An experimental test of the fetal programming hypothesis: Can we reduce child ontogenetic vulnerability to psychopathology by decreasing maternal depression?
An experimental test of the fetal programming hypothesis: Can we reduce child ontogenetic vulnerability to psychopathology by decreasing maternal depression?
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DOI：
10.1017/s0954579418000470
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发表时间：
2018-08
影响因子：
3.3
通讯作者：
Hoffman MC
中科院分区：
文献类型：
--
作者：
Davis EP;Hankin BL;Swales DA;Hoffman MC
母亲抑郁是最常见的产前并发症之一，产前母亲抑郁预示着许多儿童精神病理。在这里，我们应用胎儿程序设计假说作为一个组织框架来解决胎儿在怀孕期间暴露于母亲抑郁症状影响胎儿脆弱性和风险机制发育的可能性，这增加了随后精神病理的风险。我们考虑了四种可能的途径，通过这些途径，母亲产前抑郁可能影响后代在整个生命周期中发展后期精神病理的倾向：大脑发育、生理应激调节（下丘脑-垂体-肾上腺皮质轴）、负面情绪和认知（努力）控制。过去的大多数研究都是相关的，因此潜在的因果结论是有限的。我们采用随机对照试验（RCT）设计，描述了一项正在进行的胎儿程序设计对产前母亲抑郁症状影响的实验测试。在这项随机对照试验中，将人际关系治疗（IPT）与增强的常规护理进行比较，以评估减少产前母亲抑郁症状是否对儿童个体发育脆弱性有有益影响，从而降低后代日后出现精神病理的风险。
Maternal depression is one of the most common prenatal complications, and prenatal maternal depression predicts many child psychopathologies. Here, we apply the Fetal Programming Hypothesis as an organizational framework to address the possibility that fetal exposure to maternal depressive symptoms during pregnancy affects fetal development of vulnerabilities and risk mechanisms, which enhance risk for subsequent psychopathology. We consider four candidate pathways through which maternal prenatal depression may affect the propensity of offspring to develop later psychopathology across the lifespan: brain development, physiological stress regulation (hypothalamic pituitary adrenocortical axis), negative emotionality, and cognitive (effortful) control. The majority of past research has been correlational, so potential causal conclusions have been limited. We describe an ongoing experimental test of the fetal programming influence of prenatal maternal depressive symptoms using a randomized controlled trial (RCT) design. In this RCT, Interpersonal Therapy (IPT) is compared to enhanced usual care among distressed pregnant women to evaluate whether reducing prenatal maternal depressive symptoms has a salutary impact on child ontogenetic vulnerabilities and thereby reduces offspring’s risk for emergence of later psychopathology.