Psychology Department, University of Kentucky, Lexington, USA.
Psychiatry Department, Oregon Health & Sciences University, Portland, USA.
Res Child Adolesc Psychopathol. 2022 Aug;50(8):1055-1066. doi: 10.1007/s10802-022-00902-8. Epub 2022 Feb 1.
The current investigation extended prior cross-sectional mapping of etiological factors, transdiagnostic effortful and affective traits, and ADHD symptoms to longitudinal pathways extending from two etiological domains: polygenic and prenatal risk. Hypotheses were (1) genetic risk for ADHD would be related to inattentive ADHD symptoms in adolescence and mediated by childhood effortful control; (2) prenatal smoking would be related to hyperactive-impulsive ADHD symptoms during childhood and mediated by childhood surgency; and (3) there would be age-related variation, such that mediation of genetic risk would be larger for older than younger ages, whereas mediation of prenatal risk would be larger in earlier childhood than at later ages. Participants were 849 children drawn from the Oregon ADHD-1000 Cohort, which used a case control sample and an accelerated longitudinal design to track development from childhood (at year 1 ages 7-13) through adolescence (at year 6 ages 13-19). Results showed the mediational pathway from prenatal smoking through surgency to hyperactivity-impulsivity at Year 1 was significant (indirect effect estimate = .053, p < .01). The mediational pathway from polygenic risk through effortful control to inattention at Year 6 was also significant (indirect effect estimate = .084, p < .01). Both results were independent of the association between inattention and hyperactivity-impulsivity and control for the alternative etiological input and held across parent- and teacher-report of ADHD symptoms. In line with dual pathway models of ADHD, early prenatal risk for hyperactivity-impulsivity appears to operate through surgency, while polygenic genetic risk for inattention appears mediated by effortful control.
当前的研究扩展了先前对病因因素、跨诊断努力和情感特征以及 ADHD 症状的横断面研究，将其扩展到从两个病因领域（多基因和产前风险）延伸而来的纵向途径。假设如下：(1) ADHD 的遗传风险与青春期的注意力不集中 ADHD 症状相关，且由儿童期努力控制来介导；(2)产前吸烟与儿童期多动冲动 ADHD 症状相关，且由儿童期精力旺盛来介导；(3)存在与年龄相关的变化，即遗传风险的中介作用在年龄较大时比年龄较小时更大，而产前风险的中介作用在年幼时比年龄较大时更大。参与者是从俄勒冈 ADHD-1000 队列中抽取的 849 名儿童，该队列使用病例对照样本和加速纵向设计来追踪从儿童期（第 1 年，年龄 7-13 岁）到青春期（第 6 年，年龄 13-19 岁）的发展情况。结果表明，产前吸烟通过精力旺盛向第 1 年的多动冲动传递的中介途径是显著的（间接效应估计值 = .053，p < .01）。多基因风险通过努力控制向第 6 年的注意力不集中传递的中介途径也是显著的（间接效应估计值 = .084，p < .01）。这两个结果都独立于注意力不集中和多动冲动之间的关联，并且在 ADHD 症状的替代病因输入和家长及教师报告的控制方面都是成立的。与 ADHD 的双重途径模型一致，多动冲动的早期产前风险似乎通过精力旺盛来运作，而注意力不集中的多基因遗传风险似乎通过努力控制来介导。
