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Association and Familial Coaggregation of Type 1 Diabetes and Eating Disorders: A Register-Based Cohort Study in Denmark and Sweden

posted on 06.04.2021, 22:12 by Ashley E. Tate, Shengxin Liu, Ruyue Zhang, Zeynep Yilmaz, Janne T. Larsen, Liselotte V Petersen, Cynthia M. Bulik, Ann-Marie Svensson, Soffia Gudbjörnsdottir, Henrik Larsson, Agnieszka Butwicka, Ralf Kuja-Halkola

To ascertain the association and co-aggregation of eating disorders and childhood-onset type 1 diabetes in families.


Using population samples from national registers in Sweden (n= 2 517 277) and Demark (n= 1 825 920) we investigated the within-individual association between type 1 diabetes and EDs, and their familial co-aggregation among full siblings, half-siblings, full cousins, and half-cousins. Based on clinical diagnoses we classified eating disorders (EDs) into: any eating disorder (AED), anorexia nervosa and atypical anorexia nervosa (AN), and other eating disorder (OED). Associations were determined with hazard ratios (HR) with confidence intervals (CI) from Cox regressions.


Swedish and Danish individuals with a type 1 diabetes diagnosis had a greater risk of receiving an ED diagnosis (HR [95% CI] Sweden: AED 2.02 [1.80 – 2.27], AN 1.63 [1.36 – 1.96], OED 2.34 [2.07 – 2.63]; Denmark: AED 2.19 [1.84 – 2.61], AN 1.78 [1.36 – 2.33], OED 2.65 [2.20 – 3.21]). We also meta-analyzed the results: AED 2.07 [1.88 – 2.28], AN 1.68 [1.44 – 1.95], OED 2.44 [2.17 – 2.72]. There was an increased risk of receiving an ED diagnosis in full siblings in the Swedish cohort (AED 1.25 [1.07 – 1.46], AN 1.28 [1.04 – 1.57], OED 1.28 [1.07 – 1.52]), these results were non-significant in the Danish cohort.


Patients with 1 diabetes are at a higher risk of subsequent EDs; however, there is conflicting support for the relationship between having a sibling with type 1 diabetes and ED diagnosis. Diabetes healthcare teams should be vigilant for disordered eating behaviors in children and adolescents with type 1 diabetes.


Tate has received funding from the European Union’s Horizon 2020 Research and Innovation Programme under the Marie Sklodowska-Curie CAPICE Project grant agreement number 721567. (https://www.capice-project.eu/) Butwicka was supported by the Swedish Research Council (2017-00788), Stockholm Region (clinical research appointment 20180718) and Karolinska Institutet, Strategic Research Programme in Neuroscience (StratNeuro) while working on this project. Larsen and Petersen were supported by the Lundbeck Foundation (R276-2017-4581). Bulik acknowledges funding from the Swedish Research Council (Vetenskapsrådet, award: 538-2013-8864). Bulik acknowledges funding from the U.S. National Institute of Mental Health (R01MH119084; U01 MH109528). Bulik and Petersen acknowledge funding from the U.S. National Institute of Mental Health (R01MH120170) and Lundbeckfonden. Yilmaz is funded by NIMH (K01MH109782; R01MH105500; R01MH120170) and a Brain and Behavior Research Foundation NARSAD Young Investigator Award (28799)