Reynolds R M, Pesonen A-K, O'Reilly J R, Tuovinen S, Lahti M, Kajantie E, Villa P M, Laivuori H, Hämäläinen E, Seckl J R, Räikkönen K
Endocrinology Unit,University/BHF Centre for Cardiovascular Science, Queen's Medical Research Institute,47 Little France Crescent,Edinburgh,UK.
Institute of Behavioral Sciences, University of Helsinki,00014 University of Helsinki,Helsinki,Finland.
Psychol Med. 2015 Jul;45(10):2023-30. doi: 10.1017/S003329171400316X. Epub 2015 Jan 28.
Maternal prenatal depression predicts post-partum depression and increases risk of prematurity and low birth weight. These effects may be mediated by altered placental function. We hypothesized that placental function would be influenced by the gestational week of experiencing depressive symptoms and aimed to examine associations between maternal depressive symptoms during pregnancy and placental expression of genes involved in glucocorticoid and serotonin transfer between mother and fetus.
We studied women participating in a prospective pregnancy cohort: the Prediction and Prevention of Preeclampsia (PREDO) Study, Helsinki, Finland. Maternal depressive symptoms were assessed at 2-week intervals throughout pregnancy in 56 healthy women with singleton, term pregnancies. Messenger ribonucleic acid (mRNA) levels of glucocorticoid (GR) and mineralocorticoid (MR) receptors and serotonin transporter (SLC6A4), 11β-hydroxysteroid dehydrogenase type 1 (HSD1) and 2 (HSD2) were quantified in placental biopsies.
In adjusted analyses women who reported higher depressive symptoms across the whole pregnancy had higher mRNA levels of GR [effect size 0.31 s.d. units, 95% confidence interval (CI) 0.01-0.60, p = 0.042] and MR (effect size 0.34 s.d. units, 95% CI 0.01-0.68, p = 0.047). These effects were significant for symptoms experienced in the third trimester of pregnancy for GR; findings for MR were also significant for symptoms experienced in the second trimester. GR and MR mRNA levels increased linearly by having the trimester-specific depressive symptoms scores 0, 1 or 2-3 times above the clinical cut-off for depression (p = 0.003, p = 0.049, respectively, and p = 0.004, p = 0.15 in adjusted analyses).
Our findings offer potential gestational-age-specific mechanisms linking maternal depressive symptoms during pregnancy via placental biology. Future studies will test whether these also link with adverse offspring outcomes.
孕期母亲抑郁可预测产后抑郁,并增加早产和低出生体重的风险。这些影响可能是由胎盘功能改变介导的。我们假设胎盘功能会受到出现抑郁症状时孕周的影响,并旨在研究孕期母亲抑郁症状与参与母婴之间糖皮质激素和血清素转运的基因的胎盘表达之间的关联。
我们研究了参与一项前瞻性妊娠队列研究的女性:芬兰赫尔辛基的先兆子痫预测与预防(PREDO)研究。在整个孕期,每隔2周对56名单胎足月妊娠的健康女性进行母亲抑郁症状评估。对胎盘活检样本中的糖皮质激素(GR)和盐皮质激素(MR)受体、血清素转运体(SLC6A4)、11β-羟基类固醇脱氢酶1型(HSD1)和2型(HSD2)的信使核糖核酸(mRNA)水平进行定量分析。
在调整分析中,整个孕期报告有较高抑郁症状的女性,其GR的mRNA水平较高[效应量为0.31标准差单位,95%置信区间(CI)为0.01 - 0.60,p = 0.042],MR的mRNA水平也较高(效应量为0.34标准差单位,95%CI为0.01 - 0.68,p = 0.047)。对于GR,这些影响在妊娠晚期出现的症状中显著;对于MR,在妊娠中期出现的症状中也显著。GR和MR的mRNA水平随着特定孕周的抑郁症状评分高于临床抑郁临界值0、1或2 - 3倍而呈线性增加(在调整分析中,p分别为0.003、0.049,以及p = 0.004、0.15)。
我们的研究结果提供了潜在的、与孕周相关的机制,通过胎盘生物学将孕期母亲抑郁症状联系起来。未来的研究将测试这些是否也与不良的子代结局相关。