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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 [rg], 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 (rg = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN (rg = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating (rg = 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 (rgs = −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.
Shared genetic risk between eating disorder- and substance-use-related phenotypes: Evidence from genome-wide association studies
Munn-Chernoff M. A.;Johnson E. C.;Chou Y. -L.;Coleman J. R. I.;Thornton L. M.;Walters R. K.;Yilmaz Z.;Baker J. H.;Hubel C.;Gordon S.;Medland S. E.;Watson H. J.;Gaspar H. A.;Bryois J.;Hinney A.;Leppa V. M.;Mattheisen M.;Ripke S.;Yao S.;Giusti-Rodriguez P.;Hanscombe K. B.;Adan R. A. H.;Alfredsson L.;Ando T.;Andreassen O. A.;Berrettini W. H.;Boehm I.;Boni C.;Boraska Perica V.;Buehren K.;Burghardt R.;Cassina M.;Cichon S.;Clementi M.;Cone R. D.;Courtet P.;Crow S.;Crowley J. J.;Danner U. N.;Davis O. S. P.;de Zwaan M.;Dedoussis G.;Degortes D.;DeSocio J. E.;Dick D. M.;Dikeos D.;Dina C.;Dmitrzak-Weglarz M.;Docampo E.;Duncan L. E.;Egberts K.;Ehrlich S.;Escaramis G.;Esko T.;Estivill X.;Farmer A.;Favaro A.;Fernandez-Aranda F.;Fichter M. M.;Fischer K.;Focker M.;Foretova L.;Forstner A. J.;Forzan M.;Franklin C. S.;Gallinger S.;Giegling I.;Giuranna J.;Gonidakis F.;Gorwood P.;Gratacos Mayora M.;Guillaume S.;Guo Y.;Hakonarson H.;Hatzikotoulas K.;Hauser J.;Hebebrand J.;Helder S. G.;Herms S.;Herpertz-Dahlmann B.;Herzog W.;Huckins L. M.;Hudson J. I.;Imgart H.;Inoko H.;Janout V.;Jimenez-Murcia S.;Julia A.;Kalsi G.;Kaminska D.;Karhunen L.;Karwautz A.;Kas M. J. H.;Kennedy J. L.;Keski-Rahkonen A.;Kiezebrink K.;Kim Y. -R.;Klump K. L.;Knudsen G. P. S.;La Via M. C.;Le Hellard S.;Levitan R. D.;Li D.;Lilenfeld L.;Lin B. D.;Lissowska J.;Luykx J.;Magistretti P. J.;Maj M.;Mannik K.;Marsal S.;Marshall C. R.;Mattingsdal M.;McDevitt S.;McGuffin P.;Metspalu A.;Meulenbelt I.;Micali N.;Mitchell K.;Monteleone A. M.;Monteleone P.;Nacmias B.;Navratilova M.;Ntalla I.;O'Toole J. K.;Ophoff R. A.;Padyukov L.;Palotie A.;Pantel J.;Papezova H.;Pinto D.;Rabionet R.;Raevuori A.;Ramoz N.;Reichborn-Kjennerud T.;Ricca V.;Ripatti S.;Ritschel F.;Roberts M.;Rotondo A.;Rujescu D.;Rybakowski F.;Santonastaso P.;Scherag A.;Scherer S. W.;Schmidt U.;Schork N. J.;Schosser A.;Seitz J.;Slachtova L.;Slagboom P. E.;Slof-Op't Landt M. C. T.;Slopien A.;Sorbi S.;Swiatkowska B.;Szatkiewicz J. P.;Tachmazidou I.;Tenconi E.;Tortorella A.;Tozzi F.;Treasure J.;Tsitsika A.;Tyszkiewicz-Nwafor M.;Tziouvas K.;van Elburg A. A.;van Furth E. F.;Wagner G.;Walton E.;Widen E.;Zeggini E.;Zerwas S.;Zipfel S.;Bergen A. W.;Boden J. M.;Brandt H.;Crawford S.;Halmi K. A.;Horwood L. J.;Johnson C.;Kaplan A. S.;Kaye W. H.;Mitchell J.;Olsen C. M.;Pearson J. F.;Pedersen N. L.;Strober M.;Werge T.;Whiteman D. C.;Woodside D. B.;Grove J.;Henders A. K.;Larsen J. T.;Parker R.;Petersen L. V.;Jordan J.;Kennedy M. A.;Birgegard A.;Lichtenstein P.;Norring C.;Landen M.;Mortensen P. B.;Polimanti R.;McClintick J. N.;Adkins A. E.;Aliev F.;Bacanu S. -A.;Batzler A.;Bertelsen S.;Biernacka J. M.;Bigdeli T. B.;Chen L. -S.;Clarke T. -K.;Degenhardt F.;Docherty A. R.;Edwards A. C.;Foo J. C.;Fox L.;Frank J.;Hack L. M.;Hartmann A. M.;Hartz S. M.;Heilmann-Heimbach S.;Hodgkinson C.;Hoffmann P.;Hottenga J. -J.;Konte B.;Lahti J.;Lahti-Pulkkinen M.;Lai D.;Ligthart L.;Loukola A.;Maher B. S.;Mbarek H.;McIntosh A. M.;McQueen M. B.;Meyers J. L.;Milaneschi Y.;Palviainen T.;Peterson R. E.;Ryu E.;Saccone N. L.;Salvatore J. E.;Sanchez-Roige S.;Schwandt M.;Sherva R.;Streit F.;Strohmaier J.;Thomas N.;Wang J. -C.;Webb B. T.;Wedow R.;Wetherill L.;Wills A. G.;Zhou H.;Boardman J. D.;Chen D.;Choi D. -S.;Copeland W. E.;Culverhouse R. C.;Dahmen N.;Degenhardt L.;Domingue B. W.;Frye M. A.;Gabel W.;Hayward C.;Ising M.;Keyes M.;Kiefer F.;Koller G.;Kramer J.;Kuperman S.;Lucae S.;Lynskey M. T.;Maier W.;Mann K.;Mannisto S.;Muller-Myhsok B.;Murray A. D.;Nurnberger J. I.;Preuss U.;Raikkonen K.;Reynolds M. D.;Ridinger M.;Scherbaum N.;Schuckit M. A.;Soyka M.;Treutlein J.;Witt S. H.;Wodarz N.;Zill P.;Adkins D. E.;Boomsma D. I.;Bierut L. J.;Brown S. A.;Bucholz K. K.;Costello E. J.;de Wit H.;Diazgranados N.;Eriksson J. G.;Farrer L. A.;Foroud T. M.;Gillespie N. A.;Goate A. M.;Goldman D.;Grucza R. A.;Hancock D. B.;Harris K. M.;Hesselbrock V.;Hewitt J. K.;Hopfer C. J.;Iacono W. G.;Johnson E. O.;Karpyak V. M.;Kendler K. S.;Kranzler H. R.;Krauter K.;Lind P. A.;McGue M.;MacKillop J.;Madden P. A. F.;Maes H. H.;Magnusson P. K. E.;Nelson E. C.;Nothen M. M.;Palmer A. A.;Penninx B. W. J. H.;Porjesz B.;Rice J. P.;Rietschel M.;Riley B. P.;Rose R. J.;Shen P. -H.;Silberg J.;Stallings M. C.;Tarter R. E.;Vanyukov M. M.;Vrieze S.;Wall T. L.;Whitfield J. B.;Zhao H.;Neale B. M.;Wade T. D.;Heath A. C.;Montgomery G. W.;Martin N. G.;Sullivan P. F.;Kaprio J.;Breen G.;Gelernter J.;Edenberg H. J.;Bulik C. M.;Agrawal A.;Tortorella A.
2020
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 [rg], 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 (rg = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN (rg = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating (rg = 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 (rgs = −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.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11391/1459720
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simulazione ASN
Il report seguente simula gli indicatori relativi alla propria produzione scientifica in relazione alle soglie ASN 2023-2025 del proprio SC/SSD. Si ricorda che il superamento dei valori soglia (almeno 2 su 3) è requisito necessario ma non sufficiente al conseguimento dell'abilitazione. La simulazione si basa sui dati IRIS e sugli indicatori bibliometrici alla data indicata e non tiene conto di eventuali periodi di congedo obbligatorio, che in sede di domanda ASN danno diritto a incrementi percentuali dei valori. La simulazione può differire dall'esito di un’eventuale domanda ASN sia per errori di catalogazione e/o dati mancanti in IRIS, sia per la variabilità dei dati bibliometrici nel tempo. Si consideri che Anvur calcola i valori degli indicatori all'ultima data utile per la presentazione delle domande.
La presente simulazione è stata realizzata sulla base delle specifiche raccolte sul tavolo ER del Focus Group IRIS coordinato dall’Università di Modena e Reggio Emilia e delle regole riportate nel DM 589/2018 e allegata Tabella A. Cineca, l’Università di Modena e Reggio Emilia e il Focus Group IRIS non si assumono alcuna responsabilità in merito all’uso che il diretto interessato o terzi faranno della simulazione. Si specifica inoltre che la simulazione contiene calcoli effettuati con dati e algoritmi di pubblico dominio e deve quindi essere considerata come un mero ausilio al calcolo svolgibile manualmente o con strumenti equivalenti.
