Background: Both experimental and observational studies have provided conflicting evidence on the associations of selenium with incidence and mortality of cardiovascular disease (CVD). The aim of this study was to evaluate the association between selenium status in the body and incidence and mortality of CVD by performing a systematic review and meta-analysis of observational studies and randomized controlled trials. Methods: A systematic search for articles in MEDLINE (Ovid), Embase, Web of Science (Thomson Reuters) and Cochrane library (Wiley) was conducted. Thirteen of the 1811 articles obtained from the databases met our inclusion criteria and were considered in the final analysis. The effect sizes were presented as weighted relative risk (RR) and 95% confidence intervals (CIs) using random-effects model. To detect dose-response relationships, we used meta-regression. Results: Overall, there was a reduced risk of CVD incidence (RR ¼ 0.66; 95% CI: 0.40-1.09) and mortality (RR ¼ 0.69; 95% CI: 0.57-0.84) in physiologically high selenium status compared to low selenium status in the body. There was a 15% (RR ¼ 0.85, 95% CI: 0.76-0.94) decreased risk of CVD incidence per 10 mg increment in blood selenium concentration. In addition, a statistically significantly nonlinear dose-response relationship was found between CVD mortality and increased blood selenium concentration with the lowest risk at the 30-35 mg increment in blood selenium. Conclusions: Physiologically high selenium levels in the body are associated with decreased risk for CVD incidence and mortality, however, people should be cautious about the potential harmful effects from excessive intake of selenium.
ObjectiveThis study aimed to demonstrate the association between adverse life events (ALEs) and the risk of late‐life cognitive decline in older community‐dwelling individuals in China.MethodsWe prospectively followed up 1657 dementia‐free participants with ALE data at baseline in the Shanghai Aging Study. The cohort was categorized into four subgroups (depression with ALEs, depression without ALEs, no depression with ALEs, and no depression without ALEs). Cox regressions were conducted to estimate the hazard ratio (HR) for incident dementia stratified by all participants and depressed and nondepressed participants.ResultsWe identified 168 incident dementia cases over a mean period of 5.2 years. The cumulative dementia incidence in nondepressed participants with ALEs was the lowest among the four subgroups. Nondepressed participants with ALEs had a lower risk of incident dementia (HR [95% CI]: 0.50 [0.27‐0.92], P = .0267) than those without ALEs, adjusted for age, sex, education, apolipoprotein E ε4 (APOE ε4), body mass index, cigarette smoking, heart disease, hypertension, diabetes, stroke, Mini‐Mental State Examination (MMSE) at baseline, and anxiety.ConclusionsThis study explored a significant inverse association between ALEs and the risk of incident cognitive decline among older adults without depression in China. Interventions for depression prevention immediately after ALEs may reduce the risk of cognitive decline later in life.
Background: The relationship between body mass index (BMI) and dementia is inconclusive. Undesirable loss of fat-free mass is a risk factor for cognitive decline while obesity is also a risk factor for cardio-metabolic disorders among the older adults. Objective: This study aimed to examine the association between BMI and incident all-cause dementia among Chinese older adults using a prospective study. Methods: Participants were 1,627 community residents aged 60 or older without dementia from the Shanghai Aging Study. Cox regression models, incorporated with restricted cubic splines, were used to explore a nonlinear association between baseline BMI and risk of all-cause dementia as measured by hazard ratio (HR) using both frequentist and Bayesian approach. Results: We diagnosed 136 incident dementia cases during the mean follow-up of 5.3 years. Compared with moderate BMI (18.5–24.0 kg/m2), low BMI (< 18.5 kg/m2) were related to an increased risk of dementia with the HR as 3.38 (95% CI 1.50–7.63), while high BMI (≥24.0 kg/m2) showed a decreased risk of dementia without statistical significance (HR = 0.91, 95% CI 0.60 to 1.39). Sensitivity analysis in participants without central obesity indicated that the association was still significant with even higher HR. Bayesian approach presented the similar results. Conclusion: Our result indicates that low BMI may contribute to high risk of incident dementia, even in individuals without central obesity.
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