A Comparison of Inflammatory Markers in Depressed and Nondepressed Smokers
Authors:
- Sandra Odebrecht Vargas NunesSNSandra Odebrecht Vargas Nunes
- M. R. P. D. CastroMCM. R. P. D. Castro
- Seetal DoddSDSeetal Dodd
- Michael BerkMBMichael Berk
- 16 December 2011
- journal article
- research article
- Published by Oxford University Press (OUP) in Nicotine & Tobacco Research
- Vol. 14 (5) , 540-546
Abstract
Introduction: Both smoking and depression have been associated with increased inflammatory markers. As there are few studies on inflammatory markers that distinguish between depressed and nondepressed smokers, it is unclear if there is a cumulative impact of these mediators of inflammation. The aim of this study was to investigate inflammatory markers in tobacco smokers and compare depressed and nondepressed smokers. Methods: Smokers (n = 155) were recruited from the Cigarette Smoking Cessation Service, Londrina. Mental health status was assessed using the Diagnostic Interview for Research, in accordance with the International Classification of the Disorders-10th (ICD-10). Demographic information was collected by self-report questionnaire, and the Fagerström Test for Nicotine Dependence was administered. Blood specimens were simultaneously collected and measured for C-reactive protein (hs-CRP), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). Results: Depressed smokers had significantly higher levels of hs-CRP (p = .05), IL-6 (p = .039), and TNF-α (p = .021) compared with nondepressed smokers. Depressed smokers were also significantly more likely than nondepressed smokers to have been hospitalized in the previous month (p < .032), to suffer from cardiovascular disease (p < .001) and lung disease (p < .003), and to have more work-related disability (p = .001). Conclusions: These findings demonstrate that depressed smokers had higher hs-CRP, IL-6, and TNF-α levels than nondepressed smokers and had worse physical health outcomes and greater work-related disability. This may have important implications in identifying shared risk pathways for depressive and somatic disorders.Keywords
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