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
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
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.