14 Mar 2022 | 10.00 - 11.00Online
For unknown reasons, T1D incidence has stabilised in the last decade, particularly in the Nordic countries. Environmental triggers and specific co-morbidities that are often implicated in T1D, e.g., enterovirus infection, diet, and obesity, cannot explain this trend. However, the time trend of human exposure levels to two widely-used industrial chemicals, perfluorooctane sulfonate and perfluorooctanoic acid (PFOS and PFOA), does follow T1D incidence.
In a mother-child cohort, we recently found that high prenatal exposure to per- and polyfluoroalkyl substances (PFAS) associated with postnatal progression to islet autoantibody positivity and decreased levels of the same lipids previously found to be associated with progression to T1D. These and other recent and ongoing investigations suggest that early-life exposure to various environmental chemicals contributes to the pathogenesis of T1D as well as potentially to other diseases via the impact said exposures have on the interplay between genetic background, the gut microbiome, and lipid metabolism, which, in turn, impact host metabolism and immune system status.
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School of Medical Sciences, Örebro University, Örebro, Sweden
Turku Bioscience Centre, University of Turku, Turku, Finland
The environment we live in has a dominant impact on our health. It explains an estimated seventy percent of the chronic disease burden. Where we live, what we eat, how much we exercise, the air we breathe and whom we associate with; all of these environmental factors play a role. The combination of these factors over the life course is called the exposome. There is general (scientific) consensus that understanding more about the exposome will help explain the current burden of disease and that it provides entry points for prevention and ...Read More