There have been mixed results regarding the relationship among short chain fatty acids (SCFAs), microbiota, and obesity in human studies. We selected studies that provided data on SCFA levels or fecal microbiota abundance in obese and nonobese individuals and then combined the published estimates using a random-effects meta-analysis. Obese individuals had significantly higher fecal concentrations of acetate (SMD (standardized mean differences) = 0.87, 95% CI (confidence interva) = 0.24–1.50, I² (I–squared) = 88.5), propionate (SMD = 0.86, 95% CI = 0.35–1.36, I² = 82.3%), and butyrate (SMD = 0.78, 95% CI = 0.29–1.27, I² = 81.7%) than nonobese controls. The subgroup analyses showed no evidence of heterogeneity among obese individuals with a BMI >30 kg/m² (I² = 0.0%). At the phylum level, the abundance of fecal microbiota was reduced in obese compared to nonobese individuals, but the difference was not statistically significant (Bacteroidetes phylum, SMD = −0.36, 95% CI = −0.73–0.01; Firmicutes phylum, SMD = −0.10, 95% CI = −0.31–0.10). The currently available human case-control studies show that obesity is associated with high levels of SCFA but not gut microbiota richness at the phylum level. Additional well-designed studies with a considerable sample size are needed to clarify whether this association is causal, but it is also necessary to identify additional contributors to SCFA production, absorption, and excretion in humans.

There is increasing evidence regarding the relationship between metabolic syndrome and mortality. However, previous research examining metabolic syndrome and mortality in older populations has produced mixed results. In addition, there is a clear need to identify and manage individual components of metabolic syndrome to decrease cardiovascular disease (CVD) mortality. In this meta-analysis, we searched the MEDLINE databases using PubMed, Cochrane Library, and EMBASE databases. Based on 20 prospective cohort studies, metabolic syndrome was associated with a higher risk of all-cause mortality [relative risk (RR), 1.23; 95% confidence interval (CI), 1.15–1.32; I2 = 55.9%] and CVD mortality (RR, 1.24; 95% CI, 1.11–1.39; I2 = 58.1%). The risk estimates of all-cause mortality for single components of metabolic syndrome were significant for higher values of waist circumference or body mass index (RR, 0.94; 95% CI, 0.88–1.00), higher values of blood glucose (RR, 1.19; 95% CI, 1.05–1.34), and lower values of high-density lipoprotein (HDL) cholesterol (RR, 1.11; 95% CI, 1.02–1.21). In the elderly population, metabolic syndrome was associated with an increased risk of all-cause and CVD mortality. Among the individual components of metabolic syndrome, increased blood glucose and HDL cholesterol levels were significantly associated with increased mortality. However, older obese or overweight individuals may have a decreased mortality risk. Thus, the findings of the current meta-analysis raise questions about the utility of the definition of metabolic syndrome in predicting all-cause mortality and CVD mortality in the elderly population.

No quantitative systematic review or meta-analysis of population-based epidemiological studies has been conducted to assess the association between serum 25-hydroxyvitamin D (25(OH)D) levels and the risk of depression. This study aimed to summarize the current evidence from cross-sectional and prospective cohort studies that have evaluated the association between 25(OH)D levels and the risk of depression. Relevant studies were identified by systematically searching the PubMed, EMBASE, Web of Science, and PsycINFO databases through April 2012. Cross-sectional and cohort studies that reported adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for the association of interest were included. The reported risk estimates for 25(OH)D categories were recalculated, employing a comprehensive trend estimation from summarized dose-response data. A pooled OR was calculated separately for cross-sectional and cohort studies using random-effects models. In the meta-analysis, 25(OH)D levels were significantly inversely associated with depression in 5 of 11 case-control studies and 2 of 5 cohort studies. The pooled estimate of the adjusted OR of depression in 11 cross-sectional studies (n = 43,137) was 0.96 (95% CI = 0.94-0.99, I2 = 63%) for a 10 ng/ml increase in 25(OH)D levels. The 5 included cohort studies comprised 12,648 participants, primarily elderly individuals, whose serum 25(OH)D levels were measured, and 2,663 experienced depression events during follow-up. The pooled adjusted OR of depression was 0.92 (95% CI = 0.87-0.98, I2 = 50%) for a 10 ng/ml increase in 25(OH)D levels. Our results indicate an inverse association between serum 25(OH)D levels and the risk of depression. Further studies are warranted to establish whether this association is causal.

Objective: Epidemiological studies have repeatedly investigated the association between sleep duration and metabolic syndrome. However, the results have been inconsistent. This meta-analysis aimed to summarize the current evidence from cross-sectional and prospective cohort studies that evaluated this. Data sources: Relevant studies were identified by systematically searching the PubMed, Cochrane CENTRAL, EMBASE and PsycINFO databases through November 2012 without language restriction. Study selection: We identified 12 cross-sectional studies with 76 027 participants including 14 404 cases of metabolic syndrome, and 3 cohort studies with 2055 participants and 283 incident cases of metabolic syndrome. Results: For short sleep durations (8 to 10 h), the OR was 1.23 (95% CI=1.02–1.49, I²=75.8%) in the 11 cross-sectional studies and 1.62 (95% CI=0.86–3.04, I²=0.0%) in the 2 cohort studies. Conclusions: Short and long sleep durations are risky behaviors for increasing the risk of metabolic syndrome and thus have important public health implications, as sleep habits are amenable to behavioral interventions. The available data are sparse, and further studies, especially longitudinal studies, are needed to facilitate a better understanding of these associations.

Increasing evidence has suggested an association between blood vitamin D levels and metabolic syndrome. Our objective was to determine the relationship between blood vitamin D status and metabolic syndrome in the general adult population, using a dose-response meta-analysis. We searched the PubMed, EMBASE, Web of Science, and Cochrane Library databases through July 2013 to identify relevant studies. Observational studies, reporting risk ratios with a 95% confidence interval (CI) for metabolic syndrome in ≥3 categories of blood 25-hydroxyvitamin D [25(OH)D] levels, were selected. Data extraction was performed independently by 2 authors, and the quality of the studies was evaluated using the risk of bias assessment tool for nonrandomized studies. The pooled odds ratio of metabolic syndrome per 25 nmol/L increment in the serum/plasma 25(OH)D concentration was 0.87 (95% CI = 0.83-0.92, I(2) = 85%), based on 16 "cross-sectional studies" and 1.00 (95% CI = 0.98-1.02, I(2) = 0%) for 2 "cohort and nested case-control studies." The dose-response meta-analysis showed a generally linear, inverse relationship between 25(OH)D levels and metabolic syndrome in the cross-sectional studies (P for linear trend < .001). Blood vitamin D levels were associated with a risk of metabolic syndrome in cross-sectional studies but not in longitudinal studies. Randomized, clinical trials will be necessary to address the issue of causality and to determine whether vitamin D supplementation is effective for the prevention of metabolic syndrome.

Vitamin D deficiency and frailty are common with aging. Previous studies examining vitamin D status and frailty have produced mixed results, and in particular, the shape of the association has not been well established. We examined the association between 25-hydroxyvitamin D (25OHD) serum levels and frailty by performing a systematic review and dose-response meta-analysis. We searched the PubMed, EMBASE and Cochrane Library databases of Elsevier through February 2017. Cross-sectional and cohort studies that reported adjusted risk ratios with 95% confidence intervals (CI) for frailty with ≥3 categories of 25OHD serum levels were selected. Data extraction was performed independently by two authors. The reported risk estimates for 25OHD categories were recalculated, employing a comprehensive trend estimation from summarized dose-response data. The pooled risk estimate of frailty syndrome per 25 nmol/L increment in serum 25OHD concentration was 0.88 (95% CI = 0.82–0.95, I2 = 86.8%) in the 6 cross-sectional studies and 0.89 (95% CI = 0.85–0.94, I2 = 0.0%) in the 4 prospective cohort studies. Based on the Akaike information criteria (AIC), a linear model was selected (AIC for the nonlinear model: − 5.4, AIC for the linear model: − 6.8 in the prospective cohort studies; AIC for the linear model: − 13.6, AIC for the nonlinear model: − 1.77 in the cross-sectional studies). This dose-response meta-analysis indicates that serum 25OHD levels are significantly and directly associated with the risk of frailty. Further studies should address the underlying mechanisms to explain this relationship and to determine whether vitamin D supplementation is effective for preventing frailty syndrome.