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":"2026-01-17","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 : 2026-01-15DOI: 10.1016/j.jnha.2026.100781
Fangyu Cheng , Zongshuai Wang , Yueyuan Li , Peng Wang , Chunping Wang
Background and objectives
Chronic pain is a significant risk factor for limitations in activities of daily living (ADL). However, previous studies have mostly assessed pain severity at a single time point, overlooking its temporal variability. This study aims to explore the longitudinal associations between trajectories of chronic generalized pain severity, the number of pain sites, and trajectories of chronic site-specific pain severity with the risk of developing ADL limitations.
Methods
This study utilized longitudinal data from individuals aged 50 and above in two cohorts: the English Longitudinal Study of Ageing (ELSA) and the Korean Longitudinal Study of Aging (KLoSA). By analyzing dynamic changes in pain severity states, trajectories of chronic generalized pain severity, the number of pain sites, and chronic site-specific pain severity were identified. Cox proportional hazards models were applied to assess the associations between various pain severity trajectories and the incidence of ADL limitations. Mediation analysis was conducted to investigate the mediating effect of depression.
Results
The Cox proportional hazards models showed that, among trajectories of chronic generalized pain severity and pain severity at the back, feet, and knees, the persistent high-level pain and worsening pain trajectory groups exhibited the highest increased risk of ADL limitations. Additionally, all trajectories of the number of pain sites were positively associated with ADL limitation risk, with the increasing number of pain sites trajectory showing the strongest association (HR = 2.738, 95% CI: 2.147–3.492). Depression mediated the associations between various pain severity trajectories and ADL limitations.
Conclusion
The research findings underscore the significant role of long-term, persistently high levels and progressively worsening severity of chronic systemic and localized pain in the limitations of ADL functions in older adults. Incorporating longitudinal monitoring of chronic pain severity trajectories into ADL function limitation management programs is crucial for enhancing preventive and therapeutic interventions.
{"title":"Longitudinal associations of chronic pain severity trajectories and number of pain site trajectories with risk of limitations in ability in daily activities: Evidence from two 10-year prospective cohort studies","authors":"Fangyu Cheng , Zongshuai Wang , Yueyuan Li , Peng Wang , Chunping Wang","doi":"10.1016/j.jnha.2026.100781","DOIUrl":"10.1016/j.jnha.2026.100781","url":null,"abstract":"<div><h3>Background and objectives</h3><div>Chronic pain is a significant risk factor for limitations in activities of daily living (ADL). However, previous studies have mostly assessed pain severity at a single time point, overlooking its temporal variability. This study aims to explore the longitudinal associations between trajectories of chronic generalized pain severity, the number of pain sites, and trajectories of chronic site-specific pain severity with the risk of developing ADL limitations.</div></div><div><h3>Methods</h3><div>This study utilized longitudinal data from individuals aged 50 and above in two cohorts: the English Longitudinal Study of Ageing (ELSA) and the Korean Longitudinal Study of Aging (KLoSA). By analyzing dynamic changes in pain severity states, trajectories of chronic generalized pain severity, the number of pain sites, and chronic site-specific pain severity were identified. Cox proportional hazards models were applied to assess the associations between various pain severity trajectories and the incidence of ADL limitations. Mediation analysis was conducted to investigate the mediating effect of depression.</div></div><div><h3>Results</h3><div>The Cox proportional hazards models showed that, among trajectories of chronic generalized pain severity and pain severity at the back, feet, and knees, the persistent high-level pain and worsening pain trajectory groups exhibited the highest increased risk of ADL limitations. Additionally, all trajectories of the number of pain sites were positively associated with ADL limitation risk, with the increasing number of pain sites trajectory showing the strongest association (HR = 2.738, 95% CI: 2.147–3.492). Depression mediated the associations between various pain severity trajectories and ADL limitations.</div></div><div><h3>Conclusion</h3><div>The research findings underscore the significant role of long-term, persistently high levels and progressively worsening severity of chronic systemic and localized pain in the limitations of ADL functions in older adults. Incorporating longitudinal monitoring of chronic pain severity trajectories into ADL function limitation management programs is crucial for enhancing preventive and therapeutic interventions.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 3","pages":"Article 100781"},"PeriodicalIF":4.0,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145963114","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 : 2026-01-15DOI: 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":"2026-01-15","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}
The combined effect of vitamin mixture on biological aging, along with the specific contribution of individual components, remains unclear. This study investigated the associations between a mixture of 11 dietary vitamins and biological aging.
Methods
This cross-sectional study included 15050 adults from NHANES 2007–2018. Daily intakes of 11 vitamins were estimated using the multiple source method to account for within-person variation from two 24 -h recalls, incorporating both food and supplement contributions. Total vitamin intake was calculated as their sum. Biological aging was assessed using three established indicators: KDM-acceleration and PhenoAge-acceleration (derived as regression residuals of biological age on chronological age), and homeostatic dysregulation (HD, a composite physiological score). Multiple linear regression, restricted cubic spline regression, and quantile g-computation were used to assess individual and joint associations.
Results
The median age was 51.0 years, and 51.5% were female. Higher total vitamin intake was significantly associated with reduced biological aging (KDM-acceleration: β = −1.281; PhenoAge-acceleration: β = −1.379; HD: β = −0.046). Dose-response relationships were linear (all Pnonlinear > 0.05). Stratified analyses revealed stronger associations in males and individuals with comorbidity. Vitamin C was the primary protective component, followed by vitamin B2.
Conclusions
Higher intake of dietary vitamin mixture was associated with slower biological aging, with vitamin C as the key protective driver. These findings support recommending vitamin-rich diets to promote healthy aging.
{"title":"Association between vitamin intake and biological aging: evidence from NHANES 2007–2018","authors":"Xinyu Zhang , Yujie Xu , Xiaoyu Wang , Mengxue Chen , Jingyuan Xiong , Guo Cheng","doi":"10.1016/j.jnha.2026.100776","DOIUrl":"10.1016/j.jnha.2026.100776","url":null,"abstract":"<div><h3>Background</h3><div>The combined effect of vitamin mixture on biological aging, along with the specific contribution of individual components, remains unclear. This study investigated the associations between a mixture of 11 dietary vitamins and biological aging.</div></div><div><h3>Methods</h3><div>This cross-sectional study included 15050 adults from NHANES 2007–2018. Daily intakes of 11 vitamins were estimated using the multiple source method to account for within-person variation from two 24 -h recalls, incorporating both food and supplement contributions. Total vitamin intake was calculated as their sum. Biological aging was assessed using three established indicators: KDM-acceleration and PhenoAge-acceleration (derived as regression residuals of biological age on chronological age), and homeostatic dysregulation (HD, a composite physiological score). Multiple linear regression, restricted cubic spline regression, and quantile g-computation were used to assess individual and joint associations.</div></div><div><h3>Results</h3><div>The median age was 51.0 years, and 51.5% were female. Higher total vitamin intake was significantly associated with reduced biological aging (KDM-acceleration: β = −1.281; PhenoAge-acceleration: β = −1.379; HD: β = −0.046). Dose-response relationships were linear (all <em>P</em><sub>nonlinear</sub> > 0.05). Stratified analyses revealed stronger associations in males and individuals with comorbidity. Vitamin C was the primary protective component, followed by vitamin B2.</div></div><div><h3>Conclusions</h3><div>Higher intake of dietary vitamin mixture was associated with slower biological aging, with vitamin C as the key protective driver. These findings support recommending vitamin-rich diets to promote healthy aging.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 2","pages":"Article 100776"},"PeriodicalIF":4.0,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977546","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 : 2026-01-14DOI: 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":"2026-01-14","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 : 2026-01-14DOI: 10.1016/j.jnha.2026.100778
Kai Wei , Xiaotong Chen
Background
Global marijuana use has risen markedly in recent decades. Although prior research suggests that marijuana use is associated with epigenetic alterations, its relationship with biological aging remains unclear. This study aimed to examine the association between marijuana use and accelerated aging and explore the mediating role of metal exposure.
Methods
Using data from 12,806 U.S. adults (NHANES 2005–2018), biological age (BA) was calculated using two validated algorithms, phenotypic age (PhenoAge) and Klemera–Doubal biological age (KD-BioAge), with aging acceleration defined as the residuals from linear regression of BA on chronological age (CA). Marijuana use status was ascertained via standardized interviews. Analyses included survey-weighted multivariable linear regression, stratified subgroup analyses, joint exposure assessments, and mediation analyses.
Results
Current marijuana users exhibited significantly accelerated aging versus never users: PhenoAge acceleration (β = 0.72, 95% CI: 0.41–1.02, P < 0.001) and KD-BioAge acceleration (β = 0.36, 95% CI: 0.14–0.59, P = 0.002), after full adjustment. Subgroup and joint exposure analyses showed consistent associations, with evidence of additive associations among dual users of marijuana and tobacco. Mediation analyses identified blood cadmium as a partial mediator, explaining 15.6% and 8.3% of aging acceleration for PhenoAge and KD-BioAge, respectively.
Discussion
This study provides robust epidemiological evidence linking marijuana use to accelerated biological aging, with blood cadmium identified as a potential mechanistic link. These findings highlight the public health importance of understanding the long-term physiological correlates of marijuana use.
{"title":"Current marijuana use is cross-sectionally associated with accelerated biological aging among U.S. adults: exploring mediating effect of blood cadmium","authors":"Kai Wei , Xiaotong Chen","doi":"10.1016/j.jnha.2026.100778","DOIUrl":"10.1016/j.jnha.2026.100778","url":null,"abstract":"<div><h3>Background</h3><div>Global marijuana use has risen markedly in recent decades. Although prior research suggests that marijuana use is associated with epigenetic alterations, its relationship with biological aging remains unclear. This study aimed to examine the association between marijuana use and accelerated aging and explore the mediating role of metal exposure.</div></div><div><h3>Methods</h3><div>Using data from 12,806 U.S. adults (NHANES 2005–2018), biological age (BA) was calculated using two validated algorithms, phenotypic age (PhenoAge) and Klemera–Doubal biological age (KD-BioAge), with aging acceleration defined as the residuals from linear regression of BA on chronological age (CA). Marijuana use status was ascertained via standardized interviews. Analyses included survey-weighted multivariable linear regression, stratified subgroup analyses, joint exposure assessments, and mediation analyses.</div></div><div><h3>Results</h3><div>Current marijuana users exhibited significantly accelerated aging versus never users: PhenoAge acceleration (β = 0.72, 95% CI: 0.41–1.02, <em>P</em> < 0.001) and KD-BioAge acceleration (β = 0.36, 95% CI: 0.14–0.59, <em>P</em> = 0.002), after full adjustment. Subgroup and joint exposure analyses showed consistent associations, with evidence of additive associations among dual users of marijuana and tobacco. Mediation analyses identified blood cadmium as a partial mediator, explaining 15.6% and 8.3% of aging acceleration for PhenoAge and KD-BioAge, respectively.</div></div><div><h3>Discussion</h3><div>This study provides robust epidemiological evidence linking marijuana use to accelerated biological aging, with blood cadmium identified as a potential mechanistic link. These findings highlight the public health importance of understanding the long-term physiological correlates of marijuana use.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 3","pages":"Article 100778"},"PeriodicalIF":4.0,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145963128","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 : 2026-01-13DOI: 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":"2026-01-13","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 : 2026-01-10DOI: 10.1016/j.jnha.2026.100773
Xiaoming Zhang , Deji Xu , Yunzhi Yang , Yufei Zeng , Huilin Yu , Tengfei Fang , Ke Zhu , Yi Xiao , Jiang Wang , Qingli Dou , Wenwu Zhang
Background
Hip fracture poses a substantial threat to the quality of life in older adults. Evidence regarding the association between intrinsic capacity (IC) and hip fracture is limited. This study aimed to investigate the relationship between IC and hip fracture risk in older populations.
Methods
This multi-cohort study included five nationally representative aging cohorts: the China Health and Retirement Longitudinal Study (CHARLS), the Health and Retirement Study (HRS), the Mexican Health and Aging Study (MHAS), the Survey of Health, Ageing and Retirement in Europe (SHARE), and the English Longitudinal Study of Ageing (ELSA). Participants aged 60 years and older with baseline IC assessments and at least two follow-ups were included. Individuals with baseline hip fracture, missing hip fracture data, missing covariate data, or lost to follow-up were excluded. IC was comprehensively evaluated across five domains: cognition, locomotion, vitality, sensory function, and psychological function. Hip fractures were identified through self-report or physician diagnosis. Cox proportional hazards regression models were used to estimate the association between IC and hip fracture, and results were pooled across cohorts using a common-effects meta-analysis.
Results
A total of 37,267 participants were included, with hip fracture prevalence ranging from 1.40% in SHARE to 4.64% in CHARLS. Higher IC was significantly associated with lower hip fracture risk in all cohorts: CHARLS (HR = 0.75, 95% CI [0.67–0.84]), HRS (HR = 0.65, 95% CI [0.53–0.78]), MHAS (HR = 0.77, 95% CI [0.63–0.95]), SHARE (HR = 0.83, 95% CI [0.72–0.95]), and ELSA (HR = 0.74, 95% CI [0.57–0.98]). The pooled estimate from the common-effects model was HR = 0.76 (95% CI [0.71–0.81], I² = 10.7%). In addition, Sensitivity analyses further supported the robustness of these findings.
Conclusions
Higher IC is associated with a lower risk of hip fracture among older adults. IC may serve as an early predictive indicator of hip fracture, supporting preventive strategies to reduce the economic and societal burden of hip fractures and to preserve quality of life in aging populations.
{"title":"Intrinsic capacity and risk of hip fracture in older adults: evidence from five multinational aging cohorts","authors":"Xiaoming Zhang , Deji Xu , Yunzhi Yang , Yufei Zeng , Huilin Yu , Tengfei Fang , Ke Zhu , Yi Xiao , Jiang Wang , Qingli Dou , Wenwu Zhang","doi":"10.1016/j.jnha.2026.100773","DOIUrl":"10.1016/j.jnha.2026.100773","url":null,"abstract":"<div><h3>Background</h3><div>Hip fracture poses a substantial threat to the quality of life in older adults. Evidence regarding the association between intrinsic capacity (IC) and hip fracture is limited. This study aimed to investigate the relationship between IC and hip fracture risk in older populations.</div></div><div><h3>Methods</h3><div>This multi-cohort study included five nationally representative aging cohorts: the China Health and Retirement Longitudinal Study (CHARLS), the Health and Retirement Study (HRS), the Mexican Health and Aging Study (MHAS), the Survey of Health, Ageing and Retirement in Europe (SHARE), and the English Longitudinal Study of Ageing (ELSA). Participants aged 60 years and older with baseline IC assessments and at least two follow-ups were included. Individuals with baseline hip fracture, missing hip fracture data, missing covariate data, or lost to follow-up were excluded. IC was comprehensively evaluated across five domains: cognition, locomotion, vitality, sensory function, and psychological function. Hip fractures were identified through self-report or physician diagnosis. Cox proportional hazards regression models were used to estimate the association between IC and hip fracture, and results were pooled across cohorts using a common-effects meta-analysis.</div></div><div><h3>Results</h3><div>A total of 37,267 participants were included, with hip fracture prevalence ranging from 1.40% in SHARE to 4.64% in CHARLS. Higher IC was significantly associated with lower hip fracture risk in all cohorts: CHARLS (HR = 0.75, 95% CI [0.67–0.84]), HRS (HR = 0.65, 95% CI [0.53–0.78]), MHAS (HR = 0.77, 95% CI [0.63–0.95]), SHARE (HR = 0.83, 95% CI [0.72–0.95]), and ELSA (HR = 0.74, 95% CI [0.57–0.98]). The pooled estimate from the common-effects model was HR = 0.76 (95% CI [0.71–0.81], I² = 10.7%). In addition, Sensitivity analyses further supported the robustness of these findings.</div></div><div><h3>Conclusions</h3><div>Higher IC is associated with a lower risk of hip fracture among older adults. IC may serve as an early predictive indicator of hip fracture, supporting preventive strategies to reduce the economic and societal burden of hip fractures and to preserve quality of life in aging populations.</div></div>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 2","pages":"Article 100773"},"PeriodicalIF":4.0,"publicationDate":"2026-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939213","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 : 2026-01-10DOI: 10.1016/j.jnha.2026.100772
Guillaume Chambinaud, Aurore Fayosse, Aline Dugravot, Benjamin Landré, Alexis Schnitzler, Archana Singh-Manoux, Séverine Sabia, Louis Jacob
Objectives: The determinants of functional limitation trajectories after stroke remain scarce. This study aimed to investigate the association of early body mass index (BMI) changes with trajectories of activities of daily living (ADLs) and instrumental activities of daily living (IADLs) following stroke.
Design: Three cohorts from Europe and the United States.
Setting: Community.
Participants: Stroke survivors.
Measurements: BMI changes were assessed 1-4 years after self-reported stroke and categorized as decreased (≤-5% initial BMI), increased (≥5% initial BMI), and stable. An alternate cut-point of 2% was also used. Functional limitations were measured as the number of ADL and IADL limitations, which were repeatedly measured for up to 24 years after stroke. Associations were evaluated using segmented linear mixed-effects models after adjusting for demographic, behavioral, and medical factors.
Results: The study population comprised 2544 adults with stroke (mean [standard deviation] age 70.0 [10.9] years; 52.0% women). Based on a 5% cutoff, the number of ADL and IADL limitations was higher in the groups of decreased (ADL: 0.56 [95% CI = 0.28, 0.85]; IADL: 0.66 [95% CI = 0.38, 0.94]) and increased BMI (ADL: 0.55 [95% CI = 0.28, 0.81]; IADL: 0.59 [95% CI = 0.33, 0.85]) compared to stable BMI, respectively. Similar findings were obtained for a 2% cutoff. These differences frequently persisted for 24 years for decreased BMI and 6-12 years for increased BMI.
Conclusion: Early decreased BMI, and to a lesser extent increased BMI, following stroke could be a marker of long-term adverse trajectories of physical functioning, underlying the importance of nutritional and physical activity management after a stroke.
目的：中风后功能限制轨迹的决定因素仍然很少。本研究旨在探讨脑卒中后早期身体质量指数（BMI）变化与日常生活活动（ADLs）和日常生活工具活动（IADLs）轨迹的关系。设计：来自欧洲和美国的三个队列。设置:社区。参与者：中风幸存者。测量方法：在自我报告卒中后1-4年评估BMI变化，并将其分为下降（≤-5%初始BMI）、增加（≥5%初始BMI）和稳定。还使用了2%的替代分割点。功能限制测量为ADL和IADL限制的数量，在卒中后24年内反复测量。在调整了人口统计、行为和医学因素后，使用分段线性混合效应模型评估相关性。结果：研究人群包括2544名成年脑卒中患者（平均[标准差]70.0[10.9]岁；52.0%为女性）。基于5%的临界值，与BMI稳定组相比，BMI下降组（ADL: 0.56 [95% CI = 0.28, 0.85]; IADL: 0.66 [95% CI = 0.38, 0.94]）和BMI升高组（ADL: 0.55 [95% CI = 0.28, 0.81]; IADL: 0.59 [95% CI = 0.33, 0.85]）的ADL和IADL限制数量更高。在2%的临界值下也得到了类似的结果。这些差异通常持续24年的BMI下降和6-12年的BMI增加。结论：中风后早期BMI下降，以及在较小程度上BMI升高，可能是身体功能长期不良轨迹的标志，表明中风后营养和身体活动管理的重要性。
{"title":"The association of post-stroke changes in body mass index with activity of daily living and instrumental activity of daily living trajectories: A multi-cohort analysis.","authors":"Guillaume Chambinaud, Aurore Fayosse, Aline Dugravot, Benjamin Landré, Alexis Schnitzler, Archana Singh-Manoux, Séverine Sabia, Louis Jacob","doi":"10.1016/j.jnha.2026.100772","DOIUrl":"https://doi.org/10.1016/j.jnha.2026.100772","url":null,"abstract":"<p><strong>Objectives: </strong>The determinants of functional limitation trajectories after stroke remain scarce. This study aimed to investigate the association of early body mass index (BMI) changes with trajectories of activities of daily living (ADLs) and instrumental activities of daily living (IADLs) following stroke.</p><p><strong>Design: </strong>Three cohorts from Europe and the United States.</p><p><strong>Setting: </strong>Community.</p><p><strong>Participants: </strong>Stroke survivors.</p><p><strong>Measurements: </strong>BMI changes were assessed 1-4 years after self-reported stroke and categorized as decreased (≤-5% initial BMI), increased (≥5% initial BMI), and stable. An alternate cut-point of 2% was also used. Functional limitations were measured as the number of ADL and IADL limitations, which were repeatedly measured for up to 24 years after stroke. Associations were evaluated using segmented linear mixed-effects models after adjusting for demographic, behavioral, and medical factors.</p><p><strong>Results: </strong>The study population comprised 2544 adults with stroke (mean [standard deviation] age 70.0 [10.9] years; 52.0% women). Based on a 5% cutoff, the number of ADL and IADL limitations was higher in the groups of decreased (ADL: 0.56 [95% CI = 0.28, 0.85]; IADL: 0.66 [95% CI = 0.38, 0.94]) and increased BMI (ADL: 0.55 [95% CI = 0.28, 0.81]; IADL: 0.59 [95% CI = 0.33, 0.85]) compared to stable BMI, respectively. Similar findings were obtained for a 2% cutoff. These differences frequently persisted for 24 years for decreased BMI and 6-12 years for increased BMI.</p><p><strong>Conclusion: </strong>Early decreased BMI, and to a lesser extent increased BMI, following stroke could be a marker of long-term adverse trajectories of physical functioning, underlying the importance of nutritional and physical activity management after a stroke.</p>","PeriodicalId":54778,"journal":{"name":"Journal of Nutrition Health & Aging","volume":"30 2","pages":"100772"},"PeriodicalIF":4.0,"publicationDate":"2026-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145953978","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}
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":"2026-01-10","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}
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