The Gonda Brain Sciences Center,Bar-Ilan University,Ramat-Gan,Israel.
Department of Psychology,Bar-Ilan University,Ramat-Gan,Israel.
Psychol Med. 2018 Apr;48(6):1020-1033. doi: 10.1017/S0033291717002550. Epub 2017 Sep 11.
Chronic early trauma alters children's stress reactivity and increases the prevalence of anxiety disorders; yet the neuroendocrine and immune mechanisms underpinning this effect are not fully clear. Animal studies indicate that the mother's physiology and behavior mediate offspring stress in a system-specific manner, but few studies tested this external-regulatory maternal role in human children exposed to chronic stress.
We followed a unique cohort of children exposed to continuous wartime trauma (N = 177; exposed; N = 101, controls; N = 76). At 10 years, maternal and child's salivary immunoglobulin A (s-IgA) and oxytocin (OT), biomarkers of the immune and affiliation systems, were assayed, maternal and child relational behaviors observed, mother and child underwent psychiatric diagnosis, and child anxiety symptoms assessed.
War-exposed mothers had higher s-IgA, lower OT, more anxiety symptoms, and their parenting was characterized by reduced sensitivity. Exposed children showed higher s-IgA, more anxiety disorders and post traumatic stress disorder, and more anxiety symptoms. Path analysis model defined three pathways by which maternal physiology and behavior impacted child anxiety; (a) increasing maternal s-IgA, which led to increased child s-IgA, augmenting child anxiety; (b) reducing maternal OT, which linked with diminished child OT and social repertoire; and (c) increasing maternal anxiety, which directly impacted child anxiety.
Our findings, the first to measure immune and affiliation biomarkers in mothers and children, detail their unique and joint effects on children's anxiety in response to stress; highlight the relations between chronic stress, immune activation, and anxiety in children; and describe how processes of biobehavioral synchrony shape children's long-term adaptation.
慢性早期创伤会改变儿童的应激反应，增加焦虑障碍的患病率；然而，支撑这一效应的神经内分泌和免疫机制尚不完全清楚。动物研究表明，母亲的生理和行为以特定于系统的方式调节后代的应激，但很少有研究在暴露于慢性应激的人类儿童中测试这种外部调节的母亲作用。
我们跟踪了一组经历持续战争创伤的独特儿童队列（N=177；暴露组；N=101，对照组；N=76）。在 10 岁时，检测了母亲和儿童的唾液免疫球蛋白 A（s-IgA）和催产素（OT），这是免疫和附属系统的生物标志物，观察了母亲和儿童的关系行为，对母亲和儿童进行了精神病诊断，并评估了儿童的焦虑症状。
经历战争的母亲 s-IgA 较高，OT 较低，焦虑症状更多，育儿方式的敏感性降低。暴露组的儿童 s-IgA 较高，焦虑障碍和创伤后应激障碍更多，焦虑症状更多。路径分析模型定义了三种途径，通过这些途径，母亲的生理和行为影响儿童的焦虑；（a）增加母亲的 s-IgA，导致儿童的 s-IgA 增加，从而增加儿童的焦虑；（b）减少母亲的 OT，这与儿童 OT 和社交能力的减少有关；（c）增加母亲的焦虑，这直接影响儿童的焦虑。
我们的研究结果首次测量了母亲和儿童的免疫和附属生物标志物，详细说明了它们对儿童应激反应中焦虑的独特和共同影响；强调了慢性应激、免疫激活和儿童焦虑之间的关系；并描述了生物行为同步如何塑造儿童的长期适应。
