Prusty talks about his upcoming research on a podcast

[lyran]

Prusty did say that a drug that is already available is being trialed, and he also alluded on Twitter that a supplement won't do it, which rules out some possibilities.

That is really a shame as getting a prescription for a drug for CFS/ME or LC is very, very difficult. Even getting a prescription for LDN is nearly impossible, at least in here. And if this drug shows promise, we need years or even decades of larger studies with funding to prove it works and then of course Big Pharma will try to ban it if it's too effective. Sorry to sound so pessimistic but we have seen how things go in the past. Hopefully this time things are different.

 

[BrightCandle]

That is really a shame as getting a prescription for a drug for CFS/ME or LC is very, very difficult. Even getting a prescription for LDN is nearly impossible, at least in here. And if this drug shows promise, we need years or even decades of larger studies with funding to prove it works and then of course Big Pharma will try to ban it if it's too effective. Sorry to sound so pessimistic but we have seen how things go in the past. Hopefully this time things are different.

It might not actually be the case. In practice we might be able to find a pathway from a supplement that does impact on the protein. Maybe its not possibly directly but anything being depleted in the body by the fight with HHV6 in sufficient intake of a precursor to it the body may be able to climb it up. More slowly than drugs but I wouldn't rule out the possibility until we see the Protein and research all the pathways and then decide that the body doesn't have the capacity to impact it from intake and its going to require drugs.

 

[Vlad83]

PS I sort of love how Chat GPT has become a helper in this type of research, its a useful tool although it may be confidently lying to us!

Yes, these language models can "hallucinate" where they can't tell fact from fiction. There's apparently no way to control it in the current generation.

This is from GPT 3.5:

 

[Vlad83]

Hmm.. just been reading about how mitochondria work, and apparently it's normal for them to fragment under excess metabolic supply. So constant caloric excess can promote fragmentation, and conversely, fasting can promote fusion. In Prusty's theory, mitochondrial fragmentation is central to viral reactivation. Does it mean people who chronically overeat are susceptible to it, and all we need to do is restrict calories?

 

[Belbyr]

Hmm.. just been reading about how mitochondria work, and apparently it's normal for them to fragment under excess metabolic supply. So constant caloric excess can promote fragmentation, and conversely, fasting can promote fusion. In Prusty's theory, mitochondrial fragmentation is central to viral reactivation. Does it mean people who chronically overeat are susceptible to it, and all we need to do is restrict calories?

I highly doubt it. Fasting does seem to be a craze lately amongst the healthy and unhealthy.

 

[sb4]

Hmm.. just been reading about how mitochondria work, and apparently it's normal for them to fragment under excess metabolic supply. So constant caloric excess can promote fragmentation, and conversely, fasting can promote fusion. In Prusty's theory, mitochondrial fragmentation is central to viral reactivation. Does it mean people who chronically overeat are susceptible to it, and all we need to do is restrict calories?

I did a 30 day water fast with no noticable improvement in symptoms.

I do find it interesting though in the sense that the virus is causing cells to take in excess nutrients in order to feed it's own growth.

I would imagine other things also promote mitochondrial fragmentation.

 

[BrightCandle]

Based on Prustys 2020 paper one of the consequences of the fragmentation is the cells become very resistant to certain other viruses like Flu! Fragmentation appears to be part of the innate immune response of cells. So the fragmentation while promoting HHV6 and HHV7 it also reduces other infections.

I can see now how Covid19 might cause ME/CFS and yet ME/CFS is not maintained by an actual ongoing infection. The body responds to C19 with fragmentation and we loose energy as a result but it reduces the number of cells C19 takes over. This lasts for weeks maybe months and the entire time HHV6 is partially waking up in a bunch of cells and spreads more. HHV6 maintains the fragmentation since it allows it to continue and we stay low energy. The body then is missing the protein it needs to fission the mitochondria and we stay sick and its cell death that slowly changes the situation. Any infection could cause the problem and anything that makes the fusion worse can worsen the condition.

 

[Belbyr]

Based on Prustys 2020 paper one of the consequences of the fragmentation is the cells become very resistant to certain other viruses like Flu! Fragmentation appears to be part of the innate immune response of cells. So the fragmentation while promoting HHV6 and HHV7 it also reduces other infections.

I can see now how Covid19 might cause ME/CFS and yet ME/CFS is not maintained by an actual ongoing infection. The body responds to C19 with fragmentation and we loose energy as a result but it reduces the number of cells C19 takes over. This lasts for weeks maybe months and the entire time HHV6 is partially waking up in a bunch of cells and spreads more. HHV6 maintains the fragmentation since it allows it to continue and we stay low energy. The body then is missing the protein it needs to fission the mitochondria and we stay sick and its cell death that slowly changes the situation. Any infection could cause the problem and anything that makes the fusion worse can worsen the condition.

You might be right

 

[Sizzle]

Some more possibilities:

List any drugs that affect molecular pathways related to mitochondrial fission, fusion or quality control.

Mitochondrial dynamics and quality control are essential processes for maintaining cellular homeostasis and proper mitochondrial function. Several drugs and compounds have been identified that modulate these processes by targeting the molecular pathways involved in mitochondrial fission, fusion, or quality control. Some of these drugs include:

1. Mdivi-1 (Mitochondrial Division Inhibitor-1): Mdivi-1 is a selective inhibitor of the mitochondrial fission protein, Drp1 (dynamin-related protein 1). By inhibiting Drp1, Mdivi-1 reduces mitochondrial fission and promotes mitochondrial elongation.
2. Leflunomide: This immunomodulatory drug is known to inhibit mitochondrial fusion by targeting the Mfn1 (mitofusin 1) and Mfn2 (mitofusin 2) proteins.
3. Metformin: Metformin, a widely prescribed antidiabetic drug, has been shown to affect mitochondrial dynamics by promoting fusion and inhibiting fission, potentially through the activation of AMP-activated protein kinase (AMPK) pathway.
4. P110: P110 is a peptide that promotes mitochondrial fusion by targeting the OPA1 (optic atrophy 1) protein, which is involved in the regulation of mitochondrial inner membrane fusion.
5. SS-31 (Elamipretide): A mitochondria-targeting peptide that has been shown to improve mitochondrial function and reduce oxidative stress, it is thought to act by stabilizing cardiolipin, an essential phospholipid in the inner mitochondrial membrane.
6. Spermidine: Spermidine is a natural polyamine that has been shown to induce mitophagy, the selective degradation of damaged mitochondria by autophagy, thereby promoting mitochondrial quality control.
7. Rapamycin: This immunosuppressive drug has been shown to induce mitophagy and promote mitochondrial quality control through the activation of the mTOR (mammalian target of rapamycin) pathway.
8. NAD+ precursors (e.g., Nicotinamide Riboside, Nicotinamide Mononucleotide): These compounds can boost cellular NAD+ levels, which in turn can promote mitochondrial quality control by enhancing the activity of sirtuins, a family of NAD+-dependent protein deacetylases that regulate various cellular processes, including mitochondrial biogenesis and dynamics.

We are looking for drugs that promote fusion and inhibit fission, so that points to:

1. Mdivi-1
2. Metformin
3. P110

Just leave this here, seems relevant, maybe not

 

[junkcrap50]

Just leave this here, seems relevant, maybe not

I saw those tweets. Who the heck is Gina Henderson? And who is Pete? I searched for a bit and couldn't find them.

 

[Dude]

I saw those tweets. Who the heck is Gina Henderson? And who is Pete? I searched for a bit and couldn't find them.

I thougt exactly the same

 

[keepontruckin]

I hope BC007 is not what they are talking about. I heard from someone I consider a reliable source that it will not work, will be a big money maker and at least not cause harm.

 

[Sizzle]

I saw those tweets. Who the heck is Gina Henderson? And who is Pete? I searched for a bit and couldn't find them.

Searched but haven't found anything that made sense

 

[Sizzle]

The Reddit post is a summary of the interview and Dr. Prusty's theory. I quoted it below to save people a click. Make sure to click expand to read the whole thing.

This sentence; Prusty believes that there is only one theory and one explanation. He does not believe in a replicating SARS-COV-2 virus, but thinks it could be a small possibility. His main argument against it is that LC should then be present more often in people with severe actue Covid. However, it is more common in people with a mild disease.

Is this somehow possible to trace back to vax injured LC ?

 

[Forummember9922]

Listening to this, he has two key ideas
1. the whole thing is caused by herpesvirus reactivation, rather than SARS persistence
2. the symptoms are caused by a "switch" which is the depletion of a key protein.

He says it's something we've never thought of. And it's a protein we can re-introduce, but it will be slow, not an overnight solution.

He didn't give much away, but he does say this:
"the bone marrow is the key because the source of the cells is the bone marrow"
idk, maybe this is about a protein deficiency in platelets, or b-cells, or monocytes?

I'm personally afraid that the treatment implication would be stem cells or bone marrow transplant as that's not something that a lot of people will get prescribed, or would be able to afford.

Here's another older video from Prusty, which again his ideas are brilliant, but 24 minutes in he talks about C1Q as being important.

Maybe the ideas are outdated so forgive me if I am going back in time. C1Q is shown to be higher in CFS patients so that would not be the missing protein. I bring it up for thought because methods used to address c1q issues can be stem cells or bone marrow transplants and he mentioned bone marrow is a key factor. Some discussion on c1q was had on phoenixrising already when these findings came out.

He also (in that video) talks about high levels of ECP (Eosinophil Catonic Protein) and credits that high ECP was noted in CFS in a much earlier study, I think referring to this one in 1996. https://pubmed.ncbi.nlm.nih.gov/8738520/

So since both of these are high I don't think either are the missing thing but it's just another interesting video to watch if you want to learn more about his ideas.

I'm not sure how strong I am as far as how long we would have to wait for a fix. I guess theres people here who have had it for decades so I hope I can at least find that positive attitude. You guys are strong.

 

[Osaca]

To quote Prusty from your video on C1Q "I believe C1Q Protein activity goes down in ME/CFS patients".

 

[BrightCandle]

This sentence; Prusty believes that there is only one theory and one explanation. He does not believe in a replicating SARS-COV-2 virus, but thinks it could be a small possibility. His main argument against it is that LC should then be present more often in people with severe actue Covid. However, it is more common in people with a mild disease.

Is this somehow possible to trace back to vax injured LC ?

The data shows more people with severe Covid have PASC than those from a mild disease. However there are a lot more people who have mild disease than end up hospitalised and so the ones with it from mild are vastly more numerous. Its also somewhat different too, a lot of PASC from severe could be from detectable organ damage so it may be they have a somewhat different condition.

Saying this it might not actually be the case that severe results in more sufferers as a percentage. The reason the data on this might be garbage is that the vast majority of (97.5%) Long Covid sufferers can't get a diagnosis, so they are not counted by the medical system. Whereas a much higher percentage of PASC from severe Covid are counted. So to some extent I don't believe the studies on PASC prevalence in Severe v Mild, I don't think it is what we are seeing out in the real world and most estimates of prevalence have had very wide ranges across countries. But that is what the official medical opinion is currently that severe disease leads to more post acute covid syndrome.

 

[BrightCandle]

ChatGPT on C1Q:

C1q is a protein that plays an important role in the complement system, which is a part of the immune system. It helps to clear foreign pathogens and damaged cells from the body. If you are looking to boost the levels of C1q protein in your body, there are a few things you can do:

1. Exercise regularly: Studies have shown that exercise can increase the levels of C1q in the body. Aim for at least 30 minutes of moderate to intense exercise most days of the week.
2. Eat a healthy diet: Eating a balanced diet rich in fruits, vegetables, and lean protein sources can also help to boost C1q levels.
3. Get enough sleep: Lack of sleep can lead to decreased levels of C1q in the body. Make sure to get 7-9 hours of sleep per night.
4. Reduce stress: Chronic stress can also decrease C1q levels. Try to find ways to manage stress, such as meditation, yoga, or deep breathing exercises.
5. Talk to your doctor: If you are concerned about your C1q levels, talk to your doctor. They may be able to recommend additional steps you can take or suggest other treatments.

So nothing actionable that it knows of for this protein! I didn't have much luck finding routes to boost this one.

 

[Forummember9922]

FWIW On that previous list of proteins responsible for fusion (or responsible for preventing fission) i asked gpt to make a list for each individual protein showing what might then improve mitochondria, and Resveratrol and melatonin came up the most. Obvi not the cfs cure but perhaps worth a stack consideration

 

[Osaca]

I saw an earlier mention of the protein pyruvate dehydrogenase (PDH) which ticks some of the boxes Prusty mentioned even though it doesn’t seem revolutionary, I doubt it's the right one and it isn't directly involved with fission/fusion. Here’s the boxess it ticks:

1. Prusty’s 2020 paper mentioned the down regulation of this protein.
2. It has often / previously appeared in the ME/CFS literature (https://pubmed.ncbi.nlm.nih.gov/28018972/). Pyruvate dehydrogenase deficiency causes many problems including lactic acidosis, progressive neurological and neuromuscular degeneration and if it’s induced by a genetic mutation (not a reactivated virus) death during childhood https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4003492/. As such it is something that has been found before, but maybe only he was able to connect the dots as he mentioned in his interview?
3. Furthermore, it’s stimulation reverses the induction of itaconate https://jlb.onlinelibrary.wiley.com/doi/full/10.1002/JLB.3MR0322-692RR.
4. Finally, it was also part of a treatment that was partially successful https://sci-hub.se/https://doi.org/10.1016/j.mehy.2018.08.014 even though this treatment is not really confirmed and could be b.s. It was Frank Comhaire’s treatment with sodium dichloroacetate (DCA) to increase pyruvate dehydrogenase (PDH) which allegedly works well for some, but not for others.