Search

Objects: Previous studies have suggested a potential correlation between rheumatoid arthritis (RA) and biological aging, but the intricate connections and mechanisms remain elusive. Methods: In our study, we focused on two specific measures of biological age (PhenoAge and BioAge), which are derived from clinical biomarkers. The residuals of these measures, when compared to chronological age, are defined as biological age accelerations (BAAs). Utilizing the extensive UK Biobank dataset along with various genetic datasets, we conducted a thorough assessment of the relationship between BAAs and RA at both the individual and aggregate levels. Results: Our observational studies revealed positive correlations between the two BAAs and the risk of developing both RA and seropositive RA. Furthermore, the genetic risk score (GRS) for PhenoAgeAccel was associated with an increased risk of RA and seropositive RA. Linkage disequilibrium score regression (LDSC) analysis further supported these findings, revealing a positive genetic correlation between PhenoAgeAccel and RA. PLACO analysis identified 38 lead pleiotropic single nucleotide polymorphisms linked to 301 genes, providing valuable insights into the potential mechanisms connecting PhenoAgeAccel and RA. Conclusion: In summary, our study has successfully revealed a positive correlation between accelerated biological aging, as measured by BAAs, and the susceptibility to RA. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to identify novel genetic factors that contribute to body surface area (BSA) and explore its relationship with complex traits and diseases. Methods: Based on more than 330,000 European individuals in the UK Biobank, the first large‐scale genome‐wide association study for BSA was performed. Comprehensive genetic analysis and enrichment analysis were then performed to explore the biological function of the identified loci. The genetic correlations and causal associations between BSA and other anthropometry parameters, early growth indices, and later‐life diseases, respectively, were assessed by complex genetic approaches. Results: Genome‐wide association study analysis identified a total of 456 conditionally independent single‐nucleotide polymorphism mapping genes with known functions in the regulation of adipogenesis and metabolism and enriched in adipogenesis‐related pathways. BSA was highly genetically correlated with obesity phenotypes, and all the studied anthropometry parameters from the UK Biobank were significantly positively associated with BSA. BSA was phenotypically associated with 13 chronic diseases and genetically associated with 6 diseases. Mendelian randomization analyses showed that BSA has a causal effect in increasing the risk of some diseases. Conclusions: These findings increase understanding of genetic determinants for BSA and its relationship with complex traits and diseases, and BSA could be regarded as a potential obesity trait. [ABSTRACT FROM AUTHOR]

Purpose: To reveal relationship between air pollution exposure and osteoporosis (OP) risk., Methods: Based on large-scale data from the UK Biobank, we evaluated the relationship between OP risk and several air pollutants. Then air pollution scores (APS) were constructed to assess the combined effects of multiple air pollutants on OP risk. Finally, we constructed a genetic risk score (GRS) based on a large genome-wide association study of femoral neck bone mineral density and assessed whether single or combined exposure to air pollutants modifies the effect of genetic risk on OP and fracture risk., Results: PM 2.5 , NO 2 , NO x , and APS were significantly associated with an increased risk of OP/fracture. OP and fracture risk raised with increasing concentrations of air pollutants: compared to the lowest APS quintile group, subjects in the highest quintile group had a hazard ratio (HR) (95% CI) estimated at 1.140 (1.072-1.213) for OP and 1.080 (1.026-1.136) for fracture. Moreover, participants with low GRS and the highest air pollutant concentration had the highest risk of OP, the HRs (95% CI) of OP were 1.706 (1.483-1.964), 1.658 (1.434-1.916), 1.696 (1.478-1.947), 1.740 (1.506-2.001) and 1.659 (1.442-1.908), respectively, for PM 2.5 , PM 10 , PM 2.5-10 , NO 2 , and NO x . Similar results were also observed for fractures. Finally, we assessed the joint effect of APS and GRS on the risk of OP. Participants with higher APS and lower GRS had a higher risk of developing OP. Similar results were observed in the joint effect of GRS and APS on fracture., Conclusions: We found that exposure to air pollution, individually or jointly, could improve the risk of developing OP and fractures, and increased the risk by interacting with genetic factors., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Yu, Cao, Bo, Lei and Deng.)