**5. Conclusions**

Results from this meta-analysis showed no large effect of a genetically determined reduction in 25(OH)D concentrations by selected polymorphisms on T1D risk, despite the strong association seen in some observational studies. Although the hypothesis that a different SNP distribution from vitamin D related genes is associated with T1D was not confirmed by this study, small effects cannot be discounted. To make conclusive estimates in complex diseases, such as T1D, further characterization of complex interactions between genetic and environmental factors, like the included variants affecting serum 25(OH)D concentrations, need to be considered.

**Supplementary Materials:** The following are avaiable online at https://www.mdpi.com/2072-6643/ 13/12/4260/s1, Supplementary Figure S1. Funnel plot analysis for publication bias; Supplementary Figure S2. Subgroup analysis of Caucasian participants for the association between selected genetic variants affecting serum 25-hydroxyvitamin concentrations and type 1 diabetes with the random effects model (coded by 25-hydroxyvitamin D increasing alleles). Squares represent the individual odds ratio estimate. Diamonds show the pooled effect. Horizontal bars represent the 95% confidence intervals; Supplementary Table S1. Ovid: MEDLINE search strategy—the database coverage was 1946 to present, and the database was last searched on 1 April 2021; Supplementary Table S2. Ovid: Embase Classic and Embase search strategy—the database coverage was 1947 to present, and the database was last searched on 1 April 2021; Supplementary Table S3. Web of Science search strategy—the database coverage was 1947 to present, and the database was last searched on 1 April 2021; Supplementary Table S4. OpenGWAS search strategy –annotated R script using R package. The database coverage was 2020 to present, and the database was last searched on 1 April 2021; Supplementary Table S5. Quality assessment of the included studies: summary of critical appraisal using CASP tools; Supplementary Material S1 Author ICMJE disclosure forms.

**Author Contributions:** L.N.: Conceptualization, Methodology, Software, Validation, Formal analysis, Investigation, Data curation, Writing—original draft preparation, Writing—reviewing and editing, Visualization, Project administration. E.H.: Conceptualization, Methodology, Resources, Writing—reviewing and editing, Supervision, Project administration, Funding acquisition. A.Z.: Conceptualization, Methodology, Software, Formal analysis, Writing—reviewing and editing, Supervision. J.S.: Investigation, Writing—reviewing and editing, Supervision. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research was in part supported by National Health and Medical Research Council, Australia (GNT11123603).

**Institutional Review Board Statement:** Not applicable.

**Informed Consent Statement:** Not applicable.

**Data Availability Statement:** Not applicable, due to being systematic review with meta-analyses. All data is available in primary studies.

**Acknowledgments:** We want to acknowledge the participants and investigators of the FinnGen study, and all the participants and investigators of the UK Biobank.

**Conflicts of Interest:** The authors declare no potential duality of interest associated with this study. All authors have completed the ICMJE uniform disclosure form (see Supplementary Materials).
