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My dummest farfetched UC theory yet.

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Posted 9/3/2014 5:49 PM (GMT 0)
This might be my own theory,not sure if anyone else has thought of it for IBD.

Probably has no basis in reality,but what the heck,just spitballing here.

NSAIDS cause a form of colitis/IBD one's like Ibuprofen inhibit both cox1 and cox2 which seems to be the worst case.

As opposed to specific cox1 or cox2 inhibitors,by themselves at lower doses.

Just suppose a what if. Guess what, there are dietary cox inhibitors.

You eat enough of certain foods,veggies,fruits that inhibit cox1 or cox2,and perhaps take some nsaids along the way,and also happen to eat a lot of fats.

Any help from the forum biochemists appreciated to sort this out,if there is any validity.

Totally out of the box.
So if you suppress cox might get colitis,if you continue to suppress cant resolve inflammation,once inflammation
resolved then need to suppress,anything make sense here.
No I have not been drinking.

Old Mike
if this is going on with gluten what else is going on
http://www.greenmedinfo.com/blog/could-popular-pain-killer-be-causing-celiac-disease

Cox2 seems to be necessary to resolve inflammation,but prolonged

upregulation is a problem.

http://gut.bmj.com/content/52/12/1714.long

human uc PGD2 prolonged upregulation in remission

http://www.pnas.org/content/107/26/12023.full.pdf

nsaids also mess with B cells and antibody production

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2693360/

and human colitis read down

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1664160/pdf/bmj00203-0051c.pdf

curcumin

http://www.ncbi.nlm.nih.gov/pubmed/11566484

more dietary

http://www.chiro.org/nutrition/FULL/Natural_COX-2_Inhibitors.shtml

vitamin D
http://www.ncbi.nlm.nih.gov/pubmed/24619416
vitamin c
http://www.jimmunol.org/cgi/content/meeting_abstract/178/MeetingAbstracts/S88-a
B6
http://www.spandidos-publications.com/etm/2/3/419

more dietary see table one the lower the number the less it takes to inhibit

http://webcache.googleusercontent.com/search?q=cache:aYK0_G7af6UJ:www.plosone.org/article/info%253Adoi%252F10.1371%252Fjournal.pone.0076452+&cd=5&hl=en&ct=clnk&gl=us

more see table 5

http://www.itmonline.org/arts/lox.htm

cox2 mice

http://www.luzimarteixeira.com.br/wp-content/uploads/2009/09/artigo28-nutricao.pdf

cox2 mucosal protection and healing,just click on PDF to get full paper

http://www.hindawi.com/journals/tswj/2006/941592/abs/

cox 2 inhibitors human ibd, short term does not seem to be a problem,or not enough data

http://www.ibdwatch.com/symptoms/role-selective-cox-2-inhibitors-exacerbation-ibd/

more after all these studies they are still not sure

http://hal.archives-ouvertes.fr/docs/00/53/49/90/PDF/PEER_stage2_10.1007%252Fs00228-009-0719-3.pdf

cox2 and colon cancer

http://www.ncbi.nlm.nih.gov/pubmed/16251413
Posted 9/3/2014 7:37 PM (GMT 0)
Hey, that's how you solve problems, by thinking outside the box. I see nothing wrong with the theory, particularly in my case. Most here know that I believe my UC came about by the use of broad spectrum antibiotics. I was going through a period of extremely high stress and went to the hospital one night with sore throat, migraine headache, and a temperature which couldn't get under control. They really couldn't figure out what was wrong with me and put me on broad spectrum antibiotics and high dose Ibuprofen (I always avoided NSAIDS due to my previous autoimmune disease). I got better and was released. I started having diarrhea right there in the hospital, which they chalked up to the antibiotics and said it would go away once off them. It didn't and later on we finally figured out that I had mono (EBV) and a couple of months later still having diarrhea, was diagnosed with UC. I still blame the antibiotics but who knows, maybe I had the perfect storm of triggers, including Ibuprofen.
Posted 9/3/2014 7:59 PM (GMT 0)
Doesn't sound dumb..

This small study says " All patients experienced flare-up of their underlying IBD within 6 weeks of initiating COX-2 therapy" onlinelibrary.wiley.com/doi/10.1097/00054725-200407000-00005/full "The spectrum of gastrointestinal toxicity and effect on disease activity of selective cyclooxygenase-2 inhibitors in patients with inflammatory bowel disease"

What is confusing to me though is that I thought aspirin was a cox inhibitor yet mesalazines help UC for many, this extract may help explain the difference though as mesalazine is salicylic acid rather than full aspirin
qjmed.oxfordjournals.org/content/94/8/445.long "Salicylic acid: a link between aspirin, diet and the prevention of colorectal cancer"

Trying to read this one but finding it really confusing www.annalsgastro.gr/index.php/annalsgastro/article/viewFile/295/264 "Cyclooxygenase-2 inhibitors and inflammatory bowel disease" - possibly something got lost in translation!
Posted 9/3/2014 8:45 PM (GMT 0)
Just so we are on the same page here.
We all know that NSAIDS can induce colitis,or cause flairs.
Depending on the NSAID can inhibit cox1 or cox2 or at a high enough dose both.

What I am trying to say is that perhaps dietary cox inhibitors if you eat enough might also
cause a problem.
Perhaps why they cant figure out good ibd diets,or why vegens get UC,or why if you switch to paleo
some go into remission.
Perhaps some just eat the wrong high cox inhibiting veggies and fruits,along with high fat.
Since say 1900 we are exposed to many more fruits and veggies from other parts of the world,
than we were prior,also food supplementation from about 1950 or so.
Like I said up front,may have no basis in reality.

Old Mike
Posted 9/3/2014 8:48 PM (GMT 0)
Which foods are cox inhibitors?
Posted 9/3/2014 9:06 PM (GMT 0)

I posted these above in that mess of studies.

OM

more dietary see table one the lower the number the less it takes to inhibit

http://webcache.googleusercontent.com/search?q=cache:aYK0_G7af6UJ:www.plosone.org/article/info%253Adoi%252F10.1371%252Fjournal.pone.0076452+&cd=5&hl=en&ct=clnk&gl=us

more see table 5

http://www.itmonline.org/arts/lox.htm

citrus compounds

http://li123-4.members.linode.com/files/Citrus%20Compounds%20Inhibit%20Inflammation-%20and%20Obesity-Related%20Colon%20Carcinogenesis%20in%20Mice.pdf

curcumin

http://www.ncbi.nlm.nih.gov/pubmed/11566484

more dietary

http://www.chiro.org/nutrition/FULL/Natural_COX-2_Inhibitors.shtml


vitamin D

http://www.ncbi.nlm.nih.gov/pubmed/24619416

vitamin c

http://www.jimmunol.org/cgi/content/meeting_abstract/178/MeetingAbstracts/S88-a

B6

http://www.spandidos-publications.com/etm/2/3/419

Posted 9/3/2014 9:15 PM (GMT 0)
Well - I do recall that they are kinda like the serotonin and dopamine thing - There is an "up one" and down "one". So if you decrease one then the other increases and visa versa... It's all about balance to maintain or signal certain cellular processes. I'm not 100% on this but pretty darn sure.

I think things like bacteria cause an increase in COX-2 yet a decrease in Cox-1 or visa-versa.... If you effect both however, like decrease substantially both, that's where the trouble would start to occur.........

So like you said, at a high enough dose some NSAID's I guess effect both (I didn't know this). So this would be why they maybe set-up trouble for bacteria invasion etc.

I have to look it up in my text later on. See what it says to verify.

QUICK EDIT: I think when both are inhibited it reduces response to bacteria via inflammation etc and effects the permeability of the mucus barrier - or epithelial barrier... Not sure if food would be able to do this as well - effect both that is.
Posted 9/3/2014 10:35 PM (GMT 0)

This idea probably a waste of time since the Faroe Islands have the highest rate of IBD in the world,yet

not a lot of veggies in the diet.

But then again now that I think about it,their whale meat mess may just be another cause.

We are also exposed to this stuff but, don't eat it at the same concentrations that I expect they do if

they eat a lot of whale meat. I have been trying to find reasons for their high IBD incidence,perhaps

the toxic whales. The also import a lot of meat from Denmark, high MAP.

Highest IBD incidence in the world. Gee you would think the docs might look at this more.

http://www.ncbi.nlm.nih.gov/pubmed/23695429

OM

http://en.wikipedia.org/wiki/Faroese_cuisine

but they eat a lot of whale meat contaminated with mercury,pesticides and pcb's, also have MAP in herds.

Looks like this toxic mix is really wrecking their immune systems.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3417701/

http://www.newscientist.com/article/dn16159-faroe-islanders-told-to-stop-eating-toxic-whales.html#.VAeYs2d0wq0


Post Edited (Old Mike) : 9/3/2014 5:50:41 PM (GMT-6)

Posted 9/4/2014 3:19 AM (GMT 0)
www.theglobeandmail.com/report-on-business/beekeepers-plan-to-sue-pesticide-makers-over-bee-deaths/article20319629/

So finally we have a law suit against the two big pesticide manufactures - who knows where it will go. Anyway, I was curious if you ever came across anything in regards to a route similar this in all the COX stuff. Or I wonder what pesticide use is like in the Faroe Islands. Reason I mention it is because in the article above it mentions that Neonicotinoids are suspected of making bees more susceptible to pathogens....... and they become present in all parts of the plant.... So maybe they have a similar effect on us.

Canada is number #1 or #2 in IBD incidence in the world and it clusters around agriculture here.
Posted 9/4/2014 5:08 AM (GMT 0)
Hadn't used many NSAIDs, if any, when I got my UC. Sounds like a long shot to me, but certainly a valid theory, i might have counsumed one NSAID or two prior my diagnosis, nothing I recall tho. Im more into my own theory that it has got something to do with hormones...
Posted 9/4/2014 6:58 AM (GMT 0)
Mark have not ran across anything specific,but we do know that pesticides are endocrine disruptors,in humans. The whales since they are at the top of the food chain bio-accumulate all these toxins.
Both Canada and the Faroe Islands are north, so less sun,so less vitamin D which acts as a hormone.
OM
Posted 9/4/2014 8:56 PM (GMT 0)
natural cox 2 inhibitors seem to help me..cabbage, curcumin, vitamin d.
Posted 9/6/2014 11:21 PM (GMT 0)
/www.youtube.com/watch?v=EpMvDe8-qsM

Posted this on another thread but then watched it again as I have not for some time. Upon watching it, I came across their reference to the Fareo Islands near the end of it so though I'd put it here as well. The whole thing all the way through just reminds me so much of the MAP thing.
Posted 9/7/2014 3:56 AM (GMT 0)
I was living on Advil prior to UC, migraines.

I too often wondered about a simple cause like this.
For example, something environmental or dietary causes minor mucus barrier compromise, which sets of a snowball effect cascade to full blown UC though only in people genetically susceptible to an immune overreaction. They give meds to decrease the inflammation but they do not fix the root cause.

Not everyone who is generically susceptible gets uc, but what if their mucus membranes were to be experimentally compromised, with that chemical they give rats, would they then get chronic uc? Whereas non susceptible people would heal and go on healthy? Anyone know the answer?

What ir it were as simple as 1. Use meds to stop inflammation and allow environment for proper bacteria to flourish. 2. Feed these bacteria substrate for butyrate; rebuild mucus membrane; remove original offending substance(or activity)(if such applies or can be identified) After many months, stop meds and live healthily ever after.
Wishful thinking, I know
Posted 9/7/2014 10:31 AM (GMT 0)
CDN26:


Why yes,maybe,this guy had colitis induced by too much ibuprofen, he recovered,even after quitting smoking

7 years prior to getting sick.  This is a barrier disruption and recovery. I will try and dig around for more

chemically induced colitis.  A question might be is this really ulcerative colitis as we know it or something like it.

Never the less it is a barrier disruption.  Perhaps the trick here is that the offending agent is removed quickly or it is only a one time event, and treatment starts immediately. Where in some cases UC starts kind of gradually and people may go for years before it is diagnosed. A key might be immediate treatment before lots of damage is done,but if you don't know your colon is sick until it is too late,then perhaps a problem.

So it would seem as in the WT wild type mice when exposed to DSS then recover, also most humans recover

from a chemically induced colitis,unless the damage is so severe that the colon is actually destroyed.


This thread not useless after all.  What else might this mean.

Genetics/epigenetic changes, unknown infection,poor immune response, MAP infection,over aggressive immune response, immune response will not shut off, continuous exposure to some dietary factor,combined disruption from say antibiotics which thin mucus and also kill of bacteria which take a long time to recover. Probably many other possibles that I have not though of right now.

So this takes us back to full circle,don't know,but until MAP is finally ruled out once and for all,who knows.

The multiple effect of antibiotics is interesting,where you get at least two types of disruptions, at once.


Old Mike

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1664160/pdf/bmj00203-0051c.pdf

this might be a good one but cant get the paper,but the abstract does say most recover

http://www.ncbi.nlm.nih.gov/pubmed/18209577

http://www.ncbi.nlm.nih.gov/pubmed/19104938

http://www.ncbi.nlm.nih.gov/pubmed/16498283

coffee enema

http://www.ncbi.nlm.nih.gov/pubmed/19077527

soap

http://www.ncbi.nlm.nih.gov/pubmed/3489329

as you can see depending on what is used the colon can be pretty much destroyed,I always say watch

what the hell you put up your butt.

http://www.ncbi.nlm.nih.gov/pubmed/16615621

here is a hydrogen peroxide enema where the guy fully recovered.

Take note that before they invented DSS colitis for mouse studies back in the 1950's or so, the would induce

colitis in the mice with hydrogen peroxide.

http://www.ncbi.nlm.nih.gov/pubmed/21873825

another soap enema

http://www.ncbi.nlm.nih.gov/pubmed/3775481

could list more

 

Post Edited (Old Mike) : 9/7/2014 10:01:51 AM (GMT-6)

Posted 9/7/2014 2:00 PM (GMT 0)
I was thinking about it this morning - Has anyone ever tired or have you ever come across a case study for someone with Ulcerative Colitis that has responded to multiple long term antibiotics? So not bacterial colitis, but Ulcerative Colitis.

We know there's been some success with Crohn's in this area. Was curious. For some reason long term Vancomycin rings a bell but what about other antibiotics with it as well.
Posted 9/7/2014 2:25 PM (GMT 0)
Well here is one from our site.

But did she really have UC like the rest of us, or some unknown bowel infection,or do we have some unknown

bowel infection.

Antibiotics seem to work better for chohns, but in the small intestine the bacteria loads are so much lower than what is going on in the colon. We also have biofilms to contend with in the colon,makes it hard for antibiotics to get

at everything.  There is some medical info on antibiotics and UC but not that much,and not too many great results.

OM

https://www.healingwell.com/community/?f=38&m=1689855

Posted 9/7/2014 3:15 PM (GMT 0)
It interesting that in Miracles post on that thread she was normal within 2 days.... But only for 2 days. We all know how rough a go she has had with it.

I wonder what would have happened if she were able to continue it long term.
Posted 9/7/2014 3:22 PM (GMT 0)
I think in real cases of true UC antibiotics aren't going to be of much help. If something bacterial is going on that would respond to antibiotics (such as C-Diff) then antibiotics might help. It's also possible that some or many cases of UC that are bacterial in origin may not respond to any antibiotics at all because there might not be any known antibiotic that would work, even if you knew exactly what the bacteria (or virus) was. I was originally afraid my UC might be a response to EBV (might still be) but there is no known way to eliminate the EBV virus. Also, one theory of the immune system failure is that antibiotic use has forced a mutation in some bacteria or virus that is normally present in our systems and this mutation continues to be the norm and our immune system is forever trying to attack and kill this "new" mutated virus or bacteria, never being able to kill it off.
Posted 9/7/2014 3:55 PM (GMT 0)
I've seen some threads here where people claim to have been helped by antibiotics. Flagyl cleared up all my symptoms while I was on it, but that was short term. We know probiotics and fecal transplants CAN have an effect...the effect is not the same all across the board, but the effects can result in remission.

I've been looking up what research has been done on bacterial antigens in UC. Seeing as how with that recent IgA coating study, it has been really difficult to identify what sorts of bacteria are being reacted with in UC in general, and the fact pANCA antibodies do, in fact, react with major species of commensal bacteria... I honestly think it is possible that there is a bacterial cause of UC if not in all people, then just a subset of those with what is now called UC and it's just extremely difficult to figure out what is going on because we are only just discovering the intricacies of our gut's microbial makeup. I think the reason a bacterial cause has been so difficult to identify is because we have not had the tools to properly visualize and assess these things

This is the pANCA study i'm reading right now, btw: http://iai.asm.org/content/68/3/1542.full

I would guess that if UC is microbial in nature, then the efficacy of probiotics and fecal transplants depends on what the makeup of your gut, and what is contained in the fecal matter or probiotics that will determine how you respond.

Another probably weak connection i've made, but interesting to me anyway, is that often those with UC have extra-intestinal symptoms, like arthritis, which has been linked with certain gut bacteria. I had an episode of reactive arthritis after my gut infection last year, and its a known phenomenon. I suspect some sort of molecular mimicry (immune system reacts to antigen on bacteria, and then the immune system attacks similar looking antigens all across the body) situation is going on with the appearance of extra intestinal symptoms in UC.

Post Edited (Tunnelvisionary) : 9/7/2014 9:58:25 AM (GMT-6)

Posted 9/7/2014 4:27 PM (GMT 0)
This thread got me thinking again,antibiotics of course kill bacteria,but when the bacteria lyse they release

lots of endotoxin,just suppose we react not only to antibiotic released endotoxin,but exogenous endotoxin.

 I may start a separate endotoxin thread. I also know that it is very difficult to remove

endotoxin from water,and yes it may be in your normal tap or bottled water.

Will have to do more research before I start another thread, but out of the box we go.


As a side thought,suppose our immune system is killing off lots of bacteria,these will release endotoxins this making us sick,more bacteria penetration more killing,more endotoxins.

Suppress the immune cascade with pred,and 5asa drugs which are biostatic and we can go into remission.

So immune suppression,less bacteria killing,less endotoxin,less inflammation.

Have not read enough yet to make any real concrete theory.

Old Mike

here is something on endotoxin and absorbants, you will also notice one way to lower the colon load is lavage.

http://gut.bmj.com/content/34/1/51.full.pdf


and from my alkaline phosphatase thread

http://onlinelibrary.wiley.com/doi/10.1002/ibd.21161/full


will use this post as a storage area for endotoxin papers,so if I decide to start a new one info will be

easy to find.

http://www.biostrategics.com/kpmgendo.pdf


exogenous endotoxins

http://nutritionfacts.org/video/the-exogenous-endotoxin-theory/


as an exohormone

http://www.ncbi.nlm.nih.gov/pubmed/16237650


fat

http://diabetes.diabetesjournals.org/content/57/6/1470.full


and fever,interesting when I get sick anymore I don't really get much of a fever

http://jp.physoc.org/content/548/3/929.long


 

Post Edited (Old Mike) : 9/7/2014 12:34:07 PM (GMT-6)

Posted 9/8/2014 6:41 AM (GMT 0)
Endotoxin is an interesting angle to view IBD from... will check out these papers

OM, I remember a while back you asking why UC starts in the rectum. I came across this abstract suggesting a hypothesis as to why UC starts in the rectum. www.ncbi.nlm.nih.gov/pubmed/11768558

Also interesting that they mention colitis doesn't happen in a germ-free environment in animal models.

Don't know if this is helpful, but thought you might find it interesting.

Post Edited (Tunnelvisionary) : 9/8/2014 12:44:30 AM (GMT-6)

Posted 9/8/2014 12:32 PM (GMT 0)
Interesting, but from 2001. I wonder what their definition of a germ is?
Posted 9/8/2014 3:43 PM (GMT 0)
I have mentioned this before - but the interesting thing about Ulcertive-Colitis is that in germ free mice, even though they don't get Colitis, they still have a very thin layer of MUC2 type firm mucus (or the inner layer). It's quite thin due to the lack of any bacteria present in the colon.

All it takes is not even the bacteria itself, but simply exposure to endotoxin, so this can be either LPS (lipopolysaccharides) or PGN (Peptidoglycan) to generate a normal inner layer.

So within 40 minutes of exposure of Germ Free mice to bacterial exotoxin they spontaneously develop a firm inner layer of mucus that is exactly the same as conventional mice.

This to me, shows one of the main problems in Ulcerative-Coltis - this response isn't working. Something is effecting this ability to generate a protective firm inner mucus layer - or any mucus at all really. To me I have always thought of "infection" versus this process just shutting off one day.
Posted 9/8/2014 4:17 PM (GMT 0)

garylouisville said...
Interesting, but from 2001. I wonder what their definition of a germ is?

It's from 2001, not the 18th century Gary tongue

No but really, what do you mean by that question? Like what their definition of germ-free environment is?

Canada Mark said...
I have mentioned this before - but the interesting thing about Ulcertive-Colitis is that in germ free mice, even though they don't get Colitis, they still have a very thin layer of MUC2 type firm mucus (or the inner layer). It's quite thin due to the lack of any bacteria present in the colon.

All it takes is not even the bacteria itself, but simply exposure to endotoxin, so this can be either LPS (lipopolysaccharides) or PGN (Peptidoglycan) to generate a normal inner layer.

So within 40 minutes of exposure of Germ Free mice to bacterial exotoxin they spontaneously develop a firm inner layer of mucus that is exactly the same as conventional mice.

This to me, shows one of the main problems in Ulcerative-Coltis - this response isn't working. Something is effecting this ability to generate a protective firm inner mucus layer - or any mucus at all really. To me I have always thought of "infection" versus this process just shutting off one day.

I remember reading this! But I forget where.

Can they remove a mouse's ability to generate mucus very well? Are there mice with defects in mucus production available for UC study? That seems like it would be more useful to study than the DSS models they use right now.
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