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Maternal distress in late pregnancy alters obstetric outcomes and the expression of genes important for placental glucocorticoid signalling
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Accepted Version
Supplementary Figure 1
Date
2017-05-08
Authors
Togher, Katie L.
Treacy, Eimear
O'Keeffe, Gerard W.
Kenny, Louise C.
Journal Title
Journal ISSN
Volume Title
Publisher
Elsevier B.V.
Published Version
Abstract
The experience of maternal distress in pregnancy is often linked with poorer obstetric outcomes for women as well as adverse outcomes for offspring. Alterations in placental glucocorticoid signalling and subsequent increased fetal exposure to cortisol have been suggested to underlie this relationship. In the current study, 121 pregnant women completed the Perceived Stress Scale, State Trait Anxiety Inventory and Edinburgh Postnatal Depression Scale in the third trimester of pregnancy. Placental samples were collected after delivery. Maternal history of psychiatric illness and miscarriage were significant predictors of poorer mental health in pregnancy. Higher anxiety was associated with an increase in women delivering via elective Caesarean Section, and an increase in bottle-feeding. Birth temperature was mildly reduced among infants of women with high levels of depressive symptomology. Babies of mothers who scored high in all stress (cumulative distress) measures had reduced 5-min Apgar scores. High cumulative distress reduced the expression of placental HSD11B2 mRNA and increased the expression of placental NR3C1 mRNA. These data support a role for prenatal distress as a risk factor for altered obstetric outcomes. The alterations in placental gene expression support a role for altered placental glucocorticoid signalling in the relationship between maternal prenatal distress and adverse outcomes.
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Keywords
Anxiety , Depression , Maternal , Obstetric , Placenta , Pregnancy , Prenatal , Stress
Citation
Togher, K. L., Treacy, E., O’Keeffe, G. W. and Kenny, L. C. (2017) ‘Maternal distress in late pregnancy alters obstetric outcomes and the expression of genes important for placental glucocorticoid signalling’, Psychiatry Research, 255, pp. 17-26. doi:10.1016/j.psychres.2017.05.013