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Perceived Stress, Reproductive Hormones, and Ovulatory Function
Perceived Stress, Reproductive Hormones, and Ovulatory Function
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Perceived Stress, Reproductive Hormones, and Ovulatory Function
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Perceived Stress, Reproductive Hormones, and Ovulatory Function
Perceived Stress, Reproductive Hormones, and Ovulatory Function
Journal Article

Perceived Stress, Reproductive Hormones, and Ovulatory Function

2015
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Overview
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.

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