Background: Among people with diabetes, depression is more common and is associated with greater morbidity and mortality. A better understanding of mechanisms underlying the link between poor health and depression is needed. Pain and functional impairment may account for the effect of poor health on depression in diabetes.
Purpose: The purpose of the study was to examine whether pain and functional impairment mediate the association between diabetes-related medical symptoms and depression in type 2 diabetes.
Method: Adults diagnosed with type 2 diabetes (N = 77) completed the following measures: Patient Health Questionnaire (PHQ), Diabetes Symptom Checklist (DSC), and Medical Outcomes Study 12-item Short-Form Health Survey (SF-12). Body mass index (BMI) was computed using height and weight data from medical records. Mediation and linear regression analyses were conducted.
Results: Pain and functional impairment made significant, independent contributions to depression. Functional impairment mediated the link between diabetes-related medical symptoms and depression. Pain mediated the association between higher BMI and depression.
Conclusion: Pain and functional impairment appear to play important, independent roles in depression in type 2 diabetes. Mediation analyses suggest the following: 1. diabetes-related medical problems increase functional impairment, which in turn leads to greater depression; and 2. the burden of carrying greater body mass (higher BMI) increases pain, which leads to increased depression.
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http://dx.doi.org/10.1007/s12529-011-9210-5 | DOI Listing |
Cell Commun Signal
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Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, 100191, China.
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School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong S.A.R., China.
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January 2025
Laboratory of Human Physiology and Pathology, Faculty of Pharmaceutical Sciences, Teikyo University, Tokyo, Japan.
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January 2025
Institute of Animal Reproduction and Food Research, Polish Academy of Sciences in Olsztyn, 10-748, Olsztyn, Poland.
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The involvement of B lymphocytes in the pathogenesis of rheumatoid arthritis (RA) is well-established, with their early and aberrant activation being a crucial factor. However, the mechanisms underlying this abnormal activation in RA remain incompletely understood. In this study, we identified a significant reduction in MAPK4 expression in both RA patients and collagen-induced arthritis (CIA) mouse models, which correlates with disrupted B cell activation.
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