Abstract
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 g ], 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 g = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN (r g = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating (r g = 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 gs = -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.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | e12880 |
| Tidsskrift | Addiction Biology |
| Vol/bind | 26 |
| Nummer | 1 |
| Antal sider | 20 |
| ISSN | 1355-6215 |
| DOI | |
| Status | Udgivet - jan. 2021 |
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I: Addiction Biology, Bind 26, Nr. 1, e12880, 01.2021.
Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avis › Tidsskriftartikel › Forskning › peer review
TY - JOUR
T1 - Shared genetic risk between eating disorder- and substance-use-related phenotypes
T2 - Evidence from genome-wide association studies
AU - Munn-Chernoff, Melissa A
AU - Johnson, Emma C
AU - Chou, Yi-Ling
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AU - Kendler, Kenneth S
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AU - Magnusson, Patrik K E
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AU - Penninx, Brenda W J H
AU - Porjesz, Bernice
AU - Rice, John P
AU - Rietschel, Marcella
AU - Riley, Brien P
AU - Rose, Richard J
AU - Shen, Pei-Hong
AU - Silberg, Judy
AU - Stallings, Michael C
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AU - Vanyukov, Michael M
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AU - Wall, Tamara L
AU - Whitfield, John B
AU - Zhao, Hongyu
AU - Neale, Benjamin M
AU - Wade, Tracey D
AU - Heath, Andrew C
AU - Montgomery, Grant W
AU - Martin, Nicholas G
AU - Sullivan, Patrick F
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AU - Gelernter, Joel
AU - Edenberg, Howard J
AU - Bulik, Cynthia M
AU - Agrawal, Arpana
PY - 2021/1
Y1 - 2021/1
N2 - 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 g ], 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 g = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN (r g = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating (r g = 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 gs = -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.
AB - 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 g ], 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 g = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN (r g = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating (r g = 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 gs = -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.
KW - Alcoholism/genetics
KW - Depressive Disorder, Major/genetics
KW - Feeding and Eating Disorders/genetics
KW - Genome-Wide Association Study
KW - Humans
KW - Linkage Disequilibrium
KW - Phenotype
KW - Polymorphism, Single Nucleotide
KW - Risk Factors
KW - Schizophrenia/genetics
KW - Substance-Related Disorders/genetics
KW - Tobacco Use Disorder/genetics
UR - http://www.scopus.com/inward/record.url?scp=85079714981&partnerID=8YFLogxK
U2 - 10.1111/adb.12880
DO - 10.1111/adb.12880
M3 - Journal article
C2 - 32064741
AN - SCOPUS:85079714981
SN - 1355-6215
VL - 26
JO - Addiction Biology
JF - Addiction Biology
IS - 1
M1 - e12880
ER -