Diabetes Epidemiology : Collaborative Analysis Of Diagnostic Criteria In Europe Research Articles

Possible Ways to Improve Postprandial Glucose Control in Type 1 Diabetes.

Possible Ways to Improve Postprandial Glucose Control in Type 1 Diabetes.

Association of metabolic syndrome with coronary artery calcification.

Association of metabolic syndrome with coronary artery calcification.

Postprandial Glucose: Marker or Risk Factor?

Postprandial glucose (PPG) has a noxious effect on the vascular endothelium, which is mainly mediated by oxidative stress. This condition leads to endothelial activation and dysfunction, two prerequisites for the onset of cardiovascular disease (CVD) (1). The importance of PPG is reflected in the creation of guidelines by the International Diabetes Federation (IDF) for the management of postmeal glucose (http://www.idf.org/guidelines/postmeal-glucose). In these guidelines, the statement “Postmeal and postchallenge hyperglycaemia are independent risk factors for macrovascular disease” was rated as Level 1+, i.e., the data were derived from well-conducted meta-analyses, systematic reviews of randomized controlled trials (RCTs), or RCTs with a low risk of bias. The relationship between postchallenge hyperglycemia and CVD has been addressed by several studies. In the Honolulu Heart Program, the risk of coronary heart disease was increased in Japanese American men aged 45–68 years who had an abnormal oral glucose tolerance test (2). Comparable results were observed in the Chicago Heart Association Detection Project in Industry Study (3), the Paris Prospective Study (4), the Baltimore Longitudinal Study of Aging (5), and the Diabetes Epidemiology: Collaborative Analysis of Diagnostic Criteria in Europe (DECODE) study (6). Furthermore, two meta-analyses provided evidence that hyperglycemia in the nondiabetic range was associated with a higher risk of fatal and nonfatal CVD. They also showed that CVD events increased linearly, with no threshold, along with 2-h postmeal plasma glucose levels (7,8). Relatively few studies have analyzed postmeal hyperglycemia as a risk factor in CVD development. In the Diabetes Intervention Study (DIS), in type 2 diabetic patients who were monitored for 11 years, postbreakfast glucose levels, rather than fasting glucose, were related to myocardial infarction and death (9). In this issue of Diabetes Care , Cavalot et al. (10) add further evidence of the harmful relationship between postmeal glucose levels and …

UKPDS Risk Engine, Decode and Diabetes PHD Models for the Estimation of Cardiovascular Risk in Patients with Diabetes

Individuals with type 2 diabetes have a two to four fold increased risk for developing cardiovascular disease than persons without diabetes. The presence of traditional and nontraditional risk factors that frequently coexist with type 2 diabetes are associated with this higher cardiovascular risk. Diabetes itself has been considered a cardiovascular disease equivalent. Nevertheless, the American Diabetes Association has recognized that absolute risk for cardiovascular disease varies among individuals with diabetes and has recommended the use of designed models and algorithms to estimate risk, especially in younger patients (<40 years). Cardiovascular risk is best evaluated with an estimation that takes into account the individual's characteristics and risk factors. The algorithms and models that have been designed specifically for the assessment of cardiovascular risk in individuals with diabetes will be the subject of this review. Specifically, the DECODE (Diabetes Epidemiology: Collaborative analysis of Diagnostic criteria in Europe) equation has been shown to have discriminative capacity of 0.67; the UKPDS Risk Engine model is reported to have a sensitivity of around 90% and specificity of 33%; and the Diabetes Personal Health Decisions (PHD) in our study had a sensitivity of 67% and specificity of 41%. In this review we will discuss the pros and cons of each model, their use in clinical practice and the application of the UKPDS risk engine and PHD model in a Mexican population.

Does diagnosis of the metabolic syndrome detect further men at high risk of cardiovascular death beyond those identified by a conventional cardiovascular risk score? The DECODE Study: The Diabetes Epidemiology: Collaborative analysis Of Diagnostic Criteria in Europe (DECODE) Study Group

It is not known whether the metabolic syndrome detects further individuals at high risk of death from cardiovascular disease (CVD), beyond those identified by a conventional cardiovascular risk score. A prospective study. A total of 2790 men without diabetes, aged 50–69 years from seven population-based European cohorts participating in the DECODE Study, were followed for CVD mortality over 10 years. Some 51% of the men had an estimated 10-year risk of fatal CVD under 5%, using the European SCORE project equation, and 22% of them had the metabolic syndrome, as defined by the National Cholesterol Education Program Adult Treatment Panel III. In the low-risk men, the hazards ratio for fatal CVD, after adjusting for age and study centre, was 2.71 (1.33–5.51) for men with the syndrome (P<0.01) compared with men without the syndrome. A large waist circumference (>102cm) carried an odds ratio of 2.24 (1.05–4.76) in the low CVD risk men. Men with a low cardiovascular risk score and the metabolic syndrome had a significantly higher risk of fatal CVD than those without the syndrome. The use of the metabolic syndrome in clinical practice is thus justified in men, but waist circumference provided a simpler diagnostic tool with similar fatal CVD risk in these low-risk men. A large waist circumference could be used for prescreening, and could be included in CVD risk scores.

Framingham, SCORE, and DECODE Risk Equations Do Not Provide Reliable Cardiovascular Risk Estimates in Type 2 Diabetes

Accurate cardiovascular disease (CVD) risk estimates can inform choice of therapeutic strategies for individuals, provided they have been appropriately validated (1). Risk calculators are of particular relevance in diabetic patients given their 2–4 times higher CVD risk compared with the nondiabetic population (2). Framingham Study (3) risk equations for coronary heart disease (CHD) and CVD, based on age, sex, blood pressure, cholesterol (total and HDL), and smoking, with diabetes status as a categorical variable, have been validated prospectively in general populations (4,5) but not in diabetic subjects (6). The Systematic Coronary Risk Evaluation (SCORE) Project risk scores for fatal CHD and CVD (7) appear to overestimate risk in the general population (8,9) and have not been evaluated in diabetes. Following recognition of glycemia as a CVD risk factor (10), the Diabetes Epidemiology: Collaborative Analysis of Diagnostic Criteria in Europe (DECODE) Study Group developed a fatal CVD risk equation incorporating glucose tolerance status and fasting plasma glucose (11). We have evaluated these three risk equations in patients with type 2 diabetes using UK Prospective Diabetes Study (UKPDS) data (12). The UKPDS (12,13) recruited 5,102 of 7,616 people with newly diagnosed type 2 diabetes in 23 U.K. centers and followed them for median 10.4 years (range 6–20). Exclusion criteria included severe vascular disease, myocardial infarction, or stroke within 1 year and major systemic illness. The study received ethical committee approval, conformed to Declaration of …

Strategies for the prevention of type 2 diabetes and cardiovascular disease

The DECODE (Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe) study provides a clear overview of the outcomes of metabolic syndrome and type 2 diabetes in terms of cardiovascular mortality in a European population. The study demonstrates that the presence of the metabolic syndrome doubles the risk of cardiovascular mortality, with a stronger effect in women than in men.1 Although each individual component of the metabolic syndrome confers an increased risk of cardiovascular mortality, this is not as pronounced as when the metabolic syndrome itself is present. The more the components of the metabolic syndrome, the higher cardiovascular mortality.1 In addition, DECODE also demonstrates that the combination of metabolic syndrome and type 2 diabetes leads to a significantly increased risk of cardiovascular or all-cause mortality, with this risk again being higher in women ( Table 1 ). Life expectancy for people with type 2 diabetes is decreased by 5–10 years and adults with diabetes have an annual mortality of about 5.4%, which is double the rate for non-diabetic adults.2,3 View this table: Table 1 Relative risk for mortality in subjects with either metabolic syndrome, or diabetes, or both1 The often devastating impact of these conditions has led to much interest in how outcomes for people with type 2 diabetes can be improved and how type 2 diabetes can be prevented in the first place. ### Lifestyle interventions A number of studies have now demonstrated the efficacy of specific, goal-oriented lifestyle interventions in the prevention of type 2 diabetes. This is clearly demonstrated by the Finnish Diabetes Prevention Study (DPS),4 in which 522 middle-aged, overweight subjects with impaired glucose tolerance (IGT)5 were randomly assigned to either the intervention group or the control group. Each subject in the intervention group received individualized counselling6 aimed at reducing weight and intake of total and …

SCREENING FOR DIABETES IN GENERAL PRACTICE

SCREENING FOR DIABETES IN GENERAL PRACTICE

Inflammation and insulin resistance.

This Is the second of two articles describing a symposium on the relationship between inflammation and insulin resistance that was held in Niagra Falls, NY, 20–21 September 2002. Antonio Ceriello (Udine, Italy) discussed the role of glucose intake and postprandial hyperglycemia in the development of diabetes complications, as well as the relationship of hyperglycemia to oxidative stress. The DECODE (Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe) study showed high 2-h postload glucose to be associated with increased mortality independent of fasting glucose (1), and the Pacific and Indian Ocean Study showed isolated 2-h hyperglycemia to double the risk of mortality (2). The Funagata Diabetes Study showed that impaired glucose tolerance (IGT) but not impaired fasting glucose was a risk factor for cardiovascular disease (CVD) (3). There is evidence that lowering postprandial glucose improves outcome. Post hoc analysis of the STOP-type 2 diabetes study showed that myocardial infarction and hypertension decrease with use of the prandial glucose-lowering agent acarbose (4). In the Kumamoto study, postprandial hyperglycemia strongly predicted retinopathy and nephropathy (5). Endothelial dysfunction (ED) is a potential mediator of the effect of prandial glycemia, with altered vasodilation and procoagulant abnormalities. ED can be induced by hyperglycemia following a 75-g oral glucose load in persons with normal or IGT or with diabetes, with reduction of flow-mediated brachial artery dilation proportional to the degree of hyperglycemia (6). In a study of 225 persons with hypertension followed for 32 months, forearm ED was a marker of future CVD events (7), with a 4.5-year follow-up of 281 persons showing both ED and measures of oxidative stress to predict CVD events (8). Acute hyperglycemia may suppress vasodilation, which may involve oxidant stress, as it is reversed with antioxidant or l-arginine treatment (9). Glucose increases endothelial cell free radical production leading …

Inflammation and insulin resistance.

This Is the second of two articles describing a symposium on the relationship between inflammation and insulin resistance that was held in Niagra Falls, NY, 20–21 September 2002. Antonio Ceriello (Udine, Italy) discussed the role of glucose intake and postprandial hyperglycemia in the development of diabetes complications, as well as the relationship of hyperglycemia to oxidative stress. The DECODE (Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe) study showed high 2-h postload glucose to be associated with increased mortality independent of fasting glucose (1), and the Pacific and Indian Ocean Study showed isolated 2-h hyperglycemia to double the risk of mortality (2). The Funagata Diabetes Study showed that impaired glucose tolerance (IGT) but not impaired fasting glucose was a risk factor for cardiovascular disease (CVD) (3). There is evidence that lowering postprandial glucose improves outcome. Post hoc analysis of the STOP-type 2 diabetes study showed that myocardial infarction and hypertension decrease with use of the prandial glucose-lowering agent acarbose (4). In the Kumamoto study, postprandial hyperglycemia strongly predicted retinopathy and nephropathy (5). Endothelial dysfunction (ED) is a potential mediator of the effect of prandial glycemia, with altered vasodilation and procoagulant abnormalities. ED can be induced by hyperglycemia following a 75-g oral glucose load in persons with normal or IGT or with diabetes, with reduction of flow-mediated brachial artery dilation proportional to the degree of hyperglycemia (6). In a study of 225 persons with hypertension followed for 32 months, forearm ED was a marker of future CVD events (7), with a 4.5-year follow-up of 281 persons showing both ED and measures of oxidative stress to predict CVD events (8). Acute hyperglycemia may suppress vasodilation, which may involve oxidant stress, as it is reversed with antioxidant or l-arginine treatment (9). Glucose increases endothelial cell free radical production leading …

Should postprandial glucose be routinely measured and treated to a particular target? No!

Diabetes is a serious medical condition associated with disability, premature death, and enormous medical costs (1). Arguably more important is the insidious way in which the diagnosis of diabetes afflicts people with worry and despair over the loss of health as well as the burden of self-care. As health care professionals, our recommendations to patients regarding methods and targets of treatment can dramatically influence the quality of patients’ lives. The issue at hand is this: Should postprandial glucose (PPG) be routinely measured and treated to a particular target? I will answer this from the perspective of guidelines generally applicable in the medical community, with the recognition that for particular patients, very different approaches could be appropriate. The problem with attempting to answer this question is that there is essentially no direct clinical trial evidence to inform the decision, leaving a great deal to opinion. There are numerous epidemiological studies, such as DECODE (Diabetes Epidemiology: Collaborative Analysis Of Diagnostic Criteria in Europe), suggesting that 2-h glucose levels >140 mg/dl obtained after a 75-g oral glucose load are associated with increased risk of cardiovascular disease (CVD), in excess of the risk defined by fasting glucose (2). These results have been used as the primary evidence that patients and providers should work to attain glucose levels <140 mg/dl 2 h after meals in patients with diabetes. At face value, it seems illogical to base the clinical care of people with diabetes eating several meals a day on single glucose measurements obtained during an oral glucose tolerance test in “normal” individuals. Furthermore, interpretation of these epidemiologic studies is confounded by the fact that postchallenge glucose is also a marker of insulin resistance and the metabolic syndrome (3). Since other components of the metabolic syndrome cosegregate with postchallenge glucose in these studies, it leaves unanswered …

Is the current definition for diabetes relevant to mortality risk from all causes and cardiovascular and noncardiovascular diseases?

To assess the relation between fasting plasma glucose (FPG) or 2-h plasma glucose (2hPG) and mortality from all causes, cardiovascular disease (CVD), and non-CVD and to determine whether the relationship is graded or threshold. Diabetes Epidemiology: Collaborative Analysis Of Diagnostic Criteria in Europe (DECODE) is a collaborative prospective study of 22 cohorts in Europe with baseline glucose measurements for 29714 subjects aged 30-89 years who were followed-up for 11 years (329050 person-years). Hazard ratio (HR) for death was estimated using Cox regression analysis. High glucose concentrations as well as very low glucose levels were associated with increased risk of death. Compared with an FPG of 4.50-6.09 mmol/l, the multivariate-adjusted HR (95% CI) for FPG <4.50 mmol/l was 1.2 (1.0-1.4) for all-cause, 1.3 (1.0-1.8) for CVD, and 1.1 (0.9-1.4) for non-CVD mortality; the corresponding HRs for diabetes (FPG >or=7.0 mmol/l) were 1.6 (1.4-1.8), 1.6 (1.3-1.9), and 1.6 (1.4-1.9), respectively. For a 2hPG of 3.01-4.50 mmol/l, as compared with a 2hPG of 4.51-5.50 mmol/l, the HRs were 1.1 (1.0-1.2), 1.1 (0.9-1.3), and 1.1 (1.0-1.3), respectively; the corresponding HRs for diabetes (2hPG >or=11.1 mmol/l) were 2.0 (1.7-2.3), 1.9 (1.5-2.4), and 2.1 (1.7-2.5), respectively. The HR for previously undetected diabetes defined by 2hPG was not significantly different from that for known diabetes, which was significantly higher than that for undetected diabetes based on FPG. Subjects with a 2hPG of 10.01-11.09 mmol/l had mortality risks similar to those diabetic subjects defined by an FPG >or=7.0 mmol/l. The relation between mortality and glucose was J shaped rather than showing threshold effect at high glucose levels, except for CVD mortality and 2hPG, where the relation was graded and increasing.

Impaired Glucose Tolerance

Impaired glucose tolerance (IGT) is determined by measuring plasma glucose levels 2 hours after glucose loading in the oral glucose tolerance test. There is good evidence from epidemiologic and prospective trials [e.g. Diabetes Epidemiology: Collaborative Analysis of Diagnostic Criteria in Europe (DECODE)] linking IGT with the development of type 2 diabetes mellitus and cardiovascular disease (CVD). IGT is characterized by an increase in postprandial glucose levels, which is considered the earliest metabolic abnormality in type 2 diabetes mellitus. It is one of a series of risk factors for CVD (hypertension, high triglyceride levels, low high-density lipoprotein-cholesterol and central obesity), known as the metabolic syndrome. The different factors making up this syndrome are intimately related. An impaired lipid profile can contribute to insulin resistance, as IGT may play a pathogenic role on other cardiovascular risk factors. IGT is the first easily identifiable step in the pathophysiology of type 2 diabetes mellitus. It is associated with high risk for type 2 diabetes mellitus and subsequent vascular morbidity and mortality. It is currently unknown whether treating IGT will reduce the incidence of macrovascular complications, as studies addressing this issue have yet to be conducted. Therefore, the main reason to identify and treat IGT is to prevent or delay the onset of type 2 diabetes mellitus. It has been demonstrated that lifestyle intervention with diet and exercise can reduce the incidence of type 2 diabetes mellitus. Pharmacologic intervention with metformin and acarbose is also effective. Other drugs, such as those indicated to treat other parameters of the metabolic syndrome, may also be useful. We can now be assured that prevention or delay of onset of type 2 diabetes mellitus is possible in individuals with IGT, either by changes in lifestyle or by pharmacotherapy.

American Diabetes Association 60th Scientific Sessions, 2000: glucose tolerance, diabetes and cancer, glycemic control, monitoring, and related topics.

This is the sixth in a continuing series of articles on the American Diabetes Association (ADA) 60th Scientific Sessions held in San Antonio, TX, in June 2000. It covers topics related to use of fasting versus 2-h glucose for diagnosis of diabetes, diabetes and cancer, glycemic control, monitoring, and hypoglycemia. ### Postload Glycemia in the Diagnosis of Diabetes At a symposium on diagnostic criteria for diabetes James Gavin, Chevy Chase, MD, discussed the dilemma that fasting and post–glucose load glucose levels are differently regulated and that diagnosis based on the two criteria therefore define somewhat different populations. The use of fasting glucose has several advantages. It is more convenient to perform and limits a missed diagnosis of diabetes. Gavin noted that microvascular complications begin to occur above a fasting glucose of 126 mg/dl. A concern, however, is that more than half of patients with diabetes diagnosed by a glucose tolerance test have a fasting glucose below 126 mg/dl. Given new data showing that the fasting glucose level is less predictive of cardiovascular disease (CVD) risk than postchallenge glucose level, Gavin concluded that “fundamentally, we are back at ‘square one’ in asking ‘What is diabetes?’” Daniel Porte, San Diego, CA, noted that “cause and effect is not necessary when we see associations,” an important caveat in the new emphasis on glucose tolerance testing and postchallenge glycemia for diabetes diagnosis. Jaakko Tuomilehto, Helsinki, Finland, reviewed data from the Diabetes Epidemiology Collaborative Analysis of Diagnostic Criteria in Europe (DECODE) Study of 18,048 men and 7,316 women aged 30 years or older followed for an average of 7 years after glucose tolerance testing, addressing the question of whether fasting glucose or 2-h postload glucose better predicts mortality (1) There were a total of 1,836 deaths. The World Health Organization (WHO) criteria for diabetes, based mainly on 2-h glucose >200 mg/dl, and the …

Glucose peaks – the hidden danger in type 2 diabetes

Glucose peaks – the hidden danger in type 2 diabetes