Stress, infection and preterm birth: a biobehavioural perspective

Preterm birth is currently the most important problem in maternal-child hea lth in the United States. Epidemiological studies have suggested that two f actors, maternal stress and maternal urogenital tract infection, are signif icantly and independently associated with an increased risk of spontaneous preterm birth. These factors are also more prevalent in the population of s ociodemographically disadvantaged women who are at increased risk for prete rm birth. Studies of the physiology of parturition suggest that neuroendocr ine and immune processes play important roles in the physiology and pathoph ysiology of normal and preterm parturition. However, not all women with hig h levels of stress and/or infection deliver preterm, and little is understo od about factors that modulate susceptibility to pathophysiological events of the endocrine and immune systems in pregnancy. We present here a compreh ensive, biobehavioural model of maternal stress and spontaneous preterm del ivery. According to this model, chronic maternal stress is a significant an d independent risk factor for preterm birth. The effects of maternal stress on preterm birth may be mediated through biological and/or behavioural mec hanisms. We propose that maternal stress may act via one or both of two phy siological pathways: (a) a neuroendocrine pathway, wherein maternal stress may ultimately result in premature and/or greater degree of activation of t he maternal-placental-fetal endocrine systems that promote parturition; and (b) an immune/inflammatory pathway, wherein maternal stress may modulate c haracteristics of systemic and local (placental-decidual) immunity to incre ase susceptibility to intrauterine and fetal infectious-inflammatory proces ses and thereby promote parturition through proinflammatory 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 ex tensively cross-regulate one another, we further posit that exposure to bot h high levels of chronic stress and infectious pathogens in pregnancy may p roduce an interaction and multiplicative effect in terms of their combined risk for preterm birth. Finally, we hypothesise that the effects of materna l stress are modulated by the nature, duration and timing of occurrence of stress during gestation. A discussion of the components of this model, incl uding a theoretical rationale and review of the available empirical evidenc e, 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 com prehensive 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 characterist ics of pregnant women who are especially susceptible to stress and/or infec tion, and to broaden our understanding of biological (endocrine, immune, an d endocrine-immune interactions) mechanisms that may translate social adver sity during pregnancy into pathophysiology, thereby suggesting intervention strategies.