OBJECTIVE: Up-regulated levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) are common to both type 2 diabetes mellitus (T2DM) and elevated depressive symptoms, yet little attention has been given to the biological mechanisms associated with these co-morbidities. This study examined the association between inflammation and both T2DM and elevated depressive symptoms. METHODS: Baseline data were analyzed from 3009 adults, aged 70-79, participating in the Health, Aging, and Body Composition Study. Diabetes was assessed per self-report, medication use, fasting glucose and/or glucose tolerance tests. Elevated depressive symptoms were categorized using the Center for Epidemiologic Studies Depression scale (cut-score≥20). Log-transformed IL-6, TNF-α, and CRP were analyzed using ANCOVA. RESULTS: Participants with T2DM and elevated depressive symptoms (T2DM+DEP n=14) demonstrated significantly (p<.05) higher IL-6 compared to (T2DM Only n=628), (DEP Only n=49), and (No T2DM or DEP n=2067) groups following covariate adjustment. Similarly, participants with T2DM+DEP (n=14) had significantly (p<.05) higher CRP, after covariate adjustment, compared to DEP Only (n=50) and No T2DM or DEP groups (n=2153). No association was observed for TNF-α. CONCLUSIONS: These findings provide evidence that inflammation is associated with T2DM and elevated depressive symptoms. Participants with T2DM+DEP demonstrated the highest IL-6 levels compared to all other groups. Greater CRP levels were also observed in T2DM, but not elevated depressive symptoms, which may suggest that differential associations between T2DM and depressive symptoms exist for various inflammatory markers. Further investigation into these associations could aid in understanding the biological pathways underlying both T2DM and depressive symptoms.
OBJECTIVE: Up-regulated levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) are common to both type 2 diabetes mellitus (T2DM) and elevated depressive symptoms, yet little attention has been given to the biological mechanisms associated with these co-morbidities. This study examined the association between inflammation and both T2DM and elevated depressive symptoms. METHODS: Baseline data were analyzed from 3009 adults, aged 70-79, participating in the Health, Aging, and Body Composition Study. Diabetes was assessed per self-report, medication use, fasting glucose and/or glucose tolerance tests. Elevated depressive symptoms were categorized using the Center for Epidemiologic Studies Depression scale (cut-score≥20). Log-transformed IL-6, TNF-α, and CRP were analyzed using ANCOVA. RESULTS:Participants with T2DM and elevated depressive symptoms (T2DM+DEP n=14) demonstrated significantly (p<.05) higher IL-6 compared to (T2DM Only n=628), (DEP Only n=49), and (No T2DM or DEP n=2067) groups following covariate adjustment. Similarly, participants with T2DM+DEP (n=14) had significantly (p<.05) higher CRP, after covariate adjustment, compared to DEP Only (n=50) and No T2DM or DEP groups (n=2153). No association was observed for TNF-α. CONCLUSIONS: These findings provide evidence that inflammation is associated with T2DM and elevated depressive symptoms. Participants with T2DM+DEP demonstrated the highest IL-6 levels compared to all other groups. Greater CRP levels were also observed in T2DM, but not elevated depressive symptoms, which may suggest that differential associations between T2DM and depressive symptoms exist for various inflammatory markers. Further investigation into these associations could aid in understanding the biological pathways underlying both T2DM and depressive symptoms.
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