Serum Homocysteine Levels and All-Cause and Cause-Specific Mortality in Korean Adult Men: A Cohort Study
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SUBMITTER: Kim M
PROVIDER: S-EPMC11357046 | biostudies-literature | 2024 Aug
REPOSITORIES: biostudies-literature
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Project description:Erythritol occurs naturally in some fruits and fermented foods, and has also been used as an artificial sweetener since the 1990s. Although there have been questions and some studies regarding its potential adverse health effects, the association between serum erythritol and long-term mortality has not been evaluated. To examine the association between serum erythritol's biochemical status and risk of overall and cause-specific mortality, a prospective cohort analysis was conducted using participants in the ATBC Study (1985-1993) previously selected for metabolomic sub-studies. The analysis included 4468 participants, among whom 3377 deaths occurred during an average of 19.1 years of follow-up. Serum erythritol was assayed using an untargeted, global, high-resolution, accurate-mass platform of ultra-high-performance liquid and gas chromatography. Cause-specific deaths were identified through Statistics Finland and defined by the International Classification of Diseases. After adjustment for potential confounders, serum erythritol was associated with increased risk of overall mortality (HR = 1.50 [95% CI = 1.17-1.92]). We found a positive association between serum erythritol and cardiovascular disease mortality risk (HR = 1.86 [95% CI = 1.18-2.94]), which was stronger for heart disease mortality than for stroke mortality risk (HR = 3.03 [95% CI = 1.00-9.17] and HR = 2.06 [95% CI = 0.72-5.90], respectively). Cancer mortality risk was also positively associated with erythritol (HR = 1.54 [95% CI = 1.09-2.19]). The serum erythritol-overall mortality risk association was stronger in men ≥ 55 years of age and those with diastolic blood pressure ≥ 88 mm Hg (p for interactions 0.045 and 0.01, respectively). Our study suggests that elevated serum erythritol is associated with increased risk of overall, cardiovascular disease, and cancer mortality. Additional studies clarifying the role of endogenous production and dietary/beverage intake of erythritol in human health and mortality are warranted.
| S-EPMC11434845 | biostudies-literature
Project description:BackgroundThe liver plays critical roles in human health. Circulating level of liver function biomarkers may associate with the long-term and short-term mortality in general population.MethodsWe used data from US National Health and Nutrition Examination Survey 1988-94 and 1999-2014. People aged ≥ 20 years with measured serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), alkaline phosphatase (ALP), total bilirubin (TB), and albumin (ALB) at baseline were included. All-cause and cause-specific mortality was identified from the National Death Index through 31 December 2015. Additive Cox regression models were applied to assess the correlation patterns between the serum level of these analytes and mortality risk.ResultsA total of 44,508 participants were included; among them, 9,721 deaths occurred during a mean follow-up of 12.5 years. A "J-shaped" correlation was found between serum levels of ALT, AST, and TB and all-cause mortality. The risk of mortality monotonically increased with increasing GGT and ALP levels when their levels exceeded the valley points. A "L-shaped" correlation was found between the serum level of ALB and all-cause mortality. The correlation patterns were comparable among deaths from different causes and were consistent in subgroup and sensitivity analyses. While the integration of all six liver function biomarkers did not yield an optimal predictive performance for mortality (area under ROC curve = 0.706), it demonstrated a significantly better performance compared to any single biomarker..ConclusionCirculating liver function biomarkers showed diverse nonlinear correlations with mortality and may be utilized as part of a screening process to help identify individuals who may be at elevated risk of mortality.
| S-EPMC11600561 | biostudies-literature
Project description:Hyperphosphatemia has been associated with increased mortality in chronic kidney disease but the nature of such a relation in the general population is unclear. To investigate the association between phosphate (P) levels and all-cause and cause-specific mortality, we assessed two cohorts from the Rotterdam Study, with follow-up of 14.5 (RS-I) and 10.9 (RS-II) years until January 2012 with availability of fasting phosphate levels. Deaths were classified according to International Classification of Diseases into 7 groups: cardiovascular, cancer, infections, external, dementia, chronic lung diseases and other causes. Sex-stratified Weibull and competing-risks models were adjusted for age, BMI and smoking. Hazard ratios are expressed per 1 mg/dL increase in phosphate levels. The total number of participants included 3731 (RS-I, 2154 women) and 2494 (RS-II, 1361 women) subjects. The main outcome measures were all-cause and cause-specific mortality. A significant positive association was found between phosphate and all-cause mortality in men (pooled HR (95% CI): 1.46 (1.26-1.69)) but not in women (0.90 (0.77-1.05)). In men, higher phosphate increased the risk for cardiovascular mortality (1.66 (1.29-2.14)), other causes (1.67 (1.16-2.40)) and chronic lung disease mortality (1.94 (1.02-3.72)), the latter driven by mortality due to chronic obstructive pulmonary disease (COPD) (4.44 (2.08-9.49)). No relations were found for mortality due to infections, cancer, dementia or external causes. In conclusion, serum P is associated with increased all-cause, cardiovascular and COPD mortality in men but not women. The association with COPD mortality is novel and needs further research on underlying mechanisms.
| S-EPMC6133003 | biostudies-literature
Project description:BackgroundHomocysteine (Hcy) was implicated in oxidative stress and diabetes biologically. However, the clinical evidence on the link between Hcy level and diabetes is limited and controversial. This study is aimed at investigating the association of serum Hcy with all-cause and cardiovascular mortality in diabetic patients.MethodsSerum Hcy was measured among 2,286 adults with type 2 diabetes in NHANES 1999-2006. Cox proportional hazard regression was used to estimate hazard ratios (HR) and 95% CIs for the association of Hcy with all-cause and cause-specific mortality.ResultsOver a median follow-up of 11.0 (interquartile range, 8.9-13.4) years, 952 of the 2286 patients with diabetes died, covering 269 (28.3%) cardiovascular deaths and 144 (15.2%) cancer deaths. Restricted cubic spline showed the linear relationship between Hcy and all-cause mortality risk. After multivariate adjustment, higher serum Hcy levels were independently associated with increased risk of all-cause and cardiovascular mortality. Compared with participants in the bottom tertile of Hcy, the multivariate-adjusted HRs and 95% CI for participants in the top quartile were 2.33 (1.64-3.30) for all-cause mortality (p trend < 0.001), 2.24 (1.22-4.10) for CVD mortality (p trend = 0.017), and 2.05 (0.90-4.69) for cancer mortality (p trend = 0.096). The association with total mortality was especially stronger among patients with albuminuria. Serum Hcy significantly improved reclassification for 10-year mortality in diabetic patients (net reclassification index = 0.253 and integrated discrimination improvement = 0.011).ConclusionsSerum Hcy was associated with risks of all-cause and cardiovascular mortality in diabetic adults. Our results suggested that Hcy was a promising biomarker in risk stratification among diabetic patients.
| S-EPMC9578792 | biostudies-literature
Project description:BackgroundThe most effective way to halt the advancement of COPD is smoking cessation. However, limited data are available on the question of whether quitting smoking within two years after COPD diagnosis reduces the risk of mortality. The goal of our research was to analyze the relationship between quitting smoking after COPD diagnosis and the risks of all-cause and cause-specific mortality, using the Korean National Health Insurance Service (NHIS) database.MethodsThis study included 1,740 male COPD patients aged 40 years or more who had been newly diagnosed within the 2003-2014 time period and had smoked prior to their COPD diagnosis. The patients were categorized into two groups according to their smoking status after COPD diagnosis: (i) persistent smokers (ii) quitters (smoking cessation within two years of COPD diagnosis). Multivariate Cox proportional hazard regression was performed to determine the adjusted hazard ratio (HR) and 95% confidence interval (CI) for both all-cause and cause-specific mortality.ResultsAmong 1,740 patients (mean age, 64.6 years; mean follow-up duration, 7.6 years), 30.5% stopped smoking after COPD diagnosis. Quitters gained a 17% risk reduction in all-cause mortality (aHR, 0.83; 95% CI, 0.69-1.00) and a 44% risk reduction in cardiovascular mortality (aHR, 0.56; 95% CI, 0.33-0.95) compared with persistent smokers.ConclusionOur study found that patients who quit smoking within two years after COPD diagnosis had lower risks of all-cause and cardiovascular mortality relative to persistent smokers. These results can be used to encourage newly diagnosed COPD patients to stop smoking.
| S-EPMC10316560 | biostudies-literature
Project description:Unlike hemodialysis (HD), peritoneal dialysis (PD) is a continuous therapy and does not induce myocardial stunning. Yet, the death risk in HD and PD patients is similar. This study tested the hypothesis that serum potassium abnormalities contribute more to the death risk in PD patients than in HD patients.Data from patients treated in DaVita facilities between July 1, 2001 and June 30, 2006 (n=10,468 PD patients; n=111,651 HD patients) were used to determine association of serum potassium with mortality.PD patients were significantly more likely to have serum potassium < 4 mEq/L, with an adjusted odds ratio of 3.30 (95% confidence interval [95% CI], 3.05, 3.56). There was a U-shaped relationship between time-averaged serum potassium and all-cause and cardiovascular mortality of PD patients, with adjusted hazards ratios of 1.51 for all-cause mortality for potassium < 3.5 mEq/L (95% CI, 1.29, 1.76) and 1.52 for potassium ? 5.5 mEq/L (95% CI, 1.32, 1.75). The population-attributable risks for all-cause mortality for serum potassium < 4.0 and ? 5.5 mEq/L were 3.6% and 1.9%, respectively, in PD patients, and 0.8% and 1.5%, respectively, in HD patients.Abnormalities in serum potassium contribute disproportionately to the high death risk in PD patients. This may, in part, account for the equivalent cardiac risk seen with the two therapies.
| S-EPMC3408121 | biostudies-literature
Project description:ObjectivesPrevious studies have reported controversial findings regarding the association of testosterone with mortality in older men. This heterogeneity might be partially explained by comorbidities and the presence of metabolic syndrome, as well as differential associations according to causes of death.MethodsWe used data from a random subsample of the Three-City study, in which hormone levels were measured in 338 men ≥65 years without metabolic syndrome who were followed-up for 12 years. Vital status was determined for all participants from different sources. We used inverse-probability-weighted Cox regression to estimate the hazard ratios (HRs) of cause-specific mortality and 95% confidence intervals (CIs).ResultsOver the follow-up period, 130 men died (30 from cardiovascular disease, 45 from cancer, 55 from other causes). The association of testosterone with mortality showed significant heterogeneity across causes of death (p=0.027 and p=0.022 for total and bioavailable testosterone, respectively). Higher testosterone levels were associated with increased cardiovascular mortality (HR for 1-standard deviation increase, 1.86; 95% CI, 1.28 to 2.71 and 1.50; 95% CI, 1.04 to 2.17 for total and bioavailable testosterone, respectively). By contrast, there were no significant associations of testosterone with mortality from cancer and other causes.ConclusionsOur data suggest that the association of testosterone with mortality in men without metabolic syndrome might be differential according to the cause of death. These findings may partially explain the heterogeneity across studies on the relationship between testosterone levels and mortality.
| S-EPMC7644941 | biostudies-literature
Project description:ImportanceThe associations of levels of diverse serum carotenoids ascertained via repeated measurements with all-cause, cancer, and cardiovascular disease (CVD) mortality risk have not been considered in previous prospective studies.ObjectiveTo investigate the association between repeated measurement of serum carotenoid levels and all-cause and cause-specific mortality risk.Design, setting, and participantsThis cohort study's baseline data were collected using information from physical examinations from 1990 to 1999. Eligible participants were followed up until December 2017, with a median (interquartile range) follow-up period of 22.3 (15.5-25.3) years. Included individuals were age 40 years or older at the baseline data collection, were residents of the study site in the town of Yakumo, Hokkaido, Japan, and participated in a physical examination at least once from 1990 to 1999. Among eligible participants, after excluding 332 individuals, 3116 individuals were included in the analysis. Data analysis was conducted in April 2020.ExposuresRepeated measurements of 6 serum carotenoid levels and 4 associated indices.Main outcomes and measuresAll-cause, cancer, and CVD mortality, categorized by International Classification of Diseases, Ninth Revision and International Statistical Classification of Diseases and Related Health Problems, Tenth Revision codes, were recorded. A time-dependent Cox regression model was performed to examine associations between time-varying serum carotenoid levels and mortality.ResultsAmong 3116 individuals who received physical examinations, the mean (SD) age was 54.7 (10.6) years and 1883 (60.4%) were women. During the follow-up period, 762 deaths from all causes, 253 deaths from cancer, and 210 deaths from CVD were ascertained. In a time-dependent Cox regression analysis, for every 25% higher serum levels of total carotenoids, risks were statistically significantly lower for all-cause mortality (hazard ratio [HR], 0.85; 95% CI, 0.82-0.87; P < .001), cancer mortality (HR, 0.82; 95% CI, 0.78-0.87; P < .001), and CVD mortality (HR, 0.86; 95% CI, 0.81-0.91; P < .001). Using only baseline measures, for every 25% higher serum levels of total carotenoids, risks were also statistically significantly lower for all-cause mortality (HR, 0.92; 95% CI, 0.89-0.95; P < .001), cancer mortality (HR, 0.87; 95% CI, 0.83-0.93; P < .001), and CVD mortality (HR, 0.93; 95% CI, 0.88-0.99; P = .03) but with larger HRs than those associated with repeated measurements.Conclusions and relevanceThis study found that higher levels of serum carotenoids in analysis using repeated measurements were associated with significantly lower all-cause and cause-specific mortality over a follow-up period of 25 years.
| S-EPMC8196342 | biostudies-literature
Project description:ObjectiveTo investigate the association of predicted lean body mass, fat mass, and body mass index (BMI) with all cause and cause specific mortality in men.DesignProspective cohort study.SettingHealth professionals in the United States PARTICIPANTS: 38 006 men (aged 40-75 years) from the Health Professionals Follow-up Study, followed up for death (1987-2012).Main outcome measuresAll cause and cause specific mortality.ResultsUsing validated anthropometric prediction equations previously developed from the National Health and Nutrition Examination Survey, lean body mass and fat mass were estimated for all participants. During a mean of 21.4 years of follow-up, 12 356 deaths were identified. A J shaped association was consistently observed between BMI and all cause mortality. Multivariable adjusted Cox models including predicted fat mass and lean body mass showed a strong positive monotonic association between predicted fat mass and all cause mortality. Compared with those in the lowest fifth of predicted fat mass, men in the highest fifth had a hazard ratio of 1.35 (95% confidence interval 1.26 to 1.46) for mortality from all causes. In contrast, a U shaped association was found between predicted lean body mass and all cause mortality. Compared with those in the lowest fifth of predicted lean body mass, men in the second to fourth fifths had 8-10% lower risk of mortality from all causes. In the restricted cubic spline models, the risk of all cause mortality was relatively flat until 21 kg of predicted fat mass and increased rapidly afterwards, with a hazard ratio of 1.22 (1.18 to 1.26) per standard deviation. For predicted lean body mass, a large reduction of the risk was seen within the lower range until 56 kg, with a hazard ratio of 0.87 (0.82 to 0.92) per standard deviation, which increased thereafter (P for non-linearity <0.001). For cause specific mortality, men in the highest fifth of predicted fat mass had hazard ratios of 1.67 (1.47 to 1.89) for cardiovascular disease, 1.24 (1.09 to 1.43) for cancer, and 1.26 (0.97 to 1.64) for respiratory disease. On the other hand, a U shaped association was found between predicted lean body mass and mortality from cardiovascular disease and cancer. However, a strong inverse association existed between predicted lean body mass and mortality from respiratory disease (P for trend <0.001).ConclusionsThe shape of the association between BMI and mortality was determined by the relation between two body components (lean body mass and fat mass) and mortality. This finding suggests that the "obesity paradox" controversy may be largely explained by low lean body mass, rather than low fat mass, in the lower range of BMI.
| S-EPMC6028901 | biostudies-literature
Project description:BackgroundIncreasing mortality among men from drugs, alcohol and suicides is a growing public health concern in many countries. Collectively known as "deaths of despair", they are seen to stem from unprecedented economic pressures and a breakdown in social support structures.MethodsWe use high-quality population wide Scottish data to calculate directly age-standardized mortality rates for men aged 15-44 between 1980 and 2018 for 15 leading causes of mortality. Absolute and relative inequalities in mortality by cause are calculated using small-area deprivation and the slope and relative indices of inequality (SII and RIIL) for the years 2001-2018.ResultsSince 1980 there have been only small reductions in mortality among men aged 15-44 in Scotland. In that period drug-related deaths have increased from 1.2 (95% CI 0.7-1.4) to 44.9 (95% CI 42.5-47.4) deaths per 100,000 and are now the leading cause of mortality. Between 2001 and 2018 there have been small reductions in absolute but not in relative inequalities in all-cause mortality. However, absolute inequalities in mortality from drugs have doubled from SII = 66.6 (95% CI 61.5-70.9) in 2001-2003 to SII = 120.0 (95% CI 113.3-126.8) in 2016-2018. Drugs are the main contributor to inequalities in mortality, and together with alcohol harm and suicides make up 65% of absolute inequalities in mortality.ConclusionsContrary to the substantial reductions in mortality across all ages in the past decades, deaths among young men are increasing from preventable causes. Attempts to reduce external causes of mortality have focused on a single cause of death and not been effective in reducing mortality or inequalities in mortality from external causes in the long-run. To reduce deaths of despair, action should be taken to address social determinants of health and reduce socioeconomic inequalities.
| S-EPMC7716282 | biostudies-literature