Rita Rastogi Kalyani1, Nan Ji2, Mercedes Carnethon3, Alain G Bertoni4, Elizabeth Selvin5, Edward W Gregg6, Mario Sims7, Sherita Hill Golden8. 1. Department of Medicine, Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, MD 21287, USA; Welch Center for Prevention, Epidemiology, and Clinical Research, 2024 East Monument Street, Suite 333, Baltimore, MD 21287, USA. Electronic address: rrastogi@jhmi.edu. 2. Department of Medicine, Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, MD 21287, USA. Electronic address: nancyji0702@gmail.com. 3. Department of Preventive Medicine-Epidemiology, Northwestern University Feinberg School of Medicine, 680 N Lake Shore Drive, Suite 1400, Chicago, IL 60611, USA. Electronic address: carnethon@northwestern.edu. 4. Department of Epidemiology and Prevention Wake Forest School of Medicine, 1 Medical Center Blvd, Winston-Salem, NC 27157, USA. Electronic address: abertoni@wfubmc.edu. 5. Department of Medicine, Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, MD 21287, USA; Welch Center for Prevention, Epidemiology, and Clinical Research, 2024 East Monument Street, Suite 333, Baltimore, MD 21287, USA. Electronic address: lselvin@jhsph.edu. 6. Centers for Disease Control, Division of Diabetes Translation, 4770 Buford Hwy., NE Mailstop K-10, Atlanta, GA 30341, USA. Electronic address: edg7@cdc.gov. 7. Department of Medicine, University of Mississippi Medical Center, Jackson Medical Mall Suite 701, 350 W. Woodrow Wilson Drive, Jackson, MS 39213, USA. Electronic address: msims2@umc.edu. 8. Department of Medicine, Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, MD 21287, USA; Welch Center for Prevention, Epidemiology, and Clinical Research, 2024 East Monument Street, Suite 333, Baltimore, MD 21287, USA. Electronic address: sahill@jhmi.edu.
Abstract
AIMS: To investigate the degree to which comorbid depression contributes to the relationship of diabetes with functional disability in African Americans (AAs), a population at high-risk for complications. METHODS: We examined 2989 African Americans (AAs) in the Jackson Heart Study who had diabetes and depressive symptoms (CES-D) assessed at baseline. Overall functional disability was defined as the inability to perform at least one task of daily living. Multivariable logistic regression models explored the association of diabetes and depressive symptoms with functional disability. RESULTS: Prevalence of overall functional disability was highest with both diabetes and depressive symptoms (54%), similar with diabetes alone (31%) or depressive symptoms alone (33%), and lowest with neither (15%). Adjusting for demographics, smoking, BMI, cardiovascular comorbidities, and hsCRP, the association of depressive symptoms alone (OR=2.30,95% CI 1.75-3.03) and both diabetes and depressive symptoms (OR=2.75,1.88-4.04) with overall functional disability was significant, but not for diabetes alone (OR=1.26,0.95-1.67), compared to neither. In regression analyses including any diabetes and any depressive symptoms together in models, the main effect of depressive symptoms but not diabetes was associated with overall functional disability, and the interaction term was not significant (p-value=0.84). CONCLUSIONS: Functional disability was highest among AAs who have both diabetes and depressive symptoms; the latter was a stronger contributor. Future studies should explore mechanisms underlying functional disability in diabetes, particularly the role of depression.
AIMS: To investigate the degree to which comorbid depression contributes to the relationship of diabetes with functional disability in African Americans (AAs), a population at high-risk for complications. METHODS: We examined 2989 African Americans (AAs) in the Jackson Heart Study who had diabetes and depressive symptoms (CES-D) assessed at baseline. Overall functional disability was defined as the inability to perform at least one task of daily living. Multivariable logistic regression models explored the association of diabetes and depressive symptoms with functional disability. RESULTS: Prevalence of overall functional disability was highest with both diabetes and depressive symptoms (54%), similar with diabetes alone (31%) or depressive symptoms alone (33%), and lowest with neither (15%). Adjusting for demographics, smoking, BMI, cardiovascular comorbidities, and hsCRP, the association of depressive symptoms alone (OR=2.30,95% CI 1.75-3.03) and both diabetes and depressive symptoms (OR=2.75,1.88-4.04) with overall functional disability was significant, but not for diabetes alone (OR=1.26,0.95-1.67), compared to neither. In regression analyses including any diabetes and any depressive symptoms together in models, the main effect of depressive symptoms but not diabetes was associated with overall functional disability, and the interaction term was not significant (p-value=0.84). CONCLUSIONS: Functional disability was highest among AAs who have both diabetes and depressive symptoms; the latter was a stronger contributor. Future studies should explore mechanisms underlying functional disability in diabetes, particularly the role of depression.
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