Publication Description
OBJECTIVE: Glycated hemoglobin (HbA1c), a standard measure of chronic glycemia for managing diabetes, has been proposed to diagnose diabetes and identify people at risk. The Diabetes Prevention Program (DPP) was a 3.2-year randomized clinical trial of preventing type 2 diabetes with a 10-year follow-up study, the DPP Outcomes Study (DPPOS). We evaluated baseline HbA1c as a predictor of diabetes and determined the effects of treatments on diabetes defined by an HbA1c >/=6.5% (48 mmol/mol). RESEARCH DESIGN AND METHODS: We randomized 3,234 nondiabetic adults at high risk of diabetes to placebo, metformin, or intensive lifestyle intervention and followed them for the development of diabetes as diagnosed by fasting plasma glucose (FPG) and 2-h postload glucose (2hPG) concentrations (1997 American Diabetes Association [ADA] criteria). HbA1c was measured but not used for study eligibility or outcomes. We now evaluate treatment effects in the 2,765 participants who did not have diabetes at baseline according to FPG, 2hPG, or HbA1c (2010 ADA criteria). RESULTS: Baseline HbA1c predicted incident diabetes in all treatment groups. Diabetes incidence defined by HbA1c >/=6.5% was reduced by 44% by metformin and 49% by lifestyle during the DPP and by 38% by metformin and 29% by lifestyle throughout follow-up. Unlike the primary DPP and DPPOS findings based on glucose criteria, metformin and lifestyle were similarly effective in preventing diabetes defined by HbA1c. CONCLUSIONS: HbA1c predicted incident diabetes. In contrast to the superiority of the lifestyle intervention on glucose-defined diabetes, metformin and lifestyle interventions had similar effects in preventing HbA1c-defined diabetes. The long-term implications for other health outcomes remain to be determined.
Primary Author
Diabetes Prevention Program Research Group
Author Address
National Institute of Diabetes and Digestive and Kidney Diseases, Phoenix, AZ dppmail@bsc.gwu.edu.; Biostatistics Center, George Washington University, Rockville, MD.; University of Miami, Miami, FL.; Northwestern University, Chicago, IL.; Albert Einstein College of Medicine, New York, NY.; Massachusetts General Hospital and Harvard Medical School, Boston, MA.; Biostatistics Center, George Washington University, Rockville, MD.; University of Michigan, Ann Arbor, MI.; Joslin Diabetes Center and Harvard Medical School, Boston, MA.; VA Puget Sound Health Care System and University of Washington, Seattle, WA.; Indiana University, Indianapolis, IN.; Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Publisher
by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered
Author Address
National Institute of Diabetes and Digestive and Kidney Diseases, Phoenix, AZ dppmail@bsc.gwu.edu.; Biostatistics Center, George Washington University, Rockville, MD.; University of Miami, Miami, FL.; Northwestern University, Chicago, IL.; Albert Einstein College of Medicine, New York, NY.; Massachusetts General Hospital and Harvard Medical School, Boston, MA.; Biostatistics Center, George Washington University, Rockville, MD.; University of Michigan, Ann Arbor, MI.; Joslin Diabetes Center and Harvard Medical School, Boston, MA.; VA Puget Sound Health Care System and University of Washington, Seattle, WA.; Indiana University, Indianapolis, IN.; Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Secondary Authors
* prepared by
Knowler,W. C.
Edelstein,S. L.
Goldberg,R. B.
Ackermann,R. T.
Crandall,J. P.
Florez,J. C.
Fowler,S. E.
Herman,W. H.
Horton,E. S.
Kahn,S. E.
Mather,K. J.
Nathan,D. M.
