Chicago Childhood Diabetes Registry

The goal of this study is to investigate the epidemiology and natural history of childhood-onset diabetes, whether of autoimmune, non-autoimmune, or mixed etiology. The following research questions are to be addressed:

1. Is it feasible to distinguish type 1 from early-onset type 2 diabetes at diagnosis?
2. What proportion of diabetic children carry susceptibility genes for diabetes (MODY, type 1 or type 2) and/or obesity? How do these susceptibility alleles assort themselves within families?
3. Is change in the incidence of childhood diabetes occurring uniformly across all age-, sex- and ethnic strata?
4. Are secular changes in type 2 incidence rates continuing, and is this occurring in all age-, sex- and ethnic strata?
5. Do young people with diabetes who demonstrate signs and symptoms of early complications have greater insulin resistance or other characteristics that distinguish them from those patients who are free of complications, controlled for disease duration and metabolic control?
6. Do young patients with early signs/symptoms of complications have more parents who themselves have elevated cardiovascular disease risk factors, than patients who are free of chronic complications, controlled for disease duration and metabolic control?

Childhood diabetes is an urgent public health challenge. Affected children and their families face major intrusions on quality of life, financial burdens, and limitations in achieving their educational and vocational goals. Recent increases in childhood diabetes herald a substantial jump in the diabetes-related public health burden in years to come, unless effective primary and secondary prevention efforts are mounted. It is therefore essential to understand in detail the mechanisms underlying the current epidemic among children and adolescents. We believe that the most critical area of research at this point in time is to unravel the role of genetic susceptibility to diabetes and obesity, and its interaction with the changing epidemiology of behavioral risk factors. The few available population-based studies show that a substantial minority of children with diabetes are affected by type 2, particularly in population subgroups where adult type 2 diabetes rates are high. Increases in the traditional risk factors for type 2 diabetes (obesity, physical inactivity) are documented to be increasing in US, suggesting that the rates of childhood type 2 diabetes are likely to continue to increase apace. In direct contrast to the situation among adults, screening results in those under age 18 show that virtually all childhood diabetes is detected within a short time after its onset. Interest has recently revived in the interplay of type 1 and type 2 risk factors in the etiology of childhood diabetes and its chronic sequelae. Geneticists have made important progress in identifying the multiple variants associated with risk of type 2 diabetes and obesity, and they have confirmed the strong influence of HLA and insulin promoter loci in susceptibility to type 1. In short, we are currently poised to embed genetic studies in an epidemiologically defined population to efficiently investigate the etiology of glucose intolerance.