The recent increase in T1D incidence points to a changing global environment rather than variation in the gene pool, which require the passage of multiple generations (1).
Twin studies also provide evidence for the importance of environmental risk factors for T1D.
Environmental risk factors are thought to act as either ‘initiators’ or ‘accelerators’ of beta cell autoimmunity, or ‘precipitators’ of overt symptoms in individuals who already have evidence of beta cell destruction (1).
The T1D environmental risk factors that have received most attention are viruses and infant nutrition.
The role of hygiene in the aetiology of T1D is also currently being explored
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