The Effect of Excess Weight Gain with Intensive Diabetes Treatment on Cardiovascular Disease Risk Factors and Atherosclerosis in Type 1 Diabetes: Results from the Diabetes Control and Complications Trial / Epidemiology of Diabetes Interventions and Complications Study (DCCT/EDIC) Study
Background—Intensive diabetes therapy of type 1 diabetes (T1DM) reduces diabetes complications but can be associated with excess weight gain, central obesity, and dyslipidemia. The purpose of this study was to determine if excessive weight gain with diabetes therapy of T1DM is prospectively associated with atherosclerotic disease.
Methods and Results—Subjects with T1DM (97% Caucasian, 45% female, mean age 35 years) randomly assigned to intensive (INT) or conventional (CONV) diabetes treatment during the Diabetes Control and Complications Trial (DCCT) underwent intima-media thickness (IMT) (n=1015) and coronary artery calcium (CAC) score (n=925) measurements during follow-up in the Epidemiology of Diabetes Interventions and Complications (EDIC) Study. INT subjects were classified by quartile of BMI change during the DCCT. Excess gainers (4th quartile, including CONV subjects meeting this threshold) maintained greater BMI and waist circumference (WC), needed more insulin, had greater IMT (+5%, P<0.001 EDIC year 1, P=0.003 EDIC year 6), and trended towards greater CAC scores (OR 1.55, CI 0.97 – 2.49, P=0.07) than minimal gainers. DCCT subjects meeting metabolic syndrome criteria for WC and blood pressure had greater IMT in both EDIC years (P=0.02 to <0.001); those meeting HDL criteria had greater CAC scores (OR 1.6 and CI 1.1 – 2.4, P=0.01) during follow-up. Increasing frequency of a family history of diabetes, hypertension, and hyperlipidemia was associated with greater IMT thickness with INT but not CONV.
Conclusions—Excess weight gain in DCCT is associated with sustained increases in central obesity, insulin resistance, dyslipidemia and blood pressure, as well as more extensive atherosclerosis during EDIC.
- Received October 31, 2011.
- Accepted November 2, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited