My latest UC theory-Call it part X

Isn't DMSO a poison?!

So just figured I'd share this...

I haven't been on antibiotics in over 10 years. I haven't eaten any meat in 25 years. And yes... one day I woke up 4 years ago with the beginning of my first flare.

That said, my mother has been taking enbrel for the last 10 years for psoriatric arthritis, my father has hypothydroidism...  so clearly... auto-immune conditions are a part of my genetic make-up.

 

I guess JC193's post points right at Old Mikes other post today.....

Prenatal methyl-donor supplementation augments colitis in young adult mice. As well as a bunch of other studies showing the same.

www.healingwell.com/community/default.aspx?f=38&m=2835280

So genetic susceptibility triggered by something...

I really wrote this thread to show what is going on with the gut bugs,and why they
might lead to never ending UC.
We can discuss triggers,but might be hundreds or even thousands,who knows.
What we may be able to figure out is how to fix the dysbiosis which I suspect will
take more than what is currently being done.
FT might be the quick way,but again does not work on everyone.
Makes me want to spend the money to see what gut bugs are gone,I know my poo
has no odor like it should have. So I have to suspect a mass extinction of bacteroides.
Old Mike

89 bucks

OM

http://ubiome.com/

They say IBD is a familial disease,even spouses that live in the same house one can have crohn's while the other

will have a more leaky gut than normal.

The onset has also changed over the past say 50 years where it is hitting younger and younger people.

I got UC at 32,my son at 21.

I hope your son responds to the meds.

Old Mike

http://www.sciencedaily.com/releases/2012/09/120913123512.htm

 

Post Edited (Old Mike) : 8/28/2013 8:29:28 AM (GMT-6)

Canada Mark, I was disgustingly healthy and ate very healthy (and atypical) American diet. I was pooping fine and no IBS at all and early 30's and started to see a bit of blood in my stool, which I ignored/denied as knew could NOT be colon cancer. Was training to do big bike trip and instead of increasing fitness it dropped dramatically. One day woke up and put on shorts to run outside to pick up paper and they were like 4 sizes too big. Holy crap! I never weighed myself so no idea where I started but borrowed neighbor's scale and knew I had lost significant weight. After that it was the exponential downhill slide with multiple trips to doctors (it took them a while to figure it out) increase in pain, blood and total loss of appetite...more weight loss.... really miserable. Then came the diagnosis. Asked 99 year old grandmother if any family members had history of this and she said no. (got those long-lived genes in me, too and low BP)
I have no clue where this came from.....my doc thinks I was exposed to novel organism (as posted earlier have drunk untreated and questionable water multiple times on bike and backpacking trips) and system went nuts. Who knows? Totally out of the blue.
BTW, the thoughts are IBD is not just the two diseases- they just lump us together based on symptoms and etiology of illness could be completely different. So one model could indeed be illness triggered/caused by ab's, but there could be multiple other mechanism's going on here.
Who knows? Totally out of the blue.

Mark: Make sure you don't miss this part of my last post.

This may sound like Pseudoscience but its not.

Our colon should have very little oxygen and a low ORP.

There might be something going on with these alkaline water machines to produce negative

ORP water.

 

Huh What:

 Need to find out if they induced colitis with drinking water or enema.

No more out there on this study,unless want to pay.

Redox potential,might be what this whole thread is about,basically oxygen content of water.

This gives me a really really wild thought. You know on your faucet at the end it mixes the water with air,

this will increase the ORP, Oxidation Reduction Pontential, so all/most of our tap water is highly oxygenated

thus a high ORP.

Will look into this more.

http://sciencelinks.jp/j-east/article/200012/000020001200A0321909.php

Not quite the same thing. Want reduced ORP. You don't happen to have an ORP meter do you.

Looking for negative millivolts.

OM

http://www.betterhealthcompany.com/id117.html

To expand on this thread and Old Mikes line of thinking:

Here's some thoughts I had recently:

First it appears as Old Mike has been saying for a long time that there's an imbalance of bacteria, and breakdown if the mucus barrier.

Second it appears that identifying bacteria is still in its infancy and different sampling and analysis techniques are yielding different results. Same with sample site and so on... this topic can get long on it's own. Bottom line though is that regardless of the testing and analysis type there is always a large difference in the bacteria make-up. Some older sampling says an explosion in proteobacteria in the gut lumen samples and a colapase in bacteriodetes - and some say there is a high presence of bacteriodetes in the mucus membrane of people with UC... and others say different results altogether.

In any case it points to perhaps the issue at hand. Bacterial imbalance.

--------------------------------------

A Normal Immune reaction to an Abnormal Gut Microbiome


1) Reduction in gut bacteria due to inhibition by one or more environmental factors, for instance: dietary chemicals, low dose exposure to pesticides, air pollution, oxygen in the colon, antibiotics, genetics, c-diff, ecoli infection, disease, etc etc… This list goes on forever.

2) This reduction or initial imbalance or functional “dysbiosis” can eventually manifest in one or more of the following when the balance of the microbiome is shifted in a particular direction:

So my current thinking is there is three states:

The Three States of Dysbiosis:

1. Luminal Dysbiosis
2. Mucosal Dysbiosis
3. Cellular Dysbiosis or “Cellular Infection” which I'll get to further on

Luminal being associated with IBS
Mucosal being associated with Ulcerative Colitis
Cellular being associated with Crohns

All of these can overlap each other and one or more can be present at the same time.

3) In IBS there is a slight shift in the reduction of bacteriodetes, and a slight increase in proteobateria
4) In Ulcerative Colitis there is an explosion of proteobacteria and a significant decrease in Bacteriodetes
5) In Crohn’s there is a complete collapse or “Mass Extinction” of Bacteriodetes

BUT here is the important factor:

6) In IBS there is a slight shift in the reduction of bacteriodetes, and a slight increase in proteobateria – This shift takes place in the Gut Lumen and affects the luminal balance of microbes. The mucosal balance remains protected by a healthy population of bacteriodetes. (or whatever turns out to be normally present in healthy people int he gut lumen)

7) In Ulcerative Colitis there is an explosion of proteobacteria and a significant decrease in Bacteriodetes – This shift takes place not only in the Gut Lumen, but has crossed into the Mucosal Barrier or Mucus Membrane. So there is now substantially less bacteriodetes present in the outer most mucus membrane of the colon. (or again whatever bacteria turns out to be normally present in healthy people within the mucosa)


8) In Crohn’s there is a complete collapse or “Mass Extinction” of Bacteriodetes, dysbiosis has occurred in the Gut Lumen, the Mucus Membrane and disbyosis or “cellular Infection” has penetrated into the epithelial and immune cells and occurs anywhere in the digestive track. (or again whatever turns out to be normally present in healthy people - in this case probably none, or no bacteria)

This “Dysbiosis” is a perfectly normal response to an abnormal gut microbiome. Or alternatively, it could be more correctly stated as a perfectly normal immune response to an increase in certain “opportunistic commensal bacteria” and a decrease in other commensal bacteria.


Regardless of how bacterial analysis eventually plays out as the variables are endless. Something has occurred or a "shift" has taken place in one the three locations (lumen, mucus membrane, cellular)

-------------


Commensal bacteria help keep our bodies healthy in many ways: they help us to digest foods and acquire nutrients such as vitamins B and K, encourage your immune system to develop and prevent the colonization of bacterial pathogens that cause disease by competing with them. This system is held in place by a series of “checks and balances”. With three main or parent aspects:

i) Poulation Control - The microbiome make-up itself. Each species keeps one or more other species from being completely dominant. “Self -regulation” would be an appropriate term.

ii) Hormonal Response – or the Adaptive Immune system

iii) Innate Immune System Response

These three “balance and check” properties are important because the effects of alteration to one can affect the balance and/or response of the others. All three play a pivotal role in the pathogenisis of the three states of dysbiosis. The Hormonal Response or "Adaptive Immune Response I personally think being of paramount significance.

--------------------------------

IBS

IBS is associated with abdominal pain and cramping, as well as changes in the functionality of the bowel. It is a disorder of dichotomous extremes, with many patients experiencing predominantly constipation, diarrhea, or both. Alterations in gut motility are paramount to this disorder and contribute to prevalence of both diarrhea and constipation.

IBD

IBD includes two chronic GI diseases, ulcerative colitis and Crohn's disease, which are relapsing inflammatory conditions of unknown etiology. Approximately 50% of patients with IBD in long-standing remission have IBS-like symptoms.

Let’s look at what differentiates the three conditions and first let’s focus on IBS:

IBS

Currently the gastro community states the following in regards to IBS; Irritable bowel syndrome (IBS) is a functional gastrointestinal (GI) disorder, meaning it is a problem caused by changes in how the GI tract works. People with a functional GI disorder have frequent symptoms, but the GI tract does not become damaged. “IBS is not a disease; it is a group of symptoms that occur together.” is their current line of thinking. This is at least an upgrade from the prior statements that IBS was a product of a person’s “imagination”… seriously…

In the past, IBS was called colitis, mucous colitis, spastic colon, nervous colon, and spastic bowel. The name was changed to reflect the understanding that the disorder has both physical and mental causes and is not a product of a person’s imagination.

At this point in time it’s hard to believe that anyone would state that IBS is the product of a person’s imagination – yet even today there are many doctors who still reiterate this very statement to their patients. It’s quite sad.

Let’s look at the most common symptoms:

• IBS with constipation (IBS-C)
- hard or lumpy stools at least 25 percent of the time
- loose or watery stools less than 25 percent of the time

• IBS with diarrhea (IBS-D)
- loose or watery stools at least 25 percent of the time
- hard or lumpy stools less than 25 percent of the time

• Mixed IBS (IBS-M)
- hard or lumpy stools at least 25 percent of the time
- loose or watery stools at least 25 percent of the time

• Unsubtyped IBS (IBS-U)
- hard or lumpy stools less than 25 percent of the time
- loose or watery stools less than 25 percent of the time

Other symptoms of IBS may include:

Diarrhea—having loose, watery stools three or more times a day and feeling urgency to have a bowel movement

Constipation—having hard, dry stools; three or fewer bowel movements in a week; or straining to have a bowel movement.

Feeling that a bowel movement is incomplete

Passing mucus, a clear liquid made by the intestines that coats and protects tissues in the GI tract
abdominal bloating

IBD

Now let’s look at Crohn’s Disease and Ulcerative Colitis:

Crohn's Disease
location: Inflammation may occur anywhere along the digestive tract. Inflammation is continuous throughout affected areas
Ulcerative Colitis
location: Inflammation may occur in patches. Large intestine (colon) is typically the only affected site.

Crohn's Disease
Pain: Pain is commonly experienced in the lower right abdomen
Ulcerative Colitis
Pain: Pain is common in the lower left part of the abdomen

Crohn's Disease
Appearance: Colon wall may be thickened and may have a rocky appearance. Ulcers along the digestive track are deep and may extend into all layers of the bowel wall
Ulcerative Colitis
Appearance: Colon wall is thinner and shows continuous inflammation. Mucus lining of large intestine may have ulcers, but they do not extend beyond the inner lining

Crohn's Disease
Bleeding: Bleeding from the rectum during bowel movements is not common
Ulcerative Colitis
Bleeding: Bleeding from the rectum during bowel movements

Symptoms of Crohn's Disease / Ulcerative Colitis

• Abdominal pain, cramping or swelling / • Abdominal pain or discomfort
• Anemia / • Anemia caused by severe bleeding
• Fever / • Fever
• Gastrointestinal bleeding / • Rectal bleeding
• Joint pain / • Joint pain
• Malabsorption / • Malabsorption
• Persistent or recurrent diarrhea / • Bloody diarrhea
• Weight loss / • Weight loss

Other Non-Similar Symptoms:

Crohn's Disease / Ulcerative Colitis

• Stomach ulcers / • Dehydration
• Vomiting / • Fatigue
/ • Loss of appetite
/ • Urgent bowel movements

I feel it’s again important to stress that anyone with IBD commonly has one type of IBS subtype symptom present at all times even during periods of clinical remission. There are cases of patients in remission being completely “asymptomatic”, so no IBD or IBS symptoms at any time, but this is more of a rarity.


Now here's why currently I think this is all important:

CONT'D ON NEXT POST

Now

Again, what the heck... I'm all confused again! This is some pretty complex stuff...

So before I get to the really good stuff, let's focus on a few other things:

- We learned that the immune system is always in a constant state of inflammation and this is essentially regulated through the Master Channels of Dopamine and Serotonin.

- We learned and are still are learning that there is some kind of an imbalance or "dysbiosis" in bacteria within our gut and that this imbalance can not only be different in the Gut Lumen, The Mucus Membrane and Cellular (epithelial or gut lining cells cells and Immune Cells themselves) (which again I'll get to soon!)

- We learned that Pathogenic Bacteria (Food born E-coli) down regulate SERT and this causes an increase in 5HT and this is exactly how they effect our bodies and cause the symptoms they do

- We learned that levels of 5HT is for some unknown reason high in people with IBS and IBD and that SERT expression is low in people with IBS/IBD

- We learned that even commensal bacteria (common bacteria) generate an immune response and our bodies "tolerate" this. Again eventually through the Master Channels.

- We learn that Proteoacteria (such as C-diff) cause the release of IKF and NFKB and the release of TNF-a and Chemokines as an immune response and that proteobacteria are part of our normal gut microbiome but are kept under control through the series of balances and checks -Population Control "Self Regulation" due to the diversity, Adaptive or Hormonal Immune Response, and Innate Immune Response.

- And this one, I currently think is REALLY, REALLY important - there is an off switch to TNF-a thought I don't know what it is and seems to be a very complex issue and I haven't looked into it fully yet. But in any case there will be one, I'm sure of this.

Now we all have these varying responses to things such as food, and we read about things like SERT or Butyrate, or the effects of nicotine, as well as Protease that Old Mike talks about a lot and so on. So let's go down this path a little as they popped up when I was reading these papers and their citations.

Nicotine - Nicotine and serotonin in immune regulation and inflammatory processes: a perspective:

Nicotine and serotonin modulate the innate and adaptive immune responses and the inflammatory states. Several nicotinic cholinergic and serotonergic receptor subtypes have been characterized in B and T lymphocytes, monocytes, macrophages, and dendritic cells. The use of knockout mice has allowed a better characterization of nicotinic receptors and their role in anti-inflammatory processes in these cells. Cytokines play a crucial role in controlling inflammatory reactions. Nicotine and serotonin have been reported to regulate cytokine release. Cholinergic mechanisms also play an important role in inflammation through endogenous acetylcholine. Nicotine mimics this effect by activating the cholinergic anti-inflammatory pathways. New concepts of reciprocal interactions between nicotine and serotonin are emerging. The role of nicotine as an anti-inflammatory agent has been established, whereas that of serotonin remains more controversial.
www.ncbi.nlm.nih.gov/pubmed/17108054

- So now we can look at why perhaps nicotine has the suppression effects from smoking that a lot of people find, but after quitting or upon quitting, wham UC strikes as the levels of 5HT rise again.


Butyrate
Absorption of SCFAs is important for colonocyte health and metabolism, epithelial integrity, as well as colonic fluid and electrolyte balance. Butyrate, a key SCFA, is known to have multiple regulatory roles in the mammalian colon, including stimulation of fluid and electrolyte absorption. Butyrate has also been implicated in suppressing mucosal inflammation (16). Decreased production or availability of butyrate has been shown to result in chronic inflammation and acute diarrhea (6). However, to date, the effects of enteric pathogens on the absorption of SCFAs have not been examined. We speculate that decreased butyrate availability caused by EPEC (Food borne e-coli - my words) infection might compromise colonic epithelial integrity, resulting in inflammation of the epithelium
eanimal.snu.ac.kr/aboutus/seminar/070110%ED%9D%AC%EC%98%81EcoilMCT12005.pdf

- and here we can learn how the balance or "dysibiosis" of gut bacteria effect Butyrate and why it may be important to include resistant starch as part of a therapy. Also fiber from a resistant starch diet has been shown to prevent the adherence of e-coli and other proteobacteria to to the mucosal lining"


Trypsine
Trypsine - is a serine protease found in the digestive system. This study shows that its also a signal molecule - "Mast cells containing tryptase are normally found in the intestine, and their number increases during inflammation (29), suggesting that PAR-2 mediates some effects of mast cell proteases. PAR-2 is up-regulated by interleukin 1α and tumor necrosis factor, supporting its role in inflammation (30).

We conclude that pancreatic trypsin activates PAR-2 at the apical membrane of enterocytes and regulates the intestinal epithelium. Thus, in addition to its digestive function, trypsin should also be considered an intestinal signaling molecule that specifically regulates enterocytes through PAR-2."

- so now we can look at excess protease in the gut as a problem from an immune perspective in response to bacteria present in the gut and generated from the "immune cascade", not so much or further exaggerated by food source protease and protease additives


There's many others that I have crossed paths with as well... But these are some of the main ones. Same with upstream effect like Methylation... and well the list goes on again. Altering one of the The Three States of Dysbiosis:

1. Luminal Dysbiosis
2. Mucosal Dysbiosis
3. Cellular Dysbiosis or “Cellular Infection”

Altering one of the states of Dysbiosis alters any one of the main three "check and balances" as I have come to cal them.

i) Population Control - The microbiome make-up itself. Each species keeps one or more other species from being completely dominant. “Self -regulation” would be an appropriate term.

ii) Hormonal Response – or the Adaptive Immune system

iii) Innate Immune System Response

And this causes all of the wild and crazy effects we all see and and perhaps contributes to why we are all different in our responses as the bacteria make-up in us all will ultimately be unique to us.

So again, what seems so complex on the surface to us and these huge chain reactions is really, very, very simple - A normal response to an abnormal gut microbiome. - and this is nothing new whatsoever - think SCD, GAPS, and even current traditional medical research... they all center around bacteria at the heart of the problem. I'm just trying to offer up some new or recent research and perhaps some ideas to ponder over for those interested.

Now...


Cellular Dysbiosis or “Cellular Infection” as I have come to call it


First let's learn about this:

Here www.ncbi.nlm.nih.gov/pmc/articles/PMC3542012/ we learn Mucosa associated but not luminal Escherichia coli is augmented in Crohn’s disease and ulcerative colitis - Their Conclusion: In CD and UC patients only the mucosa associated population of E. coli is augmented and the proliferation is prominent in the ileum of CD and rectum and sigmoid of both UC and CD patients which are sites where the lesions usually are observed. The augmented E. coli population in these sites presented a low number of the virulence markers, possibly meaning that they are not relevant for the disease process.

- This study intrigued the heck outa me...

And based on what was learned previously from all of the above I did some more digging on this particular topic.

So from the above we see for the first time the separation between luminal and mucosa infection. i.e the balance in the lumen is perhaps normal whereas the balance in the mucosa is abnormal. And this correlates to what I keep calling the "Three States of Dysbiosis" - mainly cause I have no idea what else to call them at the moment!


Anyway - Obviously if there's an increased presence or screwy balance of e-coli in the mucosa well they had to get there somehow, and this get's back to all of the above that I wrote. There's multiple pathways set up by a variety of environmental factors and/or genetic factors etc...

Now there's many other papers suggesting not only e-coli, but other proteobacteria as well that have made their way into the mucosa. And one could go on and on, but the bottom line I think is this: They really shouldn't be there - or at least not in large quantities. At least from all of the above you can begin to see how they might get in there....

So more digging and thinking about the effects of pathogenic e-coli as well as what we learned about the immune response to normal c-diff and all that good stuff....

Looking into e-coli I came across a term -and at the very same time I was thinking about the increase in TNF-a that is always talked about from remicade discussions and papers and talks and explainations from my GI...

My line of thinking was quite simple - I thought to myself "it's obvious there's some kind of infection going on in my body" and it probably has to do with a response to bacteria being were they should not be - OR, simply a higher number of certain bacteria that is constantly throwing the normal "check and balance" procedure out of whack. And this is causing an influx or higher amount of TNF-a to be present where it normally shouldn't be or preventing the "off" switch for inflammation from activating causing a cascade of crazy effects... and now knowing the effects of TNF-a on the SERT expression and how this causes the increase in 5HT and how things all go really wonky from this first "chick and balance" point - and I'm crapping mucus all the time but this AA therapy seems to have tackled that to a degree and.... well, I became curious about e-coli and came across the following term:

Adherent and Invasive Escherichia Coli (AIEC)

THIS SCARED THE CRAP OUT OF ME.... I had not seen or heard of this before, even when i was reading about E-coli effects on SERT

Firstly, before you even read this let's remember that for sure we all have to much TNF-a. Which has always assumed to be from the immune cascade that people get lot's in as Old Mike says and wich is more likely from the immune response and all the stuff we learned from above... Also let's remember once again that TNF-a Down-regulates SERT and causes and increase in 5HT....

And we all have talked about or read about the increase of macrophages and so on... and we all (or at least I have) been told many times that there is a wonky autoimmune response going on and that our body does not know how to shut off inflammation 'Flip the off switch".... And this is why I need to take Remicade and so on... to deal with the chronic inflammation and prevent further damage. And so on and so on...

Soooooooo, in the words of Old Mike: "Let's look at this mess" and ugggg.... this is NOT good at all!

"Adherent and invasive Escherichia coli (AIEC) associated with Crohn's disease are able to survive and to replicate extensively in active phagolysosomes within macrophages. AIEC-infected macrophages release large amounts of tumour necrosis factor-alpha (TNF-α) and do not undergo cell death. The aim of the present study was to determine what benefit AIEC bacteria could gain from inducing the release of large amounts of TNF-α by infected macrophages and to what extent the neutralization of TNF-α could affect AIEC intramacrophagic replication. Our results showed that the amount of TNF-α released by infected macrophages is correlated with the load of intramacrophagic AIEC bacteria and their intracellular replication. TNF-α secretion was not related to the number of bacteria entering host cells because when the number of bacteria internalized in macrophage was decreased by blocking lipid raft-dependent and clathrin-coated pits-dependent endocytosis, the amount of TNF-α secreted by infected macrophages was not modified. Interestingly, dose-dependent increases in the number of intracellular AIEC LF82 bacteria were observed when infected macrophages were stimulated with exogenous TNF-α, and neutralization of TNF-α secreted by AIEC-infected macrophages using anti-TNF-α antibodies induced a significant decrease in the number of intramacrophagic bacteria. These results indicate that AIEC bacteria use TNF-α as a Trojan horse to ensure their intracellular replication because replication of AIEC bacteria within macrophages induces the release of TNF-α, which in turn increases the intramacrophagic replication of AIEC. Neutralizing TNF-α secreted by infected macrophages may represent an effective strategy to control AIEC intracellular replication.
www.nature.com/labinvest/journal/v92/n3/full/labinvest2011156a.html

and www.plosone.org/article/info:doi/10.1371/journal.pone.0012714


sooooo...

I don't like were this mess is going one bit.... the whole Crohn's-Coltis thing I have and all... Seriously... this is bad news.

On the plus side - I have read that fiber prevents this adhesion... but really, aside from that how does one deal immediately with an issue like this inside the immune cells themselves...

PS - this all took me nine bazillion hours to type out so please excuse any spelling and grammar etc...

Just my thoughts on an extension of what Old Mike has been saying.

My only thought as of today is really to continue with this Amino Acid Therapy to see if I can relieve some of the symptoms and get the 5HT things under control, then use diet and health and maybe fecal transplant or something to try and correct an imbalance.

ALSO one last thing. Adherent and invasive Escherichia coli (AIEC) and other Adhesive and Invasive Bacteria are found in normal people as well... So maybe a fecal transplant when in a major flare from someone with these present in it leads to infection and a dramatic worsening of symptoms??? MAYBE...

big thank you OM for all this, much I want to read in it. So hoping for you that you find something that helps your situation.

On the pickles...I am still amazed how good I feel each time I eat raw fermented cabbage. My colon is doing really well, still not really well in my body as a whole though, constantly fatigued, trying to find out what else is going on for me.

The stress element is very interesting. For me, flares seem to come sometime post stress, not during stress. I wonder if it is because my adrenals are trying to rest after over production of cortisol and hence body loses that anti-inlammatory help and the autoimmune tendency is no longer subdued at all. Research seems to be showing that bacteria are needed to activate all hormones in the gut, I wonder if somehow these gut bacteria are also exhausted by the demand to produce more hormones and therefore when they are weakened others take over.....all speculation for now of course....

Edited to add: Thanks to Canada Mark too, your post x-post with mine so hadn't seen it when wrote my reply

oh yeah, that reminds me. I forgot to post this.

Nitric Oxide Can Regulate Gene Expression
www.sciencedaily.com/releases/2013/08/130824131400.htm

Functions of histone modifications
Serine/Threonine/Tyrosine phosphorylation
Addition of a negatively charge phosphate group can lead to major changes in protein structure, leading to the well-characterised role of phosphorylation in controlling protein function. It is not clear what structural implications histone phosphorylation has, but histone phosphorylation has clear functions as a post-translational modification, and binding domains such as BRCT have been characterised.

Just thinking back to how E-coli cause tyrosine phosphorylation and maybe there's a genetic effect or something from this - have no idea... in any case just found it an odd coincidence.

Also about e-coli/c-diff etc being able to switch from anerobic to aerobic in certain conditions. Which monky's with NO I think.

Not really sure, again I just thought the article would interest you

Post Edited (Canada Mark) : 8/29/2013 6:13:35 PM (GMT-6)