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Stress, infection and preterm birth: a biobehavioural perspective
P D Wadhwa1, J F Culhane, V Rauh
1Department of Psychiatry & Human Behavior, University of California-Irvine, 3117 Gillespie Neuroscience Building, Zot Code 4260, Irvine, CA 92697, USA. pwadhwa@uci.edu
Paediatric and Perinatal Epidemiology
|August 25, 2001
Summary
Chronic maternal stress and urogenital infections increase preterm birth risk. This biobehavioral model explores how stress impacts pregnancy via neuroendocrine and immune pathways, potentially interacting with infection to heighten risk.
Area of Science:
- Reproductive biology and maternal-fetal medicine.
- Neuroendocrinology and immunology in pregnancy.
- Behavioral science and public health.
Background:
- Preterm birth is a leading maternal-child health issue in the US.
- Maternal stress and urogenital infections are linked to spontaneous preterm birth.
- These risk factors disproportionately affect socioeconomically disadvantaged women.
Purpose of the Study:
- To present a comprehensive biobehavioral model of maternal stress and spontaneous preterm delivery.
- To elucidate the neuroendocrine and immune pathways mediating stress effects on parturition.
- To explore how stress and infection interact to influence preterm birth risk.
Main Methods:
- Theoretical model development integrating existing epidemiological and physiological data.
- Review of neuroendocrine and immune system roles in parturition.
- Hypothesizing mechanisms of stress, infection, and their interaction on preterm birth.
Main Results:
- Chronic maternal stress is a significant, independent risk factor for preterm birth.
- Stress may activate maternal-placental-fetal endocrine systems prematurely.
- Stress can also modulate immune responses, increasing susceptibility to infection-induced inflammation.
Conclusions:
- Maternal stress influences preterm birth through neuroendocrine and immune pathways.
- Placental corticotropin-releasing hormone may be a key mediator.
- Combined stress and infection may have multiplicative effects on preterm birth risk, modulated by stress timing and duration.
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