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Aims Methods Results Conclusions The relationship between α‐Klotho (αK) and mortality is controversial and has not been examined in a large, diverse cohort. We investigated the association between serum αK protein levels with all‐cause and cause‐specific mortality in a cohort representative of the US population.We used National Health and Nutrition Examination Survey (NHANES) data from 2007 to 2016. A nonlinear association between mortality and αK levels as a quadratic variable were examined using Cox proportional hazard models and competing risk models. Multivariable models were adjusted for age, gender, race, hypertension, diabetes, smoking, alcohol use, physical activity, body mass index (BMI), serum cholesterol, estimated glomerular filtration rate, highest educational status attained and family income to poverty threshold ratio.Of the 13 749 participants, 1569 (11%) died, 7092 (52%) were female, and 5918 (43%) were Caucasian. The mean (SD) of age was 58 (11) years, BMI 29.7 (6.7) kg/m2, and αK was 0.85 (0.31) ng/mL. In the adjusted Cox proportional hazards model with quadratic αK, we found a U‐shaped relationship between all‐cause mortality and αK levels (continuous αK hazard ratio [HR] = 0.56, 95% confidence interval [CI]: 0.37, 0.85; P = .007; squared‐αK HR = 1.25, 95% CI: 1.11, 1.41; P < 0.001). A similar U‐shaped relationship was noted between αK and cancer mortality in the adjusted Cox proportional hazards model (continuous αK HR = 0.45, 95% CI: 0.19, 1.06; P = 0.07; squared αK HR = 1.32, 95% CI: 1.07, 1.61; P = 0.009). No relationship was present with cardiovascular or other‐cause mortality.In this large diverse cohort, we report a U‐shaped relationship between αK with all‐cause and cancer mortality. Further research to elucidate the underlying biological mechanism of these relationships is needed. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders, but few studies have evaluated mortality risks among individuals with IBS. We explored the association between IBS and all-cause and cause-specific mortality in the UK Biobank. METHODS: We included 502,369 participants from the UK Biobank with mortality data through 2022. IBS was defined using baseline self-report and linkage to primary care or hospital admission data. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and cause-specific mortality using multivariable Cox proportional hazards regression models within partitioned follow-up time categories (0-5, >5-10, and >10 years). RESULTS: A total of 25,697 participants (5.1%) had a history of IBS at baseline. After a median follow-up of 13.7 years, a total of 44,499 deaths occurred. Having an IBS diagnosis was strongly associated with lower risks of all-cause (HR50.70,95%CI50.62-0.78) and all-cancer (HR50.69,95%CI50.60-0.79) mortality in the first 5 years of follow-up. These associations were attenuated over follow-up, but even after 10 years of follow-up, associations remained inverse (all-cause: HR5 0.89, 95%CI5 0.84-0.96; all-cancer: HR 5 0.87, 95% CI 5 0.78-0.97) after full adjustment. Individuals with IBS had decreased risk of mortality from breast, prostate, and colorectal cancers in some of the follow-up time categories. DISCUSSION: We found that earlier during follow-up, having diagnosed IBS was associated with lower mortality risk, and the association attenuated over time. Additional studies to understand whether specific factors, such as lifestyle and healthcare access, explain the inverse association between IBS and mortality are needed. [ABSTRACT FROM AUTHOR]

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: Serum albumin levels and cancer mortality are closely related, yet large-sample studies encompassing a broad spectrum of cancer types are lacking. Methods: This study encompassed patients diagnosed with cancer across the continuous 10 cycles of NHANES surveys from 1999 to 2018. The study population was stratified into two groups based on median albumin levels (≤ 4.2g/dL and > 4.2 g/dL) or cancer aggressiveness (well-survived cancers and poorly-survived cancers). Survival rates were estimated using the Kaplan-Meier method. The Cox proportional hazards model was employed to evaluate the association between serum albumin levels and cancer mortality. Restricted cubic spline (RCS) analysis was conducted to assess the nonlinear relationship between serum albumin levels and the risk of cancer mortality. Results: Kaplan-Meier curves demonstrated that patients with albumin levels ≤ 4.2 g/dL exhibited lower survival rates compared to those with levels > 4.2 g/dL, irrespective of cancer aggressiveness. Following adjustment for confounders, decreased albumin levels were associated with an elevated risk of cancer mortality across all groups [all cancers, HR (95%CI) = 2.03(1.73, 2.37); well survived cancers, HR (95%CI) = 1.78(1.38, 2.32); and poorly survived cancers, HR (95%CI) = 1.99(1.64, 2.42)]. RCS analyses revealed a stable nonlinear negative association between albumin levels and cancer mortality in all groups, regardless of confounder adjustment. Conclusion: Low serum albumin levels predict higher cancer mortality. Furthermore, a nonlinear negative association was observed between serum albumin levels and the risk of cancer mortality. [ABSTRACT FROM AUTHOR]

Background: Socioeconomic status (SES) is associated with a range of health outcomes, including cancer diagnosis and survival. However, the evidence for this association is inconsistent between countries with and without single‐payer health care systems. In this study, the relationships between neighborhood‐level income, cancer stage at diagnosis, and cancer‐specific mortality in Alberta, Canada, were evaluated. Methods: The Alberta Cancer Registry was used to identify all primary cancer diagnoses between 2010 and 2020. Average neighborhood income was determined by linking the Canadian census to postal codes and was categorized into quintiles on the basis of income distribution in Alberta. Multivariable multinomial logistic regression was used to model the association between income quintile and stage at diagnosis, and the Fine–Gray proportional subdistribution hazards model was used to estimate the association between SES and cancer‐specific mortality. Results: Out of the 143,818 patients with cancer included in the study, those in lower income quintiles were significantly more likely to be diagnosed at stage III (odds ratio [OR], 1.07; 95% CI [confidence interval], 1.06–1.09) or IV (OR, 1.12; 95% CI, 1.11–1.14) after adjusting for age and sex. Lower income quintiles also had significantly worse cancer‐specific survival for breast, colorectal, liver, lung, non‐Hodgkin lymphoma, oral cavity, pancreas, and prostate cancers. Conclusions: Disparities were observed in cancer outcomes across neighborhood‐level income groups in Alberta, which demonstrates that health inequities by SES exist in countries with single‐payer health care systems. Further research is needed to better understand the underlying causes and to develop strategies to mitigate these disparities. The association between socioeconomic status and cancer outcomes in countries with single‐payer health care systems is inconsistent. In this analysis, lower socioeconomic status was found to be associated with both stage at diagnosis and cancer‐specific mortality of major cancer types in a Canadian province. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease (IBD) has a rising global prevalence. However, the understanding of its impact on mortality remains inconsistent so we explored the association between IBD and all-cause and cause-specific mortality. This study included 502,369 participants from the UK Biobank, a large, population-based, prospective cohort study with mortality data through 2022. IBD was defined by baseline self-report or from primary care or hospital admission data. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and cause-specific mortality in multivariable Cox proportional hazards regression models. A total of 5799 (1.2%) participants had a history of IBD at baseline. After a median follow-up of 13.7 years, 44,499 deaths occurred. Having IBD was associated with an increased risk of death from all causes (HR = 1.16, 95% CI = 1.07–1.24) and cancer (HR = 1.16, 95% CI = 1.05–1.30), particularly colorectal cancer (CRC) (HR = 1.56, 95% CI = 1.17–2.09). We observed elevated breast cancer mortality rates for individuals with Crohn's disease, and increased CRC mortality rates for individuals with ulcerative colitis. In stratified analyses of IBD and all-cause mortality, mortality risk differed by individuals' duration of IBD, age at IBD diagnosis, body mass index (BMI) (P Heterogeneity = 0.03) and smoking status (P Heterogeneity = 0.01). Positive associations between IBD and all-cause mortality were detected in individuals diagnosed with IBD for 10 years or longer, those diagnosed before the age of 50, all BMI subgroups except obese individuals, and in never or current, but not former smokers. We found that having IBD was associated with increased risks of mortality from all causes, all cancers, and CRC. This underscores the importance of enhanced patient management strategies and targeted prevention efforts in individuals with IBD. [ABSTRACT FROM AUTHOR]

Background: Different ages for diagnosis of diabetes have diverse effects on risks of cardiovascular disease, dementia, and mortality, but there is little evidence of cancer. This study investigated the relationship between diabetes at different diagnostic ages and risks of cancer incidence and mortality in people aged 37--73 years. Methods: Participants with diabetes in the UK Biobank prospective cohort were divided into four groups: ≤40, 41--50, 51--60, and >60 years according to age at diagnosis. A total of 26,318 diabetics and 105,272 controls (1:4 randomly selected for each diabetic matched by the same baseline age) were included. We calculated the incidence density, standardized incidence, and mortality rates of cancer. Cox proportional hazard model was used to examine the associations of diabetes at different diagnostic ages with cancer incidence and mortality, followed by subgroup analyses. Results: Compared to corresponding controls, standardized incidence and mortality rates of overall and digestive system cancers were higher in diabetes diagnosed at age 41--50, 51--60, and >60 years, especially at 51--60 years. Individuals diagnosed with diabetes at different ages were at higher risk to develop site-specific cancers, with a prominently increased risk of liver cancer since the diagnosis age of >40 years. Significantly, participants with diabetes diagnosed at 51--60 years were correlated with various site-specific cancer risks [hazard ratio (HR) for incidence: 1.088--2.416, HR for mortality: 1.276--3.269]. Moreover, for mortality of digestive system cancers, we observed an interaction effect between smoking and diabetes diagnosed at 51--60 years. Conclusion: Our findings highlighted that the age at diagnosis of diabetes, especially 51--60 years, was critical risks of cancer incidence and mortality and may represent a potential preventative window for cancer. [ABSTRACT FROM AUTHOR]

Background: Kidney function is associated with clinical outcomes in patients with cancer. Objectives: This study aimed to assess the association between kidney function decline and cancer‐related mortality among community‐dwelling elderly individuals. Design: This was a retrospective longitudinal cohort study. Participants: The 61,988 participants were from an elderly health examination database in Taipei City from 2005 to 2012. Measurements Multivariable logistic regression was used to assess the association between baseline covariates and rapidly deteriorating estimated glomerular filtration rate (eGFR). In addition, Cox proportional hazards model and the Fine–Gray model were used to quantify the effects of covariates on total cancer mortality and six specific cancer mortalities. Results: During the follow‐up period, 1482 participants died of cancer. Their baseline average eGFR was 73.8 ± 19.9 mL/min/1.73 m2, and 18.3% had rapid renal function decline (≥5 mL/min/1.73 m2 per year). Rapid renal function decline was positively related to age, baseline eGFR, proteinuria, hypertension, waist circumferences, high log triglyceride levels, and diabetes mellitus (DM) history. In Cox proportional hazard models, participants with rapid eGFR decline had an increased risk of cancer mortality [hazard ratio (95% CI): 1.97 (1.73, 2.24); p < 0.001] compared to those without rapid eGFR decline. In the analysis of site‐specific cancer mortality risk, rapid eGFR decline was associated with six site‐specific cancer mortality, namely gastrointestinal tract, hepatobiliary, lung, prostate, urinary tract, and hematological malignancies. Conclusions: Elderly individuals with rapid kidney function decline had higher cancer mortality risks. Serial assessments of dynamic changes in eGFR might provide information relevant for cancer prognosis. [ABSTRACT FROM AUTHOR]

Aim: To estimate the risk of cancer incidence and mortality among patients with alcoholic liver disease in South Korea. Methods: A matched cohort study was conducted, including 1,042,185 men (alcoholic liver disease cases: 208,437; controls: 833,748) and 100,400 women (alcoholic liver disease cases: 20,080; controls: 80,320), matched for sex, age, smoking, alcohol consumption, and body mass index at a 1:4 ratio. The risk of cancer incidence and mortality in the alcoholic liver disease group was assessed using Cox proportional hazards regression models. Results: Both men and women with alcoholic liver disease had an elevated risk of all‐cancer and liver cancer incidence and mortality in comparison with the control group. In men, alcoholic liver disease was associated with a significantly higher risk of development of 10 cancer types, including lip, oral cavity, and pharynx; esophagus; liver; gallbladder and biliary tract; pancreas; larynx; lung; kidney; thyroid gland; and leukemia. Subgroup analysis by hepatitis B and C infection showed increased hazard ratios of all cancer incidences and mortality in the alcoholic liver disease group, regardless of hepatitis B or C infection status. In both sexes, a higher number and more years of hospital or clinic visits for alcoholic liver disease were associated with an increased risk of incidence and mortality from all cancers and liver cancer. A more profound dose–response relationship between alcoholic liver disease and alcohol consumption was observed in women than in men. Conclusions: Our findings emphasize the need for a clinical surveillance program and the early detection of cancer in patients with alcoholic liver disease. [ABSTRACT FROM AUTHOR]

Purpose: We investigated the risk of mortality from cancers attributable to modifiable risk factors across representative transport, rescue, and security industries.Methods: We used nationwide Danish registries to identify all 307,605 workers from these industries from 2001 through 2015 and 2,278,363 other economically active individuals aged 18-64 years at the baseline for comparison. Adjusted hazard ratios (HR) and 95% confidence intervals (CI) for site-specific cancer deaths were calculated using Cox regression. Site-specific cancers were categorized by using population-attributable fraction (PAF) estimates derived from the previous literature.Results: During an average follow-up of 12.8 years, 5977 cancer deaths were registered in these industries. Cancer mortality with a high proportion of avoidable deaths (i.e., high PAF) was elevated in male seafarers (1.37; 1.16-1.62), in men of land transport (1.44; 1.35-1.52), in women of land transport (1.51; 1.29-1.77), and in women of defense forces (1.43; 1.13-1.81). In contrast, cancer mortality with a high PAF was reduced in men of police force (0.63; 0.51-0.78). The total cancer mortality was higher in seafarers (1.24; 1.12-1.37), workers in land transport (1.31; 1.27-1.36), and workers in defense forces (1.14; 1.07-1.22).Conclusions: We observed considerable cancer mortality disparities associated with modifiable risk factors across transport, rescue, and security industries. [ABSTRACT FROM AUTHOR]

Sleep duration is emerging as an important modifiable risk factor for morbidity and mortality. We assessed the association between sleep duration and cancer incidence and mortality among Japanese adults using data from six population‐based cohorts with 271 694 participants. During a total follow‐up period of about 5.9 million person‐years, we identified 40 751 incident cancer cases and 18 323 cancer deaths. We computed study‐specific hazard ratios (HRs) and 95% confidence intervals (CIs) using Cox proportional hazards regression models and pooled the estimates using random‐effects meta‐analysis. Sleep duration of ≥10 hours (vs 7 hours) was associated with increased risk of cancer incidence among women (HR 1.19, 95% CI 1.02‐1.38), but not men, and increased risk of cancer mortality among men (HR 1.18, 95% CI 1.00‐1.39) and women (HR 1.44, 95% CI 1.20‐1.73). Sleep duration of ≤5 hours (vs 7 hours) was not associated with cancer incidence and mortality. However, among postmenopausal women, sleep durations of both ≤5 and ≥10 hours (vs 7 hours) were associated with an increased risk of cancer mortality. Among Japanese adults, sleep duration of ≥10 hours is associated with increased risk of cancer incidence and mortality among women and cancer mortality among men. [ABSTRACT FROM AUTHOR]

Background: The relationship between vitamin D status and mortality in patients with osteoarthritis (OA) is unknown. This study investigated the associations of serum 25-hydroxyvitamin D [25(OH)D] concentrations with all-cause and cause-specific mortality among American adults with OA.Methods: This study included 2556 adults with OA from the National Health and Nutrition Examination Survey (2001-2014). Death outcomes were ascertained by linkage to National Death Index (NDI) records through 31 December 2015. Cox proportional hazards model and two-piecewise Cox proportional hazards model were used to elucidate the nonlinear relationship between serum 25(OH)D concentrations and mortality in OA patients, and stratified analyses were performed to identify patients with higher mortality risk.Results: During 16,606 person-years of follow-up, 438 all-cause deaths occurred, including 74 cardiovascular disease (CVD)-related and 78 cancer deaths. After multivariable adjustment, lower serum 25(OH)D levels were significantly and nonlinearly associated with higher risks of all-cause and CVD mortality among participants with OA. Furthermore, we discovered L-shaped associations between serum 25(OH)D levels and all-cause and CVD mortality, with mortality plateauing at 54.40 nmol/L for all-cause mortality and 27.70 nmol/L for CVD mortality. Compared to participants with 25(OH)D levels below the inflection points, those with higher levels had a 2% lower risk for all-cause mortality (hazard ratio [HR] 0.98, 95% confidence interval [CI] 0.96-0.99) and 17% lower risk for CVD mortality (HR 0.83, 95% CI 0.72-0.95).Conclusions: Nonlinear associations of serum 25(OH)D levels with all-cause and CVD mortality were observed in American patients with OA. The thresholds of 27.70 and 54.40 nmol/L for CVD and all-cause mortality, respectively, may represent intervention targets for lowering the risk of premature death and cardiovascular disease, but this needs to be confirmed in large clinical trials. [ABSTRACT FROM AUTHOR]

Introduction: Air pollutants are classified as carcinogens by the International Agency for Research on Cancer. Long-term exposure to ambient particulate matter with an aerodiameter of 2.5 μm or lower (PM2.5) has been reported to be linked with increased mortality due to hepatocellular carcinoma (HCC). However, the effects of air pollutants other than PM2.5 on HCC-related mortality have not been fully investigated. Accordingly, we conducted this study to assess the effect of long-term exposure to air pollutants (PM2.5 and nitrogen dioxide [NO2]) on HCC-related mortality. Method: In 2005, the Taiwan Liver Cancer Network (TLCN) was established by the National Research Program for Genomic Medicine to recruit liver cancer patients from 5 major medical centers in northern, central, and southern Taiwan. The TLCN had successfully recruited 9,344 patients by the end of 2018. In this study, we included 1,000 patients randomly sampled from the TLCN to assess the effect of exposure to air pollutants on HCC mortality after HCC diagnosis. Daily averages of PM2.5 and NO2 concentrations were retrieved from 77 air quality-monitoring stations and interpolated to the townships of patients' residences by using the Kriging method. The effect of air pollutants on HCC survival was assessed using a Cox proportional hazards model. Results: A total of 940 patients were included in the analysis. After adjusting for potential confounders and mutually adjusting for co-pollutants, we observed that the hazards ratio (95% confidence interval) for HCC-related mortality for every 1-μg/m3 increase in PM2.5 concentration was 1.11 (1.08–1.14) and that for every 1-ppb increase in NO2 concentration was 1.08 (1.03–1.13). Conclusion: Our study suggests that long-term exposure to PM2.5 and NO2 was associated with decreased survival time in patients with HCC in Taiwan. [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]

We examined whether secondhand smoke exposure during childhood was associated with cancer mortality in adulthood among never smokers. In the Japan Collaborative Cohort Study for Evaluation of Cancer Risk, we analyzed data from 45,722 Japanese lifetime nonsmokers aged 40–79 years with no history of cancer at baseline (1988–1990) who had completed a lifestyle questionnaire, including information on the number of family members who had smoked at home during their childhood (0, 1, 2, or ≥3 family members). A Cox proportional hazards model and competing-risks regression were used to calculate multivariable hazard ratios and subdistribution hazard ratios with 95% confidence intervals for overall and site-specific cancer mortality according to the number of family members who smoked during the participant's childhood, after adjusting for potentially confounding factors. During a median follow-up period of 19.2 years, a total of 2,356 cancer deaths were documented. Secondhand smoke exposure was positively associated with the risk of mortality from pancreatic cancer in adulthood; the multivariable hazard ratio for having 3 or more family members who smoked (as compared with none) was 2.32 (95% confidence interval: 1.14, 4.72). Associations were not evident for total cancer risk or risk of other types of smoking-related cancer. In this study, secondhand smoke exposure during childhood was associated with an increased risk of pancreatic cancer mortality in adulthood. [ABSTRACT FROM AUTHOR]

Purpose: We aimed to investigate the relationship between overall nutritional status and cancer mortality. Methods: A total of 12 262 US adults from six consecutive surveys of the National Health and Nutrition Examination Survey (NHANES 2003–2014) were analyzed. The overall health nutritional biomarkers index (HNBI) score, capturing characteristics of 17 biomarkers was developed to assess the overall nutritional status. The lower the HNBI score, the healthier nutritional status would be. Hazard ratio (HR) and 95% confidence intervals (95% CIs) were calculated by Cox proportional hazards regression models to evaluate the association between the HNBI score and cancer mortality. Results: The lower overall HNBI score was associated with decreased risk of cancer mortality, compared with participants in the 4th quartile of overall HNBI score, the HR (95% CIs) for participants in the 1st quartiles was 0.54 (0.33–0.89) (P-trend = 0.019). Healthier lifestyle habits and not obesity interacted with HNBI score, compared with participants with higher HNBI score and smoking currently/not exercising regularly/obesity, participants with lower HNBI score and not smoking currently/exercising regularly/not obesity were associated with lower risk of cancer mortality, the HR (95% CIs) were 0.43 (0.26–0.73), 0.57 (0.33–0.97), and 0.62 (0.47–0.97), respectively. These significant associations remained among participants who were followed-up more than 2 years. Conclusion: Our findings suggested that healthier overall nutritional status was associated with lower risk of cancer mortality among US adults. Not smoking, exercise regularly and not obesity interacted with overall nutritional status. Adherence to better overall nutritional status, lifestyle habits and optimal weight would prevent premature death from cancer. [ABSTRACT FROM AUTHOR]

Background: It is currently unknown if within high-quality dietary intake there exist distinct dietary patterns associated with health benefits that are identifiable with multidimensional dietary pattern analyses. The purpose of this study was to identify specific dietary patterns and groups therein and their associations with all-cause, CVD, and cancer mortality.Methods: We conducted sex-specific k-means cluster analyses within Healthy Eating Index 2015 (HEI-2015) quintile 5 in 3 US cohorts [NIH-American Association of Retired Persons Diet and Health Study (AARP), the Multiethnic Cohort (MEC), Women's Health Initiative Observational Study (WHI OS)], clusters ranging from n = 1190 to n = 12,007. Characterizations incorporated HEI-2015 overall and component-specific percentage adherence goals, using untruncated and truncated radar graphs and shape analyses. Using cohort- and sex-specific Cox proportional hazards models, associations of quintile 5 clusters with all-cause, cardiovascular disease (CVD), and cancer mortality were evaluated relative to quintile 1.Results: In each cohort sex-specific sample, 3 identified clusters included 16%-62% of participants, providing evidence for variation within high-quality dietary intake. Clusters revealed commonalities in total fruits and whole fruits intakes that exceeded goals and high sodium intake. Dairy and whole grain intakes oftentimes fell below goal. Some clusters were in addition characterized by total vegetables, greens & beans, and seafood & plant protein intakes exceeding goals. All high-quality dietary patterns were associated with a multivariable-adjusted significant 15%-26% lower risk of all-cause death than diet intake in quintile 1 (except for cluster 2 in WHI OS), and with a 16%-25% lower risk of CVD mortality in the AARP and MEC cohorts. Cancer mortality results were inconsistent.Conclusions: Multiple ways to achieve a high-quality diet were identified and significant associations with lower all-cause and CVD mortality were seen in some cohorts. [ABSTRACT FROM AUTHOR]

Background: Social determinants of health (SDOHs) cluster together and can have deleterious impacts on health outcomes. Individually, SDOHs increase the risk of cancer mortality, but their cumulative burden is not well understood. The authors sought to determine the combined effect of SDOH on cancer mortality. Methods: Using the Reasons for Geographic and Racial Differences in Stroke (REGARDS) cohort, the authors studied 29,766 participants aged 45+ years and followed them 10+ years. Eight potential SDOHs were considered, and retained SDOHs that were associated with cancer mortality (P <.10) were retained to create a count (0, 1, 2, 3+). Cox proportional hazard models estimated associations between the SDOH count and cancer mortality through December 31, 2017, adjusting for confounders. Models were age‐stratified (45‐64 vs 65+ years). Results: Participants were followed for a median of 10.6 years (interquartile range [IQR], 6.5, 12.7 years). Low education, low income, zip code poverty, poor public health infrastructure, lack of health insurance, and social isolation were significantly associated with cancer mortality. In adjusted models, among those <65 years, compared to no SDOHs, having 1 SDOH (adjusted hazard ratio [aHR], 1.39; 95% CI, 1.11‐1.75), 2 SDOHs (aHR, 1.61; 95% CI, 1.26‐2.07), and 3+ SDOHs (aHR, 2.09; 95% CI, 1.58‐2.75) were associated with cancer mortality (P for trend <.0001). Among individuals 65+ years, compared to no SDOH, having 1 SDOH (aHR, 1.16; 95% CI, 1.00‐1.35) and 3+ SDOHs (aHR, 1.26; 95% CI, 1.04‐1.52) was associated with cancer mortality (P for trend =.032). Conclusions: A greater number of SDOHs were significantly associated with an increased risk of cancer mortality, which persisted after adjustment for confounders. Individually, social determinants of health increase the risk of cancer mortality, but their cumulative burden is not well understood. A greater number of social determinants of health in the same individual are found to be significantly associated with an increased risk of cancer mortality, even after adjustment for a variety of confounders. [ABSTRACT FROM AUTHOR]

Background The risk of cancer in adulthood can be influenced by exposure to environmental factors (e.g. food shortage and stress) in early life. Objectives This study compared the risk of cancer morbidity and mortality between Chinese adults who were or were not exposed to the Great Chinese Famine (1959–1961) in utero or during early childhood. Methods The Kailuan Study participants (n  = 101,095) were classified into 5 famine exposure groups by birth year collected at study baseline (2006–2007): after 1961 (unexposed), 1959–1961 (in utero exposed), 1956–1958 (infancy and early childhood exposed, aged 0.1–2.9 y), 1953–1955 (childhood exposed, aged 3.0–5.9 y), and before 1953 (exposed, aged 6+ y). They were further classified by the severity of famine exposure. Cancer and cancer mortality cases from 2006 to 2016 were confirmed by reviewing medical records. Cox proportional hazard models were computed, adjusting for sex, socioeconomic status, and other time-varying cancer-related covariates. Results During a median follow-up of 10.0 y, we identified 3560 incident cancer cases and 1749 cancer deaths. Famine exposure at all ages was positively associated with the risk of cancer morbidity and mortality (P  < 0.001 for all, compared with unexposed). Severe exposure to famine in early childhood, but not other ages, had a higher risk of composite cancer events [adjusted HR = 2.04 (95% CI: 1.47, 2.84) for 0.1–2.9 y; and 1.61 (95% CI: 1.15, 2.25) for 3.0–5.9 y], relative to the less severely exposed groups of the same age range. When cancer morbidity and mortality were studied separately, similar patterns were observed. Conclusions In utero and early childhood exposures to famine, especially severe famine, were associated with a higher risk of cancer morbidity and mortality in adulthood. Awareness should be raised regarding the long-term effect of early life nutritional status. Trial registration number: ChiCTR-TNRC-11001489 (http://www.chictr.org.cn/showprojen.aspx?proj=8050). [ABSTRACT FROM AUTHOR]

Sixty-four percent of adults in America drink coffee daily, and caffeine is the main reason people tend to drink coffee habitually. Few studies have examined the association between caffeine and all-cause and cause-specific mortality. The objective of this study was to examine the association between caffeine and all-cause and cause-specific mortality using the National Health and Nutrition Examination Survey (NHANES) 1999-2014 database. The multivariate Cox proportional hazards regression model was used to examine 23,878 individuals 20 years and older. Daily caffeine intake was measured once at baseline. A total of 2206 deaths occurred, including 394 cardiovascular (CVD) deaths and 525 cancer deaths. Compared to those with a caffeine intake of <100 mg/day, the hazard ratios (HRs) for CVD mortality were significantly lower in the participants with a caffeine intake of 100-200 mg/day (HR, 0.63; 95% confidence interval [CI], 0.45-0.88), and those with a caffeine intake of >200 mg/day (HR, 0.67; 95% CI, 0.50-0.88) after adjusting for potential confounders. The HRs for all-cause mortality were significantly lower in the participants with a caffeine intake of 100-200 mg/day (HR, 0.78; 95% CI, 0.67-0.91), and those with a caffeine intake of >200 mg/day (HR, 0.68; 95% CI, 0.60-0.78). Subgroup analyses showed that caffeine may have different effects on all-cause mortality among different age and body mass index (BMI) groups. In conclusion, higher caffeine intake was associated with lower all-cause and CVD mortality. [ABSTRACT FROM AUTHOR]

• Elevated SII levels linked to higher frailty and mortality risk. • U-shaped relationship found between SII levels and mortality. • Critical SII thresholds identified for all-cause and cancer-related mortality. • Maintaining low SII levels may reduce frailty and mortality risk. Frailty is a state of heightened vulnerability to stress, whether from within the body or external factors. We aim to assess the prognostic value of the Systemic Immune-Inflammation Index (SII) in middle-aged and older frail adults. We used data from the 2003–2018 National Health and Nutrition Examination Survey (NHANES) linked to the 2019 National Death Index (NDI) to study mortality. Cox proportional hazards model and two-piecewise Cox proportional hazards model were used to elucidate the nonlinear relationship between SII level and mortality. Our study included 7,446 frail patients (mean age 65.6) with 2,524 deaths (726 from cardiovascular disease and 458 from cancer) over 49,565 person-years. Elevated SII levels were associated with an increased risk of all-cause, cardiovascular disease (CVD)-related and cancer-related mortality, even after adjusting for potential confounders (adjusted HR (95 % CI) = 1.35 (1.25, 1.46), 1.42 (1.22, 1.65) and 1.26 (1.05, 1.51), respectively). Moreover, a U-shaped correlation was discerned between SII levels and the risks of all-cause and cancer-related mortality, with respective thresholds identified at 334.96 and 348.28. Our findings reveal SII levels positively correlate with frailty, all-cause mortality, CVD-related mortality, and cancer-related mortality in middle-aged and elderly frail individuals in the U.S. The critical thresholds for SII index were 334.96 for all-cause mortality and 348.28 for cancer-related mortality. This study underscores the potential benefits of maintaining a certain low level of SII to effectively mitigate the incidence of frailty and mortality among frail patients. [ABSTRACT FROM AUTHOR]

Occupational polycyclic aromatic hydrocarbons (PAHs) exposure has been shown to increase the risk of various cancers and may be associated with carcinogenic mortality. However, no study has explored the relationship between environmental PAH exposure and mortality in general population. The aim of our study was to explore the association between PAH exposure and all-cause, cardiovascular, and cancer mortality in a general US adult population. We analyzed data from the National Health and Nutrition Examination Survey (NHANES 2001–2006) based on the information in this dataset on 692 males and 717 females. PAH exposure was detected using biomarkers from urine samples. Follow-up data on mortality were derived from initial examination of the subjects until death or 31 December 2006 in the NHANES database. We calculated hazard ratios (HRs) of PAH metabolites among all-cause, cardiovascular, and cancer mortality using the multivariate Cox proportional hazards regression model after adjusting for covariates. Among males, 3-phenanthrene was positively associated with increased risk of all-cause mortality (HR 1.043, 95%CI 1.019–1.066). Female participants with higher 2-napthol (HR 1.043, 95%CI 1.014–1.072), 3-fluorene (HR 2.159, 95%CI 1.233–3.779), and 1-phenanthrene (HR = 1.259, 95%CI 1.070–1.481) levels had increased all-cause mortality. In addition, high 3-phenanthrene (HR 1.333, 95%CI 1.008–1.763) and 1-phenanthrene (HR 1.463, 95%CI 1.126–1.900) levels increased the risk of cardiovascular mortality. However, there were no significant findings for cancer mortality in both genders. Environmental PAH exposure among the adult population is associated with non-carcinogenic but not cancer mortality. Future studies are warranted to determine the underlying mechanisms related to these findings. [ABSTRACT FROM AUTHOR]

Background: The health consequences of the use of Swedish snus, including its relationship with mortality, have not been fully established. We investigated the relationship between snus use and all-cause and cause-specific mortality (death due to cardiovascular diseases, cancer diseases and all other reasons, respectively) in a nationwide collaborative pooling project.Methods: We followed 169 103 never-smoking men from eight Swedish cohort studies, recruited in 1978-2010. Shared frailty models with random effects at the study level were used in order to estimate adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) of mortality associated with snus use.Results: Exclusive current snus users had an increased risk of all-cause mortality (aHR 1.28, 95% CI 1.20-1.35), cardiovascular mortality (aHR 1.27, 95% CI 1.15-1.41) and other cause mortality (aHR 1.37, 95% CI 1.24-1.52) compared with never-users of tobacco. The risk of cancer mortality was also increased (aHR 1.12, 95% CI 1.00-1.26). These mortality risks increased with duration of snus use, but not with weekly amount.Conclusions: Snus use among men is associated with increased all-cause mortality, cardiovascular mortality, with death from other causes and possibly with increased cancer mortality. [ABSTRACT FROM AUTHOR]

The potential of physical activity (PA) to attenuate the effects of alcohol consumption on the risks of alcohol‐related cancer mortality is unknown. We used data from participants aged 30 years and over in 10 British population‐based surveys (Health Surveys for England 1994, 1997, 1998, 1999, 2003, 2004, 2006 and 2008 and the Scottish Health Surveys 1998 and 2003). Alcohol‐related cancer mortality included oral cavity, throat, larynx, oesophagus, liver, colorectal, stomach and female breast (conservative definition), and additionally pancreas and lung (broad definition). Alcohol consumption was categorised into six groups based on the UK units/week: (a) never‐drinkers, (b) ex‐drinkers, (c) occasional drinkers, (d) within guidelines (<14 UK units/week [women]; <21 UK units/week [men]), (e) hazardous (14‐35 [women]; 21‐49 [men]) and (f) harmful (>35 [women]; >49 [men]). PA was categorised using two dichotomous classifications based on the lower (7.5 Metabolic Equivalent Task [MET]‐hours/week) and upper (15 MET‐hours/week) recommended limits. Using Cox proportional hazard models, we found a strong direct association between alcohol consumption and mortality risk of alcohol‐related cancers, with a significantly higher risk among ex‐drinkers (Hazard ratio [HR] = 1.46, 95% confidence interval [CI] = [1.09, 1.94]), drinkers who consumed hazardous (HR = 1.39, 95% CI = [1.06, 1.83]) and harmful amounts of alcohol (HR = 1.62, 95% CI = [1.13, 2.30]) compared to never‐drinkers in the fully adjusted model. The increased mortality risks were substantially attenuated when participants in these drinking groups exercised >7.5 MET‐hours/week. PA could be promoted as an adjunct risk minimisation measure for alcohol‐related cancer prevention. What's new? While alcohol consumption contributes to cancer mortality and is pervasive worldwide, many people who drink also engage in physical activity, which has numerous health benefits. The combined impact of these behaviors on cancer mortality risk is unknown. Here, alcohol consumption was strongly associated with alcohol‐related cancer mortality risk among participants from 10 British population‐based studies. This risk, however, was significantly reduced in physically active participants who met at least the lower recommended limit of activity per week. The findings suggest that adopting physical activity as a healthy lifestyle behavior could lessen the impact of alcohol consumption on cancer mortality. [ABSTRACT FROM AUTHOR]

Health insurance availability and affordability are vital elements in diagnosis and treatment of patients with cancer and thus constitute clinical significance as well. Although past studies have explored the disparity in mortality figures for patients with different insurance statuses, this population-based study is pioneering in analyzing the changes in cancer mortality risks over time amid macroeconomic shifts. The study uses Surveillance Epidemiology and End Results (SEER) data of 424,889 non-elderly patients with breast, cervical, ovarian, and uterine cancer diagnosed during 2007–2010 and 2011–2015. In addition to discussing incidence figures and insurance patterns, the study uses Kaplan-Meier and Cox's proportional hazard models to examine the changes in survival probability and mortality risks for insurance-stratified patients with female-specific cancer across the two time periods. Patients without insurance have an increased risk of mortality over time relative to insured patients. Moreover, uninsured patients face this heightened risk more than Medicaid patients. Despite public policy measures as well as advancements in diagnostic facilities and treatment technology, the increased relative mortality of patients without insurance limits the long-term affordability of cancer treatment for economically vulnerable patients in comparison with insured patients. • Recession caused lower ratio of insured patients, limiting treatment affordability. • Patients with cancer without insurance have higher relative mortality risk than before. • Uninsured patients face the heightened risk more than Medicaid-covered patients. • Over time, mortality gap between patients with and without insurance has widened. [ABSTRACT FROM AUTHOR]

Objective: Cancer patients exhibit disparity in mortality risks across demographic divisions as well as insurance groups. The effects of macroeconomic environment also vary for such strata. This study analyses the gaps between mortality risks for male and female cancer patients with and without insurance and examines how such gaps transform over time with macroeconomic shifts. Methods: Demographic, clinical and treatment records of 45,750 melanoma and 91,157 lung cancer patients diagnosed in 2007–2009 and 2011–2013 were extracted from Surveillance, Epidemiology and End Results (SEER) database. Kaplan–Meier test was applied to ascertain survival probability of each insurance group, while Cox proportional hazard model was used to assess relative mortality risk for Medicaid and uninsured patients, for the whole data as well as separately for both time periods and genders. Results: Both the hazard ratios and change thereof over time are greater for female patients without insurance, than for male patients. More than any insurance–gender subgroup, uninsured female patients of melanoma have much increased hazard ratios, from 1.41 [95% confidence interval (CI), 1.04–1.92] to 2.22 [95% CI, 1.67–2.94]. Conclusion: Despite diagnostic improvements and technology advancements, the adverse effects of macroeconomic crisis are associated with increased relative mortality risks for cancer patients without insurance, more for women than men. [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]

The objective of this study was to investigate whether leukocyte telomere length (LTL) predicts the risk for cancer mortality among American Indians participating in the Strong Heart Study (1989–1991). Participants (aged 45–74 years) were followed annually until December 2015 to collect information on morbidity/mortality. LTL was measured by qPCR using genomic DNA isolated from peripheral blood. The association between LTL and risk for cancer mortality was examined using a multivariable Cox proportional hazard model, adjusting for age, gender, education, study site, smoking, alcohol use, physical activity, systolic blood pressure, fasting blood glucose, obesity, and low- and high-density lipoprotein. Of 1945 participants (mean age 56.10 ± 8.17 at baseline, 57% women) followed for an average 20.5 years, 220 died of cancer. Results showed that longer LTL at baseline significantly predicts an increased risk of cancer death among females (HR 1.57, 95% CI 1.08–2.30), but not males (HR 0.74, 95% CI 0.49–1.12) (p for interaction 0.009). Specifically, compared with the women with the longest LTL (fourth quartile), those in the third, second, and first quartiles showed 53%, 41%, and 44% reduced risk for cancer death, respectively. The findings highlight the importance of sex-specific analysis in future telomere research. [ABSTRACT FROM AUTHOR]

Studies have indicated that transportation noise is associated with higher cardiovascular mortality, whereas evidence of noise as a risk factor for respiratory and cancer mortality is scarce and inconclusive. Also, knowledge on effects of low-level noise on mortality is very limited. We aimed to investigate associations between road and railway noise and natural-cause and cause-specific mortality in the Danish population. We estimated address-specific road and railway noise at the most (LdenMax) and least (LdenMin) exposed façades for all residential addresses in Denmark from 1990 to 2017 using high-quality exposure models. Using these data, we calculated 10-year time-weighted mean noise exposure for 2.6 million Danes aged >50 years, of whom 600,492 died from natural causes during a mean follow-up of 11.7 years. We analyzed data using Cox proportional hazards models with adjustment for individual and area-level sociodemographic variables and air pollution (PM 2.5 and NO 2). We found that a 10-year mean exposure to road LdenMax and road LdenMin per 10 dB were associated with hazard ratios (95% confidence intervals) of, respectively, 1.09 (1.09; 1.10) and 1.10 (1.10; 1.11) for natural-cause mortality, 1.09 (1.08; 1.10) and 1.09 (1.08; 1.10) for cardiovascular mortality, 1.13 (1.12; 1.14) and 1.17 (1.16; 1.19) for respiratory mortality and 1.03 (1.02; 1.03) and 1.06 (1.05; 1.07) for cancer mortality. For LdenMax, the associations followed linear exposure-response relationships from 35 dB to 60–<65 dB, after which the function levelled off. For LdenMin, exposure-response relationships were linear from 35 dB and up, with some levelling off at high noise levels for natural-cause and cardiovascular mortality. Railway noise did not seem associated with higher mortality in an exposure-response dependent manner. In conclusion, road traffic noise was associated with higher mortality and the increase in risk started well below the current World Health Organization guideline limit for road traffic noise of 53 dB. [Display omitted] • Road noise was associated with higher cardiovascular, respiratory and cancer mortality. • Results were robust to adjustment for air pollution. • Increase in mortality risk started below current guideline limits for road noise. • Railway noise was not associated with mortality. [ABSTRACT FROM AUTHOR]

Our goal is to evaluate the strengths of the associations between area-level deprivation and survival time for a variety of cancers. A total of 145 585 subjects were diagnosed with various cancers in Busan, Korea, and an area-level deprivation index constructed from several important socioeconomic variables. A multilevel Cox model was used in the analysis to investigate the effects of multiple risk factors. After adjusting for gender and age, an increased area-level deprivation index was found to be significantly associated with a higher hazard rate for major cancers. Estimated hazard ratios (95% confidence interval) were 1.08 (1.06, 1.11), 1.15 (1.13, 1.18), and 1.22 (1.18, 1.25) for the second, third, and fourth quartiles of deprivation index groups, respectively, when compared with the least deprived group. When compared with the least deprived group, the more deprived group showed significant decrease in survival time for major cancers. This finding highlights the importance of preventive and care services incorporating socioeconomic characteristics of areas. [ABSTRACT FROM AUTHOR]

Background: We examined the association between metabolic dysregulation and cancer mortality in a prospective cohort of Black and White adults.Methods: A total of 25,038 Black and White adults were included in the analysis. Metabolic dysregulation was defined in two ways: 1) using the joint harmonized criteria for metabolic syndrome (MetS) and 2) based on factor analysis of 15 variables characterizing metabolic dysregulation. We estimated hazards ratios (HRs) and 95% confidence intervals (CIs) for the association of MetS and metabolic dysregulation with cancer mortality during follow-up using Cox proportional hazards models.Results: About 46% of Black and 39% of White participants met the criteria for MetS. Overall, participants with MetS (HR: 1.22, 95% CI: 1.03-1.45) were at increased risk of cancer-related death. In race-stratified analysis, Black participants with MetS had significantly increased risk of cancer mortality compared with those without MetS (HR: 1.32, 95% CI: 1.01-1.72), increasing to more than a 2-fold risk of cancer mortality among those with five metabolic syndrome components (HR: 2.35, 95% CI: 1.01-5.51).Conclusions: There are marked racial differences in the prevalence of metabolic dysregulation defined as MetS based on the harmonized criteria. The strong positive associations between MetS and cancer mortality suggests that efforts to improve cancer outcomes in general, and racial disparities in cancer outcomes specifically, may benefit from prevention and management of MetS and its components. [ABSTRACT FROM AUTHOR]

Aim: Our study aims to investigate the association between dietary acrylamide exposure and cancer mortality among Chinese elderly. Methods: A prospective cohort of 4000 elderly men and women aged 65 years and above (Mr. and Ms. OS Hong Kong study) was recruited from local communities from 2001 to 2003. Dietary exposure to acrylamide was evaluated at baseline based on a validated food frequency questionnaire and an acrylamide database from the 1st Hong Kong Total Diet Study. Data on mortality statistics through March 2014 were obtained from the Death Registry of the Department of Health of Hong Kong with a median follow-up of 11.1 years. Cox proportional hazards models were used to examine the association between the acrylamide exposure and cancer mortality. Sex hormones were assessed in men. Results: During a median follow-up of 11.1 years (39,271 person-years), we ascertained 330 cancer deaths. Vegetables (43.7%) and cereals (28.9%) products were the major contributors to dietary acrylamide. Compared with the lowest quartile of acrylamide intake (<9.9 µg/day), the multivariable hazard ratios for the highest quartile (>17.1 µg/day) were 1.9 (95% CI 1.3-2.8; P < 0.01), 1.9 (95% CI 1.0-3.6; P = 0.05), and 2.0 (95% CI 1.0-4.0; P = 0.06) for the cancer mortality from overall, digestive and respiratory system, respectively. The associations were attenuated to null after further adjustment for circulating free estradiol in men. No statistically significant interactions were observed between acrylamide exposure and sex, obesity and overall lifestyle pattern scores. Conclusions: The longitudinal data provided evidence that dietary acrylamide, in amounts that Chinese elderly are typically exposed to, was associated with increased cancer mortality. Circulating free estradiol may mediate the association in men. [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]

Observational studies suggest that low concentrations of serum 25-hydroxyvitamin D (25(OH)D) and high concentrations of parathyroid hormone (PTH) are associated with a higher risk of mortality. The aim of this study was to examine whether 25(OH)D and PTH concentrations are independently associated with overall and disease-specific (cardiovascular and cancer-related) mortality in a large, prospective population-based cohort of older adults. Data from 1317 men and women (65–85 years) of the Longitudinal Aging Study Amsterdam were used. Cox proportional hazard analyses were used to examine whether 25(OH)D and PTH at baseline were associated with overall mortality (with a follow-up of 18 years) and disease-specific mortality (with a follow-up of 13 years). Compared to persons in the reference category of ≥75 nmol/L, persons with serum 25(OH)D <25 nmol/L (HR 1.46; 95% CI: 1.12–1.91) and 25–49.9 nmol/L (HR 1.24; 95% CI: 1.01–1.53) had a significantly higher risk of overall mortality, as well as men with baseline PTH concentrations ≥7 pmol/L (HR 2.54 (95% CI: 1.58–4.08)), compared to the reference category of <2.33 pmol/L. The relationship of 25(OH)D with overall mortality was partly mediated by PTH. Furthermore, men with PTH concentrations of ≥7 pmol/L (HR 3.22; 95% CI: 1.40–7.42) had a higher risk of cardiovascular mortality, compared to the reference category. No significant associations of 25(OH)D or PTH with cancer-related mortality were observed. Both 25(OH)D and PTH should be considered as important health markers. [ABSTRACT FROM AUTHOR]

Residing in greener areas may decrease the burden of chronic diseases, but the association with cancer is unclear. We studied the associations between residential green spaces and site-specific cancer mortality in urban Belgium. We linked the 2001 Belgian census, register mortality data for 2001–2014, and environmental information (green spaces and air pollution) at baseline residence (2001). We included residents from the largest Belgian urban areas aged ≥ 30 years at baseline. Exposure to residential green spaces was assessed using the Normalized Difference Vegetation Index (NDVI), Urban Atlas, and perceived neighbourhood greenness (from the census). We used Cox proportional hazards models to obtain hazard ratios (HR) and their 95 % confidence intervals (95 %CI) of the mortality risk from lung, colorectal, breast (in women) and prostate cancer (in men) per interquartile range increment in residential green spaces. We further analyzed the role of outdoor air pollution and effect modification by age and socioeconomic position (SEP) in main associations. 2,441,566 individuals were included at baseline. During follow-up, 1.2 % died from lung cancer, 0.6 % from colorectal cancer, 0.8 % from breast cancer, and 0.6 % from prostate cancer. After adjustment, higher exposure to green spaces was associated with a reduced mortality risk from lung cancer and breast cancer [e.g., for NDVI within 300 m, HR:0.946 (95 %CI:0.924,0.970), and HR:0.927 (95 %CI:0.892,0.963), respectively], but not with colorectal or prostate cancer mortality. For the latter, a suggestive hazardous effect of green spaces was found. Air pollution seemed to have only a marginal role. Beneficial effects of greenspace were generally stronger in < 65-year-old, but no clear trend by SEP was found. Our findings suggest that residing in green areas could decrease mortality risk from lung and breast cancer, potentially independent from air pollution. Future studies should consider different indicators of greenspace exposure and investigate potential pathways underlying the associations. [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]

Purpose: Racial disparities in cancer mortality may be greater for cancers that are amenable to available early detection and treatment (amenability level). We investigated whether these patterns vary by age at cancer diagnosis.Methods: Using 5-year relative survival rates (5Y-RSR), we classified 51 cancer sites into least amenable, partly amenable, and mostly amenable cancers (<40%, 40-69%, ≥70% 5-YRS, respectively). We examined whether racial disparities in mortality rates (African-Americans, Asian/Pacific Islanders, Hispanics, whites), as estimated through Cox regression models, were modified by age at diagnosis and amenability level in 516,939 cancer cases diagnosed in 1995-1999.Results: As compared with whites, all racial minority groups experienced higher cancer mortality rates in the youngest age group of 20-34 years. African-Americans and Hispanics diagnosed with partly and mostly amenable cancers had higher mortality rates relative to whites with cancers of the same amenability levels; further, these differences decreased in magnitude or reversed in direction with increasing age. In contrast, the racial differences in mortality were smaller and remained fairly constant across age groups for least amenable cancers. For example, in the youngest (20-34) and oldest (80-99) age groups, the adjusted hazard ratios (HRs) for African-Americans versus whites with least amenable cancers were, respectively, 1.26 (95% CI 1.02, 1.55) and 0.90 (95% CI 0.85, 0.96), while the HRs for African-Americans versus whites with mostly amenable cancers were 2.77 (95% CI 2.38, 3.22) and 1.07 (95% CI 0.98, 1.17).Conclusions: Cancer survival disadvantage for racial minorities is larger in younger age groups for cancers that are more amenable to medical interventions. [ABSTRACT FROM AUTHOR]

Cancer mortality is higher among residents of low-socioeconomic status (SES) areas than those of high- SES areas; however, the contribution of modifiable risk factors to this disparity is not known. We used data from 54,737 participants in the VITamins And Lifestyle (VITAL) Study, aged 50e76 with no history of cancer at baseline (2000e2002). Of these, 1488 died of cancer over an average of 7.7 years of follow-up. Data on modifiable risk factors including body mass index (BMI), physical activity, diet, alcohol, smoking and screening were taken from baseline questionnaires. We constructed a block group-level SES index using data from the 2000 United States Census and fit Cox proportional hazards models estimating the association between area-level SES and total cancer mortality with and without control for modifiable risk factors. All statistical tests are 2-sided. Cancer mortality was 77% (95% CI: 50%, 111%) higher in the lowest-SES areas compared with the highest. Modifiable risk factors accounted for 45% (95% CI: 34%, 62%) of this association. Smoking explained the greatest proportion (29%; 95% CI: 22%, 40%) of the observed association, followed by diet (11%; 95% CI: 7%, 17%), physical activity (10%; 95% CI: 7%, 16%), screening (9%; 6%, 13%), and BMI (5%; 95% CI: 1%, 10%). Results were similar in models controlling for individual education and income. The association between area-level SES and cancer mortality is partially explained by modifiable risk factors, which could suggest the appropriate targets to reduce socioeconomic disparities. [ABSTRACT FROM AUTHOR]

Background: Adults in the United States (U.S) can be simultaneously exposed to more than one social risk factor over their lifetime. However, cancer epidemiology tends to focus on single social risk factors at a time. We examined the prospective association between cumulative social risk exposure and deaths from cancer in a nationally representative sample of U.S. adults.Methods: The study included 8745 adults (aged≥40 years) in the NHANES Survey III Mortality Study over a median follow-up of 13.5 years (1988-1994 enrollment dates and 1988 through 2006 for mortality data). Social risk factors (low family income, low education level, minority race, and single-living status) were summed to create a cumulative social risk score (0 to ≥3). We used Cox proportional hazard models to estimate age- and sex-adjusted hazard ratios (HRs) and 95% confidence intervals (95% CI) for the association between cumulative social risk with deaths from all-cancers combined, tobacco-related cancers, and screening-detectable cancers.Results: Deaths from all-cancers combined (P for trend=0.001), tobacco-related cancers (P for trend=<0.001), and lung cancer (P for trend=0.01) increased with an increasing number of social risk factors. As compared with adults with no social risk factors, those exposed to ≥3 social risk factors were at increased risk of deaths from all-cancers combined (HR=1.8, 95% CI=1.3-2.4), tobacco-related cancers (HR=2.6, 95% CI: 1.6-4.0), and lung cancer (HR=2.3, 95% CI=1.3-4.1).Conclusions: U.S. adults confronted by higher amounts of cumulative social risk appear to have increased mortality from all-cancers combined, tobacco-related cancers, and lung cancer. An enhanced understanding of the cumulative effect of social risk factors may be important for targeting interventions to address social disparities in cancer mortality. [ABSTRACT FROM AUTHOR]

Objectives To estimate the all-cause, cardiovascular, and cancer mortality risks associated with serum uric acid levels in elderly adults. Design Cohort study. Setting The Annual Geriatric Health Examination Program database from 2006 to 2010. Paticipants Community-dwelling Taipei citizens aged 65 and older (N = 77,541). Measurements Stratified according to sex, serum uric acid levels were analyzed in quartiles and as normal versus high categories. Mortality was determined by matching cohort identifications with national death files. Results Men had significantly higher uric acid levels than women ( P < .001), and mean levels increased with age ( P < .001). Serum uric acid levels (normal vs high) were an independent risk factor for all-cause and cardiovascular mortality in men and women, with the strongest association found for cardiovascular mortality. The association between serum uric acid levels and cardiovascular mortality was independent of other cardiovascular risk factors such as hypertension, diabetes mellitus, hyperlipidemia, and glomerular filtration rate levels. When levels were analyzed as quartiles, men with levels in the second quartile had the lowest hazard ratios for all-cause and cardiovascular mortality. Conclusion High serum uric acid levels are associated with greater risk of all-cause and cardiovascular mortality but not cancer mortality in elderly adults. Further studies are warranted to investigate the prognostic implications and potential utility in the monitoring of therapy. [ABSTRACT FROM AUTHOR]

Leukocyte telomere length (LTL) is related to the aging of somatic cells. We hypothesized that LTL is inversely associated with mortality in elderly men. LTL was measured in 2744 elderly men (mean age 75.5, range 69–81 years) included in the prospective population-based MrOS-Sweden study. Mortality data were obtained from national health registers with no loss of follow-up. During the follow-up (mean 6.0 years), 556 (20%) of the participants died. Using Cox proportional hazards regression, tertile of LTL did not associate with all-cause mortality [tertile 1 (shortest) or 2 (middle) vs. tertile 3 (longest); hazard ratio (HR) = 1.05, 95% confidence interval (CI) 0.85–1.28 and HR = 0.97, 95% CI 0.79–1.19, respectively]. Furthermore, LTL did not associate with cancer (197 events) or cardiovascular disease (CVD, 206 events) mortality (tertile 1 vs. tertile 3; HR = 0.94, 95% CI 0.67–1.34 and HR = 0.94, 95% CI 0.68–1.30, respectively). The lack of association between LTL and mortality remained also after adjustment for multiple covariates. Our results demonstrate that LTL is not associated with all-cause mortality or mortality due to cancer or CVD in elderly men. Further studies are needed to determine whether LTL can predict the risk of mortality in elderly women. [ABSTRACT FROM AUTHOR]

Introduction: Both baseline cardiorespiratory fitness and adiposity predict the risk of cancer mortality. However, the effects of changes in these two factors over time have not been evaluated thoroughly. The aim of this study was to examine the independent and joint associations of changes in cardiorespiratory fitness and body composition on cancer mortality. Methods: The cohort consisted of 13,930 men (initially cancer-free) with two or more medical examinations from 1974 to 2002. Cardiorespiratory fitness was assessed by a maximal treadmill exercise test, and body composition was expressed by body mass index (BMI) and percent body fat. Changes in cardiorespiratory fitness and body composition between the baseline and the last examination were classified into loss, stable, and gain groups. Results: There were 386 deaths from cancer during an average of 12.5 yr of follow-up. After adjusting for possible confounders and BMI, change hazard ratios (95% confidence intervals) of cancer mortality were 0.74 (0.57-0.96) for stable fitness and 0.74 (0.56-0.98) for fitness gain. Inverse dose-response relationships were observed between changes in maximal METs and cancer mortality (P for linear trend = 0.05). Neither BMI change nor percent body fat change was associated with cancer mortality after adjusting for possible confounders and maximal METs change. In the joint analyses, men who became less fit had a higher risk of cancer mortality (P for linear trend = 0.03) compared with those who became more fit, regardless of BMI change levels. Conclusions: Being unfit or losing cardiorespiratory fitness over time was found to predict cancer mortality in men. Improving or maintaining adequate levels of cardiorespiratory fitness appears to be important for decreasing cancer mortality in men. [ABSTRACT FROM AUTHOR]

Aims: We aimed to evaluate the association between HbA1c variability and mortality due to all causes, cancer, and non-cancer in patients with type 2 diabetes independently of mean HbA1c levels. Methods: We enrolled 754 patients with type 2 diabetes who first visited our hospital between 1995 and 1996, had been followed for at least 2 years, and had undergone four or more HbA1c determinations. Patients were followed through June 2012. The standard deviation (SD) or coefficient of variation (CV) was used as a measure of HbA1c variability. Risk of death was evaluated by multivariate Cox proportional hazard models. Results: Through June 2012, 63 patients died. Hazard ratios (HRs) for all-cause mortality and non-cancer mortality including cardiovascular diseases (CVD) increased across tertiles of both HbA1cSD and HbA1cCV. HRs for cancer mortality did not increase across tertiles of either HbA1cSD or HbA1cCV. Using a stepwise regression method, both HbA1cSD and HbA1cCV predicted all-cause mortality, especially non-cancer mortality. In contrast, mean HbA1c predicted cancer mortality. Conclusions: HbA1c variability is a predictor of all-cause mortality, especially non-cancer mortality including CVD, in patients with type 2 diabetes, independent of mean HbA1c level. In contrast, mean HbA1c, but not HbA1c variability, might predict cancer mortality. [ABSTRACT FROM AUTHOR]