@misc{10481/75717, year = {2022}, month = {6}, url = {http://hdl.handle.net/10481/75717}, abstract = {Background: Attention deficit/hyperactivity disorder (ADHD) is a highly prevalent neurodevelopmental disorder caused by a combination of genetic and environmental factors and is often thought as an entry point into a negative life trajectory, including risk for comorbid disorders, poor educational achievement or low income. In the present study, we aimed to clarify the causal relationship between ADHD and a comprehensive range of related traits. Methods: We used genome-wide association study (GWAS) summary statistics for ADHD (n¼53 293) and 124 traits related to anthropometry, cognitive function and intelligence, early life exposures, education and employment, lifestyle and environment, longevity, neurological, and psychiatric and mental health or personality and psychosocial factors available in the MR-Base database (16 067 n 766 345). To investigate their causal relationship with ADHD, we used two-sample Mendelian randomization (MR) with a range of sensitivity analyses, and validated MR findings using causal analysis using summary effect estimates (CAUSE), aiming to avoid potential false-positive results. Results: Our findings strengthen previous evidence of a causal effect of ADHD liability on smoking and major depression, and are consistent with a causal effect on odds of decreased average total household income [odds ratio (OR)¼0.966, 95% credible interval (CrI)¼(0.954, 0.979)] and increased lifetime number of sexual partners [OR¼1.023, 95% CrI¼(1.013, 1.033)]. We also found evidence for a causal effect on ADHD for liability of arm predicted mass and weight [OR¼1.452, 95% CrI¼(1.307, 1.614) and OR¼1.430, 95% CrI¼(1.326, 1.539), respectively] and time spent watching television [OR¼1.862, 95% CrI¼(1.545, 2.246)], and evidence for a bidirectional effect for age of first sexual intercourse [beta¼ 0.058, 95% CrI¼( 0.072, 0.044) and OR¼0.413, 95% CrI¼(0.372, 0.457), respectively], odds of decreased age completed full-time education [OR¼0.972, 95% CrI¼(0.962, 0.981) and OR¼0.435, 95% CrI¼(0.356, 0.533), respectively] and years of schooling [beta¼-0.036, 95% CrI¼( 0.048, 0.024) and OR¼0.458, 95% CrI¼(0.411, 0.511), respectively]. Conclusions: Our results may contribute to explain part of the widespread co-occurring traits and comorbid disorders across the lifespan of individuals with ADHD and may open new opportunities for developing preventive strategies for ADHD and for negative ADHD trajectories.}, organization = {European Union H2020 Programme (H2020/2014-2020) 667302 728018 848228 2020604}, organization = {Instituto de Salud Carlos III European Commission PI18/01788 PI19/00721 P19/01224 PI20/00041 FI18/00285 CD15/00199 CP09/00119 CPII15/00023}, organization = {Pla estrategic de recerca i innovacio en salut (PERIS), Generalitat de Cata-lunya (METAL-Cat) SLT006/17/287}, organization = {Agencia de Gestio D'Ajuts Universitaris de Recerca Agaur (AGAUR)}, organization = {Generalitat de Catalunya 2017SGR1461 2016FI_B00899}, organization = {Ministry of Science, Innovation and Universities IJC2018-035346-I}, organization = {European Commission}, organization = {`la Marato' de TV3 092330/31}, organization = {ECNP Network `ADHD across the Lifespan'}, publisher = {Oxford University Press}, keywords = {ADHD}, keywords = {Mendelian randomization}, keywords = {Causal analysis using summary effect estimates}, title = {Mendelian randomization analysis for attention deficit/hyperactivity disorder: studying a broad range of exposures and outcomes}, doi = {10.1093/ije/dyac128}, author = {Soler Artigas, María and Rovira, Paula}, }