scholarly journals A socially patterned Biological Health Score and mortality in Understanding Society and UKBiobank

2019 ◽  
Vol 29 (Supplement_4) ◽  
Author(s):  
M Chadeau-Hyam ◽  
M Karimi ◽  
R Castagné ◽  
B Bodinier ◽  
C Delpierre ◽  
...  

Abstract Background It now established that social factors impact the quality of ageing, through the lifecourse stimulation/dysregulation of key physiological systems. Composite scores such as allostatic load, focusing on the response to stress, can be used to measure individual physiological wear-and-tear. Methods Using data from the Understanding Society study, a cross-sectional panel study including 9,088 participants representative of the UK population, we defined a synthetic biological health score (BHS) capturing the wear-and-tear of four physiological systems (endocrine, inflammatory, cardiovascular, and metabolic systems), and of two key organs (liver and kidney). We used 16 established blood-derived biomarkers of these systems to calculate the BHS and explored the relative contribution of socio-economic position to the BHS and its main components across age groups. Using data from UK biobank, including over 400,000 UK participants in whom similar biomarkers have been assayed in blood, we sought validation of our results and investigated the role of the BHS on all-cause and disease specific mortality, and disease incidence. Results We identified a systematic decreasing education-related gradient of the BHS (p < 0·001) leading to lower biological risk in participants with higher educational attainment. Education-related differences in the BHS were detected early in life, and were not attributable to lifestyle and behavioural factors. Analyses of the UK biobank data validated these findings and also showed that the BHS contributed in turn, irrespective of established health risk factors, to all-cause and disease specific mortality. Interpretation Our findings highlight the social-to-biological processes ultimately leading to health inequalities, and suggest that such disparities can already be detected in the 20-40 year age group.

2013 ◽  
Vol 31 (6_suppl) ◽  
pp. 67-67 ◽  
Author(s):  
Michael K. Brawer ◽  
Matthew R. Cooperberg ◽  
Stephen J. Freedland ◽  
Gregory P. Swanson ◽  
Steven Stone ◽  
...  

67 Background: Prostate cancer outcomes are variable and difficult to predict. Improved tools are needed to appropriately match treatment to a patient’s risk of progression. We developed and validated a multivariate model to predict disease−specific mortality (DSM) by combining clinical parameters (CAPRA score) with a score based on measuring the expression level of cell cycle progression (CCP) genes. Methods: A multivariate prediction model was trained using patients from 4 retrospective cohorts with median clinical follow up of 7.6 years. We used 200 men from the UK diagnosed after TURP, 353 from Scott & White and 388 from UCSF treated with radical prostatectomy, and 118 men from Durham VA treated with EBRT. CCP score was derived from fixed tumor tissue (biopsy or surgical resection). Outcome was either time from treatment to biochemical recurrence (US cohorts) or time from diagnosis to disease specific mortality (UK cohort). The model was validated for predicting time from diagnosis to DSM in 180 men from the UK diagnosed by needle biopsy with clinically localized prostate cancer and managed conservatively (mean/median CAPRA score = 6). Results: A model combining CAPRA with CCP score was fit in the training set by a Cox Proportional Hazards analysis stratified by cohort. The Combined score was defined as 0.39*CAPRA+0.57*CCP score. There were no significant interactions between cohort and CAPRA or CCP score. This suggests that both CCP score and CAPRA confer similar prognostic information regardless of cohort composition, treatment, or specific outcome. In the validation cohort the Combined score was highly prognostic (HR= 2.27, 95%CI: (1.63, 3.16), p = 1.2 x 10−7). By likelihood ratio testing, the Combined score was a better predictor of DSM than CAPRA alone (p = 0.0028). The c−index of the Combined score was 0.75, which was an improvement over CAPRA (c−index 0.71). Conclusions: This multivariate model predicts DSM in a conservatively treated cohort. The model provides prognostic information beyond clinical variables, and can be used to help differentiate aggressive from indolent cancer at diagnosis.


BMC Cancer ◽  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Jun Kasuga ◽  
Takashi Kawahara ◽  
Daiji Takamoto ◽  
Sachi Fukui ◽  
Takashi Tokita ◽  
...  

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1287
Author(s):  
Inken Behrendt ◽  
Gerrit Eichner ◽  
Mathias Fasshauer

Prospective studies and randomized controlled trials elucidating the impact of antioxidants supplementation on mortality risk are inconclusive. The present analysis determined association between regular antioxidants use and all-cause (primary objective), as well as cause-specific, mortality in 345,626 participants of the UK Biobank cohort using Cox proportional hazard models. All models were adjusted for confounders and multiple testing. Antioxidants users were defined as participants who indicated to regularly use at least one of the following: multivitamins, vitamin C, vitamin E, selenium, and zinc. Median age of antioxidants users (n = 101,159) and non-users (n = 244,467) at baseline was 57 years. During 3.9 million person-years and a median follow-up of 11.5 years, 19,491 deaths occurred. Antioxidants use was not significantly associated with all-cause, cancer, and non-cancer mortality including several cancer and non-cancer subtypes. Interestingly, mortality risk from respiratory disease was significantly 21% lower among antioxidants users as compared to non-users (hazard ratio: 0.79; 95% confidence interval: 0.67, 0.92). In conclusion, the present study findings do not support recommendations for antioxidants supplementation to prevent all-cause, cancer, or non-cancer mortality on a population level. The significant inverse association between antioxidants use and respiratory disease mortality needs further study.


2019 ◽  
Vol 101 (7) ◽  
pp. 441-452 ◽  
Author(s):  
J On ◽  
J Shim ◽  
EH Aly

Introduction The ‘watch and wait’ approach has recently emerged as an alternative approach for managing patients with complete clinical response in rectal cancer. However, less is understood whether the intervention is associated with a favourable outcome among patients who require salvage therapy following local recurrence. Materials and methods A comprehensive systematic search was performed using EMBASE, PubMed, MEDLINE, Journals@Ovid as well as hand searches; published between 2004 and 2018, to identify studies where outcomes of patients undergoing watch and wait were compared with conventional surgery. Study quality was assessed using the Newcastle–Ottawa assessment scale. The main outcome was relative risks for overall and disease specific mortality in salvage therapy. Results Nine eligible studies were included in the meta-analysis. Of 248 patients who followed the watch and wait strategy, 10.5% had salvage therapy for recurrent disease. No statistical heterogeneity was found in the results. The relative risk of overall mortality in the salvage therapy group was 2.42 (95% confidence interval 0.96–6.13) compared with the group who had conventional surgery, but this was not statistically significant (P > 0.05). The relative risk of disease specific mortality in salvage therapy was 2.63 (95% confidence interval 0.81–8.53). Conclusion Our findings demonstrated that there was no significant difference in overall and disease specific mortality in patients who had salvage treatment following recurrence of disease in the watch and wait group compared with the standard treatment group. However, future research into the oncological safety of salvage treatment is needed.


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