Is Crohn’s disease tied to cattle germ?

[mf15]

Is Crohn’s disease tied to cattle germ?

FYI:There are people working on this.
Old Mike
http://westernfarmpress.com/management/crohn-s-disease-tied-cattle-germ

 

[PaulPhoenix]

Thanks for this. I wonder if anyone (Kiny?) knows whether you can starve out the MAP through EN for a few weeks?

Edit: also- where's that vaccine?!!

 

[kiny]

Think you would die before you can starve it. It depends on iron acquisition to survive (they use mycobactin to culture it), maybe deprivation of iron or iron abundance interferes with it's survival, I dunno, but EN prolly has no effect on it. EN might be able to modulate commensal microflora though because it's low in fibers, I don't think it influences MAP is any way.

You would need to find MAP too, MAP isn't easily found in people with crohn's disease, only reasons I can think of is because the bacterial load of MAP is so small it is so hard to find, because detection methods are still so bad, or because they're looking in the wrong spot and should be looking at the lymphatic system, or maybe because like some study suggested, the response is against MAP antigen, not live MAP. Or because it has nothing to do with crohn's disease ~ They don't know because they get 0 funding.

The question is also, how important is finding it in every person if you developed decent antimicrobials, no one seems to have an issue with the fact that M Leprae, another mycobacteria, is not found in everyone and you can't culture it, but they still treat people for it. They don't know how well antibiotics work because for one you would need one that works well against non-dividing cells (because of how slow MAP reproduces), and you would need one specific for crohn's disease that is safe and tested, but if you don't test it, give no funding, and simply ignore it (thanks in most part because of very stubborn GI, not because of lack of interest from the scientific community), how are you going to know.

 

[kiny]

The first reply to that link is how many GI respond. Why would TNF-α blockers work if crohn's disease was related to mycobacteria, wouldn't it make crohn's disease worse like with tuberculosis.

TNF-α blockers cause apoptosis, which would hinder the growth of macrophage penetrating MAP. TNF-α blockers are in a way an antimicrobial. Also many documented bacteria thrive in an inflammatory environment.

The fact that something which lowers the inflammatory response might actually hurt the proliferation of a bacteria is something most GI can't even wrap their head around.

Not only that, the fact TNF-α blockers are detrimental for MAP survival is documented: http://www.ncbi.nlm.nih.gov/pubmed/22398081

What you do have to wonder is that when people go off the TNF-α blockers, what happens then. And all the potential risks involved with them.

 

[PaulPhoenix]

I wonder what happened to the MAP vaccine then - was being done in London IIRC.

I only drink UHT milk and avoid processed food. I wonder if there have been studies of remission lengths with relation to food or exclusion of particular chemicals?

I bet there aren't studies comparing after the TNF-a drugs stop working with flare ups in never treated people.

 

[kiny]

I bet there aren't studies comparing after the TNF-a drugs stop working with flare ups in never treated people.

Right, there are no studies specifically looking at what happens if someone goes off a TNF-α blocker, which is a shame really.

 

[Dave Watson]

Couple of further points to add to kiny's excellent responses.

This study found 92% of CD sufferers infected with MAP (link).

This study demonstrated that MAP-infected macrophages produce excess amounts of of TNF (link).

Another bug linked to CD is AIEC. Again, AIEC-infected macrophages also produce excess TNF (link).

We have two bugs linked to CD and both invade immune cells and the invaded immune-cells produce excess amounts of TNF. Could this excess TNF cause the inflammation and ulcers in CD?

In one way or another, CD drugs reduce/inhibit TNF in the gut.

• Corticosteroids can improve Crohn’s and corticosteroids inhibit TNF (link).
• Naltrexone can improve Crohn’s and Naltrexone inhibits TNF (link).
• Mesalamine can improve Crohn’s and Mesalamine inhibits TNF (link).
• Enbrel, Remicade and Humira can all improve Crohn’s and all are anti-TNF drugs.
• Ect.

So, how would the excess TNF cause the inflammation/ulcers in CD - what's the elusive disease-causing mechanism ?

This article (link) discusses the miss-labelling of Crohn's as an autoimmune disease, when really it's a chronic inflammatory disorder of unknown cause; in others words, drop the autoimmune-disease label because it's not so! Even Wiki (lol) is saying CD is not an autoimmune disease: "Crohn's disease has wrongly been described as an autoimmune disease in the past; recent investigators have described it as an immune deficiency state"

Again, could the excess TNF from infected immune cells cause CD?

Excess TNF affects the functioning of immune cells (link)... and immune cells protect the gut-lining from damage by normal gut bacteria.

Additionally, there's an aspect of Crohn's missed by everyone... why doesn't the damn inflammation/ulcers/fistulas heal? (Keep in mind that CD is NOT an autoimmune disease)

Excess TNF is linked to non-healing wounds (and obviously non-healing inflammation). Excess TNF up-regulates MMIF (Macrophage migration inhibitory factor). MMIF plays a central role in wound healing. EMPHASIS: MMIF plays a central role in wound healing!

So, could the excess TNF play a dual role in CD?

1. Indirectly cause the gut damage by preventing immune cells from clearing bacteria from the gut-lining.

2. Prevent/delay the gut damage (inflammation/ulcers) from healing.

Food for thought...

(Can't include links 'cause I've got less than 10 posts).

 

[Dave Watson]

Lauric acid has been found to be effective against MAP.

In in vivo experiments with cows, 10 registered Jersey cows with clinical paratuberculosis were given lauric acid mixed with their protein supplement feed in an amount equal to 1 gram per kilogram per day. The cows showed cessation of thesymptoms of paratuberculosis and improvement in physical condition within 21 days. Four of these cows died from causes other than paratuberculosis before the conclusion of the tests. The six remaining cows, after receiving lauric acid in their feed forintervals varying from 48 days to 122 days, had corresponding survival times of 157 days to 332 days. The feces of these six cows were negative for Mycobacterium paratuberculosis within 41 to 112 days. Details of the tests and the results therefrom aredescribed below.

Source: patentgenius dot com/patent/4223040.html

Thanks for this. I wonder if anyone (Kiny?) knows whether you can starve out the MAP through EN for a few weeks?

Edit: also- where's that vaccine?!!