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A Brief Note On Type 1 Diabetes ( T1d )

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Type 1 diabetes (T1D) is an autoimmune disorder in which the β-cells in the pancreatic islets have been destroyed, leaving the body with very little or completely without endogenous insulin. There are many proposed etiologies to this auto-destruction, some of which are genetic susceptibilities and environmental factors. The incidence of T1D has steadily increased in developed countries, suggesting that exposure to various environmental factors may lead to β-cell autoimmunity; namely the intake of milk, sucrose, meat, and overall caloric intake (Rowe, Campbell-Thompson, Schatz, & Atkinson, 2011). An “overload hypothesis” by Dahlquist points to accelerated growth as a main factor. Dahlquist suggests overfeeding, especially from sugar sources, leads to high insulin demand, and expedites the destruction and autoimmune process. There is a known association between obesity and type 2 diabetes, however recent growth data from a population-based study shows that children diagnosed with T1D were growing faster than their age-matched controls, prior to diagnosis (Dahlquist, 2006). Obesity has recently been linked to T1D, with early height and weight increase starting as early as the first two years of life (Dahlquist, 2006). Children with low birth weight also had a lower risk for childhood T1D in contrast to their high birth weight counterpart.
Chronically elevated inflammation is also a proposed factor for T1D. IL-1β (Interleukin-1 beta), IFN-γ (interferon gamma), and TNF-α (tumor

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