Lahey Benjamin B, Van Hulle Carol A, Singh Amber L, Waldman Irwin D, Rathouz Paul J
Department of Health Studies, University of Chicago, Chicago, Illinois 60637, USA.
Arch Gen Psychiatry. 2011 Feb;68(2):181-9. doi: 10.1001/archgenpsychiatry.2010.192.
It is necessary to understand the etiologic structure of child and adolescent psychopathology to advance theory and guide future research.
To test alternative models of the higher-order structure of etiologic effects on 11 dimensions of child and adolescent psychopathology using confirmatory factor analyses of genetic and environmental covariances.
Representative sample of twins.
Home interviews.
A total of 1571 pairs of 9- to 17-year-old twins.
Structured assessments of psychopathology using adult caregivers and youth as informants.
The best-fitting genetic model revealed that most genetic factors nonspecifically influence risk for either all 11 symptom dimensions or for dimensions of psychopathology within 1 of 2 broad domains. With some notable exceptions, dimension-specific genetic influences accounted for modest amounts of variance.
To inform theory and guide molecular genetic studies, an etiologic model is offered in which 3 patterns of pleiotropy are hypothesized to be the principal modes of genetic risk transmission for common forms of child and adolescent psychopathology. Some common environmental influences were found, but consistent with a "generalist genes, specialist environments" model, there was little sharing of environmental influences. This implies that prevalent dimensions of child and adolescent psychopathology mostly share their genetic liabilities but are differentiated by nonshared experiences.
有必要了解儿童和青少年精神病理学的病因结构，以推动理论发展并指导未来研究。
使用遗传和环境协方差的验证性因素分析，检验对儿童和青少年精神病理学11个维度的病因效应高阶结构的替代模型。
双胞胎代表性样本。
家庭访谈。
共1571对9至17岁的双胞胎。
使用成年照料者和青少年作为信息提供者对精神病理学进行结构化评估。
拟合度最佳的遗传模型显示，大多数遗传因素非特异性地影响所有11个症状维度或两个广泛领域之一内精神病理学维度的风险。除了一些显著的例外情况，维度特异性遗传影响解释的方差量适中。
为了为理论提供信息并指导分子遗传学研究，提出了一种病因模型，其中假设三种多效性模式是儿童和青少年常见形式精神病理学遗传风险传递的主要模式。发现了一些共同的环境影响，但与“通才基因，专才环境”模型一致，环境影响几乎没有共享。这意味着儿童和青少年精神病理学的普遍维度大多共享其遗传易感性，但通过非共享经历而有所区分。
