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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]

Aim: To test the association of alcohol consumption with total and cause‐specific mortality risk. Design Prospective observational multi‐centre population‐based study. Setting: Sixteen cohorts (15 from Europe) in the MOnica Risk, Genetics, Archiving and Monograph (MORGAM) Project. Participants: A total of 142 960 individuals (mean age 50 ± 13 years, 53.9% men). Measurements Average alcohol intake by food frequency questionnaire, total and cause‐specific mortality. Findings In comparison with life‐time abstainers, consumption of alcohol less than 10 g/day was associated with an average 11% [95% confidence interval (CI) = 7–14%] reduction in the risk of total mortality, while intake > 20 g/day was associated with a 13% (95% CI = 7–20%) increase in the risk of total mortality. Comparable findings were observed for cardiovascular (CV) deaths. With regard to cancer, drinking up to 10 g/day was not associated with either mortality risk reduction or increase, while alcohol intake > 20 g/day was associated with a 22% (95% CI = 10–35%) increased risk of mortality. The association of alcohol with fatal outcomes was similar in men and women, differed somewhat between countries and was more apparent in individuals preferring wine, suggesting that benefits may not be due to ethanol but other ingredients. Mediation analysis showed that high‐density lipoprotein cholesterol explained 2.9 and 18.7% of the association between low alcohol intake and total as well as CV mortality, respectively. Conclusions: In comparison with life‐time abstainers, consuming less than one drink per day (nadir at 5 g/day) was associated with a reduced risk of total, cardiovascular and other causes mortality, except cancer. Intake of more than two drinks per day was associated with an increased risk of total, cardiovascular and especially cancer mortality. [ABSTRACT FROM AUTHOR]

Purpose: The health benefits of the Mediterranean diet (MedDiet) have been widely studied. However, controversy remains for one of its components: alcohol intake. We aimed to assess the joint effect of adherence to the MedDiet and alcohol-drinking pattern on all-cause mortality. Methods: We used data from 20,506 subjects from a prospective cohort of Spanish university graduates, the Seguimiento Universidad de Navarra (SUN) cohort. Adherence to the MedDiet was operationalized using four different dietary indexes and then categorized in low or high adherence, according to the median score. Alcohol-drinking pattern was evaluated with the previously defined the Mediterranean alcohol-drinking pattern (MADP), grouped into three categories of adherence (low, moderate and high adherence) and a fourth category for abstainers. The outcome was all-cause mortality. Results: During a median follow-up of 12.1 years, we observed 460 deaths. No statistically significant supra-multiplicative interaction between the two exposures was found. Low adherence to both the MedDiet and MADP was associated with higher all-cause mortality compared to high adherence to both exposures [multivariable-adjusted hazard ratio (HR) = 2.02, 95% confidence interval (CI): 1.33–3.07]. Similar results were found for cancer mortality and cardiovascular mortality. Conclusions: Although the combined effect of the MedDiet and MADP was not significantly higher than the product of their individual effects, a low adherence to both the MedDiet and MADP was associated with higher rates of all-cause mortality. This report also shows the usefulness of the dietary pattern approach applied to alcohol intake and of including the drinking pattern as another component of the MedDiet. [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]

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]