Lars Libuda1,2, Roaa Naaresh3, Christine Ludwig3, Björn-Hergen Laabs4, Jochen Antel3, Manuel Föcker5, Johannes Hebebrand3, Anke Hinney3, Triinu Peters3. 1. Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Essen, University of Duisburg-Essen, Virchowstr. 174, 45147, Essen, Germany. lars.libuda@uni-due.de. 2. Research Institute for the Prevention of Allergies and Respiratory Diseases in Childhood, Department of Pediatrics, Marien-Hospital Wesel, 46483, Wesel, Germany. lars.libuda@uni-due.de. 3. Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Essen, University of Duisburg-Essen, Virchowstr. 174, 45147, Essen, Germany. 4. Institut für Medizinische Biometrie und Statistik, Universität zu Lübeck, Universitätsklinikum Schleswig-Holstein, 23562, Lübeck, Germany. 5. Department of Child and Adolescent Psychiatry, University of Münster, 48149, Münster, Germany.
Abstract
BACKGROUND: While observational studies revealed an inverse association between serum 25(OH)vitamin D (25(OH)D) and the risk of attention deficit/hyperactivity disorder (ADHD), the causality of this relationship remains unclear. METHODS: We conducted a bidirectional two-sample Mendelian Randomization (MR) study to examine whether 25(OH)D has an effect on the risk to develop ADHD or vice versa. Information on single nucleotide polymorphisms (SNP) associated with serum 25(OH)D was obtained from a genome-wide association study (GWAS) considering phenotype data from 79,366 individuals of European ancestry. Data on risk for ADHD were derived from a GWAS analysis with 20,183 individuals diagnosed with ADHD and 35,191 controls. For our analysis, we considered effect sizes based on the European participants (19,099 cases and 34,194 controls). RESULTS: Single SNP analyses showed a causal effect of vitamin D on ADHD risk for only one SNP (rs12785878, p = 0.024). The overall MR estimates did not reveal a causal effect of 25(OH)D on risk for ADHD. In the reverse analysis, neither any single nor the multi-SNP MR analyses showed a causal effect of ADHD on 25(OH)D. CONCLUSION: Results from this two-sample MR study did not confirm a causal effect of 25(OH)D on ADHD or vice versa. Accordingly, our study does not provide evidence that improving 25(OH)D via supplementation could reduce the risk of developing ADHD.
BACKGROUND: While observational studies revealed an inverse association between serum 25(OH)vitamin D (25(OH)D) and the risk of attention deficit/hyperactivity disorder (ADHD), the causality of this relationship remains unclear. METHODS: We conducted a bidirectional two-sample Mendelian Randomization (MR) study to examine whether 25(OH)D has an effect on the risk to develop ADHD or vice versa. Information on single nucleotide polymorphisms (SNP) associated with serum 25(OH)D was obtained from a genome-wide association study (GWAS) considering phenotype data from 79,366 individuals of European ancestry. Data on risk for ADHD were derived from a GWAS analysis with 20,183 individuals diagnosed with ADHD and 35,191 controls. For our analysis, we considered effect sizes based on the European participants (19,099 cases and 34,194 controls). RESULTS: Single SNP analyses showed a causal effect of vitamin D on ADHD risk for only one SNP (rs12785878, p = 0.024). The overall MR estimates did not reveal a causal effect of 25(OH)D on risk for ADHD. In the reverse analysis, neither any single nor the multi-SNP MR analyses showed a causal effect of ADHD on 25(OH)D. CONCLUSION: Results from this two-sample MR study did not confirm a causal effect of 25(OH)D on ADHD or vice versa. Accordingly, our study does not provide evidence that improving 25(OH)D via supplementation could reduce the risk of developing ADHD.
Authors: Jie Zheng; Denis Baird; Maria-Carolina Borges; Jack Bowden; Gibran Hemani; Philip Haycock; David M Evans; George Davey Smith Journal: Curr Epidemiol Rep Date: 2017-11-22
Authors: Johannes Hebebrand; Triinu Peters; Dick Schijven; Moritz Hebebrand; Corinna Grasemann; Thomas W Winkler; Iris M Heid; Jochen Antel; Manuel Föcker; Lisa Tegeler; Lena Brauner; Roger A H Adan; Jurjen J Luykx; Christoph U Correll; Inke R König; Anke Hinney; Lars Libuda Journal: Mol Metab Date: 2018-04-03 Impact factor: 7.422