Type 1 Diabetes (T1D) is one of the most prevalent chronic diseases with childhood onset. The incidence of T1D has increased with 25% during the last three years, and threefold during the last generation. The disease has a multifactorial aetiology and app ears after a long period where the immune system destroys the insulin producing beta-cells in the pancreas, but we still do not know what starts the disease process. We know that the most important genetic factor is a combination of alleles in the HLA cla ss II complex. Since the genetic background of the population is stable, the changes in incidence must be attributed to changes in the environment or its interaction with genes. Infections are among the prime suspects for environmental triggers of Type 1 Diabetes. Although several viruses have been linked to type 1 diabetes, most studies have focused on enterovirus with mixed results. On the other hand, part of the risk for T1D may be due to lack of exposure to protective factors. The so-called hygiene hy pothesis proposes that the decline in microbial exposure has caused the concomitant increase in atopic disorders and probably also Type 1 Diabetes. Maybe the timing of infection in pregnancy and early childhood and the total number of infections are of i mportance for TID risk. In this project helminths and parasites, and common symptomatic virus infections will be studied. The large cohort studies Environmental Triggers of Type 1 Diabetes: The MIDIA Study and The Norwegian Mother and Child Cohort are int ernationally unique since children can be followed from mothers life during childhood with biological samples and questionnaire information. In the MIDIA study children with high genetic risk for Type 1 Diabetes are followed with stool samples every month s the first three years of life, with questionnaires and blood samples every third month in the first year, and thereafter annually to 15 years of age.