Wechsler Daniel L, Rijsdijk Fruhling V, Adamo Nicoletta, Eilertsen Espen M, Ahmadzadeh Yasmin I, Badini Isabella, Hannigan Laurie J, Ystrom Eivind, McAdams Tom A
Department of Psychology, Institute of Psychiatry, Psychology and Neuroscience, King's College London, UK.
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, UK; and Department of Psychology, Faculty of Social Sciences, Anton de Kom University, Suriname.
BJPsych Open. 2023 Sep 6;9(5):e169. doi: 10.1192/bjo.2023.554.
Several longitudinal studies have cast doubt on the aetiological overlap between child and adult attention-deficit hyperactivity disorder (ADHD). However, a lack of genetically sensitive data following children across adulthood precludes direct evaluation of aetiological overlap between child and adult ADHD.
We circumvent the existing gap in longitudinal data by exploring genetic overlap between maternal (adult) and offspring (child) ADHD and comorbid symptoms in an extended family cohort.
Data were drawn from the Norwegian Mother, Father and Child Cohort Study, a Norwegian birth registry cohort of 114 500 children and their parents. Medical Birth Registry of Norway data were used to link extended families. Mothers self-reported their own ADHD symptoms when children were aged 3 years; reported children's ADHD symptoms at age 5 years; and children's ADHD, oppositional defiant disorder (ODD), conduct disorder, anxiety and depression symptoms at age 8 years. Genetic correlations were derived from Multiple-Children-of-Twins-and-Siblings and extended bivariate twin models.
Phenotypic correlations between adult ADHD symptoms and child ADHD, ODD, conduct disorder, anxiety and depression symptoms at age 8 years were underpinned by medium-to-large genetic correlations (child ADHD: = 0.55, 95% CI 0.43-0.93; ODD: = 0.80, 95% CI 0.46-1; conduct disorder: = 0.44, 95% CI 0.28-1; anxiety: = 0.72, 95% CI 0.48-1; depression: = 1, 95% CI 0.66-1). These cross-generational adult-child genetic correlations were of a comparable magnitude to equivalent child-child genetic correlations with ADHD symptoms at age 5 years.
Our findings provide genetically sensitive evidence that ADHD symptoms in adulthood share a common genetic architecture with symptoms of ADHD and four comorbid disorders at age 8 years. These findings suggest that in the majority of cases, ADHD symptoms in adulthood are not aetiologically distinct from in childhood.
多项纵向研究对儿童与成人注意力缺陷多动障碍（ADHD）之间的病因重叠提出了质疑。然而，缺乏跟踪儿童至成年期的基因敏感性数据，使得无法直接评估儿童与成人ADHD之间的病因重叠情况。
我们通过在一个大家庭队列中探索母亲（成人）与后代（儿童）ADHD及共病症状之间的基因重叠，来弥补纵向数据方面存在的差距。
数据取自挪威母亲、父亲与儿童队列研究，这是一个挪威出生登记队列，包含114500名儿童及其父母。利用挪威医学出生登记处的数据来关联大家庭。母亲们在孩子3岁时自我报告自己的ADHD症状；在孩子5岁时报告孩子的ADHD症状；在孩子8岁时报告孩子的ADHD、对立违抗障碍（ODD）、品行障碍、焦虑和抑郁症状。基因相关性通过多子女双胞胎和兄弟姐妹模型以及扩展的双变量双胞胎模型得出。
8岁时成人ADHD症状与儿童ADHD、ODD、品行障碍、焦虑和抑郁症状之间的表型相关性，由中等至高度的基因相关性所支撑（儿童ADHD：=0.55，95%置信区间0.43 - 0.93；ODD：=0.80，95%置信区间0.46 - 1；品行障碍：=0.44，95%置信区间0.28 - 1；焦虑：=0.72，95%置信区间0.48 - 1；抑郁：=1，95%置信区间0.66 - 1）。这些跨代的成人 - 儿童基因相关性与5岁时儿童之间ADHD症状的等效基因相关性程度相当。
我们的研究结果提供了基因敏感性证据，表明成年期的ADHD症状与8岁时ADHD及四种共病的症状具有共同的基因结构。这些结果表明，在大多数情况下，成年期的ADHD症状在病因上与儿童期并无不同。
