Pub Date : 2026-02-01Epub Date: 2026-01-12DOI: 10.1016/j.jnha.2026.100774
Xianlin Zhang, Wenbo Tang, Pinfang Kang, Bi Tang, Zhongyan Du, Wenke Cheng
Background: Biological aging and dietary fatty acid balance may influence the bidirectional progression between atrial fibrillation (AF) and heart failure (HF); however, most studies focus on single endpoints, overlooking intermediate states.
Objective: To evaluate the independent and joint associations of phenotypic age acceleration (PhenoAgeAccel) and the plasma omega-6/omega-3 (ω-6/ω-3) polyunsaturated fatty acid (PFUA) ratio with AF-HF transitions, and to examine mediation by lipids and C-reactive protein.
Methods: In a retrospective cohort of 191,091 UK Biobank participants free of baseline cardiovascular disease, PhenoAgeAccel was calculated as the residual from regressing phenotypic age on chronological age. The ω-6/ω-3 ratio was quantified by nuclear magnetic resonance. Incident AF and HF were modeled using clock-forward multistate Markov models for four transitions: baseline to AF, baseline to HF, AF to HF, and HF to AF. These transitions represent sequential disease progression, where either AF or HF may occur first and later progress to AF-HF comorbidity. Hazard ratios (HRs) were estimated per 1-SD increment. Joint exposure and mediation analyses were performed.
Results: Over a median 15.4 years, 10,084 developed AF and 3,117 H F; 1,335 transitioned from AF to HF and 426 from HF to AF. Per 1-SD higher PhenoAgeAccel, risks increased for baseline-to-AF (HR 1.12 [95% CI 1.10-1.15]), baseline-to-HF (1.24 [1.21-1.26]), AF-to-HF (1.12 [1.09-1.15]), and HF-to-AF (1.06 [1.01-1.12]). Per 1-SD higher ω-6/ω-3 ratio, risks rose for baseline-to-AF (1.04 [1.02-1.06]), baseline-to-HF (1.07 [1.05-1.10]), AF-to-HF (1.12 [1.07-1.18]), and HF-to-AF (1.10 [1.01-1.20]). Mediation occurred via triglycerides (up to 38.5% of ω-6/ω-3-AF association) and CRP (up to 10.7% of PhenoAgeAccel-HF association).
Conclusion: Higher PhenoAgeAccel and ω-6/ω-3 PFUA ratios were independently associated with higher risks of AF-HF transitions, with these associations partly explained by lipid and inflammatory pathways.
{"title":"Phenotypic age acceleration and omega-6/omega-3 PUFA ratio in dynamic atrial fibrillation-heart failure transitions: a multistate analysis.","authors":"Xianlin Zhang, Wenbo Tang, Pinfang Kang, Bi Tang, Zhongyan Du, Wenke Cheng","doi":"10.1016/j.jnha.2026.100774","DOIUrl":"10.1016/j.jnha.2026.100774","url":null,"abstract":"<p><strong>Background: </strong>Biological aging and dietary fatty acid balance may influence the bidirectional progression between atrial fibrillation (AF) and heart failure (HF); however, most studies focus on single endpoints, overlooking intermediate states.</p><p><strong>Objective: </strong>To evaluate the independent and joint associations of phenotypic age acceleration (PhenoAgeAccel) and the plasma omega-6/omega-3 (ω-6/ω-3) polyunsaturated fatty acid (PFUA) ratio with AF-HF transitions, and to examine mediation by lipids and C-reactive protein.</p><p><strong>Methods: </strong>In a retrospective cohort of 191,091 UK Biobank participants free of baseline cardiovascular disease, PhenoAgeAccel was calculated as the residual from regressing phenotypic age on chronological age. The ω-6/ω-3 ratio was quantified by nuclear magnetic resonance. Incident AF and HF were modeled using clock-forward multistate Markov models for four transitions: baseline to AF, baseline to HF, AF to HF, and HF to AF. These transitions represent sequential disease progression, where either AF or HF may occur first and later progress to AF-HF comorbidity. Hazard ratios (HRs) were estimated per 1-SD increment. Joint exposure and mediation analyses were performed.</p><p><strong>Results: </strong>Over a median 15.4 years, 10,084 developed AF and 3,117 H F; 1,335 transitioned from AF to HF and 426 from HF to AF. Per 1-SD higher PhenoAgeAccel, risks increased for baseline-to-AF (HR 1.12 [95% CI 1.10-1.15]), baseline-to-HF (1.24 [1.21-1.26]), AF-to-HF (1.12 [1.09-1.15]), and HF-to-AF (1.06 [1.01-1.12]). Per 1-SD higher ω-6/ω-3 ratio, risks rose for baseline-to-AF (1.04 [1.02-1.06]), baseline-to-HF (1.07 [1.05-1.10]), AF-to-HF (1.12 [1.07-1.18]), and HF-to-AF (1.10 [1.01-1.20]). Mediation occurred via triglycerides (up to 38.5% of ω-6/ω-3-AF association) and CRP (up to 10.7% of PhenoAgeAccel-HF association).</p><p><strong>Conclusion: </strong>Higher PhenoAgeAccel and ω-6/ω-3 PFUA ratios were independently associated with higher risks of AF-HF transitions, with these associations partly explained by lipid and inflammatory pathways.</p>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 2","pages":"100774"},"PeriodicalIF":4.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12901530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145953888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study assesses the association between exposure to volatile organic compounds (VOCs) and phenotypic age acceleration, and evaluates the potential synergistic interaction by dietary micronutrient intake.
Methods
A total of 7,209 participants were chosen from the National Health and Nutrition Examination Survey (NHANES) conducted between 2005–2006 and 2011−2018. The VOCs metabolites were quantitatively evaluated using ultra-performance liquid chromatography-electrospray ionization tandem mass spectrometry. The dietary micronutrient intake was assessed through interviews that involved recalling a 24-h diet. To measure biological aging, the "BioAge" R package was utilized to calculate PhenoAge. Various statistical analyses such as weighted multiple linear regression, weighted quantile sum (WQS) regression, restricted cubic spline models, subgroup analyses, and interaction analyses were employed to assess the impact of VOCs metabolites on PhenoAge acceleration while considering the influence of dietary micronutrient intake.
Results
The participants' average age was 47.37 years, and females accounted for 51.5% of the sample. Through weighted multivariate linear regression analysis, we discovered significant positive connections between CEMA, 3HPMA, DHBMA, MHBMA3, HPMMA, PGA, and PhenoAge acceleration. Our WQS analysis indicated a noteworthy positive correlation between VOCs metabolite mixtures and PhenoAge acceleration (β = 0.693, P < 0.001), with DHBMA, HPMMA, and PGA identified as the most influential metabolites. By employing restricted cubic spline models, we established a linear relationship between DHBMA, HPMMA, PGA,and PhenoAge acceleration. Subgroup analyses consistently demonstrated positive associations for DHBMA, HPMMA, PGA with PhenoAge acceleration across various subgroups. Furthermore, dietary micronutrient intake exhibited significant synergistic interaction with these metabolites.
Conclusions
This study confirms that VOC exposure contributes to phenotypic age acceleration. Critically, we find that some dietary micronutrients appear to interact with VOC exposure, mitigating its effect and providing evidence that aging is jointly driven by synergistic environmental and nutritional stressors.
目的研究挥发性有机化合物（VOCs）暴露与表型年龄加速之间的关系，并评估膳食微量营养素摄入可能产生的协同作用。方法从2005-2006年和2011 - 2018年进行的全国健康与营养检查调查（NHANES）中选取7209名参与者。采用超高效液相色谱-电喷雾串联质谱法对VOCs代谢物进行定量评价。通过回顾24小时饮食的访谈来评估膳食微量营养素摄入量。为了测量生物老化，使用“BioAge”R软件包计算PhenoAge。采用加权多元线性回归、加权分位和（WQS）回归、限制三次样条模型、亚组分析和相互作用分析等统计分析方法，在考虑膳食微量营养素摄入影响的情况下，评估VOCs代谢物对表型加速的影响。结果研究对象平均年龄47.37岁，女性占51.5%。通过加权多元线性回归分析，我们发现CEMA、3HPMA、DHBMA、MHBMA3、HPMMA、PGA与表型加速之间存在显著正相关。我们的WQS分析表明，VOCs代谢物混合物与表型加速之间存在显著的正相关（β = 0.693, P < 0.001），其中DHBMA、HPMMA和PGA被认为是影响最大的代谢物。通过限制三次样条模型，我们建立了DHBMA、HPMMA、PGA与表型加速之间的线性关系。亚组分析一致表明，DHBMA、HPMMA、PGA与不同亚组的表型加速呈正相关。此外，膳食微量营养素摄入量与这些代谢物表现出显著的协同作用。结论：本研究证实，VOC暴露有助于表型年龄加速。关键的是，我们发现一些膳食微量营养素似乎与VOC暴露相互作用，减轻了其影响，并提供证据表明衰老是由协同环境和营养压力共同驱动的。
{"title":"Associations of volatile organic compound exposure with phenotypic age acceleration and the synergistic interaction of dietary micronutrients","authors":"Huanrui Zhang , Wen Tian , Guoxian Qi , Baosen Zhou , Yujiao Sun","doi":"10.1016/j.jnha.2026.100770","DOIUrl":"10.1016/j.jnha.2026.100770","url":null,"abstract":"<div><h3>Objective</h3><div>This study assesses the association between exposure to volatile organic compounds (VOCs) and phenotypic age acceleration, and evaluates the potential synergistic interaction by dietary micronutrient intake.</div></div><div><h3>Methods</h3><div>A total of 7,209 participants were chosen from the National Health and Nutrition Examination Survey (NHANES) conducted between 2005–2006 and 2011−2018. The VOCs metabolites were quantitatively evaluated using ultra-performance liquid chromatography-electrospray ionization tandem mass spectrometry. The dietary micronutrient intake was assessed through interviews that involved recalling a 24-h diet. To measure biological aging, the \"BioAge\" R package was utilized to calculate PhenoAge. Various statistical analyses such as weighted multiple linear regression, weighted quantile sum (WQS) regression, restricted cubic spline models, subgroup analyses, and interaction analyses were employed to assess the impact of VOCs metabolites on PhenoAge acceleration while considering the influence of dietary micronutrient intake.</div></div><div><h3>Results</h3><div>The participants' average age was 47.37 years, and females accounted for 51.5% of the sample. Through weighted multivariate linear regression analysis, we discovered significant positive connections between CEMA, 3HPMA, DHBMA, MHBMA3, HPMMA, PGA, and PhenoAge acceleration. Our WQS analysis indicated a noteworthy positive correlation between VOCs metabolite mixtures and PhenoAge acceleration (β = 0.693, P < 0.001), with DHBMA, HPMMA, and PGA identified as the most influential metabolites. By employing restricted cubic spline models, we established a linear relationship between DHBMA, HPMMA, PGA,and PhenoAge acceleration. Subgroup analyses consistently demonstrated positive associations for DHBMA, HPMMA, PGA with PhenoAge acceleration across various subgroups. Furthermore, dietary micronutrient intake exhibited significant synergistic interaction with these metabolites.</div></div><div><h3>Conclusions</h3><div>This study confirms that VOC exposure contributes to phenotypic age acceleration. Critically, we find that some dietary micronutrients appear to interact with VOC exposure, mitigating its effect and providing evidence that aging is jointly driven by synergistic environmental and nutritional stressors.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 2","pages":"Article 100770"},"PeriodicalIF":4.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-01-08DOI: 10.1016/j.jnha.2026.100771
Chenfei Zhang, Yonghao Wu, Yinan Liang, Kaifeng Wang
Background
Low back pain (LBP) is a leading cause of global disability. While frailty is a known risk factor, previous studies have been largely cross-sectional, thus the impact of dynamic changes in frailty on incident LBP is unclear. This study aimed to investigate the association of changes in frailty status with incident LBP.
Methods
This prospective cohort study utilized data from the China Health and Retirement Longitudinal Study (CHARLS), including 9,174 participants aged ≥45 years without LBP at the start of follow-up. Frailty status (robust, pre-frail, frail) was determined using a 30-item Frailty Index (FI) at baseline (2011) and two years later (2013). Dynamic changes were defined by transitions between these states. Incident LBP was the primary outcome, ascertained via follow-up until 2020. Multivariable Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs).
Results
The study included 9,174 participants (mean age 59.2 years; 47.9% female) followed for a median of 7.48 years, during which 3,437 incident LBP cases were identified. Compared with participants who remained robust, those who progressed to a pre-frail or frail status had a significantly increased risk of incident LBP (HR 1.48, 95% CI 1.32−1.66). Progression from pre-frail to frail also increased risk (HR 1.51, 95% CI 1.35−1.69) compared to remaining pre-frail. Conversely, recovery was protective; participants improving from pre-frail to robust (HR 0.69, 95% CI 0.61−0.78) or from frail to less frail status (HR 0.77, 95% CI 0.66−0.90) had significantly lower risks than their stable counterparts.
Conclusions
Frailty is a dynamic and powerful predictor of incident LBP. Progression towards frailty significantly elevates LBP risk, while recovery is protective. These findings establish a temporal relationship, positioning frailty as a critical, modifiable target for LBP prevention. Integrating frailty assessment into routine clinical care may be a key strategy to reduce the burden of LBP in aging populations.
背景：腰痛（LBP）是全球致残的主要原因。虽然虚弱是一个已知的危险因素，但以前的研究大多是横断面的，因此虚弱的动态变化对LBP事件的影响尚不清楚。本研究旨在探讨虚弱状态变化与腰痛事件的关系。方法本前瞻性队列研究利用中国健康与退休纵向研究（CHARLS）的数据，纳入9174名随访开始时年龄≥45岁、无LBP的参与者。在基线（2011年）和两年后（2013年）使用30项虚弱指数（FI）确定虚弱状态（强健、体弱、体弱）。动态变化是由这些状态之间的转换定义的。通过随访至2020年，偶发性腰痛是主要结局。采用多变量Cox比例风险模型计算风险比（hr）和95%置信区间（ci）。结果本研究纳入9174名参与者（平均年龄59.2岁，女性47.9%），随访时间中位数为7.48年，期间发现3437例LBP事件。与保持健康的参与者相比，那些进展到体弱或体弱状态的参与者发生LBP的风险显著增加（HR 1.48, 95% CI 1.32 - 1.66）。从虚弱前期到虚弱的进展也增加了风险（HR 1.51, 95% CI 1.35−1.69）。相反，复苏是保护性的；从虚弱到健壮（HR 0.69, 95% CI 0.61 - 0.78）或从虚弱到不那么虚弱（HR 0.77, 95% CI 0.66 - 0.90）的参与者的风险显著低于稳定的参与者。结论虚弱是腰痛发生的动态、有效的预测因子。虚弱的进展显著增加了腰痛的风险，而恢复是保护性的。这些发现建立了一种时间关系，将虚弱定位为预防腰痛的关键、可改变的目标。将衰弱评估纳入常规临床护理可能是减轻老年人群腰痛负担的关键策略。
{"title":"Dynamic changes in frailty status and the risk of incident low back pain: a nationwide cohort study based on the China health and retirement longitudinal study","authors":"Chenfei Zhang, Yonghao Wu, Yinan Liang, Kaifeng Wang","doi":"10.1016/j.jnha.2026.100771","DOIUrl":"10.1016/j.jnha.2026.100771","url":null,"abstract":"<div><h3>Background</h3><div>Low back pain (LBP) is a leading cause of global disability. While frailty is a known risk factor, previous studies have been largely cross-sectional, thus the impact of dynamic changes in frailty on incident LBP is unclear. This study aimed to investigate the association of changes in frailty status with incident LBP.</div></div><div><h3>Methods</h3><div>This prospective cohort study utilized data from the China Health and Retirement Longitudinal Study (CHARLS), including 9,174 participants aged ≥45 years without LBP at the start of follow-up. Frailty status (robust, pre-frail, frail) was determined using a 30-item Frailty Index (FI) at baseline (2011) and two years later (2013). Dynamic changes were defined by transitions between these states. Incident LBP was the primary outcome, ascertained via follow-up until 2020. Multivariable Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs).</div></div><div><h3>Results</h3><div>The study included 9,174 participants (mean age 59.2 years; 47.9% female) followed for a median of 7.48 years, during which 3,437 incident LBP cases were identified. Compared with participants who remained robust, those who progressed to a pre-frail or frail status had a significantly increased risk of incident LBP (HR 1.48, 95% CI 1.32−1.66). Progression from pre-frail to frail also increased risk (HR 1.51, 95% CI 1.35−1.69) compared to remaining pre-frail. Conversely, recovery was protective; participants improving from pre-frail to robust (HR 0.69, 95% CI 0.61−0.78) or from frail to less frail status (HR 0.77, 95% CI 0.66−0.90) had significantly lower risks than their stable counterparts.</div></div><div><h3>Conclusions</h3><div>Frailty is a dynamic and powerful predictor of incident LBP. Progression towards frailty significantly elevates LBP risk, while recovery is protective. These findings establish a temporal relationship, positioning frailty as a critical, modifiable target for LBP prevention. Integrating frailty assessment into routine clinical care may be a key strategy to reduce the burden of LBP in aging populations.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 2","pages":"Article 100771"},"PeriodicalIF":4.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-01-13DOI: 10.1016/j.jnha.2026.100775
Shuai Xiang , Yixuan Li , Yunlong Li , Shuzhe Xie , Chengfeng Wang , Xu Che , Yongxing Du
Background
Phenotypic age acceleration (PhenoAgeAccel) is a promising biological aging metric, but its associations with chronic digestive disease risk are unclear. This study evaluated these associations and assessed modification by genetic risk and lifestyle.
Methods
We analyzed 292,639 UK Biobank participants. PhenoAge and PhenoAgeAccel were calculated using a validated algorithm based on clinical biomarkers. Cox proportional hazards models estimated associations of PhenoAgeAccel, genetic risk, and lifestyle with incident chronic digestive diseases, including interaction and stratified analyses. Variance decomposition quantified contributions of aging, genetics, and lifestyle.
Results
Over a median 13.67-year follow-up, PhenoAgeAccel > 0 (accelerated aging) was independently associated with higher risk of most chronic digestive diseases, notably Crohn’s disease (HR per 5-year increase, 1.36; 95%CI, 1.30–1.42) and liver cirrhosis (HR, 1.35; 95%CI, 1.30–1.40). Significant additive interactions occurred between PhenoAgeAccel and genetic risk for diverticulosis, Crohn’s disease, ulcerative colitis, liver cirrhosis, and chronic pancreatitis; among biologically older individuals at high genetic risk, interaction-attributable excess risk reached 42.8% of total risk. A healthy lifestyle attenuated aging-related risk for all outcomes except Crohn's disease and ulcerative colitis. Variance decomposition revealed disease-specific risk contribution profiles: biological aging contributed most to Crohn’s disease and chronic pancreatitis, genetic risk to diverticulosis and ulcerative colitis, and lifestyle to gastroesophageal reflux disease and nonalcoholic fatty liver.
Conclusions
Higher PhenoAgeAccel was associated with higher risks of chronic digestive diseases, with associations modified by genetic risk and lifestyle. PhenoAgeAccel may be a useful risk marker and warrants further investigation of aging-targeted strategies.
{"title":"Associations of phenotypic age acceleration, genetic risk, and lifestyle with chronic digestive diseases: A large-scale longitudinal cohort study","authors":"Shuai Xiang , Yixuan Li , Yunlong Li , Shuzhe Xie , Chengfeng Wang , Xu Che , Yongxing Du","doi":"10.1016/j.jnha.2026.100775","DOIUrl":"10.1016/j.jnha.2026.100775","url":null,"abstract":"<div><h3>Background</h3><div>Phenotypic age acceleration (PhenoAgeAccel) is a promising biological aging metric, but its associations with chronic digestive disease risk are unclear. This study evaluated these associations and assessed modification by genetic risk and lifestyle.</div></div><div><h3>Methods</h3><div>We analyzed 292,639 UK Biobank participants. PhenoAge and PhenoAgeAccel were calculated using a validated algorithm based on clinical biomarkers. Cox proportional hazards models estimated associations of PhenoAgeAccel, genetic risk, and lifestyle with incident chronic digestive diseases, including interaction and stratified analyses. Variance decomposition quantified contributions of aging, genetics, and lifestyle.</div></div><div><h3>Results</h3><div>Over a median 13.67-year follow-up, PhenoAgeAccel > 0 (accelerated aging) was independently associated with higher risk of most chronic digestive diseases, notably Crohn’s disease (HR per 5-year increase, 1.36; 95%CI, 1.30–1.42) and liver cirrhosis (HR, 1.35; 95%CI, 1.30–1.40). Significant additive interactions occurred between PhenoAgeAccel and genetic risk for diverticulosis, Crohn’s disease, ulcerative colitis, liver cirrhosis, and chronic pancreatitis; among biologically older individuals at high genetic risk, interaction-attributable excess risk reached 42.8% of total risk. A healthy lifestyle attenuated aging-related risk for all outcomes except Crohn's disease and ulcerative colitis. Variance decomposition revealed disease-specific risk contribution profiles: biological aging contributed most to Crohn’s disease and chronic pancreatitis, genetic risk to diverticulosis and ulcerative colitis, and lifestyle to gastroesophageal reflux disease and nonalcoholic fatty liver.</div></div><div><h3>Conclusions</h3><div>Higher PhenoAgeAccel was associated with higher risks of chronic digestive diseases, with associations modified by genetic risk and lifestyle. PhenoAgeAccel may be a useful risk marker and warrants further investigation of aging-targeted strategies.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 2","pages":"Article 100775"},"PeriodicalIF":4.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-01-09DOI: 10.1016/j.jnha.2025.100768
Yi Zou, Qi Yang, Xiaokun Tang, Mei Yang
{"title":"Limitations in Clinical Translation of the Age-Friendly Environment and Sarcopenia Association","authors":"Yi Zou, Qi Yang, Xiaokun Tang, Mei Yang","doi":"10.1016/j.jnha.2025.100768","DOIUrl":"10.1016/j.jnha.2025.100768","url":null,"abstract":"","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 2","pages":"Article 100768"},"PeriodicalIF":4.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-01-28DOI: 10.1016/j.jnha.2026.100797
Renato Bandeira de Mello , Vitor Pelegrim de Oliveira
{"title":"Hearing loss associated with mobility and cognitive impairment: comorbid condition, an intrinsic capacity-aligned vulnerability cluster or a syndromic clustering?","authors":"Renato Bandeira de Mello , Vitor Pelegrim de Oliveira","doi":"10.1016/j.jnha.2026.100797","DOIUrl":"10.1016/j.jnha.2026.100797","url":null,"abstract":"","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 2","pages":"Article 100797"},"PeriodicalIF":4.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-20DOI: 10.1016/j.jnha.2025.100758
Li Zhang , Yiwen Xing , Yiming Pan , Yiwei Zhao , Zhibin Wang , Yue Wu , Xue Gao , Xiaxia Li , Yu Wang , Yumin Wang , Yansu Guo , Yi Tang , Lina Ma
Objective
To explore the association between hearing impairment, as detected by the whisper test, and physio-cognitive decline syndrome (PCDS) in older adults.
Design
Cross-sectional study.
Setting
Community.
Participants
Data were derived from the Beijing Disability Risk and Ageing Monitoring Study (BEAM), including 1,117 community-dwelling older adults. PCDS was defined as the concurrent presence of mobility impairment no disability (MIND) and cognitive impairment no dementia (CIND). Mobility impairment was defined as weakness and/or slowness, while cognitive impairment was defined as performance below 1.5 standard deviations in any cognitive domain, adjusted for age and education.
Results
The prevalence of PCDS was 14.50%. Compared with older adults in the non-PCDS group, participants with PCDS were older, had lower educational level, experienced more chronic diseases, took more medications, and exhibited a higher prevalence of hearing impairment as detected by the whisper test. In terms of mobility and cognition, participants with PCDS demonstrated slower gait speed, weaker grip strength, and lower scores on the Mini-Mental State Examination, particularly in the domains of immediate memory, delayed memory, and attention and computation. After adjusting for confounders, multivariate logistic regression analysis showed that hearing impairment detected by the whisper test was significantly associated with PCDS (odds ratio = 2.121, 95% confidence interval: 1.009–1.459) when compared to the non-PCDS group.
Conclusion
Hearing impairment, as identified by the whisper test, is closely correlated with PCDS in community-dwelling older adults. The comprehensive management of older adults should not only focus on general conditions such as educational level and medication use, but also pay attention to functional status such as hearing, in order to screen for PCDS in the early stage and delay function decline.
{"title":"Hearing impairment detected by the whisper test is associated with physio-cognitive decline syndrome in community-dwelling older adults","authors":"Li Zhang , Yiwen Xing , Yiming Pan , Yiwei Zhao , Zhibin Wang , Yue Wu , Xue Gao , Xiaxia Li , Yu Wang , Yumin Wang , Yansu Guo , Yi Tang , Lina Ma","doi":"10.1016/j.jnha.2025.100758","DOIUrl":"10.1016/j.jnha.2025.100758","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the association between hearing impairment, as detected by the whisper test, and physio-cognitive decline syndrome (PCDS) in older adults.</div></div><div><h3>Design</h3><div>Cross-sectional study.</div></div><div><h3>Setting</h3><div>Community.</div></div><div><h3>Participants</h3><div>Data were derived from the Beijing Disability Risk and Ageing Monitoring Study (BEAM), including 1,117 community-dwelling older adults. PCDS was defined as the concurrent presence of mobility impairment no disability (MIND) and cognitive impairment no dementia (CIND). Mobility impairment was defined as weakness and/or slowness, while cognitive impairment was defined as performance below 1.5 standard deviations in any cognitive domain, adjusted for age and education.</div></div><div><h3>Results</h3><div>The prevalence of PCDS was 14.50%. Compared with older adults in the non-PCDS group, participants with PCDS were older, had lower educational level, experienced more chronic diseases, took more medications, and exhibited a higher prevalence of hearing impairment as detected by the whisper test. In terms of mobility and cognition, participants with PCDS demonstrated slower gait speed, weaker grip strength, and lower scores on the Mini-Mental State Examination, particularly in the domains of immediate memory, delayed memory, and attention and computation. After adjusting for confounders, multivariate logistic regression analysis showed that hearing impairment detected by the whisper test was significantly associated with PCDS (odds ratio = 2.121, 95% confidence interval: 1.009–1.459) when compared to the non-PCDS group.</div></div><div><h3>Conclusion</h3><div>Hearing impairment, as identified by the whisper test, is closely correlated with PCDS in community-dwelling older adults. The comprehensive management of older adults should not only focus on general conditions such as educational level and medication use, but also pay attention to functional status such as hearing, in order to screen for PCDS in the early stage and delay function decline.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 2","pages":"Article 100758"},"PeriodicalIF":4.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145798820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-10DOI: 10.1016/j.jnha.2025.100754
Gebretsadkan Gebremedhin Gebretsadik , Bo Yang , Andrea J. Glenn , Ai-Min Yang , Jie Li , Vicky Wai-Ki Chan , Man-Sau Wong , Simin Liu , Ka-Hei Kenneth Lo
Objectives
To examine the association of dietary Manganese (Mn) intake with type 2 diabetes (T2D) incidence, total cardiovascular disease (CVD), and CVD mortality by analyzing data from the UK Biobank and conducting a meta-analysis of available prospective cohorts.
Design
Prospective analysis of a primary cohort with a dose-response meta-analysis of prospective cohorts.
Setting
The UK Biobank cohort and the meta-analysis of prospective cohorts.
Participants
UK Biobank participants aged 40–69 years at baseline were enrolled between 2006 and 2010 and followed until December 2022. We included 165,194 participants in T2D analytic cohort and 164,111 individuals in CVD analytic cohort. Our systematic review and meta-analysis of six studies comprised over 270,000 participants.
Exposure
Dietary manganese (Mn) intake.
Measurements
The outcome measurements were T2D incidence, total CVD, and CVD mortality. Dietary intake was assessed using 24-h dietary instrument. Cox proportional hazards models were used to assess associations of Mn intake with T2D and CVD risk. Effect estimates were presented in hazard ratios (HR) with 95% confidence intervals (CI). In meta-analysis, a pooled risk for a 1 mg/day increase in Mn intake was estimated using restricted maximum likelihood (REML).
Results
High Mn intake (Q5) was not significantly associated with lower risk of T2D as compared to Q1 (adjusted HR 0·91; 95% CI 0·82, 1.01, Ptrend = 0·07). The dose-response meta-analysis revealed a 4% reduction in T2D risk with each mg/day increase in Mn intake (pooled RR 0·96; 95% CI 0·94, 0·99), with potential non-linearity (Pnonlinear< 0.01). Q5 Mn intake was not significantly associated with reduced risk of CVD (adjusted HR 0·99; 95% CI 0·92, 1.05; Ptrend = 0·61) or CVD mortality (adjusted HR 0·85; 95% CI 0·64, 1.13; Ptrend = 0·66).
Conclusions
Our meta-analysis suggested that increasing Mn intake may lower T2D risk, potentially exhibiting a dose-response non-linear pattern, although not corroborated by UK Biobank analysis.
目的通过分析英国生物银行（UK Biobank）的数据并对现有前瞻性队列进行荟萃分析，研究膳食锰（Mn）摄入量与2型糖尿病（T2D）发病率、总心血管疾病（CVD）和CVD死亡率之间的关系。设计对主要队列进行前瞻性分析，并对前瞻性队列进行剂量-反应荟萃分析。英国生物银行队列和前瞻性队列的荟萃分析。2006年至2010年期间，基线年龄为40-69岁的suk生物银行参与者入组，随访至2022年12月。我们纳入了165,194名T2D分析队列参与者和164,111名CVD分析队列参与者。我们对六项研究进行了系统回顾和荟萃分析，其中包括27万多名参与者。暴露膳食中锰（Mn）的摄入量。结果测量为T2D发生率、CVD总发生率和CVD死亡率。采用24 h膳食仪评估日粮摄入量。Cox比例风险模型用于评估锰摄入量与T2D和CVD风险的关系。效果估计以95%可信区间（CI）的风险比（HR）表示。在荟萃分析中，使用限制最大似然（REML）估计了锰摄入量增加1 mg/天的综合风险。结果高锰摄入量（Q5）与T2D风险较Q1降低无显著相关性（调整后危险度0.91;95% CI 0.82, 1.01， p趋势= 0.07）。剂量-反应荟萃分析显示，锰摄入量每增加mg/天，T2D风险降低4%（合并RR 0.96; 95% CI 0.94, 0.99），存在潜在的非线性（pnonlinearity < 0.01）。Q5 Mn摄入量与降低CVD风险（调整后危险度0.99;95% CI 0.92, 1.05; Ptrend = 0.61）或CVD死亡率（调整后危险度0.85;95% CI 0.64, 1.13; Ptrend = 0.66）无显著相关性。我们的荟萃分析表明，增加锰摄入量可能会降低T2D风险，可能表现出剂量-反应非线性模式，尽管没有得到UK Biobank分析的证实。
{"title":"Dietary manganese, type 2 diabetes, and cardiovascular disease: A UK Biobank cohort study and meta-analysis of over 270,000 individuals","authors":"Gebretsadkan Gebremedhin Gebretsadik , Bo Yang , Andrea J. Glenn , Ai-Min Yang , Jie Li , Vicky Wai-Ki Chan , Man-Sau Wong , Simin Liu , Ka-Hei Kenneth Lo","doi":"10.1016/j.jnha.2025.100754","DOIUrl":"10.1016/j.jnha.2025.100754","url":null,"abstract":"<div><h3>Objectives</h3><div>To examine the association of dietary Manganese (Mn) intake with type 2 diabetes (T2D) incidence, total cardiovascular disease (CVD), and CVD mortality by analyzing data from the UK Biobank and conducting a meta-analysis of available prospective cohorts.</div></div><div><h3>Design</h3><div>Prospective analysis of a primary cohort with a dose-response meta-analysis of prospective cohorts.</div></div><div><h3>Setting</h3><div>The UK Biobank cohort and the meta-analysis of prospective cohorts.</div></div><div><h3>Participants</h3><div>UK Biobank participants aged 40–69 years at baseline were enrolled between 2006 and 2010 and followed until December 2022. We included 165,194 participants in T2D analytic cohort and 164,111 individuals in CVD analytic cohort. Our systematic review and meta-analysis of six studies comprised over 270,000 participants.</div></div><div><h3>Exposure</h3><div>Dietary manganese (Mn) intake.</div></div><div><h3>Measurements</h3><div>The outcome measurements were T2D incidence, total CVD, and CVD mortality. Dietary intake was assessed using 24-h dietary instrument. Cox proportional hazards models were used to assess associations of Mn intake with T2D and CVD risk. Effect estimates were presented in hazard ratios (HR) with 95% confidence intervals (CI). In meta-analysis, a pooled risk for a 1 mg/day increase in Mn intake was estimated using restricted maximum likelihood (REML).</div></div><div><h3>Results</h3><div>High Mn intake (Q5) was not significantly associated with lower risk of T2D as compared to Q1 (adjusted HR 0·91; 95% CI 0·82, 1.01, P<sub>trend</sub> = 0·07). The dose-response meta-analysis revealed a 4% reduction in T2D risk with each mg/day increase in Mn intake (pooled RR 0·96; 95% CI 0·94, 0·99), with potential non-linearity (P<sub>nonlinear</sub>< 0.01). Q5 Mn intake was not significantly associated with reduced risk of CVD (adjusted HR 0·99; 95% CI 0·92, 1.05; <em>P<sub>trend</sub></em> = 0·61) or CVD mortality (adjusted HR 0·85; 95% CI 0·64, 1.13; <em>P<sub>trend</sub></em> = 0·66).</div></div><div><h3>Conclusions</h3><div>Our meta-analysis suggested that increasing Mn intake may lower T2D risk, potentially exhibiting a dose-response non-linear pattern, although not corroborated by UK Biobank analysis.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 2","pages":"Article 100754"},"PeriodicalIF":4.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145711919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-11-18DOI: 10.1016/j.jnha.2025.100727
Cheng Huang , Yuan Yu , Weihao Liang , Jiayong Li , Yilong Wang , Fangfei Wei , Tianyu Xu , Yu Ning , Zhe Zhen , Jia Liu , Wengen Zhu , Yugang Dong , Chen Liu , Peisen Huang
Background
The association between high protein intake and cardiovascular diseases (CVD) was conflicting and the role of age in this relationship was rarely studied. This study aimed to examine the association of high protein diet with the risk of CVD and the interaction of age in this association.
Methods
Participants from UK biobank (2007–2023) with at least 1 dietary questionnaire and without history of chronic diseases at baseline were included. High-protein diet was defined as protein intake ≥1.8 g·kg−1·day−1. The primary outcome was major adverse cardiovascular events (MACE). Cox regression analyses and restricted cubic spline (RCS) regression analyses were performed.
Results
Among 19420 participants, the median (IQR) age was 54 (14) years and 14137 (72.8%) were women. With a follow-up of 256258.9 person-years, 967 MACEs occurred. After adjusting for sociodemographic and cardiovascular risk factors, participants with high-protein intake had higher risk of MACE compared with participants with low-protein intake (HR = 1.21, 95% CI, 1.02–1.44, P = 0.027). High-protein diet was also associated with higher risk of all-cause mortality, heart failure, myocardial infarction and CVD death (HR = 1.39, 95% CI, 1.17–1.65, P < 0.001; HR = 1.43, 95% CI, 1.07–1.92, P = 0.015; HR = 1.50, 95% CI, 1.07–2.10, P = 0.019; HR = 1.73, 95% CI, 1.12–2.65, P = 0.013, respectively). Among participants aged over 55 years, high protein intake was associated with higher risk of MACE (HR = 1.36, 95% CI, 1.13-1.63, P = 0.001). Whereas, among participants younger than 55 years, the association was not significant (HR = 0.75, 95% CI, 0.51–1.11, P = 0.099, Pinteraction = 0.003). Similar interaction between age and high protein diet was witnessed in the association of high protein intake and stroke (Pinteraction = 0.019).
Conclusions
Higher protein intake was related to higher incidence of MACE in participants over 55 years old, but the association was not evident in their counterparts younger than 55 years old.
背景：高蛋白摄入与心血管疾病（CVD）之间的关系是相互矛盾的，年龄在这种关系中的作用很少被研究。本研究旨在探讨高蛋白饮食与心血管疾病风险的关系以及年龄在这种关系中的相互作用。方法：受试者来自英国生物银行（2007-2023），至少有1份饮食问卷，基线时无慢性疾病史。高蛋白饮食定义为蛋白质摄入量≥1.8 g·kg-1·day-1。主要终点为主要不良心血管事件（MACE）。采用Cox回归分析和限制性三次样条（RCS）回归分析。结果：在19420名参与者中，中位（IQR）年龄为54（14）岁，14137（72.8%）为女性。随访256258.9人年，发生967例mace。在调整了社会人口统计学和心血管危险因素后，高蛋白摄入的参与者与低蛋白摄入的参与者相比，MACE的风险更高（HR = 1.21, 95% CI, 1.02-1.44, P = 0.027）。高蛋白饮食还与全因死亡率、心力衰竭、心肌梗死和心血管疾病死亡的高风险相关（HR = 1.39, 95% CI, 1.17-1.65, P < 0.001; HR = 1.43, 95% CI, 1.07-1.92, P = 0.015; HR = 1.50, 95% CI, 1.07-2.10, P = 0.019; HR = 1.73, 95% CI, 1.12-2.65, P = 0.013）。在55岁以上的参与者中，高蛋白摄入与MACE的高风险相关（HR = 1.36, 95% CI, 1.13-1.63, P = 0.001）。然而，在年龄小于55岁的参与者中，相关性不显著（HR = 0.75, 95% CI, 0.51-1.11, P = 0.099, P - interaction = 0.003）。高蛋白饮食与脑卒中的关系中，年龄与高蛋白饮食之间也存在类似的相互作用（p - interaction = 0.019）。结论：在55岁以上的参与者中，较高的蛋白质摄入量与较高的MACE发生率相关，但在55岁以下的参与者中，这种关联并不明显。
{"title":"Associations between High Protein Intake and Cardiovascular Diseases by Age Groups: A Cohort Study","authors":"Cheng Huang , Yuan Yu , Weihao Liang , Jiayong Li , Yilong Wang , Fangfei Wei , Tianyu Xu , Yu Ning , Zhe Zhen , Jia Liu , Wengen Zhu , Yugang Dong , Chen Liu , Peisen Huang","doi":"10.1016/j.jnha.2025.100727","DOIUrl":"10.1016/j.jnha.2025.100727","url":null,"abstract":"<div><h3>Background</h3><div>The association between high protein intake and cardiovascular diseases (CVD) was conflicting and the role of age in this relationship was rarely studied. This study aimed to examine the association of high protein diet with the risk of CVD and the interaction of age in this association.</div></div><div><h3>Methods</h3><div>Participants from UK biobank (2007–2023) with at least 1 dietary questionnaire and without history of chronic diseases at baseline were included. High-protein diet was defined as protein intake ≥1.8 g·kg<sup>−1</sup>·day<sup>−1</sup>. The primary outcome was major adverse cardiovascular events (MACE). Cox regression analyses and restricted cubic spline (RCS) regression analyses were performed.</div></div><div><h3>Results</h3><div>Among 19420 participants, the median (IQR) age was 54 (14) years and 14137 (72.8%) were women. With a follow-up of 256258.9 person-years, 967 MACEs occurred. After adjusting for sociodemographic and cardiovascular risk factors, participants with high-protein intake had higher risk of MACE compared with participants with low-protein intake (HR = 1.21, 95% CI, 1.02–1.44, <em>P</em> = 0.027). High-protein diet was also associated with higher risk of all-cause mortality, heart failure, myocardial infarction and CVD death (HR = 1.39, 95% CI, 1.17–1.65, <em>P</em> < 0.001; HR = 1.43, 95% CI, 1.07–1.92, <em>P</em> = 0.015; HR = 1.50, 95% CI, 1.07–2.10, <em>P</em> = 0.019; HR = 1.73, 95% CI, 1.12–2.65, <em>P</em> = 0.013, respectively). Among participants aged over 55 years, high protein intake was associated with higher risk of MACE (HR = 1.36, 95% CI, 1.13-1.63, <em>P</em> = 0.001). Whereas, among participants younger than 55 years, the association was not significant (HR = 0.75, 95% CI, 0.51–1.11, <em>P</em> = 0.099, <em>P<sub>interaction</sub></em> = 0.003). Similar interaction between age and high protein diet was witnessed in the association of high protein intake and stroke (<em>P<sub>interaction</sub></em> = 0.019).</div></div><div><h3>Conclusions</h3><div>Higher protein intake was related to higher incidence of MACE in participants over 55 years old, but the association was not evident in their counterparts younger than 55 years old.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 1","pages":"Article 100727"},"PeriodicalIF":4.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145558459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01Epub Date: 2025-11-21DOI: 10.1016/j.jnha.2025.100733
Bingxuan Weng , Jin Jin , Lixue Huang , Yu Wang , Wenshu Jiao , Jingnan Li , Meng Ma , Mengyuan Wang , Xunliang Tong , Yanming Li
Objective
Frailty is increasingly recognized in older adults with lower respiratory tract infections (LRTIs), yet the optimal assessment tool and its prognostic value remain unclear. This study evaluates the prevalence, inter-tool agreement, and predictive performance of four frailty measures in this population.
Methods
Older adults hospitalized with LRTIs were prospectively enrolled. Frailty was assessed using the Clinical Frailty Scale (CFS), Fried Frailty Phenotype (FFP), FRAIL Scale (FS), and Short Physical Performance Battery (SPPB). The primary outcome was 1-year mortality; secondary outcomes included in-hospital mortality and decline in activities of daily living (ADL) at discharge and 1 year. Inter-tool agreement was assessed using Cohen’s kappa, and predictive performance was evaluated by the area under the receiver operating characteristic curve (AUROC).
Results
Of 361 patients (median age 74 years; 61.5% male), frailty prevalence ranged from 18.0% (CFS) to 57.3% (SPPB), with fair to moderate inter-tool agreement. In-hospital and 1-year mortality were 1.4% and 11.5%, respectively. ADL decline occurred in 18.3% at discharge and 21.6% at 1 year. All tools were associated with 1-year mortality, but only the FFP and SPPB were associated with ADL decline.
The FFP demonstrated the the most consistent discriminative performance, with relatively high AUC and a good trade-off between sensitivity and specificity. The CFS exhibited high specificity (0.823–0.881), whereas the SPPB demonstrated high sensitivity (0.724–1.000) across different outcomes. None of the tools adequately predicted 1-year ADL decline (AUC < 0.600).
Conclusions
Frailty is prevalent and prognostic in older adults with LRTIs. The FFP provided consistent prediction of mortality and short-term ADL decline, the CFS was effective for confirming high-risk patients, and the SPPB was useful for early risk screening. The limited prediction of long-term functional decline highlights the need for LRTIs-specific frailty assessment instruments.
{"title":"Comparing various frailty instruments for predicting adverse outcomes in older patients hospitalized with lower respiratory tract infections","authors":"Bingxuan Weng , Jin Jin , Lixue Huang , Yu Wang , Wenshu Jiao , Jingnan Li , Meng Ma , Mengyuan Wang , Xunliang Tong , Yanming Li","doi":"10.1016/j.jnha.2025.100733","DOIUrl":"10.1016/j.jnha.2025.100733","url":null,"abstract":"<div><h3>Objective</h3><div>Frailty is increasingly recognized in older adults with lower respiratory tract infections (LRTIs), yet the optimal assessment tool and its prognostic value remain unclear. This study evaluates the prevalence, inter-tool agreement, and predictive performance of four frailty measures in this population.</div></div><div><h3>Methods</h3><div>Older adults hospitalized with LRTIs were prospectively enrolled. Frailty was assessed using the Clinical Frailty Scale (CFS), Fried Frailty Phenotype (FFP), FRAIL Scale (FS), and Short Physical Performance Battery (SPPB). The primary outcome was 1-year mortality; secondary outcomes included in-hospital mortality and decline in activities of daily living (ADL) at discharge and 1 year. Inter-tool agreement was assessed using Cohen’s kappa, and predictive performance was evaluated by the area under the receiver operating characteristic curve (AUROC).</div></div><div><h3>Results</h3><div>Of 361 patients (median age 74 years; 61.5% male), frailty prevalence ranged from 18.0% (CFS) to 57.3% (SPPB), with fair to moderate inter-tool agreement. In-hospital and 1-year mortality were 1.4% and 11.5%, respectively. ADL decline occurred in 18.3% at discharge and 21.6% at 1 year. All tools were associated with 1-year mortality, but only the FFP and SPPB were associated with ADL decline.</div><div>The FFP demonstrated the the most consistent discriminative performance, with relatively high AUC and a good trade-off between sensitivity and specificity. The CFS exhibited high specificity (0.823–0.881), whereas the SPPB demonstrated high sensitivity (0.724–1.000) across different outcomes. None of the tools adequately predicted 1-year ADL decline (AUC < 0.600).</div></div><div><h3>Conclusions</h3><div>Frailty is prevalent and prognostic in older adults with LRTIs. The FFP provided consistent prediction of mortality and short-term ADL decline, the CFS was effective for confirming high-risk patients, and the SPPB was useful for early risk screening. The limited prediction of long-term functional decline highlights the need for LRTIs-specific frailty assessment instruments.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 1","pages":"Article 100733"},"PeriodicalIF":4.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145571659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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