Fasting plasma glucose variability and all-cause mortality among type 2 diabetes patients: a dynamic cohort study in Shanghai, China.
Ontology highlight
ABSTRACT:
SUBMITTER: Xu D
PROVIDER: S-EPMC5177938 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:AIMS/HYPOTHESIS:The aim of this study was to determine whether long-term intra-individual variability in fasting glucose (FG) during young adulthood is associated with incident diabetes, cardiovascular disease (CVD) and mortality. METHODS:We included participants from the Coronary Artery Risk Development in Young Adults (CARDIA) study, ages 18-30 years at baseline (1985-1986) and followed with eight examinations for up to 30 years. Long-term glucose variability was assessed using the CV (CV-FG) and the absolute difference between successive FG measurements (average real variability; ARV-FG). For participants who developed any event (diabetes, CVD or mortality), FG variability measurement was censored at the examination prior to event ascertainment. We estimated HRs for incident diabetes, CVD and mortality with adjustment for demographics, baseline FG, change in FG (censor - baseline) and time-varying education, smoking, alcohol consumption, BMI, physical activity, systolic BP, BP medications, LDL-cholesterol and cholesterol medications (and incident diabetes and diabetes medications for CVD and mortality outcomes). RESULTS:Among 3769 black and white participants, there were 317 incident diabetes cases (102,677 person-years), 159 incident CVD events (110,314 person-years) and 174 deaths (111,390 person-years). After adjustment, HRs per 1 SD higher ARV-FG were 1.64 (95% CI 1.52, 1.78) for diabetes, 1.15 (95% CI 1.01, 1.31) for CVD and 1.25 (95% CI 1.11, 1.40) for mortality. The HRs per 1 SD higher CV-FG were 1.39 (95% CI 1.21, 1.58) for diabetes, 1.32 (95% CI 1.13, 1.54) for CVD and 1.08 (95% CI 0.92, 1.27) for mortality, after adjustment. The cause-specific HRs per 1 SD higher ARV-FG were 1.29 (95% CI 1.14, 1.47) for non-CVD death and 1.05 (95% CI 0.76, 1.45) for CVD death. We did not observe evidence for effect modification of any association by sex or race. CONCLUSIONS/INTERPRETATION:Our results suggest that higher intra-individual FG variability during young adulthood before the onset of diabetes is associated with incident diabetes, CVD and mortality.
| S-EPMC7235631 | biostudies-literature
Project description:BACKGROUND:This study investigated whether visit-to-visit fasting plasma glucose (FPG) variability, as measured by the coefficient of variation (CV), increased peripheral artery disease (PAD) risk. METHODS:Individuals with type 2 diabetes from the National Diabetes Care Management Program during the period 2002-2004, ??30 years of age, and free of PAD (n?=?30,932) were included and monitored until 2011. Cox proportional hazards regression models were implemented to analyze related determinants of PAD. RESULTS:A total of 894 incident cases of PAD were identified during an average 8.2 years of follow-up, resulting in a crude incidence rate of 3.53 per 1000 person-years. Both FPG-CV and HbA1c were significantly associated with PAD after multivariate adjustment, with corresponding hazard ratios of 1.24 [95% confidence interval (CI) 1.04-1.47] for FPG-CV in the third tertile and 1.50 (95% CI 1.10-2.04) for HbA1c???10%. The findings of the sensitivity analysis remained consistent after excluding potential confounders, demonstrating the consistency of the results. CONCLUSIONS:The associations between HbA1c, variability in FPG-CV, and PAD suggest a linked pathophysiological mechanism, suggesting the crucial role of glycemic variability in clinical management and therapeutic goals in preventing PAD in type 2 diabetes.
| S-EPMC6945758 | biostudies-literature
Project description:BACKGROUND:The extent to which diabetes mellitus or hyperglycemia is related to risk of death from cancer or other nonvascular conditions is uncertain. METHODS:We calculated hazard ratios for cause-specific death, according to baseline diabetes status or fasting glucose level, from individual-participant data on 123,205 deaths among 820,900 people in 97 prospective studies. RESULTS:After adjustment for age, sex, smoking status, and body-mass index, hazard ratios among persons with diabetes as compared with persons without diabetes were as follows: 1.80 (95% confidence interval [CI], 1.71 to 1.90) for death from any cause, 1.25 (95% CI, 1.19 to 1.31) for death from cancer, 2.32 (95% CI, 2.11 to 2.56) for death from vascular causes, and 1.73 (95% CI, 1.62 to 1.85) for death from other causes. Diabetes (vs. no diabetes) was moderately associated with death from cancers of the liver, pancreas, ovary, colorectum, lung, bladder, and breast. Aside from cancer and vascular disease, diabetes (vs. no diabetes) was also associated with death from renal disease, liver disease, pneumonia and other infectious diseases, mental disorders, nonhepatic digestive diseases, external causes, intentional self-harm, nervous-system disorders, and chronic obstructive pulmonary disease. Hazard ratios were appreciably reduced after further adjustment for glycemia measures, but not after adjustment for systolic blood pressure, lipid levels, inflammation or renal markers. Fasting glucose levels exceeding 100 mg per deciliter (5.6 mmol per liter), but not levels of 70 to 100 mg per deciliter (3.9 to 5.6 mmol per liter), were associated with death. A 50-year-old with diabetes died, on average, 6 years earlier than a counterpart without diabetes, with about 40% of the difference in survival attributable to excess nonvascular deaths. CONCLUSIONS:In addition to vascular disease, diabetes is associated with substantial premature death from several cancers, infectious diseases, external causes, intentional self-harm, and degenerative disorders, independent of several major risk factors. (Funded by the British Heart Foundation and others.).
| S-EPMC4109980 | biostudies-literature
Project description:ObjectiveTo investigate the association of normal fasting plasma glucose (FPG) and the risk for type 2 diabetes.Research design and methodsData concerning 13,845 subjects, aged 40-69 years, who had their FPG measured at least three times between 1992 and 2008 were extracted from a database. Three FPG groups were defined (51-82, 83-90, and 91-99 mg/dL). A Cox proportional hazards analysis was applied to estimate the risk of incident diabetes adjusted for other risk factors.ResultsDuring 108,061 person-years of follow-up (8,110 women and 5,735 men), 307 incident cases of type 2 diabetes were found. The final model demonstrated a hazard ratio of 2.03 (95% CI 1.18-3.50) for 91-99 mg/dL and 1.42 (0.42-4.74) for 83-90 mg/dL.ConclusionsOur data suggest that FPG between 91 and 99 mg/dL is a strong independent predictor of type 2 diabetes and should be used to identify people to be further investigated and aided with preventive measures.
| S-EPMC3114342 | biostudies-literature
Project description:IntroductionLong-term glycemic variability is associated with various adverse health outcomes in patients with diabetes mellitus (DM). However, the relationship between glycemic variability and gastric cancer remains unclear. We aimed to investigate the association between glycemic variability and gastric cancer incidence in individuals without DM.MethodsWe used the Korean National Health Insurance Service data sets of claims and health checkups and included 202,562 individuals without DM. Fasting plasma glucose (FPG) variability was measured using the variability independent of the mean (VIM), coefficient of variation, SD, and average successive variability. The association between FPG variability and gastric cancer incidence was analyzed using Cox regression adjusting for age, sex, body mass index, smoking status, alcohol consumption, regular exercise, income level, family history of cancer, mean FPG level, and number/mean interval of FPG measurements.ResultsIn total, 1,920 patients developed gastric cancer (0.95%) within a median follow-up of 5.6 (5.3, 6.4) years. The fully adjusted hazard ratio and 95% confidence interval for gastric cancer were 1.26 and 1.18-1.34, respectively, in the highest quartile of FPG variability assessed by VIM compared with that in the lowest quartile. Similar results were obtained in the normal and impaired fasting glucose groups and when using the variability indexes, including coefficient of variation, SD, and average successive variability. There was a sequential increase in the incidence of gastric cancer according to the increase in the deciles of FPG variability (P for linear trend <0.001). A 1-SD increase in FPG variability assessed by VIM was significantly associated with a 10.0% increase in gastric cancer risk in the fully adjusted model.DiscussionIn a DM-free population, high variability in visit-to-visit FPG levels was independently associated with an increased risk of gastric cancer.
| S-EPMC7455226 | biostudies-literature
Project description:BackgroundWhile the association between hypoglycaemia and poor outcomes in diabetes is well established, it is unclear whether such an association is generalizable to those without diabetes.MethodsA total of 8497 participants free of cardiovascular disease and diabetes from the Third National Health and Nutrition Examination Survey were included. We examined the relationship between baseline low (<80 mg/dL) and high (⩾126 mg/dL) fasting plasma glucose compared to normal levels (80-99 mg/dL).ResultsOver a median follow-up of 14 years, 2101 deaths occurred, of which 570 were due to cardiovascular disease. In a model adjusted for sociodemographic and cardiovascular disease risk factors, individuals with low fasting plasma glucose were at increased risk of cardiovascular disease and all-cause mortality [hazard ratio = 1.79 (95% confidence interval = 1.04-3.08) and hazard ratio = 1.35 (95% confidence interval = 1.02-1.78), respectively], compared to those with normal fasting plasma glucose. These associations were stronger among men than women for both cardiovascular disease mortality and all-cause mortality.ConclusionLow fasting plasma glucose in individuals without diabetes is a risk factor for cardiovascular disease and all-cause mortality, especially in men.
| S-EPMC7607395 | biostudies-literature
Project description:Background and aimsThe aim of this study is to investigate the association between visit-to-visit variability in fasting plasma glucose (FPG) and the risk of digestive cancers among individuals with and without diabetes.MethodsUsing data from Kailuan cohort, a prospective population-based study, individuals who had at least two measurements of FPG between 2006 and 2012 without prior cancer were included in this study. Four indexes of variability were used, including standard deviation (SD), coefficient of variation (CV), variability independent of the mean (VIM), and average successive variability (ARV). Cox regression was used to evaluate the relationship between the quartiles of FPG variability and digestive cancers.ResultsA total of 98,161 individuals were studied. Over a mean follow-up of 9.32 ± 0.81 years, 1103 individuals developed incident digestive cancer (1.21 per 1000 person-years). Compared to the individuals in the lowest quartile, those in the highest quartile of FPG variability by SD had 38.7% higher risk of developing overall digestive cancers after adjusting for the significant confounders (hazard ratio, 1.387; 95% confidence interval, 1.160-1.659; P = 0.0003). Higher FPG variability was associated with significantly higher risks of colorectal cancer (fully adjusted HR 1.432, 95% CI [1.073-1.912], P = 0.015) and pancreatic cancer (fully adjusted HR 2.105, 95% CI [1.024-4.329], P = 0.043), but not liver cancer (fully adjusted HR 1.427, 95% CI [0.973-2.092], P = 0.069) or esophageal and gastric cancer (fully adjusted HR 1.139, 95% CI [0.776-1.670], P = 0.506). Subgroup analyses showed that individuals who were younger (<65 years), male, and those without diabetes experienced a predominantly higher risk of developing digestive cancers. Similar results were observed when using CV, VIM, and ARV.ConclusionsFPG variability was significantly associated with increasing risk of digestive cancers, especially for pancreatic and colorectal cancer. Our study suggested a potential role of FPG variability in risk stratification of digestive cancers. Approaches that reduce FPG variability may lower the risks of incident digestive cancers among the general population. This trial is registered with ChiCTR-TNRC-11001489.
| S-EPMC9301759 | biostudies-literature
Project description:Nearly 4.3 million deaths worldwide were attributable to exposure to household air pollution in 2012. However, household coal use remains widespread.We investigated the association of cooking coal and all-cause and cause-specific mortality in a prospective cohort of primarily never-smoking women in Shanghai, China.A cohort of 74,941 women were followed from 1996 through 2009 with annual linkage to the Shanghai vital statistics database. Cause-specific mortality was identified through 2009. Use of household coal for cooking was assessed through a residential history questionnaire. Cox proportional hazards models estimated the risk of mortality associated with household coal use.In this cohort, 63% of the women ever used coal (n = 46,287). Compared with never coal use, ever use of coal was associated with mortality from all causes [hazard ratio (HR) = 1.12; 95% confidence interval (CI): 1.05, 1.21], cancer (HR = 1.14; 95% CI: 1.03, 1.27), and ischemic heart disease (overall HR = 1.61; 95% CI: 1.14, 2.27; HR for myocardial infarction specifically = 1.80; 95% CI: 1.16, 2.79). The risk of cardiovascular mortality increased with increasing duration of coal use, compared with the risk in never users. The association between coal use and ischemic heart disease mortality diminished with increasing years since cessation of coal use.Evidence from this study suggests that past use of coal among women in Shanghai is associated with excess all-cause mortality, and from cardiovascular diseases in particular. The decreasing association with cardiovascular mortality as the time since last use of coal increased emphasizes the importance of reducing use of household coal where use is still widespread.Kim C, Seow WJ, Shu XO, Bassig BA, Rothman N, Chen BE, Xiang YB, Hosgood HD III, Ji BT, Hu W, Wen C, Chow WH, Cai Q, Yang G, Gao YT, Zheng W, Lan Q. 2016. Cooking coal use and all-cause and cause-specific mortality in a prospective cohort study of women in Shanghai, China. Environ Health Perspect 124:1384-1389;?http://dx.doi.org/10.1289/EHP236.
| S-EPMC5010399 | biostudies-other
Project description:ObjectivesAbout 11%-30% of individuals with impaired fasting plasma glucose (IFG) have type 2 diabetes mellitus (T2DM), diagnosed by the 75 g oral glucose tolerance test (75 g OGTT). This study investigated (1) the prevalence and cut-off levels for fasting plasma glucose (FPG) and glycated haemoglobin A1c (HbA1c) in IFG individuals that most effectively predict the presence of T2DM diagnosed by a 75 g OGTT; (2) the predictors associated with T2DM; and (3) the pathophysiological characteristics of patients with IFG.Materials and methodsA single-centre, cross-sectional study was conducted in a primary care setting. A standard 75 g OGTT was performed on 123 subjects with IFG. Their beta-cell function and insulin resistance were calculated through plasma glucose and insulin levels monitored during the 75 g OGTT.ResultsIn the IFG subjects, the prevalence of T2DM using the 2-hour postload plasma glucose (2hPG) criterion was 28.5%. Pre-diabetes and normal glucose metabolism were found in 48.7% and 22.8%, respectively, by 75 g OGTT. An HbA1c level ≥6.0% or FPG ≥5.9 mmol/L were the optimal cut-off thresholds for the prediction of the presence of T2DM. HbA1c had a sensitivity of 76.7% and specificity of 55.7% (95% CI 57.7% to 90.1% and 95% CI 43.3% to 67.6%, respectively), while FPG had a sensitivity of 85.7% and specificity of 23.9% (95% CI 69.7% to 95.2% and 95% CI 15.4% to 34.1%, respectively). The presence of metabolic syndrome, a higher HbA1c and higher FPG levels were associated with the risk of T2DM in the Thai IFG population.ConclusionsAlmost one-third of the people with IFG had T2DM diagnosed by the 2hPG criterion. HbA1c was more effective than FPG in predicting the presence of T2DM in the IFG subjects. IFG individuals with HbA1c≥6.0% or FPG≥5.9 mmol/L should be advised to undergo a 75 g OGTT to detect T2DM earlier than otherwise.
| S-EPMC7656954 | biostudies-literature
Project description:Genome-wide association studies (GWAS) in White Europeans have shown that genetic variation rs10830963 in melatonin receptor 1B gene (MTNR1B) is associated with fasting glucose and type 2 diabetes, which has also been replicated in several Asian populations. As a variant in the gene involved in the regulation of circadian rhythms, the effect of the variant on sleep status remains unknown. This study aimed to investigate the effects of MTNR1B rs10830963 on fasting glucose, type 2 diabetes and sleep status in Chinese Hans.MTNR1B rs10830963 was genotyped in a population-based cohort including 3,210 unrelated Chinese Hans from Beijing and Shanghai, and tested for associations with risk of type 2 diabetes, diabetes-related traits and sleep status.We confirmed the associations of MTNR1B rs10830963 with fasting glucose (beta = 0.11 mmol/l, 95%CI [0.03, 0.18], P = 0.005), glycated hemoglobin (HbA1c) (beta = 0.07%, 95%CI [0.02,0.12], P = 0.004) and homeostasis model assessment of beta-cell function (HOMA-B) (beta = -5.01%, 95%CI [-8.24,-1.77], P = 0.003) in the Shanghai, but not in the Beijing subpopulation (P >or= 0.58). The effect size of MTNR1B rs10830963 on fasting glucose in Shanghai Chinese Hans was comparable to that reported from other Asian populations. We found no evidence of associations with type 2 diabetes (OR 1.05 [0.90-1.23], P = 0.54), homeostasis model assessment of insulin sensitivity (HOMA-S) (P = 0.86) or sleep status (P >or= 0.44).A common variant in MTNR1B was associated with fasting glucose, HbA1C and HOMA-B but not with sleep status in Chinese Hans from Shanghai, strengthening the role of MTNR1B rs10830963 in fasting glycemia and impaired beta-cell function.
| S-EPMC2873324 | biostudies-literature