Lack of Immune Supression Capability

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Re: Lack of Immune Supression Capability

Postby thisisalex » Wed Sep 22, 2010 11:07 am

Direct-MS wrote:The abstract below demonstrates that persons with MS have a decreased capacity for immune suppression. I put this on to emphasize the point that MS is not simply a normal immune system invading the CNS due to CCSVI effects.
There is no doubt that CCSVI plays a major role in MS and needs to be treated as soon as possible. However, the data tell us that MS is best seen as being caused by CCSVI in concert with a faulty immune system (genetics plus environmental effects). A reduced capacity for immune suppression is one element of such immune dysregulation that helps to drive MS.

i think its too early to draw consequences...
... and what if the immune system gets defected because of CCSVI?
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Postby David1949 » Wed Sep 22, 2010 2:06 pm

mose wrote:sounds like a potential explanation for why Buffalo found CCSVI in a decent clip of non-MS. CCSVI + immune dysfunction in conjunction could contribute to what is known as MS.

Somewhere I read that Buffalo's healthy control group included relatives of the MS group. So if CCSVI is inherited then that could create a higher percentage of people with CCSVI in the control group than would be expected in the general public. I'll see if I can find a link to that.
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Postby David1949 » Wed Sep 22, 2010 4:03 pm

Based on the numbers posted here by Direct-MS, the family members in the healthy control group had only a slightly higher incidence of CCSVI than the non-family members. The difference is not statistically significant. So the inclusion of them in the healthy control group would not cause a significant bias.
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Postby 1eye » Thu Sep 23, 2010 8:18 am

Direct-MS wrote:Possibly up to 20% of the population is born with venous malformations which result in CCSVI.

Another smaller group of the population (1% ?) ends up with an immune dysregulation due to gentic susceptibity and environmental factors such as a virulent EBV infection during a time of low vitamin D and an overall poor immune education due to ultra-hygienic conditions.

Occam is starting to get a bit nervous.

Those with both CCSVI and acquired immune dysregulation (perhaps .2% of the population [1% of 20%]) get MS because CCSVI opens up the BBB and once the immune system gains access to the CNS, the immune dysregulation results in a poorly controlled immune/CNS interaction and ongoing damage. Other factors related to CCSVI can explain accompanying neurodegeneration.

Or, the tricuspid valve has problems in 1% of people and 50% of the time is asymptomatic, and 1% of the 20% with this and CCSVI have symptoms related to intermittent posture-related reflux to the brain which as we have seen in Schelling causes Dawson's fingers.

There are probably a few other possible scenarios. Research will find out the truth, but especially if everyone gets Liberated, and the big $ are not available anymore, will we ever know?
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Postby concerned » Thu Sep 23, 2010 10:58 am

That's quite a bit of faith in Ockham, for certainly there is plurality at play here.

I've always felt that "if something sounds too good to be true, it probably is" was a better motto to live by.

Postby MegansMom » Thu Sep 23, 2010 3:26 pm

I am new to MS but I have been an RN for close to 40 yrs.

I have been to be a somewhat focused "nerd" type of nurse. Now CCSVI seems to be ( as reported by Zamboni) a host of different blockages, stenosis, atresia, anular rings, webs, location and degree they seem to have degrees in the interference of normal flow and location. He documented in the initial study dated Dec 5 2008 that he had lumped them into 4 types A,B,C, D....... the anomalies causing reflux but the amount of involved vessels (locations) and extent of blockage being different & in amount of reflux being different . The locations of MS lesions ( on MRI) created by the flow of the reflux could also be seen to be in patterns.

Now we get to the why......if congenital, don't we get MS until later and varying ages........this might have to do with the amount of the debris deposited ( iron, etc) Think of a partially clogged sink- think of dish water- water in ,used and dirty and slow out- leaves dirty residue.........the slower the drain the more time for crap to be on the sink walls. Then you add the sheer stress of reverse flow and interupted endothelium which has the debris ground into it. I think the lesions may have formed as the bodies way to try to protect itself from the encroachment. The macrophages ( the garbage men of WBCs) are often found in MS people to be laden with iron. Maybe they are attempting to remove it?

Now remember the human body wants to be efficient.....and its immune system compensates well and for a long time in a young & otherwise healthy person, but when pushed it has a tipping point. Some people have great immunity and some do not.....this is inherited but can be suppressed or boosted dependent on environment- ie smoking, diet, exercise,etc

I think the immune system tries hard to keep up and remove the debris (remember this is over years) thus over a long time the immune picture. We see in the snapshot of a hematological examination done after the fact- we are talking about and over active- stressed immune system potentially from quite early on in life its been on overdrive.This seems more plausible to me.

As for the twins ,their DNA is the same ( thus their anomalous stenotic anatomy) but the debris would be different in them depending on exposure- esp to heavy metals, diet, and everything that has entered the individual and influences ones immune system. This may explain why only one twin develops MS. Congenital anomalies of all sorts are seen in families yet to differing degrees.

I am very hopeful that CCSVI and angioplasty will impactand potentially change MS as we know it now. Some day it might be just a minor inconvenience with an easy low risk "cure", that needs occasional monitoriing and an immune system that needs a boost after being chronically over worked.

I can not wait to find out.

The things that will be found out post CCSVI discovery have just begun.

These are exciting times.

Bravo to all the pioneers!
Cat (Catherine Somerville on FB)
My 35 yo daughter is newly dx 8/19/10 (had 12 symptoms)
Dx with Type A CCSVI- 1 IJV & double "candy wrapper" appearance of her Azygos
Venoplasty done Sept 21, 2010
Doing extremely well-
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