If gluteomorphin is what binds to the receptors and not the antibodies, how do these two play a role in the opiate-like symptoms someone may experience?

This may be explained by the “Opioid hypothesis.” The incomplete digestion of proteins derived by wheat and milk produces peptides called gliadinomorphin-7 and exorphins (gliadorphin aka gluteomorphin, rubiscolin, casomorphin). The lack of protease DPP-IV favors the conversion of gliadinomorphin-7 in exorphins. Exorphins can be transferred across the intestinal epithelium, transported via the blood stream, and can cross the blood brain barrier where it can exert its opiate-like effects (morphine-like activity) in the central nervous system.


Both gluten-sensitive and non-sensitive patients could have varying levels of gluteomorphin/gluten, and Uhde et al (2020) observed that these patients may "differ in the types of antibodies produced to gluten molecules, which would influence the inflammatory responses these antibodies can instigate...B cells of celiac disease patients produced a subclass profile of IgG antibodies with a strong inflammatory potential that is linked to autoimmune activity and intestinal cell damage...In contrast, the patients with non-celiac gluten sensitivity produced IgG antibodies that are associated with a more restrained inflammatory response."


Thus, not everyone will have the same levels of gluteomorphin to start off with to cross the BBB and experience the same level of opiate effects, and when gluteomorphins do cross over, the immune response to the gluten/gluteomorphin will vary depending on which antibody the person produces.



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