Diabetes in Veterans is usually presumed to be T2D because T1D precludes enlistment, but T1D may present in adults; how T1D genetic risk impacts different racial/ethnic groups is unknown. To assess the contributions of T1D genetic risk, we examined 109,954 Veterans in the VA's Million Veteran Program (MVP), using a 30 SNP T1D genetic risk score (GRS) for those with European, Hispanic, and Asian ancestry, and a separate 7-SNP GRS for those of African ancestry. High T1D genetic risk (GRS ≥90th percentile) was characterized according to age at diabetes onset (20-39, 40-59, and 60+ years). High T1D genetic risk was more common with the earliest onset group (13.2%, 10.0% and 9.0%, respectively), and that group had the highest proportion of minority ancestry (47%, 37%, and 25%), all p<0.001. The three high T1D risk groups had similar follow-up (13, 12, and 11 years), GAD antibodies if tested (39%, 41%, and 40%), and low C-peptide levels if measured (36%, 23%, and 33%). However, typical T1D features were more common with earlier onset: use of insulin (80%, 63%, and 43%), time to insulin (0.2, 2.4, and 1.4 yr), diabetic ketoacidosis (11%, 3%, and 0.8%), and severe hypoglycemia prompting an ED visit (10%, 5%, and 3%), all p<0.001. While earlier age of onset groups had more use of T1D ICD codes (50%, 25% and 13%), testing for GAD antibodies (18%, 4%, and 2%), and testing for C-peptide (24%, 9%, and 3%), respectively, all p<0.001, less than half of any group had diagnostic testing for T1D. Conclusions: Increased T1D genetic risk is associated with earlier age of diabetes onset in adults and increased prevalence of typical T1D characteristics, but similar GAD antibodies and C-peptide levels. Since individuals with high T1D risk and early diabetes onset are disproportionately of minority ancestry, health policies aimed to improve T1D recognition and management are needed to remedy this health disparity. Disclosure P. K. Yang: None. L. S. Phillips: Other Relationship; Diasyst Inc., Research Support; Abbott Diabetes, Janssen Pharmaceuticals, Inc., Pfizer Inc., Kowa Pharmaceuticals America, Inc., GlaxoSmithKline plc. Y. Sun: None. S. Raghavan: None. E. M. Litkowski: None. B. T. Legvold: None. M. K. Rhee: Research Support; Kowa Research Institute, Inc. M. Vujkovic: None. P. Reaven: Research Support; Dexcom, Inc. A. Leong: Other Relationship; Merck & Co., Inc. Funding National Institutes of Health (U01DK098245, P30DK111024, AI156161, DK127083); U.S. Department of Veterans Affairs (I01-CX001025, I01-BX005831, I01-BX003340, CX001899, I01CX001737)
Read full abstract