scholarly journals The association of energy and macronutrient intake with all-cause mortality, cardiovascular disease, and dementia: findings from 120,963 women and men in the UK Biobank

2021 ◽  
pp. 1-24
Author(s):  
Briar L McKenzie ◽  
Katie Harris ◽  
Sanne A E Peters ◽  
Jacqui Webster ◽  
Mark Woodward
Keyword(s):  
Cardiovascular Disease ◽  
Sex Differences ◽  
Energy Intake ◽  
Lower Risk ◽  
Premature Death ◽  
Uk Biobank ◽  
Risk Of Death ◽  
Hazard Ratios ◽  
Reference Cluster ◽  
The Uk

Abstract This study aimed to investigate the association between individual, and combinations of, macronutrients with premature death, cardiovascular disease (CVD) and dementia. Sex differences were investigated. Data were utilised from a prospective cohort of 120,963 individuals (57% female) within the UK Biobank, who completed ≥two 24-hour diet recalls. The associations of macronutrients, as percentages of total energy intake, with outcomes were investigated. Combinations of macronutrients were defined using k-means cluster analysis, with clusters explored in association with outcomes. There was a higher risk of death with high carbohydrate intake (Hazard ratios (HRs), 95% confidence intervals (95% CI) upper v lowest third 1.13 (1.03, 1.23)), yet a lower risk with higher intakes of protein (upper v lowest third 0.82 (0.76, 0.89)). There was a lower risk of CVD with moderate intakes (middle v lowest third) of energy and protein (sub distribution HRs (SHR), 0.87 (0.79, 0.97) and (0.87 (0.79, 0.96)) respectively). There was a lower risk of dementia with moderate energy intake (SHR 0.71 (0.52, 0.96)). Sex differences were identified. The dietary cluster characterised by low carbohydrate, low fat and high protein was associated with a lower risk of death (HR 0.84 (0.76, 0.93)) compared to the reference cluster, and a lower risk of CVD for men (SHR 0.83 (0.71, 0.97)). Given that associations were evident, both as single macronutrients and for combinations with other macronutrients for death, and for CVD in men, we suggest that the biggest benefit from diet-related policy and interventions will be when combinations of macronutrients are targeted.

scholarly journals Unhealthy Lifestyle, Genetics and Risk of Cardiovascular Disease and Mortality in 76,958 Individuals from the UK Biobank Cohort Study

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4283
Author(s):  
Katherine M. Livingstone ◽  
Gavin Abbott ◽  
Joey Ward ◽  
Steven J. Bowe
Keyword(s):  
Cardiovascular Disease ◽  
Cohort Study ◽  
Polygenic Risk Score ◽  
Nucleotide Polymorphisms ◽  
Uk Biobank ◽  
Unhealthy Lifestyle ◽  
Hazard Ratios ◽  
All Cause Mortality ◽  
The Uk ◽  
Cvd Mortality

To examine associations of unhealthy lifestyle and genetics with risk of all-cause mortality, cardiovascular disease (CVD) mortality, myocardial infarction (MI) and stroke. We used data on 76,958 adults from the UK Biobank prospective cohort study. Favourable lifestyle included no overweight/obesity, not smoking, physical activity, not sedentary, healthy diet and adequate sleep. A Polygenic Risk Score (PRS) was derived using 300 CVD-related single nucleotide polymorphisms. Cox proportional hazard ratios (HR) were used to model effects of lifestyle and PRS on risk of CVD and all-cause mortality, stroke and MI. New CVD (n = 364) and all-cause (n = 2408) deaths, and stroke (n = 748) and MI (n = 1140) events were observed during a 7.8 year mean follow-up. An unfavourable lifestyle (0–1 healthy behaviours) was associated with higher risk of all-cause mortality (HR: 2.06; 95% CI: 1.73, 2.45), CVD mortality (HR: 2.48; 95% CI: 1.64, 3.76), MI (HR: 2.12; 95% CI: 1.65, 2.72) and stroke (HR:1.74; 95% CI: 1.25, 2.43) compared to a favourable lifestyle (≥4 healthy behaviours). PRS was associated with MI (HR: 1.35; 95% CI: 1.27, 1.43). There was evidence of a lifestyle-genetics interaction for stroke (p = 0.017). Unfavourable lifestyle behaviours predicted higher risk of all-cause mortality, CVD mortality, MI and stroke, independent of genetic risk.

scholarly journals Accelerometer measured physical activity and the incidence of cardiovascular disease: Evidence from the UK Biobank cohort study

PLoS Medicine ◽  
2021 ◽  
Vol 18 (1) ◽  
pp. e1003487
Author(s):  
Rema Ramakrishnan ◽  
Aiden Doherty ◽  
Karl Smith-Byrne ◽  
Kazem Rahimi ◽  
Derrick Bennett ◽  
...  
Keyword(s):  
Physical Activity ◽  
Cardiovascular Disease ◽  
Lower Risk ◽  
Cox Regression ◽  
Moderate Intensity ◽  
Inverse Association ◽  
Uk Biobank ◽  
Reverse Causality ◽  
Vigorous Intensity ◽  
The Uk

Background Higher levels of physical activity (PA) are associated with a lower risk of cardiovascular disease (CVD). However, uncertainty exists on whether the inverse relationship between PA and incidence of CVD is greater at the highest levels of PA. Past studies have mostly relied on self-reported evidence from questionnaire-based PA, which is crude and cannot capture all PA undertaken. We investigated the association between accelerometer-measured moderate, vigorous, and total PA and incident CVD. Methods and findings We obtained accelerometer-measured moderate-intensity and vigorous-intensity physical activities and total volume of PA, over a 7-day period in 2013–2015, for 90,211 participants without prior or concurrent CVD in the UK Biobank cohort. Participants in the lowest category of total PA smoked more, had higher body mass index and C-reactive protein, and were diagnosed with hypertension. PA was associated with 3,617 incident CVD cases during 440,004 person-years of follow-up (median (interquartile range [IQR]): 5.2 (1.2) years) using Cox regression models. We found a linear dose–response relationship for PA, whether measured as moderate-intensity, vigorous-intensity, or as total volume, with risk of incident of CVD. Hazard ratios (HRs) and 95% confidence intervals for increasing quarters of the PA distribution relative to the lowest fourth were for moderate-intensity PA: 0.71 (0.65, 0.77), 0.59 (0.54, 0.65), and 0.46 (0.41, 0.51); for vigorous-intensity PA: 0.70 (0.64, 0.77), 0.54 (0.49,0.59), and 0.41 (0.37,0.46); and for total volume of PA: 0.73 (0.67, 0.79), 0.63 (0.57, 0.69), and 0.47 (0.43, 0.52). We took account of potential confounders but unmeasured confounding remains a possibility, and while removal of early deaths did not affect the estimated HRs, we cannot completely dismiss the likelihood that reverse causality has contributed to the findings. Another possible limitation of this work is the quantification of PA intensity-levels based on methods validated in relatively small studies. Conclusions In this study, we found no evidence of a threshold for the inverse association between objectively measured moderate, vigorous, and total PA with CVD. Our findings suggest that PA is not only associated with lower risk for of CVD, but the greatest benefit is seen for those who are active at the highest level.

scholarly journals Social deprivation as a risk factor for COVID-19 mortality among women and men in the UK Biobank: nature of risk and context suggests that social interventions are essential to mitigate the effects of future pandemics

2021 ◽  
pp. jech-2020-215810
Author(s):  
Mark Woodward ◽  
Sanne A E Peters ◽  
Katie Harris
Keyword(s):  
Cardiovascular Disease ◽  
Sex Differences ◽  
Risk Factor ◽  
Social Deprivation ◽  
Linear Trend ◽  
Population Based ◽  
Lifestyle Factors ◽  
Uk Biobank ◽  
The Uk ◽  
Log Linear

ObjectivesTo investigate sex differences in the effects of social deprivation on COVID-19 mortality and to place these effects in context with other diseases.DesignProspective population-based study.SettingUK Biobank.Participants501 865 participants (54% women).Main outcome measureCOVID-19 as the underlying cause of death.ResultsOf 472 946 participants alive when COVID-19 was first apparent in the UK (taken as 1 February 2020), 217 (34% women) died from COVID-19 over the next 10 months, resulting in an incidence, per 100 000 person years, of 100.65 (95% CI 79.47 to 121.84) for women and 228.59 (95% CI 194.88 to 262.30) for men. Greater social deprivation, quantified using the Townsend Deprivation Score, was associated with greater risk of fatal COVD-19. Adjusted for age and ethnicity, HRs for women and men, comparing those in the most with the least deprived national fifths, were 3.66 (2.82 to 4.75) for women and 3.00 (2.46 to 3.66) for men. Adjustments for key baseline lifestyle factors attenuated these HRs to 2.20 (1.63 to 2.96) and 2.62 (2.12 to 3.24), respectively. There was evidence of a log-linear trend in the deprivation–fatal COVID-19 association, of similar magnitude to the equivalent trends for the associations between deprivation and fatal influenza or pneumonia and fatal cardiovascular disease. For all three causes of death, there was no evidence of a sex difference in the associations.ConclusionsHigher social deprivation is a risk factor for death from COVID-19 on a continuous scale, with two to three times the risk in the most disadvantaged 20% compared with the least. Similarities between the social gradients in COVID-19, influenza/pneumonia and cardiovascular disease mortality, the lack of sex differences in these effects, and the partial mediation of lifestyle factors suggest that better social policies are crucial to alleviate the general medical burden, including from the current, and potential future, viral pandemics.

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.

Advanced cardiometabolic & inflammatory markers for prediction of cardiovascular disease and cancer

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
D Radenkovic ◽  
S.C Chawla ◽  
G Botta ◽  
A Boli ◽  
M.B Banach ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Risk Score ◽  
Cancer Incidence ◽  
Risk Function ◽  
Patient Characteristics ◽  
Risk Scores ◽  
Uk Biobank ◽  
Training Set ◽  
All Cause Mortality ◽  
The Uk

Abstract   The two leading causes of mortality worldwide are cardiovascular disease (CVD) and cancer. The annual total cost of CVD and cancer is an estimated $844.4 billion in the US and is projected to double by 2030. Thus, there has been an increased shift to preventive medicine to improve health outcomes and development of risk scores, which allow early identification of individuals at risk to target personalised interventions and prevent disease. Our aim was to define a Risk Score R(x) which, given the baseline characteristics of a given individual, outputs the relative risk for composite CVD, cancer incidence and all-cause mortality. A non-linear model was used to calculate risk scores based on the participants of the UK Biobank (= 502548). The model used parameters including patient characteristics (age, sex, ethnicity), baseline conditions, lifestyle factors of diet and physical activity, blood pressure, metabolic markers and advanced lipid variables, including ApoA and ApoB and lipoprotein(a), as input. The risk score was defined by normalising the risk function by a fixed value, the average risk of the training set. To fit the non-linear model >400,000 participants were used as training set and >45,000 participants were used as test set for validation. The exponent of risk function was represented as a multilayer neural network. This allowed capturing interdependent behaviour of covariates, training a single model for all outcomes, and preserving heterogeneity of the groups, which is in contrast to CoxPH models which are traditionally used in risk scores and require homogeneous groups. The model was trained over 60 epochs and predictive performance was determined by the C-index with standard errors and confidence intervals estimated with bootstrap sampling. By inputing the variables described, one can obtain personalised hazard ratios for 3 major outcomes of CVD, cancer and all-cause mortality. Therefore, an individual with a risk Score of e.g. 1.5, at any time he/she has 50% more chances than average of experiencing the corresponding event. The proposed model showed the following discrimination, for risk of CVD (C-index = 0.8006), cancer incidence (C-index = 0.6907), and all-cause mortality (C-index = 0.7770) on the validation set. The CVD model is particularly strong (C-index >0.8) and is an improvement on a previous CVD risk prediction model also based on classical risk factors with total cholesterol and HDL-c on the UK Biobank data (C-index = 0.7444) published last year (Welsh et al. 2019). Unlike classically-used CoxPH models, our model considers correlation of variables as shown by the table of the values of correlation in Figure 1. This is an accurate model that is based on the most comprehensive set of patient characteristics and biomarkers, allowing clinicians to identify multiple targets for improvement and practice active preventive cardiology in the era of precision medicine. Figure 1. Correlation of variables in the R(x) Funding Acknowledgement Type of funding source: None

scholarly journals Sex differences in the association between major cardiovascular risk factors in midlife and dementia: a cohort study using data from the UK Biobank

BMC Medicine ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jessica Gong ◽  
Katie Harris ◽  
Sanne A. E. Peters ◽  
Mark Woodward
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
Sex Differences ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Sex Difference ◽  
Incidence Rates ◽  
Cox Proportional Hazards ◽  
Uk Biobank ◽  
The Uk

Abstract Background Sex differences in major cardiovascular risk factors for incident (fatal or non-fatal) all-cause dementia were assessed in the UK Biobank. The effects of these risk factors on all-cause dementia were explored by age and socioeconomic status (SES). Methods Cox proportional hazards models were used to estimate hazard ratios (HRs) and women-to-men ratio of HRs (RHR) with 95% confidence intervals (CIs) for systolic blood pressure (SBP) and diastolic blood pressure (DBP), smoking, diabetes, adiposity, stroke, SES and lipids with dementia. Poisson regression was used to estimate the sex-specific incidence rate of dementia for these risk factors. Results 502,226 individuals in midlife (54.4% women, mean age 56.5 years) with no prevalent dementia were included in the analyses. Over 11.8 years (median), 4068 participants (45.9% women) developed dementia. The crude incidence rates were 5.88 [95% CI 5.62–6.16] for women and 8.42 [8.07–8.78] for men, per 10,000 person-years. Sex was associated with the risk of dementia, where the risk was lower in women than men (HR = 0.83 [0.77–0.89]). Current smoking, diabetes, high adiposity, prior stroke and low SES were associated with a greater risk of dementia, similarly in women and men. The relationship between blood pressure (BP) and dementia was U-shaped in men but had a dose-response relationship in women: the HR for SBP per 20 mmHg was 1.08 [1.02–1.13] in women and 0.98 [0.93–1.03] in men. This sex difference was not affected by the use of antihypertensive medication at baseline. The sex difference in the effect of raised BP was consistent for dementia subtypes (vascular dementia and Alzheimer’s disease). Conclusions Several mid-life cardiovascular risk factors were associated with dementia similarly in women and men, but not raised BP. Future bespoke BP-lowering trials are necessary to understand its role in restricting cognitive decline and to clarify any sex difference.

scholarly journals Gout, Rheumatoid Arthritis, and the Risk of Death Related to Coronavirus Disease 2019: An Analysis of the UK Biobank

2021 ◽  
Author(s):  
Ruth K. Topless ◽  
Amanda Phipps‐Green ◽  
Megan Leask ◽  
Nicola Dalbeth ◽  
Lisa K. Stamp ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Uk Biobank ◽  
Risk Of Death ◽  
The Uk

scholarly journals Coffee Consumption and Cardiovascular Diseases: A Mendelian Randomization Study

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2218
Author(s):  
Shuai Yuan ◽  
Paul Carter ◽  
Amy M. Mason ◽  
Stephen Burgess ◽  
Susanna C. Larsson
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Diseases ◽  
Intracerebral Hemorrhage ◽  
Genetic Variants ◽  
Odds Ratio ◽  
Observational Studies ◽  
Mendelian Randomization ◽  
Coffee Consumption ◽  
Uk Biobank ◽  
The Uk

Coffee consumption has been linked to a lower risk of cardiovascular disease in observational studies, but whether the associations are causal is not known. We conducted a Mendelian randomization investigation to assess the potential causal role of coffee consumption in cardiovascular disease. Twelve independent genetic variants were used to proxy coffee consumption. Summary-level data for the relations between the 12 genetic variants and cardiovascular diseases were taken from the UK Biobank with up to 35,979 cases and the FinnGen consortium with up to 17,325 cases. Genetic predisposition to higher coffee consumption was not associated with any of the 15 studied cardiovascular outcomes in univariable MR analysis. The odds ratio per 50% increase in genetically predicted coffee consumption ranged from 0.97 (95% confidence interval (CI), 0.63, 1.50) for intracerebral hemorrhage to 1.26 (95% CI, 1.00, 1.58) for deep vein thrombosis in the UK Biobank and from 0.86 (95% CI, 0.50, 1.49) for subarachnoid hemorrhage to 1.34 (95% CI, 0.81, 2.22) for intracerebral hemorrhage in FinnGen. The null findings remained in multivariable Mendelian randomization analyses adjusted for genetically predicted body mass index and smoking initiation, except for a suggestive positive association for intracerebral hemorrhage (odds ratio 1.91; 95% CI, 1.03, 3.54) in FinnGen. This Mendelian randomization study showed limited evidence that coffee consumption affects the risk of developing cardiovascular disease, suggesting that previous observational studies may have been confounded.

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