To assess dementia risk after incident type 2 diabetes (T2D) by age at diagnosis and evaluate modification by treatment, genetic susceptibility, and mitochondrial function.
Design
Prospective 1:1 age- and sex-matched cohort study using inverse-probability-weighted Cox models.
Setting
Kunshan Aging Research with E-health (KARE) cohort in China (2018–2024).
Participants
42,514 adults without diabetes or dementia at baseline, including 21,257 incident T2D cases and 21,257 non-diabetic controls.
Measurements
Outcomes were all-cause dementia, Alzheimer’s disease (AD), and vascular dementia (VaD) from linked medical records and annual examinations. T2D onset age was grouped as 45–54 years, 55–64 years, and persons 65 years and older. In genotyped participants (n = 14,455), a T2D polygenic risk score (PRS) and blood mitochondrial DNA copy number (mtDNA-CN) were examined.
Results
Over a median 3.67 years, incident T2D was associated with higher risks of all-cause dementia (adjusted hazard ratio [AHR] 1.95, 95% CI 1.71–2.21), AD (2.21, 1.88–2.59), and VaD (1.57, 1.20–2.07). Glucose-lowering treatment was associated with lower dementia risk versus no treatment. Among patients aged 55–64 years, the low-PRS/low-mtDNA-CN subgroup had the highest AD risk (AHR 2.41, 95% CI 1.12–5.19).
Conclusion
Age at T2D onset was associated with variation in dementia risk. Earlier diagnosis and treatment were associated with lower observed cognitive risk, while genetic susceptibility and mitochondrial function may inform individualised risk stratification.
目的通过诊断年龄评估2型糖尿病（T2D）发生后痴呆的风险，并评估治疗、遗传易感性和线粒体功能的改变。设计前瞻性1:1年龄和性别匹配队列研究，采用反概率加权Cox模型。基于电子健康（KARE）队列的中国昆山老龄化研究（2018-2024）参与者：42,514名基线时无糖尿病或痴呆的成年人，包括21,257例T2D病例和21,257例非糖尿病对照。测量结果为全因痴呆、阿尔茨海默病（AD）和血管性痴呆（VaD），来自相关医疗记录和年度检查。T2D发病年龄分为45-54岁、55-64岁和65岁及以上。在基因型参与者（n = 14,455）中，检测了T2D多基因风险评分（PRS）和血线粒体DNA拷贝数（mtDNA-CN）。结果在平均3.67年的时间里，T2D的发生与全因痴呆（校正风险比[AHR] 1.95, 95% CI 1.71-2.21）、AD（2.21, 1.88-2.59）和VaD（1.57, 1.20-2.07）的高风险相关。降糖治疗与不治疗相比，痴呆风险更低。在55-64岁的患者中，低prs /低mtdna - cn亚组的AD风险最高（AHR 2.41, 95% CI 1.12-5.19）。结论T2D发病年龄与痴呆风险变化相关。早期诊断和治疗与观察到的较低认知风险相关，而遗传易感性和线粒体功能可能为个体化风险分层提供信息。
{"title":"Age at type 2 diabetes onset and risk of dementia: The modifying role of genetic susceptibility and mitochondrial function","authors":"Wanqing Dong , Qibin Yuan , Benrui Wu , Shiteng Gao , Yingyu Zhang , Ying Pan , Kaixin Zhou , Hongwei Jiang","doi":"10.1016/j.jnha.2026.100780","DOIUrl":"10.1016/j.jnha.2026.100780","url":null,"abstract":"<div><h3>Objectives</h3><div>To assess dementia risk after incident type 2 diabetes (T2D) by age at diagnosis and evaluate modification by treatment, genetic susceptibility, and mitochondrial function.</div></div><div><h3>Design</h3><div>Prospective 1:1 age- and sex-matched cohort study using inverse-probability-weighted Cox models.</div></div><div><h3>Setting</h3><div>Kunshan Aging Research with E-health (KARE) cohort in China (2018–2024).</div></div><div><h3>Participants</h3><div>42,514 adults without diabetes or dementia at baseline, including 21,257 incident T2D cases and 21,257 non-diabetic controls.</div></div><div><h3>Measurements</h3><div>Outcomes were all-cause dementia, Alzheimer’s disease (AD), and vascular dementia (VaD) from linked medical records and annual examinations. T2D onset age was grouped as 45–54 years, 55–64 years, and persons 65 years and older. In genotyped participants (<em>n</em> = 14,455), a T2D polygenic risk score (PRS) and blood mitochondrial DNA copy number (mtDNA-CN) were examined.</div></div><div><h3>Results</h3><div>Over a median 3.67 years, incident T2D was associated with higher risks of all-cause dementia (adjusted hazard ratio [AHR] 1.95, 95% CI 1.71–2.21), AD (2.21, 1.88–2.59), and VaD (1.57, 1.20–2.07). Glucose-lowering treatment was associated with lower dementia risk versus no treatment. Among patients aged 55–64 years, the low-PRS/low-mtDNA-CN subgroup had the highest AD risk (AHR 2.41, 95% CI 1.12–5.19).</div></div><div><h3>Conclusion</h3><div>Age at T2D onset was associated with variation in dementia risk. Earlier diagnosis and treatment were associated with lower observed cognitive risk, while genetic susceptibility and mitochondrial function may inform individualised risk stratification.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 3","pages":"Article 100780"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145981149","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 : 2026-03-01Epub Date: 2026-02-10DOI: 10.1016/j.jnha.2026.100801
Alexandre Cornic , Dan Caraman , Olivier Briere , Jennifer Gautier , Cédric Annweiler , Alexis Bourgeais , on behalf of the BACK-UPUG study group
Background
Post-Emergency Geriatric Units (PEGUs) aim to reduce hospital length of stay (LOS) and prevent functional decline by facilitating earlier discharge.
Aims
This study aim to identify factors linked to prolonged hospitalization to improve patient selection for PEGU.
Methods
In this retrospective study at the University Hospital of Angers (Dec 2022–Feb 2024), 590 eligible PEGU patients were analyzed. LOS was categorized as short (0–5 days) or prolonged (6 or more days). Sociodemographic, clinical, and biological data were assessed using univariate and multivariate logistic regression.
Results
Median age was 88, 62.2% were female, and 69% lived at home; 42% had prolonged LOS. Prolonged stay was associated in univariate analysis with higher Charlson Comorbidity Index (OR: 1.10 [1.02−1.19],p = 0.015), elevated CRP > 64 mg/L (2.07 [1.46−2.92], p < 0.001), and higher Clinical Frailty Scale (1.79 [1.23−2.59], p = 0.002). The multivariate analysis showed that a CRP levels ≥64 mg/L (OR 1.92 [1.35−2.75], p < 0.001) and a CFS equal to or superior to 7 (OR 1.59 [1.07−2.36], p = 0.022) were associated with prolonged LOS.
Discussion
Frailty and inflammation independently predict longer stays. Limitations include retrospective design and patient exclusions.
Conclusion
Frailty and elevated CRP are key predictors of prolonged PEGU stay. Although causality cannot be established due to the retrospective design and potential biases, these findings may help to better characterize older patients who could potentially benefit from PEGU interventions
{"title":"Frailty and inflammation predict prolonged stay in post-emergency geriatric units: a retrospective cohort study","authors":"Alexandre Cornic , Dan Caraman , Olivier Briere , Jennifer Gautier , Cédric Annweiler , Alexis Bourgeais , on behalf of the BACK-UPUG study group","doi":"10.1016/j.jnha.2026.100801","DOIUrl":"10.1016/j.jnha.2026.100801","url":null,"abstract":"<div><h3>Background</h3><div>Post-Emergency Geriatric Units (PEGUs) aim to reduce hospital length of stay (LOS) and prevent functional decline by facilitating earlier discharge.</div></div><div><h3>Aims</h3><div>This study aim to identify factors linked to prolonged hospitalization to improve patient selection for PEGU.</div></div><div><h3>Methods</h3><div>In this retrospective study at the University Hospital of Angers (Dec 2022–Feb 2024), 590 eligible PEGU patients were analyzed. LOS was categorized as short (0–5 days) or prolonged (6 or more days). Sociodemographic, clinical, and biological data were assessed using univariate and multivariate logistic regression.</div></div><div><h3>Results</h3><div>Median age was 88, 62.2% were female, and 69% lived at home; 42% had prolonged LOS. Prolonged stay was associated in univariate analysis with higher Charlson Comorbidity Index (OR: 1.10 [1.02−1.19],<em>p = 0.015</em>), elevated CRP > 64 mg/L (2.07 [1.46−2.92], <em>p < 0.001</em>), and higher Clinical Frailty Scale (1.79 [1.23−2.59], <em>p = 0.002)</em>. The multivariate analysis showed that a CRP levels ≥64 mg/L (OR 1.92 [1.35−2.75], p < 0.001) and a CFS equal to or superior to 7 (OR 1.59 [1.07−2.36], p = 0.022) were associated with prolonged LOS.</div></div><div><h3>Discussion</h3><div>Frailty and inflammation independently predict longer stays. Limitations include retrospective design and patient exclusions.</div></div><div><h3>Conclusion</h3><div>Frailty and elevated CRP are key predictors of prolonged PEGU stay. Although causality cannot be established due to the retrospective design and potential biases, these findings may help to better characterize older patients who could potentially benefit from PEGU interventions</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 3","pages":"Article 100801"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146168107","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 : 2026-03-01Epub Date: 2026-01-17DOI: 10.1016/j.jnha.2026.100782
Ruiyang Wang , Jiamin Wang
{"title":"Sarcopenia and metabolomics: mind the gap between biomarker discovery and clinical application","authors":"Ruiyang Wang , Jiamin Wang","doi":"10.1016/j.jnha.2026.100782","DOIUrl":"10.1016/j.jnha.2026.100782","url":null,"abstract":"","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 3","pages":"Article 100782"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145999820","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 : 2026-03-01Epub Date: 2026-01-15DOI: 10.1016/j.jnha.2026.100779
Xianzhi Li , Yajie Li , Li Yin , Qian Zhu , Shunjin Liu , Xiangyi Xing , Zonglei Zhou
Background
The combined impact of specific PM2.5 components and ozone (O₃) on sarcopenic obesity (SO) remains unclear. This study examined the effects of PM2.5 constituents and O₃ on SO risk and explored inflammation as a potential mediator.
Methods
We analyzed data from the China Health and Retirement Longitudinal Study (CHARLS, 2011–2015). SO was defined as the co-occurrence of obesity (body mass index [BMI] ≥ 28 kg/m²) and sarcopenia, the latter characterized by low muscle mass plus either low muscle strength or impaired physical performance. Air pollution data (PM2.5, its components, and O₃) were derived from the Tracking Air Pollution in China database. Systemic inflammation was operationalized as a composite z-score from C-reactive protein and white blood cell count. We employed Cox regression and quantile-based g-computation to evaluate the air pollution-SO relationship, and performed causal mediation analysis to quantify the mediating role of inflammatory pathways.
Results
Long-term exposure to a mixture of PM2.5 constituents was significantly associated with an increased risk of SO (HR = 1.10, 95%CI: 1.06–1.14). Ammonium contributed most substantially to this effect (71%), followed by black carbon (22%) and organic matter (7%). In contrast, O₃ exhibited no independent association with SO risk. A significant positive synergistic interaction was observed between the PM2.5 constituents and O₃, indicating a compounded adverse effect. Mediation analysis revealed that systemic inflammation accounted for 14–26% of the effect of PM2.5 exposure on SO development. These associations were more pronounced among older adults, men, and urban residents.
Conclusions
This study provides novel insights into environmental triggers of SO, highlighting the need for integrated air quality policies targeting specific PM2.5 components and personalized prevention strategies addressing inflammatory pathways in at-risk populations.
{"title":"Air pollution and muscle-fat imbalance: How PM2.5 components and ozone drive sarcopenic obesity through inflammation","authors":"Xianzhi Li , Yajie Li , Li Yin , Qian Zhu , Shunjin Liu , Xiangyi Xing , Zonglei Zhou","doi":"10.1016/j.jnha.2026.100779","DOIUrl":"10.1016/j.jnha.2026.100779","url":null,"abstract":"<div><h3>Background</h3><div>The combined impact of specific PM<sub>2.5</sub> components and ozone (O₃) on sarcopenic obesity (SO) remains unclear. This study examined the effects of PM<sub>2.5</sub> constituents and O₃ on SO risk and explored inflammation as a potential mediator.</div></div><div><h3>Methods</h3><div>We analyzed data from the China Health and Retirement Longitudinal Study (CHARLS, 2011–2015). SO was defined as the co-occurrence of obesity (body mass index [BMI] ≥ 28 kg/m²) and sarcopenia, the latter characterized by low muscle mass plus either low muscle strength or impaired physical performance. Air pollution data (PM<sub>2.5</sub>, its components, and O₃) were derived from the Tracking Air Pollution in China database. Systemic inflammation was operationalized as a composite z-score from C-reactive protein and white blood cell count. We employed Cox regression and quantile-based g-computation to evaluate the air pollution-SO relationship, and performed causal mediation analysis to quantify the mediating role of inflammatory pathways.</div></div><div><h3>Results</h3><div>Long-term exposure to a mixture of PM<sub>2.5</sub> constituents was significantly associated with an increased risk of SO (<em>HR</em> = 1.10, 95%<em>CI</em>: 1.06–1.14). Ammonium contributed most substantially to this effect (71%), followed by black carbon (22%) and organic matter (7%). In contrast, O₃ exhibited no independent association with SO risk. A significant positive synergistic interaction was observed between the PM<sub>2.5</sub> constituents and O₃, indicating a compounded adverse effect. Mediation analysis revealed that systemic inflammation accounted for 14–26% of the effect of PM<sub>2.5</sub> exposure on SO development. These associations were more pronounced among older adults, men, and urban residents.</div></div><div><h3>Conclusions</h3><div>This study provides novel insights into environmental triggers of SO, highlighting the need for integrated air quality policies targeting specific PM<sub>2.5</sub> components and personalized prevention strategies addressing inflammatory pathways in at-risk populations.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 3","pages":"Article 100779"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145963113","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 : 2026-03-01Epub Date: 2026-01-14DOI: 10.1016/j.jnha.2026.100777
Duo Lv , Tingting Wang , Jiayao Fan , Dongsheng Hong , Zhiyi Chen , Qianchun Xu , Dan Zhou , Xishao Xie
Objective
The association between adherence to the planetary health diet and chronic kidney disease (CKD) remains under characterized. This study aim to investigate the association of planetary health diet index (PHDI) with the risk of CKD and assess potential effect modification by genetic predisposition.
Design, setting, and participants
A large, population-based cohort study was conducted using data from UK Biobank. Eligible participants included those without a history of CKD who completed at least one 24 -h dietary recall questionnaire.
Measurements
Three distinct planetary health diet indexes (PHDIs) were used to assess dietary adherence. A polygenic risk score (PRS) for CKD was calculated to evaluate genetic susceptibility. Cox proportional hazards models were used to estimate the associations between the PHDI and the risk of incident CKD. The joint effects of PHDI and genetic susceptibility were further examined. Sensitivity analyses were conducted to evaluate the robustness of the findings.
Results
A total of 139,165 participants were included in the primary analysis. Over a median follow-up of 13.3 years, 6,391 incident CKD cases were identified. Compared with participants in the lowest adherence category, the hazard ratios (HRs) of incident CKD for those in highest adherence were 0.827 (95% CI, 0.757−0.904), 0.865 (95% CI, 0.805−0.929), and 0.891 (95% CI, 0.821−0.996) for Stubbendorff PHDI, Colizzi PHDI and Knuppel PHDI, respectively. Participants with highest adherence to planetary health diet and low genetic risk showed the lowest risk of CKD, with HRs of 0.707 (95% CI, 0.600−0.832), 0.682 (95% CI, 0.597−0.778), and 0.770 (95% CI, 0.663−0.893) across the three different PHDIs. These associations remained robust in several sensitivity analyses.
Conclusions
Higher adherence to the planetary health diet was associated with lower risk of CKD, and these effects were enhanced by jointing with genetic susceptibility. Promoting this sustainable dietary pattern may play a key strategy for CKD prevention.
{"title":"Planetary health diet index, genetic susceptibility and incident chronic kidney disease: a cohort study from the UK Biobank","authors":"Duo Lv , Tingting Wang , Jiayao Fan , Dongsheng Hong , Zhiyi Chen , Qianchun Xu , Dan Zhou , Xishao Xie","doi":"10.1016/j.jnha.2026.100777","DOIUrl":"10.1016/j.jnha.2026.100777","url":null,"abstract":"<div><h3>Objective</h3><div>The association between adherence to the planetary health diet and chronic kidney disease (CKD) remains under characterized. This study aim to investigate the association of planetary health diet index (PHDI) with the risk of CKD and assess potential effect modification by genetic predisposition.</div></div><div><h3>Design, setting, and participants</h3><div>A large, population-based cohort study was conducted using data from UK Biobank. Eligible participants included those without a history of CKD who completed at least one 24 -h dietary recall questionnaire.</div></div><div><h3>Measurements</h3><div>Three distinct planetary health diet indexes (PHDIs) were used to assess dietary adherence. A polygenic risk score (PRS) for CKD was calculated to evaluate genetic susceptibility. Cox proportional hazards models were used to estimate the associations between the PHDI and the risk of incident CKD. The joint effects of PHDI and genetic susceptibility were further examined. Sensitivity analyses were conducted to evaluate the robustness of the findings.</div></div><div><h3>Results</h3><div>A total of 139,165 participants were included in the primary analysis. Over a median follow-up of 13.3 years, 6,391 incident CKD cases were identified. Compared with participants in the lowest adherence category, the hazard ratios (HRs) of incident CKD for those in highest adherence were 0.827 (95% CI, 0.757−0.904), 0.865 (95% CI, 0.805−0.929), and 0.891 (95% CI, 0.821−0.996) for Stubbendorff PHDI, Colizzi PHDI and Knuppel PHDI, respectively. Participants with highest adherence to planetary health diet and low genetic risk showed the lowest risk of CKD, with HRs of 0.707 (95% CI, 0.600−0.832), 0.682 (95% CI, 0.597−0.778), and 0.770 (95% CI, 0.663−0.893) across the three different PHDIs. These associations remained robust in several sensitivity analyses.</div></div><div><h3>Conclusions</h3><div>Higher adherence to the planetary health diet was associated with lower risk of CKD, and these effects were enhanced by jointing with genetic susceptibility. Promoting this sustainable dietary pattern may play a key strategy for CKD prevention.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 3","pages":"Article 100777"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145963129","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 : 2026-03-01Epub Date: 2026-01-28DOI: 10.1016/j.jnha.2026.100796
Jung-Hwan Kim , Seok-Jae Heo , Yu-Jin Kwon , Ji-Won Lee
{"title":"Response to the Letter to the Editor concerning “Associations of Individual Beverage Types and Substitution with Dementia Risk”","authors":"Jung-Hwan Kim , Seok-Jae Heo , Yu-Jin Kwon , Ji-Won Lee","doi":"10.1016/j.jnha.2026.100796","DOIUrl":"10.1016/j.jnha.2026.100796","url":null,"abstract":"","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 3","pages":"Article 100796"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146079938","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 : 2026-03-01Epub Date: 2026-01-22DOI: 10.1016/j.jnha.2026.100784
Ting Liao , Ting-Ying Wang , Meng-Chun Lu , Huey-Liang Kuo , Yu-Lung Chen , Kuo-Cheng Lin , Yi-Ling Chen , Ying Hsiao , Yi-Chen Huang
Objectives
This study assessed musculoskeletal outcomes of a combined intervention comprising food-based protein supplementation, nutrition education (NE), and resistance exercise in older adults; comparing milk and soy milk as protein sources.
Design
Quasi-experimental study.
Setting and participants
Eighty-two community-dwelling adults aged ≥60 years completed the intervention.
Intervention
This 8-week cluster-based intervention assigned participants to 1 of 4 groups: exercise alone (Group 1), exercise plus NE (Group 2), exercise plus NE with milk supplementation (Group 3), and exercise plus NE with soy milk supplementation (Group 4). All groups engaged in resistance training 3 times per week, and all groups received weekly NE, except for Group 1.
Measurements
Body composition, and physical performance were measured using dual-energy X-ray absorptiometry and standardized tests at baseline and after the intervention.
Results
Within-group analyses showed that all groups experienced significant improvements in walking speed. Additionally, Group 3 exhibited improvements in handgrip strength (mean change: +4.41 kg), 5-time sit-to-stand performance (−1.94 s). Compared with other groups, Group 3 achieved greater gains in handgrip strength than Group 2 (−0.84 kg) and Group 4 (+0.52 kg), and showed a borderline significant improvement in total bone mineral density (BMD; +0.01 vs. −0.06 g/cm2) compared with Group 1. Furthermore, Groups 2 − 4 exhibited greater increases in upper-limb BMD (+0.04, +0.02, +0.01 g/cm2, respectively) compared with Group 1 (−0.02 g/cm2).
Conclusions
Exercise combined with NE and protein supplementation, particularly milk, may be associated with favorable bone health in older adults.
{"title":"Muscle performance and bone density following a multi-intervention program with milk or soy milk supplementation in older adults: quasi-experimental study","authors":"Ting Liao , Ting-Ying Wang , Meng-Chun Lu , Huey-Liang Kuo , Yu-Lung Chen , Kuo-Cheng Lin , Yi-Ling Chen , Ying Hsiao , Yi-Chen Huang","doi":"10.1016/j.jnha.2026.100784","DOIUrl":"10.1016/j.jnha.2026.100784","url":null,"abstract":"<div><h3>Objectives</h3><div>This study assessed musculoskeletal outcomes of a combined intervention comprising food-based protein supplementation, nutrition education (NE), and resistance exercise in older adults; comparing milk and soy milk as protein sources.</div></div><div><h3>Design</h3><div>Quasi-experimental study.</div></div><div><h3>Setting and participants</h3><div>Eighty-two community-dwelling adults aged ≥60 years completed the intervention.</div></div><div><h3>Intervention</h3><div>This 8-week cluster-based intervention assigned participants to 1 of 4 groups: exercise alone (Group 1), exercise plus NE (Group 2), exercise plus NE with milk supplementation (Group 3), and exercise plus NE with soy milk supplementation (Group 4). All groups engaged in resistance training 3 times per week, and all groups received weekly NE, except for Group 1.</div></div><div><h3>Measurements</h3><div>Body composition, and physical performance were measured using dual-energy X-ray absorptiometry and standardized tests at baseline and after the intervention.</div></div><div><h3>Results</h3><div>Within-group analyses showed that all groups experienced significant improvements in walking speed. Additionally, Group 3 exhibited improvements in handgrip strength (mean change: +4.41 kg), 5-time sit-to-stand performance (−1.94 s). Compared with other groups, Group 3 achieved greater gains in handgrip strength than Group 2 (−0.84 kg) and Group 4 (+0.52 kg), and showed a borderline significant improvement in total bone mineral density (BMD; +0.01 vs. −0.06 g/cm<sup>2</sup>) compared with Group 1. Furthermore, Groups 2 − 4 exhibited greater increases in upper-limb BMD (+0.04, +0.02, +0.01 g/cm<sup>2</sup>, respectively) compared with Group 1 (−0.02 g/cm<sup>2</sup>).</div></div><div><h3>Conclusions</h3><div>Exercise combined with NE and protein supplementation, particularly milk, may be associated with favorable bone health in older adults.</div><div>(Clincaltrials.gov as NCT06173271)</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 3","pages":"Article 100784"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146039536","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 : 2026-03-01Epub Date: 2026-02-19DOI: 10.1016/j.jnha.2026.100812
Philipe de Souto Barreto , Jorge G. Ruiz
{"title":"Nutrition for healthy longevity: the past, the present and the future","authors":"Philipe de Souto Barreto , Jorge G. Ruiz","doi":"10.1016/j.jnha.2026.100812","DOIUrl":"10.1016/j.jnha.2026.100812","url":null,"abstract":"","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 3","pages":"Article 100812"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146260092","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 : 2026-03-01Epub Date: 2026-01-22DOI: 10.1016/j.jnha.2026.100785
Zongjie Luo , Hangyu Chen , Shuqian Huang , Qihua Lai , Xiaoying Hu , Yuan Wang , Yuanqin Wang , Jing Wang , Yanni Li , Fengqiong Liu
Background
Diet and nutrition affect chronic diseases, but large-scale evidence on nutrient patterns and disease risk is limited. This study aims to explore nutrient-based dietary patterns and their links to major chronic diseases and multimorbidity risk.
Methods
Dietary intake was assessed via dietary questionnaires in 208,312 UK Biobank participants. Principal component analysis (PCA) was used to derive principal components (PCs) of 63 nutrients. Cox regression was used to analyze hazard ratios (HRs) for 36 chronic conditions, and negative binomial regression was applied to examine associations of multimorbidity with nutrients.
Results
A total of 15 distinct nutrient patterns were identified, covering a broad range of nutritional characteristics, including macronutrients, vitamins, minerals, and pure energy food items. A total of 540 associations (15 PCs × 36 disease outcomes) were tested, with 66 associations met the FDR-adjusted (false discovery rate) significance threshold (P < 0.01). Nutrient patterns, especially those characterized by macronutrients, are closely associated with the risk of chronic conditions, including cardiometabolic disorders, neurodegenerative and mental health disorders, chronic liver diseases, as well as respiratory, genitourinary and musculoskeletal system diseases. The conditions most closely associated with dietary nutrients include cardiometabolic diseases (hypertension, diabetes, myocardial infarction), chronic obstructive pulmonary disease (COPD), chronic kidney disease (CKD), mental/behavioural disorders, hepatitis/cirrhosis, prostate problems, osteoporosis, and anemia. No nutrient patterns showed significant effects on cancer, autoimmune diseases, or nervous system disorders. Additionally, specific and distinct roles of proteins, fats, free sugars, alcohol, and salt in multimorbidity were identified in the population.
Conclusion
Diverse patterns of nutrient intake have been observed in the population. Nutrient patterns are closely linked to chronic diseases, with distinct disease spectra corresponding to different nutrient patterns. Some patterns correlate significantly with the number of multimorbidities. Our findings highlight balanced nutrient intake’s role in managing chronic disease risk and inform evidence-based dietary interventions.
{"title":"An atlas of associations between dietary nutrients and the risk of 36 major chronic diseases","authors":"Zongjie Luo , Hangyu Chen , Shuqian Huang , Qihua Lai , Xiaoying Hu , Yuan Wang , Yuanqin Wang , Jing Wang , Yanni Li , Fengqiong Liu","doi":"10.1016/j.jnha.2026.100785","DOIUrl":"10.1016/j.jnha.2026.100785","url":null,"abstract":"<div><h3>Background</h3><div>Diet and nutrition affect chronic diseases, but large-scale evidence on nutrient patterns and disease risk is limited. This study aims to explore nutrient-based dietary patterns and their links to major chronic diseases and multimorbidity risk.</div></div><div><h3>Methods</h3><div>Dietary intake was assessed via dietary questionnaires in 208,312 UK Biobank participants. Principal component analysis (PCA) was used to derive principal components (PCs) of 63 nutrients. Cox regression was used to analyze hazard ratios (HRs) for 36 chronic conditions, and negative binomial regression was applied to examine associations of multimorbidity with nutrients.</div></div><div><h3>Results</h3><div>A total of 15 distinct nutrient patterns were identified, covering a broad range of nutritional characteristics, including macronutrients, vitamins, minerals, and pure energy food items. A total of 540 associations (15 PCs × 36 disease outcomes) were tested, with 66 associations met the FDR-adjusted (false discovery rate) significance threshold (<em>P</em> < 0.01). Nutrient patterns, especially those characterized by macronutrients, are closely associated with the risk of chronic conditions, including cardiometabolic disorders, neurodegenerative and mental health disorders, chronic liver diseases, as well as respiratory, genitourinary and musculoskeletal system diseases. The conditions most closely associated with dietary nutrients include cardiometabolic diseases (hypertension, diabetes, myocardial infarction), chronic obstructive pulmonary disease (COPD), chronic kidney disease (CKD), mental/behavioural disorders, hepatitis/cirrhosis, prostate problems, osteoporosis, and anemia. No nutrient patterns showed significant effects on cancer, autoimmune diseases, or nervous system disorders. Additionally, specific and distinct roles of proteins, fats, free sugars, alcohol, and salt in multimorbidity were identified in the population.</div></div><div><h3>Conclusion</h3><div>Diverse patterns of nutrient intake have been observed in the population. Nutrient patterns are closely linked to chronic diseases, with distinct disease spectra corresponding to different nutrient patterns. Some patterns correlate significantly with the number of multimorbidities. Our findings highlight balanced nutrient intake’s role in managing chronic disease risk and inform evidence-based dietary interventions.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 3","pages":"Article 100785"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146039535","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 : 2026-03-01Epub Date: 2026-01-28DOI: 10.1016/j.jnha.2026.100793
Alejandro Álvarez-Bustos , Cristina Andres-Lacueva , Ignacio Ara , María Angeles Arévalo , Juan P. Bolaños , Ana Coto-Montes , José Antonio Enriquez , Germaine Escames , Francisco José García-García , María Carmen Gómez-Cabrera , Oriol Grau-Rivera , Mikel Izquierdo , Nicolás Martínez Velilla , Ander Matheu , Rocío Menéndez Colino , Manuel Muñoz Torres , Xavier Nogués , Juan Oliva , María Isabel Orts-Cortés , Ignacio Párraga Martínez , Pedro Abizanda
Background
The lack of a universally accepted definition, a gold-standard assessment tool, and sufficient evidence-based interventions has hindered the integration of frailty into routine clinical practice, particularly outside geriatric medicine. For clinicians, health professionals, policymakers, and aging researchers, a unified framework based on robust evidence has become essential.
Objectives
To provide a consensus on relevant aspects of frailty, including definition, attributes, misunderstandings, pathophysiology, phenotypes, assessment, biomarkers, management, stigmas and future challenges, useful for epidemiological, clinical and research application across Europe.
Design
Consensus document.
Setting
25 research centers on frailty and healthy aging.
Measurements
Relevant aspects on frailty.
Results
In this document we present a consensus regarding what frailty is, what frailty is not, what is aging, which are the most common misunderstandings related to frailty, which is the pathophysiology and which are the biomarkers of frailty, how should frailty be assessed and who should assess frailty, how should frailty be managed, the presence or absence of frailty subphenotypes or subtypes, how is the stigma of been considered frail, which are the gender considerations, and which are the current challenges and future directions. We support that frailty is the expression of an age-associated clinical phenotypic syndrome driven by the biology of aging, life-course environmental exposures, and disease burden. Its physiological basis lies in a heterogeneous decline of functional reserve across organ systems, accompanied by impaired homeostasis and reduced capacity to respond to stressors, ultimately predisposing to adverse health outcomes, mainly disability.
Conclusions
We present a consensus document on frailty, useful for epidemiological, clinical and research application across Europe.
{"title":"Consensus document on frailty: conceptualization, detection, multidisciplinary management and future roadmap","authors":"Alejandro Álvarez-Bustos , Cristina Andres-Lacueva , Ignacio Ara , María Angeles Arévalo , Juan P. Bolaños , Ana Coto-Montes , José Antonio Enriquez , Germaine Escames , Francisco José García-García , María Carmen Gómez-Cabrera , Oriol Grau-Rivera , Mikel Izquierdo , Nicolás Martínez Velilla , Ander Matheu , Rocío Menéndez Colino , Manuel Muñoz Torres , Xavier Nogués , Juan Oliva , María Isabel Orts-Cortés , Ignacio Párraga Martínez , Pedro Abizanda","doi":"10.1016/j.jnha.2026.100793","DOIUrl":"10.1016/j.jnha.2026.100793","url":null,"abstract":"<div><h3>Background</h3><div>The lack of a universally accepted definition, a gold-standard assessment tool, and sufficient evidence-based interventions has hindered the integration of frailty into routine clinical practice, particularly outside geriatric medicine. For clinicians, health professionals, policymakers, and aging researchers, a unified framework based on robust evidence has become essential.</div></div><div><h3>Objectives</h3><div>To provide a consensus on relevant aspects of frailty, including definition, attributes, misunderstandings, pathophysiology, phenotypes, assessment, biomarkers, management, stigmas and future challenges, useful for epidemiological, clinical and research application across Europe.</div></div><div><h3>Design</h3><div>Consensus document.</div></div><div><h3>Setting</h3><div>25 research centers on frailty and healthy aging.</div></div><div><h3>Measurements</h3><div>Relevant aspects on frailty.</div></div><div><h3>Results</h3><div>In this document we present a consensus regarding what frailty is, what frailty is not, what is aging, which are the most common misunderstandings related to frailty, which is the pathophysiology and which are the biomarkers of frailty, how should frailty be assessed and who should assess frailty, how should frailty be managed, the presence or absence of frailty subphenotypes or subtypes, how is the stigma of been considered frail, which are the gender considerations, and which are the current challenges and future directions. We support that frailty is the expression of an age-associated clinical phenotypic syndrome driven by the biology of aging, life-course environmental exposures, and disease burden. Its physiological basis lies in a heterogeneous decline of functional reserve across organ systems, accompanied by impaired homeostasis and reduced capacity to respond to stressors, ultimately predisposing to adverse health outcomes, mainly disability.</div></div><div><h3>Conclusions</h3><div>We present a consensus document on frailty, useful for epidemiological, clinical and research application across Europe.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 3","pages":"Article 100793"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146079941","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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