Department of Child and Adolescent Psychiatry, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Department of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behavior, Nijmegen, The Netherlands.
J Abnorm Child Psychol. 2018 Oct;46(7):1427-1437. doi: 10.1007/s10802-017-0377-3.
Literature suggests that life stressors predict attention-deficit/hyperactivity disorder (ADHD) symptoms and that this relationship is moderated by the serotonin transporter polymorphism (5-HTTLPR). It is less clear whether, on reverse, ADHD symptoms may influence the risk of exposure to life stressors. Furthermore, the role of life stressors may vary across development depending on the type of life stressor. We used threewave longitudinal data of 1,306 adolescents from the general population and clinicreferred cohort of the TRacking Adolescents' Individual Lives Survey. The 5-HTTLPR genotype (SS, LS, LL), parent-reported ADHD symptoms at three time points (T1: Mage = 11.2; T2: Mage = 13.5; T3: Mage = 16.2 years), and the number of personrelated ('dependent') and environment-related ('independent') life stressors occurring between measurements (T1-T2, T2-T3) were assessed. Using path analyses, we examined bidirectional relations between exposure to these life stressors and ADHD symptoms between the separate waves moderated by 5-HTTLPR status. Exposure to life stressors did not predict ADHD symptoms. Rather, we found that in 5-HTTLPR Sallele homozygotes, ADHD symptoms in middle adolescence (T2) predicted exposure to the number of person-related life stressors later in adolescence (T2-T3, p = 0.001). There was no relation with environment-related life stressors. Our study suggests that S-allele homozygotes with higher levels of ADHD symptoms in middle adolescence are more vulnerable to becoming exposed to person-related ('dependent') life stressors in late adolescence. Findings emphasize the need to be aware of social-emotional adversities that may occur in genetically vulnerable adolescents with ADHD symptoms in the transition into adulthood.
文献表明,生活应激源可预测注意缺陷多动障碍(ADHD)症状,而这种关系受 5-羟色胺转运体多态性(5-HTTLPR)调节。相反,ADHD 症状是否会影响生活应激源暴露的风险则不太清楚。此外,根据生活应激源的类型,生活应激源的作用在不同的发展阶段可能有所不同。我们使用了来自一般人群和诊所的青少年个体生活跟踪调查(TRacking Adolescents' Individual Lives Survey)的队列的三波纵向数据,共涉及 1306 名青少年。5-HTTLPR 基因型(SS、LS、LL)、父母在三个时间点报告的 ADHD 症状(T1:Mage=11.2;T2:Mage=13.5;T3:Mage=16.2 岁)以及在两次测量之间发生的人与环境相关的(“依赖”)生活应激源的数量(T1-T2、T2-T3)。通过路径分析,我们在分别的波次中,检验了生活应激源暴露与 ADHD 症状之间的双向关系,这种关系受到 5-HTTLPR 状态的调节。生活应激源暴露并不能预测 ADHD 症状。相反,我们发现,在 5-HTTLPR S 等位基因纯合子中,青少年中期(T2)的 ADHD 症状预测了青少年后期(T2-T3)与人相关的生活应激源数量的增加(p=0.001)。与环境相关的生活应激源无关。我们的研究表明,在青少年中期 ADHD 症状较高的 S 等位基因纯合子中,更易受到青春期后期与人相关的(“依赖”)生活应激源的影响。这些发现强调了需要注意可能在具有 ADHD 症状的遗传易感性青少年过渡到成年期时出现的社会情感逆境。