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Prof Trevor Marshall
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Prof Rolf Zinkernagel, 1996 Nobel Laureate, gave the keynote at the DMM2006 conference at the Karolinska Institute last May.

The theme of his keynote was: 'you guys/gals forget about autoimmunity - these diseases are due to pathogens' (my paraphrase, of course)

I was so delighted to have the conference kick off in that way that I didn't go straight to the library and pull the text of the paper he was discussing. During the conference I had a number of detailed conversations with him about his work, trying to understand what importance it had to the "Marshall Pathogenesis." I knew it must be important but wasn't sure why:X

Back in California I pulled the paper, and printed the key diagram, which he had caricatured on the whiteboard during his presentation - Figure 8. Here is just the graphics from that figure:



Look. I am a slow learner. I admit it. I am going to hide behind the excuse that I am "thorough":):):)

What Rolf's team had done was to take mice in the first few days after they were born, before their immune systems were producing T-lymphocytes, and inject a virus into their brains. Because their immune systems were unable to fight the virus, or make antibodies to it, the virus persisted in the brains. When those mice were challenged by infection with the same virus later in life they couldn't fight it, and they died (see the sad picture on the top line there...)

The top graph line shows the dotted black line rising at about day 7, when the T-lymphocytes started to be manufactured by the mice immune system.

When other mice were not challenged with the virus until they were grown, and had normally functioning immune systems, they fought the virus, and lived (graph line 2).

So what has this all got to do with the 'Marshall Pathogenesis,' and persistent bacterial infections? Well it has taken me 2 months to realize that here is one mechanism by which babies could be infected at birth.

The human adaptive immune system takes even longer to become fully functional, although the mother is supposed to pass some immune function to the infant by breast feeding.

Worse, if the baby was being bottle-fed (in the 1950's onwards) Nestle was fortifying that milk with Vitamin D, perverting innate immunity. Therefore only adaptive immunity could protect the infant, and the T-lymphocytes associated with adaptive immunity don't appear until weeks after birth (mice live and die at an accelerated rate compared with humans).

Breast fed-babies would eventually get supplemented baby-food as well. But when? Before or after immunity had been acquired? How much sunshine would the infants get? Hmm...

Now if certain bacterial species were able to persistently infect the neo-natal brain in the same way as Rolf's CMV did, then it could be expected that those folk might well experience a greater degree of difficulty clearing a challenge later in life, just like the mice did... Hmmm...

Eureka!...

So we don't need to postulate placental transmission of the pathogens, just normal spread between the family members (and pets) during those first few weeks of life... Ah, that's much more sensible... and there we have the familial aggregation... ("Please pass the baby for a cuddle, Mom")

..Trevor..

ps: Not everybody reacts violently to insect bites.. only a minority.. Only about 5% of tickbite events progress to chronic Lyme... Hmmm...

pps: you don't really want to know this, but hospitals here in California have started to give Hepatitis B immunization to new-borns, even before they are discharged from the maternity ward:X

Reenie
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Trevor,

Wow... that is a real eye opener. :shock:

I was bottle fed and Mom was only allowed to breast feed my older sister one day, then told she couldn't breast feed due to having a different Rh blood factor than us.  Mom's Rh is negative while mine and sis' are positive.  

I wonder how much help that one day gave sis' immune system over mine.  I always seemed to be more sickly than my sis.   

It'll be interesting to see how mine and sis' children do healthwise, being breast fed babies. :cool:

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Trevor-

Why would the mouse survive the virus injection in the first few days but the same virus kill the mouse later in life? In neither case does the innate immune system function so why the differing outcomes?

JCB

Prof Trevor Marshall
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JCB:
They used a lower dose at birth, not enough to kill, only enough to 'plant' the virus.
They also used different (although related) species of virus.

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In reference to the Hep B immunization, here on the East Coast, the birth mother has to sign permission for the shot.  The permission slip is brought in during labor or shortly after giving birth and most of the young mothers don't know enough not to sign.  And why does a newborn need Hep B?  They're not sexually active or have STD, etc.  That shot is terrible for a newborn!!!  So many unknowns associated with it.  This is just my opinion.

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Trevor,
It seems like the paper also proposes that the prior infection increases the inflammatory response to the related virus (via the cytotoxic T cells arising from the early infection), and the increased inflammation can cause inflammatory damage (a hypothesis somewhat in line with the autoimmune view, but with the idea of the long term presence of a microbial trigger).  Is that correct?

It seems to me that the infant would also acquire infections just by sharing the same blood supply with the mother, wouldn't it?  Or is there a problem with that aspect of transmission?

Joyce Waterhouse

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Dr Trevor Marshall wrote: When the same mice were not challenged with the virus until they were grown, and had normally functioning immune systems, they fought the virus, and lived (graph line 2).

Trevor, this is not exactly clear to me. You say: the same mice. Do you mean the ones infected in the first few days after they were born?

Thanks, Frans

From Trevor: Fixed Frans, thanks:)

Last edited on Fri Jul 28th, 2006 13:44 by Prof Trevor Marshall

Prof Trevor Marshall
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Joyce,
Whenever I try to advance the concept that pathogens can be acquired through the placental barrier I hit a lot of resistance, even though I have seen studies showing Mycobacterium tuberculosis transmission via that pathway, and also transmission in sperm (thereby presumably straight into the embryo).

It is certainly easy to see how a wide range of (eg, air-borne or skin-borne) pathogens could be transfered in the first few weeks of life, while acquired immunity is still being built up.

Additionally, this is a persuasive demonstration that a (supposedly pathogenic) virus can persist in the brain throughout life, which, in itself, is a radical departure from conventional thinking. I don't think anybody has given enough thought to persistence, let alone what happens in the first few days and weeks of life.

I think Rolf's attempt to show that the cytotoxic T-cells might be more active is because he didn't have the missing piece of the puzzle (L-forms), we had that...

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Trevor,

I was working on an analogy these last days to explain how the innate immunesystem differs from the acquired one.

To make it extremely short at this time I would make the analogy of building a house (growth of embryo to baby to (even older) child).

When one builds a house, normally there is an overseer making sure that all the materials are in proper order. Eg no rot in the wood or concrete used.

This overseer is the immunesystem.

The problem is that when the overseer trusts the one who is delivering the materials (the mother), but that person is really trying to rip you and your overseer off, you might end up with materials that are rotten to the core.

In this instance it is the virus/L-form that is in the materials that stem from the mother (or, as you point out above, anyone (in the family) who takes the child on her/his lap).

Now, when we keep on using the same overseer for the rest of our lives, the building (the body) will fall apart, since he (the immune system) is convinced the materials used are ok (not infected).

What the MP in fact does, is appoint another overseer who starts inspecting the materials used and finds them faulty (immunesystem starts recognizing the pathogens) and he starts to replace them (herx).

Is this about the drift of what you are saying? I know it is oversimplifying things, but still works for me as an analogy  :D

Sincerely, Frans

Prof Trevor Marshall
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Frans,
I think the MP is like a new boss for the overseer, who retrains him/her to recognize what rot really looks like:)

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You are right, of course, never heard of transplanting a whole immunesystem....

Frans

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Trevor, there is something I don't understand.

When these mice were infected in the first few days, why didn't innate immunity take care of the pathogens.

If innate immunity develops later on, why didn't the innate immunity of these mice get rid of the pathogens after it was fully functional.

How do the pathogens shield themselves from innate immunity in these mice is the right question I guess.

Frans

Prof Trevor Marshall
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Frans, that is the $64,000 question which Rolf's group was posing. They were showing that persistent infection is possible, and how to recreate it in the lab. At least, I think that was what they set out to do. Or maybe it just happened that way, because they were also clearly focused on proving that autoimmunity is not the immune system attacking "self."

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To those of you who are concerned about newborn vaccinations, you should know that parents can postpone the baby's vaccinations. The policy to vaccinate in the hospital was put in place to increase compliance because many parents do not return for clinic visits in a timely manner. Check on the hospital policy before the birth to avoid hassles if a doctor's signed permission is needed.

If parents decide to vaccinate, they can delay the start until the baby is older and also space them out. Not getting more than one vaccination at a time will allow the baby's immune system to cope with the challenge.

Best,

Meg

Toni D
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Meg, this is exactly what my daughter is now doing with her two.  The oldest who received the shot at birth and is now 4 years old is just overcoming speech and language delay.  Some say is related to the Hep B vaccine before he was even a day old.  Others don't know.  The great news is that he's almost completely back on track in all areas of his precious life.

The youngest did not receive the shot, only because my daughter's pediatrician read her the riot act about the oldest one getting it at birth, and all the cons associated thereto.  She is fine, thank God.  Both children receive one shot at a time, even now, mercury free.  It costs more because she (daughter) has more copays, but it's your child's life at stake here.  If there's a reaction, we know immediately what it's from.  There's no guessing games going on.  There's always so much to learn--at any age.

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We were fortunate in having a doctor for our babies who thought it was too much for an infant to get so many vaccinations so early in life.  He just pushed the time table forward, and spaced things out. We had no trouble with having the appropriate vaccinations in time for school attendance.

In terms of breast-fed infants being exposed to vitamin D - friends from Brazil whose brunette daughters were born in Denmark were told that they needed to give their babies vitamin D supplements as they would not get enough vitamin D from the sun in Denmark.  Breast-fed babies in other places were probably also prescribed vitamin D supplements.

I'm surprised that people still think that the placenta will protect against disease transmission.  Babies are certainly born HIV positive, for example, and can also suffer from the mother's case of rubella.

Margo

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Toni D,
Children with learning, attention and relationship difficulties are responding well to the MP. Remember that these Th1 diseases aggregate in the family, especially down the maternal line. Take a look at the parent's forum and see how young Matt, and also Margo's daughter, have overcome their difficulties.

ps: I am not convinced that mercury is the problem. Remember the paper by the scientist who discovered L-forms in 1934: "Filterable Forms of Bacteria."
http://www.marshallprotocol.com/forum39/6844.html
What she meant is that the L-forms are so small they go right through the filters used to ensure purity in pharmaceutical manufacturing. I think you get the picture...

Toni D
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Thank you, Dr. Marshall.  I went to the site, but will have to print it out to read.  My eyes are doing better reading on paper, as opposed to the screen, about right now.  Can then use my magnifying glass;).

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Trevor,

As I understand it, they found that after introducing the virus just after birth, the virus only persisted in the brain, but was eridicated by innate immunity in the other parts of the body.

This seems to me as if the viruses have a preference for certain cells (maybe even bodyparts) which very much reminds me of bacteria who have a preference for certain human cells (bodyparts).

I know you think that the different th1-diseases differ, amongst others, because the different bacteria involved have a liking for different cells/tissues.

Taking this further, it would be of great importance for prof. Z in future experimants, to use other species of viruses or rather, bacteria, to see if they survive in the same way as the virus in this paper of prof. Z.

Furthermore, on cell-level, one should investigate which molecules of the pathogens and the host (human) interact in such a way that they, synergistically (together), evade the innate immune response.

Can you explain how the immunesystem recognizes intracellular infection? I mean what happens if a muscle-cell gets infected. How does the immunesystem 'see' that invader?

Do even 'normal' cells have the ability to show pathogenic proteins/molecules on their surface?

It seems to me that that might be a weak spot.

Sincerely, Frans

Prof Trevor Marshall
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Each family of cells is specialized by not only what is inside its membrane, but the particular set of receptors in its membrane. I think the complexity is probably too great to quantify the cells operation, but not too much to get a broad overview of what is happening.

I wouldn't attempt to guess why the neo-natal mice can't clear the CMV from their brains. But it certainly is a big signpost for us on our quest for an understanding of the precise manner in which Th1 disease manifests itself in so many different ways.

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Owwww, I have looked around a little and see that (most) cells have the MHC molecules that indicate that an invader is present or not, it is simplifying things I know, but do I understand that correctly?

Thank you Trevor.

Prof Trevor Marshall
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It is simplifying things. Everybody thought we understood the immune system. Thats why you'all are still sick:X

Right now there is focus on what happens inside the cell to signal intracellular pathogens. Virtually nothing is known, although there were recent reports that the nuclear membrane apparently also carries receptors, including TLR (Toll-Like-Receptors).

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Dr Trevor Marshall wrote: Frans,
I think the MP is like a new boss for the overseer, who retrains him/her to recognize what rot really looks like:)

Is this a permanent retraining?  In other words, once we finish the MP will our immune system be "fixed" so that it recognizes invaders appropriately.  Or is that what the yearly "cleanup" is for?

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A clearer understanding of horizontal DNA transfer and just which plasmids get "shared" between host and pathogen, how, and impact of timing and innate immune response for initial transfer and subsequent L-form colonization look like a great new horizon for study to build on the MP foundation. Molecular modeling, in vitro and animal studies like Dr Z's are providing clues, but human in vivo descriptions must be the obvious goal.  

As an aside, all those prenatal vitamins I took for each pregnancy and while I was nursing each child for a year or more do not make me feel great as a mother. Never mind the gallons of milk I chugged or those awful green vitamin drops I gave my babies. Who needed formula for dietary D? I also know both my husband (adopted, formula fed) and I had Th1 symptoms well before we married.

Last edited on Sat Jul 29th, 2006 10:39 by jrfoutin

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" Any immune response involves, firstly, recognition of the pathogen or other foreign material, and secondly, a reaction to eliminate it"

We know that microbes, especially zoonotic, have sophisticated means to avoid detection.

"Broadly, the different types of immune response fall into two categories: innate ( or non-adaptive ) immune reponses and adaptive immune responses. The important difference between these is that an adaptive immune response is highly specific for a particular pathogen. Moreover, although the innate response does not alter on repeated exposure to a given infectious agent, the adaptive response improves with each succesive encounter with the same pathogen: in effect the adaptive immune system 'remembers' the infectious agent, and can prevent it from causing disease later."
"Phagocytes and innate immune responses - One important group of leucocytes is the phagocytic cells, such as the monocytes, macrophages and polymorphonuclear neutrophils. These cells bind to microorganisms, internalize them and then kill them."

NOT ALWAYS as we know.

"Because they use primitive non-specific recognition systems which allow them to bind to a variety of microbial products, they mediate innate immune response. In effect, they act as a first line of defence against infection."
"In practice there is considerable interaction between the lymphocytes (adaptive immunity) and phagocytes (innate immunity). For example, some phagocytes can take up antigens and show them to T lymphocytes in a form they can recognize, a process which is called antigen presentation. In turn, the T lymphocytes release soluble factors ( cytokines ), which activate the phagocytes and cause them to destroy the pathogens they have internalized. In another interaction, phagocytes use antibodies released by B lymphocytes to allow them to recognize pathogens more effectively. One consequence of these interactions is that most immune responses to infectious organisms are made up of a variety of innate and adaptive components. In the earliest stages of infection, innate response predominate, but later the lymphocytes start to generate adaptive immune responses. They then 'remember' the pathogen, and mount more effective and rapid responses should the individual become reinfected with the same pathogen at a later date."

With this in mind, besides early innoculations with vaccines ( prior to maturation of the adaptive immune system ), the routine use of innate immune suppressing drugs - called anti-inflammatories, anti-pyretic or anti-histamines, for early infections is IMO the major culprit in the epidemic of chronic illness.

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"...the innate response does not alter on repeated exposure to a given infectious agent, the adaptive response improves with each succesive encounter with the same pathogen..."

"...most immune responses to infectious organisms are made up of a variety of innate and adaptive components. In the earliest stages of infection, innate response predominate, but later the lymphocytes start to generate adaptive immune responses. They then 'remember' the pathogen, and mount more effective and rapid responses should the individual become reinfected with the same pathogen at a later date."

So are you saying this is why Dr Z's early innoculated mouse died upon subsequent introduction of "similar" infection?

You also suggest pinning down the full complexity of the chronic disease epidemic beyond dietary conditions that create a lush environment for opportunistic pathogens to thrive. Routine use of innate immune suppressing drugs like anti-inflammatories, anti-pyretic, or anti-histimines (as well as to a lesser degree dietary D suppressed innate immune function + ample folate food source in the host) and spreading pathogens with
"early innoculations with vaccines ( prior to maturation of the adaptive immune system )..."
"...Is IMO the major culprit in the epidemic of chronic illness."

Then wouldn't looking at environments that had one of the elements along with chronic disease but not the other might be of some value. (Somewhere that D additives have not been popular, but chronic disease exists because of anti-inflamatories, anti-pyretic,or anti-histimines or the opposite countries that have not used anti-inflammatories, anti-pyretic, or anti-histimines but they do use dietary D and have chronic disease).

Zinkernagel's mouse had no D or anti-etc's? and the onset of death was accute after the second challenge?

Prof Trevor Marshall
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Janet,
They don't say what the mice were being fed on, but I imagine it was only the best quality pre-packaged mouse-food, and a few minutes searching through Google should reveal the constituents of that (remember this is Swiss mouse-food). I have little doubt it would be fortified, to give the mice a good start in life.

We use only the finest baby frogs, dew picked and flown from Iraq, cleansed in finest quality spring water, lightly killed, and then sealed in a succulent Swiss quintuple smooth treble cream milk chocolate envelope and lovingly frosted with glucose."

"(Monty Python, 'Crunchy Frog' sketch)


That is actually a very good point, you know, Janet:) Google, someone?

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Hmm, it seems to me dr Z. should also test the D-metabolites next time...

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Sorry about the last loose canon of a post, now something more serious.

Something occurred to me. The virus dr Z. used was only persistent in the brain, but got killed in the rest of the body by innate immunity. This seems to rule out anything suppressing innate immunity.

Another thought, or question rather, is if it is known if certain parts of the body develop innate immunity earlier than others?  If the brain's innate immunity develops slower, this might account for the susceptibility (of the brain in this instance).

Sincerely, Frans

Last edited on Sat Jul 29th, 2006 16:56 by Frans

Prof Trevor Marshall
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Frans,
Look at the graph in my FDA presentation slides. You will see that there is a decade of concentrations over which a drug is replaced on a receptor. It is not a simple ON/OFF switch, it is a gradual suppression, which increases with dose.

http://autoimmunityresearch.org/fda_visiting-professor_7mar06.pdf

Also, it is certainly possible that the immune system behaves differently in the brain, and in the rest of the body, at any concentration.

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I may be a slow study, and there are quite alot of things that I did not understand when reading the good doctor's paper, but what I did notice is that he starts off by saying that many autoimmune diseases are precipitated by viral infections. Throughout the paper he continually makes references to viral infections. As such, is he saying that there is a viral component to sarcoidosis? If that is the case, obviously anitbiotics would not help that "portion" of the disease. What are we to make of this paper then and how does it help us?

I am wondering if the cd's will be ready since I would like to see Dr Eishi's theory of sarcoidosis. I am guessing, however, that nobody here believes strictly in Dr. Eishi's work?  It is interesting that many people have had acne problems, but then again, some have not. What are we to make of his findings?

Are we to think that sarc  likely has a 100% bacterial cause, or is there a possibility that there are viral components to this disease?

Lastly, this question might be more appropriate for another area but here goes:

I am on stage 3...d levels still low I suspect, but not much herxing that I can tell - nothing intolerable at any rate. My acne that started after the MP began has stayed pretty much the same, 2 small lesions have developed, and an existing one has stayed exactly the same. Wouldn't we expect them to start to decline (go away) at some point in time?  Why wouldn't we want to up the M just a little ( to say 150 eod)  to see if this helped at all ? I think this is within the normal amts given to teenagers for acne anyway.

Thanks,
Norman

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Sorry...one more question: If there is a viral component to sarcoidosis as the good doctor suggests, are we therefore "S*** out of luck" for a complete cure? I didn't think the body was able to get rid of many of these viruses on its own.

Thanks again,

Norman

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Frans, maybe a 3 arm double blind study?

  • Add D chow on purpose to one group of mice + vaccinate/challenge.
  • The next group anti-inflamatories, anti-pyretic, or anti-histimines + vaccinate/challenge and no D chow.
  • The next just eat D-free lightly killed baby frogs + vaccinate/challenge (hold the glucose).
Dr Marshall, from a simple Google search I found a rodent chow list. From this short list, one can see diet has (*wink*) nothing (*wink*) to do with controlled clinical animal studies. 

Interesting article also turned up by David G. Baker, Natural Pathogens of Laboratory Mice, Rats, and Rabbits and Their Effects on Research (Division of Laboratory Animal Medicine, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana 70810).

Abstract:
Laboratory mice, rats, and rabbits may harbor a variety of viral, bacterial, parasitic, and fungal agents. Frequently, these organisms cause no overt signs of disease. However, many of the natural pathogens of these laboratory animals may alter host physiology, rendering the host unsuitable for many experimental uses. While the number and prevalence of these pathogens have declined considerably, many still turn up in laboratory animals and represent unwanted variables in research. Investigators using mice, rats, and rabbits in biomedical experimentation should be aware of the profound effects that many of these agents can have on research.
..........................

So I'm back at wanting to see some molecular modeling and a little more evidence from human populations. The FDA CPI opportunity 53 of natural history databases, and also compare/contrast of dietary D to anti-histamine and other anti's mentioned by Blaney (OTC?) or combo of both (hello USA!), with mega-analysis data for chronic disease sounds interesting.
..........................

Norman, My understanding is that sarcoidosis and other Th1 diseases respond to the MP because the innate immune system becomes enabled. The exact pathogen or complexity of pathogens and layering of pathoghens over time vary. Some have more bugs per square inch maybe. I can think of several ph3 folks besides myself that still have skin Herxing from time to time and ongoing. It takes time.

Last edited on Sat Jul 29th, 2006 18:11 by jrfoutin

Prof Trevor Marshall
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Norman,
Once the Th1 bacterial pathogens are killed off, the immune system deals with the viruses it couldn't clear while the bacteria were present. That's why folks lose warts, psoriasis, and other things as they recover on the MP. Relaaaaax...

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LOL.........thanks for the quick response. You always seem to zing me ! LOL !

rick
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  Reenie wrote:” I wonder how much help that one day gave sis' immune system over mine.  I always seemed to be more sickly than my sis.”  

 Jrfoutin wrote; “Who needed formula for dietary D? I also know both my husband (adopted, formula fed) and I had Th1 symptoms well before we married.”  

I find the above two quotes similar to my experience and observations, I was adopted in the nineteen fifties and was taken away from my birth mother at birth.

What I find interesting is that for the first 7-8 years of my life I remember nothing but pain in my bones, primarily the legs and feet which I would describe now as like piano wire being pulled through the marrow.

I know my adoptive parents took me to specialist after specialist with no reasonable explanation for this pain. I remember asking later in life; did they ever think that perhaps this could have been because I was deprived of Colostrum at birth and did this give me a predisposition to a deprived immune system?  The answer of course was no because I was supplemented with formulas etc. My adoptive mother confirmed I was supplemented with Vitamin D because of the severe aching in the bones.

Later in life I met my birth mother and four siblings, two children stayed with her and the other two were also adopted out, guess which three have Th1 illness now? Coincidence?

Does this suggest that the immune system is genetically predisposed to these illnesses later in life because of being colostrum deprived in those first few days? Or perhaps the c-jun gene does remain active after our bodies have developed instead of staying dormant, or even reawakens in the event of pathogen challenges we acquire over the next 40 years.

What Trevor says about it not being one specific pathogen but a host of pathogens acquired over a lifetime including some just being “at the scene of the crime”, that statement is ringing in my ears!     

Maybe acquisition started from day 1. 

                                                  Rick 

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Trevor - John and I have been reading this thread with much interest, particulary when you say:

Now if certain bacterial species were able to persistently infect the neo-natal brain in the same way as Rolf's CMV did, then it could be expected that those folk might well experience a greater degree of difficulty clearing a challenge later in life, just like the mice did... Hmmm...


We thought you might be interested in hearing about the first few weeks of Matt's life nearly 14 years ago.....

Matt was 5 weeks premature and spent his first few days in a humidicrib.  I breast-fed him but he was supplemented with formula and was given quite a few feeds with a tube.  We were in hospital for 10 days and then allowed home once he was OK out of the humidicrib and I had established his feeding and he was over a bit of jaundice (my memory is a bit hazy but that is the jist of it). 

All was well for a few days until he started sleeping through feed times.  I got worried and called our pediatrician - to cut a long story short, he ended up in the neonatal intensive care unit for 10 days and tested for all kinds of things.  He stopped breathing a couple of times that night we took him to hospital, but he was revived each time and put on a cocktail of antibiotics while they tried to work out what was wrong.  He responded favourably to the antibiotics and we were later told that he had an E. coli urinary tract infection that ended up in sceptacemia.  He probably picked up the infection in hospital (I always worried about that tube-feeding...).

We have always wondered why, out of the 1600 boys in Matt's school, he is the only one in recent momory who has missed a couple of years of schooling due to a chronic disease.  We are sure he is not the only one to be bitten by an insect or tick in the Canberra/South Coast region in the past few years.  Sure, the school has its share of autistic kids and others with asthma and ADD, but none with an illness like Matt's that has put him out of action for such a long period of time.  Matt keeps asking, "Why me?" - do you think we may be beginning to find an answer for him??? 

Regards, Robyn and John

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Trevor,

Just an FYI that I wasn't upset in the least last night, just a bit confused. I think it's sometimes hard to judge a person's thoughts without speaking to him, and that often leads to misunderstandings :o).

I would still like to know if I can find any of Dr. Eishi's work anywhere so I can look at it. It does seem, however, that you would be leaning to a combination of bacteria and viruses as a combined force causing the immune reaction of sarc.

I understand the position that you are trying to reset the immune response, but here's my question that I am fuzzy about:  With respect to  my acne breakout and newly developed lesions since starting the MP , and ( i believe) a stronger herx reaction when I previously ( and mistakenly I will admit) took a greater than recommended dose of minocycline, why would you not suggest taking a larger dose if a person could handle it and it was under the recommended dosage of the drug given to teenagers for acne?  It's just that it seems to me if the doctor is perscribing a certain dosage to teenagers, why would one think a much lesser dose would work just as well or better?  Would taking more M somehow lessen the degree to which the MP works in some way? Would taking any topical medications help?

I am not sure what relation this acne breakout and the two newer skin lesions (about the size of your pinky nail) has to do with my sarcoidosis...whether it's a large part of the cause (the primary cause) or if there are many other bacterial and viral infections going on, but I'm wondering if at least trying to hit the acne would help somewhat? Lastly, would you take the acne breakout ( which has not resolved in a year or more) and the skin lesions as a good sign ...possibly a sign that the bacteria is not "comfortable" remaining in hiding...or that the immune system is now responding to the bacteria ....OR..that the bacteria is getting worse somehow ( in effect getting worse)?

Lastly, my sinus condition still seems to be about the same...any thoughts? I would have thought that this would have cleared a bit by phase 3.

Just trying to understand........sorry if these questions seem simple minded or repetetive in nature. Thanks for your time and I appreciate the help very much.

Norman

 

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Norman, Please move these questions to your progress report discussion, it is not relevant to the discussion about Professor Zinkernagel's work.

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After reading this thread and reviewing the 1951 paper by Klieneberger-Nobel, can one assume that the viruses mentioned by Dr. Z and the L forms discussed by Klieneberger are the same pathogen? 

In other words, do viruses REALLY exist or are they L forms of bacteria? 

Sherry

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Sherry,
Viruses typically have small genomes, say 70,000 base-pairs, while bacterial genomes typically span several million base-pairs.

There are many other differences too:):)

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     On twenty-first century Earth, what was typical can no longer be taken for granted. Myriad novel life forms are possible if able to combine parts from viruses and bacteria......and who-knows-what else (fungi, nematodes, arthropods?).....whether accidental or engineered.:shock: 

     To go back to the beginning again, from the information presented; it appears the mice brains present a different pathogenesis model than the mice bodies when infected with the same virus. This makes sense. "Life" is as diverse as it is tenacious. Using Darwin's platform, the lifeform which benignly parasitizes and lives symbiotically with a host has a greater advantage for survival and proliferation than a more destructive invader. This virus has hit on a winning set of mutations that guarantee the survival and proliferation of itself and it's host. For the most part, these lifeforms (or parts thereof) are smaller than most have bothered to look. We should expect there to be a thriving, diverse, and and storied history of infectious agents of this type. Especially in the reproductive and nervous systems. Call them L-forms, CWD or pleomorphic bacteria, "self-determining" DNA/RNA pieces, viruses................this world is truly their oyster! :dude:

     Drs. Blaney and Marshall: Whether part of the innate or adaptive immunity systems, how does the body get rid of infectious agents which are sequestered inside living host cells on the MP? Do these pathogens get induced to leave the cell, leaving the host cell alive? Or are the host cells killed along with the pathogens? What are the specific sequence of events which take place, on the cellular level?

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Steve
You may be interested in this Information:
CELL WALL DEFICIENT BACTERIA AND THE MARSHALL PROTOCOL
Thanks, Barb ...

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Infants vaccines make me nervous.  Which vaccines would you suggest for babies and in what order? My first grandchild is coming soon and if some of what my family members have gone through could be prevented I would be grateful.

Thanks, Rosie

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Rosie,

The question of whether or not to vaccinate is fraught with controversy. We cannot advise on particular vaccines. Parents should study the issues and decide for themselves.

Vaccines are given in a certain pattern to promote their effectiveness. The baby's pediatrician or the public health office are two resources to ask how long immunizations can be delayed and how far apart they can be spaced.

Best,

Meg

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Trevor, another question I have that relates loosely to this thread:

I understand from another thread that you have been busy with molecularly 'shooting' Beni's molecule at several bacterial genomes with success.

Would it be perhaps interesting to do the same with viral genomes? Looks to me that might be an interesting exercise.

Sincerely, Frans

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This thread is very interesting to me.  I don't ever remember a tickbite but I did get sick right after my Rabies Vaccine (required in veterinary school).  My mother also had Bell's Palsy when she was pregnant with me, but my identical twin sister is fine.  She doesn't get vaccinated for anything...

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This thread has got me thinking (I haven't been doing alot of that lately).

My first thought is that I am considered a hepatitis B carrier. This was discovered after I got the first two out of three hep B vaccinations. Could I have actually developed the disease from the vaccination if my immune system didn't work properly? I say that I am considered a Hepatits B carrier because I test positive for the antigen but I test negative for the hepatitis B DNA.

Secondly, since I am considered a Hep B carrier, both of my children were vaccinated the day they were born. Could this have been a big mistake? But if they now test positive for Hepatitis B antigen, would that indicate that thier immune systems were able the convert it? Maybe because I breast fed them, the innate immunity was given to them throught the breast milk.

Thirdly, you had discussed earlier about the transmission of bacteria and viruses through the placenta. I believe that this has been speculated in mothers that are HIV positive. This is why it is so highly recommended that these mothers take certain antiviral medications during the pregnancy. If the threat was only due to transmission at birth, they would just have to give them the treatment starting at the time of the exposure(during delivery) just as they do anyone who has an HIV exposure. I don't know if placental transfer has been proven in HIV pregnancies, but they do treat it as if it were.

If HIV can transfer through the placenta, isn't it pretty likely that other bacteria do as well?

MPolson

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Since this thread talks a lot about vaccines I thought I would post here. Feel free to move it somewhere more relative.

Scientists Identify Immune System Trigger For Fighting Lyme Disease

News article dated August 23, 2006

Anyway, so what? They've found a glycolipid which triggers an immune response from the body's natural killer (NK) T cells. Surely this isn't the only receptor that borrelia communicate with. How on earth would this help?:? I guess these guys are just behind the times still. They've figured out a wierd way in which a parent form stimulates T cells. Whoopee doo.

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greg,
Every young biochemist who graduates these days is trying to make a million - by discovering a drug that can be commercially marketed. They are typically given 0.1% (or so) of the profits - and so their life goal becomes to try and fit disease into the constraints of commercial drug discovery.

I am sure these folks are thinking about a vaccine, or something they can market.

Of course, it won't work. That is why we keep getting promises for our research tax dollars, and not results. Meanwhile, we keep giving them money...

norman
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Hi,

I was trying to read a bit of Dr. Z's paper, and I think I asked this before ( not sure), but why does he always refer to autoimmune diseases as being caused by viruses? Do you think there are any viral components to any cases of sarcoidosis or other Th! inflamatory diseases?

Thanks,

Norman

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I was wondering myself. Here is what Dr Marshall wrote in a paper

Antibiotics in Sarcoidosis - Reflections on the First Year (8-3-03)
http://www.joimr.org/phorum/read.php?f=2&i=38&t=38

The SARS Coronavirus is a pathogen with the apparent ability to virulently hyper-activate the immune system in this manner [9,10,11,12]. While the granuloma of sarcoidosis are formed by an accumulation of considerably less virulent pathogens than SARS, the anomalous T-cell Receptor alpha-beta V protein is similarly present [13].

Last edited on Tue Nov 14th, 2006 11:00 by wrotek

MarkN
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Speaking of vaccines I know two people whose health was never the same after having adult vaccinations.

Freddie Ash
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HI MARKN

This is Fred in WV.  Mark, please tell us more.

Remember, we are all in this together and I am pulling for us.

Your friend in sarcoidosis

Freddie

MarkN
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Hi Freddie

One man was very athletic in his 40's and had Hep. booster and some other shots for going overseas. He got a rash and noticed his swimming and biking endurance suddenly went down. He never used to get sick but for the past two winters has had walking pneumonia. Also an older woman, already in poor health but getting worse, and her dementia seems to have doubled overnight after some shots. So no vaccines for me - who knows the risks involved between the viruses, bacteria, mercury etc.

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Mark,
The mercury is not a factor. Mercury has become associated with these chronic diseases because the body cannot clear heavy metals when the immune system becomes overloaded with Th1 pathogens. But once patients recover on the MP they no longer exhibit elevated mercury or lead levels. So mercury is just another "co-infection," if you like, just like Babesia and the other things that are often observed with Th1 disease, but are not causative, just 'associated.'

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Here's an interesting article about a study in Germany. After thinking about it, it appears that it really, really makes sense if one follows Dr. Marshall's and Rolf Zinkernagel's studies/ideas about how early infection affects one's ability to respond when re-infected later in life.

Younger Siblings May Boost Brain Tumor Risk

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Trevor, something just hit me regarding infected stem cells.

If innate immunity is suppressed from birth on and babies start gathering infections, it would only be logical to assume the stem cells get infected also, since I would think they are also wholly dependant on innate immunity ?

Sincerely, Frans

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That is correct, Frans.

Frans
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Trevor, you once stated here on the forum that the world wasn't ready yet to face the consequences of vitamin D being immunosuppressive.

I understand fully now...

It's mind boggling really, this will shake the world of medicin to its core once the meaning of this sinks in...

wow....

Phil Schoner
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Here is a thought regarding why the innate immune system of Dr. Z's mice never attacked the virus in the brain after the few weeks it took to develop (Trevor's $64,000 question). 

The virus was there before the IIS developed, and the IIS said to itself, "Hey, this thing is supposed to be here, I'll leave it alone".  And the virus said, "Hey, IIS, I belong here, and I won't bother you.  I'll just sit here in the corner of the castle.  You go ahead and develop yourself to fight foreign invaders.  We both know that I'm not foreign, I predated you."  So the virus and the IIS lived happily ever after, until the virus received reinforcements in that second challenge.

Phil

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Trevor,

I have been reading this paper again and again and am starting to get it, I hope.

One question comes to mind though.

From the way dr Zinkernagel presents his theory, I get the impression that what we call autoimmunity is just a theory.

Have there ever been foud antibodies to self? Or is autoimmunity as we knew it just a hypothesis ?

Sincerely, Frans

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Antibodies are non-specific, as to their target. I am not aware of any definite 'antibodies to self'. In any case, if there was such a thing, the organism would quickly degenerate to a pile of blubber.

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Thanks Trevor, that's clear.

dr Zinkernagel probably cracked another problem of autoimmunity, delivering a proven alternative.

What I was wondering about:  I have heard some talk about HERV's maybe being part of the problem, or at least delivering more dna to the pea soup.

But if we consider that stem cells probably are infected, what remains of herv's? Are they indeed in our DNA, or do they get there in this first extremely vulnerable period of life?

Sincerey, Frans

Last edited on Fri Feb 2nd, 2007 10:09 by Frans

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Trevor, a much more important question on my mind is:

how is Interferon upregulated/activated?

I am looking at the following, the pathway of the TLR's:

- http://tinyurl.com/2kmsy7

It looks to me like the TLR's also have a direct link to the IFN's? And perhaps thereby: viruses also, as well as bacteria?

Sincerely, Frans

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Sorry, Frans, I am occupied sorting through some new stuff right now. Remind of this in a week or two's time, please.

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Thanks Trevor, I'll try to remember, but am on the 2nd abx now... :D:D:D

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Vaccinations were mentioned frequently on this thread and so I've decided to post the following here.

I found the video on this site to be most interesting (note also at the 53 min mark, diseases linked to particular vaccines), although there are things said, particularly near the end that would be contrary to the MP: http://heartspring.net/flu_shot_side_effects.html  

Also at this link you can find (directly under the video) an interesting article written by Dr. Alan Cantwell, Jr., entitled Are Vaccines Causing More Disease Than They are Curing?

While the MP may be the only real cure for many of us with Th1 illness, perhaps vaccinations may be one the leading causes of the infections that cause our illnesses. 

Claire

Last edited on Fri Mar 16th, 2007 06:18 by eClaire

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Breast feeding may make some difference to the development of TH 1 disease but i found the speed of development in my 3 children had much more to do with sunlight exposure than any other thing. The son who developed the condition last was a computer junkie and rarely left his room for years. His outdoor loving sister and brother developed the disease 6 years before him....His sister was breastfed for a year......the longest BF child.

stella



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