Diabetes 56:1502-1507, 2007 DOI: 10.2337/db07-0140 © 2007 by the American Diabetes Association
(How) Can We Prevent Type 2 Diabetes?From the Department of Medicine, University of Southern California Keck School of Medicine, Los Angeles, California Address correspondence and reprint requests to Thomas A. Buchanan, MD, Room 6602, General Hospital, 1200 N. State St., Los Angeles, CA 90033. E-mail: buchanan@usc.edu
Abbreviations:
DPP, Diabetes Prevention Program; DPS, Diabetes Prevention Study; DREAM, Diabetes REduction Assessment with rosiglitazone and ramapril Medication; PIPOD, Pioglitazone in Prevention of Diabetes; TRIPOD, Troglitazone in Prevention of Diabetes
In the past 6 years, several randomized controlled trials have been conducted to test the impact of behavioral and pharmacological interventions on rates of development of type 2 diabetes in high-risk groups (1–7). The studies have demonstrated that it is possible to reduce the number of people who develop diabetes by 25–62% over 3- to 6-year time frames. As a result, discussions on mitigating the growing public health problem of type 2 diabetes have expanded from a relatively narrow focus on disease treatment to a broader focus on disease prevention. Ultimately, the broader focus is relevant to prevention and early treatment, both aimed at stabilization or reversal of an otherwise progressive disease process. Optimal strategies for disease modification at the stages of pre-diabetes and early diabetes remain to be defined. However, existing information is sufficient to begin to sort out the relative effectiveness of interventions and to make some recommendations for clinical care. In this article, I discuss both the concept of and evidence for diabetes prevention in the context of the biology of type 2 diabetes. I also suggest an approach for clinical care that is based on a combination of knowledge about disease biology and the results of clinical trials.
Hyperglycemia results from an insulin supply that is insufficient to meet the body's needs. Diabetes is hyperglycemia that exceeds the threshold where the risk of diabetic retinopathy is currently thought to begin. In type 2 diabetes, insufficient insulin supply occurs in a setting of increased insulin demands—chronic insulin resistance. Longitudinal studies of insulin secretion and insulin action in Pima Indians (8), Hispanic women with prior gestational diabetes (9), and Hispanic, white, and African-American participants in the Insulin Resistance Atherosclerosis Study (10) reveal that abnormalities in insulin secretion and
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