Risk Of Cause-specific Mortality Research Articles

All-cause and cause-specific mortality risk and loss in life expectancy associated with incident type 2 diabetes onset age and duration.

Evidence on type 2 diabetes onset age and duration on mortality risk has been limited by short follow-up, inadequate control for confounding, missing repeated measurements, and inability to cover the full range of onset age, duration, and major causes of death. Moreover, scarce data dissect how type 2 diabetes onset age and duration shape life expectancy. We evaluate prospectively these topics based on 270,075 eligible participants in the Nurses' Health Studies and Health Professionals Follow-up Study, leveraging repeated measurements throughout up to 40 years of follow-up. Cox models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). In fully adjusted analyses, incident early onset type 2 diabetes (diagnosed <40 years of age) was associated with significantly higher mortality from all-causes (HR, 95% CI was 3.16, 2.64-3.79; vs. individuals without type 2 diabetes), cardiovascular disease (6.56, 4.27-10.1), respiratory disease (3.43, 1.38-8.51), neurodegenerative disease (5.13, 2.09-12.6), and kidney disease (8.55, 1.98-36.9). The relative risk elevations declined dramatically with each higher decade of age at diagnosis for deaths from most of these causes, though the absolute risk difference increased continuously. A substantially higher cumulative incidence of mortality and a greater loss in life expectancy were associated with younger age at type 2 diabetes diagnosis. Longer disease duration was associated with generally higher relative and absolute risk of mortality. Early onset of type 2 diabetes and longer disease duration are associated with substantially increased risk of all-cause and cause-specific mortality and greater loss in life expectancy.

Association Among Vitamin D Supplementation, Serum 25(OH)D Concentrations, and Mortality Risk: A Prospective Cohort Study Using NHANES 2007-2018 Data.

To determine the associations among self-reported vitamin D (VD) supplementation, measured serum 25-hydroxyvitamin D (25[OH]D) concentrations, and all-cause and cause-specific mortality risks. Self-reported VD supplementation, serum 25(OH)D concentration, and all-cause and cause-specific mortality data from the National Health and Nutrition Examination Survey 2007-2018 were examined for 10,793 adults ≥20 years from the United States. VD dosage was categorized as <800 or ≥800 IU/d. The mortality status and causes of mortality up to 2019 were determined using the National Death Index. The relationships among VD, 25(OH)D levels, and mortality were analyzed using Cox regression before and after propensity score matching (PSM). Over a median of 6.6 years, 915 deaths were recorded, 230 because of cardiovascular disease (CVD), 240 because of cancer, and 445 because of other specific causes. Mortality risk did not differ between VD <800 IU/d and ≥800 IU/d before or after PSM. However, serum 25(OH)D concentrations were statistically different before and after PSM. The upper 2 quartiles of 25(OH)D levels were associated with lower all-cause mortality, and the fourth quartile was associated with reduced other-specific mortality before and after PSM. No correlation was found between the 25(OH)D concentration and CVD- or cancer-specific mortality after PSM. The inverse 25(OH)D-mortality relationship was consistent across subgroups. Based on this large cohort study, higher 25(OH)D levels are robustly associated with reduced all-cause and other specific mortality but not CVD- or cancer-specific mortality. These findings support the benefits of maintaining adequate VD status for longevity. Further research is required to elucidate these mechanisms and define the optimal VD concentration to reduce mortality. These results underscore the importance of public health strategies for preventing VD deficiency.

Mortality Disparities Among Arrestees by Race, Sentencing Disposition, and Place

Understanding mortality disparities among justice system-involved populations is crucial for public health and policy, especially for marginalized racial groups such as American Indian/Alaska Native persons. To examine racial disparities in mortality within the broader justice system-involved population in South Dakota, focusing on different sentencing dispositions and the role of place. This observational study used administrative criminal records linked to mortality data from January 2000 to December 2016. The statewide data linked data from South Dakota Attorney General's Office and South Dakota Department of Health. Individuals aged 18 years and older with arrests were analyzed in this population-based sample. Data were analyzed from August 1, 2022, to July 30, 2023. Sentencing dispositions were categorized as arrest only, fine, probation, jail, and prison. The main outcomes were mortality rates (both all-cause and cause-specific) calculated using Poisson regression models, adjusted for demographic and county variables. Of 182 472 individuals with 422 987 arrests, the study sample included 29 690 American Indian/Alaska Native arrestees (17 900 [60%] male; mean [SD] age, 29.4 [11.0] years) and 142 248 White arrestees (103 471 [73%] male; mean [SD] age, 32.6 [12.9] years). American Indian/Alaska Native persons accounted for 16% of arrestees and 26% of arrests, but only 9% of the population in South Dakota. Across dispositions, mortality risk was greater for White individuals sentenced to probation, jail, and prison relative to White individuals who were arrested only. In terms of racial disparities, all-cause mortality risk was 2.37 (95% CI, 1.95-2.88) times higher for American Indian/Alaska Native than White arrestees in the arrest-only disposition. Disparities persisted across all dispositions but narrowed substantially for probation and prison. Results were similar for cause-specific mortality risk, except for cancer risk. In urban areas, mortality risk was 2.70 (95% CI, 1.29-2.44) times greater for American Indian/Alaska Native individuals relative to White individuals among those with arrest-only dispositions. In this population-based observational study, mortality risk and associated racial disparities among justice system-involved individuals differed substantially across dispositions and places, underscoring the need for public health interventions tailored to these factors. Further research is needed to understand the mechanisms through which sentencing and place shape these disparities.

Contributions of causes of death to differentials in life expectancy by internal migrant status in the Netherlands. A population register based study, 2015–2019

Important health differences exist in the context of international migration and residential mobility. Less is known about health differences regarding the medium-distance level of internal migration. This study examines life expectancy gaps between internal movers and stayers in the Netherlands and their underlying processes by assessing the contribution of different causes of death by age and sex. It uses individually-linked death counts and population exposures extracted from population registers, covering the native Dutch population aged 10+ from 2015 to 2019. The pooled data were disaggregated by causes-of-death group (neurodegenerative diseases, cardiovascular diseases, lifestyle-related mortality, external causes, and other causes), internal migrant status (movers and stayers, based on past 10-year residence in the 40 NUTS-3 [Nomenclature of Territorial Units for Statistics, level 3] regions), age, and sex. Comparing movers and stayers, we computed life expectancy at age 10 (e10), age- and cause-specific mortality risks, and applied decomposition methods to assess contributions of causes of death to e10 gaps. In the Netherlands in 2015–2019, e10 was lower for movers between NUTS-3 regions than stayers (males: 2.49 years; females: 3.51 years), due to excess mortality for movers at most ages. Movers only had a lower mortality than stayers at younger working ages (males: ages 20–44; females: ages 20–34). Mortality from neurodegenerative diseases and cardiovascular diseases were the largest contributors to the e10 gap, especially at ages 75+ and for females. Mortality from lifestyle-related and external causes of death contributed less, with the largest contributions for females aged 75–89 and males aged 45–69. The lower e10 of movers in the Netherlands is likely explained by health selection effects–in particular care-related moves as coping behaviour–rather than by causal effects through risk accumulation. Research focusing on regional or spatial heterogeneity of the mover-stayer health gap would be insightful to further understand these processes.

Circadian rhythm analysis using wearable-based accelerometry as a digital biomarker of aging and healthspan

Recognizing the pivotal role of circadian rhythm in the human aging process and its scalability through wearables, we introduce CosinorAge, a digital biomarker of aging developed from wearable-derived circadian rhythmicity from 80,000 midlife and older adults in the UK and US. A one-year increase in CosinorAge corresponded to 8–12% higher all-cause and cause-specific mortality risks and 3–14% increased prospective incidences of age-related diseases. CosinorAge also captured a non-linear decline in resilience and physical functioning, evidenced by an 8–33% reduction in self-rated health and a 3–23% decline in health-related quality of life score, adjusting for covariates and multiple testing. The associations were robust in sensitivity analyses and external validation using an independent cohort from a disparate geographical region using a different wearable device. Moreover, we illustrated a heterogeneous impact of circadian parameters associated with biological aging, with young (<45 years) and fast agers experiencing a substantially delayed acrophase with a 25-minute difference in peak timing compared to slow agers, diminishing to a 7-minute difference in older adults (>65 years). We demonstrated a significant enhancement in the predictive performance when integrating circadian rhythmicity in the estimation of biological aging over physical activity. Our findings underscore CosinorAge’s potential as a scalable, economic, and digital solution for promoting healthy longevity, elucidating the critical and multifaceted circadian rhythmicity in aging processes. Consequently, our research contributes to advancing preventive measures in digital medicine.

Hepatic steatosis, metabolic dysfunction and risk of mortality: findings from a multinational prospective cohort study.

Non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MetS) are implicated in the aetiology of non-communicable diseases. Our study aimed to evaluate associations between NAFLD and MetS with overall and cause-specific mortality. We used dietary, lifestyle, anthropometric and metabolic biomarker data from a random subsample of 15,784 EPIC cohort participants. NAFLD was assessed using the fatty liver index (FLI) and MetS using the revised definition. Indices for metabolic dysfunction-associated fatty liver disease (MAFLD) were calculated. The individual associations of these indices with overall and cause-specific mortality were assessed using multivariable Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (95%CIs). As a subobjective, risk associations with adaptations of new classifications of metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic and alcohol-related liver disease (MetALD) were also assessed. Among the 15,784 sub-cohort participants, a total of 1997 deaths occurred (835 due to cancer, 520 to CVD, 642 to other causes) over a median 15.6 (IQR, 12.3-17.1) years of follow-up. Compared to an FLI < 30, FLI ≥ 60 was associated with increased risks of overall mortality (HR = 1.44, 95%CI = 1.27-1.63), and deaths from cancer (HR = 1.32, 95%CI = 1.09-1.60), CVD (HR = 2.06, 95% CI = 1.61-2.63) or other causes (HR = 1.21, 95%CI = 0.97-1.51). Mortality risk associations were also elevated for individuals with MAFLD compared to those without. Individuals with MetS were at increased risk of all mortality endpoints, except cancer-specific mortality. MASLD and MetALD were associated with higher risk of overall mortality. Our findings based on a prospective cohort suggest that individuals with hepatic steatosis or metabolic dysfunction have a higher overall and cause-specific mortality risk.

Lung cancer among patients with secondhand smoke exposure: A systematic review.

e22506 Background: Smoking tobacco is recognized as the leading cause of lung cancer. However, it is imperative to note that 10–15% of lung cancer patients have no history of smoking, and that lung cancer remains the leading cause of cancer deaths among non-smokers. Since passive smokers are exposed to many carcinogenic compounds in the exhaled smoke, it is naturally plausible that secondhand smoking (SHS) is a risk factor for lung cancer. However, current USPSTF screening guidelines for lung cancer with low dose CT (LDCT) do not include patients exposed to SHS. We performed a systematic review to highlight SHS as an etiology of lung cancer and insights for inclusion in cancer screening criteria. Methods: We utilized the PubMed, Medline, Science Direct, and ClinicalTrials.gov databases to search for relevant literature using keywords ('low Dose CT,' 'secondhand smoke,' 'lung cancer'). The search strategy was designed to ensure a comprehensive retrieval of pertinent literature, minimizing the possibility of omitting articles due to insignificant spelling and/or semantic variations. Eligible studies had to be published between 2010 and 2023 and focused on examining the effect of SHS in populations at risk of lung cancer or those undergoing lung cancer screening. Articles not available in English were excluded from this systematic review. In total, 239 relevant articles were retrieved from all databases, narrowing down to 14 articles after the initial screening and further reducing to 4 articles after the second round of screening. Results: Three of the four articles included in our systemic review were conducted in Asia. A study by He et al. showed a substantial increase in the relative risk of lung cancer among SHS (RR 2.00; 95% CI, 0.62-6.40), with significant dose-response relationships between cumulative SHS exposure at home and work and the increased risk of cause-specific and total mortality. Another observational study on the use of LDCT in Japan has interestingly shown a shifting landscape of lung cancer demographics, with 49.6% of patients identified as never-smokers and 70.0% of the never-smoker lung cancer patients having SHS exposure. Secondhand smoking has also been reported to increase the risk of pulmonary nodules (HR 1.17; 95% CI, 1.01-1.35) and pulmonary emphysema (OR 13.6; 95% CI, 1.70-106.1) in those with moderate-to-high SHS exposure, which was the population where lung cancer was more prevalent. Conclusions: Our findings suggest a critical gap in current healthcare recommendations, specifically addressing the absence of guidelines for LDCT screening in individuals with moderate-to-high SHS exposure despite established evidence linking SHS to a significant increase in the risk of lung cancer development. More studies are needed to formulate evidence-based guidelines for lung cancer screening and detection in this population, given the expected mortality reduction benefit.

Ratio of Red Blood Cell Distribution Width to Albumin Level and Risk of Mortality.

The ratio of red blood cell distribution width (RDW) to albumin concentration (RAR) has emerged as a reliable prognostic marker for mortality in patients with various diseases. However, whether RAR is associated with mortality in the general population remains unknown. To explore whether RAR is associated with all-cause and cause-specific mortality and to elucidate their dose-response association. This population-based prospective cohort study used data from participants in the 1998-2018 US National Health and Nutrition Examination Survey (NHANES) and from the UK Biobank with baseline information provided from 2006 to 2010. Included participants had complete data on serum albumin concentration, RDW, and cause of death. The NHANES data were linked to the National Death Index records through December 31, 2019. For the UK Biobank, dates and causes of death were obtained from the National Health Service Information Centre (England and Wales) and the National Health Service Central Register Scotland (Scotland) to November 30, 2022. Potential associations between RAR and the risk of all-cause and cause-specific mortality were evaluated using Cox proportional hazards regression models. Restricted cubic spline regressions were applied to estimate possible nonlinear associations. In NHANES, 50 622 participants 18 years of age or older years were included (mean [SD] age, 48.6 [18.7] years; 26 136 [51.6%] female), and their mean (SD) RAR was 3.15 (0.51). In the UK Biobank, 418 950 participants 37 years of age or older (mean [SD], 56.6 [8.1] years; 225 038 [53.7%] female) were included, and their mean RAR (SD) was 2.99 (0.31). The NHANES documented 7590 deaths over a median (IQR) follow-up of 9.4 (5.1-14.2) years, and the UK Biobank documented 36 793 deaths over a median (IQR) follow-up of 13.8 (13.0-14.5) years. According to the multivariate analysis, elevated RAR was significantly associated with greater risk of all-cause mortality (NHANES: hazard ratio [HR], 1.83 [95% CI, 1.76-1.90]; UK Biobank: HR, 2.08 [95% CI, 2.03-2.13]), as well as mortality due to malignant neoplasm (NHANES: HR, 1.89 [95% CI, 1.73-2.07]; UK Biobank: HR, 1.93 [95% CI, 1.86-2.00]), heart disease (NHANES: HR, 1.88 [95% CI, 1.74-2.03]; UK Biobank: HR, 2.42 [95% CI, 2.29-2.57]), cerebrovascular disease (NHANES: HR, 1.35 [95% CI, 1.07-1.69]; UK Biobank: HR, 2.15 [95% CI, 1.91-2.42]), respiratory disease (NHANES: HR, 1.99 [95% CI, 1.68-2.35]; UK Biobank: HR, 2.96 [95% CI, 2.78-3.15]), diabetes (NHANES: HR, 1.55 [95% CI, 1.27-1.90]; UK Biobank: HR, 2.83 [95% CI, 2.35-3.40]), and other causes of mortality (NHANES: HR, 1.97 [95% CI, 1.86-2.08]; UK Biobank: HR, 2.40 [95% CI, 2.30-2.50]) in both cohorts. Additionally, a nonlinear association was observed between RAR levels and all-cause mortality in both cohorts. In this cohort study, a higher baseline RAR was associated with an increased risk of all-cause and cause-specific mortality in the general population. These findings suggest that RAR may be a simple, reliable, and inexpensive indicator for identifying individuals at high risk of mortality in clinical practice.

Associations of early retirement and mortality risk: a population-based study in Taiwan

BackgroundEarly retirement is highly prevalent in Taiwan. This study assesses the association between early retirement and all-cause and cause-specific mortality risks while exploring the modifying effect of sociodemographic factors.MethodsUsing Taiwan’s...

The prevalence and mortality risks of PRISm and COPD in the United States from NHANES 2007–2012

BackgroundWe estimated the prevalence and mortality risks of preserved ratio impaired spirometry (PRISm) and chronic obstructive pulmonary disease (COPD) in the US adult population.MethodsWe linked three waves of pre-bronchodilator spirometry data from the US National Health and Nutritional Examination Survey (2007–2012) with the National Death Index. The analytic sample included adults ages 20 to 79 without missing data on age, sex, height, BMI, race/ethnicity, and smoking status. We defined COPD (GOLD 1, 2, and 3–4) and PRISm using FEV1/FVC cut points by the Global Initiative for Chronic Obstructive Lung Disease (GOLD). We compared the prevalence of GOLD stages and PRISm by covariates across the three waves. We estimated adjusted all-cause and cause-specific mortality risks by COPD stage and PRISm using all three waves combined.ResultsPrevalence of COPD and PRISm from 2007–2012 ranged from 13.1%-14.3% and 9.6%-10.2%, respectively. We found significant differences in prevalence by sex, age, smoking status, and race/ethnicity. Males had higher rates of COPD regardless of stage, while females had higher rates of PRISm. COPD prevalence increased with age, but not PRISm, which was highest among middle-aged individuals. Compared to current and never smokers, former smokers showed lower rates of PRISm but higher rates of GOLD 1. COPD prevalence was highest among non-Hispanic White individuals, and PRISm was notably higher among non-Hispanic Black individuals (range 31.4%-37.4%). We found associations between PRISm and all-cause mortality (hazard ratio [HR]: 2.3 95% CI: 1.9—2.9) and various cause-specific deaths (HR ranges: 2.0–5.3). We also found associations between GOLD 2 (HR: 2.1, 95% CI: 1.7–2.6) or higher (HR: 4.2, 95% CI: 2.7–6.5) and all-cause mortality. Cause-specific mortality risk varied within COPD stages but typically increased with higher GOLD stage.ConclusionsThe prevalence of COPD and PRISm remained stable from 2007–2012. Greater attention should be paid to the potential impacts of PRISm due to its higher prevalence in minority groups and its associations with mortality across various causes including cancer.

Ambient air pollution, lifestyle, and genetic predisposition on all-cause and cause-specific mortality: A prospective cohort study

BackgroundAlthough it is widely acknowledged that long-term exposure to ambient air pollution is closely related to the risk of mortality, there were inconsistencies in terms of cause-specific mortality and it is still unknown whether lifestyle and genetic susceptibility could modify the association. MethodsThis population-based prospective cohort study involved 461,112 participants from the UK Biobank. The land-use regression model was used to estimate the concentrations of particulate matter (PM2.5, PMcoarse, PM10), and nitrogen oxides (NO2 and NOx). The association between air pollution and mortality was evaluated using Cox proportional hazard models. Furthermore, a lifestyle score incorporated with smoking status, physical activity, alcohol consumption, and diet behaviors, and polygenic risk score using 12 genetic variants, were developed to assess the modifying effect of air pollution on mortality outcomes. ResultsDuring a median follow-up of 14.0 years, 33,903 deaths were recorded, including 17,083 (2835; 14,248), 6970, 2429, and 1287 deaths due to cancer (lung cancer, non-lung cancer), cardiovascular disease (CVD), respiratory and digestive disease, respectively. Each interquartile range (IQR) increase in PM2.5, NO2 and NOx was associated with 7 %, 6 % and 5 % higher risk of all-cause mortality, respectively. Specifically, for cause-specific mortality, each IQR increase in PM2.5, NO2 and NOx was also linked to mortality due to cancer (lung cancer and non-lung cancer), CVD, respiratory and digestive disease. Furthermore, additive and multiplicative interactions were identified between high ambient air pollution and unhealthy lifestyle on mortality. In addition, associations between air pollution and mortality were modified by lifestyle behaviors. ConclusionLong-term exposure to air pollutants increased the risk of all-cause and cause-specific mortality, which was modified by lifestyle behaviors. In addition, we also revealed a synergistically detrimental effect between air pollution and an unhealthy lifestyle, suggesting the significance of joint air pollution management and adherence to a healthy lifestyle on public health.

Association of composite dietary antioxidant index with mortality in adults with hypertension: evidence from NHANES.

The objective of this study is to assess the correlation between composite dietary antioxidant index (CDAI) with all-cause mortality and cause-specific mortality in adults with hypertension. The cohort study comprised adult participants with hypertension from the NHANES database, spanning 9 cycles from 2001 to 2018. Follow-up was conducted until December 31, 2019. Multi-variable Cox regression analysis was utilized to ascertain hazard ratios (HR) and their corresponding 95% confidence intervals, evaluating the relationship between CDAI and the risks of all-cause and cause-specific mortality. To further investigate the association between CDAI and mortality rates in adults with hypertension, Kaplan-Meier survival curves, restricted cubic splines (RCS), subgroup analyses and sensitivity analyses were employed. The analysis included 16,713 adults with hypertension (mean age 56.93 ± 0.23 years, 8,327 [49.61%] male). During the mean follow-up time 102.11 ± 1.22 months, with 3,908 (18.08%) all-cause mortality occurred, 1,082 (4.84%) cardiovascular mortality and 833 (3.80%) cancer mortality. Compared to the lowest quartile of CDAI, the weighted multivariate hazard ratios of participants in the highest quartile was 0.77 (95% CI, 0.68-0.87) for all-cause mortality, 0.83 (95% CI, 0.67-1.04) for cardiovascular mortality, and 0.64 (95% CI, 0.50-0.82) for cancer mortality. RCS analysis demonstrated a nonlinear association of CDAI with all-cause and cancer mortality, and a linear association between CDAI and cardiovascular mortality. The results were robust in subgroup analyses and sensitivity analyses. Higher CDAI is associated with reduced all-cause mortality, cardiovascular mortality, and cancer mortality in hypertensive adults. Our findings highlight the importance of an antioxidant diet in improving outcomes in adults with hypertension.

MASLD/MetALD and mortality in individuals with any cardio-metabolic risk factor: A population-based study with 26.7 years of follow-up.

A new term, metabolic dysfunction-associated steatotic liver disease (MASLD), has been proposed by a multi-society expert panel. However, it remains unclear whether hepatic steatosis per se in MASLD contributes to an increased risk of mortality in individuals with any cardio-metabolic risk factor (CMRF), which is also a significant risk factor for increased mortality. This study aimed to compare all-cause and cause-specific mortality between the "MASLD/MetALD" and "no steatotic liver disease (SLD)" groups in individuals with any CMRF. A population-based cohort study was conducted using 10,750 participants of the Third National Health and Nutrition Examination Survey. All-cause and cause-specific (cardiovascular, cancer, diabetes, and liver) mortality risks were compared between the "MASLD," "MetALD," and "no SLD" groups using the Cox proportional hazards model with complex survey design weights, adjusted for confounders. Over 26 years, the "MASLD" group did not show significantly increased all-cause (adjusted HR 1.04[95% CI: 0.95-1.14], p = 0.413), cardiovascular (0.88 [0.75-1.04], p = 0.139), or cancer (1.06[0.84-1.33], p = 0.635) mortality risk compared to the "no SLD" group in individuals with any CMRF. The MetALD group was associated with increased all-cause (1.41 [1.05-1.89], p = 0.022), cancer (2.35 [1.33-4.16], p = 0.004), and liver (15.04 [2.96-76.35], p = 0.002) mortality risk compared with the no SLD group. This trend was more pronounced in the MetALD group with advanced fibrosis assessed by Fibrosis-4 (FIB-4). In individuals with CMRF, the presence of steatotic liver disease (MASLD) alone did not increase the risk of mortality, except in cases with more alcohol consumption (MetALD). Therefore controlling metabolic risk factors and reducing alcohol consumption in people with MASLD or MetALD will be crucial steps to improve long-term health outcomes.

Association of diabetic retinopathy on all-cause and cause-specific mortality in older adults with diabetes: National Health and Nutrition Examination Survey, 2005–2008

To evaluate the effect of diabetic retinopathy (DR) status or severity on all-cause and cause-specific mortality among diabetic older adults in the United States using the most recent National Health and Nutrition Examination Survey (NHANES) follow-up mortality data. The severity of DR was graded according to the Early Treatment Diabetic Retinopathy Study (ETDRS) grading scale. Multiple covariate-adjusted Cox proportional hazards regression models, Fine and Gray competing risk regression models, and propensity score matching (PSM) methods were used to assess the risk of all-cause and cause-specific mortality in individuals with diabetes. All analyses adopted the weighted data and complex stratified design approach proposed by the NHANES guidelines. Time to death was calculated based on the time between baseline and date of death or December 31, 2019, whichever came first. Ultimately 1077 participants, representing 3,025,316 US non-hospitalized individuals with diabetes, were included in the final analysis. After a median follow-up of 12.24 years (IQR, 11.16–13.49), 379 participants were considered deceased from all-causes, with 43.90% suffering from DR, including mild DR (41.50%), moderate to severe DR (46.77%), and proliferative DR (PDR) (67.21%). DR was associated with increased all-cause, cardiovascular disease (CVD) and diabetes mellitus (DM)-specific mortality, which remained consistent after propensity score matching (PSM). Results of DR grading assessment suggested that the presence of mild, moderate to severe NPDR was significantly associated with increased risk of all-cause and CVD-specific mortality, while the presence and severity of any DR was associated with increased DM-specific mortality, with a positive trend. The presence of DR in elderly individuals with diabetes is significantly associated with the elevated all-cause and CVD mortality. The grading or severity of DR may reflect the severity of cardiovascular disease status and overall mortality risk in patients with diabetes.

The clustering effects of current smoking status, overweight/obesity, and physical inactivity with all-cause and cause-specific mortality risks in U.S. adults

ObjectiveTo estimate the associations of smoking, weight status and physical inactivity with all-cause and cause-specific deaths, and the advanced rate period (RAP) to determine how early death was advanced among United States (U.S.) adults aged 18 years or older. MethodsWe used data from the third National Health and Nutrition Examination Survey (NHANES III) and the 2019 Linked Mortality File (LMF) with a follow-up period of 21.6 years (n = 16,612, including 7,278 deaths). Smoking, weight status, and physical inactivity were obtained from NHANES III and mortality outcomes from the 2019 LMF. Cox regression was used to estimate hazard ratios, RAPs and their corresponding confidence intervals. ResultsFor adults who currently smoke, were obese and physically inactive, the rate of dying from all-cause, CVD, and cancer was at least 231 % greater than for those who never smoked, were normal weight and physically active. The RAPs associated with the clustering of these risk factors for all cause, CVD- and cancer-specific cause of deaths were 13.0, 12.1 and 18.9 years older, respectively. ConclusionsOur findings underscore the need to focus on modifiable risk factors for illness prevention and health promotion and call attention to the increasing clustering of unhealthy risk factors in the U.S. population.

Exposure to volatile organic compounds and mortality in US adults: A population-based prospective cohort study

Volatile organic compounds (VOCs) are ubiquitous in both indoor and outdoor environments. Evidence on the associations of individual and joint VOC exposure with all-cause and cause-specific mortality is limited. Measurements of 15 urinary VOC metabolites were available to estimate exposure to 12 VOCs in the National Health and Nutritional Examination Survey (NHANES) 2005–2006 and 2011–2018. The environment risk score (ERS) was calculated using LASSO regression to reflect joint exposure to VOCs. Follow-up data on death were obtained from the NHANES Public-Use Linked Mortality File through December 31, 2019. Cox proportional hazard models and restricted cubic spline models were applied to evaluate the associations of individual and joint VOC exposures with all-cause and cause-specific mortality. Population attributable fractions were calculated to assess the death burden attributable to VOC exposure. During a median follow-up of 6.17 years, 734 (8.34 %) deaths occurred among 8799 adults. Urinary metabolites of acrolein, acrylonitrile, 1,3-butadiene, and ethylbenzene/styrene were significantly associated with all-cause, cardiovascular disease (CVD), respiratory disease (RD), and cancer mortality in a linear dose-response manner. Linear and robust dose-response relationships were also observed between ERS and all-cause and cause-specific mortality. Each 1-unit increase in ERS was associated with a 33.6 %, 39.1 %, 109.8 %, and 67.8 % increase for all-cause, CVD, RD, and cancer mortality risk, respectively. Moreover, joint exposure to VOCs contributed to 17.95 % of all-cause deaths, 13.49 % of CVD deaths, 35.65 % of RD deaths, and 33.85 % of cancer deaths. Individual and joint exposure to VOCs may enhance the risk of all-cause and cause-specific mortality. Reducing exposure to VOCs may alleviate the all-cause and cause-specific death burden.

Low-dose colchicine for atherosclerosis: long-term safety.

Low-dose colchicine (0.5 mg daily) is now FDA-approved for secondary prevention in patients with coronary disease and will be increasingly prescribed in clinical practice. In this State-of-the-Art Review, data were collated from contemporary systemic reviews of case reports, drug registries, and placebo-controlled trials that assessed specific issues of safety related to the continuous use of colchicine in a range of clinical settings to inform physicians, pharmacists, and patients of the absolute risks of continuous use of low-dose colchicine, including among individuals taking statin therapy. Based upon these collective data, it is concluded that aside mild diarrhoea on initiation of colchicine that typically subsides in the vast majority of patients within a week of therapy, continuous use of low-dose colchicine is well tolerated and very safe. It does not affect renal, liver, or cognitive function, has no adverse effects on bleeding, wound healing, fertility, or pregnancy, and does not increase risks of cancer, serious infection, or cause-specific mortality. When appropriately prescribed to patients without significant renal or hepatic impairment, reports of myelosuppression, myotoxicity, and serious drug-drug interactions are rare and no more frequent than placebo, including in patients taking statin therapy. Physicians, pharmacists, and patients can be reassured that in the absence of significant renal or hepatic impairment continuous use of low-dose colchicine can be used safely in patients with atherosclerosis for the purpose of reducing cardiovascular risk.

Exposure to Polybrominated Diphenyl Ethers and Risk of All-Cause and Cause-Specific Mortality

Polybrominated diphenyl ethers (PBDEs) are an important group of persistent organic pollutants with endocrine-disrupting properties. However, prospective cohort studies regarding the association of PBDE exposure with long-term health outcomes, particularly mortality, are lacking. To examine the association of environmental exposure to PBDEs with risk of all-cause and cause-specific mortality. This nationally representative cohort study used data from the National Health and Nutrition Examination Survey 2003 to 2004 and linked mortality information through December 31, 2019. Adults aged 20 years or older with available data on PBDE measurements and mortality were included. Statistical analysis was performed from February 2022 to April 2023. PBDE analytes in serum samples were measured using solid phase extraction and isotope dilution gas chromatography high-resolution mass spectrometry. All-cause mortality, cancer mortality, and cardiovascular mortality. This study included 1100 participants (mean [SE] age, 42.9 [0.6] years; proportion [SE] female, 51.8% [1.6%]; proportion [SE] Hispanic, 12.9% [2.7%]; proportion [SE] non-Hispanic Black, 10.5% [1.6%]; proportion [SE] non-Hispanic White, 70.8% [3.7%]; proportion [SE] other race and ethnicity, 5.8% [1.1%]). During 16 162 person-years of follow-up (median [IQR] follow-up, 15.8 [15.2-16.3] years; maximum follow-up, 17 years), 199 deaths occurred. Participants with higher serum PBDE levels were at higher risk for death. After adjustment for age, sex, and race and ethnicity, lifestyle and socioeconomic factors, and body mass index, participants with the highest tertile of serum PBDE levels had an approximately 300% increased risk of cancer mortality (HR, 4.09 [95% CI, 1.71-9.79]) compared with those with the lowest tertile of serum PBDE levels. No significant association of PBDE exposure with all-cause mortality (HR, 1.43 [95% CI, 0.98-2.07]) or cardiovascular mortality (HR, 0.92 [95% CI, 0.41-2.08]) was observed. In this nationally representative cohort study, PBDE exposure was significantly associated with an increased risk of cancer mortality. Further studies are needed to replicate the findings and determine the underlying mechanisms.

Iron Metabolic Biomarkers and the Mortality Risk in the General Population: A Nationwide Population-Based Cohort Study.

Iron is an essential element in the human body and plays a critical role in many physiological and cellular processes. However, the association between iron status and the risk of all-cause or cause-specific mortality has not been well-investigated. And it is unclear whether the association between iron metabolic biomarkers and the risk of mortality differs between people with and without diabetes mellitus (DM). This work aimed to investigate associations between iron metabolic biomarkers and all-cause and cause-specific mortality risk in the general population, and heterogeneities in the associations among population with and without DM.. A total of 29 166 adults from the National Health and Nutrition Examination Survey (NHANES) III and NHANES 1999 to 2010 were included, with linkage to the National Death Index to December 31, 2019. Cox proportional-hazard models and Fine-Gray subdistribution hazard models were used to estimate associations between iron metabolic biomarkers and outcomes. During a median follow-up of 18.83 years, 9378 deaths were observed, including 3420 cardiovascular disease (CVD) deaths and 1969 cancer deaths. A significant linear association between serum ferritin (SF) and all-cause mortality was observed among the overall population and those without DM. J-shaped associations between transferrin saturation (TSAT) and all-cause and CVD mortality were observed among all populations. In the overall population, compared to the first quartile (Q1) group, the adjusted hazard ratio (HR) (95% CI) for all-cause mortality was 1.07 (1.00-1.15), 1.05 (0.98-1.12), 1.13 (1.05-1.21) in Q2, Q3, and Q4 groups for SF, while the HR was 0.94 (0.88-0.99), 0.92 (0.86-0.97), and 0.93 (0.88-0.99) for TSAT. In individuals without DM, the adjusted HR of the Q4 of SF were 1.19 (1.03-1.37) for CVD mortality and 1.25 (1.05-1.48) for cancer mortality. In individuals with DM, the adjusted HRs of the Q4 of TSAT were 0.76 (0.62-0.93) for CVD mortality and 1.47 (1.07-2.03) for cancer mortality. Iron metabolism abnormalities increase mortality risk in the general population. The associations of iron status with mortality were significantly different between individuals with and without DM, which indicated tailored strategies for iron homeostasis are needed.

Ultra-processed food consumption and risk of chronic respiratory diseases mortality

Chronic respiratory diseases (CRDs) are diseases of the respiratory tract and are among the most prominent causes of disability and mortality globally(1). Chronic obstructive pulmonary disease (COPD) and lung cancer are among the leading cause of death among all CRDs(2). Evidence showed that diet, particularly ultra-processed foods (UPFs) are strongly associated with cardiovascular disease, diabetes, cancer, and depression(3). However, the link between UPFs intake and CRDs has rarely been investigated. we aimed to examine the association between UPF consumption and risk of mortality due to CRDs overall, COPD and lung cancer among adults in the USA. A total of 96,607 participants aged 55 years and over were obtained from Prostate, Lung, Colorectal and Ovarian (PLCO) cancer study, a randomised trial designed to investigate the effects of screening on cancer-related mortality. However, data collected also afforded the opportunity to examine the relationships between UPF intake and mortality caused by respiratory diseases. Dietary history of participants was collected at baseline using a validated food frequency questionnaire as was the presence of respiratory diseases. Food items were grouped into one of the four NOVA food classification system(4). Cox regression was fitted to estimate the risk of all-cause mortality and cause-specific mortality due to increased consumption of UPFs over time. Competing risk regression was used to account for the competing risks events and effect of participant loss. During the follow-up period of 1,379,655.5 person-years (median 16.8 years), 28700 all-cause, 4,901 all respiratory, 2,015 lung cancer and 1,536 COPD mortalities occurred. A dose-response association was found between higher UPF intake and mortality from all respiratory diseases and COPD, but not lung cancer. After considering competing events, higher intake of UPF increased the risk of mortality from all respiratory diseases by 10% (HR: 1.10; 95% CI: 1.01, 1.21) and COPD by 20% (HR: 1.20; 95% CI: 1.02, 1.42). After imputation for missing data, the risk of lung cancer increased by 25% among participants in the highest quintile of UPF intake. The PLCO trial data highlighted that consumption of UPF increased respiratory mortality, among those with COPD, however further mechanistic studies are recommended to further clarify the link between UPF and lung cancer. This study also indicated that a high intake of UPF generally increases the risk of mortality of those with respiratory diseases and contributes to a large body of evidence indicating that higher UPF consumption increases the overall risk of mortality.