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Does everyone see the post I just sent the way I see it. HD images... I need a computer that works like a old single speed bike, don't need all the extra gears. Just gets me in trouble. Help ? M

Chris as mentioned before there are many iron chelators with IP6 the most powerful and someone posted longtime ago a link to this paper: http://arxiv.org/ftp/arxiv/papers/0808/0808.1371.pdf
where the author mentions diseases correlated with iron overload and why iron chelators work so well!
In our case there are substances like IP6, pycnogenol, gingko biloba, quercetin, rutin, catechin, curcumin, xanthones etc that work as iron chelators while stabilize endothelium with microcirculatory improvement and faster healing of CCSVI!

Dr Bob Lawrence that first informed us about micronutrients like pycnogenol and their role in MS suggests in case of relapse increased daily pycnogenol even to 600-700mg (in smaller doses) along with increased Gingko, Resveratrol (although it works differently), EGCG etc probably he knows more than we do, he is doctor and PwMS 18 years now and takes only LDN and supplements, no disability, no problems at all!
Dr Aston Emphry also confirms this, it was though the first that spoke about vitamin D and it's role in MS!

skydog wrote:Does everyone see the post I just sent the way I see it. HD images... I need a computer that works like a old single speed bike, don't need all the extra gears. Just gets me in trouble. Help ? M

Change your avatar.

Rokkit

DIM wrote: Dr Aston Emphry also confirms this, it was though the first that spoke about vitamin D and it's role in MS!

Hey Dim,
So glad to hear your wife is well and stable. Aston Embry writes about CCSVI in the next issue of MS Pathways. He's very excited about the findings...also, our old friend phytic acid found in legumes, is one of the best chelators. You know I've got Jeff on all those guys!

Mark...you've lost your pic...but not your voice-
cheer

Well, Embry is against legumes in his best bet diet, so what do you do? (and I have to say, my husband does react to having eaten them which is sad, because I love beans.

whyRwehere wrote:Well, Embry is against legumes in his best bet diet, so what do you do? (and I have to say, my husband does react to having eaten them which is sad, because I love beans.

Cheer wrotte that mainly legumes contain phytic acid (IP6 or inositol exaphosphatase) not to eat legumes, you can take IP6 supplements with no allergenic ingredients!
Be careful as IP6 may remove iron from all your body not from your brain only, check regularly your blood iron status!
I prefer "easier" chelators as the others I mention above!

Thank you for the information!

Here's a link to, I believe, a funding document on SWI and its promise as a diagnostic tool.

Note more of the incredible images comparing regular technology to the new SWI.

Notice that the SWI makes a 1.5 or 3 t MRI have the capability of resolution equivalent to a 7t.
CLICK HERE

This is really REALLY great that this work in already in process with the CCSVI team. we WILL get the kind of MRI data we need, it is just a matter of time. I keep remembering that this researcher has already said that CCSVI is in harmony with his SWI work. The importance of that should not be undrestimated

mrhodes40 wrote: This is really REALLY great that this work in already in process with the CCSVI team. we WILL get the kind of MRI data we need, it is just a matter of time. I keep remembering that this researcher has already said that CCSVI is in harmony with his SWI work. The importance of that should not be undrestimated

thanks for those links, Marie...that really shows the potential for SWI. One thing I did not convey from Dr. Haacke's presentation was the smile on his face as he presented his "eureka!" revelations. He was exuberant. He has been looking at iron deposition in MS brains for awhile (just google his name) and for him, the pieces were coming together! His most recent paper on iron in MS was before the CCSVI research:
http://www.pubmedcentral.nih.gov/articl ... id=2650739

Just published six months prior to the conference- it fits together perfectly with what we are seeing in CCSVI.

Dr. Frohman made a kind of snide/funny comment about "Dr. Haacke's lack of enthusiasm..." because you could see how excited he was to see the pieces coming together.
from my notes:

Dr. Haacke states his findings in MS brains is consistent with everything presented today regarding venous structure, oxygen and iron deposition. He offers thanks to the foundation and Bologna for the openness of discussion and the freedom of ideas. He asserts that CCSVI does not go against what we know about MS....however it will further define it.

cheer
ps...nice to see your handsome face, Mark!

This Iron accumulation in brain - is very interesting. I would like to know that are there differencies with iron between ms clinical courses - rr, sp, pp?

ps. I saw Mark's photo and think "why he has Chuck Norris avatar?"

Ernst wrote:This Iron accumulation in brain - is very interesting. I would like to know that are there differencies with iron between ms clinical courses - rr, sp, pp?

ps. I saw Mark's photo and think "why he has Chuck Norris avatar?"

Yes, Dr. Haacke found direct correlation between disability and amount of iron and hypoxic injury in the brain. PPMS patients had the highest amounts. ...read Dr. Haacke's study:
http://www.pubmedcentral.nih.gov/articl ... id=2650739
And Mark may look like a tough dude...but we all know he's a sweetiepie at heart
cheer

I have a clarification and a question.

First of all, intense immune suppression does not merely reduce lesion volume but also disability progression, relapse rate, and brain volume decrease, at least in the initial stages of MS. E.g. with Campath, patients have NO disability progression (actually a slight improvement) at least for the several years duration of the trial, and an INCREASE in measured brain volume. At the same time, there are no relapses and new lesions. Of course Campath comes with major side effects, and I believe that treating CCSVI is better because it's closer to the root of the problem than the immune-system, however if we want to put all facts on the table and piece our puzzle together, we have to acknowledge that this means that the immune-system initially plays a HUGE role in exacerbating the problems caused by CCSVI, i.e. hypoxia and iron deposits, not just a side role. Otherwise immune suppression wouldn't be able to completely suppress the progression. Significant reduction of CNS volume change has also been attributed to the CRABS and to Cladribine, the latter also showing evidence of less disability progression. There is also decent-looking research on interferons showing that they delay the onset of SPMS in RRMS patients by a good amount (I think the time to onset was almost doubled). So again, during the EARLY stages of MS the immune system does play a role beyond cleaning up the trouble in that it exacerbates the problems caused by CCSVI by a LOT.

Now the question. I've been trying to come up with a theory for this but so far with no success. Why does the immune system initially respond to the damage caused by the reflux, creating the regular MRI lesions, and then stops after some years when SPMS starts?

Great question, radeck. That's another $64,000 question. Why does the immune system eventually stop trying to clean things up? And why does it never start in PPMS? Here's a guess...in the RRMS stages, the communication between the immune system and the CNS is intact. Microbleeding and hypoxic injury signal for macrophages to come in and clean up, just like in stroke-

Abstract

Lymphocytes, neutrophils and macrophages are found in the brain in areas of acute ischaemic stroke. The percentages of activated T cells and regulatory T cells were significantly increased in patients with ischemic stroke compared to healthy subjects and patients with OND. There was also an increase in the percentage of CCR7+ T cells. There were no significant differences in the activation of other cell types. In conclusion, there is evidence of immune activation and Treg cells in acute ischaemic stroke.

http://linkinghub.elsevier.com/retrieve ... 2808004578

After the damage accumulates and there is a death of enough axons- the communication between the CNS and immune system is hampered-the immune system cannot be reached or the immune system basically gives up the fight.

Not all MSers reach this stage. We have a family friend in her 70s who is just fine. I would imagine her stenosis is small compared to Jeff's double jugs, and her brain would show less iron deposition and hypoxic tissue loss.

This is only a theory. Dr. Haacke has found a correlation between iron deposition, hypoxic death and the amount of disability and progression. I would assume communication with the immune system would suffer as the brain suffers. It's all one body.
cheer

Thanks Cheer. Your two explanations, a) the Immune System (IS) giving up, and/or b) the IS loosing communication with the CNS, of course lead to the questions: what makes the IS give up, and what reduces the communication between it and the CNS? On a) Do we know from other diseases where the immune system responds to an actual pathogen that it simply gives up at some point? On b) could scar tissue caused by so many relapses reduce the contact between the IS and the CNS (i.e. the blood brain barrier becoming less transmissive to T cells)?

There's your assignment, Radeck...
Do some research for us, and find other diseases in the CNS in which the immune system is affected. What happens to the CNS in HIV-AIDS? What causes the immune system to back down in stroke? Do neurologists have any theories as to PPMS and the lack of immune activation?-
get googling and get us some research and answer some of your great questions for us!
cheer