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FMT/Anti-MAP/UC and Crohns Cause Hypothesis

Hi Everyone,
(Links are from the Centre of Digestive Diseases, written by Dr Borody)

I have been reading, and reading and just couldn't stop thinking about .
The Fact is we do not know what Causes Crohn Disease/or UC.
The two things I have looked into detail are Fecal Transplants, and Anti-Map Therapy. I do not believe there are any members on the forum who are actually undergoing any anti-map therapy. Nevertheless In the link to the journal article it states that they placed anti-biotic through a colon-scope in order to remove the blastocystsis parasite. This reminded me then of H.Polyri being called an auto-immune disease etc etc.

FACT: We can gather a healthy Fecal Donor infuse this into someone with a clostridium difficule, and they will be cured. We can do the same for someone with Ulcerative colitis and they can be in remission for up to 13 years ( could be a cure for some), or we could infuse them into someone with crohn disease and they will be in remission(please see articles).

Hypothesis:
Someone's fecal sample who has Crohn/UC/Clostridium Difficule who is infused into a healthy being that has not taken any anti-biotics for a prolonged time in their lifetime will not be infected.

Yet someone who has been taking anti-biotics constantly(5x a year or more) will be affected with an IBD due to compromised gut Flora.

This test will never be done due to the risks as im more than sure. A mice model will not work, as they can induce inflammation but not crohns disease or ulcerative colitis. It must be done on a healthy individual willing to take the risk, and I guess its against medical ethics, but I clearly remember the H.Polyri Doctor infecting himself on purpose to prove a point that stomach ulcers were not caused from stress.

Put aside the rise of processed food(never gonna change), the rise in IBD(population growth), and the rise of environmental pollution(only so much one can do) there clearly is a link which is overlooked.

Mycobacterium Avium Subspecies can be tested for via a blood test, and its accurate in diagnosing a MAP infection. Another way to prove this point is to feed somone MAP infected cow until either Crohns disease or Ulcerative colitis is visible, with constant anti-biotic abuse. Then and only then will alot of answers be answered, but at the moment I see alot of research into genes, NOD2, predisposition and it looks like thats all that been accomplished. It makes me raise eyebrows. There is no funding thats a fact, but really would you waste so much time in gene research when it doesnt get anywhere. The SSI Vaccine from Qu Bioligics holds certain ground for future treatment but what it does is eradticate a certain strain of E.Coli. Hence Anti-Map, FMT, and SSI all aim at the Gut Flora.

If people still believe it is an autoimmune disease well then they need to look and brainstrom. Because
A) there is no proof that it is an autoimmune disease
b) there is lots of facts that it is an immune deficiency.

I would appreciate it if anyone has some thoughts? Im new to this and im sure alot more people on this forum has a greater insight than me. I will ask in the treatment forum if anyone has ever undergone FMT or Anti-Map therapy.





Link 1 : Reversal of IBD By FMT
http://cdd.com.au/pdf/publications/...American College of Gastroenterology p741.pdf

Links2: Antio Biotics Fed straight through to the colon via colonscopy
http://cdd.com.au/pdf/publications/All Publications/2009-Enema Intra-Colonic infusion Abstract1.pdf

Links3: Mycoabacteria Therapy
http://cdd.com.au/pdf/publications/...age, W. Chamberlin, TJ Borody, J Campbell.pdf

Links 4: Another cause of crohn disease

http://cdd.com.au/pdf/publications/...ody et al, Am J Gastroenterol, 104(S3)990.PDF
 
I used an alternative, experimental treatment to target the MAP bacteria.
The result was that it cured my psoriasis that appeared when I had my first Crohns flare.

I do not know if the MAP was destroyed in my intestinal tract.

Dan
 
I tend to agree that microbiota/flora balancing definitely has a positive effect. I know this is the case for me if I stop taking probios for just two days. MAP may play an integral causitive role among other things. However, I also believe it could be a pathogenic mycoplasma which is apparently a very stealth critter.

This study: http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2672.2002.01531.x/full

It seems to point out that detecting mycoplasmas are harder than mycobacteria. This study lists a couple of other studies which suggest that, for some reason, mycobacteria cannot account for the appearance/structural damage in Crohn's. "However, those infective organisms that have been studied (Sartor 2000), including the atypical mycobacteria (Thompson 1994), do not explain the manifestations of CD that occur throughout the gastrointestinal tract."

About mycoplasmas:"During growth, they undergo cell lysis (Rottem et al. 1973) so that fragments of mycoplasmas with cholesterol/lipoprotein may enter mucosal enterocytes or colonocytes and reach immune cells by transcytosis (Mazumder et al. 2000). Mycoplasmas strongly stimulate macrophages to induce pro-inflammatory cytokine release (Chambaud et al. 1999). Exogenous lipids, chiefly cholesterol, and fatty acids are needed for the growth of many mycoplasmas and a number of studies have shown that decreasing the fat content in enteral formula diets has therapeutic value in CD (Roediger et al. 1993). A randomized prospective multiple centre study in Europe recently demonstrated that fat reduction is of significant therapeutic use in patients with CD (Gassull et al. 2000). Whether reduced lipid availability leads to a decrease in mycoplasmas or lipids on their own provide the therapeutic response needs to be investigated."

The study also points out that mycoplasma may be killed with long term antibiotics like: clarithromycin, rifabutin and clofazimine.
 
Moe,
last week I was in contact with Dr. Borody. I too cant help but think that he is on the right track. We are currently waiting to meet with our GI to talk over the anit-M.A. P. treatment, or fecal transplant.

It can all be a little overwhelming wondering what is the best treatment for our daughter. I believe it is the current treatment that has gotten her almost into remission, but the long term effects of biologicals is something we must consider.

autoimmune vs. immune deficiency: It sure seems the medical profession is still focusing on the disease as autoimmune. Hopefully with all the research, they will find out more about the cause very soon.
 
An offshoot in this discussion - there is a Medscape (surgery) article describing the use of synthetic faecal transplant material to treat Cl. Difficile. The more I read, the more I think there is an infective agent/micro biome imbalance at the root of CD


HD
 
The following preliminary info, please do further in-depth research yourself, was lifted from http://www.roadback.org/index.cfm/fuseaction/studies.display/display_id/93.html

I get the sense that tests can only test for specific mycoplasma which have already been identified and to which your body is detectably waging enough of an immune response.

Interesting about "gold salts" reminds me of colloidal gold/silver as a possible mycoplasma treatment.

"Mycoplasmas, unlike viruses, can grow in tissue fluids (blood, joint, heart, chest, and spinal fluids) and can grow in living tissue cell structures without killing the cells- as some viruses and bacteria do. Mycoplasmas are frequently isolated from the oral or genito-urinary tracts of normal population and are found to infect females four times more often than males, which just happens to be the same incident rate in rheumatoid arthritis and other related disorders. Mycoplasmas can attach to specific cells without killing the cells and thus their infection process can go undetected. No symptoms suggests no disease. In some people the attachment of mycoplasmas to the susceptible cell membranes acts like a living thorn, a persistent foreign substance, causing the host's immune defense mechanism to wage war. This allergic type of inflammation often results in heated, swollen, and painful inflamed tissues. In such cases the mycoplasma may not be isolated from the inflamed tissues but is detected by the host's serum antibody level. A positive response would indicate that mycoplasma has infected the host. A positive mycoplasma test would indicate further tetracycline or anti-mycoplasma treatment.

Mycoplasma growth is also suppressed by gold salts, some antimalarial drugs and even bee venom - all are which are more toxic and less effective than tetracyclines...

Unfortunately, mycoplasmas never became part of medical school curriculum or textbooks until the late 50s and were considered as some oddity until one strain (mycoplasma pneumoniae) was identified as the cause of atypical pneumonia. This strain of mycoplasma as well as others have been suggested as a contributing factor for rheumatic disease. These diseases may be considered to be the results of immune complex (mycoplasma + antibody) and also the self destructive autoimmune reaction (mycoplasma + host protein ). Recent studies are now supporting the role and mechanism of mycoplasmas as both immune complex and as an autoantigen. If this proves to be the case, we may soon see mycoplasma associated with many other immunological disorders besides rheumatoid, i.e. diabetes, multiple sclerosis, etc.

Mycoplasma Complement Fixation Test

This test, mycoplasma complement fixation or MCF, identifies antibodies to a specific mycoplasma and are reported as a titer to the specific mycoplasma (s) resident in the patient. This is more specific than the m. pneumoniae kit.

PCR (Polymerase Chain Reaction) Test

This test identifies the mycoplasma strain by its DNA or genetic makeup. Results are + or -.

How are the results interpreted?

With the MCF, low titers are significant. Sometimes disease activity is not sufficient to produce a measurable level of antibody to mycoplasma. In this case, when antibiotics are administered, the subsequent attack on the organism generates a higher level of antibodies which than can be measured. An early test which was negative may become positive after a period of antibiotic treatment

PCR testing is by individual strain and is either positive or negative. It is very sensitive."
 
Hey moe, thanks for posting this, I see you're from Sydney, I was wondering, do you go to the center of digestive diseases for treatment? I'm in qld and thinking of going to Sydney for a few weeks to see a specialist from there, I'm not too happy w the GI clinics here.
 
Hey joshuaaa.
Yes i do. and im very grateful. If your after this kind if therapy then it's definitely worth it. My own gp laughs at the map and fmt procedure.
 
I'm contemplating.
They showed me some anti-map therapy of a patient with so many fitsulas and really heavy inflammation. Then they showed 6 months post anti-map. All that was left was scar tissue, but the colon looked extremely healthy.
I have not seen fmt results first hand but from what I've read there promising to put someone in remission if constantly done. Ill ask a bit more about fmt on next consult.
 
Moe,

Dr Borody was very helpful. He sent me two links regarding the use of Remicade with anti-M.A.P therapy and more on the anti-M.A. P. treatment. He is also going to connect us to a doctor here that does this type of treatment, however we are going to see if our local GI can implement this type of therapy along with the REmicade as recommended by Dr Boroday. (we have limited funds and not sure if our ins. even covers it)

I just want to know what are options are and be ready with a plan if needed.
I can send links to articles if you would like.
 
Hi there.
Sure please send. Remicade + anti-map. Hmmm I wonder why he would recommend both. I've seen anti-map work by itself. No biologics straight map. Is the disease severe ATM.
 
Think I can explain the reasoning. There's a tiny number of cases of people who went on infliximab and antibiotics that are "cured", the few people documented show no symptoms.

You can theorise why but I think it's bad to do so because it's very few people and guessing why is stupid. The theory is that inflixmab causes apoptosis lowering intracellular MAP and so does macrophage penetrating antibiotics, if you combine them it's a more effective anti-MAP treatment.

I think the major issue is that the current antibiotics, while they work against MAP in animals, perhaps humans, are highly ineffective still. MAP reproduces slow and the antibiotics are most effective when the bacteria divides, you would need some very targeted antibiotics against non-dividing cells because MAP reproduces so slowly or a vaccine that understand how T cells target MAP.

I'm somewhat saddened that there is a chance crohn's disease is caused by MAP but many people don't think it's needed to find targeted antibiotics. Even if MAP is not the cause of the disease, the farmers are struggling immensely to rid their herds of the bacteria.
 
I think it's important to remember how nasty the MAP bug is, it's up there with one of the smartest and nastiest bugs ever discovered. The way it manages to steal iron, the way it manages to avoid apoptosis, how slow it reproduces, how it avoids detection, how it avoids pasteurisation, it's intracellular, it's slow dividing times means it probably laughs at most antibiotics, it's very hard to detect it, it's incredibly adaptive and resistant, etc.

I only wish I had tuberculosis, MAP is so much nastier if that is actually what many people have.

I like to read about MAP but I also know there is a chance it has nothing to do with crohn's disease, it makes sense it does, but detection is very disappointing, of course because you can't see it doesn't mean it's not there, maybe it's deeper in the lymphatic system or mesentery.

Also a few cases of animals where they could not detect MAP at all, the animal died confirmed paratuberculosis, they could not find the bug at all and never did. Kind of like M Leprae, often they don't find it, even though you can see the people have Leprosy.
 
Okay wow.
I know they mentioned that influximab and imuran has anti-map activity. But not to that extent. So many questions to ask thanks kiny.
 
Okay wow.
I know they mentioned that influximab and imuran has anti-map activity. But not to that extent. So many questions to ask thanks kiny.


The idea or theory is that it's causing rapid apoptosis of MAP infected cells because for whatever reason infliximab induces apoptosis. And as you mentioned all those other drugs are antimicrobial in a weird way.

All of those things are really hard to believe for most GI btw. Go tell a GI that infliximab can kill bacteria and most will say "get out" lol.
 
Location
Ohio
We struggled with c diff until Chloe started taking small amounts of colloidal silver. Now the c diff is gone along with her other crohns symptoms. I don't completely understand why but she sure did improve significantly when we set out to kill the c diff spores.
 
If people are interested I can rant some more about MAP.

There's another drug like infliximab, it's called etanercept, it blocks TNF-alpha just like infliximab.

Funny thing is, it is ineffective for crohn's disease, it is now only used for rheumatoid arthritis, no longer for crohn's disease because it doesn't work.

The difference, infliximab causes apoptosis and etanercept does not, but both block TNF-alpha but only one works for crohn's disease, infliximab.

(it has nothing to do with any differences in their ability to lower TNF-alpha btw, studies show they are both just as effective, it's purely down to one causing apoptosis and the other not)
 
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Reading over what people say, and in some studies they bunch UC and crohn's disease up.

There's this other thread where people were asking why does it matter if it's UC or crohn and I said that crohn might involve a pathogen and UC might not and that means one might be helped with antibiotics and UC will not.

I always said there is zero proof crohn is an autoimmune disease, and it's true, there is literally zero proof, but there is a lot of proof this is the case for UC, UC involves autoantibodies targeting the colon, there is autoimmunity in UC, against colonic epithelium cells, it's completely absent in crohn's disease.

There's almost no research regarding MAP and UC because in most cases in UC there are autoantibodies (in like 80% of the cases they easily find them iirc), something some people might say for crohn's disease but there is no evidence of that at all, crohn is transmural, the likelyhood of bacterial infection is extremely high for crohn's disease, it is low for UC.

UC and crohn's disease are day and night diseases, they have nothing to do with one another. They both feature inflammation, but so do a few hundres other intestinal diseases and no one bunches them together etiher. I have no idea why some studies bunch these two diseases together, it's a shame they use the word IBD, since it somehow implies these both disease are linked when they're very different. Intestinal tuberculosis is way closer to crohn's disease than UC is to crohn's disease. I would say a person with AIDS and a MAC infection is closer to crohn than someone with UC, no idea who decided to bunch UC together with crohn's disease or why people even do it. Many know these diseases are different.

I feel they make it worse each time they do IBD-day or IBD research or IBD-something, they keep implying these disease are linked when they're not.

Keeping these diseases split as much as possible would help so much, for both diseases.
 
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If people are interested I can rant some more about MAP.

There's another drug like infliximab, it's called etanercept, it blocks TNF-alpha just like infliximab.

Funny thing is, it is ineffective for crohn's disease, it is now only used for rheumatoid arthritis, no longer for crohn's disease because it doesn't work.

The difference, infliximab causes apoptosis and etanercept does not, but both block TNF-alpha but only one works for crohn's disease, infliximab.

(it has nothing to do with any differences in their ability to lower TNF-alpha btw, studies show they are both just as effective, it's purely down to one causing apoptosis and the other not)
here is another funny thing, the tnf-alpha molecule is supposedly an apoptosis inducer, that is one of its roles. i was just thinking today about the nature of biological systems and our attempts to get precise in activating one small process or event in the human body, without simultaneousy effecting(negatively or positively) other events in the body, its tough because thats not how the body seems to work.
 

Catherine

Moderator
Please correct me I am wrong MAP is known as Johne's disease when it occurs in animals. There are control programs in place for Johne's disease, so i would say it is at least in animals in Australia.
 
Please correct me I am wrong MAP is known as Johne's disease when it occurs in animals. There are control programs in place for Johne's disease, so i would say it is at least in animals in Australia.
I'm afraid I wouldn't be able to correct you as I'm not too clued on about it, although I hope that this anti MAP treatment can indeed help as many of us as possible, catherine if you don't mind me asking, I see your daughter is on azathiaporine, I think I am starting it soon, is that what's put her in remission? How is she coping on it? If I may ask.
 
Your gp needs to join the forum.
He's out of date :p.
Regarding the centre Joshua.
The fmt looks promising but you need to stay consistent. As for anti-map you would need to see them to discuss. He's booked out until October. But he's other staff are avaulable and follow the same protocol,
 
I'm right in saying that MAP lurks inside cells and therefore is hard to remove with many antibiotics, aren't I?

I remember when our Parrot was diagnosed with psittacosis, which is caused by an intracellular bacteria (sits inside the cells). The treatment was a long course if Tetracycline which had to be kept in the body long enough for the bacteria to emerge and be killed.

Would similar apply here?
 
I'm right in saying that MAP lurks inside cells and therefore is hard to remove with many antibiotics, aren't I?
Yah, it's intracellular, survives inside macrophages for a long time, it divides really slowly and it's very resistant, it can stay dorment for many years before animals actually get sick, it's really hard to detect.

It's a nasty bug in animals, animals just die when they get it, including primates, they can't fight it, they stop eating and lose too much weight and die.

In ruminants it can basically kill the herd, it will spread through feces, the control programs for MAP aren't because they suddenly care about people with crohn's disease, it's so farmers don't lose millions on cows that are dying.

The control programs don't work that well though, you only need one infected cow or an infected soil and the cows will get it again.

You don't hear about MAP that often because no one wants to talk about it, in one study a researcher described how hard it was to get farmers to even admit their herd had MAP. Can you imagine if diseases like crohn's disease and diabetes are linked to a bug in cows, everyone will stop eating meat and drinking milk, it will result in huge economic losses. And unlike other issues they had with cows in the past, this is one they cant' contain, every day there are cows dying from paratuberculosis. It's the best kept secret of farmers today. Everyone knows about it, and everyone is telling each other to be quiet about it.
 
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Hasn't some research showed that lauric acid can kill MAP. I'm sure I read that somewhere. An animal study IIRC. Maybe cooking in coconut oil might help <g>
 

Catherine

Moderator
Sarah is in clinical remission I believe aza has put her their but she has developed a small bowel fistula. She has no side effects from aza.
 
Joshua,

Dr Borody, who specialized in the anti-M.A.P. is from Australia. You may have the opportunity to talk with him yourself. He has a research lab there. I have not heard that M.A.P. doesnt exist in Australia but I do know that there is not an easy way to test for it.

He is a very nice doctor/Professor. He also specializes in fecal transplants. It is all VERY interesting and I am so glad there are people willing to look at Crohns from a different point of view. that may be the way it is cured.

By the way, how are you doing?
 
Joshua,

Dr Borody, who specialized in the anti-M.A.P. is from Australia. You may have the opportunity to talk with him yourself. He has a research lab there. I have not heard that M.A.P. doesnt exist in Australia but I do know that there is not an easy way to test for it.

He is a very nice doctor/Professor. He also specializes in fecal transplants. It is all VERY interesting and I am so glad there are people willing to look at Crohns from a different point of view. that may be the way it is cured.

By the way, how are you doing?
I'm doing a little better thanks :) 3rd day eating solid foods and feeling way better than on liquid diet :)
 
Moe,
last week I was in contact with Dr. Borody. I too cant help but think that he is on the right track. We are currently waiting to meet with our GI to talk over the anit-M.A. P. treatment, or fecal tranyou splant.

It can all be a little overwhelming wondering what is the best treatment for our daughter. I believe it is the current treatment that has gotten her almost into remission, but the long term effects of biologicals is something we must consider.

autoimmune vs. immune deficiency: It sure seems the medical profession is still focusing on the disease as autoimmune. Hopefully with all the research, they will find out more about the cause very soon.
How do reach Dr. Borody? I have tried everything. Please advise.
traci9201@me.com
 
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