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My crazy theory as to why UC starts in the rectum.

Based on my history.

UC 1980,quit smoking in 1977.

Prior history none.

Now back in 1971 Nov-Dec, a good case of Korean craps,resulting in D for about 2 weeks.

One day with the burning D, I felt something tear and a burning sensation for about 3 days, went away and did not think about it again.

Came home from Korea Jan 1972, got a rectal abscess which needed emergency surgery sometime

in the spring of 1972, since then ongoing abscess, fistula etc..

1980 my scopes showed ulceration at 6cm.

Old proctologist said the UC/proctosigmoiditis might be caused by the abscesses.

So have been thinking about this since then.

As we know UC starts in the rectum for many/most.

Ok so what might be going on, is that you get a small tare, resulting in a infection which you might not even notice, or a big one resulting in a abscess.

The consequence of this is that now the blood/immune system has been directly exposed to gut bacteria, without any of the controlling effects such as mucus, and proper antigen presentation by the colon, to the immune system.

So now the immune system is primed to commensal colon bacteria.

This is a form of autologous vaccination.

Since the immune system is now primed,it goes after commensal bacteria in the colon.

Why it mostly starts in the rectum is perhaps, the infection is from rectal bacteria where the tear was, so the immune system is primed for the rectal area rather than a more proximal location.

So in other words the immune system has lost tolerance to commensal colon bacteria, and specifically rectal bacteria, or stool that has different bacterial populations from proximal to distal.

You will find that one of the definitions of UC is a loss of tolerance to commensal bacteria.

One way to regain tolerance, or even perhaps the only way.

Oral tolerance.

That's right autologous, oral FMT.

I have a study on that, some I believe might have went into remission, have to find it.

I might think you need small, long term dosage as a way to induce tolerance.

Found it.


You can also see from the study the autologous bacteria population seems to go in the wrong direction.

But, I am not looking to correct the dysbiosis in stool bacteria,but to establish immune tolerance.

as you can see 20% of the controls went into remission.

The controls used their own poo, which means autologous.

I guess I have posted on this before, but worth a rehash.

Of course the dangers of oral FMT is infection, especially in the lungs, or if you vomit.

You might ask yourself why is there no cure except surgery.

Answer: You can't un-prime the immune system,unless tolerance to commensal bacteria is somehow reestablished.

Does this explain increased incidence in the west, or increased incidence from moving from east to west in the world,or increased incidence with a western diet.

Perhaps the immune system once primed, everything is still ok,until something such as diet,

induces leaky gut, then more bacteria or antigens are presented to the primed immune system and a sever immune attack is induced.

Also the immune attack is specific to the rectal bacteria or distal stool bacteria, so that is why you would want to use your own poo for FMT and not from someone else.

you can see here some of the ways the gut protects itself from commensal bacteria

but what if the chain is broken by direct immune contact in an abscess


some oral tolerance info


now read here where it says clinical and experimental evedience
pay particular attention where is says lack of inflammation with diversion of the fecal stream to ileal or colonic segments


I will even back myself up with a case of true autologous vaccination.

Primary manifestation of Inflammatory Bowel Disease (IBD) following subcutaneous autovaccination.

Raithel M1, Weidenhiller M2, Hahn M3, Hagel A4, Bechthold C4, Neurath MF4, Rieker RJ5, Stein J6.

Author information

•1Dept. Medicine 1, Gastroenterology, Functional Tissue Diagnostics, University of Erlangen, Germany martin.raithel@uk-erlangen.de.
•2Gastroenterological Practice, Regensburg, Germany.
•3Department of Anaesthesiology, Kantonsspital Liestal, Switzerland.
•4Dept. Medicine 1, Gastroenterology, Functional Tissue Diagnostics, University of Erlangen, Germany.
•5Department of Pathology, University of Erlangen, Germany.
•6Department of Nutritional Medicine, Sachsenhausen Hospital, Teaching Hospital of the J.W. von Goethe University, Frankfurt/Main, Germany Crohn-Colitis Centre Rhein-Main, Frankfurt/Main, Germany.


Onset of inflammatory bowel disease (IBD) is nowadays seen as an interplay or a combination of genetic susceptibility, disturbed intestinal immunity and environmental factors including gut microbiome. However, the initiation of inflammation and progression to IBD pathogenesis in a given individual is poorly understood.In this case report we describe the clinical course of a 17-year old female patient, developing symptoms suggestive of IBD after "autovaccine therapy", in which sterilized samples of the patient's own stool were injected subcutaneously for improvement of her general immunity. The patient presented with a severe onset of disease, which was firstly suspected as ulcerative colitis on outpatient examination and later corrected to IBD with Crohn's- like features in our institution, due to high systemic inflammation, mixed lymphocytic-granulocytic infiltrates in gastric biopsies and further characteristics suggestive of Crohn's disease. A prolonged and complicated course was seen subsequently with intermittent steroid dependency in the long term.Numerous publications postulate that (auto-)immune reactions against resident bacterial stool flora may play a role in IBD. It is possible that in this patient tolerance to endogenous bacteria was disrupted by systemic pro-inflammatory mechanisms induced by autovaccination.

read the last sentence again.
It is possible that in this patient tolerance to endogenous bacteria was disrupted by systemic pro-inflammatory mechanisms induced by autovaccination

Old Mike
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Not really sure why they moved my post out of the research area, its
taken me a little while but I was getting to crohn's disease.

I have also ran a search on the whole forum and do not come up with

Old Mike

Looks like this might somewhat contradict theory,there might be some hope after all, but perhaps

not long term. They did clinical trials,Oral administration of Alequel, a mixture of autologous colon-extracted proteins for the treatment of Crohn’s disease.

Wonder why they used colon extracted on crohns as opposed to UC.


clinical trial, and they did use some proteins from the ileum is some people.


ah, the plot thickens, it seems that only proteins that are not fully digested induce tolerance,

the trick is along with the proteins use sodium bicarbonate to interfere with digestion, nice trick.

This for food allergy, but who knows might apply to systemic immune response somehow.

Complete degradation of peanut via the combined effects of stomach and intestinal enzymes has been demonstrated by sequential digests of peanut extract (gastric digests followed by intestinal digests) (Vieths et al., 1999). Oral tolerance to peanut and Brazil nut was enhanced by adding sodium bicarbonate to the dosing solution. Sodium bicarbonate treatment increased the pH of the solution from 7.5 to 8.8, likely inhibiting stomach pepsin activity during oral exposure (Kopper et al., 2004). Limiting digestion of peanut and Brazil nut may have preserved the stomach labile proteins, some of which were resistant to intestinal enzymes, and therefore supplied intact antigens to the intestine for immune processing and subsequent tolerance induction


Now this brings up the thought, especially for perhaps IBD, we ingest lots of antigens,is our digestion too good,once tolerance is broken.

Should we, take some sodium bicarbonate with each meal.

The idea is partial breakdown of the proteins, not complete, or none.

Another study has shown that inhibition of digestion blocks oral tolerance to ovalbumin. Cimetidine treatment of mice prior to ingestion of ovalbumin leads to decreased tolerance, while oral administration of pepsin-treated ovalbumin to cimetidine-treated mice results in immune unresponsiveness (Jain and Michael, 1995). Taken together, these findings suggest that an intermediate level of digestion is optimal for tolerance induction
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