [ 62 ]. In addition, studies targeting biological substances that specifically function in both adipose tissue metabolism and endometriosis could help better understand the observed relationship between adiposity and the establishment or behavior of endometriosis.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

⚙ Ask this paper AI returns verbatim quotes from the full text · source: pmc-nxml ⓘ

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosischronic_pelvic_paindysmenorrhea

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (67)

Cited by (23)

Source provenance

europepmc
last seen: 2026-09-21T06:08:07.822426+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:24:03.506079+00:00
License: CC0 · commercial use OK