Department of Population Medicine, College of Medicine, QU Health, Qatar University, P. O. Box:2713, Doha, Qatar.
Department of Population Medicine, College of Medicine, QU Health, Qatar University, P. O. Box:2713, Doha, Qatar.
Psychoneuroendocrinology. 2024 Aug;166:107060. doi: 10.1016/j.psyneuen.2024.107060. Epub 2024 Apr 23.
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.
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.
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.
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.
胎盘作为一种缓冲器，通过 11-β 羟类固醇脱氢酶同工酶 2（11-β HSD2）酶来调节胎儿暴露于母体皮质醇的程度。我们进行了系统评价和荟萃分析，以评估产前心理困扰（PPD）对胎盘 11-β HSD2 基因表达的影响，并探讨与胎儿神经发育相关的潜在机制途径。
我们检索了 PubMed、Embase、Scopus、APA PsycInfo®和 ProQuest Dissertations，以评估观察性研究中 PPD 与人类胎盘 11-β HSD2 表达之间的相关性。根据三个情境 PPD 暴露组（产前抑郁、焦虑症状和感知压力），汇总调整后的回归系数（β）及其相应的 95%置信区间（CI）。
在 3159 条检索记录中，有 16 项纵向研究纳入了来自 7 个国家的 1869 名参与者。总体而言，PPD 障碍的暴露与胎盘 11-β HSD2 基因表达呈弱负相关，具体如下：产前抑郁（β=-0.01，95%CI 0.05-0.02，I²=0%）、焦虑症状（β=-0.02，95%CI 0.06-0.01，I²=0%）和感知压力（β=-0.01，95%CI 0.06-0.04，I²=62.8%）。第三孕期的 PPD 暴露与较低的胎盘 11-β HSD2 水平更为相关。PPD 和胎盘 11-β HSD2 与母亲和儿童的皮质醇反应性变化以及不良健康结局的发展有关。女性后代对 PPD 暴露更为敏感。
该研究表明，产前心理困扰在调节胎盘 11-β HSD2 基因表达方面具有适度作用。未来应计划开展前瞻性队列研究，利用更大的样本量或先进的统计方法来提高对小效应量的检测能力。此外，控制母亲的种族、PPD 暴露的孕期、分娩方式和婴儿性别等关键预测因素对于有效探讨 PPD 对胎儿编程的影响至关重要。
