Handley Elizabeth D, Rogosch Fred A, Cicchetti Dante
University of Rochester Mt. Hope Family Center.
Dev Psychopathol. 2015 Nov;27(4 Pt 2):1489-502. doi: 10.1017/S0954579415000899.
The current study examined the prospective association between child maltreatment and the development of substance use disorder in adolescence with the aim of investigating pathways underlying this relation, as well as genetic moderation of these developmental mechanisms. Specifically, we tested whether youth who experienced maltreatment prior to age 8 were at risk for the development of marijuana dependence in adolescence by way of a childhood externalizing pathway and a childhood internalizing pathway. Moreover, we tested whether variation in FK506 binding protein 5 gene (FKBP5) CATT haplotype moderated these pathways. The participants were 326 children (n =179 maltreated; n = 147 nonmaltreated) assessed across two waves of data collection (childhood: ages 7-9 and adolescence: ages 15-18). Results indicated that higher levels of child externalizing symptoms significantly mediated the effect of child maltreatment on adolescent marijuana dependence symptoms for individuals with one or two copies of the FKBP5 CATT haplotype only. We did not find support for an internalizing pathway from child maltreatment to adolescent marijuana dependence, nor did we find evidence of moderation of the internalizing pathway by FKBP5 haplotype variation. Findings extend previous research by demonstrating that whether a maltreated child will traverse an externalizing pathway toward substance use disorder in adolescence is dependent on FKBP5 genetic variation.
本研究考察了儿童期受虐与青少年物质使用障碍发展之间的前瞻性关联,旨在探究这种关系背后的潜在途径以及这些发展机制的基因调节作用。具体而言,我们测试了8岁之前经历过虐待的青少年是否会通过儿童期外化途径和儿童期内化途径而面临在青春期发展为大麻依赖的风险。此外,我们还测试了FK506结合蛋白5基因(FKBP5)CATT单倍型的变异是否会调节这些途径。研究对象为326名儿童(179名受虐儿童;147名未受虐儿童),他们在两轮数据收集过程中接受了评估(儿童期:7至9岁;青春期:15至18岁)。结果表明,只有携带一份或两份FKBP5 CATT单倍型的个体,较高水平的儿童外化症状才会显著介导儿童期受虐对青少年大麻依赖症状的影响。我们没有发现支持从儿童期受虐到青少年大麻依赖的内化途径的证据,也没有发现FKBP5单倍型变异对内化途径产生调节作用的证据。研究结果扩展了先前的研究,表明受虐儿童在青春期是否会通过外化途径发展为物质使用障碍取决于FKBP5基因变异。