Álvaro Camacho1, Britta Larsen2, Robyn L McClelland3, Cindy Morgan2, Michael H Criqui2, Mary Cushman4, Matthew A Allison2. 1. Department of Family & Preventive Medicine, University of California, San Diego, USA. Electronic address: acamacho@ucsd.edu. 2. Department of Family & Preventive Medicine, University of California, San Diego, USA. 3. Department of Biostatistics, University of Washington, Seattle, WA, USA. 4. Department of Medicine, University of Vermont, Burlington, VT, USA.
Abstract
OBJECTIVE: Depressive symptoms are associated with inflammation yet the association between inflammation and different levels of depression remains unclear. Therefore, we studied the association of subsyndromal and depressive symptoms with inflammatory markers in a large multi-ethnic cohort. METHODS: C-reactive protein (CRP) (n=6269), interleukin-6 (IL-6) (n=6135) and tumor necrosis factor-alpha (TNF-α) (n=1830) were measured in selected participants from the multi-ethnic study of atherosclerosis (MESA). Subsyndromal depressive symptoms were defined as a CES-D value from 8 to 15, depressive symptoms as a CES-D≥16 and normal as a CES-D≤7. Depressive states (subsyndromal and depressed) were entered into multivariable linear regression models incrementally adjusting for demographic, behavioral, biologic and comorbidities. RESULTS: Among 6289 participants not taking antidepressants and free from CVD, the mean age was 62.2, while 52% were women, 36.4% were Caucasian, 28.9% African-American, 22.3% Hispanics and 12.4% Chinese-American. Of the total, 24.2% had subsyndromal depression and 11.8% had depressive symptoms. Compared to the non-depressed group and after controlling for demographics, there was no association between both subsyndromal and depressive symptoms with logCRP (β=-0.01, p=0.80 and β=-0.05, p=0.25 respectively), logIL-6 (β=0.01, p=0.71 and β=-0.04, p=0.07 respectively) and logTNF-α (β=-0.03, p=0.29 and β=0.06, p=0.18 respectively). Moreover, fully adjusted models showed no significant associations for logIL-6 and logTNF-α and the different depressive categories. However, with full adjustment, we found a significant inverse association between depressive symptoms and lnCRP (β=-0.10, p=0.01) that was not present for subsyndromal depression (β=-0.05, p=0.11). CONCLUSION: Among participants not taking anti-depressants, subsyndromal depression is not associated with inflammation. However, depressive symptoms measured by CES-D≥16 are associated with a lower inflammation (CRP).
OBJECTIVE:Depressive symptoms are associated with inflammation yet the association between inflammation and different levels of depression remains unclear. Therefore, we studied the association of subsyndromal and depressive symptoms with inflammatory markers in a large multi-ethnic cohort. METHODS:C-reactive protein (CRP) (n=6269), interleukin-6 (IL-6) (n=6135) and tumor necrosis factor-alpha (TNF-α) (n=1830) were measured in selected participants from the multi-ethnic study of atherosclerosis (MESA). Subsyndromal depressive symptoms were defined as a CES-D value from 8 to 15, depressive symptoms as a CES-D≥16 and normal as a CES-D≤7. Depressive states (subsyndromal and depressed) were entered into multivariable linear regression models incrementally adjusting for demographic, behavioral, biologic and comorbidities. RESULTS: Among 6289 participants not taking antidepressants and free from CVD, the mean age was 62.2, while 52% were women, 36.4% were Caucasian, 28.9% African-American, 22.3% Hispanics and 12.4% Chinese-American. Of the total, 24.2% had subsyndromal depression and 11.8% had depressive symptoms. Compared to the non-depressed group and after controlling for demographics, there was no association between both subsyndromal and depressive symptoms with logCRP (β=-0.01, p=0.80 and β=-0.05, p=0.25 respectively), logIL-6 (β=0.01, p=0.71 and β=-0.04, p=0.07 respectively) and logTNF-α (β=-0.03, p=0.29 and β=0.06, p=0.18 respectively). Moreover, fully adjusted models showed no significant associations for logIL-6 and logTNF-α and the different depressive categories. However, with full adjustment, we found a significant inverse association between depressive symptoms and lnCRP (β=-0.10, p=0.01) that was not present for subsyndromal depression (β=-0.05, p=0.11). CONCLUSION: Among participants not taking anti-depressants, subsyndromal depression is not associated with inflammation. However, depressive symptoms measured by CES-D≥16 are associated with a lower inflammation (CRP).
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