Nestle Nutrition workshop series. Clinical & performance programme最新文献

The poor effectiveness of conventional dietary treatment for weight loss and weight maintenance in patients with type-2 diabetes may be improved by a meal replacement strategy that provides a strong structured meal plan with reasonable opportunity for dietary variety. Typical meal replacement programs fix the intake of one or two meals per day with a calorie-controlled, nutritionally balanced commercial formulation, and allow prudent additional meals and snacks. In obese subjects, diets with meal replacements have proven to be more efficient than conventional diets. Patients on the meal replacement regimen lost 7.3 and 8.4% of initial body weight after 12 weeks and 4 years, respectively, whereas the patients on the conventional diet had lost 1.4% and 3.2% of initial body weight after 12 weeks and 4 years, respectively. The meal replacement plan has also proven to be effective in patients with type-2 diabetes. After 6 and 12 months, patients in the meal replacement group achieved on average a weight loss of 5.24 and 4.35% of their initial body weight, respectively. In contrast, after 6 and 12 months, patients on the individualized diet plan achieved on average a weight loss of 2.85 and 2.36% of their initial body weight, respectively. Meal replacements offer a promising strategy for treating obese patients with type-2 diabetes.

Overproduction of superoxide by the mitochondrial electron transport chain is the common link between the various pathways of glucotoxicity. The increased oxidative byproducts in diabetes are the result of a glucose-induced increase in the production of reactive oxygen species and decreased antioxidant defense capacity. Several epidemiologic observations indicate an inverse association between vitamin E intake and coronary heart disease (CHD). There are several limitations in such studies including the fact that they rely on food questionnaires and dietary recalls. Large interventional trials have yielded inconsistent results. Of concern is that, in some of these studies there was a greater incidence of lung cancer or CHD. These observations underscore the potential hazards of consuming large amounts of antioxidants. At the present time, given the inconsistencies of the studies available, the widespread supplementation with pharmacological doses of antioxidants should be discouraged. Future studies should focus on identifying reliable markers of oxidation to incorporate these measurements in the clinical interventional trial.

Gestational diabetes mellitus (GDM), a common medical complication of pregnancy is increasing in prevalence among all populations in parallel with the global increase in obesity and type-2 diabetes mellitus (DM). Although controversy regarding the perinatal consequences of GDM continues, efforts to identify the severity of maternal glucose intolerance associated with clinically important adverse outcomes are ongoing. Medical therapies beyond the traditional 'standard' medical nutrition therapy (diet) or insulin are being explored (oral glyburide and metformin); however, less costly alternatives such as more intensive lifestyle modification need to be evaluated. Such approaches are also applicable after GDM and are known to delay or prevent progression to DM in these high-risk subjects.

Fructose is a monosaccharide which is abundant in nature. It is the sweetest naturally occurring carbohydrate. The availability of fructose increased substantially when it became possible in the 1960s to economically produce high fructose syrups from corn starch and other starches. Such high fructose syrups are now used to sweeten soft drinks, fruit drinks, baked goods, jams, syrups and candies. The most recent data available suggest that fructose consumption is increasing worldwide. Fructose presently accounts for about 10% of average total energy intake in the United States. Studies in both healthy and diabetic subjects demonstrated that fructose produced a smaller postprandial rise in plasma glucose and serum insulin than other common carbohydrates. Substitution of dietary fructose for other carbohydrates produced a 13% reduction in mean plasma glucose in a study of type-1 and type-2 diabetic subjects. However, there is concern that fructose may aggravate lipemia, particularly in men. In one study, daylong plasma triglycerides (estimated by determining the area under response curves) in healthy men was 32% greater during a high fructose diet than during a high glucose diet. There is also concern that fructose may be a factor contributing to the growing worldwide prevalence of obesity. Increasing fructose consumption is temporally associated with the increase in obesity. Moreover, on theoretical grounds, dietary fructose might increase energy intake. Fructose stimulates insulin secretion less than does glucose and glucose-containing carbohydrates. Since insulin increases leptin release, lower circulating insulin and leptin after fructose ingestion might inhibit appetite less than consumption of other carbohydrates and lead to increased energy intake. However, there is not yet any convincing experimental evidence that dietary fructose does increase energy intake. Although evidence that fructose has adverse effects is limited, adding fructose in large amounts to the diet may be undesirable, particularly for men. Fructose that occurs naturally in fruits and vegetables is a modest component of energy intake and should not be of concern.

Lifestyle modification should be the primary therapeutic intervention in individuals with the dysmetabolic syndrome, given the fact that obesity, unhealthy diet, and physical inactivity are primary underlying risk factors for its development. Most individuals with the dysmetabolic syndrome need to lose weight through dietary changes and increases in physical activity. Modest weight losses may significantly improve all aspects of the syndrome. Because individuals differ in their lifestyles, tailoring interventions to meet the specific needs of each person will maximize the chances of success. Assessment of the individual with the dysmetabolic syndrome involves quantification of obesity, diets and dietary patterns, physical activity, emotional problems, and motivation. To help individuals make lifestyle changes, a number of behavior modification strategies have shown good efficacy. These strategies include a tailored problem-solving intervention, involving goal-setting, self-monitoring, stimulus control, cognitive restructuring, stress management, relapse prevention, social support, and contracting. The frequency of self-monitoring is an especially important strategy for continued success. Research studies have clearly demonstrated the power of lifestyle modification for long-term behavioral change. Lifestyle modification appears effective in delaying or preventing the development of the dysmetabolic syndrome.

There is debate among professionals regarding the use of the glycemic index (GI) for meal planning. In type-1 diabetes, there are 4 studies (average duration approximately 4 weeks) comparing high versus low GI diets; none reported improvements in HbA1c, and although 2 reported improvements in fructosamine, 2 reported no differences. In type-2 diabetes, there are 12 studies (average duration approximately 5 weeks); 3 reported improvements in HbA1c and fructosamine, 5 reported no differences in HBA1c, and 3 reported no differences in fructosamine. In adults, there is limited evidence that a low GI diet is beneficial for weight loss or satiety. Three epidemiologic studies reported that a low GI/glycemic load (GL) is associated with a reduced risk of developing diabetes or prevalence of insulin resistance; however, 5 studies report no association between GI/GL and the risk of developing diabetes, fasting insulin or insulin resistance, or adiposity. In general, the total amount of carbohydrate in a meal is the primary meal-planning strategy for people with diabetes. The GI can be used as an adjunct for the fine tuning of postprandial blood glucose responses. Other food/meal-planning interventions have been shown to be more effective than the use of the GI.

Despite 30 years of research, the cause of type-1 diabetes remains unknown. Meanwhile, its incidence has risen three-fold, its clinical features have become increasingly difficult to distinguish from type-2 diabetes and the contribution of genes to its pathogenesis has changed. The accelerator hypothesis argues that type-1 and type-2 diabetes are the same disorder of insulin resistance set against different genetic backgrounds. It identifies three processes which variably accelerate beta cell loss: constitution, insulin resistance and the immune response to it. None of the accelerators leads to diabetes in the absence of weight gain, a trend which the hypothesis deems central to the rising incidence of all diabetes in the industrially developed and developing world. Weight gain causes an increase in insulin resistance, which results in the weakening of glucose control. The rising blood glucose accelerates beta cell apoptosis (glucotoxicity) and, by increasing beta cell immunogenicity, further accelerates apoptosis in a subset genetically predisposed to an intense immune response. Rather than overlap between the two types of diabetes, the accelerator hypothesis envisages overlay--one a subset of the other. Body mass is central to the development and rising incidence of all diabetes. Only tempo distinguishes type 1 from type 2. The control of weight gain, and with it insulin resistance, could be the means of preventing both by slowing their progression.

The increasing prevalence of diabetes is reaching epidemic proportion worldwide. Because of the associated morbidity and mortality, it is exerting major pressure on the healthcare system. With a better understanding of the pathophysiology of type-2 diabetes, the concept of primary prevention has emerged. A number of studies have confirmed that intensive lifestyle modification was very effective in the prevention of diabetes in the impaired glucose tolerance (IGT) population. However, maintaining long-term lifestyle modification is a major challenge. It is, therefore, important to have other strategies, either pharmacological or surgical, that can be used as an adjunct or alternative to lifestyle modification. The Chinese study showed that metformin and acarbose could reduce the risk of diabetes by 65 and 83%, respectively, in IGT subjects. The efficacy of metformin was confirmed by the Diabetes Prevention Program (31% risk reduction) and that of acarbose by the STOP-NIDDM trial (36% risk reduction) in a similar high-risk population. The TRIPOD study showed that troglitazone could reduce the risk of diabetes by 55% in Hispanic women with a history of gestational diabetes. And more recently, the XENDOS study showed that orlistat could reduced the risk of diabetes by 37% in obese subjects when used as an adjunct to an intensive lifestyle program. Three studies have suggested that bariatric surgery in morbidly obese subjects could reduce the risk of diabetes to near zero. Furthermore, a number of studies have examined the effect of a renin angiotensin aldosterone system inhibitor, as well as statin and hormone replacement therapy on the prevention of type-2 diabetes in high-risk subjects as secondary outcomes and have suggested that they could be of potential benefit. The accumulating evidence is now overwhelming. Yes, diabetes can be prevented or delayed in high-risk populations. With this new information, we need to design new strategies to screen high-risk populations and to implement the new treatments that have proven effective in the prevention of type-2 diabetes.