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 journalArticle

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
JournalBiological Psychiatry
DOIs
Publication statusPublished - Jan 1 2019

Fingerprint

Attention Deficit Disorder with Hyperactivity
Population
Anorexia Nervosa
Confidence Intervals
Odds Ratio
Bulimia Nervosa
Feeding and Eating Disorders
Thinness
Genetic Models
Psychiatry
Mothers

Keywords

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

ASJC Scopus subject areas

  • Biological Psychiatry

Cite this

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.

In: Biological Psychiatry, 01.01.2019.

Research output: Contribution to journalArticle

@article{873ae45140e14ff4b8acde0118dd46f3,
title = "Associations Between Attention-Deficit/Hyperactivity Disorder and Various Eating Disorders: A Swedish Nationwide Population Study Using Multiple Genetically Informative Approaches",
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.",
keywords = "ADHD, Anorexia nervosa, Bulimia nervosa, Eating disorders, Genetic epidemiology, Polygenic risk score",
author = "{Eating Disorders Working Group of the Psychiatric Genomics Consortium} and Shuyang Yao and Ralf Kuja-Halkola and Joanna Martin and Yi Lu and Paul Lichtenstein and Christopher H{\"u}bel and Catarina Almqvist and Magnusson, {Patrik K.} and Bulik, {Cynthia M.} and Henrik Larsson and Claes Norring and Andreas Birgeg{\aa}rd and Claes Norring and Andreas Birgeg{\aa}rd and Catarina Almqvist and Henrik Larsson and Joanna Martin and Christopher H{\"u}bel and Zeynep Yilmaz and Hunna Watson and Jessica Baker and Thornton, {Laura M.} and Bulik, {Cynthia M.} and Bulik, {Cynthia M.} and Roger Adan and Tetsuya Ando and Jessica Baker and Andrew Bergen and Wade Berrettini and Andreas Birgeg{\aa}rd and Claudette Boni and {Boraska Perica}, Vesna and Harry Brandt and Roland Burghardt and Matteo Cassina and Carolyn Cesta and Maurizio Clementi and Joni Coleman and Roger Cone and Philippe Courtet and Steven Crawford and Scott Crow and James Crowley and Unna Danner and Oliver Davis and {de Zwaan}, Martina and George Dedoussis and Daniela Degortes and Janiece DeSocio and Sandro Sorbi",
year = "2019",
month = "1",
day = "1",
doi = "10.1016/j.biopsych.2019.04.036",
language = "English",
journal = "Biological Psychiatry",
issn = "0006-3223",
publisher = "Elsevier USA",

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TY - JOUR

T1 - Associations Between Attention-Deficit/Hyperactivity Disorder and Various Eating Disorders

T2 - A Swedish Nationwide Population Study Using Multiple Genetically Informative Approaches

AU - Eating Disorders Working Group of the Psychiatric Genomics Consortium

AU - Yao, Shuyang

AU - Kuja-Halkola, Ralf

AU - Martin, Joanna

AU - Lu, Yi

AU - Lichtenstein, Paul

AU - Hübel, Christopher

AU - Almqvist, Catarina

AU - Magnusson, Patrik K.

AU - Bulik, Cynthia M.

AU - Larsson, Henrik

AU - Norring, Claes

AU - Birgegård, Andreas

AU - Norring, Claes

AU - Birgegård, Andreas

AU - Almqvist, Catarina

AU - Larsson, Henrik

AU - Martin, Joanna

AU - Hübel, Christopher

AU - Yilmaz, Zeynep

AU - Watson, Hunna

AU - Baker, Jessica

AU - Thornton, Laura M.

AU - Bulik, Cynthia M.

AU - Bulik, Cynthia M.

AU - Adan, Roger

AU - Ando, Tetsuya

AU - Baker, Jessica

AU - Bergen, Andrew

AU - Berrettini, Wade

AU - Birgegård, Andreas

AU - Boni, Claudette

AU - Boraska Perica, Vesna

AU - Brandt, Harry

AU - Burghardt, Roland

AU - Cassina, Matteo

AU - Cesta, Carolyn

AU - Clementi, Maurizio

AU - Coleman, Joni

AU - Cone, Roger

AU - Courtet, Philippe

AU - Crawford, Steven

AU - Crow, Scott

AU - Crowley, James

AU - Danner, Unna

AU - Davis, Oliver

AU - de Zwaan, Martina

AU - Dedoussis, George

AU - Degortes, Daniela

AU - DeSocio, Janiece

AU - Sorbi, Sandro

PY - 2019/1/1

Y1 - 2019/1/1

N2 - 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.

AB - 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.

KW - ADHD

KW - Anorexia nervosa

KW - Bulimia nervosa

KW - Eating disorders

KW - Genetic epidemiology

KW - Polygenic risk score

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U2 - 10.1016/j.biopsych.2019.04.036

DO - 10.1016/j.biopsych.2019.04.036

M3 - Article

JO - Biological Psychiatry

JF - Biological Psychiatry

SN - 0006-3223

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