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An Update on ME/CFS Research with Ronald W. Davis, PhD

Messages
31
Location
Padova, Italy

slysaint

Senior Member
Messages
2,125
Hi to everyone ! Please, how these findings (ME/CFS is caused by something in the serum and not in cells) can meet latest study from Griffith University , where a defect in a receptor which doesn't permit calcium to enter cells has been put in connection with the ME/CFS symptomatology ?
http://statements.qld.gov.au/Statem...researchers-make-chronic-fatigue-breakthrough

Thank you.
you might find this thread useful
http://forums.phoenixrising.me/index.php?posts/815540/
 
Messages
38
Location
SE USA
It adds to the proof, but ME/CFS has already been demonstrably biological for decades. Certain groups have only been able it ignore it by bending reality.

Does it persuade the hard-line quacks and the bureaucrats? No, but each study makes it harder for them to continue to ignore the nature of ME/CFS.

When Prof Davis mentioned hypothesis testing, I couldn't help but think, sure we have a “hypothesis,” ME/CFS is a result of physiological/biological dysfunction and not psychogenic. OK NIH lets fund a study.
 

TrixieStix

Senior Member
Messages
539
Persistent immune response to the persistent pathogen could be causing continuous production and systemic circulation of things like TNF-alpha, IL-1, etc. that have the ability to modify PDH function (source) and thus cause hypometabolism in cells distant from the viral reservoir. These immune messengers are what would be present in the serum causing the dysfunction(s).
Ron Davis wrote the following in August when Bob Naviaux's metabolomics study results were released.

"Another important finding from this study is that the metabolomic response observed in ME/CFS is opposite to the pattern seen in acute infection and metabolic syndrome. This result supports the controversial idea that while infection is often the initiating event for ME/CFS, it does not contribute to the ongoing illness. What is important to note is that in the absence of evidence of an active infection, it is plausible that the long-term antimicrobial treatments often used for ME/CFS patients are doing more harm than good."

I'm under the impression that the infection-driven hypothesis as the cause of the disease seems to have been abandoned or at least considered much less likely given recent research findings,

Bob Naviaux stated in September...

"In most of the cases of ME/CFS that I have seen where IgG antibody titers have been measured before, during, and after antiviral therapy, the antibody titers remain high after treatment, even though the patient may report symptomatic improvement.
I believe the symptomatic improvement after antiviral treatment may have more to do with the metabolic effects of antivirals in ME/CFS than their action on viral replication."
 
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Barry53

Senior Member
Messages
2,391
Location
UK
Ron Davis wrote the following in August when Bob Naviaux's metabolomics study results were released.

"Another important finding from this study is that the metabolomic response observed in ME/CFS is opposite to the pattern seen in acute infection and metabolic syndrome. This result supports the controversial idea that while infection is often the initiating event for ME/CFS, it does not contribute to the ongoing illness. What is important to note is that in the absence of evidence of an active infection, it is plausible that the long-term antimicrobial treatments often used for ME/CFS patients are doing more harm than good."
Could this potentially affect how some people become more severely affected? My wife is towards the milder end of moderately affected I would say, and has no medication for her ME. She does take a small amount of D-Ribose.
 

arewenearlythereyet

Senior Member
Messages
1,478
And potentially e
Could this potentially affect how some people become more severely affected? My wife is towards the milder end of moderately affected I would say, and has no medication for her ME. She does take a small amount of D-Ribose.
and potentially explain why there may be slow onset as well as rapid?
 

TrixieStix

Senior Member
Messages
539
Messages
65
Location
UK
That would be great news if you could get some interest in corporate donations. But a word of caution. Because you are in the UK and are talking about corporate London you might want to be sure they don't get the idea of donating to local ME charities of dubious value. Not to say there are not charities in UK worth supporting (there are) They might hear about the great work being done elsewhere and think that it's all good and the same and want to contribute locally in a way that could be disaster. Or perhaps I'm misunderstanding (and being concerned unnecessarily) in the specificity with which you targeted them. Certainly possible.

Anyway, appreciation for you taking the time to try and wrangle money for ME research.
Good point. Thanks.
 

ash0787

Senior Member
Messages
308
Ron says: Pyruvate is not very soluble so it's difficult to get enough of it into your cells. I mentioned the pyruvate because it is inhibiting the increase in impedance that we see when we stress cells in the presence of ME/CFS serum.

Ron has figured out that whatever is in the serum that's triggering this is a big molecule, so it could be a protein, A protein complex, or an antibody (which includes auto antibodies)

This was the type of information I was hoping for in the videos, thankyou, extremely grateful for your ongoing efforts.
 

nandixon

Senior Member
Messages
1,092
I'm a little confused by what Ron was saying, if Pyuvate Dehydrogenase is the blockade, then how does adding pyruvate to culture bypass the need for PDH?

Why pyruvate? A block is sensitive to quantity. If there is enough quantity it might force it through the block. It might also send signals to the body to change enzymatic regulation of pyruvate metabolism.
What may be happening with the addition of pyruvate inhibiting the increase in impedance in Dr Davis' device when tested with ME/CFS serum, is that the pyruvate is freeing the pyruvate dehydrogenase (PDH) complex from excess inhibition (i.e., phosphorylation) by the pyruvate dehydrogenase kinases (PDKs). This is because pyruvate is a potent inhibitor of the PDKs.

If true, this would appear very consistent with the recent Fluge & Mella study, which indicated the PDH complex to be inhibited and which also found increased mRNA expression for most of the PDKs (PDK1, 2 & 4).

I wonder if Dr Davis has tried adding insulin to one of his test runs with ME/CFS serum? If the insulin also prevents the increase in impedance, that may narrow things down to indicate that the unknown substance in the blood is having an effect somewhere in this pathway:

Insulin--> PI3K/Akt/mTOR(mTORC1)--> PDH

(This is a simplified depiction of the pathway.)
 
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AndyPR

Senior Member
Messages
2,516
Location
Guiding the lifeboats to safer waters.
Just wanted to check my understanding (or not) of Ron's little testing chip device. Am I right in thinking that a current is passed through the test subject in order for the impedance to be measured? I think I'm right but there is the odd, very slim, almost negligible chance I might be wrong. :)
 

trishrhymes

Senior Member
Messages
2,158
Just wanted to check my understanding (or not) of Ron's little testing chip device. Am I right in thinking that a current is passed through the test subject in order for the impedance to be measured? I think I'm right but there is the odd, very slim, almost negligible chance I might be wrong. :)

A current of electricity through the chip and a current of excitement through the patient...
 

Ben H

OMF Volunteer Correspondent
Messages
1,131
Location
U.K.
Just wanted to check my understanding (or not) of Ron's little testing chip device. Am I right in thinking that a current is passed through the test subject in order for the impedance to be measured? I think I'm right but there is the odd, very slim, almost negligible chance I might be wrong. :)

The 'test subject' is the patients blood @AndyPR

Is that where the confusion lay? To confirm-there arn't patients chained up at the Genome Centre with current being dealt and impedance being measured while biochemists scream 'MORE, MORE I SAY, MUWAHAHAHAHAHA'. :D

Sorry. I had to.


B
 
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A.B.

Senior Member
Messages
3,780
Is that where the confusion lay? To confirm-there arn't patients chained up at the Genome Centre with currents being dealt and impedance being measured while biochemists scream 'MORE, MORE I SAY, MUWAHAHAHAHAHA'. :D

Sorry. I had to.

Careful, the PACE authors read this forum. You could give them ideas for their next treatment, now that CBT/GET are on their way out.