Obesity as a risk factor for COVID-19 mortality in women and men in the UK biobank: Comparisons with influenza/pneumonia and coronary heart disease.
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SUBMITTER: Peters SAE
PROVIDER: S-EPMC7536945 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background Cardiorespiratory fitness may moderate the association between obesity and all-cause mortality (ie, the "fat-but-fit" hypothesis), but unaddressed sources of bias are a concern. Methods and Results Cardiorespiratory fitness was estimated as watts per kilogram from a submaximal bicycle test in 77 169 men and women from the UK Biobank cohort and combined with World Health Organization standard body mass index categories, yielding 9 unique fitness-fatness combinations. We also formed fitness-fatness combinations based on bioimpedance as a direct measure of body composition. All-cause mortality was ascertained from death registries. Multivariable-adjusted Cox regression models were used to estimate hazard ratios and 95% CIs. We examined the association between fitness-fatness combinations and all-cause mortality in models with progressively more conservative approaches for accounting for reverse causation, misclassification of body composition, and confounding. Over a median follow-up of 7.7 years, 1731 participants died. In our base model, unfit men and women had higher risk of premature mortality irrespective of levels of adiposity, compared with the normal weight-fit reference. This pattern was attenuated but maintained with more conservative approaches in men, but not in women. In analysis stratified by sex and excluding individuals with prevalent major chronic disease and short follow-up and using direct measures of body composition, mortality risk was 1.78 (95% CI, 1.17-2.71) times higher in unfit-obese men but not higher in obese-fit men (0.94 [95% CI, 0.60-1.48]). In contrast, there was no increased risk in obese-unfit women (1.09 [95% CI, 0.44-1.05]) as compared with the reference. Conclusions Cardiorespiratory fitness modified the association between obesity and mortality in men, but this pattern appeared susceptible to biases in women.
| S-EPMC8174221 | biostudies-literature
Project description:BackgroundCommencing work at an early age has been linked to various risk factors for coronary heart disease (CHD), such as shift work and intensive job strain. However, the relationship between starting work too early and CHD risk remains largely unclear. We examined the association between age at job initiation and the risk of CHD.MethodsUK Biobank participants aged 38 to 70 years without cardiovascular disease who provided data on their age at job initiation were included. The primary outcome was CHD, which was ascertained using hospital and death records. The hazard ratios (HRs) and 95% confidence interval (CIs) for the association between age at job initiation and CHD were calculated using multivariable Cox regression.ResultsOf the 501,971 participants, 114,418 eligible participants were included in the final analysis. The median age at job initiation was 19.0 years. During the mean follow-up of 12.6 years, 6,130 (5.4%) first CHD events occurred. We observed that age at job initiation was inversely associated with CHD (HR 0.98, 95% CI 0.97-0.99), and the association was potentially J-shaped. The HRs for the < 17-year, 17-18-year, and 19-21-year age groups were 1.29 (95%CI 1.18-1.41), 1.12 (95% CI 1.03-1.22) and 1.05 (95% CI 0.97-1.14), respectively, compared with those of the ≥ 22-year group.ConclusionsAge at job initiation was associated with incident CHD, which was independent of socioeconomic status. Participants who commenced employment before the age of 19 years exhibited a higher risk of developing CHD later in adulthood.
| S-EPMC10614325 | biostudies-literature
Project description:Aims: To investigate the effect of diabetes on mortality and incident heart failure (HF) according to sex, in the low risk population of UK Biobank. To evaluate potential contributing factors for any differences seen in HF end-point. Methods: The entire UK Biobank study population were included. Participants that withdrew consent or were diagnosed with diabetes after enrolment were excluded from the study. Univariate and multivariate cox regression models were used to assess endpoints of mortality and incident HF, with median follow-up periods of 9 years and 8 years respectively. Results: A total of 493,167 participants were included, hereof 22,685 with diabetes (4.6%). Two thousand four hundred fifty four died and 1,223 were diagnosed or admitted with HF during the follow up periods of 9 and 8 years respectively. Overall, the mortality and HF risk were almost doubled in those with diabetes compared to those without diabetes (hazard ratio (HR) of 1.9 for both mortality and heart failure) in the UK Biobank population. Women with diabetes (both types) experience a 22% increased risk of HF compared to men (HR of 2.2 (95% CI: 1.9-2.5) vs. 1.8 (1.7-2.0) respectively). Women with type 1 diabetes (T1DM) were associated with 88% increased risk of HF compared to men (HR 4.7 (3.6-6.2) vs. 2.5 (2.0-3.0) respectively), while the risk of HF for type 2 diabetes (T2DM) was 17% higher in women compared to men (2.0 (1.7-2.3) vs. 1.7 (1.6-1.9) respectively). The increased risk of HF in women was independent of confounding factors. The findings were similar in a model with all-cause mortality as a competing risk. This interaction between sex, diabetes and outcome of HF is much more prominent for T1DM (p = 0.0001) than T2DM (p = 0.1). Conclusion: Women with diabetes, particularly those with T1DM, experience a greater increase in risk of heart failure compared to men with diabetes, which cannot be explained by the increased prevalence of cardiac risk factors in this cohort.
| S-EPMC8057521 | biostudies-literature
Project description:ObjectiveTo define the sex, age, and disease-specific associations of resting heart rate (RHR) with cardiovascular and mortality outcomes in 502,534 individuals from the UK Biobank over 7-12 years of prospective follow-up.MethodsThe main outcomes were all-cause, cardiovascular, and ischaemic heart disease mortality. Additional outcomes included incident acute myocardial infarction (AMI), fatal AMI, and cancer mortality. We considered a wide range of confounders and the effects of competing hazards. Results are reported as hazard ratios (HR) for all-cause mortality and sub-distribution hazard ratios (SHR) for other outcomes with corresponding 95% confidence intervals (CI) per 10bpm increment of RHR.ResultsIn men, for every 10bpm increase of RHR there was 22% (HR 1.22, CI 1.20 to 1.24, p = 3×10-123) greater hazard of all-cause and 17% (SHR 1.17, CI 1.13 to 1.21, p = 5.6×10-18) greater hazard of cardiovascular mortality; for women, corresponding figures were 19% (HR 1.19, CI 1.16 to 1.22, p = 8.9×10-45) and 14% (SHR 1.14, CI 1.07 to 1.22, p = 0.00008). Associations between RHR and ischaemic outcomes were of greater magnitude amongst men than women, but with similar magnitude of association for non-cardiovascular cancer mortality [men (SHR 1.18, CI 1.15-1.21, p = 5.2×10-46); women 15% (SHR 1.15, CI 1.11-1.18, p = 3.1×10-18)]. Associations with all-cause, incident AMI, and cancer mortality were of greater magnitude at younger than older ages.ConclusionsRHR is an independent predictor of mortality, with variation by sex, age, and disease. Ischaemic disease appeared a more important driver of this relationship in men, and associations were more pronounced at younger ages.
| S-EPMC7259773 | biostudies-literature
Project description:ObjectiveTo determine the combined effects of body mass index (BMI) and body fat (BF) on prognosis in coronary heart disease (CHD) to better understand the obesity paradox.Patients and methodsWe studied 581 patients with CHD between January 1, 2000, and July 31, 2005, who were divided into low (<25) and high BMI (≥25), as well as low (≤25% men and ≤35% women) and high BF (>25% in men and >35% in women). Four groups were analyzed by total mortality during the 3-year follow-up by National Death Index: low BF/low BMI (n=119), high BF/low BMI (n=26), low BF/high BMI (n=125), and high BF/high BMI (n=311).ResultsDuring the 3-year follow-up, mortality was highest in the low BF/low BMI group (11%), which was significantly (P<.001) higher than that in the other 3 groups (3.9%, 3.2%, and 2.6%, respectively); using the high BF/high BMI group as a reference, the low BF/low BMI group had a 4.24-fold increase in mortality (confidence interval [CI], 1.76-10.23; P=.001). In multivariate logistic regression for mortality, when entered individually, both high BMI (odds ratio [OR], 0.79; CI, 0.69-0.90) and high BF (OR, 0.89; CI, 0.82-0.95) as continuous variables were independent predictors of better survival, whereas low BMI (OR, 3.60; CI, 1.37-9.47) and low BF (OR, 3.52; CI, 1.34-9.23) as categorical variables were independent predictors of higher mortality.ConclusionAlthough both low BF and low BMI are independent predictors of mortality in patients with CHD, only patients with combined low BF/low BMI appear to be at particularly high risk of mortality during follow-up. Studies are needed to determine optimal body composition in the secondary prevention of CHD.
| S-EPMC3257992 | biostudies-literature
Project description:BackgroundCurrent physical activity guidelines do not distinguish between activity accumulated in different behavioural domains but some studies suggest that occupational physical activity (OPA) may not confer health benefits and could even be detrimental. The purpose of this study was to investigate associations between OPA and mortality outcomes.MethodsFrom baseline (2006-2010), 460,901 UK Biobank participants (aged 40-69 years) were followed for a median 12.0 (IQR: 11.3-12.7) years. OPA was categorised by cross-tabulating degree of manual work and walking/standing work amongst those in paid employment (n = 267,765), and combined with categories of occupational status for those not in paid employment (n = 193,136). Cox proportional hazards models were used to estimate sex-stratified hazard ratios (HR) and 95% confidence intervals (CI) for mortality from all causes, CVD, and cancer by occupational group, and for working hours/week and non-occupational physical activity stratified by occupational group. Models included adjustment for age and a range of lifestyle, socio-economic and health-related covariates.ResultsDuring 5,449,989 person-years of follow-up, 28,740 deaths occurred. Compared to those reporting no heavy manual or walking/standing work (e.g. sedentary office workers) and adjusting for covariates, retirement was associated with lower mortality in women (HR = 0.62, CI: 0.53-0.72) and men (HR = 0.80, CI: 0.71-0.90), whereas unemployment was associated with higher mortality in men only (HR = 1.24, CI: 1.07-1.45). Within the working population, there was no evidence of differences in all-cause, CVD or cancer mortality by OPA group when comparing those reporting higher levels of OPA to the lowest OPA reference group for both women and men. Working < 35 h/week versus 35-40 h/week was associated with lower mortality in women (HR = 0.85, CI: 0.79-0.92) and men (HR = 0.83, CI: 0.78-0.89), with no interaction by OPA. Non-occupational physical activity was associated with lower mortality in working women (HR = 0.89 per 5 kJ/day/kg, CI: 0.84-0.95) and men (HR = 0.87 per 5 kJ/day/kg, CI: 0.84-0.91), with no interaction by OPA group.ConclusionsJobs classified as higher levels of OPA may not be as active as reported, or the types of physical activity performed in those jobs are not health-enhancing. Irrespective of OPA category or employment status, non-occupational physical activity appears to provide health benefits.
| S-EPMC8314512 | biostudies-literature
Project description:It is well established that psychological distress (depression and anxiety) is related to an increased risk of mortality. The personality trait of neuroticism, reflecting a relatively stable tendency towards negative emotions, has also been associated with elevated rates of death in some studies. Accordingly, we tested the possibility that it is the neuroticism trait itself, rather than the distress state, that is generating an increased risk of mortality.We used data from the UK Biobank study, a UK-wide prospective cohort study (2006-2010) in which distress was ascertained using the Patient Health Questionnaire and neuroticism using the Eysenck Personality Questionnaire-Revised Short Form.A mean of 6.2 years of follow-up of 308 721 study members gave rise to 4334 deaths. Higher neuroticism was weakly associated with total mortality (age-adjusted and sex-adjusted HR per SD increase; 95% CI 1.05; 1.02 to 1.09), and moderately strongly correlated with distress symptoms (r=0.55, p<0.0001). Distress symptoms were positively related to risk of total mortality (age-adjusted and sex-adjusted HR per SD increase in distress; 95% CI 1.23; 1.20 to 1.26). This gradient was, in fact, slightly strengthened after adding neuroticism to the multivariable model (1.30; 1.26 to 1.34) but markedly attenuated after taking into account other covariates which included health behaviours and somatic disease (1.16; 1.12 to 1.20). Similar results were apparent when cardiovascular disease, cancer and external cause of death were the end points of interest.While there was good a priori reasons to anticipate the neuroticism would at least partially explain the relation between distress symptoms and cause-specific mortality, we found no such evidence in the present study.
| S-EPMC5541175 | biostudies-other
Project description:ObjectiveThe aim of this study was to obtain estimates of the causal relationship between BMI and mortality.MethodsMendelian randomization (MR) with BMI-associated genotypic variation was used to test the causal effect of BMI on all-cause and cause-specific mortality in UK Biobank participants of White British ancestry.ResultsMR analyses supported a causal association between higher BMI and greater risk of all-cause mortality (hazard ratio [HR] per 1 kg/m2 : 1.03; 95% CI: 0.99-1.07) and mortality from cardiovascular diseases (HR: 1.10; 95% CI: 1.01-1.19), specifically coronary heart disease (HR: 1.12; 95% CI: 1.00-1.25) and those excluding coronary heart disease/stroke/aortic aneurysm (HR: 1.24; 95% CI: 1.03-1.48), stomach cancer (HR: 1.18; 95% CI: 0.87-1.62), and esophageal cancer (HR: 1.22; 95% CI: 0.98-1.53), and a decreased risk of lung cancer mortality (HR: 0.96; 95% CI: 0.85-1.08). Sex stratification supported the causal role of higher BMI increasing bladder cancer mortality risk (males) but decreasing respiratory disease mortality risk (males). The J-shaped observational association between BMI and mortality was visible with MR analyses, but the BMI at which mortality was minimized was lower and the association was flatter over a larger BMI range.ConclusionsResults support a causal role of higher BMI in increasing the risk of all-cause mortality and mortality from several specific causes.
| S-EPMC6334168 | biostudies-literature
Project description: Not available
| S-EPMC7337688 | biostudies-literature
Project description:Later chronotype (i.e. evening preference) and later timing of sleep have been associated with greater morbidity, including higher rates of metabolic dysfunction and cardiovascular disease (CVD). However, no one has examined whether chronotype is associated with mortality risk to date. Our objective was to test the hypothesis that being an evening type is associated with increased mortality in a large cohort study, the UK Biobank. Our analysis included 433 268 adults aged 38-73 at the time of enrolment and an average 6.5-year follow-up. The primary exposure was chronotype, as assessed through a single self-reported question-defining participants as definite morning types, moderate morning types, moderate evening types or definite evening types. The primary outcomes were all-cause mortality and mortality due to CVD. Prevalent disease was also compared among the chronotype groups. Analyses were adjusted for age, sex, ethnicity, smoking, body mass index, sleep duration, socioeconomic status and comorbidities. Greater eveningness, particularly being a definite evening type, was significantly associated with a higher prevalence of all comorbidities. Comparing definite evening type to definite morning type, the associations were strongest for psychological disorders (OR 1.94, 95% CI 1.86-2.02, p = < 0.001), followed by diabetes (OR 1.30, 95% CI 1.24-1.36, p = < 0.001), neurological disorders (OR 1.25, 95% CI 1.20-1.30, p = < 0.001), gastrointestinal/abdominal disorders (OR 1.23, 95% CI 1.19-1.27, p = < 0.001) and respiratory disorders (OR 1.22, 95% CI 1.18-1.26, p = < 0.001). The total number of deaths was 10 534, out of which 2127 were due to CVD. Greater eveningness, based on chronotype as an ordinal variable, was associated with a small increased risk of all-cause mortality (HR 1.02, 95% CI 1.004-1.05, p = 0.017) and CVD mortality (HR 1.04, 95% CI 1.00-1.09, p = 0.06). Compared to definite morning types, definite evening types had significantly increased risk of all-cause mortality (HR 1.10, 95% CI 1.02-1.18, p = 0.012). This first report of increased mortality in evening types is consistent with previous reports of increased levels of cardiometabolic risk factors in this group. Mortality risk in evening types may be due to behavioural, psychological and physiological risk factors, many of which may be attributable to chronic misalignment between internal physiological timing and externally imposed timing of work and social activities. These findings suggest the need for researching possible interventions aimed at either modifying circadian rhythms in individuals or at allowing evening types greater working hour flexibility.
| S-EPMC6119081 | biostudies-literature