Karen C Schliep1, Sunni L Mumford, Catherine J Vladutiu, Katherine A Ahrens, Neil J Perkins, Lindsey A Sjaarda, Kerri A Kissell, Ankita Prasad, Jean Wactawski-Wende, Enrique F Schisterman. 1. 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.
Abstract
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.
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.
Authors: Jennifer R Piazza; David M Almeida; Natalia O Dmitrieva; Laura C Klein Journal: J Gerontol B Psychol Sci Soc Sci Date: 2010-07-20 Impact factor: 4.077
Authors: N H Hjollund; T K Jensen; J P Bonde; T B Henriksen; A M Andersson; H A Kolstad; E Ernst; A Giwercman; N E Skakkebaek; J Olsen Journal: Fertil Steril Date: 1999-07 Impact factor: 7.329
Authors: Penelope P Howards; Enrique F Schisterman; Jean Wactawski-Wende; Jennifer E Reschke; Andrea A Frazer; Kathleen M Hovey Journal: Am J Epidemiol Date: 2008-10-30 Impact factor: 4.897
Authors: Jean Wactawski-Wende; Enrique F Schisterman; Kathleen M Hovey; Penelope P Howards; Richard W Browne; Mary Hediger; Aiyi Liu; Maurizio Trevisan Journal: Paediatr Perinat Epidemiol Date: 2009-03 Impact factor: 3.980
Authors: Amelia K Wesselink; Elizabeth E Hatch; Kenneth J Rothman; Jennifer L Weuve; Ann Aschengrau; Rebecca J Song; Lauren A Wise Journal: Am J Epidemiol Date: 2018-12-01 Impact factor: 4.897
Authors: Jihye Park; Joseph B Stanford; Christina A Porucznik; Kylie Christensen; Karen C Schliep Journal: Psychoneuroendocrinology Date: 2019-09-16 Impact factor: 4.905
Authors: Theresa M Hardy; Mauricio Garnier-Villarreal; Donna O McCarthy; Richard A Anderson; Rebecca M Reynolds Journal: West J Nurs Res Date: 2018-08-09 Impact factor: 1.967