Objective: Elevated sodium consumption is associated with increased risk for chronic kidney disease (CKD) and data for this disease burden attributable to high sodium intake in China from 1990 to 2019 are scarce in China. Our study aims to estimate and present the national burden of CKD attributable to high sodium intake, as well as its profile.Methods: The regional disease burden data from the China Center for Food Safety Risk Assessment (CFSA) from 1990 to 2019 were compiled based on the methodology of GBD 2019. CKD burden [deaths and disability-adjusted life years (DALYs)] was quantified according to population group (age, gender) and regions categories (province, SDI). The estimated annual percentage change (EAPC) in age-standardized mortality rate (ASMR) and age-standardized DALYs rate (ASDR) were calculated to describe long-term trends.Results: Totally, the number of deaths of CKD attributable to high sodium intake reached 95,000, with DALYs amounting to 2.59 million person-years in 2019, while the trends of ASMR (EAPC: -0.31, 95%CI: −0.46, −0.17%) and ASDR (−0.33, 95%CI: −0.48, −0.18%) were down during the observation period. The age-specific numbers and rates of deaths, as well as DALYs increase with age are higher in males than in females. Significant disparities in CKD burden attributable to high sodium intake were observed across provinces and SDI regions. In both 1990 and 2019, the number of deaths and DALYs were higher in middle SDI regions, while low-middle SDI regions had highest ASMR and ASDR. The EAPC of ASDR was found to be significantly negatively correlated with the 1990 ASDR (ρ = −0.393, p = 0.024), and the EAPC of ASMR and ASDR were also significantly negatively correlated with the 2019 SDI (ASMR:ρ = −0.571, p < 0.001; ASDR:ρ = −0.368, p = 0.035).Conclusion: High sodium intake accounted for a sizeable burden of disease from 1990 to 2019 in China, also presents sexual and geographic variations. Despite a slight decreasing trend exists, the absolute number increased as much as twofold, particularly among males and seniors. Targeting to reduce sodium intake remains a priority, and progress requires systematic monitoring and evaluation, particularly in middle SDI regions that are experiencing rising trends and low-middle SDI regions being susceptible to approaches.

Objective: To combat the harmful impacts of cardiovascular diseases (CVDs) on public health, it is crucial to understand the epidemiologic features and disease burden. The study aims to identify the trends of CVDs burden in youths aged 0–19 years from 1990 to 2021 across the global, Asian, and Chinese contexts to inform more effective strategies and actions. Methods: The data from the Global Burden of Diseases and Risk Factors Study (GBD) 2021 were analyzed, stratified by sex, age, the socio-demographic index (SDI) regions, disease subtypes, respectively. We also employed the Auto-Regressive Integrated Moving Average (ARIMA) to predict the future burden of CVDs up to 2036. Results: In 2021, DALY rate of CVDs among children and adolescents were 303.140 (268.480–343.800) globally, 268.730 (242.730–298.350) in Asia and 148.800 (126.510–173.620) in China. It exhibited significant declined trends from 1990 to 2021, with average annual percentage changes (AAPCs) of −2.447, −2.665, and −4.379, respectively (all p < 0.001). Compared with males, females had relatively higher prevalence of CVDs globally (797.060 vs. 791.140 per 100,000). Rheumatic heart disease served as the most prominent subtype across the world. Non-optimal temperatures emerged as the primary risk factor for CVDs-related disability-adjusted life years (DALYs). The CVDs incidence rate is predicted to rise to 108.861 per 100,000 globally, while the rate in Asia remains steady and decreases in China in 2036. Conclusion: A substantial global burden of CVDs in youths aged 0–19 years remains the pressing public health issue in 2021. The burden of overall and type-specific CVDs varies by age, sex, SDI, regions and countries. Current and future challenges in CVDs prevention for youngsters implied by the epidemiologic features are highlighted in this study.

Some observational studies have suggested an association between insomnia and the risk of certain gastrointestinal disorders, such as gastroesophageal reflux, irritable bowel syndrome and peptic ulcers. However, the direction and magnitude of the causal relationship are difficult to determine due to confounding and reverse causation. The aim of this study is to explore the causal association between insomnia and a variety of gastrointestinal disorders from genetic level using Mendelian randomization. We used a two-sample, two-way MR to analyze the link between insomnia and several gastrointestinal disorders (nine in total). Genetic variants used as instrumental variables were obtained from genome-wide association study (GWAS) data in the Open GWAS database. Causal effects were primarily estimated using inverse variance weighted (IVW), weighted median (WM) and MR-Egger. Horizontal pleiotropy was tested using MR-PRESSO and MR-Egger regression. Heterogeneity and sensitivity were assessed using Cochran's Q and leave-one-out. The forward MR analysis demonstrated significant causal effects of insomnia on gastroesophageal reflux disease (GERD) (IVW: OR = 1.864, 95%CI: 1.16–2.98, P = 0.009) and irritable bowel syndrome(IBS) (IVW: OR = 2.401, 95%CI:1.06–5.44, P = 0.036; WM: OR = 3.381, 95%CI:1.12–10.22, P = 0.031). Conversely, reverse MR analyses indicated protective associations against insomnia development for chronic gastritis (IVW: OR = 0.98, 95%CI: 0.97–0.99, P = 0.027), while revealing risk-enhancing effects for acute gastritis (IVW: OR = 1.013, 95% CI: 1.006–1.019, P < 0.001). No causal associations were observed between insomnia and the remaining five gastrointestinal conditions. Through bidirectional MR analysis of nine gastrointestinal disorders, we provide genetic evidence for causal effects of insomnia on four conditions: gastroesophageal reflux disease (GERD), irritable bowel syndrome (IBS), chronic gastritis, and acute gastritis.

Major airway diseases, including chronic obstructive pulmonary disease (COPD), asthma, bronchiectasis and chronic rhinosinusitis without nasal polyps (CRSsNP), frequently coexist and share inflammatory, epithelial and remodeling features. However, whether these clinically distinct airway disorders are driven by a unified genetic liability and how this shared liability maps to disease-relevant tissues, genes and immune-regulatory programs remain incompletely understood. We integrated GWAS summary statistics for COPD, asthma, bronchiectasis and CRSsNP using linkage disequilibrium score regression, local genetic correlation analysis and Genomic structural equation modeling. A latent shared airway disease factor, termed gAirwayDisease, was constructed to capture common genetic liability across the four conditions. We then applied an integrative functional genomics framework, including gsMap spatial enrichment, PoPS gene prioritization, MAGMA gene-set enrichment, GTEx v8 lung MTWAS, OneK1K and DICE immune-cell MTWAS, scMORE regulon analysis and phenome-wide Mendelian randomization. All six airway disease pairs showed positive genetic correlations, with estimates ranging from 0.508 to 0.685. Genomic SEM supported a single shared factor, with positive standardized loadings for COPD, asthma, bronchiectasis and CRSsNP and excellent model fit. Spatial mapping localized gAirwayDisease-associated signals to airway- and epithelial-associated anatomical domains. PoPS prioritized immune and airway-relevant genes, including SMAD3, GATA3, IL1R1, RUNX3 and STAT6, while MAGMA enrichment highlighted B-cell activation, T-cell activation and transcriptional regulatory pathways. Lung MTWAS identified SLC9A2 and ORMDL3 as top genetically regulated expression signals. OneK1K immune-cell MTWAS highlighted recurrent IL18R1 associations across CD4 and CD8 T-cell subsets. scMORE further identified 36 significant regulon–cell type pairs across dendritic cells, B cells, monocytes, T cells and NK cells, including BCL11A, TCF4, KLF4, RUNX1 and STAT4 regulons. MR-PheWAS linked genetically predicted gAirwayDisease to respiratory, allergic, lung function and immune-related traits. This study defines gAirwayDisease as a genetically informed latent factor capturing shared liability across major airway diseases. Integrated functional genomic analyses highlight airway epithelial and immune regulatory programs associated with shared disease susceptibility and prioritize candidate genes and regulons for future experimental validation.