Prenatal stress and balance of the child's cardiac autonomic nervous system at age 5-6 years.

Aimée E Van Dijk,Tanja G M Vrijkotte,Manon Van Eijsden,Karien Stronks,Reinoud J B J Gemke,Andrew H Kemp

doi:10.1371/journal.pone.0030413

Abstract

ObjectiveAutonomic nervous system (ANS) misbalance is a potential causal factor in the development of cardiovascular disease. The ANS may be programmed during pregnancy due to various maternal factors. Our aim is to study maternal prenatal psychosocial stress as a potential disruptor of cardiac ANS balance in the child.MethodsMothers from a prospective birth cohort (ABCD study) filled out a questionnaire at gestational week 16 [IQR 12–20], that included validated instruments for state anxiety, depressive symptoms, pregnancy-related anxiety, parenting daily hassles and job strain. A cumulative stress score was also calculated (based on 80th percentiles). Indicators of cardiac ANS in the offspring at age 5–6 years are: pre-ejection period (PEP), heart rate (HR), respiratory sinus arrhythmia (RSA) and cardiac autonomic balance (CAB), measured with electrocardiography and impedance cardiography in resting supine and sitting positions.Results2,624 mother-child pairs, only single births, were available for analysis. The stress scales were not significantly associated with HR, PEP, RSA and CAB (p≥0.17). Accumulation of maternal stress was also not associated with HR, PEP, RSA and CAB (p≥0.07).Conclusion Results did not support the hypothesis that prenatal maternal psychosocial stress deregulates cardiac ANS balance in the offspring, at least in rest, and at the age of five-six years.

Highlights

Growing evidence from multiple disciplines has led to the proposition that the risk of developing coronary heart disease partly depends on environmental factors acting in early life [1,2]
Evidence shows that chronic stress conditions significantly influence the maternal hypothalamic-pituitary-adrenal (HPA) axis, leading to hyper secretion of cortisol, which influences the development of the foetal HPA axis [3,4,5]
Maternal stress may cause a shift towards increased activation of the sympathetic nervous system (SNS) and a decrease in the parasympathetic nervous system (PNS) of the mother, together with increased secretion of catecholamines, all leading to elevated blood pressure and heart rate in the mother [6,7]

Summary

Introduction

Growing evidence from multiple disciplines has led to the proposition that the risk of developing coronary heart disease partly depends on environmental factors acting in early life [1,2]. Maternal stress may cause a shift towards increased activation of the sympathetic nervous system (SNS) and a decrease in the parasympathetic nervous system (PNS) of the mother, together with increased secretion of catecholamines, all leading to elevated blood pressure and heart rate in the mother [6,7]. This could have detrimental effects on the development of the foetal nervous system, potentially causing long-term changes in, for example, the sympatheticparasympathetic nervous system balance, which may lead to cardiovascular diseases at adult age.

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Results

Conclusion