Weight gain and hypoglycemia have been identified as the major adverse effects of intensive diabetes therapy[1,29] or improved glucose control in type 1 diabetes. The current report provides new information on the rate of weight gain for up to 9 years of intensive therapy as well as data on body composition and body fat distribution. On average, adult subjects randomly assigned to intensive therapy gained 4.8 kg more during a mean 6.0 years of follow-up than those receiving conventional treatment. In both women and men, the rate of weight gain declined markedly with longer follow-up. Whether this is a natural consequence of long-term intensive treatment or a result of greater attention to weight gain by patients and study personnel is not clear. Similarly, the mechanism(s) of the weight gain cannot be directly addressed by this study.
Results from the 1-year follow-up data from the feasibility phase established a correlation between weight gain and both a lower HbA1c and the presence of severe hypoglycemia. In a study of 6 adult type 1 diabetes patients studied before and after intensive therapy, Carlson and Campbell estimated that 70% of their weight gain could be accounted for by elimination of glycosuria, and the remaining 30% by a 5% decrease in daily energy expenditure, as assessed by whole-room calorimetry. An increase in energy expenditure associated with poor glycemic control has previously been reported[31,32].
To our knowledge, an increase in fat-free mass associated with intensive treatment has not previously been reported. In the Carlson and Campbell study, 2.4 of the 2.6 kg of increased weight was accounted for by an increase in fat mass. However, their study sample was small (n = 6) and was followed for only 2 months, and thus it lacked power to find relatively modest increases in fat-free mass. Goodship et al. found no difference in fat-free mass in 31 subjects with type 1 diabetes compared with age- and sex-matched nondiabetic volunteers. Fat-free mass was calculated from anthropometry, and the subjects represented a wide range of glycemic control. Librenti et al. found no significant difference in body composition between type 1 diabetic and nondiabetic subjects, but their subjects were not receiving intensive therapy. Body composition was assessed with BIA using standard equations. In contrast, we assessed body composition in 1,180 individuals using a BIA method specifically validated for our population.
Much attention has been focused on body fat distribution because of increasing evidence that abdominal obesity, as assessed by WHR[12,35,36] or waist circumference, may be a risk factor for macrovascular disease. We found no significant differences in WHR associated with intensive therapy, despite greater weight gain, although waist circumferences were significantly greater among intensively treated women. Whether waist circumference or WHR is a better predictor of cardiovascular disease risk is debatable. A previous report noted that the intensively treated DCCT patients in the highest quartile of weight gain had increased WHR and BMI associated with higher blood pressure and a relatively atherogenic serum lipid profile. These individuals may be predisposed to the insulin resistance syndrome associated with type 2 diabetes, and their tendency toward abdominal obesity may have been exposed by intensive insulin treatment.
In conclusion, intensive diabetes treatment is associated with weight gain for up to 9 years. The rate of increase appears to decrease with time, however, and includes an increase in fat-free mass. Given the marked benefits of improved glycemic control in preventing the microvascular complications of type 1 diabetes, the risk of weight gain should not deter initiation of intensive treatment in appropriate patients. Nonetheless, better understanding of the causes of weight gain and methods to control it are desirable. Besides the physical consequences of excessive weight, concern with body image could make the fear of weight gain an obstacle to successful implementation of intensive diabetes therapy.
The DCCT is sponsored by the Division of Diabetes, Endocrinology and Metabolic Diseases of the National Institute of Diabetes and Digestive and Kidney Diseases, the National Institutes of Health, through cooperative agreements and a research contract. Additional support was provided by the National Heart, Lung and Blood Institute; the National Eye Institute; and the General Clinical Research Program of the National Center for Research Resources.Abbreviation Notes
BIA = bioelectrical body impedance analysis; DCCT = Diabetes Control and Complications Trial; NCEP = National Cholesterol Education Program; WHR = waist-to-hip ratio
Address reprint requests to the DCCT Research Group, Box NDIC/DCCT, Bethesda, MD 20892.
Diabetes Care. 2001;24(10):1711-172. © 2001 American Diabetes Association, Inc.
Cite this: Influence of Intensive Diabetes Treatment on Body Weight and Composition of Adults With Type 1 Diabetes in the Diabetes Control and Complications Trial - Medscape - Oct 01, 2001.