Specific Causes Of Death Research Articles

Blood pressure-lowering and risk of cancer: an individual participant-level data meta-analysis and mendelian randomisation studies

Abstract Background The current body of randomised evidence concerning the effect of blood pressure lowering on the risk of cancer remains limited. Purpose We leveraged the strengths of both randomised controlled trials (RCTs) and genomic information to examine this question. Methods Individual-level data from 314,016 participants from 42 RCTs were pooled to investigate the effect of blood pressure lowering on the risk of cancer through one-stage individual participant data (IPD) meta-analysis. The primary outcome was incident cancer, defined as the first occurrence of any cancer diagnosed after randomisation. Pre-specified subgroup analyses were conducted to assess heterogeneity in effect by follow-up time and baseline age groups, sex, body mass index categories, smoking status and previous use of antihypertensive drugs. Secondary outcomes were cause-specific cancer death and site-specific cancer risk comprising breast, colorectal, kidney, lung, prostate, and skin. Cox proportional hazard regression, stratified by trials, were used for statistical analyses. For site-specific cancers, analyses were complemented with Mendelian randomisation analyses using naturally randomised genetic variants associated with blood pressure lowering, retrieved from genome-wide association studies involving participants of European ancestry. Results Over a median of 4 years (interquartile range 2), 17,954 participants in RCTs were diagnosed with cancer of any type and 4,878 participants were reported to have died with cancer as the cause of death. In the IPD meta-analysis that compared the treatment arm with the comparator, no associations were identified between reductions in either systolic or diastolic blood pressure and the risk of incident cancer (hazard ratios [HRs] per 5 mmHg reduction in systolic and per 3 mmHg diastolic blood pressure were 1.03 (95% confidence interval [CI] 0.99-1.06) and 1.03 [0.98-1.07], respectively). We also found no pattern of increasing or decreasing relative risk for incident cancer during the follow-up period, nor was there evidence of heterogeneity in treatment effects across baseline subgroups. No effect on the risk of cause-specific cancer death was identified for either systolic or diastolic blood pressure lowering. Considering site-specific cancers, we also found no evidence of effect, except for a possible link with lung cancer risk, with HRs of 1.17 [99.5% CI 1.02-1.32] for systolic blood pressure and 1.17 [99.5% CI 0.98-1.36] for diastolic blood pressure lowering. In Mendelian randomisation studies, no association was observed for genetically determined systolic and diastolic blood pressure and all the considered site-specific cancers, including overall lung cancer and its subtypes. Conclusion We found no consistent randomised evidence to suggest that blood pressure-lowering has a substantial effect, whether increasing or decreasing, on incident cancer, cause-specific cancer death, or selected site-specific cancers.

Effects of restrictive vs liberal transfusion strategies on mortality in patients with acute myocardial infarction and anemia: The 6-month follow up primary results of the MINT trial

Abstract Background The Myocardial Ischemia and Transfusion (MINT) trial identified a statistically non-significant increase in risk of 30-day death or myocardial infarction (MI) (primary endpoint) and all-cause death and a statistically significant increase in cardiac death in patients with an acute MI and anemia assigned to a restrictive transfusion strategy compared to a liberal transfusion strategy. Purpose To determine the effect of a restrictive versus a liberal transfusion strategy on all-cause and cause-specific death 6-months post-randomization (secondary endpoint). Methods The MINT trial randomized 3,504 patients with MI and hemoglobin <10 g/dL to a restrictive (hemoglobin threshold of 7 or 8 g/dL) or liberal (hemoglobin threshold of <10 g/dL) transfusion strategy implemented during the index hospitalization. Sites contacted patients at 30-days and 6-months post-randomization and recorded patient vital status, date of death, and site-reported cause of death (categorized as cardiac, non-cardiac, or unknown). A competing risk analysis (cumulative incidence estimation and Fine-Gray models) was conducted to estimate the effect of transfusion strategy on all-cause and cause-specific death. Results Patients were enrolled from 6 countries between 2017 and 2023; average age was 72 years, and 46% were female. Vital status at 6-months was obtained for 3419 (97.6%) randomized patients (restrictive: 98.1%; liberal: 97.0%); 2,690 (76.8%) patients were alive and 729 (20.8%) had died. At 6-months, all-cause death occurred in 376 patients in the restrictive arm (21.7%) and 353 in the liberal arm (20.5%), hazard ratio [HR]: 1.07, 95% CI: 0.93–1.24. Compared to the liberal arm, a greater proportion of deaths in the restrictive arm were cardiac (41.8% vs. 29.8%). The risk of cardiac death was significantly higher in patients in the restrictive arm (9.0% vs. 6.1%, HR: 1.52; 95% CI: 1.19–1.94) whereas risk of non-cardiac death (HR: 0.87; 95% CI: 0.70–1.08) and unknown cause of death (HR: 0.88; 95% CI: 0.64–1.21) did not differ between the restrictive and the liberal arms. Conclusions In patients with acute MI and anemia, the 6-month incidence of all-cause death did not differ with a restrictive versus a liberal transfusion strategy. However, the numerically higher rate of all-cause mortality, seen with the restrictive strategy at 30-days, persisted through 6-months and was driven by cardiac causes. The long-term findings from the MINT trial suggest that a restrictive transfusion strategy may be harmful for patients with MI and anemia.

A Predictive Model for Gastric Cancer-Specific Death after Gastrectomy: A Competing-Risk Nomogram

Background: We aimed to assess the likelihood of cause-specific death and other causes of death after gastrectomy for gastric cancer (GC). Additionally, a competing-risk nomogram was developed for patient counseling and decision-making. Methods: Eligible GC patients who had gastrectomy between 2007 and 2015 were included in the study from the Surveillance, Epidemiology, and End Results (SEER) database. Death from gastric cancer and death from other causes were considered as separate competing events. Cumulative incidence functions (CIF) were calculated for each event, and a competing-risk nomogram was developed. Results: Overall, 8,808 patients who underwent gastrectomy were analyzed. Among them, 4,659 (52.90%) died from gastric cancer and 1,284 (14.58%) died from other causes. The five-year cumulative incidence of cause-specific death for gastric cancer was 50.4%, and 10.2% for deaths from other causes. Several independent factors, such as age at diagnosis, tumor site, grade, size, lymph node examination results, pathological T status, pathological N status, metastatic status, Lauren classification, radiation, and chemotherapy, were found to be associated with gastric cancer-specific death. The nomogram, based on results from the competing risk regression model, demonstrated good performance. Conclusion: We have developed a nomogram aimed at predicting gastric cancer-specific mortality in patients following gastrectomy. The model has undergone internal validation, demonstrating good accuracy and reliability. It serves as useful tool that can assist physicians and patients in making more informed clinical decisions.

Estimating the burden of diseases attributed to PM2.5 using the AirQ + software in Mashhad during 2016–2021

The study used the AirQ + software developed by the World Health Organization (WHO) to evaluate the health impacts associated with long-term exposure to PM2.5 in Mashhad, Iran. For this purpose, we analyzed the daily average concentrations of PM2.5 (with a diameter of 2.5 micrometers or less) registered by the air quality monitoring stations from 2016 to 2021. The levels of PM2.5 surpassed the Air Quality Guidelines (AQG) limit value of 5 µg/m3 (annual value) established by WHO. The findings revealed that the burden of mortality (from all-natural causes) at people above 30 years old associated with PM2.5 exposures was 2093 [95% confidence interval [CI]: 1627–2314] deaths in 2016 and 2750 [95% CI: 2139–3038] deaths in 2021. In general, the attributable mortality from specific causes of deaths (e.g., COPD (chronic obstructive pulmonary diseases), IHD (ischemic heart diseases) and stroke) in people above 25 years old increased between the years, but the mortality from lung cancer was stable at 46 [95% CI: 33–59] deaths in 2016 and 48 [95% CI: 34–61] deaths in 2021. The attributable mortality from ALRI (Acute Lower Respiratory Infection) in children below 5 years old increased between the years. We also found differences in mortality cases from IHD and stroke among the age groups and between the years 2016 and 2021. It was concluded that burden of disease methodologies are suitable tools for regional and national policymakers, who must take decisions to prevent and to control air pollution and to analyze the cost-effectiveness of interventions.

Projecting future excess deaths associated with extreme precipitation events in China under changing climate: an integrated modelling study

Climate-change-induced extreme precipitation events have attracted global attention; however, the associated excess deaths burden has been insufficiently explored and remains unclear. We first defined an extreme precipitation event for each county when the daily total precipitation exceeded the county-specific 99·5th percentile of the daily precipitation from 1986 to 2005; then we estimated the associations between extreme precipitation events and cause-specific deaths in 280 Chinese counties using a two-stage time-series model. Second, we projected the excess deaths related to extreme precipitation events by combining the bias-corrected multi-model precipitation predictions derived under different combined emission-population scenarios of three representative concentration pathways (RCPs; RCP2·6, RCP4·5, and RCP8·5) and three shared socioeconomic pathways (SSP2, a business-as-usual scenario) populations (S1, low fertility rate; S2, medium fertility rate; and S3, high fertility rate). We quantified the climate and population contributions to the changes of future excess deaths nationwide and by climatic zones. Compared with the non-extreme precipitation days, the percentage increase of deaths associated with exposure to extreme precipitation days is 13·0% (95% CI 7·0-19·3) for accidental cause, 4·3% (2·0-6·6) for circulatory disease, and 6·8% (2·8-10·9) for respiratory disease. The number of annual average excess deaths related to extreme precipitation events during 1986-2005 was 2644 (95% CI 1496-3730) for accidental cause, 69 (33-105) for circulatory disease, and 181 (79-279) for respiratory disease. In the 2030s, the total number of excess deaths of these three causes will increase by 1244 (43%), 1756 (61%), and 2008 (69%) under RCP2·6, RCP4·5, and RCP8·5 scenarios combined with a medium-fertility-rate population (SSP2-S2), respectively, but will decrease by 3% under RCP2·6-SSP2-S2 and increase by 25% under RCP8·5-SSP2-S2 in the 2090s. Humid and water-limited regions in subtropical, middle-temperate, and plateau climate zones will face highly increased risks. Climate and population factors contributed disproportionally among the five climate zones. This study is the largest integrated projection exploring the disease burden associated with extreme precipitation events. The excess deaths will be amplified by climate and population changes. Improving mitigation and adaptation capacities is crucial when responding to precipitation extremes. National Natural Science Foundation of China and Wellcome Trust.

Cause-Specific Mortality Rates Among the US Black Population

This cross-sectional study examines the specific causes of death associated with the disparities in all-cause mortality between non-Hispanic Black and non-Hispanic White populations, as well as their changes over time.

Review of Local Homeless Mortality Efforts: A Call for Standardized Data and Reporting.

There are currently no national estimates of how many people die while unhoused in the US. Local jurisdictions have developed their own approaches for estimating homeless mortality. We aimed to examine these local approaches, document what is known about homeless mortality, and summarize local methodologies. We reviewed 17 publicly available homeless mortality reports (ie, gray literature). Reports were sought from government, Health Care for the Homeless, coalition to end homelessness, and other advocacy and social service websites. From each report, we extracted the number of homeless deaths, dates of observation, data source(s) used, determination of homeless status, manners and causes of death, and decedent demographics. Data collection and reporting on homeless mortality varied greatly across reports. This variation limits aggregation across reports. Medical examiner data was the most used data source. Manner of death was the most consistently collected field, with accidental deaths reported as the most prevalent manner of homeless deaths. Not all reports listed specific causes of death, but those that did reported toxicity (eg, overdose) and cardiovascular causes as most prevalent. The most granular age category of most homeless decedents was 40 to 60years. On average, 80% of decedents were of male sex. While over half of reports included race and ethnicity information, disparities could not be estimated without suitable denominators. Standardized data collection and reporting guidance is needed for homeless mortality. Health departments can work with local Health Care for the Homeless programs and Continuums of Care to establish data sharing processes. Matching vital statistics with homeless service utilization records may be one opportunity to improve these efforts. Until there is federal or national guidance on these standards, localities can consider adding housing or homelessness variables as optional or mandatory fields in electronic death reporting systems.

Cesarean delivery, labor duration, and mothers’ mortality risk over 50 years of follow-up

BackgroundPregnancy complications have been recognized as a window to future health. Though cesarean delivery is common, it is unknown whether labor duration and mode of delivery are associated with maternal long-term mortality. ObjectiveTo examine whether labor duration and mode of delivery were associated with all-cause and cause-specific mortality. Study DesignParticipants were mothers from the multisite Collaborative Perinatal Project (CPP) cohort (1959–1966; n=43,646, limited to last CPP delivery). We ascertained all-cause and specific causes of death as of 2016 via linkage to the National Death Index and Social Security Death Master File. Hazard ratios (HR) testing mode of delivery and labor duration were estimated using Cox proportional hazards models adjusted for demographic and clinical characteristics. We further stratified analyses by parity. ResultsAmong participants with a recorded delivery mode, 5.9% (2486/42,335) had a cesarean delivery. Participants who had a cesarean were older (26.9 vs 24.3 years), with higher body mass index (24.0 vs 22.7 kg/m2), were less likely to be nulliparous (21% vs 30%), and more likely to have a household income of at least $6000 (22% vs 17%), to smoke ≥1 pack/d (18% vs 15%), to have diabetes mellitus (12% vs 1%) and to have a prior medical condition (47% vs 34%), compared to participants with a vaginal delivery. Delivery mode was similar by race/ethnicity, marital status, and education. Median labor duration was 395 minutes among participants who had an intrapartum cesarean delivery and 350 minutes among participants delivered vaginally. By 2016, 52.2% of participants with a cesarean delivery and 38.5% of participants with a vaginal delivery had died. Cesarean vs vaginal delivery was significantly associated with increased risk for all-cause mortality (HR=1.16 (95% confidence interval [CI]: 1.09, 1.23); in nulliparas, HR=1.27 (95% CI: 1.09, 1.47); in multiparas, HR=1.13 (95% CI: 1.06, 1.21) as well as increased risk of death from cardiovascular disease, diabetes, respiratory disease, infection, and kidney disease. Associations with death from cardiovascular disease, infection, and kidney disease were stronger for multiparas than nulliparas, though the association with death from diabetes was stronger among nulliparas. Labor duration was not significantly related to overall mortality. ConclusionIn a historic United States cohort with a low cesarean delivery rate, cesarean delivery was an indicator for subsequent increased mortality risk, particularly related to cardiovascular disease and diabetes. Future studies with long-term follow-up are warranted given the current high prevalence of cesarean delivery.

Serum Erythritol and Risk of Overall and Cause-Specific Mortality in a Cohort of Men.

Erythritol occurs naturally in some fruits and fermented foods, and has also been used as an artificial sweetener since the 1990s. Although there have been questions and some studies regarding its potential adverse health effects, the association between serum erythritol and long-term mortality has not been evaluated. To examine the association between serum erythritol's biochemical status and risk of overall and cause-specific mortality, a prospective cohort analysis was conducted using participants in the ATBC Study (1985-1993) previously selected for metabolomic sub-studies. The analysis included 4468 participants, among whom 3377 deaths occurred during an average of 19.1 years of follow-up. Serum erythritol was assayed using an untargeted, global, high-resolution, accurate-mass platform of ultra-high-performance liquid and gas chromatography. Cause-specific deaths were identified through Statistics Finland and defined by the International Classification of Diseases. After adjustment for potential confounders, serum erythritol was associated with increased risk of overall mortality (HR = 1.50 [95% CI = 1.17-1.92]). We found a positive association between serum erythritol and cardiovascular disease mortality risk (HR = 1.86 [95% CI = 1.18-2.94]), which was stronger for heart disease mortality than for stroke mortality risk (HR = 3.03 [95% CI = 1.00-9.17] and HR = 2.06 [95% CI = 0.72-5.90], respectively). Cancer mortality risk was also positively associated with erythritol (HR = 1.54 [95% CI = 1.09-2.19]). The serum erythritol-overall mortality risk association was stronger in men ≥ 55 years of age and those with diastolic blood pressure ≥ 88 mm Hg (p for interactions 0.045 and 0.01, respectively). Our study suggests that elevated serum erythritol is associated with increased risk of overall, cardiovascular disease, and cancer mortality. Additional studies clarifying the role of endogenous production and dietary/beverage intake of erythritol in human health and mortality are warranted.

Maternal characteristics and infant and child mortality: A cohort study in England linking Census and health data

Child mortality is a common measure of the overall health of society. Maternal characteristics, such as ethnicity and socioeconomic status are known to contribute to inequalities in health and mortality in babies and children. Overall, in the UK babies born to non-white mothers have a higher risk of mortality, and there is also a strong association between deprivation and risk of death. However, population data is currently lacking for England and Wales disentangling the various socioeconomic risk factors which are known to contribute to increased risk. We utilise population level data to assess the association between socioeconomic status, ethnicity, and child mortality. Our cohort consisted of all live singleton births in England and Wales between 2011 and 2016. We linked birth notifications to mothers’ 2011 Census records using NHS number, which provides person-level sociodemographic information. Death registration data was linked to identify all-cause and cause-specific deaths in babies. Babies were followed from date-of-birth for up to 10-years, or date-of-death. We report cumulative incidence of all-cause mortality for a 10-year follow-up for neonatal, infant and child deaths based on maternal socioeconomic and ethnic groups. Cox proportional hazard models are used to estimate hazard ratios for neonatal, infant and child deaths, with both minimally adjusted (maternal age and baby sex) and fully-adjusted models (accounting for other maternal, household and birth characteristics). This presentation will give an overview of our unique linked data sources, the statistical techniques employed, the latest available analytical results, and the emerging implications of the research.

Racial/ethnic disparities in all-cause and cause-specific death among children with malignant central nervous system tumours: a registry-based cohort retrospective analysis

It is generally recognized that there is unequal mortality in childhood central nervous system (CNS) malignancy in the United States (US), but little is known about the trends and contributors of racial/ethnic disparities in death. We assessed the trends of racial/ethnic disparities in all-cause and cause-specific death, and the contributions of tumour, treatment and socioeconomic factors to this disparity. This registry-based cohort study included children (aged ≤19 years) diagnosed with malignant CNS tumours, using data from the US population-based cancer registry in the Surveillance, Epidemiology, and End Results (SEER) Program. The clinical outcomes were all-cause and cause-specific death for each racial/ethnic group (White, Black, Hispanic, non-Hispanic Asian/Pacific Islander [API], and non-Hispanic American Indian/Alaska Native [AI/AN] children). We quantified absolute disparities using absolute rate difference in 5-year cumulative incidence of death. Cox proportion risk models were used to estimate the relative racial/ethnic disparities, and the contribution of factors to disparities in death. In this study, data from 14,510 children with malignant CNS tumours (mean [SD] age, 8.5 [5.7]; 7988 [55.1%] male) were analysed. Overall, the cumulative incidence of death from CNS tumours across four racial/ethnic groups decreased from 2001 to 2020. Black patients had the highest risk of death from all causes and CNS tumours between 2001 and 2020, with adjusted hazard ratios (HR) of 1.52 (1.38-1.68) and 1.47 (1.31-1.64), respectively. The absolute disparity in all-cause death between Hispanic and White patients increased slightly (from 8.2 percentage points [ppt] to 9.4ppt), and the relative disparity in death from CNS tumours increased from 1.33 (1.15-1.55) in 2001-2005 to 1.78 (1.44-2.20) in 2016-2020. The absolute disparities in death from CNS tumours between Black and White patients (from 11.8ppt to 4.3ppt) and between API and White patients (from 10.1ppt to 5.1ppt) decreased from 2001-2005 to 2011-2015. Race/ethnicity disparities in death from CNS tumours among childhood malignant CNS tumours had reduced from 2001 to 2020, and quantifying the contribution of factors to this disparity in death could provide a basis for decreasing mortality among racial/ethnic minority patients. Shenyang Young and Middle-aged Science and Technology Innovation Talent Support Program.

Cause-specific excess mortality in Denmark, Finland, Norway, and Sweden during the COVID-19 pandemic 2020–2022: a study using nationwide population data

While there is substantial evidence on excess mortality in the first two years of the COVID-19 pandemic, no study has conducted a cause-specific analysis of excess mortality for the whole period 2020–2022 across multiple countries. We examined cause-specific excess mortality during 2020–2022 in Denmark, Finland, Norway, and Sweden—four countries with similar demographics and welfare provisions, which implemented different pandemic response policies. To this end, we utilized nationwide register-based information on annual cause-specific deaths stratified by age and sex, and applied linear regression models to predict mortality in 2020–2022 based on the reference period 2010–2019. Excess deaths were obtained by contrasting actual and expected deaths. Additional analyses employed standardization to a common population, as well as population adjustments to account for previous deaths. Our results showed that, besides deaths due to COVID-19 (a total of 32,491 during 2020–2022), all countries experienced excess deaths due to cardiovascular diseases (in total 11,610 excess deaths), and under-mortality due to respiratory diseases other than COVID-19 (in total 9878) and dementia (in total 8721). The excess mortality due to cardiovascular diseases was particularly pronounced in Finland and Norway in 2022, and the under-mortality due to dementia was particularly pronounced in Sweden in 2021–2022. In conclusion, while COVID-19 deaths emerge as the most apparent consequence of the pandemic, our findings suggest that mortality has also been influenced by substitutions between different causes of death and over time, as well as indirect consequences of COVID-19 infection and pandemic responses—albeit to different extents in the different countries.

Causes of Excess Mortality in Diabetes Patients Without Coronary Artery Disease: A Cohort Study Revealing Endocrinologic Contributions.

Diabetes mellitus (DM) patients without coronary artery disease (CAD) have a higher all-cause mortality rate than patients with neither DM nor CAD. We examined cause-specific death of DM patients with and without CAD. We conducted a cohort study of all patients who underwent CAG in Western Denmark between 2003 and 2016. Using Danish health registries, patients were followed for a maximum of 10 years and stratified according to their DM and CAD status. Outcomes included all-cause-, cancer-, circulatory-, and endocrinologic death. Ten-year cumulative risks were computed as well as adjusted and unadjusted hazard ratios (aHR and HR). A total of 132,432 patients (28,524 deaths, median follow-up of 6.2 years) were included. Compared to patients with neither DM nor CAD, DM patients without CAD had a higher 10-year risk of all-cause death (27.9% versus 19.7%, aHR 1.43 [95% CI 1.35-1.52]), cancer death (7.2% versus 5.4%, aHR 1.29 [95% CI 1.15-1.46]), circulatory death (9.1% versus 6.9%, aHR 1.35 [95% CI 1.22-1.49]), and endocrinologic death (3.9% versus 0.3%, aHR 14.02 [95% CI 10.95-17.95]). Among endocrinologic deaths, 87% were due to classical complications of DM, such as diabetic nephropathy and ketoacidosis, in DM patients without CAD. Diabetes patients without CAD exhibit a higher risk of all-cause mortality, driven primarily by elevated rates of cancer, circulatory, and endocrinologic deaths, particularly related to diabetic microvascular complications.

Association between parity and female mortality: the mediative role of depressive symptoms.

Is parity associated with all-cause and cause-specific mortality among women in a nationally representative cohort of the US population, and does depression mediate this association? Nulliparous women have a higher risk of all-cause and cause-specific mortality, with depression partially mediating the relationship between parity and women's all-cause and cause-specific mortality. Parity, a significant state in reproductive life, has enduring implications for women's health. There is also a complex relationship between depression, a prevalent mental and emotional disorder, and female fertility. Previous studies have elucidated the relationships between parity and depression, both of which are associated with mortality. However, findings from studies examining parity and women's mortality have been inconsistent. Moreover, few studies have investigated whether the effect of parity on mortality is mediated by depression. We conducted a cross-sectional study using data from seven cycles of the National Health and Nutrition Examination Survey (NHANES) spanning 2005-2018. The study cohort comprised adult women with available parity and survival follow-up data. Parity data were self-reported and sourced from the Reproductive Health Questionnaire. Depression scores were derived from the Patient Health Questionnaire 9, and cause-specific deaths were identified using the International Statistical Classification of Diseases, 10th Revision (ICD-10). Weighted multivariable Cox regression was applied to analyze the association between parity, depression, and mortality. Weighted linear regression was performed to examine the relationship between parity and depression. Mediation analyses were employed to determine whether and to what extent depression mediated the effect of parity on mortality. Our study ultimately encompassed 16962 American women. Following multivariable adjustment, compared to nulliparous women, those with one to three live births exhibited a 17% and 33% reduction in all-cause and cancer mortality, respectively (all-cause mortality: HR = 0.83, 95% CI = 0.69-0.99, P = 0.040; cancer mortality: HR = 0.67, 95% CI = 0.45-0.99, P = 0.045). Women with more than four live births demonstrated lower all-cause mortality and mortality from other (not cancer or cardiovascular disease) diseases (all-cause mortality: HR = 0.73, 95% CI = 0.58-0.93, P = 0.011; other diseases mortality: HR = 0.66, 95% CI = 0.47-0.91, P = 0.013). No correlation was detected between parity and the risk of cardiovascular disease mortality among women. Furthermore, depression was found to partially mediate the impact of parity on all-cause mortality and mortality from other diseases in women. Firstly, a single index of parity was used as an exposure factor, and other reproductive factors such as birth spacing, age at first birth, and mode of delivery were not taken into account. Secondly, despite accounting for important potentially confounders in our analysis, such as BMI, smoking status, and educational level, the influence of unmeasured confounders (e.g., social class, latent reproductive system diseases) on reproductive behavior or mortality cannot be dismissed. Thirdly, women's vulnerability to depression fluctuates across reproductive stages, and the effect of depression on female fertility varies over time. Due to data constraints, we were unable to obtain information on women's mental health status at different reproductive stages. Fourthly, due to the data accessibility limitations of NHANES, we were unable to specifically explore the relationship between parity and different specific types of cancer, a limitation that may obscure potential correlations. Additionally, despite our efforts to control for various confounding factors in subgroup analyses, the smaller sample sizes in some subgroups may limit the statistical power, affecting the ability to detect effects. Finally, studies exploring the association between parity and depression are cross-sectional designs, making it difficult to infer causality. These results should be interpreted with caution, and further research is warranted to corroborate our findings. Our study underscores the elevated risk of all-cause and cause-specific mortality in nulliparous women and reveals that depression partially mediates the negative correlation between parity and women's all-cause mortality and mortality from other diseases. These results should be interpreted with caution, and further investigation is needed to support our findings. This work was supported by the National Key Research and Development Program of China (2023YFC2705700), the Key Research & Developmental Program of Hubei Province (2022BCA042), and the Interdisciplinary Innovative Talents Foundation from Renmin Hospital of Wuhan University (JCRCWL-2022-001). The authors declare that they have no conflict of interest. N/A.

Development and validation of accelerated failure time model for cause-specific survival and prognostication of oral squamous cell carcinoma: SEER data analysis.

Oral Squamous Cell Carcinoma is the most prevalent malignancies affecting the oral cavity. Despite progress in studies and treatment options its outlook remains grim with survival prospects greatly affected by demographic and clinical factors. Precisely predicting survival rates and prognosis plays a role in making treatment choices for the best achievable overall health outcomes. To develop and validate an accelerated failure time model as a predictive model for cause-specific survival and prognosis of Oral Squamous Cell Carcinoma patients and compare its results to the traditional Cox proportional hazard model. We screened Oral cancer patients diagnosed with Squamous Cell Carcinoma from the Surveillance Epidemiology and End Results (SEER) database between 2010 and 2020. An accelerated failure time model using the Type I generalized half logistic distribution was used to determine independent prognostic factors affecting the survival time of patients with oral squamous carcinoma. In addition, accelerated factors were estimated to assess how some variables influence the survival times of the patients. We used the Akaike Information Criterion, Bayesian Information Criterion to evaluate the model fit, the area under the curve for discriminability, Concordance Index (C-index) and Root Mean Square Error and calibration curve for predictability, to compare the type I generalized half logistic survival model to other common classical survival models. All tests are conducted at a 0.05 level of significance. The accelerated failure time models demonstrated superior effectiveness in modeling (fit and predictive accuracy) the cause-specific survival (CSS) of oral squamous cell carcinoma compared to the Cox model. Among the accelerated failure time models considered, the Type I generalized half logistic distribution exhibited the most robust model fit, as evidenced by the lowest Akaike Information Criterion (AIC = 27370) and Bayesian Information Criterion (BIC = 27415) values. This outperformed other parametric models and the Cox Model (AIC = 47019, BIC = 47177). The TIGHLD displayed an AUC of 0.642 for discrimination, surpassing the Cox model (AUC = 0.544). In terms of predictive accuracy, the model achieved the highest concordance index (C-index = 0.780) and the lowest root mean square error (RMSE = 1.209), a notable performance over the Cox model (C-index = 0.336, RMSE = 6.482). All variables under consideration in this study demonstrated significance at the 0.05 level for CSS, except for race and the time span from diagnosis to treatment, in the TIGHLD AFT model. However, differences emerged regarding the significant variations in survival times among subgroups. Finally, the results derived from the model revealed that all significant variables except chemotherapy, all TNM stages and patients with Grade II and III tumor presentations contributed to the deceleration of time to cause-specific deaths. The accelerated failure time model provides a relatively accurate method to predict the prognosis of oral squamous cell carcinoma patients and is recommended over the Cox PH model for its superior predictive capabilities. This study also underscores the importance of using advanced statistical models to improve survival predictions and outcomes for cancer patients.

Age, period, and cohort trends of substance poisoning, alcohol-related disease, and suicide deaths in Australia, 1980-2019.

Deaths due to substance poisoning, alcohol-related disease, and suicide pose a critical public health issue, and have been categorized as "deaths of despair" in the US. Whether these deaths represent a distinct phenomenon requires exploration, particularly in other countries. This retrospective observational study examines age-period-cohort trends of (combined and cause-specific) substance poisoning, alcohol-related disease, and suicide deaths among Australians aged ≥15-years that occurred between 1980 and 2019 and compares trends between males and females. Combined mortality rates were initially (1980-1999) relatively stable, reflecting a reduction in alcohol-related disease deaths offset by an increase in substance poisoning deaths. A decline (2000-2006) and subsequent increase (2007-2019) in combined rates were primarily attributable to corresponding changes in both substance poisoning and suicide deaths among males. Distinct age-period-cohort trends were observed between cause of death sub-types, with net drifts: increasing for male (net drift [95% CI]: 3.33 [2.84, 3.83]) and female (2.58 [2.18, 2.98]) substance poisoning deaths; decreasing among male alcohol-related disease (-1.46 [-1.75, -1.16]) and suicide deaths (-0.52[-0.69, -0.36]); and remaining relatively stable for female alcohol-related disease (-0.28 [-0.66, 0.09]) and suicide deaths (-0.25 [-0.52, 0.01]). Although combined age-specific trends were relatively stable over the study period, different and distinct patterns were observed within cause-specific deaths, challenging the notion that these causes of death represent a distinct epidemiological phenomenon. These data indicate a critical need to review the appropriateness of guidance for clinical practice, prevention strategies, and policy initiatives aimed at preventing future deaths.

Causes and investigation of stillbirths in Brazil: A multicentre cross-sectional study in 10 referral maternity hospitals.

Understanding the local characteristics and statistics related to stillbirths may be the first step in a series of strategies associated with a reduction in stillbirth ratio. The aim of this study was to estimate the fetal mortality ratio and evaluate the investigation processes related to the causes of death, comparing the investigation according to the specific cause of death. A cross-sectional study was retrospectively conducted in 10 tertiary obstetric care centers. Medical records of women with stillbirth managed between January 1, 2009 and December 31, 2018 were analyzed and classified, according to sociodemographic characteristics, and gestational and childbirth data, culminating in stillbirth. The stillbirth ratio and its causes were presented in proportions for the study period and individually for each health facility. Cases of 3390 stillbirths were analyzed. The stillbirth ratio varied from 10.74/1000 live births (LBs) in 2009 to 9.31/1000 in 2018. "Intrauterine hypoxia and asphyxia" (ICD-10 P20) and "unspecific causes of death" (ICD-10 P95) represented 40.8% of the causes of death. Investigation for TORCHS and diabetes occurred in 90.8% and 61.4% of deaths, respectively. Placental and necroscopic tests were performed in 36.6% of the cases. The adoption of a rational and standardized investigation of stillbirth remains an unmet need; the use of additional tests and examinations are lacking, especially when unspecific causes are attributed.

Binge drinking at time of bariatric surgery is associated with liver disease, suicides, and increases long-term mortality.

Alcohol use disorder has been reported in patients undergoing bariatric procedures, but the pattern of alcohol consumption has not been evaluated. We investigated the prevalence, risk factors, and impact of binge drinking (BD) at the time of surgery and during follow-up. A prospective, longitudinal study of subjects undergoing bariatric surgery was included in the LABS-2 registry between 2006 and 2009. Participants with AUDIT questionnaire at the time of surgery and a minimum of 12 months follow-up were included. BD was defined as consuming ≥5 drinks on at least 1 occasion in the previous month. Liver biopsies were obtained during bariatric procedures in not all cases. Survival analysis was performed with the adjusted Cox regression model and competing risk. A total of 2257 subjects were included, with a median follow-up of 79 months. The prevalence of BD at time of surgery was 12%, and it raised up to 23% during follow-up. Patients with BD predominantly had a binge eating disorder (OR=1.35 [95% CI: 1.04-1.76]), regularly consumed fast food [OR=1.4 (95% CI: 1.07-1.85)] and used other drugs (OR=2.65 [95% CI: 1.74-4.04]). Within liver biopsies evaluation, BD showed higher hepatic iron deposits (OR=3.00 [95% CI: 1.25-7.21]). BD at the time of surgery was associated with a higher risk of BD during follow-up (OR=10.49 [95% CI: 7.86-14.00]) and long-term mortality (HR: 3.21 [95% CI: 1.67-6.18]). Specific causes of death in these patients with BD were liver disease (p=0.020), suicide (p=0.015), neoplasms (p=0.034), and respiratory (p=0.025). The prevalence of BD in patients undergoing bariatric surgery is high and increases the risk of postoperative liver disease, suicides, and long-term mortality.

All-cause mortality and cause-specific death in U.S. long-lived siblings: data from the Long Life Family Study.

This study compared the mortality risk of long-lived siblings with the U.S. population average and their spouse controls, and investigated the leading causes of death and the familial effect in death pattern. In the Long Life Family Study (LLFS), 1,264 proband siblings (Mean age 90.1, SD 6.4) and 172 spouses (83.8, 7.2) from 511 U.S.-based families were recruited and followed over 12 years. Their survival function was compared with a birth cohort-, baseline age-, sex-, and race-matched pseudo sample from U.S. census data. To examine underlying and contributing causes, we examined in detail 338 deaths with complete death adjudication at the University of Pittsburgh Field Center through the year 2018. A familial effect on survival and death pattern was examined using mixed effect models. The LLFS siblings had better survival than the matched U.S. population average. They also had slightly but not significantly better survival than their spouses' (HR=1.18 [95%CI 0.94-1.49]) after adjusting for age and sex. Age at death ranged from 75-104 years, mean 91.4. The leading causes of death were cardiovascular disease (33.1%), dementia (22.2%), and cancer (10.7%). Mixed effect model shows a significant random effect of family in survival, with adjustment of baseline age and sex. There was no significant familial effect in the underlying cause of death or conditions directly contributing to death among siblings recruited by the University of Pittsburgh Field Center. Our findings demonstrate a higher survival in the LLFS siblings than the U.S. census data, with a familial component of survival. We did not find significant correspondence in causes of death between siblings within families.

Plasma n6 polyunsaturated fatty acid levels and risk for total and cause-specific mortality: A prospective observational study from the UK Biobank

BackgroundThe potential role of n-6 PUFAs in major health outcomes remains controversial. ObjectivesTo examine the relationship between the major plasma n6 PUFA, linoleic acid (LA), as well as the non-LA n6 PUFAs, and total and cause-specific mortality. MethodsThis was a prospective, observational, biomarker-based study in the UK Biobank. Individuals with complete information on baseline demographic, covariate and plasma PUFA levels (percent ot total fatty acids) and mortality outcomes were included (n=257,925). Multivariable-adjusted, Cox-proportional hazards models were used to predict risk of death from all-causes, and from cardiovascular disease (CVD), cancer, and other causes as a function of plasma LA and non-LA n6 levels, both continuously and by PUFA quintile (Q). ResultsComparing LA Q5 to Q1, the hazard ratio (HR, 95% CI) for total mortality was 0.80 (0.76, 0.84; p<0.001), and this was similar for all three cause-specific death categories. On the other hand, mortality HR for non-LA n6 was 1.12 (1.08,1.17; p<0.001), and this was primarily due to increased risk for non-CVD, noncancer deaths [HR 1.29 (1.19,1.40; p<0.001)]. Exploratory analyses among the eight next most common other causes of death suggested that both the decreased risk associated with higher LA and the increased risk associated with non-LA n6 were confined to deaths from respiratory and digestive diseases. ConclusionsThese findings highlight the profound differences in mortality risk related to LA and non-LA n6 PUFA levels and underscore the inappropriateness of treating n-6 PUFAs as a homogenous class with respect to health outcomes. They also support recommendations to maintain (if not increase) current LA intakes.