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Ron Davis Update

Janet Dafoe

Board Member
Messages
867
If he's right I wonder if taking acetyl coA would give us a bit more energy. He mentions it can be bought as a supplement...I don't feel I know enough yet to try it.
Would a viral, bacterial or fungal reservoir potentially keep the shunt on? Surely in those cells only though. Could there be a cell-danger response like reaction of cells elsewhere that initiate the shunt to protect themselves? I look forward to next week's video to learn more.
You’d have to get it from the gut into the bloodstream and from the bloodstream into the cells and from the cells into the mitochondria and it’s not clear that eating it would accomplish that.
 

bthompsonjr1993

Senior Member
Messages
176
@Janet Dafoe I wonder if low GABA functioning would explain why the GABA agonist Benzos are so seemingly effective in ME

I thought the same thing, so I googled Ativan and learned this:

"Ativan belongs to a family of medications known as benzodiazepines. It binds to the GABA receptors found on nerve cells, enhancing GABA release in the brain. By increasing levels of GABA, Ativan helps relieve anxiety. Ativan is considered an intermediate-acting benzodiazepine."

I have the same experience with Ativan that Whitney has. It is the only medication I have ever taken that seems to easy my CFS symptoms. I don't take it often, for the same reasons that Whitney doesn't. But when I am forced to engage in or do something that I know has a high likelihood of causing a crash, I take Ativan and it helps me every single time.
 
Messages
246
if ammonia is high, the function medicine doctors know of a way to decrease it, namely with L-arginine alpha-ketoglutarate, no idea if it cross the BBB but it helped me to not pee anymore at night, i took 5-10 grams a day for a few weeks and the effect lasted for months. Also since NO is produced in the urea cycle, I got better erections and isn't that what's most important, haha.
 
Is the metabolic trap dead in the water or is this a drilling down into further aspect s of the trap
I don't think it's dead, they just have not been able to detect it in ME/CFS patients yet. To be fair though, they only look at blood at Stanford, and it might be present somewhere that blood doesn't touch, like the CSF. Can you imagine finding volunteers to sample that though?
 

Violeta

Senior Member
Messages
2,895
If he's right I wonder if taking acetyl coA would give us a bit more energy. He mentions it can be bought as a supplement...I don't feel I know enough yet to try it.
Would a viral, bacterial or fungal reservoir potentially keep the shunt on? Surely in those cells only though. Could there be a cell-danger response like reaction of cells elsewhere that initiate the shunt to protect themselves? I look forward to next week's video to learn more.

You could go ahead and try B5, pantothenic acid. It has been very helpful for people with lupus. I looked up lupus to see if the itaconate shunt was involved, but I'm not well enough versed on this topic to decide if it is or not.

I can get the link to the study if anyone is interested.

B5 is also helpful in raising acetylcholine levels.

You might be able to affect acetyl-coA levels just by raising the gradient of CoA. I have found pantothenic acid very helpful.
 
Messages
72
There is a molecule called 4'-phosphopantetheine that provide an accelerated precursor to CoA bypassing several regulatory steps and can even correct in-born errors of metabolism in CoA synthesis pathway. If administered intravenously it should bypass low gut absorption and dozens of milligrams will suffice for an experiment as the daily turnover of CoA is in that amount.
See nature news article https://www.nature.com/articles/nrm.2016.110 you can use sci-hub for free access, simply copy and past the doi link in the search box.
 
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Messages
72
Other than 4'-phosphopantetheine there are several molecules, some of them are on the market, and I'm pretty certain that if Rob Phair research pan out it would be easy for stakeholders to convince a pharmaceutical company to donate drugs for trials. Many of these inhibit innate immune system activation such interferon alpha receptor antibodies (available), interleukin 1 antagonists (available), JAK1 inhibitors (available), TYK2 inhibitors (phase 3), IRAK4 inhibitors (phase 2).. and several others in preclinical development.. rising tide lift all boats is my hope..
 

gregh286

Senior Member
Messages
976
Location
Londonderry, Northern Ireland.
if ammonia is high, the function medicine doctors know of a way to decrease it, namely with L-arginine alpha-ketoglutarate, no idea if it cross the BBB but it helped me to not pee anymore at night, i took 5-10 grams a day for a few weeks and the effect lasted for months. Also since NO is produced in the urea cycle, I got better erections and isn't that what's most important, haha.

Hi
Good work..you still use regularly
I pee too much as well.
Direct correlation with how bad I feel.
Major symptom for us.
Must give it a whirl
 

Alvin2

The good news is patients don't die the bad news..
Messages
2,995
I like how they plan to use carbon tracers to test if the metabolites they are expecting are present in increased concentrations.

Also if the innate immune system is not handing off then that suggests it can be turned off without the patient potentially having an infection that then rages out of control killing the patient.

If there are genetic mutations contributing to ME/CFS i hope they are mapped and those who have had genetic testing can go back and check if they have those sequences.

I forget how Manganese factors into all this?

@Janet Dafoe I wonder if low GABA functioning would explain why the GABA agonist Benzos are so seemingly effective in ME
I tried Picamilon which can cross the blood brain barrier and is cleaved to GABA, didn't help my cognitive functioning.

There is a molecule called 4'-phosphopantetheine that provide an accelerated precursor to Acetyl-CoA bypassing several regulatory steps and can even correct in-born errors of metabolism in Acetyl-CoA synthesis pathway. If administered intravenously it should bypass low gut absorption and dozens of milligrams will suffice for an experiment as the daily turnover of Acetyl-CoA is in that amount.
See nature news article https://www.nature.com/articles/nrm.2016.110 you can use sci-hub for free access, simply copy and past the doi link in the search box.
This would be interesting to try.
Also i noticed that if Glutamate is used up then we should be able to take Glutamine to replace it which is a cheap supplement.
I have tried that but it had no effect.
Perhaps we need mega doses?

I took the 5g/day recommended on the package and still have the bottle of it, perhaps i will try 10g/day.
 

Oliver3

Senior Member
Messages
846
@Oliver3 Just the nature of benzos I think. They are notoriously unsustainable
I've always thought that the body's mechanism for habituation should be studied. Perhaps it's not just the benzos but the body's need for homeostasis. Imagine if we could figure out the reasons for habituation and correct it somehow, so that Everytime you take the drug it has the most impact it should
 

Janet Dafoe

Board Member
Messages
867
I don't think it's dead, they just have not been able to detect it in ME/CFS patients yet. To be fair though, they only look at blood at Stanford, and it might be present somewhere that blood doesn't touch, like the CSF. Can you imagine finding volunteers to sample that though?
Look above in this thread for our third video which is an update on the metabolic trap. It is definitely not dead.
 

bthompsonjr1993

Senior Member
Messages
176
@Janet Dafoe Regarding the second video in the metabolic trap series (the manganese grant video), I was intrigued by Ron saying that the hair tests for CFS patients were coming back showing low manganese and low copper, both of which are very rare in the general population.
So I went and bought a hair analysis test. I sent it to the lab, and my results came back today. All of my levels were normal, except for manganese and copper, which were both low. I can't explain how happy this made me. As CFS patients, I know we are all so sick of tests constantly coming back normal. To have Ron find these abnormalities, say that they could very well play a role in the pathology of the disease, and then to find that I have these deficiencies, was exhilarating. I am feeling so happy knowing that you guys are truly discovering what is going amiss in our bodies. Something that no doctor I have ever seen in person has even come close to being able to do. Thank you thank you THANK YOU!