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Published on: June 13, 2021
Prenatal SSRI exposure alters neonatal corticosteroid binding globulin, infant cortisol levels, and emerging HPA
Jodi L Pawluski1, Ursula M Brain, Caroline M Underhill
1Early Human Experience Unit, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, Canada. j.pawluski@maastrichtuniversity.nl
Insights
Prenatal exposure to selective serotonin reuptake inhibitor (SSRI) antidepressants altered neonatal corticosteroid-binding globulin (CBG) levels. In SSRI-exposed infants, higher neonatal CBG predicted a smaller diurnal cortisol change, impacting the developing hypothalamic-pituitary-adrenal (HPA) system.
Area of Science:
- Neuroendocrinology
- Developmental Pediatrics
- Pharmacology
Background:
- Serotonin plays a crucial role in the development of the hypothalamic-pituitary-adrenal (HPA) axis.
- Prenatal exposure to selective serotonin reuptake inhibitor (SSRI) antidepressants may disrupt HPA axis development and function.
- Investigating the impact of SSRIs on neonatal and infant cortisol and corticosteroid-binding globulin (CBG) is essential.
Purpose of the Study:
- To examine the relationship between prenatal SSRI exposure, maternal mood, and neonatal/infant cortisol and CBG levels.
- To assess the long-term implications of altered CBG levels in infants exposed to SSRIs prenatally.
Main Methods:
- Assayed serum cortisol and CBG in mothers and neonates at delivery.
- Documented maternal mood symptoms during gestation.
- Measured infant salivary cortisol levels at 3 months of age.
Main Results:
- Prenatal SSRI exposure increased neonatal serum CBG levels, irrespective of maternal depression.
- Neonatal serum cortisol levels were not affected by SSRI exposure or maternal mood.
- Higher neonatal CBG in SSRI-exposed infants predicted a reduced diurnal cortisol change at 3 months.
Conclusions:
- Prenatal SSRI exposure influences the developing HPA system by altering neonatal CBG and infant cortisol diurnal patterns.
- Further research is needed on the long-term functional consequences of prenatal SSRI exposure on CBG gene expression and HPA system development.
Background:
Serotonin influences the development of the hypothalamic-pituitary-adrenal (HPA) system; therefore prenatal exposure to selective serotonin reuptake inhibitor antidepressants (SSRIs) may alter HPA axis development and function. To address this, prenatal exposure to SSRIs and maternal mood were examined in relation to neonatal and infant levels of cortisol and its binding protein, corticosteroid-binding globulin (CBG).
Methods:
Serum cortisol and CBG levels were assayed from SSRI-exposed and non-exposed mothers and their neonates at delivery. Maternal mood symptoms were documented at 36 weeks gestation. To determine the long-term implications of changes in CBG, levels of salivary cortisol were assessed in infants at 3 months of age.
Results:
Prenatal SSRI exposure significantly increased serum CBG levels in neonates after vaginal delivery (p ≤ 0.038), even when controlling for maternal depression. Neonatal serum cortisol levels did not vary with SSRI exposure or antenatal maternal mood, but were significantly higher following vaginal delivery (p ≤ 0.003). Neonatal serum CBG levels were associated with infant salivary levels of evening cortisol (p ≤ 0.051). In SSRI-exposed infants, increased levels of neonatal CBG predicted a smaller diurnal change in infant salivary cortisol (p ≤ 0.028), regardless of maternal depression.
Conclusions:
Prenatal SSRI exposure affects the developing HPA system by altering serum CBG levels in neonates and infant salivary cortisol levels. Further research is warranted on the long-term functional implications of the effect of prenatal SSRI exposure on fetal hepatic CBG gene expression and the developing HPA system.
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