This Is MS Multiple Sclerosis Knowledge & Support Community

Thank you Scott. We are definitely on the same page. Your views on recovery are well taken.

Lately, there have been some interesting publications on impaired immune response to EBV in MS.
https://www.ncbi.nlm.nih.gov/pubmed/28197337
http://www.msra.org.au/ms-immune-system ... ead%20more
http://www.ms-uk.org/scientists-discove ... ain-210317
Most certainly, EBV transformed T cells play a major role. The EBV does so for its own benefit.

Furthermore, recently there have also been published studies that suggest a relationship between T cells and long chain fatty acids where T cells no longer clean up B cells. The studies of Swank and the prevention of a transition to a secondary progressive (SP) form by an extended low saturated fat diet would seem to confirm such relationship.
https://multiplesclerosisnewstoday.com/ ... ne-system/

Moreover, here above we saw a study on protein changes in EBV-B cells, making them no longer recognized by T cells.
http://www.mstranslate.com.au/ms-epstei ... te-part-2/

I believe that this whole EBV complex is of particular importance for the progressive form of MS. The inflammatory variant (RR) is situated more in the corner of the Varicella-Zoster virus which is known as an inflammatory virus, possibly augmented by other herpes strains.

The interaction between various immune cells including regulatory cells, EBV and other herpes virinae and the fat metabolism will undoubtedly be immensely complicated and the result of many tens or even hundreds of millions of years of evolution.
[post-script: See for instance this article on Analysis of the cross-talk of Epstein–Barr virus-infected B cells with T cells in the marmoset
http://www.nature.com/cti/journal/v6/n2 ... 0171a.html
and this article from the same authors on An essential role of virus-infected B cells in the marmoset experimental autoimmune encephalomyelitis model
http://journals.sagepub.com/doi/abs/10. ... 7317690184 ]

Notwithstanding, I think the big picture is given here (the above posting of Feb 1):
http://www.thisisms.com/forum/general-d ... ml#p245692
where the above considerations would seem a logical expose explaining the transition from the inflammatory (steps 1-4) to the progressive phase (steps 5-7) of MS.

Incidently, despite the huge complexity, chemo like cyclophosphamide (or alternatively mitoxantrone that Terry Wahls used, neurologists call them "heavy immuno suppressive medications" but clearly they do the hell of a lot more to our microcosm, including most importantly a surge of new 'clean' immune cells) would seem to be able to effectively reset the immune system. So, while it may take a long long time before all the intricacies of the viral interaction with the immune system and the fat metabolism are fully understood, it may not be necessary to have to wait that long.

The chemo would then need to arrest the decline; a diet like the Wahls green diet would detoxify the body and open the cells again and perhaps help silence the HERV expression via the microbiome. Terry Wahls used several cycles of mitoxantrone (a chemo) and then the diet got her out of the wheelchair.

Last Summer, I became 60 years old. The oxidative stress caused by the EBV B cells should now gradually come down because the B-cell production will come down. As the disease is still progressing, I am exploring the possibility to get cyclosphosphamide but I am also wholeheartedly taking Scott's advice here above and on http://www.thisisms.com/forum/general-d ... ml#p246916

The programme of ECTRIMS/ACTRIMS 2017 is made up of bits and pieces and only adds to the confusion.
http://www.professionalabstracts.com/ec ... ner/#/grid
The programme needs radical change.
As patients, we should not accept to loose yet another year because of this persistent medical impasse.
http://en.wikipedia.org/wiki/Agnotology

As recent demarches around president Trump have shown, facts alone will never be sufficient and will have to be placed in a bigger story (albeit of real or fake news).
The problem with MS research is that such a grand narrative has never been constructed, rather that it has always been much of a piecemeal approach.
In fact, a first attempt of story telling during the openingsspeech of a recent ECTRIMS/ACTRIMS on the role of EBV B-cells is not being continued in any way.

Those responsible for the ECTRIMS/ACTRIMS conference should revise the programme.
It should become some sort of amalgamation of the last few pages of this thread and in particular the synopsis on the previous page pg 54
http://www.thisisms.com/forum/general-d ... ml#p245692
and the programme of the ACTRIMS Feb 2017 Forum
https://www.actrims.org/forum2017/
http://forum2017.actrims.org/forum2017/ ... t-a-glance
http://forum2017.actrims.org/forum2017/ ... -abstracts
https://multiplesclerosisnewstoday.com/ ... o-florida/

You need to get all this written down in one place. While all the would-be scientists on ThisIsMS consider themselves good writers, they are not. You need not only correct science, but a good scientific writer who can communicate well, not only in whole sentences, but whole well-connected paragraphs, chapters, sections, papers, articles, essays, books. Etcetera. Not long lists of words separated only by commas. Such lists will not get a cogent point across. Basic grammar is required. Subjects, verbs, objects, adjectives, adverbs, etcetera.

@1eye: I could not agree more. The synopsis http://www.thisisms.com/forum/general-d ... ml#p245692 is for me, to get my head around it, to construct a mindmap. As the matter is so complex and multi-factorial, I believe it is a necessary pre-requisite before things can be written down.

But over and above a good paper work, it needs a place where the new thinking can land, a conducive environment where professionals can discuss across the boundaries in conventional medicine. It needs what I sometimes call a ‘New Health Society’, a bit along the lines of what iSoC did for the Internet. https://en.wikipedia.org/wiki/Internet_Society

I see strong parallels with the development of the Internet in the early 90’s . The Internet was breaking with the old AT&T environment and the old telecom/CCITT thinking and practice. The new insights in health and disease are breaking with traditional medicine and need a similar ‘paradigm’ change. See here the challenge that we are up to.

I don't know how to organise this but I am open to any suggestions.

In 1992 I was spending a lot of time on PPP, working with the working group. I went to the IETF meeting that year, and heard Dave Clark talk about Kings, Presidents, and Voting. Now we can see what's wrong with all three, given the results democracy has been coming up with lately.

The problem back then was people like me who believed in OSI, and wanted to impose a high standard of standardness on everything.

However the Internet was a victim of its own success. I used to say that these new networks would make themselves useful to people, in direct proportion to the number of people who used them. I used to quote Lenny Bruce, saying "It's the information that makes the country strong." I used to compare routers and bridges with the Yellow Pages: the more people use them, the more useful they become.

But who uses the Yellow Pages anymore? The dream of Internet Ubiquity is now a reality, and it is rife with lawless behaviour. Good old tcp.

I think I agree. I think the scientific community could well use Internet-style working groups and organizational structure. The mailing list is a key ingredient. There can still be mailing lists, or something like them.

Maybe you could start by writing a MSRFC (Medical Science Request For Comments). A straw man which would propose a structure for a Medical Science Engineering Task Force (MSETF), and btw adopt several documents as MSETF defacto standards. Gain credibility and legitimize best practises by making standards out of stuff everybody does already, but forgot to write down, like angioplasty.

Call it engineering, to give people a good excuse to stay away. The less people involved at the beginning, the better the result will be. It need to start with technology: i.e, a strong technical foundation, preferably real-world tested by something like bake-offs.

One thing you might do is call on everyone who ever had a CCSVI procedure to submit to testing. Controls should not be hard to find. Use several standard measures, like timed walking, PASAT, etc. Try to determine if 5+ years of placebo effect have made any measureable difference compared to those who did not have a CCSVI procedure. If you design it right, and enlist the right people, it might even get funded. Publish result as an MSRFC.

Perhaps there are several Best-Practices-type documents which could be done as MSRFCs. One would be an updated and cleaned up version of whatever is the page you and several others seem to be on, your new concept and treatment options.

Another might be cheerleader's Endothelial Health document, written up as an MSRFC.

Another might be jimmylegs' diet recommendations, what test are required, what ranges you should look for, what foods contain the recommended nutrition, what supplements, and why, what you should stay away from, written up as a MSRFC.

The Internet is a real game changer. See Mary Meeker's reports on "Re-imagining ... " e.g. on
I don’t want to start here a philosophical discussion but the gist of my thinking is that the Internet will cause - besides the obvious technological advances- a new wave of Enlightment in our society that we will only understand in full in a hundred years.

In our modern world with all its entrenched interests, many things are frozen, rusted, have become part of the establishment, including our “free press”. In fact, that press is not at all as free as people might think.

Think for instance about our MS dossier. I have contacted editors, directors etc in our “free press" to ask for their attention. In the beginning some show real interest - even enthusiasm - but when it comes to a change in their believe system, they get cold feet. I suppose they ask – their rules of good practice - “the establishment” which is the MS neurologists, those who have learned the wrong thing in the first place. And these neurologists will deny, defer, deter, delay, destroy... At that point, our "free press" gets locked up in an old system, becomes part of the establishment. And the "free press" is dead.

Without the Internet, we would not have had the social media and patient fora such as this platform - as patients, we would have been literally illiterate. Apart from all the technicalities on working groups, document types, participation rules, IPR rules etc that will need to be looked at when setting up a New Health Society, we should cherish the open nature of the Internet as the greatest gift to mankind in its history. It is the Internet that will challenge old world thinking and practices in all its aspect. http://www.internetsociety.org/

Having said that, I will look at your suggestions for working groups and organizational structure. And perhaps we could start work together on a strawman MSRFC document (a Medical Science Request for Comments document).

And if anyone else reading here has ideas or would wish to participate, please don’t hesitate to let me know either by posting or pm. Thanks a whole lot.

MSRFC – Medical Science Request For Comment #2017.1001
22 Mai 2017

The etiology and pathogenesis of MS has for long been unknown. This MSRFC proposes a concept for comment.

MS has two components: the inflammatory part and the progressive part. Different mechanisms underlie both parts.

The inflammatory phase is caused by a deficient mitochondrial antiviral signaling (MAVS) which makes that intra-cellular interferon mechanisms are not adequately induced. The failure to recognize the double stranded viral DNA from herpes strains is caused by a deficiency in the working of certain Single Nucleotide Polymorphisms (SNPs) in the genome (to note different prevalence for MS in Japanese population). In periods of immune deficiency (dry eyes, herpes evades T cell immunity), herpes virinae may integrate their DNA in permissible cells, typically cells that divide fast such as OPCs (herpes survival strategy after millions of years of evolution). At some point, cells come to expression and trigger a large scale activation of HERV (endogeneous retroviral segments integrated in the human DNA during evolution) in a triangular arrangement with the genome. The enzyme Peptidyl Arginine Deiminase (PAD4) - an enzyme that converts arginine to citrulline -penetrates the mitochondria and causes a disruption of ATP production. [PADs are a prerequisite for NETosis, the neutrophil extra cellular trap a pro-inflammatory form of cell death, which mechanism causes cells to die to trap pathogens and prevent them from spreading] SNPs in PADs are associated with an inhibitory immune response and increased risk of developing the disease. With a lack of energy, the ion pump fails and motor and sensory problems start. PADs also hypercitrullinate the myelin basic protein (MBP). The immune system then cleans up failed cells causing demyelination and lesions; the remyelination process gets blocked. In the process, the virus causes evasion of T cell immunity, for its own benefit. The peak in the graph of age of onset is around 25 years. Over time, the mechanism wanes. Obviously, people who have more mitochondria per cell because of higher Vitamin D (more sun exposure) during fetal period and adolescence will be better protected. Chronic venous insufficiency (CCSVI) may breach the BBB and initiate a viral spread from the nasopharynx into CNS and spinal.

The EBV virus spreads slowly and infects B cells where T cells fail to remove the B cells. By mid age, the Peyer’s Patches are affected by immortalized EBV infected B cells resulting in an IgA deficiency leading to a faster depletion of the immunoglobuline. And people are diagnosed with an Inflammatory Bowel Syndrome (IBS). The gut microbiome configuration is affected. The epigenetic regulation of cells in the genome, which co-evolved with the microbiome for 1.5 Billion years, gets distorted. Cells that had been quiet so far (methylation signal) now come to expression with an SNP failure to recognize the HERV/virus. This then becomes again a triangular drama of HERV-virus-genome. [see pg 6 of: https://www.geneuro.com/data/documents/ ... y-2017.pdf and also my earlier thesis on http://www.mshackathon.nl/wp-content/up ... ressed.pdf which is based on different sources that can be found in the pages above] This causes a new inflammation with processes as described in the paragraph above and a second peak in the graph of the age of onset at around age 42. This episode and the former episode are not "synchronised" pointing to the involvement of different PADs/SNPs.

The CNS/spinal trauma cause an inhibited tendon reflex and disregulated parasympatic nervous system. “Speculation that CCSVI and Related MS is Caused by prolonged, Undetected Vasospasm of the OJV and Azygos Vein", Faro Owiesy, M.D. https://isnvd.org/sites/default/files/S ... inal_1.pdf Dr. Owiesy of Los Angeles has suggested that a disregulated Autonomic Nervous System (ANS) triggers spasms in the smooth muscles of stenosed or damaged veins. The ensuing blood back jets injure the tissue which leads to inflammation of the myelin sheath and an immune system response. To note: a very extensive analysis of my own blood revealed only two things that were clearly out of range: high herpes immune complexes and high smooth muscle titres (the doctor said "I was eating my own muscles").
[Post script: I don't exclude the possibility that, at least in its inception, spasticity developed a natural compensatory mechanism for nervous/muscle weakness, after 100's of millions of years of evolution]
These trauma's and diverse stressors increases the level of nitric oxide (NO), in particular through iNOS. [on inducible NOs, see also Introduction of https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3472775/ ] As a reaction of cells to stressors, the balance ADMA/SDMA changes which stimulates iNOS (vicious cycle or positive feedback loop). A steady excessive amount of immortalized EBV infected B cells gives rise to an elevation of superoxide and with that its products with iNOS induced NO, the potent oxidant peroxynitrite. And as a consequence of oxidative damage inflammatory cytokines and intracellular calcium. Because the compounds involved in the biochemistry have limited diffusion distances in biological tissue, the fundamental mechanisms are initially local. However, over time the tissue distribution is propagated indefinitely by the vicious cycle mechanism. This underlies the progressive phase. Slowly, mitochondria throughout the body will fail causing a short of ATP production, failure to break the muscle bonds and with that muscle spasticity. The disability will see a slow progression. Where an already weak nerve conduction from the CNS/spinal to muscles and sensory system aggravates the symptoms and imposes a much convoluted picture.

For the inflammatory phase, therapeutic options may include anti viral medication, mabs (EBV B cell depletion), and chemo (surge of new clean T/B cells). The progressive phase is robust and inherently more difficult to down-regulate. Some of the therapeutic options mentioned may help to break the cycle (e.g. EBV B cell depletion would stop superoxide production). In his book Explaining Unexplained Illnesses, Martin Pall has summarized a variety of agents that may be expected to down-regulate NO/OHNOO cycle biochemistry. We have seen many of these agents come across here on this forum including CoQ10 and carnitines, minocycline as a PAD inhibitor, Magnesium, Zinc, Selenium, Flavonoids, Hyperbaric Oxygen therapy, etc etc. Besides, probiotics and blocking intra cellular calcification may help. Martin Pall argues that due to its complexity and robustness the cycle mechanism will not have a magic bullet to treat, rather that a combination of multiple compounds may collectively work well enough to lower its action.

Thomas Kuhn, in his famous book The Structure of Scientific Revolutions, observed that “Novelty emerges only with difficulty, against a background provided by expectation”. This will not be different here, this time round. Skepticism is healthy; knee-jerk rejection is not. It is my hope that one day this new paradigm - or perhaps I should say the three new paradigms in casu a new viral consciousness; microbiome and epigenetics; the NO/OHNOO cycle mechanism - will be picked up by the New York Times or any other proponents of our free press, to help open the debate.

If this viral theory is correct, why do immune-depleting therapies like Lemtrada and HSCT have such promising results? Normalised brain atrophy, the end of disability progression for those who take it early enough, etc?

jackblack400 wrote:If this viral theory is correct, why do immune-depleting therapies like Lemtrada and HSCT have such promising results? Normalised brain atrophy, the end of disability progression for those who take it early enough, etc?

Lemtrada is a mab (a monoclonal anti-body), depletes the EBV infected immortalised B cells. The superoxide production drops down and so does the oxidative stress. The underlying causal mechanism is explained above. The explanation of the working mechanism by the pharma is guesswork.
HSCT is preceded by chemo. The chemo does the real thing: it resets the immune system. It depletes old virally infected T/B/regulatory immune cells and causes a surge of new clean baby immune cells. The stem cell transplant just speeds system recovery.

Both therapies are also (planned) in a 'light' version. Ocrelizumab, which is essentially the same than Rituximab, depletes the B cells. Repeated administration (every 6 months or so) will keep the wrong B cells down and create a steady new source of cash. It is already deep between the ears of the average neurologist so the promotion has done its work.
Also there is a light variant of Cyclosphosphamide which is administered 4 to 8 times about one month apart which promises to stop progression.

Chemo's like cyclophosphamide which are very small particles better penetrate the spinal and CNS than mabs which are relatively large. In case of mabs, sometimes mabs are therefore administered intrathecal.

Alemtuzumab destroys T cells as well, which is important because B cells aren't the whole story. Ocrelizumab has already been proven to be far inferior to Alemtuzumab and (obviously) HSCT.

Cladribine is like Lemtrada but can cross the blood-brain barrier, it's actually pretty unfortunate that it was pulled from the market for MS. It's something that's going to have to be explored further.

From what I've read, the idea that EBV causes MS has a lot of traction with a lot of those studying MS (it's a favourite theory on Barts MS blog, for example). The best case scenario is that EBV causes immune cells to attack something in the CNS resulting in demyelineation, if this happens enough over time it triggers some sort of neurodegenerative process, which is why immunomodulators don't work particularly well on people who have had inflammation for a long time. So to 'cure' MS you fix the immune system as fast as possible before enough damage has been done to sustain significant neurodegeneration going forward. The worst case scenario is that MS is a neurodegenerative disease and inflammation is merely a symptom of this neurodegeneration. Maybe some kind of neurodegenerative process is started in the brain causing the immune system to attack the byproducts, causing more damage. Limiting the inflammation would therefore help a bit, maybe stop relapses but underlying neurodegeneration would continue and this is still possible. We know first gen immunomodulators don't really do anything to progression.

However you mentioned many other things in your original post, are you still sticking with all of that?

jackblack400 wrote:Alemtuzumab destroys T cells as well, which is important because B cells aren't the whole story. Ocrelizumab has already been proven to be far inferior to Alemtuzumab and (obviously) HSCT.

True, the matter is more complicated than just B cells, T cells and regulatory immune cells are also involved. T cells are infected by herpes Zoster, B cells by EBV... Immunologists know very well: Zoster is an inflammatory virus, EBV is an onco virus [with high EBV B cells against onco]

jackblack400 wrote:Cladribine is like Lemtrada but can cross the blood-brain barrier, it's actually pretty unfortunate that it was pulled from the market for MS. It's something that's going to have to be explored further.

Apparently, Rituximab will be pulled from the market, for MS. I guess its to create a market for Ocrelizumab. Dark forces everywhere..

jackblack400 wrote:From what I've read, the idea that EBV causes MS has a lot of traction with a lot of those studying MS (it's a favourite theory on Barts MS blog, for example). The best case scenario is that EBV causes immune cells to attack something in the CNS resulting in demyelineation, if this happens enough over time it triggers some sort of neurodegenerative process, which is why immunomodulators don't work particularly well on people who have had inflammation for a long time.

I think the demyelination is related to the inflammation, herpes virinae in particular Zoster and PAD arginine citrullination. But also the T cells get affected so they don't clean up the EBV infect immortalised B cells anymore. I know there is a lot of controversy about Swank but if he has shown one thing, it is that with a sustained low saturated fat diet the inflammatory attacks drop down significantly and - and this is most important - the progression does not develop. I think it is because T cells work properly including to remove the faulty EBV B cells.

jackblack400 wrote: So to 'cure' MS you fix the immune system as fast as possible before enough damage has been done to sustain significant neurodegeneration going forward. The worst case scenario is that MS is a neurodegenerative disease and inflammation is merely a symptom of this neurodegeneration. Maybe some kind of neurodegenerative process is started in the brain causing the immune system to attack the byproducts, causing more damage. Limiting the inflammation would therefore help a bit, maybe stop relapses but underlying neurodegeneration would continue and this is still possible. We know first gen immunomodulators don't really do anything to progression.

However you mentioned many other things in your original post, are you still sticking with all of that?

I am not convinced that the neuro degeneration in the progressive phase is concentrated in the brain or that it is uniquely related to the inflammation. The herpes strains may work together though making things 'convoluted'.

Leonard wrote:Apparently, Rituximab will be pulled from the market, for MS. I guess its to create a market for Ocrelizumab. Dark forces everywhere.

Yeah, Rituximab is an old off-patent drug so they can't make money from it. Ocrelizumab is the same drug modified very slightly so it can be re-patented. Cladribine is also an old off-patent drug, the formulation they're currently seeking approval for is an oral pro-drug formulation that money can be made from. It was originally withdrawn after the FDA refused it based on bunk reasoning. Now it's back, and the EMA will accept it in a few months, with the rest of the world to follow. It doesn't seem to be as efficacious as Alemtuzumab though, it just doesn't annihilate enough immune cells, even if it does get into the CNS unlike Alemtuzumab.

I think the demyelination is related to the inflammation, herpes virinae in particular Zoster and PAD arginine citrullination. But also the T cells get affected so they don't clean up the EBV infect immortalised B cells anymore. I know there is a lot of controversy about Swank but if he has shown one thing, it is that with a sustained low saturated fat diet the inflammatory attacks drop down significantly and - and this is most important - the progression does not develop. I think it is because T cells work properly including to remove the faulty EBV B cells.

I agree it probably is.

I am not convinced that the neuro degeneration in the progressive phase is concentrated in the brain or that it is uniquely related to the inflammation. The herpes strains may work together though making things 'çonvolved'.

I buy the current theory that remyelination can't occur properly after repeated, sustained inflammation. The cells that do it are broken. This explains SPMS for the most part. They say the reason PPMS occurs mainly in older individuals is that their natural remyelination facilites aren't working. This explains most things but there are things left unexplained too. Why are PPMS and SPMS characterised by less inflammation, for example? And if PPMs really is simply inflammation without a working repair mechanism, that would mean stopping the inflammation early (like with HSCT) would end progression. That remains to be tested.

I think we need to step up research on neuroprotection at this point. We know from endless experiments that hormones like testosterone and estradiol are the strongest neuroprotectives out there and have a big role to play in neuronal survival as well as remyelination (an example: http://www.pnas.org/content/113/51/14829.abstract). They've made a form of estradiol that retains the remyelinating effects but doesn't have the eostrogenic effects which could be given to people today but is probably 20 + years away. The problem is that MS is not cancer; people aren't in imminent risk of death from it, so there is no sense of urgency from the research and government community.

jackblack400 wrote: I think we need to step up research on neuroprotection at this point. We know from endless experiments that hormones like testosterone and estradiol are the strongest neuroprotectives out there and have a big role to play in neuronal survival as well as remyelination (an example: http://www.pnas.org/content/113/51/14829.abstract). They've made a form of estradiol that retains the remyelinating effects but doesn't have the eostrogenic effects which could be given to people today but is probably 20 + years away. The problem is that MS is not cancer; people aren't in imminent risk of death from it, so there is no sense of urgency from the research and government community.

This hormonal path would bring us back in the old world of endocrinologists and neuroligists. It won’t solve anything, just delay things. What we need is a real paradigm change: a new viral consciousness (see e.g. link below); a new understanding of the microbiome - genome relationship; a new understanding of microcellular biochemistry under oxidative stress conditions.

Hormones are an influence, at best. And low testosterone may be found in PwMS because the body tries to regulate and thereby depletes testosterone. Administration may help a bit but it will be marginally. This matter needs a real change of thinking, decoupling all of us from old world thinking. This will be a challenge, not only for us as patients, but for the whole medical world.

https://www.geneuro.com/data/documents/ ... y-2017.pdf

Leonard wrote: This hormonal path would bring us back in the old world of endocrinologists and neuroligists. It won’t solve anything, just delay things. What we need is a real paradigm change: a new viral consciousness (see e.g. link below); a new understanding of the microbiome - genome relationship; a new understanding of microcellular biochemistry under oxidative stress conditions.

Hormones are an influence, at best. And low testosterone may be found in PwMS because the body tries to regulate and thereby depletes testosterone. Administration may help a bit but it will be marginally. This matter needs a real change of thinking, decoupling all of us from old world thinking. This will be a challenge, not only for us as patients, but for the whole medical world.

https://www.geneuro.com/data/documents/ ... y-2017.pdf

There are two aspects to MS: inflammation and neurodegeneration. As you and others have elucidated, the inflammation might be caused by EBV infected B cells attacking various parts of the CNS. So you need to switch that off with a therapy like Alemtuzumab or HSCT, something that depletes B and maybe T and plasma cells too. But neurodegeneration persist through a number of mechanism.

It's not about hormones, necessarily, but high doses of certain hormones can have extremely strong neuroprotective effects, even if the underlying neurodegeneration is not caused by lack of those hormones. The exact mechanisms are unknown, but is partly due to strong anti oxidant activity as well as upregulation of pathways involved in neurogenesis and neuronal survival. Testosterone therapy (to levels far above natural) eliminated brain atrophy in a small clinical trial.

We can also use endothelin modulators to fix the vascular component of MS. There is a particularly strong compound I am thinking of here. We need trials of things like nerve growth factor brain implants too.

I'm reading that document you linked, it's very interesting. But I think there are hugely positive things we can do with existing compounds that upregulate key factors involved in vascular and neural growth and survival, and key to that is hormones like estradiol and testosterone, and even things like IGF-1, HGH, etc.

How long until we can get access to GNbAC1?

Edit: I've also been thinking about intravenous ATP supplementation. This has been proven to relieve fatigue in cancer patients. If ATP production failure is part of MS why can't that be solved by intravenous ATP supplementation?

Seen this? http://files.shareholder.com/downloads/ ... e_2017.pdf