A new concept and treatment options for MS

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The Mind-Body Connection

Postby Leonard » Wed Jan 18, 2012 4:25 am

In Multiple Sclerosis, there is definitely a mind-body connection. The mind-body connection is perhaps one of the most difficult areas of modern medicine. I remember having read about studies conducted when Israel was under the threat of attack by Scud missiles. The effect of this sort of stress was apparently different from the effect of emotional stress.

Personalities, lifestyles, behaviours and other factors such as for example emotional stress could predispose people to illness and put them at risk of acquiring certain diseases. I am sure our subconscious mind has its role to play there.

http://www.tldp.com/issue/175-6/Nourish ... 0Body.html
http://mybrainnotes.com/memory-brain-stress.html Subcortical Brain Structures, Stress, Emotions, and Mental Illness, … in a deep evolutionary sense, many of the complex information-processing potentials of the cortex are servants (often unconscious, automatized servants) to the dictates of the affective forces that ruled behavior prior to cortical evolution

From the publications under the above links, it shows that the hypothalamus is central to this theme. But, as we can see from the above posting (11 Jan 2012, 8:14am), the prolactin secretion is regulated by the same hypothalamus. Is this the connection? Is this where some important "unfinished business", stresses, social dislocation etc come into play in biological processes? Is this why we must confront the things that we instinctive feel we should but we don't because that is easier and more comfortable?

If that is the case, this might well be the direct "biological" link explaining the mind-body connection. Where stresses and emotions could inhibit prolactin secretion with a direct effect on demyelination. And indeed, and this is important for us, the method to induce prolactin secretion (as in the patent application mention in the posting above) to stimulate oligodendrocytes precursor cells could be a way forward.

MS becomes a multi-facetted complex disease with many influences. I believe this influence is among the weaker.
Clearly, the vascular obstruction and the gut bacteria will be among the stronger influences.
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Re: I think I found it: This Is MS

Postby Taurus » Wed Jan 18, 2012 8:21 pm

Leonard Good Research. But have u ever thought why MS is most prevalent in some areas and not uniformly distributed around the globe. Then there is a gender difference also (more in women than men). Lately, people now disclose that even there minors have MS who do not get exposed to stress in life like we do. I say there are still lot of unknowns in MS equations. Your efforts in this regard are certainly admirable.
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Re: I think I found it: This Is MS

Postby Leonard » Thu Jan 19, 2012 4:04 am

Taurus wrote:Leonard Good Research. But have u ever thought why MS is most prevalent in some areas and not uniformly distributed around the globe. Then there is a gender difference also (more in women than men). Lately, people now disclose that even there minors have MS who do not get exposed to stress in life like we do. I say there are still lot of unknowns in MS equations. Your efforts in this regard are certainly admirable.


Thanks Taurus. In fact, there are answers to all your questions in the above postings. They have in some way all been seen. I think we need now to consolidate what we know.... I am still looking for the best way to do that, using the global college of this forum...

Also the reflection on vitamin D supplementation in the posting below is possibly important.
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Re: I think I found it: This Is MS

Postby Leonard » Thu Jan 19, 2012 4:19 am

I learn a few things from this presentation by Trevor Marshall:
http://vimeo.com/32641708

1. (amended) Vitamin D and in particular the active form 1,25D may have effects on many other receptors including the Thyroid receptor; the link with the the Vitamin D Receptor (VDR) might not even be so important .. see his video from 16:45 onwards.

What seems important is that active 1,25D binds to the same points on these receptors as the inactive form 25OH. The 1,25 then enables / activates these receptors to do what they must do e.g. to activate the oligodendrocytes essential for maintaining the myelin and remyelination..

Now, it could well be that in the early stages of the disease, a high 25OH inactive form (through supplementation) could be useful to help raise 1,25D and thus to help activate receptors. For this reason vitamin D 25OH supplementation could help us ...

However, in the later stage of the diseasewhen many receptors are already knocked out, a high 25OH may get in the way as it binds to the same points on the receptors as the active form 1,25D. I have seen that my body regulated 25OH down as -I guess- the body seeks ways to make extra room for active 1,25D to bind. To that end, it is known that a high 1.25D is a market of MS (we know this) and also that there actually is not only the forward path (from 25OH to 1.25D) but also a path back from the 1,25D to the passive 25OH.

2. lipids may also activate receptors...

3. I learn that the Chlamydia bacteria, just like the Bar-Eppstein virus, knocks out the VDR receptor. Of the Bar-Eppstein virus, we knew, there is also published on PubMed referred to in a posting above. Of the Chlamydia bacteria, I did not know.

These bacteria can apparently keep quiet for many years to break out - then this may give rise to flares in the first benign form ..

The bacteria may infect the brains (compromised BBB) but it may also -and that is important here- besides affecting the VDR (impair micro cellular nutrition, glucose deficiency, ion pump failure), affect many other receptors that control very important processes for maintaining our myelin (the maintenance of oligodendrocytes / remyelination).

Where the outbreak of the bacteria directly affects our myelin, as we know best..
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David Hubbard's view falls in line with this concept

Postby Leonard » Thu Jan 19, 2012 10:23 am

wow, cool http://www.youtube.com/watch?feature=pl ... fBSLdstQk#!

I think this video will fall fully in line with the concept that has been built out here already.

few quotes:
"that the myeline is breaking down in the first place"
"the immune system just comes to clean up"
"need to shift the question to why are the oligodendrocytes dying?"
"what causes the stagnation...": "perhaps insufficient drainage" "blood abnormalities"

It seems we have an ally here in Dr Hubbard. :smile: :smile: :smile:
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In summary: This Is MS

Postby Leonard » Fri Jan 20, 2012 3:32 am

In summary:

An impaired vitamin D metabolism is a factor, no question about that. The glucose transport is slowing down, causing all sort of effects on the cells including on the charging of the ion pump. But I think it's more than a just failing of the vitamin D metabolism.

Besides the Vitamin D receptor, other receptors will become contaminated by the ligans of the gut bacteria as well and stop functioning as they should. For us, those receptors that activate or transcribe the oligodendrocytes and Schwann cells (or at least the pre-cursors thereof) are particularly important.

If this process fails, we will suffer from a 'wider' problem of insufficient myelin maintenance that we also see in diabetes2 patients. These latter patients will experience many of the same symptoms as MS patients.

Besides that, many years of CCSVI will cause the protective tissue of the brain to break (compromised BBB). But then also the endothelium (the inside tissue of the vessel walls) will be damaged. The endothelium contains cells that are crucial to the process of transcription / activation of e.g. oligodendrocytes (or their pre-cursors), and therefore that process will not function properly anymore either.

And again, if this process fails, the myelin around the draining veins of MS patients (MS in the brain is veno centric - re: Torben Fog in the 60's) will not be nourished properly and disintegrate. This is more of a 'local' problem of myelin maintenance.

If we add the two together, it is exactly what we see: a 2-stage disease from RR caused by Chlamidia bacteria or Epstein-Barr virus knocking out receptors and infecting the brain causing scleroses and demyelination to a progressive form with gut commensal bacteria knocking out receptors and demyelination.
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Re: I think I found it: This Is MS

Postby jamesoeck » Fri Jan 20, 2012 10:30 am

What a boat load of information on this page. If MS is so easy to pin point in people than why is it so difficult to get your Doctor or Specialist tell you point blank when you go in for a check up that you do not feel good and after a good psychical he say "that with out a doubt you have Multiple Sclerosis" or that you have type 2. Than after a week or so you can not walk or stand and are very week and you go back and your Doctor says that you need more iron or B12. I was told by my eye doctor that I had an infection in my optic nerve and lost over 50% of my vision so I got B12 shots for 2times a week for a couple of months and than he told me that I needed to go see a specialist for a check over. After many times to see the specialist I was told after having a spinal tap that I had MS. So I say with all the information that I read above I don't think it is that easy as they say. Because each person is different in many ways, such as color of skin, male,female, and other things as to ware they live in the United States or ware it is very humid. So it is not very easy unless you have done a lots, and lots of experiments and done a lot of testing on big groups people and followed them for a period of years.
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A failing glucose/oxygen metabolism

Postby Leonard » Tue Jan 24, 2012 3:07 am

http://www.nature.com/jcbfm/journal/vao ... 1191a.html Our results of significant underutilization of oxygen in MS.... to which I would add underutilization of glucose which is the other side of the same coin.
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the other coin: failure to activate oligodendrocytes

Postby Leonard » Tue Jan 24, 2012 3:11 am

http://www.sciencedaily.com/releases/20 ... g.facebook

The results, published February 23, 2004, in the advance on-line edition of the Annals of Neurology, suggest that the earliest event is not, as previously believed, a misguided immune system attack on a brain substance called myelin. Instead, the first event appears to be the death of the brain cells that produce myelin, triggering a subsequent immune system mop-up operation to clean up the cells and the myelin, said author John W. Prineas, MBBS, of the University of Sydney in Australia. Dr. Hubbard (see posting 19 Jan 2012 4:23 above) referred to this publication in his video.
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Re: I think I found it: This Is MS

Postby SaraG » Tue Jan 24, 2012 4:38 pm

When I was diagnosed with MS I quickly went on a gluten free/low fat/low dairy diet (MS Recovery Diet). I felt much better immediately and kept telling my husband that I know somehow MS is linked to blood sugar levels. I had always suffered hypoglycemia and it was greatly improved with my new diet. However, I could never get rid of the nagging tiredness I felt. I was scared to death of fat and ate very lowfat. I then discovered Paleo which is grain free (except for occasional white rice), legume free, vegetable oil free, mostly dairy free and most definitely low sugar. I credit the higher fat content (fat is nourishing to the brain) and the low sugar/carb with regulating my blood sugar to the point that just gluten free cannot (too many carbs). This is not necessarily low carb but it is lower carb than the Standard American Diet (SAD). It is also a diet that excludes all processed foods (chemicals) unlike a low carb diet like Atkins which allows for processed food (chemicals) as long as it is low carb. I follow Paul Jaminets "Perfect Health Diet" which is more South Pacific Islander Paleo.

I am relaying this just to keep the window open that maybe fats are not a problem for us or not good fats at least (olive oil. coconut oil, butter (or ghee)and high quality fatty cuts of meat but bad fats such as rancid vegetable oils (canola,safflower, etc.).

I have never felt better in my life. I am most always bursting with energy. I have had no relapses and no new scarring on my MRI's and the only time I feel bad is if I ingest too much sugar.

I realize I am just one person saying this but I credit good fats with a substantial part of my recovery and would just like to keep that window open so we don't automatically say that fat is bad for people with MS and miss a possible piece of the puzzle that could help find the cure.
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sugar is bad

Postby Leonard » Thu Jan 26, 2012 6:36 am

SaraG wrote:When I was diagnosed with MS I quickly went on a gluten free/low fat/low dairy diet (MS Recovery Diet). I felt much better immediately and kept telling my husband that I know somehow MS is linked to blood sugar levels. I had always suffered hypoglycemia and it was greatly improved with my new diet. However, I could never get rid of the nagging tiredness I felt. I was scared to death of fat and ate very lowfat. I then discovered Paleo which is grain free (except for occasional white rice), legume free, vegetable oil free, mostly dairy free and most definitely low sugar. I credit the higher fat content (fat is nourishing to the brain) and the low sugar/carb with regulating my blood sugar to the point that just gluten free cannot (too many carbs). This is not necessarily low carb but it is lower carb than the Standard American Diet (SAD). It is also a diet that excludes all processed foods (chemicals) unlike a low carb diet like Atkins which allows for processed food (chemicals) as long as it is low carb. I follow Paul Jaminets "Perfect Health Diet" which is more South Pacific Islander Paleo.

I am relaying this just to keep the window open that maybe fats are not a problem for us or not good fats at least (olive oil. coconut oil, butter (or ghee)and high quality fatty cuts of meat but bad fats such as rancid vegetable oils (canola,safflower, etc.).

I have never felt better in my life. I am most always bursting with energy. I have had no relapses and no new scarring on my MRI's and the only time I feel bad is if I ingest too much sugar.

I realize I am just one person saying this but I credit good fats with a substantial part of my recovery and would just like to keep that window open so we don't automatically say that fat is bad for people with MS and miss a possible piece of the puzzle that could help find the cure.



Thanks SaraG, I share your view. Fats are necessary. It even seems that fats can (help) activate / transcribe oligodendrocytes so necessary for maintaining our myeline and axons. Marshall said something about this when he was in Asia, see http://vimeo.com/32641708 And about fast sugars, I agree, they are devastating.

Fast sugars grow MGmin LDL cholesterol, this is created when sugar is added to normal LDL. But it coats or "glycates" the red blood cells with sugar before the body can lower the level with insulin. In addition, receptors of cells will be blocked including the vitamin D receptor (important for the glucose metabolism and ion pump) as well as receptors of cells responsible for activating / transcribing the (pre-cursors of) oligodendrocytes that are so essential to maintain our myelin/axons.

http://www.c-reactive-protein.com/103.htm
http://en.wikipedia.org/wiki/Autophagy

Probably the MGmin LDL cholesterol and the ligands of intestinal commensal bacteria that cause VDR dysfunction are among the same category of species, may be even sharing some underlying mechanism. This explains why you must go low on sugar if you have MS.

But this may also cause you a problem because you need the fast glucose shots simply to keep going, to get enough glucose into your starving cells.. That is certainlyn the case for myself. So whilst taking the glucose shots, you are sealing your cells at the same time. And over time, you need to take more and more sugar to get the same effect until...

A common type 2 diabetes drug, metformin, may help fight the disease by blocking the transformation of normal LDL into the super-sticky LDL. It has also been suggested that metformin helps to open the glucose gates to the cells / GLUTs (links can be found in above postings). The working mechanism of metformin is still not very well understood but I am convinced that it is one of the most under-appreciated drugs for our disease. And indeed, it might well be an alternative for olmesartan that prof. Marshall is using to clean the contaminated receptors (re: Marshall Protocol).
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A huge systemic failure?

Postby Leonard » Thu Jan 26, 2012 6:40 am

if I try to oversee the situation, I believe that there is clearly something wrong with the system as a whole, world-wide.

If I as a semi-literate can come up with a plausible explanation for MS in 1 year (with the help of these fora and in my spare time, do not tell me that it's all wrong because it is not ..), why for Christ's sake can a system like ECTRIMS / ACTRIMS which met in Amsterdam in October 2011 with over 7,000 specialists and after 150 years of thinking not come up with something consistent and coherent, which gives a plausible explanation?

Can we put the blame on the pharmaceutical industry? Today there are debates (which will certainly gain further momentum) on the changing social responsibilities of corporate actors. And business ethics will gain more importance. But at the end of the day, these companies are responsible to their shareholders.

Can we blame the clinical sector, hospitals and doctors? Maybe, I'm not sure. They are to some extent also a victim of more bureaucracy and protocols, e.g. to limit responsibility / liability for their hospitals and themselves. Whilst craftmanship was lost on the way.

Can we put the blame on public health institutions? As Nigel Crisp said in his book, Turning the World Upside Down, public health has been overshadowed by the pharmaceutical and clinical sectors since the 1950s. And to some extent, officials may have been submissive because they did not have the manpower and expertise. That is bad ...

SO AS PATIENTS WE ARE LEFT OUT IN THE COLD ALREADY FOR MANY YEARS. AND WE FACE A SYSTEM THAT STAGNATES AND SUSTAINS ITSELF... What's worse, it seems we can not even find a button to press to force change ..
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the incompleteness of logical contact

Postby Leonard » Tue Jan 31, 2012 2:08 am

The problem is that all schools of thought just sit at their own base, so that the melting pot does not develop. The system stagnates and sustains itself. And we sit out in the cold..

I quote:

"when paradigms change, there are usually significant shifts in the criteria determining the legitimacy both of problems and of proposed solutions..

... that two scientific schools disagree about what is a problem and what a solution, they will inevitably talk through each other when debating the relative merits of their respective paradigms. In the partially circular arguments that regularly result, each paradigm will show to satisfy more of less the criteria that it dictates for itself and to fall short of a few of those dictated by its opponent..

... the incompleteness of logical contact consistently characterises paradigm debates.." unquote

etc. etc. etc.

Thomas S Kuhn has beautifully written down (and that is an understatement) what happens when paradigms change in "The Structure of Scientific Revolutions". This book was hailed 'a landmark in intellectual history' and it really is! It is such a pleasure to read and to find this recognition for the evolving landscape in our little world. It is a must read for all who develop new policies, for hospital directors, for doctors, for researchers, for any well-educated person. It's just beautiful in the way it characterises what is going on here...
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keep your nuclear receptors in good condition

Postby Leonard » Tue Feb 07, 2012 7:43 am

a paradigm shift from the traditional biomarkers to nuclear receptor profiling

Nuclear receptors (NRs) are major targets for drug discovery. Upon ligand binding, NRs undergo a conformational change, which alters their binding preference for coregulators. Short α-helical sequences in the coregulator proteins, LXXLL (in coactivators) or LXXXIXXXL (in corepressors), are essential for the NR-coregulator interactions. However, little is known on how specificity is dictated.

In order to obtain a comprehensive overview of NR-coregulator interactions, new technologies are being developed that allow for characterization of real-time coregulator-nuclear receptor interaction (nuclear receptor function). see for instance https://www.pamgene.com/en/company.htm

Drug R&D for elucidation of drug-target interactions and in support of clinical trials as a drug activity based biomarker platform is a paradigm shift from the more traditional biomarkers that only focus on presence of certain RNA, DNA or protein molecules and not their activity nor the interaction of the drug with these important classes of signalling molecules.

Retinoid X receptor gamma signaling accelerates CNS remyelination

I quote: The molecular basis of CNS myelin regeneration (remyelination) is poorly understood. We generated a comprehensive transcriptional profile of the separate stages of spontaneous remyelination that follow focal demyelination in the rat CNS and found that transcripts that encode the retinoid acid receptor RXR-γ were differentially expressed during remyelination. Cells of the oligodendrocyte lineage expressed RXR-γ in rat tissues that were undergoing remyelination and in active and remyelinated multiple sclerosis lesions. Knockdown of RXR-γ by RNA interference or RXR-specific antagonists severely inhibited oligodendrocyte differentiation in culture. In mice that lacked RXR-γ, adult oligodendrocyte precursor cells efficiently repopulated lesions after demyelination, but showed delayed differentiation into mature oligodendrocytes. Administration of the RXR agonist 9-cis-retinoic acid to demyelinated cerebellar slice cultures and to aged rats after demyelination caused an increase in remyelinated axons. Our results indicate that RXR-γ is a positive regulator of endogenous oligodendrocyte precursor cell differentiation and remyelination and might be a pharmacological target for regenerative therapy in the CNS. unquote see
http://www.nature.com/neuro/journal/v14 ... .2702.html

what is the right angle of attack?

R&D and progress in this matter is predominantly driven by business incentives related to the discovery of new drugs. Of course, the profit motivation is important for the further development of new drugs. However, I am not sure whether for us the drive to nuclear receptor profiling is necessarily the right angle of attack.

If MS is caused by a contamination of nuclear receptors (VDR-RXR complex and the Thyroid hormone receptor or TR) by bacterial ligands, the first question to ask is: can we prevent this from happening or reverse the situation of receptor blockage or dysfunctioning by using existing techniques or medication?

It is well known that through diet and lifestyle changes, MS is to an extent a 'manageable' disease. The experiments by Dr. Roy Swank who followed 144 MS patients for over 34 years show that those who were on a low fat diet (<20 gr of saturated fats/day) did not progress any further and the disease even somewhat reversed. I think the same is true for sugars possibly in combination with saturated or trans-fats where people on a low fat and sugar free (implied) diet stop from detoriating (= diabetes2 relation).
http://www.thelancet.com/journals/lance ... 40-6736(90)91533-G/abstract
http://en.wikipedia.org/wiki/Swank_diet
http://www.swankmsdiet.org/About%20The%20Diet
http://www.ncbi.nlm.nih.gov/pubmed/7572944

The low fat and low sugar diet, existing diabetes drugs as Metformin, Olmesartan and certain anti-biotics could therefore be a good first line of defense against our disease, primary aimed at keeping nuclear receptors (at the least those nuclear receptors we have left) alive and kicking (e.g. to sense the insulin and transport glucose, to transcribe and transactivate).
http://www.ncbi.nlm.nih.gov/pubmed/9731705

As this is not where the money in the market is, there may be an important need here for public intervention and public funding.
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Re: I think I found it: This Is MS

Postby Leonard » Mon Feb 13, 2012 5:20 am

From another topic on this forum on Researchers report potential MS breakthrough
general-discussion-f1/topic19166.html
http://www.msrc.co.uk/index.cfm/fuseact ... ageid/1104

Caltech researchers report a possible breakthrough in multiple sclerosis medicine in the latest issue of the Journal of Neuroscience of 8 February 2012. The article is titled Exogenous Leukemia Inhibitory Factor Stimulates Oligodendrocyte Progenitor Cell Proliferation and Enhances Hippocampal Remyelination
http://www.jneurosci.org/content/32/6/2100.abstract

I quote ... we identify these parenchymal glia as oligodendrocyte (OL) progenitor cells (OPCs) and show that LIF delivery stimulates their proliferation through the activation of gp130 receptor signaling within these cells. Importantly, this effect of LIF on OPC proliferation can be harnessed to enhance the generation of OLs that express myelin proteins and reform nodes of Ranvier in the context of chronic demyelination in the adult mouse hippocampus. Our findings, considered together with the known beneficial effects of LIF on OL and neuron survival, suggest that LIF has both reparative and protective activities that make it a promising potential therapy for CNS demyelinating disorders and injuries. unquote.

Here, mention is made of yet another receptor (the gp130 receptor in OPC) that, when activated, stimulates the proliferation of OPC (oligodendrocytes progenitor cells). According to the article, such activation is possible through LIF (Leukemia Inhibitory Factor) delivery.

In an above posting on this same topic (11 Jan 2012 2:14pm), the role of prolactin for the activation of the oligodendrocytes was mentioned. Where the inhibition of prolactic secretion would cause problems. I quote: A method for treating demyelinating diseases such as MS comprised of administering to an individual afflicted with a demyelinating disease a medicament that induces prolactin secretion. Prolactin secretion stimulates oligodendrocyte precurser cells, which remyelinate demyelinated nerve cells. The medicament is administered at a dosage sufficient to induce prolactin secretion resulting in a hyperprolactinemia. Estrogen, estradiol, estriol, histamine H2-receptor antagonists such as cimetidine, and vitamin D can be administered in conjunction with the prolactin-inducing medicament to further promote the remyelination of the nerve cells. uquote
http://www.faqs.org/patents/app/20080286234

The article below then suggests a link between the breakthrough reported by Caltech and the above 2008 patent on prolactin secretion. It indicates a role for LIF in loss of autocrine PRL suppression contributing to unrestrained prolactinomas PRL secretion. http://www.ncbi.nlm.nih.gov/pubmed/12574225
Also the receptors mentioned earlier in above posting i.e. the Retenoid X Receptors and prolactin receptors are related. http://www.ncbi.nlm.nih.gov/pmc/article ... 90034a.pdf

As a semi-literate, I do not understand the precise meaning or full reach of what is being said here but it is clear to me that a variety of receptors is involved in the metabolic processes/endocrine system in the brain and spinal column. Besides the VDR, RXR and TR, we note here the gp130 receptor and the D2R, a D2-like dopamine receptor.

And although sulpiride is mentioned as a D2R agonist and LIF delivery may help the proliferation of oligodendrocytes, it would occur to me that keeping the variety of receptors (or those you have left over after so many years of ccsvi) healthy is probably the first and most important thing to do.
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