Department of Psychology, Institute of Psychiatry, Psychology and Neuroscience, King's College London, UK
Fruhling V. Rijsdijk
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
Nicoletta Adamo
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, UK; and South London and Maudsley NHS Foundation Trust, London, UK
Espen M. Eilertsen
PROMENTA Research Centre, University of Oslo, Norway; and Centre for Fertility and Health, Norwegian Institute of Public Health, Oslo, Norway
Yasmin I. Ahmadzadeh
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, UK
Isabella Badini
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, UK
Laurie J. Hannigan
Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, Norway; Nic Waals Institute, Lovisenberg Diaconal Hospital, Oslo, Norway; and Medical Research Council Integrative Epidemiology Unit, University of Bristol, UK
Eivind Ystrom
PROMENTA Research Centre, University of Oslo, Norway; Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, Norway; and School of Pharmacy, University of Oslo, Norway
Tom A. McAdams
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, UK; and PROMENTA Research Centre, University of Oslo, Norway
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: rG = 0.55, 95% CI 0.43−0.93; ODD: rG = 0.80, 95% CI 0.46−1; conduct disorder: rG = 0.44, 95% CI 0.28−1; anxiety: rG = 0.72, 95% CI 0.48−1; depression: rG = 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.
