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
*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)
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.
stress miscarriage placentation fetomaternal conflict evolutionary theory
To whom correspondence should be addressed at the present address:
Epidemiology Branch, National Institute on Environmental Health Sciences, P.O. BOX 12233, MD A3-05, Room 309, 111 TW Alexander Drive, Research Triangle Park, NC 27709-2233.
Author contributions: P.A.N., B.S.L., B.I.S., and B.G.E. designed research; P.A.N., D.S.M., and B.G.E. performed research; D.S.M. and B.G.E. contributed new reagents/analytic tools; P.A.N., K.B.W., and B.G.E. analyzed data; and P.A.N., K.B.W., B.S.L., B.I.S., and B.G.E. wrote the paper.
Conflict of interest statement: No conflicts declared.
overall cortisol baseline;
human chorionic gonadotrophin.
© 2006 by The National Academy of Sciences of the USA