Background: Physical activity is beneficial to lipid profiles, however the association between sedentary behaviours and paediatric dyslipidaemia remains controversial. Understanding these associations is critical given that youth are increasingly engaging in sedentary pursuits, and are sleeping, on average, 1 h less than children were 20 years ago.
Objective and hypotheses: To investigate whether various forms of sedentary behavior/sleep predict lipid profiles in children over a 2-year period. Our hypothesis is that sedentary behavior will adversely impact lipid profiles in childhood.
Method: Data from 630 children living in Quebec, Canada, with at least one biological parent with obesity (QUALITY cohort) were collected at both 810 years and 1012 years. Sedentary behaviour, sleep time and moderate-to-vigorous physical activity (MVPA) were measured over 7 days using accelerometry, with sedentary behaviour defined as the average minutes daily at <100 counts/min. Sleep time was derived from accelerometer non-wear time. Screen time, computer/video game use and TV viewing over the past 7 days were self-reported. Adiposity was measured using DXA scan and dietary carbohydrate/fat intake by an average of three 24 h dietary recalls. Outcomes included fasting total cholesterol, triglycerides, HDL-cholesterol and LDL-cholesterol. Multivariable models adjusted for MVPA, fitness, adiposity and diet.
Results: Every additional hour of TV time at baseline predicted a 7.4% (95% CI=3.9; 10.9) increase in triglycerides and 2.1% (95% CI=−3.7; −0.5) decrease in HDL. These findings held true for triglycerides after adjusting for adiposity, dietary carbohydrate and sugar-sweetened beverages. Every additional hour of sleep predicted a 4.1% (95% CI=−7.9; −0.3) decrease in LDL even after controlling for sedentary behaviour and dietary fat intake.
Conclusion: Higher time spent engaged in TV watching and lower sleep appear to be deleterious to childhood lipid profiles over time, even when taking into account other major lifestyle habits.
Funding: This work was supported by the Canadian Institutes of Health Research (#OHF-69442, #NMD-94067, #MOP-97853, #MOP-119512), the Heart and Stroke Foundation of Canada (#PG-040291) and the Fonds de Recherche du Quebec Sante.
01 Oct 2015 - 03 Oct 2015