ObjectivesThis study aimed to compare the burden and trends of stroke attributed to dietary risk factors in the Belt and Road (“B&R”) countries from 1990 to 2019.MethodsThe 2019 Global Burden of Disease (GBD) Study was used to gather information on the burden of stroke attributable to dietary risk factors. Numbers and age-standardized rates (ASRs) of deaths, disability-adjusted life years (DALYs) were determined in 1990 and 2019 among the “B&R” countries. The average annual percent change (AAPC) was used to analyze the temporal trends of diet-induced stroke DALYs from 1990 to 2019 and in the final decade (2010–2019) by Joinpoint regression analysis.ResultsIn 2019, the absolute number of stroke deaths and DALYs attributable to dietary risk factors were 671,872 cases (95% UI 436,354–937,093) and 1.67 million cases (95% UI 1.15–2.24) in China. We found geographical differences in mortality and DALYs of diet-attributable stroke among member countries, with Bulgaria, Hungary and Serbia being the three highest countries in 1990, Bulgaria, North Macedonia and Montenegro in Central Asia in 2019. The ASRs of diet-induced stroke mortality and DALYs were generally declining in most member states from 1990 to 2019, however, the corresponding metrics in Mongolia remained high. The fastest decline in ASR of mortality and DALYs for diet-induced stroke was seen in Estonia, Eastern Europe, with AAPC values of −7.09% (95%CI: −7.72, −6.46%) and − 6.62% (95%CI: −7.20, −6.03%), respectively. We noted a substantial downward trend in ASR of mortality and DALYs from diet-induced stroke changes in the final decade (2010–2019) for most member states. The ASR of DALYs for diet-induced stroke decreased greater in females than in males. For those aged 50–74, the DALYs for stroke due to dietary risk factors in all other member countries of the “B&R” showed a decreasing trend, except for the Philippines, which rose (AAPC = 2.13, 95%CI: 1.40–2.87%) and Turkmenistan, which remained stable (AAPC = 0.05, 95%CI: −0.43–0.33%).ConclusionThe burden of diet-induced stroke varies substantially across “B&R” countries and threaten public health, relevant evidence-based policies and interventions should be adopted to address the future burden of stroke in “B&R” countries through extensive collaboration.

ObjectivesObesity is often associated with glucolipid and/or energy metabolism disorders. Ascophyllum nodosum extract (seaweed extract, SE) and Camellia sinensis-leaf extract (tea extract, TE) have been reported to promote positive metabolic effects through different mechanisms. We investigated the effects of SE and TE on metabolic homeostasis in diet-induced obese mice and discussed their functional characteristics.MethodsMale C57BL/6J mice fed with high-fat diets for 8 weeks were established as obese models and subsequently divided into different intervention groups, followed by SE, TE, and their joint interventions for 10 weeks. Body weight and food intake were monitored. Fasting glucose and oral glucose tolerance tests were interspersed during the experiment. After the intervention, the effects on obesity control were assessed based on body composition, liver pathology section, blood lipids and glucose, respiratory exchange ratio (RER), energy expenditure (EE1, EE2, and EE3), inflammatory factors, lipid anabolism enzymes, and gut flora of the obese mice.ResultsAfter continuous gavage intervention, the mice in the intervention groups exhibited lower body weight (lower ~4.93 g, vs. HFD 38.02 g), peri-testicular fat masses (lower ~0.61 g, vs. HFD 1.92 g), and perirenal fat masses (lower ~0.21 g, vs. HFD mice 0.70 g). All interventions prevented diet-induced increases in plasma levels of glucose, adiponectin, leptin, and the inflammatory factors IL-1β and TNF-α. The RER was modified by the interventions, while the rhythm of the RER was not. Blood lipids (total cholesterol, triglycerides, and LDL) decreased and were associated with lower lipid anabolism enzymes. In addition, the SE and TE interventions altered the structure and abundance of specific flora. Different interventions inhibited the growth of different genera positively associated with obesity (Escherichia–Shigella, Helicobacter, etc.) and promoted the growth of Akkermansia and Bacteroides, thus affecting the chronic inflammatory state.ConclusionSE and TE both have synergistic effects on weight control and glucolipid metabolism regulation by improving insulin sensitivity and reducing lipid synthesis-related enzyme expression, whereas the combination of SE and TE (3:1) has a better effect on regulating energy metabolism and inhibiting chronic inflammation.

BackgroundThe effect of obesity on intensive care unit outcomes among critically ill patients and whether there are sex differences have not been well investigated. We sought to determine the association between obesity and 30-day all-cause and cause-specific mortality among critically ill men and women.MethodsAdult participants who had body mass index (BMI) measurements were included from the eICU database. Participants were divided into six groups according to BMI (kg/m2) categories (underweight, <18.5; normal weight, 18.5–24.9; overweight, 25–29.9; class I obesity, 30–34.9; class II obesity, 35–39.9; class III obesity, ≥40). A multivariable adjusted logistic model was conducted with odds ratios (ORs) and 95% confidence intervals (CIs). A cubic spline curve based on the generalized additive model was used to represent the nonlinear association. Stratified analysis and sensitivity analysis were also performed.ResultsA total of 160,940 individuals were included in the analysis. Compared with the class I obesity category, the underweight and normal weight categories had higher all-cause mortality, and the multivariable adjusted ORs were 1.62 (95% CI: 1.48–1.77) and 1.20 (95% CI: 1.13–1.27) for the general population, 1.76 (95% CI: 1.54–2.01) and 1.22 (95% CI: 1.13–1.32) for men, and 1.51 (95% CI: 1.33–1.71) and 1.16 (95% CI: 1.06–1.27) for women, respectively. Accordingly, multivariable adjusted ORs for the class III obesity category were 1.14 (95% CI: 1.05–1.24) for the general population, 1.18 (95% CI: 1.05–1.33) for men, and 1.10 (95% CI: 0.98–1.23) for women. With cubic spline curves, the association between BMI and all-cause mortality was U-shaped or reverse J-shaped. Similar findings were observed for cause-specific mortality, with the underweight category associated with a higher risk of mortality. Class III obesity increased the risk of cardiovascular death among men (OR 1.51; 95% CI: 1.23–1.84) and increased the risk of other-cause death among women (OR 1.33; 95% CI: 1.10–1.61).ConclusionThe obesity paradox appears to be suitable for all-cause and cause-specific mortality among critically ill men and women. However, the protective effect of obesity cannot be extended to severely obese individuals. The association between BMI and cardiovascular mortality was sex-specific and was more pronounced among men than among women.Graphical abstract

BackgroundThe effect of vitamin K is associated with several pathological processes in fatty liver. However, the association between vitamin K levels and metabolic dysfunction-associated fatty liver disease (MAFLD) remains unclear.ObjectiveHere, we investigated the relationship between vitamin K intake and MAFLD risk by employing the American National Health and Nutrition Examination Surveys (NHANES) including 3,571 participants.MethodsMAFLD was defined as hepatic steatosis with one or more of the following: overweight or obesity, type 2 diabetes, or >2 other metabolic risk abnormalities. The total vitamin K was the sum of dietary and supplement dietary intake. The relationship of between log10(vitamin K) and MAFLD was investigated using survey-weighted logistic regression and stratified analysis, with or without dietary supplementation.ResultsThe MAFLD population had a lower vitamin K intake than the non-MAFLD population (p = 0.024). Vitamin K levels were inversely associated with MAFLD in the fully adjusted model (OR = 0.488, 95% CI: 0.302–0.787, p = 0.006). Consistent results were seen in the group without dietary supplements (OR = 0.373, 95% CI: 0.186–0.751, p = 0.009) but not in the group consuming dietary supplements (OR = 0.489, 95% CI: 0.238–1.001, p = 0.050).ConclusionVitamin K intake may be a protective factor for MAFLD, especially for individual not using dietary supplements. Nevertheless, more high-quality prospective studies are needed to clarify the causal relationship between them.