Abstract
BackgroundThe mental health status of a pregnant woman and its consequent impact on foetal well being is not given much importance compared to the risk imposed by obstetric complications and medical conditions. Maternal psychological distress is a major public health problem and needs timely detection and intervention to prevent any adverse pregnancy outcome. There is ample evidence from literature that justifies the association of prenatal maternal mental stress and elevated cortisol with delayed infant motor and cognitive development; evidence from India being rather limited. The study aim is to prospectively assess the association of maternal psychological distress and cortisol level with motor and cognitive development of the infant.MethodsA sample of 2612 eligible pregnant women who have been registered for antenatal care at selected public sector hospitals in Bengaluru will be recruited after obtaining written informed consent. They will be assessed for the presence of maternal psychological distress in the form of depression and anxiety using appropriate scales and saliva samples will be collected for cortisol estimation during early, mid and late pregnancy. Follow up visits after delivery will be done on day 10, 3 months, 8 months and 12 months. The Bayley Scales of Infant and Toddler Development [BSID] (Third edition) will be used to measure both motor and mental milestones in terms of Psychomotor Development Index (PDI) and Mental Development Index (MDI). Logistic regression model will be used to determine the association between the exposure variables and outcomes which will be reported as Odd’s Ratio (OR) and 95% confidence intervals (CI).DiscussionOur study findings could add to the growing evidence that maternal psychological distress during pregnancy adversely influences growth and development in the offspring and subsequent development of the child. While maternal anxiety and depression can be measured by using self reporting instruments, estimation of maternal endogenous cortisol levels could serve as a biomarker of prenatal psychological stress. Findings from this study could be used to focus upon the burden of mental health problems during pregnancy and to consider steps to scale up prenatal mental health services in health care settings.
Highlights
The mental health status of a pregnant woman and its consequent impact on foetal well being is not given much importance compared to the risk imposed by obstetric complications and medical conditions
There is ample evidence from literature that justifies the association of prenatal maternal stress with delayed infant motor and cognitive development wherein it has been reported that high levels of maternal stress during mid-pregnancy was significantly associated with lower scores of motor and mental development of the infant [5,6,7,8]
Prenatal maternal stress has been frequently linked with elevated levels of maternal endogenous cortisol [9]
Summary
The mental health status of a pregnant woman and its consequent impact on foetal well being is not given much importance compared to the risk imposed by obstetric complications and medical conditions. There is ample evidence from literature that justifies the association of prenatal maternal mental stress and elevated cortisol with delayed infant motor and cognitive development; evidence from India being rather limited. Women are highly vulnerable to psychological distress that includes anxiety, depression and stress [1,2,3] During this phase of complex and dynamic changes, the fetal organs and organ systems that are forming are subject to both positive and negative influences, known as foetal programming [4]. Animal studies show that exposure to prenatal stress induced a significant rise in maternal cortisol secretion by activating the maternal Hypothalamo Pituitary Axis (HPA). Elevated levels of cortisol reach the foetus and modify the activity of foetal HPA axis [15,16,17]. Prenatal stress exerts an inhibitory effect on the placental enzyme 11 βhydroxysteroid-dehydrogenase type 2 which converts maternal cortisol to inactive cortisone resulting in a rise in amniotic fluid cortisol level which affects foetal HPA functioning [21]
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