Prenatal psychological distress and 11β-HSD2 gene expression in human placentas: Systematic review and meta-analysis

Angham Ibrahim Tartour; Tawanda Chivese; Safa Eltayeb; Fatima M Elamin; Eleni Fthenou; Mohammed Seed Ahmed; Giridhara Rathnaiah Babu

doi:10.1016/j.psyneuen.2024.107060

Prenatal psychological distress and 11β-HSD2 gene expression in human placentas: Systematic review and meta-analysis

Psychoneuroendocrinology. 2024 Apr 23:166:107060. doi: 10.1016/j.psyneuen.2024.107060. Online ahead of print.

Authors

Angham Ibrahim Tartour¹, Tawanda Chivese², Safa Eltayeb³, Fatima M Elamin⁴, Eleni Fthenou³, Mohammed Seed Ahmed⁵, Giridhara Rathnaiah Babu²

Affiliations

¹ Department of Population Medicine, College of Medicine, QU Health, Qatar University, P. O. Box:2713, Doha, Qatar. Electronic address: aa1304397@qu.edu.qa.
² Department of Population Medicine, College of Medicine, QU Health, Qatar University, P. O. Box:2713, Doha, Qatar.
³ Qatar Biobank for Medical Research, Qatar Foundation, Doha, Qatar.
⁴ Office of Research Ethics and Integrity, Qatar University, P. O. Box:2713, Doha, Qatar.
⁵ Department of Basic Medical Sciences, College of Medicine, QU Health, Qatar University, P. O. Box:2713, Doha, Qatar.

PMID: 38677195
DOI: 10.1016/j.psyneuen.2024.107060

Abstract

Background: The placenta acts as a buffer to regulate the degree of fetal exposure to maternal cortisol through the 11-Beta Hydroxysteroid Dehydrogenase isoenzyme type 2 (11-β HSD2) enzyme. We conducted a systematic review and meta-analysis to assess the effect of prenatal psychological distress (PPD) on placental 11-β HSD2 gene expression and explore the related mechanistic pathways involved in fetal neurodevelopment.

Methods: We searched PubMed, Embase, Scopus, APA PsycInfo®, and ProQuest Dissertations for observational studies assessing the association between PPD and 11-β HSD2 expression in human placentas. Adjusted regression coefficients (β) and corresponding 95% confidence intervals (CIs) were pooled based on three contextual PPD exposure groups: prenatal depression, anxiety symptoms, and perceived stress.

Results: Of 3159 retrieved records, sixteen longitudinal studies involving 1869 participants across seven countries were included. Overall, exposure to PPD disorders showed weak negative associations with the placental 11-β HSD2 gene expression as follows: prenatal depression (β -0.01, 95% CI 0.05-0.02, I2=0%), anxiety symptoms (β -0.02, 95% CI 0.06-0.01, I2=0%), and perceived stress (β -0.01 95% CI 0.06-0.04, I2=62.8%). Third-trimester PPD exposure was more frequently associated with lower placental 11-β HSD2 levels. PPD and placental 11-β HSD2 were associated with changes in cortisol reactivity and the development of adverse health outcomes in mothers and children. Female-offspring were more vulnerable to PPD exposures.

Conclusion: The study presents evidence of a modest role of prenatal psychological distress in regulating placental 11-β HSD2 gene expression. Future prospective cohorts utilizing larger sample sizes or advanced statistical methods to enhance the detection of small effect sizes should be planned. Additionally, controlling for key predictors such as the mother's ethnicity, trimester of PPD exposure, mode of delivery, and infant sex is crucial for valid exploration of PPD effects on fetal programming.

Keywords: 11β-Hydroxysteroid Dehydrogenase Type 2; Early-life exposures; Fetal reprogramming; Gene expression; Placenta; Prenatal psychological distress.

Publication types

Review