OBJECTIVE: To investigate whether serum uric acid (SUA) level is associated with all-cause and cardiovascular disease (CVD) mortality among individuals with diabetes. RESEARCH DESIGN AND METHODS: In this prospective cohort study, we included patients with diabetes from the U.S. National Health and Nutritional Examination Survey (NHANES) 1999–2018. Mortality and underlying causes of death were ascertained by linkage to national death records through 31 December 2019. Weighted Cox proportional hazards regression models were used to evaluate hazard ratios (HRs) and 95% CIs for all-cause and CVD mortality. We also performed a meta-analysis of available cohort studies to combine the association between SUA level and mortality in diabetes. RESULTS: Among the 7,101 patients with diabetes from NHANES 1999–2018, the weighted mean of SUA level was 5.7 mg/dL. During 57,926 person-years of follow-up, 1,900 deaths (n = 674 deaths from CVD) occurred. In the fully adjusted model, when compared with patients with diabetes in the lowest SUA quintile, those in the highest SUA quintile had the HRs (95% CIs) of 1.28 (1.03, 1.58) for all-cause mortality and 1.41 (1.03, 1.94) for CVD mortality. We included 13 cohort studies in the meta-analysis and found that the pooled HRs (95% CIs) were 1.08 (1.05, 1.11) for all-cause mortality and 1.05 (1.03, 1.06) for CVD mortality per 1 mg/dL increment of SUA level in patients with diabetes. CONCLUSIONS: This study indicated that higher SUA levels were associated with increased risks of all-cause and CVD mortality in diabetes. Interventional studies are needed to elucidate the health effect of treatments to lower SUA levels.

Background: Mild cognitive impairment (MCI) induced the majority number of dementia patients. The prevalence of MCI in China varied across studies with different screening tools and diagnostic criteria. Objective: A systematic review and meta-analysis was conducted to estimate the pooled MCI prevalence among the population aged 55 years and older in China. Methods: PubMed, EMBASE, CNKI, Wanfang, CQVIP, and CBMdisc were searched for studies on prevalence of MCI among Chinese elderly between January 1, 1980, and February 10, 2020. The quality assessment was conducted via external validity, internal validity, and informativity, the pooled prevalence was calculated through the random-effect model, and the homogeneity was evaluated by Cochran’s Q test and I². Results: Fifty-three studies with 123,766 subjects were included. The pooled prevalence of MCI among Chinese elderly was 15.4% (95% CI: 13.5–17.4%). Subgroup analyses indicated that the prevalence calculated with different screening tools was 20.2% (95% CI: 15.1–25.9%) for Montreal Cognitive Assessment (MoCA) and 13.0% (95% CI: 10.7–15.5%) for Mini-Mental State Examination (MMSE). According to different diagnostic criteria, the prevalence was 14.8% (95% CI: 12.2–17.6%) for Petersen criteria, 15.0% (95% CI: 12.7–17.5%) for DSM-IV, and 21.2% (95% CI: 17.5–25.2%) for Chinese Expert Consensus on Cognitive Impairment (CECCI). Besides, women, older adults, illiterate people, rural residents, and those who lived with unhealthy lifestyles and morbidity showed higher prevalence. Conclusions: The prevalence of MCI in China was 15.4%, which varied by demographics, lifestyles, morbidity, screening tools, and diagnostic criteria. In further studies, screening tools and diagnosis criteria should be considered when estimating MCI prevalence.

The age‐related loss of muscle mass and muscle function known as sarcopenia is a primary contributor to the problems faced by the old people. Sarcopenia has been a major public health problem with high prevalence in many countries. The related underlying molecular mechanisms of sarcopenia are not completely understood. This review is focused on the potential mechanisms and current research strategies for sarcopenia with the aim of facilitating the recognition and treatment of age‐related sarcopenia. Previous studies suggested that protein synthesis and degradation, autophagy, impaired satellite cell activation, mitochondria dysfunction, and other factors associated with muscle weakness and muscle degeneration may be potential molecular pathophysiology of sarcopenia. Importantly, we also prospectively highlight that exosomes (small vesicles) as carriers can regulate muscle regeneration and protein synthesis according to recent researches. Dietary strategies and exercise represent the interventions that can also alleviate the progression of sarcopenia. At last, building on recent studies pointing to exosomes with the roles in increasing muscle regeneration, mediating the beneficial effects of exercise, and serving as messengers of intercellular communication and as carriers for research strategies of many diseases, we propose that exosomes could be a potential research direction or strategies of sarcopenia in the future.

Background: Current cholesterol guidelines have recommended very low low‐density lipoprotein cholesterol (LDL‐C) treatment targets for people at high risk of cardiovascular disease (CVD). However, recent observational studies indicated that very low LDL‐C levels may be associated with increased mortality and other adverse outcomes. The association between LDL‐C levels and long‐term risk of overall and cardiovascular mortality among the U.S. general population remains to be determined. Methods and Results: This prospective cohort study included a nationally representative sample of 14 035 adults aged 18 years or older, who participated in the National Health and Nutrition Examination Survey III 1988–1994. LDL‐C levels were divided into 6 categories: <70, 70–99.9, 100–129.9, 130–159.9, 160–189.9 and ≥190 mg/dL. Deaths and underlying causes of deaths were ascertained by linkage to death records through December 31, 2015. Weighted Cox proportional hazards regression models were used to estimate the hazard ratios (HR) of mortality outcomes and its 95% CIs. During 304 025 person‐years of follow up (median follow‐up 23.2 years), 4458 deaths occurred including 1243 deaths from CVD. At baseline, mean age was 41.5 years and 51.9% were women. Very low and very high levels of LDL‐C were associated with increased mortality. After adjustment for age, sex, race and ethnicity, education, socioeconomic status, lifestyle factors, C‐reactive protein, body mass index, and other cardiovascular risk factors, individuals with LDL‐C<70 mg/dL, compared to those with LDL‐C 100–129.9 mg/dL, had HRs of 1.45 (95% CI, 1.10–1.93) for all‐cause mortality, 1.60 (95% CI, 1.01–2.54) for CVD mortality, and 4.04 (95% CI, 1.83–8.89) for stroke‐specific mortality, but no increased risk of coronary heart disease mortality. Compared with those with LDL‐C 100–129.9 mg/dL, individuals with LDL‐C≥190 mg/dL had HRs of 1.49 (95% CI, 1.09–2.02) for CVD mortality, and 1.63 (95% CI, 1.12–2.39) for coronary heart disease mortality, but no increased risk of stroke mortality. Conclusions: Both very low and very high LDL‐C levels were associated with increased risks of CVD mortality. Very low LDL‐C levels was also associated with the high risks of all‐cause and stroke mortality. Further investigation is needed to elucidate the optimal range of LDL‐C levels for CVD health in the general population.

Background: Diets rich in plant-based foods are associated with lower risks of non-alcoholic fatty liver disease (NAFLD), while the prospective evidence is limited. We aimed to examine longitudinal associations of plant-based diets and genetic susceptibility with NAFLD risk. Methods: This longitudinal cohort study included 159,222 participants (58.0 ± 8.0 years old, 55.7% female) free of NAFLD in the UK Biobank. We calculated the overall plant-based diet index (PDI), the healthful plant-based diet index (hPDI), and the unhealthful plant-based diet index (uPDI). New-onset NAFLD was the primary outcome. The weighted polygenic risk score was calculated based on risk variants associated with NAFLD. Hazard ratios (HR) and 95% confidential intervals (CI) were estimated by Cox proportional hazards model. Magnetic resonance imaging-derived proton density fat fraction (MRI-PDFF) measured liver fat content in a subsample of 20,692 participants (57.5 ± 7.4 years old, 52.6% female) was the secondary outcome. The associations between plant-based diet indices and MRI-PDFF were evaluated using generalized linear models. Results: During a median follow-up of 9.5 years, 1541 new-onset NAFLD cases were documented. Compared to the lowest quintile, multivariable-adjusted hazard ratios (HRs) of NAFLD in the highest quintile were 0.78 (95% confidential intervals [CI], 0.66–0.93, p-trend =0.02), 0.74 (95% CI, 0.62–0.87, p-trend <0.0001), and 1.24 (95% CI, 1.05–1.46, p-trend = 0.02) for overall PDI, hPDI, and uPDI, respectively. For liver fat content, higher overall PDI and hPDI were associated with lower MRI-PDFF, while higher uPDI was associated with higher liver fat content. We observed a significant interaction between hPDI and PRS (p-interaction =0.03), and the NAFLD risk was lowest among participants with the highest hPDI and low genetic risk. Conclusions: Higher intake of plant-based diets especially healthful plant-based diets was associated with lower NAFLD risk and liver fat content regardless of genetic susceptibility, whereas an unhealthful plant-based diet was associated with higher NAFLD risk and intrahepatic steatosis. These results suggest that the quality of plant-based foods should be highlighted when adopting a plant-based diet.