Suchergebnisse

Background Despite an overall reduction in suicide, educational disparities in suicide have not decreased over the last decade. The mechanisms behind educational disparities in suicide, however, remain unclear: low educational status may increase the risk of suicide ("causation") or low educational status and suicide may share confounders. This paper assesses whether educational disparities in suicide (EDS) are more likely to be due to causation. Method The DEMETRIQ study collected and harmonized register-based data on mortality follow-up from forty population censuses from twelve European populations. More than 102,000 suicides were registered over 392 million person-years. Three analyses were carried out. First, we applied an instrumental variable approach that exploits changes in the legislation on compulsory educational age to instrument educational status. Second, we analyzed EDS by age under the hypothesis that increasing EDS over the life cycle supports causation. Finally, we compared EDS in men and women under the assumption that greater EDS in women would support causation. Findings The instrumental variable analysis showed no evidence for causation between higher education and suicide, for men or women. The life-cycle analysis showed that the decrease of educational inequalities in suicide between the baseline 1991 period and the 2001 follow-up period was more pronounced and statistically significant in the first three younger age groups. The gender analysis indicated that EDS were systematic and greater in men than in women: the rate ratio of suicide for men with low level of education (RR = 2.51; 95% CI:2.44–2.58) was higher than the rate ratio in women (RR = 1.32; 95CI%:1.26–1.38). Interpretation Overall, there was little support for the causation hypothesis, suggesting that the association between education and suicide is confounded. Educational inequalities in suicide should be addressed in early life by early targeting of groups who struggle to complete their education and display higher risk of mental disorder or of mental health vulnerabilities. ; publishersversion ; published

Reuse of record except for individual research requires license from Congressional Information Service, Inc. ; "Printed for the use of the Committee on Veterans' Affairs." ; "October 1978." ; At head of title: 95th Congress, 2d session. House committee print no. 169. ; CIS Microfiche Accession Numbers: CIS 78 H762-20 ; Microfiche. ; Mode of access: Internet.

Copyright © 2021 Suri, Bulte, Chiesa, Ebmeier, Jezzard, Rieger, Pitt, Griffanti, Okell, Craig, Chappell, Blockley, Kivimäki, Singh-Manoux, Khir, Hughes, Deanfield, Jensen, Green, Sigutova, Jansen, Zsoldos and Mackay. Background: It is well-established that what is good for the heart is good for the brain. Vascular factors such as hypertension, diabetes, and high cholesterol, and genetic factors such as the apolipoprotein E4 allele increase the risk of developing both cardiovascular disease and dementia. However, the mechanisms underlying the heart–brain association remain unclear. Recent evidence suggests that impairments in vascular phenotypes and cerebrovascular reactivity (CVR) may play an important role in cognitive decline. The Heart and Brain Study combines state-of-the-art vascular ultrasound, cerebrovascular magnetic resonance imaging (MRI) and cognitive testing in participants of the long-running Whitehall II Imaging cohort to examine these processes together. This paper describes the study protocol, data pre-processing and overarching objectives. Methods and Design: The 775 participants of the Whitehall II Imaging cohort, aged 65 years or older in 2019, have received clinical and vascular risk assessments at 5-year-intervals since 1985, as well as a 3T brain MRI scan and neuropsychological tests between 2012 and 2016 (Whitehall II Wave MRI-1). Approximately 25% of this cohort are selected for the Heart and Brain Study, which involves a single testing session at the University of Oxford (Wave MRI-2). Between 2019 and 2023, participants will undergo ultrasound scans of the ascending aorta and common carotid arteries, measures of central and peripheral blood pressure, and 3T MRI scans to measure CVR in response to 5% carbon dioxide in air, vessel-selective cerebral blood flow (CBF), and cerebrovascular lesions. The structural and diffusion MRI scans and neuropsychological battery conducted at Wave MRI-1 will also be repeated. Using this extensive life-course data, the Heart and Brain Study will examine how 30-year trajectories of vascular risk throughout midlife (40–70 years) affect vascular phenotypes, cerebrovascular health, longitudinal brain atrophy and cognitive decline at older ages. Discussion: The study will generate one of the most comprehensive datasets to examine the longitudinal determinants of the heart–brain association. It will evaluate novel physiological processes in order to describe the optimal window for managing vascular risk in order to delay cognitive decline. Ultimately, the Heart and Brain Study will inform strategies to identify at-risk individuals for targeted interventions to prevent or delay dementia. ; The Heart and Brain Study is funded by a UK Alzheimer's Society Research Fellowship to SS (Grant Reference: 441). This study was also supported by the Academy of Medical Sciences/the Wellcome Trust/the Government Department of Business, Energy and Industrial Strategy/the British Heart Foundation/Diabetes UK Springboard Award to SS (SBF006\1078). The pilot study was funded by the Oxford Alzheimer's Research UK Thames Valley Network Pilot Project Grant to SS. Work on this study receives institutional support from the UK National Institute of Health Research (NIHR) Oxford Health Biomedical Research Centre (BRC) and the Wellcome Centre for Integrative Neuroimaging (WIN). The WIN was supported by core funding from the Wellcome Trust (203139/Z/16/Z). The Whitehall II study was supported by the British Heart Foundation (RG/16/11/32334), UK Medical Research Council (MR/K013351/1 and MR/R024227/1 to MK), the US National Institute on Aging (RF1AG062553 and R01AG056477 to MK and AS-M), "Adult Determinants of Late Life Depression, Cognitive Decline and Physical Functioning – The Whitehall II Ageing Study" (MR/K013351/1; PI: MK), and "The Whitehall II Study: A Core Resource for Ageing Research" (MR/R024227/1; PI: MK). The Whitehall II Imaging Sub-study was supported by the UK Medical Research Council (MRC) grants "Predicting MRI abnormalities with longitudinal data of the Whitehall II Sub-study" (G1001354; PI KE; ClinicalTrials.gov Identifier: NCT03335696). The authors report the following additional funding: STC: BHF (PG/18/45/33814 and PG/19/31/34343), KE and EZ (HDH Wills 1965 Charitable Trust (1117747), and the European Commission (Horizon 2020 grant "Lifebrain", 732592), MK [UK MRC (MR/K013351/1, MR/R024227/1, and MR/S011676/1), National Institute on Aging (NIH), US (R01AG056477), NordForsk (75021), Academy of Finland (311492), Helsinki Institute of Life Science Fellowship (H970)], LG [Monument Trust Discovery Award from Parkinson's UK (J-1403), the MRC Dementias Platform UK (MR/L023784/2) and the NIHR Oxford Health BRC], AS-M [NIH (R01AG056477 and R01AG062553)], MAC and MC (Engineering and Physical Sciences Research Council UK (EP/P012361/1), MJ [grants from the Disciplinary Honours program of the Radboud University and Alzheimer Nederland (WE.04-2019-64)]. TO was supported by a Sir Henry Dale Fellowship jointly funded by the Wellcome Trust and the Royal Society (grant number 220204/Z/20/Z). NB was supported by an Early Career Fellowship from the Engineering and Physical Sciences Research Council (grant number EP/K025716/1). PJ was supported by the NIHR Oxford Biomedical Research Centre. AH receives support from the British Heart Foundation, the Economic and Social Research Council (ESRC), the Horizon 2020 Framework Programme of the European Union, the National Institute on Aging, the National Institute for Health Research University College London Hospitals Biomedical Research Centre, the UK Medical Research Council and works in a unit that receives support from the UK Medical Research Council.

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