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Type 1 diabetes is classified into two types by the American Diabetes Association; type 1A diabetes is the immune-mediated form and type 1B the non–immune mediated form of the disease, both leading to β-cell destruction and absolute insulin deficiency. It is estimated that approximately 1.5 million people in the US have type 1A diabetes. The incidence of type 1 diabetes is increasing worldwide at a rate of 3–5 % each year. Strikingly, it has doubled in each of the last two decades, children less than five years of age being the most commonly affected group.1,2 Recently, it has been reported that if the present trends continue, the number of patients younger than five years of age will have risen by 70 % by the year 2020.3 The increasing incidence of type 1 diabetes is unlikely due to genes, as the increase has occurred over a relatively short period of time. Environmental causes have been hypothesized to increase the incidence of diabetes.4,5 A number of associations are reported between an environmental stimulus and diabetes incidence, including age of gluten exposure, introduction of infant formulas to the diet and type of these formulas, change in gut microbial flora, vitamin D deficiency, viral infections, and others.6–11 Alternatively, an unknown protective element in the environment may have been removed 20–30 years ago. There are a number of large prospective studies under way to identify environmental determinants of type 1 diabetes, including The environmental determinants of diabetes in the young (TEDDY) study12 and the MIDIA (Norwegian acronym for ‘environmental triggers of type 1 diabetes’) study in Norway.13
Type 1A diabetes is a polygenic disorder and much is known about the genetics associated with it. Approximately 1/300 individuals from the general population develop type 1 diabetes while 1/20 siblings of patients with type 1 diabetes develop the disorder.14–16 It was previously thought that the concordance rate for monozygotic twins with type 1 diabetes was relatively low (<50 %); however, following a cohort of monozygotic twins for longer than 50 years, the concordance rate for type 1 diabetes development is 66 %. A recent analysis of these long-term twin data indicates that there is no age at which an initially discordant monozygotic twin is no longer at risk, with some developing type 1 diabetes in the fourth and fifth decades of life.17
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