FECAL TRANSPLANTS: A Guide

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Here is link to a recent study covering the dizzying complexity of trying to answer the question of whether microbiome alterations/disruptions are the cause or the result of IBD. It is now clear that there are major alterations in the microbiome, we just don't fully understand the implications and meaning of this data. It seems it is still possible the microbiome could be the sole cause if IBD as opposed to genetic mutations/heredity. Attempting to normalize the altered microbiome in IBD patients to appear more normal/healthy to improve or cure the disease is what Fecal Microbiota Transplants are all about.

Microbiota Alterations in Inflammatory Bowel Diseases: From Correlation to Causality
Published Online: May 14, 2016
http://www.cmghjournal.org/article/S2352-345X(16)30040-6/fulltext
 
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wildbill_52280 said:
Here is link to a recent study covering the dizzying complexity of trying to answer the question of whether microbiome alterations/disruptions are the cause or the result of IBD. It is now clear that there are major alterations in the microbiome, we just don't fully understand the implications and meaning of this data. It seems it is still possible the microbiome could be the sole cause if IBD as opposed to genetic mutations/heredity. Attempting to normalize the altered microbiome in IBD patients to appear more normal/healthy to improve or cure the disease is what Fecal Microbiota Transplants are all about.

Microbiota Alterations in Inflammatory Bowel Diseases: From Correlation to Causality
Published Online: May 14, 2016
http://www.cmghjournal.org/article/S2352-345X(16)30040-6/fulltext
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This is very interesting, thank you! I do think fecal transplants are a big piece of the puzzle as will other methods to help clear out any existing pathogens in the system. It is nice that people are researching the CAUSE of the disease now as a trend, rather than the symptoms.
 
Scared1 said:
This is very interesting - has to do with UC but a version is also being made for Crohn's based on the website....

http://www.serestherapeutics.com/clinical-trials/overview/ser-287-seres-101-study
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Scared1, you may be interested in the site thepowerofpoop.com whose original curator was somewhat of a pioneer in bringing together a lot of information regarding FMT to the web. And in particular, given the sort of companies you're linking, you might be interested in the listings on this page, where a lot of the companies that were/are doing next-generation FMT research (e.g. poop in a pill) are listed. You'll see Seres, Enterome, Second Genome, Vedanta and some other less known names. And many of these companies are now backed by the giants of the Pharma industry. True, it's an exciting field, but so far, definitely promising research in recurrent CDI, and to some extent UC, but I haven't seen anything too exciting yet for CD. I'm keeping my fingers crossed though.
 
wildbill_52280 said:
I'm pretty sure this is in this thread somewhere, but it doesnt hurt to bring it up again because it is awesome. There is also a synthetic FMT pill being studied right now for crohn's. The pills are usually a selected mixture of different types of good bacteria.
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Yeah, I didn't see it anywhere. I find this very interesting and I hope it leads to something in the next few years. I know there is a version for the pill - except the website just talks about the UC one but they are doing the same thing.

I really think the whole dysbiosis is a piece of it - not the whole piece to the puzzle. But, with that said, its a BIG piece of it and I am following so many trials and news on a daily basis (weird, it has become part of my morning coffee routine - sit and literally look at any postings/news/etc from the prior 24 hours), and it helps seeing that there are some interesting things in the pipeline:)
 
Scared1 said:
Yeah, I didn't see it anywhere. I find this very interesting and I hope it leads to something in the next few years. I know there is a version for the pill - except the website just talks about the UC one but they are doing the same thing.

I really think the whole dysbiosis is a piece of it - not the whole piece to the puzzle. But, with that said, its a BIG piece of it and I am following so many trials and news on a daily basis (weird, it has become part of my morning coffee routine - sit and literally look at any postings/news/etc from the prior 24 hours), and it helps seeing that there are some interesting things in the pipeline:)
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This article mentions an FMT pill for crohn's being studied, third paragraph from the bottom.
http://www.nytimes.com/2015/11/10/health/fecal-transplants-made-somewhat-more-palatable.html?_r=1
 
irishgal said:
Wow, that's even more antibiotics than AMAT! Shorter duration though. Not thrilled about the PEG.
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I know! All antibiotics - here is a "layman version" per the website abstract:

The available evidence suggests that it is the commensal gut microbiota responsible for the stimulation of the intestinal immune system in the inflammatory bowel diseases (IBD). Thus, many IBD researchers and providers have questioned the current therapeutic approach. For instance, if the gut flora plays a role in the development of IBD, then perhaps targeting the microbes rather than the immune system, or an approach which targets a combination of the two, would be more efficacious.

We hypothesize that immune suppressive medications lead to persistent colonization with potentially pathogenic microbes that perpetuate disease chronicity in IBD patients. Additionally, we hypothesize that host immunosuppression could allow indolent colonizers of the colonic mucosa (symbionts) to behave as pathobionts, thereby causing progressive loss of response (LOR) to immune suppression. About 50% of patients with IBD lose response to conventional, immune suppressive medications for reasons that cannot be explained by the pharmacokinetics and pharmacodynamics of the drugs. This is a major challenge faced by providers who care for patients with IBD.

This study would evaluate for microbes that become more abundant in the feces of patients with IBD who are treated with immune suppression. This alone would represent a significant advance in the field. As proof of concept, we will then attempt to fundamentally change the intestinal environment. We will change the gut microbiota with a colonoscopy preparation, antibiotics, and an anti-fungal medication. We will allow the inflamed gastrointestinal tract a “Holiday” from gut microbes that may be perpetuating the inflammatory response. We will be studying this intervention in the sickest of IBD patients, ages 3-70, who are refractory to conventional therapies, in an attempt to “reset” the luminal environment and either treat the disease itself, or rescue response to therapy. This study could lead to new therapies for IBD and it will also advance our understanding of the gut flora in this vulnerable population.

I couldn't find anything (yet) if this short term antibiotic (very aggressive) regime is intended as a "Cure" meaning no maintenance after and why these were selected - I am hoping to find some info to see. I mean why this pattern of administering these antiobiotics in a successive way and what science was behind it, curious to see if it is similar to the whole pathogen concept like SSI and MAP. At least it is encouraging to see SOME shift -I will post whatever info I find:)
 
Scared1 said:
Has anyone hears about this trial? I came across it it today and thought it was interesting - it is not yet recruiting and in phase 2 and last updated and entered in this month...

https://clinicaltrials.gov/ct2/show/NCT02765256
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I think this is a horrible idea to give someone all these antibiotics when we already suspect the destruction of the natural microbiota to be the cause of many diseases. If anything, they should try to select antibiotics specific to a certain group of pathogens and also try to verify the good bacteria will not be affected by the antibiotics.

If I were to approve such a study those would be the only criteria under which something like this would be tried. Also start in mice and rats first as usual for any groups of chemicals, and only after that perhaps on only a few patients because who knows what could happen.
 
wildbill_52280 said:
I think this is a horrible idea to give someone all these antibiotics when we already suspect the destruction of the natural microbiota to be the cause of many diseases. If anything, they should try to select antibiotics specific to a certain group of pathogens and also try to verify the good bacteria will not be affected by the antibiotics.

If I were to approve such a study those would be the only criteria under which something like this would be tried. Also start in mice and rats first as usual for any groups of chemicals, and only after that perhaps on only a few patients because who knows what could happen.
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I wouldn't rule it out - I mean, I am just curious to see what the reasoning is - perhaps they are trying to aggressively kill of the bad bacteria and these antibiotics were selected for a reason - too soon to tell. At least they are trying to look at the CAUSE as opposed to another symptom focused treatment. I do think that this is a step in the right direction from that regards, whether or not the reasoning is as sound right now - I can't tell, too premature without further data. I always check those clinical trials - I like to see what the status is and it gives you a nice overview. Interesting, I was looking at historical archives of PUD (Peptic Ulcer Disease) and here is some clips I found in scientific articles at the time (this is an article from 1985):

"Genetic factors appear to play a role and a polygenic mode of inheritance has been proposed. Emotional factors also seem to be important. Children with peptic ulcer disease tend to be of above-average intelligence, are often overachievers who have trouble dealing with frustation, and tend to internalize their feelings. Hydrochloric acid has traditionally been implicated in the pathogenesis of peptic ulcer and most therapies are directed at either "neutralizing" acid or blocking its secretion. Recently, local factors such as gastric mucus, alkaline secretion by the gastric mucosal cells, gastric blood flow, and prostaglandins have been shown to be important in local tissue resistance to acid and to digestive enzymes. The diagnosis of peptic ulcer disease depends on a high index of suspicion. Although pain is the most common symptom, there is no typical or characteristic pattern. Nausea and vomiting may also occur in conjunction with the pain."

I can't help but notice the similarities with that and how Crohn's is being looked at - i.e. genetic implications, treating the symptoms, etc...Just thought it was interesting because it seems to be history may be repeating itself. I am just glad I am seeing more and more related to treatment of actual disease rather than the manifestations of the disease - if the MAP vaccine works and SSI works - then I would push for my husband to do both treatments, honestly, because I am sure there may be more than one pathogen or maybe just one (either way), going that route makes a world of a different then living on what medication can I use next as I get worse and worse....and after reading everyone's stories on these forums, it breaks my heart all the time and hope it doesn't always have to be this way....
 
I at least like that they are moving away from immunosuppresives! I kind of agree partly with Wildbill, in that I'd be curious to see which microbes they're targeting and with what meds. I worry about damaging things with AMAT, but at least I know I am specifically targeting something that I have tested culture positive for. It's likely killing more, and I may be on to fecal transplants after AMAT, but since I feel so well and that has corresponded with a large drop in my mycobacteria culture load, I deal. I still think some of this microbiota research, while super interesting, is destracting to the debate of MAP. Wish they'd just fund the full MAP research and give us proof once and for all! Then we can move on to looking for other harmful pathogens.
 
I definitely agree Irishgirl - it is aggressive, yet I wonder why they got the funding?! I mean, you would think that if something like this can get the funding to do proof of concept and the initial trials, I am sure the evidence behind MAP is more convincing to warrant some financial backing to put this to bed. I read somewhere on the post that MAP has been suspected for way too long and it hasn't been proven conclusively yet as a cause for Crohn's and that should mean that it isn't cause otherwise, everyone would be on board. I honestly took that to mean well this must mean they HAVEN'T been able to prove conclusively it DOESN'T and so it remains a possibility, which to me, warrants some serious research investment.
 
irishgal said:
I at least like that they are moving away from immunosuppresives! I kind of agree partly with Wildbill, in that I'd be curious to see which microbes they're targeting and with what meds. I worry about damaging things with AMAT, but at least I know I am specifically targeting something that I have tested culture positive for. It's likely killing more, and I may be on to fecal transplants after AMAT, but since I feel so well and that has corresponded with a large drop in my mycobacteria culture load, I deal. I still think some of this microbiota research, while super interesting, is destracting to the debate of MAP. Wish they'd just fund the full MAP research and give us proof once and for all! Then we can move on to looking for other harmful pathogens.
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The topics of Map and the microbiome are not that much different. One of the main purposes of the natural bacteria(microbiome) in our guts is to defend against pathogens, like MAP. This defense provided by the good bacteria is called colonization resistance, the creation of short chain fattys acids is one main purpose of the bacteria when they ferment fiber from our food. This lowers intestinal PH to inhibit pathogens. other molecules are created as well like antibacterials AKA biocins. So theoretically the main cause could be a damaged microbiome that could allow map to persist in the gut.
 
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This is actually from an older article written july 2014, even though FMT has progressed or likely will progress to a pill form, I thought this was still interesting, and I wonder if this device is still in development in China.

FMT: Quality Control and Feasibility
It would be ideal to standardize FMT. If the purification of fecal microbiota
can be technically controlled it might be more available; otherwise
its application in the world would be restricted by health policy if there is
no quality control. The best solution for this problem
is to allow the procedures to be performed automatically with
machines, GenFMTer. The latest news, from my team cooperating with
Dr. Youquan Zhao and Dr. Huiquan Wang at Tianjin University Precision
Instrument College in China, is the successful development of a new
automatic system for purification of fecal microbiota from fresh feces. This
will advance the standardized FMT from a bio-safety cabinet to automatic
instruments. The operator only needs to press the buttons related to the
designated processes and all procedures can be done in less than a half
an hour. Since we do not know the changing of fecal viable organism after
the feces is expulsed from the colon, it may be the best way to transplant
those microbiota back to the gut as soon as possible.
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http://www.worldgastroenterology.org/UserFiles/file/e-wgn/e-wgn-2014-july.pdf
 
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wildbill_52280 said:
Vedanta biosciences gets 50 million to continue developing Fecal transplant pills for IBD and other health conditions.

http://www.forbes.com/sites/luketim...ionally-defined-bugs-into-drugs/#64702ff46e03
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Thanks! This is encouraging - I don't know if its me because I have just been looking into this since April (my husband's diagnosis), but it seems a lot has been going on with research regarding IBDs in general. Sorry if this is a stupid question - but for those that have had Crohn's for a long time (10+), how do you feel that research has changed and/or GI's methods personally during your treatments? My husband's GI made a statement that when he started practice, there were no options and through his lifetime, he has seen so many changes....so I wonder from your guy's perspective, have you always seen this much research/interest in this area or is this just me having been involved now in this disease that it SEEMS that way?
 
Fecal transplants can be used to clear antibiotic-resistant bacteria out of the gut:

Colonization of the gastrointestinal tract with multidrug-resistant (MDR) bacteria is a consequence of gut dysbiosis. We describe the successful utilization of fecal microbiota transplantation to inhibit Klebsiella pneumoniae MBL+ and Escherichia coli ESBL+ gut colonization in the immunocompromised host as a novel tool in the battle against MDR microorganisms.

http://link.springer.com/article/10.1007/s00005-016-0387-9
 
ppk said:
Fecal transplants can be used to clear antibiotic-resistant bacteria out of the gut:

Colonization of the gastrointestinal tract with multidrug-resistant (MDR) bacteria is a consequence of gut dysbiosis. We describe the successful utilization of fecal microbiota transplantation to inhibit Klebsiella pneumoniae MBL+ and Escherichia coli ESBL+ gut colonization in the immunocompromised host as a novel tool in the battle against MDR microorganisms.

http://link.springer.com/article/10.1007/s00005-016-0387-9
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Thanks for the article! Its time like this I love this forum - sharing knowledge and at the same time hope based on actual evidence:) Thank you!
 
Hi ppk,
Upon my first skimming of the article this seems very interesting - will need to -re-read and digest. But honestly, I do think that with any treatment down the line - any of the vaccine initiatives (MAP, SSI for AEIC, and some of the pending trials about using antibiotics directed at AEIC), that fecal transplants will be a part of the therapy to a cure. I do believe that antibiotics could lead to the dysbiosis - my husband was on antibiotics for three years (minocycline, and prior those three years, another few years of accutane), so I do believe that contributed. He may have the genetic predisposition but no one in his entire family has every had crohn's - so he would be the first. So at a certain point, I think this fecal transplant will become more of a standard treatment down the line (complimenting other therapies as well).
 
Scared - you know Accutane is linked to Crohn's. Not sure of the exact mechanism, but about a year ago I saw the research and it was crazy. There was a class action lawsuit and all. Bad stuff with Accutane and Crohn's.
 
Hi Irishgirl, yeah - I had heard about it and need to look into the exact mechanism. Its weird - I mean what doctor kept prescribing it to him for YEARS and he never questioned it, his first comment when I told him it was dangerous was - well the doctor said it was ok so I trusted him...:-|
 
Pretty typical of docs involvement in Big Pharma! They take them at their word, which is really a shame that they can't. I've found, especially with GIs, that they really minimize the side effects of everything. I've been told on three different occasions that the black box warning (for three different meds) was really not a big deal. More technical details than anything else. In one instance, it was for a med for my three year old child!! For God's sake, even the FDA, which I think does a terrible job on many things, thought it wise to put a black box warning on it. Don't tell me there's no risk!

I was never able to connect the mechanism of Accutane/CD to what I knew of MAP. Maybe it's a dysbiosis thing that acts as a trigger.
 
Scared1 said:
Hi ppk,
Upon my first skimming of the article this seems very interesting - will need to -re-read and digest. But honestly, I do think that with any treatment down the line - any of the vaccine initiatives (MAP, SSI for AEIC, and some of the pending trials about using antibiotics directed at AEIC), that fecal transplants will be a part of the therapy to a cure. I do believe that antibiotics could lead to the dysbiosis - my husband was on antibiotics for three years (minocycline, and prior those three years, another few years of accutane), so I do believe that contributed. He may have the genetic predisposition but no one in his entire family has every had crohn's - so he would be the first. So at a certain point, I think this fecal transplant will become more of a standard treatment down the line (complimenting other therapies as well).
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I also took antibiotics for years for acne, I never went ahead with accutane though because I read on forums of people taking 3-6 courses and still having acne I decided doctors don't fully understand this disease, and when I eliminated milk and reduced sugar and other dietary improvements my skin improved. But it was learning about the emerging studies on antibiotics and IBD that I made the connection the years of doxycycline most likely contributed to Crohn's diagnoses. Below is a link to one of many studies that show a connection. This study was also done to explore the theory that antibiotics were a confounding(hidden) variable which made the studies connecting accutane use to IBD and that the real culprit is antibiotics not accutane because almost everyone who had been on accutane already were given lots of antibiotics by their dermatologist.



Potential association between the oral tetracycline class of antimicrobials used to treat acne and inflammatory bowel disease.
http://www.ncbi.nlm.nih.gov/pubmed/20700115

It is a very good scientific hypothesis that we have eliminated beneficial bacteria somehow and that their restoration from a healthy person will correct the IBD disease process permanently.
 
Thanks Wildbill,
You know I wonder - the various types of Crohn's (and i am not referring to the 5 types they have) but you know, the spectrum of mild, moderate, etc...each with its own manifestations and so on and progression (i.e. some progress, some don't) if that could be stratified like drug-induced Crohn's, or certain mutations based Crohn's, etc....have you come across any articles that attempt to at least stratify the types of crohn's and associated dysbiosis based on genetics, drug use, etc...some sort of stratification? The sheer variability of this disease makes it such a trial and error issue - which is probably one of the most annoying things about it. I wonder if anyone has tried to research this at least for treatment recommendation's sake...
 
Scared1 said:
Thanks Wildbill,
You know I wonder - the various types of Crohn's (and i am not referring to the 5 types they have) but you know, the spectrum of mild, moderate, etc...each with its own manifestations and so on and progression (i.e. some progress, some don't) if that could be stratified like drug-induced Crohn's, or certain mutations based Crohn's, etc....have you come across any articles that attempt to at least stratify the types of crohn's and associated dysbiosis based on genetics, drug use, etc...some sort of stratification? The sheer variability of this disease makes it such a trial and error issue - which is probably one of the most annoying things about it. I wonder if anyone has tried to research this at least for treatment recommendation's sake...
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This here touches on the topic you mention, and it has a lot of good references to related papers.
 
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Scared1 said:
Thanks Wildbill,
You know I wonder - the various types of Crohn's (and i am not referring to the 5 types they have) but you know, the spectrum of mild, moderate, etc...each with its own manifestations and so on and progression (i.e. some progress, some don't) if that could be stratified like drug-induced Crohn's, or certain mutations based Crohn's, etc....have you come across any articles that attempt to at least stratify the types of crohn's and associated dysbiosis based on genetics, drug use, etc...some sort of stratification? The sheer variability of this disease makes it such a trial and error issue - which is probably one of the most annoying things about it. I wonder if anyone has tried to research this at least for treatment recommendation's sake...
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I don't recall there being 5 types of crohn's but levels of severity sure, but I have read studies which say they could classify the disease into different types in the future. I dont think we are at the point where we know exactly what causes what type or severity, because there are still so many factors that can cause IBD. Like vitamin d, dietary fiber, antibiotics, artificial sweeteners, animal fat, omega 6 fats, etc, and any combination of the above, but i think they will be able to classify the types by the bacterial makeup. If you looked hard enough and collected most of the latest studies you might be able to piece some of that information together, but I'm pretty sure we don't have enough studies yet, getting closer though.
 
wildbill_52280 said:
Here is a really old study i forgot about that is like a super risky form of a fecal transplant.
They tried to eliminate as much gut bacteria as they could and repopulate the IBD patients gut with just a few good bacteria. Apparently it seemed to help.

http://www.currenttherapeuticres.com/article/S0011-393X(97)80067-7/pdf
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Thanks for the article! I do think that FT are going to be a piece of the puzzle - the more I think about this dysbiosis caused by whatever the underlying reason in immune deficient hosts (i.e. my husband) due to antibiotics, a pathogen, etc.... I think once that underlying cause is gone - i.e. pathogen, then they would need to replenish or repopulate the microbiome and FT would be the way to go about it. For my husband, I think he would prefer a FT every 2 years rather than daily pills, symptoms, etc....that would be much a more ideal maintenance regime than many of the medications and their potential side effects.
 
Here is an interesting article summary from this year - very recent entitled:

Fecal transplantation: any real hope for inflammatory bowel disease?

Purpose of review: Fecal microbiota transplant (FMT) has emerged as an important treatment for antibiotic resistant or recurrent Clostridium difficile infection. There has been a great deal of media coverage of the efficacy of FMT, and patients with inflammatory bowel disease (IBD) understandably wonder if this approach would also work for them. There are also instructions on ‘do it yourself’ FMT therapy on the web. It is important to understand whether there is evidence that this approach is effective in IBD so that we can advise our patients appropriately.

Recent findings: Systematic reviews have identified four case series involving 27 ulcerative colitis patients with a pooled remission rate of 24% (95% confidence interval (CI) = 11–45%). Two randomized controlled trials evaluating a total of 123 active ulcerative colitis patients have given conflicting results but the pooled data do suggest benefit with a number needed to treat of 6 (95% CI = 3–33). There are four case series involving 38 patients with Crohn's disease with a clinical response in 60.5% (95% CI = 28–86%). There are no randomized trials in Crohn's disease.

Summary: At present there are insufficient data to recommend FMT in IBD, and patients certainly should not be administering this themselves. This remains an interesting approach to treating IBD and more studies are needed to establish the optimal method of delivery as well as randomized, placebo controlled trials to establish the efficacy of FMT.
 
Scared1 said:
Here is an interesting article summary from this year - very recent entitled:

Fecal transplantation: any real hope for inflammatory bowel disease?

Purpose of review: Fecal microbiota transplant (FMT) has emerged as an important treatment for antibiotic resistant or recurrent Clostridium difficile infection. There has been a great deal of media coverage of the efficacy of FMT, and patients with inflammatory bowel disease (IBD) understandably wonder if this approach would also work for them. There are also instructions on ‘do it yourself’ FMT therapy on the web. It is important to understand whether there is evidence that this approach is effective in IBD so that we can advise our patients appropriately.

Recent findings: Systematic reviews have identified four case series involving 27 ulcerative colitis patients with a pooled remission rate of 24% (95% confidence interval (CI) = 11–45%). Two randomized controlled trials evaluating a total of 123 active ulcerative colitis patients have given conflicting results but the pooled data do suggest benefit with a number needed to treat of 6 (95% CI = 3–33). There are four case series involving 38 patients with Crohn's disease with a clinical response in 60.5% (95% CI = 28–86%). There are no randomized trials in Crohn's disease.

Summary: At present there are insufficient data to recommend FMT in IBD, and patients certainly should not be administering this themselves. This remains an interesting approach to treating IBD and more studies are needed to establish the optimal method of delivery as well as randomized, placebo controlled trials to establish the efficacy of FMT.
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This is true, the research has a way to go yet. Doing it yourself requires an understanding of the process and the risks involved. But there is even an FMT recently done by professionals that went wrong because they didn't follow proper donor selection criteria, http://ofid.oxfordjournals.org/content/2/1/ofv004.full

So it doesn't matter who you are, even professionals mess things up. And anyone who properly educates themselves can consider themselves an educated professional and do an FMT safely, that's initially what this thread was all about when I started it. Even when taking every precaution there are unknown risks involved, it's just so new. But lots of animals naturally eat feces with seemingly no harm whatsoever, and actually their life depends on it.

https://www.youtube.com/watch?v=TrqRYSvfwhQ
http://www.bbc.co.uk/nature/adaptations/Coprophagia#p0097kyl
 
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Scared1 said:
Thanks Wildbill,
You know I wonder - the various types of Crohn's (and i am not referring to the 5 types they have) but you know, the spectrum of mild, moderate, etc...each with its own manifestations and so on and progression (i.e. some progress, some don't) if that could be stratified like drug-induced Crohn's, or certain mutations based Crohn's, etc....have you come across any articles that attempt to at least stratify the types of crohn's and associated dysbiosis based on genetics, drug use, etc...some sort of stratification?
Click to expand...

Yes, there is an interesting and very recent publication on this very question, although they looked in terms of gene expression across all of IBD and not just Crohn's. And they found that IBD really consists of three distinct diseases instead of the usual two. Instead of the usual CD/UC breakdown, their genetic data indicates that IBD should really be classified as either UC, or Colonic Crohn's, or Ileal Crohn's.

They also rank these three in terms of progression of severity over time with UC being the mildest and Ileal Crohn's being the most aggressive, which bad news for me since I have ileal Crohn's.

The paper is here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4714968/pdf/main.pdf
 
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Fecal transplants are a bit of a paradox to me in regards to Crohn's. And I'm talking about small bowel disease. The small intestine bacterial density is orders of magnitude less than the large bowel composition. The species are markedly different as well. Upper small bowel are primarily gram-positive aerobes. At the terminal ileum the composition transitions more toward a 50/50 areobes/anaerobes, and in the colon (large intestine), the bacterial diversity explodes with anaerobes. It seems at odds with nature's design to introduce fecal species into the upper gut. She wouldn't have spent millions of years evolving the the illececal valve in vertabrae if she didn't mind the mixing of small and large bowel contents. Most animals don't go around eating each other's poops.

I'll apologize in advance if my views don't align with yours. Just saying FMT may have therapeutic value for disease in the large bowel, which doesn't really cover Crohn's spectrum completely.
 
Xeridea - the points you raise are good ones, which is why much of the research into FMT is focused on UC rather than Crohn's. There is such a thing as colonic Crohn's of course. And FMT may still be able to help to some degree in the small bowel, so it's worth a try as far as research is concerned. But like other therapies it may not prove the be a cure-all for all IBD.
 
xeridea said:
Fecal transplants are a bit of a paradox to me in regards to Crohn's. And I'm talking about small bowel disease. The small intestine bacterial density is orders of magnitude less than the large bowel composition. The species are markedly different as well. Upper small bowel are primarily gram-positive aerobes. At the terminal ileum the composition transitions more toward a 50/50 areobes/anaerobes, and in the colon (large intestine), the bacterial diversity explodes with anaerobes. It seems at odds with nature's design to introduce fecal species into the upper gut. She wouldn't have spent millions of years evolving the the illececal valve in vertabrae if she didn't mind the mixing of small and large bowel contents. Most animals don't go around eating each other's poops.

I'll apologize in advance if my views don't align with yours. Just saying FMT may have therapeutic value for disease in the large bowel, which doesn't really cover Crohn's spectrum completely.
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All good theory aside, the most dramatic and effective FMT's performed to date have been through a nasogastric tube and this was in crohn's disease, in some cases just one fmt makes a big difference. FMT enemas or through colonoscope have been labor intensive and take a long time like 30-60 enemas.

The underlying universal concept here with FMT is all these intestinal disease's may develop from a lack of diversity/extinction in beneficial microbes. So regardless of the specific's of which bacteria are missing and what pathogens moved in and what genetic differences the person has, when you restore the good bacteria, everything could normalize. For the most part the scientific evidence we have supports this theory so far.

Also if the ileum is before the ileocecal valve and you claim nature intends on keeping the contents of the large intestine absolutly seperate, then how should an enema reliably reach the affected ileum of a crohn's patient? An oral FMT would have much better luck at treating every inch of the intestine large and small.
 
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Fecal Microbiota Transplantation for Ulcerative Colitis: A Systematic Review and Meta-Analysis
Published: June 13, 2016
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0157259#pone.0157259.ref016

Abstract

Background
Fecal microbiota transplantation (FMT) has been recognized as a novel treatment for ulcerative colitis (UC). However, its efficacy and safety remain unclear.

Objective
We conducted this systematic review to assess the efficacy and safety of FMT in UC.

Results
Twenty five studies (2 randomized controlled trials, 15 cohort studies, and 8 case studies) with 234 UC patients were included. Overall, 41.58% (84/202) patients achieved clinical remission (CR) and 65.28% (126/193) achieved clinical response. Among the cohort studies, the pooled estimate of patients who achieved CR and clinical response were 40.5% (95% CI 24.7%-58.7%), and 66.1% (95% CI 43.7%-83.0%). Most adverse events were slight and self-resolving. The analyses of gut microbiota in 7 studies showed that FMT could increase microbiota diversity and richness, similarity, and certain change of bacterial composition.

Conclusion
FMT provides a promising effect for UC with few adverse events. Successful FMT may be associated with an increase in microbiota diversity and richness, similarity, and certain change of bacterial composition.
 
xeridea said:
Most animals don't go around eating each other's poops.
Click to expand...

You may find this interesting.

Buffington next tested whether the specific differences in the microbiome were causative factors underlying the social impairments in offspring of mothers fed a high-fat diet. Because mice eat each other's poop, the researchers housed the animals together so that they would acquire microbiota from their cagemates. When socially impaired three-week-old mice born to mothers on a high-fat diet were paired with normal mice, a full restoration of the gut microbiome and a concurrent improvement in behavior was observed within four weeks.
Click to expand...
http://www.eurekalert.org/pub_releases/2016-06/bcom-ass061516.php
 
Not sure if this case report has been posted before in the thread. FMT on a child failing big drugs and who was on way to colectomy. stories of this kind bring tears to me eyes... Im so happy for this child and his family, I feel so hopeful on day we could all make it...:

''Repeated fecal microbiota transplantation in a child with ulcerative colitis.''

http://www.ncbi.nlm.nih.gov/pubmed/27324973
 
Lady Organic said:
Not sure if this case report has been posted before in the thread. FMT on a child failing big drugs and who was on way to colectomy. stories of this kind bring tears to me eyes... Im so happy for this child and his family, I feel so hopeful on day we could all make it...:

''Repeated fecal microbiota transplantation in a child with ulcerative colitis.''

http://www.ncbi.nlm.nih.gov/pubmed/27324973
Click to expand...

Thanks for posting Lady Organic! I definitely agree - I am so happy for that family!
 
Lady Organic said:
Not sure if this case report has been posted before in the thread. FMT on a child failing big drugs and who was on way to colectomy. stories of this kind bring tears to me eyes... Im so happy for this child and his family, I feel so hopeful on day we could all make it...:

''Repeated fecal microbiota transplantation in a child with ulcerative colitis.''

http://www.ncbi.nlm.nih.gov/pubmed/27324973
Click to expand...

thanks Lady Organic, I don't think we have seen this before so this is a good contribution to this thread. There is a study that was posted before that similarly used FMT orally in 30 patients with refractory crohn's that didn't respond well to med's. Amazing stuff. http://www.ncbi.nlm.nih.gov/pubmed/25168749
 
Lady Organic said:
another case report of long term disease resolved by FMT:

''Coordinated Hospital-Home Fecal Microbiota Transplantation via Percutaneous Endoscopic Cecostomy for Recurrent Steroid-Dependent Ulcerative Colitis.'':

http://www.ncbi.nlm.nih.gov/pubmed/27282271
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Thanks again! This is great!
I had to learn what a cecostomy was, supposedly a tube that is placed into the body to insert liquid medication into the beginning of the large intestine(cecum).
 
I'll give it to you guys. The case for FMT in UC may be there. But it's less convincing in Crohn's.

You all keep posting UC studies.
 
xeridea said:
I'll give it to you guys. The case for FMT in UC may be there. But it's less convincing in Crohn's.

You all keep posting UC studies.
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I think the studies just show there is promise - perhaps more so for UC but I think for Crohn's it will serve as a complimentary therapy to the other prospective treatments out there (SSI Vaccine & MAP Vaccine/Redhill Triple Therapy). It is still nice to hear people get better though - UC or otherwise:)
 
 
I previously was informed that bacteria made up 99% of the human Microbiome and that other organisms were lower in number and lesser in their influence. Now I believe I fell victim to possible propaganda from scientists to get funding for Microbiome research!! Joking of course but here is a recent paper that talks about this in relation to Fecal Transplants. Makes me believe a real fecal transplant will still be preferable over a FMT pill with a defined set of bacteria, but FMT pill could still hold much promise and of course over time the pills would eventually include every organism you would need to restore health, its just could be 10-20 years from now. Thankfully the bacterial FMT pills are only a few years away. http://journals.plos.org/plosbiology/article/asset?id=10.1371/journal.pbio.1002503.PDF
 
“There is no doubt that poo can save lives,” said Bordenstein. Take the case of the use of fecal transplants to treat Clostridium difficile infections. According to the literature, it has a 95 percent cure rate. “Right now fecal transplants are used as the treatment of last resort, but their effectiveness raises an important question: When will doctors start prescribing them, or some derivative, first?” Bordenstein asked.
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These days, fecal transplantation is no joke
by David Salisbury | Jul. 12, 2016, 1:30 PM
http://news.vanderbilt.edu/2016/07/these-days-fecal-transplantation-is-no-joke/
 
A completed study of FMT in U.C. shows positive results over placebo. 3x as many patients reached steroid free remission and endoscopic remission compared to placebo group. They gave the patients 40 enemas for 8 weeks from multiple donors. There were some negative responses though where 2 patients became worse in FMT where 1 patient became worse in Placebo. http://www.gastroendonews.com/In-th...Fecal-Transplant-for-Ulcerative-Colitis/37001
 
Some recent research suggests that different populations will have different gut bacteria composition due to a concept called cospeciation, that says our gut bacteria co-evolved with us,.

What I get from this is that if we get into donor bacteriotherapy, we may need to look to get them from individuals in a similar ancestral halpogroup, otherwise some species from them might get reject by our immune system.

That, he adds, could have implications for the burgeoning use of faecal transplants - often used in patients whose own gut bacteria have been suppressed with antibiotics. “It’s a very positive enterprise, but our results suggest those efforts need to consider that our bacteria are tracking our lineage.”
 
Scipio said:
A disappointing failure for the microbiome approach to controlling recurrent C. diff. infections. No better than placebo and in some cases worse.

It looks like this microbiome approach is not going ot be as quick and easy as some have predicted:

http://www.cnbc.com/2016/07/29/gut-...nge-after-microbiome-drug-fails-in-trial.html
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Thanks, I was just about to post on this. disappointing for sure. this pill from seres is just a handfull of bacteria though, spores to be precise. As a comparison a different type of FMT pills used for c diff were "full spectrum" containing a much wider range of bacteria and were just as effective as regular fecal transplants.http://www.cleveland.com/healthfit/index.ssf/2013/10/a_canadian_doctor_is_curing_st.html

these pills are made one by one with a centrifuge which seperates and concentrates the bacteria from other stool contents. It's actually a very simple process, but hard to gaurantee that's its free of any unknown risks, like the seres targeted approach could have been since they know exactly whats in it.
 
wildbill_52280 said:
Vedanta biosciences issued broad patent for microbiome therapies utilizing clostridia species of bacteria. As far as I know this means any company that wants to use them for any medications must consult with them for a period of time.
http://www.kctv5.com/story/32766682...ome-therapeutics-based-on-bacterial-consortia
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The "consultation" with Vendanta will consist almost entirely of haggling over how much the other company must pay for a license to use the technology covered by the patent.
 
Here is a piece of evidence that supports the concept of damage to the microbiome possibly involved in many diseases and not just C. diff or IBD, in this mouse experiment they used antibiotics to cause diabetes. http://www.nature.com/articles/nmicrobiol2016140

Restoration of the natural microbiome with a fecal microbiota transplant would likely be able to reverse this and that is the hopes we have for the upcoming experiments when applied to humans, many studies are happening right now. There are also 4 studies in the last 5 years linking antibiotics to increased risk of IBD, many of my serious health problems began 2 weeks after taking an antibiotic, within a year i was diagnosed with crohn's. I found a study on amoxicillin-clavulanic acid in human's and the effects it had on their gi microbiome, it pretty much obliterated the clostridia species, and these are the ones that are messed up in IBD, and this is the antibiotic i took right before my health seriously declined. These are also the species they are trying to use in FMT pills now. So much evidence now points to that antibiotic I took as the cause of my crohn's.
 
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wildbill_52280 said:
Here is a piece of evidence that supports the concept of damage to the microbiome possibly involved in many diseases and not just C. diff or IBD, in this cases using antibiotics. http://www.nature.com/articles/nmicrobiol2016140

Restoration of the natural microbiome with a fecal microbiota transplant would likely be able to reverse this and that is the hopes we have for the upcoming experiments when applied to humans, many studies are happening right now. There are also 4 studies in the last 5 years linking antibiotics to increased risk of IBD, many of my serious health problems began 2 weeks after taking an antibiotic, within a year i was diagnosed with crohn's.
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I can definitely believe that - my husband took antiobiotics (minocycline for 3-4 years before he was diagnosed), no family history, very healthy, 28 years old, never been to a doctor (literally). Plus, he is overly clean (hygiene hypothesis - not like normal clean, like obssessive). So I definitely believe that part of it.
 
Interesting article just came out in journal:

Any Future for Fecal Microbiota Transplantation as Treatment Strategy for Inflammatory Bowel Diseases?
Kump P, Högenauer C.
Abstract
Fecal microbiota transplantation (FMT) is a novel therapeutic procedure aiming at restoring a normal intestinal microbiota by application of fecal microorganisms from a healthy subject into the gastrointestinal tract of a patient. FMT is the most effective treatment for recurrent Clostridium difficile infections (CDI). These infections also occur in patients with inflammatory bowel diseases (IBDs), where case series demonstrated a successful treatment of CDI by FMT in 83-92% of patients. The effect of FMT on the activity of IBD has mainly been investigated in ulcerative colitis (UC) patients, including 3 randomized controlled trials. So far, 2 randomized controlled trials showed a superiority of FMT compared to placebo in inducing remission in UC, while 1 study found no significant difference to placebo. The variation in response to FMT between these studies as well as in the uncontrolled trials might be explained by many differences in the way of FMT application, patient pretreatment and patient and donor selection. The data for the use of FMT in Crohn's disease and pouchitis are sparse; currently, no conclusion can be drawn regarding the effectiveness of FMT in these indications. It needs to be noted that cases of IBD activation after FMT have been reported. So far, FMT can only be recommended to be used for the treatment of concomitant CDI in IBD in clinical practice. For treating IBD irrespective of CDI, FMT should be only used in clinical trials. Current forms of FMT, especially protocols using repeated application, are very time and personnel consuming. Future trends are the use of defined stable microbiota preparations, in particular oral preparations, which will enable better and larger controlled trails for investigating FMT in IBD.
 
Another anecdote: while I have lots of family with Crohn's and I am of Ashkenazi descent and my family environment was super-clean, my history of getting Crohn's directly follows repeatedly being given 2 week regimens of full-spectrum antibiotics for chronic urinary tract infections when I was in my 20s.
 
wantok said:
Another anecdote: while I have lots of family with Crohn's and I am of Ashkenazi descent and my family environment was super-clean, my history of getting Crohn's directly follows repeatedly being given 2 week regimens of full-spectrum antibiotics for chronic urinary tract infections when I was in my 20s.
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These are studies linking antibiotics to increasing the risk of developing IBD in other words "causing" the disease.

2004
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774910/
2010
http://www.ncbi.nlm.nih.gov/pubmed/20700115
2011
http://faculty.vet.upenn.edu/gastro/documents/Hwang12-19-11ajg2011304a.pdf
2012
http://pediatrics.aappublications.org/content/130/4/e794.full
2013
http://journals.lww.com/ibdjournal/...4_YI_Antibiotics_and_Risk_of_New_Onset.4.aspx

While It's hard to say antibiotics alone can cause IBD because many people take antibiotic's and do not develop IBD, it can depends on the type of antibiotic, how many times you have taken it, the length of time etc, and other risk factors that are present like diet etc. But when you look at all the scientific evidence that exists, damage to the microbiome and the correction of this damage with restoration of missing bacteria with Fecal transplants, you can see it all starts to come together and make more sense, maybe we are on the right track here, I believe we are.



More evidence that suggests a link between antibiotics as a cause of IBD and destruction of microbiome:

Antibiotic Associated Hemorrhagic Colitis: The Need to Distinguish
from Clostridium difficile Colitis!
http://www.practicalgastro.com/pdf/January09/PG_Jan09_DharmarajanArticle.pdf
(this case report strongly showing the ability of antibiotics to promote diarrhea and colitis(colonic inflammation),so to make a small analogical leap and suggest antibiotics could also cause chronic colitis such as in IBD, doesn't sound so far fetched now)


Here is another study of someone with antibiotics associated diarrhea. Quote "Antibiotic administration was associated with distinct changes in the diversity of the gut microbiota, including a marked decrease in the prevalence of butyrate-producing bacteria." (Is it just a coincidence that IBD patients are lacking in diversity of beneficial clostridia which are butyrate producing bacteria)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC356823/

Another study of microbiome changes during antibiotic associated diarrhea of someone taking amoxicillin-clavulanic acid. Clostridia species were so inhibited by antibiotics they undetectable, but grew back after removal of antibiotics. (this is the antibiotic I took before my health changed in a serious way one year later I was diagnosed with crohn's disease.)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC356823/

Clinical onset of the Crohn's disease after eradication therapy of Helicobacteria pylori infection. Does Helicobacter pylori infection interact with natural history of inflammatory bowel diseases?(this is an anecdotal report, but i think it was the amoxicillin that cause the crohn's and certain antibiotics can make a similar pattern of bacterial changes in people? i suggest some people may recover, and some may not)
http://www.ncbi.nlm.nih.gov/pubmed/11208510


Is Crohn's disease caused by antibiotics?
http://www.ncbi.nlm.nih.gov/pubmed/7721242
 
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Increased Intestinal Microbial Diversity Following Fecal Microbiota Transplant for Active Crohn's Disease.

Inflamm Bowel Dis. 2016 Sep;22
Abstract

BACKGROUND:
The microbiota in the lumen of patients with Crohn's disease (CD) is characterized by reduced diversity, particularly Firmicutes and Bacteroidetes. It is unknown whether the introduction of the intestinal microbiota from healthy individuals could correct this dysbiosis and reverse mucosal inflammation. We investigated the response to fecal microbial transplantation (FMT) from healthy individuals to subjects with active CD.

METHODS:
We performed a prospective open-label study (uncontrolled) of FMT from healthy donors to subjects with active CD. A single FMT was performed by colonoscopy. Recipients' microbial diversity, mucosal T-cell phenotypes, and clinical and inflammatory parameters were measured over 12 weeks, and safety over 26 weeks.

RESULTS:
Nineteen subjects were treated with FMT and completed the study follow-up. Fifty-eight percent (11/19) demonstrated a clinical response (Harvey-Bradshaw Index decrease >3) following FMT. Fifteen subjects had sufficient pre/postfecal samples for analysis. A significant increase in microbial diversity occurred after FMT (P = 0.02). This was greater in clinical responders than nonresponders. Patients who experienced a clinical response demonstrated a significant shift in fecal microbial composition toward their donor's profile as assessed by the Bray-Curtis index at 4 weeks (P = 0.003). An increase in regulatory T cells (CD4CD25CD127lo) was also noted in recipients' lamina propria following FMT. No serious adverse events were noted over the 26-week study period.

CONCLUSIONS:
In this open-label study, FMT led to an expansion in microbial bacterial diversity in patients with active CD. FMT was overall safe, although the clinical response was variable. Determining donor microbial factors that influence clinical response is needed before randomized clinical trials of FMT in CD.

https://www.ncbi.nlm.nih.gov/pubmed/27542133
 
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My son's diagnosis has changed from Crohn's to UC. He is cortisone dependent (at the moment on 30 mg of prednisolone per day, has been on prednisolone for 9 months now, 30-60 mg day), currently also on Humira and 75 mg of Azathpriorine, IVIG and Eusaprim antibiotics. We are considering FMT. Is he too immunocomprimised to get a FMT? Any risks for serious side effects?
 
Malgrave said:
My son's diagnosis has changed from Crohn's to UC. He is cortisone dependent (at the moment on 30 mg of prednisolone per day, has been on prednisolone for 9 months now, 30-60 mg day), currently also on Humira and 75 mg of Azathpriorine, IVIG and Eusaprim antibiotics. We are considering FMT. Is he too immunocomprimised to get a FMT? Any risks for serious side effects?
Click to expand...

As far as I recall most people who have received FMT for crohn's were refractory and failed most med's. There hasn't been much negative effects from it, some cases people who were stable went into a flare, one guy who did a home FMT with U.C. became much worse but who knows what he was doing without proper guidance. But of course, this is all early info on an experimental but promising treatment. Take the precautions of course if you DIY.
 
SO which came first? The dysbiosis or the inflammation? A new study shows it looks like the dysbiosis came first.
This evidence could further support the concept that dysbiosis is the first step in IBD development, and that could mean that it is also the cause of the disease itself and restoring dysbiosis with Fecal Microbiota transplant could be the cure.

If a dysbiosis is an instigator, then in principle it should be possible to detect this defect in otherwise healthy populations who are at increased risk for disease, such as healthy relatives of IBD patients.

In a new study published in this issue of Cellular and Molecular Gastroenterology and Hepatology, Jacobs et al 3 do exactly that. Performing a thorough analysis of fecal microbial profiles from 36 IBD patients in remission (26 with Crohn’s disease and 10 with ulcerative colitis) and 54 healthy first-degree relatives, they showed that it is possible to identify an IBD-like intestinal microbiome in at-risk healthy individuals who do not have clinically detectable inflammation.
Click to expand...
http://www.sciencedirect.com/science/article/pii/S2352345X16301060

I also recall a study examining the microbiome in crohn's patients who were in remission and on immunosuppressant therapy, a dysbiotic state was still evident when inflammation was suppressed, suggesting that the inflammatory response is not the sole cause of a dysbiotic state. But inflammation does have a strong influence on dysbiosis, so inhibiting inflammation does improve things just doesn't seem to correct things completely, I'll have to find that study though.
 
wildbill_52280 said:
SO which came first? The dysbiosis or the inflammation?
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My guess (and it's just a guess - no data) is that it's either or both. I'm thinking the dysbiosis and the inflammation form a self-feeding loop, a vicious cycle that can start with either one.
 
Scipio said:
My guess (and it's just a guess - no data) is that it's either or both. I'm thinking the dysbiosis and the inflammation form a self-feeding loop, a vicious cycle that can start with either one.
Click to expand...

Under what natural or semi natural circumstance would that happen though, inflammation is generally a response to bacterial threat, or tissues damage/repair, as far as I know. What circumstance could inflammation be triggered entirely independent of any changes in the microbiome? I'm not arguing any given position just thinking out out loud really.
Generally speaking my position is that 90% of IBD cases are not genetically determined and the condition is reversible, through a FMT. Whether dysbiosis is a cause of inflammation of inflammation is a cause of dysbiosis, I would say that these questions are important because this evidence would point to the correction of the microbiome as a therapeutic strategy, rather then the prevailing paradigm of suppressing the inflammation or immune system to influence symptoms.

I would say at this point the evidence is really good to justify treating the state of dysbiosis, perhaps affecting symptoms through that variable/pathway instead, and I do believe it will lead to the cure. I really don't know what is taking so long to get these FMT pill studies for crohn's going though, the evidence has been here for a while now, we can do it now. The colonoscopic enemas and home enemas are unreliable way of studying this, we are beyond that by now.
 
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wildbill_52280 said:
Under what natural or semi natural circumstance would that happen though, inflammation is generally a response to bacterial threat, or tissues damage/repair, as far as I know. What circumstance could inflammation be triggered entirely independent of any changes in the microbiome? I'm not arguing any given position just thinking out out loud really.
Click to expand...

There are many ways the gut can become directly inflamed without first disrupting the bacterial microbiome - celiac disease, viral enteritis, NSAIDS, all sorts of autoimmune inflammation, etc. And once inflamed the inflammation could easily result in disruption of the microbiome, which in turn could lead to more inflammation. It's a chicken and egg thing.

Successful FMT could indeed prove to be a useful tool to break this vicious cycle and restore good health, but there is no particular reason think that disruption of the microbiome is only way the process can get started in the first place.
 
Healing effect of fecal microbiota transplantation lasts for long
October 11, 2016
https://www.sciencedaily.com/releases/2016/10/161011085352.htm

The researchers in the University of Helsinki and Helsinki University Hospital have studied in detail the intestinal microbiota of 14 patients treated with a faecal microbiota transplant. The patients suffered from recurrent Clostridium difficile -infection, also known as antibiotic associated diarrhea, and they had not responded to antibiotic treatment. After the faecal microbiota transplantation therapy, the patient's microbiota was followed for a year.

The researchers found out that the patient's intestinal microbiota highly resembled the donor's microbiota and this composition remained stable through-out the 1-year follow-up period.

"Our results suggest that intestinal microbiota can be modified relatively permanently. This opens new possibilities to the use this treatment for other diseases related to microbial dysbiosis," says the Academy Research Fellow Reetta Satokari from the University of Helsinki.
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ARE YOU READY TO SWALLOW A PILL FULL OF POOP?
11.02.16

https://www.wired.com/2016/11/microbiome-therapy-making-fecal-transplants-better/

COLLEEN KELLY STARTED using fecal microbiota transplants in 2008—one of the first gastroenterologists in the US to do so. Over the years, she has noticed some strange side effects. One of her C. diff patients, for instance, also suffered from alopecia universalis. He hadn’t been able to grow any hair since he was 16: not on his head, not in his armpits, not even on his eyebrows. But when he got a stool transplant from his sister, he started sprouting fresh patches.

When Kelly told a colleague about the result, she got a second shock: He had seen a fecal transplant recipient regrow hair too. The two doctors were stuck. They didn’t have the resources to analyze their patients’ microbiomes to see what bugs might have been responsible for the change. “You don’t know how bad I wish I had that,” she says.

Tabletop robots sort through fecal samples from around the world, identify species of bacteria, and use those to grow more.
She’s not alone. It’s becoming more and more clear that the microbiome has therapeutic potential beyond the gut. Some patients undergo significant weight changes after a transplant; others say their depression goes away. Yet doctors still can’t figure out how it works.

Which is why, in early August, the National Institutes of Health announced that it would fund a fecal transplant registry, maintained by the American Gastroenterological Association. For the first time, thousands of transplant patients will have their microbiomes sequenced before and after treatment so doctors can have a better shot at identifying not only the bugs that fight C. diff but also what’s causing all those side effects. If Kelly had access to that kind of analysis with her alopecia patient, she might have stumbled onto a new, targeted microbiome therapy—delivering just the right bacteria to trigger hair growth
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Pectin fiber(for example from an apple)makes Fecal Transplants more effective.
For the sake of interpreting this abstract, a lower number on the MAYO score indicates lower amount of symptoms in U.C. This was a very small study though but since good results were observed larger studies would likely be replicated in the future and anything that makes FMT more effective is a great step forward.

BMC Microbiol. 2016 Nov 3;16(1):255.
Pectin enhances the effect of fecal microbiota transplantation in ulcerative colitis by delaying the loss of diversity of gut flora.

Abstract

BACKGROUND:
Fecal microbiota transplantation (FMT) induces remission in ulcerative colitis (UC). However, the treatment effect of FMT diminishes over time. Maintaining the diversity of the gut flora for long periods may improve the effects of FMT in UC. Pectin, which can be fermented by gut microbiota into short-chain fatty acids, is postulated to shape the composition and maintain the balance of gut microbiota following transplantation. This study investigated whether pectin could enhance the effects of FMT in UC patients.

RESULTS:
Three FMT patients and four FMTP(FMT plus Pectin fiber) patients achieved the primary outcome. The Mayo scores of the FMTP group were lower than those of the FMT group at weeks 4 and 12 (P = 0.042 and P = 0.042, respectively). There were no differences in the diversity of the gut flora between the two groups at weeks 4 and 12; however, the composition of the gut flora of the FMTP group was more similar than the FMT group to that of the donor at all-time points post-treatment.

CONCLUSIONS:
Pectin decreased the Mayo score by preserving the diversity of the gut flora following FMT for UC.
 
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WOW!!

Crit Care. 2016 Oct 18;20(1):332.
Successful treatment with fecal microbiota transplantation in patients with multiple organ dysfunction syndrome and diarrhea following severe sepsis.
Abstract
BACKGROUND:
The dysbiosis of intestinal microbiota plays an important role in the development of gut-derived infections, making it a potential therapeutic target against multiple organ dysfunction syndrome (MODS) after sepsis. However, the effectiveness of fecal microbiota transplantation (FMT) in treating this disease has been rarely investigated.

METHODS:
Two male patients, a 65-year-old and an 84-year-old, were initially diagnosed with cerebellar hemorrhage and cerebral infarction, respectively, after admission. During the course of hospitalization, both patients developed MODS, septic shock, and severe watery diarrhea. Demographic and clinical data were collected. Intestinal dysbiosis was confirmed by 16S rDNA-based molecular analysis of microbiota composition in fecal samples from the two patients. The two patients each received a single nasogastric infusion of sterile-filtered, pathogen-free feces from a healthy donor. Fecal samples were collected every two days post infusion to monitor changes in microbiota composition in response to treatment.

RESULTS:
Following FMT, MODS and severe diarrhea were alleviated in both patients. Their stool output and body temperature markedly declined and normalized. Significant modification of microbiota composition, characterized by a profound increase of commensals in the Firmicutes phylum and depletion of opportunistic organisms in the Proteobacteria phylum, was observed in both patients. Furthermore, we identified a reconstituted bacterial community enriched in Firmicutes and depleted of Proteobacteria that was associated with a decrease in the patients' fecal output and in the levels of plasma inflammation markers.

CONCLUSIONS:
The outcome of treating two patients with FMT indicates that restoration of the intestinal microbiota barrier can alleviate the infection and modulate the immune response. These findings warrant further investigation of FMT as a putative new therapy for treating microbiota-related diseases such as MODS.
 
Medicine (Baltimore). 2016 Jul;95(30):e4055. doi: 10.1097/MD.0000000000004055.

Clinical efficacy maintains patients' positive attitudes toward fecal microbiota transplantation.

Abstract
Few studies have been conducted on the attitudes of patients seeking fecal microbiota transplantation (FMT). This study aimed to investigate the reasons for patients with Crohn's disease (CD) seeking FMT and their attitude changes after FMT.In this prospective study, all included patients were diagnosed with CD for at least 6 months and intended to receive FMT. A questionnaire was designed to investigate the history of medical visits and patients' attitudes toward FMT. Only refractory patients who failed to clinically respond to previous treatment were selected for undergoing FMT. Three months after the first FMT, patients were required to complete the second questionnaire on attitudes toward the first FMT.A total of 207 patients with CD were included for questionnaire survey. In 118 refractory patients, 94.07% sought FMT because they had no other choice. In 89 nonrefractory patients, 78.65% sought FMT for the reason that they wanted to achieve better clinical results or even a cure, although the current treatment was effective for them. In all, 118 refractory patients received FMT. Three months after the first FMT, 88.98% (105/118) patients completed the questionnaire on patients' attitudes toward FMT. Of these 105 patients, 56.19% reported to have satisfactory clinical efficacy and 74.29% were willing to receive the second FMT. Moreover, 89.52% (94/105) showed their willingness to recommend FMT to other patients.In conclusion, this study at least first time demonstrated that patients with CD were willing to accept FMT due to its efficacy.
 
YouTube Video Published on Nov 4, 2016

Experts from the AGA Center for Gut Microbiome Research and Education share updates on one of the most important medical breakthroughs -- fecal transplants. Drs. Loren Laine, Colleen Kelly, and Gary Wu serve as co-principal investigators on AGA's new FMT national registry
https://www.youtube.com/watch?v=fAUUpP5HiFA
 
Inflamm Bowel Dis. 2016 Nov 7. [Epub ahead of print]
A Single Species of Clostridium Subcluster XIVa Decreased in Ulcerative Colitis Patients.


Abstract
BACKGROUND:
Imbalance of the intestinal microbiota is associated with gastrointestinal disease and autoimmune disease and metabolic syndrome. Analysis of the intestinal microbiota has recently progressed, and the association with inflammatory bowel disease has been reported at the species level. Such findings suggest that the recovery of homeostasis in the intestinal microbiota could cure inflammatory bowel disease. We aimed to search new probiotic candidates for inflammatory bowel disease through translational research by analysis of ulcerative colitis (UC) patients' intestinal microbiota and clarify the effects of them on inflammation. Here, we focused on Fusicatenibacter saccharivorans, which belongs to Clostridium subcluster XIVa and was successfully isolated and cultured in 2013. We analyzed the association of F. saccharivorans to UC patients' activity and inflammation for the first time.

METHODS:
Feces from UC patients and healthy controls were analyzed by 16S ribosomal RNA gene sequences. F. saccharivorans was administered to murine colitis model. Colitic lamina propria mononuclear cells from UC patients and mice were stimulated with F. saccharivorans.

RESULTS:
The whole fecal bacteria in active UC patients were less than that in quiescent UC patients. Furthermore, F. saccharivorans was decreased in active UC patients and increased in quiescent. The administration of F. saccharivorans improved murine colitis. F. saccharivorans induced interleukin 10 production by lamina propria mononuclear cells from not only colitis model mice but also UC patients.

CONCLUSIONS:
F. saccharivorans decreased in correlation to UC activity and suppresses intestinal inflammation. These results suggest that F. saccharivorans could lead to a novel UC treatment.
 
I already posted this study but see what I highlighted here. It's nice to hear a scientific article say this straight out, it's rare to hear it but it's high probability for FMT to correct GI microbiome to be a cure for IBD, most articles talk about FMT as a treatment but cure is a real possibilty and some cases people seemed to be cured.

wildbill_52280 said:
Inflamm Bowel Dis. 2016 Nov 7. [Epub ahead of print]
A Single Species of Clostridium Subcluster XIVa Decreased in Ulcerative Colitis Patients.


Abstract
BACKGROUND:
Imbalance of the intestinal microbiota is associated with gastrointestinal disease and autoimmune disease and metabolic syndrome. Analysis of the intestinal microbiota has recently progressed, and the association with inflammatory bowel disease has been reported at the species level. Such findings suggest that the recovery of homeostasis in the intestinal microbiota could cure inflammatory bowel disease. We aimed to search new probiotic candidates for inflammatory bowel disease through translational research by analysis of ulcerative colitis (UC) patients' intestinal microbiota and clarify the effects of them on inflammation. Here, we focused on Fusicatenibacter saccharivorans, which belongs to Clostridium subcluster XIVa and was successfully isolated and cultured in 2013. We analyzed the association of F. saccharivorans to UC patients' activity and inflammation for the first time.

METHODS:
Feces from UC patients and healthy controls were analyzed by 16S ribosomal RNA gene sequences. F. saccharivorans was administered to murine colitis model. Colitic lamina propria mononuclear cells from UC patients and mice were stimulated with F. saccharivorans.

RESULTS:
The whole fecal bacteria in active UC patients were less than that in quiescent UC patients. Furthermore, F. saccharivorans was decreased in active UC patients and increased in quiescent. The administration of F. saccharivorans improved murine colitis. F. saccharivorans induced interleukin 10 production by lamina propria mononuclear cells from not only colitis model mice but also UC patients.

CONCLUSIONS:
F. saccharivorans decreased in correlation to UC activity and suppresses intestinal inflammation. These results suggest that F. saccharivorans could lead to a novel UC treatment.
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