Cause-specific Mortality Research Articles

Body shapes of multiple anthropometric traits and all-cause and cause-specific mortality in the UK Biobank

Background: Individual traditional anthropometric measures like body mass index (BMI) and waist circumference may not fully capture the relation of adiposity to mortality. Investigating multi-trait body shapes could overcome this limitation, deepening insights into adiposity and mortality. Methods: Using UK Biobank data from 462,301 adults (40-69 years at baseline: 2006-2010), we derived four body shapes from principal component analysis on BMI, height, weight, waist and hip circumference, and waist-to-hip ratio. We then used multivariable-adjusted Cox proportional hazard models to estimate hazard ratios (HR) and 95% confidence intervals (CI) for associations between body shapes and mortality for principal component scores of +1 and -1. Results: During 6,114,399 person-years of follow-up, 28,807 deaths occurred. A generally obese body shape exhibited a U-shaped mortality association. A tall and centrally obese body shape showed increased mortality risk in a dose-response manner (comparing a score of +1 and 0: HR=1.16; 95% CI=1.14-1.18). Conversely, tall and lean or athletic body shapes displayed no increased mortality risks when comparing a score of +1 and 0, with positive relations for the comparison between a score of -1 and 0 in these shapes (short and stout shape: HR=1.12, 95% CI=1.10-1.14; non-athletic shape: HR=1.15, 95% CI=1.13-1.17). Conclusions: Four distinct body shapes, reflecting heterogeneous expressions of obesity, were differentially associated with all-cause and cause-specific mortality. Multi-trait body shapes may refine our insights into the associations between different adiposity subtypes and mortality.

Exploring educational disparities in breast cancer dynamics: a comprehensive analysis of incidence, death within 5 years of diagnosis, and mortality in the Belgian context.

Breast cancer is the most prevalent cancer worldwide. Belgium shows high age-standardized incidence rates, but also high survival rates. Like many health outcomes, breast cancer has been associated with multiple factors of socioeconomic status. This paper aims to (a) map educational differences in breast cancer incidence, mortality and death rates within 5 years of diagnosis, (b) update earlier trends in breast cancer mortality rates in Belgium for the 2004-2013 period and (c) investigate the role of fertility indicators as mediating factors in the association between education and breast cancer outcomes. Data consisted of a linkage between the 2001 Belgian Census, register data on mortality and cancer incidence data (2004-2013) from the Belgian Cancer Registry. We calculated age standardized rates, rate ratios (Poisson regression) and hazard ratios (Cox regression) and furthermore also applied the method of Excess Portion Eliminated (EPE) in a mediation analysis of the fertility indicators. We stratified our analysis by age: younger than 50 (premenopausal) and 50 or older (postmenopausal). We observed striking differences in breast cancer incidence, all-cause and cause-specific death rates 5-years after diagnosis by educational level. Higher educated women had higher breast cancer incidence, but also lower all-cause and lower cause-specific death rates; adding up to zero differences in breast cancer mortality in the postmenopausal group and lower breast cancer mortality in the premenopausal group. A notable shift in the social gradient occurred since the 1990's, favouring higher-educated women in recent years. Especially, with regards to survival after diagnosis there is potential for policy intervention. Stage at diagnosis played a crucial role, but differences between socioeconomic groups remained significant after including this parameter. While fertility indicators played a role, the impact was less pronounced than expected.

Unravelling demographic and socioeconomic patterns of COVID-19 death and other causes of death: results of an individual-level analysis of exhaustive cause of death data in Belgium, 2020.

The COVID-19 pandemic led to significant excess mortality in 2020 in Belgium. By using microlevel cause-specific mortality data for the total adult population in Belgium in 2020, three outcomes were considered in this study aiming at predicting sociodemographic (SD) and socioeconomic (SE) patterns of (1) COVID-19 specific death compared to survival; (2) all other causes of death (OCOD) compared to survival; and (3) COVID-19 specific death compared to all OCOD. Two complementary statistical methods were used. First, multivariable logistic regression models providing odds ratios and 95% confidence intervals were fitted for the three study outcomes. In addition, we computed conditional inference tree (CIT) algorithms, a non-parametric class of classification trees, to identify and rank by significance level the strongest predictors of the three study outcomes. Older individuals, males, individuals living in collectivities, first-generation migrants, and deprived SE groups experienced higher odds of dying from COVID-19 compared to survival; living in collectivities was identified by the CIT as the strongest predictor followed by age and sex. Education emerged as one of the strongest predictors for individuals not living in collectivities. Overall, similar patterns were observed for all OCOD except for first- and second-generation migrants having lower odds of all OCOD compared to survival; age group was identified by the CIT as the strongest predictor. Older individuals, males, individuals living in collectivities, first- and second-generation migrants, and individuals with lower levels of education had higher odds of COVID-19 death compared to all OCOD; living in collectivities was identified by the CIT as the strongest predictor followed by age, sex, and migration background. Education and income emerged as among the strongest predictors among individuals not living in collectivities. This study identified important SD and SE disparities in COVID-19 mortality, with living in collectivities highlighted as the strongest predictor. This underlines the importance of implementing preventive measures, particularly within the most vulnerable populations, in infectious disease pandemic preparedness to reduce virus circulation and the resulting lethality.

Abstract 4136145: All-cause and Cause-specific Mortality Disparities in the District of Columbia: Temporal Trends from 2000 to 2020

Background: A report evaluating all-cause mortality in 30 major U.S. cities documented that inequality between Black and White populations in Washington, D.C. was the greatest. However, little is known about disparities in cause-specific mortality over time or by racial groups. Aims: Evaluate trends in all-cause and cause-specific mortality in D.C. from 2000 to 2020 by race, and concurrently examine trends in cardiovascular (CV) risk factors. Methods: Using the CDC WONDER database, we calculated age-adjusted mortality rates per 100,000 persons (2000-2020) for Non-Hispanic Black and Non-Hispanic White populations in D.C. and corresponding rate ratios. Average Annual Percentage Change (AAPC) was examined with joinpoint regression. We examined the prevalence of risk factors (obesity, hypertension, diabetes, smoking, and hypercholesterolemia) using the Behavioral Risk Factor Surveillance System (2000-2020). Results: Among 102,710 deaths that occurred in D.C. (80% Black), cardiovascular diseases (CVD, 32%) and cancer (22%) accounted for over half of the deaths. All-cause mortality declined between 2000-2012 (AAPC: -2.9%, 95% CI: -5.6, 1.0) but stagnated between 2012-2018 (AAPC:-1.1%, 95% CI: -4.6, 0.9) and increased after 2018 (AAPC: 7.7%, 95% CI: 0.6, 11.9). CVD mortality declined between 2000-2011 and plateaued thereafter among Black individuals, contrasting with a monotonous decline (AAPC: -4.7%, 95% CI: -5.3, -4.0) among White individuals, resulting in a magnification of the disparities. Cancer mortality decreased over time for both White and Black individuals (AAPC: -3.4%, 95% CI: -3.9, -2.9 vs. AAPC: -1.8%, 95% CI: -2.1, -1.4, respectively), with a greater magnitude in White individuals. Risk factors were more prevalent among Black individuals over the period. Conclusion: In D.C., the mortality rate is higher in Black vs. White populations, and disparities are increasing over time. While CVD and cancer mortality rates declined overall, profound disparities remain. CVD risk factors are more common in Black populations, with persisting disparities. There is an urgent need for CVD prevention and management, tailored to Black populations in D.C.

PCSK9 inhibitor with cause-specific mortality amongst cancer survivors: a chance to kill two birds with one stone.

PCSK9 inhibitor with cause-specific mortality amongst cancer survivors: a chance to kill two birds with one stone.

Abstract 4127413: High-normal Blood Pressure (130-139/85-89mmHg) is Associated with an Increased Risk of Mortality

Background: The relationship between high-normal blood pressure (BP) and mortality lacks high-quality evidence based on large population cohort. The aim of this study was to comprehensively investigate the association of high-normal BP and its trajectory with all-cause and cause-specific mortality. Methods: In a community-based population cohort from the China Health Evaluation And risk Reduction through nationwide Teamwork (ChinaHEART) project, 3,598,940 participants aged 35-75 years with baseline BP were included. High-normal BP was defined as a systolic blood pressure (SBP) of 130-139 mmHg and/or a diastolic blood pressure (DBP) of 85-89 mmHg at baseline. Four trajectories of BP change were identified in 105,894 participants included in the study, who had more than 2 follow-up BP measurements, using latent mixture modeling. Among them, high-normal-increasing was defined as an increase in SBP from 130-139 at baseline to over 140 at the last follow-up. Findings: Compared with the optimal BP group (SBP < 120 mmHg and DBP < 80 mmHg, [18.1%]), participants with high-normal BP (18.7%) had a 4% increase in all-cause mortality risk (hazard ratio [HR] 1.04, 95% confidence interval [CI]: 1.01-1.07) and a 28% increase in CVD mortality risk (HR 1.28, 95% CI: 1.21-1.34), with the greatest increase in mortality risk observed from hemorrhagic stroke (HR 1.75, 95% CI: 1.55-1.98). Among BP trajectories, compared with participants with optimal-stable BP (25.3%), those with high-normal-increasing BP (3.5%) had a 25% increase in all-cause mortality risk (HR 1.25, 95% CI: 1.00-1.54) and a 67% increase in CVD mortality risk (HR 1.66, 95% CI: 1.21-2.30), with the greatest increase in mortality risk also observed from hemorrhagic stroke (HR 3.15, 95% CI: 1.38-7.20). In our study cohort, approximately 0.7% and 1.3% of all-cause mortality was attributable to the high-normal BP at baseline and high-normal-increasing BP trajectory, respectively. Interpretation: Individuals presenting high-normal BP at baseline or high-normal-increasing BP trajectory afterward exhibited a significantly elevated mortality risk, which is most pronounced for hemorrhagic stroke. Early management of BP in patients with high-normal BP is crucial for the prevention and treatment of hypertension.

Abstract 4147601: Associations between Accelerated Aging Phenotypes with Cancer-Specific and Cardiovascular-Specific Mortality in Long-Term Cancer Survivorship

Background: The consequences of cancer and anti-cancer treatments are often described as representing an “accelerated aging” phenotype. However, little is known about how the “accelerated aging” phenotype affects mortality risks in long-term cancer survivors. Purpose: To investigate the association between accelerated aging phenotype and cause-specific mortality in a sample of long-term cancer survivors Methods: Data for cancer survivors (CS) were extracted from the National Health and Nutrition Examination Survey between the years 1999-2010. Participants missing vital data and those diagnosed with multiple cancers, childhood cancers, cancer within the previous 5 years, or skin cancer were excluded. Mortality outcomes were collected from the National Death Index through December 2019. The Phenotype Age score was derived from blood biochemistry measures such as albumin, creatinine, and c-reactive protein. Accelerated Aging (AA) was defined as a Phenotype Age greater than the participants’ chronological age. CS were grouped by time since diagnosis: 5-10, 10-15, 15-20, and ≥20 years. Within each group, hazard ratios (HR) were derived from competing-risk hazard regression for the AA phenotype association with cancer-specific and cardiovascular-specific mortality. Regressions were modeled with participant age as the time-scale to account for the predictive nature of chronological age. Results: A total of 875 CS (65.6±12.9 years, 62% female, 31% non-white, 15.6±9.4 years from cancer diagnosis) were included. The most common cancer types were prostate (16%) and breast (21%) cancer. There were 107 cancer and 113 cardiovascular deaths over a 10.8±4.6 year follow-up. The AA phenotype was significantly associated with cardiovascular-specific mortality in each survivor group (all p<0.05). Conversely, the AA phenotype was only significantly associated with cancer-specific mortality in the 5-10 years of survivorship group (p=0.01). Results are displayed in Figure 1, along with cubic splines fit to the HR of each survivorship group. Conclusions: Present results suggest that the AA phenotype may demonstrate time-dependent associations with cancer-specific and cardiovascular-specific risks, two leading causes of death in CS.

Income-Related Disparities in Mortality Among Young Adults With Type 2 Diabetes.

Previous studies have indicated an inverse association between income and mortality. However, differences in health outcomes according to the income level of young adults with type 2 diabetes (T2D) compared with older adults with T2D have not been elucidated. To estimate the overall and cause-specific mortality risks among patients with T2D according to income and age. This retrospective nationwide cohort study in South Korea included adults aged 20 to 79 years who were diagnosed with T2D between January 1, 2008, and December 31, 2013, and followed up until December 31, 2019, and age- and sex-matched controls without diabetes. Data were analyzed between January 1, 2023, and August 27, 2024. Risks of all-cause, cardiovascular, and cancer mortality were estimated according to participants' income, which was categorized into 3 levels (low, middle, and high) based on the health insurance premium. Logistic regression analyses and Cox proportional hazard regression analyses were performed according to age groups (20-39, 40-59, and 60-79 years). A total of 1 240 780 adults (604 975 patients with T2D and 635 805 age- and sex-matched controls without diabetes) were included in the analyses. Their mean (SD) age was 56.9 (11.8) years, and 626 176 (50.5%) were men. Overall, the risk of mortality increased with lower income among patients with T2D, as well as in comparison with controls without diabetes. There was an inverse association between income and mortality risk in younger individuals (adjusted hazard ratios of all-cause mortality in the low income vs high income subgroups with T2D were 2.88 [95% CI, 2.25-3.69] in those aged 20 to 39 years, 1.90 [95% CI, 1.81-2.00] in those aged 40 to 59 years, and 1.26 [95% CI, 1.23-1.29] in those aged 60 to 79 years; P < .001 for comparing risk ratios between age groups). The pattern of income-related disparities in younger individuals was observed in cardiovascular mortality but less in cancer mortality. In this cohort study of 1 240 780 individuals aged 20 to 79 years, the risk of mortality with low income was most prominent among individuals with T2D aged 20 to 39 years. These findings highlight the need for socioeconomic support to reduce income-related health disparities in younger individuals.

Dietary amino acids intake and all-cause and cause-specific mortality: results from the Golestan Cohort Study

BackgroundLess is known whether the amino acid composition of dietary protein sources effects on long-term health outcomes. We aimed to evaluate the association between dietary amino acid composition and all-cause and cause-specific mortality.MethodsThis study used data from the Golestan Cohort Study, which was performed in the Golestan Province of Iran from January 2004 to June 2008. Mortality, which was the primary outcome, was ascertained through September 2022. The Cox proportional hazards regression models were used to determine the adjusted hazard ratios (HR) and 95% confidence intervals (CI) for mortality according to the quintiles of amino acid consumption, taking the third quintile as the reference.ResultsA total of 47,337 participants (27,293 [57.7%] women) with a mean (standard deviation) age of 51.9 (8.9) years were included. During a median follow-up of 15 years, 9,231 deaths were documented. Regarding essential amino acid intakes, the HRs of all-cause mortality were 1.16 (95% CI, 1.07–1.26) in the first quintile, compared with the reference group (P for non-linear trend < 0.001). Similarly, non-linear associations were observed between risk of all-cause mortality and intake of branched-chain, aromatic, sulfur-containing, or non-essential amino acids (P for non-linear trend < 0.001 for all comparisons), with higher HRs for participants in the first quintiles. There was an age interaction for the associations between dietary amino acids and mortality (P for interaction ˂0.05). While high amino acid diets were detrimental in middle-aged adults (< 65 years), increased hazards of mortality were observed among older adults (≥ 65 years) with low amino acid intake.ConclusionsThis study showed the non-linear trend between amino acids intake and risk of mortality in the middle-aged and older Iranian population. Overall, our findings suggest that diets lower in amino acids were associated with increased hazards of mortality, particularly among older adults.

Reproductive factors and biological aging: the association with all-cause and cause-specific premature mortality.

Are reproductive factors associated with biological aging, and does biological aging mediate the associations of reproductive factors with premature mortality? Multiple reproductive factors are related to phenotypic age acceleration (PhenoAge-Accel), while adherence to a healthy lifestyle mitigates these harmful effects; PhenoAge-Accel mediated the associations between reproductive factors and premature mortality. Accelerated aging is a key contributor to mortality, but knowledge about the effect of reproductive factors on aging is limited. This prospective cohort study included 223729 women aged 40-69years from the UK biobank in 2006-2010 and followed up until 12 November 2021. Reproductive factors were collected through a touchscreen questionnaire. Biological aging was assessed through PhenoAge-Accel. Multiple linear regression models were used to examine the relationships of reproductive factors with PhenoAge-Accel and estimate the modified effect of a healthy lifestyle. Furthermore, we applied mediation analysis to explore the mediating role of PhenoAge-Accel in the associations between reproductive factors and premature mortality. Early menarche (<12 years vs 13 years, β: 0.37, 95% CI: 0.30, 0.44), late menarche (≥15 years vs 13 years, β: 0.18, 95% CI: 0.11, 0.25), early menopause (<45 years vs 50-51 years, β: 0.62, 95% CI: 0.51, 0.72), short reproductive lifespan (<30 years vs 35-39 years, β: 0.81, 95% CI: 0.70, 0.92), nulliparity (vs two live births, β: 0.36, 95% CI: 0.30, 0.43), high parity (≥4 vs 2 live births, β: 0.49, 95% CI: 0.40, 0.59), early age at first live birth (<20 years vs 25-29 years, β: 0.66, 95% CI: 0.56, 0.75), and stillbirth (β: 0.51, 95% CI: 0.36, 0.65) were associated with increased PhenoAge-Accel. Furthermore, PhenoAge-Accel mediated 6.0%-29.7% of the associations between reproductive factors and premature mortality. Women with an unfavorable lifestyle and reproductive risk factors had the highest PhenoAge-Accel compared to those with a favorable lifestyle and without reproductive risk factors. The participants in the UK Biobank were predominantly of White ethnicity; thus, caution is warranted when generalizing these findings to other ethnic groups. Our findings reveal the harmful effects of multiple reproductive factors on biological aging and the mediating role of biological aging in the associations between reproductive factors and premature mortality. They highlight the significance of adhering to a healthy lifestyle to slow biological aging as a potential way to reduce premature mortality among women with reproductive risk factors. This study was funded by the National Natural Science Foundation of China (82003479, 82073660, 72204215), Hubei Provincial Natural Science Foundation of China (2023AFB663), Zhejiang Province Public Welfare Technology Application Research Project (GF22H269155), and China Postdoctoral Science Foundation (2019M662646, 2020T130220). The authors have no competing interests to disclose. N/A.

Wildfire Smoke: Health Effects, Mechanisms, and Mitigation.

Wildfires are becoming more frequent and intense on a global scale, raising concerns about their acute and long-term effects on human health. We conducted a systematic review of the current epidemiological evidence on wildfire health risks and a meta-analysis to investigate the association between wildfire smoke exposure and various health outcomes. We discovered that wildfire smoke increases the risk of premature deaths and respiratory morbidity in the general population. Meta-analysis of cause-specific mortality and morbidity revealed that wildfire smoke had the strongest associations with cardiovascular mortality (RR: 1.018, 95% CI: 1.014-1.021), asthma hospitalization (RR: 1.054, 95% CI: 1.026-1.082), and asthma emergency department visits (RR: 1.117, 95% CI: 1.035-1.204) in the general population. Subgroup analyses of age found that adults and elderly adults were more susceptible to the cardiopulmonary effects of wildfire smoke. Next, we systematically addressed the toxicological mechanisms of wildfire smoke, including direct toxicity, oxidative stress, inflammatory reactions, immune dysregulation, genotoxicity and mutations, skin allergies, inflammation, and others. We discuss wildfire smoke risk mitigation strategies including public health interventions, regulatory measures, and personal actions. We conclude by highlighting current research limitations and future directions for wildfire research, such as elucidating the complex interactions of wildfire smoke components on human health, developing personalized risk assessment tools, and improving resilience and adaptation strategies to mitigate the health effects of wildfires in changing climate.

Long-Term Ozone Exposure, COPD, and Asthma Mortality: A Retrospective Cohort Study in the Republic of Korea

Ozone concentrations have increased in recent decades, and several studies have reported that long-term exposure to ozone increases the mortality risk induced by respiratory conditions. However, research on cause-specific mortality related to ozone exposure and respiratory diseases remains scarce. We constructed a retrospective cohort of 5,360,032 adults aged ≥ 65 years from the National Health Insurance Service of Republic of Korea, and death certificates were obtained from Statistics Republic of Korea to determine the cause of death between 2010 and 2019. The daily maximum 8 h average levels of ozone during the warm season annually (May–September) and other air pollutants were determined for the residential district. We analyzed the data using a time-varying Cox proportional hazards model with individual- and district-level covariates, incorporating a competing risk framework to address deaths from causes other than chronic obstructive pulmonary disease (COPD) and asthma. In our single-pollutant model with a 3-year moving average, a 1 ppb increase in ozone exposure was associated with a hazard ratio (HR) of 1.011 (95% confidence interval [CI]: 1.008–1.013) for COPD mortality and an HR of 1.016 (95% CI: 1.011–1.022) for asthma mortality. In our model adjusted for the presence of underlying diseases and district-level variables, the HRs were 1.009 (95% CI: 1.008–1.014) for COPD and 1.017 (95% CI: 1.011–1.023) for asthma, respectively. These associations remained robust in our two-pollutant model, except for NO2 and COPD. A linear concentration–response relationship was identified between ozone concentration, COPD, and asthma mortality. In this large nationwide cohort study, long-term exposure to ozone was associated with an increased risk of death from COPD and asthma in older Korean adults.

The association between android-to-gynoid lean mass ratio and all-cause and specific-cause mortality in US adults: A prospective study.

The associations of lean mass distribution with mortality risk are not fully elucidated. We aimed to evaluate the effects of a new lean mass distribution indicator-android/gynoid lean mass ratio (AGLR) evaluated by dual-energy x-ray absorptiometry (DXA) on the risk of all-cause and specific-cause mortality in a NHANES cohort. This was a population-based cohort study, which included 18 542 subjects aged 20 years and older from the US National Health and Nutrition Examination Survey (US NHANES, 2003-2006 and 2011-2018). The primary outcomes of our study were all-cause mortality, cardiovascular (CVD) mortality and cancer mortality, which were obtained from the linkage to registries. Cox proportional hazard regression models were used to investigate the association between lean mass distribution and mortality risk among the US NHANES general population. Restricted cubic spline nested in Cox regression was also used to test whether there was a non-linear association of AGLR as a continuous variable with the risk of mortality. During a median follow-up of 6.9 years, 1412 participants died, of whom 435 were due to CVD and 340 were due to cancer. The multivariable-adjusted (Model 4) hazard ratios (HRs) for each SD increase in AGLR were 1.53 (95% confidence interval [CI] 1.40-1.67) for all-cause mortality, 1.56 (95% CI 1.30-1.87) for cancer mortality and 1.64 (95% CI 1.47-1.84) for CVD mortality. The associations were robust in sensitivity analyses and present in most subgroups. AGLR evaluated by DXA was associated with a higher risk of all-cause and specific-cause mortality among the general population from the US NHANES cohort.

Association of weight-adjusted waist index with all-cause and cause-specific mortality among cancer survivors: a cohort study of the NHANES 1999-2018

Association of weight-adjusted waist index with all-cause and cause-specific mortality among cancer survivors: a cohort study of the NHANES 1999-2018

CT-derived fat density as a predictor of cause-specific mortality in patients undergoing TAVI: Findings from a large registry subanalysis.

CT-derived fat density as a predictor of cause-specific mortality in patients undergoing TAVI: Findings from a large registry subanalysis.

Obesity Paradox and the Effect of NT-proBNP on All-Cause and Cause-Specific Mortality.

In heart failure patients, obesity is associated with better outcomes as compared to normal weight, a phenomenon called the obesity paradox. To examine if obesity modifies the relationship between NT-proBNP and all-cause and cause-specific mortality in adults without coronary artery disease or heart failure history. We used the National Health and Nutrition Examination Survey (NHANES) data from 1999 to 2004 and linked it with mortality through December 31, 2019. Participants > 18 years were categorized into normal weight (BMI ≤ 25 kg/m2), overweight (BMI > 25-29.9 kg/m2) and obese (BMI > 29.9 kg/m2). NT-proBNP levels were categorized as low (< 126 pg/mL) or high (≥ 126 pg/mL). Using Cox proportional hazard models, we examined effect modification by obesity using interaction, without and with adjusting for potential confounders. Of the 12 621 participants, 2794 (22%) died during 202 859 person-years follow-up. In adjusted models, normal-weight participants with high NT-proBNP had 2 times higher all-cause mortality risk than those with low NT-proBNP (HR = 2.05; 95%CI = 1.74, 2.41; p < 0.001); however, this mortality risk was 27% lower in obese participants (HR interaction = 0.73; 95%CI = 0.59, 0.92; p = 0.008). Similarly, in normal-weight participants, the difference in other-cause mortality risk between high and low NT-proBNP participants was significant in adjusted models (HR = 2.27; 95%CI = 1.81, 2.85; p < 0.001) and obese participants had 48% lower other-cause mortality risk between those with high and low NT-proBNP (interaction HR = 0.52; 95%CI = 0.36, 0.77; p = 0.001). Conversely, obesity did not modify the relationship between NT-proBNP and cardiovascular or cancer mortality. In patients free of heart failure or coronary artery disease, obesity may be protective against mortality associated with high NT-proBNP.

Association between Diet-Related Greenhouse Gas Emissions and Mortality among Japanese Adults: The Japan Collaborative Cohort Study.

Planetary and human health are highly intertwined; our current food system is associated with high greenhouse gas emissions (GHGE) and burden of disease. The aim of this study was to investigate the associations of diet-related GHGE with all-cause and cause-specific mortality in Japan. This study included 58,031 Japanese adults (35,078 women and 22,953 men) 40-79 y of age who participated in the Japan Collaborative Cohort Study during the period 1988-1990. Diet-related GHGE was calculated from dietary intake estimated by a validated food frequency questionnaire and previously developed GHGE tables of each food and beverage. Participants were classified into quintiles of diet-related GHGE per kg food/d. Hazard ratios (HRs) of all-cause and cause-specific mortality were calculated using the Cox proportional hazard and restricted cubic spline models. The average diet-related GHGE was . Over a period of 19.3 y (955,819 person-years) of median follow-up, 11,508 deaths were documented. After adjusting for lifestyle and medical history, in comparison with the fourth quintiles of diet-related GHGE, the first and fifth quintiles were associated with a higher risk of all-cause mortality: multivariable HR of all-cause mortality was 1.11 [95% confidence interval (CI): 1.05, 1.18] and 1.09 (95% CI: 1.03, 1.17) for the lowest and highest GHGE, respectively; those of cardiovascular disease mortality were 1.23 (95% CI: 1.10, 1.38) and 1.22 (95% CI: 1.08, 1.37), respectively. The diet-related GHGE range with the lowest HR of all-cause mortality was food/d ( for nonlinearity ). Replacing one serving of red meat with one serving of pulses was inversely associated with all-cause mortality (; 95% CI: 0.93, 0.99) and GHGE (mean change, ; 95% CI: , ). Diet-related GHGE was associated with all-cause and cardiovascular disease mortality in a U-shaped fashion. This finding could be useful for creating a policy for sustainable shifts in dietary habits that will benefit the population and environmental health. https://doi.org/10.1289/EHP14935.

All-cause and cause-specific mortality risks in individuals with diabetes living alone: A large-scale population-based cohort study

AimsThe rise in one-person households is a global trend. We aimed to investigate mortality risk in individuals with diabetes living alone (IDLA) using a large-scale population-based database. MethodsA total of 2,447,557 adults with type 2 diabetes were identified from the Korean National Health Information Database. One-person households were defined based on the number of registered family members. The risks of all-cause and cause-specific mortalities were estimated using a multivariable Cox proportional hazards regression model. ResultsDuring a median follow-up period of 6.0 years, 191,084 deaths (7.8 %) occurred. IDLA had a higher risk of mortality compared to those not living alone after adjusting for potential confounders (HR 1.20, 95 % CI: 1.18–1.22). This association was more prominent in younger individuals, men, and those with low income, and it was dependent on the duration of living alone. The risks of cause-specific mortality were all significantly higher in the IDLA group compared with the non-IDLA group. Adherence to favorable lifestyle behaviors was associated with a significant reduction in all-cause mortality, particularly in IDLA. ConclusionsThe elevated risk of mortality in IDLA highlights the need for tailored medical interventions and social assistance, particularly for those with unhealthy lifestyles or low income.

Heat and cause-specific cardiopulmonary mortality in Germany: a case-crossover study using small-area assessment

High temperatures have been associated with increased mortality, with evidence reported predominately in large cities and for total cardiovascular or respiratory deaths. This case-crossover study examined heat-related cause-specific cardiopulmonary mortality and vulnerability factors using small-area data from Germany. We analyzed daily counts of cause-specific cardiopulmonary deaths from 380 German districts (2000-2016) and daily mean temperatures estimated by spatial-temporal models. We applied conditional quasi-Poisson regression using distributed lag nonlinear models to examine heat effects during May-September in each district and random-effects meta-analysis to pool the district-specific estimates. Potential individual- and district-level vulnerability factors were examined by subgroup analyses and meta-regressions, respectively. Heat was associated with increased mortality risks for all cardiopulmonary sub-causes. The relative risk (RR) of total cardiovascular and respiratory mortality for a temperature increment from the 75th to the 99th percentile was 1.24 (95% confidence interval: 1.23, 1.26) and 1.34 (1.30, 1.38), respectively. The RRs of cardiovascular sub-causes ranged from 1.16 (1.13, 1.19) for myocardial infarction to 1.32 (1.29, 1.36) for heart failure. For respiratory sub-causes, the RR was 1.27 (1.22, 1.31) for COPD and 1.49 (1.42, 1.57) for pneumonia. We observed greater susceptibility related to several individual- and district-level characteristics, e.g., among females or in highly urbanized districts. Heat vulnerability factors remained consistent between urban and rural areas. Our study highlights heat-related increases in cause-specific cardiopulmonary mortality across Germany and identifies key vulnerability factors, offering insights for improving public health practices to mitigate heat-related health impacts. European Union's Horizon 2020 research and innovation program; Helmholtz Associations Initiative and Networking Fund.

The effect of median household income on the prognosis of lung adenocarcinoma: A SEER analysis.

Lung cancer is the main cause of death related to malignant tumors. Since cause-specific mortality can guide clinical decision-making, this study employed the Fine-Gray model based on the Surveillance, Epidemiology, and End Results (SEER) database to identify significantly how socio-economic status influences initial treatment decisions and survival outcomes in patients with lung adenocarcinoma. The aim of this study was to identify the predictors of lung adenocarcinoma. The U.S. Surveillance, Epidemiology, and End Results (SEER) database was used to identify patients diagnosed with lung adenocarcinoma between 2000 and 2018. Seventeen thousand four hundred forty-one patients with lung adenocarcinoma were subdivided in four socio-economic tertiles, based on median household income. Cox regression modeling explored the relationship between race, surgery, grading, and median household income on survival outcomes. The study also assessed patient demographic characteristics, age at diagnosis, and surgical interventions. Among 17441 patients with primary lung adenocarcinoma, the age distribution was as follows: less than 45 years (n=202, 1.16%), between 45 and 54 years (n=1121, 6.43%), 55 and 64 years (n=4252, 24.38%), 65 and 74 years (n=6357, 36.45%), 75 and 84 years (n=4426, 25.38%), and more than 84 years (n=1083, 6.2%). The adjusted hazard ratio (aHR) with 95% CI for ages 65-74 years, 75-84 years, and older than or equal to 85 years were 0.25 (0.11,1.29), 0.40 (0.11,1.50), and 0.72 (0.11,2.05), respectively. Multifactorial Cox regression indicated that the aHR for tumor metastasis was 0.93 (0.03, 2.54), and for patients who did not undergo surgery, it was 1.46 (0.03, 4.31). Grade IV patients exhibited the lowest survival rate [0.66(0.11, 1.93)]. A notable correlation existed between median household income and survival, with distinctly lower survival rates observed in low-income groups. Older patients, especially those who did not undergo surgery and had a higher tumor grade, had significantly reduced survival. Moreover, survival rates for black patients in lower-income brackets were worse than those for white patients in the same financial category. The quality of life of lung cancer patients is affected by low-income family.