Effects of prenatal depressive symptoms on maternal and infant cortisol reactivity
Effects of prenatal depressive symptoms on maternal and infant cortisol reactivity
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DOI：
10.1007/s00737-016-0611-y
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发表时间：
2016-08-01
影响因子：
4.5
通讯作者：
Ramchandani, Paul G.
中科院分区：
文献类型：
--
作者：
Braithwaite, Elizabeth C.;Murphy, Susannah E.;Ramchandani, Paul G.
产前抑郁症与不良的后代结果，和流行的机制理论，以解释情绪相关的影响，涉及母亲和胎儿的下丘脑-垂体-肾上腺（HPA）轴的改变。最近的研究表明，抑郁症可能与怀孕早期皮质醇反应减弱失败有关。本研究的目的是调查这种影响是否持续到妊娠中期和晚期。进一步的目的是测试是否母亲产前皮质醇反应直接预测婴儿皮质醇反应。103名孕妇在第二或第三孕期被招募。通过自我报告评估抑郁症状，并测量母亲唾液皮质醇对压力源（婴儿痛苦电影）的反应。出生后约2个月，母亲（n = 88）报告产后抑郁症和婴儿唾液皮质醇接种反应进行了测量。产前抑郁症与皮质醇对妊娠中晚期急性应激的反应性无关。同样，无论是产前抑郁症，也没有母亲产前皮质醇反应预测婴儿皮质醇反应接种2个月。如果产前抑郁症对胎儿和婴儿发育的影响是由母体和胎儿HPA轴的改变介导的，那么怀孕早期可能是一个特别脆弱的时期。或者，HPA反应性的变化可能不像以前认为的那样对这种关联起核心作用。
Prenatal depression is associated with adverse offspring outcomes, and the prevailing mechanistic theory to account for mood-associated effects implicates alterations of the maternal and foetal hypothalamic-pituitary adrenal (HPA) axes. Recent research suggests that depression may be associated with a failure to attenuate cortisol reactivity during early pregnancy. The aim of the current study is to investigate whether this effect continues into mid and late gestation. A further aim is to test whether maternal prenatal cortisol reactivity directly predicts infant cortisol reactivity. One hundred three pregnant women were recruited during either the second or third trimester. Depressive symptoms were assessed by self-report, and maternal salivary cortisol responses to a stressor (infant distress film) were measured. Approximately 2 months after birth, mothers (n = 88) reported postnatal depression and infant salivary cortisol responses to inoculation were measured. Prenatal depression was not associated with cortisol reactivity to acute stress in mid and late pregnancy. Similarly, neither prenatal depression nor maternal prenatal cortisol reactivity predicted infant cortisol reactivity to inoculation at 2 months. If the effects of prenatal depression on foetal and infant development are mediated by alterations of the maternal and foetal HPA axes, then early pregnancy may be a particularly vulnerable period. Alternatively, changes to HPA reactivity may not be as central to this association as previously thought.