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Background and aims: Various smoking behaviors, including smoking initiation, age of initiation, heaviness of smoking and smoking cessation, have been individually related to the risk of mortality; however, no study has assessed these smoking behaviors jointly in relation to mortality. Our study aimed to measure prospectively the association of panoramic smoking burden (PSB), generated from the four aforementioned smoking behaviors, with all‐cause and cause‐specific mortality, and measure whether such associations are modified by genetic variations. Design Prospective cohort study. Setting: UK Biobank. Participants: A total of 360 937 participants aged between 37 and 73 years were enrolled in 2006–10 and ‐followed‐up to 2018. Measurements The exposure was PSB, constructed based on four smoking behaviors including smoking initiation, age of initiation, heaviness of smoking and smoking cessation in a weighted method. A genetically determined PSB was also constructed with smoking‐associated single nucleotide polymorphisms (SNPs) and categorized into tertiles. The primary outcomes were all‐cause and cause‐specific mortality. Findings We identified 15 968 deaths [9022 from cancer and 5092 from cardiovascular disease (CVD)] over a median of 11.36 years' follow‐up. For all‐cause mortality, compared with participants with the PSB of zero, the hazard ratios of participants who had a PSB of one, two, three and four were 1.23 [95% confidence intervals (CI) = 1.18–1.29), 1.66 (95% CI = 1.59–1.75), 3.33 (95% CI = 3.17–3.51) and 5.76 (95% CI = 4.66–7.13), respectively. Among participants within each genetic risk category, low and intermediate PSB were associated with 45–58% reduced risk of all‐cause death compared with high PSB. Analysis of population‐attributable risk percentage indicated that 21.9, 19.1 and 24.7% of all‐cause‐, cancer‐ and CVD‐specific death could have been avoided if all ever smokers initiated smoking after age 18 years, smoked < 20 cigarettes/day and quit smoking. Conclusions: The panoramic smoking burden, based on smoking initiation, age of initiation, heaviness of smoking and smoking cessation, appears to be associated with all‐cause and cause‐specific mortality in a gradient manner with increasing panoramic smoking burden independent of other traditional and genetic risk factors. [ABSTRACT FROM AUTHOR]

Excessive 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, P interaction ≤ 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. [ABSTRACT FROM AUTHOR]

Background: A number of prior studies have examined the association between anthropometric measures and mortality, but studies investigating the sex-specific predictive value of novel anthropometric measures on mortality are scarce so far. Therefore, we investigated the sex-specific relevance of the new anthropometric measures body adiposity index (BAI) and waist to height ratio (WHtR) as well as the common measures body mass index (BMI), waist circumference (WC), and waist to hip ratio (WHR) for cause-specific mortality risk.Methods: The analysis was based on data from the German population based KORA (Cooperative Health Research in the Region of Augsburg) Augsburg cohort study. A total of 6670 men and 6637 women aged 25 to 74 years at baseline examination were included. During a mean follow-up period of 15.4 years, 2409 persons died. Via Cox proportional hazard regression, the associations between the different anthropometric measures and all cause-, cardiovascular disease (CVD)- and cancer mortality were assessed.Results: BMI, WC, and WHR were significantly associated with all-cause and CVD-mortality in both sexes. WC and WHR were particularly associated with higher all-cause and CVD-mortality risk in women, while in men especially WHtR and BAI were strongly related to these outcomes. Females with WC, WHtR, and WHR measures in the 4th quartile compared with women in the 2nd quartile had a higher risk of death from cancer. Contrary, men in the lowest quartile of WC and WHtR in comparison to men in the 2nd quartile had a significantly elevated cancer mortality risk. BAI was no risk predictor for all-cause and cause-specific mortality in women.Conclusions: Central obesity reflects higher all-cause and CVD-mortality risk particularly in women. BAI and WHtR seem to be valid as risk predictors for all-cause and especially CVD mortality in men but not women. There are marked sex-differences regarding cancer mortality risk for the different anthropometric measures. [ABSTRACT FROM AUTHOR]

Chocolate contains both potentially harmful components (ie, stearic acid and added sugar) and beneficial components (ie, phenolics and flavonoids). Despite its popularity, the long-term health effects of chocolate consumption remain unclear. The aim of this study was to examine the association of chocolate consumption with all-cause and cause-specific mortality. This was a prospective cohort study. This study included 84,709 postmenopausal women free of cardiovascular disease (CVD) and cancer at baseline in the observational study and clinical trials control arms of the prospective Women's Health Initiative cohort who were enrolled during 1993 through 1998. These women were followed through March 2018. The outcomes included all-cause mortality and cause-specific mortality from CVD, cancer, and dementia. Multivariable Cox proportional hazards models were used to estimate adjusted hazard ratios (HRs) of all-cause mortality and cause-specific mortality. During 1,608,856 person-years of follow-up (mean [SD] of 19.0 [4.2] years), 25,388 deaths occurred, including 7,069 deaths from CVD, 7,030 deaths from cancer, and 3,279 deaths from dementia. After adjustment for a variety of covariates, compared with no chocolate consumption, the HRs (95% CI) for all-cause mortality were 0.95 (0.92 to 0.98), 0.93 (0.89 to 0.96), 0.97 (0.90 to 1.04), and 0.90 (0.84 to 0.97) for <1 serving/wk, 1 to 3 servings/wk, 4 to 6 servings/wk, and ≥1 serving/d of chocolate consumption, respectively (P for trend =.02). For CVD mortality, compared with no chocolate consumption, the HRs (95% CI) were 0.96 (0.91 to 1.01), 0.88 (0.82 to 0.95), 1.06 (0.93 to 1.21), and 0.92 (0.80 to 1.05) for <1 serving/wk, 1 to 3servings/wk, 4 to 6 servings/wk, and ≥1 serving/d of chocolate consumption, respectively (P for trend =.45). For dementia mortality, compared with no chocolate consumption, the HRs (95% CI) were 0.91 (0.84 to 0.99), 0.89 (0.80 to 0.99), 0.97 (0.79 to 1.18), and 0.97 (0.80 to 1.18) for <1 serving/wk, 1 to 3 servings/wk, 4-6 servings/wk, and ≥1 serving/d of chocolate consumption, respectively (P for trend =.95). Chocolate consumption was not associated with cancer mortality. The results suggest a modest inverse association of chocolate consumption with mortality from all causes, CVD, or dementia, specifically for moderate chocolate consumption of 1 to 3 servings/wk. [ABSTRACT FROM AUTHOR]

We studied the associations of leukocyte telomere length (LTL) with all-cause, cardiovascular disease, and cancer mortality in 12,199 adults participating in 2 population-based prospective cohort studies from Europe (ESTHER) and the United States (Nurses' Health Study). Blood samples were collected in 1989-1990 (Nurses' Health Study) and 2000-2002 (ESTHER). LTL was measured by quantitative polymerase chain reaction. We calculated z scores for LTL to standardize LTL measurements across the cohorts. Cox proportional hazards regression models were used to calculate relative mortality according to continuous levels and quintiles of LTLz scores. The hazard ratios obtained from each cohort were subsequently pooled by meta-analysis. Overall, 2,882 deaths were recorded during follow-up (Nurses' Health Study, 1989-2010; ESTHER, 2000-2015). LTL was inversely associated with age in both cohorts. After adjustment for age, a significant inverse trend of LTL with all-cause mortality was observed in both cohorts. In random-effects meta-analysis, age-adjusted hazard ratios for the shortest LTL quintile compared with the longest were 1.23 (95% confidence interval (CI): 1.04,1.46) for all-cause mortality, 1.29 (95% CI: 0.83, 2.00) for cardiovascular mortality, and 1.10 (95% CI: 0.88, 1.37) for cancer mortality. In this study population with an age range of 43-75 years, we corroborated previous evidence suggesting that LTL predicts all-cause mortality beyond its association with age. [ABSTRACT FROM AUTHOR]

Background: A small change in tea consumption at population level could have large impact on public health. However, the health benefits of tea intake among Americans are inconclusive. Objective: To evaluate the association between tea consumption and all-causes, cardiovascular disease (CVD) and cancer mortality in the Aerobics Center Longitudinal study (ACLS). Methods: 11808 participants (20-82 years) initially free of CVD and cancers enrolled in the ACLS and were followed for mortality. Participants provided baseline self-report of tea consumption (cups/day). During a median follow-up of 16 years, 842 participants died. Of others, 250 died from CVD, and 345 died from cancer, respectively. A Cox proportional hazard model was used to produce hazard ratio (HR) and 95% confidence interval (CI). Results: Compared with participants consuming no tea, tea drinkers had a survival advantage ( Log-2 = 10.2, df = 3, P = 0.017); however, the multivariate hazard ratios (HRs) of all-cause mortality for those drinking 1–7, 8–14, and >14 cups/week were 0.95 (95% CI, 0.81–1.12), 1.00 (95% CI, 0.82–1.22), and 0.98 (95% CI, 0.76–1.25), respectively (P for linear trend = 0.83). The multivariate HR were 1.16 (95% CI, 0.86–1.56), 1.22 (95% CI, 0.85–1.76), and 0.94 (95% CI, 0.56–1.54) for CVD mortality (P for linear trend = 0.47), and 0.97 (95% CI, 0.75–1.25), 0.85 (95% CI, 0.60–1.16), and 0.94 (95% CI, 0.64–1.38) for cancer mortality (P for trend = 0.62). Conclusions: There were week or null relationships between tea consumption and mortality due to all-cause, CVD disease or cancer were observed in ACLS. [ABSTRACT FROM PUBLISHER]

Objectives To assess the relationship between hemoglobin concentration and cause-specific mortality. Design Cohort study. Setting Data from the government-sponsored Annual Geriatric Health Examination Program. Participants Community-dwelling Taipei citizens aged 65 and older followed up between 2006 and 2010 (N = 77,532). Measurements Mortality was determined by matching participants' medical records with national death files. Cox proportional hazards regression models were used to evaluate the relationship between hemoglobin concentration (World Health Organization ( WHO)-defined anemia and 7 hemoglobin concentrations) and cause-specific mortality. Results The mortality risk of WHO-defined anemia increased substantially in both sexes for all-cause and cancer mortalities (men, hazard ratio ( HR) = 1.86, 95% confidence interval ( CI) = 1.71-2.02 for all-cause mortality; HR = 1.94, 95% CI = 1.69-2.22 for cancer mortality; for women, HR = 1.63, 95% CI = 1.43-1.86 for all-cause mortality; HR = 1.74, 95% CI = 1.38-2.19 for cancer mortality). Men with hemoglobin concentrations of 15.0 to 15.9 g/ dL and women with hemoglobin concentrations of 13.0 to 13.9 g/ dL had the lowest risks of all-cause, cardiovascular, and cancer mortality. Risks of all-cause and cancer mortality increased significantly when hemoglobin concentrations were less than 14 g/ dL in men and less than 12 g/ dL in women. Even mild anemia (11.0-11.9 g/ dL) was associated with greater mortality risk. Stratification according to age, body mass index, estimated glomerular filtration rate, and presence of comorbidities did not lead to any substantial changes. Conclusion Hemoglobin concentrations associated with optimal survival in older adults were identified and additional data provided regarding the relationship between hemoglobin concentrations and cause-specific mortality risks in older adults. [ABSTRACT FROM AUTHOR]