Maternal prenatal depression predicts infant negative affect via maternal inflammatory cytokine levels.
Maternal prenatal depression predicts infant negative affect via maternal inflammatory cytokine levels.
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DOI：
10.1016/j.bbi.2018.06.011
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发表时间：
2018-10
期刊：
影响因子：
--
通讯作者：
Loftis JM
中科院分区：
文献类型：
--
作者：
Gustafsson HC;Sullivan EL;Nousen EK;Sullivan CA;Huang E;Rincon M;Nigg JT;Loftis JM
怀孕期间母亲的抑郁症状与后代情绪和行为问题的风险相关，但这种关联发生的机制尚不清楚。婴儿负面情绪升高（哭闹增多、烦躁、恐惧等）是未来精神病理学的一个关键风险因素，因此了解其决定因素具有预防和早期干预的潜力。一个未经充分研究但有希望的假设是，母亲的情绪通过母亲的产前炎症机制影响婴儿的情绪，但这尚未在人类中进行前瞻性研究。使用一项对从妊娠中期到产后六个月的妇女进行的试点研究的数据（N = 68），我们的目标是启动一项前瞻性研究，探讨母亲炎症细胞因子是否介导母亲抑郁症状与婴儿后代负面影响之间的关联。该研究样本旨在检查后代可能存在的一系列广泛的自我调节和情绪调节问题。为此，我们过度选择了有家族史或自身有注意力缺陷/多动症症状加重史的女性。结果支持了这一假设：妊娠晚期母体促炎细胞因子（使用包括血浆白细胞介素 6、肿瘤坏死因子 α 和单核细胞趋化蛋白 1 浓度作为指标的潜在变量进行索引）介导了这种效应，因此较高的母体抑郁症状与较高的母体炎症相关，并且这介导了对母体婴儿负面情绪报告的影响（控制婴儿期母体影响）。这是第一项人类研究证明母体炎症细胞因子介导产前抑郁症与婴儿结局之间的关联，也是第一项证明抑郁症状影响婴儿气质的生物学机制。
Maternal depressive symptoms during pregnancy are associated with risk for offspring emotional and behavioral problems, but the mechanisms by which this association occurs are not known. Infant elevated negative affect (increased crying, irritability, fearfulness, etc.) is a key risk factor for future psychopathology, so understanding its determinants has prevention and early intervention potential. An understudied yet promising hypothesis is that maternal mood affects infant mood via maternal prenatal inflammatory mechanisms, but this has not been prospectively examined in humans. Using data from a pilot study of women followed from the second trimester of pregnancy through six months postpartum (N = 68) our goal was to initiate a prospective study as to whether maternal inflammatory cytokines mediate the association between maternal depressive symptoms and infant offspring negative affect. The study sample was designed to examine a broad range of likely self-regulation and mood-regulation problems in offspring; to that end we over-selected women with a family history or their own history of elevated symptoms of attention-deficit/hyperactivity disorder. Results supported the hypothesis: maternal pro-inflammatory cytokines during the third trimester (indexed using a latent variable that included plasma interleukin-6, tumor necrosis factor-alpha and monocyte chemoattractant protein-1 concentrations as indicators) mediated the effect, such that higher maternal depressive symptoms were associated with higher maternal inflammation, and this mediated the effect on maternal report of infant negative affect (controlling for maternal affect during the infant period). This is the first human study to demonstrate that maternal inflammatory cytokines mediate the association between prenatal depression and infant outcomes, and the first to demonstrate a biological mechanism through which depressive symptoms impact infant temperament.
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