ME/CFS Research: Herpes Autoimmune Spectrum Disorder

[Rebecca under the papyrus]

I tried to comprehend what you wrote and shared with us @joshua.leisk
My question is, does anyone else has this symptom: since I started with the 4 cups green tea 3 days ago, I have this feeling as if I don't get enough air in my system, does anyone know this effect or can it to me? Does this has to do with the grean tea? It is quite unsettling, so I am not sure what to do now.

Perhaps it's simply because of the caffeine that increases cortisol and hence oxygen consumption?

 

[godlovesatrier]

Joshua by thoughts on the nausea and aches created by taking Glycine and Cysteine? Even in doses just under 500mg it's strong. I'm titrating up slowly currently on 400mg Cysteine and 300mg glycine. I did try more Glycine less Cysteine but the nausea was much worse.

I'm titrating up to 1500mg a day over a few months.

 

[Elike]

Perhaps it's simply because of the caffeine that increases cortisol and hence oxygen consumption?

Maybe, I don't know. And I just found this study: Epigallocatechin-3-gallate Increases Maximal Oxygen Uptake in Adult Humans , but I dont get why then in consequence I have the feeling that I dont get enough air...
I will stick to it, who knows maybe this is some change to the better in the long run ...

 

[Reading_Steiner]

Stayed up until about 5am reading all the new stuff, I'm gonna go out on a limb and say that this is the correct explanation for chronic fatigue syndrome, at least the form that I experience. I feel positive for the first time in a year maybe. Its hard to describe how I came to that conclusion but i've been trying to build a conceptual mechanistic relationship model from the various experiences I have had over the 5 years, somehow these old experiences and thoughts stick in my subconscious mind in a way that I can compare it to the chemical reactions describes in this paper. For a more recent example ... I've been on a bit of a downward trend recently and I can relate the sensations I've been getting to past times where it lead to me becoming extremely severe, specifically I have noticed a sporadic 'bristling' feeling in my nerves suggesting a 'balancing' issue creating aberrant noise in the absence of a viable trigger, Joshua seems to describe something that fits in his paper, which he calls " Glutamate-induced excitotoxicity " .

I've known for a little while that most cases of this illness likely work like this - there is a 'baseline', a mechanism at play that is different from normal operation of the body, if you push hard enough you can always run into this mechanism, but it might take hours of effort for someone thats doing pretty good. On top of that 'baseline' there are variabilities, multiple layers that come and go over time, one of them has something to do with the immune system and environmental chemicals. In some way this interacts with the 'baseline' and generates a new layer of problem, which can disappear or create additional layers. My guess as to what the 'baseline' is was limited to only knowing about the Metabolic Trap hypothesis, but now I have a new option,
the diverting away of CAC metabolites away from ATP creation into this process which generates these excessive nitrogen containing things. I have always felt that the body is essentially poisoning itself when it tries to generate energy, and at the same time I often hit some sort of chemical reaction limit, If I try to do a task when I don't really feel like it, I sometimes start to actually slow down my movements like one of those wind up toys, when I get to that point I have to rest a lot for days to start getting some energy capacity back. At other times this doesn't happen, I can exercise myself into a lot of trouble ! usually on those times a lot of body heat and insomnia is generated after, then I feel different in the body for weeks.

I'd say that this treatment plan is worth a try and we are very lucky that Joshua and his wife have done this work ! I have reservations still though, for example what if say 30% of our body is comprised of these infected cells, what happens if we 'delete' too much of ourselves ? would normal cells regenerate fast enough to fill in the gaps as it were ? this begs the question, what % of cells in say the liver need to be infected to cause the proposed pathogenesis ? can infected cells induce the negative effect in adjacent cells ?

 

[vision blue]

@Learner1 I admire your patience (I think ive noticed this before and commented on it) and thanks because your sanity saving posts here.

@joshua.leisk I've read all 3 papers, though when i read them carefully, i didn't have figures in front of me which perhaps may have changed my impressions.

If we consider just the mechanistic changes, not putative causes and not possible treatments, an important question is how many independent mechanisms are you suggesting are occurring simultaneously and are you the first to argue for these in CFS.

Starting with the first question then, In some places, you propose there are three: α-KGDH, PDH and beta-adrenergic cascade deficiencies but in other places you say it's actually less "Each of these α-KGDH, PDH and beta-adrenergic cascade deficiencies are able to cause both of the others" and in other places you suggest there are additional independent factors at play. So is it really one then? three? more than three? This is critical for a theory.

For the second part, Since it's already been argued in the literature for cfs and cancer that there is an increase in fermentation/ warburg effect/cytostolic glycolosis (sometimes called aerobic, somtimes anerobic) which lead to the alternations in lactate and pyruvate, the question then is how many of the other alterations you mention can follow from this one? (it's also not true by the way that the reason for this warberg effect has not been proposed but that's another issue). We know all these biochemcial changes affect one another- how far can we get in predicting all the metabolic changes by considering ramifications of just this one (already known) change?

many many other things can be asked and said, - will mention just two things that aren't clear because related to above issue. I don't recall seeing details of the: "beta andrenergic cascade deifiencies" that you refer to as part of the theory (maybe i missed it - its possible, but if i did, othes will as well.); that's important because andrenergic changes so often mentioned these days in cfs, dys etc - the devils in the details- what are the cascade deficiencies, and back to the issue i've raised, is it independent of the other mechanistic changes, and are you the first to argue for it Similar clarification for urea acid cycle . i see the claim m of defects alot across your three manuscripts but don't recall seeing details- do you mean it's "blocked" (decreased enzyme,) and if is it blocked, where, what enzyme, and does it follow from other metabolic change, are you the first.

This isn't anything you wont' get from reviewers so its worth your trouble to consider this.

 

[vision blue]

Joshua seems to describe something that fits in his paper, which he calls " Glutamate-induced excitotoxicity " .

I

That's not his. Glutimate as "excitotoxin" has been in the literature for decades.

 

[joshua.leisk]

Yes I wonder that too... I think it has to be the tea, it began two days ago, so one day after I started drinking the cups as described in his paper and simce then it's constant.
I will stick to it for another few days. I have experienced air hunger before but not this long. Last time when I tried wim hoffs breathing exercise,...after all the heavy breathing I needed even more air. So I ditched that try.

Hi! Anyone starting with the protocol would be advised to follow the directions in the 3.1 spec. In our disease model, the “air hunger” of hypoxia will go once the ROS comes down and someone can make succinate, fumarate normally. In the meantime, the B vitamins may assist in producing succinate via a backup pathway. If someone has succinate, a very small dose - eg. 25mg may also do wonders here.

3.2 spec should be released today - no major changes, just clarifying important aspects of the dietary advice which were insufficiently detailed in 3.1. This may also help people when reaching any “acute hepatic immune response” phase.

 

[joshua.leisk]

seems this is getting more interesting and I need to read it all again, have anyone started trying the proposed treatment plan ? also how does it differ from things people have tried before, is is more of a specific combination of things informed by precise knowledge of the effects ? Your work does seem to draw parallels with things that Dr Prusty has been talking about ( that guy seems to know more than he is letting on ).

simple question I suppose is, if we presume there to be some merit to all this, what did you do differently to the big labs / funded studies ? the likelihood of a 2 man casual research team making some sort of breakthrough rather than Stanford or similar seems unlikely does it not ?

Edit - Looked into this a bit, trying to see if anything lines up ...
" In human cerebral cortex, hGDH1 and hGDH2 are expressed in astrocytes, the cells responsible for removing and metabolizing transmitter glutamate, and for supplying neurons with glutamine and lactate. "
GDH thingy
In one of his cryptic tweets Dr Prusty seemed to be researching these Astrocyte things ( I never heard of it before ) Picture of the day: Astrocytes stained from a CFS brain.
A little look and you can find that someone was able to figure out that the picture shows A1 activated mode of this type of cell.

Hi! Yes, we have some people in remission right now and a number of people at various stages of recovery. It’s an interesting journey.

What I did differently..

Probably starting from scratch with a completely blank slate and no expectations.

I didn’t set out to study CFS - I just had a cluster of people I was coaching with different goals, common symptoms and markers. While digging through the problems, I realised along the way it was CFS... and as I kept digging, it got even more interesting.

Another key factor - I initially worked with a handful of people and talked to them for at least 5 hours each day, over many months. Being “retired”, I had the time to do this. There were no billable hours or pressures, just days of poking and teasing out aspects of the puzzle. I enjoy puzzles and helping people, so this was rewarding enough.

From these ongoing experiences - reactions to variables and discussions - it all became clearer and clearer.

I think also looking at this as a “biological engineering problem” rather than with a mindset honed by classical medical training also helped a lot - my skill-set has been developed around pattern recognition, pathways and problem solving.

My background was once electronics engineering and later, IT. My daily work expectations were having to dive into highly complex environments with typically unquantifiable numbers of “unknown” variables and being required to quickly zero-in on problems by using inferences from tangible behaviour / pressures / flows from related pathways / processes / functions. It was like building 3D jigsaw puzzles, by seeing the inputs/outputs, flows/pressures and feedback loops for every system and function.

This was often in a high-stress situation where a fault condition would cost >$1M/day and you ALWAYS had to locate the root cause - placing bandaids on a faulty pathway would invariably lead to unexpected behaviour and future problems. This would be completely unacceptable.

So, armed with that mindset, time/opportunity and tools from perhaps a decade or so of studying biological sciences out of sheer curiosity (I’m thoroughly in love with this topic), without simultaneously having being taught how I “should” look at things, I appear to have found myself in a fairly unique position.

It’s possible that solving this needs someone who has ample time, has lovingly studied metabolism, clinical / sports endocrinology and exercise sciences, with the mindset of an engineer, while also having (quite remarkably) fully recovered from CFS, thereby having a very personal understanding of it and desire to stamp it out.

I’m trying my best.

Prusty - PDH. There are multiple causes for this, but the main one is hypoxia / HIF. Just as we’ve seen in cancer studies, the remodelling under hypoxic conditions (which happens when a-KGDH is impaired) alters PDHK.

Disable the HIF-1a transcription factors being activated and that problem usually stops quite quickly, providing the “autoimmune antibodies” for eg. the beta-adrenergic receptor (which may/may not be present depending on the infection) have been already resolved. This is quite easy to do - there are many ways to achieve this, however the best way is to resolve the root cause.

Anaplerosis via succinate (succinate, GABA, B12, etc) or fumarate (urea cycle, aspartate) does it quickly, but does nothing to fix the underlying problem - in fact, it adds to the ROS and continues the vicious cycle.

This is the same underlying issue with nutrition / hormones in cancer treatments and was the key realisation in the third paper.

We “had the important pieces”, however were looking at the whole puzzle “through a mirror.”

The more patches you put in place, by fixing individual legs / cascades, usually accelerates the progress of the disease, without simultaneously doing something to modify the viral behaviour itself.

In a nutshell - everything you put in gets turned into viral proteins, ROS and further metabolite depletion via urine. You can/will “move the pressures around” and create new pathway impairments by healing another.

So much easier just to turn the whole thing off, instead.

 

[joshua.leisk]

@Learner1 I admire your patience (I think ive noticed this before and commented on it) and thanks because your sanity saving posts here.

@joshua.leisk I've read all 3 papers, though when i read them carefully, i didn't have figures in front of me which perhaps may have changed my impressions.

If we consider just the mechanistic changes, not putative causes and not possible treatments, an important question is how many independent mechanisms are you suggesting are occurring simultaneously and are you the first to argue for these in CFS.

Starting with the first question then, In some places, you propose there are three: α-KGDH, PDH and beta-adrenergic cascade deficiencies but in other places you say it's actually less "Each of these α-KGDH, PDH and beta-adrenergic cascade deficiencies are able to cause both of the others" and in other places you suggest there are additional independent factors at play. So is it really one then? three? more than three? This is critical for a theory.

For the second part, Since it's already been argued in the literature for cfs and cancer that there is an increase in fermentation/ warburg effect/cytostolic glycolosis (sometimes called aerobic, somtimes anerobic) which lead to the alternations in lactate and pyruvate, the question then is how many of the other alterations you mention can follow from this one? (it's also not true by the way that the reason for this warberg effect has not been proposed but that's another issue). We know all these biochemcial changes affect one another- how far can we get in predicting all the metabolic changes by considering ramifications of just this one (already known) change?

many many other things can be asked and said, - will mention just two things that aren't clear because related to above issue. I don't recall seeing details of the: "beta andrenergic cascade deifiencies" that you refer to as part of the theory (maybe i missed it - its possible, but if i did, othes will as well.); that's important because andrenergic changes so often mentioned these days in cfs, dys etc - the devils in the details- what are the cascade deficiencies, and back to the issue i've raised, is it independent of the other mechanistic changes, and are you the first to argue for it Similar clarification for urea acid cycle . i see the claim m of defects alot across your three manuscripts but don't recall seeing details- do you mean it's "blocked" (decreased enzyme,) and if is it blocked, where, what enzyme, and does it follow from other metabolic change, are you the first.

This isn't anything you wont' get from reviewers so its worth your trouble to consider this.

Thank you for writing all of this. I believe these are all answered in the 3rd paper, however the figures will definitely be needed, as it’s a ridiculously complicated disease model.

Paper 1 showed the 3 “hot-spots” at a-KGDH, PDH and beta-oxidation, along with various ways to trigger them.

Paper 2 showed a layer of metabolite depletions which creates a situation that perpetuates this.

Paper 3 showed the root cause and how to disable it. It also describes the urea cycle defects in much more detail.

I’ve elaborated on much of paper 3 here - https://forums.phoenixrising.me/thr...e-spectrum-disorder.83371/page-4#post-2335821

It’s possible that I’ll condense / refine all three articles into one paper for peer-review / publishing and take input from people like your good self to make sure my communication is clear. I’m also open to further collaborating with additional authors, if this leads to more efficient and robust communication.

Almost everything stems from the “Warburg effect” or “reverse-Warburg effect”, which appears to have more than one state, depending on the ROS being generated and availability of eg. Aspartate, P5P, B12, GABA, Acetyl-CoA.

These effects are a normal cellular response / adaptation to enhance survival when certain conditions are true. This is also very, very useful for enhanced protein synthesis under normal circumstances, when the cells aren’t viral / cancerous. There are a number of layers to this.

In my mind, the main difference between a HHV-infected cell and a cancerous HHV-infected cell is impaired cell-cell communication. Cancerous cells can “speak”, but they can’t “hear” when a neighbouring cell says “hey, stop bumping into me!”

Beta-adrenergic cascade is mostly Acetyl-CoA deficiency (and cascade) in this context. It’s also tissue-specific, causing the dysautonomia and some aspects of the orthostatic intolerance. (When succinate is low, via a-KGDH low / ROS high + aspartate low, GABA low, B5, B12 low, etc), this can also contribute via lack of agonism at the succinate receptor, in the kidneys, messing up RAAS -https://jasn.asnjournals.org/content/jnephrol/22/8/1416.full.pdf.)

 

[joshua.leisk]

I'd say that this treatment plan is worth a try and we are very lucky that Joshua and his wife have done this work ! I have reservations still though, for example what if say 30% of our body is comprised of these infected cells, what happens if we 'delete' too much of ourselves ? would normal cells regenerate fast enough to fill in the gaps as it were ? this begs the question, what % of cells in say the liver need to be infected to cause the proposed pathogenesis ? can infected cells induce the negative effect in adjacent cells ?

Thank you - a lot of effort has been put in to reach this point.

I’m currently unsure how many infected cells will be required to influence an entire organ / tissue via cell-cell communication, cytokines, lactate, etc., however existing studies on the effects of senescent cells may hold answers or clues.

Regarding cell replacement - the rate of this will be “high” in the fasting method described. We’re unlikely to get everything done on the first fast, so we continue with an ongoing therapy -

For the non-fasting method, the rate will be dictated by the capabilities of the host immune system and WBC counts -

Reishi has triterpenes which turn off most of the viral alterations and induces/allows apoptosis signalling via CtBP->SIRT4->NF-kB, p53, etc.

Reishi also contains some level of beta-glucans which further stimulate the necessary immune response.

As the rate of targeted immune response is heavily influenced by specific beta-glucans (and nutrients required to replace cells - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3678455/), we added Lion’s Mane. This adds a significant increase to ongoing efforts. By further adding oat bran (very cheap source of beta-glucans), this becomes very impressive and rather unpleasant at times - start with eg. 1/4 teaspoon / day.

If someone finds the ongoing immune response too intolerable, this can largely be dialled back (ballpark 5 day lag) by reducing beta-glucan intake.

One key point is that once the liver becomes the focus, they now have “mono part deux” - they’re going to want to be in bed, as they’ll have no energy and feel like they have a very nasty infection / flu.. which they do. (Our body doesn’t care about our feelings in this matter - it just sees the threat needing to be eliminated.)

I do have an unpublished idea about how, in a clinical setting, you could potentially resolve all CFS symptoms, antibodies and infected cells over 1-2 weeks, while avoiding symptoms equating to tumor lysis syndrome. This would also be curative.

I’m in the process of discussing this with clinicians at the moment, as it needs some unusual tools. It’ll likely be a while, if at all, before this is available.

 

[joshua.leisk]

Joshua by thoughts on the nausea and aches created by taking Glycine and Cysteine? Even in doses just under 500mg it's strong. I'm titrating up slowly currently on 400mg Cysteine and 300mg glycine. I did try more Glycine less Cysteine but the nausea was much worse.

I'm titrating up to 1500mg a day over a few months.

While glycine and cysteine are important for making glutathione, collagen synthesis, sleep, etc., cysteine is also used to make CoA, which becomes Acetyl-CoA.

If someone was taking these two without also disabling the viral alterations, you may be perpetuating the cycle and creating more nitrogen to metabolise. Without sufficient water / urination, I could see this being unpleasant. I dare say that pathology would hold quick answers to this.

 

[Marylib]

I do have an unpublished idea about how, in a clinical setting, you could potentially resolve all CFS symptoms, antibodies and infected cells over 1-2 weeks, while avoiding symptoms equating to tumor lysis syndrome. This would also be curative.

I’m in the process of discussing this with clinicians at the moment, as it needs some unusual tools. It’ll likely be a while, if at all, before this is available.

@joshua.leisk - You realize that these two paragraphs have us all really excited, don't you? Seems like for decades everyone had been examining the elephant from the part of the elephant they can feel or reach or have access to. As you wrote - fresh eyes and the time to examine it without the usual training (I may not be expressing this properly) can lead to a Eureka moment. And there are some very devoted clinicians who keep trying to stir up interest in the scientific community. I can imagine that two weeks in a clinical setting sound like heaven to many of us. As I said, I don't really have the capacity myself at the moment to take care of my needs and do the protocol at the same time. The pharmaceutical companies may not be happy about it, but we would be! Thanks again for all the information and attempts to explain it. Just think if we could train those cancer cells to stop what they are doing and get with the program...

 

[Marylib]

I'm wondering if @paolo has seen this discussion. Paolo has an interesting way of looking at things, too.

 

[godlovesatrier]

I've costed it out in the UK. The non-fast main protocol is about £150 for a months worth. I got it all on amazon apart from the liposamal gluthathione which was just really hard to find and I think will cost a small fortune if I buy the right amount. But found that on Baldwins the herbalist website.

But the diet is the tricky part I think, for me anyway, I am at 125g carbs but need to increase the fat and get the carbs down. Will probably end up sacrificing the main carbs in my meals and add in the eggs for a bit of a short fall. Haven't reacted to eggs since I was a child so will be interesting to see if the protocol does anything for that. Not going to get my hopes up about that one tho.

 

[ilmc]

Hard not to get excited, even if it is only for a clear treatment to try. Thanks for all the work. I just wish I could give this to my doctor and let him do the necessary tests + help me in sourcing the supplements. Even if I don't completely fit the profile I would still want to try it. I would welcome 1 week of agony, or a month, where my immune system is actually doing something.

When my CFS started EBV antibodies were high for at least a year. Years later my new doctor told me it was all negative. I'm not sure at which point I got 'cured'. I never completely believed it and theorized that my immune system was too weak to generate antibodies.

Still, I think my CFS started much earlier. I had a mycoplasma infection almost 15 years before the CFS. It is all very vague as it is so long ago, presumable related to a tick bite but I don't fit the lyme symptoms. Perhaps the tick transferred some other pathogens like HHV6, if that is even possible.

 

[JoeS]

I've costed it out in the UK. The non-fast main protocol is about £150 for a months worth. I got it all on amazon apart from the liposamal gluthathione which was just really hard to find and I think will cost a small fortune if I buy the right amount. But found that on Baldwins the herbalist website.

But the diet is the tricky part I think, for me anyway, I am at 125g carbs but need to increase the fat and get the carbs down. Will probably end up sacrificing the main carbs in my meals and add in the eggs for a bit of a short fall. Haven't reacted to eggs since I was a child so will be interesting to see if the protocol does anything for that. Not going to get my hopes up about that one tho.

I don't understand, does Reishi have to be alcohol tincture? Because only alcohol extract has Triterpenoids.

 

[xebex]

Still, I think my CFS started much earlier. I had a mycoplasma infection almost 15 years before the CFS. It is all very vague as it is so long ago, presumable related to a tick bite but I don't fit the lyme symptoms. Perhaps the tick transferred some other pathogens like HHV6, if that is even possible.

my thoughts on this would be that you already had HHV6 essentially not causing any problems till you got the tick bite, immune system would then try to mount a response but can’t because of the HHV6.

 

[Reading_Steiner]

Hi! Yes, we have some people in remission right now and a number of people at various stages of recovery. It’s an interesting journey.

What I did differently..

Probably starting from scratch with a completely blank slate and no expectations.

I didn’t set out to study CFS - I just had a cluster of people I was coaching with different goals, common symptoms and markers. While digging through the problems, I realised along the way it was CFS... and as I kept digging, it got even more interesting.

Another key factor - I initially worked with a handful of people and talked to them for at least 5 hours each day, over many months. Being “retired”, I had the time to do this. There were no billable hours or pressures, just days of poking and teasing out aspects of the puzzle. I enjoy puzzles and helping people, so this was rewarding enough.

From these ongoing experiences - reactions to variables and discussions - it all became clearer and clearer.

I think also looking at this as a “biological engineering problem” rather than with a mindset honed by classical medical training also helped a lot - my skill-set has been developed around pattern recognition, pathways and problem solving.

My background was once electronics engineering and later, IT. My daily work expectations were having to dive into highly complex environments with typically unquantifiable numbers of “unknown” variables and being required to quickly zero-in on problems by using inferences from tangible behaviour / pressures / flows from related pathways / processes / functions. It was like building 3D jigsaw puzzles, by seeing the inputs/outputs, flows/pressures and feedback loops for every system and function.

This was often in a high-stress situation where a fault condition would cost >$1M/day and you ALWAYS had to locate the root cause - placing bandaids on a faulty pathway would invariably lead to unexpected behaviour and future problems. This would be completely unacceptable.

So, armed with that mindset, time/opportunity and tools from perhaps a decade or so of studying biological sciences out of sheer curiosity (I’m thoroughly in love with this topic), without simultaneously having being taught how I “should” look at things, I appear to have found myself in a fairly unique position.

It’s possible that solving this needs someone who has ample time, has lovingly studied metabolism, clinical / sports endocrinology and exercise sciences, with the mindset of an engineer, while also having (quite remarkably) fully recovered from CFS, thereby having a very personal understanding of it and desire to stamp it out.

I’m trying my best.

Prusty - PDH. There are multiple causes for this, but the main one is hypoxia / HIF. Just as we’ve seen in cancer studies, the remodelling under hypoxic conditions (which happens when a-KGDH is impaired) alters PDHK.

Disable the HIF-1a transcription factors being activated and that problem usually stops quite quickly, providing the “autoimmune antibodies” for eg. the beta-adrenergic receptor (which may/may not be present depending on the infection) have been already resolved. This is quite easy to do - there are many ways to achieve this, however the best way is to resolve the root cause.

Anaplerosis via succinate (succinate, GABA, B12, etc) or fumarate (urea cycle, aspartate) does it quickly, but does nothing to fix the underlying problem - in fact, it adds to the ROS and continues the vicious cycle.

This is the same underlying issue with nutrition / hormones in cancer treatments and was the key realisation in the third paper.

We “had the important pieces”, however were looking at the whole puzzle “through a mirror.”

The more patches you put in place, by fixing individual legs / cascades, usually accelerates the progress of the disease, without simultaneously doing something to modify the viral behaviour itself.

In a nutshell - everything you put in gets turned into viral proteins, ROS and further metabolite depletion via urine. You can/will “move the pressures around” and create new pathway impairments by healing another.

So much easier just to turn the whole thing off, instead.

I understand, I have been on the fringe of that world at some times in my life so I probably have a better appreciation / imagination of whats involved than most. I feel like I am a good judge of character or something like that. I've seen these 'puzzle pieces' emerging from a sea of uncertainty and doubt over the past few years, I knew there would be someone out there with the experience necessary to make sense of it if I just wait patiently.

I asked about the state of the cells I think because my image of the overall picture of whats going on is blurry still, probably due to the veil of fatigue that hangs over my mind constantly. I seem to think in a different way now thats more intuitive as a result. Anyway much of the research claims recently has been to do with signalling, Ron Davis' "something in the blood" that affects the cells impedance, and Prusty was talking about HHV-6 doing something that caused cells to fragment their mitochondrias en masse ( as clearly as I can remember the work ). I take it you are aware of these theories ?

I will try the protocol as soon as possible, I just want to be precise about it and yet not spend more money than is necessary, as i'm not diagnosed with CFS yet by the NHS here, I have no disposable income - income at the moment. This is a big investment of 'focus' for me and I feel like doing formal documentation would be too much on top of that, sorry. I've never sent off for expensive lab tests. I know that many people have tried every therapy under the sun, I've only tried vitamins, probiotic and BCAA, and I was on Propranolol for years which seemed to help. I will let you know how it goes though.

 

[vision blue]

however the figures will definitely be needed, as it’s a ridiculously complicated disease model.

Almost everything stems from the “Warburg effect” or “reverse-Warburg effect”, which appears to have more than one state, depending on the ROS being generated and availability of eg. Aspartate, P5P, B12, GABA, Acetyl-CoA.

Thanks for the reply. I did btw look at figures- but after i read the papers rather than during. But I don't see those figures as novel to you at all. These are standard biochem pathways with well known connections between them. There are academic groups that show all these pathways at once in pictures so sort of just reinventing the wheel drawing your own- but some people out there seem to think this is new to you. (presumably folk not steeped in biochem)

When you say amost everything stems from Warberg or reverse, not sure if you mean your theory or just life in general- but as I noted, if you mean about your theroy, then still at the mechanistic level, i'm not seeing what's new about your claims. I will look though again at paper 3 to see the greater urea cycle details you mentioned are there and see if that part is anything new.

But sometimes, people can create succesful treatments even if they say nothing new in mechasism and even if their viral theory is wrong - I will hope that you are one of those. Sorry, not everyone can be a fan. I know what you need to do to make this seriously publishable (and not in a journal where you pay them to publish) but presumably you'll get there eventually with the feedback eveyrone has been giving you.

 

[YippeeKi YOW !!]

As you wrote - fresh eyes and the time to examine it without the usual training (I may not be expressing this properly) can lead to a Eureka moment

You expressed it perfectly .

I'd add that the absence of " .... the usual training...." also implies the absence of the usual medical/scientific prejudices and a more open mind, along with a willingness to wander down paths that the deeply interbred medico-scientific community would scoff at. Coupled with @joshua.leisk 's obvious deep and wide grasp of the science-y part, and I'm almost ready to believe in miracles ...