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

FMMM1

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Yes, that's it. Thanks! Interesting... wondering if anyone is doing anything further with this? Ron Davis?
There's probably a write up about this on the web (Cort Johnson etc.). There's a copy of the paper at this web address; I'm not good on links, type it into Google if it doesn't come up:

https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-018-1600-x

Yea it looks interesting but I haven't hear if anyone with more knowledge (e.g. OMF) has reviewed it.

There's some stuff at this web address:
https://www.s4me.info/threads/the-e...ome-2018-chin-an-yang-et-al.5409/#post-124059

Possibly the interest relating to prostate cancer may move this research forward.
 

FMMM1

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I'm not sure you can conclude that. They may not cause it, but those receptors are linked to dysautonomia and muscle weakness. Have a read of this regarding Carmen Scheibenbogen immunotherapy research.
Link : Recent Autoimmune Therapy Study from Ramsay 2016 & 2017 Grantee Carmen Scheibenbogen
Again were on the same side here; I have skin in the game (I assume you do to). If there was a single case of an autoimmune form of ME/CFS then that would be worth finding e.g. since it would give you an insight into the disease mechanism.

I think one of the difficulties in presenting ME/CFS as a B-cell autoimmune (autoantibody) disease is that rituximab didn't work. I.e. if ME/CFS was a B-cell autoimmune (autoantibody) disease then rituximab would have worked. T-cell autoimmunity has been suggested (Mark Davis - 2017 OMF Symposium) i.e. as the reason for the observed T-cell clonal expansion. However, Unutmaz/Oh's recent MAIT cell paper suggests changes in microbiome and increase translocation of pathogenic gut bacteria. So the clonal expansion of T-cells, observed by Davis, may be a response to pathogenic gut bugs/leaky gut not autoimmunity.

In the extract you included it was stated that the assessment of "improvement" was a based on a self reported questionnaire. Fluge and Mella used an activity monitor (electronic device measuring steps etc. I assume). The quite rightly criticised PACE trial also used a self reported questionnaire. I'd prefer to have seen the activity monitor, as per Fluge and Mella, used to assess improvement.

In my view Carmen Scheibenbogen's group should be funded by the European Union i.e. as a specialist research/treatment centre for ME/CFS. Ron Davis said that some research would fail, some would succeed [or something similar]. I think generalised autoimmune [disease causing] antibodies in ME/CFS are fading but Carmen's group have just found something interesting i.e. very long chain non-coding RNA's.

The other thing that Ron said (Invest in ME Conference 2018) is that we need data. I suggest that we (i.e. those with skin in the game) lobby our politicians to get funding for ME/CFS research - data.
 

FMMM1

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I agree. My politicians (USA) are on board. We just need more of them to create critical mass. In the USA I think it is going to take Congressional directed funding as Nancy Klimas keeps mentioning in her videos.
Interesting i.e. regarding Congressional directed funding. The veterans are getting funding, for understandable reasons. If ME/CFS gets Congressional directed funding then there could be an opportunity/lessons to learn to put pressure on the European Union to fund ME/CFS. Currently the European Union hasn't shown much interest in ME/CFS.
 
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Im asking myself why so many ppl now abandon the autoimmunity. What happened to the experiment from Ron with CFS serum. He said he used a filter and the problem is in the serum. He said its something in a kDalton rage from an autoantibody. Only because Rituximab didnt work doesnt mean its not the immune system. How often it does nothing for Ms or other diseases.

Here is a video i posted before

He measured the serum with a bio essay. So it should be very close to what really happens in your body. To be fair, i took a lot of immun suppression and it did nothing for me. But i still believe in the molecular mimicry and the failure in the immune system.
 

FMMM1

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Im asking myself why so many ppl now abandon the autoimmunity. What happened to the experiment from Ron with CFS serum. He said he used a filter and the problem is in the serum. He said its something in a kDalton rage from an autoantibody. Only because Rituximab didnt work doesnt mean its not the immune system. How often it does nothing for Ms or other diseases.

Here is a video i posted before

He measured the serum with a bio essay. So it should be very close to what really happens in your body. To be fair, i took a lot of immun suppression and it did nothing for me. But i still believe in the molecular mimicry and the failure in the immune system.
I haven't watched the video.

Mark Davis presented data at the 2017 OMF Symposium showing clonal expansion of T-cells - T-cell activation. Similarly, Unutmaz/Oh appear to have found evidence of immune activation of MAIT cells (a type of T-cell in your gut mucosal layer etc. which responds to pathogenic bacteria in the gut - microbiome). So T-cell activation i.e. "immune" problems are firmly established in ME/CFS; B-cell autoimmune antibodies kind of disappeared i.e. once the rituximab trial failed.

I think MAIT cells are now being linked to MS; i.e. they congregate at the site of inflammation and secrete proinflammatory cytokines etc. (?). MS is not straight forward i.e. I don't think that there are specific autoantibody tests for MS; I think they e.g. rely on scans (MRI) and the expression of some proteins in cerebro spinal fluid to diagnose MS. I think there's commonly a problem identifying autoantibodies in diseases labelled as autoimmune @Jonathan Edwards . Maybe Robert Phair/Ron Davis's kynurinine work will help to understand autoimmunity.

Ron Davis says, in one of his videos, that the problem in identifying the signalling factor in blood plasma (causing the switch in metabolism) is that the body can use the same chemical for different purposes. E.g. ATP inside cells is used for cellular energy production and in plasma it's a signalling factor (Naviaux/autism etc.); so if you found something like ATP in plasma in ME/CFS what's it's function?


I've been trying to lobby the European Union for funding for ME/CFS research [https://forums.phoenixrising.me/ind...re-working-for-you.61516/page-2#post-1017469] feel free to join in.
 
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knackers323

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@FMMM1 do you know if these guys are conducting further investigations or what their next planned step is?
This sounds interesting

Unutmaz/Oh appear to have found evidence of immune activation of MAIT cells (a type of T-cell in your gut mucosal layer etc. which responds to pathogenic bacteria in the gut - microbiome)
 

FMMM1

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@FMMM1 do you know if these guys are conducting further investigations or what their next planned step is?
This sounds interesting

Unutmaz/Oh appear to have found evidence of immune activation of MAIT cells (a type of T-cell in your gut mucosal layer etc. which responds to pathogenic bacteria in the gut - microbiome)
If you Google "unutmaz mait me cfs" or something similar then you'll see some background e.g. the Jackson laboratories [where Unutmaz (and Oh?) works] published an article on the recent paper*. Cort Johnson did a article regarding Unutmaz's presentation in (2018) Montreal. Science 4 ME ++++.
*Here's a web address for the full paper - https://sci-hub.se/10.1038/s41385-018-0072-x I found it quite challenging to read/understand.

Unutmaz got one of the NIH Collaborative Centre awards. I'm not clear what this Unutmaz's group are currently doing but you might be able to check the reporting requirements for the NIH award and see when they are due to report on their work. Cort Johnson did an article(s) on the NIH Collaborative Centre awards/OMF missing out and he highlighted that the reporting requirements were quite demanding. I check out the OMF site fairly regularly, so I think I know about OMF research; but I don't feel I know what Unutmaz's group are doing - hopefully they are so focused on ME/CFS they haven't had the time to do public updates.
 

FMMM1

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@Learner1 Hi check our Ron Davis's presentation at Australian Conference. He presented data for heavy metals analysis in ME. Selenium is low in some people with ME; linked to low thyroid function?

Think OMF are working on developing methods for RNA virus's.
 

Learner1

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Thank you. I heard about it but will have to wait for the replay, which I'm looking forward to.

In addition to thyroid conversion, selenium is also used to make glutathione. ME/CFS patients typically have significant oxidative stress.
 

FMMM1

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Thank you. I heard about it but will have to wait for the replay, which I'm looking forward to.

In addition to thyroid conversion, selenium is also used to make glutathione. ME/CFS patients typically have significant oxidative stress.
Yes oxidative stress was highlighted in Maureen Hanson's recent (metabolic?) study. Also Dr. Shingu [Hanson's group] has demonstrated low glutathione in ME i.e. using MRI.
 

Learner1

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What effects do glycine, glutamine or N-A-C have on you?
They are the 3 aminos that make glutathione. My labs typically say I need a lot more glycine than the other 2. Even with plenty of B vitamins and the 3 aminos, I do not make enough glutathione to keep up with my oxidative stress and lipid peroxides and 8OHdG (which damages DNA) are high. I found taking glutathione before and after exertion reduces PEM and the lipid peroxides and 8OHdG.
 

junkcrap50

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Posting here, because there's no "Nanoneedle Thread." But with the latest news about exosomes, I'm thinking about the nanoneedle and am wondering, why can't they do a quick small study of trialing dialysis on ME/CFS patients blood to filter out the "something in the blood." From reading about dialysis, you can tune it so that it filters out anything of a particular size. It probably would only provide temporary relief if it did cure or reverse ME/CFS. But if it worked, just think what a fundraising tool and research highlight to show the NIH & other researchers.
 
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