Experimental gerontology最新文献

{"title":"Pain duration as a staging variable: A conceptual framework for testing depression-pathway interventions in dementia risk","authors":"Herul Wahyudin ,&nbsp;Maria Oktasari ,&nbsp;Bagus Julian Hikmy ,&nbsp;Ma'rifatin Indah Kholili ,&nbsp;Hayu Stevani ,&nbsp;Raudah Zaimah Dalimunthe","doi":"10.1016/j.exger.2026.113089","DOIUrl":"10.1016/j.exger.2026.113089","url":null,"abstract":"<div><div>This study proposes a conceptual framework for testing the role of pain duration as a staging variable in the relationship between chronic pain and dementia risk. Chronic pain duration, often associated with an increased risk of dementia, may influence how depression interacts with cognitive decline. In this article, we propose two hypotheses for future research: (H1) In the 3–24 months period, depression-targeted care through interventions such as cognitive behavioral therapy and antidepressant medication is expected to provide the most significant cognitive benefits. (H2) After 24 months, depression care remains important, but its effectiveness may be limited without multimodal pain management, which includes physical therapy and pharmacological interventions. We also consider confounding variables such as comorbidities and sociodemographic factors that may influence study outcomes, which need to be accounted for in future research. This framework aims to provide a foundation for longitudinal research and intervention trials that test the proposed hypotheses, contributing to the development of more effective dementia prevention strategies for individuals with chronic pain.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"217 ","pages":"Article 113089"},"PeriodicalIF":4.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147388461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic associations and mediating effects of insulin resistance between hypertension and sarcopenia: A bidirectional two-sample Mendelian randomization study","authors":"Jingfeng Zou ,&nbsp;Liyin Zhang ,&nbsp;Shaotian Li ,&nbsp;Shanshan Hu ,&nbsp;Chunhui Tian ,&nbsp;Yiting Liu ,&nbsp;Yilan Yin ,&nbsp;Mi Yan ,&nbsp;Guqiao Nie ,&nbsp;Wen Peng","doi":"10.1016/j.exger.2026.113086","DOIUrl":"10.1016/j.exger.2026.113086","url":null,"abstract":"<div><h3>Objective</h3><div>Hypertension and sarcopenia are major global public health problems among the aging society. This study aims to explore the causal associations and mediating effects of insulin resistance (IR) between hypertension and sarcopenia.</div></div><div><h3>Methods</h3><div>A bidirectional two-step Mendelian randomization (MR) was applied to determine the causal mediating role of IR in the pathway between hypertension and four sarcopenia related traits (right and left handgrip strength/HGS, Appendicular lean mass/ALM, and Usual walking pace/UWP) by using single nucleotide polymorphisms as instrumental variables to predict insulin, body mass index (BMI), fasting blood glucose (FBG), glycosylated hemoglobin a1c (HbA1c) and triglycerides (TG) genetically.</div></div><div><h3>Results</h3><div>The IVW analysis indicated that there was a suggestive causality between hypertension and a reduced risk of UWP (OR = 0.952, 95% CI 0.913–0.991, <em>P</em> = 0.018), with triglycerides mediating a moderate proportion of this effect (6.985–13.666%).No significant causal associations were found between hypertension and right HGS, left HGS, or ALW (all <em>P</em> &gt; 0.05). Each 1-standard deviation decrease in genetically determined right HGS (OR 0.963, 95% CI 0.935–0.992, <em>P</em> = 0.013) increased the suggestive risk of hypertension, each 1-standard deviation decrease in genetically determined left HGS (OR 0.958, 95% CI 0.930–0.986, <em>P</em> = 0.004), and ALM (OR 0.977, 95% CI 0.969–0.986, <em>P</em> = 0.000) also increased the risk of hypertension. No significant causal association was found between UWP and hypertension (<em>P</em> &gt; 0.05). Compared with other indicators, insulin, strongly associated with the link between right HGS, left HGS, ALM and hypertension, has gained the notably total proportion mediated effect accounted from 11.378 to 21.297%. Furthermore, we systematically summarized the pathogenesis between hypertension and sarcopenia.</div></div><div><h3>Conclusion</h3><div>The study indicates the causality between hypertension and sarcopenia, potentially mediated by insulin resistance (BMI, insulin, FBG, HbA1c, and TG). It provides crucial evidence for the genetic association between hypertension and sarcopenia, while also offering insights for managing both conditions, particularly in terms of blood glucose, lipid, and weight control.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"217 ","pages":"Article 113086"},"PeriodicalIF":4.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147370618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploration of the co-regulatory mechanism of calorie restriction and endurance exercise on elderly skeletal muscle and its potential intervention targets","authors":"Donghui Zhu ,&nbsp;Xiuxiu Chen","doi":"10.1016/j.exger.2026.113083","DOIUrl":"10.1016/j.exger.2026.113083","url":null,"abstract":"<div><div>This study aims to explore the shared transcriptomic features of caloric restriction (CR) and endurance exercise in skeletal muscle among older adults. As age increases, muscle atrophy gradually becomes a common issue of functional decline in the elderly. Utilizing bioinformatics analysis, this research identified 101 overlapping differentially expressed genes (DEGs) involved in both CR and endurance exercise. These genes are primarily enriched in key biological pathways related to longevity, Apelin signaling, AMPK signaling, FoxO signaling, and cGMP-PKG signaling pathways. Additionally, we identified 10 key genes (such as LPL, PPARGC1A, and IGF1), 4 transcription factors (FOXC1, POU2F2, GATA2, and STAT3), and 4 microRNAs (miR-155-5p, miR-124-3p, miR-1-3p, and miR-16-5p) interacting with these genes. Drug-gene interaction analysis identified carotuximab as a compound with potential relevance for future investigation in the context of muscle aging. These findings provide new insights into the molecular mechanisms underlying muscle functional decline in the elderly and propose potential targets and drugs for intervention development.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"217 ","pages":"Article 113083"},"PeriodicalIF":4.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147373694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynapenic-metabolic obesity and incident stroke in middle-aged and older adults: The mediating role of intrinsic capacity and systemic inflammation.","authors":"Yang Dong, Bo Yang","doi":"10.1016/j.exger.2026.113143","DOIUrl":"https://doi.org/10.1016/j.exger.2026.113143","url":null,"abstract":"<p><strong>Background: </strong>Conventional obesity definitions overlook heterogeneity related to metabolic health and muscle strength. This study examined the associations between dynapenic-metabolic obesity (DMO) and incident stroke among middle-aged and older Chinese adults.</p><p><strong>Methods: </strong>Our study included 11,770 participants aged ≥45 years from the China Health and Retirement Longitudinal Study (CHARLS, 2011-2018) with 2011 as baseline. Dynapenia was defined by handgrip strength (<28 kg for men, <18 kg for women); metabolic dysfunction by ≥2 of 4 criteria (hypertension, dyslipidemia, impaired glycemia, or low HDL-C); and obesity by BMI ≥25 kg/m² (general obesity) or waist circumference ≥ 90 cm for men and ≥ 85 cm for women (abdominal obesity). Cox models estimated hazard ratios (HRs) for stroke, adjusting for covariates. Mediation analysis evaluated the roles of C-reactive protein (CRP) and intrinsic capacity (IC).</p><p><strong>Results: </strong>During follow-up, 787 participants (6.7%) experienced stroke. Obesity alone, without dynapenia or metabolic dysfunction, was associated with elevated stroke risk (general obesity: HR 1.50, 95% CI 1.15-1.95; abdominal obesity: HR 1.55, 95% CI 1.21-1.98). The highest risk was observed in participants with combined dynapenia and metabolic dysfunction (DMGO: HR 2.97, 95% CI 2.01-4.37; DMAO: HR 2.96, 95% CI 2.08-4.21). Mediation analyses indicated that systemic inflammation and reduced intrinsic capacity partially explained these associations. Findings were consistent across subgroups and sensitivity analyses.</p><p><strong>Conclusions: </strong>Dynapenic-metabolic obesity is strongly associated with incident stroke, but even obesity alone increases risk. Systemic inflammation and impaired intrinsic capacity partially mediate these effects, highlighting the importance of integrated strategies targeting adiposity, metabolic health, and muscle function to prevent stroke in aging populations.</p>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":" ","pages":"113143"},"PeriodicalIF":4.3,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147792975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disulfidptosis in osteoarthritis: Role of SLC2A3 downregulation and potential therapeutic implications","authors":"Ruoyang Feng ,&nbsp;Xiadiye Tuerhong ,&nbsp;Yongsong Cai ,&nbsp;Yirixiati Aihaiti","doi":"10.1016/j.exger.2026.113058","DOIUrl":"10.1016/j.exger.2026.113058","url":null,"abstract":"<div><h3>Objective</h3><div>Disulfidptosis is a newly recognized form of regulated cell death characterized by actin cytoskeleton collapse under disulfide stress. Recent studies suggest it may significantly contribute to osteoarthritis (OA), though its exact role in OA development remains unclear. This study aims to analyze the expression of disulfidptosis-related genes in OA, identifying potential biomarkers and candidate therapeutic leads.</div></div><div><h3>Methods</h3><div>Transcriptomic data from six datasets related to OA and single-cell RNA sequencing data were sourced from the GEO database. To identify differentially expressed genes (DEGs) associated with disulfidptosis, we employed robust rank aggregation. We then utilized functional enrichment analysis, constructed a protein-protein interaction network, and applied machine learning models to prioritize key genes of interest. A single-cell analysis was conducted to evaluate gene expression within specific subsets of chondrocytes. Additionally, we predicted drug-target binding affinity using the GraphDTA model and performed molecular docking studies to assess drug-to-target binding affinity. Finally, immunohistochemistry, RT-qPCR, and Western blotting were performed for experimental validation.</div></div><div><h3>Results</h3><div>We identified several DEGs related to disulfidptosis, including SLC2A3, PDLIM1, and SLC3A2, which were found to be downregulated in OA tissues, particularly in pre-fibrocartilage chondrocyte subtypes. Our functional analysis indicated that these genes were enriched in pathways associated with cytoskeleton organization and the oxidative stress response. Furthermore, machine learning models demonstrated that these genes have significant diagnostic potential across various datasets. Using GraphDTA for drug prediction and molecular docking, we discovered that talaroflavone exhibits a strong binding affinity to SLC2A3, with highest predicted affinity (13.98) and a binding energy of −8.8 kcal/mol. Experimental validation confirmed the downregulation of SLC2A3 in OA-affected cartilage. Functional assays indicated that modulating SLC2A3 could alleviate cartilage matrix degradation and oxidative stress, suggesting a potential functional association between SLC2A3 and OA progression.</div></div><div><h3>Conclusion</h3><div>This study providing functional evidence for a potential association between disulfidptosis-related genes and OA, while highlighting SLC2A3 as a potential functional regulator for further investigation. Additionally, was identified talaroflavone as a computationally predicted lead compound that warrants future experimental validation. These findings not only enhance our understanding of the molecular pathways underlying OA but also lay the groundwork for potential development of targeted therapeutic strategies.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"215 ","pages":"Article 113058"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146109270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated metabolomics and machine learning identify potential biomarkers and metabolism-related targets for MASLD in older adults","authors":"Ze Jin ,&nbsp;Mengpei Zhu ,&nbsp;Ziwen Wang ,&nbsp;Lina Xiong ,&nbsp;Zhifan Xiong","doi":"10.1016/j.exger.2026.113067","DOIUrl":"10.1016/j.exger.2026.113067","url":null,"abstract":"<div><h3>Background</h3><div>Given the high prevalence and serious health threats of Metabolic dysfunction-associated steatotic liver disease (MASLD) in older people, uncovering the pathological features of MASLD in the context of age is critically important. This study aimed to perform serum metabolomics analysis for older adults with MASLD to identify potential biomarkers and involved metabolic disturbances.</div></div><div><h3>Methods</h3><div>30 older subjects with MASLD and 30 healthy individuals were included (age &gt; 65). Sex-stratified metabolomics analysis was applied by using ultra-high-performance liquid chromatography-mass spectrometry (UHPLC-MS/MS). Partial least squares discriminant analysis (PLS-DA) was utilized to identify differential metabolites between groups. The distinct and shared pathways of MASLD in older men and older women were explored using MetaboAnalyst 6.0. Machine learning algorithms are applied to screen for optimal biomarkers. Receiver operating characteristics (ROC) curve analysis was applied to test the predictive ability of biomarkers. Spearman's correlation analysis was conducted to evaluate the correlation of metabolic biomarkers with biochemical parameters. The differences in phosphatidylcholine concentration were externally validated in other 60 older adults. Finally, in the aged mice MASLD model, the mRNA expression levels of the rate-limiting enzyme of phosphatidylcholine synthesis (PCYT1A and PEMT) were detected.</div></div><div><h3>Results</h3><div>Principal components analysis (PCA) and PLS-DA exhibited pronounced metabolic separations between the MASLD and HC groups in both older males and females. 14 shared metabolites were selected by the least absolute shrinkage and selection operator (LASSO) and Support Vector Machine-Recursive Feature Elimination (SVM-RFE) algorithms. Finally, 6 metabolites significantly dysregulated in older MASLD patients (|logFC| &gt; 0.5) would be determined as the optimal metabolic markers, including: PC 18:1_22:6, 2’-Deoxyuridine-5-monophosphate, porphobilinogen, uridine, all-trans-13,14-Dihydroretinol and D-Ribulose 1,5-bisphosphate. Notably, a marked difference in serum phosphatidylcholine levels in the elderly between the MASLD group and the healthy group was confirmed by external validation (<em>p</em> &lt; 0.001). The significant downregulation of PCYT1A mRNA expression was also found in the aged mice MASLD model.</div></div><div><h3>Conclusions</h3><div>This study depicts the metabolic features of MASLD in the older population. Our finding explores promising biomarkers for diagnosis and provides more perspectives on molecular mechanisms and potential targets for MASLD in the context of aging.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"215 ","pages":"Article 113067"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146168562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and validation of a machine learning model for frailty screening using claims data in Japan: the Longevity Improvement & Fair Evidence Study","authors":"Kengo Kawaguchi ,&nbsp;Megumi Maeda ,&nbsp;Futoshi Oda ,&nbsp;Yasuharu Nakashima ,&nbsp;Haruhisa Fukuda","doi":"10.1016/j.exger.2026.113050","DOIUrl":"10.1016/j.exger.2026.113050","url":null,"abstract":"<div><h3>Background</h3><div>Frailty is an ageing-associated multidimensional condition linked to higher long-term care (LTC) needs, healthcare expenditures, and mortality. In Japan, the Questionnaire for Medical Checkup of Old-Old (QMCOO) is used to assess frailty, but its implementation is resource-intensive. Claims-based prediction models may offer a scalable alternative for early frailty identification.</div></div><div><h3>Methods</h3><div>We developed a machine learning model using administrative claims data from older adults to predict frailty status as defined by the QMCOO. In Phase 1, the model was trained and validated using data from a single municipality. In Phase 2, the model's prognostic utility for predicting all-cause mortality was evaluated using data from seven other municipalities. We applied the eXtreme Gradient Boosting algorithm, incorporating demographic variables, LTC use, comorbidities, procedures, and medical device use. Model performance was assessed mainly using the area under the receiver operating characteristic curve (ROC-AUC). Mortality risk was estimated using Kaplan–Meier method and Cox regression models.</div></div><div><h3>Results</h3><div>In Phase 1, a total of 74,148 individuals were included (development cohort: 60,930, validation cohort: 13,218). The model achieved an ROC-AUC of 0.780 in internal validation and 0.728 in external validation. In Phase 2, external validation was conducted in a new cohort of 354,815 individuals. Frailty classification was associated with significantly higher mortality in both the development (hazard ratio: 7.03, 95% confidence interval: 6.47–7.63) and validation (6.75, 6.62–6.89) cohorts.</div></div><div><h3>Conclusion</h3><div>This claims-based frailty prediction model showed reasonable performance and prognostic value. It may support efficient, population-level frailty screenings where questionnaire-based assessments are impractical.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"215 ","pages":"Article 113050"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146081231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systems-level modelling of DNA damage, senescence, and stem cell dynamics in ageing","authors":"Anchen Che ,&nbsp;Amy E. Morgan ,&nbsp;Mark T. Mc Auley","doi":"10.1016/j.exger.2026.113063","DOIUrl":"10.1016/j.exger.2026.113063","url":null,"abstract":"<div><div>Ageing entails a variety of cellular and physiological changes that increase susceptibility to disease and death. A significant contributor to ageing is cellular senescence, a state of irreversible cell cycle arrest triggered by stressors such as DNA damage, telomere shortening, and the senescence-associated secretory phenotype. It is challenging to understand the nonlinear interactions between these complex mechanisms using conventional laboratory approaches. Mathematical modelling is capable of representing this complexity. In this study we introduce a mathematical model that captures the dynamics of cellular ageing within a population of cells. The model integrates key processes including DNA damage repair, senescence, quiescence, apoptosis, and cell division. The model was used to simulate the effects of ageing and to evaluate the efficacy of several interventions, including senolytics, telomere length preservation, and stem cell therapy. Deterministic and stochastic simulations reproduce core ageing features: progressive accumulation of senescent cells, a generation distribution centred near experimentally observed Hayflick limits, and an exponential-like age distribution of non-senescent cells. This model captures the long-lasting effects of interventions such as telomere lengthening and stem-cell therapy. It offers a quantitative, extendable platform that supports hypothesis testing and helps identify which ageing interventions warrant experimental validation. Overall, it provides a predictive framework for interpreting cellular ageing and for guiding future experimental work.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"215 ","pages":"Article 113063"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146196236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of accelerometer-measured rest-activity rhythm patterns and parameters with cardiovascular and all-cause mortality in older adults: Population-based cohort study","authors":"Shuaijie Chen ,&nbsp;Qiong Su ,&nbsp;Ruming Shen ,&nbsp;Hailin Zhang ,&nbsp;Xiaoyan Lin ,&nbsp;Shengbin Yu ,&nbsp;Mingqin Chen ,&nbsp;Yuhong Shi ,&nbsp;Feng Peng ,&nbsp;Jinxiu Lin ,&nbsp;Dajun Chai","doi":"10.1016/j.exger.2026.113043","DOIUrl":"10.1016/j.exger.2026.113043","url":null,"abstract":"<div><h3>Background</h3><div>Rest-activity rhythm (RAR) is a fundamental biomarker of age-related circadian system deterioration. However, the long-term effect of RAR patterns on mortality in older adults remains unclear.</div></div><div><h3>Methods</h3><div>This study analysed data from National Health and Nutrition Examination Survey 2011–2014. The RAR parameters were derived from wrist accelerometers, and four patterns were identified through clustering analysis using Gaussian mixture models. Cox models were used to compare the hazard ratio (HR) and 95% confidence interval (CI) of mortality among participants with different RAR parameters and patterns.</div></div><div><h3>Results</h3><div>This study included 1710 participants aged ≥60 years. The median follow-up duration was 6.67 years. In total, 269 all-cause deaths and 77 cardiovascular deaths occurred during follow-up period. Four RAR patterns were identified: ‘morning-type’, ‘earlier-type’, ‘delayed-type’, and ‘evening-type’. Compared to ‘morning-type’, ‘evening-type’ was associated with higher risks of cardiovascular (HR: 12.16, 95% CI: 4.02–36.82) and all-cause mortality (HR: 3.31, 95% CI: 1.91–5.72). Higher interdaily stability was associated with lower risks of cardiovascular (HR: 0.67, 95% CI: 0.55–0.81), and all-cause mortality (HR: 0.86, 95% CI: 0.74–1.00). Higher relative amplitude was associated with lower risks of cardiovascular (HR: 0.61, 95% CI: 0.49–0.75), and all-cause mortality (HR: 0.70, 95% CI: 0.60–0.81). Conversely, higher intradaily variability was associated with increased risk of cardiovascular (HR: 1.30, 95% CI: 1.15–1.46) and all-cause mortality (HR: 1.19, 95% CI: 1.10–1.30).</div></div><div><h3>Conclusions</h3><div>RAR patterns and parameters were significantly associated with cardiovascular and all-cause mortality in older adults. Early identification and intervention for adverse RAR patterns may help improve long-term health outcomes.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"215 ","pages":"Article 113043"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive evaluation of appendicular lean mass and sarcopenia on human health: evidence from the NHANES program","authors":"Xiao Long ,&nbsp;Ruizhi Chen ,&nbsp;Yanmin Lu ,&nbsp;Binbin Ma ,&nbsp;Yuxin Chang ,&nbsp;Zichao Jiang ,&nbsp;Ting Lei","doi":"10.1016/j.exger.2026.113049","DOIUrl":"10.1016/j.exger.2026.113049","url":null,"abstract":"<div><h3>Background</h3><div>While accumulating points have been figured out the importance of muscle function, less clinical or epidemiological evidence have been provided. This study aimed to provide new evidence on the systemic effects of muscle mass on health condition, based on the National Health and Nutrition Examination Survey (NHANES) program.</div></div><div><h3>Method</h3><div>All used data was acquired from 11 survey cycles (1999–2020) of the NHANES program. The mortality information of participants was derived from the National Death Index (NDI) website. The disease status of participants was obtained from questionnaire surveys. The metabolism-related index was obtained from examination data. Multiple regression methods, smooth curve fitting, and threshold effect models were used for association analyses.</div></div><div><h3>Result</h3><div>In this large-scale study encompassing 46,733 participants, appendicular lean mass (ALM) demonstrated significant associations with multiple health outcomes: ALM exhibited L-shaped relationships with hyperuricemia and malignancy, inverse correlations with asthma, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), nephrolithiasis, depression, and cancer-cause mortality, a positive correlation with bone mineral density (BMD), and notably, protective saturating effects against osteoarthritis (OA), all-cause mortality, and cardiovascular (CVD)-cause mortality. A significant inverse association was observed between sarcopenia and BMD, while positive correlations were identified between sarcopenia and COPD, asthma, OA, depression, and all-cause mortality.</div></div><div><h3>Conclusions</h3><div>In this study, we explored the association between ALM or sarcopenia and multiple health outcomes, highlighting the widespread impact of ALM on systemic health condition. These findings provide new epidemiological evidence on how ALM or sarcopenia influence the health status among the U.S. population.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"215 ","pages":"Article 113049"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146043331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}