A negative study for prebiotics/FOS
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
A negative study for prebiotics/FOS
It seems prebiotics don't do what researchers hoped they would in IBD. Not only do they not work, more people dropped out of the study who were in the treatment group, presumably because their symptoms got worse, not better.
I think this gives strength to the theory that you don't just feed good bacteria with prebiotics, you food all your darn critters, good and bad.
Randomised, double-blind, placebo-controlled trial of fructo-oligosaccharides in active Crohn's disease.
Gut. 2011; 60(7):923-9 (ISSN: 1468-3288)
Benjamin JL; Hedin CR; Koutsoumpas A; Ng SC; McCarthy NE; Hart AL; Kamm MA; Sanderson JD; Knight SC; Forbes A; Stagg AJ; Whelan K; Lindsay JO
Nutritional Sciences Division, King's College London, London, UK.
INTRODUCTION: The commensal intestinal microbiota drive the inflammation associated with Crohn's disease. However, bacteria such as bifidobacteria and Faecalibacterium prausnitzii appear to be immunoregulatory. In healthy subjects the intestinal microbiota are influenced by prebiotic carbohydrates such as fructo-oligosaccharides (FOS). Preliminary data suggest that FOS increase faecal bifidobacteria, induce immunoregulatory dendritic cell (DC) responses and reduce disease activity in patients with Crohn's disease.
AIMS AND METHODS: To assess the impact of FOS in patients with active Crohn's disease using an adequately powered randomised double-blind placebo-controlled trial with predefined clinical, microbiological and immunological end points. Patients with active Crohn's disease were randomised to 15 g/day FOS or non-prebiotic placebo for 4 weeks. The primary end point was clinical response at week 4 (fall in Crohn's Disease Activity Index of ≥ 70 points) in the intention-to-treat (ITT) population.
RESULTS: 103 patients were randomised to receive FOS (n = 54) or placebo (n = 49). More patients receiving FOS (14 (26%) vs 4 (8%); p = 0.018) withdrew before the 4-week end point. There was no significant difference in the number of patients achieving a clinical response between the FOS and placebo groups in the ITT analysis (12 (22%) vs 19 (39%), p = 0.067). Patients receiving FOS had reduced proportions of interleukin (IL)-6-positive lamina propria DC and increased DC staining of IL-10 (p < 0.05) but no change in IL-12p40 production. There were no significant differences in the faecal concentration of bifidobacteria and F prausnitzii between the groups at baseline or after the 4-week intervention.
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. ISRCTN50422530.
I think this gives strength to the theory that you don't just feed good bacteria with prebiotics, you food all your darn critters, good and bad.
Randomised, double-blind, placebo-controlled trial of fructo-oligosaccharides in active Crohn's disease.
Gut. 2011; 60(7):923-9 (ISSN: 1468-3288)
Benjamin JL; Hedin CR; Koutsoumpas A; Ng SC; McCarthy NE; Hart AL; Kamm MA; Sanderson JD; Knight SC; Forbes A; Stagg AJ; Whelan K; Lindsay JO
Nutritional Sciences Division, King's College London, London, UK.
INTRODUCTION: The commensal intestinal microbiota drive the inflammation associated with Crohn's disease. However, bacteria such as bifidobacteria and Faecalibacterium prausnitzii appear to be immunoregulatory. In healthy subjects the intestinal microbiota are influenced by prebiotic carbohydrates such as fructo-oligosaccharides (FOS). Preliminary data suggest that FOS increase faecal bifidobacteria, induce immunoregulatory dendritic cell (DC) responses and reduce disease activity in patients with Crohn's disease.
AIMS AND METHODS: To assess the impact of FOS in patients with active Crohn's disease using an adequately powered randomised double-blind placebo-controlled trial with predefined clinical, microbiological and immunological end points. Patients with active Crohn's disease were randomised to 15 g/day FOS or non-prebiotic placebo for 4 weeks. The primary end point was clinical response at week 4 (fall in Crohn's Disease Activity Index of ≥ 70 points) in the intention-to-treat (ITT) population.
RESULTS: 103 patients were randomised to receive FOS (n = 54) or placebo (n = 49). More patients receiving FOS (14 (26%) vs 4 (8%); p = 0.018) withdrew before the 4-week end point. There was no significant difference in the number of patients achieving a clinical response between the FOS and placebo groups in the ITT analysis (12 (22%) vs 19 (39%), p = 0.067). Patients receiving FOS had reduced proportions of interleukin (IL)-6-positive lamina propria DC and increased DC staining of IL-10 (p < 0.05) but no change in IL-12p40 production. There were no significant differences in the faecal concentration of bifidobacteria and F prausnitzii between the groups at baseline or after the 4-week intervention.
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. ISRCTN50422530.
Finally! "Official" proof of what we've always known to be true. Great find!
Here's the link, for anyone who might want to add it to your bookmarks:
http://www.ncbi.nlm.nih.gov/pubmed/21262918
Thanks,
Tex
Here's the link, for anyone who might want to add it to your bookmarks:
http://www.ncbi.nlm.nih.gov/pubmed/21262918
Thanks,
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.
Zizzle wrote:more people dropped out of the study who were in the treatment group, presumably because their symptoms got worse, not better.
That's if they're healthy. If they're not, then they are likely not helped, but probably hurt by the prebiotic. It seems that this study supports the theory behind the FODMAP diet:In healthy subjects the intestinal microbiota are influenced by prebiotic carbohydrates such as fructo-oligosaccharides (FOS).
Clinical Ramifications of Malabsorption of Fructose and Other Short-chain Carbohydrates - PRACTICAL GASTROENTEROLOGY • AUGUST 2007Fructans are also known as inulins (when the number of fructose molecules, or degree of polymerization or DP, is ≥10), or fructo-oligosaccharide (FOS) or oligofructose (when the DP is <10). Fructose has created much interest because of its possible role in contributing to the obesity epidemic in the USA (1) and for its postulated role in inducing functional gut symptoms.
Symptoms such as bloating, abdominal distension, discomfort, pain, and altered bowel habits are often described as “functional” gut symptoms since their cause is usually related to alterations in the function of the gut and enteric nervous system rather than being manifestations of structural abnormalities. Indeed, functional gut disorders (FGD) are very common, affecting at least 15% of the community across the world. These disorders have been classified into entities such as “irritable bowel syndrome” (IBS), “functional diarrhea,” “functional bloating,” and “functional dyspepsia” according to the symptom complex (2). While the definition of such syndromes is useful in the design of clinical trials, they are somewhat artificial as their overlap is considerable and they are all believed to involve similar mechanisms of visceral hypersensitivity and disorders of the gut-brain axis.
Red and bolded texts are my emphasis. This seems also to support the interview Polly heard on PBS radio.
I don't think it's any coincidence that those of us who need to totally abstain from eating fruit (and also most vegetables) are also the ones having the most difficulty obtaining remission by diet alone.
Gloria
You never know what you can do until you have to do it.
Gloria wrote:I don't think it's any coincidence that those of us who need to totally abstain from eating fruit (and also most vegetables) are also the ones having the most difficulty obtaining remission by diet alone.
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.
That always puzzled me, because I eventually figured out that bananas were causing me problems. I could sorta tolerate up to half a banana per day, but anything more than that would make me sick, and even half a banana seemed to be too much, sometimes. At the time I figured it was just the fiber, but it was probably the FOS, which I had never heard of, at the time.Zizzle wrote:Keep in mind that bananas are a major source of FOS, and many here tolerate bananas.
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.
Beth,
I think there is a correlation between being fructose intolerant and being unable to obtain remission by diet alone. I don't think it's the lack of fruit that is the problem. I suspect that a chemical, perhaps fructose, that is common to all fruit and vegetables, causes the intestines to react. I'm not implying that the lack of fruit causes the problem, but rather that the fructose in fruit and vegetables could be the culprit.
I was surprised to find that all vegetables have fructose in them and I am unable to eat most, if not all, vegetables.
It's very likely that you are not fructose intolerant. It's not a problem common to most members of the board, but most of us do have to be pretty careful to eat only cooked or canned fruits, remove skins from fruit, and avoid citrus fruit. These are not issues connected with fructose, but rather with fiber and citric acid.
Gloria
I think there is a correlation between being fructose intolerant and being unable to obtain remission by diet alone. I don't think it's the lack of fruit that is the problem. I suspect that a chemical, perhaps fructose, that is common to all fruit and vegetables, causes the intestines to react. I'm not implying that the lack of fruit causes the problem, but rather that the fructose in fruit and vegetables could be the culprit.
I was surprised to find that all vegetables have fructose in them and I am unable to eat most, if not all, vegetables.
It's very likely that you are not fructose intolerant. It's not a problem common to most members of the board, but most of us do have to be pretty careful to eat only cooked or canned fruits, remove skins from fruit, and avoid citrus fruit. These are not issues connected with fructose, but rather with fiber and citric acid.
Gloria
You never know what you can do until you have to do it.
Thanks, Gloria. This is really helpful! I've wondered for sometime if fructose was an issue because when I'm not in a flare most fruits except for berries and apples are hugely problematic. Bananas have a problem for years - and I sure do miss them! But maybe it's a combination of fructose and fiber?
When I was in my 20's I remember that I'd get D after eating fresh fruit. If I ate too much fruit, I would have looser BMs. I didn't think it was that unusual and forgot about it until I got MC. I wonder if I've always had problems with fruit and I'm just realizing it now.Beth wrote:when I'm not in a flare most fruits except for berries and apples are hugely problematic.
You can find the fructose level of various fruits and vegetables on this website:
http://nutritiondata.self.com/
Click on the button "Foods by Nutrient" and select Fructose. For a breakdown of fruits and vegetables, select either "Fruits and fruit juices" or "Vegetables and vegetable products" from the "Within" drop-down list.
Gloria
You never know what you can do until you have to do it.

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