Article: Scientists find key link between viruses and inflammatory bowel diseases

Thanks for sharing.

We all try probiotics and antibiotics with varied levels of success. What else would be an option?

To the question: "We all try probiotics and antibiotics with varied levels of success. What else would be an option?"

Well, maybe antivirals at the right time followed by the needed probiotics. The problem in my opinion is, there is no probiotic protocol for IBD, because gastros and big pharma ignore this avenue of treatment. So everyone is left to themselves to blindly experiment with probiotics. But are we taking the right ones in the right amount to rebalance? I would guess probiotic treatment would need to be customized to each patients microbiome issues. And once we do rebalance what might be the best maintenance treatment.

DBwithUC said...
you do not grasp the basic science. You seem to start with the agenda that IBD should not be auto-immune despite all the massive evidence from genetics to antigens that it is an auto-immune.

What massive evidence? Here is a public presentation on Crohn’s Disease by Dr Marcel Behr of McGill University, on May 28, 2014.

He says there is little or no evidence that IBD is an autoimmune disease. The latest scientific studies indicate that it is an immune deficiency disease, a deficiency against one particular type of bacteria. The signs point that it may be a mycobacteria, the same type of bacteria that causes tuberculosis and leprosy.

Yes immunosupressants help with IBD, but they are also effective to curb inflammation in meningitis, tuberculosis, and leprosy which clearly are infectious diseases.

I am not sure if he is correct because so far nobody has come up with a cure. But at the very least we can say that the scientific consensus is moving away from IBD as an autoimmune disease.

/www.youtube.com/watch?v=7x3lq8QEg5g&feature=youtu.be
”The latest double-blind scientific studies indicate that the theory of an overactive immune system should be discarded along with other obsolete explanations such as in the 1950's when it was assumed that IBD was 'all in your mind', a psychosomatic disorder and the recommended treatment was a psychiatrist.

"Although the autoimmune theory has been unequivocally dismissed for over 20 years, many physicians and gastroenterologists cling to this theory - the medical community has historically been slow to change"

IamCurious said...
... there is little or no evidence that IBD is an autoimmune disease. The latest scientific studies indicate that it is an immune deficiency disease, ...

this is just wrong.

The MAP camp has lobbied hard for an immune-mediated effect in Chrons, but some of their science is dodgy. But even still for UC, any auto-mediated effect is lesser than the auto-immune effect.

/inflammatoryboweldisease.net/living/ibd-autoimmune-condition/ said...
While the specific mechanisms of both of these aren’t completely understood in terms of IBD, there is evidence of both in Crohn’s and UC, with Crohn’s showing more of the immune-mediated side, and UC showing more autoimmune properties

this is a side issue, because my point was that the confirmation of commensal viruses alongside commensal bacteria, or even the evidence that the viruses are also in dysbiosis, in no way suggested that a virus was causing UC. That is a complete misreading of the research.

This is always interesting despite it often leaving more questions than answers. Any progress made in understanding IBD is good with me.

My hypothesis has been that our immune system is somehow weaken (this article suggests that a virus or some sort is responsible) and then inflammation is able to occur. I have not been exposed to anything abnormal so that makes me think it is more my ability to fight inflammation is lessen compared to my peers.

Also, not sure if anyone else saw, but RedHill Pharma presented their Phase 3 trial information for their RHB-104 treatment for Crohn's patients. Originally the data was very exciting, 26 week remission rate was 37% compared to 23% for placebo. The big problem was the 52 week remission which dropped to 27% compared to 20% for placebo. The market didn't like the news, the stock was originally up 50% on the 26 week remission news but later dropped once the 52 week news were covered on the conference call.

As it relates to us, I still think this is a good thing. You can never have too many treatment options. Doesn't this drug just show that treatment effectiveness dropped overtime like all of our meds do? I can understand why Wall Street wasn't happy, but I still think it is good news given the 26-week remission rate.

I think in the end we do not know with 100% certainty whether UC is autoimmune or is not. So I do not think there is right and wrong in that matter. It's true to say that research is trending in one direction or another, but I don't believe anything has been ruled out forever. Responding to immune-suppressing meds means there is an immune involvement in the process but doesn't necessarily mean that's the cause of all that troubles us (might be a symptom?). Same with our wacky bacteria makeup (a cause or a symptom?). Lots of what came first the chicken or the egg, kinda stuff...

I'd say that you/I are born with a genetic-deficiency related to our immune system function that when triggered epigenetically (that is exposure to antibiotics, a specific virus, a bacterium, etc. that causes a cascade of things that ultimately leads to an UC) causes our immune system to go crazy and mount and endless attack. Whether that deficiency leads to a lack of bacterium diversity, a tendency to have a permeable mucosa barrier, or a tendency to attack a common bacteria *shrug* who knows. I could be wholly wrong.

I find the research interesting, and equally find the laymans reports lacking in understanding the importance of research amusing. I just hope they figure this out in my lifetime, but not exactly hopeful.

FMT does not just replace bacteria, but fungi,yeast,phages and virus.

Too bad it does not put everyone into remission.

On the subject of MAP, most all IBD drugs also suppress MAP even biologics.

MAP may just be a bystander, or as a bystander make things worse.

They should be able to determine causes better with identical twin studies,where one has
IBD and the other does not. More work needs to be done with twins.

here is a german twin study, gut infections seem to possibly stand out.
/academic.oup.com/ecco-jcc/article/6/1/29/2392166

now this one for crohns indicates a genetic immune deficiency against mycobacteria
/www.sciencedirect.com/science/article/pii/S1521691814000535

oldmike

Post Edited (Old Mike) : 7/31/2018 8:35:24 AM (GMT-6)

There is some confusion...

The gut comprises luminal bacteria (including outer mucus layer), and mucosa associated bacteria (inner mucus layer).

FMT uses donor stool, comprising a small selection of luminal bacteria.

Only a small number of strains persist after FMT. The effect of loading the bowel with mostly transient, luminal bacteria via FMT, is unclear. However, it does not generally alter the composition of the mucosa associated bacteria.

It is effective for c-difficile, which is predominantly a luminal infiltrative bacteria.


It is a broad approach that may help a portion of UC sufferers (rarely Crohns) by re-balancing luminal populations.

The contention is whether it alters commensal mucosa associated bacterial population or diversity.

It's unlikely that UC (and certainly not Crohns) is a reaction to luminal bacteria.