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What is inside the fecal stream that is driving inflammation.

The fecal stream is behind the inflammation in crohn's disease. Rutgeerts et al. showed contact with intestinal fluids in patients caused disease within 8 days.(1) (2)

Harper confirmed this a third time (3). Small bowel effluent causes inflammation.

However, patients that received an enema of effluent that first went through a 22-nm ultrafiltrate showed no such response. Showing that fecal content larger than 0.22 micron is responsible for the inflammation. Either bacteria or large particles in the fecal stream cause the inflammation. (3)

Macrophages within the lamina propria show an immune response to E. coli, Streptococci and Listeria (4).

Serological markers like anti-OmpC can predict CD disease years before the diagnosis. (5)


(1) ''Early lesions of recurrent Crohn's disease caused by infusion of intestinal contents in excluded ileum. https://www.ncbi.nlm.nih.gov/pubmed/9453485 ''

(2) ''Effect of faecal stream diversion on recurrence of Crohn's disease in the neoterminal ileum
''

(3) ''Role of the faecal stream in the maintenance of Crohn's colitis
https://gut.bmj.com/content/gutjnl/26/3/279.full.pdf ''

(4) ''Immunocytochemical evidence of Listeria, Escherichia coli, and Streptococcus antigens in Crohn's disease.
''

(5)''Serological markers predict inflammatory bowel disease years before the diagnosis.
''
 
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I would think it is the fecal stream that feeds the existing bacteria responsible for the inflammation. In some instances I also would speculate that some foods have components that are similar to some secretions output by certain bacterium which increase inflammation. That is the hypothesis I came to regarding my adverse reaction to onions when I was ill. I can eat them without any consequences now.

It would be difficult to explain long term remission otherwise. Especially when not using a typical Crohn’s treatment.

Much of our food is both GMO and doused In glyphosate which adds another layer of complexity to it all.

Dan
 
Interesting but these studies are old. Have none of these avenues been followed since these findings were published? I had understood that there were as yet no identified antigens in Crohn’s, hence the constant speculation of different causes. And if the bug(s) is larger than 22n-m then why hasn’t it or they been identified since these publications? Frustrating! It seems like we just go around and around!
 
I think the speculation about different causes is because there are different causes and often multiple causes. Thats why its a difficult thing to get under control.

Based strictly off of my own alternative treatment results, mycoplasma pneumonia and H-Pylori were larger factors concerning inflammation than MAP and E-Coli although all were involved. The H-Pylori must have been right in the gut lining as killing it (too quickly apparently) caused a fire like burning in the gut that I have never experienced before. Once that healed though, things improved considerably.

I could be wrong, but I doubt it.

Just an opinion.

Dan
 
What do you think about the idea of low stomach acid being part of the puzzle?

Stomach acid is needed to assist the digestion of meat to extract iron and other nutrients. Its other role is to sterilise or destroy unwanted bacteria. If stomach acid is insufficient then these functions will not work properly.

Presumably loads of stomach acid is not needed to digest and sterilise EEN (which comes sterile and predigested) which could explain why EEN works.

Given that food digestion is such a main part of the digestive tract I find it quite incredible that gastroenterologists have so little concern about the saliva, acid, bile, enzymes and mechanics of a Crohn's patient and also pay little attention to the food which is being consumed. Surely both these parts have an integral role to play in the disease?

I also wonder about the role of baker's yeast. Why are so many Crohnies found to be ASCA positive? Why would anyone need/develop antibodies to yeast if it was not a problem in some way? Maybe sufficient stomach acid is needed to neutralize yeast? Removing yeast from the diet is not an easy task- it is in so many foods, not just bread.

The other thing EEN is free of is gluten. Gluten has been shown to play a big part in gut problems. It just might be that stomach acid or some other enzyme can neutralise gluten so that it is harmless.

Some crohnies have claimed that apple cider vinegar has helped them so maybe it is the PH factor doing the job.
 
Why are so many Crohnies found to be ASCA positive?

Why would anyone need/develop antibodies to yeast if it was not a problem in some way?
Right, you can detect anti-fungal IgG in the blood of crohn's disease patients. Malassezia and Candida albicans are associated with crohn's disease.

Patients with primary immunodeficiencies, often develop severe fungal infections.

Anti-OmpC implicates E. Coli.
 
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Yes Wildbill, micro-organisms can and do cause problems, inflammation being one of them, but not always. Most of the time the digestive process of saliva, acid and bile destroys the baddies while the good ones are allowed in. However, sometimes a bad one gets through the chemical bath and that's when the immune system comes into play.

A good immune system will be effective without needing to resort to inflammation so the person isn't even aware of a the bug, but it depends on the bug. Something like listeria usually makes people feel very unwell but eventually the immune system eliminates it through a combination of inflammation, flushing and fever.

The problem with CD and allergies is that the immune system does not work correctly. It attacks the wrong things or fails to attack at all.
 
couldn't any micro-organism from the external world cause inflammation? because that would be in the fecal stream.
In a patient with active inflammation, it's intestinal bacteria or fungi present in the fecal matter that is causing inflammation. They're lumen bacteria sticking to the intestinal wall that the fecal stream physically moves around.

Most people think of the intestinal mucosal tissue as static. In reality it is very mobile and moves around all the time, it does this to mitigate migration of bacteria into the lamina propria. But even an intestine with complete mucosal healing remains incredibly permeable. Bacteria and fungi can enter through peyer's patches for example.


Regarding the ''external bacteria'' question. The bacterial load of a normal diet is quite high, especially plant based diets can be very high in bacterial load. A simple piece of fruit contains thousands of bacteria. Dieticians might argue these are ''healthy'' bacteria, but what is considered healthy for a normal individual might cause inflammation in crohn's disease patients.

EN probably works by limiting the fecal stream, and its bioavailability depletes intestinal bacteria from the necessary nutrients to survive. Intestinal bacterial load decreases on EN. I think this is less important...but what EN also does is simply decrease the amount of bacteria you ingest.

3875
 
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Regarding the ''external bacteria'' question. Due to the prevalence of salmonella and campylobacter infections in the West...it is inevitable that some people with crohn's disease will at some point be (re)infected with salmonella or campylobacter. Someone with active disease and active lesions, would flare without a doubt if they come into contact with salmonella or campylobacter.

Foodborne infections of course don't explain persistent inflammation, the persistent inflammation is being caused by something perpetually present in the fecal stream, but the foodborne infection would cause lesions that allow fecal matter to come into contact with the intestine without the mucosal layer acting as a barrier.
 
(You of course can't find campylobacter or salmonella in most stool of crohn's disease patients...even with a weakened immune system, most people will overcome those infections, including crohn's disease patients....BUT....that foodborne infection would leave lesions behind...battle scars if you wish....lesions that are being crhonically penetrated by fecal matter)
 
While I'm writing. Regarding the decrease in bacterial load.

You can't mimmick crohn's disease in mice with a sterile intestine. If you could get intestinal bacterial load to zero in a crohn's disease patient, there would be no inflammation whatsoever.

All crohn's disease treatments that aren't based on immunosuppression rely on decreasing bacterial load or targeting specific bacteria or fungi.

The most straightforward way to decrease bacterial load are antibiotics right. And they work, initially, especially macrophage penetrating ones like cipro, they enter the lamina propria, penetrate macrophages and manage to kill E coli for example. But the problem with antibiotics is that the remission is transient, at some point we see that those bacteria become resistant to the antibiotic and they now have a fitness advantage due to the depletion of commensal bacteria. It's not a solution.

What is likely a much better solution is the use of bacteriophages that target specific bacteria that we know are involved in the chronic stimulation of inflammation in crohn's disease patients. There are trial underway with bacteriaophages that target AIEC for example. Also FimH blockers that target AIEC are being developed.

EN decreases bacteria load and fungal load, and it modulates bacterial population. It likely does this with nutrient depletion due to its high bioavailability.
 
The idea of ''good'' and ''bad'' bacteria is a theory that doesn't work in practice.

It works so poorly that we had to invent a new term, we don't just have commensals and pathogens anymore, we now invented the word ''pathobionts''. You'll see this word being used in studies studying the interactions of bacteria and the intestine.

Pathobionts are bacteria that are harmless ''commensals'' that act as disease causing ''pathogens'' under certain conditions.

Soon we will have another category, and then another, and then another.

The truth is that the story about good and bad bacteria falls apart in patients with primary immunodeficiencies like crohn's disease patients. The intestine is lined from top to botton with macrophages.

Any bacteria entering the lumina propria through an active lesion is considered an invading pathogen, and macrophages will respond aggressively to all of them, macrophages do not distinguish between good and bad. Unlike neutrophils they have a long lifespan and are able continue to release inflammatory cytokines for days.

Maybe it's worth considering when doctors recommend those ''million bacteria'' probiotics with ''good'' bacteria. Ingesting millions of bacteria is probably not the smartest idea for crohn's disease patients until a single study shows it is helpful, which they all failed to do.
 
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