UNASSIGNED: Current research offers limited clarity on the correlation between waist circumference and chronic pain prevalence.
UNASSIGNED: This investigation seeks to elucidate the potential relationship between waist circumference and chronic pain and their causal association.
UNASSIGNED: An observational study was conducted, leveraging data from the National Health and Nutrition Examination Survey (NHANES) collected between 2001 and 2004. The multivariable logistic regression was used to assess the relationship between waist circumference and chronic pain. Furthermore, a meta-analysis of Mendelian Randomization (MR) was applied to explore a causal relationship between waist circumference and pain.
UNASSIGNED: The observational study, post multivariable adjustment, indicated that an increase in waist circumference by 1 dm (decimeter) correlates with a 14% elevation in chronic pain risk (Odds Ratio [OR] = 1.14, 95% Confidence Interval [CI]: 1.04-1.24, p = 0.01). Moreover, the meta-analysis of MR demonstrated that an increased waist circumference was associated with a genetic predisposition to pain risk (OR = 1.14, 95%CI: 1.06-1.23, p = 0.0007).
UNASSIGNED: Observational analysis confirmed a significant relationship between increased waist circumference and the incidence of chronic pain, and results based on MR Study identified increased waist circumference as potentially causal for pain.

UNASSIGNED: This study aims to explore the causal relationships between 1400 serum metabolites (SMs) and five autoimmune diseases (Myasthenia gravis [MG], Multiple sclerosis [MS], Systemic lupus erythematosus [SLE], Type 1 diabetes mellitus [T1DM], and Ulcerative colitis [UC]) through Mendelian randomization analysis.
UNASSIGNED: Data on MG, MS, SLE, T1DM, and UC were obtained from the IEU OpenGWAS Project database, while information on 1400 SMs was extracted from GWAS summary statistics provided by Chen et al. Causal relationships were assessed using the inverse variance weighted (IVW), MR-Egger, Weighted Median (WME), and Simple median (SME) methods. The robustness of instrumental variables was verified through computation of the F-statistic. Heterogeneity was evaluated using Cochran\'s Q test and the leave-one-out (LOO) method. Horizontal pleiotropy was assessed using MR-Egger regression and MR-PRESSO.
UNASSIGNED: Following correction of the IVW P values using the False Discovery Rate (FDR) method, it was found that increased levels of 5-methyluridine (ribothymidine) (OR = 1.191, 95%CI 1.086-1.307, FDR-P = 0.000) and 2\'-deoxyuridine (OR = 1.337, 95%CI 1.127-1.586, FDR-P = 0.001) were found to be correlated with a higher risk of MS. Conversely, the ratio of S-adenosylhomocysteine (SAH) to 5-methyluridine (ribothymidine) (OR = 0.771, 95%CI 0.649-0.916, FDR-P = 0.007) was linked to a decreased risk of MS. Levels of 1,2-dilinoleoyl-GPE (18:2/18:2) (OR = 0.877, 95%CI 0.791-0.974, FDR-P = 0.003) appear to be a protective factor for T1DM. No notable correlations between SMs and MG, SLE, or UC. The study detected no heterogeneity or horizontal pleiotropy.
UNASSIGNED: Levels of 5-methyluridine (ribothymidine), 2\'-deoxyuridine, and the ratio of S-adenosylhomocysteine (SAH) to 5-methyluridine (ribothymidine) can serve as predictors for MS. Similarly, 1,2-dilinoleoyl-GPE (18:2/18:2) levels can be used to predict T1DM. However, no significant causal relationships were found between SMs and MG, SLE, or UC. This observation holds significant clinical implications for crafting tailored preventive and therapeutic approaches for ADs.

UNASSIGNED: The correlation between gut microbiota and interstitial cystitis has garnered significant attention in previous studies. Nevertheless, the causal relationship between them remains to be clarified.
UNASSIGNED: Genetic variation serves as a tool in Mendelian randomization analyses, facilitating the inference of causal relationships between exposure factors and disease outcomes. In this study, summary statistics derived from a comprehensive genome-wide association study conducted by the MiBioGen consortium were utilized as exposure factors, while interstitial cystitis data sourced from the GWAS Catalog served as the disease outcome. Then, a two-sample Mendelian randomization analysis was performed by applying inverse variance-weighted, MR-Egger, Weighted Median, Simple Mode, and Weighted Mode. In addition, heterogeneity and horizontal pleiotropy were excluded by sensitivity analysis.
UNASSIGNED: IVW results confirmed that genus Haemophilus (OR = 2.20, 95% CI: 1.16-4.15, p = 0.015), genus Butyricimonas (OR = 2.26, 95% CI: 1.15-4.45, p = 0.018), genus Bacteroides (OR = 4.27, 95% CI: 1.36-13.4, p = 0.013) and Coprococcus1 (OR = 3.39, 95% CI: 1.28-8.99, p = 0.014) had a risk effect on interstitial cystitis. Sensitivity analysis did not find outlier SNPs.
UNASSIGNED: Our analysis has identified a causal relationship between specific genera and interstitial cystitis. However, further validation through randomized controlled trials is essential to substantiate these findings.

UNASSIGNED: The intricate relationship between migraine and insomnia has been a subject of great interest due to its complex mechanisms. Despite extensive research, understanding the causal link between these conditions remains a challenge.
UNASSIGNED: This study employs a bidirectional Mendelian randomization approach to investigate the causal relationship between migraine and insomnia. Risk loci for both conditions were derived from large-scale Genome-Wide Association Studies (GWAS). The primary method of Mendelian Randomization utilized in this study is the Inverse Variance Weighted (IVW) method.
UNASSIGNED: Our findings indicate a bidirectional causal relationship between migraine and insomnia. In the discovery set, migraine had a significant effect on insomnia (OR=1.02, 95% CI=1.02 (1.01-1.03), PIVW=5.30E-04). However, this effect was not confirmed in the validation set (OR=1.03, 95% CI=1.03 (0.87-1.21), PIVW=0.77). Insomnia also had a significant effect on migraine (OR=1.02, 95% CI=1.02 (0.01-1.03), PIVW=2.67E-08), and this effect was validated in the validation set (OR=2.30, 95% CI=2.30 (1.60-3.30), PIVW=5.78E-06).
UNASSIGNED: This study provides meaningful insights into the bidirectional causality between migraine and insomnia, highlighting a complex interplay between these conditions. While our findings advance the understanding of the relationship between migraine and insomnia, they also open up new avenues for further research. The results underscore the need for considering both conditions in clinical and therapeutic strategies.

BACKGROUND: Empirical investigations have shown an association between gut microbiota and postpartum depression (PPD); nevertheless, the precise cause-and-effect relationship between these two variables remains ambiguous. This research aimed to examine the possible reciprocal causal relationship between the gut microbiota and PPD.
METHODS: In this work, we used Mendelian randomization (MR) to analyze the relationship between the gut microbiota (n = 18,340) and PPD (n = 67,205). We obtained the relevant SNPs from publicly accessible genome-wide association studies (GWAS). The SNP estimations were combined by the inverse-variance weighted (IVW) method, including sensitivity analyses such as weighted median, MR Egger, and MR Pleiotropy Residual Sum and Outlier (PRESSO).
RESULTS: We have identified strong correlations between six bacterial characteristics and the likelihood of developing PPD. Our research revealed that the genus Ruminococcaceae UCG010, the family Veillonellaceae, and the class Clostridia had a beneficial effect on preventing PPD. The class Alphaproteobacteria, genus Slackia, and order NB1n were found to have a significant negative impact on PPD. The sensitivity studies conducted on these bacterial features consistently confirmed these finding.
CONCLUSIONS: It is crucial to acknowledge that our study was conducted just within a European society, which may restrict its applicability to other groups.
CONCLUSIONS: The findings from our MR investigation indicate a potential causal relationship between certain kinds of gut bacteria and PPD. Additional investigation is required to elucidate the influence of gut microbiota on the advancement of PPD.

UNASSIGNED: To investigate the causal relationship between gut microbiota (GM) and chalazion through Mendelian randomization (MR) analysis.
UNASSIGNED: GM-related genome-wide association studies (GWAS) were obtained from the International Consortium MiBioGen. Genetic data for chalazion were sourced from the MRC Integrative Epidemiology Unit (IEU) Open GWAS database. Five MR methods, including inverse variance weighted (IVW), were employed to estimate causal relationships. Cochran\'s Q test was used to detect heterogeneity, the MR-Egger intercept test and MR-PRESSO regression were utilized to detect horizontal pleiotropy, and the leave-one-out method was employed to validate data stability.
UNASSIGNED: We identified 1,509 single nucleotide polymorphisms (SNPs) across 119 genera as instrumental variables (IVs) (p < 1 × 10-5). According to the inverse variance weighted (IVW) estimate, the Family XIII AD3011 group (OR = 1.0018, 95% CI 1.0002-1.0035, p = 0.030) and Catenibacterium (OR = 1.0013, 95% CI 1.0002-1.0025, p = 0.022) were potentially associated with increased risk of chalazion. Conversely, Veillonella (OR = 0.9986, 95% CI 0.9974-0.9999, p = 0.036) appeared to provide protection against chalazion. There was no evidence of heterogeneity or pleiotropy.
UNASSIGNED: This study uncovered the causal relationship between GM and chalazion, pinpointing Catenibacterium and Family XIII AD3011 group as potential risk contributors, while highlighting Veillonella as a protective factor. In-depth investigation into the potential mechanisms of specific bacteria in chalazion was essential for providing novel therapeutic and preventive strategies in the future.

The prevalence of thyroid dysfunction diseases (TDFDs) and osteoporosis (OP) is high. Previous studies have indicated a potential association between TDFDs and OP, yet the causal direction remains unclear. This study aimed to investigate the potential causal relationship between TDFDs and the risk of developing OP and related fractures. We obtained pooled data from genome-wide association studies (GWASs) conducted on TDFDs and OP in European populations and identified single-nucleotide polymorphisms (SNPs) with genome-wide significance levels associated with exposure to TDFDs as instrumental variables. Inverse variance weighted (IVW) was employed as the primary method for Mendelian randomization (MR) analysis, supplemented by MR‒Egger, weighted median, simple mode and weighted mode methods. Sensitivity analyses were conducted to evaluate the robustness of the findings. The IVW method demonstrated an increased risk of OP in patients with TDFDs, including hyperthyroidism and hypothyroidism (TDFDs: OR = 1.11; 95% CI 1.09, 1.13; hypothyroidism: OR = 1.14; 95% CI 1.10, 1.17; hyperthyroidism: OR = 1.09; 95% CI 1.06, 1.12). These findings were supported by supplementary analysis, which revealed a positive correlation between TDFDs and the risk of OP. Multiple sensitivity analyses confirmed the absence of horizontal pleiotropy in the study, thus indicating the robustness of our results. The causal relationship between TDFDs and increased risk of OP implies the need for early bone mineral density (BMD) screening and proactive prevention and treatment strategies for individuals with TDFDs.

OBJECTIVE: Obesity and a high body mass index (BMI) are considered as risk factors for abdominal wall hernia (AWH). However, anthropometric measures of body fat distribution (BFD) seem to be better indicators in the hernia field. This Mendelian randomization analysis aimed to generate more robust evidence for the impact of waist circumstance (WC), body, trunk, arm, and leg fat percentages (BFP, TFP, AFP, LFP) on AWH.
METHODS: A univariable MR design was employed and the summary statistics allowing for assessment were obtained from the genome-wide association studies (GWASs). An inverse variance weighted (IVW) method was applied as the primary analysis, and the odds ratio value was used to evaluate the causal relationship between BFD and AWH.
RESULTS: None of the MR-Egger regression intercepts deviated from null, indicating no evidence of horizontal pleiotropy (p > 0.05). The Cochran Q test showed heterogeneity between the genetic IVs for WC (p = 0.005; p = 0.005), TFP (p < 0.001; p < 0.001), AFP-L (p = 0.016; p = 0.015), LFP-R (p = 0.012; p = 0.009), and LFP-L (p < 0.001; p < 0.001). Taking the IVW random-effects model as gold standard, each standard deviation increment in genetically determined WC, BFP, TFP, AFP-R, AFP-L, LFP-R, and LFP-L raised the risk of AWH by 70.9%, 70.7%, 56.5%, 69.7%, 78.3%, 87.7%, and 72.5%, respectively.
CONCLUSIONS: This study proves the causal relationship between AWH and BFD, attracting more attention from BMI to BFD. It provides evidence-based medical evidence that healthy figure management can prevent AWH.

UNASSIGNED: Several reports in recent years have found an association between gut microbiota and upper urinary urolithiasis. However, the causal relationship between them remains to be clarified.
UNASSIGNED: Genetic variation is used as a tool in Mendelian randomization for inference of whether exposure factors have a causal effect on disease outcomes. We selected summary statistics from a large genome-wide association study of the gut microbiome published by the MiBioGen consortium with a sample size of 18,340 as an exposure factor and upper urinary urolithiasis data from FinnGen GWAS with 4,969 calculi cases and 213,445 controls as a disease outcome. Then, a two-sample Mendelian randomization analysis was performed by applying inverse variance-weighted, MR-Egger, maximum likelihood, and weighted median. In addition, heterogeneity and horizontal pleiotropy were excluded by sensitivity analysis.
UNASSIGNED: IVW results confirmed that class Deltaproteobacteria (OR = 0.814, 95% CI: 0.666-0.995, P = 0.045), order NB1n (OR = 0.833, 95% CI: 0.737-0.940, P = 3.15 × 10-3), family Clostridiaceae1 (OR = 0.729, 95% CI: 0.581-0.916, P = 6.61 × 10-3), genus Barnesiella (OR = 0.695, 95% CI: 0.551-0.877, P = 2.20 × 10-3), genus Clostridium sensu_stricto_1 (OR = 0.777, 95% CI: 0.612-0.986, P = 0.0380), genus Flavonifractor (OR = 0.711, 95% CI: 0.536-0.944, P = 0.0181), genus Hungatella (OR = 0.829, 95% CI: 0.690-0.995, P = 0.0444), and genus Oscillospira (OR = 0.758, 95% CI: 0.577-0.996, P = 0.0464) had a protective effect on upper urinary urolithiasis, while Eubacterium xylanophilum (OR =1.26, 95% CI: 1.010-1.566, P = 0.0423) had the opposite effect. Sensitivity analysis did not find outlier SNPs.
UNASSIGNED: In summary, a causal relationship was found between several genera and upper urinary urolithiasis. However, we still need further randomized controlled trials to validate.