Search

Background: The American Heart Association recently introduced a novel cardiovascular health (CVH) metric, Life's Essential 8 (LE8), for health promotion. However, the relationship between LE8 and cancer mortality risk remains uncertain., Methods: We investigated 17,076 participants from US National Health and Nutrition Examination Survey (US NHANES) and 272,727 participants from UK Biobank, all free of cancer at baseline. The CVH score, based on LE8 metrics, incorporates four health behaviors (diet, physical activity, smoking, and sleep) and four health factors (body mass index, lipid, blood glucose, and blood pressure). Self-reported questionnaires assessed health behaviors. Primary outcomes were mortality rates for total cancer and its subtypes. The association between CVH score (continuous and categorical variable) and outcomes was examined using Cox model with adjustments. Cancer subtypes-related polygenic risk score (PRS) was constructed to evaluate its interactions with CVH on cancer death risk., Results: Over 141,526 person-years in US NHANES, 424 cancer-related deaths occurred, and in UK Biobank, 8,872 cancer deaths were documented during 3,690,893 person-years. High CVH was associated with reduced overall cancer mortality compared to low CVH (HR 0.58, 95% CI 0.37-0.91 in US NHANES; 0.51, 0.46-0.57 in UK Biobank). Each one-standard deviation increase in CVH score was linked to a 19% decrease in cancer mortality (HR: 0.81; 95% CI: 0.73-0.91) in US NHANES and a 19% decrease (HR: 0.81; 95% CI: 0.79-0.83) in UK Biobank. Adhering to ideal CVH was linearly associated with decreased risks of death from lung, bladder, liver, kidney, esophageal, breast, colorectal, pancreatic, and gastric cancers in UK Biobank. Furthermore, integrating genetic data revealed individuals with low PRS and high CVH exhibited the lowest mortality from eight cancers (HRs ranged from 0.36 to 0.57) compared to those with high PRS and low CVH. No significant modification of the association between CVH and mortality risk for eight cancers by genetic predisposition was observed. Subgroup analyses showed a more pronounced protective association for overall cancer mortality among younger participants and those with lower socio-economic status., Conclusions: Maintaining optimal CVH is associated with a substantial reduction in the risk of overall cancer mortality. Adherence to ideal CVH correlates linearly with decreased mortality risk across multiple cancer subtypes. Individuals with both ideal CVH and high genetic predisposition demonstrated significant health benefits. These findings support adopting ideal CVH as an intervention strategy to mitigate cancer mortality risk and promote healthy aging., (© 2024. The Author(s).)

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.

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).)

Low neighborhood socioeconomic status has been linked to adverse health outcomes. However, it is unclear whether changing the neighborhood may influence health. We examined 10-year change in neighborhood socioeconomic deprivation in relation to mortality rate among 288,555 participants aged 51–70 years who enrolled in the National Institutes of Health-AARP Diet and Health Study in 1995–1996 (baseline) and did not move during the study. Changes in neighborhood socioeconomic deprivation between 1990 and 2000 were measured by US Census data at the census tract level. All-cause, cardiovascular disease, and cancer deaths were ascertained through annual linkage to the Social Security Administration Death Master File between 2000 and 2011. Overall, our results suggested that improvement in neighborhood socioeconomic status was associated with a lower mortality rate, while deterioration was associated with a higher mortality rate. More specially, a 30-percentile-point reduction in neighborhood deprivation among more deprived neighborhoods was associated with 11% and 19% reductions in the total mortality rate among men and women, respectively. On the other hand, a 30-point increase in neighborhood deprivation in less deprived neighborhoods was associated with an 11% increase in the mortality rate among men. Our findings support a longitudinal association between changing neighborhood conditions and mortality. [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: 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]

Background Urban sprawl has the potential to influence cancer mortality via direct and indirect effects on obesity, access to health services, physical activity, transportation choices and other correlates of sprawl and urbanization. Methods This paper presents a cross-sectional analysis of associations between urban sprawl and cancer mortality in urban and suburban counties of the United States. This ecological analysis was designed to examine whether urban sprawl is associated with total and obesity-related cancer mortality and to what extent these associations differed in different regions of the US. A major focus of our analyses was to adequately account for spatial heterogeneity in mortality. Therefore, we fit a series of regression models, stratified by gender, successively testing for the presence of spatial heterogeneity. Our resulting models included county level variables related to race, smoking, obesity, access to health services, insurance status, socioeconomic position, and broad geographic region as well as a measure of urban sprawl and several interactions. Our most complex models also included random effects to account for any county-level spatial autocorrelation that remained unexplained by these variables. Results Total cancer mortality rates were higher in less sprawling areas and contrary to our initial hypothesis; this was also true of obesity related cancers in six of seven U.S. regions (census divisions) where there were statistically significant associations between the sprawl index and mortality. We also found significant interactions (p < 0.05) between region and urban sprawl for total and obesity related cancer mortality in both sexes. Thus, the association between urban sprawl and cancer mortality differs in different regions of the US. Conclusions Despite higher levels of obesity in more sprawling counties in the US, mortality from obesity related cancer was not greater in such counties. Identification of disparities in cancer mortality within and between geographic regions is an ongoing public health challenge and an opportunity for further analytical work identifying potential causes of these disparities. Future analyses of urban sprawl and health outcomes should consider exploring regional and international variation in associations between sprawl and health. [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., (© 2022. The Author(s).)

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

Background: Since 1971, the annual National Ambient Air Quality Standard (NAAQS) for nitrogen dioxide (NO 2 ) has remained at 53 ppb, the impact of long-term NO 2 exposure on mortality is poorly understood., Objectives: We examined associations between long-term NO 2 exposure (12-month moving average of NO 2 ) below the annual NAAQS and cause-specific mortality among the older adults in the U.S., Methods: Cox proportional-hazard models were used to estimate Hazard Ratio (HR) for cause-specific mortality associated with long-term NO 2 exposures among about 50 million Medicare beneficiaries living within the conterminous U.S. from 2001 to 2008., Results: A 10 ppb increase in NO 2 was associated with increased mortality from all-cause (HR: 1.06; 95% CI: 1.05-1.06), cardiovascular (HR: 1.10; 95% CI: 1.10-1.11), respiratory disease (HR: 1.09; 95% CI: 1.08-1.11), and cancer (HR: 1.01; 95% CI: 1.00-1.02) adjusting for age, sex, race, ZIP code as strata ZIP code- and state-level socio-economic status (SES) as covariates, and PM 2.5 exposure using a 2-stage approach. NO 2 was also associated with elevated mortality from ischemic heart disease, cerebrovascular disease, congestive heart failure, chronic obstructive pulmonary disease, pneumonia, and lung cancer. We found no evidence of a threshold, with positive and significant HRs across the range of NO 2 exposures for all causes of death examined. Exposure-response curves were linear for all-cause, supra-linear for cardiovascular-, and sub-linear for respiratory-related mortality. HRs were highest consistently among Black beneficiaries., Conclusions: Long-term NO 2 exposure is associated with elevated risks of death by multiple causes, without evidence of a threshold response. Our findings raise concerns about the sufficiency of the annual NAAQS for NO 2 ., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Intake time of diet has recently been demonstrated to be associated with the internal clock and circadian pattern. However, whether and how the intake time of minerals would influence the natural course of cancer was largely unknown., Methods: This study aimed to assess the association of mineral intake at different periods with cancer and all-cause mortality. A total of 27,455 participants aged 18-85 years old in the National Health and Nutrition Examination Survey were recruited. The main exposures were the mineral intakes in the morning, afternoon and evening, which were categorized into quintiles, respectively. The main outcomes were mortality of cancer and all causes., Results: During the 178,182 person-years of follow-up, 2680 deaths, including 601 deaths due to cancer, were documented. After adjusting for potential confounders, compared to the participants who were in the lowest quintile(quintile-1) of mineral intakes at dinner, the participants in the highest quintile intake(quintile-5) of dietary potassium, calcium and magnesium had lower mortality risks of cancer (HRpotassium = 0.72, 95% CI:0.55-0.94, P for trend = 0.023; HRcalcium = 0.74, 95% CI:0.57-0.98, P for trend = 0.05; HRmagnesium = 0.75, 95% CI:0.56-0.99, P for trend = 0.037) and all-cause (HRpotassium = 0.83, 95% CI:0.73-0.94, P for trend = 0.012; HRcalcium = 0.87, 95% CI:0.76-0.99, P for trend = 0.025; HRmagnesium = 0.85, 95% CI:0.74-0.97, P for trend = 0.011; HRcopper = 0.80, 95%CI: 0.68-0.94, P for trend = 0.012). Further, equivalently replacing 10% of dietary potassium, calcium and magnesium consumed in the morning with those in the evening were associated with lower mortality risk of cancer (HRpotassium = 0.94, 95%CI:0.91-0.97; HRcalcium = 0.95, 95%CI:0.92-0.98; HRmagnesium = 0.95, 95%CI: 0.92-0.98)., Conclusions: This study demonstrated that the optimal intake time of potassium, calcium and magnesium for reducing the risk of cancer and all-cause mortality was in the evening., (© 2021. The Author(s).)

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.

Background: The shape of the exposure-response curve for long-term ambient fine particulate (PM 2.5 ) 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 PM 2.5 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 PM 2.5 on mortality was examined using two stage models of PM 2.5 and nitrogen dioxide (NO 2 )., Results: A 10 μg /m 3 increase in 12-month average PM 2.5 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. PM 2.5 exposures, however, were not associated with lung cancer mortality. Results were not sensitive to control for ozone exposures. PM 2.5 -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 PM 2.5 levels. Associations between PM 2.5 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 PM 2.5 were lower than that for all PM 2.5 and were null for respiratory and lung cancer-related deaths., Conclusions: PM 2.5 was associated with mortality from CVD, respiratory, and all cancer, but not lung cancer. PM 2.5 -associated risks of CVD and respiratory mortality were similar across PM 2.5 levels, with no evidence of a threshold. Blacks, urban, and younger beneficiaries were most vulnerable to the long-term impacts of PM 2.5 on mortality.

Cohort or period components of trends can provide a rationale for new research or point to clues on the effectiveness of control strategies. Graphical display of trends guides models that quantify the experience of a population. In this paper, a method for smoothing rates by single year of age and year is developed and displayed to show the contributions of period and cohort to trends. The magnitude of the contribution of period and/or cohort in a model for trends may be assessed by the percentage of deviance explained and the relative contributions of cohort (C) and period (P) individually, known as the C-P score. The method is illustrated using Surveillance, Epidemiology, and End Results data (1975-2014) on lung and bronchial cancer mortality in females and prostate and colorectal cancer incidence in males. Smoothed age-period and age-cohort rates provide a useful first step in studies of etiology and the impact of disease control without imposing a restrictive model. We found that, in this data set, cohort predominates for female lung and bronchial cancer and period predominates for male prostate cancer. However, the effects change with age for male colorectal cancer incidence, indicating an age shift in relevant exposures. These methods are applied on an interactive website for both incidence and mortality at over 20 cancer sites in the United States., (Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health 2019.)

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.

Background: Previous meta-analyses of randomized controlled trials (RCTs) of vitamin D supplementation and total cancer incidence and mortality found inconsistent results, and most included trials administered generally low doses of vitamin D (≤1100 IU/day). We updated the meta-analysis by incorporating recent RCTs that have tested higher doses of vitamin D supplements., Materials and Methods: PubMed and Embase were searched from the inception to November 2018. Summary relative risks (RRs) and 95% confidence intervals (CIs) were estimated using a random-effects model., Results: For total cancer incidence, 10 trials were included [6537 cases; 3-10 years of follow-up; 54-135 nmol/l of attained levels of circulating 25(OH) vitamin D [25(OH)D] in the intervention group]. The summary RR was 0.98 (95% CI, 0.93-1.03; P = 0.42; I2 = 0%). The results remained null across subgroups tested, including even when attained 25(OH)D levels exceeded 100 nmol/l (RR, 0.95; 95% CI, 0.83-1.09; P = 0.48; I2 = 26%). For total cancer mortality, five trials were included [1591 deaths; 3-10 years of follow-up; 54-135 nmol/l of attained levels of circulating 25(OH)D in the intervention group]. The summary RR was 0.87 (95% CI, 0.79-0.96; P = 0.005; I2 = 0%), which was largely attributable to interventions with daily dosing (as opposed to infrequent bolus dosing). No statistically significant heterogeneity was observed by attained levels of circulating 25(OH)D (Pheterogeneity = 0.83), with RR being 0.88 (95% CI, 0.78-0.98; P = 0.02; I2 = 0%) for ≤100 nmol/l and 0.85 (95% CI, 0.70-1.03; P = 0.11; I2 = 0%) for >100 nmol/l., Conclusions: In an updated meta-analysis of RCTs, vitamin D supplementation significantly reduced total cancer mortality but did not reduce total cancer incidence., (© The Author(s) 2019. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

This article summarizes cancer mortality trends and disparities based on data from the National Center for Health Statistics. It is the first in a series of articles that will describe the American Cancer Society's vision for how cancer prevention, early detection, and treatment can be transformed to lower the cancer burden in the United States, and sets the stage for a national cancer control plan, or blueprint, for the American Cancer Society goals for reducing cancer mortality by the year 2035. Although steady progress in reducing cancer mortality has been made over the past few decades, it is clear that much more could, and should, be done to save lives through the comprehensive application of currently available evidence-based public health and clinical interventions to all segments of the population. CA Cancer J Clin 2018;000:000-000. © 2018 American Cancer Society., (© 2018 American Cancer Society.)

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.

Knowledge of the cancer burden is important for informing and advocating cancer prevention and control. Mortality data are readily available for states and counties, but not for congressional districts, from which representatives are elected and which may be more influential in compelling legislation and policy. The authors calculated average annual cancer death rates during 2002 to 2011 for each of the 435 congressional districts using mortality data from the National Center for Health Statistics and population estimates from the US Census Bureau. Age-standardized death rates were mapped for all sites combined and separately for cancers of the lung and bronchus, colorectum, breast, and prostate by race/ethnicity and sex. Overall cancer death rates vary by almost 2-fold and are generally lowest in Mountain states and highest in Appalachia and areas of the South. The distribution is similar for lung and colorectal cancers, with the lowest rates consistently noted in districts in Utah. However, for breast and prostate cancers, while the highest rates are again scattered throughout the South, the geographic pattern is less clear and the lowest rates are in Hawaii and southern Texas and Florida. Within-state heterogeneity is limited, particularly for men, with the exceptions of Texas, Georgia, and Florida. Patterns also vary by race/ethnicity. For example, the highest prostate cancer death rates are in the West and north central United States among non-Hispanic whites, but in the deep South among African Americans. Hispanics have the lowest rates except for colorectal cancer in Wyoming, eastern Colorado, and northern New Mexico. These data can facilitate cancer control and stimulate conversation about the relationship between cancer and policies that influence access to health care and the prevalence of behavioral and environmental risk factors., (© 2015 American Cancer Society.)

Background: We investigated if certain persistent organic pollutants (POPs), namely polychlorinated biphenyls (PCBs) and organochlorine (OC) pesticides, predicted total, cardiovascular disease (CVD), and cancer mortality among the elderly, with the hypothesis that associations differ by the amount of fat mass., Methods: We studied serum concentrations of 11 PCBs in 633 elders (age≥70 years) and of 5 OC pesticides in 675 elders within the National Health and Nutrition Examination Survey (NHANES) 1999-2004. Mean follow-up was 4.1-years., Results: Neither PCBs nor OC pesticides were associated with total mortality when fat mass was not considered in analyses. However, associations of PCBs and OC pesticides with total mortality depended on fat mass (Pinteraction<0.01 and 0.06, respectively). PCBs associated inversely with total mortality for high fat mass, but not for lower fat mass. On the contrary, OC pesticides associated positively with total mortality for low fat mass and this association weakened at higher fat mass. The interaction was also observed with CVD mortality. In elders with low fat mass, higher PCBs associated with 2-3 fold higher risk of CVD mortality, while this association was absent in elders with more fat mass (Pinteraction=0.03). The positive association between OC pesticides and CVD mortality was also observed only among elderly with low fat mass (Pinteraction=0.03)., Conclusions: The possibility of interaction between POPs and the amount of fat mass on risk of mortality from chronic diseases is clinically important in modern societies with an obesity epidemic and requires confirmation in other studies with larger sample size., (Copyright © 2015 Elsevier Inc. All rights reserved.)