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Aims: The aim of this study was to investigate associations between having visited the theatre/cinema and an arts exhibition during the past year and all-cause, cardiovascular disease (CVD), cancer and other-cause mortality. Methods: The 2008 public health postal survey in Scania, Sweden, was distributed to a stratified random sample of the adult population (18–80 years old). The participation rate was 54.1%, and 25,420 participants were included in the present study. The baseline 2008 survey data were linked to cause-of-death register data to create a prospective cohort with 8.3-year follow-up. Associations between visit to the theatre/cinema, visit to an arts exhibition and mortality were investigated in survival (Cox) regression models. Results: Just over a quarter (26.5%) had visited both the theatre/cinema and an arts exhibition during the past year, 36.6% only the theatre/cinema, 4.9% only an arts exhibition and 32% neither of the two. Not visiting the theatre/cinema during the past year was associated with higher all-cause and CVD mortality. Not visiting an arts exhibition was associated with higher all-cause and other-cause mortality. The combination of having visited neither the theatre/cinema nor an arts exhibition during the past year was associated with higher all-cause, CVD and other-cause mortality. Conclusions: There is an association between attending arts and culture activities and a reduced risk of CVD and other-cause mortality but not cancer mortality, although model imperfections are possible. [ABSTRACT FROM AUTHOR]

Background: This study aimed to examine associations between haemoglobin A1c (HbA1c) levels over time and all-cause and cause-specific mortality in middle-aged and older Koreans. Methods: Using 16 years of follow-up data from the Korean Genome and Epidemiology Study, we analysed 9294 individuals aged 40–69 years with no history of cardiovascular disease (CVD) or cancer. Participants were divided into a known diabetes group and five groups categorized by HbA1c levels (< 5.0%, 5.0–5.4%, 5.5–5.9%, 6.0–6.4%, and ≥ 6.5%). Hazard ratios (HRs) for all-cause and cause-specific mortality associated with HbA1c levels were calculated using a conventional and a time-dependent Cox proportional hazards model. Restricted cubic spline models were fitted to investigate the relationship between continuous HbA1c levels and mortality among people without known diabetes. Subgroup analyses were performed for age, sex, smoking, hypertension, liver diseases, and red blood cell counts. Results: During a median follow-up period of 15.7 years, there were 944 deaths, including 185 deaths from CVD, 359 from cancer, and 125 from all external causes. Compared with participants with HbA1c levels of 5.5–5.9%, multivariate-adjusted HRs and 95% confidence intervals for all-cause death of participants with levels < 5.0%, 5.0–5.4%, 6.0–6.4%, and ≥ 6.5% and participants with known diabetes were 1.84 (1.35–2.51), 1.13 (0.95–1.34), 1.30 (1.04–1.62), 1.37 (0.97–1.93), and 2.03 (1.70–2.44), respectively. The risk of cancer mortality was significantly increased in HbA1c < 5.0% (HR, 2.21; 95% CI 1.42–3.44) and known diabetes (HR, 1.60; 95% CI 1.18–2.15). When we performed diverse subgroup analyses, low HbA1c levels at baseline were strongly associated with mortality in participants with liver diseases. Conclusions: We found U-shaped associations between HbA1c levels at baseline and over time and all-cause mortality in middle-aged and older Koreans. Additionally, the risk of cancer mortality increased both in low and high HbA1c groups, but CVD mortality increased only in high HbA1c group. In particular, people with liver diseases and low HbA1c levels had a high risk of all-cause mortality. Therefore, more careful management of these groups is suggested to identify any deteriorating health conditions. [ABSTRACT FROM AUTHOR]

Background: The shape of the exposure-response curve for long-term ambient fine particulate (PM2.5) exposure and cause-specific mortality is poorly understood, especially for rural populations and underrepresented minorities.Methods: We used hybrid machine learning and Cox proportional hazard models to assess the association of long-term PM2.5 exposures on specific causes of death for 53 million U.S. Medicare beneficiaries (aged ≥65) from 2000 to 2008. Models included strata for age, sex, race, and ZIP code and controlled for neighborhood socio-economic status (SES) in our main analyses, with approximately 4 billion person-months of follow-up, and additionally for warm season average of 1-h daily maximum ozone exposures in a sensitivity analysis. The impact of non-traffic PM2.5 on mortality was examined using two stage models of PM2.5 and nitrogen dioxide (NO2).Results: A 10 μg /m3 increase in 12-month average PM2.5 prior to death was associated with a 5% increase in all-cause mortality, as well as an 8.8, 5.6, and 2.5% increase in all cardiovascular disease (CVD)-, all respiratory-, and all cancer deaths, respectively, in age, gender, race, ZIP code, and SES-adjusted models. PM2.5 exposures, however, were not associated with lung cancer mortality. Results were not sensitive to control for ozone exposures. PM2.5-mortality associations for CVD- and respiratory-related causes were positive and significant for beneficiaries irrespective of their sex, race, age, SES and urbanicity, with no evidence of a lower threshold for response or of lower Risk Ratios (RRs) at low PM2.5 levels. Associations between PM2.5 and CVD and respiratory mortality were linear and were higher for younger, Black and urban beneficiaries, but were largely similar by SES. Risks associated with non-traffic PM2.5 were lower than that for all PM2.5 and were null for respiratory and lung cancer-related deaths.Conclusions: PM2.5 was associated with mortality from CVD, respiratory, and all cancer, but not lung cancer. PM2.5-associated risks of CVD and respiratory mortality were similar across PM2.5 levels, with no evidence of a threshold. Blacks, urban, and younger beneficiaries were most vulnerable to the long-term impacts of PM2.5 on mortality. [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]

Anemia and low and high levels of hemoglobin have been associated with increased mortality and morbidity. However, most studies have measured hemoglobin at only 1 time point, and few studies have considered possible reverse causation. We used data from the Women's Health Initiative, in which baseline hemoglobin was measured in 160,081 postmenopausal women and year 3 hemoglobin was measured in 75,658 participants, to examine the associations of hemoglobin concentration with total mortality, coronary heart disease mortality, and cancer mortality. Women were enrolled from 1993 to 1998 and followed for a median of 16 years. Cox proportional hazards models were used to estimate the relative mortality hazards associated with deciles of baseline hemoglobin and the mean of baseline + year 3 hemoglobin. Both low and high deciles of baseline hemoglobin were positively associated with all 3 outcomes in the total cohort. In analyses restricted to women with 2 measurements, a low mean hemoglobin level was robustly and positively associated with all 3 outcomes, after exclusion of the early years of follow-up. High mean hemoglobin was also associated with increased risk of total mortality, whereas associations with heart disease mortality and cancer mortality were weaker and inconsistent. Our results provide evidence that low and high levels of hemoglobin are associated with increased risk of mortality in otherwise healthy women. [ABSTRACT FROM AUTHOR]

[Display omitted] Our understanding of the impact of long-term exposures to PM 2.5 constituents and sources on mortality is limited. To examine associations between long-term exposures to PM 2.5 constituents and sources and cause-specific mortality in US older adults. We obtained demographic and mortality data for 15.4 million Medicare beneficiaries living within the conterminous United States (US) between 2000 and 2008. We assessed PM 2.5 constituents exposures for each beneficiary and used factor analysis and residual-based methods to characterize PM 2.5 sources and mixtures, respectively. In age-, sex-, race- and site- stratified Cox proportional hazard models adjusted for neighborhood socio-economic status (SES), we assessed associations of individual PM 2.5 constituents, sources, and mixtures and cause-specific mortality and examined modification of these associations by participant demographics and location of residence. We assessed the robustness of our findings to additional adjustment for behavioral risk factors and to alternate exposure definitions and exposure windows. Hazard ratios (HR) were highest for all causes of death, except COPD, for PM 2.5 constituents and the coal combustion-related PM 2.5 components, with no evidence of confounding by behavioral covariates. We further found Pb and metal-related PM 2.5 components to be significantly associated with increased HR of all causes of death, except COPD and lung cancer mortality, and nitrate (NO 3 –) and silicon (Si) and associated source-related PM 2.5 components (traffic and soil, respectively) to be significantly associated with increased all-cause, CVD, respiratory and all cancer-related mortality HR. Associations for other examined constituents and mortality were inconsistent or largely null. Our analyses of mixtures were generally consistent with these findings. Mortality HRs were greatest for minority, especially Black, low-income urban, younger, and male beneficiaries. PM 2.5 components related to coal combustion, traffic, and to a lesser extent, soil were strongly associated with mortality from CVD, respiratory disease, and cancer. [ABSTRACT FROM AUTHOR]