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dc.contributor.authorYao, Shuyang
dc.contributor.authorKuja-Halkola, Ralf
dc.contributor.authorMartin, Joanna
dc.contributor.authorLu, Yi
dc.contributor.authorLichtenstein, Paul
dc.contributor.authorNorring, Claes
dc.contributor.authorBirgegård, Andreas
dc.contributor.authorYilmaz, Zeynep
dc.contributor.authorHübel, Christopher
dc.contributor.authorWatson, Hunna
dc.contributor.authorBaker, Jessica
dc.contributor.authorAlmqvist, Catarina
dc.contributor.authorEating Disorders Working Group of the Psychiatric Genomics Consortium
dc.contributor.authorThornton, Laura M
dc.contributor.authorMagnusson, Patrik K
dc.contributor.authorBulik, Cynthia M
dc.contributor.authorLarsson, Henrik [incl. Karhunen, L]
dc.date.accessioned2020-01-24T11:54:28Z
dc.date.available2020-01-24T11:54:28Z
dc.date.issued2019
dc.identifier.urihttps://erepo.uef.fi/handle/123456789/7975
dc.description.abstractBackground Although attention-deficit/hyperactivity disorder (ADHD) and eating disorders (EDs) frequently co-occur, little is known about the shared etiology. In this study, we comprehensively investigated the genetic association between ADHD and various EDs, including anorexia nervosa (AN) and other EDs such as bulimia nervosa. Methods We applied different genetically informative designs to register-based information of a Swedish nationwide population (N = 3,550,118). We first examined the familial coaggregation of clinically diagnosed ADHD and EDs across multiple types of relatives. We then applied quantitative genetic modeling in full-sisters and maternal half-sisters to estimate the genetic correlations between ADHD and EDs. We further tested the associations between ADHD polygenic risk scores and ED symptoms, and between AN polygenic risk scores and ADHD symptoms, in a genotyped population-based sample (N = 13,472). Results Increased risk of all types of EDs was found in individuals with ADHD (any ED: odds ratio [OR] = 3.97, 95% confidence interval [CI] = 3.81, 4.14; AN: OR = 2.68, 95% CI = 2.15, 2.86; other EDs: OR = 4.66, 95% CI = 4.47, 4.87; bulimia nervosa: OR = 5.01, 95% CI = 4.63, 5.41) and their relatives compared with individuals without ADHD and their relatives. The magnitude of the associations decreased as the degree of relatedness decreased, suggesting shared familial liability between ADHD and EDs. Quantitative genetic models revealed stronger genetic correlation of ADHD with other EDs (.37, 95% CI = .31, .42) than with AN (.14, 95% CI = .05, .22). ADHD polygenic risk scores correlated positively with ED symptom measures overall and with the subscales Drive for Thinness and Body Dissatisfaction despite small effect sizes. Conclusions We observed stronger genetic association with ADHD for non-AN EDs than for AN, highlighting specific genetic correlation beyond a general genetic factor across psychiatric disorders.
dc.language.isoenglanti
dc.publisherElsevier BV
dc.relation.ispartofseriesBiological psychiatry
dc.relation.urihttp://dx.doi.org/10.1016/j.biopsych.2019.04.036
dc.rightsCC BY 4.0
dc.subjectADHD
dc.subjectanorexia nervosa
dc.subjectbulimia nervosa
dc.subjecteating disorders
dc.subjectgenetic epidemiology
dc.subjectpolygenic risk score
dc.titleAssociations Between Attention-Deficit/Hyperactivity Disorder and Various Eating Disorders: A Swedish Nationwide Population Study Using Multiple Genetically Informative Approaches
dc.description.versionpublished version
dc.contributor.departmentSchool of Medicine / Clinical Nutrition
uef.solecris.id67648710en
dc.type.publicationTieteelliset aikakauslehtiartikkelit
dc.relation.doi10.1016/j.biopsych.2019.04.036
dc.description.reviewstatuspeerReviewed
dc.format.pagerange577-586
dc.relation.issn0006-3223
dc.relation.issue8
dc.relation.volume86
dc.rights.accesslevelopenAccess
dc.type.okmA1
uef.solecris.openaccessHybridijulkaisukanavassa ilmestynyt avoin julkaisu
dc.rights.copyright© Society of Biological Psychiatry
dc.type.displayTypearticleen
dc.type.displayTypeartikkelifi
dc.rights.urlhttps://creativecommons.org/licenses/by/4.0/


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