Diabetes causes multiple metabolic defects, and its complications attack multiple organ systems. But it is frustratingly difficult to pin down a specific link between these metabolic derangements and long-term complications. The venerable "control and complications controversy" persists because we keep looking for one answer, one simple relationship between glycemic control and diabetic complications. But why should the relationship be simple or linear? Why should the product of blood glucose and time necessarily cause, equally, such diverse end-organ damage as neuropathy, nephropathy, retinopathy, and accelerated atherosclerosis? Factors other than blood glucose are almost certainly involved.
It should not be surprising, then, that obesity, blood pressure, high serum lipid levels, and family history play a significant role in macrovascular complications. Coexisting risk factors are especially relevant in type II, non—insulin-dependent diabetes, because this disease confers the most risk for accelerated atherosclerosis and the risk is most difficult to correlate specifically with glycemia.
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