ME/CFS International Research Symposium, March 2019, Australia

Here are the glucose subset slides - 777 patients retroactively studied!
1. Glucose tolerance test n=22 split into three subsets Flat, Trunctated, Normal
[Screenshot removed]
2. Retroactive analysis of 777 patient data [Screenshot removed]

3. How these 3 subsets related to other medical test data. Flat response is an autoimmune group. [Screenshot removed]
Is there a way to resize images?


EDIT : Screenshots removed as Emerge do not want people to share
 
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Andy said:
People can click on the images to look at a larger version if they want, is this what you wanted?
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Thanks @Andy. I still see them large on the browser I am logged in and posted with, but other windows where I am not logged in they are small. Maybe I have the images cached........ Next time I'll try and post thumbnails
 
wigglethemouse said:
Thanks @Andy. I still see them large on the browser I am logged in and posted with, but other windows where I am not logged in they are small. Maybe I have the images cached........ Next time I'll try and post thumbnails
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I see the images as a reasonable size for my tablet screen size, so I think it's safe to assume that the forum software resizes them dynamically.
 
Forbin said:
The news that was unknown to me (at least) was that the T-cell clonal expansion that had been seen in 4 ME patients turned out to also be showing up in controls at more or less the same frequency. I think they compared 12 patients with 12 controls, or something close to that.
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Jonathan Edwards said:
That is worth knowing. It does not surprise me. The question now is whether or not there is justification for looking at this more, in the UK for instance.
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Let´s see what Mark Davis has to say at the NIH Conference next April
 
JaimeS said:
Wen Zhong said actually that there were fewer viruses in pwME. It wasn't a huge difference, but it was the case. Unfortunately after a long day like today I'm not sure whether or not you have DNA & RNA the right way around, sorry. :confused:
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Hi @JaimeS I thought the low selenium and link to low T3 (thyroid) was really interesting. Is there a definitive test for thyroid function? It's just that (low) thyroid function seems to be similar to ME; however, we don't seem to be able to definitively say that people have/have not got low thyroid function.
 
Jonathan Edwards said:
That is worth knowing. It does not surprise me. The question now is whether or not there is justification for looking at this more, in the UK for instance.
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I recall your prophetic words, i.e. dismissing T-cell clonal expansion as a worthwhile research area.
 
fossil said:
The link is to an organisation that is holding the MINDD International Forum. Someone mentioned it earlier in the thread because Naviaux is going to it, not the Emerge conference.
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Thank you for your reply. I should have found a better way to phrase my question.

Maybe there is a mitochondrial element to the other conference.
 
FMMM1 said:
Hi @JaimeS I thought the low selenium and link to low T3 (thyroid) was really interesting. Is there a definitive test for thyroid function? It's just that (low) thyroid function seems to be similar to ME; however, we don't seem to be able to definitively say that people have/have not got low thyroid function.
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It's possible to test for T3 but there are some issues -- here's an article I found on that from NIH. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5113291/
 
Dissappointed about the clonal expansion, but watching this McGregor talk is actually really interesting. Seems like he's clearly understanding about how to study this illness and finding sub-groups that the metabolomic results clearly seperate. The glucose sub-groups look really interesting as well, and I can't help wonder if there might be treatment possiblities in there.
 
FMMM1 said:
Hi @JaimeS I thought the low selenium and link to low T3 (thyroid) was really interesting. Is there a definitive test for thyroid function? It's just that (low) thyroid function seems to be similar to ME; however, we don't seem to be able to definitively say that people have/have not got low thyroid function.
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The second to last slide shows high PFOS levels in many patients. PFOS has been well studied and is known to affect the thyroid. e.g.
Thyroid disruption by perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA)
CONCLUSIONS:
An accumulation of PFOS and PFOA was documented in thyroid cells, and a cytotoxic effect was observed after exposure to extremely high concentrations of these compounds. In environmentally exposed communities and in the general population, the most consistent effect of exposure to PFOA, and to a less extent to PFOS, is the occurrence of hypothyroidism. Women and children appear to be more at risk of developing mild thyroid failure.
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.
 
FMMM1 said:
Hi @JaimeS I thought the low selenium and link to low T3 (thyroid) was really interesting. Is there a definitive test for thyroid function? It's just that (low) thyroid function seems to be similar to ME; however, we don't seem to be able to definitively say that people have/have not got low thyroid function.
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There was a paper ( late 2017 or early 2018) noting low T3 in pwme - essentially a downregulated system which kind of tied in to the hibernation state hypothesis
 
JaimeS said:
Wen Zhong said actually that there were fewer viruses in pwME. It wasn't a huge difference, but it was the case. Unfortunately after a long day like today I'm not sure whether or not you have DNA & RNA the right way around, sorry. :confused:
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DNA viruses have been tested from blood, RNA have not, at least according to last October's symposium. I don't know what exactly is delaying them from the testing for RNA viruses, but RNA viruses like enteroviruses have been linked to ME/CFS more than any other viruses, so I look forward to RNA viruses being tested. One potential problem is the fact that they are only looking for the viruses in the blood. According to Ron Davis, any virus that is actively replicating should be found in the blood, but there is some ambiguity on whether this really is the case for certain type of viral infections.
 
JES said:
I don't know what exactly is delaying them from the testing for RNA viruses, but RNA viruses like enteroviruses
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Ron Davis stated yesterday that testing for RNA virus is really really hard to do so they were looking at parasites next. He spent some time explaining how they are developing tests to combine many samples while at the same time looking for multiple matches in their DNA tests. This helps with scale and expense.

EDIT: If I remember rightly I think he also said that they were collaborating with someone to look for human endogenous retrovirus (HERV) in the genome data....... (I assume much like done in the EBNA2 paper last year)
 
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Did anybody see Robert Phair's talk yesterday - and if so can you give a summary?

I'm particularly interested in whether he said anything about the mass spectrometer issues that Ron Davis briefly referred to in his Christmas message. I got the impression from Dr Davis' video that the early testing - which appeared to corroborate the metabolic trap hypothesis - was now in question. Obviously I'd like to know more, if Dr Phair provided any details.
 
JES said:
According to Ron Davis, any virus that is actively replicating should be found in the blood, but there is some ambiguity on whether this really is the case for certain type of viral infections.
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For the record, this is not a generally accepted assumption in the field of virology. In fact, there are numerous examples of persistent viral infections that leave no trace of their existence in the blood.

Ron Davis’s claim is an extraordinary claim, and extraordinary claims require extraordinary proof.

I’m not privy to Ron’s thinking, but I believe his claim was influenced by some recent preliminary findings on the existence of viral extracellular DNA and/or extracellular vesicles being discovered in the blood.

wigglethemouse said:
Ron Davis stated yesterday that testing for RNA virus is really really hard to do
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This is correct. RNA, unlike DNA, is an inherently unstable molecule and an RNA molecule will degrade on its own within minutes or hours, depending upon the chemical milieu.

A colleague of mine spent many years working in a lab with the poliovirus, which is probably the most well-studied RNA virus.
This is the way he put it:
“Working with RNA is a nightmare. If you so much as sneeze, your experiment is ruined!”
 
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Stewart said:
Did anybody see Robert Phair's talk yesterday - and if so can you give a summary?

I'm particularly interested in whether he said anything about the mass spectrometer issues that Ron Davis briefly referred to in his Christmas message. I got the impression from Dr Davis' video that the early testing - which appeared to corroborate the metabolic trap hypothesis - was now in question. Obviously I'd like to know more, if Dr Phair provided any details.
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They have DNA data from 66 doctor qualified patients and ALL of them have at least one IDO2 potentially damaging mutation. Dr Phair said many patients sent him their WES/WGS genome data and 3 patients did not have one of the mutations but did have the Tyrosine pathway mutation that is the other potential trap that he has identified (no experimental work on that yet).

Regarding the Mass Spec they found the issue was poor signal to noise ratio i.e. sample levels were at the noise floor of the instrument. They now have access to one that is at minimum 30 times more sensitive where sample levels should be above the noise threshold to give good signal to noise ratio. No data given on this.

[This is all from memory as the morning session was not archived on the livestream site]
 
Last day focused on Treatments.These are the main highlights.

Dr. Jarred Younger appeared in a video and talked about future PET/MRI studies looking for a cause for brain inflammation and try to identify activated microglia.
Also he will decode data from large longitudinal studies looking at inflammation markers and other things - lots of good data to try and define subsets.
And in Gulf War Illness and Fibromyalgia has treatment studies using botanicals and others to reduce pain and improve energy by addressing inflammation - at least three seems to be looking hopeful.

He said to expect lots of papers in 2019 :)

And he is working on developing a new medication that will be better than low dose naltrexone to calm down microglia.

Dr. Davis talked about 3 drugs that move the "needle" and one metabolite very low in some severe patients.
1. Indoleproplonate is made in the gut. It seems severe patients may be low in the bacteria that produces this. Indoleproplonate is a neuro protective agent.
[Screenshot removed]

2. He has previously talked about Ativan correcting the nanoneedle signature (IIMEC13 June 2018). Since then they have seen the same reaction on the Seahorse ($120,000 instrument). They test with activated T-Cells which happen to express GABA receptors (possible mechanism of activation).
[Screenshot removed]

3. Lastly he announced two other drugs that correct the nanoneedle impedance signature when used with a patients blood. Copaxone and a new drug called SS31.
[Screenshot removed]

He summarised to say that they don't know why these drugs have the effect they do.

Of note is that Copaxone is an MS drug. Ron Davis has talked with MS experts and they agree that their MS patients match the diagnostic criteria for ME/CFS but insist their patients do not also have ME/CFS in addition to ME..................

EDIT : Screenshots removed as Emerge do not want people to share
 
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