Abstract
Type 1 diabetes is a condition that can lead to serious long-term complications and can have significant psychological and quality of life implications. Its incidence is increasing in all parts of the world, but the reasons for this are incompletely understood. Genetic factors alone cannot explain such a rapid increase in incidence; therefore, environmental factors must be implicated.
Lifestyle factors have been classically associated with type 2 diabetes. However, there are data implicating obesity and insulin resistance to type 1 diabetes as well (accelerator hypothesis). Cholesterol has also been shown to be correlated with the incidence of type 1 diabetes; this may be mediated by immunomodulatory effects of cholesterol. There is considerable interest in early life factors, including maternal diet, mode of delivery, infant feeding, childhood diet, microbial exposure (hygiene hypothesis), and use of anti-microbials in early childhood. Distance from the sea has recently been shown to be negatively correlated with the incidence of type 1 diabetes. This may contribute to the increasing incidence of type 1 diabetes since people are increasingly living closer to the sea. Postulated mediating mechanisms include hours of sunshine (and possibly vitamin D levels), mean temperature, dietary habits, and pollution. Ozone, polychlorinated biphenyls, phthalates, trichloroethylene, dioxin, heavy metals, bisphenol, nitrates/nitrites, and mercury are amongst the chemicals which may increase the risk of type 1 diabetes. Another area of research concerns the role of the skin and gut microbiome. The microbiome is affected by many of the factors mentioned above, including the mode of delivery, infant feeding, exposure to microbes, antibiotic use, and dietary habits. Research on the reasons why the incidence of type 1 diabetes is increasing not only sheds light on its pathogenesis but also offers insights into ways we can prevent type 1 diabetes.Keywords: Type 1 diabetes, incidence, pollution, hygiene hypothesis, accelerator hypothesis, microbiome.
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