An Update on ME/CFS Research with Ronald W. Davis, PhD
- Thread starter Ben H
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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/Statement/2017/2/21/gold-coast-researchers-make-chronic-fatigue-breakthrough
http://statements.qld.gov.au/Statem...researchers-make-chronic-fatigue-breakthrough
Thank you.
http://statements.qld.gov.au/Statement/2017/2/21/gold-coast-researchers-make-chronic-fatigue-breakthrough
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/
http://forums.phoenixrising.me/index.php?posts/815540/
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.
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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."
"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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And potentially e
and potentially explain why there may be slow onset as well as rapid?
and potentially explain why there may be slow onset as well as rapid?
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This is a good read if you haven't read it. It was posted in September.
http://www.openmedicinefoundation.o...d-cfs-statement-by-ron-davis-and-bob-naviaux/
http://www.openmedicinefoundation.o...d-cfs-statement-by-ron-davis-and-bob-naviaux/
I'm not really sure. I don't belong to any Facebook ME groups. You are free to distribute it to whomever and however you like 
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I guessed you were on something
. But this time I'm blaming Storm Doris for rocking my trip to the west country
Always on something . But this time I'm blaming Storm Doris for rocking my trip to the west country
. But this time I'm blaming Storm Doris for rocking my trip to the west country
Hope you manage to get where ever you need to get to safely.
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.)
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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Here now (just outside Taunton) most annoyingly missed my connection in London despite me doing quick walking which I never do.... too windy for the train to go fast.
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.
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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.
Lol, that's a whole different market you are thinking of there I reckon Trish Might be a way of financing the research though.
Might be a way of financing the research though. 
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.
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'.
Sorry. I had to.
B
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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'.
Sorry. I had to.
Sorry. I had to.