Screening is best accomplished with a fasting plasma glucose test. Diabetes is diagnosed if the fasting plasma glucose level is 7.0 mmol/L or greater, or if the plasma glucose level is 11.1 mmol/L or ...greater in a 2-hour oral glucose tolerance test (OGTT).2 Either test should be done on 2 occasions before a diagnosis can be made. Impaired fasting glucose is diagnosed if the fasting glucose level is 6.1-6.9 mmol/L, and impaired glucose tolerance is diagnosed if the plasma glucose level is 7.8-11.0 mmol/L in a 2-hour OGTT. Although there are studies suggesting a benefit of treating people who have impaired glucose tolerance to reduce the incidence of progression of diabetes and possibly cardiovascular disease, the evidence is still inadequate to recommend screening for impaired fasting glucose or impaired glucose tolerance. However, people with the latter condition may nonetheless be identified in the course of their health care. These patients should be treated with lifestyle interventions aimed at lowering weight and increasing exercise, because such interventions may lower the incidence of diabetes (level I evidence).31-33 Acarbose treatment can also be considered for these patients, because it has been shown to reduce the incidence of cardiovascular outcomes and hypertension (level I evidence).34 Although the use of metformin33 and acarbose35 in patients with impaired glucose tolerance has been shown to reduce the incidence of diabetes over 3 years, the rate of diabetes dropped when metformin was discontinued.36 Of note, the prevention trials were all of 3 to 6 years' duration, and it is unclear whether the effects of lifestyle or pharmacologie intervention persist beyond that period. Furthermore, it is still uncertain whether diabetes can truly be prevented or whether these strategies simply delay its onset. The impact of delaying diabetes for a few years on preventing microvascular complications would likely be small, since the risk of complications is low in the first 15 years after diabetes diagnosis. The beneficial effects of lifestyle modification on cardiovascular events in people with impaired glucose tolerance also remain to be demonstrated. Finally, the cost-effectiveness of screening for impaired glucose tolerance and offering lifestyle interventions only to those with a positive test result and not to all people with diabetes risk factors has not been examined.
It is vital for individuals with type 2 diabetes (T2DM) to adhere to a healthy dietary pattern to maintain optimal blood glucose levels and overall health. Increasing costs of healthy foods, however, ...are a barrier to maintaining healthful dietary patterns, particularly for individuals with T2DM who are experiencing food insecurity. Poor diet quality may result in difficulties maintaining optimal blood glucose levels, leading to higher rates of diabetes complications, and increased acute care usage and costs. Although the adverse impacts of food insecurity on maintaining optimal blood glucose levels are well documented, effective strategies to this among individuals with T2DM are lacking. One approach is providing subsidies to purchase healthy foods through subsidized healthy food prescription programs. These programs may help reduce food insecurity and improve diet quality, thereby improving blood glucose levels and reducing diabetes complications over time.
A parallel group randomized controlled trial will examine the effectiveness of a subsidized healthy food prescription program compared to a healthy food prescription alone in improving average blood glucose levels (primary outcome), and other secondary outcomes among 404 adults who are experiencing food insecurity and persistent hyperglycemia. The subsidized healthy food prescription program consists of two core elements: 1) A one-time healthy food prescription pamphlet that outlines an evidence-based healthy dietary pattern; 2) A healthy food subsidy of $1.50/day/household member to purchase healthy foods in participating supermarkets for 6 months. At baseline and 6-month follow-up, participants will provide responses to sociodemographic and health-related items, and a variety of patient-reported outcomes. Biochemical and physical measurements will also be obtained.
The study’s theory of change posits that reducing food insecurity and improving diet quality will be key mediators in improving blood glucose levels, which may reduce diabetes complications, and healthcare usage and costs over time.
The results of this study will demonstrate if a subsidized healthy food prescription program results in meaningful changes in average blood glucose levels and other clinically relevant outcomes.
Alberta Innovates, Alberta Health Services.
Metabolic syndrome: Waist not want not Weir, Erica; Lipscombe, Lorraine
Canadian Medical Association journal (CMAJ),
2004-Apr-27, 2004-04-27, 20040427, Letnik:
170, Številka:
9
Journal Article
Recenzirano
Odprti dostop
Background and epidemiology: The metabolic syndrome refers to a constellation of clinical factors associated with an increased risk of diabetes and coronary artery disease. These factors include ...abdominal obesity, hypertension, dyslipidemia, impaired glucose metabolism, prothrombotic state and proinflammatory state. Also called the dysmetabolic syndrome, syndrome X or insulin resistance syndrome, this condition entered the scientific lexicon about 15 years ago as investigators sought to understand the link between insulin resistance and other metabolic factors in the development of coronary artery disease. Consistent, comprehensive results accumulated since then have not only confirmed that this syndrome leads to heart disease, but they have also demonstrated that modest interventions, such as changes in diet and physical activity level, may effectively control this syndrome and prevent outcomes such as diabetes. The rising prevalence of this syndrome in industrialized nations has largely been attributed to lifestyle changes in diet and physical activity, leading to higher obesity rates. In 2002 analysis of data from the Third National Health and Nutrition Examination Survey collected between 1988 and 1994 indicated that a whopping 44% of the American population aged 50 years and older had the metabolic syndrome, according to NCEP definitions.2 The prevalence increased with age, elevated body weight and membership in certain ethnic populations such as Hispanics and Native Americans. Additional research indicated that the syndrome was associated with a tripling of cardiovascular disease mortality and a doubling of overall mortality in a cohort of middle-aged Finnish men.3 Given that more than 40% of adults over age 50 are estimated to have this syndrome,2 these results have tremendous implications for future disease burden related to diabetes and coronary artery disease.
Glucose infusion can prevent the increase in glucose production (Ra) and increase glucose uptake (Rd) during exercise of moderate intensity. We postulated that 1) because in postabsorptive intense ...exercise (>80% maximal O2 uptake) the eightfold increase in Ra may be mediated by catecholamines rather than by glucagon and insulin, exogenous glucose infusion would not prevent the Ra increment, and 2) such infusion would cause greater Rd. Fit young men were exercised at >85% maximal O2 uptake for 14 min in the postabsorptive state controls (Con), n = 12 or at minute 210 of a 285-min glucose infusion. In seven subjects, the infusion was constant (CI; 4 mg . kg-1 . min-1), and in seven subjects it was varied (VI) to mimic the exercise Ra response in Con. Although glucose suppressed Ra to zero (with glycemia approximately 6 mM and insulin approximately 150 pM), an endogenous Ra response to exercise occurred, to peak increments two-thirds those in Con, in both CI and VI. Glucagon was unchanged, and very small increases in the glucagon-to-insulin ratio occurred in all three groups. Catecholamine responses were similar in all three groups, and correlation coefficients of Ra with plasma norepinephrine and epinephrine were significant in all. In all CI and VI, Rd at rest was 2x Con, increased earlier in exercise, and was higher for the 1 h of recovery with glucose infusion. Thus the Ra response was only partly attenuated, and the catecholamines are likely to be the regulators. This suggests that an acute endogenous Ra rise is possible even in the postprandial state. Furthermore, the fact that more circulating glucose is used by muscle during exercise and early recovery suggests that muscle glycogen is spared.
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