This can easily be coincidence, if she had just waited she may have gotten better anyways. Unless we have a measurable mechanism or time machine to go back and try non GET for her we don't know if it really helped her, and chances are it did not, given the millions of examples to the contrary to one example of "success".
Dr. Ronald W. Davis Answers Patient Questions: Q and A follow-up to 2/21/17 Research Update
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AshleyHalcyoneH
Open Medicine Foundation
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They are in the process of trying all of them. It will take some time and they are not done yet!
AshleyHalcyoneH
Open Medicine Foundation
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I ***
*** you guys. If you do this you can have my firstborn child. Or, since I don't intend to have one, the fluffier of my cats. She is mean but gorgeous.(I know that getting your own firstborn child back is all the reward you need xxx)
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AshleyHalcyoneH
Open Medicine Foundation
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Not sure if anyone answered you, but yes we will. We will hopefully be coming out with another video in a few weeks.
Yeah TBH I *had* thought GET was a viable path to recovery for a small minority until the PACE trial did a sterling job of disproving that
This is the problem when you have no proven mechanism for a disease, theorizing based on incomplete and massaged data leads to bad conclusions, Garbage in, garbage outYeah TBH I *had* thought GET was a viable path to recovery for a small minority until the PACE trial did a sterling job of disproving that
If researchers were objective instead of biased we would have no PACE (and many other examples of bad science). Believing diseases are psychosomatic is commonplace, until Orexin was discovered they believed Narcolepsy was psychological. Dream analysis was a popular treatment despite its nonexistent cure rate. They refused to believe it would not work despite it not working until the real cause was proven. They may have found the real cause years earlier if they actually looked for it
Hope is one of nature's survival traits
YesA thought - aided and abetted by my glass of cider
thats why i have stopped trying to figure out the etiology of this condition (something i never thought i would do), once they figure it out they will either come up with a cure or we have a solid basis to work on one for the first time
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I had a thought a few days ago but I must have forgot, I guess that tends to happen ...
when you filter out whatever the problem is then put the cells back in, run the test etc,
wouldn't the time it takes for the suppressing effect to wear off give some indication of what sort of particle it is ?
for example if u were to somehow remove all the sugar the effect would be quite noticable very quickly but if it was an antibody wouldn't it take longer because the cell has to repair previous antibody damage ?
when you filter out whatever the problem is then put the cells back in, run the test etc,
wouldn't the time it takes for the suppressing effect to wear off give some indication of what sort of particle it is ?
for example if u were to somehow remove all the sugar the effect would be quite noticable very quickly but if it was an antibody wouldn't it take longer because the cell has to repair previous antibody damage ?
If their son is still sick, I would hope their priority would be helping him get well, over following a pet theory/hypothesis.
Something i keep forgetting to ask, it seems when a new video or OMF announcement is made a new thread gets created for it, which is good, keeps threads from becoming ginormous, but can someone post in the old thread about the new one, so they are not overlooked?
I happened upon this thread by chance which is why i got the idea.
I happened upon this thread by chance which is why i got the idea.
Comet
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AndyPR
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Sorry, didn't make myself clear enough there. I was intending to highlight the difference between a $30 million donation to the Arts and Sciences and the $3.35 million funding for the foundation, and querying why, when their son's health was at stake, they couldn't find $30 million for research, whether it be for CII or OMF.
Janet Dafoe
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I think that @Ben Howell already did that. Right, Ben?
Chezboo
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I thought the same thing when reading this. It's very hard not to wonder why they gave 30 million to Arts and Sciences rather than to any ME/CFS research when the situation for many is so desperate yet totally neglected.
Murph
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Just thinking about the impedance test and the filter, and the coming drug assays.
We know extra pyruvate in the serum can make the impedance go away. There's a clue there, although as Ron says it is too early to interpret it.
Is there anything that's been added to the mix that has shown impedance to rise? Ron used the word dimensionality to describe the amount we can learn from this simple test and I can't wait for him to explore the "dimensionality" more by testing many many drugs on these cells!
For example, here's one that looks interesting. The anti-fungal drug itraconazole, (which one forum member has tried and felt 'amazing' on for a while) looks like it can inhibit mTor. Woudl that cause impedance to rise?
It seems that even though it is mainly an antifungal, it also has profound effects on mTor. This abstract is intriguing to me:
Itraconazole, a clinically used antifungal drug, was found to possess potent antiangiogenic and anticancer activity that is unique among the azole antifungals. Previous mechanistic studies have shown that itraconazole inhibits the mechanistic target of rapamycin (mTOR) signaling pathway, which is known to be a critical regulator of endothelial cell function and angiogenesis. However, the molecular target of itraconazole that mediates this activity has remained unknown.
Here we identify the major target of itraconazole in endothelial cells as the mitochondrial protein voltage-dependent anion channel 1 (VDAC1), which regulates mitochondrial metabolism by controlling the passage of ions and small metabolites through the outer mitochondrial membrane. VDAC1 knockdown profoundly inhibits mTOR activity and cell proliferation in human umbilical vein cells (HUVEC), uncovering a previously unknown connection between VDAC1 and mTOR. Inhibition of VDAC1 by itraconazole disrupts mitochondrial metabolism, leading to an increase in the cellular AMP:ATP ratio and activation of the AMP-activated protein kinase (AMPK), an upstream regulator of mTOR.
VDAC1-knockout cells are resistant to AMPK activation and mTOR inhibition by itraconazole, demonstrating that VDAC1 is the mediator of this activity. In addition, another known VDAC-targeting compound, erastin, also activates AMPK and inhibits mTOR and proliferation in HUVEC. VDAC1 thus represents a novel upstream regulator of mTOR signaling in endothelial cells and a promising target for the development of angiogenesis inhibitors.
We know extra pyruvate in the serum can make the impedance go away. There's a clue there, although as Ron says it is too early to interpret it.
Is there anything that's been added to the mix that has shown impedance to rise? Ron used the word dimensionality to describe the amount we can learn from this simple test and I can't wait for him to explore the "dimensionality" more by testing many many drugs on these cells!
For example, here's one that looks interesting. The anti-fungal drug itraconazole, (which one forum member has tried and felt 'amazing' on for a while) looks like it can inhibit mTor. Woudl that cause impedance to rise?
It seems that even though it is mainly an antifungal, it also has profound effects on mTor. This abstract is intriguing to me:
Itraconazole, a clinically used antifungal drug, was found to possess potent antiangiogenic and anticancer activity that is unique among the azole antifungals. Previous mechanistic studies have shown that itraconazole inhibits the mechanistic target of rapamycin (mTOR) signaling pathway, which is known to be a critical regulator of endothelial cell function and angiogenesis. However, the molecular target of itraconazole that mediates this activity has remained unknown.
Here we identify the major target of itraconazole in endothelial cells as the mitochondrial protein voltage-dependent anion channel 1 (VDAC1), which regulates mitochondrial metabolism by controlling the passage of ions and small metabolites through the outer mitochondrial membrane. VDAC1 knockdown profoundly inhibits mTOR activity and cell proliferation in human umbilical vein cells (HUVEC), uncovering a previously unknown connection between VDAC1 and mTOR. Inhibition of VDAC1 by itraconazole disrupts mitochondrial metabolism, leading to an increase in the cellular AMP:ATP ratio and activation of the AMP-activated protein kinase (AMPK), an upstream regulator of mTOR.
VDAC1-knockout cells are resistant to AMPK activation and mTOR inhibition by itraconazole, demonstrating that VDAC1 is the mediator of this activity. In addition, another known VDAC-targeting compound, erastin, also activates AMPK and inhibits mTOR and proliferation in HUVEC. VDAC1 thus represents a novel upstream regulator of mTOR signaling in endothelial cells and a promising target for the development of angiogenesis inhibitors.