601-P: Diabetes Self-Efficacy—Longitudinal Relationships with Diabetes Overall Self-Management, Medication Adherence, Diabetes Distress, and Glycemic Control in Adults with Type 2 Diabetes



Introduction and Objective: Self-efficacy and diabetes distress are inextricably linked to coping with diabetes. The role of diabetes distress in the relationship between diabetes self-efficacy and glycemic control in T2DM over time is understudied. The objective of this study was to evaluate the longitudinal associations of self-efficacy with overall diabetes self-management, medication adherence, diabetes distress, and glycemic control.Methods: Within the context of a randomized controlled trial comparing telephonic self-management support to enhanced standard of care among 812 predominantly socioeconomically disadvantaged ethnic minority adults with suboptimal control of T2DM (HbA1c >7.5%), we investigated between-group differences in self-efficacy and examined self-management, medication adherence, and diabetes distress, self-reported on validated scales at 6-months, as potential mediators between baseline diabetes self-efficacy and HbA1c at 12-months using multiple-linear regression.Results: Participants (M[SD] age = 59.2 [10.8], M[SD] HbA1c = 9.3 [1.8], 57% females, and 86% Hispanic/Latino) were mostly less educated (75% less than grade 12 or GED ). An increase of 4.19 points for self-efficacy relative to the baseline in the intervention group was significant (95% CI = -6.08, -2.30; p <.001 ) at 12-month follow-up. There was a significant indirect effect of baseline self-efficacy on lowered 12-month HbA1c through increased medication adherence at 6-month follow-up (ab = -0.005, 95% CI = -0.007, -0.003; p <.001). Results did not support overall self-management or diabetes distress as mediators of self-efficacy.Conclusion: These associations are consistent with Bandura’s self-efficacy theory and suggest that diabetes self-efficacy is responsive to intervention and predictive of glycemic outcomes among disadvantaged adults with suboptimal control of T2DM.

Disclosure

R. Fang: None. C. Schechter: None. E.A. Walker: None. J.S. Gonzalez: None.

Funding

This study was supported by grant R 18 DK098742 from the National Institutes of Health. This study was also partially supported by the Einstein Mount Sinai Diabetes Research Center (P30 DK020541) and the New York Regional Center for Diabetes Translation Research (P30 DK111022). Dr. Gonzalez is supported by grants R01 DK104845, R01 DK121298, R01 DK121896 and R18 DK098742 from the National Institutes of Health.



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