Intrinsische Kapazität: Fünf Fähigkeiten, die mehr über Ihr Altern verraten als eine Zahl

Age-related decline in intrinsic capacity (IC), defined as the sum of an individual's physical and mental capacities, is a cornerstone for promoting healthy aging by prioritizing maintenance of function over disease treatment. However, assessing IC is resource-intensive, and the molecular and cellular bases of its decline are poorly understood. Here we used the INSPIRE-T cohort (1,014 individuals aged 20-102 years) to construct the IC clock, a DNA methylation-based predictor of IC, trained on the clinical evaluation of cognition, locomotion, psychological well-being, sensory abilities and vitality. In the Framingham Heart Study, DNA methylation IC outperforms first-generation and second-generation epigenetic clocks in predicting all-cause mortality, and it is strongly associated with changes in molecular and cellular immune and inflammatory biomarkers, functional and clinical endpoints, health risk factors and lifestyle choices. These findings establish the IC clock as a validated tool bridging molecular readouts of aging and clinical assessments of IC.

<h4>Objectives</h4>This study aims to test a conceptual mediation model wherein periodontitis is associated with mortality through direct pathways and indirectly via accelerated biological aging.<h4>Material and methods</h4>We analyzed six cycles of National Health and Nutrition Examination Survey data with mortality follow-up of 250 months. Weighted descriptive statistics were used to compare group characteristics, Kaplan-Meier analysis to evaluate periodontitis-mortality associations and generalized linear models to examine the links between periodontitis and biological aging. Cox proportional hazards models integrated with restricted cubic splines were utilized to explore the association between biological age and mortality, and mediation analyses quantified the mediation of biological aging. Additionally, age, gender, and smoking status subgroup analyses were conducted.<h4>Results</h4>Moderate/severe periodontitis was associated with a significantly elevated all‑cause mortality risk (18.31% vs. 10.88% in no/mild periodontitis) and greater biological age advancement (PhenoAge: 1.22 years; KDM: 0.68 years). Biological age acceleration exhibited a non-linear association with mortality, with hazard ratios rising sharply beyond a threshold (PhenoAge: 16.4 years; KDM: 31.8 years). Mediation analysis showed that biological age partially mediated the periodontitis-mortality association, with indirect effect hazard ratios of 1.085 (95% CI: 1.067-1.106) for PhenoAge advance and 1.0

<h4>Objective</h4>Aging is characterized by progressive physiological and psychological changes, leading to decreased cellular metabolism and increased vulnerability to age-related diseases.<h4>Methods.</h4>In this study, we examined the relationship between circulating Klotho levels and biological age acceleration (BAA) in a representative cohort of middle-aged and older adults. Data were obtained from the National Health and Nutrition Examination Survey (NHANES, 2007-2010), including 5,654 participants aged 45-85 years. Serum Klotho concentrations were quantified using ELISA, while biological age was estimated with the BioAge R package.<h4>Result</h4>Linear regression analyses demonstrated a robust inverse association between log-transformed Klotho levels and BAA across all statistical models, with reductions of -1.06 (95% CI: -1.77 to -0.36, p = 0.005), -1.44 (95% CI: -2.15 to -0.73, p < 0.001), and -1.30 (95% CI: -2.20 to -0.40, p = 0.01). Consistent results were observed in logistic regression models, where higher Klotho concentrations were linked to lower odds of accelerated aging (OR = 0.72, 95% CI: 0.59-0.88, p = 0.002; OR = 0.63, 95% CI: 0.51-0.77, p < 0.0001; OR = 0.62, 95% CI: 0.46-0.84, p = 0.01). Subgroup analyses revealed significant associations in women, participants over 60 years of age, and individuals without chronic illnesses. Interaction analyses further indicated that age (p-interaction = 0.002), alcohol intake (p-interaction = 0.04), and diabetes status

Adverse childhood experiences (ACEs), such as abuse and neglect, are associated with poor health in adulthood. One proposed biological mechanism linking early adversity to health outcomes is epigenetic age acceleration (EAA), a measure of biological aging derived from DNA methylation. Understanding whether ACEs contribute to EAA might identify pathways linking early life stress to increased risk of morbidity and mortality.This systematic review and meta-analysis examined the relationship between cumulative ACE exposure and EAA in adults across 27 eligible observational studies from 1036 identified by comprehensive screening of the literature. Studies involved more female participants (median 56.6%) and employed a range of epigenetic clocks, most frequently Horvath, GrimAge, and PhenoAge. Risk of bias was assessed using the ROBINS-E tool, with most studies rated as having some concerns, primarily due to a lack of adjustment for key covariates. Meta-analyses of 6 studies using cumulative ACE exposure and standardised regression coefficients revealed no significant associations with EAA for first-generation clocks (Horvath: β =  - 0.03, 95% CI - 0.15 to 0.09; Hannum: β =  - 0.09, 95% CI - 0.41 to 0.23) or second-generation clocks (PhenoAge and GrimAge: both β = 0.21, 95% CIs spanning zero). Narrative synthesis of studies, including those that could not be considered in the meta-analyses, highlighted heterogeneous methodologies and mixed findings, particularly for individual ACEs