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Huge improvement in two hours

Elph68

Senior Member
Messages
598
Then what do you mean by this?
ok ... this is not scientifically correct, but for simplicity, and in this context .... when I was referring to the lymphatic system I meant the glands/nodes where the bits and pieces of the immune system are made and stored ... and the immune system in this context is the bits and pieces that attack and kill pathogens ....

I am always going to get pulled up on correct terminology .... Sorry, but I always forget the correct names ......
 

Elph68

Senior Member
Messages
598
@Elph68

"I am going for a week"

wherever you're going, and hope its somewhere nice - have a good time, don't forget to come back:)
Hi maryb,

took the kids to a nice seaside town called Bridport (NE Tasmania).... bleached white sands, warm water in a sandy bay .... and temps over 30C .... just beautiful :)

Cheers.
 

maryb

iherb code TAK122
Messages
3,602
Location
UK
Hi maryb,

took the kids to a nice seaside town called Bridport (NE Tasmania).... bleached white sands, warm water in a sandy bay .... and temps over 30C .... just beautiful :)

Cheers.

Well we've got rain, rain rain and more rain, the ground is so wet its colder at 8oC than it would be at -2. That cold damp that gets in your bones - all ages too, my cleaner who's only 36 was complaining yesterday. Horrible.
Glad someone's got the sunshine somewhere, Bridport sounds fabulous, glad you had a good time.
 
Messages
43
Hi PathogenKiller .... this is great to hear ..... just be very mindful of 1 thing though .... Don't use azithro again .... the reason being if you did not take it out completely the first time the strep will be 100% resistant to azithro now ....... Do not pulse it .... what will happen is the azithro will kill off the good bacteria, allowing the strep to regain hold ......... I have papers here on this, 7 days treatment of azithro increases strep resistance to it by up to 80% .....

To get it all .... Gentamycin/vancomycin IV ...... 2 - 4 weeks ..... Not sure which one will work best .... and chew xylitol gum flat out to stop it from coming back .....

I am so happy to hear this :)

I did Zithro for a month. I'm not going after my strep with Zithro. My doc sas youd have to be on abx for years to treat chronic strep. My titers have been coming down on herbs so I'm cool with that. Went from. 900+ down under 400 in 6 months while fighting Lyme and myco too. I already use a xylitol as a mouthwash and gargle for the strep. Im sure the Zithro was active against the strep. Also, are you familiar with pairing efflux pump inhibitors like berberine with abx? It really helps resistance. Also, serrazimes. Just took my 12 month blood tests so well see what's up. I can't believe the change in just one year. It's been amazing.
 
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maryb

iherb code TAK122
Messages
3,602
Location
UK
@PathogenKiller
glad to hear your levels are coming down, such good news. Can you tell me more about the herbs you are using and the use of berberine with abx.
also why would you choose serrazimes over serrapeptase?
thanks
 

Elph68

Senior Member
Messages
598
Unless you have references that show that destruction of epithelial cells leads to leaky gut, you shouldn't state this as a fact.


Elph68, your statements do not seem to be backed up by science or fact; rather your statements are your own speculation.

There is nothing wrong with presenting personal ideas and well-reasoned speculation, but you should make it clear what is fact, and what is speculation. If you present your own unverified ideas as an established fact, then that is misinformation. But if you make clear that these ideas are speculation, then fine.


For example, it is fine to write: "I have an idea that the destruction of epithelial cells could lead to leaky gut," and then you might explain your reasoning of why you think this might be the case.

But if you write: "the destruction of epithelial cells causes leaky gut," then it is wrong to say this, because you are presenting this as a proven fact, but really is just your personal hunch or speculative idea.


Some of the most interesting writing on this forum is speculative but with the speculation based on a foundation of scientific fact. That is how science operates: it creates a solid foundation of established fact, and then makes small speculative leaps forward from that foundation.

So this is why it is important to clearly state in your writing what is established fact, and what is a speculative leap forward from that foundation of fact.

Hi Hip,

I am very sorry that it has taken so long to reply but I have been a little busy .... If I am making a theoretical assumption, I will say so .... A scientific fact is what I have been talking about here.

You will see in this paper that destruction of the epithelial layer=increased intestinal permeability otherwise known as a 'leaky gut' .... which is what I am trying to get across here in this thread.

http://www.wjgnet.com/1007-9327/full/v19/i43/7531.htm

This talks of protease expression, which is the foundation of the 'undetectable infection' thread. Protease expression is what causes the inflammation and IgA antibodies. The biofilms also produce super oxide and hydrogen peroxide as stated in previous threads which also damages the epithelial layer .....
 
Messages
43
@PathogenKiller
glad to hear your levels are coming down, such good news. Can you tell me more about the herbs you are using and the use of berberine with abx.
also why would you choose serrazimes over serrapeptase?
thanks
My primary supplements/herbs are
Olive Leaf Extract
Berberine
Triphala
Anatumul
NAC
methyl b-12
lmthf
b-5
ubiquinol
butyrate
biotin
lactoferrin
probiotics
various enzymes

Here is a study about efflux pump inhibitors
http://jac.oxfordjournals.org/content/59/6/1247.fullhttp://jac.oxfordjournals.org/content/59/6/1247.full

I take serrazimes because it is supposedly a cleaner version. Most of these enzymes are fermented products and thus that leaves room for mold contamination, inactivity.. etc.
 

Hip

Senior Member
Messages
17,824
You will see in this paper that destruction of the epithelial layer=increased intestinal permeability otherwise known as a 'leaky gut' .... which is what I am trying to get across here in this thread.

http://www.wjgnet.com/1007-9327/full/v19/i43/7531.htm

I had a quick glance, but I cannot find anything in that paper which states that destruction of the epithelial layer leads to increased intestinal permeability. Perhaps you might want to quote the paragraph where you believe it states this.
 

knackers323

Senior Member
Messages
1,625
My primary supplements/herbs are
Olive Leaf Extract
Berberine
Triphala
Anatumul
NAC
methyl b-12
lmthf
b-5
ubiquinol
butyrate
biotin
lactoferrin
probiotics
various enzymes

Here is a study about efflux pump inhibitors
http://jac.oxfordjournals.org/content/59/6/1247.fullhttp://jac.oxfordjournals.org/content/59/6/1247.full

I take serrazimes because it is supposedly a cleaner version. Most of these enzymes are fermented products and thus that leaves room for mold contamination, inactivity.. etc.

Do you notice any effect directly from NAC, good or bad? It makes me feel worse.
 

MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
I had a quick glance, but I cannot find anything in that paper which states that destruction of the epithelial layer leads to increased intestinal permeability. Perhaps you might want to quote the paragraph where you believe it states this.

I don't have time to read the whole paper but pulled this out of the conclusion:

Proteases are essential for normal physiological development and are involved in numerous processes in our body. They are secreted by various cell types and their receptors are abundant in the gut wall, on immune cells, epithelial cells, and on neuronal cells. A growing amount of evidence supports a role for proteases and their receptors to IBD pathophysiology. The understanding that the enteric microbiota are crucial to disease initiation, and the fact that proteases are secreted by most bacteria and are considered virulence factors in infectious colitis, suggest that perhaps commensal bacterial proteases can also damage epithelial barrier function and may be involved in the initiation and perpetuation of IBD in genetically predisposed patients. Indeed, in this review we have summarized the current evidence that support this notion...
 

Hip

Senior Member
Messages
17,824
@MeSci
Thanks for that extract. It does not seem to mention anything about intestinal permeability though, or say anything about destruction of epithelial cells leading to increased intestinal permeability.

The phrase "epithelial barrier function" refers to the physical barrier provided by the cell membranes of the epithelial cells, plus the tight junctions which are responsible for "stitching" these epithelial cells together. Leaky gut is known to be caused by a failure of the "stitching," that is to say, by tight junction dysfunction. This tight junction dysfunction leads to microscopic holes at the molecular level. Leaky gut occurs at the molecular level. Leaky gut is not like some sieve or tea bag with macroscopically visible holes.

And I have never heard of leaky gut being caused by a failure in the epithelial cells themselves. If there were any destruction to epithelial cells, I would think that the self-repair processes of the epithelial layer would kick in, and rapidly fix and repair the damage, just as when you cut your skin and the skin healing process kicks in.
 
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MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
@MeSci
Thanks for that extract. It does not seem to mention anything about intestinal permeability though, or say anything about destruction of epithelial cells leading to increased intestinal permeability.

The phrase "epithelial barrier function" refers to the physical barrier provided by the cell membranes of the epithelial cells, plus the tight junctions which are responsible for "stitching" these epithelial cells together. Leaky gut is known to be caused by a failure of the "stitching," that is to say, by tight junction dysfunction. This tight junction dysfunction leads to microscopic holes at the molecular level. Leaky gut occurs at the molecular level. Leaky gut is not like some sieve or tea bag with macroscopically visible holes.

And I have never heard of leaky gut being caused by a failure in the epithelial cells themselves. If there were any destruction to epithelial cells, I would think that the self-repair processes of the epithelial layer would kick in, and rapidly fix and repair the damage, just as when you cut your skin and the skin healing process kicks in.

It does mention permeability:

proteases originating from commensal enteric bacteria also have a potential association with intestinal inflammation via increased enteric permeability.

Yes, as I understand it, leaky gut is about disruption of the tight junctions, and I have not yet seen evidence of destruction of epithelial cells.

NB the paper in question is about inflammatory bowel disease, so not sure how relevant it is to other bowel conditions.
 

Elph68

Senior Member
Messages
598
I had a quick glance, but I cannot find anything in that paper which states that destruction of the epithelial layer leads to increased intestinal permeability. Perhaps you might want to quote the paragraph where you believe it states this.

You only had to read the abstract, the 7th line in ....

Numerous reports have identified a dysbiosis in the intestinal microbiota in patients suffering from inflammatory bowel diseases (IBD), yet the mechanism(s) in which this complex microbial community initiates or perpetuates inflammation remains unclear. The purpose of this review is to present evidence for one such mechanism that implicates enteric microbial derived proteases in the pathogenesis of IBD. We highlight and discuss studies demonstrating that proteases and protease receptors are abundant in the digestive system. Additionally, we investigate studies demonstrating an association between increased luminal protease activity and activation of protease receptors, ultimately resulting in increased intestinal permeability and exacerbation of colitis in animal models as well as in human IBD. Proteases are essential for the normal functioning of bacteria and in some cases can serve as virulence factors for pathogenic bacteria. Although not classified as traditional virulence factors, proteases originating from commensal enteric bacteria also have a potential association with intestinal inflammation via increased enteric permeability. Reports of increased protease activity in stools from IBD patients support a possible mechanism for a dysbiotic enteric microbiota in IBD. A better understanding of these pathways and characterization of the enteric bacteria involved, their proteases, and protease receptors may pave the way for new therapeutic approaches for these diseases.

And if you want a broad definition .... colitis is a result of the destruction of the epithelial layer .....
 

Elph68

Senior Member
Messages
598
It does mention permeability:



Yes, as I understand it, leaky gut is about disruption of the tight junctions, and I have not yet seen evidence of destruction of epithelial cells.

NB the paper in question is about inflammatory bowel disease, so not sure how relevant it is to other bowel conditions.

Hi MeSci,

there is a likelyhood that they may find a lot of people that have IBS, in fact have IBD, it is just not easily detectable ...
 

Elph68

Senior Member
Messages
598
@MeSci
Thanks for that extract. It does not seem to mention anything about intestinal permeability though, or say anything about destruction of epithelial cells leading to increased intestinal permeability.

The phrase "epithelial barrier function" refers to the physical barrier provided by the cell membranes of the epithelial cells, plus the tight junctions which are responsible for "stitching" these epithelial cells together. Leaky gut is known to be caused by a failure of the "stitching," that is to say, by tight junction dysfunction. This tight junction dysfunction leads to microscopic holes at the molecular level. Leaky gut occurs at the molecular level. Leaky gut is not like some sieve or tea bag with macroscopically visible holes.

And I have never heard of leaky gut being caused by a failure in the epithelial cells themselves. If there were any destruction to epithelial cells, I would think that the self-repair processes of the epithelial layer would kick in, and rapidly fix and repair the damage, just as when you cut your skin and the skin healing process kicks in.

Unfortunately there are 2 basic mechanisms that prevent the total repair ....
1. protease activity
2. Super oxide and hydrogen peroxide production

So using your analogy of a cut ... if you cut your finger and then continually scrape it out with a sharp object, it never completely heals.....
 

Hip

Senior Member
Messages
17,824
@Elph68
It seems that you are right that a loss of epithelial cells can increase intestinal permeability, but the study you quoted says this happens in the context of inflammatory bowel diseases (IBD), which are a set of severe bowel conditions, such as Crohn's and ulcerative colitis (UC).

However, ME/CFS patients generally do not have Crohn's or UC or other forms of IBD, so this epithelial cell damage probably does not apply to ME/CFS, or to most other diseases. Most diseases do not involve severe bowel inflammation.

Many ME/CFS patients do have irritable bowel syndrome (IBS), myself included, but if there is any inflammation in IBS, it is very subtle and weak, not like the severe bowel inflammation found in Crohn's or UC.

I should think that outside of IBD, you will not get loss of epithelial cells, and so I would think that outside of IBD, leaky gut when it does occur will be only be caused by tight junction dysfunction in most people.



Incidentally, I have speculated that a leaky gut from tight junction dysfunction may promote the coxsackievirus B infections that are strongly linked to ME/CFS.

The receptor that many coxsackievirus B species attach to in order to enter and infect human cells is called the coxsackievirus and adenovirus receptor (CAR). The interesting thing about CAR is that it is found in an inaccessible location: CAR is actually part of the tight junction that binds together the epithelial cells in the intestinal lining, and tight junctions are normally closed, making CAR inaccessible.

So how does coxsackievirus B attach itself to CAR?

This passage explains it:
"Coxsackievirus B uses the coxsackievirus and adenovirus receptor (CAR) to attaches itself to the cell. However, the CAR remains below the surface of epithelial cells, in a seemingly inaccessible location called the tight junction.

In the new study, Drs. Bergelson and Coyne found that CVBs have evolved an indirect route of attack. The virus first attaches itself to more accessible cell receptors called decay accelerating factor receptors (DAF) that lie exposed on the upper surface of epithelial cells.

After attaching itself to a DAF receptor, the virus triggers two signals that open the door to infection. One signal causes the virus to move into the tight junction, where it can reach the CAR. A second signal leads the virus to move deeper into cells where it can release its nucleic acid payload and complete the process of infection.
"

Source: here.

So I can't help wondering whether having leaky gut, where your tight junctions are open and dysfunctional, may allow a coxsackievirus B infection in the gut to become worse than normal, as one might speculate that a leaky gut will make the CAR receptors more accessible to coxsackievirus B.

But this is all just pure speculation.
 
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MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
colitis is a result of the destruction of the epithelial layer .....

Where does it say that? There are several forms of colitis, one, interestingly, being caused by CMV, one of the exclusionary causes tested for in the diagnosis of ME/CFS. That is described here. I still haven't spotted anything in your linked abstract about proteases destroying epithelial cells - can you point me to it?

I was diagnosed with 'spastic colon' (an old name for IBS) at the age of 11, having been opened up due to suspected appendicitis. My colon was said to be inflamed.
 

MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
@Elph68
It seems that you are right that a loss of epithelial cells can increase intestinal permeability, but the study you quoted says this happens in the context of inflammatory bowel diseases (IBD), which are a set of severe bowel conditions, such as Crohn's and ulcerative colitis (UC).

However, ME/CFS patients generally do not have Crohn's or UC or other forms of IBD, so this epithelial cell damage probably does not apply to ME/CFS, or to most other diseases. Most diseases do not involve severe bowel inflammation.

Many ME/CFS patients do have irritable bowel syndrome (IBS), myself included, but if there is any inflammation in IBS, it is very subtle and weak, not like the severe bowel inflammation found in Crohn's or UC.

I should think that outside of IBD, you will not get loss of epithelial cells, and so I would think that outside of IBD, leaky gut when it does occur will be only be caused by tight junction dysfunction in most people.



Incidentally, I have speculated that a leaky gut from tight junction dysfunction may promote the coxsackievirus B infections that are strongly linked to ME/CFS.

The receptor that many coxsackievirus B species attach to in order to enter and infect human cells is called the coxsackievirus and adenovirus receptor (CAR). The interesting thing about CAR is that it is found in an inaccessible location: CAR is actually part of the tight junction that binds together the epithelial cells in the intestinal lining, and tight junctions are normally closed, making CAR inaccessible.

So how does coxsackievirus B attach itself to CAR?

This passage explains it:


So I can't help wondering whether having leaky gut, where your tight junctions are open and dysfunctional, may allow a coxsackievirus B infection in the gut to become worse than normal, as one might speculate that a leaky gut will make the CAR receptors more accessible to coxsackievirus B.

But this is all just pure speculation.

Perhaps the more crucial thing is that by attaching to this receptor the virus is able to enter the bloodstream and thus access the rest of the body. Interesting find.
 

Hip

Senior Member
Messages
17,824
Perhaps the more crucial thing is that by attaching to this receptor the virus is able to enter the bloodstream and thus access the rest of the body. Interesting find.

Or alternatively, one could speculate a leaky gut might allow the virus easier access the vagus nerve — a nerve which enervates the gut tissues and runs from gut to brain — and then travel along this nerve, and enter the brain.

Dr Chia said that this vagus nerve route may be how coxsackievirus B is able to get into the brain. There is a mechanism of transport that viruses can use to travel along nerves called retrograde axonal transport (RAT). By means of RAT, it takes just three days for a virus to travel all the way along the vagus nerve, from gut to brain.