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Does Candida Albicans Trigger the Onset of Celiac Disease?
In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease. In 1998 I foundedÂ The Gluten-Free Mall, Your Special Diet Superstore!, and I am the co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.View all articles by Scott Adams
Lancet. 2003 Jun 21;361(9375):2152-4.
Celiac.com 08/25/2003 – This interesting study compares a specific amino acid sequence found in Candida cell wall protein to a the gliadin amino acid sequence that triggers the immune response in celiac disease. The researchers found that the sequences are "identical or highly homologous to known coeliac disease-related alpha-gliadin and gamma-gliadin T-cell epitopes," and propose that Candida is the trigger for the onset of celiac disease. Below is the abstract for this study.
Is Candida albicans a trigger in the onset of coeliac disease?
Nieuwenhuizen WF, Pieters RH, Knippels LM, Jansen MC, Koppelman SJ.
Coeliac disease is a T-cell-mediated autoimmune disease of the small intestine that is induced by ingestion of gluten proteins from wheat, barley, or rye. We postulate that Candida albicans is a trigger in the onset of coeliac disease. The virulence factor of C albicans-hyphal wall protein 1 (HWP1)-contains amino acid sequences that are identical or highly homologous to known coeliac disease-related alpha-gliadin and gamma-gliadin T-cell epitopes. HWP1 is a transglutaminase substrate, and is used by C albicans to adhere to the intestinal epithelium. Furthermore, tissue transglutaminase and endomysium components could become covalently linked to the yeast. Subsequently, C albicans might function as an adjuvant that stimulates antibody formation against HWP1 and gluten, and formation of autoreactive antibodies against tissue transglutaminase and endomysium.
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