Type 1 Diabetes (T1D) is an autoimmune disease caused by the destruction of insulin-producing -cells in the islets of Langerhans by autoantibodies. Its prevalence in the population is rapidly increasing and the precise triggers and underlying mechanisms of disease onset are still not fully understood. The methylation of cytosines in cytosine – guanine dinucleotides is an important epigenetic mechanism to control gene expression. The aim of this thesis was to establish a link between DNA methylation patterns in umbilical cord blood of children with familial risk of type 1 diabetes, environmental factors and information on future events (seroconversion, T1D onset). Using multivariate regression analysis, epigenome wide association studies were conducted with children from the BABYDIET cohort. Findings support the assumption of heritable disease-associated methylation patterns and give evidence for environmentally induced epigenetic programming in utero. Further examination of the found results, enabled novel insight into epigenetic mechanisms and disease susceptibility.