Evidence is scarce regarding sensitive exposure windows of the
hypothesised association between environmental factors and the
risks of developing T1D. It has been suggested that T1D is likely to originate from gene–environment interactions during foetal de- velopment (Howard et al., 2011). Recent evidence provides a convincing link between a suboptimal gestational environment and an increased risk of onset of metabolic diseases (Joss-Moore and Lane, 2009). Most cases (94%) of T1D can be predicted by detecting multiple islet autoantibodies in children below the age of five years, supporting the hypothesis that the autoimmune processes occur early in life (Regnéll and Lernmark, 2013; Mehers
and Gillespie, 2008).