Causal Relationship between Television Viewing Time, Cardiovascular Diseases, and Potential Mechanisms

Abstract

Background:

As the predominant leisure-time sedentary behavior, television viewing was documented to increase cardiovascular diseases in observational studies, yet the causal relationship and potential mechanisms remain to be determined.

Objectives:

To systematically investigate the causal relationship between television viewing time, cardiovascular diseases, and potential mechanisms.

Methods:

We conducted a two-sample Mendelian randomization (MR) analysis to estimate causal associations with cardiovascular diseases and biomarkers of cardiometabolic risk. The random inverse-variance weighted method was used as the primary estimate. To account for multiple comparisons, a Bonferroni correction p value for cardiovascular diseases and biomarkers of cardiometabolic risk was 0.0045 and 0.0024, respectively.

Results:

Genetically instrumented television viewing time was associated with higher risks of type 2 diabetes (odd ratio [OR]=2.51; 95% confidence interval [CI]: 1.89-3.33; p<0.00001), hypertension (OR=2.11; 95% CI: 1.67-2.66; p<0.00001), coronary heart disease (OR=1.53; 95% CI: 1.23-1.91; p=0.00015), and heart failure (OR=1.42; 95% CI: 1.18-1.70; p=0.00017). Suggestive evidence of harmful associations was also observed for peripheral artery disease (OR=1.58; 95% CI: 1.07-2.34; p=0.02253) and ischemic stroke (OR=1.34; 95% CI: 1.10-1.63; p=0.00328). Biomarkers of cardiometabolic risk, including interleukin 10, leptin, visceral adipose, abdominal subcutaneous adipose, liver fat, body mass index, waist circumference, triglycerides, and C-reactive protein, were increased. Systolic blood pressure, heart rate, low-density lipoprotein, and total cholesterol were potentially increased while high-density lipoprotein was decreased. However, television viewing time had no effect on venous thromboembolism or pulmonary embolism.

Conclusion:

Television viewing time was causally associated with increased risks of cardiovascular diseases, which may be explained by metabolic and inflammatory mechanisms.