641-P: Diabetes Distress and Blood Glucose in the Function and Emotion in Everyday Life with Type 1 Diabetes (FEEL-T1D) Study—Which Comes First, the Chicken or the Egg?

Introduction: Diabetes Distress (DD) has been consistently linked with suboptimal blood glucose in T1D. However, prior studies have rarely used methods that can adequately evaluate the directionality of this relationship. This study paired ecological momentary assessment (EMA) and continuous glucose monitoring (CGM) to examine the relative strength of lagged effects of blood glucose (BG) on DD and vice versa. Methods: FEEL-T1D participants (N=182, 40±14 yrs, 54% women, 41% Latino, 29% White, 15% Black) wore blinded CGM for 10-14 days and completed 5-6 smartphone EMA surveys per day. Using multilevel cross-lagged panel modeling, we evaluated within-person lagged effects from momentary ratings of DD (scale: 0-100) to various BG metrics (BG average, Time in Range [TIR, 70-180 mg/dL], % time 181-250 mg/dL, % time > 250 mg/dL, % time 54-69 mg/dL, % time <54 mg/dL, and coefficient of variation [CV]) over the subsequent 3 hours and between 3 hours of BG metrics and subsequent DD ratings. Results: Unstandardized within-person parameter estimates and 95% confidence intervals for lagged effects of BG on subsequent DD ratings were significant for average BG (0.01; 0.01, 0.02), TIR (−0.01; −0.02, −0.004), % time 181-250 mg/dL (0.01; 0.001, 0.02), and % time > 250 mg/dL (0.02; 0.01, 0.04), but not for CV or % time in low BG; as expected, higher BG predicted subsequently higher DD. Lagged effects of DD ratings on subsequent 3-hour BG metrics were only significant for % time 54-69 mg/dL (−0.02; −0.04, −0.002); unexpectedly, DD was predictive of less % time with low BG. Conclusion: These novel findings reveal that the experience of DD is significantly influenced by preceding suboptimal BG levels, particularly high BG, even when individuals are blinded to their BG values. Results suggest that interventions that improve BG levels may reduce DD but do not support the hypothesis that reductions in DD will conversely lead to improvements in BG. Disclosure J.S.Gonzalez: Consultant; Virta Health Corp. P.Lee: None. S.Schneider: None. E.Pyatak: Research Support; Abbott Diabetes. R.Hernandez: None. D.Spruijt-metz: None. C.J.Hoogendoorn: None. G.Crespo-ramos: None. S.Agarwal: Advisory Panel; Medtronic, Consultant; Beta Bionics, Inc., Research Support; Abbott Diabetes, Dexcom, Inc. J.P.Crandall: Research Support; Abbott Diabetes. A.L.Peters: Advisory Panel; Abbott Diabetes, Medscape, Novo Nordisk, Vertex Pharmaceuticals Incorporated, Zealand Pharma A/S, Research Support; Abbott Diabetes, Dexcom, Inc., Insulet Corporation, Stock/Shareholder; Omada Health, Inc., Livongo. L.T.Pham: None. Funding National Institutes of Health (R01DK121298, P30DK111022)