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Volume 93, Issue 4, Pages 1104-1111 (1 March 2010)


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Semen quality in fertile men in relation to psychosocial stress

Audra L. Gollenberg, Ph.D.a, Fan Liu, M.S.b, Charlene Brazil, B.S.c, Erma Z. Drobnis, Ph.D.d, David Guzick, M.D., Ph.D.b, James W. Overstreet, M.D., Ph.D.c, James B. Redmon, M.D.e, Amy Sparks, Ph.D.f, Christina Wang, M.D.g, Shanna H. Swan, Ph.D.bCorresponding Author Informationemail address

Received 30 September 2008; received in revised form 5 December 2008; accepted 8 December 2008. published online 24 February 2009.

Objective

To examine the association between stressful life events and semen parameters.

Design

Cross-sectional analysis in a pregnancy cohort study.

Setting

Prenatal clinics in five U.S. cities.

Patient(s)

Fertile men (n = 744) in the Study for Future Families, a cohort study of pregnant women and their partners.

Intervention(s)

None.

Main Outcome Measure(s)

Sperm concentration, percent motile, and percent normal morphology and classification above/below World Health Organization (WHO) cutoffs for semen quality.

Result(s)

After adjusting for confounders, men reporting 2+ recent stressful life events had an increased risk of being classified below WHO thresholds for “normal” defined by concentration, motility, and morphology criteria compared with men reporting <2 stressful life events (odds ratio [OR] = 2.06; 95% confidence interval [CI], 1.18, 3.61; OR = 1.54; 95% CI, 1.04, 2.29; OR = 1.93; 95% CI, 1.02, 3.66 for concentration, motility and morphology, respectively). Men experiencing 2+ stressful life events had lower sperm concentration (log scale, β = −0.25; 95% CI, −0.38, −0.11) and lower percent motile sperm (β = −1.95; 95% CI, −3.98, 0.07), but percent normal morphology was less affected.

Conclusion(s)

These results suggest that stressful life events may be associated with decreased semen quality in fertile men. The experience of psychosocial stress may be a modifiable factor in the development of idiopathic infertility.

a Division of Biostatistics and Epidemiology, Department of Public Health, School of Public Health and Health Sciences, University of Massachusetts-Amherst, Amherst, Massachusetts

b Department of Obstetrics and Gynecology, University of Rochester School of Medicine and Dentistry, Rochester, New York

c Center for Health and the Environment, University of California, Davis, California

d Department of Obstetrics, Gynecology and Women's Health, School of Medicine, University of Missouri, Columbia, Missouri

e Departments of Medicine and Urologic Surgery, University of Minnesota Medical School, Minneapolis, Minnesota

f Department of Obstetrics and Gynecology, University of Iowa, Iowa City, Iowa

g Division of Endocrinology, Department of Medicine, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, California

Corresponding Author InformationReprint requests: Dr. Shanna H. Swan, University of Rochester School of Medicine and Dentistry, Department of Obstetrics and Gynecology, 601 Elmwood Avenue, Box 668, Rochester, New York 14642 (FAX: 585-276-2151).

 A.L.G. has nothing to disclose. F.L. has nothing to disclose. C.B. has nothing to disclose. E.Z.D. has nothing to disclose. D.G. has nothing to disclose. J.W.O. has nothing to disclose. J.B.R. has nothing to disclose. A.S. has nothing to disclose. C.W. has nothing to disclose. S.H.S. has nothing to disclose.

 This work was supported by the National Institute of Health grant nos. R01-ES09916 to the University of Missouri from the National Institute of Environmental Health Sciences (NIEHS); MO1-RR00400 to the University of Minnesota General Clinical Research Center; and MO1-RR0425 to the Research and Education Institute at Harbor-UCLA Medical Center and the Cedars-Sinai Research Institute from the National Center for Research Resources.

PII: S0015-0282(08)04660-8

doi:10.1016/j.fertnstert.2008.12.018


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