scholarly journals Association of Antioxidants Use with All-Cause and Cause-Specific Mortality: A Prospective Study of the UK Biobank

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1287
Author(s):  
Inken Behrendt ◽  
Gerrit Eichner ◽  
Mathias Fasshauer
Keyword(s):  
Respiratory Disease ◽  
Mortality Risk ◽  
Cancer Mortality ◽  
Primary Objective ◽  
Inverse Association ◽  
Uk Biobank ◽  
Cancer Subtypes ◽  
Specific Mortality ◽  
The Uk ◽  
The Impact

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.

Vitamin D Status and Risk of All-Cause and Cause-Specific Mortality in a Large Cohort: Results From the UK Biobank

2020 ◽  
Vol 105 (10) ◽  
pp. e3606-e3619 ◽  
Author(s):  
Xikang Fan ◽  
Jiayu Wang ◽  
Mingyang Song ◽  
Edward L Giovannucci ◽  
Hongxia Ma ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cancer Mortality ◽  
Lower Risk ◽  
Premature Death ◽  
Inverse Association ◽  
Vitamin D Status ◽  
Uk Biobank ◽  
Hydroxyvitamin D ◽  
Specific Mortality ◽  
The Uk

Abstract Context Although an inverse association between vitamin D status and mortality has been reported in observational studies, the precise association shape and optimal vitamin D status remain undetermined. Objective To investigate the association between vitamin D status and risk of all-cause and cause-specific mortality and estimate optimal serum 25-hydroxyvitamin D [25(OH)D] concentrations. Design Prospective cohort study. Setting UK Biobank. Participants 365 530 participants who had serum 25(OH)D measurements and no history of cardiovascular disease (CVD), cancer, or diabetes at baseline (2006-2010). Main outcome measures All-cause and cause-specific mortality. Results During a median follow-up of 8.9 (interquartile range: 8.3-9.5) years, 10 175 deaths occurred, including 1841 (18.1%) due to CVD and 5737 (56.4%) due to cancer. The multivariate analyses revealed nonlinear inverse associations, with a decrease in mortality risk appearing to level off at 60 nmol/L of 25(OH)D for all-cause and CVD deaths and at 45 nmol/L for cancer deaths. Compared to participants with 25(OH)D concentrations below the cutoffs, those with higher concentrations had a 17% lower risk for all-cause mortality (hazard ratio [HR]: 0.83, 95% confidence interval [CI]: 0.79-0.86), 23% lower risk for CVD mortality (HR: 0.77, 95% CI: 0.68-0.86), and 11% lower risk for cancer mortality (HR: 0.89, 95% CI: 0.84-0.95). Conclusions Higher 25(OH)D concentrations are nonlinearly associated with lower risk of all-cause, CVD, and cancer mortality. The thresholds of 45 to 60 nmol/L might represent an intervention target to reduce the overall risk of premature death, which needs further confirmation in large clinical trials.

scholarly journals Prospective Association of the Portfolio Diet with All-Cause and Cause-Specific Mortality Risk in the Mr. OS and Ms. OS Study

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4360
Author(s):  
Kenneth Lo ◽  
Andrea J. Glenn ◽  
Suey Yeung ◽  
Cyril W. C. Kendall ◽  
John L. Sievenpiper ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Mortality Risk ◽  
Cancer Mortality ◽  
Lower Risk ◽  
Cox Regression ◽  
Statistical Significance ◽  
Food Sources ◽  
Inverse Association ◽  
Diet Adherence ◽  
Specific Mortality

The Portfolio Diet has demonstrated its cardiovascular benefit from interventions, but the association between Portfolio Diet adherence and the risk of all-cause and cause-specific mortality has not been examined in Chinese population. The present study has collected Portfolio Diet adherence (assessed by food frequency questionnaire), lifestyle factors and mortality status of 3991 participants in the Mr. Osteoporosis (OS) and Ms. OS Study. Cox regression models were used to examine the association between the Portfolio Diet adherence and mortality risk (all-cause, cardiovascular disease or cancer). The highest quartile of the Portfolio Diet score was associated with a 28% lower risk of all-cause (hazard ratio, HR: 0.72) and cancer (HR: 0.72) mortality, respectively. The association between Portfolio Diet adherence and cardiovascular disease mortality did not reach statistical significance (HR: 0.90, 95% CI = 0.64, 1.26). Among male participants, the highest adherence to the Portfolio Diet was also associated with a lower risk of all-cause (HR: 0.63) and cancer mortality (HR: 0.59), and there was an inverse association between food sources of plant protein and the risk of cardiovascular mortality (HR: 0.50). However, most associations between the Portfolio Diet and mortality were not significant among females. The protection for cancer mortality risk might reach the plateau at the highest adherence to the Portfolio Diet for females. To conclude, greater adherence to the Portfolio Diet was significantly associated with a lower risk of mortality in Hong Kong older adults, and the associations appeared stronger among males.

Gluten Intake and All-Cause and Cause-Specific Mortality: Prospective Findings from the UK Biobank

2020 ◽  
Author(s):  
Inken Behrendt ◽  
Mathias Fasshauer ◽  
Gerrit Eichner
Keyword(s):  
Heart Disease ◽  
Celiac Disease ◽  
Ischemic Heart Disease ◽  
Primary Objective ◽  
Ischemic Heart ◽  
Uk Biobank ◽  
Disease Mortality ◽  
Specific Mortality ◽  
Ischemic Heart Disease Mortality ◽  
The Uk

ABSTRACT Background Gluten has been linked to adverse effects on metabolic and vascular health. Objectives The present study determines the association between dietary gluten intake and all-cause (primary objective), as well as cause-specific, mortality in people without celiac disease. Methods Gluten intake was estimated in 159,265 participants of the UK Biobank which is a large multicenter, prospective cohort study initiated in 2006. Cox proportional hazard regression models were used and HRs were determined for all-cause and cause-specific mortality. All models were adjusted for confounders and multiple testing. Results Median (IQR) age was 57 (49–62) y with 52.1% of participants being female. Gluten intake was 8.5 (5.1–12.4) g/d with significantly higher consumption in males [10.0 (6.3–14.1) g/d] than in females [7.2 (4.6–10.7) g/d] (P < 0.0001). During a median follow-up of 11.1 (10.6–11.9) y and 1.8 million person-years, 6259 deaths occurred. Gluten intake was not significantly associated with all-cause mortality after adjusting for confounders (HR: 1.00; 95% CI: 1.00, 1.01; P = 0.59). Dietary gluten was not significantly associated with cancer (HR: 1.00; 95% CI: 1.00, 1.01; raw P = 0.24) or noncancer (HR: 1.00; 95% CI: 0.99, 1.01; raw P = 0.56) mortality. However, gluten intake was positively associated with ischemic heart disease mortality (HR: 1.02; 95% CI: 1.01, 1.04; raw P = 0.003, Holm-adjusted P = 0.04). Conclusions Gluten intake is not significantly associated with all-cause and cancer mortality in adults without celiac disease. The findings support the hypothesis that limiting gluten intake is unlikely to provide significant overall survival benefits on a population level. The positive association between gluten intake and ischemic heart disease mortality requires further study.

scholarly journals 699 Sleep Health Traits and COVID-19: Mortality Risk from the UK Biobank

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A273-A273
Author(s):  
Xi Zheng ◽  
Ma Cherrysse Ulsa ◽  
Peng Li ◽  
Lei Gao ◽  
Kun Hu
Keyword(s):  
Risk Factors ◽  
Sleep Apnea ◽  
Sleep Duration ◽  
Sex Education ◽  
Mortality Risk ◽  
Self Report ◽  
Severe Illness ◽  
Uk Biobank ◽  
Sleep Health ◽  
The Uk

Abstract Introduction While there is emerging evidence for acute sleep disruption in the aftermath of coronavirus disease 2019 (COVID-19), it is unknown whether sleep traits contribute to mortality risk. In this study, we tested whether earlier-life sleep duration, chronotype, insomnia, napping or sleep apnea were associated with increased 30-day COVID-19 mortality. Methods We included 34,711 participants from the UK Biobank, who presented for COVID-19 testing between March and October 2020 (mean age at diagnosis: 69.4±8.3; range 50.2–84.6). Self-reported sleep duration (less than 6h/6-9h/more than 9h), chronotype (“morning”/”intermediate”/”evening”), daytime dozing (often/rarely), insomnia (often/rarely), napping (often/rarely) and presence of sleep apnea (ICD-10 or self-report) were obtained between 2006 and 2010. Multivariate logistic regression models were used to adjust for age, sex, education, socioeconomic status, and relevant risk factors (BMI, hypertension, diabetes, respiratory diseases, smoking, and alcohol). Results The mean time between sleep measures and COVID-19 testing was 11.6±0.9 years. Overall, 5,066 (14.6%) were positive. In those who were positive, 355 (7.0%) died within 30 days (median = 8) after diagnosis. Long sleepers (>9h vs. 6-9h) [20/103 (19.4%) vs. 300/4,573 (6.6%); OR 2.09, 95% 1.19–3.64, p=0.009), often daytime dozers (OR 1.68, 95% 1.04–2.72, p=0.03), and nappers (OR 1.52, 95% 1.04–2.23, p=0.03) were at greater odds of mortality. Prior diagnosis of sleep apnea also saw a two-fold increased odds (OR 2.07, 95% CI: 1.25–3.44 p=0.005). No associations were seen for short sleepers, chronotype or insomnia with COVID-19 mortality. Conclusion Data across all current waves of infection show that prior sleep traits/disturbances, in particular long sleep duration, daytime dozing, napping and sleep apnea, are associated with increased 30-day mortality after COVID-19, independent of health-related risk factors. While sleep health traits may reflect unmeasured poor health, further work is warranted to examine the exact underlying mechanisms, and to test whether sleep health optimization offers resilience to severe illness from COVID-19. Support (if any) NIH [T32GM007592 and R03AG067985 to L.G. RF1AG059867, RF1AG064312, to K.H.], the BrightFocus Foundation A2020886S to P.L. and the Foundation of Anesthesia Education and Research MRTG-02-15-2020 to L.G.

scholarly journals Cardiovascular-related deaths at the beginning of the COVID-19 outbreak: a prospective analysis based on the UK Biobank

BMJ Open ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. e046931
Author(s):  
Junren Wang ◽  
Jianwei Zhu ◽  
Huazhen Yang ◽  
Yao Hu ◽  
Yajing Sun ◽  
...  
Keyword(s):  
Primary Diagnosis ◽  
Secondary Outcome ◽  
Hospital Inpatient ◽  
Reference Period ◽  
Stress Reactions ◽  
Uk Biobank ◽  
The Uk ◽  
The Impact ◽  
Distinct Increase ◽  
Related Mortality

ObjectiveTo assess the impact of the COVID-19 outbreak on cardiovascular disease (CVD) related mortality and hospitalisation.DesignCommunity-based prospective cohort study.SettingThe UK Biobank.Participants421 372 UK Biobank participants who were registered in England and alive as of 1 January 2020.Primary and secondary outcome measuresThe primary outcome of interest was CVD-related death, which was defined as death with CVD as a cause in the death register. We retrieved information on hospitalisations with CVD as the primary diagnosis from the UK Biobank hospital inpatient data. The study period was 1 January 2020 to June 30 2020, and we used the same calendar period of the three preceding years as the reference period. In order to control for seasonal variations and ageing of the study population, standardised mortality/incidence ratios (SMRs/SIRs) with 95% CIs were used to estimate the relative risk of CVD outcomes during the study period, compared with the reference period.ResultsWe observed a distinct increase in CVD-related deaths in March and April 2020, compared with the corresponding months of the three preceding years. The observed number of CVD-related deaths (n=218) was almost double in April, compared with the expected number (n=120) (SMR=1.82, 95% CI 1.58 to 2.07). In addition, we observed a significant decline in CVD-related hospitalisations from March onwards, with the lowest SIR observed in April (0.45, 95% CI 0.41 to 0.49).ConclusionsThere was a distinct increase in the number of CVD-related deaths in the UK Biobank population at the beginning of the COVID-19 outbreak. The shortage of medical resources for hospital care and stress reactions to the pandemic might have partially contributed to the excess CVD-related mortality, underscoring the need of sufficient healthcare resources and improved instructions to the public about seeking healthcare in a timely way.

Association of a Healthy Lifestyle With All-Cause and Cause-Specific Mortality Among Individuals With Type 2 Diabetes: A Prospective Study in UK Biobank

2021 ◽  
Author(s):  
Han Han ◽  
Yaying Cao ◽  
Chengwu Feng ◽  
Yan Zheng ◽  
Klodian Dhana ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Respiratory Disease ◽  
Digestive Disease ◽  
Diabetes Management ◽  
Healthy Lifestyle ◽  
Population Attributable Risk ◽  
Uk Biobank ◽  
All Cause Mortality ◽  
Specific Mortality

<a>Objective: </a><a></a><a></a><a></a><a></a><a>To evaluate the association of a healthy lifestyle, involving seven low-risk factors mentioned in diabetes management guidelines (no current smoking, moderate alcohol consumption, regular physical activity, healthy diet, less sedentary behavior, adequate sleep duration, and appropriate social connection), with all-cause and cause-specific mortality among individuals with type 2 diabetes.</a> <p>Research Design and Methods: This study included 13,366 participants with baseline type 2 diabetes from the UK Biobank free of CVD or cancer. Lifestyle information was collected through a baseline questionnaire.</p> <p><a>Results: During a median follow-up of 11.7 years, 1,561 deaths were documented, with 625 from cancer, 370 from CVD, 115 from respiratory disease, 81 from digestive disease, and 74 from neurodegenerative disease.</a><a> In multivariate-adjusted model, each lifestyle factor was significantly associated with all-cause mortality and hazard ratios (95% CIs) associated with the lifestyle score (scoring 6-7 vs. 0-2 unless specified) were 0.42 (0.34, 0.52) for all-cause mortality, 0.57 (0.41, 0.80) for cancer mortality, 0.35 (0.22, 0.56) for CVD mortality, 0.26 (0.10, 0.63) for respiratory mortality, and 0.28 (0.14, 0.53) for digestive mortality (scoring 5-7 vs. 0-2). In the population-attributable-risk analysis, 27.1% (95% CI: 16.1, 38.0%) death was attributable to a poor lifestyle (scoring 0-5). </a><a>The association between a healthy lifestyle and all-cause mortality was consistent, irrespective of factors reflecting diabetes severity (diabetes duration, glycemic control, diabetes-related microvascular disease, and diabetes medication)</a>.</p> <p>Conclusions: <a></a><a></a>A healthy lifestyle was associated with a lower risk of mortality due to all-cause, CVD, cancer, respiratory disease, and digestive disease among individuals with type 2 diabetes. <b></b></p>

Abstract 021: C-reactive Protein Partially Mediates The Inverse Association Between Coffee Consumption And Risk Of Type 2 Diabetes: Findings From The UK Biobank And The Rotterdam Studies

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Carolina Ochoa-Rosales ◽  
Niels van der Schaft ◽  
Kim V Braun ◽  
Frederick Ho ◽  
Fanny Petermann ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Coffee Consumption ◽  
Inverse Association ◽  
Statistical Regression ◽  
Uk Biobank ◽  
C Reactive Protein ◽  
Coffee Intake ◽  
Reactive Protein ◽  
The Uk

Background: Coffee intake has been linked to lower type 2 diabetes (T2D) risk. We hypothesized this may be mediated by coffee’s effects on inflammation. Methods: Using participants from the UK Biobank (UKB n=145370) and Rotterdam Study (RS n=7172) cohorts, we studied associations of coffee intake with incident T2D; longitudinally measured insulin resistance (HOMA IR); serum levels of inflammation markers; and the mediating role of inflammation. Statistical regression models were adjusted for sociodemographic, lifestyle and health factors. Results: The median follow up was 7 (UKB) and 9 (RS) years. An increase of one coffee cup/day was associated with 4-6% lower T2D risk (RS HR=0.94 [95% CI 0.90; 0.98]; UKB HR=0.96 [0.94; 0.98]); lower HOMA IR (RS β=-0.017 [-0.024; -0.010]); with lower C reactive protein (CRP) and higher adiponectin (Figure1). Consumers of filtered coffee had the lowest T2D risk (UKB HR=0.88 [0.83; 0.93]). CRP levels mediated 9.6% (UKB) and 3.4% (RS) of the total effect of coffee on T2D (Figure 1). Conclusions: We suggest that coffee’s beneficial effects on lower T2D risk are partially mediated by improvements in systemic inflammation.Figure 1. a CRP and a adiponectin refer to the effect of coffee intake on CRP and adiponectin levels. a CRP RS : β=-0.014 (-0.022; -0.005); UKBB a CRP UKB : β=-0.011 (-0.012; -0.009) and RS a adiponectin : β=0.025 (0.007; 0.042). b CRP and b adiponectin refer to the effect of coffee related levels in CRP and adiponectin on incident T2D, independent of coffee. RS b CRP : HR=1.17 (1.04; 1.31); UKB b CRP : HR=1.45 (1.37; 1.54); and b adiponectin : HR=0.58 (0.32; 0.83). c′ refers to coffee’ effect on T2D going directly or via others mediators. UKB c′ independent of CRP : HR=0.96 (0.94; 0.99); RS c′ independent of CRP : HR=0.94 (0.90; 0.99); and RS c′ independent of CRP+adiponectin : HR=0.90 (0.80; 1.01). Coffee related changes in CRP may partially explain the beneficial link between coffee and T2D, mediating a 3.4% (0.6; 4.8, RS) and 9.6% (5.7; 24.4, UKB). Evidence of mediation was also found for adiponectin.

scholarly journals Association of supplemental calcium and dairy milk intake with all-cause and cause-specific mortality in the UK Biobank: a prospective cohort study

2019 ◽  
Vol 123 (5) ◽  
pp. 574-582 ◽  
Author(s):  
L. C. Stasinopoulos ◽  
A. Zhou ◽  
E. Hyppönen
Keyword(s):  
Hormone Replacement Therapy ◽  
Replacement Therapy ◽  
Cancer Mortality ◽  
Hormone Replacement ◽  
Sensitivity Analyses ◽  
Milk Consumption ◽  
Inverse Association ◽  
Uk Biobank ◽  
Supplement Use ◽  
Increased Risk

AbstractExcessive Ca intakes have been proposed to associate with vascular calcification and a higher risk of prostate cancer. We investigated the associations of supplemental and dietary Ca intake with mortality using data from 497 828 UK Biobank participants. The average follow-up was 4·2 years and 14 255 participants died, 8297 from cancer, 2959 from CVD and 572 from respiratory disease. The use of Ca supplements and milk consumption were associated with differences in mortality in younger (≤65 years) but not in older participants (>65 years, Pinteraction ≤ 0·04 for all comparisons). Among participants <65 years, there was an inverse association between Ca supplementation (OR 0·91, 95 % CI 0·83, 0·99) and milk consumption (OR 0·93, 95 % CI 0·86, 1·00) with respect to all-cause mortality. In the same age group, milk drinkers had lower odds of cancer mortality (OR 0·89, 95 % CI 0·80, 0·98) but Ca supplement use was associated with increased odds of respiratory mortality (OR 1·69, 95 % CI 1·16, 2·74). All associations in participants aged ≥65 years were null after full adjustment. In sensitivity analyses stratified by hormone replacement therapy, Ca supplement use was associated with decreased odds of cancer mortality in users but increased risk in other women (OR 0·81, 95 % CI 0·69, 0·94 v. OR 1·17, 95 % CI 1·01, 1·35, respectively). To conclude, we saw little evidence for harm with dietary or supplemental Ca. Further studies are required to confirm the proposed interaction with hormone replacement therapy and to exclude reverse causation as a determinant in the association between Ca supplements and increased risk of respiratory diseases.

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 ◽  
...  
Keyword(s):  
Uk Biobank ◽  
Health Score ◽  
Specific Mortality ◽  
Wear And Tear ◽  
Disease Specific Mortality ◽  
Biological Health ◽  
Using Data ◽  
The Uk ◽  
Disease Specific ◽  
Physiological Systems

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 &lt; 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.

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