It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
Attention Deficit-Hyperactivity Disorder (ADHD) is a complex psychiatric and neurodevelopmental disorder that develops during childhood and spans into adulthood. ADHD’s aetiology is complex, and evidence about its cause and risk factors is limited. We leveraged genetic data from genome-wide association studies (GWAS) and performed latent causal variable analyses using a hypothesis-free approach to infer causal associations between 1387 complex traits and ADHD. We identified 37 inferred potential causal associations with ADHD risk. Our results reveal that genetic variants associated with iron deficiency anemia (ICD10), obesity, type 2 diabetes, synovitis and tenosynovitis (ICD10), polyarthritis (ICD10), neck or shoulder pain, and substance use in adults display partial genetic causality on ADHD risk in children. Genetic variants associated with ADHD have a partial genetic causality increasing the risk for chronic obstructive pulmonary disease and carpal tunnel syndrome. Protective factors for ADHD risk included genetic variants associated with the likelihood of participating in socially supportive and interactive activities. Our results show that genetic liability to multiple complex traits influences a higher risk for ADHD, highlighting the potential role of cardiometabolic phenotypes and physical pain in ADHD’s aetiology. These findings have the potential to inform future clinical studies and development of interventions.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 QIMR Berghofer Medical Research Institute, Department of Genetics and Computational Biology, Brisbane, Australia (GRID:grid.1049.c) (ISNI:0000 0001 2294 1395); The University of Queensland, School of Biomedical Sciences, Faculty of Medicine, Brisbane, Australia (GRID:grid.1003.2) (ISNI:0000 0000 9320 7537)
2 The University of Queensland, The University of Queensland Diamantina Institute, Woolloongabba, Australia (GRID:grid.1003.2) (ISNI:0000 0000 9320 7537); 23andMe, Inc, Sunnyvale, USA (GRID:grid.420283.f) (ISNI:0000 0004 0626 0858)
3 QIMR Berghofer Medical Research Institute, Department of Genetics and Computational Biology, Brisbane, Australia (GRID:grid.1049.c) (ISNI:0000 0001 2294 1395)
4 Duke University, Department of Psychiatry & Behavioral Sciences, School of Medicine, Durham, USA (GRID:grid.26009.3d) (ISNI:0000 0004 1936 7961); Holmusk Technologies, Inc., New York, USA (GRID:grid.26009.3d)