DOI: 10.5061/dryad.ns8q3
title: Data from: Childhood adiposity and type 1 diabetes: a Mendelian randomization study

description: BACKGROUND: The incidence of type 1 diabetes (T1D) is increasing globally.
 One hypothesis is that increasing childhood obesity rates may explain part
 of this increase, but, as T1D is rare, intervention studies are
 challenging to perform. The aim of this study was to assess this
 hypothesis with a Mendelian randomization approach that uses genetic
 variants as instrumental variables to test for causal associations.
 METHODS AND FINDINGS: We created a genetic instrument of 23 single
 nucleotide polymorphisms (SNPs) associated with childhood adiposity in
 children aged 2-10 years. Summary-level association results for these 23
 SNPs with childhood-onset (&lt;17 years) T1D were extracted from a
 meta-analysis of genome-wide association study with 5,913 T1D cases and
 8,828 reference samples. Using inverse-variance weighted Mendelian
 randomization analysis, we found support for an effect of childhood
 adiposity on T1D risk (odds ratio 1.32, 95% CI 1.06-1.64 per standard
 deviation score in body mass index [SDS-BMI]). A sensitivity analysis
 provided evidence of horizontal pleiotropy bias (p = 0.04) diluting the
 estimates towards the null. We therefore applied Egger regression and
 multivariable Mendelian randomization methods to control for this type of
 bias and found evidence in support of a role of childhood adiposity in T1D
 (odds ratio in Egger regression, 2.76, 95% CI 1.40-5.44). Limitations of
 our study include that underlying genes and their mechanisms for most of
 the genetic variants included in the score are not known. Mendelian
 randomization requires large sample sizes, and power was limited to
 provide precise estimates. This research has been conducted using data
 from the Early Growth Genetics (EGG) Consortium, the Genetic Investigation
 of Anthropometric Traits (GIANT) Consortium, the Tobacco and Genetics
 (TAG) Consortium, and the Social Science Genetic Association Consortium
 (SSGAC), as well as meta-analysis results from a T1D genome-wide
 association study. CONCLUSIONS: This study provides genetic support for a
 link between childhood adiposity and T1D risk. Together with evidence from
 observational studies, our findings further emphasize the importance of
 measures to reduce the global epidemic of childhood obesity and encourage
 mechanistic studies.
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