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The region of Campania, South Italy rose to prominence in the mid-2000s due to the illegal disposal of waste by the Camorra during the local waste management crisis. Several lines of evidence have identified a link between exposure to toxic waste and adverse health outcomes in the local populations. Critically, studies since 2017 have strongly suggested that this link is causal in nature. The uncertainty of evidence polarised the Italian epidemiological community and partly undermined the precautionary principle in public health policy, leading to years of delay in the deployment of appropriate interventions. The crisis also sparked concerns about pollution of soil, water, and agricultural products. The contrast between political responses and protests from local communities shows analogies with environmental emergencies of a larger scale. Beyond law enforcement actions to prosecute illegal waste disposal activity, future mitigation of risks for affected populations will require coordinated efforts in environmental policy (land reclamation, improved waste management) and public health (i.e. extensive epidemiological surveillance, screening and prevention programs). By summarising evidence over the last two decades, this review aims to construct a cohesive interdisciplinary narrative of the events in the Campanian waste crisis.

Background: 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. Methodology: 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. Results: 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

Introduction: Previous randomized controlled trials (RCTs) and meta-analyses of RCTs evaluating vitamin D supplementation for the prevention of cancer incidence and mortality have found inconsistent results and no meta-analysis has assessed the quality of the evidence available. We, therefore, aimed to perform an updated meta-analysis by including recent large-scale RCTs and assessing the quality of the pooled evidence. Methods: We searched several databases and trial registers from inception to April 2022. We used a random-effects model to estimate pooled risk ratios (RRs) and 95% confidence intervals (CIs). We used the Grades of Recommendation, Assessment, Development, and Evaluation (GRADE) considerations to evaluate the certainty of evidence. Results: We included 13 RCTs in our study. Vitamin D supplementation had no effect on the risk of total cancer incidence (RR 0.99, 95% CI: 0.94–1.04; I2 = 0%), total cancer mortality (RR 0.93, 95% CI: 0.84–1.03; I2 = 24%) and total mortality (RR 0.92, 95% CI: 0.82–1.04; I2 = 36%). The overall quality of evidence was high for all outcomes. Discussion: Vitamin D supplementation is ineffective in reducing total cancer incidence and mortality in largely vitamin D-replete older adult populations. Future research should be based on populations with a higher prevalence of vitamin D deficiency and should involve more extended follow-up periods. Study protocol: PROSPERO database, CRD42021285401.

The association between acrylamide (AA) and the development of cancer has been extensively discussed but the results remained controversial, especially in population studies. Large prospective epidemiological studies on the relationship of AA exposure with cancer mortality were still lacking. Therefore, we aimed to assess the association between AA biomarkers and cancer mortality in adult population from National Health and Nutrition Examination Survey (NHANES) 2003-2014. We followed 3717 participants for an average of 10.3 years. Cox regression models with multivariable adjustments were performed to determine the relationship of acrylamide hemoglobin adduct (HbAA) and glycidamide hemoglobin adduct (HbGA) with cancer mortality. Mediation analysis was conducted to demonstrate the mediated role of low-grade inflammation score (INFLA-score) in this correlation. Compared with the lowest quintile, participants with the highest quintile of HbAA, HbGA and HbAA+HbGA had increased cancer mortality risk, and the hazard ratios(HRs) were 2.07 (95%CI:1.04-4.14) for HbAA, 2.39 (95%CI:1.29-4.43) for HbGA and 2.48 (95%CI:1.28-4.80) for HbAA+HbGA, respectively. And there was a considerable non-linearity association between HbAA and cancer mortality (p for non-linearity = 0.0139). We further found that increased INFLAscore significantly mediated 71.67% in the effect of HbGA exposure on increased cancer mortality risk. This study demonstrates that hemoglobin biomarkers of AA are positively associated with cancer mortality in adult American population and INFLA-score plays a mediated role in this process. Our findings can raise public awareness of environmental and dietary exposure to acrylamide and remind people to refrain from smoking or having acrylamide-rich foods. [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]

Background Patients with kidney failure have a higher cancer risk compared with the age-matched general population. However, the outcomes of incident dialysis patients with a prior cancer history are unknown. Methods Using Australia and New Zealand Dialysis and Transplant Registry data (2000–2019), the outcomes and survival probabilities of incident dialysis patients with prior cancers and having experienced a cancer recurrence or having developed a new cancer after dialysis commencement were described. Results Of 4912 patients with prior cancers before dialysis commencement, 323 (7%) and 343 (7%) patients experienced cancer recurrence or developed new cancers after dialysis initiation, respectively. The median time from dialysis commencement to cancer recurrence was 1.2 years [interquartile range (IQR) 0.5–2.8] and was 2.0 years (IQR 0.7–4.0) for new cancer occurrence. Of those with cancer recurrence, 80% presented with metastatic disease and one in two patients died from cancer, with a median time from cancer recurrence to death of 0.5 years (IQR 0.2–1.7). Of those who developed new cancer, urinary tract and respiratory cancers were the most frequent cancer types, with a median time from new cancer diagnosis to death of 1.3 years (IQR 0.4–3.1). The 3-year survival probabilities on dialysis following cancer recurrence and new cancer were 19% [95% confidence interval (CI) 15–24] and 41% (35–47), respectively. Conclusion Among incident dialysis patients with a prior cancer history, 14% experienced cancer recurrence or developed a new cancer. Patients who experienced cancer recurrence or developed new cancer have poor outcomes, with ˂50% surviving beyond 3 years. These findings suggest the need to have a greater understanding of the characteristics, cancer screening, treatment responses and reasons for commencing dialysis in patients with kidney failure and prior cancer history, which may help in the shared clinical decision-making process when considering dialysis for these patients. [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]

Simple Summary: It has been questioned whether vitamin D supplements can reduce the mortality and incidence of tumors. In this systematic review and meta-analysis of 12 randomized controlled trials with a total of 72,669 participants, vitamin D supplementation could not reduce the cancer mortality or cancer incidence. Our results suggest a reconsideration of the previous view that vitamin D supplementation could reduce overall cancer mortality is needed. Background: Vitamin D deficiency is related to increased cancer risk and deaths. However, whether vitamin D supplementation reduces cancer mortality remains unclear, and several randomized controlled trials yield inconsistent results. Methods: Medline, Embase, and the Cochrane Central Register of Controlled Trials were searched from their inception until 28 June 2022, for randomized controlled trials investigating vitamin D supplementation. Pooled relative risks (RRs) and their 95% confidence intervals (CIs) were estimated. Trials with vitamin D supplementation combined with calcium supplementation versus placebo alone and recruiting participants with cancer at baseline were excluded in the present study. Results: This study included 12 trials with a total of 72,669 participants. Vitamin D supplementation did not reduce overall cancer mortality (RR 0.96, 95% CI 0.80–1.16). However, vitamin D supplementation was associated with a reduction in lung cancer mortality (RR 0.63, 95% CI 0.45–0.90). Conclusions: Vitamin D supplementation could not reduce cancer mortality in this highly purified meta-analysis. Further RCTs that evaluate the association between vitamin D supplementation and total cancer mortality are still needed. [ABSTRACT FROM AUTHOR]

Carotenoids are abundant pigments mainly contained in vegetables and fruits, and show antioxidant properties by quenching free radicals in human body. Few studies have investigated associations between serum carotenoid levels and premature mortality. The objective of this study was to investigate the association between serum carotenoid level and premature mortality in a Japanese population. This study included 446 Japanese adults (174 men, aged of 40–64) recruited as participants in the Japan Collaborative Cohort (JACC) Study. Serum carotenoid level was measured by high-performance liquid chromatography. Premature mortality was defined as death before 65 years old during the follow-up period. Premature mortality was ascertained in 60 men (34.5%) and 65 women (23.9%). In men, compared to the 1st tertile of serum b-cryptoxanthin and provitamin A, those who were in the 3rd tertile had lower risks of premature all-cause mortality (OR, 95% CI: 0.19, 0.07–0.47 for b-cryptoxanthin, and 0.24, 0.09–0.61 for provitamin A). In women, compared to the 1st tertile of serum b-cryptoxanthin, those who were in the 3rd tertile had higher risks of premature all-cause mortality (OR, 95% CI: 1.94, 1.00–4.03). These significant associations were observed in analyses for premature cancer mortality. We found significant associations between higher levels of serum b-cryptoxanthin and provitamin A and lower risks of premature mortality among Japanese men, while a different directional association was found in women. Although these findings suggest roles of serum carotenoids on premature mortality, further studies are needed to validate this association in other populations. [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: There has been an increase in certain cancers among young adults (YA) aged 20-39, particularly in Latin America. This is the first study to examine cancer incidence and mortality in YA in Costa Rica, focusing on sex-specific patterns., Methods: Invasive cancer cases (excluding non-melanoma skin cancer) in YA from 2006 to 2015 were obtained from the Costa Rican National Registry of Tumors. Utilising SEER∗Stat software, age-standardized incidence rates (IRs) and incidence rate ratios (IRRs) were calculated. Trends and annual percent changes (APCs) in IRs were estimated using the Joinpoint regression analysis program. Cancer deaths from 2000 to 2021 were obtained from the Costa Rican National Institute of Statistics and Census. Age-standardised mortality rates were calculated using STATA®17., Findings: YA comprised 10.7% of all invasive cancer cases diagnosed from 2006 to 2015. The age-standardized incidence rate (ASIR) of invasive cancer in YA was 50.9/100,000 person-years. The ASIR was twofold higher for females compared to males (IRR = 2.03, 95% CI:1.94, 2.13). This difference increased with age, peaking in the 35-39-year age group (IRR = 2.84, 95% CI:2.62, 3.10). Thyroid, breast, and cervical cancer were the most common in females. Testicular cancer was the most common in males. Leading causes of cancer-related deaths included cervical and breast cancer in females and stomach and brain/nervous system cancer in males., Interpretation: The study highlights sex-specific patterns in cancer incidence and mortality among YA in Costa Rica to increase understanding and improve cancer outcomes in this age group., Funding: This study was funded by the Intramural Research Program of the National Cancer Institute., Competing Interests: The authors have declared no conflicts of interest., (© 2024 The Authors.)

Objective: In this study, we examined associations between county-level measures of structural racism and county-level cancer incidence and mortality rates between race groups while accounting for factors associated with cancer rates and county-level measures of environmental burden., Methods: To explore this relationship, we conducted multiple linear regression analyses. Data for these analyses came from an index of county-level structural racism and publicly available data on 2015 to 2019 age-adjusted cancer rates from the US Cancer Statistics Data Visualization Tool, 2019 County Health Rankings and Roadmaps, the Environmental Protection Agency's 2006 to 2010 Environmental Quality Index, and 2015 to 2019 estimates from the US Census American Community Survey., Results: County-level structural racism was associated with higher county cancer incidence rates among Black (adjusted incidence rate: 17.4, 95% confidence interval [95% CI]: 9.3, 25.5) and Asian/Pacific Islander populations (adjusted incidence rate: 9.3, 95% CI: 1.8, 16.9) and higher mortality rates for American Indian/Alaskan Native (adjusted mortality rate [AMR]: 17.4, 95% CI: 4.2, 30.6), Black (AMR: 11.9, 95% CI: 8.9, 14.8), and Asian/Pacific Islander (AMR: 4.7, 95% CI: 1.3, 8.1) populations than White populations., Conclusion: Our findings highlight the detrimental impact of structural racism on cancer outcomes among minoritized populations. Strategies aiming to mitigate cancer disparities must embed processes to recognize and address systems, policies, laws, and norms that create and reproduce patterns of discrimination., Competing Interests: Conflict of Interest: No conflict of interest reported by the authors.

Nationwide estimates of the impact of common modifiable risk factors on mortality remain crucial. We aim to assess the influence of social determinants, lifestyle, and metabolic factors on mortality in 174,004 adults aged ≥40 years from the China Cardiometabolic Disease and Cancer Cohort (4C) Study. We reveal that 17 modifiable factors are independently associated with mortality, accounting for 64.8% of all-cause mortality, 77.4% of cardiovascular mortality, and 44.8% of cancer mortality. Low education emerges as the leading factor for both all-cause and cancer mortality, while hypertension is predominant for cardiovascular mortality. Moreover, low gross domestic product per capita and high ambient particulate matter with a diameter of <2.5 μm (PM 2 .5 ) air pollution account for 7.8% and 4.3% for all-cause mortality, respectively, using a different method. Gender-specific analyses reveal distinct patterns, with women's mortality primarily associated with social determinants and men exhibiting stronger associations with lifestyle factors. Targeted health interventions are essential to mitigate mortality risks effectively in China., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Purpose: We aimed to compare cancer mortality among foreign- and Colombian populations in Colombia during the period of 2006-2020., Methods: This retrospective study utilized vital statistics from the Colombian National Department of Statistics (DANE). The dataset included variables such as age group, sex, country of permanent residency, insurance, education level, marital status, ethnicity, and cause of death. The population data to calculate rates was obtained from the Colombian census and the United Nations. Crude and adjusted rates as well as proportional mortality rates were calculated., Results: A total of 561,932 cancer deaths occurred in Colombia from 2006 to 2020. The foreign population (country of permanent residency different to Colombia) had a lower crude cancer mortality rate (31.1 per 100,000 inhabitants) than the Colombian population (81.9 per 100,000 inhabitants). However, the age-adjusted cancer mortality rate among the foreign population was 253.6 per 100,000, compared to 86.1 per 100,000 among the Colombian population. The proportional cancer mortality was 10.4 % among foreign population compared to 17.4 % among Colombian population., Conclusions: The proportional cancer mortality shows that the proportion of cancer-related deaths is greater among the Colombian population compared to the immigrant population. However, immigrants in Colombia have a higher age-adjusted cancer mortality rate than Colombians, indicating that immigrants have worse cancer outcomes than the Colombians even though the immigrant population is younger. This is likely due to the frequent barriers that immigrants encounter in accessing health care in Colombia. Future research needs to focus on access to care for the immigrant population by investigating cancer-related risk factors among immigrants and addressing their barriers to cancer prevention and treatment., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2024 The Authors. Published by Elsevier Ltd.)

Introduction: The purpose of this study was to investigate the association of central lean mass distribution with the risk of mortality., Methods: This cohort study included 40,283 UK Biobank participants. Cox proportional hazards regression models were used to estimate the association of central lean mass distribution, i.e., trunk-to-leg lean mass ratio, assessed by dual-energy X-ray absorptiometry, with the risk of mortality., Results: The median age of the participants was 65 years, and 52% were women. During a median follow-up of 4.18 years, 674 participants died, of whom 366 were due to cancer and 126 were due to cardiovascular causes. Compared with the lowest tertile of a trunk-to-leg lean mass ratio, the multivariable-adjusted (age, sex, ethnicity, lifestyle, comorbidities, body mass index, and appendicular muscle mass index) hazards ratios of the highest tertile of trunk-to-leg lean mass ratio were 1.55 (95% CI: 1.23-1.94), 1.69 (95% CI: 1.26-2.26), and 1.14 (95% CI: 0.72-1.80) for all-cause, cancer, and cardiovascular mortality, respectively. Neutrophil-to-lymphocyte ratio mediated 9.3% (95% CI: 3.3%-40.4%) of the association of trunk-to-leg lean mass ratio with all-cause mortality. There was evidence for additive interactions of trunk-to-leg lean mass ratio with older age and poor diet quality for all-cause mortality., Conclusion: Trunk-to-leg lean mass ratio, assessed by dual-energy X-ray absorptiometry, was positively associated with the risks of all-cause and cancer mortality, independent of general obesity and central obesity, in UK middle-aged and older adults. Central lean mass distribution may interact synergistically with aging and poor diet quality to further increase the risk of death., (© 2024 The Author(s). Published by S. Karger AG, Basel.)

Background: There is evidence indicating that both lipoprotein(a) [Lp(a)] and fibrinogen (FIB) are associated with mortality, However, the impact of their combination on mortality has not been determined. Thus, the aim of this study was to examine the association between the combination of Lp(a) and FIB with all-cause and cause-specific mortality., Methods: This prospective cohort study enrolled 4,730 participants from the third National Health and Nutrition Examination Survey. The exposure variables included Lp(a), FIB and their combination, while the outcome variables consisted of all-cause, cardiovascular disease (CVD) and cancer-related mortality. Multivariate COX regression, subgroup analysis, sensitivity analysis and restricted cubic spline (RCS) were used to investigate the association between Lp(a), FIB and their combination with all-cause, CVD and cancer-related mortality., Results: Over a median follow-up period of 235 months, 2,668 individuals died, including 1,051 deaths attributed to CVD and 549 deaths due to cancer. Multivariate Cox regression analyses revealed independent associations between both Lp(a) and FIB with all-cause, CVD, and cancer-related mortality. Compared to participants in the 1st to 50th percentiles of both Lp(a) and FIB, those in the 90th to 100th percentiles exhibited multivariable adjusted HRs of 1.813 (95% CI: 1.419-2.317, P < 0.001), 2.147 (95% CI: 1.483-3.109, P < 0.001) and 2.355 (95% CI: 1.396, 3.973, P = 0.001) for all-cause, CVD and cancer-related mortality, respectively. Subgroup and sensitivity analyses did not substantially attenuate the association between the combination of high Lp(a) and high FIB with the risk of all-cause and CVD-related mortality. Additionally, the RCS analysis showed that the relationship between Lp(a) and the risk of all-cause and cancer-related mortality, as well as the relationship between FIB and the risk of cancer-related mortality, were linear (P for nonlinearity > 0.05). Conversely, the relationship between Lp(a) and the risk of CVD-related mortality, as well as the relationship between FIB and the risk of all-cause and CVD-related mortality, were nonlinear (P for nonlinearity < 0.05)., Conclusions: High levels of Lp(a) and FIB together conferred a greater risk of mortality from all-cause, CVD and cancer., (© 2024. The Author(s).)

Recent meta‐analyses of randomized controlled trials (RCTs) have demonstrated significant reduction in cancer mortality by vitamin D supplementation. We estimated costs and savings for preventing cancer deaths by vitamin D supplementation of the population aged 50+ years in Germany. Our analysis is based on national data on cancer mortality in 2016. The number of preventable cancer deaths was estimated by multiplying cancer deaths above age 50 with the estimated proportionate reduction in cancer mortality derived by vitamin D supplementation according to meta‐analyses of RCTs (13%). Saved costs were estimated by multiplying this number by estimated end‐of‐life cancer care costs (€40 000). Annual costs of vitamin D supplementation were estimated at 25€ per person above age 50. Comprehensive sensitivity analyses were conducted. In the main analysis, vitamin D supplementation was estimated to prevent almost 30 000 cancer deaths per year at approximate costs of €900 million and savings of €1.154 billion, suggesting net savings of €254 million. Our results support promotion of supplementation of vitamin D among older adults as a cost‐saving approach to substantially reduce cancer mortality.

Abstract Background Numerous studies have suggested that fasting plasma glucose (FPG) was associated with the risk of mortality. However, relationship on longitudinal changes of FPG with the risk of mortality remained inconsistent. Methods We examined the association of FPG at baseline and its longitudinal changes with risk of mortality based on a cohort study in Yinzhou, China, during 2010–2018. Cox regression models and competing risk models were separately used to examine the association of FPG levels and long‐term fluctuation with risk of total and cause‐specific mortality. Results Subjects who had an impaired fasting glucose or diabetes suffered a higher risk of total mortality than subjects who had a normal fasting glucose (HRs and 95% CIs: 1.17 [1.01–1.35], 1.30 [1.10–1.53], respectively). The HR for total mortality was 1.54 (95% CI: 1.29–1.84) and for cancer mortality was 1.41 (95% CI: 1.04–1.92) in the highest quartile of coefficient of variation of FPG. Trajectory analysis indicated that subjects with a significantly changed FPG suffered a higher risk of total mortality. Conclusion According to this cohort study, we found that long‐term fluctuation of FPG was significantly associated with the risk of total and cancer mortality. Our findings suggest that long‐term fluctuation of FPG could be used as an efficient indicator for predicting the subsequent risk of mortality.

Abstract Background This study evaluates the role of social isolation on inflammation and cancer mortality among women. Methods Data were abstracted from the U.S. National Health and Nutrition Examination Survey from 1988 to 1994. The Social Network Index was used to assess participants’ degree of social isolation. C-reactive protein and fibrinogen levels were included as markers of inflammation. We used the National Death Index to identify causes and dates of mortality. Chi-square and multivariable Cox regressions were employed for statistical analyses. Results Of 3360 women (median age: 54 years), the most isolated, very isolated, somewhat isolated, and not isolated comprised 14.5, 30.2, 37.1, and 18.2% of the sample, respectively. The most isolated participants were more likely to have low income (56.8% vs 12.2%, p

Many cancers are associated with poor diet, lack of physical activity, and excess weight. Improving any of these three lifestyle factors would likely reduce cancer deaths. However, modifications to each of these—better nutrition, enhanced activity and fitness, and loss of extra body fat—have different effect sizes on cancer mortality. This review will highlight the relative benefit that each lifestyle change, enacted prior to a diagnosis of cancer, might impart on cancer-related deaths, as well as attempt to quantify the changes required to derive such a benefit. The review relies primarily on epidemiological data, with meta-analyses serving as the backbone for comparisons across interventions and individual studies within the larger meta-analyses providing the data necessary to form more quantitative conclusions. The reader can then use this information to better understand, recommend, and implement behaviors that might ultimately reduce cancer mortality. Of all the interventions, it seems clear that exercise, specifically improving cardiorespiratory fitness, is the best way to decrease the risk of dying from cancer.

Purpose: Insulin levels play an important role in cancer development. However, the link between an insulinogenic diet and cancer is still unclear. Therefore, we performed a systematic review with meta-analysis to investigate the association between dietary insulin index (II) and load (IL) with cancer risk and mortality. Methods: A comprehensive search between electronic databases (Web of Science, PubMed/Medline, Scopus, and Google Scholar) was conducted to identify relevant studies up to January 2022. The relative risks (RR) and Odds ratios (OR) were extracted from eligible studies, and meta-analysis was performed to calculate the pooled effect size. Result: 12 papers including 14 studies (10 cohorts and 4 case–control) were included for the meta-analysis. Among them, 10 studies reported effect size for the risk of cancer, and 4 studies reported effect size for cancer mortality. We observed no significant association between II and IL with cancer overall (RRII: 1.03, 95%CI: 0.91–1.17, RRIL: 1.16, 95%CI: 0.94–1.42) and in cohort studies, however, in case–control studies was related with higher odds of cancer (ORII: 2.30, 95%CI: 1.21–4.38, ORIL: 2.57, 95%CI: 1.64–4.02). Higher II and IL scores were associated with the increased risk of total (RRII: 1.29, 95%CI: 1.02–1.63) and (RRIL: 1.39, 95%CI: 1.06–1.83) and colorectal cancer mortality (RRII: 1.29, 95%CI: 1.13–1.48) and (RRIL: 1.37, 95%CI: 1.18–1.60). Conclusion: Higher dietary II and IL were not associated with cancer risk in overall and cohort studies, whereas related with a higher risk of cancer in case–control studies. We observed a significant positive relation of II and IL with cancer mortality, especially CRC mortality. [ABSTRACT FROM AUTHOR]

Background: At present, "Belt and Road" ("B&R") member states (accounting for about 61.78% of the world's population) face different types of cancer threats to varying degrees. We analyzed the incidence and mortality and risk factors of cancer in the member countries of the "B&R" to explore the basis of health and medical cooperation between countries and provide a foundation for formulating cancer prevention and control policies for building a healthy "B&R."Methods: Data were derived from the Global Cancer Observatory and Cancer Country Profiles in 2020. Incidence and mortality were age-standardized rates (ASRs). Population attributable fractions (PAFs) was applied to measure risk factors of cancers in the "B&R" countries. The mortality-to-incidence ratio (MIR) was calculated by dividing the mortality rate by the incidence rate.Results: A total of 26 cancers were included in the study. Lung, breast, colorectal, stomach, liver, prostate, cervical, esophageal, thyroid, and uterine cancers were the most common and highest in age-standardized mortality in the "B&R" countries. For men, Hungary had the highest cancer age-standardized incidence and mortality (ASR, 289.3 per 100,000 and ASR, 235.7 per 100,000, respectively), followed by Latvia (ASR, 288.6 per 100,000 and ASR, 196.5 per 100,000, respectively). In females, the highest incidence rates were estimated in Greece (ASR, 238.7 per 100,000), and the highest mortality rate was Brunei (ASR, 192.3 per 100,000). All countries were in the middle or high HDI range, with about half (46.88%) of countries achieving high HDI, mostly in Central and Eastern Europe (13 countries) and West Asia (10 countries). The United Arab Emirates had the highest MIR in male and female (1.59 vs 2.19). Tobacco products, infectious factors, and ultraviolet rays were the three main cancer risk factors in the "B&R" countries.Conclusion: The overall burden of cancer in the countries along the "B&R" remains substantial, while the corresponding cancer prevention and control policies need to be improved. Strengthening health cooperation among member countries will contribute to a joint response to the risks and challenges posed by cancer. [ABSTRACT FROM AUTHOR]

Background: There is extensive interest in understanding how neighborhood socioeconomic status (nSES) may affect cancer incidence or survival. However, variability regarding items included and approaches used to form a composite nSES index presents challenges in summarizing overall associations with cancer. Given recent calls for standardized measures of neighborhood sociodemographic effects in cancer disparity research, the objective of this systematic review was to identify and compare existing nSES indices studied across the cancer continuum (incidence, screening, diagnosis, treatment, survival/mortality) and summarize associations by race/ethnicity and cancer site to inform future cancer disparity studies. Methods: Using PRISMA guidelines, peer‐reviewed articles published between 2010 and 2019 containing keywords related to nSES and cancer were identified in PubMed. Results: Twenty‐four nSES indices were identified from 75 studies. In general, findings indicated a significant association between nSES and cancer outcomes (n = 64/75 studies; 85.33%), with 42/64 (65.63%) adjusting for highly‐correlated individual SES factors (e.g., education). However, the direction of association differed by cancer site, race/ethnicity, and nSES index. Conclusions: This review highlights several methodologic and conceptual issues surrounding nSES measurement and potential associations with cancer disparities. Recommendations pertaining to the selection of nSES measures are provided, which may help inform disparity‐related disease processes and improve the identification of vulnerable populations in need of intervention. [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]

Abstract Background Cancer has become a global health problem, and assessments of cancer mortality are important for effective public health policy‐making and adequate resource allocation. In this study, we aimed to predict the mortality rates and numbers of deaths related to four common cancers (lung, liver, stomach, and esophagus) in China from 2020 to 2030 and to estimate the corresponding cancer burden caused by population aging and tobacco smoking. Methods Cancer mortality data (2004–2017) were extracted from China's death surveillance datasets, and China's population figures (2020–2030) were obtained from the United Nations population projections. Smoking prevalence data were retrieved from a World Health Organization global report, and relative risks of smoking and cancers were derived from large‐scale Asian studies. We predicted the deaths related to the four major cancers and age‐standardized mortality rates using joinpoint regression and linear regression models. The tobacco smoking‐related burden of these four major cancers was estimated using the population attributable fraction. Results Unlike lung cancer mortality which was predicted to continue to increase, the age‐standardized mortality rates for digestive cancers (liver, stomach, and esophageal cancers) are predicted to decline over the next decade. The number of deaths caused by the four major cancers is predicted to increase from 1,490,304 in 2020 to 1,823,960 in 2030. The age‐specific mortality rates of the four major cancers are predicted to increase with age after 40–45 years, peaking in the age groups of 80–84 and ≥85 years. In 2030, the combined number of deaths from the four examined cancers among adults aged ≥65 years is predicted to be 1,167,153, accounting for 64% of all deaths from these cancers. Tobacco smoking is predicted to contribute to nearly 29% of deaths from these cancers, corresponding to 527,577 deaths. Conclusions The overall trend in the combined total mortality from four major cancers is predicted to decline over the next decade; however, the corresponding death toll is expected to surge, in the context of China's population aging and high smoking prevalence. These estimates provide data‐driven evidence for China to implement effective cancer control measures in the future.

Chronic health conditions are commonplace in older populations. The process of aging impacts many of the world's top health concerns. With the average life expectancy continuing to climb, understanding patterns of morbidity in aging populations has become progressively more important. Cancer is an age-related disease, whose risk has been proven to increase with age. Limited information is published about the epidemiology of cancer and the cancer contribution to mortality in the 85+ age group, often referred to as the oldest-old. In this review, we perform a comprehensive assessment of the most recent (2011-2016) literature on cancer prevalence, incidence and mortality in the oldest-old. The data shows cancer prevalence and cancer incidence increases until ages 85-89, after which the rates decrease into 100+ ages. However the number of overall cases has steadily increased over time due to the rise in population. Cancer mortality continues to increase after age 85+. This review presents an overview of plausible associations between comorbidity, genetics and age-related physiological effects in relation to cancer risk and protection. Many of these age-related processes contribute to the lowered risk of cancer in the oldest-old, likewise other certain health conditions may "protect" from cancer in this age group.

ObjectiveThe purpose of this study was to evaluate the associations of serum biomarkers of fruit and vegetable intake (vitamin C and carotenoids) with cause–specific mortality and all–cause mortality in a nationally representative sample of US adults.MethodsWe analyzed data from 12,530 participants from the National Health and Nutrition Examination Survey III (1988–1994). The Cox proportional hazards models with restricted cubic spline were used for the analysis.ResultsDuring 246,027 person–years of follow–up, 4,511 deaths occurred, including 1,395 deaths from cardiovascular disease, 1,072 deaths from heart disease, 323 deaths from cerebral disease, and 954 deaths from cancer. The serum vitamin C was significantly associated with the cancer and all–cause mortality, with hazard ratios (HRs) (95% CIs) for each one SD of 0.80 (0.71–0.91) and 0.91 (0.86–0.96). The serum alpha–carotene was significantly associated with the cancer mortality, with HRs (95% CIs) of 0.70 (0.54–0.90), 0.68 (0.48–0.95), 0.64 (0.43–0.95), and 0.44 (0.33–0.60) for comparisons of groups 2–5 with group 1 in model 2, respectively. The change for each one SD in the composite biomarker score, equivalent to a 0.483 times/month difference in total fruits and vegetables intake, gave an HR of 0.79 (0.69–0.90) for cancer mortality.ConclusionInverse associations were found between serum vitamin C, carotenoids, and composite biomarker score and outcomes expect for cerebral disease, heart disease, and cardiovascular disease mortality. This finding supports an increase in dietary fruit and vegetable intake as a primary prevention strategy for cancer and all–cause mortality.

Background: Short and long sleep durations are associated with mortality outcomes. The association between sleep duration and mortality outcomes may differ according to sex and age. Methods: Participants of the Japan Public Health Center-based prospective study (JPHC Study) were aged 40–69 years and had completed a detailed questionnaire on lifestyle factors. Sex- and age-stratified analyses on the association between habitual sleep duration and mortality from all-causes, cardiovascular diseases (CVD), cancer and other causes included 46,152 men and 53,708 women without a history of CVD or cancer. Cox proportional hazards regression models, adjusted for potential confounders, were used to determine hazard ratios and 95% confidence intervals. Results: Mean follow-up time was 19.9 years for men and 21.0 years for women. In the multivariable sex-stratified models, some categories of sleep durations ≥8 hours were positively associated with mortality from all-causes, CVD, and other causes in men and women compared with 7 hours. The sex- and age-stratified analyses did not reveal any major differences in the association between sleep duration and mortality outcomes in groups younger and older than 50 years of age. The only exception was the significant interaction between sleep duration and age in women for mortality from other causes. Conclusions: Sleep durations ≥8 hours are associated with mortality outcomes in men and women. Age may be an effect modifier for the association between sleep duration and mortality from other causes in women.

Objective: Type 2 diabetes mellitus (T2DM) affects 10% of Americans and is associated with an increased incidence of cancer. Statins are first-line cholesterol-lowering medications in the treatment of hyperlipidemia. Several studies have demonstrated a relationship between statin use and reduced cancer incidence. We examined the cancer benefits of statin subtypes, with specific attention to disease-free survival (DFS) and overall survival (OS). Methods: This retrospective review included adults with T2DM diagnosed with solid tumors at Roswell Park Cancer Institute in Buffalo, NY, USA (2003–2010). Individuals with gestational diabetes, incomplete records, or diagnosed with rare solid tumors were excluded. Follow-up began at the date of diagnosis and ended with the first confirmed recurrence, death, or loss of contact. Demographics were assessed by Chi-square, Kaplan–Meier survival analyses, and Cox proportional hazards regression. Findings: Overall, 1102 patients met inclusion criteria, 52.1% of the study participants were female, and 578 participants (52.5%) died during the follow-up period which ranged from 0 to 156 months. Hydrophilic statin use was associated with improved DFS at 5-year follow-up (41.0% vs. 36.9%, P = 0.0077) compared to lipophilic statin use. Multivariate regression revealed that hydrophilic statins were associated with improved DFS (hazard ratio [HR]: 0.706, 95% confidence interval [CI]: 0.526–0.947) and OS (HR: 0.685, 95% CI: 0.503–0.934). Pravastatin was associated with improved OS (HR: 0.674, 95% CI: 0.471–0.964). Conclusion: In patients with T2DM and cancer, hydrophilic statins, and pravastatin in particular, are associated with improved DFS as well as OS. Further research examining the cancer-specific effects of hydrophilic and lipophilic statins is needed to better understand their beneficial effects.

Cancer is a leading cause of death worldwide, posing a huge burden upon society and individuals. The adequate intake of fruit and vegetables is reported to be an effective strategy for primary cancer prevention. Fruits and vegetables are rich in nutrients, such as vitamins and flavonoids, which may reduce the occurrence and progression of cancers. However, the importance of each flavonoid and the sub-classes remains controversial regarding cancer mortality. The population benefiting from increased flavonoid intake has not been determined. An estimation of cancer mortality by flavonoid intake is not established. We explored the association between the intake of flavonoids and cancer mortality amongst 14,029 participants in the National Health and Nutrition Examination Survey. During a median follow-up of 117 months, 405 cancer deaths were confirmed. Being in the second, third, and fourth quartiles of flavonol intake, the cancer mortality was inversely associated with the intake of flavonols (multivariate analysis HR (95% CI] 0.58 [0.36, 0.91], p = 0.02, Q1 vs. Q2; 0.55 [0.31, 0.96], p = 0.04, Q1 vs. Q3; 0.54 [0.30, 0.99], p = 0.05, Q1 vs. Q4, respectively). Potential effects of dietary flavonol intake against cancer death was observed especially in participants aged 50 or above, males, whites, former smokers, people who used to drink or drink alcohol mildly, people without hyperlipidemia, and people with hypertension. Moreover, the dietary intakes of peonidin, naringenin, and catechin were inversely associated with cancer mortality (multivariate HR [95% CI] 0.93 [0.88,0.98], p = 0.01; 0.97 (0.95,1.00), p = 0.03; 0.98 (0.96,1.00), p = 0.05, respectively). Furthermore, a nomogram based on flavonol intake is feasible for assessing cancer mortality for each participant. Taken together, our results could improve personalized nutrition amongst cancer patients.

Ecological studies showed correlations between a shift toward animal-protein-rich diets and longer life-expectancy; however, only a few studies examined individual-level association of protein source and mortality risks using appropriate iso-caloric substitution models adjusted for total energy intake. We used EPIC-Heidelberg (European Prospective Investigation into Cancer and nutrition) to create iso-caloric substitution models and determined relative all-cause, cardiovascular and cancer mortality hazards associated with dietary intake of animal protein and other macronutrients, employing Cox proportional hazard models. For comparison with other studies, we also synthesized evidence from a systematic review relating animal protein intake to mortality risk from seven prospective cohort studies in the USA, Europe and Japan. Substitution of 3% of total energy from animal protein for fat (saturated, mono-unsaturated) and carbohydrate (simple, complex) was associated with all-cause mortality (Hazard Ratios [HR] from 1.05 to 1.11), mostly driven by cardiovascular mortality (HR from 1.13 to 1.15). Independently of animal protein, substituting poly-unsaturated fat for saturated fat increased cancer-related mortality risk by 12 percent. The systematic review largely corroborated our findings. Overall, higher proportions of dietary energy from animal protein, combined with low energy intake from either carbohydrate sub-types or dietary fats, increases all-cause and cardiovascular mortality risks, but not cancer-related mortality.

We aimed to investigate the association between dietary zinc intake and total deaths, cancer, and cardiovascular disease death. In this prospective, 10-year, community-based cohort analysis, data from 143,050 adult participants (aged 40 years and older) were analyzed. Dietary zinc intake at baseline was assessed using a food frequency questionnaire. Harrell’s C-index was used to determine the optimal cut-off of dietary zinc intake with the log-rank test. Using the Cox proportional hazards regression models, the association between dietary zinc intake and all-cause, cancer, and cardiovascular disease mortality was estimated using hazard ratios and 95% confidence intervals. During the mean 10.1 years of follow-up, 5436 participants expired, of whom 2355 died due to cancer and 985 died due to cardiovascular causes. After adjustment for confounders, dietary zinc intake was inversely associated with all-cause mortality (≤5.60 mg/day vs. >7.98 mg/day; hazard ratio, 1.13; 95% confidence interval, 1.01–1.25) and cardiovascular disease mortality (≤5.12 mg/day vs. >7.28 mg/day; hazard ratio, 1.42; 95% confidence interval, 1.11–1.81) but not with cancer mortality (≤5.60 mg/day vs. >10.08 mg/day; hazard ratio, 1.09; 95% confidence interval, 0.90–1.33). Dietary zinc intake was associated with a lower risk of all-cause mortality and cardiovascular disease mortality but not with cancer mortality. Our findings could suggest that recommending optimal dietary zinc intake is helpful for human health.

Background: China has the highest number of new cancer cases and deaths worldwide, posing huge health and economic burdens to society and affected families. This study comprehensively analyzed secular trends of national cancer mortality statistics to inform future prevention and intervention programs in China. Methods: The annual estimate of overall cancer mortality and its major subtypes were derived from the National Health Commission (NHC). Joinpoint analysis was used to detect changes in trends, and we used age-period-cohort modeling to estimate cohort and period effects in Cancers between 1987 and 2020. Net drift (overall annual percentage change), local drift (annual percentage change in each age group), longitudinal age curves (expected longitudinal age-specific rate), and period (cohort) relative risks were calculated. Results: The age-standardized cancer mortality in urban China has shown a steady downward trend but has not decreased significantly in rural areas. Almost all cancer deaths in urban areas have shown a downward trend, except for colorectal cancer in men. Decreasing mortality from cancers in rural of the stomach, esophagus, liver, leukemia, and nasopharynx was observed, while lung, colorectal cancer female breast, and cervical cancer mortality increased. Birth cohort risks peaked in the cohorts born around 1920–1930 and tended to decline in successive cohorts for most cancers except for leukemia, lung cancer in rural, and breast and cervical cancer in females, whose relative risks were rising in the very recent cohorts. In addition, mortality rates for almost all types of cancer in older Chinese show an upward trend. Conclusions: Although the age-standardized overall cancer mortality rate has declined, and the urban-rural gap narrowed, the absolute cancer cases kept increasing due to the growing elderly population in China. The rising mortality related to lung, colorectal, female breast, and cervical cancer should receive higher priority in managing cancer burden and calls for targeted public health actions to reverse the trend.

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: Exercise may increase the inhalation and deposition of air pollutants, which may counteract its beneficial effects. We thus examined the combined effects of chronic exposure to fine particulate matter (PM2.5) and habitual exercise on the risk of death from cancer in Taiwan.Patients and Methods: A total of 384 128 adults (≥18 years of age) were recruited for a medical screening programme between 2001 and 2016, yielding 842 384 medical-examination records. All participants were followed up until 31 May 2019. Vital data were obtained from the National Death Registry of Taiwan and the ambient PM2.5 exposure was estimated using a satellite-based spatiotemporal model. Information on habitual exercise was collected using a standard self-administered questionnaire. The time-dependent Cox-regression model was used to evaluate the combined effects.Results: A greater amount of habitual exercise was associated with lower risk of death from cancer, whilst a higher level of PM2.5 exposure was associated with a higher risk of death from cancer. The inverse associations of habitual exercise with death from cancer were not modified by chronic exposure to PM2.5. The participants in the group with a high level of exercise and a low level of PM2.5 exposure exhibited a 35% lower risk of death from cancer than those in the group with a low level of exercise and a high level of PM2.5 exposure (95% confidence interval: 28%, 42%).Conclusions: Increased levels of exercise and reduced exposure levels of PM2.5 are associated with a lower risk of death from cancer. Habitual exercise reduces the risk of death from cancer regardless of the levels of chronic PM2.5 exposure. Our results indicate that habitual exercise is a suitable health-promotion strategy even for people who reside in moderately polluted regions. [ABSTRACT FROM AUTHOR]

Abstract Objective A previous Australian study compared the observed numbers of cancer cases and deaths in 2007 with the expected numbers based on 1987 rates. This study examines the impact of cancer rate changes over the 20-year period 1996–2015, for people aged under 75 years. Results The overall age-standardised cancer incidence rate increased from 350.7 in 1995 to 364.4 per 100,000 in 2015. Over the period 1996–2015, there were 29,226 (2.0%) more cases (males: 5940, 0.7%; females: 23,286, 3.7%) than expected numbers based on 1995 rates. Smaller numbers of cases were observed compared to those expected for cancers of the lung for males and colorectum, and cancers with unknown primary. Larger numbers of cases were observed compared to those expected for cancers of the prostate, thyroid and female breast. The overall age-standardised cancer mortality rate decreased from 125.6 in 1995 to 84.3 per 100,000 in 2015. During 1996 to 2015 there were 106,903 (− 20.6%) fewer cancer deaths (males: − 69,007, − 22.6%; females: − 37,896, − 17.9%) than expected based on the 1995 mortality rates. Smaller numbers of deaths were observed compared to those expected for cancers of the lung, colorectum and female breast, and more cancer deaths were observed for liver cancer.

Abstract Background To estimate the relationship between inflammatory biomarkers and cancer mortality in a nationally representative sample of the U.S. population while controlling for education, occupation, and income. Methods Data were obtained from the U.S. National Health and Nutrition Examination Survey from 1988 to 1994 (N = 7817) and 1999–2002 (N = 2344). We fit Cox proportional hazard models to examine the relationship between C-reactive protein (CRP) and fibrinogen with cancer mortality. Results In the full Cox multivariate model, clinically raised CRP was associated with cancer mortality in NHANES 1988–1994 (> 0.99 mg/dL: 95%CI: 1.04–2.13). However, across two inflammatory biomarkers (CRP and Fibrinogen), two NHANES time periods (1998–1994 and 1999–2002) and three income levels (12 strata in total), Hazard ratio confidence intervals did not include the null only for one association: CRP and cancer mortality among low income participants from 1988 to 1994 (HR = 1.83, 95% CI: 1.10–3.04). Conclusions We find evidence that only in one unique stratum is earlier life CRP, and not fibrinogen, associated with prospective cancer mortality. After more complete control for socioeconomic confounding, CRP and fibrinogen do not predict cancer mortality in most subpopulations.

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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]

Background: Elevated blood pressure is a major risk factor for cardiovascular (CV) disease. But the effects of sodium intake or excretion on CV mortality are uncertain. The present study aimed to investigate the association between 24 h urinary sodium excretion, as a marker of dietary salt intake, and CV or cancer mortality in a healthy Japanese population using 24 hurine collection. Methods: The baseline study was conducted in 1980. A total of 1291 participants aged 21 to 85 years, underwent health check-ups, which included blood chemistry measurements and the collection of 24 h urine samples. Enrolled 1291 participants were followed up for 27.5 years, in whom the final follow-up rate was 95.8%. Cox proportional hazards regression models were used to assess the association between 24 h urinary sodium excretion and CV or cancer mortality. Results: The mean 24 h urinary sodium excretion was 5.80 ± 2.28 g/day. There were 631 deaths: 153 (27%) from cancer, 142 (26%) from CV disease. In the Cox proportional hazard regression model after adjustment for confounding factors, systolic and diastolic blood pressures, and uric acid were positively associated with CV mortality, and the 24 h urinary sodium and potassium excretions were inversely associated with CV mortality (p < 0.05). On the other hand, there were no association between 24 h urinary sodium excretions and cancer mortality. We divided the urinary sodium excretions levels into quartiles. After adjustment for confounding factors, the hazard ratio of CV mortality in the highest quartile of 24 h urinary sodium excretion versus the lowest was 0.46 (p < 0.05). The cumulative survival rate for CV death was significantly decreased in the lowest quartile compared with the other higher groups. Conclusions: We found that impacts of 24 h sodium excretion on CV and cancer mortalities were much different in the general population. [Display omitted] • 24 h urinary sodium excretion was inversely associated with cardiovascular (CV) death. • There was no association between sodium excretion and cancer mortality. • CV death was decreased in the highest quartile compared with the lower groups. [ABSTRACT FROM AUTHOR]

OBJECTIVES: This report describes the extended follow-up (1941–2015) of a cohort of 38 549 automobile manufacturing workers with potential exposure to metalworking fluids (MWF). The outcomes of interest were mortality from cancers of the esophagus, stomach, intestine, rectum, bladder, liver, pancreas, larynx, lung, skin, prostate, brain, and female breast, as well as leukemia. This report includes 5472 deaths from cancer, more than ten times the numbers of deaths in our last summary report published 20 years ago. METHODS: Standardized mortality ratios were computed for the entire study period. Adjusted hazard ratios (HR) were estimated in Cox proportional hazard models with categorical variables for cumulative exposure to each type of MWF. RESULTS: Exposure–response patterns are consistent with prior mortality reports from this cohort. We found increased risk of skin and female breast cancer with straight fluids. For the first time, we found elevated risk of stomach cancer mortality. Overall, many of the exposure–response results did not suggest an association with MWF. CONCLUSIONS: Mortality is a poor proxy for cancer diagnosis for treatable cancers and not the optimal outcome measure in etiological studies. Although the HR presented here handle bias from the healthy worker hire effect and left truncation, they do not handle bias from healthy worker survivor effect, which likely results in underestimates of the health impacts of MWF. Although this updated summary provides some information on the risk of cancer from MWF, targeted future analyses will help clarify associations.

Abstract Background The association of high-sensitivity C-reactive protein (hsCRP) with mortality is controversial. We aimed to investigate the associations of hsCRP concentrations with the risks of all-cause and cause-specific mortality and identify potential modifying factors affecting these associations among middle-aged and elderly individuals. Methods This community-based prospective cohort study included 14,220 participants aged 50+ years (mean age: 64.9 years) from the Health and Retirement Study. Cox proportional hazard models were employed to estimate the associations between the hsCRP concentrations and the risk of all-cause and cause-specific mortality with adjustment for sociodemographic and lifestyle factors, self-reported medical history, and other potential confounders. Results In total, 1730 all-cause deaths were recorded, including 725 cardiovascular- and 417 cancer-related deaths, after an 80,572 person-year follow-up (median: 6.4 years; range: 3.6–8.1 years). The comparisons of the groups with the highest (quartile 4) and lowest (quartile 1) hsCRP concentrations revealed that the adjusted hazard ratios and 95% confidence intervals were 1.50 (1.31–1.72) for all-cause mortality, 1.44 (1.13–1.82) for cardiovascular mortality, and 1.67 (1.23–2.26) for cancer mortality. The associations between high hsCRP concentrations and the risks of all-cause, cardiovascular, and cancer mortality were similar in the men and women (P for interaction > 0.05). Conclusions Among middle-aged and older individuals, elevated hsCRP concentration could increase the risk of all-cause, cardiovascular, and cancer mortality in men and women.

Abstract Background Although long-term alcohol and tobacco use have widely been recognised as important risk factors for cancer, the impacts of alcohol and tobacco health policies on cancer mortality have not been examined in previous studies. This study aims to estimate the association of key alcohol and tobacco policy or events in Australia with changes in overall and five specific types of cancer mortality between the 1950s and 2013. Methods Annual population-based time-series data between 1911 and 2013 on per capita alcohol and tobacco consumption and head and neck (lip, oral cavity, pharynx, larynx and oesophagus), lung, breast, colorectum and anus, liver and total cancer mortality data from the 1950s to 2013 were collected from the Australian Bureau of Statistics and Cancer Council Victoria, the WHO Cancer Mortality Database and the Australian Institute of Health and Welfare. The policies with significant relations to changes in alcohol and tobacco consumption were identified in an initial model. Intervention dummies with estimated lags were then developed based on these key alcohol and tobacco policies and events and inserted into time-series models to estimate the relation of the particular policy changes with cancer mortality. Results Liquor licence liberalisation in the 1960s was significantly associated with increases in the level of population drinking and thereafter of male cancer mortality. The introduction of random breath testing programs in Australia after 1976 was associated with a reduction in population drinking and thereafter in cancer mortality for both men and women. Meanwhile, the release of UK and US public health reports on tobacco in 1962 and 1964 and the ban on cigarette ads on TV and radio in 1976 were found to have been associated with a reduction in Australian tobacco consumption and thereafter a reduction in mortality from all cancer types except liver cancer. Policy changes on alcohol and tobacco during the 1960s–1980s were associated with greater changes for men than for women, particularly for head and neck, lung and colorectum cancer sites. Conclusion This study provides evidence that some changes to public health policies in Australia in the twentieth century were related to the changes in the population consumption of alcohol and tobacco, and in subsequent mortality from various cancers over the following 20 years.

Objectives: To examine the effect of smoking status, smoking intensity, duration of smoking cessation and age of smoking initiation on the risk of all-cause and cause-specific mortality among cardiovascular disease (CVD) patients.Design: A population-based prospective cohort study.Setting: The National Health Interview Survey (NHIS) in the U.S. that were linked to the National Death Index (NDI).Participants: 66,190 CVD participants ≥ 18 years of age who were interviewed between 1997 and 2013 in the NHIS linked to the NDI through December 31, 2015.Outcome Measures: The primary outcome was all-cause mortality and the secondary outcome was cause-specific mortality including CVD mortality and cancer mortality.Results: During the mean follow-up of 8.1 years, we documented 22,518 deaths (including 6,473 CVD deaths and 4,050 cancer deaths). In the overall CVD population, former and current smokers had higher risk of all-cause (Former smokers: hazard ratios (HRs), 1.26; 95% confidence interval (CI), 1.21–1.31, P < 0.001; Current smokers: HRs, 1.96; 95%CI, 1.86–2.07, P < 0.001), CVD (Former smokers: HRs, 1.12; 95%CI, 1.05–1.21, P = 0.001; Current smokers: HRs, 1.80; 95%CI, 1.64–1.97, P < 0.001) and cancer mortality (Former smokers: HRs, 1.49; 95%CI, 1.35–1.64, P < 0.001; Current smokers: HRs, 2.78; 95%CI, 2.49–3.09, P < 0.001) than never smokers. Furthermore, similar results were observed when the study subjects were stratified according to the type of CVD. Among current smokers, the risk for cancer mortality increased as the daily number of cigarettes increased, regardless of the specific type of CVD. However, the association of the risk for all-cause and CVD mortality with smoking intensity did not present a dose-response relationship. In participants with angina pectoris or stroke, smoking intensity was inversely associated with deaths from CVD. In addition, the risk for all-cause, CVD and cancer mortality declined as years of smoking cessation increased. Finally, the relative risk of all-cause mortality was not significantly different in individuals with a younger age of smoking initiation.Conclusions: CVD patients who are smokers have an increased risk of all-cause, CVD and cancer mortality, and the risk decreases significantly after quitting smoking. These data further provide strong evidence that supports the recommendation to quit smoking for the prevention of premature deaths among individuals with CVD.

Background: Prior studies on the relationship between bowel health and mortality have generally focused on the individual association of stool frequency or consistency with mortality but did not present a joint association. Therefore, we aimed to systematically evaluate the individual and joint associations of stool frequency and consistency with all-cause and cause-specific mortality in this study. Methods: A total of 14,574 participants from the National Health and Nutrition Examination Survey 2005–2010 were incorporated in this analysis. Survey sample-weighted Cox proportional hazards models adjusted for potential confounders were used to estimate hazard ratios (HRs) between bowel health measures and mortality risks. Results: During a median of 7.6 years of follow-up, 1502 deaths occurred, including 357 cancer deaths and 284 cardiovascular disease (CVD) deaths. The bowel habit of the most participants was 7 times/week (50.7%), and the most common type was “Like a sausage or snake, smooth and soft” (51.8%). Stool frequency displayed a parabolic relationship with all-cause mortality, and less than 7 times/week is a significant risk factor for mortality (HR for 1 time/week: 1.43, p-values = 0.04. HR for 6 times/week: 1.05, p-value = 0.03). Analyzing the joint association of stool frequency and consistency on mortality clarified the limitations of only inspecting the effects of either individual factor. Compared with 7 times/week of normal stool, infrequent soft stools at 4 times/week were associated with 1.78-, 2.42-, and 2.27-times higher risks of all-cause, cancer, and CVD mortality, respectively. Conclusion: Analyses of bowel health should consider the joint effects of stool frequency and stool consistency. Self-appraisal of stool frequency and consistency may be a simple but useful tool for informing about major chronic illnesses.

Objectives: Tea consumption has been considered beneficial to human health because tea contains phytochemicals such as polyphenols and theaflavins. We conducted a systematic review and meta-analysis on the association between tea consumption and mortality from all causes, cardiovascular disease (CVD), and cancer to provide a quantitative assessment of current evidence., Methods: The PubMed, Web of Science, and Scopus databases were searched through April 2024 to identify eligible studies. Random effects models were used to combine study-specific effect estimates (ESs)., Results: A total of 38 prospective cohort data sets (from 27 papers) with 1,956,549 participants were included in this meta-analysis. The pooled ESs of the highest versus lowest categories of tea consumption were 0.90 (95% CI, 0.86-0.95) for all-cause mortality, 0.86 (95% CI, 0.79-0.94) for CVD mortality, and 0.90 (95% CI, 0.78-1.03) for cancer mortality. In the dose-response analysis, a nonlinear association was observed. The greatest risk reductions were observed for the consumption of 2 cups/day for all-cause mortality (ES, 0.91; 95% CI, 0.88-0.94) and 1.5 cups/day for cancer mortality (ES, 0.92; 95% CI, 0.89-0.96), whereas additional consumption did not show a further reduction in the risk of death. A plateau was observed for CVD mortality at moderate consumption levels (1.5-3 cups/day), but a sustained reduction in mortality risk was observed at higher intake levels., Conclusion: Moderate tea consumption (e.g., 1.5-2 cups/day) was associated with lower all-cause, CVD, and cancer mortality compared to no tea consumption. Further well-designed prospective studies are needed for a definitive Conclusion.

Aims: A higher risk of cancer among patients with heart failure (HF) has been suggested in recent community-based studies. This study aimed to investigate the impact of HF during hospitalization with acute coronary syndrome (ACS) on the long-term cancer risk., Methods and Results: The study included 572 patients admitted with ACS to three Italian hospitals, discharged cancer-free, and prospectively followed for 24 years or until death. All but three patients completed the follow-up, which represented 6440 person-years (mean age: 66 ± 12 years; 70% males). Baseline HF was diagnosed in 192 (34%) patients. A total of 129 (23%) patients developed cancer (103 without HF and 26 with HF), and 107 (19%) patients died due to it (81 without HF and 26 with HF). The incidence rates for cancer onset and cancer death were not different according to HF status. Cox regression analysis revealed no association between HF or left ventricular ejection fraction (LVEF) and cancer risk. In addition, no difference in cancer risk was observed among patients with HF with preserved ejection fraction, HF with mildly reduced ejection fraction, and HF with reduced ejection fraction. In competing risk regression analysis, the risk of cancer onset associated with HF was sub-hazard ratio (SHR) 0.47 [95% confidence interval (CI): 0.30-0.72; P = 0.001] and SHR 1.02 (95% CI: 1.01-1.04; P = 0.002) with LVEF. Results were the same in the adjusted model. Yet the fully adjusted model showed an attenuated association between cancer death and HF (SHR: 0.63; 95% CI: 0.37-1.05; P = 0.08) and LVEF (SHR: 1.02; 95% CI: 0.99-1.06; P = 0.08). Consistent results were obtained after using propensity score matching analysis that created 192 pairs. A negative interaction between age and HF and a positive interaction between age and LVEF for cancer risk have also been found., Conclusions: An inverse association between baseline HF and long-term cancer risk has been observed among the ABC Study on heart disease patients who were followed for 24 years after ACS., (© 2024 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)