Association between glycemic status and all-cause mortality among individuals with dementia: a nationwide cohort study
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SUBMITTER: Huh Y
PROVIDER: S-EPMC11340194 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
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Project description:Background and aimsBoth fasting and non-fasting levels of triglyceride have been shown positively associated with all-cause mortality. It is unknown whether fasting status modifies this association. This study aimed to address this question.MethodsThis study included 34,512 US adults (27,036 fasting and 7476 nonfasting participants). All-cause mortality was ascertained by linkage to the National Death Index records. Cox proportional hazards models were used to estimate hazard ratios of triglyceride for mortality.ResultsThis cohort was followed up for a mean of 13.0 years. During the follow-up, 8491 all-cause deaths were recorded. A 1-natural-log-unit increase in triglyceride was associated with an 8% higher multivariate-adjusted risk of all-cause mortality. Interaction analyses showed that fasting status interacted with triglyceride in predicting all-cause mortality. Sub-analyses showed that a 1-natural-log-unit increase in triglyceride was associated with a 17% higher multivariate-adjusted risk of all-cause mortality in the nonfasting subcohort; however, there lacked such an association in the fasting sub-cohort. Similarly, high (200-499 mg/dL) and very high levels of triglyceride (≥500 mg/dL) were associated with higher all-cause mortality risks compared with low normal triglyceride (<100 mg/dL) only in the nonfasting subcohort.ConclusionThis study found that, compared to fasting triglyceride, nonfasting triglyceride was more sensitive in predicting all-cause mortality. This study supports the initiatives by some guidelines to recommend the use of nonfasting triglycerides for risk assessment.
| S-EPMC9110781 | biostudies-literature
Project description:ObjectiveThe Estimated Glucose Disposal Rate (eGDR) serves as a surrogate marker for insulin resistance, with numerous studies highlighting its significant prognostic value. This paper aims to analyze the impact of eGDR on cardiovascular and all-cause mortality across different glycemic metabolic statuses, including normal fasting glucose (NFG), prediabetes, and diabetes.MethodsThis study included 46,016 American adults who underwent health examinations as part of the National Health and Nutrition Examination Survey from 1999 to 2018. Multivariable Cox regression was employed to explore the relationships between eGDR and mortality rates under varying glycemic states. Additionally, Kaplan-Meier curves were used to compare the cumulative incidence of cardiovascular and all-cause mortality across different metabolic statuses. Finally, the predictive value of eGDR for mortality was assessed using receiver operating characteristic curves.ResultsDuring an average follow-up of 115 months, a total of 6,906 (15.01%) participants experienced all-cause mortality, with 1,798 (3.91%) deaths attributed to cardiovascular causes. Kaplan-Meier analysis revealed that higher eGDR levels were associated with gradually reduced mortality rates. After adjusting for confounders, elevated eGDR levels were protective against both cardiovascular and all-cause mortality; the protective effect was notably stronger for cardiovascular mortality [Cardiovascular mortality hazard ratio: 0.92; All-cause mortality hazard ratio: 0.94]. Further interaction tests indicated that glycemic status significantly modified the protective effect of eGDR (P-interaction<0.0001); specifically, high eGDR conferred stronger protection against cardiovascular and all-cause mortality in individuals with NFG and prediabetes compared to those with diabetes. Receiver operating characteristic analysis suggested that eGDR had superior predictive value for mortality in the NFG and prediabetic populations compared to the diabetic group.ConclusioneGDR is a straightforward surrogate for insulin resistance, acting as a protective factor against cardiovascular and all-cause mortality in American adults, with glycemic status modifying this protective effect. Specifically, high eGDR levels offer stronger protection in individuals with NFG and prediabetes compared to those with diabetes; moreover, eGDR appears to be more suitable for predicting mortality events in the NFG and prediabetic populations.
| S-EPMC11790456 | biostudies-literature
Project description:Background and aimWe sought to determine the association between alanine aminotransferase (ALT) in the normal range and mortality in the absence of liver dysfunction to better understand ALT's clinical significance beyond liver injury and inflammation.MethodsA cohort of 2,708 male and 3,461 female adults aged 20-75 years without liver dysfunction (ALT<30 in males & <19 in females, negative viral serologies, negative ultrasound-based steatosis, no excess alcohol consumption) from the National Health and Nutrition Examination Survey (NHANES)-III (1988-1994) were linked to the National Death Index through December 31, 2015. Serum ALT levels were categorized into sex-specific quartiles (Females: <9, 9-11, 11-14, ≥14 IU/L, Male: <12, 12-15, 15-20, ≥20 U/L). The primary outcome was all-cause mortality. Hazard ratios (HRs) were estimated, adjusting for covariates and accounting for the complex survey design.ResultsRelative to males in the lowest quartile (Q1), males in the highest quartile (Q4) had 44% decreased risk of all-cause mortality (aHR [95% CI]: 0.56 [0.42, 0.74]). Females in Q4 had 45% decreased risk of all-cause mortality (aHR [95% CI]: 0.55 [0.40, 0.77]). Males with BMI <25 kg/m2 in Q4 had significantly lower risk of all-cause mortality than Q1; however, this association did not exist in males with BMI ≥25 (BMI<25: 0.36 [0.20, 0.64], BMI≥25: 0.77 [0.49, 1.22]). Risk of all-cause mortality was lower in males ≥50 years than in males<50 (age≥50: 0.55 [0.39, 0.77], age<50: 0.81 [0.39, 1.69]). These age- and BMI-related differences were not seen in females.ConclusionALT within the normal range was inversely associated with all-cause mortality in U.S. adults.
| S-EPMC7678955 | biostudies-literature
Project description:There have been conflicting results regarding the association between diabetes and the risk of hematologic malignancies, and its interaction with obesity is unknown. This study determined the risk of hematologic malignancies according to the glycemic status in a population-based study involving health screening 9,774,625 participants. The baseline glycemic status of the participants was categorized into no diabetes, impaired fasting glucose (IFG), newly detected diabetes, diabetes duration <5 years, and diabetes duration ≥5 year groups. The risks of overall and specific hematologic malignancies were estimated using a Cox regression analysis. During a median follow up of 7.3 years, 14,733 hematologic malignancies developed. The adjusted hazard ratio (aHR) for the risk of all the hematologic malignancies was 0.99 (95% confidence interval (CI) 0.95-1.02) for IFG, 0.99 (95% CI 0.91-1.08) for newly detected diabetes, 1.03 (95% CI 0.96-1.11) for diabetes duration <5 years, and 1.11 (95% CI 1.03, 1.20) for diabetes duration ≥5 year groups. The association was independent from obesity. The risk of non-Hodgkin's lymphoma (NHL) increased according to the progression of dysglycemia towards a longer diabetes duration, while Hodgkin's lymphoma did not. This study in Korea demonstrated diabetes to be associated with an increased risk of hematologic malignancies independent of obesity. The NHL risk increased with the diabetes duration.
| S-EPMC8507554 | biostudies-literature
Project description:BackgroundFew studies have analyzed the relationship between glucose variability (GV) and adverse health outcomes in patients with differences in glycemic status. The present study tests the hypothesis that GV predicts all-cause mortality regardless of glycemic status after simple adjustment (age and sex) and full adjustment (age, sex, cardiovascular disease, hypertension, use of aspirin, statins, GLP-1 receptor agonists, SGLT-2 inhibitors and DPP-4 inhibitors, baseline FPG and average HbA1c).MethodsProspective cohort study with 795 normoglycemic patients, 233 patients with prediabetes, and 4,102 patients with type 2 diabetes. GV was measured using the coefficient of variation of fasting plasma glucose (CV-FPG) over 12 years of follow-up. The outcome measure was all-cause mortality.ResultsA total of 1,223 patients (657 men, 566 women) died after a median of 9.8 years of follow-up, with an all-cause mortality rate of 23.35/1,000 person-years. In prediabetes or T2DM patients, the fourth quartile of CV-FPG exerted a significant effect on all-cause mortality after simple and full adjustment. A sensitivity analysis excluding participants who died during the first year of follow-up revealed the following results for the highest quartile in the fully adjusted model: overall, HR (95%CI) = 1.54 (1.26-1.89); dysglycemia (prediabetes and T2DM), HR = 1.41 (1.15-1.73); T2DM, HR = 1.36 (1.10-1.67).ConclusionWe found CV-FPG to be useful for measurement of GV. It could also be used for the prognostic stratification of patients with dysglycemia.
| S-EPMC9312379 | biostudies-literature
Project description:Previous studies investigating determinants of changes in glycemic status among individuals with prediabetes mainly focused on glucose-defined prediabetes. In this study, we examined determinants of a regression to normoglycemia or a progression to diabetes among individuals with HbA1c-defined prediabetes. The study included 817 participants (18-79 years) with prediabetes (HbA1c 5.7-6.4% (39-47?mmol/mol)) at baseline. Glycemic status at follow-up was categorized as diagnosed diabetes (self-reported physician diagnosis or antidiabetic medication), undiagnosed diabetes (HbA1c???6.5% (?48?mmol/mol)), prediabetes (as defined at baseline), and normoglycemia (HbA1c?<?5.7% (<39?mmol/mol)). Determinants of glycemic changes were identified by multinomial logistic regression (OR (95% CI)), with those remaining in the prediabetic state as reference. During a mean follow-up time of 12.0 years, 33.8% of the participants reverted to normoglycemia, 7.2% progressed to undiagnosed diabetes, 12.8% progressed to diagnosed diabetes, and 46.2% remained prediabetic. Determinants of a regression to normoglycemia were female sex (male vs. female: 0.67 (0.46; 0.98)) and higher HDL cholesterol levels (1.17 (1.02; 1.35) per 10?mg/dl). Determinants of a progression to undiagnosed or diagnosed diabetes were higher values of BMI (1.10 (1.02; 1.18); 1.13 (1.06; 1.21) per kg/m2), waist circumference (1.04 (1.01; 1.07); 1.06 (1.03; 1.09) per cm), alanine aminotransferase (1.06 (1.03; 1.09); 1.07 (1.03; 1.10) per U/l), and gamma-glutamyl transferase (1.02 (1.00; 1.03); 1.03 (1.01; 1.04) per U/l). Higher age (1.04 (1.02; 1.06) per year), female sex (male vs. female: 0.56 (0.33; 0.97)), and parental history of diabetes (yes vs. no: 1.82 (1.05; 3.15)) were further associated with a progression to diagnosed diabetes, whereas higher triglyceride levels (1.03 (1.01; 1.06) per 10?mg/dl) were associated with a progression to undiagnosed diabetes. In conclusion, among the investigated determinants, potentially modifiable anthropometric and metabolic markers were associated with glycemic changes in individuals with HbA1c-defined prediabetes. The findings of this study demonstrate the need for more refined case finding strategies for diabetes prevention.
| S-EPMC6204174 | biostudies-literature
Project description:This population-based, retrospective cohort study aimed to evaluate the association between glaucoma surgery and all-cause and cause-specific mortality among Korean elderly patients with glaucoma. A total of 16210 elderly patients (aged ≥ 60 years) diagnosed with glaucoma between 2003 and 2012 were included, and their insurance data were analyzed. The participants were categorized into a glaucoma surgery cohort (n = 487), which included individuals who had diagnostic codes for open angle glaucoma (OAG) or angle closure glaucoma (ACG) and codes for glaucoma surgery, and a glaucoma diagnosis cohort (n = 15,723), which included patients who had codes for OAG and ACG but not for glaucoma surgery. Sociodemographic factors, Charlson Comorbidity Index score, and ocular comorbidities were included as covariates. Cox regression models were used to assess the association between glaucoma surgery and mortality. The incidence of all-cause mortality was 34.76/1,000 person-years and 27.88/1,000 person-years in the glaucoma surgery and diagnosis groups, respectively. The adjusted hazard ratio (HR) for all-cause mortality associated with glaucoma surgery was 1.31 (95% confidence interval [CI], 1.05-1.62, P = 0.014). The adjusted HR for mortality due to a neurologic cause was significant (HR = 2.66, 95% CI 1.18-6.00, P = 0.018). The adjusted HRs for mortality due to cancer (HR = 2.03, 95% CI 1.07-3.83, P = 0.029) and accident or trauma (HR = 4.00, 95% CI 1.55-10.34, P = 0.004) associated with glaucoma surgery for ACG were significant as well. Glaucoma surgery was associated with an increase of mortality in elderly patients with glaucoma. In particular, the risk of mortality associated with glaucoma surgery due to neurologic causes was significant.
| S-EPMC8382742 | biostudies-literature
Project description:BackgroundAlthough diabetes is reportedly associated with the occurrence of acute pancreatitis (AP), the risk of AP according to the duration and severity of diabetes is not yet clear. We aimed to investigate the risk of AP based on glycemic status and the presence of comorbidities using a nationwide population-based study.MethodsWe enrolled 3,912,496 adults who underwent health examinations under the National Health Insurance Service in 2009. All participants were categorized by glycemic status as normoglycemic, impaired fasting glucose (IFG), or diabetes. Baseline characteristics and the presence of comorbidities at the time of health check-up were investigated, and the occurrence of AP was followed up until 31 December 2018. We estimated the adjusted hazard ratios (aHRs) for AP occurrence according to the glycemic status, duration of diabetes (new-onset, duration < 5 years, or ≥ 5 years), type and number of anti-diabetic medications, and presence of comorbidities.ResultsDuring the observation period of 32,116,716.93 person-years, 8,933 cases of AP occurred. Compared with normoglycemia, the aHRs (95% confidence interval) were 1.153 (1.097-1.212) in IFG, 1.389 (1.260-1.531) in new-onset diabetes, 1.634 (1.496-1.785) in known diabetes < 5 years, and 1.656 (1.513-1.813) in patients with known diabetes aged ≥ 5 years. The presence of comorbidities associated with diabetes severity had a synergistic effect on the relationship between diabetes and AP occurrence.ConclusionAs glycemic status worsens, the risk of AP increases, and there is a synergistic effect when comorbidities coexist. To reduce the risk of AP, active control of factors that can cause AP should be considered in patients with long-standing diabetes and comorbidities.
| S-EPMC10197233 | biostudies-literature
Project description:BackgroundDiabetes has been linked to accelerated brain aging, i.e., neuroimaging-predicted age of brain is higher than chronological age. This report evaluated whether accelerated brain aging in diabetes is associated with higher levels of glycated hemoglobin (HbA1c) and increased mortality.MethodsBrain age in Dallas Heart Study (n = 1949) was estimated using T1-weighted magnetic resonance imaging (MRI) scans and a previously-published Gaussian Processes Regression model. Accelerated brain aging (adjusted Δ brain age) was computed as follows: (brain age adjusted for chronological age)-minus-(chronological age). Mortality data until 12/31/2016 were obtained from the National Death Index. Associations of adjusted Δ brain age with diabetes in full sample and with HbA1c in individuals with diabetes were evaluated. Proportion of association between diabetes and all-cause mortality that was accounted for by adjusted Δ brain age were evaluated with mediation analyses. Covariates included Framingham 10-year risk score, race/ethnicity, income, body mass index, and history of myocardial infarction.ResultsDiabetes was associated with] higher adjusted Δ brain age [estimate= 1.79; 95% confidence interval (CI): 0.889, 2.68]. Among those with diabetes, higher HbA1c (log-base-2-transformed) was associated with higher adjusted Δ brain age (estimate=3.88; 95% CI: 1.47, 6.30). Over a median follow-up of 97.5 months, 24/246 (9.8%) with diabetes and 63/1703 (3.7%) without diabetes died. Adjusted Δ brain age accounted for 65.3 (95% CI: 39.3, 100.0)% of the association between diabetes and all-cause mortality.ConclusionAccelerated brain aging may be related to poor glycemic control in diabetes and partly account for the association between diabetes and all-cause mortality.
| S-EPMC10177664 | biostudies-literature
Project description:Changes in the DNA methylation (DNAm) landscape have been implicated in aging and cellular senescence. To unravel the role of specific DNAm patterns in late-life survival, we performed genome-wide methylation profiling in nonagenarians (n=111) and determined the performance of the methylomic predictors and conventional risk markers in a longitudinal setting. The survival model containing only the methylomic predictors was superior in terms of predictive accuracy compared with the models containing the conventional predictors body mass index and mini-mental state examination. At the 2.55-year follow-up, we identified 19 mortality-associated (false-discovery rate <0.5) CpG sites that mapped to genes functionally clustering around the nuclear factor kappa B (NF-κB) complex. Interestingly, none of the mortality-associated CpG sites overlapped with the established aging-associated DNAm sites. Our results are in line with previous findings on the role of NF-κB in controlling animal life spans and demonstrate the key role of this complex in human longevity.
2017-02-09 | GSE68194 | GEO