This Is MS Multiple Sclerosis Knowledge & Support Community

Hi Zina

I think BUMP means entering a post in a thread so that it will appear at the top of the list and consequently come to the attention of people who may have missed it. It's definitely ok to have more posts when a thread is bumped.

Sorry though, I don't know if yoga would keep your veins flexible. Sounds logical.....

Now, I'm bumping the thread because there's a new abstract (full text of the article is open access) that could be relevant to the inflammation discussion.

Role of platelets in neuroinflammation: a wide-angle perspective

The role of platelets in inflammation is well appreciated in the cardiovascular and cancer research communities but appears to be relatively neglected in neurological research.

Now, what makes this interesting (at least to me) is that one of the authors is R. Zivadinov from Buffalo. Starting on page 34 of the article there's a discussion: Platelets in multiple sclerosis: smoking gun?

I must say I don't understand the article at all, so I wanted to post it hoping someone else might. In particular, I wonder if the info in the article might shed more speculative light on Buffalo's "therapeutic angioplasty" (per their newsletter) that will be different from Dr. Zamboni's or Dr. Dake's interventions for CCSVI? Anyone care to hazard a comment? Maybe not related at all......

Thanks!

Sharon

Shayk,

It would take me a long time to fully understand this paper but it definitely looks interesting. One thing I noticed right away is that one of the authors is from Iran !!! CCSVI is truly science gone global.

ozarkcanoer

did you say PAGE 34?! yikes.

Nice bump, Sharon
I do not claim to completely understand all the platelet specifics, but it appears that Zivadinov and the other docs are explaining platelets to a neurological world which has not considered them very important. This paper illuminates more connections of MS to venous disorders. Platelets are tiny, irregularly shaped cells that do not have a nucleus w/ DNA. They circulate in the blood and control clotting.

Here is CVI research-
Note: Chronic venous insufficiency of the legs shows extreme platelet activation-

Conclusion: All classes of CVI are associated with significantly increased percentages of platelet-monocyte aggregates and increased percentages of platelet-neutrophil aggregates throughout the circulation. The presence of more of these aggregates and the increased propensity to form aggregates in the presence of platelet agonists in all classes of CVI suggests an underlying state of platelet activation and increased reactivity that is independent of the presence of ulceration.

http://cat.inist.fr/?aModele=afficheN&cpsidt=1180395

And now, from the Zivadinov paper, here are platelets in MS- also in a state of chronic activation...

The possible involvement of platelets in MS was first studied by Putnam in 1935, who considered a role for venule thrombosis in CNS demyelination [297]. In the 1950’s- 60’s, at least ten studies appeared on the relation of platelets to CNS demyelination, several of which reported augmented platelet adhesiveness in MS, which correlated with disease activity [298-301]. More recently, a number of observations of platelet abnormalities in MS patients have appeared [302-304], and others cited below. We became interested when colleague W. Sheremata encountered MS patients with severe immune thrombocytopenic purpura (ITP) [305], leading to our report of increased platelet microparticles and platelet activation marker CD62P (P-Selectin) in MS [306]. Thus, chronic platelet activation in MS may now be regarded as well established,
including by the report of Cananzi et al cited earlier [54].

http://www.jneuroinflammation.com/conte ... 4-7-10.pdf

One point Dr. Zivadinov made, emphatically, in Bologna- was that he believed the next ten years would generate thousands of new research papers explaining MS as a vascular disorder and CCSVI. This paper appears to be one of those promised papers.

If CVI of the legs is caused by venous blockage, which then signals platelet activation, the coagulation cascade, and resultant tissue damage (venous ulcers)- then CCSVI, created by venous blockage- could do the same thing to the brain. Both diseases share venous insufficiency, platelet activation, inflammation and tissue damage.
thanks for sharing it!
cheer

related abstract

Rev Diabet Stud. 2009 Fall;6(3):148-58. Epub 2009 Nov 10.
A Molecular Level Understanding of Zinc Activation of C-peptide and its Effects on Cellular Communication in the Bloodstream.
Inspired by previous reports, our group has recently demonstrated that C-peptide exerts beneficial effects upon interactions with red blood cells (RBCs). These effects can be measured in RBCs obtained from animal models of both type 1 diabetes and type 2 diabetes, though to different extents. To date, the key metrics that have been measured involving C-peptide and RBCs include an increase in glucose uptake by these cells and a subsequent increase in adenosine triphosphate (ATP) release. Importantly, to date, our group has only been able to elicit these beneficial effects when the C-peptide is prepared in the presence of Zn2+. The C-peptide-induced release of ATP is of interest when considering that ATP is a purinergic signaling molecule known to stimulate the production of nitric oxide (NO) in the endothelium and in platelets. This NO production has been shown to participate in smooth muscle relaxation and subsequent vessel dilation. Furthermore, NO is a well-established platelet inhibitor. The objective of this review is to provide information pertaining to C-peptide activity on RBCs. Special attention is paid to the necessity of Zn2+ activation, and the origin of that activation in vivo. Finally, a mechanism is proposed that explains how C-peptide is exerting its effects on other cells in the bloodstream, particularly on endothelial cells and platelets, via its ability to stimulate the release of ATP from RBCs.

Cheer wrote:

I truly hope that some PPMS patients may be able to get MRVs and stent surgery. There's been a fire lit under me, and I want to get the word out

I too am PPMS and plan to have the diagnosis at Stanford if they ever resume testing. I am a bit cautious abut stenting, though. I have been involved with stent and angioplasty in industry for 20 years, and stents are all designed essentially for arteries, not veins. Angioplasty (i.e. the liberation procedure) makes more sense to me, but PPMS definitely should be on board and I will be happy to participate in studies.

hi cheer,

thank you for bringing the platelets into the disussion. One question that I was thinking about is the possible role of platelet aggregation inhibitors in the ms treatment. Low molecular Heparins are not expansive and they don`t have severe side effects.
Anticoagulation therapy (with substances such as Warfarin) has been shown to bring no benefit in studies decades ago. But at that time, low-molecular Heparin for daily injections was not yet available. What I`m not sure about is whether inhibition of aggregation also means inhibition of (metabolic) activation of the platelets. But with the CSVI theory it probably makes sense to test the effects of long time blood thinning measures, specially when the inflammatory effects of platelet factors could be diminished.
Do you have more information about this?

lobra

Lobra-
What I've been recommending with my endothelial health research is trying proteolytic enzymes as a first step (such as serrapeptase, bromelain and nattokinase) to naturally break down platelet aggregation and calm c-reactive proteins in the inflammation/coagulation cascade. Dr. Ashton Embry has recently added these supplements to his Best Bet Diet. Since lo-molecular weight heparin is an incredibly expensive drug in the US (although not the rest of the world), it's a good first step for folks in America.
That said, if heparin were available to you for your wife....it might be an interesting test to see how she did on it-
cheer

Hi Sharon,

Thank you for your prompt response...and for the info you posted..and I just remembered something(as I have been reading these latest posts on blood clotting and platelets etc ). Prior to diagnosis 10 yrs ago, the yr I had my first real major attack, I had had, 2 months prior, a miscarriage. I was in my 4th month of pregnancy. When I eventually went to a neurologist and began testing for MS, he later told me, after I gave him my medical history, that it was his feeling the miscarriage was because of the MS. At the time (and all this time until lately with the introduction of the CCSVI paradigm shift for MS)I did not understand how these two events could be related. I had guessed that it was the miscarriage, the trauma of that event, that had brought on the symptoms. I do remember saying something about blood clotting, and that my blood was prone to clotting. But I do not recall him saying this was the case with MS patients in general.
Now this is all starting to make sense!

peace,
zina

cheerleader wrote:Lobra-
What I've been recommending with my endothelial health research is trying proteolytic enzymes as a first step (such as serrapeptase, bromelain and nattokinase) to naturally break down platelet aggregation and calm c-reactive proteins in the inflammation/coagulation cascade. Dr. Ashton Embry has recently added these supplements to his Best Bet Diet. Since lo-molecular weight heparin is an incredibly expensive drug in the US (although not the rest of the world), it's a good first step for folks in America.
That said, if heparin were available to you for your wife....it might be an interesting test to see how she did on it-
cheer

I was taking rather large doses of nattokinase, serrapaptase, bromelain, rutin, CQ10... (a product called Neprinol) for about 8 months for a non-MS fibrin issue. I thought that it would also benefit the MS by breaking down the plaques in the brain. Everything was fine for a while, but then I started having an MS relapse - crushing fatigue, extreme dizziness, vision stuff... I was not too worried, because I have been RR for a long, long time, and I thought that it would pass. It did not. I have been in relapse since August 2009.

I started to think about the plaques in the brain, and began to wonder if they were protective lesions, rather than reactive lesions, and that perhaps dissolving them was re-opening breaches in the BBB, and actually making the MS worse. When I learned about CCSVI, I thought that I was right, and stopped the enzymes. I am very slowly remitting, but I have decided to not take them again until after liberation.

I mentioned this idea to the neurologist last week, and he implied that it was a reasonable assumption.

I'm not saying not to take the enzymes - Joan is absolutely right in her research, but I want to share my own experience with them, and suggest caveat.

Maybe I am going SP...

Hi J,

I took 14 bottles of Serrapeptase at the highest dosage level per tablet (Enerex - 90,000 I.U.'s, 750 mg's, 120 caplets) at a rate of 3 to 5 caps a day, focusing on taking most of the dosage in the wee small hours of 3 -7am.

The sole purpose of this venture was to investigate the difference between the "before" (3 years ago) & "after" (this past June) Serrapeptase MRI's. My neurologist was genuinely intrigued by the idea and carefully compared them.

He stated that there was no change whatsoever in the lesions. In his opinion, Serrapeptase did not cross the BBB and chew on the lesions.

Am now undergoing a rare exacerbation period and have run out. Wanting to get back on it because I was relapse-free during the time taking it.

Itsa