ABSTRACT
OBJECTIVE@#To assess the relationship between yogurt intake and mortality risk from prospective cohort studies.@*METHODS@#The PubMed, EMBASE, and Web of Science databases were searched for all records related to yogurt intake and mortality risk [all-cause or cardiovascular disease (CVD) or cancer mortality] before October 1, 2018. The Newcastle-Ottawa Quality Scale was used to estimate the quality of all eligible articles. The results of the highest and lowest categories of yogurt intake in each study were collected and the effect size was pooled using a random effects model. The dose-response analysis was calculated using the generalized least squares trend estimation model.@*RESULTS@#Eight eligible cohort studies were included in this meta-analysis. There were 235,676 participants in the 8 studies, and the number of deaths was 14,831. Compared with the lowest category, the highest category of yogurt intake was not significantly related with all-cause mortality [hazard ratio (HR)=0.93; 95% confidence interval (CI): 0.85, 1.01], CVD mortality (HR=0.92; 95% CI: 0.81, 1.03) and cancer mortality (HR=0.97; 95% CI: 0.83, 1.12). These studies were homogenous, since the homogeneity test showed that I was 28.7%, 15.1% and 11.8%, respectively. However, yogurt intake ⩾200 g/d was significantly associated with a lower all-cause mortality (HR=0.88; 95% CI: 0.80, 0.96) and CVD mortality (HR=0.87; 95% CI: 0.77, 0.99) in the subgroup analysis. The dose-response analysis showed that yogurt intake of 200 g/d was inversely associated with all-cause mortality (P=0.041, HR=0.95, 95% CI: 0.92, 1.00) and CVD mortality (P=0.009, HR=0.92, 95% CI: 0.86, 0.98), and all of which were linear relationship (P>0.05).@*CONCLUSIONS@#This review provided the evidence regarding yogurt intake can reduce all-cause and CVD mortality. Although some positive findings were identified, more high-quality cohort studies and randomized controlled trials are warranted on a possible protective effect of yoghurt on health.
ABSTRACT
Observational studies between magnesium int- ake and risk of type 2 diabetes yielded inconsistent results. We conducted a system literature search of PubMed database through March 2015 for prospective cohort studies of magnesium intake and type 2 diabetes risk. Study-specific results were pooled in a random-effects model. Subgroup and sensitivity analysis were performed to assess the potential sources of heterogeneity and the robustness of the pooled estimation. Generalized least squares trend estimation was used to investigate the dose-response relationship. A total of 15 papers with 19 analyses were identified with 539,735 participants and 25,252 incident diabetes cases. Magnesium intake was associated with a significant lower risk of type 2 diabetes (RR: 0.77; 95% CI: 0.71-0.82) for the highest compared with lowest category. This association was not significantly modified by the pre-specified study characteristics. In the dose-response analysis, a magnesium intake increment of 100 mg/day was associated with a 16% reduction in type 2 diabetes risk (RR: 0.84; 95% CI: 0.80-0.88). A nonlinear relationship existed between magnesium intake and type 2 diabetes (P-nonlinearity=0.003). This meta-analysis further verified a protective effect of magnesium intake on type 2 diabetes in a nonlinear dose-response manner.