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Perceived Stress, Reproductive Hormones, and Ovulatory Function: A Prospective Cohort Study

Schliep, Karen C.a; Mumford, Sunni L.a; Vladutiu, Catherine J.b; Ahrens, Katherine A.a; Perkins, Neil J.a; Sjaarda, Lindsey A.a; Kissell, Kerri A.a,c; Prasad, Ankitaa; Wactawski-Wende, Jeand; Schisterman, Enrique F.a

doi: 10.1097/EDE.0000000000000238
Reproduction

Background: Stress has been shown to suppress ovulation in experimental models, but its effect on human reproduction at the population level is unclear.

Methods: Healthy women (n = 259), aged 18–44 years from Western New York, were followed for 2 menstrual cycles (2005–2007). Women completed daily perceived stress assessments, a 4-item Perceived Stress Scale (PSS-4) up to 4 times each cycle, and a 14-item PSS at baseline. Mixed model analyses were used to assess effects of stress on log reproductive hormone concentrations and sporadic anovulation.

Results: High versus low daily stress was associated with lower estradiol (−9.5% [95% confidence interval (CI) = −15.6% to −3.0%]), free estradiol (−10.4% [−16.5% to −3.9%]), and luteinizing hormone (−14.8% [−21.3% to −7.7%]) and higher follicle-stimulating hormone (6.2% [95% CI = 2.0% to 10.5%]) after adjusting for age, race, percent body fat, depression score, and time-varying hormones and vigorous exercise. High versus low daily stress was also associated with lower luteal progesterone (−10.4% [95% CI = −19.7% to −0.10%]) and higher odds of anovulation (adjusted odds ratio = 2.2 [95% CI = 1.0 to 4.7]). For each unit increase in daily stress level, women had a 70% higher odds of an anovulatory episode (odds ratio = 1.7 [1.1 to 2.4]). Similar but attenuated results were found for the association between the PSS-4 and reproductive hormones, while null findings were found for the baseline PSS.

Conclusion: Daily perceived stress does appear to interfere with menstrual cycle function among women with no known reproductive disorders, warranting further research to explore potential population-level impacts and causal biologic mechanisms.

From the aEpidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health & Human Development, Rockville, MD; bDepartment of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC; cProgram of Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD; and dEpidemiology and Environmental Health, University at Buffalo, Buffalo, NY.

Submitted 26 June 2014; accepted 4 October 2014.

Supported by the Intramural Research Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development and National Institutes of Health (contract number: HHSN275200403394C).

K.C.S., S.L.M., K.A.A., N.J.P., L.A.S., K.A.K., A.P., and E.F.S. received support from the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health for the submitted work. C.J.V. received support from grant T32-HL007055 from the National Heart, Lung, and Blood Institute, National Institutes of Health.

Disclosure: The authors report no conflicts of interest.

Correspondence: Sunni L. Mumford, Epidemiology Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, 6100 Executive Boulevard, 7B03, Rockville, MD 20852. E-mail: mumfords@mail.nih.gov.

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