Shared genetic risk between eating disorder- and substance-use-related phenotypes: Evidence from genome-wide association studies.
Détails
ID Serval
serval:BIB_9F7C7C4CB90A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Shared genetic risk between eating disorder- and substance-use-related phenotypes: Evidence from genome-wide association studies.
Périodique
Addiction biology
ISSN
1369-1600 (Electronic)
ISSN-L
1355-6215
Statut éditorial
Publié
Date de publication
01/2021
Peer-reviewed
Oui
Volume
26
Numéro
1
Pages
e12880
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural
Publication Status: ppublish
Publication Status: ppublish
Résumé
Eating disorders and substance use disorders frequently co-occur. Twin studies reveal shared genetic variance between liabilities to eating disorders and substance use, with the strongest associations between symptoms of bulimia nervosa and problem alcohol use (genetic correlation [r <sub>g</sub> ], twin-based = 0.23-0.53). We estimated the genetic correlation between eating disorder and substance use and disorder phenotypes using data from genome-wide association studies (GWAS). Four eating disorder phenotypes (anorexia nervosa [AN], AN with binge eating, AN without binge eating, and a bulimia nervosa factor score), and eight substance-use-related phenotypes (drinks per week, alcohol use disorder [AUD], smoking initiation, current smoking, cigarettes per day, nicotine dependence, cannabis initiation, and cannabis use disorder) from eight studies were included. Significant genetic correlations were adjusted for variants associated with major depressive disorder and schizophrenia. Total study sample sizes per phenotype ranged from ~2400 to ~537 000 individuals. We used linkage disequilibrium score regression to calculate single nucleotide polymorphism-based genetic correlations between eating disorder- and substance-use-related phenotypes. Significant positive genetic associations emerged between AUD and AN (r <sub>g</sub> = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN (r <sub>g</sub> = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating (r <sub>g</sub> = 0.27; q = 0.0016). Conversely, significant negative genetic correlations were observed between three nondiagnostic smoking phenotypes (smoking initiation, current smoking, and cigarettes per day) and AN without binge eating (r <sub>gs</sub> = -0.19 to -0.23; qs < 0.04). The genetic correlation between AUD and AN was no longer significant after co-varying for major depressive disorder loci. The patterns of association between eating disorder- and substance-use-related phenotypes highlights the potentially complex and substance-specific relationships among these behaviors.
Mots-clé
Alcoholism/genetics, Depressive Disorder, Major/genetics, Feeding and Eating Disorders/genetics, Genome-Wide Association Study, Humans, Linkage Disequilibrium, Phenotype, Polymorphism, Single Nucleotide, Risk Factors, Schizophrenia/genetics, Substance-Related Disorders/genetics, Tobacco Use Disorder/genetics, eating disorders, genetic correlation, substance use
Pubmed
Web of science
Création de la notice
20/02/2020 15:40
Dernière modification de la notice
02/12/2023 7:15