Abstract
OBJECTIVE - The effectiveness of intentional weight loss in reducing cardiovascular disease (CVD) events in type 2 diabetes is unknown. This report describes 1-year changes in CVD risk factors in a trial designed to examine the long-term effects of an intensive lifestyle intervention on the incidence of major CVD events. RESEARCH DESIGN AND METHODS - This study consisted of a multicentered, randomized, controlled trial of 5,145 individuals with type 2 diabetes, aged 45-74 years, with BMI >25 kg/m2 (>27 kg/m 2 if taking insulin). An intensive lifestyle intervention (ILI) involving group and individual meetings to achieve and maintain weight loss through decreased caloric intake and increased physical activity was compared with a diabetes support and education (DSE) condition. RESULTS - Participants assigned to ILI lost an average 8.6% of their initial weight vs. 0.7% in DSE group (P < 0.001). Mean fitness increased in ILI by 20.9 vs. 5.8% in DSE (P < 0.001). A greater proportion of ILI participants had reductions in diabetes, hypertension, and lipid-lowering medicines. Mean A1C dropped from 7.3 to 6.6% in ILI (P < 0.001) vs. from 7.3 to 7.2% in DSE. Systolic and diastolic pressure, triglycerides, HDL cholesterol, and urine albumin-to-creatinine ratio improved significantly more in ILI than DSE participants (all P < 0.01). CONCLUSIONS - At 1 year, ILI resulted in clinically significant weight loss in people with type 2 diabetes. This was associated with improved diabetes control and CVD risk factors and reduced medicine use in ILI versus DSE. Continued intervention and follow-up will determine whether these changes are maintained and will reduce CVD risk.
Original language | English (US) |
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Pages (from-to) | 1374-1383 |
Number of pages | 10 |
Journal | Diabetes care |
Volume | 30 |
Issue number | 6 |
DOIs | |
State | Published - May 2007 |
Bibliographical note
Funding Information:This work was supported in part by the National Institutes of Health [grants T32MH020030 to M.J.L.; R01MH106595 to L.E.D., A.X.M., C.M.N.; R01HD059835 to B.G.; R01MH105379 to N.R.N.; R01MH108641 to N.R.N., and K02AA023239 to A.B.A.]. This work was funded by NIMH/U.S. Army Medical Research and Material Command [R01MH106595] and NIH 5U01MH109539. This work would have not been possible without the financial support provided by Stanley Center for Psychiatric Genetics at the Broad Institute, One Mind, and Cohen Veterans Bioscience.