Theoretical Immunology

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tara97
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Post by tara97 »

yeah cortisol also stimulates the secretion of gastric acid this may effect the intrinsic factor for b12 absorbsion. another thing that can cause low blood pressure is overstimulation of the vagus nerve. I have low blood pressure yet I can feel my heart pulsate in my head and my teeth and my eyes.
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Leonard
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Post by Leonard »

Let's just assume that micro-cellular nutrition is the problem in MS. Let’s also assume as well that in addition to a local problem (close to the narrowings of the neck veins) there can also develop a global problem (a whole body problem of poor GLUT translocation, insulin resistance). In fact, the double peak in the graph of the age of onset suggests two different underlying mechanisms are at work here.

People with MS have a high glucose demand; their cells are screaming for energy. Sugars and glucose are the easiest to get out of the bloodstream. Some people with MS have a high sugar consumption.

We know too much sugar is bad. On this thread, several publications may be found that argue that a prolonged use of sugar may be linked to increasing insulin resistance. Sugar gives a short boost but in the long run high sugar consumption does the opposite and you need to take ever more for the same effect. You get into a vicious circle.

In the newspaper and Internet today a new type of cholesterol is presented that is more dangerous than LDL, called MGmin-LDL. It's denser and stickier than LDL. Well, cholesterol (HDL / LDL) is not as bad as previously thought, but this particular version is. And this ultra bad cholesterol uses sugar to grow.
http://www.nursinginpractice.com/articl ... identified
and many other links can be found by Googling on MGmin-LDL.

The risk of cholesterol is always related to the narrowing of arteries where plaques reduce the passages and passages may get completely blocked. With catastrophic consequences. Of course it is. But once again I think conceptually we may looked at the issue broader. I think these sticky micro-structured plaques could also block the fine "pores" of veins and capillaries, closing them off for glucose and oxygen transport. Thus hindering the transport of micro-cellular nutrition! It is another way of looking at the effects of cholesterol, but potentially just as disastrous in particular if you already have poor or malnourished cells/neurons.

Metformin stimulates an enzyme that allows the GLUTs to work better, and thereby promotes cellular nutrition (and thus helps to overcome "insulin resistance"). Metformin is also said to have the ability to lower glucose levels. I think because glucose is better absorbed by the cells, and thus the level in the blood drops.

But an article in a local paper also suggests that Metformin helps to block the formation of the ultra bad cholesterol. Thus, Metformin could be a useful drug (fully apart from diabetes2) to keep open the fine "pores" in the vessel walls and thereby promote micro-cellular feeding.
Last edited by Leonard on Mon May 30, 2011 3:05 am, edited 1 time in total.
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Leonard
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Post by Leonard »

<shortened url>

This is an interview with Dr. Vogl from Frankfurt, Germany. As you may know, dr. Vogl was one of the first doctors performing ccsvi treatment.
Quote dr. Vogl: Treatment of the veins is no causal treatment of MS, but an action to improve the consequences of this circulation problem. Unquote
I would agree. Liberation from ccsvi can not be an end in itself.

What then is affected by the poor circulation? Right,

- the cells become malnourished, weakened, virusses (EBV, herpes) get to grips, the immune system turns on ..

- the mitochondria of the nerve cells become undernourished, the ion pumps of the cells can not maintain their equilibrium, the transmission of the nerve signals becomes weaker ..

The auto-immune hypothesis should be reconsidered. Micro-cellular nutrition (local and global) becomes important. Besides angioplasty of local strictures in the neck, healthy vessels and clean vessel walls becomes of overriding importance. Low sugar consumption and low blood glucose levels would seem important ..
Last edited by Leonard on Mon May 30, 2011 3:06 am, edited 2 times in total.
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Leonard
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Post by Leonard »

With reference to the previous posting: The weakened cells may also fall victim to the Hepatitis B vaccine, see e.g. http://weeksmd.com/?p=664
Here multiple sclerosis is allegedly linked to the Hepatitis B vaccine.
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Leonard
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Post by Leonard »

CCSVI is no end in itself; there must be something else that underlies the MS. A lack of oxygen and glucose in the draining veins of the cerebro-spinal caused by a low blood flow would be a very plausible candidate. Here, cells called astrocytes malfunctioning could indeed be an important first step that triggers a chain of reactions that ultimately shows up as MS...

The debate in the medical world is in any case going in the right direction with statements like these:

A controversial new theory that doctors have failed to cure multiple sclerosis (MS) becauses they are treating the wrong disease has split medical opinion. Neurologists at Glasgow University claim conventional wisdom about MS is based on a differential conditioning altogether, which explains why no cure has been found for the disease.

Professor Peter Behan and Dr. Abhijit Chaudhuri, who worked with Dr. Bart Roep, from Leiden in the Netherlands, believe the century-old view prevailing that MS is caused by immune cells attacking a protein that insulates nerves is wrong. They claim instead that MS is caused by support cells called astrocytes malfunctions, may possibly be due to a combination of environmental and genetic factors.

http://www.sclerosi.org/articoli/theory ... gnosis.php
http://www.smh.com.au/national/research ... 15sfw.html

I wonder when they will reach the point of undernourished cells ... :D
In any event, the double peak on the graph of the age of onset and the typical recovery times involved linking the disease to a malfunctioning ion pump are real and can be well explained by the low glocose concept.
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tara97
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Post by tara97 »

WOW to the hep B vaccine. I came out of a 5 year remission after a hep B vaccine. I suspected that it might have kicked it off.
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Leonard
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Post by Leonard »

I was vaccinated for Hep B in 2/99 and 4/99 before a world trip and later in 4/2000.
Diagnosed with MS in 2004 at 47 years; clear first symptoms in 2002.
Coincidence???
I probably had a weak micro-cellular feeding condition already due to the stenoses (earlier symptoms as early as 14 years of age..), besides the active lesions two old inactive scars when diagnosed.
The Hep B vaccination may well have triggered the (or should I say the new) inflammation ..
Last edited by Leonard on Thu Jun 02, 2011 8:24 am, edited 1 time in total.
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Post by jimmylegs »

hep vaccination was part of my constellation of pre-dx circumstances. the docs told me it was a coincidence. it kind of makes sense, and i did have neuropathic stuff going on prior.

there is no doubt that my immune system was very weak, but the acute dx attack definitely initiated after a physical trauma to the head.
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Leonard
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Post by Leonard »

From Joan's facebook page on Research on Glutamate excitotoxicity in MS:
<shortened url>

This link is very interesting
http://www.nature.com/nrn/journal/v4/n8 ... 4_BX1.html

This is a point where neuro-theories come together with the low glucose / low oxygen hypothesis .. whow

From a posting here on TIMS a while ago I learned that cell death itself does not trigger the immune system. There is still a virus or something else needed to set the thing on fire.

If you push this theory a little further out, you come to the conclusion that the inflammation of MS and our mobility functions are not primarily linked. I.e. the fact that we wind down, fatigue comes etc. is the primary process where the neuro cells can not maintain their equilibrium. The typical MS lesions etc are caused by an inflammation of weakened or died cells where viruses get to grips and perhaps the immune is trying to do what it can to save, to correct ..
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Re: cell death

Post by NHE »

Leonard wrote:From a posting here on TIMS a while ago I learned that cell death itself does not trigger the immune system.
Apoptotic cell death doesn't. However, necrotic cell death is likely a different game altogether.


NHE
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Leonard
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Re: cell death

Post by Leonard »

NHE wrote:
Leonard wrote:From a posting here on TIMS a while ago I learned that cell death itself does not trigger the immune system.
Apoptotic cell death doesn't. However, necrotic cell death is likely a different game altogether.

NHE
Is MS the result of programmed cell death rather than necrotic cell death mechanisms? This article would seem to suggest so:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2230017/

Quote from wikipedia: http://en.wikipedia.org/wiki/Necrosis
Necrosis is caused by factors external to the cell or tissue, such as infection, toxins, or trauma. This is in contrast to apoptosis, which is a naturally occurring cause of cellular death. While apoptosis often provides beneficial effects to the organism, necrosis is almost always detrimental and can be fatal.

Cells that die due to necrosis do not usually send the same chemical signals to the immune system that cells undergoing apoptosis do. This prevents nearby phagocytes from locating and engulfing the dead cells, leading to a build-up of dead tissue and cell debris at or near the site of the cell death. For this reason, it is often necessary to remove necrotic tissue surgically, a process known as debridement. unquote

I believe that necrosis could be particularly dangerous and could possibly end fatally. We know that MS is not like that. So from this, may we say that MS is probably more of a programmed cell death?

Excitotoxic cell death as suggested by Hubbard/Joan may be both apoptotic and necrotic.
http://www.nature.com/nrn/journal/v4/n8 ... 4_BX1.html
There may be something flawed here, possibly ...

Or perhaps the models that we have here are not fit to adequately represent what is happening in reality. And we need new concepts altogether..
Last edited by Leonard on Sat Jun 04, 2011 1:12 pm, edited 1 time in total.
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Post by mrbarlow »

Hep B - 1991, Booster 2003/4

CIS diagnosis - 2010

BTW - EBV - 1989
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CVfactor
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Post by CVfactor »

Neuroparalytic accdents were more prevalent in the early Rabies vaccines.

These are basically the equivalent of EAE in humans.

I'm not sure if this can be said for Hepatitis vaccines though.
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Post by Talisker »

I link on apoptosis
http://users.rcn.com/jkimball.ma.ultran ... tosis.html

Apoptosis requires a base level of energy to start the process
http://nro.sagepub.com/content/4/5/345.abstract
http://www.nature.com/nrm/journal/v3/n3 ... rm762.html
http://www.mitochondrial.net/showabstra ... d=10366439

Possible evidence of apoptosis in ms
http://www.ncbi.nlm.nih.gov/pubmed/10498820
http://www.ncbi.nlm.nih.gov/pubmed/18566024 **
http://www.ncbi.nlm.nih.gov/pubmed/10498820
**
Taken together, these results suggest that patterns of inhibitor of apoptosis expression in immune cells may have value in distinguishing between MS subtypes and offer insight into the mechanisms responsible for their distinct clinical courses
I dissaree that the apoptosis inhibinators was acting on the immune cells, but on the astrocytes that are starved of glucose and nuerons and oligodendrocytes that are starved of lactate.

I did have a bookmarked link to an article that said mitochondrial that are energy deficient produce a positive NO feedback loop that leads to cell death but can't find it.

CPn Help/files/Ref1_Annals04.pdf
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Leonard
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Post by Leonard »

se1956 wrote:Here
<shortened url>

the EDSS of a woman decreased from 5 to less than 2 after a liver transplant. After 3 years she was symptom free.

I think this may not be the result of the immunosuppression, that is necessary after the transplant, but the result of a "normal" liver metabolism.

R.
I would like to elaborate a bit here on the story of the person who underwent a liver transplant and cured of MS. In fact, I think it is not the immuno suppressive mediation but the liver itself that changed the metabolism.

The liver makes our cholesterol, an absolutely essential part of our metabolism. There is HDL and LDL cholesterol, which in their ratio is known as our cholesterol value. Cholesterol is not as bad as often thought; the book titled the Cholesterol Hype by Malcolm Kendrick is a real winner. In Japan, a high cholesterol is seen as a good sign of a healthy life.

Recently a new form of cholesterol was discovered: MGmin-LDL. It seems to be super sticky, and grows on sugar. It also seems to have a very fine structure.

http://www.healthhabits.ca/2011/05/27/m ... -kill-you/

<shortened url>

http://reuptake.org/2011/05/27/mgmin-ld ... t-disease/

I think that besides forming the famous plaques, this super sticky cholesterol can block the fine pores of our normal veins with disastrous consequences for patients who already have a poor nutritional condition. And possibly (according to an article in a local paper), people would benefit when taking Metformin as Metformin seems to break down this ultrabad cholesterol.

I think this is also closely related to a recent posting on the biofilms on a Dutch web forum http://www.lymediseaseresource.com/Serrapetase.html
This might in fact point to exactly the same mechanism. In other words, that it is this super-sticky MG-min LDL cholesterol that puts a biofilm in our veins. Where another liver by transplant (which is quite something...) or a sugar-free diet with Metformin (diabetes therapy 2) would improve the vascular condition so that the micro-cellular nutrition condition is strengthened.

If the biofilm in our veins inhibits or impairs the normal feeding, cells will die. This of course will be a controlled process (apoptosis which means that a calcification of the cells occurs). And finally, this is just like atherosclerosis, but also coupled with the micro-cellular nutrition falling sharply.

THIS IS PRECISELY THE POINT WHERE THE SQUARE IS ROUNDED AND WE ARE BACK AT THE FIRST POSTING OF THIS THREAD. I THINK WITH THIS THREAD, WE HAVE PRETTY MUCH UNRAVELLED WHAT IS MS.
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