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Meg Mangin R.N.
Research Team
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Posted: Sun Mar 27th, 2005 02:09 |
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Simple explanation of the Marshall Protocol
The Marshall Protocol was developed by Professor Trevor Marshall, Ph.D in 2002 to treat certain diseases that involve Th1 immune system dysfunction.
Prof. Marshall's papers describe how numerous Th1 diseases such as sarcoidosis, Lyme disease, chronic fatigue syndrome, fibromyalgia, lupus and rheumatoid arthritis (among others) are caused by Cell Wall Deficient (CWD) bacteria of various species.
These bacteria are able to hide safely inside phagocytes (large white blood cells in the body's immune system which are designed to engulf and digest foreign invaders) instead of being "digested" (killed) by the phagocytic cells that ingested them.
These infected white blood cells are themselves the source of the elevated 1,25-D levels in our bodies. Normally, 25-D is converted to 1,25-D only in the kidneys, where the body has distinct processes that regulate the conversion rate. White blood cells that host CWD bacteria, however, convert 25-D to 1,25-D on their own. The process is self-perpetuating, because with higher levels of 1,25-D circulating in our bodies it becomes easier for still more CWD bacteria to penetrate white blood cells.
Detection of inflammation caused by these bacteria is accomplished with two basic blood tests....the D metabolites:
1,25 dihydroxyvitamin-D and 25 hydroxyvitamin-D.
The body normally regulates the amount of 1,25-D it generates. This is a secosteroid hormone and is critical to many functions throughout the body.
But 1,25-D is also a paracrine mediator, a cytokine. The concentration in inflamed tissue builds up to many times greater than it is in the bloodstream, and the kidneys cannot regulate its level in the tissue. The kidneys do try to regulate the level in the blood, however.
An essential part of the Marshall Protocol is avoidance of foods and supplements containing vitamin D to reduce the level of 25-D which suppresses the immune system.
The aim of cutting your 25-D down is to prevent it from displacing the active metabolite from the Vitamin D Receptor, thus preventing normal immune system function.
The kidneys will try and regulate the levels of 1,25-D which reach the bloodstream. In acute Th1 disease they can't do that, there is just too much 1,25-D being created for the kidneys to regulate it.
It may be necessary for many people, but not all, to avoid exposure to natural light and bright lights.
A key part of the protocol is the establishment of an inflammatory blockade of the hormone Angiotensin II with an Angiotensin Receptor Blocker (ARB), Benicar (olmesartan medoxomil).
The protocol also includes the introduction of carefully, selected low dose antibiotics in a pulsed schedule.
For detailed information on implementing the Marshall Protocol, see the MP Phase 1 Document.pdf
See also:
What is the Marshall Protocol?
About the Marshall ProtocolLast edited on Thu Jul 31st, 2008 18:34 by
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Aussie Barb
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Posted: Wed May 11th, 2005 17:24 |
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Simple explanation of the Marshall Pathogenesis
* Once a disease pathogenesis is understood, that pathogenesis determines the treatment.
* The Marshall Protocol is the treatment of choice for patients with many chronic illnesses.
* The common denominator in these illnesses is the invasion of white blood cells by tiny cell-wall-deficient bacteria. These bacteria activate the immune cells they penetrate, stimulating production of inflammatory cytokines. Because the bacteria are stimulating the T-helper 1 process of the immune system, the result is called Th1 inflammation.
* Elevated levels of 1,25-D - the active hormone metabolized from Vitamin D - is a defining characteristic of Th1 inflammation.
* In healthy people, Vitamin D (25-D) is converted to 1,25-D in the kidneys, where the levels are regulated to match the body's needs.
* In people with Th1 inflammation, infected white blood cells convert 25-D to 1,25-D independently of the kidneys, causing levels to rise above what the body requires.
* Elevated 1,25-D makes it easier for the bacteria to move in and out of cells, protecting them from the immune system. As more bacteria are able to parasitize white blood cells, they in turn produce still more 1,25-D. This vicious cycle largely accounts for the chronic nature of Th1 illnesses.
* Elevated 1,25-D has direct adverse effects on well-being, and is capable of causing a truly astonishing variety of symptoms in its own right.
* Reducing 1,25-D is imperative to recover your health.
* Dietary changes are essential. Strict avoidance of dietary sources of Vitamin D, including supplements, reduces the amount of 25-D available to be converted into 1,25-D. It is also vital to reduce the level of 25-D because it is a secosteroid that suppresses the innate immune system.
* Many folks may be photosensitive. Sunlight on skin triggers the production of additional 1,25-D. Light in they eyes may cause neurological symptoms. Folks who are photosensitive must avoid exposure to natural light and bright lights to prevent symptoms that may decrease their ability to tolerate the immunopathology of the MP recovery process.
* The MP requires a high degree of commitment. If you follow the Marshall Protocol with diligence, you have an excellent chance of getting well.
This graphic illustrates The Disease Process of Cell Wall Deficient (CWD) Bacteria
Thanks to Gary Kays.....
Last edited on Wed Mar 12th, 2008 03:34 by Meg Mangin R.N.
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Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| 24+ years not Dx| ABCofMP
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Aussie Barb
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Posted: Fri Jul 22nd, 2005 16:41 |
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Simple explanation of the pathogenesis of Th1 inflammation
-The CWD-bacteria create the dysregulation. They create 1,25-D in quantities that your body can't handle.
-The latest research as pointed out by Dr Marshall clearly indicates that it is not just one bacteria making you sick, but an accumulation of bacteria and the changes they provoke in the cells they infect.
-You get these bacteria in all sorts of ways; by water, soil, milk, sperm, blood transfusion, etc.
-Research found that a cell that was invaded by one bacteria led to 70 new genes and 368 altered genes.
-An immunecell is programmed to kill and destroy invaders
-A bacteria getting in that cell alters that program, making it possible for more bacteria to get in by producing 1,25-D which affects the proteins in the cell's wall, creating gaps where they can sneak in
-If a second bacteria of another species gets in, that leads to even more reprogramming. Possibly that new program makes the immunecell create the cytokine-cascade (the actual inflammation)
-Dr Marshall believes that there are many new programs possible if even more species enter/infect the cells
-Some of these new programs are called RA, some are called Lyme, some CFS etc.
-In other words: the constant reprogramming of the genes in your cells by the different species of CWD-bacteria and possibly the order in which they infect the cells leads to the different Th1-illnesses, not an initial genetic defect
(BTW, On the DVDs Dr Marshall pointed out that the research of Prof. Bach showed that cumulative infection/ gathering of CWD-bacteria had a definite impact)
Cell Wall Deficient Bacteria (CWD)
Cell Wall Deficient bacteria act in four ways:
1. they produce 1,25-D to 'hide' from the immunes ystem
2. they produce 1,25-D to weaken the cell walls of the immune system cells
3. they produce excess 1,25-D which is the hormone that is like the 'fuel' for inflammation (it is needed for the immune-cells to differentiate)
4. they directly stimulate the phagocytes (nucleus) to start a cytokine cascade (the actual inflammation)
CWD bacteria need angiotensin II to do the first 3 and Benicar blocks that, thereby turning it all around:
1. they are less able to hide
2. they can't slip in and out of the cells of the immune system so easily
3. there is less 1,25-D, so less 'fuel' for the inflammation, therefore bringing the inflammation down
-Benicar blocks only angiotensin II type one receptors to inhibit bacterial growth.
-Benicar does not inhibit the good effects of angiotensin II type 2 receptors and this allows the immune system to function normally.
Successive intracellular infection
-We all get invaded/infected by CWD-bacteria constantly.
-These CWD-bacteria alter the genes in the invaded/infected cells (not the human genes/DNA, but only the genes in the infected cells' nucleus).
-If you are first invaded/infected by CWD # 1 you may have 70 genes that are altered (this is shown by research).
-If you are then invaded/infected by bacteria #2, there will be even more genes altered, as well as the ones that are already altered.
-You can see that if you get invaded/infected by more and more species, you can get enormous changes.
-You, and also everyone else on this planet, will give CWD-bacteria to other people.
Biofilms
-Several sorts of bacteria make biofilms. Our 'beloved' CWD too.
-Biofilms consist of colonies of bacteria. This makes up the DNA pea soup, since these colonies consist of all sorts of bacteria, probably also the CWD forms we know.
-Several sorts of bacteria manufacture capnine.
The order in which things seem to develop:
- Bacterium 1 enters cell
- Innate immunity cannot kill it: this might be because vitamin D is too high, but also because of the capnine some bacteria manufacture, so there are now at least two mechanisms the bacteria use to evade being killed by the host (that's us)
- Bacterium 1 starts making biofilm, thereby further evading being killed (this might in fact be mechanism number three)
- Bacterium 1 also starts de-regulating the host (our) DNA
- Now bacterium 2 (might be and probably is of a totally different species) enters the cell and also enters the biofilm, and helps bacterium 1 to make more biofilm
- Even more changes in host (our) DNA are being made
- The bacteria start mutiplying, more capnine is produced, more biofilm, and then the kids move out, so to speak, and move to other cells, etc, etc
(This might be what we are observing under the microscope, once the bacteria's "food has run out", those long strings of pearls, they are probably trying to move to other cells to survive)
- etcetera
 Frans
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Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| 24+ years not Dx| ABCofMP
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Meg Mangin R.N.
Research Team
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Posted: Sat Sep 10th, 2005 02:59 |
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(filename)
Simplified guide to the Marshall Protocol
- Inflammation is bad.
- Chronic inflammation is caused by bacteria inside the cells of the immune system.
- Hormone D increases with inflammation and protects the bacteria.. Chronic intracellular infection causes a dysregulation of how Vitamin D is metabolized and too much Hormone D is produced by the body.
- Eating too much vitamin D fuels the inflammation and shuts down the bug killing and causes a host of other symptoms.
- Up to a point increased inflammation may make us feel better, because it suppresses the immune system, sort of like prednisone, which helps relieve symptoms at the expense of crippling the immune system.
- We can't get WELL until ALL the intracellular bacteria are killed.
- Benicar helps the immune system 'see' the intracellular bacteria.
- Inflammation increases when pathogens are killed because the immune system reacts to the dying bacteria.
- This is called immunopathology (Herx) and it produces symptoms that can make you feel BAD.
- Benicar protects the body from the effects of inflammation-helps you feel better and prevents tissue damage.
- We may have an immune system reaction on antibiotics alone because SOME pathogens are being killed, but some pathogens may still be hiding in the cells.
- Benicar reveals ALL the pathogens to the immune system.
- We may initially feel confused and disappointed because we feel worse when we hoped to get relief from symptoms.
- We need to remember that Benicar potentiates the killing of pathogens.
- If it were possible to kill intracellular bacteria as effectively without Benicar we wouldn't be able to tolerate the immune system reaction.
- We're killing more pathogens, but the immune system reaction is controlled with Benicar.
- Is it worth it? I submit that we're getting far more 'bang for the buck', so YES, IT'S DEFINITELY WORTH IT!
- We also need to discourage intracellular bacteria from taking hold again in the future; once we get healthy we're going to want to STAY HEALTHY.
- We're pioneers here. We need to work together, and we need to thank Dr. Marshall and his fellow sarcoidosis patients who have scattered the seeds to make a trail for people with other Th1 diseases to follow. ~Sujay,MD
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Meg Mangin R.N.
Research Team
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Posted: Wed Nov 8th, 2006 03:33 |
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Simple explanation of the action of Benicar
Action of Benicar, 25-D and 1,25-D on the Vitamin D Receptor
-The VDR (Vitamin D Receptor) must be turned on for innate immunity to work.
-Vitamin D and 25-D are antagonists, only 1,25-D is the agonist.
-The only thing which turns the VDR on is 1,25D. So, you need some 1,25D but not a lot (20pg/mL is a good number). If you get too much 1,25D = BAD (starts to affect other receptors and makes you ill, that's why you're here).
-One of the reasons we need Benicar is to compete with 25D to bind with the VDR. There are plenty more reasons we need Benicar (antimicrobial, helps reduce angiotensin II, etc).
-Benicar acts upon the palliative receptors only at high doses, as its affinity isn't as high for them as it is for the VDR and AG2R.
-25-D blocks the action of the VDR and suppresses the immune system (not good).
Why Benicar is important to the immune system
-DNA forms a sort of blueprint of our bodies.
-There is, however, a distinction to be made between DNA for the whole body (chromosomal DNA, found e.g. in our stem cells) and DNA per cell (cellular DNA).
-Each cell has its own DNA, carrying the blueprint of what function this particular cell can perform. You can imagine that a braincell needs different DNA than a muscle cell.
But how does DNA work its magic?
-Each cell contains so called receptors. These are big molecules that react with molecules that enter our bodies via food or drinks.
-For example: if you eat fatty food, you ingest a lot of vitamin D molecules. These molecules are transformed to 1,25D in the kidneys. This 1,25D reacts especially with a receptor called the vitamin D receptor (VDR).
-This reaction leads to the receptor activating DNA (DNA transcription), which in turn leads to the creation of certain ligands and molecules.
-Our immunesystem consists roughly of two different parts, the so called innate immunesystem and the adaptive immunesystem.
-The adaptive part, which works with antibodies, protects you from getting the same disease twice.
-The innate immunesystem, however, is just as important!
-The innate immunesystem consists of several parts. The most important part you need to know in relation to the MarshallProtocol and innate immunity is that every cell contains its own, small (innate) immunesystem.
-Why? Because bacteria, viruses and other microbes can invade the cells of our bodies, like muscle cells and braincells.
-The cell’s own little immunesystem ‘sees’ the microbes and start signalling to the rest of the body that it is invaded by a microbe. This recruits other white bloodcells to the scene, that eat up the invaded cell including the microbe that is in there.
-To describe this a little more complicated: the innate immunesystem in each cell consists, among other things, of several receptors that react with molecules of the invading microbe, eg with lipopolysaccharides (LPS) in the cell wall of bacteria. This reaction of the receptor with the parts of microbes leads, in fact, to DNA transcription by the receptor which leads to the creation of, eg, chemical substances that recruit other white blood cells (eg macrophages) to the scene. These chemicals consist of, eg, the so-called cytokines.
-To maintain a healthy body, it is therefore imperative that this innate immunesystem works!
-Recent research has shown the crucial role of the VDR in this innate immunity and is revealing more and more every day.
-Why? Because the DNA transcription by the VDR is responsible for the creation of several of these receptors of the innate immunesystem. (eg the Toll Like Receptors (TLR’s)
-So, if the VDR doesn’t work properly, our cells get invaded and lack the ability to react with parts of the invading microbes, which should lead to the cells and microbes getting killed. In other words: one is infected for life… also called chronic disease.
-So, what is the significance of this theoretic excercise?
-One: eg Wirostko has shown bacteria in cells where they shouldn’t be able to live if our innate immunesystems worked, showing that innate immunity is somehow compromised;
-Two: Olmesartan (Benicar) enables the innate immune system to work again as planned! Benicar therefore acts as a sort of anti-microbial! ~Frans
See also:
Inside the cell
Cell biology animation
Infectious diseases: animation
Cell Wall Deficient Bacteria and the Marshall Protocol
Bactera vs genes: the spread of chronic disease in families
Last edited on Wed Mar 5th, 2008 14:04 by Meg Mangin R.N.
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Meg Mangin R.N.
Research Team
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Posted: Tue Jan 30th, 2007 01:18 |
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(filelink)
Simple explanation of innate immunity
Innate immunity is the part of the general immunity each individual is born with.
Innate immunity is different from acquired immunity, which develops specifically over time as our body is challenged by pathogens. Acquired immunity is also called adaptive immunity because the body develops a "memory" of specific pathogens it has identified in the past.
Innate immunity protects the body against microorganisms in general, either before they can gain entry (skin, coughing and sneezing are examples) or by killing them or protecting us from them after they have entered our body. Innate immunity includes chemicals that are produced by the body to disable or kill invaders (this includes inflammation) and special immune system cells that attack invaders. Phagocytosis, ingestion and killing of foreign particles, is an example of innate immunity. The body doesn't have to identify the specific particle; it only has to identify it as an invader that isn't supposed to be there.
 Belinda
See also A Brief Overview of Innate and Adaptive Immunity in Relation to the Marshall Protocol
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Meg Mangin R.N.
Research Team
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Posted: Fri May 4th, 2007 19:50 |
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[filelink]
Simple explanation of new research
The understanding of the science behind infection by CWD organisms has been evolving over the last few years. However, the following facts have remained:
1) CWD bacteria suppress the innate immune system. Benicar reactivates it so it can kill the bacteria and pulsed antibiotics can be effective.
2) 1,25D activates the immune system by docking onto the VDRs as an agonist. However, an infection with CWD organisms results in the production of extrarenal 1,25D, which when excessive, leads to problems such as osteoporosis, immune suppression and hormonal irregularities.
Now, from more recent research, I would add to these the following:
1) CWD organisms inactivate the innate immune system by directly providing antagonist ligands to dock to the VDRs.
2) The body responds to CWD organisms by producing extrarenal 1,25D. However, this extrarenal 1,25D is blocked from the VDRs by these bacterially produced antagonist ligands, so it is not as capable of activating the innate immune system. Instead the 1,25D concentration increases until it affects other receptors causing the problems described above.
3) Sunshine and dietary vitamin D when converted to 1,25D can activate the innate immune system in healthy individuals and thus help to treat infection. However, sunshine and dietary vitamin D can harm those who are already seriously infected by providing the source for an excess of 1,25D (i.e. a higher concentration than is useful for activating the VDRs).
4) A high concentration of 25D (dietary vitamin D) provides antagonist ligands to the VDRs, blocking 1,25D from docking to them. This prevents the innate immune system from being activated.
The strategy for treatment remains the same:
1) Reduce dietary vitamin D until the concentration of 25-D is below the level that would interfere with the reactivation of the innate immune system.
2) Reduce dietary vitamin D until the concentration of 1,25-D is within the normal range. Dietary vitamin D is the precursor to 1,25-D.
3) Take Benicar to activate the innate immune system and to provide suppression of inflammation.
4) Reduce light in response to photosensitivity and to reduce the concentration of 1,25-D to within the normal range.
5) Take antibiotics in such as way as to produce tolerable herxing/immunopathology.
6) Look after your yourself and your disease symptoms (get plenty of rest, drink plenty of fluids, etc.). ~KenC
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Meg Mangin R.N.
Research Team
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Posted: Tue Feb 5th, 2008 05:01 |
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[filelink]Simple explanation of vitamin D metabolism
There are two forms of Vitamin D.....active and inactive.
Vitamin D is not a vitamin. Vitamins are substances the body cannot make (lack of Vitamin C causing scurvy is a good example).
Vitamin D is a secosteroid hormone with a function similar to that which prednisone performs. It was misidentified when it was discovered (at the University of Wisconsin) and the name has stuck. Vitamin D (a secosteroid hormone) is an immune-suppressant.
The body makes the inactive form of Vitamin D in the cells of the skin.
The Vitamin D made in the skin is inactive and easy to measure. It's only function is as a precursor for the body to make the active form of Vitamin D.
People do not need to take Vitamin D in any form (food or supplements) to have enough of the active form in their body because the body makes it in the kidneys and other cells using the inactive form made in the skin.
It only takes a few minutes of natural light to produce enough inactive Vitamin D which is stored by the body for use when natural light is scarce.
The active form of Vitamin D is used by the Vitamin D Receptors (VDR) in almost every cell in the body, including immune system cells, for many vital functions including activating the immune system.
Most chronic disease is caused by inflammation. Inflammation is caused by intracellular bacteria that live within the white cells of the immune system.
These bacteria block activation of the Vitamin D Receptors in the cells, so that key antimicrobial peptides cannot be manufactured by the immune system, and in the process cause the body to produce too much active Vitamin D to accumulate in the cells.
Thus, the bacteria can continue to live and multiply within the cells of the immune system.
People who are ill with inflammatory diseases make too much of the active hormone but scientists rarely measure this because it is difficult and expensive.
People who are ill and have too much of the active Vitamin D will have a low level of the inactive Vitamin D because of a complicated feedback mechanism in the cells that manufacture the active Vitamin D. In other words, the high active Vitamin D reduces the level of the inactive Vitamin D....remember this is the only form scientists usually bother to measure.....erroneously thinking that a low inactive level means a low active level.
Scientists have ignored this crucial fact and base conclusions about disease on the measurement of only the inactive Vitamin D which is low because of the disease process.
When people with chronic disease have their active Vitamin D level measured it is found to be high.
Low inactive Vitamin D does not cause diseases. The diseases cause the low inactive Vitamin D.
Studies of Vitamin D need to measure both inactive Vitamin D (which will be low in chronic disease) and the active Vitamin D which will be high in chronic disease in order to come to accurate conclusions about chronic disease.
People with chronic disease who take Vitamin D (food and supplements) will suppress the action of the Vitamin D Receptor and thus turn-off the immune system's response so it cannot fight the intra-phagocytic bacteria that cause chronic inflammatory diseases.
Cancer is caused by inflammation. Taking supplemental vitamin D will not prevent cancer.
Some people feel better in the short-term when they take Vitamin D because bacteria are not being killed which often causes temporary symptoms due to increased toxins, but they will succumb to the chronic diseases which are caused by intracellular infection more rapidly in the long-run.
Many people with chronic diseases feel ill when they take too much Vitamin D or spend too much time in the sun where their skin makes Vitamin D.
Too much active vitamin D has the effect of taking calcium from the bones and depositing it in the heart or lungs or kidneys (kidney stones), reducing their function.
Too much active Vitamin D causes calcium to leech from bones which results in osteoporosis.
Rickets is caused by too little calcium not lack of Vitamin D.
Last edited on Sat Feb 16th, 2008 04:45 by Meg Mangin R.N.
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