Associations Between Attention-Deficit/Hyperactivity Disorder and Various Eating Disorders: A Swedish Nationwide Population Study Using Multiple Genetically Informative Approaches

Eating Disorders Working Group of the Psychiatric Genomics Consortium

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

Background: 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.

Original languageEnglish (US)
Pages (from-to)577-586
Number of pages10
JournalBiological psychiatry
Volume86
Issue number8
DOIs
StatePublished - Oct 15 2019

Bibliographical note

Funding Information:
SY acknowledges financial support from the China Scholarship Council. JM was supported by the Wellcome Trust (Grant No. 106047). ZY was supported by the National Institutes of Health (Grant No. K01MH109782). CMB acknowledges funding from the Swedish Research Council (Grant No. 538-2013-8864). HL acknowledges financial support from the Swedish Research Council (Grant No. 2014-3831). The project has also received funding from the Swedish Initiative for Research on Microdata in the Social and Medical Sciences framework (Grant No. 340-2013-5867). The CATSS was supported by funding from the Swedish Research Council for Health, Working Life and Welfare and the Swedish Research Council. The Swedish Twin Registry is acknowledged for access to data. The Swedish Twin Registry is managed by Karolinska Institutet and receives funding through the Swedish Research Council under Grant No. 2017-00641. We gratefully acknowledge the contribution of the participants in the Child and Adolescent Twin Study in Sweden and their families. The following consortia provided genome-wide association study summary statistics: Psychiatric Genomics Consortium (Attention-Deficit/Hyperactivity Disorder Working Group and Eating Disorders Working Group), Lundbeck Foundation Initiative for Integrative Psychiatric Research (iPSYCH), and iPSYCH-Broad Work Group. PL has served as a speaker for Medice. CN is a consultant on a research grant from Shire. CMB has been a grant recipient from and served on scientific advisory boards for Shire and has received royalties from Pearson and Walker. HL has received educational speaking fees from Eli Lilly and Shire and has received a research grant from Shire, all outside the submitted work. All other authors report no biomedical financial interests or potential conflicts of interest.

Funding Information:
SY acknowledges financial support from the China Scholarship Council . JM was supported by the Wellcome Trust (Grant No. 106047 ). ZY was supported by the National Institutes of Health (Grant No. K01MH109782 ). CMB acknowledges funding from the Swedish Research Council (Grant No. 538-2013-8864 ). HL acknowledges financial support from the Swedish Research Council (Grant No. 2014-3831 ). The project has also received funding from the Swedish Initiative for Research on Microdata in the Social and Medical Sciences framework (Grant No. 340-2013-5867 ). The CATSS was supported by funding from the Swedish Research Council for Health, Working Life and Welfare and the Swedish Research Council . The Swedish Twin Registry is acknowledged for access to data. The Swedish Twin Registry is managed by Karolinska Institutet and receives funding through the Swedish Research Council under Grant No. 2017-00641 .

Funding Information:
PL has served as a speaker for Medice. CN is a consultant on a research grant from Shire. CMB has been a grant recipient from and served on scientific advisory boards for Shire and has received royalties from Pearson and Walker. HL has received educational speaking fees from Eli Lilly and Shire and has received a research grant from Shire, all outside the submitted work. All other authors report no biomedical financial interests or potential conflicts of interest.

Publisher Copyright:
© 2019 Society of Biological Psychiatry

Keywords

  • ADHD
  • Anorexia nervosa
  • Bulimia nervosa
  • Eating disorders
  • Genetic epidemiology
  • Polygenic risk score

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