Interactive effects of corticotropin releasing hormone receptor 1, serotonin transporter linked polymorphic region, and child maltreatment on diurnal cortisol regulation and internalizing symptomatology.
Interactive effects of corticotropin releasing hormone receptor 1, serotonin transporter linked polymorphic region, and child maltreatment on diurnal cortisol regulation and internalizing symptomatology.
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DOI：
10.1017/s0954579411000599
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发表时间：
2011-11
影响因子：
3.3
通讯作者：
Oshri A
中科院分区：
文献类型：
--
作者：
Cicchetti D;Rogosch FA;Oshri A
在等静负荷框架内，研究了基因与环境(GxE)的相互作用对皮质醇的昼夜调节和内化症状的影响。对参加夏令营的受虐儿童(238例，21.4%)和未受虐儿童(男10.08岁)的CRHR1TAT单倍型和5-HTTLPR进行了检测。内化和抑郁症状通过他人和自我报告进行评估。观察到CRHR1的GxE效应以及虐待和早期虐待对皮质醇昼夜调节的影响；CRHR1的变异仅在受虐待的儿童中与皮质醇失调有关。早期滥用和高度内化症状也相互作用，预测非典型的昼夜皮质醇调节。CRHR1、5-HTTLPR和儿童虐待(GxGxE)的相互作用确定了一组具有高度内化症状的虐待儿童，他们共享这两个基因的相同组合。这一发现支持了一种平衡负荷的观点，即与虐待儿童相关的慢性应激对皮质醇调节和内化症状的影响受遗传变异的影响。
Within an allostatic load framework, the effect of gene by environment (GxE) interactions on diurnal cortisol regulation and internalizing symptomatology were investigated. Variation in the CRHR1 TAT haplotype and 5-HTTLPR was determined in a sample of maltreated (n = 238, 21.4% with early physical and sexual abuse) and nonmaltreated (n = 255) children (M age = 10.08) participating in a summer research camp. Internalizing and depressive symptoms were assessed by other- and self-report. GxE effects for CRHR1 and maltreatment and early abuse on diurnal cortisol regulation were observed; CRHR1 variation was related to cortisol dysregulation only among maltreated children. Early abuse and high internalizing symptoms also interacted to predict atypical diurnal cortisol regulation. The interaction of CRHR1, 5-HTTLPR, and child maltreatment (GxGxE) identified a subgroup of maltreated children with high internalizing symptoms who shared the same combination of the two genes. The findings support an allostatic load perspective on the effects of the chronic stress associated with child maltreatment on cortisol regulation and internalizing symptomatology as moderated by genetic variation.