Priya Palta1, Sherita Hill Golden2, Jeanne A Teresi3, Walter Palmas4, Paula Trief5, Ruth S Weinstock6, Steven Shea7, Jennifer J Manly8, Jose A Luchsinger9. 1. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA; Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. 2. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA; Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins University, Baltimore, MD, USA; Department of Medicine, Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 3. Research Division, Hebrew Home at Riverdale, Bronx, NY, USA; Morris W. Stroud, III, Center for Studies on Quality of Life, and New York State Psychiatric Institute, Columbia University, New York, NY, USA. 4. Department of Medicine, Division of General Medicine, Columbia University School of Medicine, New York, NY, USA. 5. Department of Psychiatry and Behavioral Sciences, SUNY Upstate Medical University, Syracuse, NY, USA; Department of Medicine, SUNY Upstate Medical University, Syracuse, NY, USA. 6. Department of Medicine, SUNY Upstate Medical University, Syracuse, NY, USA. 7. Department of Medicine, Division of General Medicine, Columbia University School of Medicine, New York, NY, USA; Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, USA. 8. Department of Neurology and Taub Institute, Division of Cognitive Neuroscience, Columbia University College of Physician and Surgeons, NY, USA; Gertrude H. Sergievksy Center, Columbia University Medical Center, New York, NY. 9. Department of Medicine, Division of General Medicine, Columbia University School of Medicine, New York, NY, USA; Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, USA. Electronic address: jal94@columbia.edu.
Abstract
AIMS: We investigated the longitudinal association of depression, with and without cognitive dysfunction, with hemoglobin A1c (HbA1c), systolic blood pressure (SBP), and low-density lipoprotein (LDL) in a predominantly minority cohort. METHODS: There were 613 participants. Presence of depression was defined by a score ≥7 on the Short-CARE depression scale. We tested participants for executive dysfunction using the Color Trails Test (CTT), part 2, and for memory dysfunction using the total recall task of the Selective Reminding Test (TR-SRT). We classified performance in these tests as abnormal based on standardized score cutoffs (<16th percentile and one standard deviation below the sample mean). Random effects models were used to compare repeated measures of the diabetes control measures between those with depression versus those without depression and ever versus never cognitively impaired. RESULTS:Baseline depression was present in 36% of participants. Over a median follow-up of 2 years, depression was not related to worse HbA1c, SBP, or LDL. The presence of (1) abnormal performance on a test of executive function and depression (n=57) or (2) abnormal performance on a test of verbal recall and depression (n=43) was also not associated with clinically significant worse change in diabetes control. CONCLUSIONS: Depression, with or without low performance in tests of executive function and memory, may not affect clinically significant measures of diabetes control in the elderly.
RCT Entities:
AIMS: We investigated the longitudinal association of depression, with and without cognitive dysfunction, with hemoglobin A1c (HbA1c), systolic blood pressure (SBP), and low-density lipoprotein (LDL) in a predominantly minority cohort. METHODS: There were 613 participants. Presence of depression was defined by a score ≥7 on the Short-CARE depression scale. We tested participants for executive dysfunction using the Color Trails Test (CTT), part 2, and for memory dysfunction using the total recall task of the Selective Reminding Test (TR-SRT). We classified performance in these tests as abnormal based on standardized score cutoffs (<16th percentile and one standard deviation below the sample mean). Random effects models were used to compare repeated measures of the diabetes control measures between those with depression versus those without depression and ever versus never cognitively impaired. RESULTS: Baseline depression was present in 36% of participants. Over a median follow-up of 2 years, depression was not related to worse HbA1c, SBP, or LDL. The presence of (1) abnormal performance on a test of executive function and depression (n=57) or (2) abnormal performance on a test of verbal recall and depression (n=43) was also not associated with clinically significant worse change in diabetes control. CONCLUSIONS:Depression, with or without low performance in tests of executive function and memory, may not affect clinically significant measures of diabetes control in the elderly.
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