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Fecal Transplants
- Thread starter Cat-a-Tonic
- Start date
If anyone is looking for a dr who does the procedure, I contacted Dr Shepard in Tampa FL and he is doing the procedure for many patients, C-diff, Crohn's and Colitis.
when you mention Colities, does dr. shepard specifically treat ulcerative colitis??
when you mention Colities, does dr. shepard specifically treat ulcerative colitis??
[QUOTE steve55]If anyone is looking for a dr who does the procedure, I contacted Dr Shepard in Tampa FL and he is doing the procedure for many patients, C-diff, Crohn's and Colitis.
when you mention Colities, does dr. shepard specifically treat ulcerative colitis??
when you mention Colities, does dr. shepard specifically treat ulcerative colitis??
Are you still feeling good?
- Location
- United States
I teared up when I read this. Still reading the thread but I pray it continues to work for you.
- Location
- United States
I am crying with joy right now reading this.
Just the thought that there is hope.
I'm not sure where I will begin in researching this but since I'm facing the prospect of surgery, I will do anything, even drink the shit if I have to.
Someone pinch me. Hope is an amazing thing.
<3
Just the thought that there is hope.
I'm not sure where I will begin in researching this but since I'm facing the prospect of surgery, I will do anything, even drink the shit if I have to.
Someone pinch me. Hope is an amazing thing.
<3
Its been a while since i've updated how im doing. Ive had a health issue going on lately. I haven't done the FT for several months, been doing very well no crohns, D, no trouble except some occational pain on my left side. Well, it flared up and turned out to be diverticulitus! The most painful thing ive ever experienced. Went into the hospital got iV's with cipro and flagyl for a few days.,i went back to doing the FT for a while. I was afraid my crohns might return after taking all those antibiotics. So far everythings great. Bree
That sounds great!! except for the diverticulitis. i was wondering what was your diet like during the fecal transplants? and what is it like now?
Also, do you think you may have developed diverticulitis from transplanting from your donor?
thanks!
I'm currently doing the FMT again. I currently am eating a low fiber diet because of the pain as food passes by my inflamed colon. I'm getting a colonoscopy next week so I'll update what they find. I feel like the fmt really helps heal the lower colon very well. But I think a colonoscopy delivery would work much better. I've thought seriously of traveling to Florida or California to try it. I think probiotics are great to take, but nothing can take the place of real human probiotics. If you do try this yourself, expect gas, bloating at first. All the probiotics are foreign invaders to your colon. After a while, a week or two, the bacteria seems to be adapted to your own, at least that's what I think. I did have two large abscesses heal in two weeks and I had two fistulas close. Which is unbelievable! I haven't had a bit of problem down there since the FMT. Now the trouble is higher up on the left side under my ribs. A CT scan shows diverticulitus, I think I've had it a long time. I'll update on the colonoscopy results . Bree
Glad your doing well please keep us posted
It is recommended when doing fecal transplants to consume a high fiber diet. only in the beginning before the transplants begin, during the antibiotics, are the patients advised to follow a low fiber diet, specifically to discourage ALL bacterial growth, the antibiotic course is meant to lower all bacteria so that they may be more easily replaced by the transplants. The good bacteria use fiber, mainly fibers classified as soluble, to ferment and to grow. The volume/bulk of a bowel movement is basically, the result of proper fermentation. it is the products of fermentation like the short chain fatty acids which can drive out the bad bacteria and are anti-inflammatory/control the inflammatory response.
A major issue with the enema route of a transplant is that you are using someone elses BM which is at the end stage of fermentation, and most or all of the soluble fibers that encouraged growth may have been utilized. So when it is now introduced to your colon, there isnt much encouragement for the new bacteria to grow and once again dominate its niche within the community, of course this is somewhat theoretical but based on science. I also believe your donor should be on a high fiber diet as well, to encourage the numbers of good bacteria that you need, to also dominate in their flora, all of which, may make the transplant much more effective, theoretically. even without doing any of this you will likely have results but do you really want to do 30-60 fecal enemas? personally id rather do 10 and be done with it. Good luck!!
Yes hilarious as well as shocking, I just came across this and had a good laugh over the comment of the husband telling his wife "thought you said you weren't going to take anymore of my shit"LOL:rof: However, I would do this in a heartbeat! Its not like you're eating it. You have poop in you as it is. Whats the difference? Would just be going into the same place as the rest! and if it has a high rate of curing. I wouldn't even think twice about it!
Andrea, i totally agree. We have this one on the list of possibilities for our daughter.
Right now I want to try Kefir. I think it is the same idea: introduce good bacteria into the gut. It may take a little longer, and I heard you have to introduce them slowly into the system.
I wouldnt think twice about it either. Let me know if you do it.
Right now I want to try Kefir. I think it is the same idea: introduce good bacteria into the gut. It may take a little longer, and I heard you have to introduce them slowly into the system.
I wouldnt think twice about it either. Let me know if you do it.
I read this paragraph a while ago and found it a little creepy.
"Possible Other Consequences of Fecal Transplant
What other traits might be transmitted with a fecal transplant?
Obviously, lifestyle, personal behavior, and sense of wellbeing
are dependent on regularity, but other behavioral changes
may also. For example, the composition of the gut flora in
Drosophila is influenced by diet, as in humans, and transfer of
the gut flora to germ-free recipients also transferred the mating
preferences of the flies, whereas antibiotic treatment of the flies
caused them to lose their mating preferences.12 Human gut flora
also may determine our appetites, scent, and possibly moods
(reviewed in13)." -K Rosenthal article (Infect Dis Clin Pract 2011;19: 276Y278) entitled
Fecal Transplants Transfer More Than Microbiota
Abstract: Fecal transplants are being used to repopulate the colon
as a treatment for antibiotic-associated chronic diarrhea. In addition
to treating the diarrhea, the transferred microbiota carries functions
that affect the metabolism, immune system, and potentially, the behavior
of the recipient. Screening of fecal donors may be just as necessary as
screening organ donors to ensure that unwanted traits are not transferred
with the transplant.
Key Words: fecal transplant, obesity, metabolic syndrome,
autoimmunity, immunotolerance
Something to think about anyhow...
"Possible Other Consequences of Fecal Transplant
What other traits might be transmitted with a fecal transplant?
Obviously, lifestyle, personal behavior, and sense of wellbeing
are dependent on regularity, but other behavioral changes
may also. For example, the composition of the gut flora in
Drosophila is influenced by diet, as in humans, and transfer of
the gut flora to germ-free recipients also transferred the mating
preferences of the flies, whereas antibiotic treatment of the flies
caused them to lose their mating preferences.12 Human gut flora
also may determine our appetites, scent, and possibly moods
(reviewed in13)." -K Rosenthal article (Infect Dis Clin Pract 2011;19: 276Y278) entitled
Fecal Transplants Transfer More Than Microbiota
Abstract: Fecal transplants are being used to repopulate the colon
as a treatment for antibiotic-associated chronic diarrhea. In addition
to treating the diarrhea, the transferred microbiota carries functions
that affect the metabolism, immune system, and potentially, the behavior
of the recipient. Screening of fecal donors may be just as necessary as
screening organ donors to ensure that unwanted traits are not transferred
with the transplant.
Key Words: fecal transplant, obesity, metabolic syndrome,
autoimmunity, immunotolerance
Something to think about anyhow...
The below sentence came from the linked article talking about nitrates fueling bad bacteria in IBD patients.
"This also may be why stool transplants or super probiotics (containing huge and diverse amounts of bacteria) may be needed to overwhelm what is going on in the colon, and to re-establish the balance quickly."
http://blog.brendawatson.com/general/dysbiosis-in-ibd-nitrates-the-culprit/
"This also may be why stool transplants or super probiotics (containing huge and diverse amounts of bacteria) may be needed to overwhelm what is going on in the colon, and to re-establish the balance quickly."
http://blog.brendawatson.com/general/dysbiosis-in-ibd-nitrates-the-culprit/
kiny
Well-known member
Wouldn't surprise me if this worsened crohn's disease.
There is no evidence this works, there is no reason for me to believe why a fecal transplant would work for CD. You're giving an unknown amount of bacteria to someone without any knowledge of what bacteria are present and without any proof that the gut flora is related to crohn's disease.
The gut flora is an organ, it communicates with the immune system 24/7, and it took years of finetuning of the adaptive immune system and gut-brain barrier to get to a point of homeostasis. It's not something you want to mess with without knowing that it will have positive effect.
No one knows what you are getting when you take a fecal transplant, most species from the gut flora are unknown at this point, let alone that we don't even understand their function to begin with, nor do we even know if the indigenous gut flora is related to crohn's disease.
People should keep the idea open that this could make crohn's disease worse. C Difficile is not crohn's disease.
I read that somewhere that some group wants to collect stool samples from a wide segement of the populastion because they really don't know much about the gut bacteria.
Also I have crohn's colitis and while I have no idea if this would help me, some folks do in fact have Crohn's in the large bowel and so it may well beneift. I take lialda and it helps me, lialda targets the large intestine.
All that said i appreciate your words of caution. Not only woud you transfer all sort of organics, there is a good chance you wil get some blood and could be exposed to various virus. If this is a vlaid treatment for any condition, it stands to reason they find what is good in poop, isolate it and provide it as a capsule or some sort of enima where you only get the good stuff and not yesterday's cheesebuerger. lol (sorry)
- Location
- United States
Do you have any references that support your words of caution? Please share if so.
At the moment, all I have seen is that it works great in C. Diff cases and potentially others; while I don't recall seeing any reports of negative reactions, even in the clinical studies.
I hope you don't have any evidence to suggest otherwise because I like this little glimpse of hope
Your perspective on this is still appreciated, thank you.
Fecal transplants and personality traits:
There are certainly some unanswered questions with this treatment, but that is like believing you take on the personality of the cow when you drink her milk--lol:ylol2:
This may or may not be the answer for improving the health of IBD patients, although it has shown to help many. But we dont have all the answers to any of the drugs given to us or our children. It is the best they have right now... (just my opinion)
I love the debates, and any info we can add to any treatments. It helps us make our choices about treatments and ask more questions.
There are certainly some unanswered questions with this treatment, but that is like believing you take on the personality of the cow when you drink her milk--lol:ylol2:
This may or may not be the answer for improving the health of IBD patients, although it has shown to help many. But we dont have all the answers to any of the drugs given to us or our children. It is the best they have right now... (just my opinion)
I love the debates, and any info we can add to any treatments. It helps us make our choices about treatments and ask more questions.
They are doing double blind studies on fecal transplants now, and not just for C. difficile.
There's one in progress with 130 UC patients, following a smaller sample study, in which 7 out of 8 UC patients who received fecal transplants responded well, and 6 remained well a year following treatment. See link. http://www.ccfc.ca/site/c.ajIRK4NLLhJ0E/b.8343767/
It will be at least another year or two Before the study is concluded and the results are published, but it does look promising.
There's one in progress with 130 UC patients, following a smaller sample study, in which 7 out of 8 UC patients who received fecal transplants responded well, and 6 remained well a year following treatment. See link. http://www.ccfc.ca/site/c.ajIRK4NLLhJ0E/b.8343767/
It will be at least another year or two Before the study is concluded and the results are published, but it does look promising.
Here is an article regarding gut flora and fecal transplants
Microbial catalog of metagenomic sequencing.pdf
http://cmbi.bjmu.edu.cn/news2/report/2010/pdf/gut_3.pdf
It has been estimated that the microbes in our bodies collectively
make up to 100 trillion cells....
Microbial catalog of metagenomic sequencing.pdf
http://cmbi.bjmu.edu.cn/news2/report/2010/pdf/gut_3.pdf
It has been estimated that the microbes in our bodies collectively
make up to 100 trillion cells....
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The difference between 'good' bacteria and 'bad' bacteria is often not the bacteria themselves but the location of the bacteria, the environment in which they live, and the quantity of the bacteria present.
A healthy immune system 'actively' ignores potentially harmful bacteria in the intestine because immune system 'knows' the balance of other bacteria will maintain homeostasis
With crohns that balance is gone and the immune system is hyperactive so reactions are more likely
On top of that there is intestinal permeability, ranging from a de-regulation of tight junctions allowing bacterial proteins and bacteria into the bloodstream to lesions and ulcerated sores smeared with shit (which would both provoke an immune response)
Dumping a whole heap of bacteria on top of that seems a bit hit and miss........
Anyone who has looked at the diets that work (for many people) will know that removing the food for bad bacteria leads to a degree of healing that allows the reintroduction of other formerly problematic foods.
I would suggest that the same is true of bacteria.
Crohn's patients have been shown to be lacking in about 25% of the bacteria present in 'healthy' gut flora.
There may be an adverse reaction to some bacteria but this can be minimised buy adopting a paleo diet prior to the faecal enema
I was using a probiotic claiming to have a massive 14 strains of bacteria, but if it doesn't contain the strains that i'm missing it won't add then to my gut.
The average gut has about 400 out of a known possible 1000 species.
At least half the bacteria present cannot be cultured by conventional techniques.
Most shop bought probiotics are Lactobacillus or Bifidobacterium species, Great for helping digest milk but they don't even appear among the 57 most abundant species in the gut.
The only way to reintroduce an absent species is to get a live population of that species into the gut.
Killing everything and taking an ineffectual pill is typical of the arrogance and ignorance of modern medicine.
This is like saying 'I tried to get pregnant but it didn't work'
First question – were you doing it properly?
Second question – Are you sure?
Third – was your donor viable?
Fourth – did you do everything you could in preparation (diet, supplements, THEN fecal transplants)?
fifth – when are you trying again?
Without a serious change of diet you are wasting your time (in my humble opinion).
The health of the donor and their stool should always be verified before the transplant
“ without any proof that the gut flora is related to crohn's disease”
WTF?????? there is a proven well established relationship, the intricacies and nuances might not be fully understood but it is just ridiculous to claim that there is no relationship.
Gut flora either regulates or modulated almost every stage of immune function and Crohn's patients have 25% less variety of bacterial species.
If you have IBD the obviously the homeostasis is already messed up, and it took years of abuse (diet, stress, antibiotics etc) to deregulate.
How does this finetuned organ respond to the antibiotics and probiotics option - it's a bit like naplaming a jungle and then planting soy and wheat
Once again emphasising the uselessness of a probiotic pill,
While we don't understand their functions, we do know that they are present and in homeostasis in a healthy gut and missing or unbalanced in an IBD gut...
DIET, SUPPLEMENTS then FAECAL TRANSPLANT
Yes we do, we don't know the precise nature of the relationship, but we do know that the are related
I just would like to say that the current state of the research on ibd as far as i understand, is very focused on the probable proposition that intestinal flora are playing a prime causative role and the question they have been trying to answer with different studies have been whether or not the state of dysbiosis is a cause or an effect of the disease process itself. in other words, does some malfunction of the human body itself make certain bacterial species unable to survive? or is the missing bacteria that is causing all the dysfunction in the first place.
which came first, the inflammation or missing bacteria?(chicken or the egg) they are trying to find out which one may be the cause of the other.
so they have looked at people the are in remission and on drugs and studied the flora, then they have looked at people recently diagnosed who are not on any drugs and have full blown natural disease state, so what did they find?? regardless of the state of inflammation the dysbiosis still persists, so this still suggests and point in the direction that the bacteria/state of dysbiosis may play a causative role. and the inflammation doesnt seem to be causing the dysbiosis.
I believe at this point the only way to now conclusively answer the question as to whether the state of dysbiosis is the cause or result of the disease, is to start performing fecal transplants as they have been proven to be safe for c. difficile.
it is my opinion that the success rates for fecal transplant will at first not be that great for crohn's but better for UC, and over time we will only learn more and soon it will be shown that, this is the solution for us all, and we will find easier and more efficient ways to correct the dysbiosis in IBD. this disease will then be as unheard of as it is in non industrialized nations that have 98% less crohn's cases.
now to find the causes, whew!!
which came first, the inflammation or missing bacteria?(chicken or the egg) they are trying to find out which one may be the cause of the other.
so they have looked at people the are in remission and on drugs and studied the flora, then they have looked at people recently diagnosed who are not on any drugs and have full blown natural disease state, so what did they find?? regardless of the state of inflammation the dysbiosis still persists, so this still suggests and point in the direction that the bacteria/state of dysbiosis may play a causative role. and the inflammation doesnt seem to be causing the dysbiosis.
I believe at this point the only way to now conclusively answer the question as to whether the state of dysbiosis is the cause or result of the disease, is to start performing fecal transplants as they have been proven to be safe for c. difficile.
it is my opinion that the success rates for fecal transplant will at first not be that great for crohn's but better for UC, and over time we will only learn more and soon it will be shown that, this is the solution for us all, and we will find easier and more efficient ways to correct the dysbiosis in IBD. this disease will then be as unheard of as it is in non industrialized nations that have 98% less crohn's cases.
now to find the causes, whew!!
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kiny
Well-known member
You must know more than most research. If the relationship between the indigenous flora and crohn's disease has been established, which commensal is the inflammation directed at?
There is a T cell inflammatory response in the intestine in people with crohn's disease. This is only possible if an antigen presenting cell presented the antigen to a T cell.
So which gut flora commensal is the antigen?
kiny
Well-known member
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1234104/pdf/0601-05.pdf
"In this study, the dominant microbiotas of CD patients did not differ qualitatively between ulcerated and nonulcerated mucosae. Biodiversity was preserved, and no particular dominant microbiota appeared to be associated with ulceration. This does not support a pathological role of qualitative dysbiosis in CD-associated ulceration.
In our study, no bacterial species was found to be specifically associated with CD ulceration, and ulceration did not qualitatively modify the dominant associated microbiota."
The only leeway I would grant here is specific invasive species of E Coli, LF82, but they are no longer part of the indigenous gut flora, they are extremely pathogenic species.
Any dysbiosis prior to acute disease might facilitate penetration through the cell wall, the gut flora is a major form of defense, but this in no way implies that the gut flora is directly involved in the actual inflammatory process.
That the gut flora is directly involved in the pathogenesis of crohn's disease is anything but established.
"In this study, the dominant microbiotas of CD patients did not differ qualitatively between ulcerated and nonulcerated mucosae. Biodiversity was preserved, and no particular dominant microbiota appeared to be associated with ulceration. This does not support a pathological role of qualitative dysbiosis in CD-associated ulceration.
In our study, no bacterial species was found to be specifically associated with CD ulceration, and ulceration did not qualitatively modify the dominant associated microbiota."
The only leeway I would grant here is specific invasive species of E Coli, LF82, but they are no longer part of the indigenous gut flora, they are extremely pathogenic species.
Any dysbiosis prior to acute disease might facilitate penetration through the cell wall, the gut flora is a major form of defense, but this in no way implies that the gut flora is directly involved in the actual inflammatory process.
That the gut flora is directly involved in the pathogenesis of crohn's disease is anything but established.
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kiny
Well-known member
No we don't.
There are major issues with the gut flora theory, one of them is the fact there are skip lesions.
http://www.ncbi.nlm.nih.gov/pubmed/?term=Crohn%27s+Disease+May+Be+Differentiated+Into+2+Distinct+Biotypes+Based+on+the+Detection+of+Bacterial+Genomic+Sequences+and+Virulence+Genes+Within+Submucosal+Tissues.
"dysbiosis and leaky gut are common manifestations of gastrointestinal upset and cannot explain “skip lesions""
In fact dysbiosis is a manifestation of intestinal TB, even though TB is not directly related to the gut flora, you can find dysbiosis in a number of diseases, they're just a manifestation of the disease state.
Another question you should ask yourself, is why the inflammation would be localised in the small intestine, instead of the colon. The colon has many more commensals than the small intestine.
So why is the colon in many people with crohn's disease unaffacted. My colon is clean and never had inflammation, if my body had a directed immune response against the gut flora, my colon should be inflamed, but it's not, the part with the highest concentration of gut flora commensals is not inflamed at all, which completely contradicts your theory.
If your theory of stress and dysbiosis and "abuse" as you call it, leads to crohn's disease, then why is the part which would be most affected, the colon, free of any inflammation?
Another question for you, for a number of years they thought the gut flora was a purely pathogenic organ, they went to great lenghts to remove these bacteria before they realised they were commensals. These people didn't develop crohn's disease at all, they got more infections, but they didn't develop crohn's disease. How come if the dysbiosis is so central in your theory?
The dysbiosis and directed immune response at gut flora is a theory with a lot of unresolved questions. Either because they're extremely hard to explain, or because the theory is wrong.
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sorry? Which specific bacteria causes crohns? Is that really the question?
Your claim was that there is no relationship.
I haven't claimed that bacteria cause crohns, and certainly not that a specific bacteria causes crohns which seems to be what you are claiming (that I am claiming).
I said there is a relationship, and that this has been established in many studies,
Relationship does not mean cause, it means that bacteria are involved in the development or expression or continuation of the disease. As causative factors? probably, As victims? Possibly.
Research suggests that it may be an absence of (specific) bacteria
There is a T cell inflammatory response. OK, all that mean is the normal immunicological tolerance has been lost or disrupted.
The immune system has a normal tolerance of many antigens expressed in three ways.
Central tolerance, whereby T cells are deleted before they mature,
Peripheral tolerance where active T cells are released but neutralised, and
an Acquired tolerance, in this case specifically Oral tolerance which can be described as “ an active non-response to antigens delivered via the oral route” [1].
In other words, the healthy immune system knows it's there but ignores it, the unhealthy immune system mounts an attack
“Commensal microorganisms are not ignored by the intestinal immune system. Recent evidence shows that commensals actively participate in maintaining intestinal immune homeostasis by interacting with intestinal epithelial cells and delivering tolerogenic signals that are transmitted to the underlying cells of the immune system.”[2]
Get it? The commensals are what prevents the T cell response, the absence of which promotes immune reaction
“These results suggest that the balance tolerance/immuno-reaction in the gut is achieved through self-regulatory cycles where suppression by negative regulators, such as pims, is triggered as soon as a specific threshold of immuno activation is reached.”[3]
“Oral tolerance is an active process, leading to the generation of antigen-specific T lymphocytes that suppress further immune stimulation. It is defined by the antigen-specific suppression of both cellular and humoral immune responses to orally administered antigens. In addition to the generation of suppressive T cells, anergy and T cell deletion have been described as mechanisms underlying oral tolerance “ [3a]
“Consequently, mucosal tolerance protects the mucosa from detrimental inflammatory immune responses. “[3a]
Balanced – not too much, not too little, there is ALWAYS inflammation in the gut, but if it is the right amount then we are healthy
So, what a tedious read that is
They did a study, comparing the bacteria at ulcerated sites and at
That's all very sciency, but meaningless.
We've already established that crohns have appox 25% less species of bacteria than normal [4], and that we don't know functions and interactions between bacteria and the immune system, let alone the interactions between bacteria themselves, so while they didn't think there was much in it, they didn't really find anything out, did they?
If I dig a hole am I going to get a blister all over my hand, or just one or two places?
If I throw a handful of seeds in the garden are they all going to sprout?
If I eat lots of lollies are all my teeth going to get holes in them?
Then you go on to point out one bacteria that is implicated, LF82
“These findings indicate that AIEC, strain LF82 disrupts the integrity of the polarized epithelial cell barrier. This disruption enables bacteria to penetrate into the epithelium and replicate in the host cell cytoplasm. These findings provide important links between microbes related to IBD, the intestinal epithelial cell barrier and disease pathogenesis. “ [5]
If that's not a relationship then i'm a pink elephant wearing a tutu
hmmmmmm, we are speaking different languages,
I say “relationship”, you hear “causal relationship“ (not casual).
“ directly involved in the pathogenesis”, not that i'm not saying it isn't (directly involved in the pathogenesis),, just that i'm not saying it is....
We certainly don't know that it isn't, but double negative get a bit clumsy.
There IS a relationship between gut flora and crohns, we don't know it's extent and we don't know who's on top.
Argggghhhhh, why do you make me read this stuff.....
I didn't see that extract in the abstract, was it the right link
So not all crohns are the same? OK, and?
“This study is the first to examine the microbial populations of submucosal tissues during intestinal disease and provide evidence of a distinct submucosal microbiome and biotypes within Crohn's disease”,
there's a relationship,
ok, there is a 'relationship', not a causal relationship, TB may lead to gut disbiosis
That the Peyers Patches are specifically targeted for inflammation...
“This correlation suggests that Crohn's disease may develop as an inflammatory process specifically targeting these important lymphoid structures.”[6]
“Peyer's patches play a major role in intestinal immunity, are portals of entry for significant pathogens, and may be important in Crohn's disease” [7]
“ PPs are the first places of T-cell-specific priming and proliferation in the gut”[3a]
There are normally far greater quantities of bacteria in the colon than the small intestine .
That area is affected the most because it is more sensitive, not because there are more bacteria there
That the Peyer's Patches suffer the inflammation has been addressed, This doesn't contradict the theory at all (only in your head)
The part most affected is the part most sensitive.
Too simple to understand?
Why are numbers of ALL immune diseases increasing at a staggering rate?
Diet probably
Disbiosis is central to 'my' theory of crohns, but I don't give a rat's arse for the 'cause'.
Disbiosis is central to crohn's but not the whole story,
It's the part of the story (along with diet) that we can take control of and effect changes to our own health.
Good luck on your wait for a scientific breakthrough and a magic bullet
What directed immune response? If anything – misdirected, wild and uncontrolled maybe
Gee wizz, a theory with unresolved questions? in science?
I don't know which branch of science you subscribe to, the magic fairyland version?
Bullshit, we just don't know yet,
Add it to the list
kiny
Well-known member
You mix a lot of things up which is why I get annoyed and wanted to reply. People are somehow convinced the gut flora and therefore fecal transplants are going to strongly impact their disease, I don't want to see them disappointed if that's not the case.
A T cell response doesn't mean the tolerance to the gut flora is lost, it's possible but it's just as likely that an APC presented a pathogen to a T cell in a lymph node.
Regarding the peyer's patches, M Cells sample pathogens that are able to bind to the epithelial barrier or go through the epithelial barrier, they don't sample the indigenous gut flora. You're trying to use that as a reason for a directed immune response against the indigenous flora, that's not right. I have posted the studies here about the peyer's patches and talked about them, which I assume is why you mention it, but correctly explain what they do. They are not directing immune responses against the gut flora commensals, they are purely looking for pathogenic bacteria who can pass through the epithelial barrier.
Gut flora commensals and pathogens are not the same thing. Even in the case of LF82, LF82 in a susceptible host is a pathogen, it is no longer a commensal, that distinction needs to be made if you want to talk about fecal transplants, a fecal transplant is going to do nothing for people if it involves pathogens that penetrate the intestinal wall. It's probably not going to help at all or make matters worse. I used the word indigenous gut flora specifically so you won't use them interchargeably but you still do since you make no distinction between peyer's parches sampling pathogens vs gut flora, or infections of the submucosa or a gut flora response.
Regarding the microbiome in submucosa you mentioned, they tested mycobacteria and invasive E Coli, that's not the gut flora, it has nothing to do with the indigenous gut flora.
One of the other things to understand is the autophagy issue, NOD2 directs autophagy through ATG16L1 activation, mutations in these result in dysfunctional phagocytosis. Both these genes are implicated in crohn's disease. Mutations would result in inability to control intracellular pathogens, not the gut flora.
There are plenty of issues like that which is why there is serious doubt cast over the idea that the immune response would be directed at the gut flora, I really doubt it is.
A T cell response doesn't mean the tolerance to the gut flora is lost, it's possible but it's just as likely that an APC presented a pathogen to a T cell in a lymph node.
Regarding the peyer's patches, M Cells sample pathogens that are able to bind to the epithelial barrier or go through the epithelial barrier, they don't sample the indigenous gut flora. You're trying to use that as a reason for a directed immune response against the indigenous flora, that's not right. I have posted the studies here about the peyer's patches and talked about them, which I assume is why you mention it, but correctly explain what they do. They are not directing immune responses against the gut flora commensals, they are purely looking for pathogenic bacteria who can pass through the epithelial barrier.
Gut flora commensals and pathogens are not the same thing. Even in the case of LF82, LF82 in a susceptible host is a pathogen, it is no longer a commensal, that distinction needs to be made if you want to talk about fecal transplants, a fecal transplant is going to do nothing for people if it involves pathogens that penetrate the intestinal wall. It's probably not going to help at all or make matters worse. I used the word indigenous gut flora specifically so you won't use them interchargeably but you still do since you make no distinction between peyer's parches sampling pathogens vs gut flora, or infections of the submucosa or a gut flora response.
Regarding the microbiome in submucosa you mentioned, they tested mycobacteria and invasive E Coli, that's not the gut flora, it has nothing to do with the indigenous gut flora.
One of the other things to understand is the autophagy issue, NOD2 directs autophagy through ATG16L1 activation, mutations in these result in dysfunctional phagocytosis. Both these genes are implicated in crohn's disease. Mutations would result in inability to control intracellular pathogens, not the gut flora.
There are plenty of issues like that which is why there is serious doubt cast over the idea that the immune response would be directed at the gut flora, I really doubt it is.
kiny
Well-known member
It's not a relationship, learn the difference between a pathogen and a commensal. LF82 is a pathogen in susceptible hosts, it's an invasive form of E Coli that penetrates macrophages and disrupts phagocytosis at the autophagy step. It sticks onto the epithelial cells and breaks through them. No fecal transplant is going to help you if LF82 is causing the inflammation.
Do you see the difference and understand that no amount of probiotics, or fecal transplants are going to help you if a bacteria is present in submucosa causing inflammation.
There is a clear difference between directed response against the indigenous gut flora and a pathogenic infection. I keep using the word indigenous so you would start to make that distinction. They are 2 different things. Do not bunch them together, fecal transplants would help the former but not the later.
LF82 sticking to and breaking through intestinal barrier:
- Location
- United States
I have heard promising results about fecal transplants as well( especially for C-diff related infections). The only issue I would have is that I think you have to make sure your donor is a relative. I mean everyones body has different bacteria that their bodies are used too. I think it is possible that by adding a bacteria that your body is not accustomed to could set the stage for almost any problem or an immune resopnse. But over all I think it is worth looking into at least. I read about a woman who had such severe C-diff, she was literally close to dying. She could not get rid of it. She had no health insurance or anything so she could not really run to the hospital. Her husband read up on the fecal transplants and he became her fecal donor, they did the procedure at home themselves( via enema bag) and she was well within days! C-diff was under control! So I do think it can work in some cases.
As far as the relationship when it comes to gut flora and the development of crohns, well that is the million dollar question. Nobody knows what causes crohns. I mean gut flora "may" have something to do with it, but there is no proof of that. I mean you can take a bunch of people out there that abuse themselves and suck antibiotics down like candy and they never have any gut issues or health problems. But then you can have someone who eats healthy as possible and hardly ever touched antibiotics and they get crohns disease or UC. For all we know crohns can be caused by a virus! I mean most viruses literally Cannot be killed. They do go dormant from time to time though but stress and illness can wake the up. I mean there are so many theories out there regarding causes for crohns. One day in the very far off distant future they may come close to finding a cause, but for right now, nobody knows... Just like a lot of the other orphan diseases out there, Nobody knows....
As far as the relationship when it comes to gut flora and the development of crohns, well that is the million dollar question. Nobody knows what causes crohns. I mean gut flora "may" have something to do with it, but there is no proof of that. I mean you can take a bunch of people out there that abuse themselves and suck antibiotics down like candy and they never have any gut issues or health problems. But then you can have someone who eats healthy as possible and hardly ever touched antibiotics and they get crohns disease or UC. For all we know crohns can be caused by a virus! I mean most viruses literally Cannot be killed. They do go dormant from time to time though but stress and illness can wake the up. I mean there are so many theories out there regarding causes for crohns. One day in the very far off distant future they may come close to finding a cause, but for right now, nobody knows... Just like a lot of the other orphan diseases out there, Nobody knows....
kiny
Well-known member
Ask access through your school or institution and you can read the full studies.
The distinction is made here too. There is nothing to discuss if you don't make a distinction between commensals and pathogens.
If you want to discuss fecal transplants you should ask yourself not only if it would work but why it would work, if the gut flora and dysbiosis is not directly involved in the inflammatory process then a fecal transplant would do nothing for people, in fact it could cause a lot of unwanted issues. So it's important to make distinctions and to define what you're talking about.
If crohn's disease involves one or more pathogens taking advantage of a susceptible host, then a fecal transplant will likely not help. No one uses a fecal transplat to treat intestinal tuberculosis, so you need to be very very sure of yourself that the gut flora is causing the inflammation before you experiment with fecal transplants, you can cause a lot of issues too with it. You should be especially careful with people who have crohn's disease, since we know people with NOD2 and ATG16L1 mutations have issues with bacterial clearance.
Firstly, sorry, all my referenced on the last post were not added, lost in the copy and paste.
I think the correct expression is “Can't see the wood for the trees”
That it WON'T do any good.
I also feel that it is only part of a strategy to combat the dis-ease, and I too don't want them disappointed so I recommend that they alter their diet (which has repeatedly been demonstrated effective, and you have also repeatedly denounced) , supplement as required, and then try this if it is still felt to be necessary.
“Crohn's disease and graft-versus-host disease are thought to be driven by an abnormal response toward the commensal flora. They have been associated with NOD2 mutations and PP dysfunction........”
“.......Commensal microorganisms are not ignored by the intestinal immune system. Recent evidence shows that commensals actively participate in maintaining intestinal immune homeostasis by interacting with intestinal epithelial cells and delivering tolerogenic signals that are transmitted to the underlying cells of the immune system......”
“........Consequently, mucosal tolerance protects the mucosa from detrimental inflammatory immune response. “[1]
It's not my theory - “mucosal tolerance [of commensal bacteria] protects the mucosa from detrimental inflammatory immune responses” - take it or leave it, I don't care
These bacteria “that bind to the epithelial barrier or go through the epithelial barrier”, they just pop out of thin air do they?
I'm no sciency guy, but when I read this.....
“The follicle-associated epithelium (FAE) differs from the epithelium of the villus mucosa: the production of mucus is weak; the membrane-bound digestive enzymes are lightly expressed and the enterocyte brush border glycocalyx has different glycosylation patterns [15–17]. FAE is also characterized by a large number of infiltrated B-cells, T-cells, macrophages and DCs. Finally, the FAE lacks the subepithelial myofibroblast sheath and, the basal lamina is more porous compared with the regular epithelium …...
…....The cellular composition of the FAE (i.e., the proportion of enterocytes and M-cells) may be modulated by bacteria present in the gut lumen........
….....M-cells are specialized in the transcytosis of intact luminal material like soluble proteins, antigens, bacteria and viruses “[1]
…....“transcytosis of intact luminal material” sounds like sampling to me, but hey, big words and all
If you remember correctly you will recall that I just took exception to your claims....
“and without any proof that the gut flora is related to crohn's disease”,
I see a relationship, I don't claim to understand it, but I can see it
We obviously read different things, as you will see from above,
“transcytosis of intact luminal material” sounds like sampling to me, Whether directly from the lumen or indirectly through the mucosal barrier, who gives a toss?
Firstly commensal implies that one party benefits ant the other is not affected.
This is not the case, both parties benefit.
Secondly you take them from one category to the other without acknowledging that what has changed is the (previously mentioned) 'active tolerance'.
Lets try 4 categories,
-essential/beneficial
-opportunistic
-transitional
-pathogenic,
and all the bacteria in the first three categories can theoretically transition into the forth category, - particularly if the immune system is functioning inappropriately
(which will happen why? Diet and disbiosis?)
The 'susceptible host' became susceptable – why? Diet and disbiosis?
Peyer's patchs (according to my sources) do both, induction of tolerance [to beneficial gut flora] and defence against pathogens
“PPs functions, like induction of immune tolerance or defense against pathogens result from the complex interplay between immune cells located in the lymphoid follicles and the follicle-associated epithelium.....”[1]
In my world “Gut Flora” means all gut flora, beneficial gut flora means good bugs only (if such a thing can exist as location, quantity and interaction with other bacteria will be what determines if they are good or not)
You mean in a healthy gut it is suppressed by 'good' bacteria
Wow, i'm starting to understand that whether something is 'commensal' or 'pathogenic' depends on so many factors, Thank you for helping me understand......
Wait.....
Wasn't that my point?
Wow this is tricky stuff, so glad you can tell me right from wrong.....
So, no amount of probiotics will change any of these factors?
Hmmmm, if you say so....
“........Consequently, mucosal tolerance protects the mucosa from detrimental inflammatory immune responses. “[1]
Impaired immune response (lack of tolerance) mean all bets are off
I'm still happy with the “Crohn's disease is caused by interactions between environmental, immunological and bacterial factors in genetically susceptible individuals” theory,
All that is needed is to remove the interaction between “unidentified persistent bacterial pathogen” and the host, and a healthy (varied) gut flora will suppress growth of (potentially) pathogenic bacteria, help maintain an effective physical barrier, and support an effective adaptive response.
I don't give a rat's arse if this “unidentified persistent bacterial pathogen”
turns out to be a good one gone bad or a bad one gone bad.
It doesn't affect the theory at all,
[1] http://f1000.com/prime/reports/b/1/9/
You separate a lot of things that are inextricably linked and focus on a specific breakdown in the third layer of a complex interactive system and completely ignore the breakdown and ineffectiveness of the first two layers which lead to the breakdown of the third.
I think the correct expression is “Can't see the wood for the trees”
That's reasonable, but completely different to what you have been asserting......
That it WON'T do any good.
I also feel that it is only part of a strategy to combat the dis-ease, and I too don't want them disappointed so I recommend that they alter their diet (which has repeatedly been demonstrated effective, and you have also repeatedly denounced) , supplement as required, and then try this if it is still felt to be necessary.
I agree , might be an APC presenting a pathogen, but my money is on an antigen from something previously tolerated....
“Crohn's disease and graft-versus-host disease are thought to be driven by an abnormal response toward the commensal flora. They have been associated with NOD2 mutations and PP dysfunction........”
“.......Commensal microorganisms are not ignored by the intestinal immune system. Recent evidence shows that commensals actively participate in maintaining intestinal immune homeostasis by interacting with intestinal epithelial cells and delivering tolerogenic signals that are transmitted to the underlying cells of the immune system......”
“........Consequently, mucosal tolerance protects the mucosa from detrimental inflammatory immune response. “[1]
It's not my theory - “mucosal tolerance [of commensal bacteria] protects the mucosa from detrimental inflammatory immune responses” - take it or leave it, I don't care
the only reason I brought up Peyer's Patches is because you keep droning on about them and the predominance of inflammation in the terminal ileum and that inflammation here somehow proves that it is not related to bacteria (strangely, because the colon, which is designed to tolerate larger numbers of bacteria, can do so better than the terminal ileum)
These bacteria “that bind to the epithelial barrier or go through the epithelial barrier”, they just pop out of thin air do they?
I'm no sciency guy, but when I read this.....
“The follicle-associated epithelium (FAE) differs from the epithelium of the villus mucosa: the production of mucus is weak; the membrane-bound digestive enzymes are lightly expressed and the enterocyte brush border glycocalyx has different glycosylation patterns [15–17]. FAE is also characterized by a large number of infiltrated B-cells, T-cells, macrophages and DCs. Finally, the FAE lacks the subepithelial myofibroblast sheath and, the basal lamina is more porous compared with the regular epithelium …...
…....The cellular composition of the FAE (i.e., the proportion of enterocytes and M-cells) may be modulated by bacteria present in the gut lumen........
….....M-cells are specialized in the transcytosis of intact luminal material like soluble proteins, antigens, bacteria and viruses “[1]
…....“transcytosis of intact luminal material” sounds like sampling to me, but hey, big words and all
While I think a “directed immune response against the indigenous flora” may be a possibility, i've never claimed this to be a fact or even the most likely 'cause or causative factor',
If you remember correctly you will recall that I just took exception to your claims....
“and without any proof that the gut flora is related to crohn's disease”,
I see a relationship, I don't claim to understand it, but I can see it
I'm so lucky to have you to tell me what is correct and what is not.....
We obviously read different things, as you will see from above,
“transcytosis of intact luminal material” sounds like sampling to me, Whether directly from the lumen or indirectly through the mucosal barrier, who gives a toss?
You seem to put bacteria in two categories, commensals and pathogenic,
Firstly commensal implies that one party benefits ant the other is not affected.
This is not the case, both parties benefit.
Secondly you take them from one category to the other without acknowledging that what has changed is the (previously mentioned) 'active tolerance'.
They were 'commensal', now they are 'pathogenic', but that only happens when YOU want it to?
Lets try 4 categories,
-essential/beneficial
-opportunistic
-transitional
-pathogenic,
and all the bacteria in the first three categories can theoretically transition into the forth category, - particularly if the immune system is functioning inappropriately
(which will happen why? Diet and disbiosis?)
The 'susceptible host' became susceptable – why? Diet and disbiosis?
But as you have shown, there is an interchangeablity, and that seems to be at the discretion of the immune system, and sometimes the immune system does not work properly.
Peyer's patchs (according to my sources) do both, induction of tolerance [to beneficial gut flora] and defence against pathogens
“PPs functions, like induction of immune tolerance or defense against pathogens result from the complex interplay between immune cells located in the lymphoid follicles and the follicle-associated epithelium.....”[1]
There are ALWAYS opportunistic, transitional and pathogenic bacteria present in the lumen, one role of beneficial gut flora is to suppress their growth,
In my world “Gut Flora” means all gut flora, beneficial gut flora means good bugs only (if such a thing can exist as location, quantity and interaction with other bacteria will be what determines if they are good or not)
Not even close to casting doubt, you are focusing on the end of a cascade and ignoring everything that lead to that point
really?, so it's a 'commensal' in a host with a healthy microflora, and a pathogen in a host with an unhealthy microflora?
You mean in a healthy gut it is suppressed by 'good' bacteria
Wow, i'm starting to understand that whether something is 'commensal' or 'pathogenic' depends on so many factors, Thank you for helping me understand......
Wait.....
Wasn't that my point?
Ohh, thanks again, indiginous means 'only the good ones', not actually the ones that are indigenous (normally present, suppressed or not), and pathogenic means only the 'bad' ones even though they might be good in someone else or somewhere else or in smaller quantities or if other bacteria were there to modulate their effects or if the immune system wasn't hyperactive.
Wow this is tricky stuff, so glad you can tell me right from wrong.....
So, no amount of probiotics will change any of these factors?
Hmmmm, if you say so....
You're still on about this artificial distinction, although I tend to agree, there is nothing to discuss
“........Consequently, mucosal tolerance protects the mucosa from detrimental inflammatory immune responses. “[1]
Impaired immune response (lack of tolerance) mean all bets are off
I don't have a problem with any of those eitiologic theories, but I don't see them as being mutually exclusive, and certainly they don't excluding other factors.If you want to discuss fecal transplants you should ask yourself not only if it would work but why it would work, if the gut flora and dysbiosis is not directly involved in the inflammatory process then a fecal transplant would do nothing for people, in fact it could cause a lot of unwanted issues. So it's important to make distinctions and to define what you're talking about
I'm still happy with the “Crohn's disease is caused by interactions between environmental, immunological and bacterial factors in genetically susceptible individuals” theory,
All that is needed is to remove the interaction between “unidentified persistent bacterial pathogen” and the host, and a healthy (varied) gut flora will suppress growth of (potentially) pathogenic bacteria, help maintain an effective physical barrier, and support an effective adaptive response.
I don't give a rat's arse if this “unidentified persistent bacterial pathogen”
turns out to be a good one gone bad or a bad one gone bad.
It doesn't affect the theory at all,
[1] http://f1000.com/prime/reports/b/1/9/
Last edited:
kiny
Well-known member
People with genetic predisposition to crohn's disease suffer from frustrated phagocytosis through NOD2, ATG16L1 mutations. They hinder correct autophagy, and LF82 is able to exploit the autophagy step. It leaves you susceptible to intracellular bacteria, which is why most of the research trying to find bacteria which could cause the immune response are directed at research towards intracellular bacteria. That's why you'll see studies trying to find AIEC (lf82), listeria, yersinia, mycoplasma, bartonella, borrelia, mycobacteria (Map, Mac) , because they're intracellular and a candidate pathogen.
We know people with crohn's disease are more susceptible to only certain types of bacteria, because of the NOD2 and ATG16L1 genes, the candidate bacteria is likely going to be one that penetrates a cell. That's what I meant with susceptible.
IMPORTANT: Fecal Transplants Outperform Antibiotics In Clinical Trial
WRITTEN BY ROBOPANDA / 01.18.13
We are nothing if not exceptionally mature.
If you’ve listened to any random episode of the FilmDrunk Frotcast, you already know that fecal transplants are totally rad. These procedures, in which feces from a person with healthy gut bacteria is transplanted into a patient with an unhealthy bacterial profile, have shown significant promise but haven’t been studied in a randomized clinical trial . . . until now. Over 500 people with the typically antibiotic-resistant bacterium Clostridium difficile have been treated with fecal transplants in the past 50 years, but all evidence until recently has be anecdotal. Ed Yong writes (in Nature) about the first fecal transplant randomized clinical trial.
The first results from a faecal transplant trial have been published in the New England Journal of Medicine, and they are a resounding vindication for the technique. The infusions of faeces cured 94% of patients who received it (15 out of 16), all of whom had already suffered at least one relapse of C.difficile. By comparison, the standard antibiotic — Vancomycin — only cured 27% of patients (7 out of 26). The difference was so great that the Dutch team behind the study had to stop the trial early. Everyone eventually received the faecal transplants. [NERS]
And YOU get a fecal transplant!
And YOU get a fecal transplant!
EVERYBODY GETS A FECAL TRANSPLANT!
Anyway, the only negative side effects (constipation or diarrhea shortly after the transplant) were rare and preferable to having C. diff. There are some interesting things to note about this study. Fecal transplants are usually done via an enema, also known in scientific nomenclature as “butt-chugging” the donor feces. Els van Nood and Josbert Keller at the University of Amsterdam instead opted to thread a tube through the nose and into the small intestine. (A different clinical study using the enema method is in progress with Lawrence Brandt at the Albert Einstein School of Medicine.)
Els Van Nood noted it may be easier to gain regulatory approval if the feces used came from pre-screened healthy donors whose feces was frozen until needed. (By all means, use the break room refrigerator.) A new clinical trial is underway comparing frozen and fresh fecal samples for effectiveness. Els Van Nood also noted that some of her test subjects expressed a desire to be in the fecal transplant group instead of the antibiotic group, with older patients being the most adamant.
It seems many people are enthusiastic about fecal transplants. Jim Romenesko received an email from an unnamed editor who says a fecal transplant story in The New York Times is on track to possibly become the most-emailed NYT article of all time. Someday, you can tell your grandkids that you were alive when articles about poop transplants were not yet the most-emailed Times articles. Those were dark times indeed.
Read more: http://www.uproxx.com/gammasquad/2013/01/fecal-transplants-clinical-trial-study/#ixzz2NijZSUHa
WRITTEN BY ROBOPANDA / 01.18.13
We are nothing if not exceptionally mature.
If you’ve listened to any random episode of the FilmDrunk Frotcast, you already know that fecal transplants are totally rad. These procedures, in which feces from a person with healthy gut bacteria is transplanted into a patient with an unhealthy bacterial profile, have shown significant promise but haven’t been studied in a randomized clinical trial . . . until now. Over 500 people with the typically antibiotic-resistant bacterium Clostridium difficile have been treated with fecal transplants in the past 50 years, but all evidence until recently has be anecdotal. Ed Yong writes (in Nature) about the first fecal transplant randomized clinical trial.
The first results from a faecal transplant trial have been published in the New England Journal of Medicine, and they are a resounding vindication for the technique. The infusions of faeces cured 94% of patients who received it (15 out of 16), all of whom had already suffered at least one relapse of C.difficile. By comparison, the standard antibiotic — Vancomycin — only cured 27% of patients (7 out of 26). The difference was so great that the Dutch team behind the study had to stop the trial early. Everyone eventually received the faecal transplants. [NERS]
And YOU get a fecal transplant!
And YOU get a fecal transplant!
EVERYBODY GETS A FECAL TRANSPLANT!
Anyway, the only negative side effects (constipation or diarrhea shortly after the transplant) were rare and preferable to having C. diff. There are some interesting things to note about this study. Fecal transplants are usually done via an enema, also known in scientific nomenclature as “butt-chugging” the donor feces. Els van Nood and Josbert Keller at the University of Amsterdam instead opted to thread a tube through the nose and into the small intestine. (A different clinical study using the enema method is in progress with Lawrence Brandt at the Albert Einstein School of Medicine.)
Els Van Nood noted it may be easier to gain regulatory approval if the feces used came from pre-screened healthy donors whose feces was frozen until needed. (By all means, use the break room refrigerator.) A new clinical trial is underway comparing frozen and fresh fecal samples for effectiveness. Els Van Nood also noted that some of her test subjects expressed a desire to be in the fecal transplant group instead of the antibiotic group, with older patients being the most adamant.
It seems many people are enthusiastic about fecal transplants. Jim Romenesko received an email from an unnamed editor who says a fecal transplant story in The New York Times is on track to possibly become the most-emailed NYT article of all time. Someday, you can tell your grandkids that you were alive when articles about poop transplants were not yet the most-emailed Times articles. Those were dark times indeed.
Read more: http://www.uproxx.com/gammasquad/2013/01/fecal-transplants-clinical-trial-study/#ixzz2NijZSUHa
I have Crohn's disease and was on Flagyl and Cipro for over two weeks and got three abscesses. I figured i had nothing to lose by trying the transplant. I waited three weeks after finishing the antibiotics and was in bad shape. abscesses were terrible. I did the transplant daily for a while and the abscesses, Two which were large, Began to shrink every day. After a month they were gone, and made NO fistula! I haven't had one bit of trouble down there since. I believe the transplants work. I don't know if it works all through the colon, but it worked on me in my lower colon and i was a complete mess. Bree
- Location
- United States
HYFR! That is awesome!! Thank you for trying it and thank you for sharing your feedback.
- Location
- United States
That is great to hear. I mean in a way it does make sense. I mean you are taking bacteria and putting it up there where it will reproduce. The only bad thing is that if you even need antibitoics wont they all be killed off again? But I think it is great that it has helped you. I mean honestly you ca do this at home yourself if you have a family member who is a donor. I knew of a lady who had BAD C-diff infection and she and her hubby did it and it worked!
I understand that research shows people with some variations of the NOD2 gene are more prone to developing crohns disease. There are about 40 variations on NOD2 currently associated with crohns.
The current theory “suggests that changes in the NOD2 gene prevent the protein from recognizing bacteria, allowing these microbes to grow unchecked and invade cells that line the intestine. “
OK, no problem with that,
My problem is that NOD2 variations have probably been with us for thousands of years, (and certainly not a new explosion of mutations in the last hundred or so years).
-It is probable that some of these variations have benefits that will/would show up in other circumstances, rather than just being a 'bad' mutation, 'our bodies turning on us', etc
Likewise, the theory that here is some new bacteria that is suddenly running rampant doesn't seen like the most obvious explanation.
-The bacteria (bacterium?, bacterial protien?) has probably been around for a long while.
The 'new' factor leading to the explosion of this (and sooooo many other) disease is that the two are being brought together
This would be why there have been low levels of IBD for hundreds of years (only a few people managed to achieve the interaction between these particular genes and these particular bacterial antigens.)
In most of the healthy population there was an intact physical barrier, a healthy population of bacteria suppressing the growth of the pathogens, and a correctly functioning immune system (to handle the very few pathogens that got past the first two)
This would account for the enormous range of theories for crohns, -antibiotics, saccharin, wheat, antibacterial soap, stress, carbohydrates, surfactants .........
Any breakdown in the immune function (beginning with disbiosis and permeability) can lead to the interaction between the specific gene and the specific protein/bacterium causing a specific disease.
Perpetuating the search for 'the specific cause' at the wrong end of the etiology is a pharmaceutical companies wet dream,
Thousands of copyrighted treatments and a general public with no understanding of what's going on.
For ever time they isolate a gene related to a disease, they get closer to a treatment with it's own host of side effects, and further away from the most effective, least invasive, and least profitable intervention.
I agree, that person is susceptible, because a gene that probably hasn't caused problems for (?) decades/centuries/thousands of years (?), is coming into contact with a bacteria that probably hasn't caused problems for (?) decades/centuries/thousands of years (?).
I'm interested in what is bringing the two together, and why the same intervention has repeatedly proved beneficial in crohns, lupus, high cholesterol, multiple sclerosis, hashimotos ,obesity, psoriasis, diabetes, polycystic ovary syndrome, etc etc
Note, i did say beneficial, not cured, obviously time for a few more studies, But i'm not expecting anyone to fund a study that shows big pharma is making money by treating us for illness due to the side effects of big ag, big pharma and big 'processedfood' corporations
Sorry if i drifted too far off topic.......
Did you do anything else to complement the the transplants?
This is great to hear, congrats.
Did you do anything else to complement the the transplants?
kiny
Well-known member
Many people with the NOD2 mutation do not have crohn's disease.
But I put very high value on the NOD2 and ATG16L1 (the autophagy gene directed by NOD2) mutations because that is concrete evidence, it differentiates crohn's disease from UC, it's consistent in the West, it's seen in adults and in the increasing number of new onset pediatric patients.
There are very few things that are certain in crohn's disease where someone can hold onto to build an understanding from, NOD2 and ATG16L1 mutations as risk factors for crohn's disease are one of the few things that have been reproduced thousands of times now, so I value this evidence a lot.
- Location
- United States
I hope the flare inducing controversy does not discourage first hand feedback from the community.
Hi everyone,
I wanted to drop a quick line, as my friend has Crohn's Disease, and he mentioned to me he'd heard fecal transplants were being considered as a potential treatment. Now, I can't speak to fecal transplant's viability for Crohn's Disease, but I can provide first-hand testimony to its legitimacy as a treatment for other GI conditions. My wife had c.diff for several months, and after trying literally everything else, a fecal transplant from my daughter was like a miracle cure.
Shortly before my son was born, some medical miscommunication resulted in my wife getting overloaded on antibiotics, killing off all of the good bacteria in her system. As a result, c.diff took over and was wreaking havoc. I'm sure many of you can identify with her experience: crippling pain, having to nurse our son on the toilet because she was going ALL the time, etc, etc. They tried Flagyl, no effect. They tried the maximum dose of Vancocin (which, at over 2 grand a bottle, was thankfully covered by our insurance), no effect. They tried mixing in probiotics with these treatments, nothing worked.
So, in desperation, she'd been reading about a fecal transplant. She talked to her doctor about it, as well as a doctor over in Seattle (several hours away) that had experience with the treatment. Her doctor was unable to do it (I can't remember the exact reasoning, but I believe it had something to do with not being recognized as an acceptable form of treatment), but seeing as the procedure is so ridiculously simple you could do it in your own home, one of her incredibly gracious nurses volunteered to do it off the books.
So, the gross part is below (you have been warned). And yes, the procedure is incredibly gross. But I can honestly say my wife has never regretted doing it, and only wishes she had done it sooner.
My wife ordered a used blender online, scrubbed it thoroughly. We had to get our then-four-year-old daughter to poop into a collection bowl the hospital gave us (this took a couple days). She was the most viable candidate because, as a young child, her immune system had the least exposure to bacterial or parasitic infections. We then had to put the stool in a zip-lock and rush over to the doctor's office because the procedure has to be done within 30 minutes or the stool isn't viable. Once there, the nurse blended the stool (and yes, we immediately threw out the blender), put it in what could best be described as a turkey baster, and gave my wife a poop enema. My wife had to lay on her side and hold it in for a good 10-15 minutes.
And that was it. One treatment. Disease gone. Completely. Now, I know c.diff is completely different from Crohn's Disease, but if people are talking about considering it for your condition, I'd have to say: get over the ick factor and give it some serious thought. Because now, three years later, my wife hasn't had a single flare-up.
I wanted to drop a quick line, as my friend has Crohn's Disease, and he mentioned to me he'd heard fecal transplants were being considered as a potential treatment. Now, I can't speak to fecal transplant's viability for Crohn's Disease, but I can provide first-hand testimony to its legitimacy as a treatment for other GI conditions. My wife had c.diff for several months, and after trying literally everything else, a fecal transplant from my daughter was like a miracle cure.
Shortly before my son was born, some medical miscommunication resulted in my wife getting overloaded on antibiotics, killing off all of the good bacteria in her system. As a result, c.diff took over and was wreaking havoc. I'm sure many of you can identify with her experience: crippling pain, having to nurse our son on the toilet because she was going ALL the time, etc, etc. They tried Flagyl, no effect. They tried the maximum dose of Vancocin (which, at over 2 grand a bottle, was thankfully covered by our insurance), no effect. They tried mixing in probiotics with these treatments, nothing worked.
So, in desperation, she'd been reading about a fecal transplant. She talked to her doctor about it, as well as a doctor over in Seattle (several hours away) that had experience with the treatment. Her doctor was unable to do it (I can't remember the exact reasoning, but I believe it had something to do with not being recognized as an acceptable form of treatment), but seeing as the procedure is so ridiculously simple you could do it in your own home, one of her incredibly gracious nurses volunteered to do it off the books.
So, the gross part is below (you have been warned). And yes, the procedure is incredibly gross. But I can honestly say my wife has never regretted doing it, and only wishes she had done it sooner.
My wife ordered a used blender online, scrubbed it thoroughly. We had to get our then-four-year-old daughter to poop into a collection bowl the hospital gave us (this took a couple days). She was the most viable candidate because, as a young child, her immune system had the least exposure to bacterial or parasitic infections. We then had to put the stool in a zip-lock and rush over to the doctor's office because the procedure has to be done within 30 minutes or the stool isn't viable. Once there, the nurse blended the stool (and yes, we immediately threw out the blender), put it in what could best be described as a turkey baster, and gave my wife a poop enema. My wife had to lay on her side and hold it in for a good 10-15 minutes.
And that was it. One treatment. Disease gone. Completely. Now, I know c.diff is completely different from Crohn's Disease, but if people are talking about considering it for your condition, I'd have to say: get over the ick factor and give it some serious thought. Because now, three years later, my wife hasn't had a single flare-up.
Artisan105
Yondaime
no comment
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DenJensen:
thank you so much for sharing the success your wife had with fecal transplant. I have heard that so many times with regards to C. diff. that is so great that she responded so well. It is also something I had not considered using a young child for the sample.
Our daughter has Crohns Colitis, and we have considered the transplants as a possibility if the standard medical treatment does not work for her.
I have been following this thread and appreciate all of the input from the forum members. there is a lot more to consider when doing a fecal transplant than I orginally thought. With Crohns colitis and fecal transplants, it involves daily treatments from 3 months to 6 months. Dr Borody of Australia has helped many Crohns patients with this procedure and it is something worth considering.
thank you so much for sharing the success your wife had with fecal transplant. I have heard that so many times with regards to C. diff. that is so great that she responded so well. It is also something I had not considered using a young child for the sample.
Our daughter has Crohns Colitis, and we have considered the transplants as a possibility if the standard medical treatment does not work for her.
I have been following this thread and appreciate all of the input from the forum members. there is a lot more to consider when doing a fecal transplant than I orginally thought. With Crohns colitis and fecal transplants, it involves daily treatments from 3 months to 6 months. Dr Borody of Australia has helped many Crohns patients with this procedure and it is something worth considering.
QUestions:
Does anyone know if the transplants are being done outside of trials yet?
I saw that the Mayo Clinic talks about it as a treatment option. I was wondering if they really offer it and if so would they offer it to children?
My son is 13, he has been through so many treatments and has had such bad reactions (often worse in intensity to the illness) While he is desperate to get better & get back to school he has very little faith in the more potent drugs and even docs. (after steroid hell for nine months )He reacts to almost everything within a few day even antibiotics. SO I have trouble trying to convince him that any of the second or third tier crohns drugs would be safe for him. He already has bone tumors.
He has said he would rather do the fecal transfer than try imurin, or humira, which are likely what the docs will suggest next. I dont think our docs our that open minded about the fecal transplants or even possibly LDN ?
Can someone tell me if these things are now offered anywhere or are becoming mainstream enough for a child to be treated with either?
having trouble finding time to do all the research. Widowed mom with 2 kids who want a lot of attention. Need to help my son. We live in the Maryland area, but I would travel to get him the right treatment. Want to do the right thing by him and don't want to miss. His childhood is ticking away in his bedroom. He is a bright, happy, active kid by nature and deserves more. All ideas welcome. thanks.
Liz
Son currently on GF diet and 2000mg pentasa 2x /day b12 vitamins and magnesium.
failed flagyl, prednisone, budesonide, with horrible side effects (took 6 months to flush out ) DX 2/2012 "early Crohns: top to bottom" and enlarged lower colon which cannot be viewed as it is "cavernous". suffers from chronic constipation, inability to absorb nutrients, and extreme fatigue.
Does anyone know if the transplants are being done outside of trials yet?
I saw that the Mayo Clinic talks about it as a treatment option. I was wondering if they really offer it and if so would they offer it to children?
My son is 13, he has been through so many treatments and has had such bad reactions (often worse in intensity to the illness) While he is desperate to get better & get back to school he has very little faith in the more potent drugs and even docs. (after steroid hell for nine months )He reacts to almost everything within a few day even antibiotics. SO I have trouble trying to convince him that any of the second or third tier crohns drugs would be safe for him. He already has bone tumors.
He has said he would rather do the fecal transfer than try imurin, or humira, which are likely what the docs will suggest next. I dont think our docs our that open minded about the fecal transplants or even possibly LDN ?
Can someone tell me if these things are now offered anywhere or are becoming mainstream enough for a child to be treated with either?
having trouble finding time to do all the research. Widowed mom with 2 kids who want a lot of attention. Need to help my son. We live in the Maryland area, but I would travel to get him the right treatment. Want to do the right thing by him and don't want to miss. His childhood is ticking away in his bedroom. He is a bright, happy, active kid by nature and deserves more. All ideas welcome. thanks.
Liz
Son currently on GF diet and 2000mg pentasa 2x /day b12 vitamins and magnesium.
failed flagyl, prednisone, budesonide, with horrible side effects (took 6 months to flush out ) DX 2/2012 "early Crohns: top to bottom" and enlarged lower colon which cannot be viewed as it is "cavernous". suffers from chronic constipation, inability to absorb nutrients, and extreme fatigue.
Artisan105
Yondaime
- Location
- United States
An important nudge here.. For those of you thinking this is not mainstream or black magic..think again.
I learned first hand that these are being done and being done often at my local hospital, by GI's.
While prepping for surgery I asked my nurse if she had heard of it.. She actually had a patient who had received one just two days prior. Astonished, I asked my surgeon and he too was familiar and said GI groups perform these often.
I know in one if the cases mentioned it was for colitis, not c diff, as I specifically asked for confirmation.
Don't hesitate to call around.. Especially for your children.
Never ever ever just assume doctors mainstream path of prescriptions is the way. The drugs they give us are horrific.. There is no amount of feces that could cause the side effects experienced by taking prednisone and such.
Our body's are amazing and leveraging a loved ones stomach bacteria should be a compelling option.
I learned first hand that these are being done and being done often at my local hospital, by GI's.
While prepping for surgery I asked my nurse if she had heard of it.. She actually had a patient who had received one just two days prior. Astonished, I asked my surgeon and he too was familiar and said GI groups perform these often.
I know in one if the cases mentioned it was for colitis, not c diff, as I specifically asked for confirmation.
Don't hesitate to call around.. Especially for your children.
Never ever ever just assume doctors mainstream path of prescriptions is the way. The drugs they give us are horrific.. There is no amount of feces that could cause the side effects experienced by taking prednisone and such.
Our body's are amazing and leveraging a loved ones stomach bacteria should be a compelling option.
M30, thank you for the post. We are keeping this treatment in mind, and so glad to hear it has become more mainstream. I know it works for C.diff and colitis, but would love to hear more about it working for Crohns and Crohns Colitis in our case.
Our daughter is currently on her 8th dose of REmicade, which had to be doubled, using Cortifoam and Asacol, but is symptom free!!!!! (almost one month) First time in 2 years.
Along the same lines (somewhat), I believe strongly in Probiotics and feel they might accomplish the same thing when used correctly and along with necessary medications.
(But that would be on another thread )
Our daughter is currently on her 8th dose of REmicade, which had to be doubled, using Cortifoam and Asacol, but is symptom free!!!!! (almost one month) First time in 2 years.
Along the same lines (somewhat), I believe strongly in Probiotics and feel they might accomplish the same thing when used correctly and along with necessary medications.
(But that would be on another thread
)
- Location
- United States
How old is your daughter again?
Easier said than done, I completely empathize with you in opting for the biologics.
However I think for those new to IBD or those seeing no benefit from medications otherwise, I would strongly recommend pursuing it.
Taking into to account short and long term side effects of medication, my gut instinct tells me the risk / reward is worth trying first, not last.
Throughout the animal kingdom, many a turd is eaten naturally, even see dogs do it. Arbitrary inhibiting TNFs never occurs, except we humans decide to use biologics - as I did 4 months before needing surgery.
Sorry if I sound like an anti-biologics person. I'm really not.
I just think the increase in IBD globally is likely the result of environmental ignorance and carelessness of mankind (preservatives, papermills, etc)
Trusting ourselves to pack a solution into a pill or injection is hard for me..
Sorry to rant. I am really, really glad your little one is in remission. That is what matters most and you are succeeding.
Best of all, FT is always an option should you need it
Easier said than done, I completely empathize with you in opting for the biologics.
However I think for those new to IBD or those seeing no benefit from medications otherwise, I would strongly recommend pursuing it.
Taking into to account short and long term side effects of medication, my gut instinct tells me the risk / reward is worth trying first, not last.
Throughout the animal kingdom, many a turd is eaten naturally, even see dogs do it. Arbitrary inhibiting TNFs never occurs, except we humans decide to use biologics - as I did 4 months before needing surgery.
Sorry if I sound like an anti-biologics person. I'm really not.
I just think the increase in IBD globally is likely the result of environmental ignorance and carelessness of mankind (preservatives, papermills, etc)
Trusting ourselves to pack a solution into a pill or injection is hard for me..
Sorry to rant. I am really, really glad your little one is in remission. That is what matters most and you are succeeding.
Best of all, FT is always an option should you need it
My daughter is 14, and started having symptoms at 12.
I believe that the biologicals play a an important role, but our hope is that fecal transplants care cure it
It is so important to get the disease under control. Even when I was talking with Dr Borody, he believes that the fecal transplants work well with the Remicade. then you eventually get off of everything.
yes, fecal transplant should be an option. Hopefully the Gi's will start to see the success rate and recommend them. However, I am not even sure that they can since it isnt FDA... not sure how all of that works.
I believe that the biologicals play a an important role, but our hope is that fecal transplants care cure it
It is so important to get the disease under control. Even when I was talking with Dr Borody, he believes that the fecal transplants work well with the Remicade. then you eventually get off of everything.
yes, fecal transplant should be an option. Hopefully the Gi's will start to see the success rate and recommend them. However, I am not even sure that they can since it isnt FDA... not sure how all of that works.
- Location
- United States
Just read this...
I just stumbled on this article.. had to share it
Human Pee Added to Compost Boosts Crops:
http://newswatch.nationalgeographic.com/2013/04/10/human-pee-added-to-compost-boosts-crops/
I just stumbled on this article.. had to share it
Human Pee Added to Compost Boosts Crops:
http://newswatch.nationalgeographic.com/2013/04/10/human-pee-added-to-compost-boosts-crops/
- Location
- Sydney Australia
Faecal transplants are definitely moving into the mainstream arena - there was an article about in Medscape in the last few days.. As for having one's own 4 year old as a donor,well, that seems about as comfortable as possible for a somewhat uncomfortable topic ( after all, she was integral to that mum not so long ago..!!)
HD
HD
- Location
- United States
Not sure why but stories like this are tear jerkers for me. I am so happy for you!!
- Location
- United States
I agree, I think the fecal transplants are a very good option. I knew of a lady who actually did one at home with her husbands help! This was because back then not many hospitals or doctors were performing this and insurance would Not cover it. She had a nasty case of C-diff that would not go away. She was literally dying. So I remember reading that her husband became her fecal donor and they did the transplant using the fecal matter mixed in saline. It worked! It cured her C-diff. I mean I honestly would try this before taking some of those other meds out there. They are scary and have soo many consequences it seems. ( at least for me, I have MCS(multiple chemical sensitivities), so I do not do well with drugs). The Fecal transplant sounds like the least invasive anyhow.
Of course you pee on your compost pile. Doesn't everyone? No, really.I just stumbled on this article.. had to share it
Human Pee Added to Compost Boosts Crops:
http://newswatch.nationalgeographic.com/2013/04/10/human-pee-added-to-compost-boosts-crops/
But if that really does come as a surprise, then you may not know about composting toilets, the contents of which are then used to fertilize, well, not veggies, but shrubs and lawns. Yes! Really!
Such as this self-contained unit from Envirolet.
These have been used in remote cabins for many,many years, are virtually odorless, and require very little maintenance. You just add a little sawdust and pump or crank the handle once after each use, and they can accommodate 6-10 people a day, for months on end, depending on the model selected. After a few months of composting, the waste is converted into fertilizer, to throw on your shrubs. See link for more info. http://www.envirolet.com/enwatsel.html
For those who cringe at composting their waste, there's incinerating toilets as well. https://en.wikipedia.org/wiki/Incinerating_toilet
I would appreciate the reference for your quote.
Something you have not addressed is that Crohn’s is not limited to the alimentary canal. It can also affect the skin, eyes, and synovial tissue (Ankylosing Spondylitis). The one thing these locations have in common is epithelial cells. I think the root cause is not a T cell response to intestinal bacteria, but to a self antigen on certain epithelial cells.
T cells are created with the ability to attack cells with a wide range of antigens, including the body’s own cells. To prevent a systemic autoimmune attack, T cells strongly attracted to “self” are killed in the thymus. The rest are released into the body, where they must not attack the body or the beneficial microbiota in the body. Since the thymus cannot screen against all self antigens on all cell types, much less the microbiotal antigens, there must be a second level of T cell mediation.
I think the initial autoimmune response may even be beneficial. It alerts the body to an inappropriate T cell response that needs to be fixed. It would be logical that the colon and microbiome are the primary source of T cell mediation in the periphery. However, if the correct microbiota aren’t present, the autoimmune response continues. The result is an autoimmune disease.
If this is true, two important points are:
1. Auto immune diseases are not caused by the presence of bad bacteria, but the absence of good bacteria (and/or other parts of the microbiome).
2. The auto immune mediation is not limited to IBD. (Wen L, Ley RE, Volchkov PY, Stranges PB, Avanesyan L, Stonebraker AC, Hu C, Wong FS, Szot GL, Bluestone JA, Gordon JI, Chervonsky AV (October 2008). "Innate immunity and intestinal microbiota in the development of Type 1 diabetes". Nature 455 (7216): 1109–13. doi:10.1038/nature07336. PMC 2574766. PMID 18806780)
Unfortunately we can’t yet tell what part(s) of the microbiome are missing, and it probably varies from person to person depending on the self antigen and T cell response. Matching fecal transplants is more complicated than matching organ transplants. In this case, it is a transplant to prevent the body from rejecting itself.
The microbiota are primarily inherited from a person’s mother. However, half of the Major Histocompatability Complex and other antigens are inherited from the father. This could result in an inadequate microbiome in some people and explain the non-Mendelian inheritance of auto immune diseases. It also implies that the father might be the best FMT donor for his children (provided he passes donor testing).
I would like to see a trial with FMT between identical twins where only one has IBD. If an inadequate microbiome is the root cause, this study could prove it because many of the other variables would be eliminated.
@pungineer
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920680/
The interactions are so complex that i doubt we will ever fully understand them,
rather than micromanage everything we should let our bodies maintain homeostasis by not interfering (with bad food, drugs etc) unless essential,
That and a breakdown in the mucosal layer-
" It is not clear, however, whether this is a direct interaction, as epithelial cells are covered by a mucus layer that imposes a physical and electrically charged barrier to bacteria."
But there's more money in treatment than yougurt :ybatty::ybatty:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920680/
The interactions are so complex that i doubt we will ever fully understand them,
rather than micromanage everything we should let our bodies maintain homeostasis by not interfering (with bad food, drugs etc) unless essential,
My thoughts exactly......
That and a breakdown in the mucosal layer-
" It is not clear, however, whether this is a direct interaction, as epithelial cells are covered by a mucus layer that imposes a physical and electrically charged barrier to bacteria."
But there's more money in treatment than yougurt :ybatty::ybatty:
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7 clinical trials right now all around the world including the united states on both forms of IBD crohn's and UC. they will be completed by the end of 2014, possibly bringing the treatment mainstream by 2015. thats a hopeful estimate, its likely to take a few more years then that, but hard to say. and thats if they are proven to be successful for crohn's disease, which in smaller preliminary studies, they have been.
- Location
- Colorado
Oh my David! I'm still laughing out loud, and it feels great! I'm actually imagining it the way you wrote it. Too funny!
Saw this evening information about a letter to be published in the New England Journal of Medicine, today i believe, from a Dr. Trevor Van Schooneveld concerning his review of fecal transplant study.
"'Poop transplants': How well do they really work?"
http://www.foxnews.com/health/2013/05/29/poop-transplants-how-well-do-really-work/?test=latestnews
"'Poop transplants': How well do they really work?"
http://www.foxnews.com/health/2013/05/29/poop-transplants-how-well-do-really-work/?test=latestnews
kiny
Well-known member
There's plenty of reasons why this doesn't make any sense:
-You would have inflammation all over the organ, like with UC, you don't with crohn's disease. Crohn's disease is patchy like intestinal TB. UC looks very different from Crohn's disease. Crohn's disease has skip lesions you see in TB too often, same type of apthous ulcers. It looks nothing like a self-antigen respone. It looks like an infection, it's transmular all through the organ, but it's confined to specific spots and parts of the organ, nothing like UC at all, it's a very different disease.
It's not just the difference between ileum / colon involvement. UC is focused on the inner lumen, it's not transmular, people dont get the fistulas, they don't have skip lesions like in intestinal TB and crohn's disease. It's totally nothing like a self-antigen response.
-You don't have a self-antigen reaction in crohn's disease like one that is readily found in UC
-Macrophage penetrating antibiotics work for crohn's disease. They don't seem to cure people, but they consistently show results
-Genetic predisposition actually point to bacterial involvement. NOD2 and ATG16L1 are involved in bacterial sensing and autophagy
Saying that bacteria aren't involved is throwing the only concrete evidence about crohn's disease overboard, the genetic predisposition. 6 out of 8 loci in crohn's disease overlap with Leprosy loci. It might not be the gut flora, but bacteria are certainly involved.
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kiny
Well-known member
Why would they be the primary source. If the primary source of inflammation is the indigenous microbiome how come people with crohn's disease often have little to no inflammation in their colon. You'd expect to have the most inflammation where the highest concentration of gut flora is, that's the colon, crohn's disease is primarily the ileum.
You don't even need the microbiome to have intestinal inflammation in the small intestine.
-Intestinal TB has nothing to do with the microbiome, and there's inflammation in the small intestine.
-Ptb has nothing to do with the microbiome, and there's inflammation in the small intestine
there is alot more evidence then just this study, this is spin press trying to create doubt out of a great study.
here's the deal, treating c diff with antibiotics can be profitable, so there going to be reports like this causing doubt on a super cheap and effective treatment that competes with antibiotics.
i vaguely recall it costs like 1000.00 a week in antibiotics to keep someon e alive with c diff.
either that or this person is just talking nonsense. how much further doubt can you draw onto a well designed scientific study? after they study it, there should be very little room for doubt.
its funny they tried to suggest the fact that the study was stopped early to mean they somehow messed it up or something, but they stopped it early to give the people on vancomycin the fecal transplants, because they obviouly worked so fast and so completly.
total spin and misinterpretation of the facts.
Oh! I was a bit tired last night when I read the article. The impression I got from it is that the doctors that did the review thought well of fecal transplants. The procedure got results that worked for many. It was thought though that the study could have been done better, and slightly different results might be found with a larger study group.
In some respects his criticism is standard protocol. I don't read all that many studies, but of those that I do often mentioned at the end is a "but". If I was to guess, in the published letter Dr. Schooneveld is trying to set the stage for a larger study to look into fecal transplants. Whether that is needed is left up to interpretation.
Probably in 20 to 30 years from now it will be said that there is a clearer eye on the topic of fecal transplants. Yes, it is true I'm afraid, I have an optimistic personality.
- Location
- United States
ft ftw
This is all so interesting! We need to keep tabs on these trials.
Thank you for responding to my post. Although I agree with your observations, I’m not sure I know what your ultimate point is. It seems you are saying that Crohn’s disease is not an autoimmune disease, which is not anything I have read before. The treatments are almost all based on suppressing an autoimmune response.
I don’t know that there is a definitive appearance of tissue subject to an autoimmune response, e.g. diabetes, M.S., etc. A general inflammation assumes that the antigens the T cells are responding to exist on every cell. This may be true of UC. However, the antigen for Crohn’s would be different. Crohn’s can also attack skin, eyes, and synovial tissue in Ankylosing Spondylitis. All have epithelial cells, and not every cell in an organ is a clone of every other cell. Multiple cells in the fetus differentiate into different organs. Some may have the antigen and others would not.
I did not say bacteria are not involved. I said that the presence of certain bacteria is not the root cause. As in c-dif, the absence of the correct microbiome might allow the overgrowth of bacteria that make symptoms worse. This would explain why antibiotics sometimes help, but do not cure. Genetic factors could have a direct affect on the microbiome. However, genetics are not the root cause either. When one identical twin has IBD, the other would have to have it as well if it were genetic. This is not so. Understanding why or seeing if an FMT would be a cure in this situation could provide vital information.
It would logical for it to be the primary source because the thymus cannot delete T-cells with high avidity for the entities in the microbiome. The thymus also allows T-cells with moderate avidity for self antigens to be released into the periphery. The mediation for the T-cells with avidity for the entities in the microbiome would probably have to be in close proximity to microbiome antigens. Mediation for other T-cells would occur there as well just for efficiency.
Again, the indigenous microbiome is not the source of the inflammation. It is an insufficient indigenous microbiome that is unable to mediate the autoimmune response of the T-cells.
If Crohn’s were intestinal tb, I think the bacterium would have been found by now, as well as a cure. I wish you were right.
kiny
Well-known member
Avidity relates to binding strength, it has nothing to do with T cell being present in the intestine of people.
You need to explain how those lymphocytes are now in intestinal tissue, and if it's not through an APC, explain why they're there. And for an APC to activate you need an antigen. And if you don't have an antigen, you have no APC and you have no T cells.
Where do you suggest T cells are coming from if it isn't from the lymphatics? They just wander about and just all decide to pay a visit to the intestine or something?
You need to explain how those lymphocytes are now in intestinal tissue, and if it's not through an APC, explain why they're there. And for an APC to activate you need an antigen. And if you don't have an antigen, you have no APC and you have no T cells.
Where do you suggest T cells are coming from if it isn't from the lymphatics? They just wander about and just all decide to pay a visit to the intestine or something?
kiny
Well-known member
T cells don't just wander about, they're not just sitting in tissue sleeping, that's the job of neutrophils and macrophages, T cell are activated in lymphatics, they don't have "proximity" or "efficiency". They get activated during the adaptive immune response, and to activate them you need an antigen, and that antigen is either a self-antigen, in the cause of an autoimmune reaction, which has never been found in CD, or it's a bacterial antigen that makes it into the lymphatics through an APC.
So when you say that bacteria aren't involved, or that they have "avidity" for the microbiome, you make 0 sense. There is a particular antigen that activates a T cell. And if the whole microbiome would be the antigen, you would have inflammation everywhere, which in CD doesn't happen, you don't have inflammation everywhere, and if it's a particular bacteria from the indigenous flora, then it's not longer part of the microbiome, it's now a pathogen.
kiny
Well-known member
Really, start reading more:
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2810%2960282-6/fulltext
The (mis)labelling of Crohn's as an autoimmune disease
http://jem.rupress.org/content/206/9/1839.full
Although CD is immune mediated, it is not an autoimmune disease, as the immunological process appears to be triggered by the content of the gut lumen rather than a self-antigen.
To have an autoimmune disease you need a self-antigen, like in UC, that's not there in CD. And if was there you would have inflammation all over the affected organ...like...in UC...and you don't in crohn's disease.
Repeating something 20 times doesn't make it any more true.
kiny
Well-known member
And they don't in CD, NOD2, ATG16L1, VDR and many others are related to handling of intracellular bacteria, they have nothing to do with the indigenous gut flora.
If there were genetic factors that had a direct effect on the microbiome, the most obvious organ that would be involved would be the colon, and in most people with CD, the disease is located in the small intestine, which has much lower bacterial load than the colon.
kiny
Well-known member
And if these experiments worsen crohn's disease in people?
Dude where have you been? you know borody has already tried Fecal transplants in patients decades ago with no bad effects, and most of them improve, no sign of disease, and no need for medications. as far as we can tell, they are cured. we dont have to speculate what might happen, when we already know what HAS happened, people got better. i thought you were on top of every scientific advancement in IBD?
and in the latest study just completed we are seeing the same results, no one is getting worse, and most get better. ITs true for ulcerative colitis and crohn's disease. that's why larger studies are being conducted, its been shown to be safe.
To everyone reading this thread here is some info on fecal transplants http://www.crohnsforum.com/showthread.php?t=52400
kiny
Well-known member
It's possible that many people with crohn's disease who aren't followed up regularly, or people who spend large amounts of time in hospitals, have enterococcus or c diff or other secondary infections. If you give them a stool transplant you would help them get rid of the secondary infection. But that doesn't mean it's a treatment for crohn's disease, it's a brute force method for people who should have been treated for the secondary infection with traditional means.
- Location
- United States
I do not know much about the fecal transplant, but I did talk to my gastro doc about it. My gastro doc is at one of the top hospitals here ( a Huge teaching University Hospital) and one of the only hospitals here that offer stem cell transplants for Crohns disease. Well I brought up the whole fecal transplant and he did say they are still doing trials right now. They originally have used it for complicated cases of C-diff and that had a very good success rate. He said they are now doing some trials on people who have UC and IBD and he said eventually they will be doing trials on IBS as well most likely. He said depending on the results of the trials, if all goes well, fecal transplants will likely become more widely available one day in the future... But he did say that there are some areas of concern. He said that there is a chance that the donor person's fecal matter could contain bacteria that another person ( the recipient) would not react well too. This is a possibility. We are all built differently, where one person could live fine with a certain bacteria in them, where you put it in another person, their immune system may not react well. But all in all, I think it is a good thing. I mean if it turns out that it helps a lot of people, or even cures people, it is good. I mean right now all there is to depend on is toxic drugs that most assuredly are going to have negative effects on the whole body in the long run.
people with crohn's disease already have 10x the amount of pathogenic bacteria compared to healthy controls, and harbor pathogenic species that healthy control's do not have. the concern about getting more new pathogens, is a good one, but nothing to critical, we already have tons of that stuff inside us. its not the kind of concern that should stop us from studying or doing fecal transplants, especially when we can easily test the stool and select healthy donors to prevent anything like this from occuring.
Wildbill, have you had fecal transfer before?
- Location
- United States
I haven't. But I have had the defacto treatment. 
not yet, but if everything goes as planned in about 5 weeks from now i will be doing it.
I think the term "brute force method" is a bit much here. Is it possible your emotions are getting in the way of seeing this treatment as viable? I dont think this is only for people who aren't followed up on regularly. A lot of people are actually damaged from traditional treatments available to them. Instead of getting better the drugs make them sicker. As a mother of a child who has had bad reactions to just about every drug ( including antibiotics, and all the Crohns drugs he has tried so far, except Pentasa which does nothing as far as I can tell) this option looks much less invasive and less risky then the side effects of the next level of drugs we are looking at. I assume you are so defensive because you have found some treatment that has allowed you to experience remission. Please keep in mind that not everyone has, and the same treatment does not work for everyone. I am grateful that researchers are doing everything they can to think outside the box to make strides to help all the people who are suffering from Crohns/colitis for whatever reason they have it. Perhaps you don't know all the facts on the subject, even the researchers don't yet. It is not just about Cdif. I know someone who is working on this study, there are so many types of flora in any given GI tract, medicine cant replace what is lost in a compromised system and neither can probiotics. So far this si the closest thing. And it may be better than you think. Please don't judge people that are still seeking answers just because you may have found one that works for you.
Why are you waiting five weeks? Are you waiting for a donor?
- Location
- United States
I agree with you, I think it should be easy enough for them to culture the stool in order to see what types of bacteria are present in it. I mean I really think we are going to see that fecal transplants are going to become a normal and widely used treatment in the not so far off future. It has already helped lots of people. I know I read of a lady who was suffering a nasty C-diff infection and she was literally at deaths door. I mean the traditional antibiotics used to eradicate it were not working. She and her husband did the fecal transplant at home via enema! I am assuming there was no hospital where they lived or anywhere near them that did the transplant. This lady went from being so very sick to being able to eat and not having diarrhea anymore within days of doing this. So there has to be something to it. I myself would rather have it done in a hospital, but hey, if I was in a situation where I was so sick and nothing was working, I would do it! What have you got to lose at that point??
I mean sure, there can be side effects or adverse effects, but there also is with medications too( probably worse side effects with the medications in my opinion). I think doctors have to start thinking "outside" of the box when it comes to treating chronic illness, especially chronic illnesses that they do not know much about( like crohns and other various chronic illnesses).
I mean sure, there can be side effects or adverse effects, but there also is with medications too( probably worse side effects with the medications in my opinion). I think doctors have to start thinking "outside" of the box when it comes to treating chronic illness, especially chronic illnesses that they do not know much about( like crohns and other various chronic illnesses).
- Location
- United States
That is awesome! I hope it goes perfectly!!! Good luck buddy.
Hi everybody, and thanks for the forum. I was very committed to the idea of a fecal transplant, and had researched it for a few years. Dr Thomas Borody, at the CDD in five dock, Sydney. Had a really bad relapse/visit to the hospital over christmas, and realised I had nothing to loose. Did it end of March (you have to do a course of antibiotics and the first infusion is done when a colonoscopy is performed. No 'Yuk" factor at all! You can have donor or your family/own donor. Was very disappointed to suffer a further relapse end of may. Still think it has great potential, and if you can try it do. there is nothing to lose, has the potential to get you off all drugs/side effects, and of course give you back your life. I still believe it was just bad timing for me, and I still have my new "friends" on board willing to help me through. I havn't given up yet. (has UC//crohn's for 20 years)
- Location
- United States
Hmm, I am quite surprised they would have you do antibiotics before the transfusion. That in my opinion would hinder the whole process. The antibiotics would kill most of the good bugs being introduced into the gut. In any event, I am sorry to hear it did not work out great for you. I believe I also read you have it done a few times, not only once. I thought it was like 3 transfusions over a period of a month or two. Don't quote me on that, but I remember reading that you have a better outcome this way.
thanks for your story barbarian. since we dont know everything about FT yet like how many transplants it takes to reach a remission and what the dosage should be for each enema etc, im hoping we will soon be able to explain why some maintain long remissions after doing fecal transplants(up to 13 years), and why we have stories such as your own.
how many enemas did you do? and how frequently did you do them?
did you change your diet while doing them? its suggested a high fiber diet is essential for it to take hold. some people go on SCD while doing them.
Thought this an interesting writing by psychiatrist Emily Deans. It discusses a study in which one group was given probiotics and how that was found to improve anxiety and depression symptoms. It additionally has a short mention about fecal transplants and the effect the procedure could have on improving brain health.
"Gut and Brain Again"
http://evolutionarypsychiatry.blogspot.com/2013/06/gut-and-brain-again.html
"Gut and Brain Again"
http://evolutionarypsychiatry.blogspot.com/2013/06/gut-and-brain-again.html
i have a strict dietary regimen. therefore, any change in the pattern allows me to come up with good hypothesis as to why some function of my body seems to change and how dietary variables affect my body. when i eat certain nuts which tend to have strange organisms on them fungus and bacteria etc., it can lead to severe depression and mood changes. i wonder if it is these organisms that are having the effect. i now believe some psychiatric disorders may have something to do with bacteria.
in ibd, we may have a reduced capacity to deal with bacteria, and this leads to chronic inflammation, chronic enteric infections leading to diarhea. i wonder if any other damage to the gut allows some of these organisms or the chemicals they produce to get into the brain. but they may not have to as your gut itself creates neurotranmitters and even bacteria that live in your gut can signal to your brain along the vagus nerve.
did anyone see this post over in the diet section
http://www.crohnsforum.com/showthread.php?p=676449#post676449
link to this article
Bacterial molecules may prevent inflammatory bowel disease
http://www.sciencenews.org/view/gen...ecules_may_prevent_inflammatory_bowel_disease
"Common molecules made by bacteria in the gut may act as chill pills for the immune system. Molecules secreted by intestinal bacteria work to prevent misplaced immune attacks in inflammatory bowel diseases like colitis, a new study finds."
Early days but suggests that an absence of certain bacteria plays a part in IBD
Have to disagree with the proposal (in the article about the report) that more fibre is the way to go, feeding bad bacteria won't help,
http://www.crohnsforum.com/showthread.php?p=676449#post676449
link to this article
Bacterial molecules may prevent inflammatory bowel disease
http://www.sciencenews.org/view/gen...ecules_may_prevent_inflammatory_bowel_disease
"Common molecules made by bacteria in the gut may act as chill pills for the immune system. Molecules secreted by intestinal bacteria work to prevent misplaced immune attacks in inflammatory bowel diseases like colitis, a new study finds."
Early days but suggests that an absence of certain bacteria plays a part in IBD
Have to disagree with the proposal (in the article about the report) that more fibre is the way to go, feeding bad bacteria won't help,
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im not trying to dismiss your post as insignificant, but this is really old news about butyric acids role in the intestine and immune function. what i was hoping for was for them to examine other molecules these bacteria may make. butyric acid seems to have been now obviously beneficial to things likes intestinal permeability and some roles in regulating inflammation.
to me it seems pointless to re-establish its beneficial role. lets try restoring these butyric acid producing bacteria that are extinct in the intestines of IBD patients with a fecal transplant and se if it corrects the dysregulated inflammation(immune response).
the time for Fecal microbiota transplant for IBD has seriously come. no more collecting small facts we already know, scientists sometimes go overboard with the irrelevant fact collecting, and the re-confirmation of old facts. we have enough evidence to supprt trying fecal transplants, lets get-r-done.
http://www.crohnsforum.com/showthread.php?t=52400