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 - Yao, Shuyang
AU - Kuja-Halkola, Ralf
AU - Martin, Joanna
AU - Lu, Yi
AU - Lichtenstein, Paul
AU - Norring, Claes
AU - Birgegård, Andreas
AU - Yilmaz, Zeynep
AU - Hübel, Christopher
AU - Watson, Hunna
AU - Baker, Jessica
AU - Almqvist, Catarina
AU - Thornton, Laura M.
AU - Magnusson, Patrik K.
AU - Bulik, Cynthia M.
AU - Larsson, Henrik
AU - Eating Disorders Working Group of the Psychiatric Genomics Consortium
AU - Davis, Oliver S.P.
PY - 2019/10/15
Y1 - 2019/10/15
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
UR - http://www.scopus.com/inward/record.url?scp=85068526535&partnerID=8YFLogxK
U2 - 10.1016/j.biopsych.2019.04.036
DO - 10.1016/j.biopsych.2019.04.036
M3 - Article (Academic Journal)
C2 - 31301758
AN - SCOPUS:85068526535
SN - 0006-3223
VL - 86
SP - 577
EP - 586
JO - Biological Psychiatry
JF - Biological Psychiatry
IS - 8
ER -