Mechanisms underlying the effects of prenatal psychosocial stress on child outcomes: beyond the HPA axis

Abstract

Accumulating evidence from preclinical and clinical studies indicates that maternal psychosocial stress and anxiety during pregnancy adversely affect child outcomes. However, knowledge on the possible mechanisms underlying these relations is limited. In the present paper, we review the most often proposed mechanism, namely that involving the HPA axis and cortisol, as well as other less well-studied but possibly relevant and complementary mechanisms. We present evidence for a role of the following mechanisms: compromised placental functioning, including the 11β-HSD2 enzyme, increased catecholamines, compromised maternal immune system and intestinal microbiota, and altered health behaviors including eating, sleep, and exercise. The roles of (epi)genetics, the postnatal environment and the fetus are also discussed. We conclude that maternal prenatal psychosocial stress is a complex phenomenon that affects maternal emotions, behavior and physiology in many ways, and may influence the physiology and functioning of the fetus through a network of different pathways. The review concludes with recommendations for future research that helps our understanding of the mechanisms by which maternal prenatal stress exerts its effect on the fetus.

Consequences and Possible Predictors of Health-damaging Behaviors and Mental Health Problems in Pregnancy – A Review

“…This review will therefore also limit itself to looking only at these factors. It is basically assumed that chronic, excessively emotional stress experienced by the pregnant woman can lead to dysregulation of maternal and fetal hypothalamic-pituitary-adrenal axis activity [113]. In the placental barrier, the presence of 11β-hydroxysteroid dehydrogenase (11β-HSD) type 2, an enzyme that catalyzes the conversion of cortisol into biologically inactive cortisone, normally protects the fetus from excessive concentrations of cortisol [15].…”

“…In the placental barrier, the presence of 11β-hydroxysteroid dehydrogenase (11β-HSD) type 2, an enzyme that catalyzes the conversion of cortisol into biologically inactive cortisone, normally protects the fetus from excessive concentrations of cortisol [15]. However, it has been postulated that chronically increased levels of stress hormones could result in increased permeability through downregulation of the 11β-HSD2 enzyme, allowing more cortisol to reach the fetal blood stream [113]. Prenatal exposure to excessively high levels of stress hormones can adversely affect the neural, immunological and behavioral development of the child, predisposing it to be more susceptible to psychological and physical disease(s) in later life [114].…”

Editorial: what are the concerns of a European child and adolescent psychiatrist?

“…Whilst an easy definition is young people up to the age of 18 years, this is now extending in many places to include young adults-particularly in the case of psychosis, where it can make more sense to take an early intervention approach spanning from 14 to 30 years, rather than a cutoff at 18 years. At the other end of the age spectrum, we are increasingly understanding more about the risk factors associated with pregnancy and the early years-for example, high levels of maternal anxiety in pregnancy being associated with an increased risk of psychiatric outcomes for offspring [1,2]. So, the boundaries between perinatal psychiatry and early child psychiatry become more blurred.…”

Prenatal risk factors and postnatal central nervous system function

“…7. In their review, Beijers et al [7] take a look at putative mechanisms involved in fetal programing via maternal stress during pregnancy. It is thought that the respective epigenetic alterations may even be transmitted from the offspring to the subsequent generation.…”