No bidirectional relationship between inflammatory bowel disease and diverticular disease: a genetic correlation and Mendelian randomization study

Background: Although previous studies found that inflammatory bowel disease (IBD) and diverticular disease (DD) usually co-exist clinically, studies examining the relationship are spare.Aim: Our study aspires to investigate the causal correlation between the IBD [including ulcerative colitis (UC) and Crohn’s disease (CD)] and DD using the Mendelian randomization (MR) analysis.Methods: We conducted a two-sample bidirectional MR analysis using publicly available genome-wide association studies (GWAS) summary data. The single nucleotide polymorphism (SNP) data associated with DD and IBD were obtained from the Finnish Biobank and UK Biobank, respectively. Through secondary data analysis of all GWAS summary data, we systematically screened genetic instrumental variables. To address the impact of horizontal pleiotropy, several methods were employed, including the inverse variance-weighted method (IVW), maximum likelihood method, Egger regression method, weighted median method, and simple median method. These approaches aimed to detect and correct for the potential bias caused by horizontal pleiotropy.Results: Genetically predicted DD did not have a causal effect on IBD (OR 1.06, 95% CI 0.98–1.17, p = 0.15), and had no causal effect on UC (OR 1.10, 95% CI 0.94–1.20, p = 0.36) and CD (OR 1.03, 95% CI 0.92–1.16, p = 0.62) either. Furthermore, in the reverse MR analysis, we did not observe any significant causal effect of IBD on DD. Results of complementary methods showed consistent results with those of the IVW method.Conclusion: This study’s findings do not provide evidence for a causal relationship between IBD and DD, which contradicts the majority of observational studies

Table2_No bidirectional relationship between inflammatory bowel disease and diverticular disease: a genetic correlation and Mendelian randomization study.xlsx

Background: Although previous studies found that inflammatory bowel disease (IBD) and diverticular disease (DD) usually co-exist clinically, studies examining the relationship are spare.Aim: Our study aspires to investigate the causal correlation between the IBD [including ulcerative colitis (UC) and Crohn’s disease (CD)] and DD using the Mendelian randomization (MR) analysis.Methods: We conducted a two-sample bidirectional MR analysis using publicly available genome-wide association studies (GWAS) summary data. The single nucleotide polymorphism (SNP) data associated with DD and IBD were obtained from the Finnish Biobank and UK Biobank, respectively. Through secondary data analysis of all GWAS summary data, we systematically screened genetic instrumental variables. To address the impact of horizontal pleiotropy, several methods were employed, including the inverse variance-weighted method (IVW), maximum likelihood method, Egger regression method, weighted median method, and simple median method. These approaches aimed to detect and correct for the potential bias caused by horizontal pleiotropy.Results: Genetically predicted DD did not have a causal effect on IBD (OR 1.06, 95% CI 0.98–1.17, p = 0.15), and had no causal effect on UC (OR 1.10, 95% CI 0.94–1.20, p = 0.36) and CD (OR 1.03, 95% CI 0.92–1.16, p = 0.62) either. Furthermore, in the reverse MR analysis, we did not observe any significant causal effect of IBD on DD. Results of complementary methods showed consistent results with those of the IVW method.Conclusion: This study’s findings do not provide evidence for a causal relationship between IBD and DD, which contradicts the majority of observational studies.</p

Table1_No bidirectional relationship between inflammatory bowel disease and diverticular disease: a genetic correlation and Mendelian randomization study.xls

Background: Although previous studies found that inflammatory bowel disease (IBD) and diverticular disease (DD) usually co-exist clinically, studies examining the relationship are spare.Aim: Our study aspires to investigate the causal correlation between the IBD [including ulcerative colitis (UC) and Crohn’s disease (CD)] and DD using the Mendelian randomization (MR) analysis.Methods: We conducted a two-sample bidirectional MR analysis using publicly available genome-wide association studies (GWAS) summary data. The single nucleotide polymorphism (SNP) data associated with DD and IBD were obtained from the Finnish Biobank and UK Biobank, respectively. Through secondary data analysis of all GWAS summary data, we systematically screened genetic instrumental variables. To address the impact of horizontal pleiotropy, several methods were employed, including the inverse variance-weighted method (IVW), maximum likelihood method, Egger regression method, weighted median method, and simple median method. These approaches aimed to detect and correct for the potential bias caused by horizontal pleiotropy.Results: Genetically predicted DD did not have a causal effect on IBD (OR 1.06, 95% CI 0.98–1.17, p = 0.15), and had no causal effect on UC (OR 1.10, 95% CI 0.94–1.20, p = 0.36) and CD (OR 1.03, 95% CI 0.92–1.16, p = 0.62) either. Furthermore, in the reverse MR analysis, we did not observe any significant causal effect of IBD on DD. Results of complementary methods showed consistent results with those of the IVW method.Conclusion: This study’s findings do not provide evidence for a causal relationship between IBD and DD, which contradicts the majority of observational studies.</p

Image2_No bidirectional relationship between inflammatory bowel disease and diverticular disease: a genetic correlation and Mendelian randomization study.tiff

Background: Although previous studies found that inflammatory bowel disease (IBD) and diverticular disease (DD) usually co-exist clinically, studies examining the relationship are spare.Aim: Our study aspires to investigate the causal correlation between the IBD [including ulcerative colitis (UC) and Crohn’s disease (CD)] and DD using the Mendelian randomization (MR) analysis.Methods: We conducted a two-sample bidirectional MR analysis using publicly available genome-wide association studies (GWAS) summary data. The single nucleotide polymorphism (SNP) data associated with DD and IBD were obtained from the Finnish Biobank and UK Biobank, respectively. Through secondary data analysis of all GWAS summary data, we systematically screened genetic instrumental variables. To address the impact of horizontal pleiotropy, several methods were employed, including the inverse variance-weighted method (IVW), maximum likelihood method, Egger regression method, weighted median method, and simple median method. These approaches aimed to detect and correct for the potential bias caused by horizontal pleiotropy.Results: Genetically predicted DD did not have a causal effect on IBD (OR 1.06, 95% CI 0.98–1.17, p = 0.15), and had no causal effect on UC (OR 1.10, 95% CI 0.94–1.20, p = 0.36) and CD (OR 1.03, 95% CI 0.92–1.16, p = 0.62) either. Furthermore, in the reverse MR analysis, we did not observe any significant causal effect of IBD on DD. Results of complementary methods showed consistent results with those of the IVW method.Conclusion: This study’s findings do not provide evidence for a causal relationship between IBD and DD, which contradicts the majority of observational studies.</p

Image1_No bidirectional relationship between inflammatory bowel disease and diverticular disease: a genetic correlation and Mendelian randomization study.tiff

Background: Although previous studies found that inflammatory bowel disease (IBD) and diverticular disease (DD) usually co-exist clinically, studies examining the relationship are spare.Aim: Our study aspires to investigate the causal correlation between the IBD [including ulcerative colitis (UC) and Crohn’s disease (CD)] and DD using the Mendelian randomization (MR) analysis.Methods: We conducted a two-sample bidirectional MR analysis using publicly available genome-wide association studies (GWAS) summary data. The single nucleotide polymorphism (SNP) data associated with DD and IBD were obtained from the Finnish Biobank and UK Biobank, respectively. Through secondary data analysis of all GWAS summary data, we systematically screened genetic instrumental variables. To address the impact of horizontal pleiotropy, several methods were employed, including the inverse variance-weighted method (IVW), maximum likelihood method, Egger regression method, weighted median method, and simple median method. These approaches aimed to detect and correct for the potential bias caused by horizontal pleiotropy.Results: Genetically predicted DD did not have a causal effect on IBD (OR 1.06, 95% CI 0.98–1.17, p = 0.15), and had no causal effect on UC (OR 1.10, 95% CI 0.94–1.20, p = 0.36) and CD (OR 1.03, 95% CI 0.92–1.16, p = 0.62) either. Furthermore, in the reverse MR analysis, we did not observe any significant causal effect of IBD on DD. Results of complementary methods showed consistent results with those of the IVW method.Conclusion: This study’s findings do not provide evidence for a causal relationship between IBD and DD, which contradicts the majority of observational studies.</p

Data_Sheet_1_Association between frailty and hepatic fibrosis in NAFLD among middle-aged and older adults: results from NHANES 2017–2020.docx

BackgroundAlthough previous studies found that frailty is prevalent in NAFLD patients with advanced liver fibrosis and cirrhosis, studies examining the relationship are spare.AimOur study aspires to investigate the potential correlation between the Frailty Index (FI) and hepatic fibrosis among middle-aged and older adults with NAFLD.MethodsData from the 2017–2020.03 National Health and Nutrition Examination Survey (NHANES) were utilized for this study, with a final of 2,383 participants aged 50 years and older included. The quantification of frailty was executed employing a 49-item frailty index. The recognition of hepatic steatosis and fibrosis was accomplished through the utilization of the controlling attenuation parameter (CAP) and transient elastography (TE). The relationship between the FI and hepatic fibrosis were investigated employing univariable and multivariable-adjusted logistic regression analyses. A subgroup analysis was conducted, dividing the subjects based on gender, Body Mass Index (BMI), and the presence of hyperlipidemia.ResultsThe findings demonstrated a positive correlation between the FI and significant hepatic fibrosis in NAFLD, even after using multivariate logistic regression models adjusting for potential confounding factors (OR = 1.022, 95% CI, 1.004–1.041) and in tertiles (Q3vs Q1: OR = 2.004, 95% CI, 1.162–3.455). In the subgroup analysis, the correlation was more statistically significant in male (OR = 1.046, 95% CI, 1.022–1.071), under/normal weight (OR = 1.077, 95% CI, 1.009–1.150), overweight (OR = 1.040, 95% CI, 1.010–1.071), and subjects without hyperlipidemia (OR = 1.054, 95% CI, 1.012–1.097). The area under the Receiver Operating Characteristic (ROC) curve for the FI in assessing the existence of substantial fibrosis in NAFLD was 0.612 (95% CI, 0.596–0.628).ConclusionThis study demonstrated a positive correlation between significant hepatic fibrosis and frailty, particularly among males aged 50 years and older, who were non-obese and did not have hyperlipidemia with NAFLD. Additional studies are required to further validate these findings.</p