BackgroundChina’s health system has shown remarkable progress in health provision and health outcomes in recent decades, however inequality in health care utilization persists and poses a serious social problem. While government pro-poor health policies addressed affordability as the major obstacle to equality in health care access, this policy direction deserves further examination. Our study examines the issue of health care inequalities in China, analyzing both regional and individual socioeconomic factors associated with the inequality, and provides evidence to improve governmental health policies.MethodsThe China Health and Nutrition Survey (CHNS) 1991–2011 data were used to analyze the inequality of health care utilization. The random effects logistic regression technique was used to model health care utilization as the dependent variable, and income and regional location as the independent variables, controlling for individuals’ age, gender, marital status, education, health insurance, body mass index (BMI), and period variations. The dynamic trend of 1991–2011 regional disparities was estimated using an interaction term between the regional group dummy and the wave dummy.ResultsThe probability of using outpatient service and inpatient services during the previous 4 weeks was 8.6 and 1.1% respectively. Compared to urban residents, suburban (OR: 0.802, 95% CI: 0.720–0.893), town (OR: 0.722, 95% CI: 0.648–0.804), rich (OR: 0.728, 95% CI: 0.656–0.807) and poor village (OR: 0.778, 95% CI: 0.698–0.868) residents were less likely to use outpatient service; and rich (OR: 0.609, 95% CI: 0.472–0.785) and poor village (OR: 0.752, 95% CI: 0. 576–0.983) residents were less likely to use inpatient health care. But the differences between income groups were not significant, except the differences between top and bottom income group in outpatient service use.ConclusionRegional location was a more important factor than individual characteristics in determining access to health care. Besides demand-side subsidies, Chinese policy makers should pay enhanced attention to health care resource allocation to address inequity in health care access.
Background We have previously shown that vitamin D supplementation increases telomerase activity, suggesting an anti-aging effect. In this study, we aim to test the hypothesis that vitamin D supplementation would slow down epigenetic aging, a new marker of biological aging. Methods A randomized clinical trial was previously conducted among 70 overweight/obese African Americans with serum 25-hydroxyvitamin D [25(OH)D] < 50 nmol/L, who were randomly assigned into four groups of 600 IU/d, 2,000 IU/d, 4,000 IU/d of vitamin D3 supplements or placebo followed by 16-week interventions. Whole genome-wide DNA methylation analysis was conducted in 51 participants. DNA methylation ages were calculated according to the Horvath and the Hannum methods. Methylation-based age acceleration index (∆Age) is defined as the difference between DNA methylation age and chronological age in years. Mixed-effects models were used to evaluate the treatment effects. Results Fifty-one participants (aged 26.1 ± 9.3 years, 16% are male) were included in the study. After the adjustment of multi-covariates, vitamin D3 supplementation of 4,000 IU/d was associated with 1.85 years decrease in Horvath epigenetic aging compared with placebo (p value = .046), and 2,000 IU/d was associated with 1.90 years decrease in Hannum epigenetic aging (p value = .044). Serum 25(OH)D concentrations were significantly associated with decreased Horvath ∆Age only (p values = .002), regardless of treatments. Conclusions Our results suggest that vitamin D supplementation may slow down Horvath epigenetic aging. But the effect on Hannum epigenetic aging is not conclusive. Large-scale and longer duration clinical trials are needed to replicate the findings.
High-sodium diet may modulate the gut microbiome. Given the circulating short-chain fatty acids (SCFAs) are microbial in origin, we tested the hypothesis that the modest sodium reduction would alter circulating SCFA concentrations among untreated hypertensives, and the changes would be associated with reduced blood pressure and improved cardiovascular phenotypes. A total of 145 participants (42% blacks, 19% Asian, and 34% females) were included from a randomized, double-blind, placebo-controlled cross-over trial of sodium reduction with slow sodium or placebo tablets, each for 6 weeks. Targeted circulating SCFA profiling was performed in paired serum samples, which were collected at the end of each period, so as all outcome measures. Sodium reduction increased all 8 SCFAs, among which the increases in 2-methylbutyrate, butyrate, hexanoate, isobutyrate, and valerate were statistically significant ( P s<0.05). Also, increased SCFAs were associated with decreased blood pressure and improved arterial compliance. There were significant sex differences of SCFAs in response to sodium reduction ( P s<0.05). When stratified by sex, the increases in butyrate, hexanoate, isobutyrate, isovalerate, and valerate were significant in females only ( P s<0.05), not in males ( P s>0.05). In females, changes in isobutyrate, isovalerate, and 2-methylbutyrate were inversely associated with reduced blood pressures ( P s<0.05). Increased valerate was associated with decreased carotid-femoral pulse wave velocity ( P =0.040). Our results show that dietary sodium reduction increases circulating SCFAs, supporting that dietary sodium may influence the gut microbiome in humans. There is a sex difference in SCFA response to sodium reduction. Moreover, increased SCFAs are associated with decreased blood pressures and improved arterial compliance. Registration— URL: https://www.clinicaltrials.gov . Unique identifier: NCT00152074.
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