Environmental determinants of type 1 diabetes

Abstract

Type 1 diabetes (T1D) accounts for 5–10% of all forms of diabetes and results from the autoimmune destruction of pancreatic beta cells, leading to severe insulin deficiency¹. The progression to T1D is a complex process involving interactions between genetic factors (susceptibility) and environmental factors, which are implicated both in the initiation and progression of islet autoimmunity².

Evidence to support the role of enviromental factors continues to expand. T1D concordance rates between monozygotic twins is less than 50%; the incidence of T1D shows significant geographic variation, with the highest incidence observed in Nordic countries, and migration studies have demonstrated that individuals tend to acquire the incidence risk of their new environment. The rising incidence of T1D in recent decades is too rapid to be explained by genetic changes alone. The greatest increases in incidence have been observed in countries that previously had a low incidence and in those experiencing the highest economic growth^2,3.

The Environmental Determinants of Diabetes in the Young (TEDDY) Study is an international, multicenter prospective cohort study that enrolled 8,667 newborns with genetic susceptibility to T1D, between 2004 and 2010 at six centers (three in the United States and three in Europe), and followed them from birth until 15 years of age to evaluate the development of islet autoimmunity and diabetes. TEDDY has evaluated multiple environmental factors operating prenatally and in childhood as candidate triggers, drivers or modifiers of autoimmunity. Its main findings, showed that viral infections, including enterovirus B infections, may trigger islet autoimmunity when persistent. Vitamin D, vitamin C, omega-3 fatty acids, probiotics, and iron may play a modulatory role in genetically susceptible children. Excessive weight gain and a high-protein diet may accelerate progression to clinical diabetes, while physical activity may delay it.