This study aimed to identify latent classes of intrinsic capacity (IC) among older adults undergoing total knee arthroplasty (TKA) and to examine the association between IC patterns and short-term postoperative functional outcomes assessed by the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC). Following the Integrated Care for Older People framework, IC was assessed across five domains—cognition, psychology, vitality, locomotion, and sensory function—using validated instruments. WOMAC scores were evaluated preoperatively and at 3 months postoperatively. Latent class analysis was performed to identify IC patterns, and multinomial logistic regression was used to examine factors associated with IC pattern classification. Three IC patterns were identified in older adults undergoing TKA: C1 “Low impairment” (59.34%), C2 “Vit + Psy” (10.75%), and C3 “Loc + Sen” (29.91%). Age, manual labour occupations, and use of walking assistive devices were significantly associated with IC pattern classification (all P < 0.05). After adjustment for baseline WOMAC and other covariates, no statistically significant differences were observed among IC pattern groups in WOMAC scores at 3 months postoperatively or ΔWOMAC (P > 0.05). Identification of IC patterns may enhance the understanding of multidimensional functional heterogeneity among older adults undergoing TKA and provide a potential framework for personalised perioperative assessment and future longitudinal research.

Sarcopenia, characterized by an age-associated decline in skeletal muscle mass and strength/function, is associated with multiple adverse clinical outcomes. Dietary nutrition and exercise interventions are effective ways to prevent and improve sarcopenia. Therefore, Huadong Hospital affiliated to Fudan University, Shanghai Elderly Nutrition and Health Quality Control Center, together with the Geriatric Nutrition Branch of China Nutrition Society convened experts from nutrition, geriatrics, sports medicine, rehabilitation medicine, traditional Chinese medicine and general practice medicine to jointly set up a working group to supplement and revise the 2015 edition of China Expert Consensus on Nutrition and Exercise Intervention for Sarcopenia based on evidence-based medicine evidence in the past ten years to form this consensus. The aim is to provide practical guidelines to prevent and treat the disease.

Rebleeding is a severe complication following recovery from esophageal variceal bleeding (EVB), yet robust predictive tools for assessing post-treatment risk after endoscopic variceal ligation (EVL) therapy remain scarce. This study developed and independently validated a machine learning (ML) model using multidimensional clinical data to predict 1-year rebleeding risk. Two independent cohorts were included: a retrospective cohort (n = 373) for model development and a prospective cohort (n = 119) for validation, with a one-year rebleeding endpoint. Predictors were identified using Recursive Feature Elimination (RFE), and eight ML algorithms were evaluated. Each algorithm was optimized via 5-fold cross-validation. The model with optimal performance was chosen to develop an online computational platform. RFE identified eight key predictors. The XGBoost model demonstrated superior predictive performance in both the training and validation cohorts, achieving AUCs of 0.883 and 0.887, respectively. This model was subsequently implemented in an online clinical platform for individualized 1-year rebleeding risk assessment. Our findings establish XGBoost as an effective tool for predicting EVB rebleeding risk, providing an evidence-based decision aid for post-EVL management.

OBJECTIVES:Appendicular skeletal muscle mass (ASM), a core parameter for sarcopenia diagnosis, is difficult to measure in primary care facilities lacking specialized equipment. This study was conducted to develop and validate an ASM prediction equation based on simple anthropometric and demographic indices. DESIGN:Cross-sectional study. SETTING AND PARTICIPANTS:The study included 5016 community-dwelling older adults (mean age, 71.0 ± 5.6 years; women, 55.9%). METHODS:Anthropometric and demographic data were collected by uniformly trained medical staff. ASM was measured through bioelectrical impedance analysis (BIA). The participants were randomly divided (4:1) into a development group (n = 4013) and a validation group (n = 1003). Stepwise multivariate linear regression was performed to establish the ASM prediction equation. RESULTS:The equation for predicting ASM was as follows: ASM (kg) = 0.232 × height (cm) + 0.128 × weight (kg) + 0.128 × calf circumference (cm) - 2.039 × sex (men: 1, women: 2) - 0.021 × age (years) - 27.129. It exhibited an adjusted R2 value of 0.90 and a standard error of estimate value of 1.34 kg. In the validation group, a strong correlation was observed between ASM measured using our equation and that measured through BIA (r = 0.952; P < .001). The Bland-Altman plot showed that the mean difference between the results for our equation and for BIA was -0.03 kg, with limits of agreement (mean 1.96 SD) of -2.4 to 2.3 kg. The intraclass correlation coefficient was 0.951 (95% CI, 0.945-0.957), indicating excellent between-method consistency. CONCLUSIONS AND IMPLICATIONS:Our equation appears to have high predictive power. With rapid and simple measurement of anthropometric and demographic indices, the equation can be used to evaluate ASM in primary care facilities lacking specialized equipment.

Background Osteoarthritis (OA), a debilitating joint disorder lacking disease-modifying therapies, involves ferroptosis-an iron-dependent cell death. While ferroptosis contributes to OA progression, its autophagy-dependent mechanisms remain undefined. This study reveals DMT1 (divalent metal transporter 1) as a central regulator of autophagic ferroptosis in OA pathogenesis. Methods OA-related ferroptosis genes were screened by LASSO regression and random forest models. IL-1β/Erastin-stimulated chondrocytes and DMM-induced OA mice were used to investigate DMT1 function. Ferroptosis and autophagy were assessed by lipid peroxidation, autophagic flux, Western blot, and modulators. Micro-CT, OARSI scoring and behavioral tests evaluated joint damage. Regulatory mechanisms were examined by miR-17-5p mimic, luciferase assays and NEDD4-mediated ubiquitination. Results DMT1 was upregulated in OA cartilage and IL-1β-stimulated chondrocytes, correlating with ferroptosis activation. Genetic DMT1 suppression attenuated ferroptosis in vitro and in vivo, whereas overexpression exacerbated lipid peroxidation and impaired cartilage repair post-DMM surgery in mice. Mechanistically, DMT1 overexpression activated autophagy, linking it to ferroptosis execution – pharmacological autophagy inhibition reduced DMT1-driven ferroptosis, while autophagy inducers amplified its effects. Conclusions We identified a DMT1–autophagy–ferroptosis axis as a critical OA mechanism. Ferroptosis inhibitors and upstream regulators (miR-17-5p, NEDD4) show promise as disease-modifying strategies for OA. The translational potential of this article This study not only elucidates a novel DMT1-autophagy-ferroptosis axis but also identifies NEDD4 as upstream therapeutic targets. The demonstration that Lip-1 treatment alleviates DMT1-driven OA exacerbation in vivo highlights translational potential of ferroptosis inhibition as a disease-modifying strategy for OA. Moreover, NEDD4 overexpression represents promising gene-based interventions with potential for precision therapy in OA.

To investigate the prevalence of sarcopenia among community-dwelling older adults and provide scientific evidence for the prevention of sarcopenia. This cross-sectional study included 5016 community-dwelling older adults (mean age, 71.0 ± 5.6 years). Sarcopenia was diagnosed according to the Asian Working Group for Sarcopenia 2019 Consensus. A nutritional risk assessment was also conducted. Multivariate logistic regression analysis was used to explore factors associated with sarcopenia. Our study comprised 5016 participants (71.0 ± 5.6 years). Sarcopenia prevalence was 11.8

Neutrophil-associated inflammatory markers (NPR, NHR, SII, and SIRI) have been implicated in various metabolic diseases. However, studies on these markers with metabolic dysfunction-associated steatotic liver disease (MASLD) and advanced liver fibrosis (ALF), as well as their impact on all-cause mortality, remain limited. In this historical cohort study, data from 8051 adults aged 20 years and older were analysed. Weighted logistic regression was used to investigate the associations of neutrophil-associated inflammatory markers with MASLD and ALF. Nonlinear associations were described via restricted cubic spline regression. The diagnostic utility was assessed via receiver operating characteristic (ROC) curves. Furthermore, weighted Kaplan‒Meier survival curves and Cox proportional hazards models were employed to assess all-cause mortality risk. Sensitivity analyses were employed to guarantee the robustness of the findings. Following adjustment for confounding factors, there was a significant positive association between the ln-transformed NPR, NHR, SII, and SIRI and the risk of MASLD (P < 0.001). Conversely, an inverse association was noted between the ln-transformed SII, SIRI and ALF (P < 0.05). Nonlinear relationships were identified between ln-transformed NPR, NHR, and SIRI and the risk of MASLD (P < 0.001), as well as between ln-transformed NPR, SII, and SIRI and the risk of ALF (P < 0.001). Furthermore, the ln-transformed NHR (cut-off value: − 2.571) exhibited the highest diagnostic accuracy for MASLD (AUC 0.71, 95

BACKGROUND Rebleeding after recovery from esophagogastric variceal bleeding (EGVB) is a severe complication that is associated with high rates of both incidence and mortality. Despite its clinical importance, recognized prognostic models that can effectively predict esophagogastric variceal rebleeding in patients with liver cirrhosis are lacking. AIM To construct and externally validate a reliable prognostic model for predicting the occurrence of esophagogastric variceal rebleeding. METHODS This study included 477 EGVB patients across 2 cohorts: The derivation cohort (n = 322) and the validation cohort (n = 155). The primary outcome was rebleeding events within 1 year. The least absolute shrinkage and selection operator was applied for predictor selection, and multivariate Cox regression analysis was used to construct the prognostic model. Internal validation was performed with bootstrap resampling. We assessed the discrimination, calibration and accuracy of the model, and performed patient risk stratification. RESULTS Six predictors, including albumin and aspartate aminotransferase concentrations, white blood cell count, and the presence of ascites, portal vein thrombosis, and bleeding signs, were selected for the rebleeding event prediction following endoscopic treatment (REPET) model. In predicting rebleeding within 1 year, the REPET model exhibited a concordance index of 0.775 and a Brier score of 0.143 in the derivation cohort, alongside 0.862 and 0.127 in the validation cohort. Furthermore, the REPET model revealed a significant difference in rebleeding rates (P < 0.01) between low-risk patients and intermediate- to high-risk patients in both cohorts. CONCLUSION We constructed and validated a new prognostic model for variceal rebleeding with excellent predictive performance, which will improve the clinical management of rebleeding in EGVB patients.

OBJECTIVE:Sarcopenia and knee osteoarthritis (KOA) are common conditions in older adults, but their relationship is controversial. We aimed to examine the potential role of sarcopenia in KOA progression and subsequent knee replacement (KR). METHODS:Using data from the Osteoarthritis Initiative, baseline sarcopenia was first screened according to the EWGSOP2 algorithm using the SARC-F (Strength, Assistance with walking, Rise from a chair, Climb stairs, and Falls) questionnaire (screened sarcopenia [Scre-S]), then further assessed combined with the five times chair-stand-test (probable sarcopenia [Prob-S]). Radiographic KOA progression was evaluated by changes in Kellgren-Lawrence Grade and Osteoarthritis Research Society International atlas scores from baseline to the 24- and 48-month follow-ups. Symptomatic progression was evaluated similarly using the Western Ontario McMaster Osteoarthritis Index. The associations of sarcopenia with radiographic or symptomatic progression and subsequent KR were analyzed before and after adjusting for potential confounders and propensity score (PS) matching. RESULTS:A total of 4,316 participants were included; 27.2% were Scre-S and 16.8% were Prob-S. Baseline Scre-S and Prob-S were positively associated with both radiographic and symptomatic progression in KOA over 24 and 48 months. Both Scre-S and Prob-S were associated with a higher risk of subsequent KR (Scre-S: hazard ratio [HR] 3.84, 95% confidence interval [CI] 3.18 to 4.62; Prob-S: HR 2.29, 95% CI 1.87 to 2.81). These results remained significant in the PS-matched cohort. CONCLUSION:Scre-S and Prob-S were significantly and longitudinally associated with both radiographic and symptomatic progression in KOA and subsequent KR. Our findings indicated a potential causal role of sarcopenia in KOA progression and highlighted its potentially therapeutic effect in KOA management.

This retrospective study aimed to compare the predictive efficacy of the shortness of breath with daily activities (SOBDA) and ventilatory response to exercise questionnaire (VSRQ) in forecasting respiratory-related adverse events in elderly patients with chronic obstructive pulmonary disease (COPD) over a 6-month follow-up period post-discharge. A total of 92 COPD patients, treated according to the 2022 GOLD report and Chinese National COPD treatment guidelines, were enrolled. SOBDA and VSRQ scores were collected upon admission and assessed daily for the first 7 days. A random forest model was used to evaluate the predictive value of these scores in relation to respiratory adverse events, with a training/testing group split at a 4:1 ratio. Five patients were excluded due to loss to follow-up or death, resulting in 87 patients in the final analysis. The primary endpoint was the occurrence of COPD exacerbations and respiratory failure. The random forest model using VSRQ scores as the response variable outperformed the SOBDA model in terms of predictive accuracy (AUC: 0.84 vs 0.65) and error rate (21.74% vs 22%). Both models demonstrated high accuracy in predicting the absence of adverse events (VSRQ: 85.72%, SOBDA: 83.67%) but showed limited sensitivity in predicting their occurrence (VSRQ: 35%, SOBDA: 40%). The VSRQ questionnaire demonstrated superior predictive performance compared to SOBDA, suggesting that VSRQ may be a useful tool for identifying high-risk elderly COPD patients and guiding clinical decision-making. Further studies are needed to confirm these findings and explore the broader applicability of VSRQ in COPD prognosis.

Osteoarthritis (OA) is a cartilage-degenerative joint disease. Mitophagy impacts articular cartilage damage. tRNA-derived small RNAs (tsRNAs) are one of the contents of adipose mesenchymal stem cell (AMSC)-derived exosomes (AMSC-exos) and are involved in disease progression. However, whether tsRNAs regulate mitophagy and whether tsRNA-modified AMSC-exos improve OA via mitophagy remain unclear. We performed small RNA sequencing to identify OA-related tsRNAs, which were then loaded into AMSC-exos, exploring the function and mechanisms related to mitophagy in vitro and in vivo. Overall, 53 differentially expressed tsRNAs (DEtsRNAs) were identified between OA and normal cartilage tissues, among which 42 DEtsRNAs, including tsRNA-12391, were downregulated in the OA group. Target genes of tsRNA-12391 mainly participated in mitophagy-related pathways such as Rap1 signaling pathway. Compared to the control group, tsRNA-12391 mimics significantly promoted mitophagy, as shown by the upregulated expression of PINK1 and LC3 and the co-localization of Mito-Tracker Green and PINK1. Furthermore, tsRNA-12391 mimics effectively enhanced chondrogenesis in chondrocytes, as demonstrated by the elevated expression of collagen II and ACAN. AMSC-exos with tsRNA-12391 overexpression also facilitated mitophagy and chondrogenesis in vitro and in vivo. Mechanistically, tsRNA-12391 bound to ATAD3A restricted ATAD31 from degrading PINK1, leading to PINK1 accumulation. ATAD31 overexpression reversed the effects of tsRNA-12391 mimics on mitophagy and chondrogenesis. AMSC-exos loaded with tsRNA-12391 promoted mitophagy and chondrogenesis by interacting with ATAD31; this may be a novel therapeutic strategy for OA.

BACKGROUND:We sought to: (1) develop a new method in measuring spino-pelvic tilt (SPT) from antero-posterior pelvic (AP pelvis) radiographs and computed tomography scans, and examine its reliability and validity; (2) use Z-scores to evaluate patients' SPT based on an established asymptomatic norm; and (3) examine whether a compensatory mechanism of anterior pelvic tilt exists for borderline hips, denoted as differences in anterior wall indices both between standing and supine positions, and between borderline hip dysplasia (BHD) patients and asymptomatic norms. METHODS:After the inclusion and exclusion criteria, 24 patients were finally included. Patients who had unilateral or bilateral borderline hips were included. A supine computed tomography scan, standing AP pelvis, and standing full spine radiograph were obtained. Digitally reconstructed radiographs with various SPTs were generated. Regression models were fitted to predict SPT for standing AP pelvis, and subsequently to calculate Z-scores based on an established asymptomatic norm. Wilcoxon signed rank tests were applied to test the deviation of SPT from the asymptomatic norm. Generalized estimating equations were used to model Z-scores for SPT and between-position/between-population anterior acetabular coverage. RESULTS:The SPT prediction had excellent reliability with intraclass correlation coefficient > 0.99 (0.99 to 1.00) and interobserver reliability with intraclass correlation coefficient > 0.99 (0.99 to 1.00). The mean Z-score was -1.09 (0.94), and its difference from zero was statistically significant (P < 0.001). The generalized estimating equation modeling reveals a negative correlation between SPT and anterior acetabular coverage compensation, denoted as differences in anterior wall indices, both between standing and supine in BHD patients and between standing BHD patients and the standing asymptomatic norm. CONCLUSIONS:Patients who have BHD have greater anterior pelvic tilt compared with the asymptomatic norm. Anterior acetabular coverage may be overestimated on the standing AP pelvis for BHD patients.

With the exacerbation of global population aging, sarcopenia has become an increasingly recognized public health issue. Sarcopenia, characterized by a progressive decline in skeletal muscle mass, strength, and function, significantly impacts the quality of life in the elderly. Herein, we explore the role of chroniclow-gradeinflammation in the development of sarcopenia and its underlying molecular mechanisms, including chronic inflammation-associated signaling pathways, immunosenescence, obesity and lipid infiltration, gut microbiota dysbiosis and intestinal barrier disruption, and the decline of satellite cells. The interplay and interaction of these molecular mechanisms provide new perspectives on the complexity of the pathogenesis of sarcopenia and offer a theoretical foundation for the development of future therapeutic strategies.

The effectiveness and risks of anticoagulant therapy in cirrhotic patients with non-symptomatic portal vein thrombosis (PVT) remain unclear. We conducted a multicenter, Zelen-designed randomized controlled trial to determine the effectiveness of warfarin in cirrhotic patients with non-symptomatic PVT during a one-year follow-up. In brief, 64 patients were 1:1 randomly divided into the anticoagulation group or the untreated group. The probability of recanalization was significantly higher in the anticoagulation group than those untreated in both ITT analysis (71.9% vs 34.4%, p = 0.004) and PP analysis (76.7% vs 32.4%, p < 0.001). Anticoagulation treatment was the independent predictor of recanalization (HR 2.776, 95%CI 1.307-5.893, p = 0.008). The risk of bleeding events and mortality were not significantly different. A significantly higher incidence of ascites aggravation was observed in the untreated group (3.3% vs 26.5%, p = 0.015). In conclusion, warfarin was proved to be an effective and safe as an anticoagulation therapy for treating non-symptomatic PVT in cirrhotic patients.

Existing studies have presented limited and disparate findings on the nexus between immune cells, plasma metabolites, and metabolic dysfunction-associated steatotic liver disease (MASLD). The aim of this study was to investigate the causal relationship between immune cells and MASLD. Additionally, we aimed to identify and quantify the potential mediating role of metabolites. A Mendelian randomization (MR) analysis was conducted using two samples of pooled data from genome-wide association studies on MASLD that included 2568 patients and 409,613 control individuals. Additionally, a mediated MR study was employed to quantify the metabolite-mediated immune cell effects on MASLD. In this study, eight immunophenotypes were linked to the risk of MASLD, and thirty-five metabolites/metabolite ratios were linked to the occurrence of MASLD. Furthermore, a total of six combinations of immunophenotypic and metabolic factors demonstrated effects on the occurrence of MASLD, although the mediating effects of metabolites were not significant. Our study demonstrated that certain immunophenotypes and metabolite/metabolite ratios have independent causal relationships with MASLD. Furthermore, we identified specific metabolites/metabolite ratios that are associated with an increased risk of MASLD. However, their mediating role in the causal association between immunophenotypes and MASLD was not significant. It is important to consider immune and metabolic disorders among patients with MASLD in clinical practice.

Osteoarthritis (OA) progression is highly associated with chondrocyte mitochondrial dysfunction and disorders of catabolism and anabolism of the extracellular matrix (ECM) in the articular cartilage. The mitochondrial unfolded protein response (UPRmt), which is an integral component of the mitochondrial quality control (MQC) system, is essential for maintaining chondrocyte homeostasis. We successfully validated the pivotal role of activating transcription factor 5 (ATF5) in upregulating the UPRmt, mitigating IL-1β-induced inflammation and mitochondrial dysfunction, and promoting balanced metabolism in articular cartilage ECM, proving its potential as a promising therapeutic target for OA. Modified mRNAs (modRNAs) have emerged as novel and efficient gene delivery vectors for nucleic acid therapeutic approaches. In this study, we combined Atf5-modRNA (modAtf5) with engineered exosomes derived from bone mesenchymal stem cells (ExmodAtf5) to exert cytoprotective effects on chondrocytes in articular cartilage via Atf5. However, the rapid localized metabolization of ExmodAtf5 limits its application. PLGA-PEG-PLGA (Gel), an injectable thermosensitive hydrogel, was used as a carrier of ExmodAtf5 (Gel@ExmodAtf5) to achieve a sustained release of ExmodAtf5. In vitro and in vivo, the use of Gel@ExmodAtf5 was shown to be a highly effective strategy for OA treatment. The in vivo therapeutic effect of Gel@ExmodAtf5 was evidenced by the preservation of the intact cartilage surface, low OARSI scores, fewer osteophytes, and mild subchondral bone sclerosis and cystic degeneration. Consequently, the combination of ExmodAtf5 and PLGA-PEG-PLGA could significantly enhance the therapeutic efficacy and prolong the exosome release. In addition, the mitochondrial protease ClpP enhanced chondrocyte autophagy by modulating the mTOR/Ulk1 pathway. As a result of our research, Gel@ExmodAtf5 can be considered to be effective at alleviating the progression of OA.

Aerobic glycolysis has pleiotropic roles in the pathogenesis of hepatocellular carcinoma (HCC).Emerging studies revealed key promoters of aerobic glycolysis, however, little is known about its negative regulators in HCC.In this study, an integrative analysis identifies a repertoire of differentially expressed genes (DNASE1L3, SLC22A1, ACE2, CES3, CCL14, GYS2, ADH4, and CFHR3) that are inversely associated with the glycolytic phenotype in HCC.ACE2, a member of the rennin-angiotensin system, is revealed to be downregulated in HCC and predicts a poor prognosis.ACE2 overexpression significantly inhibits the glycolytic flux as evidenced by reduced glucose uptake, lactate release, extracellular acidification rate, and the expression of glycolytic genes.Opposite results are noticed in loss-of-function studies.Mechanistically, ACE2 metabolizes Ang II to Ang-(1-7), which activates Mas receptor and leads to the phosphorylation of Src homology 2-containing inositol phosphatase 2 (SHP-2).SHP2 activation further blocks reactive oxygen species (ROS)-HIF1α signaling.Addition of Ang-(1-7) or the antioxidant N-acetylcysteine compromises in vivo additive tumor growth and aerobic glycolysis induced by ACE2 knockdown.Moreover, growth advantages afforded by ACE2 knockdown are largely glycolysis-dependent.In clinical settings, a close link between ACE2 expression and HIF1α or the phosphorated level of SHP2 is found.Overexpression of ACE2 significantly retards tumor growth in patient-derived xenograft model.Collectively, our findings suggest that ACE2 is a negative glycolytic regulator, and targeting the ACE2/Ang-(1-7)/Mas receptor/ROS/HIF1α axis may be a promising therapeutic strategy for HCC treatment.

BACKGROUND AND OBJECTIVES:Older adults residing in senior homes are at a high risk of malnutrition. In this study, we investigated the nutritional status of these individuals and factors associated with malnutrition in this population.METHODS AND STUDY DESIGN:This cross-sectional study (September 2020-January 2021) included a total of 583 older adults residing in a senior home in Shanghai (mean age, 85.0±6.6 years). The Mini Nutritional Assessment Short Form (MNA-SF) questionnaire was administered to assess the nutritional status of the participants. Patients with possible sarcopenia were identified according to the guidelines recommended by the Asian Working Group for Sarcopenia in its 2019 consensus (AWGS 2019). Moreover, the factors influencing malnutrition were determined through multivariate analyses.RESULTS:The likelihoods of having malnutrition and being at a risk of malnutrition were noted in 10.5% and 37.4% of the participants, respectively. In both male and female participants, handgrip strength (HGS) and calf circumference (CC) increased significantly with increasing scores on the aforementioned questionnaire (p<0.001). Among the participants, 44.6% had ≥3 chronic diseases and 48.2% used multiple medicines. Multivariate analyses revealed that dys-phagia (OR, 3.8; 95% CI, 1.7-8.5), possible sarcopenia (OR, 3.6; 95% CI, 2.2-5.6), and dementia (OR, 4.5; 95% CI, 2.8-7.0) were correlated with a relatively high prevalence of malnutrition/malnutrition risk. Exercise (at least thrice a week) reduced malnutrition risk.CONCLUSIONS:Malnutrition is common among older adults residing in senior homes; therefore, the associated factors must be identified, and appropriate interventions should be administered.

ObjectivesSarcopenia is well known to be associated with mortality, but there is a lack of evidence on the estimates of life expectancy (LE) for sarcopenia in China. This study aims to estimate total life expectancy (TLE) and sarcopenia-specific LE in community-dwelling older Chinese adults with and without sarcopenia.MethodsThis study included participants aged 60 years and older who enrolled in the cohort in 2011 and 2013 and at least completed one follow-up until 2015 as part of the China Health and Retirement Longitudinal Study (CHARLS). The criteria for defining sarcopenia were based on the guidelines established by the Asian Working Group on Sarcopenia in 2019. TLE and sarcopenia-specific LE were estimated for the total population and subgroups using continuous-time multistate modeling.ResultsA total of 6,029 participants (49.2% women) with an average age of 68.4 (SD: 6.56) years were included in the study. The baseline prevalence of sarcopenia and possible sarcopenia was 19.5 and 44.9%, respectively. We observed that sarcopenia stages naturally deteriorated to worse stages (including death, by 24.4%) and returned to better stages (17.1%) during a median follow-up of 3.92 years (IQR: 2.00 ~ 4.00). The average TLE at the age of 60 was 20.9 [95% CI: 20.2–21.5] years (22.1 [95% CI: 19.6–24.6] for non-sarcopenic older adults, 20.9 [95% CI: 19.5–22.3] for possible sarcopenic, and 18.7 [95% CI: 16.4–21.1] for sarcopenic). Men, former and current smokers, and those living in northwest China had less TLE. Sarcopenic older adults, those with lower education, those who are unmarried, those with agriculture hukou, and those living in rural and northwest China were expected to live fewer years with non-sarcopenia. Sarcopenic older people, men, those with agriculture hukou, and those living in rural and southwest China were expected to live more years with sarcopenia.DiscussionThe results improved our understanding of the relationship between sarcopenia and life expectancy. We suggested that targeted strategies should be considered in high-risk populations and underdeveloped regions to prevent sarcopenia and improve non-sarcopenic life years for the older population.