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Crohn's Disease Forum » Diet, Fitness, and Supplements » SCD and Paleo Diets » Rush University Medical Center recruiting participants for study on the SCD diet


02-13-2013, 07:55 PM   #1
Ya noy
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Rush University Medical Center recruiting participants for study on the SCD diet

Rush University Medical Center is recruiting participants to take part in a clinical study to determine whether the SCD diet changes the intestinal flora. Home study, no travel required,


See link: http://www.rush.edu/rumc/page-1298328953440.html


details below



Clinical Trial Protocol ID
10051005-IRB01

Clinical Trial Investigator Name
Ece Mutlu, MD

Clinical Trial Title
The Specific Carbohydrate Diet: Does it change the intestinal microbiota and metabolome?



Clinical Trial Protocol Description
This study is currently recruiting subjects who are not on the Specific Carbohydrate Diet or a similar diet. Each subject must fill out surveys and send in two stool samples and one urine sample. This study can be done completely from home and does not require presence at Rush University Medical Center. All subjects will receive results of DNA analysis of stool.



Clinical Trial Eligibility Criteria
Subjects must be 8 years old or older, have a mailing address in the USA and have a formal diagnosis of either Crohn's disease, ulcerative colitis or indeterminate colitis.
02-13-2013, 08:05 PM   #2
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I hope you don't mind, but I've moved this to the SCD/Paleo section we now have!
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02-13-2013, 10:51 PM   #3
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wow! Very own sub forum
02-14-2013, 09:18 AM   #4
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That's nice of Rush University Medical Center. Hope some members here sign up and give it a go. Would be nice to hear about their experience with the trial.
02-14-2013, 10:55 AM   #5
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I just found out that the trials are already underway and have been now for over a year. They recruited several hundred participants and I don't know if they're still recruiting. Rush Medical is here in downtown Chicago, and I participated in one of their studies some years back. It was fairly time consuming, but I'm glad I did it.
02-15-2013, 08:52 AM   #6
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Changes in diet tend to change the microflora but not enough to go from one type to another. Theres a number of classifications, interestingly they are not bound to geography. For example a person in Japan can have the same gut flora as someone in Germany they found out even though they do not share a similar diet.

I think maybe a more interesting question is, does changing the gut flora from one type to another matter at all for crohn's disease. There isn't much evidence that the immune response is directed at the gut flora to begin with.

I think if SCD has any efect it might be more down to changes in medium-chain triglycerides and it's effect on the lymphatics, and less with changes in carbohydrate intake. I don't know, I just don't think that if SCD works at all it has to do with changes in the gut flora or because of changes in carbohydrate intake.

If a test does ever research the gut flora after SCD they will likely see changes, any change in diet tends to cause shifts in gut flora, but the question is if it matters for crohn's disease at all.
02-15-2013, 09:56 AM   #7
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I recently did see that a project began looking at the gut microflora of many Americans, with a variety of diets, paleo, vegetarian, vegan, Weight Watchers, etc. Should be interesting to see if they come up with anything related to IBD, that might be helpful for us.

Laura Dolson has a write up on it:

"American Gut Project: What's in Your Gut?"

http://lowcarbdiets.about.com/b/2013...n-your-gut.htm

& the sight can be seen at:

"American Gut - what's in your gut?"

http://www.indiegogo.com/americangut
02-15-2013, 11:32 AM   #8
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If a test does ever research the gut flora after SCD they will likely see changes, any change in diet tends to cause shifts in gut flora, but the question is if it matters for crohn's disease at all.
That is the million dollar question, or maybe more accurately, the multibillion dollar question.

If find it reassuring that this type of research is now being performed, in an effort to determine whether evidence exists or not.

What I feel this forum has made evident to me, is the wide variation in symptoms, as well as in the effectiveness of current medications and other treatments.

Even steroids, prednisone in particular, seems to effect different people in different ways. Causing some to gain energy and lose weight, while it seems to produce the exact opposite effect in others. The cause remains unknown.
02-15-2013, 11:33 AM   #9
Ya noy
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I recently did see that a project began looking at the gut microflora of many Americans, with a variety of diets, paleo, vegetarian, vegan, Weight Watchers, etc. Should be interesting to see if they come up with anything related to IBD, that might be helpful for us.

Laura Dolson has a write up on it:

"American Gut Project: What's in Your Gut?"

http://lowcarbdiets.about.com/b/2013...n-your-gut.htm

& the sight can be seen at:

"American Gut - what's in your gut?"

http://www.indiegogo.com/americangut
Beach,

I read about that study, on this very forum a little while back, and have it bookmarked in my computer, pending the results.
02-17-2013, 07:02 PM   #10
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"There isn't much evidence that the immune response is directed at the gut flora to begin with."

hmmmm, sorry, gotta dispute that, microbes are what the immune system is all about.
The gut microbiota shapes intestinal immune responses during health and disease
http://www.nature.com/nri/journal/v9...l/nri2515.html
"Finally, we present recent evidence to support that disturbances in the bacterial microbiota result in dysregulation of adaptive immune cells, and this may underlie disorders such as inflammatory bowel disease. This raises the possibility that the mammalian immune system, which seems to be designed to control microorganisms, is in fact controlled by microorganisms."

there is plenty of discussion going on about the role of bacteria in jast about every auto-immune diseases , as a protective factor,as a major causative factor and also as a cause
(for example http://www.ncbi.nlm.nih.gov/pubmed/19758226 - "it is proposed that the lower levels [of Vit D] result from chronic infection with intracellular bacteria that dysregulate vitamin D metabolism" [leading to autoimmune disease] )

just five minutes with google schollar and.......

"To establish and maintain a mutually beneficial relationship, the mucosal immune system must enforce tolerance toward the vast non-pathogenic microbiota while simultaneously remaining reactive to potentially pathogenic microbes; the disruption of this delicate balance results in inflammatory bowel diseases"
"These results suggest that counterbalancing dysbiosis using F. prausnitzii as a probiotic is a promising strategy in CD treatment."
"These results show that molecules of the bacterial microbiota can mediate the critical balance between health and disease."
"we describe how the intestinal microbiota is able to influence the balance between pro-inflammatory and regulatory responses and shape the host's immune system"
"Our findings suggest that novel lipids from commensal bacteria may be newly identified triggers promoting the onset and severity of autoimmune diseases"
"One of the major impacts of the mammalian microbiota is its
effect on the development and function of the immune system."
"It seems that we normally develop tolerance to our own flora. Breaking of that tolerance might be involved in the pathogenesis of inflammatory bowel disease."


Trying to isolate a single factor as the 'cause' or 'cure' is pretty simplistic.

I'm liking this theory.

"These diseases probably develop through a hierarchy of causes:

Food toxins damage the intestine and make it leaky to gut bacteria and bacterial proteins.
Malnutrition impairs the immune response to toxins and slows the healing of intestinal injuries. This makes the intestine even more leaky and damaged.
Damaged immunity allows bacteria to penetrate the gut mucosa and infect intestinal cells, and to enter the body and create systemic infections including intracellular infections of immune cells. The immune response to these infections creates an inflammatory environment which makes the gut even leakier. The infections also weaken the ability of the immune system to heal the gut.
Entry of toxins and bacteria into the body leads to autoimmunity. Food toxins conjugate with human proteins and provoke antibodies against the human protein; bacterial proteins that are ‘molecular mimics’ of human proteins engender antibodies that strike both the bacterial and human proteins.
Autoimmunity leads to further damage to the gut and to other tissues, like the thyroid, which are important for immune function and wound healing. Hypothyroidism, for instance, promotes disease progression.
In its early stages, development of the disease may be accelerated by a long course of antibiotics or an infection that causes severe diarrhea. These kill healthful gut bacteria and facilitate their replacement by pathogens.

If we prioritize these in terms of damage caused, then ulcerative colitis is an infectious and autoimmune disease, since these two factors do the most severe damage. It is generally unclear which is doing the most damage. Food toxins and malnutrition continue to be secondary sources of damage.

On the other hand, if we prioritize chronologically in terms of the original causes, the disease is originally caused by food toxins and malnutrition and sometimes antibiotics, which cause intestinal damage and infections, followed by autoimmunity."

http://perfecthealthdiet.com/2010/07...g-gut-disease/
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Last edited by hugh; 02-18-2013 at 06:59 PM.
02-18-2013, 07:10 PM   #11
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If find it reassuring that this type of research is now being performed, in an effort to determine whether evidence exists or not.
remember when they sequenced the genome and decided most of it was 'junk',because it's function wasn't obvious?
Surprise, surprise, it wasn't junk, rather than containing instructions for making proteins, they contain instructions for the genes that make the proteins ("an elaborate patchwork of regulatory sequences that act as a huge operating system")
Likewise it will be a while after the results of this study are published before the mainstream has the faintest clue what it all means.
02-19-2013, 09:48 PM   #12
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but the question is if it matters for crohn's disease at all.
Reduced diversity of faecal microbiota in Crohn's disease revealed by a metagenomic approach
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856500/
-"The most striking difference was a global loss of microbial diversity in CD"
-"the indigenous intestinal microbiota is considered a major if not the main trigger of inflammation"
-"We share the current concept that the onset of CD could be due to an altered microbiota and that a dysbiosis could enhance the risk of disease.
"

"Mucosal inflammation in inflammatory bowel disease is associated with loss of normal anaerobic bacteria"
http://gut.bmj.com/content/53/5/685

"Using a molecular approach, we observed that the faecal microflora in patients with both inactive and active colonic CD differed from the faecal microflora of healthy subjects, containing significantly more enterobacteria. In addition, approximately 30% of the dominant bacteria did not belong to the usual dominant phylogenetic groups.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774977/

All that being said, the big issue (to me) isn't so much the change in gut microbia ( although the two issues are probably inseparable), It's those bacteria triggering an immune response. They can do this from inside the intestine, but it really goes into overdrive when they get past the "single layer of polarised intestinal epithelial cells [that] separate the lumen of the gastrointestinal tract from the underlying gut-associated lymphoid tissue" and into the body
Single layer of cell? Leaky gut anybody?

One of the main reasons for SCD is the repair of the gut lining

Last edited by hugh; 02-20-2013 at 04:14 AM.
02-20-2013, 05:30 AM   #13
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If find it reassuring that this type of research is now being performed, in an effort to determine whether evidence exists or not.
.
Absolutely!

I am currently eating a paleo diet and feel pretty darn good.

I'm going to look into the Rush study and see if I can be of any service.
02-20-2013, 05:46 AM   #14
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@hugh You're mixing many things together that I like to keep split. You are mixing three things together.

-a self-directed response invoked by an autoantigen resulting in autoimmunity

-a response against indigenous gut flora

-a response against pathogens

It might help explain my previous post, one of those is causative in crohn's disease, not all 3. You can support one of those 3 but you can not support all 3 at once. The book about Elaine regarding SCD deals mostly with the gut flora, not with autoimmunity or a directed response against a pathogen.

Personally I am not convinced that we somehow lost tolerance for the indigenous gut flora, it's an explanation with a number of flaws which I and many people have explained in the multimedia section (crohn's disease is transmural, it features patchy inflammation, loss of tolerance to the gut flora isn't a feature found in any other diseases etc)

The immune system has specific barriers in place that prevent an overreactive response against the content of the gut lumen, there are many checks the adapative immune system goes through before it is activated, may I also remind that I know of no other disease in history where loss of tolerance to the gut flora has ever been a feature.

I am critical of this theory, that is all.

Last edited by kiny; 02-20-2013 at 06:13 AM.
02-20-2013, 06:11 AM   #15
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double post
02-20-2013, 11:20 AM   #16
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remember when they sequenced the genome and decided most of it was 'junk',because it's function wasn't obvious?
Surprise, surprise, it wasn't junk, rather than containing instructions for making proteins, they contain instructions for the genes that make the proteins ("an elaborate patchwork of regulatory sequences that act as a huge operating system")
Likewise it will be a while after the results of this study are published before the mainstream has the faintest clue what it all means.
People have been treating ailments with natural remedies since the dawn of time, many of which work. Neither scientists or physicians have been able to figure out all the reasons for this, or why certain treatments work for some, and not for others. These remedies have persisted, because at least for some, they've obtained results.

Only a little over 10 years ago, studies were performed to determine whether chicken soup had anything other than a "placebo effect" on colds, and while the results are not conclusive, they do indicate that, more than likely, it does have more than a placebo effect. A number of theories have been developed, but they haven't yet isolated the cause, or even the exact ingredients.

see link http://well.blogs.nytimes.com/2007/1...-chicken-soup/

Scientific advancements have made it possible for modern medicine to successfully transplant major organs, and even clone entire animals, but still can't cure the common cold.
02-21-2013, 07:48 AM   #17
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"@hugh You're mixing many things together that I like to keep split. You are mixing three things together.
-a self-directed response invoked by an autoantigen resulting in autoimmunity
-a response against indigenous gut flora
-a response against pathogens"


I'm not sure how you can separate them, It's like pulling one piece of cotton out of the Bauer tapestry and saying “Look. Yellow”

There are many of the microbes and other gut flora that can be classed as 'opportunistic pathogens', They are a normal part of a healthy gut flora but become pathogens when their numbers are out of control or when the immune system is compromised, -stress, malnutrition antibiotics, even a simple breach (leaky gut)).
Autoantigens are a different beast but only that they are a few more steps along in the chain.

"It might help explain my previous post, one of those is causative in crohn's disease, not all 3. You can support one of those 3 but you can not support all 3 at once. The book about Elaine regarding SCD deals mostly with the gut flora, not with autoimmunity or a directed response against a pathogen."


I assume that no.1 is the one that you feel is causative- the 'self directed response' but in my thinking that's not the cause, that is a result of toxins, damaged immunity, opportunistic pathogens, malnutrition.
It's the endproduct of a cascade that begins (in part) with food.

It's a while since I read 'BTVC' but as I understand it, Elaine proposed that since di- and polysaccharides could not be (as) readily absorbed in the small intestine they were available for 'bad' bacteria to breed, and in her theory it was by-products of the 'bad' bacteria that caused damage to the villi, so my interpretation is that these acidic and toxic wastes from the out of control party in the gut (along with lectins from grains, legumes -the thinking from paleo) causes permeability (allowing access to gut bacteria and bacterial proteins and eventually leading to autoimmunity).

Elaine stopped there because if it is stopped at this stage then the rest doesn't happen,
If it isn't stopped there.....
“Malnutrition impairs the immune response to toxins and slows the healing of intestinal injuries. This makes the intestine even more leaky and damaged.
Damaged immunity allows bacteria to penetrate the gut mucosa and infect intestinal cells, and to enter the body and create systemic infections including intracellular infections of immune cells. The immune response to these infections creates an inflammatory environment which makes the gut even leakier. The infections also weaken the ability of the immune system to heal the gut.
Entry of toxins and bacteria into the body leads to autoimmunity. Food toxins conjugate with human proteins and provoke antibodies against the human protein; bacterial proteins that are ‘molecular mimics’ of human proteins engender antibodies that strike both the bacterial and human proteins.”

http://perfecthealthdiet.com/2010/07...g-gut-disease/

There's been quite a bit of research suggesting that once the permeability is addressed then ALL aotoimmune diseases stop.
A new paradigm replacing that old one “your body has turned on itself, we don't know why but you will have it forever” - which should always be translated as doctorspeak for ”we don't know”

"Personally I am not convinced that we somehow lost tolerance for the indigenous gut flora, it's an explanation with a number of flaws which I and many people have explained in the multimedia section (crohn's disease is transmural, it features patchy inflammation, loss of tolerance to the gut flora isn't a feature found in any other diseases etc)
The immune system has specific barriers in place that prevent an overreactive response against the content of the gut lumen, there are many checks the adapative immune system goes through before it is activated, may I also remind that I know of no other disease in history where loss of tolerance to the gut flora has ever been a feature."


This is getting a bit long and it's late but i'm gonna press on.

I don't mind if you are not convinced, and wish you well in your management of your health.

'Indigenous gut flora' refers to one of the most complex and little understood ecosystems in existence,
A healthy balance is crucial for both nutrition and immunity.

The main purpose of the whole immune system is to regulate the contact between the world outside the body (including inside the gut) and the world outside the body.

The mucosal layer supported by a healthy gut flora are the first level of a three tiered system and are constantly monitored by the second layer, the innate immune system, which is a generic response to whatever makes it through the physical barriers.
The third layer, the adaptive immune system learns to deal with the situations not covered by the first two but over-activity can lead to pathological inflammation and/or autoimmunity.

My thought is rather than focusing on the failings of the overstressed last line of defence, time and effort is better spent on the repairing or preventing the breakdown of the first line of defence, the gut lining and associated flora.

As far as “ no other disease in history where loss of tolerance to the gut flora has ever been a feature” is concerned......
WHAT!!!!, that's a whole 'nother 10 pages......
The words 'loss of tolerance" are a bit confusing,
You're looking for a direct one step, bacteria in/disease out, not steps in between?
Abnormal microbia are linked to so many diseases, Crohns and colitis, lupis, obesity, diabeties (1 and 2), hashimotos, autism, asthma and on and on, cause? result? coincidence? i don't know

If your looking for a simple 'person with gene X has excess bacteria B that is causing antibody Y leading to autoimmune disease Z then I don't think it's ever going to happen.

Last edited by hugh; 02-21-2013 at 08:06 AM.
02-21-2013, 07:59 AM   #18
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[I]
I assume that no.1 is the one that you feel is causative- the 'self directed response'
I have issues with the autoimmune theory and the self-directed response directed at the indigenous flora.

Autoimmunity requires an autoantigen, if there's not autoantigen there's no autoimmunity, there is no known autoantigen in crohn's disease. UC for example does have an autoantigen response, you can find it in 80% of the people with UC and you can see it, it's a colon autoantigen and that's why their whole colon is inflamed. Crohn's disease is patchy, which isn't a feature of autoimmunity, it's a feature of infectious diseases.
02-21-2013, 08:04 AM   #19
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my mistake, i was just taking a guess.
the point is both autoimmunity and chronic inflammation can be the result of an overworked andstressed immune system
02-21-2013, 08:10 AM   #20
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I never ruled autoimmunity out it just seems unlikely to me.

People with tuberculosis have a stressed immune system too but this never results in autoimmunity in those people, even if they have been infected with TB for years.

Crohn's disease features inflammation in the form of experienced T cells, frustrated phagocytosis from dendritic cells and macrophages, and inflamed peyer's patches. This is easily explained with an infection, antigen presenting cell like a dendritic cells or a peyer's patch not draining properly would explain the inflammation. As long as the infection is not cleared you would have non-stop inflammation. And genetic predispostion points to our inability to deal with phagocytosis and autophagy.

The only missing thing in this theory is the actual pathogen, everything else is there. Studies keep looking for the pathogen, it would be an intracellular one, so you will see many studies looking for MAP, AIEC, Listeria, Yersinia, etc.

We also know antibiotics are somewhat successful in crohn's disease, but they tend to lose effectiveness over time, antibiotics wouldn't be helpful if it was autoimmunity.
02-21-2013, 08:30 AM   #21
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There's some questions people need to answer too who claim the gut flora is responsible for the inflammation. For example, a question I would like to ask is:

If the inflammation is directed at the gut flora, why is it localised in the small intestine in most people with crohn's disease? Why isn't the inflammation in the colon where most of the gut flora bacteria are?
02-22-2013, 03:07 AM   #22
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@kiny, I think i'm catching up to your main point,
that crohns doesn't have many characteristics of an autoimmune disease, and is more likely an infectious disease and the result of an either inadequate or misdirected immune system's failure to cope?
(a defective innate immunity and/or overaggressive adaptive immune response)
I'm not up to speed on that issue, and doesn't affect the BTVC theory

Both (autoimmune/infectious) are the end product of a cascade that probably started with bacterial overgrowth/intestinal permeability.

"As long as the infection is not cleared you would have non-stop inflammation."
The infection can't clear as long as bacteria and bacterial proteins, along with food toxins are continually causing infections
If the first level of the immune system is functioning properly then there is less work for the second and third.

"Studies keep looking for the pathogen, it would be an intracellular one"
Whatever the pathogen, it didn't just appear in the cell, In this case it most likely came through the gut lining.
The problem is the immuneresponse.
It might not due be 'normal gut bacteria', it might be due to a lack or excess of a particular bacteria or their byproducts or lack of byproducts, or a combination of all three, reacting with a specific genetic predisposition (and another million interactions continually occurring)

The hosts genetics are going to predispose someone to specific diseases, but without the leaky gut , the pathogen can't be introduced to the gene.
Some bacterial are 'conditionally pathogenic' ie pathogenic under certain conditions, (leaky gut, malnutrition, damaged immunity, genetic predisposition, other infections, a combination).

"If the inflammation is directed at the gut flora, why is it localised in the small intestine in most people with crohn's disease? Why isn't the inflammation in the colon where most of the gut flora bacteria are?"

The inflammation isn't necessarily directed AT the gut flora,
Disbiosis (+food toxins) damage the intestine,
-leading to malnutrition and impaired immune response,
-allowing bacteria to penetrate the mucosa and infect intestinal cells,
-leading to systemic infections including intracellular infections of immune cells
-The infection leads to inflammation and further leakiness,
-and further inhibit the ability to heal the gut.

and then it spirals downward, either to autoimmunity or chronic infection,

that's the theory anyway.......
02-22-2013, 04:14 AM   #23
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The inflammation isn't necessarily directed AT the gut flora,
Disbiosis (+food toxins) damage the intestine,
-leading to malnutrition and impaired immune response,
-allowing bacteria to penetrate the mucosa and infect intestinal cells,
-leading to systemic infections including intracellular infections of immune cells
-The infection leads to inflammation and further leakiness,
-and further inhibit the ability to heal the gut.

and then it spirals downward, either to autoimmunity or chronic infection,

that's the theory anyway.......


These are the first signs of crohn's disease seen in a colonoscopy from a study done in Germany, it's very rare to get a glimpse at the earliest events since most people who come in with crohn's disease are at a much later stage.

They're lymphoid follicles that become tiny ulcers that look like aphthae you would find in your mouth. These are the peyer's patches that are exclusive to the small intestine becoming inflamed. the mucusal breakdown happens around them.

These follicles are not covered by mucosa, and on top they are covered by "M Cells", M cell look for pathogenic bacteria, peyer's patches are miniature lymph nodes.

This picture to me does not look like primary mucosal breakdown, Picture C is a pretty damn healthy intestine outside of the inflamed peyer's patches.

So when people say that there's an immune response directed at the indigenous gut flora, I take issue with that, since this looks like an infection and a pathogen interacting with peyer's patches, which has nothing to do with the gut flora. The gut flora tends to stay nicely in the lumen and doesn't interact with peyer's patches.

The inflammation in people with crohn's disease is not in places with high bacterial load, it's not in places where the gut flora is most active, that would be the colon, but the inflammation is in the ileum where the peyer's patches are.

Dysbiosis, well, there's dysbiosis in the colon too and in /most/ people with crohn's disease there is no inflammation in the colon. It's a disease that is primarily related to that specific last few cm of the small intestine, the ileum.


Last edited by kiny; 02-22-2013 at 04:40 AM.
02-22-2013, 08:16 AM   #24
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These are the first signs of crohn's disease seen in a colonoscopy from a study done in Germany, it's very rare to get a glimpse at the earliest events since most people who come in with crohn's disease are at a much later stage.
It is interesting, but there is no way of knowing how long it took to get to this stage, the immune system may have been trying to handle a 'situation' for a long time already.
http://farncombe.mcmaster.ca/documen...11961740-4.pdf
In this case the woman had been identified with intestinal permeability eight years before she was diagnosed with crohns. It doesn't prove anything, but it is food for thought....
“In this case, a permeability defect was clearly identified to precede the onset of Crohn's disease in a subject at increased risk. This observation provides support for the hypothesis that increased gut permeability to macromolecules is an early step in the pathogenesis of this disorder.”

They're lymphoid follicles that become tiny ulcers that look like aphthae you would find in your mouth. These are the peyer's patches that are exclusive to the small intestine becoming inflamed. the mucusal breakdown happens around them.

These follicles are not covered by mucosa, and on top they are covered by "M Cells", M cell look for pathogenic bacteria, peyer's patches are miniature lymph nodes
Had to read up on that....
The microfold cells over the peyer's patches sample the contents of the intestine, and deliver pathogens to the APC (dendritic antigen presenting cells). Antigens stimulate the T-cells, B-cells, and macrophages.
So the third layer of the immune system kicked into play by the second layer ?

Swollen lymph nodes are a common sign of infection, that's one of the first things a doctor will check by feeling your neck or groin. It doesn't indicate that that is the location of the problem, just that the immune system is 'activated'.
“Certain diseases affect lymph nodes with characteristic consistency and location.” so maybe the inflammation and eventual ulceration is a classic sign of crohns, but not that necessarily that it began there or that it was initiated in that location.

So when people say that there's an immune response directed at the indigenous gut flora, I take issue with that, since this looks like an infection and a pathogen interacting with peyer's patches, which has nothing to do with the gut flora. The gut flora tends to stay nicely in the lumen and doesn't interact with peyer's patches.
I'm just explaining a theory, and am way out of my depth with the complexity of the immune system and happy to say so.
Many smart people clearly believe that there IS an immune response directed at the gut flora, but that it is a result of inappropriate stimulation of the immune system (and may perpetuate said stimmulation), but is not the cause of it

Tolerance exists towards resident intestinal flora but is broken in active inflammatory bowel disease (IBD)
http://www.mendeley.com/catalog/tole...l-disease-ibd/
“These results show that tolerance selectively exists to intestinal flora from autologous but not heterologous intestine, and that tolerance is broken in intestinal inflammation. This may be an important mechanism for the perpetuation of chronic IBD.”

http://www.formatex.org/microbio/pdf/pages705-718.pdf
“Despite inflammatory bowel disease (IBD) is a multi-factorial disease, it is generally assumed that damage of the intestinal barrier results in inappropriate stimulation of the immune system by the endogenous intestinal microflora thus promoting and nourishing the inflammatory process.”

None of this takes anything away from Elaine's theory (which may or may not be valid)
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