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Assessing aetiological overlap between child and adult attention-deficit hyperactivity disorder symptoms in an extended family design
BACKGROUND: 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...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cambridge University Press
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10617499/ https://www.ncbi.nlm.nih.gov/pubmed/37671545 http://dx.doi.org/10.1192/bjo.2023.554 |
Sumario: | BACKGROUND: 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. AIMS: 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. METHOD: 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. RESULTS: 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: r(G) = 0.55, 95% CI 0.43−0.93; ODD: r(G) = 0.80, 95% CI 0.46−1; conduct disorder: r(G) = 0.44, 95% CI 0.28−1; anxiety: r(G) = 0.72, 95% CI 0.48−1; depression: r(G) = 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. CONCLUSIONS: 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. |
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