& u sota code); and a Rose Questionnaire positive for claudication or angina pectoris in the absence of clinical diagnosis of angina pectoris or claudication. Subclinical disease was present in 60% of participants with IGT. One can interpret these types of data to provide the following chronology. The insulin resistance syndrome starts at a relatively young age (young adulthood) and causes accelerated atherosclerosis. By middle age, subclinical macrovascular disease is present. In those individuals with the genetic propensity, beta-cell insulin secretory function decreases and impaired glucose tolerance and finally type 2 diabetes develop. By the time type 2 diabetes does develop, subclinical and, in some cases, clinical macrovascular disease is well established and will continue to progress. Poorly controlled hyperglycemia even further accelerates the rate of atherosclerosis.

The implications of this hypothesis have far-reaching clinical implications. It means that accelerated atherosclerosis starts at a relatively young age, long before there is any clinical disease and before we would traditionally intervene. This is the stage at which treatment of insulin resistance and cardiovascular risk factors are likely to be most effective in reducing macrovascular disease. At the time of diagnosis of type 2 diabetes, many or perhaps most patients will already have moderately advanced subclinical or even clinical cardiovascular disease. Intervention strategies to reduce cardiovascular risk factors in type 2 diabetic patients will be of value but may have somewhat limited effectiveness since the subclinical cardiovascular abnormalities may be more important in determining the future course of the CVD than the risk factors themselves.

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