New Post by Dr. Chamberlin: Microbial Infection and Dysbiosis - All Part of the Same Process

[irishgal]

Thought some of you may find this new post by Dr. Chamberlin interesting. He attempts to use complexity theory to reconcile the dysbiosis and infectious theories of Crohn's disease. I know I've had this question many times: Is it a single infectious cause that AMAT fixes or is it the overall microbiome that benefits from AMAT.

This is not a research study, but more of an editorial opinion. Still, he is knowledgeable and progressive in his treatment of Crohn's disease, and I think he's a valuable source of information.

http://thecrohnsinfection.org/presenter-blog/

 

[wild_one353]

both scenarios are plausible, and in fact both are eventually true simultaneously in IBD. and infection by bacteria could overcome some good bacteria in the gut and render them extinct or vice versa, the good have been damaged and eventually you'll encounter a pathogen which further mess things up.

Scientists are still working out the terms on this new area of research and a differentiation between the terms dysbiosis and lack of diversity in good bacteria/extinction must be acknowledged. and also there is a increased diversity of pathogens as well that there has not been any terms coined yet by scientists that im aware of, all these can be generally referred to as dysbiosis, where a healthy gut ecosystem is known as eubiosis.

I'm still believing that a fecal Transplant that restores the healthy diversity that was lost, will overcome any pathogen. But getting rid of the pathogen by any other means, is only another treatment and not a cure.

 

[D Bergy]

Unless the pathogen or pathogens are responsible for more than just symptoms.

No one knows for certain.

Dan

 

[JMC]

I'm still believing that a fecal Transplant that restores the healthy diversity that was lost, will overcome any pathogen.

Except if you have a genetic mutation which means that your innate immune system cannot eliminate certain intracellular pathogens, in which case it will not.

 

[xeridea]

Except if you have a genetic mutation which means that your innate immune system cannot eliminate certain intracellular pathogens, in which case it will not.

I'm on board with this, except I don't understand why the dramatic growth in incidence of the disease. We don't evolve that fast for the mutations to take off at that pace.

 

[JMC]

I'm on board with this, except I don't understand why the dramatic growth in incidence of the disease. We don't evolve that fast for the mutations to take off at that pace.

I think this is a question that still requires a good answer. From my perspective, there are a number of possibilities:

1. The introduction of anti-biotics has caused rapid mutations of the bacteria causing disease. I believe this is what John Aitken is hinting at.
2. As we have dealt with one mycobacterial infection, Tuberculosis, the next one has appeared. I think it is telling, that in countries where you have a high incidence of Tuberculosis, you do not have Crohn's and vice versa. Viewed like that, the stats look different.

 

[irishgal]

Speaking of TB, the second half of The Forgotten Plague is here:
http://thecrohnsinfection.org/presenter-blog/

From my perspective, reading this book with Crohns disease and being successful with AMAT, the parallels are scary. I wonder if Crohn's and TB are bit mutually exclusive since they are both intracellular macrophage infections. Maybe only one mycobacteria can inhabit the same space at once. In fact, I hope this is the case since having both would be a nightmare. These mycobacteria are nothing to be trifled with.

 

[JMC]

I wonder if Crohn's and TB are bit mutually exclusive since they are both intracellular macrophage infections. Maybe only one mycobacteria can inhabit the same space at once.

I think this is probably right, you get one or the other. I also believe this is how Dietzia may work. If you get infected with a harmless mycobacteria, it "crowds out" the nasty ones.

 

[irishgal]

I was thinking about MAP/TB and competitive inhibition, and while it makes sense in some regards, I'm not sure if it's the case. I recall early in my AMAT research coming across a study which showed when people were treated for TB their Crohn's improved. Wish I could find the reference!

 

[irishgal]

New post by John Aitken: Victory
http://thecrohnsinfection.org/presenter-blog/

 

[kiny]

The chicken or the egg problem, is dysbiosis causing inflammation and allowing pathogens to colonize, or is the pathogen the precursor to inflammation and does inflammation-induced dysbiosis follow...is not an interesting question I think.

It doesn't help us patients. It won't help prevent future patients. Are we going to preemptively screen everyone's stool for a possible microbial unbalance? Without even understanding what that balance should be? Give everyone stool transplants without really understanding what we're doing? Risk of bacteremia and worsening of the disease? Check every foodsource, mental state and lifestyle that might lead to dysbiosis? That's a monumental task that probably isn't going to lead to real treatment.

A lot of money and research grants have gone into studying the gut flora of people with crohn's disease, and this has lead to exactly 0 treatment.

We know people with crohn's disease have both dysbiosis and opportunistic pathogens. AIEC takes advantage of dysbiosis, rats with antibiotic-induced dysbiosis are easily colonized with AIEC, rats without are not. But once these pathogens are present, they are intracellular, they infiltrate the peyer's patches and infiltrate macrophages in the intestinal wall, I do not believe that the microbiome is very relevant at that point.

The treatment needs to directly target these pathogens, not indirectly through altering the microbiome, which could lead to more problems than solutions.

People with crohn's disease often go into remission with treatment, and this is accompanied with normalization of the gut flora, yet the disease is still there. It is likely just a side effect of the inflammation subsiding. Normalization of the gut flora does not cure this disease. The inflammation is transmural, it is deep within the intestines, it is not caused simply by dysbiosis.

 

[JMC]

A lot of money and research grants have gone into studying the gut flora of people with crohn's disease, and this has lead to exactly 0 treatment.

YES! This is exactly the point I keep making. The microbiome research is too vague with no clear objective or direction leading to treatment. A research scientist dream, some might say, and a patients nightmare.

 

[irishgal]

Kiny and JMC - yes yes yes!! Exactly. Very frustrated by the microbiome research myself. Target the pathogen, make the patient better. People need help NOW, not in ten years. AMAT has worked beautifully in my case. Gave me a life I never thought I would have. If it worked for me, maybe it would work for a percentage of other patients too. Why not at least consider the option, imo.

 

[D Bergy]

I don't disagree with the above, but there might be something to be learned over time by studying the microbiome. For instance, preventing the disease in the first place.

I agree that killing the suspect bacterium directly is likely the only real hope of resolving symptoms and more importantly future damage from an already entrenched disease.

I believe that applies to most disease.

Dan

 

[mf15]

Early onset crohn's seem to be dysbiotic from the get go.
I could guess that the symptoms don't get bad enough,to realize there is a gut problem until the dysbiosis reaches a certain tipping point.
Old Mike

http://www.ncbi.nlm.nih.gov/pubmed/24629344

 

[kiny]

Early onset crohn's seem to be dysbiotic from the get go.

Well, inflammation tends to lead to dysbiosis. There is dysbiosis in intestinal TB, but no one blames the disease on dysbiosis, everyone agrees the dysbiosis is a symptom of the inflammation, not the other way around.

Relatives of people with crohn's disease, at high risk of developing crohn's disease do not simply have dysbiosis leading to disease. They have a very specific immune response to E Coli prior to disease: http://www.ncbi.nlm.nih.gov/pubmed/16618402 . There is no data associating OmpC antibodies with AIEC, but it is associated with ileal disease. OmpC could very well be associated with AIEC.

Early inflammation in crohn's disease is very specific, nothing that can be easily explained with dysbiosis. Very specific inflamed lymph follicles.

Genetic studies in crohn's disease point to specific genes, NOD2 and ATG16L1. Intracellular expression.

The age of onset in crohn's disease is not random, it's around the age of 13-18, the ages when the peyer's patches and m-cells are the most active.

The place of disease is not random either, the majority of people with crohn's disease have ileal involvement, not everywhere in the body, like you would expect with dysbiosis. No, the ileum, a very specific region. One of the interesting things about the ileum is that it is in the only place where peyer's patches occur.

 

[kiny]

Why do people with crohn's disease have deep transmural inflammation? Why do some people have fistula? Why are so many of the genetic predispositions related to intracellular bacteria. Why do people often develop aphthous ulcers in their mouth? Why do the tiny wounds created by biopsies, heal slower and differently in people with crohn's disease?

Why does bloodflow affect the outcome of the disease? Why does giving Viagra to crohn's disease patients, increasing blood flow, help them?

 

[D Bergy]

The sticky blood pretty much covers the reason for the slow wound healing.

Having read quite a lot on biofilm involvement in Lyme disease caused me to thin out my blood using supplements. That and the tendency in my family to get blood clots in random places. Also being the slowest blood donor in history. I knew before my diagnosis my blood was like pancake syrup.

I don't know all the reasons, but you can correct some of these things without drastic measures.

As far as the disbiosis thing, there could be just one strain of some unknown bacterium that tips the scales one way or another. All these organisms compete for space. It is possible one strain of bacterium X kills invasive E-Coli or limits it's spread. It is way too early into the research to really draw any conclusions one way or another.

Like you said already, it doesn't help anyone in the here and now.

It is interesting, but if I can't test it or make use of it, then it's just pure speculation and has no practical value at this time. I guess the home fecal transplant is always an option, but I am doing good now so I am not going to upset that apple cart.

I do think important things could be learned, but they may not necessarily be of any use to us in particular. Who knows?

Dan