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German Metabolic Academy - A Forum for the scientific Exchange between Diabetologists and Cardiologists: Lifestyle modification for the Prevention of Type 2-Diabetes and coronary Heart disease

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Objective: The Diabetes Prevention Program (DPP) and its Outcomes Study (DPPOS) demonstrated that either intensive lifestyle intervention or metformin could prevent type 2 diabetes in high-risk adults for at least 10 years after randomization. We report the 10-year within-trial cost-effectiveness of the interventions. Research design and methods: Data on resource utilization, cost, and quality of life were collected prospectively. Economic analyses were performed from health system and societal perspectives. Results: Over 10 years, the cumulative, undiscounted per capita direct medical costs of the interventions, as implemented during the DPP, were greater for lifestyle ($4,601) than metformin ($2,300) or placebo ($769). The cumulative direct medical costs of care outside the DPP/DPPOS were least for lifestyle ($24,563 lifestyle vs. $25,616 metformin vs. $27,468 placebo). The cumulative, combined total direct medical costs were greatest for lifestyle and least for metformin ($29,164 lifestyle vs. $27,915 metformin vs. $28,236 placebo). The cumulative quality-adjusted life-years (QALYs) accrued over 10 years were greater for lifestyle (6.81) than metformin (6.69) or placebo (6.67). When costs and outcomes were discounted at 3%, lifestyle cost $10,037 per QALY, and metformin had slightly lower costs and nearly the same QALYs as placebo. Conclusions: Over 10 years, from a payer perspective, lifestyle was cost-effective and metformin was marginally cost-saving compared with placebo. Investment in lifestyle and metformin interventions for diabetes prevention in high-risk adults provides good value for the money spent.
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The K121Q (rs1044498) single nucleotide polymorphism (SNP) in the ENPP1 gene has shown association with insulin resistance and type 2 diabetes in various ethnic populations. We hypothesised that K121Q may predict the success of lifestyle intervention in terms of improvement of insulin sensitivity. We genotyped 1,563 participants with an increased risk of type 2 diabetes for K121Q and performed correlational analyses with anthropometric data and variables of insulin sensitivity. For metabolic characterisation, all participants underwent an OGTT. A subgroup of 506 participants additionally underwent a euglycaemic-hyperinsulinaemic clamp. In 342 participants, metabolic traits and anthropometric data were re-evaluated after a 9 month lifestyle intervention. In the overall cohort, K121Q was not associated with measures of obesity, indices of glucose tolerance during OGTT and insulin sensitivity estimated from the OGTT or derived from a euglycaemic-hyperinsulinaemic clamp after appropriate adjustment. However, K121Q did significantly influence the change in insulin sensitivity during lifestyle intervention after appropriate adjustment (p (additive) = 0.0067, p (dominant) = 0.0027). Carriers of the minor allele had an impaired increase in OGTT-derived insulin sensitivity. A similar trend was obtained for clamp-derived insulin sensitivity, but did not reach significance. In our population of European ancestry, the ENPP1 SNP K121Q influenced the change in insulin sensitivity during lifestyle intervention. Thus, this SNP may determine susceptibility to environmental changes and could predict the success of lifestyle intervention.
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The impact of the diabetes risk gene transcription factor 7-like 2 (TCF7L2) on body weight is unclear. As TCF7L2 is expressed in adipose tissue and involved in Wnt-dependent regulation of adipogenesis, we studied the impact of TCF7L2 variants on body composition and weight loss during lifestyle intervention. We genotyped 309 German subjects at increased risk for type 2 diabetes for single nucleotide polymorphisms (SNPs) rs7903146, rs12255372, rs11196205, and rs7895340 in TCF7L2 and performed oral glucose tolerance tests before and after a 9-month lifestyle intervention. Fat distribution was quantified using whole-body magnetic resonance imaging/spectroscopy in a subgroup of 210 subjects. After adjustment for confounding variables, we observed a negative impact of the type 2 diabetes allele of SNP rs7903146 on change in BMI (P = 0.0034) and on changes in nonvisceral (P = 0.0032) and visceral fat (P = 0.0165) during lifestyle intervention. An association of rs7903146 with lifestyle intervention-induced changes in insulin secretion, glucose concentrations, liver fat, or insulin sensitivity were not detected (all P > 0.2). Essentially the same results were obtained with SNP rs1255372. In contrast, we found no effects of SNPs rs11196205 and rs7895340 on change in BMI (all P > or = 0.5). Our data reveal that diabetes-associated alleles of TCF7L2 are associated with less weight loss in response to lifestyle intervention. Thus, diabetes-associated TCF7L2 gene variation predicts the success of lifestyle intervention in terms of weight loss and determines individual susceptibility toward environmental factors.
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Research on the cause of coronary heart disease has been ongoing for approximately a century.1 From the beginning, diet played a prominent role in research on the origin of coronary heart disease. The original diet-heart hypothesis was very simple. Cholesterol is a constituent of the atherosclerotic plaque. Therefore, it was thought that there was a direct relation between cholesterol in the diet (ie, eggs), cholesterol in the blood, cholesterol in the plaque, and its clinical complications, such as myocardial infarction. In the second part of the past century, it became clear that dietary cholesterol played a minor role in regulating serum cholesterol levels. It was also shown that dietary fatty acids are the major determinants of serum cholesterol.2 The study of lipoprotein metabolism showed that the cholesterol-rich LDL fraction, not total cholesterol, was most strongly related to the development of atherosclerosis and its sequelae.3 Experimental research was essential to understand the mechanisms by which genes, hormones, and diet interact to regulate the serum cholesterol level.4 LDL cholesterol levels can be increased by saturated fatty acids, especially those with 12 to 16 carbon atoms, and by trans fatty acids.5 Several hypotheses have been proposed to explain the initiating events in atherogenesis, eg, the response-to-injury, response-to-retention, and oxidation hypotheses.6–8⇓⇓ These hypotheses are not mutually exclusive and may even be compatible with each other. The oxidation hypothesis emphasizes the importance of oxidative modification in the atherosclerotic process, because compared with native LDL, oxidized LDL is preferentially taken up in the arterial wall.8 This hypothesis makes a role of diet and lifestyle in atherogenesis likely, because LDL can be oxidized by smoking, for example, and oxidation can be prevented by dietary antioxidants, eg, vitamins and polyphenols. There is overwhelming evidence that smoking, alcohol, and physical …
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Die globale Diabetesprävalenz liegt heute bei 246Millionen Menschen. Hochrechnungen für das Jahr 2025 sagen 380Millionen Diabetiker voraus. In Deutschland haben 7 bis 8% der Bevölkerung einen Diabetes. Allerdings geht man von einer hohen Dunkelziffer an unerkanntem Diabetes aus. Die tatsächliche Zahl dürfte in Deutschland bei 7 bis 8Millionen Diabetikern liegen, was bedeutet, dass etwa jeder 10.Bundesbürger betroffen ist. In den vergangenen Jahren haben mehrere Studien gezeigt, dass eine Prävention des Typ-2-Diabetes möglich ist. Vor allem eine Lebensstilintervention erbrachte diesbezüglich die besten Erfolge. Es gibt sowohl Menschen, die gut auf eine Lebensstilintervention ansprechen, als auch Personen, die hiervon nur wenig profitieren. Die erste Gruppe kann man als „Responder“, letztere als „Non-Responder“ bezeichnen. Mittlerweile gibt es sowohl genetische als auch phänotypische Merkmale, die den Erfolg einer Lebensstilintervention vorhersagen. Somit wird eine individualisierte Prävention des Typ-2-Diabetes möglich. The global estimated prevalence of diabetes today is 246 million people. By 2025, the figure is expected to rise to 380 million. In Germany about 7 to 8% of the population is diagnosed with diabetes. However, there are a large proportion of people with unknown diabetes and the total number of subjects with diabetes is estimated at 7 to 8 million, indicating that every tenth individual is affected by the disease. Several recent studies unanimously revealed that it is possible to prevent type 2 diabetes. Particularly lifestyle intervention showed promising results. However, there is large variability in the effect of the intervention, and people with a good response (responders) and with a low response (non-responders) can be identified. Meanwhile, several genetic and phenotypic markers have been identified, which can help predict the success of the lifestyle intervention, allowing for a more effective individualized prevention of type 2 diabetes.
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A high intake of saturated fat is an important risk factor for coronary heart disease (CHD) and type 2 diabetes. However the declining rates of CHD in many affluent societies and the steady increase in type 2 diabetes worldwide suggest that these important causes of serious morbidity and premature mortality have differing risk or protective factors worldwide. Changed macronutrient composition, reduced cigarette smoking, and improved treatment of risk factors and acute cardiac events might explain the reduction in risk of CHD, whereas the increasing rates of obesity are probably the most important explanation for the increase in diabetes. Coronary risk factors associated with diabetes could outweigh improvements in conventional cardiovascular risk factors such that the decline in CHD could be stopped or reversed unless rates of obesity can be reduced. Reduced intake of saturated fatty acids and other lifestyle interventions aimed at lowering rates of obesity are the changes most likely to reduce the epidemic numbers of people with type 2 diabetes and CHD.
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This statement was reviewed by and has received the endorsement of the American College of Sports Medicine. Regular physical activity using large muscle groups, such as walking, running, or swimming, produces cardiovascular adaptations that increase exercise capacity, endurance, and skeletal muscle strength. Habitual physical activity also prevents the development of coronary artery disease (CAD) and reduces symptoms in patients with established cardiovascular disease. There is also evidence that exercise reduces the risk of other chronic diseases, including type 2 diabetes,1 osteoporosis,2 obesity,3 depression,4 and cancer of the breast5 and colon.6 This American Heart Association (AHA) Scientific Statement for health professionals summarizes the evidence for the benefits of physical activity in the prevention and treatment of cardiovascular disease, provides suggestions to healthcare professionals for implementing physical activity programs for their patients, and identifies areas for future investigation. This statement focuses on aerobic physical activity and does not directly evaluate resistance exercises, such as weight lifting, because most of the research linking physical activity and cardiovascular disease has evaluated aerobic activity. Whenever possible, the writing group has cited summary articles or meta-analyses to support conclusions and recommendations. This evidence supports the recommendation from the Centers for Disease Control and Prevention (CDC) and the American College of Sports Medicine (ACSM) that individuals should engage in 30 minutes or more of moderate-intensity physical activity on most (preferably all) days of the week.7 Physical activity is defined as any bodily movement produced by skeletal muscles that results in energy expenditure beyond resting expenditure. Exercise is a subset of physical activity that is planned, structured, repetitive, and purposeful in the sense that improvement or maintenance of physical fitness is the objective. Physical fitness includes cardiorespiratory fitness, muscle strength, body composition, and flexibility, comprising a set of attributes that people …
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Guidelines for lifestyle and dietary modification in patients with coronary artery disease (CAD) are mainly supported by evidence from general population studies. CAD patients, however, differ from the general population in age (older) and treatment with preventive drugs. This review seeks to provide evidence for a prognostic benefit of lifestyle and dietary recommendations from studies in CAD patients. A literature search was performed on the effect of lifestyle and dietary changes on mortality in CAD patients. Prospective cohort studies and randomized controlled trials of patients with established CAD were included if they reported all-causes mortality and had at least 6 months of follow-up. The effect estimates of smoking cessation (relative risk [RR], 0.64; 95% CI, 0.58 to 0.71), increased physical activity (RR, 0.76; 95% CI, 0.59 to 0.98), and moderate alcohol use (RR, 0.80; 95% CI, 0.78 to 0.83) were studied most extensively. For the 6 dietary goals, data were too limited to provide reliable effect size estimates. Combinations of dietary changes were associated with reduced mortality (RR, 0.56; 95% CI, 0.42 to 0.74). Available studies show convincingly the health benefits of lifestyle changes in CAD patients. Effect estimates of combined dietary changes look promising. Future studies should confirm these findings and assess the contribution of the individual dietary factors.