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Stress and reproductive failure: past notions, present insights and future directions Journal Journal of Assisted Reproduction and Genetics
Publisher Springer Netherlands
ISSN 1058-0468 (Print) 1573-7330 (Online)
Issue Volume 25, Numbers 2-3 / March, 2008
Category REPRODUCTIVE IMMUNOLOGY
DOI 10.1007/s10815-008-9206-5
Pages 47-62
Subject Collection Medicine
SpringerLink Date Friday, February 15, 2008

Katrina Nakamura1 , Sam Sheps2, 3 and Petra Clara Arck4, 5(1) Interdisciplinary Studies Graduate Program, University of British Columbia, 6201 Cecil Green Park Road, Vancouver, BC, V6T 1Z1, Canada
(2) Department of Health Care and Epidemiology, University of British Columbia, Vancouver, Canada
(3) Western Regional Training Center for Health and Policy Research, University of British Columbia, Vancouver, Canada
(4) Charité University Medicine, Berlin, Germany
(5) Brain Body Institute, McMaster University, Hamilton, Canada

Received: 24 January 2008 Accepted: 25 January 2008 Published online: 15 February 2008
Abstract
Problem Maternal stress perception is frequently alleged as a cause of infertility, miscarriages, late pregnancy complications or impaired fetal development. The purpose of the present review is to critically assess the biological and epidemiological evidence that considers the plausibility of a stress link to human reproductive failure.
Methods All epidemiological studies published between 1980 and 2007 that tested the link between stress exposure and impaired reproductive success in humans were identified. Study outcomes were evaluated on the basis of how associations were predicted, tested and integrated with theories of etiology arising from recent scientific developments in the basic sciences. Further, published evidence arising from basic science research has been assessed in order to provide a mechanistic concept and biological evidence for the link between stress perception and reproductive success.
Results Biological evidence points to an immune–endocrine disequilibrium in response to stress and describes a hierarchy of biological mediators involved in a stress trigger to reproductive failure. Epidemiological evidence presents positive correlations between various pregnancy failure outcomes with pre-conception negative life events and elevated daily urinary cortisol. Strikingly, a relatively new conceptual approach integrating the two strands of evidence suggests the programming of stress susceptibility in mother and fetus via a so-called pregnancy stress syndrome.

Conclusions: An increasing specificity of knowledge is available about the types and impact of biological and social pathways involved in maternal stress responses. The present evidence is sufficient to warrant a reconsideration of conventional views on the etiology of reproductive failure. Physicians and patients will benefit from the adaptation of this integrated evidence to daily clinical practice.

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Cortisol levels and very early pregnancy loss (miscarriage) in humans
Pablo A. Nepomnaschy , Kathleen B. Welch , Daniel S. McConnell, Bobbi S. Low, Beverly I. Strassmann , and Barry G. England

Author Affiliations
*Department of Anthropology, 1085 South University Avenue,
Reproductive Sciences Program, Department of Obstetrics and Gynecology, L4000 Women’s Hospital,
School of Natural Resources and Environment, 430 East University Street,
Center for Statistical Consultation and Research, 915 East Washington Street,
Department of Epidemiology, School of Public Health, 109 Observatory Street,
**Research Center for Group Dynamics, Institute for Social Research, 426 Thompson Street, and
††Department of Pathology, Medical Science I, 1301 Catherine Street, University of Michigan, Ann Arbor, MI 48109

Communicated by Richard D. Alexander, University of Michigan, Ann Arbor, MI, December 27, 2005 (received for review December 17, 2004)
Abstract

Maternal stress is commonly cited as an important risk factor for spontaneous abortion. For humans, however, there is little physiological evidence linking miscarriage to stress. This lack of evidence may be attributable to a paucity of research on maternal stress during the earliest gestational stages. Most human studies have focused on “clinical” pregnancy (>6 weeks after the last menstrual period). The majority of miscarriages, however, occur earlier, within the first 3 weeks after conception (?5 weeks after the last menstrual period). Studies focused on clinical pregnancy thus miss the most critical period for pregnancy continuance. We examined the association between miscarriage and levels of maternal urinary cortisol during the first 3 weeks after conception. Pregnancies characterized by increased maternal cortisol during this period (within participant analyses) were more likely to result in spontaneous abortion or miscarriage (P < 0.05). This evidence links increased levels in this stress marker with a higher risk of early pregnancy loss in humans.

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