Objective: To determine whether glycemia early in the course of type 1 diabetes changed between 2002 and 2016 across discrete youth cohorts.

Research Design and Methods: Data from 3,956 youth in the SEARCH for Diabetes in Youth study were used to test whether glycemia worsened between 2002 and 2016 among successive cohorts of youth with type 1 diabetes examined within 30 months of diagnosis. We used linear regression for hemoglobin A1c (HbA1c) and logistic regression for poor glycemic control (HbA1c>9%) stratified by diabetes duration (<6 months, 6-12 months, and 12-30 months) at the time of measurement. Models included survey weights and were adjusted for potential demographic confounders.

Results: Fully adjusted models revealed that mean HbA1c and frequency of poor glycemic control remained stable over time across successive youth cohorts with type 1 diabetes. Overall mean unadjusted HbA1c was 7.9% ± 1.5 (63 mmol/mol ± 16.4) in 2002 and 7.8% ± 2.4 (62 mmol/mol ± 26.2) in 2016, p=0.6 for trend. Estimates from weighted linear regression models found no overall change in HbA1c with index year, but a small linear reduction in HbA1c with each index year in the <6 months diabetes duration stratum, which was no longer statistically significant after adjusting for age, sex, race/ethnicity, and clinical site. No time trends were found for either of the other two duration strata (6-12 and 12-30 months). Although interaction effects with race/ethnicity and gender were not detected, the proportion of youth with poor glycemic control was higher among non-white (mean 28.9%, range 24.9-33.7%) than among white youth (mean 12.5%, range 8.8-17.8%) across all years.

Conclusions: HbA1c levels remained stable but higher than recommended across discrete cohorts of SEARCH youth with type 1 diabetes duration ≤ 30 months, particularly among non-white youth. Future studies should elucidate predictors of elevated glycemia among youth early in the course of type 1 diabetes.


D. Igudesman: None. F. Malik: None. E. J. Mayer-davis: None. B. A. Reboussin: None. K. J. Souris: None. C. Pihoker: None. L. M. Dolan: None. S. Saydah: None. D. Dabelea: None. N. Clouet-foraison: None. S. M. Marcovina: None.


National Institute for Health Research (1UC4DK108173-01); Centers for Disease Control and Prevention (RFPDP15-002); Kaiser Permanente Southern California (U18DP006133, U48/CCU919219, U01DP000246, U18DP002714); University of Colorado Denver (U18DP006139, U48/CCU819241-3, U01DP000247, U18DP000247-06A1); Cincinnati Children’s Hospital Medical Center (U18DP006134, U48/CCU519239, U01DP000248, 1U18DP002709); University of North Carolina at Chapel Hill (U18DP006138, U48/CCU419249, U01DP000254, U18DP002708); Seattle Children’s Hospital (U18DP006136, U58/CCU019235-4, U01DP000244, U18DP002710-01); Wake Forest University School of Medicine (U18DP006131, U48/CCU919219, U01DP000250, 200-2010-35171); South Carolina Clinical and Translational Research Institute at the Medical University of South Carolina (UL1TR001450); Seattle Children’s Hospital and the University of Washington (UL1TR00423); University of Colorado Pediatric Clinical and Translational Research Center (UL1TR000154); Barbara Davis Center for Diabetes at the University of Colorado Denver (P30-DK-57516); University of Cincinnati (UL1TR001425); Ohio Department of Health

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