Ramachandiran Cooppan

Joslin Diabetes Center, Boston, Massachusetts, U.S.A.

Diabetes mellitus is a chronic disease that results in major morbidity and mortality. As with any chronic illness the goals of therapy are to alleviate the acute symptoms and complications and then focus on preventing the long-term consequences. While the initial goals can be reasonably achieved in most instances, the long-term complications can prove to be more of a challenge. This is in part due to the fact that the disease is not a single entity but a complex metabolic syndrome that results in hyperglycemia. This can be due to an absolute deficiency of insulin or either defects in insulin secretion and insulin action or a combination of both. Clinically, it is convenient to classify the patient as having either type 1 or type 2 diabetes mellitus. This approach is based more on the underlying pathophysiology than on treatment, since many patients with type 2 diabetes will eventually require insulin for treatment.

Several different pathogenic processes may cause the development of diabetes and range from an autoimmune destruction of the beta cells in type 1 diabetes mellitus to alterations in insulin secretory capacity and peripheral insulin resistance in type 2 diabetes. In general type 1 diabetes develops in younger individuals while type 2 disease occurs in adults. However, there is a recent increase in the prevalence of type 2 diabetes mellitus in children. In the Pima Indians the prevalence has increased from 1% in subjects aged 15 to 24 1979 to 5%, and has also emerged in the 10- to 15-year-olds (1). In addition there has been an increase in African American and Mexican American youth. This increase is also seen in other parts of the world such as Japan, Bangladesh, Libya, and New Zealand (2). The issue of an increase in type 2 diabetes in the young makes it even more important to diagnose and treat the disease earlier as the long-term microvascular complications are related to both the degree of hyperglycemia as well as the duration of the disease. Dating the onset of clinical type 1 diabetes may be easier because of the acute onset of symptoms in general. However it is more difficult to do this in type 2 diabetes because the onset of symptoms is preceded by many years of asymptomatic hyperglycemia. Many patients with adult type 2 diabetes already have evidence of complications at diagnosis (3). It is estimated that these patients have had their disease for at least 10 years before it is diagnosed.

Another major issue that challenges our strategies and overall approach to therapy has to do with the long-term complications of diabetes. While microvascular disease affecting the eye, kidney, and nerves can occur in both type 1 and type 2 diabetes, patients with type 2 disease have a greater risk of developing macrovascular disease, especially coronary artery disease. Cardiovascular disease is the most important cause of death in patients with type 2 diabetes and the risk starts very early during the stage of impaired glucose tolerance well before the clinical diagnosis of diabetes mellitus (4).

These clinical issues therefore have important implications as we address the issue of glycemic control and the goals we set for our patients. If controlling the blood glucose to normal levels resulted in preventing the development and progression of both microvascular and macrovascular disease then the situation would be clear. We could approach our patients with confidence and encourage them to control the disease, while reassuring them that the time and effort they put in would be rewarded with no complications. However, the data is not as clear-cut as this, especially in regard to macrovascular disease, though recent data indicates that early glycemic control can affect the later development of heart disease in type 1 patients. The situation for the microvascular disease is far more compelling, especially with data from studies completed in the last decade.

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