ESPEYB16 8. Adrenals Food for Thought (2 abstracts)
8.20. Associations of prenatal depressive symptoms with DNA methylation of HPA axis-related genes and diurnal cortisol profiles in primary school-aged children
Stonawski V , Frey S , Golub Y , Rohleder N , Kriebel J , Goecke TW , Fasching PA , Beckmann MW , Kornhuber J , Kratz O , Moll GH , Heinrich H & Eichler A
University Hospital Erlangen, Germany
To read the full abstract: De Psychopathol. 2019; 31(2): 419–431.
Environmental stimuli, especially in the pre- and postnatal periods, can have long-lasting effects on offspring development and health. Prenatal exposure to maternal depression, anxiety or stress may alter functioning of the hypothalamic-pituitary-adrenal (HPA) axis. Here, epigenetic modifications of DNA in genes related to the HPA axis are investigated as a mechanism underlying the association between prenatal depression and altered child HPA activity.
In a longitudinal study, the authors investigated DNA methylation changes in children related to prenatal depressive symptoms, as well as associations with the child’s basal HPA activity. Children exposed to prenatal depressive symptoms in their mothers showed lower bedtime cortisol and a steeper diurnal slope. Regarding total cortisol release, prenatal exposure was related to lower cortisol release in boys, and higher cortisol release in girls. Furthermore, prenatal depressive symptoms were associated with altered methylation in the glucocorticoid receptor gene (NR3C1), the mineralocorticoid receptor gene (NR3C2), and the serotonin receptor gene (SLC6A4), with some sex-specific effects. In boys, prenatal depressive symptoms predicted bedtime cortisol mediated by NR3C2 methylation.
This study provides evidence that alterations in DNA methylation, here found especially in the NR3C2 (the mineralocorticoid receptor gene), is an underlying mediating mechanism between prenatal exposure to maternal depression and offspring outcome.
Volume 16
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ESPE Yearbook of Paediatric Endocrinology
ISSN 1662-4009 (Online)
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