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Cited by 310Preterm Birth and ChorioamnionitisMaternal Mental Health During Pregnancy and PostpartumInfant Development and Preterm Care

Stress, infection and preterm birth: a biobehavioural perspective

Wadhwa, Pathik D., Culhane, Jennifer F., Rauh, Virginia, Barve, Shirish S., Hogan, Vijaya, Sandman, Curt A., Hobel, Calvin J., Chicz‐DeMet, Aleksandra +3 more·2001·Paediatric and Perinatal Epidemiology
DOI 10.1046/j.1365-3016.2001.00005.x
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Abstract

Preterm birth is currently the most important problem in maternal‐child health in the United States. Epidemiological studies have suggested that two factors, maternal stress and maternal urogenital tract infection, are significantly and independently associated with an increased risk of spontaneous preterm birth. These factors are also more prevalent in the population of sociodemographically disadvantaged women who are at increased risk for preterm birth. Studies of the physiology of parturition suggest that neuroendocrine and immune processes play important roles in the physiology and pathophysiology of normal and preterm parturition. However, not all women with high levels of stress and/or infection deliver preterm, and little is understood about factors that modulate susceptibility to pathophysiological events of the endocrine and immune systems in pregnancy. We present here a comprehensive, biobehavioural model of maternal stress and spontaneous preterm delivery. According to this model, chronic maternal stress is a significant and independent risk factor for preterm birth. The effects of maternal stress on preterm birth may be mediated through biological and/or behavioural mechanisms. We propose that maternal stress may act via one or both of two physiological pathways: (a) a neuroendocrine pathway, wherein maternal stress may ultimately result in premature and/or greater degree of activation of the maternal‐placental‐fetal endocrine systems that promote parturition; and (b) an immune/inflammatory pathway, wherein maternal stress may modulate characteristics of systemic and local (placental‐decidual) immunity to increase susceptibility to intrauterine and fetal infectious‐inflammatory processes and thereby promote parturition through pro‐inflammatory mechanisms. We suggest that placental corticotropin‐releasing hormone may play a key role in orchestrating the effects of endocrine and inflammatory/immune processes on preterm birth. Moreover, because neuroendocrine and immune processes extensively cross‐regulate one another, we further posit that exposure to both high levels of chronic stress and infectious pathogens in pregnancy may produce an interaction and multiplicative effect in terms of their combined risk for preterm birth. Finally, we hypothesise that the effects of maternal stress are modulated by the nature, duration and timing of occurrence of stress during gestation. A discussion of the components of this model, including a theoretical rationale and review of the available empirical evidence, is presented. A major strength of this biobehavioural perspective is the ability to explore new questions and to do so in a manner that is more comprehensive than has been previously attempted. We expect findings from this line of proposed research to improve our present state of knowledge about obstetric risk assessment for preterm birth by determining the characteristics of pregnant women who are especially susceptible to stress and/or infection, and to broaden our understanding of biological (endocrine, immune, and endocrine–immune interactions) mechanisms that may translate social adversity during pregnancy into pathophysiology, thereby suggesting intervention strategies.

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Authors
Wadhwa, P. D., Culhane, J. F., Rauh, V., Barve, S. S., Hogan, V., Sandman, C. A., Hobel, C. J., Chicz‐DeMet, A., Dunkel‐Schetter, C., Garite, T. J., & Glynn, L.
Affiliations
  • University of California, Irvine (US)
  • Thomas Jefferson University (US)
  • Columbia University (US)
  • University of Kentucky (US)
  • Centers for Disease Control and Prevention (US)
  • Cedars-Sinai Medical Center (US)
  • University of California, Los Angeles (US)
Corresponding author
Wadhwa, Pathik D.
ORCID
Venue
Paediatric and Perinatal Epidemiology
Publisher
Wiley
Published
2001-07
Volume
15
Issue
s2
Pages
17-29
ISSN
  • 0269-5022 (ISSN-L)
  • 1365-3016
DOI
10.1046/j.1365-3016.2001.00005.x
OpenAlex
W2064368889
Cited by
309
References
121
Citations by year
2026: 2 · 2025: 5 · 2024: 10 · 2023: 11 · 2022: 9 · 2021: 7 · 2020: 6 · 2019: 13 · 2018: 10 · 2017: 8 · 2016: 5 · 2015: 17 · 2014: 14 · 2013: 17 · 2012: 14
FWCI
6.59
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 175 d)
Locations
  • Paediatric and Perinatal Epidemiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • Centers for Disease Control and Prevention (TS31215/15)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD028413, R29HD033506, HD-28413, HD 33506)
Topics
  • Health Sciences › Medicine › Epidemiology › Preterm Birth and Chorioamnionitis
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Maternal Mental Health During Pregnancy and Postpartum
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Infant Development and Preterm Care
Keywords
preterm birth, maternal stress, urogenital infections, neuroendocrine pathways, immune-inflammatory pathways, childbirth, placental immunity, obstetric risk assessment
MeSH terms
Female, Forecasting, Humans, Infant, Newborn, Obstetric Labor, Premature, Neurosecretory Systems, Pregnancy, Pregnancy Complications, Infectious, Research, Stress, Physiological, Vaginosis, Bacterial

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