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Summary: Calcium intake is widely recommended, but its association with mortality remains unclear. This study indicated higher levels of calcium intake were associated with lower mortality in American adults. However, a nonlinear association between calcium intake and mortality suggested that excessive calcium intake beyond a certain threshold may increase mortality risk. Purpose: The study aimed to investigate the association of total, dietary, or supplemental calcium intake with all-cause, cardiovascular, and cancer mortality in American adults. Methods: This prospective cohort study used the National Health and Nutrition Examination Survey from 2005 to 2018. Participants were categorized into tertiles based on calcium intake. Risks of all-cause, cancer, or cardiovascular mortality and the dose–response relationship were estimated using weighted Cox proportional hazard regression and restricted cubic splines, with adjustments for demographic characteristics, comorbidities, laboratory parameters, and dietary data. Results: In total, 6172 participants were included (median age: 61 years), and 869 had died (CVD:217, cancer:224) during a median follow-up of 81 months. After adjusting for confounders, higher total calcium(≥ 1660mg/d) [HR, 95%CI: 0.867 (0.865–0.869)], dietary calcium(≥ 1075mg/d) [HR, 95%CI: 0.711 (0.709–0.713)], and supplemental calcium (≥ 600mg/d) [HR, 95%CI: 0.786 (0.784–0.787)] intake groups were associated with lower all-cause mortality risk compared to the lowest intake group. Similar beneficial associations were found for cardiovascular, cancer mortality, and across subgroups of various ages, genders, races and body mass indexes. In the dose–response analysis, a 'J-shaped' nonlinear relationship was observed between calcium intake and the risk of all-cause, cardiovascular, and cancer mortality. Conclusions: Higher levels of total, dietary, or supplemental calcium were associated with lower all-cause, cardiovascular, or cancer mortality. However, a nonlinear association between calcium intake and mortality suggested that excessive calcium intake beyond a certain threshold may increase mortality risk. [ABSTRACT FROM AUTHOR]

Objective This study examined the relationship between cystatin C (CysC) levels and all-cause, cardiovascular disease (CVD), and cancer mortality in US metabolic syndrome (MetS) patients. Methods The 1999-2002 National Health and Nutrition Examination Survey (NHANES) prospective cohort research included 1980 MetS participants. To assess CysC levels and all-cause, CVD, and cancer mortality, fitted curves, Kaplan-Meier survival curves, Cox regression analysis, and receiver operating characteristic curves were performed. Results During a mean follow-up of 15.3 ± 5.4 years, a total of 819 deaths occurred. The fitted and Kaplan-Meier survival curves revealed that greater CysC levels were linked to higher all-cause, CVD, and cancer mortality rates (P <.05). After adjusting for variables, CysC level was associated with all-cause, CVD, and cancer mortality at 1.63 (1.42-1.88), 1.53 (1.19-1.95), and 1.53 (1 ∼ 2.32), respectively (P <.05). Tertile models showed consistent results: high CysC Tertile participants showed higher risk of all-cause mortality (HR 1.87; 1.43-2.45), CVD mortality (HR 1.97, 1.15 ∼ 3.38), and cancer mortality (HR 1.72, 1.01 ∼ 2.91) compared to those in the lowest tertile (P <.05). Subgroup studies by sex and other characteristics confirmed the findings. CysC demonstrated the higher predictive efficacy across mortality outcomes, followed by eGFR, outperforming urea nitrogen, creatinine, uric acid, and C-reactive protein. CysC alone exhibited substantial predictive value for all-cause (AUC 0.773; P <.05) and CVD mortality (AUC 0.726; P <.05). Combining CysC with age enhanced predictive value for all-cause mortality to 0.861 and CVD mortality to 0.771 (P <.05). Conclusion MetS patients with elevated CysC levels have a higher risk of all-cause, CVD, and cancer death. CysC may predict MetS all-cause and CVD mortality. [ABSTRACT FROM AUTHOR]

Background: The associations of weight change with all-cause and cause-specific mortality stratified by age remains unclear. We evaluated the age-stratified (< 65 vs ≥ 65 years) associations of weight change with all-cause and cause-specific mortality in a large sample of Chinese adults. Methods: Our cohort study included 746,991 adults aged at least 45 years from the Shenzhen Healthcare Big Data Cohort in China. BMI change were categorized as change within 5% (stable), decrease by 5% to 10%, decrease by > 10%, increase by 5% to 10%, and increase by > 10%. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause, non-communicable disease, cardiovascular disease (CVD), and cancer mortality according to BMI change, with adjustment for potential confounders. Results: During a median follow-up of 2.2 years (2,330,180 person-years), there were 10,197 deaths. A notable interaction emerged between weight change and age. For participants ≥ 65 years, compared with stable BMI, more than a 10% decrease in BMI was associated with higher risk of all-cause mortality (HR: 1.69, 95% CI: 1.54–1.86), non-communicable disease mortality (HR: 1.67, 95% CI: 1.52–1.84), CVD mortality (HR: 1.55, 95% CI: 1.34–1.80), and cancer mortality (HR: 1.59, 95% CI: 1.33–1.92). Similar patterns of results for 5% to 10% decrease in BMI were observed. More than a 10% increase in BMI was associated with increased risk of all-cause mortality (HR: 1.13, 95% CI: 1.04–1.24), non-communicable disease mortality (HR: 1.14, 95% CI: 1.04–1.25), and CVD mortality (HR: 1.27, 95% CI: 1.12–1.44). For participants < 65 years, only more than a 10% decrease in BMI was associated with higher risk of all-cause mortality (HR: 1.41, 95% CI: 1.12–1.77), non-communicable disease mortality (HR: 1.43, 95% CI: 1.13–1.81), and cancer mortality (HR: 1.79, 95% CI: 1.29–2.47). Conclusions: Weight loss and excessive weight gain were associated with increased risks of mortality among older adults, while only excessive weight loss was associated with increased risks of mortality among middle-aged adults. [ABSTRACT FROM AUTHOR]

Introduction: Cardiovascular disease (CVD) is a major health concern worldwide, particularly in low- and middle-income countries. The COVID-19 pandemic that emerged in late 2019 may have had an impact on the trend of CVD mortality. This study aimed to investigate the trend and changes in CVD mortality rates in Malaysia, using age-standardized mortality rates (ASMR) from 2010 to 2021. Methods: The Malaysian population and mortality data from 2010 to 2021 were obtained from the Department of Statistics Malaysia (DOSM). ASMRs from CVD per 100,000 population were calculated based on the World Health Organization (2000–2025) standard population using the direct method. The ASMRs were computed based on sex, age groups (including premature mortality age, 30–69 years), and CVD types. The annual percent change (APC) and average annual percent change (AAPC) of the ASMR with corresponding 95% confidence intervals (95% CI) were estimated from joinpoint regression model using the Joinpoint Regression Program, Version 4.9.1.0. Results: Throughout the study period (2010–2021), ASMRs for CVD exhibited an increase from 93.1 to 147.0 per 100,000, with an AAPC of 3.6% (95% CI: 2.1 to 5.2). The substantial increase was observed between 2015 and 2018 (APC 12.6%, 95% CI: 5.4%, 20.3%), with significant changes in both sexes, and age groups 50–69, 70 years and over, and 30–69 (premature mortality age). Notably, the ASMR trend remained consistently high in the premature mortality age group across other age groups, with males experiencing higher rates than females. No significant changes were detected before or after the COVID-19 pandemic (between 2019 and 2021), except for females who died from IHD (10.3% increase) and those aged 0–4 (25.2% decrease). Conclusion: Overall, our analysis highlights the persistently high burden of CVD mortality in Malaysia, particularly among the premature mortality age group. These findings underscore the importance of continued efforts to address CVD risk factors and implement effective prevention and management strategies. Further research is needed to fully understand the impact of the COVID-19 pandemic on CVD mortality rates and to inform targeted interventions to reduce the burden of CVD in Malaysia. [ABSTRACT FROM AUTHOR]

Background/Objective: We investigated the relationship between daily adequate FV intake and risk of all-cause, cardiovascular disease (CVD), and cancer mortalities among Malaysian adults. Methods: Data from a total of 18,211 Malaysian adults aged 18 years and above whom participated in the National Health and Morbidity Survey 2011 were analyzed. The participants were followed up for approximately 11 years, and mortality data were ascertained through record linkages with the death registry from the Malaysian National Registration Department. Multiple Cox regression was applied to assess the association between daily adequate FV intake and risk of all-cause, CVD, and cancer mortalities, adjusting for sociodemographic, lifestyle, and health conditions. Results: During the follow-up period, we observed a total of 1809 all-cause, 374 CVD, and 216 cancer mortalities. No significant association between daily adequate FV intake with all-cause mortality (adjusted hazard ratio (aHR): 1.01, 95% confidence interval (CI: 0.79–1.31), CVD mortality (aHR: 0.91, 95% CI: 0.57–1.47), and cancer mortality (aHR: 1.27, 95% CI: 0.74–2.17) were observed, even after excluding deaths that occurred in the first two years of observation. Conclusions: Further investigation on the type of FV intake and its preparation method with risk of mortality will provide a holistic insight into the causal relationship between FV intake and mortality. [ABSTRACT FROM AUTHOR]

Step cadence‐based and machine‐learning (ML) methods have been used to classify physical activity (PA) intensity in health‐related research. This study examined the association of intensity‐specific PA duration with all‐cause (ACM) and CVD mortality using the cadence‐based and ML methods in 68 561 UK Biobank participants wearing wrist‐worn accelerometers. The two‐stage‐ML method categorized activity type and then intensity. The one‐level‐cadence‐method (1LC) derived intensity‐specific duration using all detected steps (including standing utilitarian steps) and cadence thresholds of ≥100 steps/min (moderate intensity) and ≥130 steps/min (vigorous intensity). The two‐level‐cadence‐method (2LC) detected ambulatory steps (i.e., walking and running) and then applied the same cadence thresholds. The 2LC exhibited the most pronounced association at the lower end of duration spectrum. For example, the 2LC showed the smallest minimum moderate‐to‐vigorous‐PA (MVPA) duration (amount associated with 50% of optimal risk reduction) with similar corresponding ACM hazard ratio (HR) to other methods (2LC: 2.8 min/day [95% CI: 2.6, 2.8], HR: 0.83 [95% CI: 0.78, 0.88]; 1LC, 11.1[10.8, 11.4], 0.80 [0.76, 0.85]; ML, 14.9 [14.6, 15.2], 0.82 [0.76, 0.87]). The ML elicited the greatest mortality risk reduction. For example, the medians and corresponding HR in VPA‐ACM association: 2LC, 2.0 min/day [95% CI: 2.0, 2.0], HR, 0.69 [95% CI: 0.61, 0.79]; 1LC, 6.9 [6.9, 7.0], 0.68 [0.60, 0.77]; ML, 3.2 [3.2, 3.2], 0.53 [0.44, 0.64]. After standardizing durations, the ML exhibited the most pronounced associations. For example, the standardized minimum durations in MPA‐CVD mortality association were: 2LC, −0.77; 1LC, −0.85; ML, −0.94; with corresponding HR of 0.82 [0.72, 0.92], 0.79 [0.69, 0.90], and 0.77 [0.69, 0.85], respectively. The 2LC exhibited the most pronounced association with all‐cause and CVD mortality at the lower end of the duration spectrum. The ML method provided the most pronounced association with all‐cause and CVD mortality, thus might be appropriate for estimating health benefits of moderate and vigorous intensity PA in observational studies. [ABSTRACT FROM AUTHOR]

Individual beverages have varying associations with cardiometabolic outcomes, but little is known about overall beverage quality and cardiometabolic risk after myocardial infarction (MI). We created the Beverage Quality Index (BQI) to assess beverage quality and examined its association with cardiometabolic outcomes after MI. We included 4365 Dutch post-MI patients from the Alpha Omega Cohort, aged 60–80 years. Diet was assessed at baseline (2002–2006) with a 203-item FFQ. The BQI included eight components (coffee, tea, milk, juices, sugar-sweetened beverages, alcohol, added sugar to coffee and tea, and energy from beverages), and ranged from 0 to 80. Multivariable Cox models were used to estimate HRs for the BQI in relation to incident diabetes mellitus (DM), major adverse cardiovascular events (MACE), recurrent cardiovascular disease (CVD) and fatal CVD over 3.4 y of follow-up, with follow-up for fatal CVD extended through 2018 (12.4 y). The average BQI was 50.0 ± 12.5. During 3.4 y of follow-up, we identified 186 incident cases of DM, 601 of MACE, 310 of recurrent CVD and 140 of fatal CVD. In multivariable models, a higher BQI (T3 vs. T1) was associated with lower risk of MACE [HR: 0.73 (0.59–0.90)], and recurrent CVD [HR: 0.67 (0.50–0.91)], but not with DM or CVD mortality. After 12.4 y of follow-up, 903 CVD deaths occurred. A significant inverse association with CVD mortality during long-term follow-up was found [HR: 0.81 (0.68–0.96)]. Overall beverage intake quality, as assessed by the BQI, may represent an important target for the prevention of recurrent CVD. • We developed the beverage quality index (BQI) to assess overall beverage quality. • Higher BQI was associated with lower risk of CVD recurrence and mortality in Dutch post-MI patients. • Overall beverage quality may be an important target for the secondary prevention of CVD. • The BQI could be used as a tool to guide healthy beverage choices in clinical settings but needs validation in other cohorts. [ABSTRACT FROM AUTHOR]

Abstract Background The associations of weight change with all-cause and cause-specific mortality stratified by age remains unclear. We evaluated the age-stratified ( 10%, increase by 5% to 10%, and increase by > 10%. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause, non-communicable disease, cardiovascular disease (CVD), and cancer mortality according to BMI change, with adjustment for potential confounders. Results During a median follow-up of 2.2 years (2,330,180 person-years), there were 10,197 deaths. A notable interaction emerged between weight change and age. For participants ≥ 65 years, compared with stable BMI, more than a 10% decrease in BMI was associated with higher risk of all-cause mortality (HR: 1.69, 95% CI: 1.54–1.86), non-communicable disease mortality (HR: 1.67, 95% CI: 1.52–1.84), CVD mortality (HR: 1.55, 95% CI: 1.34–1.80), and cancer mortality (HR: 1.59, 95% CI: 1.33–1.92). Similar patterns of results for 5% to 10% decrease in BMI were observed. More than a 10% increase in BMI was associated with increased risk of all-cause mortality (HR: 1.13, 95% CI: 1.04–1.24), non-communicable disease mortality (HR: 1.14, 95% CI: 1.04–1.25), and CVD mortality (HR: 1.27, 95% CI: 1.12–1.44). For participants

Abstract Introduction Cardiovascular disease (CVD) is a major health concern worldwide, particularly in low- and middle-income countries. The COVID-19 pandemic that emerged in late 2019 may have had an impact on the trend of CVD mortality. This study aimed to investigate the trend and changes in CVD mortality rates in Malaysia, using age-standardized mortality rates (ASMR) from 2010 to 2021. Methods The Malaysian population and mortality data from 2010 to 2021 were obtained from the Department of Statistics Malaysia (DOSM). ASMRs from CVD per 100,000 population were calculated based on the World Health Organization (2000–2025) standard population using the direct method. The ASMRs were computed based on sex, age groups (including premature mortality age, 30–69 years), and CVD types. The annual percent change (APC) and average annual percent change (AAPC) of the ASMR with corresponding 95% confidence intervals (95% CI) were estimated from joinpoint regression model using the Joinpoint Regression Program, Version 4.9.1.0. Results Throughout the study period (2010–2021), ASMRs for CVD exhibited an increase from 93.1 to 147.0 per 100,000, with an AAPC of 3.6% (95% CI: 2.1 to 5.2). The substantial increase was observed between 2015 and 2018 (APC 12.6%, 95% CI: 5.4%, 20.3%), with significant changes in both sexes, and age groups 50–69, 70 years and over, and 30–69 (premature mortality age). Notably, the ASMR trend remained consistently high in the premature mortality age group across other age groups, with males experiencing higher rates than females. No significant changes were detected before or after the COVID-19 pandemic (between 2019 and 2021), except for females who died from IHD (10.3% increase) and those aged 0–4 (25.2% decrease). Conclusion Overall, our analysis highlights the persistently high burden of CVD mortality in Malaysia, particularly among the premature mortality age group. These findings underscore the importance of continued efforts to address CVD risk factors and implement effective prevention and management strategies. Further research is needed to fully understand the impact of the COVID-19 pandemic on CVD mortality rates and to inform targeted interventions to reduce the burden of CVD in Malaysia.

Abstract This study explores the association between LE8 scores and mortality risks among individuals diagnosed with cardiovascular disease (CVD). Utilizing data from the NHANES conducted between 2005 and 2018, survey-weighted multivariable Cox proportional hazards regression models were utilized. Life’s Essential 8 (LE8) scores dose–response associations were assessed using restricted cubic spline regression. Sub-analyses were performed for different categories of CVD. The study consisted of 2164 participants diagnosed with CVD, ranging in age from 20 to 80 years (weighted mean [SE] age, 61.47 [0.34] years; The average total LE8 was 64.97 [0.54]. 499 participants experienced mortality, with 350 deaths attributed to CVD. After accounting for potential covariates, LE8 score was found to be associated with a decreased both all-cause mortality (OR 0.34, CI 0.22–0.51) and CVD mortality (OR 0.40, CI 0.23–0.68). A survey-weighted multivariable Cox model with restricted cubic splines identified the lowest all-cause mortality (P

Abstract The serum uric acid to serum creatinine ratio (SUA/sCr) is a standardized index of renal function. More importance was attached to the significance of this ratio in the progression of hypertension. While the association between the prognosis of hypertension and SUA/sCr is unknown. Therefore, we aimed to prospectively examine the associations of serum uric acid to serum creatinine ratio and all-cause and CVD mortality in adults with hypertension. Participants with hypertension from NHANES 1999–2018 (n = 15,269) were included. They were stratified by 1 increment of SUA/sCr ratio and categorized into 6 groups as ≤ 4, > 4 to 5, > 5 to 6, > 6 to 7, > 7 to 8, and > 8. The reason for categorization in 6 groups was to analyze the influence of different ratios on outcomes accurately and provide more precise guidance. The sample size is large enough that even if divided into 6 groups, it does not affect the statistical power. The primary outcomes were all-cause and CVD mortality. Weighted multivariable Cox proportional hazards regression models were used to estimate hazard ratio (HRs) of mortality. Restricted cubic spline regression models were utilized to examine dose–response associations between the serum uric acid to serum creatinine ratio and all-cause and CVD mortality. Relatively comprehensive stratified analyses were conducted to confirm the accuracy and stability of the results. There were 15,269 total participants, 49.4% of whom were men, with an average age of 56.6 years. Weighted multivariable Cox proportional hazards regression models demonstrated participants in the lowest group (≤ 4) had the HRs (95% CIs) of 1.43 (1.18, 1.73) for all-cause mortality and 2.8 (1.92, 4.10) for CVD mortality when compared to the reference group. Participants in the highest group (> 8) had the HRs (95% CIs) of 0.47 (0.25, 0.89) for CVD mortality when compared to the reference group. There were progressively lower risks for all-cause and CVD mortality with the SUA/sCr ratio increased (both P trend

Abstract Background The presence of depression related to an increased risk of all-cause and cardiovascular disease (CVD) mortality has been reported. However, studies conducted on certain specific depressive symptoms are scarce. Our purpose was to assess the effect of both depressive symptoms scores and certain specific depressive symptoms on all-cause and CVD mortality. Methods In the present cohort study, all participants, aged 18 years or older, were enrolled in the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2014. Depressive symptoms score was assessed using the validated 9-item Patient Health Questionnaire Depression Scale (PHQ-9), which ranges from 0 to 27, with a PHQ-9 score ≥ 10 diagnosed as depression. The outcome events were all-cause and CVD mortality, which were followed up from 2005 to 2014. The associations of both depressive symptoms score and certain specific depressive symptoms with all-cause and CVD mortality were examined by weighted multivariable proportional hazards models. Results A total of 26,028 participants aged ≥ 18 years were included in the statistical analysis, including 12,813 (49.2%) males and 13,215 (50.8%) females, with a mean (SD) age of 47.34 (18.86) years. During the 9.32 (3.20) years of mean (SD) follow-up, 3261 deaths were recorded, of which 826 were cardiovascular deaths. All-cause mortality was 16.87/1000 person-years in subjects with depression. In terms of CVD mortality, these figures were 4.53/1000 person-years. In the full model (model 3), elevated depressive symptoms scores were independently associated with an increased risk of all-cause mortality (Highest depression symptom score group: adjusted hazard ratio, 1.63; 95% CI 1.44–1.85) and CVD mortality (Highest depression symptom score group: adjusted hazard ratio, 1.73; 95% CI 1.34–2.24). All 9 specific depressive symptoms that make up the PHQ-9 were related to an increased risk of all-cause mortality. However, only 3 symptoms, including trouble sleeping or sleeping too much, poor appetite or overeating, and suicidal ideation, were no significantly associated with an increased risk of CVD mortality. Conclusions The elevated depressive symptoms scores were strongly associated with an increased risk of all-cause and CVD mortality in US adults. Furthermore, all 9 specific depressive symptoms were associated with high all-cause mortality. However, trouble sleeping or sleeping too much, poor appetite or overeating, and suicidal ideation might not increase the risk of CVD mortality.

Previous studies have found direct associations between glycaemic index (GI) and glycaemic load (GL) with chronic diseases. However, this evidence has not been consistent in relation to mortality, and most data regarding this association come from high-income and low-carbohydrate-intake populations. The aim of this study was to evaluate the association between the overall GI and dietary GL and all-cause mortality, CVD and breast cancer mortality in Mexico. Participants from the Mexican Teachers' Cohort (MTC) study in 2006–2008 were followed for a median of 10 years. Overall GI and dietary GL were calculated from a validated FFQ. Deaths were identified by the cross-linkage of MTC participants with two national mortality registries. Cox proportional hazard models were used to estimate the impact of GI and GL on mortality. We identified 1198 deaths. Comparing the lowest and highest quintile, dietary GI and GL appeared to be marginally associated with all-cause mortality; GI, 1·12 (95 % CI: 0·93, 1·35); GL, 1·12 (95 % CI: 0·87, 1·44). Higher GI and GL were associated with increased risk of CVD mortality, GI, 1·30 (95 % CI: 0·82, 2·08); GL, 1·64 (95 % CI: 0·87, 3·07) and with greater risk of breast cancer mortality; GI, 2·13 (95 % CI: 1·12, 4·06); GL, 2·43 (95 % CI: 0·90, 6·59). It is necessary to continue the improvement of carbohydrate quality indicators to better guide consumer choices and to lead the Mexican population to limit excessive intake of low-quality carbohydrate foods. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular disease (CVD) and depression have a bidirectional association, with inflammation and metabolic factors being common important triggers for both conditions. However, as a novel inflammatory and metabolic marker, platelet-to-HDL-C ratio (PHR) has not been established in relation to depression and cardiovascular disease. Materials and methods: Participants aged 20 years and older were included in the 2005-2018 NHANES database. PHR was calculated as the ratio of platelet count (1000 cells/mL) to HDL-C (mmol/L). The Patient Health Questionnaire (PHQ-9) was used to diagnose depression, with a cutoff value of 10. Weighted logistic regression analysis and restricted cubic spline (RCS) analysis were employed to examine the association between PHR and depression-related features. Additionally, weighted COX regression and RCS were used to analyze the association of PHR with CVD mortality in patients with depression. Receiver operating characteristic curves were used to assess whether PHR had an advantage over HDL-C in predicting depression. Finally, the mediating role of PHR in the latest cardiovascular health indicator Life's Essential 8 and depression was explored. Results: A total of 26,970 eligible participants were included, including 2,308 individuals with depression, representing approximately 160 million U.S. adults when weighted. After full adjustment, we estimated that the odds ratio (OR) of depression associated with a per standard deviation (SD) increase in PHR was 1.06 (95% CI: 1.01-1.12, P=0.03). The restricted cubic spline (RCS) analysis indicated a linear association (Nonlinear P=0.113). When PHR was divided into four groups based on quartiles and included in the model after full adjustment for depression risk factors, participants in quartile 2, quartile 3, and quartile 4 of PHR showed a trend of increasing risk of depression compared to the lowest quartile group (P trend=0.01). In addition, weighted COX regression and RCS revealed that a per SD increase in PHR was associated with a higher risk of CVD mortality among patients with depression (HR: 1.38, 95% CI: 1.05-1.81, P=0.02, Nonlinear P=0.400). Subgroup analyses showed that current alcohol consumption enhanced the association between PHR and depression (P for interaction=0.017). Furthermore, the areas under the ROC curves (AUC) were 0.556 (95% CI, 0.544-0.568; P < 0.001) for PHR and 0.536 (95% CI, 0.524-0.549; P < 0.001) for HDL-C (PDeLong = 0.025). Finally, mediation analysis indicated that PHR was an intermediate mechanism between LE8 and depression (mediation proportion=5.02%, P=0.02). Conclusion: In U.S. adults, an increase in PHR linearly increases the risk of depression and CVD mortality among individuals with depression. Additionally, PHR has a better predictive advantage for depression compared to HDL-C. Furthermore, PHR significantly mediates the association between LE8 scores and depression. [ABSTRACT FROM AUTHOR]

This study explores the association between LE8 scores and mortality risks among individuals diagnosed with cardiovascular disease (CVD). Utilizing data from the NHANES conducted between 2005 and 2018, survey-weighted multivariable Cox proportional hazards regression models were utilized. Life's Essential 8 (LE8) scores dose–response associations were assessed using restricted cubic spline regression. Sub-analyses were performed for different categories of CVD. The study consisted of 2164 participants diagnosed with CVD, ranging in age from 20 to 80 years (weighted mean [SE] age, 61.47 [0.34] years; The average total LE8 was 64.97 [0.54]. 499 participants experienced mortality, with 350 deaths attributed to CVD. After accounting for potential covariates, LE8 score was found to be associated with a decreased both all-cause mortality (OR 0.34, CI 0.22–0.51) and CVD mortality (OR 0.40, CI 0.23–0.68). A survey-weighted multivariable Cox model with restricted cubic splines identified the lowest all-cause mortality (P < 0.001) and CVD mortality (P < 0.001) risk when LE8 reach at 63.75 (P < 0.001). The results highlight the association between LE8 scores and reduced mortality in CVD patient population. The implementation of comprehensive initiatives that prioritize healthy dietary patterns, will play a crucial role in alleviating the impact of cardiovascular disease and improving cardiovascular health outcomes. [ABSTRACT FROM AUTHOR]

The serum uric acid to serum creatinine ratio (SUA/sCr) is a standardized index of renal function. More importance was attached to the significance of this ratio in the progression of hypertension. While the association between the prognosis of hypertension and SUA/sCr is unknown. Therefore, we aimed to prospectively examine the associations of serum uric acid to serum creatinine ratio and all-cause and CVD mortality in adults with hypertension. Participants with hypertension from NHANES 1999–2018 (n = 15,269) were included. They were stratified by 1 increment of SUA/sCr ratio and categorized into 6 groups as ≤ 4, > 4 to 5, > 5 to 6, > 6 to 7, > 7 to 8, and > 8. The reason for categorization in 6 groups was to analyze the influence of different ratios on outcomes accurately and provide more precise guidance. The sample size is large enough that even if divided into 6 groups, it does not affect the statistical power. The primary outcomes were all-cause and CVD mortality. Weighted multivariable Cox proportional hazards regression models were used to estimate hazard ratio (HRs) of mortality. Restricted cubic spline regression models were utilized to examine dose–response associations between the serum uric acid to serum creatinine ratio and all-cause and CVD mortality. Relatively comprehensive stratified analyses were conducted to confirm the accuracy and stability of the results. There were 15,269 total participants, 49.4% of whom were men, with an average age of 56.6 years. Weighted multivariable Cox proportional hazards regression models demonstrated participants in the lowest group (≤ 4) had the HRs (95% CIs) of 1.43 (1.18, 1.73) for all-cause mortality and 2.8 (1.92, 4.10) for CVD mortality when compared to the reference group. Participants in the highest group (> 8) had the HRs (95% CIs) of 0.47 (0.25, 0.89) for CVD mortality when compared to the reference group. There were progressively lower risks for all-cause and CVD mortality with the SUA/sCr ratio increased (both P trend < 0.01). The SUA/sCr ratio was (P for nonlinearity < 0.01) nonlinearly correlated with all-cause mortality, with inflection points of 6.25. In addition, the restricted cubic splines results indicated that the SUA/sCr ratio (P for nonlinearity = 0.32) showed linear and negative associations with cardiovascular mortality with inflection points of 6.54. The inverse associations between SUA/sCr ratio and all-cause mortality were consistent across all subgroups except for the subgroup of eGFR < 45 ml/min/1.73 m2 and never smokers (P trend = 0.20 and 0.13, respectively), and the inverse associations between low SUA/sCr ratio and CVD mortality were consistent across all subgroups (P trend < 0.01). Contrary to previous studies, outcomes suggest that lower SUA/sCr ratio was associated with higher risks of all-cause and CVD mortality in adults with hypertension. [ABSTRACT FROM AUTHOR]

Background: The presence of depression related to an increased risk of all-cause and cardiovascular disease (CVD) mortality has been reported. However, studies conducted on certain specific depressive symptoms are scarce. Our purpose was to assess the effect of both depressive symptoms scores and certain specific depressive symptoms on all-cause and CVD mortality. Methods: In the present cohort study, all participants, aged 18 years or older, were enrolled in the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2014. Depressive symptoms score was assessed using the validated 9-item Patient Health Questionnaire Depression Scale (PHQ-9), which ranges from 0 to 27, with a PHQ-9 score ≥ 10 diagnosed as depression. The outcome events were all-cause and CVD mortality, which were followed up from 2005 to 2014. The associations of both depressive symptoms score and certain specific depressive symptoms with all-cause and CVD mortality were examined by weighted multivariable proportional hazards models. Results: A total of 26,028 participants aged ≥ 18 years were included in the statistical analysis, including 12,813 (49.2%) males and 13,215 (50.8%) females, with a mean (SD) age of 47.34 (18.86) years. During the 9.32 (3.20) years of mean (SD) follow-up, 3261 deaths were recorded, of which 826 were cardiovascular deaths. All-cause mortality was 16.87/1000 person-years in subjects with depression. In terms of CVD mortality, these figures were 4.53/1000 person-years. In the full model (model 3), elevated depressive symptoms scores were independently associated with an increased risk of all-cause mortality (Highest depression symptom score group: adjusted hazard ratio, 1.63; 95% CI 1.44–1.85) and CVD mortality (Highest depression symptom score group: adjusted hazard ratio, 1.73; 95% CI 1.34–2.24). All 9 specific depressive symptoms that make up the PHQ-9 were related to an increased risk of all-cause mortality. However, only 3 symptoms, including trouble sleeping or sleeping too much, poor appetite or overeating, and suicidal ideation, were no significantly associated with an increased risk of CVD mortality. Conclusions: The elevated depressive symptoms scores were strongly associated with an increased risk of all-cause and CVD mortality in US adults. Furthermore, all 9 specific depressive symptoms were associated with high all-cause mortality. However, trouble sleeping or sleeping too much, poor appetite or overeating, and suicidal ideation might not increase the risk of CVD mortality. [ABSTRACT FROM AUTHOR]

Dyslipidemia is an independent and modifiable risk factor for aging and age-related disorders. Routine lipid panel cannot capture all individual lipid species in blood (i.e., blood lipidome). To date, a comprehensive assessment of the blood lipidome associated with mortality is lacking in large-scale community-dwelling individuals, especially in a longitudinal setting. Using liquid chromatograph-mass spectrometry, we repeatedly measured individual lipid species in 3,821 plasma samples collected at two visits (~ 5.5 years apart) from 1,930 unique American Indians in the Strong Heart Family Study. We first identified baseline lipids associated with risks for all-cause mortality and CVD mortality (mean follow-up period: 17.8 years) in American Indians, followed by replication of top hits in European Caucasians in the Malmö Diet and Cancer-Cardiovascular Cohort (n = 3,943, mean follow-up period: 23.7 years). The model adjusted age, sex, BMI, smoking, hypertension, diabetes, and LDL-c at baseline. We then examined the associations between changes in lipid species and risk of mortality. Multiple testing was controlled by false discovery rate (FDR). We found that baseline levels and longitudinal changes of multiple lipid species, e.g., cholesterol esters, glycerophospholipids, sphingomyelins, and triacylglycerols, were significantly associated with risks of all-cause or CVD mortality. Many lipids identified in American Indians could be replicated in European Caucasians. Network analysis identified differential lipid networks associated with risk of mortality. Our findings provide novel insight into the role of dyslipidemia in disease mortality and offer potential biomarkers for early prediction and risk reduction in American Indians and other ethnic groups.

BackgroundNon-alcoholic Fatty Liver Disease (NAFLD) is a prevalent condition characterized by the accumulation of fat in the liver, often linked with increased risk for multi-systemic diseases. This study aims to investigate the relationship between NAFLD and mortality, particularly all-cause and cardiovascular mortality, among United States adults.MethodsData from the National Health and Nutrition Examination Survey (NHANES) were utilized, encompassing 80,312 participants from 2003–2004 to 2017–2018. After exclusions for incomplete data, potential other liver diseases, and significant alcohol consumption, the final analytical cohort included 32,698 participants. The Fatty Liver Index (FLI), a non-invasive diagnostic tool, was used to identify NAFLD. Covariates included demographic characteristics, lifestyle factors, and biochemical parameters. Survival analysis was conducted using a weighted Cox proportional hazards regression model to quantify the impact of NAFLD on mortality.ResultsThe study revealed that NAFLD was significantly associated with increased risks of all-cause and cardiovascular disease (CVD) mortality. The hazard ratios (HRs) from the survival analysis consistently indicated a higher risk among participants with NAFLD compared to those without. Subgroup analyses further confirmed the association, with notable exceptions in certain subgroups such as those with high school education and diabetes. Additionally, a nonlinear relationship between serum uric acid (SUA) levels and mortality risk was identified among NAFLD participants.ConclusionNon-alcoholic Fatty Liver Disease is a significant risk factor for all-cause and CVD mortality in US adults. The findings underscore the importance of early detection and intervention for NAFLD to mitigate its impact on public health. Further research is needed to explore the complex interactions between NAFLD, SUA levels, and mortality, particularly in high-risk subgroups.

ObjectiveA systematic analysis was conducted to determine the relationship between a plant-based diet and all-cause mortality.MethodsThe PubMed, Embase and Web of Science databases were searched. Two authors selected English documents from the database. Then the other two authors extracted the data and evaluated the Newcastle–Ottawa Scale (NOS). This study adhered to the guidelines of the Preferred Reporting Project (PRISMA) and the PROSPERO Registry protocols. A mixed-effects model combined maximum adjusted estimates, with heterogeneity measured using the I2 statistic. The sensitivity analysis validated the analysis’s robustness, while publication bias was assessed.ResultsThe results of the meta-analysis of 14 articles revealed that a plant-based diet (PDI) can reduce cancer mortality (RR = 0.88, [95% CI 0.79–0.98], τ2: 0.02, I2: 84.71%), cardiovascular disease (CVD) mortality (RR = 0.81, [95% CI 0.76–0.86], τ2: 0.00, I2: 49.25%) and mortality (RR = 0.84, [95% CI 0.79–0.89], τ2: 0.01, I2: 81.99%) risk. Adherence to a healthy plant-based diet (hPDI) was negatively correlated with cancer mortality (RR = 0.91, [95% CI 0.83–0.99], τ2:0.01, I2:85.61%), CVD mortality (RR = 0.85, [95% CI 0.77–0.94], τ2: 0.02, I2: 85.13%) and mortality (RR = 0.85, [95% CI 0.80–0.90], τ2: 0.01, I2: 89.83%). An unhealthy plant-based diet (uPDI) was positively correlated with CVD mortality (RR = 1.19, [95% CI 1.07–1.32], τ2: 0.02, I2: 80.03%) and mortality (RR = 1.18, [95% CI 1.09–1.27], τ2: 0.01, I2: 89.97%) and had a certain correlation with cancer mortality (RR = 1.10, [95% CI 0.97–1.26], τ2: 0.03, I2: 93.11%). Sensitivity analysis showed no contradictory results.ConclusionThe hPDI was negatively associated with all-cause mortality, and the uPDI was positively associated with all-cause mortality.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/#loginpage.

Aim: To determine the associations between the Chinese visceral adiposity index (CVAI) and the risks of all‐cause and cause‐specific mortality. Materials and Methods: A total of 3 916 214 Chinese adults were enrolled in a nationwide population cohort covering all 31 provinces of mainland China. The CVAI was calculated based on age, body mass index, waist circumference, and triglyceride and high‐density lipoprotein cholesterol concentrations. We used a Cox proportional hazards regression model to determine the hazard ratios and 95% confidence intervals (CIs) for risk of mortality associated with different CVAI levels. Results: The median follow‐up duration was 3.8 years. A total of 86 158 deaths (34 867 cardiovascular disease [CVD] deaths, 29 884 cancer deaths, and 21 407 deaths due to other causes) were identified. In general, after adjusting for potential confounding factors, a U‐shaped relationship between CVAI and all‐cause mortality was observed by restricted cubic spline (RCS). Compared with participants in CVAI quartile 1, those in CVAI quartile 4 had a 23.0% (95% CI 20.0%–25.0%) lower risk of cancer death, but a 23.0% (95% CI 19.0–27.0) higher risk of CVD death. In subgroup analysis, a J‐shaped and inverted U‐shaped relationship for all‐cause mortality and cancer mortality was observed in the group aged < 60 years. Conclusions: The CVAI, an accessible indicator reflecting visceral obesity among Chinese adults, has predictive value for all‐cause, CVD, and cancer mortality risks. Moreover, the CVAI carries significance in the field of health economics and secondary prevention. In the future, it could be used for early screening purposes. [ABSTRACT FROM AUTHOR]

Abstract Background Prehypertension affects 25–50% of adults worldwide and no prior study has examined the relationship between serum 25-hydroxyvitamin D [25(OH)D] concentrations and mortality risk in individuals with prehypertension. This study aims to investigate the association of serum 25(OH)D concentrations with all-cause and CVD mortality among prehypertensive adults by utilizing data from the US National Health and Nutrition Examination Survey (NHANES) 2007–2014 and linked 2019 mortality file. Methods We included 4345 prehypertensive adults who participated in the NHANES between 2007 and 2014 and were followed up until 31 December 2019. Weighted Cox proportional hazards models were used with adjustments for multiple covariates to calculate the hazard ratio (HR) and 95% confidence interval (CI) for the risks of dying from any cause and CVD. Results During a median follow-up of 8.8 years, 335 deaths from any causes were documented, of which 88 participants died from CVD. Compared with participants with sufficient 25(OH)D (≥ 75 nmol/L), the multivariate-adjusted HRs and 95% CIs for participants with severe deficiency (

ObjectiveResearch is limited regarding the predictive utility of the RAND-36 questionnaire and physical performance tests in relation to all-cause, cardiovascular disease (CVD), and total-cancer mortality in older women.MethodsData on the RAND-36 questionnaire, gait speed, and chair stand performance were assessed in 5,534 women aged ≥65 years at baseline. A subset (n = 298) had physical function assessments additionally at follow-up (years 1, 3, or 6). Multivariable Cox proportional hazards regression models estimated associations (HR) for a 1-standard deviation (SD) difference in baseline RAND-36 scores and performance tests (alone and combined) with mortality outcomes in the overall cohort and in models stratified by enrollment age (

Background: Prehypertension affects 25–50% of adults worldwide and no prior study has examined the relationship between serum 25-hydroxyvitamin D [25(OH)D] concentrations and mortality risk in individuals with prehypertension. This study aims to investigate the association of serum 25(OH)D concentrations with all-cause and CVD mortality among prehypertensive adults by utilizing data from the US National Health and Nutrition Examination Survey (NHANES) 2007–2014 and linked 2019 mortality file. Methods: We included 4345 prehypertensive adults who participated in the NHANES between 2007 and 2014 and were followed up until 31 December 2019. Weighted Cox proportional hazards models were used with adjustments for multiple covariates to calculate the hazard ratio (HR) and 95% confidence interval (CI) for the risks of dying from any cause and CVD. Results: During a median follow-up of 8.8 years, 335 deaths from any causes were documented, of which 88 participants died from CVD. Compared with participants with sufficient 25(OH)D (≥ 75 nmol/L), the multivariate-adjusted HRs and 95% CIs for participants with severe deficiency (< 25 nmol/L), moderate deficiency (25–49.9 nmol/L), and insufficient concentrations (50–74.9 nmol/L) of serum 25(OH)D for all-cause death were 2.83 (1.46–5.52), 1.17 (0.74–1.86), and 1.36 (0.93–1.98), respectively. Similarly, the multivariable-adjusted HRs and 95%CIs for CVD death were 4.14 (1.10–15.51), 1.23 (0.46–3.28), and 1.73 (0.96–3.14), respectively. We found that there was a 9% reduction in the risk of death from all causes and a 14% reduction in the risk of death from CVD for every 10 nmol/L increase in serum 25(OH)D concentrations. Conclusion: Severe serum 25(OH)D deficiency among prehypertensive adults was associated with increased risk of mortality from all causes as well as from CVD. Our work suggests that supplementing with vitamin D may prevent premature death in severely deficient individuals with prehypertension. [ABSTRACT FROM AUTHOR]

Background: Type 2 diabetes mellitus (T2DM) was a major global health threat. As a chronic low-grade inflammatory disease, the prognosis of diabetes was associated with inflammation. The advanced lung cancer inflammation index (ALI) served as a comprehensive index to assess inflammation. This study aimed to estimate the association between ALI and all-cause, cardiovascular disease (CVD), and cancer mortality in T2DM patients. Methods: We extracted cohort data from the National Health and Nutrition Examination Survey (NHANES) spanning 1999-2018 for analysis. The weighted Kaplan-Meier analysis and multivariate-adjusted Cox analysis were utilized to evaluate the relationship between ALI and all-cause, CVD, and cancer mortality in T2DM patients. Restricted cubic spline (RCS) analysis was employed to assess their non-linear relationship. Stratified analysis and interaction analysis were conducted to enhance the robustness of the results. Results: The study incorporated a total of 3,888 patients. An increase in ALI was associated with a reduced risk of all-cause and CVD mortality in T2DM patients, but not related to cancer mortality. There were J-shaped and L-shaped non-linear relationships between ALI and all-cause, CVD mortality in T2DM patients, respectively. The inflection points were 90.20 and 93.06, respectively. For values below the inflection point, every 10U increase in ALI, both all-cause and CVD mortality risk decreased by 9%. Beyond the inflection point, all-cause mortality rose by 3%, while CVD mortality remained unaffected. Gender-stratified RCS analysis indicated a linear negative relationship between CVD mortality and ALI in female T2DM patients, whereas the trend in males aligned with the overall population. Conclusion: Our research initially identified a significant correlation between increased ALI levels with decreased all-cause and CVD mortality in T2DM patients. There were J-shaped and L-shaped non-linear relationships between ALI and all-cause, CVD mortality in T2DM patients, respectively. For female patients, there was a linear negative relation between CVD mortality and ALI, whereas the trend in males aligned with the overall population. These findings suggested that maintaining ALI (for example, control body weight and keep albumin in the normal range) within a certain range in the clinical settings was crucial for improving all-cause and CVD mortality in T2DM patients. [ABSTRACT FROM AUTHOR]

Cardiovascular disease remains a leading cause of morbidity and mortality in the United States (US). Although high-quality data are accessible in the US for cardiovascular research, digital literacy (DL) has not been explored as a potential factor influencing cardiovascular mortality, although the Social Vulnerability Index (SVI) has been used previously as a variable in predictive modeling. Utilizing a large language model, ChatGPT4, we investigated the variability in CVD-specific mortality that could be explained by DL and SVI using regression modeling. We fitted two models to calculate the crude and adjusted CVD mortality rates. Mortality data using ICD-10 codes were retrieved from CDC WONDER, and the geographic level data was retrieved from the US Department of Agriculture. Both datasets were merged using the Federal Information Processing Standards code. The initial exploration involved data from 1999 through 2020 (n = 65,791; 99.98% complete for all US Counties) for crude cardiovascular mortality (CCM). Age-adjusted cardiovascular mortality (ACM) had data for 2020 (n = 3118 rows; 99% complete for all US Counties), with the inclusion of SVI and DL in the model (a composite of literacy and internet access). By leveraging on the advanced capabilities of ChatGPT4 and linear regression, we successfully highlighted the importance of incorporating the SVI and DL in predicting adjusted cardiovascular mortality. Our findings imply that just incorporating internet availability in the regression model may not be sufficient without incorporating significant variables, such as DL and SVI, to predict ACM. Further, our approach could enable future researchers to consider DL and SVI as key variables to study other health outcomes of public-health importance, which could inform future clinical practices and policies. [ABSTRACT FROM AUTHOR]

BackgroundStroke was a major global public health challenge, and its prognosis was remarkably associated with inflammation levels and nutritional status. The advanced lung cancer inflammation index (ALI) was a comprehensive indicator that combined inflammation and nutritional status. Currently, the relationship between ALI and the prognosis of stroke patients was not yet known. The purpose of the current study was to estimate their relationship.MethodsCohort data from the National Health and Nutrition Examination Survey (NHANES) 1999–2018 were collected. The association between ALI and all-cause and cardiovascular disease (CVD) mortality in stroke patients was estimated using a multivariable adjusted Cox model. Their non-linear relationship was analyzed by restricted cubic spline analysis. Sensitivity analysis was constructed through stratified analysis and interaction analysis.Results1,440 stroke patients were included in this study. An elevated ALI was significantly related to a reduced risk of all-cause mortality in stroke patients but not related to CVD mortality. A reverse J-shaped non-linear association between ALI and all-cause mortality in stroke patients, with an inflection point at 83.76 (the lowest of the mortality risk). On the left side of the inflection point, for each 10 U increase in ALI, there was a 16% reduction in the risk of all-cause mortality. However, on the right side, the risk increased by 6%. There was no remarkable interaction between stratified variables and ALI.ConclusionThis was the first study on the relationship between ALI and all-cause and CVD mortality in stroke patients. Elevated ALI was closely associated with a reduced risk of all-cause mortality. A reverse J-shaped non-linear relationship existed between the two, with an inflection point at 83.76. These findings implied that controlling the ALI of stroke patients within an appropriate range was crucial for their prognosis (such as weight management, albumin supplementation, anti-inflammatory treatment). The dynamic variation in ALI was also advantageous for clinicians in establishing personalized ALI criteria to maximize the long-term survival of stroke patients.

BackgroundThe focus of this survey is on survey data for adults aged 20 and above, covering nine survey cycles from 2001 to 2018. Additionally, the present study explored the correlation between vitamin D concentrations and both cardiovascular disease (CVD) and all-cause mortality.ObjectiveThe objectives of this study were to evaluate the trend of changes in the serum 25(OH)D concentration changes in US adults during the survey period, the prevalence of vitamin D deficiency, and the current status of vitamin D dietary intake and supplementation.MethodsIn-home health interviews were performed using meticulously designed questionnaires that gathered information on demographic details, socioeconomic conditions, dietary patterns, and overall health status. Health assessments were conducted in specially designed mobile centers.1ResultsSurvey data from 2001 to 2018 revealed a rise in serum 25(OH)D levels, from a weighted mean (95% CI) of 65.6 (63.8–67.4) nmol/L during 2001–2002 to 73.5 (70.4–76.5) nmol/L during 2017–2018, among US adults, while overall vitamin D deficiency rates remained stable (p = 0.152). Notably, in adults aged 20–39, 25(OH)D levels decreased (p = 0.002 for trend), and 25(OH)D deficiency increased (p = 0.003 for trend), especially among those with low incomes (deficiency >30%). Upon multivariable adjustment, an L-shaped relationship was found between serum 25(OH)D concentrations and both CVD and all-cause mortality (p

The findings of previous studies investigating the association between dietary glycemic index, glycemic load, and the risk of mortality have been inconsistent. We performed a meta-analysis to evaluate this association. A systematic search in PubMed and Web of Science databases was conducted to identify prospective cohort studies on dietary glycemic index and load with risk of mortality through January 2023. Study-specific relative risks (RR) were combined by using random effects models. Fifteen prospective cohort studies with a total of 527,650 participants and 48,598 all-cause and cause-specific deaths were included in the current meta-analysis. Pooled analyses indicated a higher risk of all-cause mortality (RR = 1.10, 95% CI: 1.00–1.20) and stroke mortality (RR = 1.30, 95% CI: 1.04–1.62) for the highest versus lowest levels of glycemic index. A significant non-linear association was found between glycemic index and mortality of all-causes (P for non-linearity = 0.02) and CVD (P for non-linearity <0.001), indicating increased risk at high levels of glycemic index (≥63.1 for all-cause mortality; ≥72.8 for CVD mortality). Glycemic load was positively associated with risk of CVD mortality (RR = 1.18, 95% CI: 1.09–1.27) and stroke mortality (RR = 1.30, 95% CI: 1.05–1.60) in the highest versus lowest meta-analysis. For cancer mortality, there was no significant association with glycemic index, but the association with glycemic load differed by sex. Our results indicated that high glycemic index and glycemic load was associated with an increased risk of mortality from CVD and stroke. Further large prospective studies are warranted to provide definitive evidence in subgroups. [ABSTRACT FROM AUTHOR]

Platelet distribution width (PDW), a marker of platelet size heterogeneity used as a readout of processes leading to platelet production and destruction, was recently reported to tag platelet activation variability. As platelets participate in the pathogenesis of many acute and chronic diseases, we evaluated PDW as a predictor of all-cause and cause-specific mortality. Longitudinal analysis was performed on 17,334 participants (52% women, mean age 55.6±12 years) in the Moli-sani study cohort, without a history of hematological diseases. Baseline PDW measurements were categorized in tertiles, the lowest acting as the reference. A multivariable Cox-proportional hazard model was used to estimate the association between PDW and mortality. Over a median follow-up of 11.6 years (interquartile range 10.7-12.5), 1,535 deaths [37.7% cardiovascular disease (CVD) and 36.5% cancer] were ascertained. As compared to those in the first PDW tertile (14.6-16.0 fL), individuals within the highest tertile (16.6-20.4 fL) had an increased risk of all-cause [hazard ratios (HR):1.20; 95% CI: 1.04-1.37] and CVD mortality (HR:1.29; 1.03-1.62). No association between PDW and cancer mortality was found in the whole sample. Subgroup analyses by two age classes (35-65y, ≥65y) showed that the association of PDW with both all-cause and cancer mortality was more apparent in the elderly (HR:1.34; 1.14-1.58, P for interaction =0.028 and HR:1.37; 1.01-1.85, P for interaction =0.020, respectively). We conclude that PDW-associated increase in CVD mortality risk could be related to accelerated/altered activation, production, or destruction of platelets, leading to several clinical conditions and death. In the elderly, PDW involvement in all-cause and cancer mortality should be further investigated. *Moli-sani investigators Steering committee: Licia Iacoviello, Giovanni de Gaetano, Maria Benedetta Donati. Scientific secretariat: Marialaura Bonaccio, Americo Bonanni, Chiara Cerletti, Simona Costanzo, Amalia De Curtis, Augusto Di Castelnuovo, Alessandro Gialluisi, Francesco Gianfagna, Mariarosaria Persichillo, Teresa Di Prospero. Safety and ethical committee: Jos Vermylen, Renzo Pegoraro, Antonio Spagnolo. External event adjudicating committee: Deodato Assanelli, Livia Rago. Baseline and follow-up data management: Simona Costanzo, Marco Olivieri, Teresa Panzera. Data analysis: Augusto Di Castelnuovo, Marialaura Bonaccio, Simona Costanzo, Simona Esposito, Alessandro Gialluisi, Francesco Gianfagna, Sabatino Orlandi, Emilia Ruggiero, Alfonsina Tirozzi. Biobank, molecular and genetic laboratory: Amalia De Curtis, Sara Magnacca, Fabrizia Noro, Alfonsina Tirozzi. Recruitment staff: Mariarosaria Persichillo, Francesca Bracone, Teresa Panzera. Communication and press office: Americo Bonanni. Regional institutions: Direzione Generale per la Salute - Regione Molise; Azienda Sanitaria Regionale del Molise; Agenzia Regionale per la Protezione Ambientale del Molise; Molise Dati Spa; Offices of vital statistics of the Molise region. Hospitals: Presidi Ospedalieri ASReM: Ospedale A. Cardarelli, Campobasso; Ospedale F. Veneziale, Isernia; Ospedale San Timoteo, Termoli (CB); Ospedale Ss. Rosario, Venafro (IS); Ospedale Vietri, Larino (CB); Ospedale San Francesco Caracciolo, Agnone (IS); Casa di Cura Villa Maria, Campobasso; Ospedale Gemelli Molise, Campobasso; IRCCS Neuromed, Pozzilli (IS), Italy.

ObjectiveTo investigate the association between handgrip strength (HGS) with all-cause and cardiovascular disease (CVD) mortality in US adults.MethodWe analyzed data from the National Health and Nutrition Examination Survey (NHANES) prospective cohort study (2011–2014) with 10,470 participants. The cox regression analysis, Kaplan–Meier survival curves, fitted curves, ROC curves, and propensity score-matched analysis (PSM) with inverse probability of treatment weighting (IPTW), SMRW (PSM with repeated weights), PA (pairwise algorithm), and OW (overlap weighting) regression analysis were performed to assess the relationship between HGS and all-cause and CVD mortality.ResultsThe low HGSs (men

Background: Cardiovascular disease may be the main reason for stagnant growth in life expectancy in the United States since 2010. The American Heart Association recently released an updated algorithm for evaluating cardiovascular health (CVH)—Life's Essential 8 (LE8) score. We aimed to quantify the associations of CVH levels, estimated by the LE8 score, with life expectancy in a nationally representative sample of US adults. Methods: We included 23 003 nonpregnant, noninstitutionalized participants aged 20 to 79 years who participated in the National Health and Nutrition Examination Survey from 2005 to 2018 and whose mortality was identified through linkage to the National Death Index through December 31, 2019. The overall CVH was evaluated by the LE8 score (range, 0–100), as well as the score for each component of diet, physical activity, tobacco/nicotine exposure, sleep duration, body mass index, non–high-density lipoprotein cholesterol, blood glucose, and blood pressure. Life table method was used to estimate life expectancy by levels of the CVH. Results: During a median of 7.8 years of follow-up, 1359 total deaths occurred. The estimated life expectancy at age 50 years was 27.3 years (95% CI, 26.1–28.4), 32.9 years (95% CI, 32.3–33.4), and 36.2 years (95% CI, 34.2–38.2) in participants with low (LE8 score <50), moderate (50≤ LE8 score <80), and high (LE8 score ≥80) CVH, respectively. Equivalently, participants with high CVH had an average 8.9 (95% CI, 6.2–11.5) more years of life expectancy at age 50 years compared with those with low CVH. On average, 42.6% of the gained life expectancy at age 50 years from adhering to high CVH was attributable to reduced cardiovascular disease death. Similarly significant associations of CVH with life expectancy were observed in men and women, respectively. Similarly significant associations of CVH with life expectancy were observed in White participants and Black participants but not in Mexican participants. Conclusions: Adhering to a high CVH, defined as the LE8 score, is related to a considerably increased life expectancy in US adults, but more research needs to be done in other races and ethnicities (eg, Hispanic and Asian). [ABSTRACT FROM AUTHOR]

Dietary intake is a determining factor in the morbidity and mortality of chronic disorders. However, not many documents have investigated this relationship. The aim of this study was to evaluate the associations of the Mediterranean dietary score (MDS), Alternative Healthy Eating Index (AHEI), Dietary Inflammatory Index (DII), DASH score, and dietary acid load with cardiovascular disease (CVD) mortality. A total of 2158 CVD patients (mean age of 54.73 ± 8.62 years) from the Fasa cohort study, Iran, participated in the current study. Diet quality indices including DII, AHEI, MDS, DASH, and dietary acid load (NEAP score) were computed using a validated 125‐item Food Frequency Questionnaire (FFQ). Cox regression analyses were used to determine HRs and 95% CIs. During a follow‐up of 3 years, we documented 59 CVD deaths. After adjusting for relevant confounders (age, gender, family history of CVD, smoking, physical activity, alcohol intake, and HTN) in the final model, we found that higher DII scores and dietary acid load were significantly related to increased mortality due to CVD (HR = 1.11; 95% CI = 1.01–1.24; and HR = 1.02; 95% CI = 1.01–1.03). However, the DASH score was insignificantly associated with decreased CVD mortality by 20.4% (HR = 0.79; 95% CI = 0.57–1.09). There was no significant relationship among AHEI score, MDS, and CVD mortality. This study showed that increasing dietary acidity and the use of inflammatory food compounds could contribute to CVD mortality. Also, adherence to the DASH diet may be associated with reduced CVD mortality. [ABSTRACT FROM AUTHOR]

BackgroundOptimal blood pressure (BP) management strategy among the elderly remains controversial, with insufficient consideration of long-term BP trajectory. This study aimed to identify BP trajectory patterns as well as terminal BP trajectory among the Chinese elderly and to explore the relationships between BP trajectories and all-cause mortality and cardiovascular disease (CVD) mortality.MethodsWe included 11,181 participants older than 60 at baseline (mean age, 80.98 ± 10.71) with 42,871 routine BP measurements from the Chinese Longitudinal Healthy Longevity Survey. Latent class trajectory analysis and Cox proportional hazard model were conducted to identify trajectory patterns and their associations with mortality. Furthermore, we also applied mixed-effects model to identify terminal BP trajectories among the elderly.ResultsCompared with stable at normal high level trajectory, excess systolic BP (SBP) trajectory with decreasing trend was associated with a 34% (HR = 1.34, 95% CI: 1.23–1.45) higher risk of all-cause mortality. Considering the competing risk of non-CVD death, excess BP trajectory with decreasing trend had a more pronounced effect on CVD mortality, in which HR (95% CI) was 1.67 (1.17, 2.37). Similar results were also found in diastolic BP (DBP), pulse pressure (PP), and mean arterial pressure (MAP) trajectories. We further conducted a mixed-effects model and observed that SBP and PP trajectories first increased and began to decline slightly six years before death. In contrast, DBP and MAP showed continuous decline 15 years before death.ConclusionLong-term BP trajectory was associated with all-cause mortality, especially CVD mortality. Keeping a stable BP over time may be an important way for CVD prevention among the elderly.

AimsApnoea-hypopnoea index (AHI), the universal clinical metric of sleep apnoea severity, poorly predicts the adverse outcomes of sleep apnoea, potentially because the AHI, a frequency measure, does not adequately capture disease burden. Therefore, we sought to evaluate whether quantifying the severity of sleep apnoea by the 'hypoxic burden' would predict mortality among adults aged 40 and older.Methods and resultsThe samples were derived from two cohort studies: The Outcomes of Sleep Disorders in Older Men (MrOS), which included 2743 men, age 76.3 ± 5.5 years; and the Sleep Heart Health Study (SHHS), which included 5111 middle-aged and older adults (52.8% women), age: 63.7 ± 10.9 years. The outcomes were all-cause and Cardiovascular disease (CVD)-related mortality. The hypoxic burden was determined by measuring the respiratory event-associated area under the desaturation curve from pre-event baseline. Cox models were used to calculate the adjusted hazard ratios for hypoxic burden. Unlike the AHI, the hypoxic burden strongly predicted CVD mortality and all-cause mortality (only in MrOS). Individuals in the MrOS study with hypoxic burden in the highest two quintiles had hazard ratios of 1.81 [95% confidence interval (CI) 1.25-2.62] and 2.73 (95% CI 1.71-4.36), respectively. Similarly, the group in the SHHS with hypoxic burden in the highest quintile had a hazard ratio of 1.96 (95% CI 1.11-3.43).ConclusionThe 'hypoxic burden', an easily derived signal from overnight sleep study, predicts CVD mortality across populations. The findings suggest that not only the frequency but the depth and duration of sleep related upper airway obstructions, are important disease characterizing features.

Abstract Background The association between osteocalcin and mortality has been scantly studied. We aimed to investigate the association between osteocalcin along with its trajectories and mortality based on long-term longitudinal data. Methods We performed a retrospective cohort study of 9413 type 2 diabetic patients with at least three measurements of total serum osteocalcin within 3 years since their first inpatient diagnosis of type 2 diabetes. Baseline, mean values of osteocalcin levels and their trajectories were used as exposures. A multivariable-adjusted Cox proportional hazards model was used to estimate the association of osteocalcin levels and their trajectories with mortality. Results During a mean follow-up of 5.37 years, 1638 patients died, of whom 588 were due to cardiovascular events. Multivariable-adjusted hazard ratios (HRs) across quintiles of baseline osteocalcin levels were 2.88 (95% confidence interval (CI) 2.42–3.42), 1.65 (95% CI 1.37–1.99), 1.17 (95% CI 0.96–1.42), 1.00, and 1.92 (95% CI 1.60–2.30) for all-cause mortality, and 3.52 (95% CI 2.63–4.71), 2.00 (95% CI 1.46–2.73), 1.03 (95% CI 0.72–1.47), 1.00, 1.67 (95% CI 1.21–2.31) for CVD mortality, respectively. When we used the mean values of osteocalcin as the exposure, U-shaped associations were also found. These U-shaped associations were consistent among patients of different baseline characteristics. Patients with a stable or even increasing trajectory of osteocalcin may have a lower risk of both all-cause and CVD mortality. Conclusions A U-shape association between baseline osteocalcin and mortality was observed among patients with type 2 diabetes. Patients with lower levels of serum osteocalcin during follow-ups had higher risks for all-cause and cardiovascular mortality.

BackgroundAsia has experienced a large increase in meat intake in the past decade, yet the health impact of meat intake is not well studied.ObjectiveWe examined the association of meat intake with all-cause, cancer and cardiovascular disease (CVD) mortality in an Asian country.MethodsParticipants were 113,568 adults with dietary data at recruitment (2004–2013) of the Health Examinees-Gem (HEXA-G) study, a prospective cohort study conducted in 8 regions of Korea. Participants were followed until 31 December 2020. Total, red, white, and organ meat intake were computed based on a 106-item questionnaire. Multivariable Cox proportional hazard models were implemented using the lowest quintile of meat intake as the reference category.FindingsFor 1,205,236 person-years, 3,454 deaths were recorded. High intake of processed red meat was positively associated with all-cause mortality [men: hazard ratio (HR) 1.21, 95% confidence interval (95% CI) 1.07–1.37; women: HR 1.32, 95% CI 1.12–1.56]. Increased risk of all-cause mortality (HR 1.21, 95% CI 1.05–1.39) and cancer mortality (HR 1.24, 95% CI 1.03–1.50) was observed in women with high intake of organ meat. Moderate intake of pork belly was associated with reduced risk of all-cause mortality in men (HR 0.76, 95% CI 0.62–0.93) and women (HR 0.83, 95% 0.69–0.98) but high intake was associated with increased risk of CVD mortality in women (HR 1.84, 95% CI 1.20–2.82). Low beef intake decreased the risk of CVD mortality in men (HR 0.58, 95% CI 0.40–0.84), but roasted pork increased cancer mortality in women (HR 1.26, 95% CI 1.05–1.52).ConclusionThere was increased risk of all-cause mortality associated with intake of processed red meat in men and women, increased risk of all-cause and cancer mortality with intake of organ meat in women, and increased risk of cancer mortality with intake of roasted pork intake in women. High intake of pork belly increased the risk of CVD mortality in women, but moderate intake was inversely associated with mortality from all-causes in both men and women.

Aim: To investigate the association between periodontitis and edentulism with cardiovascular disease (CVD) and all-cause mortality. Methods: Baseline data of 506 subjects including 256 angiographically verified coronary artery disease patients and 250 matched participants in cardiovascular health from the Kuopio Oral Health and Heart study were collected from 1995–1996. Mortality data were accrued until May 31, 2015, and related to baseline periodontal health and edentulism, assessed as exposure and collected by means of clinical and radiographic examination by a single examiner. Cox proportional hazards regression models were fit using covariates such as age, gender, smoking, BMI, and education. The final sample size for the periodontitis models ranged from 358 to 376, while the edentate models included 413 to 503 subjects for CVD and all-cause mortality, respectively with no missing values in the predictor, confounders, and outcome. Results: The strongest association was found between edentulism and CVD and all-cause mortality (HR: 1.9 CVD, HR: 1.6all-cause; p < .01). Conclusions: Edentulism considered as a poor oral health marker was associated strongly with CVD mortality while periodontitis was not. [ABSTRACT FROM AUTHOR]

Background: Women with one lifetime singleton pregnancy have increased risk of cardiovascular disease (CVD) mortality compared with women who continue reproduction particularly if the pregnancy had complications. Women with twins have higher risk of pregnancy complications, but CVD mortality risk in women with twin pregnancies has not been fully described. Objectives: We estimated risk of long‐term CVD mortality in women with naturally conceived twins compared to women with singleton pregnancies, accounting for lifetime number of pregnancies and pregnancy complications. Methods: Using linked data from the Medical Birth Registry of Norway and the Norwegian Cause of Death Registry, we identified 974,892 women with first pregnancy registered between 1967 and 2013, followed to 2020. Adjusted hazard ratios (aHR) with 95% confidence intervals (CI) for maternal CVD mortality were estimated by Cox regression for various reproductive history (exposure categories): (1) Only one twin pregnancy, (2) Only one singleton pregnancy, (3) Only two singleton pregnancies, (4) A first twin pregnancy and continued reproduction, (5) A first singleton pregnancy and twins in later reproduction and (6) Three singleton pregnancies (the referent group). Exposure categories were also stratified by pregnancy complications (pre‐eclampsia, preterm delivery or perinatal loss). Results: Women with one lifetime pregnancy, twin or singleton, had increased risk of CVD mortality (adjusted hazard [HR] 1.72, 95% confidence interval [CI] 1.21, 2.43 and aHR 1.92, 95% CI 1.78, 2.07, respectively), compared with the referent of three singleton pregnancies. The hazard ratios for CVD mortality among women with one lifetime pregnancy with any complication were 2.36 (95% CI 1.49, 3.71) and 3.56 (95% CI 3.12, 4.06) for twins and singletons, respectively. Conclusions: Women with only one pregnancy, twin or singleton, had increased long‐term CVD mortality, however highest in women with singletons. In addition, twin mothers who continued reproduction had similar CVD mortality compared to women with three singleton pregnancies. [ABSTRACT FROM AUTHOR]

The association between intakes of riboflavin and mortality has not been examined intensively in general populations. In this study, 10,480 adults in the 2005–2016 National Health and Nutrition Examination Survey (NHANES) were followed-up until 2019 for their vital status. Riboflavin and folate were assessed by two-day 24 h recall. The date and cause of death were obtained from the US Mortality Registry. The risks of all-cause mortality and cardiovascular disease (CVD) mortality were investigated using a Cox regression analysis. During a mean of 8.5 years follow-up, there were 1214 deaths registered (including 373 deaths from CVD and 302 from cancer). Compared to low level (quartile 1, Q1) of riboflavin intake, the hazard ratios (HRs) (95% confidence interval (CI)) for high level (quartile 4, Q4) were 0.53 (0.31–0.90) for CVD mortality and 0.62 (0.48–0.81) for all-cause mortality. The inverse association between riboflavin intake and CVD mortality was only significant among those with a high intake of folate (p for interaction 0.045). Those with a high folate intake (Q4) and low intake of riboflavin (Q1) had the highest risk of CVD mortality (HR 4.38, 95% CI 1.79–10.72), as compared with a high intake of both riboflavin and folate. In conclusion, riboflavin intake was inversely associated with all-cause mortality and CVD mortality, and the association was modified by folate intake. [ABSTRACT FROM AUTHOR]

Abstract Background Plasticizers, also called phthalates, are a group of chemicals widely used in daily life. A previous report showed no significant association between phthalate metabolite concentrations and mortality. We investigated the association of urinary phthalate levels and individual phthalate metabolite levels with all-cause and cardiovascular disease (CVD) mortality after standardizing the phthalate concentration. Methods A total of 6,625 participants were recruited from a nationally representative sample of adults aged 40 years or older who were enrolled in the National Health and Nutrition Examination Survey (NHANES) between 2003 and 2014 and were followed up through December 31, 2015. Data were analyzed from January 2021 to June 2021. NHANES-linked updated National Death Index public access files were used to acquire information on mortality status and cause of death. The present study conducted extended follow-up of an earlier analysis. Cox proportional hazard models were performed to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs) of covariate-adjusted creatinine standardization urinary phthalate concentrations with all-cause and CVD mortality after adjusting for demographics, lifestyle factors and comorbidity variables. Results The mean ± standard deviation age of all participants in the final study was 59.9±12.6 years old, and 49.6% of the participants were male. The median follow-up time was 73 months (range 1-157 months). At the censoring date of December 31, 2015, 3,023 participants were identified as deceased (13.4%). A fully adjusted Cox model showed that a urinary di(2-ethylhexyl) phthalate (DEHP) concentration >= 83.4 ng/mL was associated with a slight increase in all-cause mortality (HR 1.27, 95% CI 1.03, 1.57, P for trend= 0.014) and CVD mortality (HR 2.19, 95% CI 1.35, 3.54, P for trend= 0.002). Similarly, urinary mono-2-ethyl-5-carboxypentyl phthalate (MECPP) levels >= 39.2 ng/mL were associated with increased CVD mortality (HR 2.33, 95% CI 1.45, 3.73, P for trend < 0.001). Restricted cubic spline analyses suggested linear associations of DEHP and MECPP levels with all-cause and CVD mortality. Conclusion In this large nationally representative sample of American adults, high urinary DEHP and MECPP were significantly associated with all-cause and CVD mortality after adjusting for demographics, lifestyle factors and comorbidity variables.

Objective: A systematic analysis was conducted to determine the relationship between a plant-based diet and all-cause mortality., Methods: The PubMed, Embase and Web of Science databases were searched. Two authors selected English documents from the database. Then the other two authors extracted the data and evaluated the Newcastle-Ottawa Scale (NOS). This study adhered to the guidelines of the Preferred Reporting Project (PRISMA) and the PROSPERO Registry protocols. A mixed-effects model combined maximum adjusted estimates, with heterogeneity measured using the I 2 statistic. The sensitivity analysis validated the analysis's robustness, while publication bias was assessed., Results: The results of the meta-analysis of 14 articles revealed that a plant-based diet (PDI) can reduce cancer mortality (RR = 0.88, [95% CI 0.79-0.98], τ 2 : 0.02, I 2 : 84.71%), cardiovascular disease (CVD) mortality (RR = 0.81, [95% CI 0.76-0.86], τ 2 : 0.00, I 2 : 49.25%) and mortality (RR = 0.84, [95% CI 0.79-0.89], τ 2 : 0.01, I 2 : 81.99%) risk. Adherence to a healthy plant-based diet (hPDI) was negatively correlated with cancer mortality (RR = 0.91, [95% CI 0.83-0.99], τ 2 :0.01, I 2 :85.61%), CVD mortality (RR = 0.85, [95% CI 0.77-0.94], τ 2 : 0.02, I 2 : 85.13%) and mortality (RR = 0.85, [95% CI 0.80-0.90], τ 2 : 0.01, I 2 : 89.83%). An unhealthy plant-based diet (uPDI) was positively correlated with CVD mortality (RR = 1.19, [95% CI 1.07-1.32], τ 2 : 0.02, I 2 : 80.03%) and mortality (RR = 1.18, [95% CI 1.09-1.27], τ 2 : 0.01, I 2 : 89.97%) and had a certain correlation with cancer mortality (RR = 1.10, [95% CI 0.97-1.26], τ 2 : 0.03, I 2 : 93.11%). Sensitivity analysis showed no contradictory results., Conclusion: The hPDI was negatively associated with all-cause mortality, and the uPDI was positively associated with all-cause mortality., Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/#loginpage., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Tan, Zhang, Jiang, Li and Yang.)

Background: High blood pressure (BP) induces left atrial structural and functional remodeling that increases susceptibility to atrial arrhythmia. We hypothesized that lower systolic BP (SBP) levels are associated with a lower prevalence of premature atrial contractions (PACs) in patients with hypertension., Methods: This analysis included 4,697 participants (mean age 62±13.1 years, 50% women, 25.6% blacks) with hypertension from the Third National Health and Nutrition Examination Survey who did not have a prior history of cardiovascular disease (CVD). Multivariable logistic regression was used to examine the cross-sectional association between SBP and prevalence of PACs ascertained from 12-lead resting electrocardiograms. Multivariable Cox proportional hazard analysis was used to examine the association between baseline PACs and CVD mortality., Results: Approximately 1.6% (n=74) of participants had baseline PACs. Patients with SBP ≤140 mmHg had a lower prevalence of PACs than those with SBP ≥140 mmHg (1.1% vs. 1.9%, p-value=0.01). In a multivariable logistic regression model, each 10 mmHg decrease in SBP was associated with a 12% lower odds of PACs (OR (95%CI): 0.88 (0.77-0.99)). During 14 years of follow-up, 645 CVD deaths occurred. In a multivariable-adjusted Cox model, presence of PACs was associated with a 78% increased risk of CVD mortality (HR (95%CI): 1.78 (1.23-2.60))., Conclusions: In patients with hypertension, lower SBP levels are associated with a lower prevalence of PACs, and presence of PACs is associated with a higher risk of CVD mortality risk. These findings highlight the potential role of BP lowering in the management of cardiac arrhythmias., Competing Interests: Declaration of competing interest None declared., (Copyright © 2024 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Aims: Recognizing the rising concern of environmental impacts on health, the study aims to explore how specific environmental factors such as air pollution, humidity, and temperature variations contribute to the prevalence of cardiovascular disease (CVD) mortality, emphasizing the role of air quality, climate variables, and lifestyle factors in the disease mortality specifically., Methods and Results: Analysis of province-level data on CVD mortality in Turkey from 2010 to 2019, assessing the correlations with environmental and lifestyle factors like particulate matter, sulfur dioxide, meteorological variables, and smoking and alcohol consumption. The study employs the SAS TRAJ procedure and Ordinal Logistic Regression for statistical analysis. The multiplicity correction was done through Benjamini-Hoechberg false discovery rate (FDR) approach. As expected, both smoking and alcohol consumption were found to be significantly associated with CVD mortality (odds ratio (OR): 1.10, 95% CI: 1.08, 1.11, P-value < 0.0001). While median Air Pressure and Humidity were among the most significant markers with OR of 1.10 indicating an increasing CVD mortality, their variability metrics such as coefficient of variation (CV) showed significant protective effects with OR of 0.37 and 0.89, respectively. Temperature and its variability seemed to be protective overall., Conclusions: Our research highlights the significant influence of environmental factors on cardiovascular health, especially air pressure and humidity, beyond the known factors such as smoking and alcohol consumption. These findings suggest the need for comprehensive public health strategies that address both environmental and lifestyle risk factors to effectively reduce the burden of cardiovascular diseases., (© 2024 The Author(s). ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

BackgroundCurrent studies on the protective effects of dietary spermidine (SPD) on cardiovascular disease (CVD) are mainly limited to animal studies, and the relationship between dietary SPD and CVD mortality remains inconclusive.ObjectiveThis study aims to evaluate the association between dietary SPD intake and CVD and all-cause mortality.MethodsA total of 23,894 people enrolled in the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2014 were recruited for this study. The dietary intake of SPD from 11 specific food origins and total SPD was categorized into tertiles or quartiles. Cox proportional hazard regression models were developed to evaluate the association of SPD intake with CVD and all-cause mortalities.ResultsAmong the 23,894 participants, 2,365 deaths, including 736 deaths due to CVD, were documented. After adjustment for potential confounders, compared with participants in the lowest quartile, participants in the highest quartile of total SPD had a significantly lower risk of CVD mortality (HR = 0.68, 95% CI: 0.51–0.91) and all-cause mortality (HR = 0.70, 95% CI: 0.60–0.82); participants in the highest tertiles or quartiles of vegetable-derived SPD, cereal-derived SPD, legume-derived SPD, nut-derived SPD, and cheese-derived SPD had a lower risk of CVD mortality (HR vegetable − derivedSPD = 0.68, 95% CI: 0.54–0.86; HR cereal − derivedSPD = 0.75, 95% CI: 0.57–0.97; HR legume − derivedSPD = 0.68, 95% CI: 0.52–0.88; HR nut − derivedSPD = 0.66, 95% CI: 0.53–0.80; HR cheese − derivedSPD = 0.68, 95% CI: 0.52–0.88) and all-cause mortality (HR vegetable − derivedSPD = 0.73, 95% CI: 0.64–0.84; HR cereal − derivedSPD = 0.80, 95% CI: 0.69–0.93; HR legume − derivedSPD = 0.70, 95% CI: 0.60–0.80;HR nut − derivedSPD = 0.72, 95% CI: 0.64–0.81; HR cheese − derivedSPD = 0.70, 95% CI: 0.61–0.81) than those in the lowest tertiles or quartiles. Moreover, subgroup analysis showed consistent associations among the people with hypertension and hyperlipidemia.ConclusionHigher intake of dietary SPD is associated with decreased risk of CVD and all-cause mortality, and among specific food origin SPD, SPD derived from vegetables, cereals, legumes, nuts, and cheese was associated with reduced CVD and all-cause mortality.

Background Understanding the genetic predisposition to cardiovascular disease (CVD) may help to improve clinical intervention strategies. Lifestyle factors, such as diet, may differ among ethnic groups and may, in turn, modify individuals' risks to diseases. Objectives We examined the genetic predisposition to ever smoking in relation to CVD mortality and assessed whether such an association could be modified by dietary intake. Methods A total of 23,760 Chinese adults from the Singapore Chinese Heath Study who were free of cancer and CVD at recruitment (1993–1998) were included in the study. A weighted genetic risk score (wGRS) was calculated to define the genetically determined regular smoking behavior (never or ever). Multivariable-adjusted Cox regression models were used to assess the association between the wGRS and CVD mortality. We also conducted a 1-sample Mendelian randomization analysis for ever smoking and CVD mortality. Results Over a mean of 22.6 years of follow-up, 2301 CVD deaths were identified. A genetic predisposition to ever smoking was significantly associated with CVD mortality; the multivariable-adjusted HR of CVD mortality was 1.07 (95% CI: 1.03–1.12), with a per-SD increment in the wGRS. However, the Mendelian randomization analysis did not support a causal relationship between ever smoking and CVD mortality (OR, 1.13; 95% CI: 0.87–1.45). Additionally, the Dietary Approaches to Stop Hypertension (DASH) score significantly modified the association between the smoking wGRS and CVD mortality; the association between a genetic predisposition to smoking and CVD mortality was only observed among individuals with a low DASH score (P- interaction = 0.004). Conclusions A genetic predisposition to smoking was associated with CVD mortality in the Chinese population. In addition, we detected a significant interaction showing higher CVD mortality related to genetically determined smoking among those with lower DASH scores. [ABSTRACT FROM AUTHOR]

Objectives: To study the role of high R waves predicting cardiovascular (CVD) and all-cause mortality in a male middle-aged population followed-up 45 years.Material and Methods: A total of 7985 CVD-free men aged 40-59 years were enrolled in 13 cohorts in seven countries (USA, Finland, the Netherlands, Italy, Serbia, Greece, Japan) and high R waves were classified by Minnesota Code 3.1 (as a dichotomous variable) from baseline resting otherwise normal ECG at entry examination together with other personal characteristics. Cox models were solved to detect the possible predictive role of high R waves for CVD and all-cause mortality.Results: In Cox models high R waves were predictive of 45-year major CVD deaths with a hazard ratio of 1.17 (95% confidence intervals of 1.03-1.33) after adjustment for 6 major CVD risk factors (age, systolic blood pressure, serum cholesterol, cigarette smoking, physical activity and body mass index). The predictive role of high R wave was less evident for 45-year all-cause mortality and after adjustment for the 6 covariates the HR of high R wave lost its significance. A multiple logistic model indicated that body mass index, serum cholesterol, systolic blood pressure and mainly vigorous physical activity were directly related to high R wave prevalence while heart rate, subscapular skinfold, laterality index and shoulder pelvis shape did so in an inverse way.Conclusion: High R waves seem associated with an excess CVD mortality in a 45-year follow-up of middle-aged men, while their role is diluted when the end-point is all-cause mortality. [ABSTRACT FROM AUTHOR]

Aims: This study aims to investigate whether food intake time across 3 meals is associated with long-term survival among the people with diabetes. Materials and Methods: This study included 4642 diabetic patients participating in the National Health and Nutrition Examination Survey from 2003 to 2014. Food consumed across a day including the forenoon, afternoon, and evening was divided into quantiles based on their distribution. Cox proportional hazards regression models were used to analyze the survival relationship between food intakes time and mortality. Results: In the forenoon, compared to the participants in the lowest quantile of potato and starchy vegetable, participants in the highest quantile had lower mortality risk of cardiovascular disease (CVD) [hazard ratio (HR)potato = 0.46, 95% CI 0.24-0.89; HRstarchy-vegetable = 0.32, 95% CI 0.15-0.72]. In the afternoon, participants who consumed whole grain had lower mortality of CVD (HRwhole grain = 0.67, 95% CI 0.48-0.95). In the evening, the highest quantile of dark vegetable and milk intake is related to lower mortality risk of CVD (HRdark vegetable = 0.55, 95% CI 0.35-0.87; HRmilk = 0.56, 95% CI 0.36-0.88) and all-cause mortality (HRmilk = 0.71, 95% CI 0.54-0.92), whereas participants in the highest quantile of intakes of processed meat are more likely to die due to CVD (HRprocessed-meat = 1.74, 95% CI 1.07-2.82). Isocalorically switching 0.1 serving potato or starchy vegetable consumed in the afternoon or evening to the forenoon, 0.1 serving dark vegetable consumed in the afternoon to the evening, and 0.1 serving whole grain consumed in the forenoon to the afternoon reduced the risk of CVD mortality. Conclusions: Higher intake of potato or starchy vegetable in forenoon, whole grain in the afternoon, and dark vegetable and milk in the evening and lower intake of processed meat in the evening was associated with better long-term survival in people with diabetes. [ABSTRACT FROM AUTHOR]

Background: The association between osteocalcin and mortality has been scantly studied. We aimed to investigate the association between osteocalcin along with its trajectories and mortality based on long-term longitudinal data. Methods: We performed a retrospective cohort study of 9413 type 2 diabetic patients with at least three measurements of total serum osteocalcin within 3 years since their first inpatient diagnosis of type 2 diabetes. Baseline, mean values of osteocalcin levels and their trajectories were used as exposures. A multivariable-adjusted Cox proportional hazards model was used to estimate the association of osteocalcin levels and their trajectories with mortality. Results: During a mean follow-up of 5.37 years, 1638 patients died, of whom 588 were due to cardiovascular events. Multivariable-adjusted hazard ratios (HRs) across quintiles of baseline osteocalcin levels were 2.88 (95% confidence interval (CI) 2.42–3.42), 1.65 (95% CI 1.37–1.99), 1.17 (95% CI 0.96–1.42), 1.00, and 1.92 (95% CI 1.60–2.30) for all-cause mortality, and 3.52 (95% CI 2.63–4.71), 2.00 (95% CI 1.46–2.73), 1.03 (95% CI 0.72–1.47), 1.00, 1.67 (95% CI 1.21–2.31) for CVD mortality, respectively. When we used the mean values of osteocalcin as the exposure, U-shaped associations were also found. These U-shaped associations were consistent among patients of different baseline characteristics. Patients with a stable or even increasing trajectory of osteocalcin may have a lower risk of both all-cause and CVD mortality. Conclusions: A U-shape association between baseline osteocalcin and mortality was observed among patients with type 2 diabetes. Patients with lower levels of serum osteocalcin during follow-ups had higher risks for all-cause and cardiovascular mortality. [ABSTRACT FROM AUTHOR]