Talk:Intestinal permeability
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Crohn's disease
[edit]I noticed a mistake in the article today. The article's current wording "Excessive intestinal permeability is a factor in several autoimmune conditions such as Crohn's disease, celiac disease, ..." implies that Crohn's disease is an autoimmune condition. It would be quite helpful if one of the authors involved so far could correct that. --Chris Howard (talk) 18:06, 29 December 2014 (UTC)
- it is in part. see the second paragraph of the lead of the Crohn's article and the sources cited there. Jytdog (talk) 22:26, 29 December 2014 (UTC)
- "Although CD [Crohn's disease] is immune mediated, it is not an autoimmune disease, as the immunological process appears to be triggered by the content of the gut lumen rather than a self-antigen." (PMID 19687225) --Chris Howard (talk) 23:14, 29 December 2014 (UTC)
- see PMID 24321565 (a 2013 review) "Crohn's disease is an autoimmune disorder that affects nearly 1.4 million Americans." The article goes into some detail into the evidence for auto-antigens, etc. I can send it to you if you don't have access. PMID 25075198 has a PMC article, and you can see it treats Crohn's and ulcerative colitis as the two main forms of inflammatory bowel disorders, all of which the authors state are autoimmune. see also PMID 24231127 which is a 2014 review focused on autoantigens in Crohn's.Jytdog (talk) 23:32, 29 December 2014 (UTC)
- You have a valid argument there. The PMID I cited and the parts of the Crohn's article (the one you referenced: "While Crohn's is an immune related disease, it does not appear to be an autoimmune disease (in that the immune system is not being triggered by the body itself)" and further down: "There was a prevailing view that Crohn's disease is a primary T cell autoimmune disorder, however, a newer theory hypothesizes that Crohn's results from an impaired innate immunity") do not present it as an autoimmune disease. The more recent review articles you cite present it differently. At this point, is it the Crohn's disease article that needs an update? In terms of expertise I do not see myself in a position to do that. --Chris Howard (talk) 00:20, 30 December 2014 (UTC)
- P.S.: In fact also the article Autoimmune disease lists Crohn's disease and specifies it not as "accepted" [auto-immune] but as "immune-related", citing as reference PMID 18806708. That is in line with your statement that "it is in part". --Chris Howard (talk) 13:33, 11 January 2015 (UTC)
- You have a valid argument there. The PMID I cited and the parts of the Crohn's article (the one you referenced: "While Crohn's is an immune related disease, it does not appear to be an autoimmune disease (in that the immune system is not being triggered by the body itself)" and further down: "There was a prevailing view that Crohn's disease is a primary T cell autoimmune disorder, however, a newer theory hypothesizes that Crohn's results from an impaired innate immunity") do not present it as an autoimmune disease. The more recent review articles you cite present it differently. At this point, is it the Crohn's disease article that needs an update? In terms of expertise I do not see myself in a position to do that. --Chris Howard (talk) 00:20, 30 December 2014 (UTC)
- see PMID 24321565 (a 2013 review) "Crohn's disease is an autoimmune disorder that affects nearly 1.4 million Americans." The article goes into some detail into the evidence for auto-antigens, etc. I can send it to you if you don't have access. PMID 25075198 has a PMC article, and you can see it treats Crohn's and ulcerative colitis as the two main forms of inflammatory bowel disorders, all of which the authors state are autoimmune. see also PMID 24231127 which is a 2014 review focused on autoantigens in Crohn's.Jytdog (talk) 23:32, 29 December 2014 (UTC)
- "Although CD [Crohn's disease] is immune mediated, it is not an autoimmune disease, as the immunological process appears to be triggered by the content of the gut lumen rather than a self-antigen." (PMID 19687225) --Chris Howard (talk) 23:14, 29 December 2014 (UTC)
glutamine
[edit]so about this...
Glutamine is presently the best known compound for reducing excessive intestinal permeability and nutritional depletion is known to result in increased IP. Low levels of glutamine can lead to excessive intestinal permeability and excessive intestinal permeability is known to lower levels of glutamine. Glutamine is the preferred food source for enterocytes. Prebiotics and certain probiotics such as Escherichia coli Nissle 1917 have been found to reduce increased intestinal permeability. (ref for all that is PMID 20613941)
I have a few issues with this:
- I haven't seen any other good MEDRS sources that treat intestinal permability as something to be treated itself; in other articles like PMID 25734736 (a review in JAMA of IBS discussed IP as a sort of symptom - (occurs with IBS with diarrhea more than with constipation) and not something to be treated itself
- i have not seen any other review that makes the strong claim that this source about glutamine. other sources talk about modifying gut flora with probiotics in the context of associated diseases, so that is stronger. but nothing like this about glutamine
- the source, PMID 20613941 is not strong. from its home page it is well indexed which is great. its impact factor is 1.42.
This was added by WholeNewJourney. Would you mind waiting to see if further reviews come out with similar approaches? Thanks. Jytdog (talk) 00:28, 27 April 2015 (UTC)
- Thanks for your comments Jytdog. Lots of sources talk about the need to find treatments for increased intestinal permeability as bacteria translocation due to increased permeability is correlated with many serious medical disorders including chronic gastrointestinal disorders and up to septicemia. You have just read different sources from me. :-P I would mind removing it from the article. However, your point about it not being widely discussed in other secondary sources is making me think... Would you accept a compromise of changing the treatment section to 'research' and toning down some of the wording? Treatments for this condition is still all largely at the research stage.--WholeNewJourney (talk) 01:12, 27 April 2015 (UTC)
- thanks for kindly discussing. i would much more comfortable with this being moved to research and with the claims toned down. yes. thanks. Jytdog (talk) 02:21, 27 April 2015 (UTC)
- I'd agree with that: the present text seems too definitive given the sourcing. Alexbrn (talk) 02:24, 27 April 2015 (UTC)
- I agree with Alexbrn --Ozzie10aaaa (talk) 07:35, 27 April 2015 (UTC)
- I'd agree with that: the present text seems too definitive given the sourcing. Alexbrn (talk) 02:24, 27 April 2015 (UTC)
- thanks for kindly discussing. i would much more comfortable with this being moved to research and with the claims toned down. yes. thanks. Jytdog (talk) 02:21, 27 April 2015 (UTC)
- The source for that piece is a "scientific paper" that is clearly coming from a "leaky gut" pseudoscientist as they state that all sorts of things can be the result of this permeability. This doesn't appear to be a credible source. 68.113.54.226 (talk) 01:06, 26 January 2016 (UTC)
Off topic: gut brain axis and gut flora
[edit]The role of the gut-brain axis in developmental and psychiatric disorders such as autism and schizophrenia has been active area of research; many of the environmental factors thought to be relevant to the development of these conditions would also affect the gut flora, leaving open the question of whether specific developments in the gut flora drive the development of autism or whether problems with the intestinal mucosa happen concurrently with the development of autism.[1][2][3][4] The fact that gastrointestinal symptoms are common in children with autism and are probably undercounted, shows that autism and gut issues are probably at least related.[5] There is evidence that gene mutations or insults that can lead to autism affect both the brain and the enteric nervous system, meaning that problems in both systems develop concurrently.[5] The belief that a "leaky gut" might actually cause autism is widespread among the public, but the evidence is weak and what evidence there is, is conflicting.[5]
Jytdog did a very good job of wording and referencing this text. However, it is WP:OFFTOPIC. I propose to include it in the corresponding pages of gut-brain axis, gut flora and autism.
Best regards. --BallenaBlanca (talk) 08:00, 7 September 2016 (UTC)
- Here is the rest of it:
- Gastrointestinal symptoms are common in children with autism, but are often overlooked.[5] Currently is hypothesised that they are not simply comorbidities, but can play a role in the pathogenesis of autism.[5] The hypothesis that increased intestinal permeability may be a cause of autism is controversial, because both increased and normal intestinal permeability in children with autism have been reported.[5] One study concluded that intestinal permeability was abnormal in 36.7% of children with autism, but was always normal in children without autism.[5] There is also evidence in mouse experiments which provides some support for the "leaky gut" hypothesis.[5]
References
- ^ Dinan, T.G; Cryan, 2015 (2015). "The impact of gut microbiota on brain and behavior: implications for psychiatry". Curr Opin Clin Nutr Metab Care. 18: 552–558. doi:10.1097/MCO.0000000000000221. PMID 26372511.
{{cite journal}}
:|first2=
has numeric name (help) - ^ Buie, T (May 2015). "Potential Etiologic Factors of Microbiome Disruption in Autism". Clin Ther. 37 (5): 976–83. doi:10.1016/j.clinthera.2015.04.001. PMID 26046240.
- ^ Cite error: The named reference
ViggianoIaniro2015
was invoked but never defined (see the help page). - ^ Yarandi SS, Peterson DA, Treisman GJ, Moran TH, Pasricha PJ (2016). "Modulatory Effects of Gut Microbiota on the Central Nervous System: How Gut Could Play a Role in Neuropsychiatric Health and Diseases". J Neurogastroenterol Motil (Review). 22 (2): 201–12. doi:10.5056/jnm15146. PMC 4819858. PMID 27032544.
- ^ a b c d e f g h Rao M, Gershon MD (2016). "The bowel and beyond: the enteric nervous system in neurological disorders". Nat Rev Gastroenterol Hepatol (Review). 13 (9): 517–28. doi:10.1038/nrgastro.2016.107. PMID 27435372.
- I added the stuff I added to give the whole picture. We need to give the whole picture. The 2016 review you found (nice find) makes it clear that for some things (some mutations and insult with valproic acid) there is an underlying cause that effects both systems. We are pretty certain that the "co-occurence" actually happens. The permability causing autism is very contested as that source indicates. Also pulling out the 37% figure (and especially saying "always normal" when it was "normal in the children without autism who were tested" is not good...
- Let's work this out here on Talk instead of in the article, so we don't disrupt it. Jytdog (talk) 08:15, 7 September 2016 (UTC)
- Clearly it is speaking about the results in the context of the study, is a common wording in these cases: "One study reported that the permeability of the intestine to lactulose and mannitol was abnormal in 36.7% of children with ASD, in 21.2% of their first-degree relatives and in 4.8% of healthy adults as controls, but was always normal in children without ASD60."
- It is the research section, so is suitable to extend in the research to date. I propose to add your text, to put in context, and mine (which I already have shortened since the previous edition).
- Best regards. --BallenaBlanca (talk) 08:31, 7 September 2016 (UTC)
PKD (paleolithic ketogenic diet)
[edit]PKD has been demonstrated to be useful. Surprised there is no mention of it in Wikipedia. https://www.youtube.com/watch?v=nDPM8o9jcFA — Preceding unsigned comment added by 174.92.38.139 (talk) 00:34, 17 June 2019 (UTC)
Physical Activity & Gut Microbiota
[edit]search: exhaustive physical activity leads to small intestinal injury and short-term loss of gut barrier function
- many papers. any relevence? .... 0mtwb9gd5wx (talk) 00:10, 31 January 2023 (UTC)