Environmental Trigger(s) of Type 1 Diabetes: Why Is It So Difficult to Identify?

Type 1 diabetes (T1D) is one of the most common chronic diseases with childhood onset, and the disease incidence has increased from two-to fivefold over the past half century from, as of yet, unknown reasons. T1D occurs when the body's immune system turns against itself, destroying in a very specific and targeted way the pancreatic beta cells. T1D results from poorly defined interactions between susceptibility genes and environmental determinants. In contrast to the rapid progress in finding T1D genes, the identification and confirmation of environmental trigger(s) remain a formidable challenge. The identification of environmental determinant(s) responsible for the development of or protection against T1D is crucial from that point of view that they may be modifiable and might ultimately be used in disease prevention. The high costs of the disease both to the society and to the affected individuals and their families imply that preventing a fraction of cases, or even delaying the onset, will be of high value. This special issue contains original research articles as well as review articles that could stimulate the continuing efforts in the identification of exogenous triggers in the development of T1D. New data on environmental factors associated with progression to clinical T1D was of particular interest. Articles using bioinformatics to evaluate the number of cases (either autoantibody positivity or clinically recognized disease as the case definition) needed for the identification of a certain environmental trigger were as well very interesting. In addition, this special issue includes articles presenting autoantibody patterns in the prediction of T1D and cellular and molecular mechanisms in the disease pathogenesis. Here we give a short overview of the content of the current special issue. In original research articles, the hygiene hypothesis and risk for T1D were studied prospectively in the Diabetes Autoimmunity Study in the Young (DAISY) by examining daycare attendance during the first 2 years of life. Altogether 1783 children were available with complete daycare and breastfeeding data. For the first time, the data obtained suggest that breastfeeding may modify the effect of daycare on the risk of T1D. The goal of the other DAISY study included was to demonstrate methods for identifying exposures that differentially influence the disease process at certain ages by testing for age-related heterogeneity. The DAISY study has followed 2547 children at increased risk for T1D from birth, and 188 have developed islet autoimmunity (IA). Ethnicity, maternal age, and erythrocyte membrane n-3 fatty acid …