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The Marshall Protocol Study Site > PROF. MARSHALL'S PERSPECTIVE > Prof. Marshall's Perspective > Different bacteria in the gut of autistic children


Different bacteria in the gut of autistic children
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Prof Trevor Marshall
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 Posted: Fri Jan 13th, 2012 07:24

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"Bacteria in the gut of autistic children different from non-autistic children"

http://www.microbeworld.org/index.php?option=com_jlibrary&view=article&id=8088

http://www.microbeworld.org/index.php?option=com_jlibrary&view=article&task=download&id=8088

http://mbio.asm.org/content/3/1/e00261-11


"the study was uniquely powerful because they used tissue samples from the guts of patients"

"We detected either IgG or IgM antibodies against Sutterella wadsworthensis proteins in ~48% (11/23) of AUT-GI children"  "One Control-GI child had very weak IgG immunoreactivity against S. wadsworthensis proteins." {the other controls were negative}

..Trevor..
 

Russ
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 Posted: Fri Jan 13th, 2012 09:34

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Thanks for posting this Dr. Marshall.  I'd be curious to hear what your insights from it are.  Thanks.



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 Posted: Fri Jan 13th, 2012 11:55

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Russ, I am not sure whether the modification to the gut flora is a result of a compromised innate immune system, or whether the gut flora significantly contribute to the intraphagocytic microbiota. I suspect it is a little of each.

What this paper does demonstrate is that Autism and immune dysfunction occur in association. It is my opinion that the Autism Spectral Disorders are all syndromes of the immune-mediated dysfunction we call the 'Th1' syndromes.

..trevor..
 

Russ
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 Posted: Fri Jan 13th, 2012 14:57

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What do you make of the fact that a single species stood out so prominently?

To me, if difference in gut bacteria was just the result of a compromised immunue system, you'd think you'd see many different bacteria showing up in higher levels in the autistic kids, and no one particular species standing out so prominently. 

Here's a different study that did find that species, Sutterella wadsworthensis, to be commonly found in controls/healthy individuals.   The study was investigating a link between this bacteria and inflammatory bowel disease.  It used PCR instead of antibodies.

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0027076

 

Last edited on Fri Jan 13th, 2012 14:58 by Russ



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Prof Trevor Marshall
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 Posted: Fri Jan 13th, 2012 15:27

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Russ, no single species is causal for specific diseases. What was interesting was this one group, which compared controls and diseased with the same methodology, identified a significant difference.

PCR is a very imprecise tool. Antibodies are worse. We discussed the potential for both errors in our recent book chapter. Every group will likely get different results. That's why it is important not to try and "collect knowledge" from PubMed, but to carefully examine each study methodology and results. Often their conclusions have to be discarded, but, oh well...
 

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 Posted: Sat Jan 14th, 2012 00:57

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This study proposes some of the mechanisms for the interactions:

http://www.annualreviews.org/doi/abs/10.1146/annurev-med-012510-175505



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Prof Trevor Marshall
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 Posted: Sat Jan 14th, 2012 05:07

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Their mechanisms are not the key, Nick. The key is to understand that once the microbiota invade the phaogocytes - the monocytes, macrophages, lymphocytes and neutrophils - then the pathogens can interact directly with each other, and with the transcription of the human genome.

They can then directly alter the interactome.

Most scientists don't realize that microbes can live inside cells, even though mycobacteria, rickettsia, EBV and a host of others have been documented over the years. It is this lack of understanding which prevents them from understanding what is really happening. They need to read the Wirostko papers... Or ours...

Liz and I published a (crude) paper way back in 2003 explaining this:

Marshall TG, Marshall FE: Sarcoidosis succumbs to antibiotics - implications for autoimmune disease. Autoimmunity Reviews,2004; 3(4):295-3001.
Available from URL http://dx.doi.org/10.1016/j.autrev.2003.10.001
PMID: 15246025 or access FullText at author website

..Trevor..

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 Posted: Mon Jan 16th, 2012 17:19

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On the autism thread, I have posted a few times about GI studies and ASD.

Clostridia bacteria were once thought to be the culprit bugs which caused ASD, especially because vancomycin used to kill clostridia caused temporary improvement in symptoms until the vancomycin was stopped. Now the main researcher interested in this, Sidney Finegold, has moved onto to another species, namely, desulfovibrio – see http://cogentbenger.com/autism/interviews/finegold-interview/. Finegold has been looking directly for bugs in stool samples.

Others, less well known, have found other fecal flora abnormalities in stool samples. My son Jason’s fecal flora was grossly abnormal for what researchers (Tim Roberts of the University of Newcastle) thought were streptococcal species of bacteria. Treatment to address this led nowhere as did a course in vancomycin therapy followed up with probiotics.

I am therefore a bit blasé about new studies which purport to find a putative gut brain connection.

Indeed, there is an overwhelming number and diversity of abnormalities found with ASD subjects compared to controls in relation to a host of markers, of which stool bacteria studies is just one. Abnormalities with respect to serology markers and urinary excretions are even more diverse and extensive among ASD sufferers than differences in findings with respect to gut flora.

John



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Prof Trevor Marshall
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 Posted: Mon Jan 16th, 2012 17:32

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john,
In Singapore I addressed this issue. there can be no single pathogen, and there can be no single pathway for the disease causality. The body is too complex to allow that.

http://vimeo.com/32641708

I am sorry if I didn't make it clear, but all I see in this paper is the confirmation that a Th1 weakened immune system allows different flora to flourish in a gut. No more than that. Some of the species will join the microbiota, but the person is already ill when their gut shows this dysbiosis :)

The Interactome will determine the dysfunction which a person suffers from. Or combination of dysfunctions.

I hope that helps,
Trevor

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 Posted: Wed Feb 22nd, 2012 04:31

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While the previous reports have examined fecal specimens, Williams and coworkers (20) took a new approach and included intestinal gene expression and identification of the microbiota in the intestinal mucoepithelium. Their study revealed deficiencies in the enzymatic activity of disaccharidases and hexose transporters among the ASD patient group. These deficiencies suggest that impaired digestion and transport of intestinal carbohydrates may contribute to ASD GI symptoms. Consistent with the notion that the intestinal microbiota contributes to the enzymatic activities of the human intestine needed to degrade carbohydrates, there were also changes in the microbiota identified among the ASD group. Metagenomic analyses disclosed a significant dysbiosis with reductions in Bacteroidetes and increases in the ratio of Firmicutes to Bacteroidetes, as well as in Betaproteobacteria.
Williams et al. (13) report detecting Sutterella 16S rRNA gene sequences in ileal mucosal biopsy specimens from 12 of 23 patients diagnosed with autism and GI symptoms but in none of the specimens from 9 control children with GI symptoms. Sutterella wadsworthensis sp. nov. was described 15 years ago from clinical isolates from patients with infections that were below the diaphragm (21). In addition to the molecular taxonomy that Williams et al. describe (13), Sutterella can be identified fairly easily in the laboratory by its resistance to bile and its fatty acid profile (21).

http://mbio.asm.org/content/3/1/e00019-12.long



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 Posted: Sun Mar 18th, 2012 07:52

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Treating autism with antibiotics

http://www.youtube.com/watch?v=yOno_2m_8LY&feature=youtu.be



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Gary
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 Posted: Wed Apr 4th, 2012 20:19

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Another study that puzzles some but completely aligns with Marshall Pathogenesis.

http://www.mercurynews.com/science/ci_20328655/rare-gene-mutations-found-heighten-risk-autism



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 Posted: Thu Apr 5th, 2012 05:33

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And a day later, another one that aligns with the Marshall Pathogenesis

http://timesofindia.indiatimes.com/articleshow/12547017.cms



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 Posted: Fri Apr 20th, 2012 09:45

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bugs from day 1 - the fetus is not sterile....

http://www.newscientist.com/article/mg21428603.800-babies-are-born-dirty-with-a-gutful-of-bacteria.html



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Prof Trevor Marshall
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 Posted: Fri Apr 20th, 2012 09:53

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First, though, doctors will have to come to terms with the fact that we are born with our own set of bacteria. "Standard medical teaching is that the fetus is sterile," says Kinross. "The notion that gut development is influenced by maternal bugs will come as a shock. It's a completely new way of thinking about human disease.
 

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 Posted: Fri Apr 20th, 2012 14:31

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So how do we change the gut microbe composition we've inherited? 

Seems like the alternative medicine community has known this is an important part of the puzzle for a while but all attempts to alter the microbial community in the gut have proved temporary at best (probiotics, antibiotics, anti-candida treatments, etc.). 



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 Posted: Fri Apr 20th, 2012 16:55

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The bacteria in the GI tract do not directly cause chronic disease. Over months and years they move into the bloodstream and circulate throughout the body, adding to the microbiome. Alternative Medicine actually have the wrong concept :)

Intervening in GI tract composition, and expecting short-term results, is futile.

A single course of Cipro knocks out all GI tract bacteria for months. Dave Relman (Stanford) gave a presentation at the Paris and Seattle microbiome conferences giving data on this.
(can somebody search and see if he has published his data, otherwise I will have to see if I have a video of the presentations)

Russ
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 Posted: Fri Apr 20th, 2012 17:45

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Is this is the study you were referring to?
http://med.stanford.edu/ism/2010/september/relman.html

So I guess you are saying that the microbiota in the gut are less important than the intracellular microbes in the brains, organs, etc., at least as far as the disease process is concerned?  And the diseases can be reversed without having to change the gut ecosystem? 



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 Posted: Fri Apr 20th, 2012 18:03

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Russ, that citation looks like one of the papers :)

The GI tract ecosystem affects whether the Th1 system is exhausted dealing with microbes in the gut (which gives system-wide palliation). It also affects the cytokine storm levels, so it is very significant.

But altering the gut microbiota, once one is sick, has not been able to reverse any disease process in man :)

Antibiotics profoundly change the gut flora :)

 

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 Posted: Fri Apr 20th, 2012 18:41

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Dr Trevor Marshall wrote: But altering the gut microbiota, once one is sick, has not been able to reverse any disease process in man :)

But I wonder about the opposite.  For diseases like autism, where the gut microbiotia is suspected to play a major role, is it possible to reverse the disease process without altering the gut microbiota?



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