METHODS: The systematic review and meta-analysis were performed according to the previously published protocol. The PubMed, Web of Sciences, and Scopus databases were meticulously searched for relevant data, without time or language restriction, up to June 1, 2017. All clinical trials which assessed the effect of Se supplementation on antioxidant markers, including oxidative stress index (OSI), antioxidant potency composite (APC) index, plasma malonaldehyde (MDA), total antioxidant capacity (TAC), antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT)), and total antioxidant plasma (TAP), were included. The effect of Se supplementation on antioxidant markers was assessed using standardized mean difference (SMD) and 95% confidence interval (CI). The random-effect meta-analysis method was used to estimate the pooled SMD.
RESULTS: In total, 13 studies which assessed the effect of Se supplementation on antioxidant markers were included. The random-effect meta-analysis method showed that Se supplementation significantly increased GPX (SMD = 0.54; 95% CI = 0.21-0.87) and TAC (SMD = 0.39, 95% CI = 0.13, 0.66) levels and decreased MDA levels (SMD = - 0.54, 95% CI = - 0.78, - 0.30). The effect of Se supplementation on other antioxidant markers was not statistically significant (P > 0.05).
CONCLUSION: The findings showed that Se supplementation might reduce oxidative stress by increasing TAC and GPX levels and decreasing serum MDA, both of which are crucial factors for reduction of oxidative stress.
OBJECTIVES: The GBD (Global Burden of Disease) 2015 study integrated data on disease incidence, prevalence, and mortality to produce consistent, up-to-date estimates for cardiovascular burden.
METHODS: CVD mortality was estimated from vital registration and verbal autopsy data. CVD prevalence was estimated using modeling software and data from health surveys, prospective cohorts, health system administrative data, and registries. Years lived with disability (YLD) were estimated by multiplying prevalence by disability weights. Years of life lost (YLL) were estimated by multiplying age-specific CVD deaths by a reference life expectancy. A sociodemographic index (SDI) was created for each location based on income per capita, educational attainment, and fertility.
RESULTS: In 2015, there were an estimated 422.7 million cases of CVD (95% uncertainty interval: 415.53 to 427.87 million cases) and 17.92 million CVD deaths (95% uncertainty interval: 17.59 to 18.28 million CVD deaths). Declines in the age-standardized CVD death rate occurred between 1990 and 2015 in all high-income and some middle-income countries. Ischemic heart disease was the leading cause of CVD health lost globally, as well as in each world region, followed by stroke. As SDI increased beyond 0.25, the highest CVD mortality shifted from women to men. CVD mortality decreased sharply for both sexes in countries with an SDI >0.75.
CONCLUSIONS: CVDs remain a major cause of health loss for all regions of the world. Sociodemographic change over the past 25 years has been associated with dramatic declines in CVD in regions with very high SDI, but only a gradual decrease or no change in most regions. Future updates of the GBD study can be used to guide policymakers who are focused on reducing the overall burden of noncommunicable disease and achieving specific global health targets for CVD.