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The research indicated that gluten, when added to the diet of mice, caused inflammation in the hypothalamic region of the brain.
Mice models are deemed valuable for studying human physiology due to similarities in various systems, suggesting potential implications for humans.
While the exact reason for the inflammation is still unknown, one theory suggests that indigestible components of gluten may trigger an immune response similar to that seen in celiac patients.
Child's gluten intake during infancy, rather than mother's during pregnancy, linked to increased risk of developing type 1 diabetes -- ScienceDaily
New research presented at the Annual Meeting of the European Association for the Study of Diabetes (EASD) in Barcelona, Spain (16-20 September) shows that a child's intake of gluten at age 18 months is associated with a 46% increased risk of developing type 1 diabetes for each extra 10g of gluten consumed per day.
Columbia researchers find biological explanation for wheat sensitivity | EurekAlert! Science News
In the new study, the CUMC team examined 80 individuals with NCWS, 40 individuals with celiac disease, and 40 healthy controls. Despite the extensive intestinal damage associated with celiac disease, blood markers of innate systemic immune activation were not elevated in the celiac disease group. This suggests that the intestinal immune response in celiac patients is able to neutralize microbes or microbial components that may pass through the damaged intestinal barrier, thereby preventing a systemic inflammatory response against highly immunostimulatory molecules.
The NCWS group was markedly different. They did not have the intestinal cytotoxic T cells seen in celiac patients, but they did have a marker of intestinal cellular damage that correlated with serologic markers of acute systemic immune activation. The results suggest that the identified systemic immune activation in NCWS is linked to increased translocation of microbial and dietary components from the gut into circulation, in part due to intestinal cell damage and weakening of the intestinal barrier.
