BACKGROUND: While there is evidence that physical activity, sedentary behaviour (SB) and sleep may all be associated with modified levels of inflammatory markers in adolescents and children, associations with one movement behaviour have not always been adjusted for other movement behaviours, and few studies have considered all movement behaviours in the 24-hour day as an exposure. PURPOSE: The aim of the study was to explore how longitudinal reallocations of time between moderate-to-vigorous physical activity (MVPA), light physical activity (LPA), SB and sleep are associated with changes in inflammatory markers in children and adolescents. METHODS: A total of 296 children/adolescents participated in a prospective cohort study with a 3-year follow-up. MVPA, LPA and SB were assessed by accelerometers. Sleep duration was assessed using the Health Behavior in School-aged Children questionnaire. Longitudinal compositional regression models were used to explore how reallocations of time between movement behaviours are associated with changes in inflammatory markers. RESULTS: Reallocations of time from SB to sleep were associated with increases in C3 levels (difference for 60 min/d reallocation [d60] = 5.29 mg/dl; 95% confidence interval [CI] = 0.28, 10.29) and TNF-α (d60 = 1.81 mg/dl; 95% CI = 0.79, 15.41) levels. Reallocations from LPA to sleep were also associated with increases in C3 levels (d60 = 8.10 mg/dl; 95% CI = 0.79, 15.41). Reallocations from LPA to any of the remaining time-use components were associated with increases in C4 levels (d60 ranging from 2.54 to 3.63 mg/dl; p < 0.05), while any reallocation of time away from MVPA was associated with unfavourable changes in leptin (d60 ranging from 3088.44 to 3448.07 pg/ml; p < 0.05). CONCLUSIONS: Reallocations of time between 24-h movement behaviours are prospectively associated with some inflammatory markers. Reallocating time away from LPA appears to be most consistently unfavourably associated with inflammatory markers. Given that higher levels of inflammation during childhood and adolescence are associated with an increased risk of chronic diseases in adulthood, children and adolescents should be encouraged to maintain or increase the level of LPA to preserve a healthy immune system.
Cannabinoids, a class of compounds derived from Cannabis sativa L., have recently become more widely accessible for public consumption in the form of diverse cannabis products, in parallel with weakening the measures that so far restricted their availability. The US Food and Drug Administration has approved several cannabis-derived drugs for management of various diseases as well as chemotherapy-induced nausea and vomiting. Besides the attenuation of adverse effects of chemotherapy, numerous reports about cannabinoid-mediated anticancer effects further motivate cancer patients to support their therapy with such products. Here we present a set of preclinical data with human cell culture models, suggesting that cannabidiol and cannabis extracts may effectively counteract the anticancer effects of the clinically widely used standard-of-care platinum-based drugs. We show that even low concentrations of cannabinoids reduced the toxicity of cisplatin, oxaliplatin, and carboplatin, an effect which was accompanied by decreased platinum adduct formation and a set of commonly used molecular markers. Mechanistically, our results excluded the possibility that the observed enhanced survival of cancer cells was mediated transcriptionally. Instead, trace metal analyses strongly indicate an inhibitory impact of cannabinoids on intracellular platinum accumulation, thereby implicating changes in cellular transport and/or retention of these drugs as the likely cause of the observed biological effects. Our study raises the possibility that the desirable effect of counteracting adverse effects of chemotherapy might, at least for some cannabinoids, reflect impaired cellular availability, and consequently attenuation of the anticancer effects of platinum drugs. DATA AVAILABILITY: All data supporting the conclusions are available in the article and supplementary files. Raw data are available upon request from the corresponding author.
