Early life factors and endometriosis risk
In a population-based case–control study, we observed increased endometriosis risk with regular infant soy formula feeding. Our data suggested that intrauterine diethylstilbestrol exposure and premature birth were associated with endometriosis.
Kristen Upson, Ph.D., Sheela Sathyanarayana, M.D., Delia Scholes, Ph.D., Victoria L. Holt, Ph.D.
Volume 104, Issue 4, Pages 964-971
To study early-life factors in relation to endometriosis risk in adulthood.
Population-based, case–control study. The Women’s Risk of Endometriosis study was conducted among female enrollees aged 18–49 years of a large, integrated healthcare system in western Washington State.
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.
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.
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.
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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