Yang Peng

Although excessive manganese (Mn) exposure is known to cause neuromotor function in cases of poisoning, its effect on grip strength (a neuromotor marker) in older adults at environmental levels remains unclear. To investigate this issue, we conducted an integrated investigation combining epidemiology and animal experimentation to examine the association between urinary manganese and grip strength. A cross-sectional study of 375 elderly men (60–74 years) was conducted in Guangxi, China, from 2016 to 2017. Urinary Mn concentrations were determined by ICP-MS, and their associations with grip strength were evaluated using generalized linear models and restricted cubic splines. In parallel, 32 six-week-old male C57BL/6J mice were exposed to 0, 5, 10, or 15 mg/kg MnCl₂·4H₂O via intraperitoneal injection for 6 weeks. Forelimb grip strength of the mice was measured after the final exposure, and mRNA expression of inflammatory markers and cytokines (C reactive protein (CRP), interleukin (IL)-6, and tumor necrosis factor (TNF)-α in triceps) in triceps tissue was quantified. The median urinary Mn concentration in the study population was 0.22 μg/g creatinine. After adjusting for confounders, urinary Mn was inversely associated with hand grip strength (highest vs. lowest tertile: β = −3.57 kg; 95% CI: −5.68 to −1.47; p-trend = 0.007). Similarly, in male C57BL/6J mice, grip strengths declined significantly with increasing Mn exposure (p-trend < 0.0001), accompanied by upregulation of the mRNA levels of CRP, IL-6 and TNF-α in muscle tissue. Together, our findings suggest that environmental manganese exposure is inversely associated with grip strength in elderly men. While the manganese doses used in the animal study exceeded typical human environmental exposure, the experimental results further indicate that such grip strength reduction may be linked to muscle inflammation.

Background: Hypertension is linked to elevated cardiovascular morbidity and mortality. Research findings regarding cardiovascular benefits of polyunsaturated fatty acids (PUFAs) are inconsistent, possibly due to unbalanced N6FA/N3FA (omega-6 to omega-3 polyunsaturated fatty) ratios and genetic predispositions in PUFAs utilization and cardiovascular disease (CVD) risk. This study investigates the association between plasma PUFAs and CVD risk among hypertensive adults, stratified by the polygenic risk score (PRS) for PUFAs and CVD. Methods: The study analyzed 135,969 hypertensive adults from the UK Biobank. Cox regression models were employed to assess the links between PUFAs and cardiovascular outcomes, as well as the moderating effect of PRS. Results: During the follow-up, 22,084 (16.2%) of participants experienced CVD events, and 2,336 (1.7%) and 13,823 (10.2%) died from CVD and all causes, respectively. Higher blood levels of total polyunsaturated fatty acids (Total PUFA), N3FA, N6FA, docosahexaenoic acid (DHA), and linoleic acid (LA) were associated with lower CVD incidence and mortality, for instance, the hazard ratio for N3FA was 0.745 [95% confidence interval (0.698, 0.796)]. Furthermore, the N6FA/N3FA ratio showed a positive association with CVD incidence and mortality, with the point of minimum risk estimated at approximately 8.70 based on restricted cubic spline analysis. Protective associations of Total PUFA, N6FA, and LA with CVD incidence were stronger in individuals with lower CVD – PRS scores. Conclusion: Despite the general cardiovascular benefits of PUFAs, a higher N6FA/N3FA ratio was associated with an elevated risk of CVD in hypertensive participants. The benefits of PUFAs are greater in those with lower genetic CVD risk. This emphasizes the need to consider N6FA/N3FA balance and genetic predisposition when assessing health impact of PUFAs on CVD.

Introduction: The relationship between sleep duration and metabolic syndrome (MetS) remains debatable. In the present study, we analysed the link between total sleep duration (including nighttime sleep and nap duration) and MetS as well as its components among the Chinese population. Material and methods: This was a cross-sectional study from a prospective population cohort including 8616 participants over 40 years in Guangxi, China, evaluated from April 2011 to January 2012. MetS was diagnosed using modified criteria from the National Cholesterol Education Program’s Adult Treatment Panel III. Sleep information was obtained through a standard self-report-based questionnaire. The connection between sleep duration and MetS prevalence as well as its components was evaluated using a logistic regression model. Results: After adjusting for potential confoundings, the longer daily sleep duration (≥ 10 hours) group was observed to have the higher odds of having MetS than the reference group with ≥ 7 and < 8 hours of sleep [odds ratio (OR): 1.25, 95% confidence interval (CI): 1.03–1.52, p = 0.023], as well as the highest odds of having elevated triglycerides (OR: 1.25, 95% CI: 1.03–1.52) and fasting blood glucose (OR: 1.21, 95% CI: 1.01–1.45). Further analysis demonstrated that sleeping > 9 hours per night was correlated to MetS in females (OR: 1.27, 95% CI: 1.02–1.58), while napping ≥ 90 minutes was correlated to MetS (OR: 1.44, 95% CI: 1.11–1.87) in males. Conclusion: Both longer nighttime sleep duration and longer naps may be associated with the development of MetS. Introduction: The relationship between sleep duration and metabolic syndrome (MetS) remains debatable. In the present study, we analysed the link between total sleep duration (including nighttime sleep and nap duration) and MetS as well as its components among the Chinese population. Material and methods: This was a cross-sectional study from a prospective population cohort including 8616 participants over 40 years in Guangxi, China, evaluated from April 2011 to January 2012. MetS was diagnosed using modified criteria from the National Cholesterol Education Program’s Adult Treatment Panel III. Sleep information was obtained through a standard self-report-based questionnaire. The connection between sleep duration and MetS prevalence as well as its components was evaluated using a logistic regression model. Results: After adjusting for potential confoundings, the longer daily sleep duration (≥ 10 hours) group was observed to have the higher odds of having MetS than the reference group with ≥ 7 and < 8 hours of sleep [odds ratio (OR): 1.25, 95% confidence interval (CI): 1.03–1.52, p = 0.023], as well as the highest odds of having elevated triglycerides (OR: 1.25, 95% CI: 1.03–1.52) and fasting blood glucose (OR: 1.21, 95% CI: 1.01–1.45). Further analysis demonstrated that sleeping > 9 hours per night was correlated to MetS in females (OR: 1.27, 95% CI: 1.02–1.58), while napping ≥ 90 minutes was correlated to MetS (OR: 1.44, 95% CI: 1.11–1.87) in males. Conclusion: Both longer nighttime sleep duration and longer naps may be associated with the development of MetS.