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Treating the Wrong Surrogate End Point?

Mark O. Goodarzi, MD, PhD; Bruce M. Psaty, MD, PhD

JAMA. 2008;300(17):2051-2053.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

In the 1920s, the use of insulin to treat type 1 diabetes was lifesaving for children in diabetic ketoacidosis. Among the surviving patients with diabetes, the microvascular and macrovascular disease complications proved to be nonetheless devastating. The treatment of type 1 diabetes was revolutionized by the discovery that intensive glycemic control could prevent or delay the development of the microvascular complications of retinopathy, neuropathy, and nephropathy. Indeed, for patients with type 1 diabetes, aggressive insulin treatment also reduced the long-term risk of cardiovascular disease.¹

Therapeutic enthusiasm for intensive treatment expanded to include patients with type 2 diabetes, who typically have insulin resistance rather than the absence of insulin production characteristic of type 1 diabetes. Elevated glucose levels in patients with type 2 diabetes, like the high white blood cell counts in patients with bacterial pneumonia, are a consequence of insulin . . . [Full Text of this Article]

Author Affiliations: Division of Endocrinology, Diabetes and Metabolism, Medical Genetics Institute, Cedars-Sinai Medical Center, and Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California (Dr Goodarzi); and Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology, and Health Services, University of Washington, and Center for Health Studies, Group Health, Seattle, Washington (Dr Psaty).

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