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Updated: Apr 6, 2026

Establishment of an Experimental Mouse Model of Endometrioma to Study its Related Infertility
Published on: April 5, 2024
Early-life factors and endometriosis risk
Kristen Upson1, Sheela Sathyanarayana2, Delia Scholes3
1Department of Epidemiology, School of Public Health, University of Washington, Seattle, Washington; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington; Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina.
Objective:
To study early-life factors in relation to endometriosis risk in adulthood.
Design:
Population-based case-control study.
Setting:
Integrated healthcare system.
Patient(S):
Cases (n = 310) were women diagnosed for the first time with endometriosis between the years 1996 and 2001, and controls (n = 727) were women without a diagnosis of endometriosis randomly selected from the healthcare system population.
Intervention(S):
None.
Main Outcome Measure(S):
Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) for the associations between intrauterine diethylstilbestrol (DES) exposure, maternal smoking, mother's age at delivery, firstborn status, birth weight, fetal number, prematurity, and regular soy formula feeding during infancy and endometriosis were estimated using unconditional logistic regression, adjusting for frequency matching and confounding variables. Information on early-life factors was ascertained retrospectively by in-person interview, with information on maternal DES use and regular soy formula feeding directly gathered from the participant's mother or other family member.
Result(S):
We observed that women who were regularly fed soy formula as infants had more than twice the risk of endometriosis compared with unexposed women (aOR 2.4, 95% CI 1.2-4.9). Our data also suggested increased endometriosis risk with prematurity (aOR 1.7, 95% CI 0.9-3.1) and maternal use of DES (OR 2.0, 95% CI 0.8-4.9, adjusting only for frequency matching variables), although these confidence intervals included the null.
Conclusion(S):
Our results support the hypothesis that disruption of development during fetal and infant periods may increase the risk of endometriosis in adulthood.
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