Pub Date : 2025-12-01DOI: 10.1016/j.lanepe.2025.101539
Emer Cooke , Pamela Rendi-Wagner
{"title":"Rising antimicrobial resistance in Europe: EMA and ECDC outline urgent actions to achieve EU targets","authors":"Emer Cooke , Pamela Rendi-Wagner","doi":"10.1016/j.lanepe.2025.101539","DOIUrl":"10.1016/j.lanepe.2025.101539","url":null,"abstract":"","PeriodicalId":53223,"journal":{"name":"Lancet Regional Health-Europe","volume":"59 ","pages":"Article 101539"},"PeriodicalIF":13.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145693684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01DOI: 10.1016/j.lanepe.2025.101559
The Lancet Regional Health – Europe
{"title":"COP30: still failing to meet the challenge","authors":"The Lancet Regional Health – Europe","doi":"10.1016/j.lanepe.2025.101559","DOIUrl":"10.1016/j.lanepe.2025.101559","url":null,"abstract":"","PeriodicalId":53223,"journal":{"name":"Lancet Regional Health-Europe","volume":"59 ","pages":"Article 101559"},"PeriodicalIF":13.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145693798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01DOI: 10.1016/j.lanepe.2025.101528
Ivana Nedic
{"title":"European Society for Medical Oncology (ESMO) congress 2025","authors":"Ivana Nedic","doi":"10.1016/j.lanepe.2025.101528","DOIUrl":"10.1016/j.lanepe.2025.101528","url":null,"abstract":"","PeriodicalId":53223,"journal":{"name":"Lancet Regional Health-Europe","volume":"59 ","pages":"Article 101528"},"PeriodicalIF":13.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145693797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01DOI: 10.1016/j.lanepe.2025.101470
Clémentine Prioux , Emmanuelle Kesse-Guyot , Bernard Srour , Léopold K. Fézeu , Julia Baudry , Sandra Wagner , Serge Hercberg , Mathilde Touvier , Benjamin Allès
Background
Few studies have evaluated the effects of plant-based diets combined with ultra-processed food on cardiovascular diseases (CVD). The objective of this study was to assess associations between CVD risk and novel diet indices that integrate balance between plant-based and animal-based foods, nutritional quality and processing level.
Methods
We analyzed data from the French NutriNet-Santé prospective cohort. First, the two original healthy Plant-Based Diet and unhealthy Plant-Based Diet Indices (hPDI and uPDI) were computed. Four new indices were then built, based on the hPDI and uPDI computation, but with a multiplying factor to account for (i) the contribution of unprocessed food (UnPF) and (ii) the contribution of ultra-processed food (UPF), using the NOVA classification, culturally adapted. These two contributions (UnPF and UPF) were estimated using dietary data from 24 h records as percentages of total food consumed (g.day−1). The association between each of the six resulting index scores and cardiovascular disease (cerebrovascular and coronary) was estimated using multivariate Cox proportional hazards models adjusted for confounding factors. Sensitivity analyses were also performed to assess the robustness of these novel indices.
Findings
Among 63,835 participants, median follow-up time 9.0 years, IQR: 5–13 years, 76% women, mean age 51.4, SD = 10.2, no statistically significant protective or deleterious association was observed between those adhering to a nutritionally healthy but ultra-processed plant-based diet (hPDI-UPF), and a nutritionally unhealthy but unprocessed plant-based diet (uPDI-UnPF). When comparing participants with the highest adherence to a nutritionally healthy and unprocessed plant-based diet (hPDI-UnPF), to those with the lowest, we observed a 44% lower incidence of coronary heart disease (HRD10 vs. D1: 0.56, 95% CI: [0.42–0.75]) and 32% lower risk for CVD (HRD10 vs. D1: 0.68, 95% CI: [0.53–0.88]). Similarly, participants with the highest adherence to an unhealthy and ultra-processed plant-based diet (uPDI-UPF) had a 46% higher incidence of coronary heart disease (HRD10 vs. D1: 1.46, 95% CI: [1.11–1.93]), and a 38% higher incidence of CVD (HRD10 vs. D1: 1.38, 95% CI: [1.09–1.76]). This was the strongest association observed in our study.
Interpretation
The findings of this study mark the importance of considering not only balance between plant-based and animal-based foods, but also nutritional quality and degree of processing when evaluating association between diet and cardiovascular risk.
Funding
French National Research Agency (ANR, ANR-22-CE36-0012).
很少有研究评估植物性饮食结合超加工食品对心血管疾病(CVD)的影响。本研究的目的是评估心血管疾病风险与新型饮食指标之间的关系,这些指标综合了植物性和动物性食物之间的平衡、营养质量和加工水平。方法我们分析来自法国nutrinet - sant前瞻性队列的数据。首先,计算健康植物性饮食指数和不健康植物性饮食指数(hPDI和uPDI)。然后建立了四个新的指数,基于hPDI和uPDI的计算,但使用一个乘法因子来解释(i)未加工食品(UnPF)的贡献和(ii)超加工食品(UPF)的贡献,使用NOVA分类,适应文化。这两个贡献(UnPF和UPF)是使用24小时记录的饮食数据作为总食物消耗的百分比(g.day - 1)来估计的。使用校正了混杂因素的多变量Cox比例风险模型,估计6项结果指数得分与心血管疾病(脑血管和冠状动脉)之间的关联。还进行了敏感性分析,以评估这些新指标的稳健性。在63,835名参与者中,中位随访时间为9.0年,IQR为5-13年,76%为女性,平均年龄51.4岁,SD = 10.2,坚持营养健康但超加工的植物性饮食(hPDI-UPF)和营养不健康但未加工的植物性饮食(uPDI-UnPF)之间没有统计学上显著的保护或有害关联。当将坚持营养健康和未加工植物性饮食(hPDI-UnPF)的参与者与坚持营养健康和未加工植物性饮食(hPDI-UnPF)的参与者进行比较时,我们观察到冠心病发病率降低44% (HRD10 vs. D1: 0.56, 95% CI:[0.42-0.75]),心血管疾病风险降低32% (HRD10 vs. D1: 0.68, 95% CI:[0.53-0.88])。同样,坚持不健康和超加工植物性饮食(uPDI-UPF)的参与者冠心病发病率高出46% (HRD10 vs. D1: 1.46, 95% CI:[1.11-1.93]),心血管疾病发病率高出38% (HRD10 vs. D1: 1.38, 95% CI:[1.09-1.76])。这是我们研究中观察到的最强关联。这项研究的结果表明,在评估饮食与心血管风险之间的关系时,不仅要考虑植物性和动物性食物之间的平衡,还要考虑营养质量和加工程度。资助法国国家研究机构(ANR, ANR-22- ce36 -0012)。
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Pub Date : 2025-12-01DOI: 10.1016/j.lanepe.2025.101523
Martina Sester , Neus Altet-Gomez , Åse Bengaard Andersen , Miguel Arias-Guillén , Korkut Avsar , Anne-Marte Bakken Kran , Graham Bothamley , Anne Christine Nordholm Breschel , James Brown , Dumitru Chesov , Nelly Ciobanu , Daniela Maria Cirillo , Valeriu Crudu , Malu de Souza Galvao , Asli Görek Dilektasli , José Dominguez , Raquel Duarte , Anne Ma Dyrhol-Riise , Delia Goletti , Harald Hoffmann , Christoph Lange
{"title":"Correction to Diagnostic accuracy and predictive value of the QuantiFERON-TB gold plus assay for tuberculosis in immunocompromised individuals: a prospective TBnet study Lancet Reg Health Eur 57 (2025) 101416 LLRHEUROPE-D-25-00310","authors":"Martina Sester , Neus Altet-Gomez , Åse Bengaard Andersen , Miguel Arias-Guillén , Korkut Avsar , Anne-Marte Bakken Kran , Graham Bothamley , Anne Christine Nordholm Breschel , James Brown , Dumitru Chesov , Nelly Ciobanu , Daniela Maria Cirillo , Valeriu Crudu , Malu de Souza Galvao , Asli Görek Dilektasli , José Dominguez , Raquel Duarte , Anne Ma Dyrhol-Riise , Delia Goletti , Harald Hoffmann , Christoph Lange","doi":"10.1016/j.lanepe.2025.101523","DOIUrl":"10.1016/j.lanepe.2025.101523","url":null,"abstract":"","PeriodicalId":53223,"journal":{"name":"Lancet Regional Health-Europe","volume":"59 ","pages":"Article 101523"},"PeriodicalIF":13.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145624030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01DOI: 10.1016/j.lanepe.2025.101472
Siméon de Bruijn , Anne J. Huiberts , Stijn P. Andeweg , Christina E. Hoeve , Maarten Schipper , Diederick E. Grobbee , Hester E. de Melker , Janneke H.H.M. van de Wijgert , Susan van den Hof , Mirjam J. Knol , Cees C. van den Wijngaard
Background
Post-COVID-19 condition (PCC) risk may have changed due to vaccination status, virus variants, prior infections, and other factors. We aimed to estimate PCC prevalence for one year in individuals infected with SARS-CoV-2 during autumn 2023, controlling for pre-infection symptoms and prevalence in recently uninfected participants.
Methods
VASCO, a Dutch ongoing prospective cohort, collects three-monthly questionnaires and six-monthly SARS-CoV-2 serology. Participants indicated severity of 23 symptoms on a five-point Likert scale, and of fatigue and concentration problems on the Checklist Individual Strength. We matched participants who did with those who did not report a SARS-CoV-2 infection between September 25, 2023 and January 7, 2024, and censored follow-up time for both upon serological or antigen test evidence of infection. We estimated PCC-prevalence as the excess prevalence of at least one PCC-related symptom between matched infected and uninfected participants at 90, 180, 270, and 360 days post-infection. Additionally, participants could self-attribute long-term symptoms to SARS-CoV-2.
Findings
We 1:1 matched 5621 infected to 5621 uninfected participants. The PCC prevalence, estimated as the marginal mean excess prevalence of PCC-related symptoms between infected and uninfected participants, was 0.2% (95% confidence interval: −1.9 to 2.3, p = 0.84) at 90 days, 0.5% (−1.6 to 2.6, p = 0.63) at 180 days, 0.7% (−1.3 to 2.8, p = 0.48) at 270 days, and 0.0% (−2.1 to 2.1, p = 0.99) at 360 days. Excess prevalence of new mild and severe long-term symptoms self-attributed to SARS-CoV-2 between infected and uninfected participants were both elevated at 90 days (mild: 7.2% (5.1–9.2), severe: 0.6% (0.4–0.8)) and 180 days (mild: 3.2% (2.0–4.4), severe: 0.3% (0.2–0.4)) post-infection (all p-values <0.0001), but no longer thereafter.
Interpretation
This double-controlled study, incorporating pre- versus post-infection and uninfected symptom data, found a low risk of PCC among a community-dwelling adult population infected during the autumn 2023 SARS-CoV-2 wave. The prevalence of PCC-related symptoms in infected and uninfected individuals was not significantly different at 90–360 days post-infection. The excess prevalences of self-attributed long-term symptoms were elevated at 90 and 180 days post-infection but no longer from 270 days onwards. These findings suggest that the 2023 wave inferred a lower PCC risk than during the pandemic period.
Funding
Funded by the Dutch Ministry of Health, Welfare and Sport.
{"title":"Post-COVID-19 condition in individuals infected with SARS-CoV-2 in autumn 2023 in the Netherlands: a prospective cohort study with pre- and post-infection data","authors":"Siméon de Bruijn , Anne J. Huiberts , Stijn P. Andeweg , Christina E. Hoeve , Maarten Schipper , Diederick E. Grobbee , Hester E. de Melker , Janneke H.H.M. van de Wijgert , Susan van den Hof , Mirjam J. Knol , Cees C. van den Wijngaard","doi":"10.1016/j.lanepe.2025.101472","DOIUrl":"10.1016/j.lanepe.2025.101472","url":null,"abstract":"<div><h3>Background</h3><div>Post-COVID-19 condition (PCC) risk may have changed due to vaccination status, virus variants, prior infections, and other factors. We aimed to estimate PCC prevalence for one year in individuals infected with SARS-CoV-2 during autumn 2023, controlling for pre-infection symptoms and prevalence in recently uninfected participants.</div></div><div><h3>Methods</h3><div>VASCO, a Dutch ongoing prospective cohort, collects three-monthly questionnaires and six-monthly SARS-CoV-2 serology. Participants indicated severity of 23 symptoms on a five-point Likert scale, and of fatigue and concentration problems on the Checklist Individual Strength. We matched participants who did with those who did not report a SARS-CoV-2 infection between September 25, 2023 and January 7, 2024, and censored follow-up time for both upon serological or antigen test evidence of infection. We estimated PCC-prevalence as the excess prevalence of at least one PCC-related symptom between matched infected and uninfected participants at 90, 180, 270, and 360 days post-infection. Additionally, participants could self-attribute long-term symptoms to SARS-CoV-2.</div></div><div><h3>Findings</h3><div>We 1:1 matched 5621 infected to 5621 uninfected participants. The PCC prevalence, estimated as the marginal mean excess prevalence of PCC-related symptoms between infected and uninfected participants, was 0.2% (95% confidence interval: −1.9 to 2.3, p = 0.84) at 90 days, 0.5% (−1.6 to 2.6, p = 0.63) at 180 days, 0.7% (−1.3 to 2.8, p = 0.48) at 270 days, and 0.0% (−2.1 to 2.1, p = 0.99) at 360 days. Excess prevalence of new mild and severe long-term symptoms self-attributed to SARS-CoV-2 between infected and uninfected participants were both elevated at 90 days (mild: 7.2% (5.1–9.2), severe: 0.6% (0.4–0.8)) and 180 days (mild: 3.2% (2.0–4.4), severe: 0.3% (0.2–0.4)) post-infection (all p-values <0.0001), but no longer thereafter.</div></div><div><h3>Interpretation</h3><div>This double-controlled study, incorporating pre- versus post-infection and uninfected symptom data, found a low risk of PCC among a community-dwelling adult population infected during the autumn 2023 SARS-CoV-2 wave. The prevalence of PCC-related symptoms in infected and uninfected individuals was not significantly different at 90–360 days post-infection. The excess prevalences of self-attributed long-term symptoms were elevated at 90 and 180 days post-infection but no longer from 270 days onwards. These findings suggest that the 2023 wave inferred a lower PCC risk than during the pandemic period.</div></div><div><h3>Funding</h3><div>Funded by the <span>Dutch Ministry of Health, Welfare and Sport</span>.</div></div>","PeriodicalId":53223,"journal":{"name":"Lancet Regional Health-Europe","volume":"59 ","pages":"Article 101472"},"PeriodicalIF":13.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145693681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01DOI: 10.1016/j.lanepe.2025.101534
Hans Henri P. Kluge, Natasha Azzopardi-Muscat, David Novillo-Ortiz
{"title":"Now is the time: turning the promise of AI into health for all","authors":"Hans Henri P. Kluge, Natasha Azzopardi-Muscat, David Novillo-Ortiz","doi":"10.1016/j.lanepe.2025.101534","DOIUrl":"10.1016/j.lanepe.2025.101534","url":null,"abstract":"","PeriodicalId":53223,"journal":{"name":"Lancet Regional Health-Europe","volume":"59 ","pages":"Article 101534"},"PeriodicalIF":13.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145693683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01DOI: 10.1016/j.lanepe.2025.101502
Barnaby Roberts , James Riley , Thomas J. Evans , Richard Knight , Jean Manson , Graham Medley , Manisha Upadhyay , Katy Sinka , Simon Mead
Background
Variant Creutzfeldt–Jakob disease (vCJD) is a fatal prion disorder linked to dietary exposure to bovine spongiform encephalopathy (BSE). The epidemic peaked in the early 2000s, and no new cases have been reported in the UK since 2016. However, uncertainties remain regarding potential future cases, particularly in individuals with non-MM prion protein gene codon 129 genotypes, and possible secondary transmission via blood transfusion. We aimed to update risk estimates with recent data, informed by a probabilistic modelling approach.
Methods
We developed a cohort-based probabilistic model for variant CJD incidence incorporating genotype-specific attack rates and incubation periods, accounting for competing mortality risks. Model parameters were calibrated using historical case data and life-table analyses. We explored multiple scenarios, including sensitivity analyses with alternative incubation period distributions and potential missed diagnoses. Secondary transmission risk was assessed using historical transfusion-linked cases and epidemiological data.
Findings
In the base-case scenario, our model estimates a 48% probability that no further vCJD cases will occur, with a mean forecast of 2.7 additional cases. Allowing for missed past cases, estimates increased to a mean of 3.0 cases (one missed case) and 4.9 cases (four missed cases). Sensitivity analysis using a Cauchy incubation period distribution rather than a log-normal distribution increased estimates to 6.6, 9.4, and 17.9 cases, respectively. A plausible worse-case scenario, assuming very long incubation times and higher susceptibility in non-MM individuals, projected up to 65 cases of vCJD over coming decades, peaking in the 2030s. Secondary transmission risk remains negligible given transfusion safety measures, including leukodepletion since 1999.
Interpretation
Our findings suggest that vCJD is unlikely to re-emerge at significant levels. However, ongoing case ascertainment and scrutiny remains critical due to uncertainties in non-MM incubation and potentially, the emergence of previously unrecognised prion strains. Continued neuropathological case investigation, maintenance of core blood safety policies, and periodic risk reassessments are essential to ensure public health preparedness and avoid unnecessary restrictions.
Funding
No specific funding other than salaries of the authors.
{"title":"Estimating future variant Creutzfeldt-Jakob disease cases in the UK: a cohort-based probabilistic model","authors":"Barnaby Roberts , James Riley , Thomas J. Evans , Richard Knight , Jean Manson , Graham Medley , Manisha Upadhyay , Katy Sinka , Simon Mead","doi":"10.1016/j.lanepe.2025.101502","DOIUrl":"10.1016/j.lanepe.2025.101502","url":null,"abstract":"<div><h3>Background</h3><div>Variant Creutzfeldt–Jakob disease (vCJD) is a fatal prion disorder linked to dietary exposure to bovine spongiform encephalopathy (BSE). The epidemic peaked in the early 2000s, and no new cases have been reported in the UK since 2016. However, uncertainties remain regarding potential future cases, particularly in individuals with non-MM prion protein gene codon 129 genotypes, and possible secondary transmission via blood transfusion. We aimed to update risk estimates with recent data, informed by a probabilistic modelling approach.</div></div><div><h3>Methods</h3><div>We developed a cohort-based probabilistic model for variant CJD incidence incorporating genotype-specific attack rates and incubation periods, accounting for competing mortality risks. Model parameters were calibrated using historical case data and life-table analyses. We explored multiple scenarios, including sensitivity analyses with alternative incubation period distributions and potential missed diagnoses. Secondary transmission risk was assessed using historical transfusion-linked cases and epidemiological data.</div></div><div><h3>Findings</h3><div>In the base-case scenario, our model estimates a 48% probability that no further vCJD cases will occur, with a mean forecast of 2.7 additional cases. Allowing for missed past cases, estimates increased to a mean of 3.0 cases (one missed case) and 4.9 cases (four missed cases). Sensitivity analysis using a Cauchy incubation period distribution rather than a log-normal distribution increased estimates to 6.6, 9.4, and 17.9 cases, respectively. A plausible worse-case scenario, assuming very long incubation times and higher susceptibility in non-MM individuals, projected up to 65 cases of vCJD over coming decades, peaking in the 2030s. Secondary transmission risk remains negligible given transfusion safety measures, including leukodepletion since 1999.</div></div><div><h3>Interpretation</h3><div>Our findings suggest that vCJD is unlikely to re-emerge at significant levels. However, ongoing case ascertainment and scrutiny remains critical due to uncertainties in non-MM incubation and potentially, the emergence of previously unrecognised prion strains. Continued neuropathological case investigation, maintenance of core blood safety policies, and periodic risk reassessments are essential to ensure public health preparedness and avoid unnecessary restrictions.</div></div><div><h3>Funding</h3><div>No specific funding other than salaries of the authors.</div></div>","PeriodicalId":53223,"journal":{"name":"Lancet Regional Health-Europe","volume":"59 ","pages":"Article 101502"},"PeriodicalIF":13.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145693685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01DOI: 10.1016/j.lanepe.2025.101498
Fiona F. Stanaway , Saman Khalatbari-Soltani , Lin Zhu , Thulashigan Sreeharan , Naomi Noguchi , Anupa Pathak , Erin Mathieu , Raj Bhopal
<div><h3>Background</h3><div>Ethnic inequalities in health outcomes are a persistent concern in the United Kingdom (UK) and internationally. In this systematic review and meta-analysis, we aimed to quantify ethnic differences in all-cause mortality across the UK and explore the potential modifying roles of socioeconomic position (SEP) and country of birth.</div></div><div><h3>Methods</h3><div>We searched Medline, Embase, Scopus, and Web of Science from inception to April 20, 2024, and identified grey literature via EThOS, ProQuest, Google, and data-sharing platforms. Eligible studies reported all-cause mortality by ethnicity or other commonly used measures such as country of birth or person or parents and surname in UK populations. Two reviewers independently conducted screening, data extraction, and risk of bias assessment using the ROBINS-E tool. Certainty of evidence was evaluated using GRADE. The review was registered with PROSPERO (CRD42019146143).</div></div><div><h3>Findings</h3><div>Of 7672 records screened, 32 studies met inclusion criteria, supplemented by unpublished data from three cohort studies. Age-adjusted all-cause mortality was consistently lower among females of Bangladeshi (Relative Risk = 0.80, 95% CI 0.67–0.95), Indian (0.78, 0.68–0.88), Pakistani (0.85, 0.79–0.91), Black Caribbean (0.83, 0.81–0.85), Chinese (0.64, 0.61–0.69), and Mixed ethnicity (0.94, 0.90–0.98), and among males of Bangladeshi (0.89, 0.86–0.93), Indian (0.78, 0.69–0.88), Pakistani (0.76, 0.69–0.83), Black Caribbean (0.89, 0.85–0.93), and Chinese ethnicity (0.66, 0.50–0.87)), compared with White British individuals. In contrast, White Irish (1.20, 1.06–1.34) and White Scottish males (1.19, 1.11–1.27), and White Scottish females (1.18, 1.08–1.29), had higher mortality than other White British. Evidence on the role of SEP was inconclusive due to methodological heterogeneity. Evidence on the role of country of birth was also limited with wide and overlapping confidence intervals around the results stratified by country of birth (UK-born vs non-UK-born) in each ethnic group. However, the UK-born Black Caribbean population had higher relative mortality rate compared to the UK-born White British population (1.49; 0.98–2.28), although this did not quite reach statistical significance.</div></div><div><h3>Interpretation</h3><div>Inequalities in mortality by ethnic group were consistent and substantial. The contribution of SEP to observed inequalities is complex and the quality of evidence is impacted by methodological heterogeneity. However, SEP disadvantage is unlikely to explain the lower relative mortality of non-white groups. The potential for inequalities within ethnic groups by country of birth has important policy implications, as this suggests the need to tailor public health strategies within ethnic groups by country of birth. However, more evidence is needed for most ethnic groups. As a result, we call for greater reporting of both ethnicity and country o
在健康结果方面的种族不平等是联合王国和国际上一个长期关注的问题。在这项系统回顾和荟萃分析中,我们旨在量化英国全因死亡率的种族差异,并探讨社会经济地位(SEP)和出生国家的潜在调节作用。方法检索Medline、Embase、Scopus和Web of Science自成立以来至2024年4月20日,通过EThOS、ProQuest、谷歌和数据共享平台识别灰色文献。符合条件的研究报告了英国人口中按种族或其他常用措施(如出生国家或个人或父母和姓氏)划分的全因死亡率。两位审稿人使用ROBINS-E工具独立进行筛选、数据提取和偏倚风险评估。使用GRADE评价证据的确定性。该审查已在PROSPERO注册(CRD42019146143)。在筛选的7672条记录中,32项研究符合纳入标准,另外还有来自3项队列研究的未发表数据。孟加拉国女性(相对危险度= 0.80,95% CI 0.67-0.95)、印度(0.78,0.68-0.88)、巴基斯坦(0.85,0.79-0.91)、加勒比黑人(0.83,0.81-0.85)、中国(0.64,0.61-0.69)和混合种族(0.94,0.90-0.98),以及孟加拉国男性(0.89,0.86-0.93)、印度(0.78,0.69-0.88)、巴基斯坦(0.76,0.69-0.83)、加勒比黑人(0.89,0.85 - 0.93)和中国(0.66,0.50-0.87))的年龄调整全因死亡率均较低。与英国白人相比相比之下,爱尔兰白人(1.20,1.06-1.34)、苏格兰白人男性(1.19,1.11-1.27)和苏格兰白人女性(1.18,1.08-1.29)的死亡率高于其他英国白人。由于方法的异质性,关于SEP作用的证据尚无定论。关于出生国作用的证据也很有限,在每个种族群体中,按出生国(英国出生与非英国出生)分层的结果周围有很宽且重叠的置信区间。然而,与英国出生的英国白人人口相比,英国出生的加勒比黑人人口的相对死亡率更高(1.49;0.98-2.28),尽管这并没有达到统计学意义。不同种族死亡率的不平等是一致的和实质性的。SEP对观察到的不平等的贡献是复杂的,证据的质量受到方法异质性的影响。然而,SEP劣势不太可能解释非白人群体的相对死亡率较低。族裔群体内部按出生国划分的不平等可能具有重要的政策意义,因为这表明需要按出生国划分族裔群体内部的公共卫生战略。然而,需要更多的证据来证明大多数种族。因此,我们呼吁在英国的种族不平等研究中更多地报道种族和出生国家。澳大利亚研究理事会人口老龄化研究卓越中心(资助编号:CE170100PRO005)。
{"title":"Inequalities in all-cause mortality by ethnicity in the United Kingdom: a systematic review and meta-analysis","authors":"Fiona F. Stanaway , Saman Khalatbari-Soltani , Lin Zhu , Thulashigan Sreeharan , Naomi Noguchi , Anupa Pathak , Erin Mathieu , Raj Bhopal","doi":"10.1016/j.lanepe.2025.101498","DOIUrl":"10.1016/j.lanepe.2025.101498","url":null,"abstract":"<div><h3>Background</h3><div>Ethnic inequalities in health outcomes are a persistent concern in the United Kingdom (UK) and internationally. In this systematic review and meta-analysis, we aimed to quantify ethnic differences in all-cause mortality across the UK and explore the potential modifying roles of socioeconomic position (SEP) and country of birth.</div></div><div><h3>Methods</h3><div>We searched Medline, Embase, Scopus, and Web of Science from inception to April 20, 2024, and identified grey literature via EThOS, ProQuest, Google, and data-sharing platforms. Eligible studies reported all-cause mortality by ethnicity or other commonly used measures such as country of birth or person or parents and surname in UK populations. Two reviewers independently conducted screening, data extraction, and risk of bias assessment using the ROBINS-E tool. Certainty of evidence was evaluated using GRADE. The review was registered with PROSPERO (CRD42019146143).</div></div><div><h3>Findings</h3><div>Of 7672 records screened, 32 studies met inclusion criteria, supplemented by unpublished data from three cohort studies. Age-adjusted all-cause mortality was consistently lower among females of Bangladeshi (Relative Risk = 0.80, 95% CI 0.67–0.95), Indian (0.78, 0.68–0.88), Pakistani (0.85, 0.79–0.91), Black Caribbean (0.83, 0.81–0.85), Chinese (0.64, 0.61–0.69), and Mixed ethnicity (0.94, 0.90–0.98), and among males of Bangladeshi (0.89, 0.86–0.93), Indian (0.78, 0.69–0.88), Pakistani (0.76, 0.69–0.83), Black Caribbean (0.89, 0.85–0.93), and Chinese ethnicity (0.66, 0.50–0.87)), compared with White British individuals. In contrast, White Irish (1.20, 1.06–1.34) and White Scottish males (1.19, 1.11–1.27), and White Scottish females (1.18, 1.08–1.29), had higher mortality than other White British. Evidence on the role of SEP was inconclusive due to methodological heterogeneity. Evidence on the role of country of birth was also limited with wide and overlapping confidence intervals around the results stratified by country of birth (UK-born vs non-UK-born) in each ethnic group. However, the UK-born Black Caribbean population had higher relative mortality rate compared to the UK-born White British population (1.49; 0.98–2.28), although this did not quite reach statistical significance.</div></div><div><h3>Interpretation</h3><div>Inequalities in mortality by ethnic group were consistent and substantial. The contribution of SEP to observed inequalities is complex and the quality of evidence is impacted by methodological heterogeneity. However, SEP disadvantage is unlikely to explain the lower relative mortality of non-white groups. The potential for inequalities within ethnic groups by country of birth has important policy implications, as this suggests the need to tailor public health strategies within ethnic groups by country of birth. However, more evidence is needed for most ethnic groups. As a result, we call for greater reporting of both ethnicity and country o","PeriodicalId":53223,"journal":{"name":"Lancet Regional Health-Europe","volume":"59 ","pages":"Article 101498"},"PeriodicalIF":13.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145693680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}