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Correction
to
Sinha et al.,
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Thus, the association of obesity with impaired glucose tolerance and type 2 diabetes in children may not be a new phenomenon. However, the number of obese children is increasing rapidly, especially in some ethnic groups.3 Thus, the absolute number of children in the population who have impaired glucose tolerance and type 2 diabetes is increasing because of the increased numbers of obese children. Future research should focus on why an accumulation of excess body fat becomes detrimental to health. Public health efforts should focus on reducing the prevalence of obesity among children, since this factor alone is likely to have a major effect on the current and future risk of type 2 diabetes.
Michael I. Goran, Ph.D.
University of Southern California
Los Angeles, CA 90033
goran{at}usc.edu
References
We evaluated glucose tolerance in substantially overweight black children and white children (6 to 11 years old) who were recruited from the local community and whose parents were not seeking treatment for the weight problem. The prevalence of impaired glucose tolerance was much lower in this group of children (4.1 percent; 95 percent confidence interval, 2 to 9 percent), even though they had significantly greater insulin resistance and a significantly higher index of beta-cell function than did children who were not overweight (Table 1). An evaluation of children in our cohort who had a mean (±SD) body-mass index of 32±5 (calculated as the weight in kilograms divided by the square of the height in meters), which was similar to the mean value in the cohort described by Sinha et al., showed that only 3 of 48 children had impaired glucose tolerance (6.3 percent; 95 percent confidence interval, 1 to 17 percent).
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Gabriel I. Uwaifo, M.D.
Jane Elberg, B.S.
Jack A. Yanovski, M.D., Ph.D.
National Institutes of Health
Bethesda, MD 20892
uwaifog{at}mail.nih.gov
References
Cecilia Invitti, M.D.
Luisa Gilardini, M.D.
Istituto Auxologico Italiano
20145 Milan, Italy
invitti{at}auxologico.it
Giancarlo Viberti, M.D.
Guy's Hospital
London SE1 9RT, United Kingdom
Phyllis W. Speiser, M.D.
Schneider Children's Hospital
New Hyde Park, NY 11042
pspeiser{at}lij.edu
In my opinion, the solution to the obesity epidemic must be based on much broader public health and clinical strategies. The time has come to develop comprehensive national obesity-prevention programs that include educational, behavioral, and environmental components analogous to those already in place for tobacco use. Examples of effective prevention programs that focus on children and adolescents are school-based interventions designed to increase physical activity and consumption of healthier foods and home-based interventions designed to reduce television viewing.2,3 Physicians and other health care professionals, elected officials, educators, and parents need to recognize the impact of this major health problem and have the will and energy to correct it through preventive approaches.
Hannes Gaenzer, M.D.
University of Innsbruck
A-6020 Innsbruck, Austria
hannes.gaenzer{at}uibk.ac.at
References
To the Editor: I agree with Dr. Goran that prevalence rates are best derived from non–clinic-based samples. Of note is the recent school-based study by Grey et al.,1 involving 42 obese adolescents whose parents were not seeking treatment. In this group, the prevalence of impaired glucose tolerance was 21.4 percent, and the prevalence of type 2 diabetes was 4.6 percent — findings that are very similar to ours. I disagree with Dr. Goran's statement that our findings were very similar to those reported by Paulsen et al. in 1968; they did not use the same ADA definitions that we used. When we recalculated the prevalence of impaired glucose tolerance in their study using the ADA criteria that we had used in our study, impaired glucose tolerance was present in 11 percent of the children, and 6 percent had type 2 diabetes mellitus.
The low prevalence of impaired glucose tolerance (6.3 percent) reported by Uwaifo et al. in obese children recruited from the community is probably due to a low insulin-resistance index. In fact, the mean insulin-resistance index in their obese children was 3.4±2.7, whereas in our children it was 5±0.6 in children with normal glucose tolerance and 7.2±1 in those with impaired glucose tolerance.
Interestingly, Invitti et al. report that the cohort of children they studied, although grossly obese, had a considerably lower insulin-resistance index than our obese American cohort. As in our study, insulin resistance was found to be strongly and independently related to the glucose level at two hours. However, in contrast to our findings, the insulinogenic index was related to the glucose level at two hours. It is conceivable that our cohort was not large enough for us to detect differences in beta-cell function in patients with impaired glucose tolerance. We concur that differences in insulin resistance related to ethnic background and lifestyle may explain the striking disparity in the prevalence of impaired glucose tolerance between the two cohorts.
In response to Dr. Speiser's two important questions: we suggest that children with marked obesity undergo screening for fasting hyperinsulinemia and other features of the metabolic syndrome. The reproducibility of the insulin-resistance index (determined by homeostatic model assessment) is not known and varies greatly according to the method used to measure insulin and glucose levels. Furthermore, its predictive value in children needs to be determined.
We would also like to note that in our report, the values for proinsulin and for the ratio of proinsulin to insulin on page 806 and in Figure 2 are incorrect. All reported values for proinsulin and for the ratio of proinsulin to insulin should be divided by a factor of 10. In addition, the second part of the last sentence of the legend to Figure 2 should read, "to convert values for proinsulin to picomoles per liter, divide by 0.00939."
Sonia Caprio, M.D.
Yale School of Medicine
New Haven, CT 06520-8064
sonia.caprio{at}yale.edu
References
To the Editor: There are two commonly used strategies to combat a major public health problem such as adolescent obesity. One is a population-based strategy, as suggested by Dr. Gaenzer. The other strategy is to identify persons at high medical risk (e.g., obese adolescents with impaired glucose tolerance) and target them for disease-specific therapy. The population-based strategy works well when the program is both effective in preventing or curing the problem and low in cost. An excellent example of an outstanding population-based strategy is the use of vaccinations to prevent childhood diseases. However, there is no effective low-cost treatment for childhood obesity. I agree with Dr. Gaenzer that the time has come to develop comprehensive national obesity-prevention programs similar to programs aimed at tobacco use. However, until we have a prevention program that has been proved to reduce the incidence of childhood obesity significantly, I stand by my recommendation to identify obese children who are at high risk for diabetes and target them for intensive weight-loss treatment.
Albert P. Rocchini, M.D.
University of Michigan Medical Center
Ann Arbor, MI 48109
rocchini{at}med.umich.edu
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