Television (TV) viewing time is associated with increased risk of all-cause, cardiovascular and cancer mortality. Although TV time is detrimentally associated with key inflammatory markers, the associations of TV time with other inflammatory-related mortality (with a predominant inflammatory, oxidative or infectious component, but not attributable to cancer or cardiovascular causes), are unknown.
Among 8933 Australian adults (4593 never-smokers) from the baseline (1999–2000) Australian Diabetes, Obesity and Lifestyle Study (median follow-up, 13.6 yr), we examined TV time in relation to noninflammatory and inflammatory-related mortality (not attributable to cancer or cardiovascular causes, hereafter “inflammatory-related” mortality). Because smoking has a significant inflammatory component, we also examined this relationship in never-smokers.
Of 896 deaths, 248 were attributable to cardiovascular disease, 346 to cancer, 130 to other inflammatory-related causes (71 for never-smokers), and 172 to noninflammatory-related causes (87 for never-smokers). After multivariate adjustment for age, sex, education, household income, smoking status, alcohol intake, energy intake, diet, and cardiometabolic risk biomarkers (model 3), every additional hours per day of TV time was associated with increased risk of inflammatory-related mortality in the overall population (hazard ratio, 1.12; 95% confidence interval, 1.00–1.25) and in never-smokers (1.18; 1.00, 1.40). These results were attenuated after additional adjustment for leisure-time physical activity. After multivariate adjustment (model 3), no association was observed for noninflammatory mortality in the overall population (0.95; 0.85, 1.07), but risk tended to decrease for never-smokers (0.85; 0.75, 1.02).
In summary, before adjustment for leisure-time physical activity, TV time was associated with increased risk of inflammatory-related mortality. This is consistent with the hypothesis that high TV viewing may be associated with a chronic inflammatory state.
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1Baker Heart and Diabetes Institute, Melbourne, VIC, AUSTRALIA; 2Department of Physiology, School of Medicine, Nursing and Health Sciences, Monash University, Melbourne, VIC, AUSTRALIA; 3School of Health and Biomedical Sciences, RMIT University, Bundoora, Melbourne, AUSTRALIA; 4Menzies School of Health Research, Darwin, NT, AUSTRALIA; 5Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD; 6Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, Bethesda, MD; 7Melbourne School of Population and Global Health, University of Melbourne, VIC, AUSTRALIA; 8Swinburne University of Technology, Melbourne VIC, AUSTRALIA; 9School of Public Health, University of Queensland, Brisbane, QLD, AUSTRALIA; 10School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia; and 11Mary MacKillop Institute for Health Research, Australian Catholic University, Melbourne, VIC, AUSTRALIA
Address for correspondence: Doctor Megan Grace, Ph.D., Baker Heart and Diabetes Institute, Level 4 Alfred Centre, 99 Commercial Road, Melbourne 3004, Australia; E-mail: email@example.com.
Submitted for publication January 2017.
Accepted for publication April 2017.
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