Community symposium on molecular basis of ME/CFS at Stanford Discussion Thread

[junkcrap50]

Both the anti-purinergic drug Suramin, and more recently, the Multiple Sclerosis drug Copaxone, make the cells healthier when tested in the nanoneedle.

Reminder of @Cort 's article about Copaxone completely curing a woman with ME/CFS, who was thought to have had MS. Because she was "cured" of her MS, doctors said she couldn't have had MS and so insurance refused to pay for Copaxone, causing her ME/CFS to return.

His article:
"Rachel had ME/CFS but she’d been misdiagnosed with multiple sclerosis. That might sound like bad news but it wasn’t. She ended up responding so well to an MS drug that her doctors didn’t know what to think about it. They’d never seen anything like it."
https://www.healthrising.org/forums...ltiple-sclerosis-drug-what-does-it-mean.4028/

 

[Ben H]

What is in the serum that causes the cells to become unhealthy ? Is this connected with the metabolic trap ? Or is it some micro RNA in the serum which is causing the cells to go unhealthy.. So does that mean energy starvation can be due to either metabolic trap or something in the serum (micro RNA). Can any individual have both unhealthy serum and metabolic trap ? Very confusing.

To play devil's advocate, it could also be something(s) that are missing from the serum that are absent in ME/CFS patients but not in healthy controls.

The application of suramin may be 'normalising' (deliberate vague because the mechanism is unknown as of yet) the impedance signal because it is attenuating the deficit(s) of that which may be missing.



B

 

[SherDa]

Reminder of @Cort 's article about Copaxone completely curing a woman with ME/CFS, who was thought to have had MS. Because she was "cured" of her MS, doctors said she couldn't have had MS and so insurance refused to pay for Copaxone, causing her ME/CFS to return.

His article:
"Rachel had ME/CFS but she’d been misdiagnosed with multiple sclerosis. That might sound like bad news but it wasn’t. She ended up responding so well to an MS drug that her doctors didn’t know what to think about it. They’d never seen anything like it."
https://www.healthrising.org/forums...ltiple-sclerosis-drug-what-does-it-mean.4028/

And Copaxone is a mix of 4 amino acids, right? I don't understand how Copaxone works. How does it deliver these aminos differently than diet would? (Besides being injected instead of ingested)

 

[wigglethemouse]

From PR post Apr 1st

Rachel told me that Ron Davis is looking into the Copaxone link.

https://forums.phoenixrising.me/ind...hors-call-for-more-funding.58532/#post-967506

 

[Tally]

To play devil's advocate, it could also be something(s) that are missing from the serum that are absent in ME/CFS patients but not in healthy controls.

Didn't Dr. Davis say that when he filtered the ME/CFS serum the impedance became normal, equal to healthy controls? Which means whatever was filtered out has to be bigger than the “sieve” they used?

 

[ljimbo423]

Didn't Dr. Davis say that when he filtered the ME/CFS serum the impedance became normal, equal to healthy controls? Which means whatever was filtered out has to be bigger than the “sieve” they used?

Yes, I think Ron said most of the problems with the cells disappear after it's filtered. This is what Janet said about the size of the filter and what it might be filtering out.....

Big = larger than 10,000 molecular weight. Proteins, protein groups or antibodies (including autoantibodies). Amino acids are smaller, around 300 molecular weight.

Post #115
LINK

 

[wigglethemouse]

What @Ben H said still holds true. Maybe the "damaging" thing that is filtered out is neutralized by the something missing. So the cause could still be something missing.

 

[ljimbo423]

Reminder of @Cort 's article about Copaxone completely curing a woman with ME/CFS, who was thought to have had MS. Because she was "cured" of her MS, doctors said she couldn't have had MS and so insurance refused to pay for Copaxone, causing her ME/CFS to return.

His article:
"Rachel had ME/CFS but she’d been misdiagnosed with multiple sclerosis. That might sound like bad news but it wasn’t. She ended up responding so well to an MS drug that her doctors didn’t know what to think about it. They’d never seen anything like it."

This paper talks about how Copaxone (Glatiramer acetate-GA) works in Multiple Sclerosis...

GA treatment induces an in vivo change of the frequency, cytokine secretion pattern and the effector function of GA-specific CD4+ and CD8+ T cells, probably by affecting the properties of antigen-presenting cells such as monocytes and dendritic cells.

As demonstrated extensively in animal experiments, GA-specific, mostly, T helper 2 cells migrate to the brain and lead to in situ bystander suppression of the inflammatory process in the brain.

Furthermore, GA-specific cells in the brain express neurotrophic factors like the brain-derived neurotrophic factor (BDNF) in addition to anti-inflammatory T helper 2-like cytokines.

This sounds like it might further validate Jarrod Younger's hypothesis of brain inflammation causing symptoms.

LINK

 

[Tally]

Maybe the "damaging" thing that is filtered out is neutralized by the something missing.

This is too much for me to figure out through my brain fog

 

[Ben H]

What @Ben H said still holds true. Maybe the "damaging" thing that is filtered out is neutralized by the something missing. So the cause could still be something missing.

Yep. Exactly.

What @Tally has said is true, however that which is filtered out and seemingly relieving the impedance signal in me/cfs may be kept in check/normalised by factors which are present in healthy serum but not in me/cfs serum. Thus as @wigglethemouse says it does not exclude something missing. They are not mutually exclusive.

I'm not saying this is what is happening, at all, I do not know.


B

 

[Badpack]

Besides Carmen Scheibenbogen another researcher in Germany named Gerd Wallukat is working with g-coupled autoantibodies and identifies these AABs with a very sensitive Bioessay. First he found this AAB in Chagas especially Beta 1 adrenergic, m2 muscarinergic and in a group also Beta2.

Chagas is a Trypanosome triggered disease. Whats interresting about this is that Ron just said in his IIMEC speech that CFS looks like a trypanosome infection ( 30min+

). So i think the link here is the same production of g-coupled AABs.

Now the clue: Wallukat researched a group of dysautonomia patients ( a lot of them have cfs Symptoms ) with b2 and m2. Wallukat found this pattern in over 80% , Scheibenbogen in 40% with the unsensitive elisa test.
In chagas and in dysautonomia , maybe in CfS,this is the brigde to the immundysfunction and because of this all this illnesses seem to be similar!
Now its gonna be exciting: the link below explains why suramin blocks the g-coupled proteins and why this could be factor x in plasma and why it works in the nano needle try.

The g- coupled study with suramin
https://www.ncbi.nlm.nih.gov/m/pubmed/15626724/

The wallukat study in Chagas and the evidence of aabs

https://www.ncbi.nlm.nih.gov/m/pubmed/20117461/

 

[frozenborderline]

Naviaux discussed the IDO pathway a couple times in his paper on the Cell Danger Response (not his paper on CFS)

I think his work is good, but I also wonder about the inconsistencies between this and his recommendation in paper on CFS that possible interventions could be aimed at increasing B6. is it definite that lower B6 leads to increased kynurenine/tryptophan ratio?

Anyway, he has also said that the acute CDR is the opposite of CFS in some ways. iirc B6 is important for at least one other metabolic pathway, producing acetylcoa.

https://www.sciencedirect.com/science/article/pii/S1567724913002390

 

[wastwater]

Did the woman who responded to copaxone get a further diagnosis
I wondered about genetic leukodystrophy
It can sometimes be misdiagnosed as MS
Or ADEM/TM and EAE does copaxone work well for those

The mystery protein might be naturally present just not folded or cleaved properly

 

[GodGenghis]

Saint John's Wort big no-no

https://www.ncbi.nlm.nih.gov/pubmed/30033402

Whereas Ketamine which is sometimes touted as a treatment could potentially help?

https://www.ncbi.nlm.nih.gov/pubmed/30213652

Interesting about the St. John's Wort. I took a squirt of the tincture a few months back, and it slammed me for three days. I felt like my M.E had suddenly become much worse. And for the first day or so I was baffled. Then I remembered I had taken the SJW. The interesting variable here is that I am using a tricyclic antidepressant. In the past, before using this drug, I never noticed SJW hitting me like that.

I also used some low dose ketamine a year or so ago, and that, too, made me much worse.

 

[GodGenghis]

Regarding the recent Nanoneedle results from the drug Copaxone.

This was posted to the Facebook group "MECFS for the Slightly Irreverent" by Rachel Riggs, who is a patient, and the study coordinator / community liaison for Dr Robert Naviaux's lab.

"** Something really important happened this week at the Symposium, and I'd like to share it with all of you!! ‍

Last March, after writing quite a few other scientists (including Younger and Zaher Nahle of Solve ME/CFS) and Teva, the maker of Copaxone about my experience with the MS drug Copaxone, I talked to Dr. Naviuax about it, and he connected me with Ron Davis' team. I sent them this email:

On Mar 13, 2018, at 11:18 AM, rriggs wrote:

I was asked to be in touch with you to arrange a meeting and a blood draw. I was able to obtain two syringes of Copaxone for you, and I will be in Palo Alto next week!

I'm not sure how much you were told, so here are the details of my Copaxone experience:

I was initially misdiagnosed in January 2010 as having MS and was prescribed a daily injectable called Copaxone. I didn't give it much consideration when my energy levels improved, because it coincided with the sale of my business and I attributed this change to "retirement".

By improvement I mean I was spending two hours at the gym each day doing BodyPump and Zumba. It didn't touch symptoms such as heat intolerance, but it returned my energy levels to about 75+%.

Two years later, I had a post-injection reaction which I was told
occurs in about 5% of people who take Copaxone. Always in anticipation of that scary reaction, I eventually stopped taking it.

In late 2013, (still thinking I had MS) my symptoms became much more acute so I decided it would be prudent to resume the Copaxone in an effort to slow what seemed like rapidly progressing MS symptoms.

After approximately three weeks, I noted a lifestyle change. I was leaving the house and doing things with a new ease. My husband and I observed a pattern, in that I was now taking a new injection protocol which required only 3x weekly injections. We wanted to make sure we were not imagining this symptom improvement because in MS, this drug is not effective in treating symptoms -- its use is in slowing disease progression.

A few more weeks went by and we continued to marvel at its effects, until one day I had a post injection reaction which involved my throat tightening and large welts on my torso. My neurologist asked me to stop taking it and my allergist
confirmed via skin test that I was indeed allergic to the active ingredients. My symptoms came flooding back.

Fast forward to a diagnosis of CFS at The Mayo Clinic in late 2015, and a ton of research online to find a connection that made my experience with Copaxone make sense to me! I found this paper:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4335670/

This convinced me that it would be a really effective, relatively
innocuous treatment for the subset of patients who also respond to Rituxan, making Copaxone a Rituxan "light" in effect. At the very least, it could be used as a means of identifying a certain subset of patients and provide additional insight, to know that simply modifying B-cells in this way has such a profound effect on symptoms (I know very little about Rituxan, I say this simply because my understanding is that it too modifies B-cells).

Note: "This study describes what is, to our knowledge, the previously unknown effect of glatiramer acetate therapy on B cells in patients with relapsing-remitting multiple sclerosis (MS)."

Best,
Rachel Riggs

On Saturday, when I arrived to the Symposium, Dr. Naviaux pulled me aside immediately to tell me that when tested in the Nanoneedle Copaxone did indeed change ME/CFS blood to healthier blood. The only two drugs that have ever shown that result are Suramin, and Copaxone. I spoke to Ron Davis who also confirmed that. Later in the day, I ran into Rahim, the developer of the nanoneedle, who further confirmed that was the case."

If this post deserves its own thread, admin is welcome to move it

 

[junkcrap50]

Did the woman who responded to copaxone get a further diagnosis
I wondered about genetic leukodystrophy
It can sometimes be misdiagnosed as MS

The mystery protein might be naturally present just not folded or cleaved properly

I don't know, but in my link above in the Health Rising article, she shows up in the comments and answers questions. Also, she's in touch with Ron Davis as you see in pose #335.

 

[Badpack]

Again, i think this is the effect on g-coupled receptors aka ß2;m2 and so on. Thats why Copaxone also works with the nano needle.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3750109/

 

[wigglethemouse]

Again, i think this is the effect on g-coupled receptors aka ß2;m2 and so on. Thats why Copaxone also works with the nano needle.

In his 2017 presentation Neil McGregors genetic sub cluster analysis found anomalies in G-protein coupled receptor proteins to be very significant

Once we had identified these 38 genes, we then wanted to see if there was a relationship between them. To do this, we used factor analysis (which is a statistical process which is used to identify underlying clusters within data). We found that there were at least 7 major clusters within the data. The first cluster was an anomaly in G-protein coupled receptor protein. The 2nd and 3rd clusters also had the anomaly in the G-protein couple receptor protein, in combination with variations in a couple of additional genes. These other genes are probably amplifiers or modifiers of other genes, and we think they may be related to symptom expression.

LINK

 

[frozenborderline]

Interesting about the St. John's Wort. I took a squirt of the tincture a few months back, and it slammed me for three days. I felt like my M.E had suddenly become much worse. And for the first day or so I was baffled. Then I remembered I had taken the SJW. The interesting variable here is that I am using a tricyclic antidepressant. In the past, before using this drug, I never noticed SJW hitting me like that.

I also used some low dose ketamine a year or so ago, and that, too, made me much worse.

SJW is an MAOI on top of being serotonergic. using it with a serotonergic antidepressant, esp. since there are some theories about increased serotonin being responsible for CFS symptoms, could be intense

 

[frozenborderline]

Yep. Exactly.

What @Tally has said is true, however that which is filtered out and seemingly relieving the impedance signal in me/cfs may be kept in check/normalised by factors which are present in healthy serum but not in me/cfs serum. Thus as @wigglethemouse says it does not exclude something missing. They are not mutually exclusive.

I'm not saying this is what is happening, at all, I do not know. But talking to Ron a lot has taught me to think in different ways!


B

what is the process of figuring out what the "thing" in the blood that causes symptoms is like? Is it just trial and error with matching the general molecular weight to diff. things that could cause serum to make other cells behave like me/cfs cells? that sounds difficult! or are there any imaging things they can use to look at blood up close and identify the shape of a molecule