Background Asthma is a public health problem worldwide. However, only a few studies have reported the epidemiology of asthma in various age groups in East Asia. The present study aimed to analyze and predict trends in the incidence of asthma in East Asia through the Global Burden of Disease 2019 (GBD 2019) study and provide information for prevention and control strategies. Methods The estimates of incidence, deaths, disability-adjusted life years (DALYs), and risk factors of asthma in China, South Korea, Japan, and the world from 1990–2019 were retrieved from the GBD 2019 study. The age-standardized rates (ASRs) and the average annual percentage changes (AAPCs) assessed the incidence, deaths, and DALYs of asthma, and the projection was assessed by applying the age-period-cohort model. Results The burden of asthma in South Korea and Japan was slightly higher than in China and slightly lower than that worldwide. The age-standardized incidence rate (ASIR) of asthma in China decreased slightly from 394.58/100,000 in 1990 to 355.33/100,000 in 2019 (with an AAPC of −0.59), while the age-standardized death rate (ASDR) and the age-standardized DALY rate (ASDALR) decreased significantly (with a AAPCs of −5.22 and −2.89, respectively), which were lower than those in South Korea and Japan. Moreover, males in China, South Korea, and Japan were significantly more affected by tobacco and environmental/occupational factors than females, while the proportion of metabolic factors in females was higher than that in males. The prediction for the burden of asthma in the three East Asian countries continued to decline or stabilize until 2030, especially in China and Japan. Conclusions Although the overall asthma burden has a downward trend according to GBD 2019, it is still heavy in East Asia, especially South Korea. In addition, increased concern and control measures are needed for the disease burden in elderly patients.

Background: Coffee is one of the most consumed beverages in the world, coffee consumption has been growing in the United States over the past 20 years. Periodontitis is defined by the pathologic loss of the periodontal ligament and destruction of the connective tissue attachment and alveolar bone loss and is related to different systemic diseases and conditions. However, the causality has remained unclarified, thus we regarded discovering the causal relationship between coffee consumption and the infection risk of periodontitis as the objective of the study. Methods: Coffee consumption was subdivided into binary coffee consumption and continuous coffee consumption to refine the study design. Genetic instruments were stretched from the MRC-IEU (MRC Integrative Epidemiology Unit)analysis on the UK Biobank, the Gene-Lifestyle Interactions in Dental Endpoints (GLIDE) project, and the joint meta-analysis of a recent GWAS. The IVW (Inverse Variance Weighted) method, MR-Egger regression, and Weighted Median method were introduced to estimate the causality, a scatter plot revealed the intuitive result, and a Leave-One-Out plot was used to test the stability. Heterogeneity and pleiotropy analyses were also conducted to test outlier SNPs (Single Nucleotide Polymorphisms). Results: An effect of continuous coffee consumption on the risk of periodontitis was found (IVW: OR = 1.0104, 95%CI: 1.0016-1.0193, P = 0.0212; MR-Egger: OR = 1.0004, 95%CI: 0.9753-1.0303, P = 0.98; Weighted Median: OR = 1.0077, 95%CI: 0.9963-1.0191, P = 0.19), while the effect of binary coffee consumption on periodontitis did not meet the requirement of indicating a strong causal association, neither were the reverse causality analyses. Conclusions: The study indicated the causality of continuous coffee consumption to the risk of periodontitis with no strong evidence for an effect of binary coffee-consuming behavior on periodontitis. There was also no intensive evidence suggesting reverse causality.

Objectives In this study, assessing whether coffee consumption and caffeine intake were associated with periodontitis infection separately was set as the objective. Materials and Methods Divided into binary and continuous categories, coffee consumption was set as the exposure variable along with caffeine intake and periodontitis infection as the outcome variables. Other covariables were regarded as potential confounders. The cross-sectional study was conducted based on the National Health and Nutrition Examination Survey, with multivariate regression models, subgroup analyses, smooth fitting curves, and threshold effect examinations conducted to pursue a definite correlation between exposures and the outcome. Results Negative associations were discovered between binary coffee consumption and caffeine intake and periodontitis infection, with all confounders adjusted. In subgroup analyses stratified by sex, diabetes mellitus status, and hypertension status, interaction and threshold effects were observed, which were revealed intuitively by smooth-fitting curves. Conclusions Significant negative associations between binary consumption and caffeine intake and periodontitis infection separately were indicated, with no evidence suggesting a credible correlation between continuous coffee consumption and periodontitis infection risk. The benefits of the behavior of consuming coffee and consuming caffeine were more obvious among males and individuals who do not suffer from diabetes or hypertension.

Objectives This investigation aimed to examine the correlation between coffee and caffeine intake with the risk of COPD and lung function based on NHANES 2007–2012.Materials and Methods Exposure variables were established as coffee and caffeine consumption, while the risk of COPD and lung function were considered as the outcome variables. Other covariates were deemed potential confounders. A cross-sectional study was conducted using data from the NHANES to determine a definitive correlation between exposure variables and outcome variables.Results Multivariable regression models revealed positive associations between coffee and caffeine consumption and the risk of COPD and lung function. Subgroup analyses, stratified by sex, DM, hypertension status, and smoking habits, identified potential effect modifiers, as well as infection points from threshold effect examinations.Conclusions The results of this cross-sectional study indicated significant positive associations between coffee and caffeine consumption and the risk of COPD. Additionally, positive associations between exposure variables and FEV1 and FVC were discovered. Among the stratification factors, smoking status exhibited the most potential for modifying effects.

Background: Chronic obstructive pulmonary disease (COPD) patients often exhibit gastrointestinal symptoms, and COPD is potentially associated with colorectal cancer (CRC). Methods: We collected COPD and CRC data from the National Health and Nutrition Examination Survey, genome-wide association studies, and RNA sequence for a comprehensive analysis. We used weighted logistic regression to explore the association between COPD and CRC incidence risk. Mendelian randomization analysis was performed to assess the causal relationship between COPD and CRC, and cross-phenotype meta-analysis was conducted to pinpoint crucial loci. Multivariable mendelian randomization was used to uncover mediating factors connecting the two diseases. Our results were validated using both NHANES and GEO databases. Results: In the NHANES dataset, we found that COPD serves as a contributing factor in the development of CRC. MR analysis revealed that COPD increased the risk of CRC onset and progression (OR: 1.16, 95% CI: 1.01–1.36). Cross-phenotype meta-analysis identified four critical genes associated with both CRC and COPD. Multivariable mendelian randomization results indicated that body fat percentage, omega-3, omega-6, and the omega-3 to omega-6 ratio may be mediating factors impacting both CRC and COPD; these findings were confirmed in the NHANES dataset. In the RNA expression data for COPD and CRC, weighted gene co-expression network analysis and Kyoto Encyclopedia of Genes and Genomes enrichment results demonstrated a strong correlation between fatty acid–related modules in both diseases. Conclusions: Our findings suggest that COPD may contribute to an elevated risk of CRC development through fatty acid–related pathways.