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Abstract Background The process of biological aging in patients diagnosed with chronic liver disease remains unclear. Aim The current study aims to investigate if there is an accelerated biological aging process in participants with advanced fibrosis (AF) and metabolic dysfunction-associated steatotic liver disease (MASLD). Methods Data from the 2017–2018 NHANES cycle were analyzed. AF was determined based on the values of liver stiffness measurement (LSM) and MASLD was defined according to new consensus nomenclature. Klemera-Doubal method biological age (KDM bioage) and Phenotypic age (Phenoage) were adopted to quantify biological age. Phenoage advancement (Phenoage_advance) and KDM advancement (KDM_advance) were generated as the difference between the calculated biological age and chronological age, and a positive residual was regarded as an indicator of accelerated biological aging. Results A total of 3974 participants was enrolled. The weight mean KDM_advance and phenoage_advance in AF group was 4.22 years (95%CI: 2.96–5.49 years) and 2.61 years (95%CI: 1.80–3.41 years), while in MASLD group was 0.37 years (95%CI: -0.28–1.03 years) and 0.04 years (95%CI: -0.64–0.72 years), respectively. Multivariate linear regression analysis showed that participants with AF had older KDM_advance and phenoage_advance compared with those without AF (1.50 years (95%CI: 0.23–2.77 years), P = 0.02; 1.00 years (95%CI: 0.18–1.82 years), P = 0.02; respectively), in models adjusting demographic characteristics, socioeconomic status, lifestyle factors, and comorbidities. No significant association was found between MASLD and KDM_advance and phenoage_advance. Conclusions AF, not MASLD, was independently associated with accelerated biological aging in adults from a US representative sample.

Abstract Background Evidence for the relationship between individual and combined volatile organic compounds (VOCs) and cardiovascular disease (CVD) is limited. Besides, the mediating role of biological aging (BA) has not been studied. Therefore, this study aimed to examine the association between VOCs and CVD risk and to explore the mediating effects of BA. Methods Logistic regression models were used to investigate the relationships of metabolites of volatile organic compounds (mVOCs) and BA with CVD. In addition, weighted quantile sum (WQS) regression, adaptive elastic networks, and Environmental Risk Score (AENET-ERS) were utilized to assess overall associations of mixed VOCs co-exposure with CVD. Mediation analyses were used to identify potential mediating effects of BA. Results In the single-pollutant model, CYMA was shown to be associated with an increased risk of CVD. Additionally, we identified significantly positive associations between the WQS index and CVD (odds ratio (OR) = 1.292, 95% confidence interval (CI): 1.006, 1.660), and DHBMA had the greatest contribution for CVD (0.246). Furthermore, the AENET-ERS results showed that 8 mVOCs were significantly associated with CVD, and ERS was related to an elevated risk of CVD (OR = 1.538, 95%CI: 1.255, 1.884). Three BA indicators mediated the association of the mVOCs mixture with CVD, with mediating effect proportions of 11.32%, 34.34%, and 7.92%, respectively. Conclusion The risk of CVD was found to increase with both individual and combined exposure to VOCs. BA mediates the positive effects of VOCs on CVD, suggesting that this pathway may be one of the mechanisms of CVD.

Background: The process of biological aging in patients diagnosed with chronic liver disease remains unclear. Aim: The current study aims to investigate if there is an accelerated biological aging process in participants with advanced fibrosis (AF) and metabolic dysfunction-associated steatotic liver disease (MASLD). Methods: Data from the 2017–2018 NHANES cycle were analyzed. AF was determined based on the values of liver stiffness measurement (LSM) and MASLD was defined according to new consensus nomenclature. Klemera-Doubal method biological age (KDM bioage) and Phenotypic age (Phenoage) were adopted to quantify biological age. Phenoage advancement (Phenoage_advance) and KDM advancement (KDM_advance) were generated as the difference between the calculated biological age and chronological age, and a positive residual was regarded as an indicator of accelerated biological aging. Results: A total of 3974 participants was enrolled. The weight mean KDM_advance and phenoage_advance in AF group was 4.22 years (95%CI: 2.96–5.49 years) and 2.61 years (95%CI: 1.80–3.41 years), while in MASLD group was 0.37 years (95%CI: -0.28–1.03 years) and 0.04 years (95%CI: -0.64–0.72 years), respectively. Multivariate linear regression analysis showed that participants with AF had older KDM_advance and phenoage_advance compared with those without AF (1.50 years (95%CI: 0.23–2.77 years), P = 0.02; 1.00 years (95%CI: 0.18–1.82 years), P = 0.02; respectively), in models adjusting demographic characteristics, socioeconomic status, lifestyle factors, and comorbidities. No significant association was found between MASLD and KDM_advance and phenoage_advance. Conclusions: AF, not MASLD, was independently associated with accelerated biological aging in adults from a US representative sample. [ABSTRACT FROM AUTHOR]

Background: Evidence for the relationship between individual and combined volatile organic compounds (VOCs) and cardiovascular disease (CVD) is limited. Besides, the mediating role of biological aging (BA) has not been studied. Therefore, this study aimed to examine the association between VOCs and CVD risk and to explore the mediating effects of BA. Methods: Logistic regression models were used to investigate the relationships of metabolites of volatile organic compounds (mVOCs) and BA with CVD. In addition, weighted quantile sum (WQS) regression, adaptive elastic networks, and Environmental Risk Score (AENET-ERS) were utilized to assess overall associations of mixed VOCs co-exposure with CVD. Mediation analyses were used to identify potential mediating effects of BA. Results: In the single-pollutant model, CYMA was shown to be associated with an increased risk of CVD. Additionally, we identified significantly positive associations between the WQS index and CVD (odds ratio (OR) = 1.292, 95% confidence interval (CI): 1.006, 1.660), and DHBMA had the greatest contribution for CVD (0.246). Furthermore, the AENET-ERS results showed that 8 mVOCs were significantly associated with CVD, and ERS was related to an elevated risk of CVD (OR = 1.538, 95%CI: 1.255, 1.884). Three BA indicators mediated the association of the mVOCs mixture with CVD, with mediating effect proportions of 11.32%, 34.34%, and 7.92%, respectively. Conclusion: The risk of CVD was found to increase with both individual and combined exposure to VOCs. BA mediates the positive effects of VOCs on CVD, suggesting that this pathway may be one of the mechanisms of CVD. Highlights: Individual and mixed exposure to VOCs were associated with elevated CVD risk. DHBMA dominates mixtures of mVOCs for increased CVD risk. BA mediates the effect of VOCs mixture exposure on CVD. [ABSTRACT FROM AUTHOR]

Abstract Introduction Even though cadmium (Cd) exposure and cellular senescence (telomere length) have been linked in previous studies, composite molecular aging biomarkers are more significant and reliable factors to consider when examining the connection between metal exposure and health outcomes. The purpose of this research was to assess the association between urinary cadmium (U-Cd) and whole-body aging (phenotypic age). Methods Phenotypic age was calculated from chronological age and 9 molecular biomarkers. Multivariate linear regression models, subgroup analysis, and smoothing curve fitting were used to explore the linear and nonlinear relationship between U-Cd and phenotypic age. Mediation analysis was performed to explore the mediating effect of U-Cd on the association between smoking and phenotypic age. Results This study included 10,083 participants with a mean chronological age and a mean phenotypic age of 42.24 years and 42.34 years, respectively. In the fully adjusted model, there was a positive relationship between U-Cd and phenotypic age [2.13 years per 1 ng/g U-Cd, (1.67, 2.58)]. This association differed by sex, age, and smoking subgroups (P for interaction

Introduction: Even though cadmium (Cd) exposure and cellular senescence (telomere length) have been linked in previous studies, composite molecular aging biomarkers are more significant and reliable factors to consider when examining the connection between metal exposure and health outcomes. The purpose of this research was to assess the association between urinary cadmium (U-Cd) and whole-body aging (phenotypic age). Methods: Phenotypic age was calculated from chronological age and 9 molecular biomarkers. Multivariate linear regression models, subgroup analysis, and smoothing curve fitting were used to explore the linear and nonlinear relationship between U-Cd and phenotypic age. Mediation analysis was performed to explore the mediating effect of U-Cd on the association between smoking and phenotypic age. Results: This study included 10,083 participants with a mean chronological age and a mean phenotypic age of 42.24 years and 42.34 years, respectively. In the fully adjusted model, there was a positive relationship between U-Cd and phenotypic age [2.13 years per 1 ng/g U-Cd, (1.67, 2.58)]. This association differed by sex, age, and smoking subgroups (P for interaction < 0.05). U-Cd mediated a positive association between serum cotinine and phenotypic age, mediating a proportion of 23.2%. Conclusions: Our results suggest that high levels of Cd exposure are associated with whole-body aging. [ABSTRACT FROM AUTHOR]