Prebiotics: How to feed your family's friendly gut flora.
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
Prebiotics: How to feed your family's friendly gut flora.
Hi, I found an interesting article about prebiotic oligosaccharides. www.parentingscience.com/prebiotics.html Jon
Hi Jon,
First off, rest assured that I don't dispute that the right choice of probiotics (and even prebiotics), might be beneficial for some people who are healthy, and who do not have an inflammatory bowel disease. But articles such as the one you cited are very misleading, unfortunately, because they focus on the use of probiotics and/or prebiotics for healthy people, and they never contain a disclaimer that the information does not apply to those who have an inflammatory bowel disease. As a result, far too many people who develop an IBD naturally assume that probiotics and/or prebiotics should be beneficial for them, and so they waste their hard-earned money helping to make the manufacturers and sellers of probiotics and prebiotics wealthy, without helping themselves one bit.
Oh sure, maybe a half-dozen people out of several hundred who have an IBD, will actually be helped by these products, and so promoters will pounce on that miniscule percentage of success to promote the products. But for the vast majority of sufferers of IBDs, including microscopic colitis, probiotics and prebiotics are pretty much a waste of time and money. That has been been demonstrated time and time again over the years by the vast majority of the members of this board who have tried them, and if you need further proof, look at the research article cited below (which is 2 years more recent than the article you cited). To save some time and space, I'll just quote from my book:
15. Benjamin, J. L., Hedin, C. R., Koutsoumpas, A., Ng, S. C., McCarthy, N. E., Hart, A. L., . . . Lindsay, J. O. (2011). Randomised, double-blind, placebo-controlled trial of fructo-oligosaccharides in active Crohn's disease. Gut, 60(7), 923–929. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21262918
Quoting the conclusion from that study:
The bottom line is that while these products might help to maintain a decent balance of gut bacteria in healthy individuals (who probably don't need any help in the first place), they are worthless for people who have an IBD, and in many cases, they make symptoms worse for IBD patients.
Tex
First off, rest assured that I don't dispute that the right choice of probiotics (and even prebiotics), might be beneficial for some people who are healthy, and who do not have an inflammatory bowel disease. But articles such as the one you cited are very misleading, unfortunately, because they focus on the use of probiotics and/or prebiotics for healthy people, and they never contain a disclaimer that the information does not apply to those who have an inflammatory bowel disease. As a result, far too many people who develop an IBD naturally assume that probiotics and/or prebiotics should be beneficial for them, and so they waste their hard-earned money helping to make the manufacturers and sellers of probiotics and prebiotics wealthy, without helping themselves one bit.
Oh sure, maybe a half-dozen people out of several hundred who have an IBD, will actually be helped by these products, and so promoters will pounce on that miniscule percentage of success to promote the products. But for the vast majority of sufferers of IBDs, including microscopic colitis, probiotics and prebiotics are pretty much a waste of time and money. That has been been demonstrated time and time again over the years by the vast majority of the members of this board who have tried them, and if you need further proof, look at the research article cited below (which is 2 years more recent than the article you cited). To save some time and space, I'll just quote from my book:
This is reference 15 from that quote:Prebiotics, which are soluble fiber products that pass undigested through the stomach and small intestine, into the colon, where they are fermented by bacteria, include fructo-oligosaccharides (FOS) and inulin fiber. The theory is that the fermentation of these items should help to feed beneficial bacteria and thereby help to reestablish healthy populations of beneficial gut bacteria. Unfortunately, no valid scientific research exists to show that prebiotics are any more likely to promote the growth of beneficial bacteria than pathogenic bacteria. In fact, a random, double blind trial, using FOS as a proposed treatment for Crohn’s disease, showed absolutely no benefits.15 Almost four times as many participants receiving FOS, compared with controls, withdrew from the trial before the end of the period. That implies a significant percentage of adverse results for the FOS group. Consequently, it should not be surprising that the use of prebiotics by someone with MC usually results in unpredictable effects at best, and undesirable effects at worst.
15. Benjamin, J. L., Hedin, C. R., Koutsoumpas, A., Ng, S. C., McCarthy, N. E., Hart, A. L., . . . Lindsay, J. O. (2011). Randomised, double-blind, placebo-controlled trial of fructo-oligosaccharides in active Crohn's disease. Gut, 60(7), 923–929. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21262918
Quoting the conclusion from that study:
The red emphasis is mine, of course.CONCLUSION: An adequately powered placebo-controlled trial of FOS showed no clinical benefit in patients with active Crohn's disease, despite impacting on DC function.
The bottom line is that while these products might help to maintain a decent balance of gut bacteria in healthy individuals (who probably don't need any help in the first place), they are worthless for people who have an IBD, and in many cases, they make symptoms worse for IBD patients.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Hi Tex, Thank you for your response. You mentioned Crohn's disease in your post. Should I assume that Crohn's disease and MC is from the same etiology. I have read many research reports about the connection of MAP and Crohn's disease. One explained clusters of Crohn's disease caused by exposure to water polluted with MAP. Jon
Hi Jon,
That's certainly possible, IMO, because MC and Crohn's do have much in common (for one thing, they can affect any part of the digestive system, from mouth to anus, and that's not true for UC). And of course probiotics have been shown to be worthless for treating or preventing Crohn's disease but helpful for UC. And our own experience here on the board has shown that very few MC patients derive any benefit from probiotics. Nicotine has a similar effect — it's protective of UC, but antagonistic for Crohn's, and we haven't found it helpful for treating MC, either. And while it's possible to trigger MC by stopping a long-term smoking habit, that's probably due to the resulting stress, more than anything else.
And while I believe that stess is the primary driving force behind MC, I haven't ruled out MAP, either. There are a lot of "coincidences" between the development of IBDs and the world-wide distribution of Johne's disease in livestock. Pasteurization does not kill MAP bacteria.
Tex
That's certainly possible, IMO, because MC and Crohn's do have much in common (for one thing, they can affect any part of the digestive system, from mouth to anus, and that's not true for UC). And of course probiotics have been shown to be worthless for treating or preventing Crohn's disease but helpful for UC. And our own experience here on the board has shown that very few MC patients derive any benefit from probiotics. Nicotine has a similar effect — it's protective of UC, but antagonistic for Crohn's, and we haven't found it helpful for treating MC, either. And while it's possible to trigger MC by stopping a long-term smoking habit, that's probably due to the resulting stress, more than anything else.
And while I believe that stess is the primary driving force behind MC, I haven't ruled out MAP, either. There are a lot of "coincidences" between the development of IBDs and the world-wide distribution of Johne's disease in livestock. Pasteurization does not kill MAP bacteria.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Hi Tex, Thank you. The fact that pasteurization does not kill MAP is scary. Do you know of any people that have developed Crohn's disease after the dx of MC? My colonoscopy showed MC on all three levels. I suspect that it has gone past the flap and damaged the villi, caused malabsorption and past the blood barrier into the cells. Dr Fasano, has found high levels of zonolin in patients with MS. I sent him an e-mail and asked if he has tested people for zonolin with muscular dystrophy. No response yet. Jon
Jon,
I'm not personally aware of anyone who has developed Crohn's disease after an MC diagnosis, but at least one of our members (Joe) was diagnosed with both Crohn's disease and MC at the same time, if my memory isn't playing tricks on me. Some medical authorities claim that it is possible for MC to lead to UC, but I'm not sure what that speculation is based upon. It would appear that anyone who has MC would have at least the same statistical chance of developing Crohn's or UC as anyone else in the general population, so obviously it's certainly not impossible, even though there might be no connection between the etiology of the individual diseases.
Most of us have some degree of small intestinal involvement, and in my book I cite references that verify that both the colon and small intestine are typically affected by MC, and there are also references that verify that the colon is affected by celiac disease.
One of Dr. Fasano's articles (published in the Scandinavian Journal of Gastroenterology) concludes that everyone (not just celiacs) produces zonulin in response to exposure to gluten, and gut permeability is also affected for everyone. However, for most people, the increase in permeability is slight. As celiac disease progresses, the tight junctions progressively open wider, until gut permeability eventually becomes a major problem. This proves (beyond question, IMO) that absolutely no one should be eating gluten.
You're most welcome,
Tex
I'm not personally aware of anyone who has developed Crohn's disease after an MC diagnosis, but at least one of our members (Joe) was diagnosed with both Crohn's disease and MC at the same time, if my memory isn't playing tricks on me. Some medical authorities claim that it is possible for MC to lead to UC, but I'm not sure what that speculation is based upon. It would appear that anyone who has MC would have at least the same statistical chance of developing Crohn's or UC as anyone else in the general population, so obviously it's certainly not impossible, even though there might be no connection between the etiology of the individual diseases.
Most of us have some degree of small intestinal involvement, and in my book I cite references that verify that both the colon and small intestine are typically affected by MC, and there are also references that verify that the colon is affected by celiac disease.
One of Dr. Fasano's articles (published in the Scandinavian Journal of Gastroenterology) concludes that everyone (not just celiacs) produces zonulin in response to exposure to gluten, and gut permeability is also affected for everyone. However, for most people, the increase in permeability is slight. As celiac disease progresses, the tight junctions progressively open wider, until gut permeability eventually becomes a major problem. This proves (beyond question, IMO) that absolutely no one should be eating gluten.
Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell linesConclusions. Based on our results, we concluded that gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules.
You're most welcome,
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Jon,
In case you don't have a copy of the book, here's a quote from pages 110–112 of the book that discusses the overlap between celiac disease and MC:
11. Biagi, F., Luinetti, O., Campanella, J., Klersy, C., Zambelli, C., Villanacci, V., . . . Corazza, G. R. (2004). Intraepithelial lymphocytes in the villous tip: Do they indicate potential coeliac disease? Journal of Clinical Pathology, 57(8), 835–839. Retrieved from http://jcp.bmj.com/content/57/8/835.full
12. Dickey, W. (2008, September). Celiac disease and the colon. Practical Gastroenterology 44(1), 40–45. Retrieved from http://www.practicalgastro.com/pdf/Sept ... rticle.pdf
13. Wolber, R., Owen, D., & Freeman, H. (1990). Colonic lymphocytosis in patients with celiac sprue. Human Pathology, 21(11), 1092–1096. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/2227917
14. Fine, K. D., Lee, E. L., & Meyer, R. L. (1998). Colonic histopathology in untreated celiac sprue or refractory sprue: is it lymphocytic colitis or colonic lymphocytosis? Human Pathology, 29(12), 1433–1440. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/9865829
15. Simondi, D., Pellicano, R., Reggiani, S., Pallavicino, F., David, E., Sguazzini, C., . . . Astegiano, M. (2010). A retrospective study on a cohort of patients with lymphocytic colitis. Spanish Journal of Gastroenterology, 102(6), 381–384. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/20575599
16. Moayyedi, P., O'Mahony, S., Jackson, P., Lynch, D. A., Dixon, M. F., & Axon, A. T. (1997). Small intestine in lymphocytic and collagenous colitis: mucosal morphology, permeability, and secretory immunity to gliadin. Journal of Clinical Pathology, 50(6), 527–529. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC500002/
17. Tagkalidis, P. P., Gibson, P. R., & Bhathal, P. S. (2007). Microscopic colitis demonstrates a T helper cell type 1 mucosal cytokine profile. Journal of Clinical Pathology, 60(4), 382–387. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2001106/
18. Vande Voort, J. L., Murray, J. A., Lahr, B. D., Van Dyke, C. T., Kroning, C. M., Moore, B., & Wu, T-T. (2009). Lymphocytic duodenosis and the spectrum of celiac disease. American Journal of Gastroenterology, 104(1), 142–148. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2608723/
19. Koskela, R. (2011). Microscopic colitis: Clinical features and gastroduodenal and immunogenic findings. (Doctoral dissertation, University of Oulu). Retrieved from http://herkules.oulu.fi/isbn97895142941 ... 294150.pdf
20. Stewart, M., Andrews, C. N., Urbanski, S., Beck, P. L., & Storr, M. (2011). The association of coeliac disease and microscopic colitis: A large population-based study. Alimentary Pharmacology & Therapeutics, 33(12), 1340–1349. Retrieved from http://www.medscape.com/viewarticle/743 ... mp&spon=20
21. Green, P. H., Yang, J., Cheng, J., Lee, A. R., Harper, J. W., & Bhagat, G. (2009). An association between microscopic colitis and celiac disease. Clinical Gastroenterology and Hepatology, 7(11), 1210–1216. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/19631283
Tex
In case you don't have a copy of the book, here's a quote from pages 110–112 of the book that discusses the overlap between celiac disease and MC:
Here are the references from that quote:Are celiac disease and microscopic colitis actually symptoms of another disease?
Many research reports point out that the laboratory markers and the clinical symptoms of the two syndromes are very similar. Both celiac disease and microscopic colitis are associated with an elevated lymphocyte count in the mucosa of the intestine. With celiac disease, the lymphocytic infiltration eventually leads to villus atrophy in the small intestine. This is typically true if the patient has either a DQ2 or a DQ8 gene.11 Note that an early stage of celiac disease, known as Marsh stage 1 enteropathy, is marked by an intraepithelial lymphocyte count greater than 30 lymphocytes per 100 enterocytes.12
However, even though histological changes in the colon are not a diagnostic criteria for celiac disease, researchers have long known that with celiac disease, not only is the small intestine inflamed, but typically so is the colon and the stomach.13 As evidence of this, Wolber et al. (1990) stated:
These findings indicate that sprue-associated colonic lymphocytosis and lymphocytic colitis are histologically, quantitatively, and immunohistochemically indistinguishable, that the epithelial T cell infiltration of celiac sprue occurs in glandular mucosa at all levels of the gastrointestinal tract, and that colonic subepithelial collagen deposition in patients with celiac sprue is an infrequent occurrence. These findings also suggest that gastrointestinal epithelial T cell infiltration may be an immunologic response that is common in individuals sensitized to absorbed lumenal antigens, and that colonic lymphocytosis may occur as a response to a number of antigens, including gluten. (p. 1092)
In 1998 Fine et al. concluded, “In contrast, colonic histopathology in refractory sprue is indistinguishable from lymphocytic colitis, although immunohistochemical differences do exist.” (p. 1433).14 Clearly then, both celiac disease and microscopic colitis cause identical cellular changes in the mucosa of the colon.
And even though no mention of the small intestine is made in the diagnostic criteria for microscopic colitis, researchers have found that lymphocytic infiltration is frequently present in the small intestine of MC patients, and in some cases, villus damage is sufficient to justify a diagnosis of celiac disease. Even when the formal diagnostic criteria for celiac disease are not met, a significant number (over 10 %) of microscopic colitis patients show at least a Marsh 1 level of villus damage upon biopsy analysis of their small intestine.15
In fact, small intestinal involvement is quite common with MC.16 Other researchers have noted that the T helper cell type 1 mucosal cytokine response pattern exhibited by microscopic colitis is very similar to the response pattern of celiac disease.17 Most researchers have been unsure how to classify this type of information, since it implies non-celiac gluten sensitivity.18 Often, biopsy samples of the terminal ileum are taken during a colonoscopy exam, and upon examination under a microscope, those samples typically show lymphocytic infiltration for most patients who have MC.19
Koskela (2011) even noted that in general, the duodenum of patients with MC, excluding any patients who have celiac disease, have shorter villi than controls.19 Of course since no villi exist in the colon, villus atrophy cannot occur in the colon, but that is irrelevant to this comparison. According to Stewart et al. (2011) the association between celiac disease and microscopic colitis is so strong, that for someone diagnosed with either of the two diseases, the odds that they will also meet the diagnostic criteria of the other disease, has been shown to be approximately 50 times the level that would typically be expected in the general population.20
Other research shows that the correlation between MC and celiac disease may be much higher, as high as 70 times the probability that would normally be expected, when compared with the risk of someone in the general population developing microscopic colitis.21 In such cases, the diagnosis of MC is almost six times as likely to be made after the celiac diagnosis when compared with the odds of being diagnosed prior to the celiac diagnosis, and between two and three times as likely to be diagnosed later, compared with the odds of a simultaneous diagnosis. We can only venture a guess as to whether this is due to a failure of many GI specialists to rule out microscopic colitis during the initial testing, or whether it is because MC often develops later as a result of untreated or inadequately-treated gluten sensitivity.
11. Biagi, F., Luinetti, O., Campanella, J., Klersy, C., Zambelli, C., Villanacci, V., . . . Corazza, G. R. (2004). Intraepithelial lymphocytes in the villous tip: Do they indicate potential coeliac disease? Journal of Clinical Pathology, 57(8), 835–839. Retrieved from http://jcp.bmj.com/content/57/8/835.full
12. Dickey, W. (2008, September). Celiac disease and the colon. Practical Gastroenterology 44(1), 40–45. Retrieved from http://www.practicalgastro.com/pdf/Sept ... rticle.pdf
13. Wolber, R., Owen, D., & Freeman, H. (1990). Colonic lymphocytosis in patients with celiac sprue. Human Pathology, 21(11), 1092–1096. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/2227917
14. Fine, K. D., Lee, E. L., & Meyer, R. L. (1998). Colonic histopathology in untreated celiac sprue or refractory sprue: is it lymphocytic colitis or colonic lymphocytosis? Human Pathology, 29(12), 1433–1440. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/9865829
15. Simondi, D., Pellicano, R., Reggiani, S., Pallavicino, F., David, E., Sguazzini, C., . . . Astegiano, M. (2010). A retrospective study on a cohort of patients with lymphocytic colitis. Spanish Journal of Gastroenterology, 102(6), 381–384. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/20575599
16. Moayyedi, P., O'Mahony, S., Jackson, P., Lynch, D. A., Dixon, M. F., & Axon, A. T. (1997). Small intestine in lymphocytic and collagenous colitis: mucosal morphology, permeability, and secretory immunity to gliadin. Journal of Clinical Pathology, 50(6), 527–529. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC500002/
17. Tagkalidis, P. P., Gibson, P. R., & Bhathal, P. S. (2007). Microscopic colitis demonstrates a T helper cell type 1 mucosal cytokine profile. Journal of Clinical Pathology, 60(4), 382–387. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2001106/
18. Vande Voort, J. L., Murray, J. A., Lahr, B. D., Van Dyke, C. T., Kroning, C. M., Moore, B., & Wu, T-T. (2009). Lymphocytic duodenosis and the spectrum of celiac disease. American Journal of Gastroenterology, 104(1), 142–148. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2608723/
19. Koskela, R. (2011). Microscopic colitis: Clinical features and gastroduodenal and immunogenic findings. (Doctoral dissertation, University of Oulu). Retrieved from http://herkules.oulu.fi/isbn97895142941 ... 294150.pdf
20. Stewart, M., Andrews, C. N., Urbanski, S., Beck, P. L., & Storr, M. (2011). The association of coeliac disease and microscopic colitis: A large population-based study. Alimentary Pharmacology & Therapeutics, 33(12), 1340–1349. Retrieved from http://www.medscape.com/viewarticle/743 ... mp&spon=20
21. Green, P. H., Yang, J., Cheng, J., Lee, A. R., Harper, J. W., & Bhagat, G. (2009). An association between microscopic colitis and celiac disease. Clinical Gastroenterology and Hepatology, 7(11), 1210–1216. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/19631283
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Hi Tex. Thank you for the site. I found interesting research about MAP. I sure you will find it interesting. " Ulcerative colitis and Crohn's disease: is mycobacterium avium subspecies paratuberculosis the common villian?" http://www.gutpathogens.com/content/2/1/21 Jon