Television viewing time, independent of leisure time physical activity, has cross-sectional relationships with the metabolic syndrome and its individual components. We examined whether baseline and 5-yr changes in self-reported television viewing time are associated with changes in continuous biomarkers of cardiometabolic risk (waist circumference, triglycerides, HDL-cholesterol, systolic and diastolic blood pressure, fasting plasma glucose, and a clustered cardiometabolic risk score) in Australian adults.
The Australian Diabetes, Obesity and Lifestyle Study (AusDiab) is a prospective, population-based cohort study with biological, behavioral, and demographic measures collected in 1999-2000 and 2004-2005. Noninstitutionalized adults aged ≥25 yr were measured at baseline (11,247; 55% of those completing an initial household interview); 6400 took part in the 5-yr follow-up biomedical examination, and 3846 met the inclusion criteria for this analysis. Multiple linear regression analysis was used, and unstandardized B coefficients (95% confidence intervals (CI)) are provided.
Baseline television viewing time (10 h·wk−1 unit) was not significantly associated with change in any of the biomarkers of cardiometabolic risk. Increases in television viewing time over 5 yr (10 h·wk−1 unit) were associated with increases in waist circumference (men: 0.43 cm, 95% CI = 0.08-0.78 cm, P = 0.02; women: 0.68 cm, 95% CI = 0.30-1.05, P < 0.001), diastolic blood pressure (women: 0.47 mm Hg, 95% CI = 0.02-0.92 mm Hg, P = 0.04), and the clustered cardiometabolic risk score (women: 0.03, 95% CI = 0.01-0.05, P = 0.007). These associations were independent of baseline television viewing time and baseline and change in physical activity and other potential confounders.
These findings indicate that an increase in television viewing time is associated with adverse cardiometabolic biomarker changes. Further prospective studies using objective measures of several sedentary behaviors are required to confirm causality of the associations found.
1Cancer Prevention Research Centre, School of Population Health, the University of Queensland, Herston, Queensland, AUSTRALIA; 2Medical Research Council Epidemiology Unit, Cambridge, England, UNITED KINGDOM; 3Baker IDI Heart and Diabetes Institute, Melbourne, AUSTRALIA; 4Institute of Health and Biomedical Innovation and School of Public Health, Queensland University of Technology, Brisbane, AUSTRALIA; and 5School of Exercise and Nutrition Sciences, Deakin University, Melbourne, AUSTRALIA
Address for correspondence: Neville Owen, Ph.D., Cancer Prevention Research Centre, School of Population Health, Level 3, Public Health Building, The University of Queensland, Herston Road, Herston, Queensland 4006, Australia; E-mail: firstname.lastname@example.org.
Submitted for publication August 2009.
Accepted for publication January 2010.