Jump to content

Talk:Leaky gut

Page contents not supported in other languages.
From Wikipedia, the free encyclopedia

This is an old revision of this page, as edited by Feyre (talk | contribs) at 01:45, 8 December 2013. The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.


Citations

(Part discussion moved from from 'leaky gut syndrome.)

Thanks, it seems to me that this subject is not Alt Med as a check on Pubmed shows whilst there are only 12 hits for Leaky gut syndrome, there are 51 for 'leaky gut' including 21 reviews, where as there are 54 reviews for 'bowel permeability and tight junctions' So it seems that the science is there and probably no longer an 'alternative med' subject. However SBOS does not seem appropriate as only one cause among many possible. I will leave it to more experienced to decide. In the meantime the Article needs improvement.
Depression, re PMID 19085093 it is not a Review but as the edit is close to the article wording, it seems to comply with edits that rely on primary sources should only describe the conclusions of the source, In particular, this description should follow closely to the interpretation of the data given by the authors, PMID 18580840 may be better ref as it is secondary source from a reputable publisher will be written by an expert in the field and be editorially or peer reviewed. The author has some 242 pubmed articles on depression. The journal has a formal peer review process satisfactory to NIH, as shown here in 'instructions to authors[1] and published articles are distinct from 'letters to the editor' Peerev (talk) 21:58, 26 April 2009 (UTC)[reply]
As far as I'm aware, leaky gut is considered psueoscience. Number of hits on alt med does not prove anything (and 51 is very low for a recognised syndrome. Try searching for "chronic fatigue" and you'll get a lot more!) Both PMID 18580840 and 19085093 are hypotheses. --sciencewatcher (talk) 22:26, 26 April 2009 (UTC)[reply]
I said Pubmed not Alt med? Maybe a new Article, Leaky gut or Bowel permability appropriate? From Wiki article its not pseudoscience as it has a testable hypothesis, the fact that there are hypotheses in mainsteam journals attests that. Much of the published science also attests and 75 reviews is not trivial. Hypothesis yes, based on evidence thats why edits were placed in hypotheses section of Article!
Diabetes, PMID 18820210 is again a review in the journal 'Diabetes' ditto. Heart, PMID 18685461 is a review, to which can be added another review PMID 15980032. Hepatitis etc, PMID 18626795 is a review. Somatization and CFS, PMID 19127706 is another review, supported by PMID 19112401, which shows the hypothesis is testable. Peerev (talk) 21:31, 27 April 2009 (UTC)[reply]
Ok, it looks like you know more about this than me. Looking at these and other reviews there is genuine research into "leaky gut". The problem is that the "leaky gut syndrome" that is diagnosed by naturopaths isn't the same thing as the leaky gut that we see in the reviews. So you just need to be careful that you separate the "real" leaky gut from the quackery version.
Also, while hypotheses are fine in the hypotheses section, you just need to be careful about two things. First of all, don't give them too much WP:Weight. Generally one sentence max is sufficient for an untested hypothesis. Also you shouldn't be putting in anything too speculative even in the hypotheses section. For example, 19127706, which says "SUMMARY: 'Functional' symptoms, as occurring in CFS and somatization, have a genuine organic cause". That's a bit of a stretch, don't you think? He says "have a genuine organic cause", not "may have a genuine organic cause". Because of this, I'm now a bit suspicious about all of Maes' work. --sciencewatcher (talk) 22:25, 27 April 2009 (UTC)[reply]
From his website it seems Maes is a psychiatrist and researcher, this article is in journal 'Curr Opin Psychiatry' so opinion might be operative word? He has four published papers on Leaky gut and depression so it seems he possibly is refering to his own findings? Although not strictly MEDRS I agree with adding the word 'may' as you suggest.
The article title "Leaky gut' already redirects here, so I concur it is probably meant to cover both, but agree needs differentiating? Maybe constrasting these two in the lead might help, PMID 17182488, PMID 16092447. This Google scholar abstract might also be useful rerence [2] unless a better definition is possible, I will attempt a rewording?Peerev (talk) 21:51, 28 April 2009 (UTC)[reply]
Yes, just go ahead and improve the article, and I'll not revert unless there is an obvious issue. Sounds like you know what you're doing. --sciencewatcher (talk) 22:19, 28 April 2009 (UTC)[reply]
I recommend putting the material on "leaky gut", disruptions of tight junctions, into leaky gut rather than redirect. both articles linking to one another (and elsewhere) as necessary. There's plainly a difference between "leaky gut" per se on the one hand, and "leaky gut syndrome" on the other hand. If I understand the lay of the land correctly, the latter is asserted -- without much if any clear experimental evidence in support to date -- to be related to a cluster of symptoms so as to essentially constitute a defined spectrum disorder (i.e., "leaky gut syndrome") that is considered pseudoscientific. The former ("leaky gut") is still under experimental investigation without much of a clear understanding of its full implications within the medical community. IOW, best to split this new material into the title leaky gut. ... Kenosis (talk) 23:11, 1 May 2009 (UTC)[reply]
I've moved the new material over to Leaky gut, where it more appropriately belongs. TBH, it's far too much primary-source material-- please see also WP:Summary style. Nonetheless I've kept the just-added material intact for now at leaky gut, until one or more editors have a chance to deal with it and hopefully it can get sorted out so as not to confuse "leaky gut syndrome" with the more straightforward and far less speculative term "leaky gut". ... Kenosis (talk) 22:45, 3 May 2009 (UTC)[reply]

I will leave it to others to decide whether split is best. However most material in 'Leaky gut' complies with WP:MEDRS. If however you want please discuss specifics and not generalise. Meanwhile i will add to 'leaky gut'Peerev (talk) 23:24, 3 May 2009 (UTC)[reply]

Autism edits

Problem with 'autism' ref's you have now added to lead is they are definately not WP:MEDRS Peerev (talk) 21:45, 4 May 2009 (UTC)Removed such material sourced to media reports , primary studies etc. Peerev (talk) 22:03, 7 May 2009 (UTC)[reply]
The Johnson reference includes a research summary, and as such is a secondary source that reviews primary published studies. I've replaced the statement in the lead, and added another research review by Christison. This is too much of a "hot-button" issue subject to widespread popular misconceptions since the Wakefield false alarm. It's appropriately placed the lead because of its wide public exposure. The advanced reader likely will readily discern the difference between "leaky gut" and "leaky gut syndrome", but the layperson, it seems to me, needs to be squared up on the lack of evidence as a cause of autism at the outset of the article. ... Kenosis (talk) 21:45, 8 May 2009 (UTC)[reply]
Reincluding material until consensus reached is a breach of BRD, will not be tolerated further. You have a specific view that is not WP:NPOV certainly not for a lead. The cites you have added are not WP:MEDRS and the edit amounts to WP:OR. The Johnson article you have linked to is a consumer website and a nurses information site. From what i can find the Article is not a review and not cited by NIH. PMID 1668583 is not a review but an animal study, PMID 18337276 is a primary source. Media reports are not Medrs either. Find a review cited by NIH that is MEDRS, that says what your edit says, and it will be considered. Peerev (talk) 22:01, 11 May 2009 (UTC)[reply]

Leaky Gut in Celiac Disease

An article has appeared on Scientific American magazine that makes a connection between Celiac Disease and a Leaky Gut. It seems like this connection might be more solid than any connection between Leaky Gut and Autism. I have not seen in this Wikipedia article on Leaky Gut any reference to Celiac Disease. I think this should be mentioned. This article discusses two mechanisms that can loosen tight junctions : (1) a toxin called Zot which is produced by bacteria (2) Zonulin, a protein secreted by cells in the body. The article claims that in people with Celiac Disease, Gluten stimulates the production of zonulin, which in turn loosens tight junctions. The loosening of tight junctions causes a leaky gut which enables gluten fragments to cross the intestinal ligning and to come in contact with immune system cells thus generating an immune reaction which damages the intestinal lining cells.

The Article: "Surprises from Celiac Disease" by Alessio Fasano in Scientific American, August 2009

This article also list as a reference two Journal Articles: (1) "Mechanisms of Disease: The Role of Intestinal Barrier Function in the Pathogenesis of Gastrointestinal Autoimmune Diseases" by Alessio Fasano and Terez Shea-Donohue in Nature Clinical Practice Gastroenterology & Hepatology, Vol 2 , No 9, pages 416-422; September 2005. (2) "Diagnosis and Treatment of Celiac Disease" by L.M. Sollid and K.E.A. Lundin in Mucosal Immunology, Vol 2 No.1 Pages 3-7; January 2009.

The first journal article is already listed in the references section of this Wikipedia article. I don't know if the second reference by Sollid includes enough discussion about the roll a leaky gut plays in celiac disease in order to be listed in this WP article. But the Scientific American article is very appropriate and it is written at a level that makes it easy to understand by non-specialists. —Preceding unsigned comment added by Alex Pascual (talkcontribs) 15:52, 27 July 2009 (UTC)[reply]

Merger proposal

I propose that Leaky gut syndrome be merged into Leaky gut. I think that the content in the "Leaky gut syndrome" article can easily be explained in the context of "Leaky gut", and the "Leaky gut" article is of a reasonable size that the merging of "Leaky gut syndrome" will not cause any problems as far as article size or undue weight is concerned. There is too much repetition between the two articles to merit them being two separate articles, and they are both discussing virtually the same condition and the same treatments. Not to mention that by now there are over 65 articles on "Leaky gut" in PubMed. Softlavender (talk) 03:22, 14 March 2013 (UTC)[reply]

  • Support. There are insufficient differences between the articles to warrant two separate articles, which creates an undue WP:CONTENTFORK. The description and treatment in both articles are virtually the same. There are also over 65 articles on Leaky Gut in PubMed. Softlavender (talk) 03:34, 14 March 2013 (UTC)[reply]

Result: Merged per consensus and lack of discussion. Softlavender (talk) 06:54, 5 April 2013 (UTC)[reply]

References

(moved from "Leaky gut syndrome" Talk page)

Per the requests for references and citations, 150+ drawn upon by Galland, M.D. Res q68 02:29, 9 July 2006 (UTC)[reply]

BIBLIOGRAPHY

1. Crissinger, K.D., P.R. Kvietys, and D.N. Granger, Pathophysiology of gastrointestinal mucosal permeability. J Intern Med Suppl, 1990. 732: p. 145-54.

2. Anderson, K.E., Dietary Regulation of Cytochrome P450. Ann. Rev. Nutr., 1991. 11: p. 141-167.

3. Paine, A.J., Excited states of oxygen in biology: their possible involvement in cytochrome P450 linked oxidations as well as in the induction of the P450 system by many diverse compounds. Biochem. Pharmacol., 1978. 27: p. 1805-1813.

4. Braganza, J.M., et al., Lipid-peroxidation (free-radical-oxidation) products in bile from patients with pancreatic disease. Lancet, 1983. ii: p. 375-378.

5. Braganza, J.M., Pancreatic disease: a casualty of hepatic "detoxification"? Lancet, 1983. ii: p. 1000-1002.

6. Deitch, E.A., The role of intestinal barrier failure and bacterial translocation in the development of systemic infection and multiple organ failure. Arch. Surgery, 1990. 125: p. 403-404.

7. Hazenberg, M.P., et al., Are intestinal bacteria involved in the etiology of rheumatoid arthritis? Review article. Apmis, 1992. 100(1): p. 1-9.

8. Peters, T.J. and I. Bjarnason, Uses and abuses of intestinal permeability measurements. Can. J. Gastroenterol., 1988. 2: p. 127-132.

9. Rooney, P.J., R.T. Jenkins, and W.W. Buchanan, A short review of the relationship between intestinal permeability and inflammatory joint disease. Clin Exp Rheumatol, 1990. 8(1): p. 75-83.

10. Walker, W.A., Antigen absorption from the small intestine and gastrointestinal disease. Pediatr Clin North Am, 1975. 22(4): p. 731-46.

11. Bloembergen, P., et al., Endotoxin-induced auto-immunity in mice. I. Time and dose dependence of production and serum levels of antibodies against bromelain-treated mouse erythrocytes and circulating immune complexes. Int Arch Allergy Appl Immunol, 1987. 84(3): p. 291-7.

12. Bloembergen, P., et al., Endotoxin-induced auto-immunity in mice. II. Reactivity of LPS-hyporesponsive and C5-deficient animals. Int Arch Allergy Appl Immunol, 1988. 86(4): p. 370-4.

13. Bloembergen, P., et al., Endotoxin-induced auto-immunity in mice. III. Comparison of different endotoxin preparations. Int Arch Allergy Appl Immunol, 1990. 92(2): p. 124-30.

14. Katz, K.D., et al., Intestinal permeability in patients with Crohn's disease and their healthy relatives. Gastroenterology, 1989. 97(4): p. 927-31.

15. Pearson, A.D., et al., Intestinal permeability in children with Crohn's disease and coeliac disease. Br Med J, 1982. 285(6334): p. 20-1.

16. Pironi, L., et al., Relationship between intestinal permeability to [51Cr]EDTA and inflammatory activity in asymptomatic patients with Crohn's disease. Dig Dis Sci, 1990. 35(5): p. 582-8.

17. Munkholm, P., et al., Intestinal permeability in patients with Crohn's disease and ulcerative colitis and their first degree relatives. Gut, 1994. 35(1): p. 68-72.

18. Hollander, D., et al., Increased intestinal permeability in patients with Crohn's disease and their relatives. A possible etiologic factor. Ann Intern Med, 1986. 105(6): p. 883-5.

19. Teahon, K., et al., Intestinal permeability in patients with Crohn's disease and their first degree relatives. Gut, 1992. 33(3): p. 320-3.

20. Jenkins, R.T., et al., Increased intestinal permeability in patients with rheumatoid arthritis: a side-effect of oral nonsteroidal anti-inflammatory drug therapy? Br J Rheumatol, 1987.26(2): p. 103-7.

21. Mielants, H., Reflections on the link between intestinal permeability and inflammatory joint disease [letter; comment].

Clin Exp Rheumatol, 1990. 8(5): p. 523-4.

22. Morris, A.J., et al., Increased intestinal permeability in ankylosing spondylitis--primary lesion or drug effect? [see comments]. Gut, 1991. 32(12): p. 1470-2.

23. Smith, M.D., R.A. Gibson, and P.M. Brooks, Abnormal bowel permeability in ankylosing spondylitis and rheumatoid arthritis. J Rheumatol, 1985. 12(2): p. 299-305.

24. Sk:oldstam, L. and K.E. Magnusson, Fasting, intestinal permeability, and rheumatoid arthritis. Rheum Dis Clin North Am, 1991. 17(2): p. 363-71.

25. Juhlin, L. and C. Vahlquist, The influence of treatment on fibrin microclot generation in psoriasis. Br J Dermatol, 1983. 108(1): p. 33-7.

26. Juhlin, L. and G. Micha:elsson, Fibrin microclot formation in patients with acne. Acta Derm Venereol, 1983. 63(6): p. 538-40.

27. Hamilton, I., et al., Small intestinal permeability in dermatological disease. Q J Med, 1985. 56(221): p. 559-67.

28. Belew, P.W., et al., Endotoxemia in psoriasis [letter]. Arch Dermatol, 1982. 118(3): p. 142-3.

29. Jackson, P.G., et al., Intestinal permeability in patients with eczema and food allergy. Lancet, 1981. 1(8233): p. 1285-6.

30. Scadding, G., et al., Intestinal permeability to 51Cr-labelled ethylenediaminetetraacetate in food-intolerant subjects. Digestion, 1989. 42(2): p. 104-9.

31. Jacobson, P., R. Baker, and M. Lessof, Intestinal permeability in patients with eczema and food allergy. Lancet, 1981. i: p. 1285-1286.

32. F:alth-Magnusson, K., et al., Gastrointestinal permeability in children with cow's milk allergy: effect of milk challenge and sodium cromoglycate as assessed with polyethyleneglycols (PEG 400 and PEG 1000). Clin Allergy, 1986. 16(6): p. 543-51.

33. F:alth-Magnusson, K., et al., Gastrointestinal permeability in atopic and non-atopic mothers, assessed with different-sized polyethyleneglycols (PEG 400 and PEG 1000). Clin Allergy, 1985. 15(6): p. 565-70.

34. F:alth-Magnusson, K., et al., Intestinal permeability in healthy and allergic children before and after sodium-cromoglycate treatment assessed with different-sized polyethyleneglycols (PEG 400 and PEG 1000). Clin Allergy, 1984. 14(3): p. 277-86.

35. Jalonen, T., Identical intestinal permeability changes in children with different clinical manifestations of cow's milk allergy. J Allergy Clin Immunol, 1991. 88(5): p. 737-42.

36. Barau, E. and C. Dupont, Modifications of intestinal permeability during food provocation procedures in pediatric irritable bowel syndrome. J Pediatr Gastroenterol Nutr, 1990. 11(1): p. 72-7.

37. Paganelli, R., et al., Intestinal permeability in irritable bowel syndrome. Effect of diet and sodium cromoglycate administration. Ann Allergy, 1990. 64(4): p. 377-80.

38. Batash, S., et al., Intestinal permeability in HIV infection: proper controls are necessary [letter]. Am J Gastroenterol, 1992. 87(5): p. 680.

39. Lim, S.G., et al., Intestinal permeability and function in patients infected with human immunodeficiency virus. Scand J Gastroenterol, 1993. 28(7): p. 573-580.

40. Tepper, R.E., et al., Intestinal permeability in patients infected with human immunodeficiency virus. Am J Gastroenterol, 1994. 89: p. 878-882.

41. Lichtman, S.N., et al., Hepatic injury associated with small bowel bacterial overgrowth in rats is prevented by metronidazole and tetracycline. Gastroenterology, 1991. 100(2): p. 513-9.

42. Mack, D.R., et al., Correlation of intestinal lactulose permeability with exocrine pancreatic dysfunction. J. Pediatr., 1992. 120: p. 696-701.

43. Lahesmaa-Rantala, R., et al., Intestinal permeability in patients with yersinia triggered reactive arthritis. Ann Rheum Dis, 1991. 50(2): p. 91-4.

44. Serrander, R., K.E. Magnusson, and T. Sundqvist, Acute infections with Giardia lamblia and rotavirus decrease intestinal permeability to low-molecular weight polyethylene glycols (PEG 400). Scand J Infect Dis, 1984. 16(4): p. 339-44.

45. Serrander, R., et al., Acute yersinia infections in man increase intestinal permeability for low-molecular weight polyethylene glycols (PEG 400). Scand J Infect Dis, 1986. 18(5): p. 409-13.

46. Lim, S.G., et al., Intestinal permeability and function in patients infected with human immunodeficiency virus. A comparison with coeliac disease. Scand J Gastroenterol, 1993. 28(7): p. 573-80.

47. Bjarnason, I., R. Wise, and T. Peters, The leaky gut of alcoholism: Possible route of entry for toxic compounds. Lancet, 1984. i: p. 79-82.

48. Worthington, B.S., L. Meserole, and J.A. Syrotuck, Effect of daily ethanol ingestion on intestinal permeability to macromolecules. Am J Dig Dis, 1978. 23(1): p. 23-32.

49. Bjarnason, I., et al., Effect of non-steroidal anti-inflammatory drugs on the human small intestine. Drugs, 1986. 1: p. 35-41.

50. Rooney, P.J. and R.T. Jenkins, Nonsteroidal antiinflammatory drugs (NSAID's) and the bowel mucosa: changes in intestinal permeability may not be due to changes in prostaglandins [letter]. Clin Exp Rheumatol, 1990. 8(3): p. 328-9.

51. Ohri, S.K., et al., Cardiopulmonary bypass impairs small intestinal transport and increases gut permeability. Ann Thorac Surg, 1993. 55(5): p. 1080-6.

52. Ohri, S.K., et al., The effect of intestinal hypoperfusion on intestinal absorption and permeability during cardiopulmonary bypass. Gastroenterology, 1994. 106(2): p. 318-23.

53. Grisham, M.B., et al., Effects of neutrophil-derived oxidants on intestinal permeability, electrolyte transport, and epithelial cell viability. Inflammation, 1990. 14(5): p. 531-42.

54. Bjarnason, I., et al., Intestinal permeability to 51Cr-EDTA in rats with experimentally induced enteropathy. Gut, 1985. 26(6): p. 579-85.

55. Lifschitz, C.H. and D.H. Mahoney, Low-dose methotrexate-induced changes in intestinal permeability determined by polyethylene glycol polymers. J Pediatr Gastroenterol Nutr, 1989. 9(3): p. 301-6.

56. Berg, R.D., The translocation of the normal flora bacteria from the gastrointestinal tract to the mesenteric lymph nodes and other organs. Microecology Therapy, 1981. 11: p. 27-34.

57. Andr:e, C., [Food allergy. Objective diagnosis and test of therapeutic efficacy by measuring intestinal permeability]. Presse Med, 1986. 15(3): p. 105-8.

58. Andr:e, C., F. Andr:e, and L. Colin, Effect of allergen ingestion challenge with and without cromoglycate cover on intestinal permeability in atopic dermatitis, urticaria and other symptoms of food allergy. Allergy, 1989. 9: p. 47-51.

59. Andre, C., et al., Measurement of intestinal permeability to mannitol and lactulose as a means of diagnosing food allergy and evaluating therapeutic effectiveness of disodium cromoglycate. Ann Allergy, 1987. 59(5 Pt 2): p. 127-30.

60. Barau, E. and C. Dupont, Allergy to cow's milk proteins in mother's milk or in hydrolyzed cow's milk infant formulas as assessed by intestinal permeability measurements. Allergy, 1994. 49(4): p. 295-8.

61. Doe, W.F., An overview of intestinal immunity and malabsorption. Am J Med, 1979. 67(6): p. 1077-84.

62. Williamson, R.C., Intestinal adaptation (first of two parts). Structural, functional and cytokinetic changes. N Engl J Med, 1978. 298(25): p. 1393-402.

63. Williamson, R.C., Intestinal adaptation (second of two parts). Mechanisms of control. N Engl J Med, 1978. 298(26): p. 1444-50.

64. Lunn, P.G., C.A. Northrop-Clewes, and R.M. Downes, Recent developments in the nutritional management of diarrhoea. 2. Chronic diarrhoea and malnutrition in The Gambia: studies on intestinal permeability. Trans R Soc Trop Med Hyg, 1991. 85(1): p. 8-11.

65. Behrens, R.H., et al., Factors affecting the integrity of the intestinal mucosa of Gambian children. Am J Clin Nutr, 1987. 45(6): p. 1433-41.

66. Galland, L. and S. Barrie, Intestinal dysbiosis and the causes of disease. J. Advancement Med., 1993. 6: p. 67-82.

67. Avakian, H., et al., Ankylosing spondylitis, HLA-B27 and Klebsiella. II. Cross-reactivity studies with human tissue typing sera. Br J Exp Pathol, 1980. 61(1): p. 92-6.

68. Ebringer, R., et al., Ankylosing spondylitis: klebsiella and HL-A B27. Rheumatol Rehabil, 1977. 16(3): p. 190-6.

69. Ebringer, A. and M. Ghuloom, Ankylosing spondylitis, HLA-B27, and klebsiella: cross reactivity and antibody studies [letter]. Ann Rheum Dis, 1986. 45(8): p. 703-4.

70. Ebringer, A., The relationship between Klebsiella infection and ankylosing spondylitis. Baillieres Clin Rheumatol, 1989. 3(2): p. 321-38.

71. Geczy, A.F., et al., Cross-reactivity of anti-Klebsiella K43 BTS 1 serum and lymphocytes of patients with ankylosing spondylitis: antipodean curiosity? [letter]. Lancet, 1985. 1(8438): p. 1169.

72. Geczy, A.F., et al., HLA-B27, molecular mimicry, and ankylosing spondylitis: popular misconceptions. Ann Rheum Dis, 1987. 46(2): p. 171-2.

73. Husby, G., et al., Cross-reactive epitope with Klebsiella pneumoniae nitrogenase in articular tissue of HLA-B27+ patients with ankylosing spondylitis. Arthritis Rheum, 1989. 32(4): p. 437-45.

74. Ilowite, N.T., et al., The rheumatoid factor cross-reactive idiotype in juvenile rheumatoid arthritis: role of the CD5-positive B cell. Clin Immunol Immunopathol, 1993. 67(3 Pt 2): p. S74-82.

75. Khalafpour, S., et al., Antibodies to Klebsiella and Proteus microorganisms in ankylosing spondylitis and rheumatoid arthritis patients measured by ELISA. Br J Rheumatol, 1988. 2: p. 86-9.

76. Phillips, P.E., Evidence implicating infectious agents in rheumatoid arthritis and juvenile rheumatoid arthritis. Clin. Exper. Rheumatol., 1988. 6: p. 87-94.

77. Ramakrishnan, T.P., et al., The major rheumatoid factor crossreactive idiotype and IgA rheumatoid factor in juvenile rheumatoid arthritis. J Rheumatol, 1991. 18(7): p. 1068-72.

78. Sullivan, J.S., et al., Cross-reacting bacterial determinants in ankylosing spondylitis. Am J Med, 1988. 85(6A): p. 54-5.

79. Trull, A.K., et al., IgA antibodies to Klebsiella pneumoniae in ankylosing spondylitis. Scand J Rheumatol, 1983. 12(3): p. 249-53.

80. Welsh, J., et al., Ankylosing spondylitis, HLA-B27 and Klebsiella. I. Cross-reactivity studies with rabbit antisera. Br J Exp Pathol, 1980. 61(1): p. 85-91.

81. Yu, D.T., S.Y. Choo, and T. Schaack, Molecular mimicry in HLA-B27-related arthritis [see comments]. Ann Intern Med, 1989. 111(7): p. 581-91.

82. Katz, K.D. and D. Hollander, Intestinal mucosal permeability and rheumatological diseases. Baillieres Clin Rheumatol, 1989. 3(2): p. 271-84.

83. Davies, G.R., M.E. Wilkie, and D.S. Rampton, Effects of metronidazole and misoprostol on indomethacin-induced changes in intestinal permeability. Dig Dis Sci, 1993. 38(3): p. 417-25.

84. Bjarnason, I., et al., Effect of prostaglandin on indomethacin-induced increased intestinal permeability in man. Scand J Gastroenterol Suppl, 1989. 164: p. 97-102.

85. Bjarnason, I., et al., Misoprostol reduces indomethacin-induced changes in human small intestinal permeability. Dig Dis Sci, 1989. 34(3): p. 407-11.

86. Bjarnason, I., et al., Metronidazole reduces intestinal inflammation and blood loss in non-steroidal anti-inflammatory drug induced enteropathy. Gut, 1992. 33: p. 1204-1208.

87. O'Dwyer, S.T., et al., A single dose of endotoxin increases intestinal permeability in healthy humans. Arch Surg, 1988. 123(12): p. 1459-64.

88. Severijnen, A.J., et al., Intestinal flora of patients with rheumatoid arthritis: induction of chronic arthritis in rats by cell wall fragments of Eubacterium aerofaciens strain. Br J Rheumatol, 1990. 29: p. 433-439.

89. Dearlove, M., et al., The effect of non-steroidal anti-inflammatory drugs of faecal flora and bacterial antibody levels in rheumatoid arthritis. Br J Rheumatol, 1992. 31: p. 443-447.

90. Alarcon, G.S. and I.S. Mikhail, Antimicrobials in the treatment of rheumatoid arthritis and other arthritides: a clinical perspective. Am. J. Med. Sci., 1994. 309: p. 201-209.

91. Brown, The puzzling problem of the rheumatic diseases. Maryland State Med. J., 1856. 2: p. 88-109.

92. Caperton, E.M., et al., Ceftriaxone therapy of chronic inflammatory arthritis. A double-blind placebo controlled trial. Arch. Intern. Med., 1990. 150: p. 1677-1682.

93. Brown, T.M., et al., Antimycoplasma approach to the mechanism and the control of rheumatoid disease. Inflammatory Diseases anbd Copper. edited by J.R.J. Sorenson., 1982. Humana Press, Clifton, N.J.

94. Porter, D., et al., Prospective trial comparing the use of sulphasalazine and auranofin as second line drugs in patients with rheumatoid arthritis. Ann Rheum Dis, 1992. 51(4): p. 461-4.

95. Porter, D.R. and H.A. Capell, The use of sulphasalazine as a disease modifying antirheumatic drug. Baillieres Clin Rheumatol, 1990. 4(3): p. 535-51.

96. Pybus, P.K., Metronidazole in rheumatoid arthritis. S. African Med. J., 1982. (February 20): p. 261-262.

97. Tilley, B.C., et al., Minocycline in rheumatoid arthritis. A 48-week, double-blind, placebo-controlled trial. Ann Int Med, 1995. 122(2): p. 81-89.

98. Wojtulewski, J.A., P.J. Gow, and J. Waller, Clotrimazole in rheumtoid arthritis. Ann Rheum Dis, 1980. 39: p. 469-472.

99. Kloppenburg, M., et al., Antibiotics as disease modifiers in arthritis. Clin. Exp. Rheumatol., 1993. 11 Suppl 8: p. S113-S115.

100. Peltonen, R., et al., Changes of faecal flora in rheumatoid arthritis during fasting and one-year vegetarian diet. Br J Rheumatol, 1994. 33: p. 638-643.

101. Whitcomb, D.C. and G.D. Block, Association of acetaminophen hepatotoxicity with fasting and ethanol use. JAMA, 1994. 272(23): p. 1845-1850.

102. Sudduth, W.H., The role of bacteria and enterotoxemia in physical addiction to alcohol. Microecology and Therapy, 1989. 18: p. 77-81.

103. Ukabam, S.O. and B.T. Cooper, Small intestinal permeability as an indicator of jejunal mucosal recovery in patients with celiac sprue on a gluten-free diet. J Clin Gastroenterol, 1985. 7(3): p. 232-6.

104. Cobden, I., J. Rothwell, and A.T. Axon, Intestinal permeability and screening tests for coeliac disease. Gut, 1980. 21(6): p. 512-8.

105. Hamilton, I., et al., Intestinal permeability in coeliac disease: the response to gluten withdrawal and single-dose gluten challenge. Gut, 1982. 23(3): p. 202-10.

106. Mulder, C.J., et al., Coeliac disease. Diagnostic and therapeutic pitfalls. Scand J Gastroenterol Suppl, 1993. 200: p. 42-7.

107. Hallert, C. and T. Derefeldt, Psychic disturbances in adult coeliac disease. I. Clinical observations. Scand J Gastroenterol, 1982. 17(1): p. 17-9.

108. Hallert, C. and J. Astr:om, Psychic disturbances in adult coeliac disease. II. Psychological findings. Scand J Gastroenterol, 1982. 17(1): p. 21-4.

109. Hallert, C., J. Astr:om, and G. Sedvall, Psychic disturbances in adult coeliac disease. III. Reduced central monoamine metabolism and signs of depression. Scand J Gastroenterol, 1982. 17(1): p. 25-8.

110. Hallert, C., J. Astr:om, and A. Walan, Reversal of psychopathology in adult coeliac disease with the aid of pyridoxine (vitamin B6). Scand J Gastroenterol, 1983. 18(2): p. 299-304.

111. Singh, M.M. and S.R. Kay, Wheat gluten as a pathogenic factor in schizophrenia. Science, 1976. 191(4225): p. 401-2.

112. Storms, L.H., J.M. Clopton, and C. Wright, Effects of gluten on schizophrenics. Arch Gen Psychiatry, 1982. 39(3): p. 323-7.

113. Wood, N.C., et al., Abnormal intestinal permeability. An aetiological factor in chronic psychiatric disorders? Br J Psychiatry, 1987. 150: p. 853-6.

114. Dohan, F.C., et al., Is schizophrenia rare if grain is rare? Biol Psychiatry, 1984. 19(3): p. 385-99.

115. O'Farrelly, C., et al., Association between villous atrophy in rheumatoid arthritis and a rheumatoid factor and gliadin-specific IgG. Lancet, 1988. 2(8615): p. 819-22.

116. Wyatt, J., et al., Intestinal permeability and the prediction of relapse in Crohn's disease. Lancet, 1993. 341(8858): p. 1437-9.

117. Vanderhoof, J.A., et al., Effects of berberine, a plant alkaloid, on the growth of anaerobic protozoa in axenic culture. Tokai J Exp Clin Med, 1990. 15(6): p. 417-23.

118. Gupte, S., Use of berberine in treatment of giardiasis. Am J Dis Child, 1975. 129(7): p. 866.

119. Rabbani, G.H., et al., Randomized controlled trial of berberine sulfate therapy for diarrhea due to enterotoxigenic Escherichia coli and Vibrio cholerae. J Infect Dis, 1987. 155(5): p. 979-84.

120. Subbaiah, T.V. and A.H. Amin, Effect of berberine sulphate on Entamoeba histolytica. Nature, 1967. 215(100): p. 527-8.

121. Buchanan, H.M., et al., Is diet important in rheumatoid arthritis? [see comments]. Br J Rheumatol, 1991. 30(2): p. 125-34.

122. Darlington, L.G. and N.W. Ramsey, Is diet important in rheumatoid arthritis? [letter; comment]. Br J Rheumatol, 1991. 30(4): p. 315-6.

123. Darlington, L.G. and N.W. Ramsey, Review of dietary therapy for rheumatoid arthritis. Br J Rheumatol, 1993. 6: p. 507-14.

124. Prudden, J.F. and L.L. Balassa, The biological activity of bovine cartilage preparations. Sem Arthritis Rheumatism, 1974. 3(4): p. 287-321.

125. Sperling, R.I., Dietary omega-3 fatty acids: effects on lipid mediators of inflammation and rheumatoid arthritis. Rheum Dis Clin North Am, 1991. 17(2): p. 373-89.

126. Bjarnason, I., et al., Importance of local versus systemic effects of non-steroidal anti-inflammatory drugs in increasing small intestinal permeability in man. Gut, 1991. 32(3): p. 275-7.

127. Kirsch, M., Bacterial overgrowth. Am. J. Gastroenterol., 1990. 85: p. 231-237.

128. Stockbrugger, R.W. and U. Armbrecht, Bacterial overgrowth in the upper gastrointestinal tract and possible consequences: report of a workshop in Brussels, Belgium, 9-10 February, 1990. Microb. Ecol. Health Dis., 1991. 4: p. i-vii.

129. Brandt, J., B. L.H., and A. Wagle, Production of vitamin B12 analogues in patients with small-bowel bacterial overgrowth. Ann. Int. Med., 1977. 87: p. 546-551.

130. Giannella, R.A., S.A. Broitman, and N. Zamcheck, Competition between bacteria and intrinsic factor for vitamin B 12 : implications for vitamin B 12 malabsorption in intestinal bacterial overgrowth. Gastroenterology, 1972. 62(2): p. 255-60.

131. Playford, R.J., et al., Effect of luminal growth factor preservation on intestinal growth [see comments]. Lancet, 1993. 341(8849): p. 843-8.

132. Surawicz, C.M., et al., Treatment of recurrent Clostridium difficile colitis with vancomycin and Saccharomyces boulardii. Am J Gastroenterol, 1989. 84(10): p. 1285-7.

133. Surawicz, C.M., et al., Prevention of antibiotic-associated diarrhea by Saccharomyces boulardii: a prospective study. Gastroenterology, 1989. 96(4): p. 981-8.

134. Buts, J.-P., et al., Stimulation of secretory IgA and secretory component of immunoglobulins in small intestine of rats treated with Saccharomyces boulardii. 1990. .

135. Eibl, M.M., et al., Prophylaxis of necrotizing enterocolitis by oral IgA-IgG: review of a clinical study in low birth weight infants and discussion of the pathogenic role of infection. J Clin Immunol, 1990. 10(6 Suppl): p. 77S-79S.

136. Siitonen, S., et al., Effect of Lactobacillus GG yoghurt in prevention of antibiotic associated diarrhoea. Ann Med, 1990. 22(1): p. 57-9.

137. Salminen, E., et al., Preservation of intestinal; integrity during radiotherapy using live Lactobacillus acidophilus cultures. Clin Radiol, 1988. 39: p. 435-437.

138. Oksanen, P.J., et al., Prevention of travellers' diarrhoea by Lactobacillus GG. Ann Med, 1990. 22(1): p. 53-6.

139. Gorbach, S.L., T.W. Chang, and B. Goldin, Successful treatment of relapsing Clostridium difficile colitis with Lactobacillus GG [letter]. Lancet, 1987. 2(8574): p. 1519.

140. Klimberg, V.S., et al., Oral glutamine accelerates healing of the small intestine and improves outcome after whole abdominal radiation. Arch Surg, 1990. 125(8): p. 1040-5.

141. Souba, W.W., The gut-a key metabolic organ following surgical stress:Benefits of glutamine supplementation. Contem Surg, 1989. 35(5A): p. 5-13.

142. Souba, W.W., Glutamine: a key substrate for the splanchnic bed,. Annu. Rev. Nutr., 1991. 11: p. 285-308.

143. van der Hulst, R.R., et al., Glutamine and the preservation of gut integrity. Lancet, 1993. 341(8857): p. 1363-5.

144. Hagen, T.M., et al., Fate of dietary glutathione: disposition in the gastrointestinal tract. A,. J. Physiol., 1990. 259: p. G530-G535.

145. Cody, V., et al., ed. Plant Flavonoids in Biology and Medicine II. Biochemical, Cellular and Medicinal Properties. Progress in Clinical and Biological Research, Vol. 280. 1988, Aland R. liss, Inc.: New York. 481.

146. Vanderhoof, J.A., et al., Effect of dietary menhaden oil on normal growth and development and on ameliorating mucosal injury in rats. Am J Clin Nutr, 1991. 54(2): p. 346-50.

147. Stark, J.M. and S.K. Jackson, Sensitivity to endotoxin is induced by increased membrane fatty-acid unsaturation and oxidant stress. J Med Microbiol, 1990. 32(4): p. 217-21.

148. Eisenhans, B. and W.F. Caspary, Differential changes in the urinary excretion of two orally administered polyethylene glycol markers (PEG 900 and PEG 4000) in rats after feeding various carbohydrate gelling agents. J Nutr, 1989. 119: p. 380-387.

149. Gyory, C.P. and G.W. Chang, Effects of bran, lignin and deoxycholic acid on the permeability of the rat cecum and colon. J Nutr, 1983. 113: p. 2300-2307.

150. Shiau, S.Y. and G.W. Chang, Effects of certain dietary fibers on apparent permeability of the rat intestine. J Nutr, 1986. 116(2): p. 223-32.

151. Spaeth, G., et al., Food without fiber promotes bacterial translocation from the gut. Surgery, 1990. 108(2): p. 240-6.

152. Fukushi, T., Studies on edible rice bran oils. Part 3. Antioxidant effects of oryzanol. Rep Hokaido Inst Pub Health, 1966. 16: p. 111.

153. Yagi, K. and N. Ohishi, Action of ferulic acid and its derivatives as anti-oxidants. J Nutr Sci Vitaminol, 1979. 205: p. 127-135.


Fringe claims

The article is claiming that this syndrome has "inspired" some fringe (and other) kinds of "dietary treatments". Because this is dubious (there is no evidence whatsoever in the linked-to articles) and in the domain of health information I have removed this, but User:Softlavender has twice reinserted it in an unsourced, untagged state. Because this looks highly likely to be fringe misinformation, I think it needs to be deleted immediately. What evidence of verifiability is there? Alexbrn talk|contribs|COI 09:46, 23 October 2013 (UTC)[reply]

If you want citations for information in any article, please put [citation needed] tags. Softlavender (talk) 09:55, 23 October 2013 (UTC)[reply]
That's not strictly true. Our policy states there "any material lacking a reliable source directly supporting it may be removed", and in some circumstances (in BLPs for example) editors are required to do so. There is a spectrum, and editors view things differently. My view is that {{cn}} tags are appropriate for uncontentious material, but for anything that encroaches into the area of health information, dubious material needs immediate deletion. Anyway, irrespective of our editorial views about what should and shouldn't be deleted, it is also policy that "The burden of evidence lies with the editor who adds or restores material" (bolding in original) ... which is why I asked for evidence here. Alexbrn talk|contribs|COI 10:14, 23 October 2013 (UTC)[reply]
Oh, it is definitely true. If you've looked into any kind of quackery you'll know that Leaky Gut is a magnet for all types of quacky treatments for IBS, CFS, candida, autism, etc. If you can't find a ref it means you haven't bothered looking :) --sciencewatcher (talk) 15:45, 23 October 2013 (UTC)[reply]
There seemed a lot of material out there, but I'm not sure how much is RS; but then we get into how WP:FRINGE applies and whether it's undue to mention it ... but that's the next step :-) Alexbrn talk|contribs|COI 18:15, 23 October 2013 (UTC)[reply]
Yes, the problem is that the entirety of "leaky gut syndrome" is fringe, so perhaps an article from a reputable science magazine might be appropriate. --sciencewatcher (talk) 23:23, 23 October 2013 (UTC)[reply]
Oh okay, searching around I see that's right; this wasn't very evident from the article itself, which probably signals a wider neutrality problem here? Alexbrn talk|contribs|COI 05:36, 24 October 2013 (UTC)[reply]
(add) Actually this article is a bit of a disaster, with a load of rather dubious material trying to ride on the coat-tails of the fact that "leaky gut" is (apparently) a thing in real medicine. It was hard to know there was quackery in here because of the lack of mainstream views. Alexbrn talk|contribs|COI 08:15, 24 October 2013 (UTC)[reply]
(add) In fact I'm half-thinking this article was some kind of hoax, with random bits of vaguely-related journal articles copied and pasted together into a jargon-rich confused mess. I'm having a bit of a tidy-up. Alexbrn talk|contribs|COI 09:58, 24 October 2013 (UTC)[reply]
Leaky gut syndrome used to be a different article to Leaky gut, but they were merged a while ago. Leaky Gut Syndrome is definitely fringe/quackery. I'm not sure about Leaky Gut - there seems to be some reasonable research there, although I'm slightly suspicious. It would be good if a medical expert could take a look. --sciencewatcher (talk) 13:42, 24 October 2013 (UTC)[reply]
Not sure how much of an "expert" I am, but I am a physician. "Leaky gut" is increased permeability of the intestinal wall, which is a real phenomenon that has actually been observed. The question is whether this "leaking" has any clinical significance. Those who say it does theorize that it may be the cause of numerous diseases, such as psoriasis, arthritis, Crohn's disease, etc., etc. They have also proposed an entity that they call "leaky gut syndrome", which is said to have symptoms including bloating, gas, cramps, food sensitivities, and aches and pains. These are very nebulous symptoms that can be caused by a variety of diseases, or by simple stress and strain. Whether they can also be caused by increased permeability of the intestinal wall is, from an MD’s standpoint, a very gray area. The simple fact is, we don’t know enough about the gut, which is our biggest immune system organ. Obviously there is a lot of room for jumping to unproven conclusion, which then leads to the advocacy of untested treatments and other quackery, as others have pointed out. So in summary, "leaky gut" is real, but whether increased gut permeability leads to psoriasis or arthritis or Crohn's or food sensitivities or "leaky gut syndrome" is an open question -- and that's why I restored the sourced sentence in the lede that says precisely that. It's good that the dubious & unsourced claims are being removed, but we need to be careful not to let the pendulum swing to the other extreme and flat out label it a hoax -- because we don't know that either. NPOV is the key. Cheers, DoctorJoeE review transgressions/talk to me! 14:44, 24 October 2013 (UTC)[reply]
I think the problem with that lede sentence is that it was generalizing the view of a GP (with a history of misconduct) to stand for "doctors", as if this was a live controversy in mainstream medicine. I know this is what newspapers do, but it probably isn't NPOV here, especially since WP:FRINGE applies. Alexbrn talk|contribs|COI 14:50, 24 October 2013 (UTC)[reply]
No, that lede sentence summarized the situation, which is that gut permeability is real, but whether or not it causes disease (or perhaps vice versa, or both) is an open question that has not yet been answered. If your problem is with the source, I will replace it with a scholarly article that makes the same point. DoctorJoeE review transgressions/talk to me! 16:25, 24 October 2013 (UTC)[reply]
I think there are a few issues here:
  • Easy one first: the lede should summarize the body and not contain novel information; so anything new should be added to the body first.
  • Yes, I think it would be helpful to have a good source showing that "leaky gut" was, in the mainstream, synonymous with "gut permeability". (But - is it?)
  • I don't think characterizing the claims around the adverse causes of "leaky gut" as giving rise "an open question" is neutral. The claim for example, that it causes autism? That seems to be about as open a question as the Wakefield stuff. The NHS site it pretty down on it, implying it is implausible too (if it were true, people who drank a lot of alcohol would have the ill effects claimed, e.g.). Its pseudoscience giving rise to quackery and per WP:FRINGE we need to be careful not to give a false balance here. Alexbrn talk|contribs|COI 16:56, 24 October 2013 (UTC)[reply]
I don't really care about this topic enough to engage in a protracted debate -- but it appears to me that you are falling into the common WP trap of "neutral POV = my POV". I happen to agree with you that this is "pseudoscience giving rise to quackery", but we are not here to push our POV; we are here to write a neutral article. How is the disputed lede sentence "novel information"? I just re-read the article, and it seems to me that it is fair to summarize it by saying that the phenomenon of gut permeability is not in dispute, but the theory that it gives rise to disease, or even a series of nonspecific symptoms, is. And that is exactly what the lede sentence that you took out (twice) says. Perhaps, instead of saying that it's an "open question", you would be amenable to saying that it "lacks credible scientific support"? I agree that we should not create a false balance, but POV pushing is equally inappropriate. That will only fuel the contention of alternative medicine advocates that mainstream medicine rejects anything "new". DoctorJoeE review transgressions/talk to me! 18:40, 24 October 2013 (UTC)[reply]
There's no need to personalize it. I have no POV on leaky gut. A day ago I don't think I'd ever even heard the term. My concern is just to get the article presenting reliable information neutrally. Saying the syndrome "lacks credible scientific support" would look good to me; but I think we do that, in effect, already. (BTW, by "novel information" I meant novel-to-the-lede, but not-in-the-body). Our policy on pseudoscience requires us to describe pseudoscientific things clearly as such; saying the matter is "in dispute" would be less than ideally clear on that point. Alexbrn talk|contribs|COI 18:51, 24 October 2013 (UTC)[reply]
Exactly -- "we say that already" -- which means that it's already in the article body, and therefore appropriate to summarize in the lede. In my view, the most important point to convey in this article is that any discussion of a connection between increased intestinal permeability and pathology of any sort is only at the level of hypothesis, with (as yet) no credible scientific support. DoctorJoeE review transgressions/talk to me! 20:14, 24 October 2013 (UTC)[reply]
Then I think we are in violent agreement :-) It's probably just a matter of wording/sourcing. I am slightly uneasy that I've equated "leaky gut" with "gut permeability" without strong RS backing. Do you know of anything that will suffice here? Alexbrn talk|contribs|COI 20:43, 24 October 2013 (UTC)[reply]
Violent agreement; I like it! I've never cared for imprecise lay terms like "leaky gut", but it seems to be regarded as synonymous with "intestinal wall permeability" in every source I've looked at so far, so I think you're on firm ground there. DoctorJoeE review transgressions/talk to me! 22:41, 24 October 2013 (UTC)[reply]

It appears in a very limited context the term "leaky gut" might be used to refer to general gut permeability; however, in nearly all the material out there it appears to be used in association with the supposed systemic health effects which flow from that, which takes us firmly into fringe territory (which is not to say that investigating it is necessarily fringe, as the evidence needs to be finally settled). The NHS article luckily gives us a reliable steer on this. I think the merger wasn't a great idea, as having a "two-in-one" article complicates the categorization and content in a bad way. I think the small bit of legitimate content could probably be moved to articles about the gut, or about the conditions where there is legitimate treatment, leaving this article to focus on "leaky gut syndrome". I'll raise a query at WT:MED. Alexbrn talk|contribs|COI 14:47, 24 October 2013 (UTC)[reply]

I respectfully disagree. I think it is reasonable that the two be combined, so that we can distinguish one from the other directly, and make the point that gut permeability is a real phenomenon, but whether or not it causes symptomatology is unproven. (See also my response to your reverting my restoration, above.) DoctorJoeE review transgressions/talk to me! 16:25, 24 October 2013 (UTC)[reply]

WT:MED

FYI, I have raised a query about this article at WT:MED. Alexbrn talk|contribs|COI 15:00, 24 October 2013 (UTC)[reply]

It was suggested on WTMED that this article should be merged/redirected to the above article. I was unable to find any MEDRS source which explicitly states these two are the same. Google yields some non MEDRS sources linking the two, but suggest need a reliable source to decide what is best. Lesion (talk) 21:07, 24 October 2013 (UTC)[reply]

Bias and Skepticism

This article needs extensive revision.

It links "leaky gut" to "intestinal permeability." "Leaky gut" is an alternative medicine concept that attempts to connect various symptoms with intestinal hyperpermeability. "intestinal permeability" is a well established mechanism of the gut and there are thousands of papers on the subject, as you'll see on pubmed. Many of the papers on intestinal permeability validate some of the claims often made about leaky gut syndrome. It is reasonable to question some of the claims made regarding intestinal hyperpermeability (that it causes autism, for instance), but that it exists and can cause various symptoms has been shown extensively.

A touch of skepticism is appropriate in the absence of evidence, and still more so with contradictory evidence. However, in this instance a well-studied medical subject (intestinal permeability) is being maligned due to it still being under investigation, and its popularization as a catch-all ailment. A properly unbiased article on either leaky gut or intestinal permeability would explain intestinal permeability, mention the experimentally discovered findings, and then bring up the points of contention that have yet to be proven (and may not ever be.)

In its current state, this article feels like a Vatican attack on Galileo's heliocentric model of the solar system. — Preceding unsigned comment added by 172.56.3.119 (talk) 04:20, 16 November 2013 (UTC)[reply]

As the opening of the article says, "leaky gut" is a recognized biomedical phenomenon. But the altmed diagnosis of "leaky gut syndrome" is fringe/quackery (as the mainstream sources say) - so that's what Wikipedia says. Alexbrn talk|contribs|COI 05:58, 16 November 2013 (UTC)[reply]
Knowledge as metanarrative vis a vis "mainstream". Interesting. I agree with the comment above; this article reads like it was written by an angry teen rebelling against their parents. Not very becoming. Could be reframed in a big way. — Preceding unsigned comment added by 74.137.23.120 (talk) 03:28, 30 November 2013 (UTC)[reply]
The article is a mess, it doesn't differentiate properly between leaky gut and the supposed syndrome, perhaps splitting it in two articles fixes the issues. Interweaving unproven bs in an article about an actual condition doesn't make sense.Feyre (talk) 01:45, 8 December 2013 (UTC)[reply]

Supposed Tests/Diagnosis Methods

I have found information from a (M.D.) proponent's perspective on diagnosing/testing for leaky gut. Of course, I recognized it as unscientific and wrote it as such. But seeing as my edit got reverted, I'm guessing Dr. Oz's website is not a reliable source for the believer's perspective? I don't buy any of that stuff, but I saw that the article needed things besides "this isn't an actual condition" in the section; it was already emphasized in the background section.

Perhaps I've been away from Wikipedia too long. What would be considered a reliable source for pulling what proponents of the syndrome say?--Jade Harley (talk) 01:09, 25 November 2013 (UTC)[reply]

It's always a tricky to describe "the fringe thing" without giving it undue space; the problem here is trickier because our reliable source (NHS) call LGS "vague" - we wouldn't want to contradict that by stating something specific. We already give about as much information as that source does ... Alexbrn talk|contribs|COI 04:49, 25 November 2013 (UTC)[reply]
I see. In that case, would just a sentence or two mentioning the range of supposed diagnoses and treatments be better?--Jade Harley (pester) 14:22, 25 November 2013 (UTC)[reply]