Evidencing the gap between health expectancy and life expectancy for ethnic groups in Scotland

Background Recent evidence has shown that ethnic minorities live longer than the majority population in Scotland. This mortality advantage in ethnic minorities is not unique to Scotland. However, whether morbidity patterns by ethnicity align with mortality patterns by ethnicity is unknown. Thus, this study explores ethnic differences in health expectancies (HE) in Scotland and contrasts HE with life expectancy (LE) findings. Methods The Scottish Health and Ethnicity Linkage study anonymously links the Scottish Census 2001 for 4.6 million people to mortality records. The Scottish Census 2001 collected two measures of self-assessed health, self-declared ethnicity, age, and sex. Utilising the life tables used to calculate life expectancy by ethnicity and sex in Scotland, the Sullivan method was employed to calculate two measures of health expectancy (healthy life expectancy and disability-free life expectancy) by ethnicity and sex. 95% confidence intervals were calculated to detect significant differences compared to the majority White Scottish population, taken as reference. Results Longer health expectancies were found in males and females of Other White British, Other White, and Chinese origins as well as in Indian males compared to White Scottish populations. Any Mixed Background and Pakistani populations had the shortest healthy life expectancies. Patterns of health expectancy by ethnicity mostly aligned with patterns of life expectancy by ethnicity with the clear exception of the Pakistani population who showed among the longest life expectancies with the shortest health expectancies. Contrasting HE with LE findings, the number of years in an unhealthy state was greater in females than in males for each ethnic group. In relation to ethnicity, Pakistani and Indian populations had the highest number of years in an unhealthy state in Scotland. Pakistani females showed the strong-est disadvantage in this respect. Conclusion Pakistani populations had the shortest health expectancies contrasting with the longest life expectancies in Scotland. Future research should aim to understand why such a discrepancy occurs while policy makers ensure that fair and adapt-ed care is provided to offer better quality of life for the most vulnerable.Publisher PDFPeer reviewe

Ethnic variations in upper gastrointestinal hospitalizations and deaths:the Scottish Health and Ethnicity Linkage Study

BACKGROUND: Upper gastrointestinal (GI) diseases are common, but there is a paucity of data describing variations by ethnic group and so a lack of understanding of potential health inequalities. We studied the incidence of specific upper GI hospitalization and death by ethnicity in Scotland.METHODS: Using the Scottish Health and Ethnicity Linkage Study, linking NHS hospitalizations and mortality to the Scottish Census 2001, we explored ethnic differences in incidence (2001-10) of oesophagitis, peptic ulcer disease, gallstone disease and pancreatitis. Relative Risks (RRs) and 95% confidence intervals were calculated using Poisson regression, multiplied by 100, stratified by sex and adjusted for age, country of birth (COB) and socio-economic position. The White Scottish population (100) was the reference population.RESULTS: Ethnic variations varied by outcome and sex, e.g. adjusted RRs (95% confidence intervals) for oesophagitis were comparatively higher in Bangladeshi women (209; 124-352) and lower in Chinese men (65; 51-84) and women (69; 55-88). For peptic ulcer disease, RRs were higher in Chinese men (171; 131-223). Pakistani women had higher RRs for gallstone disease (129; 112-148) and pancreatitis (147; 109-199). The risks of upper GI diseases were lower in Other White British and Other White [e.g. for peptic ulcer disease in men, respectively (74; 64-85) and (81; 69-94)].CONCLUSION: Risks of common upper GI diseases were comparatively lower in most White ethnic groups in Scotland. In non-White groups, however, risk varied by disease and ethnic group. These results require consideration in health policy, service planning and future research.</p

Impact of vaccination on the association of COVID-19 with cardiovascular diseases:An OpenSAFELY cohort study

Infection with SARS-CoV-2 is associated with an increased risk of arterial and venous thrombotic events, but the implications of vaccination for this increased risk are uncertain. With the approval of NHS England, we quantified associations between COVID-19 diagnosis and cardiovascular diseases in different vaccination and variant eras using linked electronic health records for ~40% of the English population. We defined a 'pre-vaccination' cohort (18,210,937 people) in the wild-type/Alpha variant eras (January 2020-June 2021), and 'vaccinated' and 'unvaccinated' cohorts (13,572,399 and 3,161,485 people respectively) in the Delta variant era (June-December 2021). We showed that the incidence of each arterial thrombotic, venous thrombotic and other cardiovascular outcomes was substantially elevated during weeks 1-4 after COVID-19, compared with before or without COVID-19, but less markedly elevated in time periods beyond week 4. Hazard ratios were higher after hospitalised than non-hospitalised COVID-19 and higher in the pre-vaccination and unvaccinated cohorts than the vaccinated cohort. COVID-19 vaccination reduces the risk of cardiovascular events after COVID-19 infection. People who had COVID-19 before or without being vaccinated are at higher risk of cardiovascular events for at least two years.</p

Impact of vaccination on the association of COVID-19 with cardiovascular diseases: An OpenSAFELY cohort study

Acknowledgements: This study was supported by the COVID-19 Longitudinal Health and Wellbeing National Core Study, funded by the UKRI Medical Research Council (MC_PC_20059); the COVID-19 Data and Connectivity National Core Study, funded by the UKRI Medical Research Council; and by the CONVALESCENCE long COVID study, funded by the UK National Institute for Health and Care Research (COVID-LT-009). This work was also supported by Health Data Research UK, which is funded by the UK Medical Research Council, Engineering and Physical Sciences Research Council, Economic and Social Research Council, Department of Health and Social Care (England), Chief Scientist Office of the Scottish Government Health and Social Care Directorates, Health and Social Care Research and Development Division (Welsh Government), Public Health Agency (Northern Ireland), British Heart Foundation and Wellcome. GC, SI and AWo are supported by the British Heart Foundation (RG/13/13/30194; RG/18/13/33946), BHF Cambridge Centre of Research Excellence (RE/18/1/34212) and NIHR Cambridge Biomedical Research Centre (BRC-1215-20014; NIHR203312). RK, GDS, and VW are supported by the Medical Research Council Integrative Epidemiology Unit at the University of Bristol [MC_UU_00011/1; MC_UU_00011/4]. RK and JACS are supported by the NIHR Bristol Biomedical Research Centre and by Health Data Research UK South-West. YW was supported by a UKRI MRC Fellowship (MC/W021358/1) and received funding from the UKRI EPSRC Impact Acceleration Account (EP/X525789/1). SI and AWo were funded by a British Heart Foundation–Turing Cardiovascular Data Science Award (BCDSA/100005). SI is funded by the International Alliance for Cancer Early Detection, a partnership among Cancer Research UK C18081/A31373, Canary Center at Stanford University, the University of Cambridge, OHSU Knight Cancer Institute, University College London, and the University of Manchester. RK and JM were supported by NIHR ARC West. RD and JACS were supported by Health Data Research UK. WW is supported by the Chief Scientist’s Office (CAF/01/17). AWo and WW are supported by the Stroke Association (SA CV 20/100018). AWo is part of the BigData@Heart Consortium, funded by the Innovative Medicines Initiative-2 Joint Undertaking under grant agreement No 116074. The views expressed are those of the authors and not necessarily those of the NIHR or the Department of Health and Social Care. We are very grateful for all the support received from the OpenSAFELY team and the TPP Technical Operations team throughout this work, and for generous assistance from the information governance and database teams at NHS England and the NHS England Transformation Directorate. We thank the CONVALESCENCE Study Long Covid PPIE group for their input and for sharing their experiences and expertise throughout the duration of the project.Funder: UKRI Medical Research Council (MC_PC_20059) UK National Institute for Health and Care Research (COVID-LT-009)AbstractInfection with SARS-CoV-2 is associated with an increased risk of arterial and venous thrombotic events, but the implications of vaccination for this increased risk are uncertain. With the approval of NHS England, we quantified associations between COVID-19 diagnosis and cardiovascular diseases in different vaccination and variant eras using linked electronic health records for ~40% of the English population. We defined a ‘pre-vaccination’ cohort (18,210,937 people) in the wild-type/Alpha variant eras (January 2020-June 2021), and ‘vaccinated’ and ‘unvaccinated’ cohorts (13,572,399 and 3,161,485 people respectively) in the Delta variant era (June-December 2021). We showed that the incidence of each arterial thrombotic, venous thrombotic and other cardiovascular outcomes was substantially elevated during weeks 1-4 after COVID-19, compared with before or without COVID-19, but less markedly elevated in time periods beyond week 4. Hazard ratios were higher after hospitalised than non-hospitalised COVID-19 and higher in the pre-vaccination and unvaccinated cohorts than the vaccinated cohort. COVID-19 vaccination reduces the risk of cardiovascular events after COVID-19 infection. People who had COVID-19 before or without being vaccinated are at higher risk of cardiovascular events for at least two years.</jats:p

Impact of vaccination on the association of COVID-19 with cardiovascular diseases:an OpenSAFELY cohort study

Infection with SARS-CoV-2 is associated with an increased risk of arterial andvenous thrombotic events, but the implications of vaccination for this increasedrisk are uncertain. With the approval of NHS England, we quantified associationsbetween COVID-19 diagnosis and cardiovascular diseases in different vaccination and variant eras using linked electronic health records for ~40% of theEnglish population. We defined a ‘pre-vaccination’ cohort (18,210,937 people) inthe wild-type/Alpha variant eras (January 2020-June 2021), and ‘vaccinated’ and‘unvaccinated’ cohorts (13,572,399 and 3,161,485 people respectively) in theDelta variant era (June-December 2021). We showed that the incidence of eacharterial thrombotic, venous thrombotic and other cardiovascular outcomes wassubstantially elevated during weeks 1-4 after COVID-19, compared with beforeor without COVID-19, but less markedly elevated in time periods beyond week 4.Hazard ratios were higher after hospitalised than non-hospitalised COVID-19and higher in the pre-vaccination and unvaccinated cohorts than the vaccinatedcohort. COVID-19 vaccination reduces the risk of cardiovascular events afterCOVID-19 infection. People who had COVID-19 before or without being vaccinated are at higher risk of cardiovascular events for at least two year

Impact of vaccination on the association of COVID-19 with cardiovascular diseases: An OpenSAFELY cohort study.

Infection with SARS-CoV-2 is associated with an increased risk of arterial and venous thrombotic events, but the implications of vaccination for this increased risk are uncertain. With the approval of NHS England, we quantified associations between COVID-19 diagnosis and cardiovascular diseases in different vaccination and variant eras using linked electronic health records for ~40% of the English population. We defined a 'pre-vaccination' cohort (18,210,937 people) in the wild-type/Alpha variant eras (January 2020-June 2021), and 'vaccinated' and 'unvaccinated' cohorts (13,572,399 and 3,161,485 people respectively) in the Delta variant era (June-December 2021). We showed that the incidence of each arterial thrombotic, venous thrombotic and other cardiovascular outcomes was substantially elevated during weeks 1-4 after COVID-19, compared with before or without COVID-19, but less markedly elevated in time periods beyond week 4. Hazard ratios were higher after hospitalised than non-hospitalised COVID-19 and higher in the pre-vaccination and unvaccinated cohorts than the vaccinated cohort. COVID-19 vaccination reduces the risk of cardiovascular events after COVID-19 infection. People who had COVID-19 before or without being vaccinated are at higher risk of cardiovascular events for at least two years