Anthony T Vesco1, Kelsey R Howard2, Lindsay M Anderson3, Jaclyn L Papadakis4, Korey K Hood5, Jill Weissberg-Benchell4. 1. Pritzker Department of Psychiatry and Behavioral Health, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois, United States; Department of Psychiatry & Behavioral Sciences, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States. Electronic address: avesco@luriechildrens.org. 2. Pritzker Department of Psychiatry and Behavioral Health, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois, United States. 3. Department of Psychology, Barrow Neurological Institute, Phoenix Children's Hospital, Phoenix, Arizona, United States. 4. Pritzker Department of Psychiatry and Behavioral Health, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois, United States; Department of Psychiatry & Behavioral Sciences, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States. 5. Department of Pediatrics, Stanford University School of Medicine, Stanford, California, United States.
Abstract
OBJECTIVES: In this study, we examined the indirect effects of anxiety on glycated hemoglobin (A1C) via automatic negative thinking and diabetes distress among adolescents with type 1 diabetes (T1D) during the follow-up interval of a randomized controlled trial of an intervention targeting resilience promotion/depression prevention. METHODS: Adolescents (N=264) participating in the Supporting Teen Problem Solving clinical trial were included and assessed at 8, 12, 16 and 28 months postbaseline. A serial, double-mediation model was used to examine path effects from anxiety to A1C through automatic negative thinking, through diabetes distress and through both automatic negative thinking and diabetes distress. Relevant demographic and clinical covariates were included. RESULTS: Anxiety significantly predicted increases in both automatic negative thinking and diabetes distress. Automatic negative thinking was not found to mediate the association between anxiety and A1C, but diabetes distress did mediate the association. The double-mediation path through automatic negative thinking and diabetes distress together was significant. The indirect effect of anxiety on A1C through diabetes distress was significant and greater than the indirect effect of the double-mediator path. Anxiety did not predict A1C independent of its effects on automatic negative thinking and diabetes distress. Inclusion of demographic covariates did not substantively change the results. CONCLUSIONS: Analyses suggest that automatic negative thinking and diabetes distress mediate the relationship between anxiety and A1C among adolescents with T1D. Diabetes distress appears to be a robust factor linking anxiety to A1C. Diabetes distress should be further examined as a mediator of glycemic variability in anxious youth with T1D.
OBJECTIVES: In this study, we examined the indirect effects of anxiety on glycated hemoglobin (A1C) via automatic negative thinking and diabetes distress among adolescents with type 1 diabetes (T1D) during the follow-up interval of a randomized controlled trial of an intervention targeting resilience promotion/depression prevention. METHODS: Adolescents (N=264) participating in the Supporting Teen Problem Solving clinical trial were included and assessed at 8, 12, 16 and 28 months postbaseline. A serial, double-mediation model was used to examine path effects from anxiety to A1C through automatic negative thinking, through diabetes distress and through both automatic negative thinking and diabetes distress. Relevant demographic and clinical covariates were included. RESULTS: Anxiety significantly predicted increases in both automatic negative thinking and diabetes distress. Automatic negative thinking was not found to mediate the association between anxiety and A1C, but diabetes distress did mediate the association. The double-mediation path through automatic negative thinking and diabetes distress together was significant. The indirect effect of anxiety on A1C through diabetes distress was significant and greater than the indirect effect of the double-mediator path. Anxiety did not predict A1C independent of its effects on automatic negative thinking and diabetes distress. Inclusion of demographic covariates did not substantively change the results. CONCLUSIONS: Analyses suggest that automatic negative thinking and diabetes distress mediate the relationship between anxiety and A1C among adolescents with T1D. Diabetes distress appears to be a robust factor linking anxiety to A1C. Diabetes distress should be further examined as a mediator of glycemic variability in anxious youth with T1D.
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