Pub Date : 2024-07-01DOI: 10.1016/S2666-7568(24)00092-8
Juan Luis Sánchez-Sánchez PhD , Wan-Hsuan Lu PhD , Daniel Gallardo-Gómez MSc , Borja del Pozo Cruz PhD , Philipe de Souto Barreto PhD , Alejandro Lucia MD , Pedro L Valenzuela PhD
<div><h3>Background</h3><p>Together with environmental factors, intrinsic capacity (the composite of all the physical and mental capacities of an individual) has been proposed as a marker of healthy ageing. However, whether intrinsic capacity predicts major clinical outcomes is unclear. We aimed to explore the association of intrinsic capacity with functional decline and mortality in older adults.</p></div><div><h3>Methods</h3><p>In this systematic review and meta-analysis, we conducted a systematic search in MEDLINE (via PubMed), Scopus, and Web of Science from database inception to Feb 14, 2024, of observational longitudinal studies conducted in older adults (age ≥60 years) assessing the association of intrinsic capacity with impairment in basic activities of daily living (BADL) or instrumental activities of daily living (IADL) or risk of mortality. Estimates were extracted by two reviewers (JLS-S and W-HL) and were pooled using three-level meta-analytic models. The quality of each study was independently assessed by two authors (JLS-S and PLV) using the Newcastle–Ottawa Scale for longitudinal studies. Heterogeneity was evaluated using the <em>I</em><sup>2</sup> indicator at two levels: within-study (level 2) and between-study (level 3) variation. For associations between intrinsic capacity and IADL and BADL, we transformed data (standardised β coefficients and odds ratios [ORs]) into Pearson product moment correlation coefficients (<em>r</em>) using Pearson and Digby formulas to allow comparability across studies. For associations between intrinsic capacity and risk of mortality, hazard ratios (HRs) with 95% CIs were extracted from survival analyses. This study is registered with PROSPERO, CRD42023460482.</p></div><div><h3>Findings</h3><p>We included 37 studies (206 693 participants; average age range 65·3–85·9 years) in the systematic review, of which 31 were included in the meta-analysis on the association between intrinsic capacity and outcomes; three studies (2935 participants) were included in the meta-analysis on the association between intrinsic capacity trajectories and longitudinal changes in BADL or IADL. Intrinsic capacity was inversely associated with longitudinal impairments in BADL (Pearson's <em>r</em> –0·12 [95% CI –0·19 to –0·04]) and IADL (–0·24 [–0·35 to –0·13]), as well as with mortality risk (hazard ratio 0·57 [95% CI 0·51 to 0·63]). An association was also found between intrinsic capacity trajectories and impairment in IADL (but not in BADL), with maintained or improved intrinsic capacity over time associated with a lower impairment in IADL (odds ratio 0·37 [95% CI 0·19 to 0·71]). There was no evidence of publication bias (Egger's test p>0·05) and there was low between-study heterogeneity (<em>I</em><sup>2</sup>=18·4%), though within-study (<em>I</em><sup>2</sup>=63·2%) heterogeneity was substantial.</p></div><div><h3>Interpretation</h3><p>Intrinsic capacity is inversely associated with functional decline and mortality
背景：内在能力（个人所有体能和智能的综合）与环境因素一起被认为是健康老龄化的标志。然而，内在能力是否能预测主要临床结果尚不清楚。我们旨在探索内在能力与老年人功能衰退和死亡率之间的关系：在这项系统性综述和荟萃分析中，我们在 MEDLINE（通过 PubMed）、Scopus 和 Web of Science 中进行了系统性检索，检索时间从数据库建立之初至 2024 年 2 月 14 日，检索对象为老年人（年龄≥60 岁），检索内容为评估内在能力与基本日常生活活动（BADL）或工具性日常生活活动（IADL）损伤或死亡风险之间关系的观察性纵向研究。估算值由两位评审员（JLS-S 和 W-HL）提取，并使用三级荟萃分析模型进行汇总。每项研究的质量由两位作者（JLS-S 和 PLV）使用纽卡斯尔-渥太华纵向研究量表进行独立评估。异质性采用两个级别的 I2 指标进行评估：研究内变异（第 2 级）和研究间变异（第 3 级）。对于内在能力与 IADL 和 BADL 之间的关系，我们使用 Pearson 和 Digby 公式将数据（标准化 β 系数和几率比 [ORs]）转换为皮尔逊积矩相关系数 (r)，以实现不同研究之间的可比性。对于内在能力与死亡风险之间的关系，则从生存分析中提取了带有 95% CI 的危险比 (HR)。本研究已在 PROSPERO 注册，编号为 CRD42023460482：我们在系统综述中纳入了 37 项研究（206 693 名参与者；平均年龄范围为 65-3-85-9 岁），其中 31 项纳入了内在能力与结果之间关系的荟萃分析；3 项研究（2935 名参与者）纳入了内在能力轨迹与 BADL 或 IADL 纵向变化之间关系的荟萃分析。内在能力与 BADL（Pearson's r -0-12 [95% CI -0-19 to -0-04]）和 IADL（-0-24 [-0-35 to -0-13]）的纵向损伤以及死亡风险（危险比 0-57 [95% CI 0-51 to 0-63]）成反比。研究还发现了内在能力轨迹与 IADL（而非 BADL）损伤之间的关系，随着时间的推移，内在能力的保持或提高与 IADL 损伤的降低有关（几率比 0-37 [95% CI 0-19 至 0-71]）。没有证据表明存在发表偏倚（Egger 检验 p>0-05），研究间异质性较低（I2=18-4%），但研究内异质性很大（I2=63-2%）：解释：内在能力与老年人的功能衰退和死亡风险成反比。这些研究结果可以支持将内在能力作为健康老龄化的标志，不过还需要进一步研究，以完善这一概念在不同环境和人群中的结构和可操作性：无：摘要的西班牙文和法文译文见 "补充材料 "部分。
{"title":"Association of intrinsic capacity with functional decline and mortality in older adults: a systematic review and meta-analysis of longitudinal studies","authors":"Juan Luis Sánchez-Sánchez PhD , Wan-Hsuan Lu PhD , Daniel Gallardo-Gómez MSc , Borja del Pozo Cruz PhD , Philipe de Souto Barreto PhD , Alejandro Lucia MD , Pedro L Valenzuela PhD","doi":"10.1016/S2666-7568(24)00092-8","DOIUrl":"10.1016/S2666-7568(24)00092-8","url":null,"abstract":"<div><h3>Background</h3><p>Together with environmental factors, intrinsic capacity (the composite of all the physical and mental capacities of an individual) has been proposed as a marker of healthy ageing. However, whether intrinsic capacity predicts major clinical outcomes is unclear. We aimed to explore the association of intrinsic capacity with functional decline and mortality in older adults.</p></div><div><h3>Methods</h3><p>In this systematic review and meta-analysis, we conducted a systematic search in MEDLINE (via PubMed), Scopus, and Web of Science from database inception to Feb 14, 2024, of observational longitudinal studies conducted in older adults (age ≥60 years) assessing the association of intrinsic capacity with impairment in basic activities of daily living (BADL) or instrumental activities of daily living (IADL) or risk of mortality. Estimates were extracted by two reviewers (JLS-S and W-HL) and were pooled using three-level meta-analytic models. The quality of each study was independently assessed by two authors (JLS-S and PLV) using the Newcastle–Ottawa Scale for longitudinal studies. Heterogeneity was evaluated using the <em>I</em><sup>2</sup> indicator at two levels: within-study (level 2) and between-study (level 3) variation. For associations between intrinsic capacity and IADL and BADL, we transformed data (standardised β coefficients and odds ratios [ORs]) into Pearson product moment correlation coefficients (<em>r</em>) using Pearson and Digby formulas to allow comparability across studies. For associations between intrinsic capacity and risk of mortality, hazard ratios (HRs) with 95% CIs were extracted from survival analyses. This study is registered with PROSPERO, CRD42023460482.</p></div><div><h3>Findings</h3><p>We included 37 studies (206 693 participants; average age range 65·3–85·9 years) in the systematic review, of which 31 were included in the meta-analysis on the association between intrinsic capacity and outcomes; three studies (2935 participants) were included in the meta-analysis on the association between intrinsic capacity trajectories and longitudinal changes in BADL or IADL. Intrinsic capacity was inversely associated with longitudinal impairments in BADL (Pearson's <em>r</em> –0·12 [95% CI –0·19 to –0·04]) and IADL (–0·24 [–0·35 to –0·13]), as well as with mortality risk (hazard ratio 0·57 [95% CI 0·51 to 0·63]). An association was also found between intrinsic capacity trajectories and impairment in IADL (but not in BADL), with maintained or improved intrinsic capacity over time associated with a lower impairment in IADL (odds ratio 0·37 [95% CI 0·19 to 0·71]). There was no evidence of publication bias (Egger's test p>0·05) and there was low between-study heterogeneity (<em>I</em><sup>2</sup>=18·4%), though within-study (<em>I</em><sup>2</sup>=63·2%) heterogeneity was substantial.</p></div><div><h3>Interpretation</h3><p>Intrinsic capacity is inversely associated with functional decline and mortality","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 7","pages":"Pages e480-e492"},"PeriodicalIF":13.4,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000928/pdfft?md5=b688ecb698cd1d4ebbeecbdf43357fce&pid=1-s2.0-S2666756824000928-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141471218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01DOI: 10.1016/S2666-7568(24)00096-5
Dina Goodman-Palmer PhD , Prof Carolyn Greig PhD , Sandra Agyapong-Badu PhD , Prof Miles D Witham PhD , Collin F Payne PhD , Mamadou Bountogo MD , Boubacar Coulibaly PhD , Pascal Geldsetzer ScD , Guy Harling ScD , Maxime Inghels PhD , Jennifer Manne-Goehler ScD , Lucienne Ouermi MD , Ali Sie PhD , Prof Justine I Davies MD
<div><h3>Background</h3><p>Little is known about ageing and frailty progression in low-income settings. We aimed to describe frailty changes over time in individuals living in rural Burkina Faso and to assess which sociodemographic, disability, and multimorbidity factors are associated with frailty progression and mortality.</p></div><div><h3>Methods</h3><p>This longitudinal, population-based study was conducted at the Nouna Health and Demographic Surveillance Systems (HDSS) site in northwestern Burkina Faso. Eligible participants were aged 40 years or older and had been primarily resident in a household within the HDSS area for at least the past 6 months before the baseline survey and were selected from the 2015 HDSS household census using a stratified random sample of adults living in unique households within the area. Participants were interviewed in their homes in 2018 (baseline), 2021 (follow-up), or both. We derived the Fried frailty score for each participant at each timepoint using data on grip strength, gait speed, self-reported weight loss, self-reported exhaustion, and physical activity, and described changes in frailty status (no frailty, pre-frailty, or frailty) between 2018 and 2021. We used multivariate regression models to assess factors (ie, sex, age, marital status, educational attainment, wealth quintile, WHO Disability Assessment Schedule (WHODAS) score, and multimorbidity) associated with frailty progression (either worsening frailty status or dying, compared with frailty status remaining the same or improving) and with mortality, and developed sequential models: unadjusted, adjusting for sociodemographic factors (sex, age, marital status, educational attainment, and wealth quintile), and adjusting for sociodemographic factors, disability, and multimorbidity.</p></div><div><h3>Findings</h3><p>Between May 25 and July 19, 2018, and between July 1 and Aug 22, 2021, 5952 individuals were invited to participate: 1709 (28·7%) did not consent, 1054 (17·8%) participated in 2018 only and were lost to follow-up, 1214 (20·4%) participated in 2021 only, and 1975 (33·2%) were included in both years or died between years. Of 1967 participants followed up with complete demographic data, 190 (9·7%) were frail or unable to complete the frailty assessment in 2018, compared with 77 (3·9%) in 2021. Between 2018 and 2021, frailty status improved in 567 (28·8%) participants and worsened in 327 (16·6%), and 101 (5·1%) participants died. The relative risk of frailty status worsening or of dying (compared with frailty impRoving or no change) increased with age and WHODAS score, whereas female sex appeared protective. After controlling for all sociodemographic factors, multimorbidity, and WHODAS score, odds of mortality were 1·07 (odds ratio 2·07, 95% CI 1·05–4·09) times higher among pre-frail individuals and 1·1 (2·21, 0·90–5·41) times higher among frail individuals than among non-frail individuals.</p></div><div><h3>Interpretation</h3><p>Frailty sta
{"title":"Frailty progression in adults aged 40 years and older in rural Burkina Faso: a longitudinal, population-based study","authors":"Dina Goodman-Palmer PhD , Prof Carolyn Greig PhD , Sandra Agyapong-Badu PhD , Prof Miles D Witham PhD , Collin F Payne PhD , Mamadou Bountogo MD , Boubacar Coulibaly PhD , Pascal Geldsetzer ScD , Guy Harling ScD , Maxime Inghels PhD , Jennifer Manne-Goehler ScD , Lucienne Ouermi MD , Ali Sie PhD , Prof Justine I Davies MD","doi":"10.1016/S2666-7568(24)00096-5","DOIUrl":"10.1016/S2666-7568(24)00096-5","url":null,"abstract":"<div><h3>Background</h3><p>Little is known about ageing and frailty progression in low-income settings. We aimed to describe frailty changes over time in individuals living in rural Burkina Faso and to assess which sociodemographic, disability, and multimorbidity factors are associated with frailty progression and mortality.</p></div><div><h3>Methods</h3><p>This longitudinal, population-based study was conducted at the Nouna Health and Demographic Surveillance Systems (HDSS) site in northwestern Burkina Faso. Eligible participants were aged 40 years or older and had been primarily resident in a household within the HDSS area for at least the past 6 months before the baseline survey and were selected from the 2015 HDSS household census using a stratified random sample of adults living in unique households within the area. Participants were interviewed in their homes in 2018 (baseline), 2021 (follow-up), or both. We derived the Fried frailty score for each participant at each timepoint using data on grip strength, gait speed, self-reported weight loss, self-reported exhaustion, and physical activity, and described changes in frailty status (no frailty, pre-frailty, or frailty) between 2018 and 2021. We used multivariate regression models to assess factors (ie, sex, age, marital status, educational attainment, wealth quintile, WHO Disability Assessment Schedule (WHODAS) score, and multimorbidity) associated with frailty progression (either worsening frailty status or dying, compared with frailty status remaining the same or improving) and with mortality, and developed sequential models: unadjusted, adjusting for sociodemographic factors (sex, age, marital status, educational attainment, and wealth quintile), and adjusting for sociodemographic factors, disability, and multimorbidity.</p></div><div><h3>Findings</h3><p>Between May 25 and July 19, 2018, and between July 1 and Aug 22, 2021, 5952 individuals were invited to participate: 1709 (28·7%) did not consent, 1054 (17·8%) participated in 2018 only and were lost to follow-up, 1214 (20·4%) participated in 2021 only, and 1975 (33·2%) were included in both years or died between years. Of 1967 participants followed up with complete demographic data, 190 (9·7%) were frail or unable to complete the frailty assessment in 2018, compared with 77 (3·9%) in 2021. Between 2018 and 2021, frailty status improved in 567 (28·8%) participants and worsened in 327 (16·6%), and 101 (5·1%) participants died. The relative risk of frailty status worsening or of dying (compared with frailty impRoving or no change) increased with age and WHODAS score, whereas female sex appeared protective. After controlling for all sociodemographic factors, multimorbidity, and WHODAS score, odds of mortality were 1·07 (odds ratio 2·07, 95% CI 1·05–4·09) times higher among pre-frail individuals and 1·1 (2·21, 0·90–5·41) times higher among frail individuals than among non-frail individuals.</p></div><div><h3>Interpretation</h3><p>Frailty sta","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 7","pages":"Pages e493-e502"},"PeriodicalIF":13.4,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000965/pdfft?md5=47de85b8a01f69fad948af73b6c0f100&pid=1-s2.0-S2666756824000965-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141471219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01DOI: 10.1016/S2666-7568(24)00087-4
Prof Mika Kivimäki FMedSci , Philipp Frank PhD , Jaana Pentti MSc , Xiaolin Xu PhD , Prof Jussi Vahtera MD , Jenni Ervasti PhD , Solja T Nyberg PhD , Joni V Lindbohm MD , Prof Markus Jokela PhD , Prof Linda Partridge FMedSci
<div><h3>Background</h3><p>Ageing hallmarks, characterising features of cellular ageing, have a role in the pathophysiology of many age-related diseases. We examined whether obesity is associated with an increased risk of developing such hallmark-related diseases.</p></div><div><h3>Methods</h3><p>In this multicohort study, we included people aged 38–72 years with data on weight, height, and waist circumference measured during a clinical examination at baseline between March 13, 2006, and Oct 1, 2010, from the UK Biobank with follow-up until Nov 12, 2021. To test reproducibility of the findings (replication analysis), we used data from people aged 40 years or older included in the Finnish Public Sector study and the Finnish Health and Social Support study who responded to the study surveys, had data on BMI, and were successfully linked to electronic health records from national registers up to Dec 31, 2016. Obesity and clinical characteristics were assessed at baseline. Via linkage to national health records, participants were followed up for 83 diseases related to nine ageing hallmarks (genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication). Outcomes were the first instance of hallmark-related disease, in addition to co-occurrence of three or more hallmark-related diseases and mortality.</p></div><div><h3>Findings</h3><p>496 530 adults (mean age 57·0 years [SD 8·1]) from the UK Biobank were included in the primary analysis, and 83 249 (mean age 48·2 years [6·4]) adults from the Finnish cohorts were included in the replication analysis. Median follow-up was 12·7 years (IQR 12·0–13·4) in the UK Biobank and 14·0 years (8·0–15·0) in the Finnish cohorts. After adjusting for demographic characteristics, lifestyle factors, and depression, UK Biobank participants with obesity (BMI ≥30·0 kg/m<sup>2</sup>) had a 1·40 (95% CI 1·38–1·41) times higher hazard ratio for the first hallmark-related disease than those with a healthy weight (BMI 18·5–24·9 kg/m<sup>2</sup>). The corresponding hazard ratios for three co-occurring diseases were 2·92 (95% CI 2·64–3·22) for deregulated nutrient sensing, 2·73 (2·46–3·02) for telomere attrition, 2·33 (2·10–2·60) for epigenetic alterations, 2·30 (2·14–2·48) for mitochondrial dysfunction, 2·23 (2·04–2·45) for stem cell exhaustion, 2·02 (1·89–2·16) for altered intercellular communication, 2·01 (1·89–2·15) for cellular senescence, 1·83 (1·67–2·00) for loss of proteostasis, and 1·39 (1·27–1·52) for genomic instability. These findings were replicated in the Finnish cohorts. In both studies, the associations between other risk factors (low education, unhealthy dietary factors [available only in the UK Biobank], smoking, high alcohol consumption, physical inactivity, and depression) and hallmark-related diseases were weaker than those with obesity. 45–60% of t
{"title":"Obesity and risk of diseases associated with hallmarks of cellular ageing: a multicohort study","authors":"Prof Mika Kivimäki FMedSci , Philipp Frank PhD , Jaana Pentti MSc , Xiaolin Xu PhD , Prof Jussi Vahtera MD , Jenni Ervasti PhD , Solja T Nyberg PhD , Joni V Lindbohm MD , Prof Markus Jokela PhD , Prof Linda Partridge FMedSci","doi":"10.1016/S2666-7568(24)00087-4","DOIUrl":"10.1016/S2666-7568(24)00087-4","url":null,"abstract":"<div><h3>Background</h3><p>Ageing hallmarks, characterising features of cellular ageing, have a role in the pathophysiology of many age-related diseases. We examined whether obesity is associated with an increased risk of developing such hallmark-related diseases.</p></div><div><h3>Methods</h3><p>In this multicohort study, we included people aged 38–72 years with data on weight, height, and waist circumference measured during a clinical examination at baseline between March 13, 2006, and Oct 1, 2010, from the UK Biobank with follow-up until Nov 12, 2021. To test reproducibility of the findings (replication analysis), we used data from people aged 40 years or older included in the Finnish Public Sector study and the Finnish Health and Social Support study who responded to the study surveys, had data on BMI, and were successfully linked to electronic health records from national registers up to Dec 31, 2016. Obesity and clinical characteristics were assessed at baseline. Via linkage to national health records, participants were followed up for 83 diseases related to nine ageing hallmarks (genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication). Outcomes were the first instance of hallmark-related disease, in addition to co-occurrence of three or more hallmark-related diseases and mortality.</p></div><div><h3>Findings</h3><p>496 530 adults (mean age 57·0 years [SD 8·1]) from the UK Biobank were included in the primary analysis, and 83 249 (mean age 48·2 years [6·4]) adults from the Finnish cohorts were included in the replication analysis. Median follow-up was 12·7 years (IQR 12·0–13·4) in the UK Biobank and 14·0 years (8·0–15·0) in the Finnish cohorts. After adjusting for demographic characteristics, lifestyle factors, and depression, UK Biobank participants with obesity (BMI ≥30·0 kg/m<sup>2</sup>) had a 1·40 (95% CI 1·38–1·41) times higher hazard ratio for the first hallmark-related disease than those with a healthy weight (BMI 18·5–24·9 kg/m<sup>2</sup>). The corresponding hazard ratios for three co-occurring diseases were 2·92 (95% CI 2·64–3·22) for deregulated nutrient sensing, 2·73 (2·46–3·02) for telomere attrition, 2·33 (2·10–2·60) for epigenetic alterations, 2·30 (2·14–2·48) for mitochondrial dysfunction, 2·23 (2·04–2·45) for stem cell exhaustion, 2·02 (1·89–2·16) for altered intercellular communication, 2·01 (1·89–2·15) for cellular senescence, 1·83 (1·67–2·00) for loss of proteostasis, and 1·39 (1·27–1·52) for genomic instability. These findings were replicated in the Finnish cohorts. In both studies, the associations between other risk factors (low education, unhealthy dietary factors [available only in the UK Biobank], smoking, high alcohol consumption, physical inactivity, and depression) and hallmark-related diseases were weaker than those with obesity. 45–60% of t","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 7","pages":"Pages e454-e463"},"PeriodicalIF":13.4,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000874/pdfft?md5=5dbd86ff2a160f3a1ac7676bb4fa3351&pid=1-s2.0-S2666756824000874-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141471222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01DOI: 10.1016/S2666-7568(24)00094-1
Jinqiao Zhu MMed , Yusha Cui MMed , Junjiao Zhang MMed , Rui Yan MMed , Dongning Su MD , Prof Dong Zhao PhD , Anxin Wang PhD , Prof Tao Feng MD
<div><h3>Background</h3><p>Parkinson's disease is the second most common neurodegenerative disorder, exhibiting an upward trend in prevalence. We aimed to investigate the prevalence of Parkinson's disease, temporal trends between 1980 and 2023, and variations in prevalence by location, age, sex, survey period, sociodemographic index (SDI), human development index (HDI), and study characteristics (sample size, diagnostic criteria, and data source).</p></div><div><h3>Methods</h3><p>In this systematic review and meta-analysis we searched PubMed, Cochrane, Web of Science, Embase, Scopus, and Global Health for observational studies that reported Parkinson's disease prevalence in the general population from database inception to Nov 1, 2023. We included studies if they were original observational investigations, had participants from the general population or community-based datasets, and provided numerical data on the prevalence of Parkinson's disease either with 95% CIs or with sufficient information to calculate 95% CIs. Studies were excluded if they were conducted in a specific population, had a sample size smaller than 1000, or were review articles, case reports, protocols, meeting abstracts, letters, comments, short communications, posters, and reports. The publication characteristics (first author and publication year), study location (countries, WHO regions, SDI, and HDI), survey period, study design, diagnostic criteria, data source, participant information, and prevalence data were extracted from articles using a standard form. Two authors independently evaluated eligibility, and discrepancies were resolved through discussion with the third author. We used random effect models to pool estimates with 95% CIs. Estimated annual percentage change (EAPC) was calculated to assess the temporal trend in prevalence of Parkinson's disease. The study was registered with PROSPERO, CRD42022364417.</p></div><div><h3>Findings</h3><p>83 studies from 37 countries were eligible for analysis, with 56 studies providing all-age prevalence, 53 studies reporting age-specific prevalence, and 26 studies providing both all-age and age-specific prevalence. Global pooled prevalence of Parkinson's disease was 1·51 cases per 1000 (95% CI 1·19–1·88), which was higher in males (1·54 cases per 1000 [1·17–1·96]) than in females (1·49 cases per 1000 [1·12–1·92], p=0·030). During different survey periods, the prevalence of Parkinson's disease was 0·90 cases per 1000 (0·48–1·44; 1980–89), 1·38 cases per 1000 (1·17–1·61; 1990–99), 1·18 cases per 1000 (0·77–1·67; 2000–09), and 3·81 cases per 1000 (2·67–5·14; 2010–23). The EAPC of Parkinson's disease prevalence was significantly higher in the period of 2004–23 (EAPC 16·32% [95% CI 6·07–26·58], p=0·0040) than in the period of 1980–2003 (5·30% [0·82–9·79], p=0·022). Statistically significant disparities in prevalence were observed across six WHO regions. Prevalence increased with HDI or SDI. Considerable variations were observed in t
{"title":"Temporal trends in the prevalence of Parkinson's disease from 1980 to 2023: a systematic review and meta-analysis","authors":"Jinqiao Zhu MMed , Yusha Cui MMed , Junjiao Zhang MMed , Rui Yan MMed , Dongning Su MD , Prof Dong Zhao PhD , Anxin Wang PhD , Prof Tao Feng MD","doi":"10.1016/S2666-7568(24)00094-1","DOIUrl":"10.1016/S2666-7568(24)00094-1","url":null,"abstract":"<div><h3>Background</h3><p>Parkinson's disease is the second most common neurodegenerative disorder, exhibiting an upward trend in prevalence. We aimed to investigate the prevalence of Parkinson's disease, temporal trends between 1980 and 2023, and variations in prevalence by location, age, sex, survey period, sociodemographic index (SDI), human development index (HDI), and study characteristics (sample size, diagnostic criteria, and data source).</p></div><div><h3>Methods</h3><p>In this systematic review and meta-analysis we searched PubMed, Cochrane, Web of Science, Embase, Scopus, and Global Health for observational studies that reported Parkinson's disease prevalence in the general population from database inception to Nov 1, 2023. We included studies if they were original observational investigations, had participants from the general population or community-based datasets, and provided numerical data on the prevalence of Parkinson's disease either with 95% CIs or with sufficient information to calculate 95% CIs. Studies were excluded if they were conducted in a specific population, had a sample size smaller than 1000, or were review articles, case reports, protocols, meeting abstracts, letters, comments, short communications, posters, and reports. The publication characteristics (first author and publication year), study location (countries, WHO regions, SDI, and HDI), survey period, study design, diagnostic criteria, data source, participant information, and prevalence data were extracted from articles using a standard form. Two authors independently evaluated eligibility, and discrepancies were resolved through discussion with the third author. We used random effect models to pool estimates with 95% CIs. Estimated annual percentage change (EAPC) was calculated to assess the temporal trend in prevalence of Parkinson's disease. The study was registered with PROSPERO, CRD42022364417.</p></div><div><h3>Findings</h3><p>83 studies from 37 countries were eligible for analysis, with 56 studies providing all-age prevalence, 53 studies reporting age-specific prevalence, and 26 studies providing both all-age and age-specific prevalence. Global pooled prevalence of Parkinson's disease was 1·51 cases per 1000 (95% CI 1·19–1·88), which was higher in males (1·54 cases per 1000 [1·17–1·96]) than in females (1·49 cases per 1000 [1·12–1·92], p=0·030). During different survey periods, the prevalence of Parkinson's disease was 0·90 cases per 1000 (0·48–1·44; 1980–89), 1·38 cases per 1000 (1·17–1·61; 1990–99), 1·18 cases per 1000 (0·77–1·67; 2000–09), and 3·81 cases per 1000 (2·67–5·14; 2010–23). The EAPC of Parkinson's disease prevalence was significantly higher in the period of 2004–23 (EAPC 16·32% [95% CI 6·07–26·58], p=0·0040) than in the period of 1980–2003 (5·30% [0·82–9·79], p=0·022). Statistically significant disparities in prevalence were observed across six WHO regions. Prevalence increased with HDI or SDI. Considerable variations were observed in t","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 7","pages":"Pages e464-e479"},"PeriodicalIF":13.4,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000941/pdfft?md5=77b7538399b16d8364f00a2ba4e3b3da&pid=1-s2.0-S2666756824000941-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141471224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<div><h3>Background</h3><p>A standard treatment for fit, older patients with recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) is yet to be established. In the previous EXTREME trial, few older patients were included. We aimed to evaluate the efficacy and tolerance of an adapted EXTREME regimen in fit, older patients with recurrent or metastatic HNSCC.</p></div><div><h3>Methods</h3><p>This single-arm, phase 2 study was done at 22 centres in France. Eligible patients were aged 70 years or older and assessed as not frail (fit) using the ELAN Geriatric Evaluation (EGE) and had recurrent or metastatic HNSCC in the first-line setting that was not eligible for local therapy (surgery or radiotherapy), and an Eastern Cooperative Oncology Group performance status of 0–1. The adapted EXTREME regimen consisted of six cycles of fluorouracil 4000 mg/m<sup>2</sup> on days 1–4, carboplatin with an area under the curve of 5 on day 1, and cetuximab on days 1, 8, and 15 (400 mg/m<sup>2</sup> on cycle 1–day 1, and 250 mg/m<sup>2</sup> subsequently), all intravenously, with cycles starting every 21 days. In patients with disease control after two to six cycles, cetuximab 500 mg/m<sup>2</sup> was continued once every 2 weeks as maintenance therapy until disease progression or unacceptable toxicity. Granulocyte colony-stimulating factor was systematically administered and erythropoietin was recommended during chemotherapy. The study was based on the two-stage Bryant and Day design, combining efficacy and toxicity endpoints. The primary efficacy endpoint was objective response rate at week 12 after the start of treatment, assessed by central review (with an unacceptable rate of ≤15%). The primary toxicity endpoint was morbidity, defined as grade 4–5 adverse events, or cutaneous rash (grade ≥3) that required cetuximab to be discontinued, during the chemotherapy phase, or a decrease in functional autonomy (Activities of Daily Living score decrease ≥2 points from baseline) at 1 month after the end of chemotherapy (with an unacceptable morbidity rate of >40%). Analysis of the coprimary endpoints, and of safety in the chemotherapy phase, was based on the per-protocol population, defined as eligible patients who received at least one cycle of the adapted EXTREME regimen. Safety in the maintenance phase was assessed in all patients who received at least one dose of cetuximab as maintenance therapy. The study is registered with <span>ClinicalTrials.gov</span><svg><path></path></svg>, <span>NCT01864772</span><svg><path></path></svg>, and is completed.</p></div><div><h3>Findings</h3><p>Between Sept 27, 2013, and June 20, 2018, 85 patients were enrolled, of whom 78 were in the per-protocol population. 66 (85%) patients were male and 12 (15%) were female, and the median age was 75 years (IQR 72–79). The median number of chemotherapy cycles received was five (IQR 3–6). Objective response at week 12 was observed in 31 patients (40% [95% CI 30–51]) and morbidit
{"title":"Adapted EXTREME regimen in the first-line treatment of fit, older patients with recurrent or metastatic head and neck squamous cell carcinoma (ELAN-FIT): a multicentre, single-arm, phase 2 trial","authors":"Prof Joël Guigay MD , Hervé Le Caer MD , François-Régis Ferrand MD , Lionel Geoffrois MD , Esma Saada-Bouzid MD , Jérôme Fayette MD , Christian Sire MD , Didier Cupissol MD , Emmanuel Blot MD , Pierre Guillet MD , Julien Pavillet MD , Laurence Bozec MD , Olivier Capitain MD , Frédéric Rolland MD , Philippe Debourdeau MD , Yoann Pointreau MD , Claire Falandry MD , Stéphane Lopez MD , Alexandre Coutte MD , Thierry Chatellier MD , Anne Aupérin PhD","doi":"10.1016/S2666-7568(24)00048-5","DOIUrl":"10.1016/S2666-7568(24)00048-5","url":null,"abstract":"<div><h3>Background</h3><p>A standard treatment for fit, older patients with recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) is yet to be established. In the previous EXTREME trial, few older patients were included. We aimed to evaluate the efficacy and tolerance of an adapted EXTREME regimen in fit, older patients with recurrent or metastatic HNSCC.</p></div><div><h3>Methods</h3><p>This single-arm, phase 2 study was done at 22 centres in France. Eligible patients were aged 70 years or older and assessed as not frail (fit) using the ELAN Geriatric Evaluation (EGE) and had recurrent or metastatic HNSCC in the first-line setting that was not eligible for local therapy (surgery or radiotherapy), and an Eastern Cooperative Oncology Group performance status of 0–1. The adapted EXTREME regimen consisted of six cycles of fluorouracil 4000 mg/m<sup>2</sup> on days 1–4, carboplatin with an area under the curve of 5 on day 1, and cetuximab on days 1, 8, and 15 (400 mg/m<sup>2</sup> on cycle 1–day 1, and 250 mg/m<sup>2</sup> subsequently), all intravenously, with cycles starting every 21 days. In patients with disease control after two to six cycles, cetuximab 500 mg/m<sup>2</sup> was continued once every 2 weeks as maintenance therapy until disease progression or unacceptable toxicity. Granulocyte colony-stimulating factor was systematically administered and erythropoietin was recommended during chemotherapy. The study was based on the two-stage Bryant and Day design, combining efficacy and toxicity endpoints. The primary efficacy endpoint was objective response rate at week 12 after the start of treatment, assessed by central review (with an unacceptable rate of ≤15%). The primary toxicity endpoint was morbidity, defined as grade 4–5 adverse events, or cutaneous rash (grade ≥3) that required cetuximab to be discontinued, during the chemotherapy phase, or a decrease in functional autonomy (Activities of Daily Living score decrease ≥2 points from baseline) at 1 month after the end of chemotherapy (with an unacceptable morbidity rate of >40%). Analysis of the coprimary endpoints, and of safety in the chemotherapy phase, was based on the per-protocol population, defined as eligible patients who received at least one cycle of the adapted EXTREME regimen. Safety in the maintenance phase was assessed in all patients who received at least one dose of cetuximab as maintenance therapy. The study is registered with <span>ClinicalTrials.gov</span><svg><path></path></svg>, <span>NCT01864772</span><svg><path></path></svg>, and is completed.</p></div><div><h3>Findings</h3><p>Between Sept 27, 2013, and June 20, 2018, 85 patients were enrolled, of whom 78 were in the per-protocol population. 66 (85%) patients were male and 12 (15%) were female, and the median age was 75 years (IQR 72–79). The median number of chemotherapy cycles received was five (IQR 3–6). Objective response at week 12 was observed in 31 patients (40% [95% CI 30–51]) and morbidit","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 6","pages":"Pages e392-e405"},"PeriodicalIF":13.1,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000485/pdfft?md5=062ae4d43cb205d5927b8c841bb6c7de&pid=1-s2.0-S2666756824000485-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140959269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-01DOI: 10.1016/S2666-7568(24)00091-6
Honglian Luo , Jiafeng Zhang , Xianhua Li , Tuo Li , Wei Shen
{"title":"Eldecalcitol for sarcopenia prevention in adults with prediabetes","authors":"Honglian Luo , Jiafeng Zhang , Xianhua Li , Tuo Li , Wei Shen","doi":"10.1016/S2666-7568(24)00091-6","DOIUrl":"10.1016/S2666-7568(24)00091-6","url":null,"abstract":"","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 6","pages":"Page e389"},"PeriodicalIF":13.1,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000916/pdfft?md5=23158a79062520c12e030fee64338dd5&pid=1-s2.0-S2666756824000916-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-01DOI: 10.1016/S2666-7568(24)00095-3
Janice M Ranson
{"title":"Are mobile health applications the answer to dementia risk reduction?","authors":"Janice M Ranson","doi":"10.1016/S2666-7568(24)00095-3","DOIUrl":"10.1016/S2666-7568(24)00095-3","url":null,"abstract":"","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 6","pages":"Pages e386-e387"},"PeriodicalIF":13.1,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000953/pdfft?md5=37bbf2a12ba3ac72bc042f0528b4b9ed&pid=1-s2.0-S2666756824000953-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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