Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
JAMA Psychiatry. 2013 Mar;70(3):311-8. doi: 10.1001/jamapsychiatry.2013.287.
CONTEXT: The genetic and environmental link between attention-deficit/hyperactivity disorder in childhood and the adult manifestation of the disorder is poorly understood because of a lack of longitudinal studies with cross-informant data. OBJECTIVE: To explore the relative contribution of genetic and environmental influences on symptoms of attention problems from childhood to early adulthood. DESIGN: Analysis was conducted using longitudinal structural equation modeling with multiple informants. SETTING: The Swedish Twin Study of Child and Adolescent Development. PARTICIPANTS: One thousand four hundred eighty twin pairs were prospectively followed up from childhood to young adulthood. MAIN OUTCOME MEASURES: Symptoms were obtained using parent and self-ratings of the Attention Problems Scale at ages 8 to 9, 13 to 14, 16 to 17, and 19 to 20 years. RESULTS: The best-fitting model revealed high heritability of attention problems as indexed by parent and self-ratings from childhood to early adulthood (h² = 0.77-0.82). Genetic effects operating at age 8 to 9 years continued, explaining 41%, 34%, and 24% of the total variance at ages 13 to 14, 16 to 17, and 19 to 20 years. Moreover, new sets of genetic risk factors emerged at ages 13 to 14, 16 to 17, and 19 to 20 years. CONCLUSIONS: The shared view of self- and informant-rated attention problems is highly heritable in childhood, adolescence, and early adulthood, suggesting that the previous reports of low heritability for attention-deficit/hyperactivity disorder in adults are best explained by rater effects. Both genetic stability and genetic innovation were present throughout this developmental stage, suggesting that attention problems are a developmentally complex phenotype characterized by both continuity and change across the life span.
背景:由于缺乏具有跨报告者数据的纵向研究,因此对于儿童时期的注意力缺陷/多动障碍与该障碍成年表现之间的遗传和环境联系知之甚少。
目的:探讨遗传和环境因素对从儿童期到成年早期注意力问题症状的相对贡献。
设计:使用具有多个报告者的纵向结构方程模型进行分析。
设置:瑞典儿童和青少年发展双胞胎研究。
参与者:1480 对双胞胎前瞻性地从儿童期随访到成年早期。
主要观察指标:使用父母和自我评定的注意力问题量表在 8 至 9 岁、13 至 14 岁、16 至 17 岁和 19 至 20 岁时评估症状。
结果:最佳拟合模型显示,父母和自我评定的注意力问题在整个儿童期到成年早期具有较高的遗传性(h²=0.77-0.82)。8 至 9 岁时的遗传效应持续存在,可解释 13 至 14 岁、16 至 17 岁和 19 至 20 岁时总方差的 41%、34%和 24%。此外,在 13 至 14 岁、16 至 17 岁和 19 至 20 岁时出现了新的遗传风险因素。
结论:自我和报告者评定的注意力问题的共同观点在儿童期、青春期和成年早期具有高度遗传性,这表明先前报告的成人注意力缺陷/多动障碍遗传性低最好通过评定者效应来解释。遗传稳定性和遗传创新在整个发育阶段都存在,这表明注意力问题是一种具有发展复杂性的表型,其特征是整个生命历程中既有连续性又有变化。
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