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Map treatment?
- Thread starter mreyn
- Start date
I am curious about this as well. Just saw this article last night -- http://www.myfoxorlando.com/story/23943890/ucf-researchers-closing-in-cure-for-crohns-disease
kiny
Well-known member
I've been tested for MAP by IS900, which is a DNA test for the bacteria, negative. Because of how unreliable the tests are, and because the bacteria wold likely be deep into tissue, it doesn't tell you much. A positive test tells you something, a negative test tells you they didn't find it, which means it might not be there, or which means it might be there but it wasn't detected.
There are no "natural treatments" for MAP, whoever says there are is trying to sell you something that doesn't work.
There are antibiotics that are able to kill MAP, but this isn't as simple as it seems.
You need a macrophage penetrating antibiotics, why you need a macrophage penetrating type is because MAP invades macrophages. Macrophages are immune cells, of the innate immune system, and your first line of defense against invading pathogens. MAP has found a way to exploit these macrophages and is able to replicate inside them, it's one of the few bacteria that doesn't mind a highly inflammatory environment. Regular antibiotics will do nothing against MAP. Antibiotics that are effective against MAP are azithromycin, cipro, rifampicin, rifabutin, clarithromycin and a few others.
So just use one of them and kill MAP?
Well, not so fast, mycobacteria like MAP are vulnerable during cell division, but because of how slow MAP divides, it's really hard to kill it. This slow division is also the reason why you can't simply culture MAP like you can culture other bacteria. Culutring MAP, while possible, will take 6 months and more minimum. For many bacteria this is a matter of days or hours.
What you would need to kill MAP are antibiotics that are able to target non-dividing cells specific for MAP.
With current antibiotic there's a high chance you eventually run into resistance.
There's another reason why you should be careful with regular antibiotics that are not specific for MAP and that is that like I said, MAP is a mycobacteria, and the antibiotics used against MAP are used not only for MAP, but also for other mycobacteria, for example, TB (tuberculosis). It's not "wise" to put someone on antibiotics that overlap with anti-TB antibiotics for extended periods of time. If that person gets TB, you basically have no ammo left since you've been creating resistance with your MAP cocktail.
But when you have crohn's disease and no treatment works, it is completely reasonable to do use antibitics cocktails (and you'll need a cocktail to target MAP, a single antibiotic will run into resistance), since crohn's disease is such a serious disease for many people that the risk of developing other infections or creating resistance is an "acceptable" risk.
I think it's interesting to discuss MAP. Because MAP means a cure, simple as that, if MAP is actually the primary trigger for the inflammation, when you wipe out MAP, you would cure people. It's entirely possible that a single pathogen is responsible for the inflammation in people and has been for years, because this same thing happened in tuberculosis in people before treatment, those people had years of inflammation, once they were treated, they were cured.
I do think it's also just as likely that MAP has nothing at all to do with crohn's disease. I do read and talk to people who study MAP, but I have never suggested or said MAP is the cause of crohn's disease, I think it is "interesting" and a road that needs to be explored simply because if it is MAP, it does mean cure eventually.
It is frustrating that some people discount intracellular bacteria just because not every test or biopsy shows the presence of a bacteria. Because we've been down this road before. We've seen it with H. pyroli......most doctors refused to accept the stomach ulcers were caused by a bacteria...they were very wrong. Leprosy....they couldn't detect the bacteria and concluded it wasn't related to a bacteria...the reason was simply because it was extremely hard to find. AIDS, many many people refused to accept it was related to a virus, now we know it does. This is not the first time in history this happened.
Even more frustrating is that the overwhelming scientific evidence does point to an intracellular bacteria.
I do think there are multiple candidates for bacteria related to crohn's disease, I have linked many papers about AIEC also, which is in a way a more likely candidate than MAP, because the prevalence of AIEC in tests has been more consistent than MAP.
.
.
For the question, why would crohn's disease be caused by a bacteria in the first place? Why isn't it an "autoimmune disease" or why isn't it "a reaction against the gut flora".
Very simple, because the genetic predispositions all have to do with handling of intracellular bacteria.
NOD2, IL23, IRGM, ATG16L1, VDR, all these genes related to crohn's disease, are all, every single one, related to handling of intracellular bacteria. In fact many overlap with lerposy predisposition.
That is the reason why studies keep searching for that holy grail bacteria and why there is constant "talk" about "curing crohn's disease", which is possible if it is related to a bacteria. It is the "persistent pathogen" theory, which is different from the "loss of tolerance against the gut flora" theory.
There are no "natural treatments" for MAP, whoever says there are is trying to sell you something that doesn't work.
There are antibiotics that are able to kill MAP, but this isn't as simple as it seems.
You need a macrophage penetrating antibiotics, why you need a macrophage penetrating type is because MAP invades macrophages. Macrophages are immune cells, of the innate immune system, and your first line of defense against invading pathogens. MAP has found a way to exploit these macrophages and is able to replicate inside them, it's one of the few bacteria that doesn't mind a highly inflammatory environment. Regular antibiotics will do nothing against MAP. Antibiotics that are effective against MAP are azithromycin, cipro, rifampicin, rifabutin, clarithromycin and a few others.
So just use one of them and kill MAP?
Well, not so fast, mycobacteria like MAP are vulnerable during cell division, but because of how slow MAP divides, it's really hard to kill it. This slow division is also the reason why you can't simply culture MAP like you can culture other bacteria. Culutring MAP, while possible, will take 6 months and more minimum. For many bacteria this is a matter of days or hours.
What you would need to kill MAP are antibiotics that are able to target non-dividing cells specific for MAP.
With current antibiotic there's a high chance you eventually run into resistance.
There's another reason why you should be careful with regular antibiotics that are not specific for MAP and that is that like I said, MAP is a mycobacteria, and the antibiotics used against MAP are used not only for MAP, but also for other mycobacteria, for example, TB (tuberculosis). It's not "wise" to put someone on antibiotics that overlap with anti-TB antibiotics for extended periods of time. If that person gets TB, you basically have no ammo left since you've been creating resistance with your MAP cocktail.
But when you have crohn's disease and no treatment works, it is completely reasonable to do use antibitics cocktails (and you'll need a cocktail to target MAP, a single antibiotic will run into resistance), since crohn's disease is such a serious disease for many people that the risk of developing other infections or creating resistance is an "acceptable" risk.
I think it's interesting to discuss MAP. Because MAP means a cure, simple as that, if MAP is actually the primary trigger for the inflammation, when you wipe out MAP, you would cure people. It's entirely possible that a single pathogen is responsible for the inflammation in people and has been for years, because this same thing happened in tuberculosis in people before treatment, those people had years of inflammation, once they were treated, they were cured.
I do think it's also just as likely that MAP has nothing at all to do with crohn's disease. I do read and talk to people who study MAP, but I have never suggested or said MAP is the cause of crohn's disease, I think it is "interesting" and a road that needs to be explored simply because if it is MAP, it does mean cure eventually.
It is frustrating that some people discount intracellular bacteria just because not every test or biopsy shows the presence of a bacteria. Because we've been down this road before. We've seen it with H. pyroli......most doctors refused to accept the stomach ulcers were caused by a bacteria...they were very wrong. Leprosy....they couldn't detect the bacteria and concluded it wasn't related to a bacteria...the reason was simply because it was extremely hard to find. AIDS, many many people refused to accept it was related to a virus, now we know it does. This is not the first time in history this happened.
Even more frustrating is that the overwhelming scientific evidence does point to an intracellular bacteria.
I do think there are multiple candidates for bacteria related to crohn's disease, I have linked many papers about AIEC also, which is in a way a more likely candidate than MAP, because the prevalence of AIEC in tests has been more consistent than MAP.
.
.
For the question, why would crohn's disease be caused by a bacteria in the first place? Why isn't it an "autoimmune disease" or why isn't it "a reaction against the gut flora".
Very simple, because the genetic predispositions all have to do with handling of intracellular bacteria.
NOD2, IL23, IRGM, ATG16L1, VDR, all these genes related to crohn's disease, are all, every single one, related to handling of intracellular bacteria. In fact many overlap with lerposy predisposition.
That is the reason why studies keep searching for that holy grail bacteria and why there is constant "talk" about "curing crohn's disease", which is possible if it is related to a bacteria. It is the "persistent pathogen" theory, which is different from the "loss of tolerance against the gut flora" theory.
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