This Is MS Multiple Sclerosis Community: Knowledge & Support

Take a look at this:

Investigators at the University of Sydney have published a study suggesting that the earliest activity seen in the brain in MS is the destruction of cells that make myelin (oligodendrocytes), occurring before the onset of immune activity usually blamed for triggering the disease. This provocative study, co-funded by many sources including the National MS Society, opens up new possibilities for finding the cause of the disease and developing new treatments.

Current Study: For this study, the team used brain specimens from 11 people who had died early in the course of their MS, and the team also used comparison specimens from people with other disorders including stroke. Some of the tests focused on subsets of specimens from seven people who had lesions showing active myelin destruction. To get a sense of immune cell activity in the brain and at what stage it was occurring, the team examined newly active and resolved lesions, as well as nearby blood vessels, surrounding areas showing some disease activity and surrounding areas that appeared normal, and areas that were farther away from the lesions of interest.

Results: In tissues surrounding newly forming lesions, the investigators found evidence of the loss of oligodendrocytes with an absence of immune T or B cells that would normally be held responsible for launching the immune attack against oligodendrocytes and the myelin they produce. These and other immune cells, including scavenger cells (macrophages and microglia), were more numerous in lesions and surrounding tissues at apparently later stages of destruction and sometimes in lesions that were in the process of repair. In specimens from two very early cases of clinical onset of disease, they found few immune cells within the lesions and no evidence of activation of scavenger cells.

These and other unexpected findings from this study led the investigators to propose that the early immune activity seen in active lesions is that of macrophages and microglia, whose job it is to clean up and remove damaged myelin. They propose that lesion formation is caused by something other than destructive immune activity led by inflammatory cells against a component of myelin or oligodendrocytes.


Do i hear CCSVI in between those lines. What am thinking is that the buildup of iron, which is quite poisonous to the oligodendrocytes, causes them to die, hence lesions forming. It is then the the scavenger cells (microglia and macrophages) come in to cleanup the dead cell matter. Yes there's still a T-cell component as iron buildup will promote inflammation but probably even more damage is done by just the iron buildup.

What do you guys think?

I got this at: http://www.nationalmssociety.org/resear ... x?nid=2622

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22 yr old male located in the caribbean. Suffering with MS like symptoms from early 2008 with multiple relapses under my belt with optic neuritis. Not dx'd as yet however. Hope is to ultimately be tested for CCSVI

I think the intention or design of this study was completely unrelated to CCSVI, as it is likely that they started it before CCSVI emerged. But the outcome isn't unrelated at all, and I think it's very useful to add this study to the information you bring to your doc, esp. neuro, in case s/he's insisting in the autoimmune myth. (Now I dare to call it like this.)

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"There is only one good, knowledge, and one evil, ignorance." Socrates

I think you misunderstood what i was saying. Am not saying they had CCSVI in mind when doing that study. Am saying it further adds to evidence in support of CCSVI even if that wasn't the intention.

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22 yr old male located in the caribbean. Suffering with MS like symptoms from early 2008 with multiple relapses under my belt with optic neuritis. Not dx'd as yet however. Hope is to ultimately be tested for CCSVI

So why are the drug pushers (big pharma), making drugs to kill off Killer T-cells. They appear to be part of the repair system.
Really makes you wonder doesn't it.
I have heaps of Killer-T's because I have no spleen.
I have just found out I don't have MS, I have hereditary iron overload caused by a combination of genes. When my iron got very high I got my first and only lesion with associated symptoms similar to MS.

I'm being fixed by phlebotomy. I feel absolutely wonderful!
The fix was almost instant, 24 hours, after two years of hopelessness.

Wow....by now i think we all see how overwhelming the evidence is becoming.

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22 yr old male located in the caribbean. Suffering with MS like symptoms from early 2008 with multiple relapses under my belt with optic neuritis. Not dx'd as yet however. Hope is to ultimately be tested for CCSVI

I'm not saying what I have applies to others with MS. But surely they should rule out these types of illnesses before any diagnosis for MS.
The point is that my sister has the same gene problem as I do and she has been diagnosed with MS for twenty years.
I just couldn't accept that my MS symptoms abated during menstruation, or after a blood test, so I looked into it further.
My doctor didn't. Be your own researcher, doctors don't have the time.

All my symptoms which started over 30 years ago are on my doctors file.
They don't have time to put 2 and 2 together. I'm kind of mad about all this, but at the same time I can understand they don't know everything.

Having hemochromotosis (ironoverload) myself, I find it quite amazing that you were 'fixed' 24 hours after phlebotomy. My ferritin level was 1500 compared to the normal 50-100. It has taken me 1.5 years of bimonthly phlebotomies to get to my current level of 450. This is the normal course prescribed to lower ferritin levels that usually takes 1 to 2 years. Oh I also have MS. My lesions to this point have not changed a bit. I still have MS symptoms.

Can you share with us your course of treatment? And how do you define 'fixed'?

I have a slightly different case to you. I have PCT (Porphyria Cutanea Tarda) and one gene for hemochromatosis C282Y.
It means that I have two variables in my blood they need to fix.
I iron overload without having very high iron levels, my ferritin has never been above 175, my transferrin saturation is high, was 62% when I got my only lesion in 2008, it's around 50% now. My serum iron is highish about 28 (recommended 10-30), but non the less I overload anyway.
I have high hemaglobin too.

I have the hyperpigmentation on my arms, gums, get the fatigue and the stiff joints of HH.
The PCT can cause neurological symptoms, lesions, spasticity, epilepsy like conditions etc. oh and a nice eczema like rash, but not always. I do have that and have had it for 30 years. Doctors didn't put 2 and 2 together.

Its the interaction between the PCT and HH that causes loading at lower iron levels.
HH loads the iron and the PCT loads the porphyrins from the liver.

You need to be bled to get them both in balance, nice and low, same as in hemochromatosis so I don't load and get damage from either. Lesions are apparently reversible. I don't have as much ferritin to spare as you. They reckon you can have phlebs for a few months and that might see you right for 6-12 months with this condition. If I can't manage with the phlebs, I suppose they could chelate instead. Some iron overloaders are anemic, such as those with Thallasemia (spelling?). They use chelation to remove iron, but it's slow.

One phleb and I had all my energy back, my heart races quite a bit and I had a wild spasticity fit last week, gave me a bit of a scare, but overall I'm excellent. I'm awaiting appointments with the neuro and hematologist so they can get me on an even keel.

Phleb is the treatment for both. Maybe you should get tested for PCT.
Mine I believe is genetic (my grandfather had it), but awaiting a test. Or you acquire PCT from alcohol, hep.c., toxins (heavymetals lead etc).
Not sure how accurate the gene tests are.

I think it's about two thirds of people with PCT also have HH and one or two HH genes.

Hope I explained that OK

I am in a similar situation to paulmur as I was diagnosed with haemochromatosis in Dec 2009 and quickly commenced venesections in January 2010. My ferritin levels were very high, peaking at 2800 ug/L but since I commenced weekly venesections (450 mL of blood letting) they have reduced to 1200, however it will take at least a year for my ferritin evels to return to 'normal'.
I had a Clinically Isolated Syndrome in Dec 2007 that was confirmed by an MRI thus resulting in a single lesion on the spintal cord. Ever since that time I have had pins & needles in the hands and feet which have not abated. Next month I will be visiting my Neurologist and will likely have an MRI as my symptoms are becoming stronger.
I recently discussed CCSVI and haemochromotosis with another neurologist but he was reluctant to pass much comment until further research was carried out on CCSVI.
To date I haven't noticed any changes in my CIS symptoms since I commenced venesections but I feel that high ferritin levels are related to my other symptoms.

Bethr,

I had started a thread about CCSVI and Blood brain barrier.

I am not a specialist but just as an observer it felt that the BBB filtering is relaxed in MS patients due to some other trigger. This could be due to accumulation of dead cells in the brain triggering the immune system to clean them up and at the same time invoking some action due to which the BBB filtering is relaxed.

Normal autoimmune approach says that BBB goes haywire and at the same time the T cells attack the brain/myelin. Difficult to comprehend that two things can go wrong at the same time (though it is possible).
But CCSVI approach is more convincing than autoimmune approach.

My understanding from Zamboni's hypothesis is that shear forces of normal flow keep the endothelial cells that form the BBB tightly joined. When flow is disrupted, breaches occur, iron from de-oxygenated red blood cells enters through the BBB (not to mention CO2, and other waste), immune reaction follows.

Normal autoimmune approach has always been a sadly lacking bunch of hooey to me. I have no doubt that some auto-immune therapies help some people, sometimes, but I think it's kooky to try to knock out the T-cells, and other goodies.

I am certainly not an expert either.

So why are the drug pushers (big pharma), making drugs to kill off Killer T-cells. They appear to be part of the repair system.
Really makes you wonder doesn't it.

I veer into fringe territory, but Google up Kissinger, Useless Eaters, vaccines (newborns for Hep. B+C?), chemtrails, aspartame, flouride, thimerosol, DU, de-population, FEMA... Maybe it's not the T[cells they are trying to kill. It's drawn out though, to be sure that your treasure is transferred.

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My name is not really Johnson. MSed up since 1993

I am not very sure. I think BBB filtering happens when oxygenated blood enters the brain. I think iron from deoxygenated blood never has to breach BBB since it never went past it. It simply refluxed and settled down at venous sites in the brain.

As a side point, Dr's have found it difficult to treat brain infection since any medicine does not get past BBB.

It is still a mystery to me how PML happens when people use Tsyabri since all it is doing is to cling to T cells and avoid them getting into brain.

This means the virus responsible for PML normally does not enter brain or even if it does T cells kill them.

Given the above fact, it looks like BBB does allow some cells to enter it since normal people don't get PML and generally MS patients whose BBB is compromised do get it too. So the differentiator has to be Tsyabri.

Connect the dots ...

Of course, I am not an expert.



Again I slightly differ in my opinion. What is auto-immune. It is just our body which starts detecting our own parts foreign and starts killing them.
This could be due to malfunction in the immune system (like a mutation).
Or this could be due to change in the cell structure of the target sites (like knee tissues in the arthritis).
Remember our immune system is probably one of the most fantastic systems of our body. It differentiates foreign and local cells by looking at signatures on them. So either it starts looking incorrectly (due to its own isues) or the entity it is looking at has got the characteristics of a foreign cell. Again my own view.



Discounting that Tsyabri related deaths were not reported, I believe that these drugs do have utility and have served their purpose. But when real cure is available then these should now get into background and come into play only when real cure is not possible for whatever reasons.