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Our hypothesis is based on the homology between the 33\u2010mer gliadin peptide and a component of the NMDA glutamate receptor ion channel \u2013 the human GRINA protein \u2013 using BLASTP software. Based on this homology the 33\u2010mer may act as a natural antagonist interfering with the normal interactions of GRINA and its partners. The theory is supported by numerous independent data from the literature, and provides a mechanistic link with otherwise unrelated disorders, such as cleft lip and palate, thyroid dysfunction, restless legs syndrome, depression, ataxia, hearing loss, fibromyalgia, dermatitis herpetiformis, schizophrenia, toxoplasmosis, anemia, osteopenia, Fabry disease, Barret's adenocarcinoma, neuroblastoma, urinary incontinence, recurrent miscarriage, cardiac anomalies, reduced risk of breast cancer, stiff person syndrome, etc. The hypothesis also anticipates better animal models, and has the potential to open new avenues of research.<\/jats:p><\/jats:sec>","DOI":"10.1002\/bies.201500143","type":"journal-article","created":{"date-parts":[[2016,3,19]],"date-time":"2016-03-19T07:22:36Z","timestamp":1458372156000},"page":"427-439","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Extraintestinal manifestations of celiac disease: 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