Diet and Exercise in Type 2 Diabetes Mellitus

INTRODUCTION A National Institutes of Health (NIH) Consensus Development Conference in 1986 published a consensus statement entitled “Diet and Exercise in Noninsulin-Dependent Diabetes Mellitus.” Its report, reproduced in this journal, discussed the relationship between obesity and type 2 diabetes, appropriate dietary recommendations for type 2 diabetes, and the benefits and risks of exercise. Important questions were raised and future areas of investigation suggested. Much research has been published since 1986, and exciting studies are in progress to help answer some of these questions. This article provides an update, highlighting findings published since the Consensus Development Conference. Diabetes mellitus is a major health problem in America, with an estimated 16 million people affected. Type 2 (noninsulin-dependent) diabetes mellitus accounts for 90% of cases of diabetes. Diabetes is the leading cause of new adult blindness, renal failure, and nontraumatic distal extremity amputations and is an important risk factor for coronary, cerebral, and peripheral vascular disease. In 1992, costs attributable to diabetes in the United States were estimated to be $92 billion and the prevalence (and cost) of this disease has continued to increase.’ The incidence of type 2 diabetes increases rapidly after age 30. Native Americans have a high prevalence of type 2 diabetes. In the Pima Indian group, 13% of 2.5 to 29-y-olds have type 2 diabetes, and nearly one-half the adult population is affected. Type 2 diabetes is twice as common in African-Americans and Hispanics as in nonHispanic whites in the United States. Asian and Pacific Island Americans also have a high prevalence of diabetes. Geographic and ethnic differences appear to be related to the incidence of obesity, and lifestyle risk factors are superimposed on a susceptible genetic background. More than 60 rare genetic syndromes involving nuclear and mitochondrial genes are associated with the development of glucose intolerance.* An autosomal dominant syndrome known as maturity onset diabetes of the young (MODY) is characterized by early onset non-ketosis-prone diabetes.3 A glucokinase gene polymorphism in exon 7 was linked to MODY in 2545% of a group in France and was associated with earlier development of diabetes.4 The heterogeneity of genetic associations seen in the MODY population suggests that multiple genes are involved. Although a large number of rare genetic syndromes are associated with glucose intolerance, they account overall for only approximately 1% of type 2 diabetes. For most patients with type 2 diabetes, the specific genetic defects are unknown. Different models to explain the etiology of type 2 diabetes have been proposed. In one model, the insulin resistance syndrome develops in genetically susceptible individuals. As they progress from normal glucose tolerance to impaired glucose tolerance, increasing insulin resistance develops.’ This may be related to environmental factors, including obesity, diet, and physical inactivity. This model requires a second step, moving from impaired glucose tolerance to type 2 diabetes, due to a pancreatic /l cell defect and decreasing insulin secretion.6 A genetic basis may exist for the insulin secretory defects and insulin resistance. In another model, there are improperly functioning ,B cells that are genetically defective and/or have been injured by viruses or environmental toxins. p cell autoantibodies can be found in people with adultonset type 1 diabetes. These patients, who represent a minority of people developing diabetes as adults, are usually not overweight and require insulin therapy. In new onset type 1 diabetes, p cell production is variable, and declines over time and with increasing hyperglycemia. Unlike type 1 diabetes, the insulin secretory defect in type 2 diabetes is unrelated to autoimmunity. The etiology of the microvascular complications of diabetes (retinopathy, neuropathy, and nephropathy) is assumed to be related to hyperglycemia in both type 1 and type 2 diabetes. A landmark study, the Diabetes Control and Complications Trial (DCCT), published in 1993 demonstrated that improved glycemic control in type 1 diabetes could slow the development and progression of microvascular complications7 In this study, a team approach using intensive monitoring, diet, and insulin therapy with three or more injections per day or an insulin pump was compared with conventional insulin therapy (one or two injections per day). The results were overwhelming: there was a 40-70% reduction in risk for retinopathy, nephropathy, and neuropathy in the group with improved glycemic control, the intensively treated group. The DCCT enrolled only patients with type 1 diabetes. More recently, a similar but smaller Japanese study of insulin-treated patients with type 2 diabetes also demonstrated that improved glycemic control decreased the progression of nephropathy, retinopathy, and neuropathy.’ Since improvement in glucose