The effects of child maltreatment on early signs of antisocial behavior: genetic moderation by tryptophan hydroxylase, serotonin transporter, and monoamine oxidase A genes.
The effects of child maltreatment on early signs of antisocial behavior: genetic moderation by tryptophan hydroxylase, serotonin transporter, and monoamine oxidase A genes.
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DOI：
10.1017/s0954579412000442
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发表时间：
2012-08
影响因子：
3.3
通讯作者：
Thibodeau EL
中科院分区：
文献类型：
--
作者：
Cicchetti D;Rogosch FA;Thibodeau EL
在受虐待和未受虐待的低收入家庭儿童（N = 627，M年龄= 11.27）中调查了基因-环境交互作用对儿童后期反社会行为的预测作用。检测了TPH 1、5-HTTLPR和MAOA uVNTR三个基因的变异。除了儿童虐待状况，我们还考虑了虐待亚型的影响，虐待的发展时间和慢性。反社会行为的指标是从自我，同伴，和成人顾问报告。在一系列的ANCOVA中，儿童虐待及其参数表现出强烈的主要影响早期反社会行为的评估所有形式的报告。遗传效应主要在基因-环境相互作用的背景下起作用，调节儿童虐待对结果的影响。在这三个基因中，未受虐待的儿童在反社会行为方面没有发现基于遗传变异的差异。相比之下，在受虐儿童中，TPH 1、5-HTTLPR和MAOA的特异性多态性均与反社会行为的自我报告升高相关; 5-HTTLPR和虐待的发展时间的相互作用也表明，基于基因型，早发性和复发性虐待儿童的反社会结果更严重。TPH 1和5-HTTLPR与虐待亚型相互作用，预测反社会行为的同伴报告;遗传变异导致受虐儿童反社会行为的较大差异。TPH 1和5-HTTLPR多态性也调节了虐待亚型对成人报告反社会行为的影响;再次，遗传效应对被虐待的儿童最强。此外，TPH 1调节虐待和慢性发展时间对成人报告反社会行为的影响。这些发现阐明了遗传变异如何有助于确定哪些受虐待的儿童最容易发生反社会发展。
Gene-environment interaction effects in predicting antisocial behavior in late childhood were investigated among maltreated and nonmaltreated low-income children (N = 627, M age = 11.27). Variants in three genes, TPH1, 5-HTTLPR, and MAOA uVNTR, were examined. In addition to child maltreatment status, we also considered the impact of maltreatment subtypes, developmental timing of maltreatment, and chronicity. Indicators of antisocial behavior were obtained from self-, peer-, and adult counselor-reports. In a series of ANCOVAs, child maltreatment and its parameters demonstrated strong main effects on early antisocial behavior as assessed by all forms of report. Genetic effects operated primarily in the context of gene-environment interactions, moderating the impact of child maltreatment on outcomes. Across the three genes, among nonmaltreated children no differences in antisocial behavior were found based on genetic variation. In contrast, among maltreated children specific polymorphisms of TPH1, 5-HTTLPR, and MAOA were each related to heightened self-report of antisocial behavior; the interaction of 5-HTTLPR and developmental timing of maltreatment also indicated more severe antisocial outcomes for children with early onset and recurrent maltreatment based on genotype. TPH1 and 5-HTTLPR interacted with maltreatment subtype to predict peer-report of antisocial behavior; genetic variation contributed to larger differences in antisocial behavior among abused children. TPH1 and 5-HTTLPR polymorphisms also moderated the effects of maltreatment subtype on adult report of antisocial behavior; again genetic effects were strongest for children who were abused. Additionally, TPH1 moderated the effect of developmental timing of maltreatment and chronicity on adult report of antisocial behavior. The findings elucidate how genetic variation contributes to identifying which maltreated children are most vulnerable to antisocial development.