Myalgic Encephalomyelitis is clear to see in the blood

[Violeta]

That made me wonder: did any of the studies find significant reductions in cellular function? My analogy is a car rated at 200 hp on fuel brands A to W, and measures only 100 hp on brand X. Is there an equivalent of a dynamometer that can measure power output of muscle cells, or brain cells or whichever, and has that been done for cells of PWME vs sedentary controls?

Finding small changes in mitochondria (fragmentation ,etc) might be important in ME, or it might not. To follow the previous analogy, I can imagine a study finding that fuel X "leaves a sticky residue on the carburetor shaft, which could hamper throttle movement and thus reduce power!" ... yet dynamometer testing shows no reduction in engine power, because all stickyness does is insignificantly increase the foot pressure required. Meanwhile, the study was funded by fuel A's company, or a company that sells a really profitable fuel additive claiming to clean out sticky residue.

Measuring overall muscle power isn't adequate, because that can be affected by many factors other than mitochondrial function. For example, if the muscles were getting conflicting signals, there'd be a lot of usage byproducts (heat, lactate, etc), but reduced physical power output.

I'm questioning whether mitochondrial dysfunction has been proven to be a cause of ME symptoms, rather than just a theoretical possibility.

PKM2 accelerated the progression of chronic fatigue syndrome via promoting the H4K12la/ NF-κB induced neuroinflammation and mitochondrial damage​

https://pmc.ncbi.nlm.nih.gov/articles/PMC11953386/
This study aims to explore the effects and potential mechanisms of PKM2-mediated neuroinflammation leading to mitochondrial damage and its role in the progression of chronic fatigue syndrome (CFS)

 

[Oliver3]

https://pmc.ncbi.nlm.nih.gov/articles/PMC11852713/

There's a huge trigger warning with this one. Only read if you are up to a very depressing study of a poor young woman with severe Heds.

It reads exactly like m.e. in her symptoms.
She also had severe mitochondrial issues

Wishfu, l there are plenty of this kind of studies.lonh covid sufferers with eds is very common.
As the other study I presented shows , connective tissue problems are likely directly related to mitochondrial function.

Another study I didn't include was single case study of a girl with spinal issues that's directly related to a genetic alteration in the mitochondria. This is the thing. We are relying on the beighton score for heds diagnosis in the general public. I suspect , with good reason , for m.e. to be a form of heds. Same with fibro etc.
All the connective tissue disorders.
The tissue itself is related by mitochondrial health.


Just perhaps study some of the data provided before contributing otherwise what's the point of conversing

 

[Oliver3]

Mitochondria involved in ' brain psychiatric illnesses '
https://pmc.ncbi.nlm.nih.gov/articles/PMC8007172/

 

[Wishful]

But hey, just ignore tye vast swathes of data eh?

I wasn't ignoring it. I was asking a simple question, rather than spending hours poring over studies and probably missing important ones. People here have spent time reading the available papers, so asking if any of those studies measured cellular function rather than just theorizing that mitochondrial dysfunction would cause cellular dysfunction at a level required to cause the level of symptoms experienced.

The paper on skeletal muscle changes seems convincing, although I can't judge the quality of the research behind it. For example, the paper makes the findings about elevated sodium levels in muscles seem really important, but the study had only subjects compared to 6 healthy controls. The graph shows a clear difference, but how much of that is due to healthy and active vs inactive? I'll wait for further confirmations in larger studies.

I did notice, in that paper and others, that they said that there were strength reductions in most people (meaning others did not show this reduction). There were some other similar wordings that made me feel that if the findings are all valid, it shows a downstream effect for most PWME, but since it doesn't exist in others, it's not likely the cause of ME.

I don't have a proper feel for the biomechanics of sodium/calcium activity in muscles and nerves, so my question is: could abnormal nerve Ca/Na activity cause the abnormal levels seen in that study? Just a thought.

The PKM2 paper didn't impress me. It seems to be based on a mouse model of ME. Does a mouse swimming less vigorously mean clear proof of (complex theory about ME), or did whatever the mouse was subjected to just give it a "fuck you researcher!" attitude?

Let's just ignore all that for your car analogy...at least it's changed from the robot one.

Hey, I can't do analogies about detailed biological mechanisms. I don't have a proper feel for Na/Ca transport or fatty acid bindings. Car engines and computers I have a better feel for.

 

[Oliver3]

I wasn't ignoring it. I was asking a simple question, rather than spending hours poring over studies and probably missing important ones. People here have spent time reading the available papers, so asking if any of those studies measured cellular function rather than just theorizing that mitochondrial dysfunction would cause cellular dysfunction at a level required to cause the level of symptoms experienced.

The paper on skeletal muscle changes seems convincing, although I can't judge the quality of the research behind it. For example, the paper makes the findings about elevated sodium levels in muscles seem really important, but the study had only subjects compared to 6 healthy controls. The graph shows a clear difference, but how much of that is due to healthy and active vs inactive? I'll wait for further confirmations in larger studies.

I did notice, in that paper and others, that they said that there were strength reductions in most people (meaning others did not show this reduction). There were some other similar wordings that made me feel that if the findings are all valid, it shows a downstream effect for most PWME, but since it doesn't exist in others, it's not likely the cause of ME.

I don't have a proper feel for the biomechanics of sodium/calcium activity in muscles and nerves, so my question is: could abnormal nerve Ca/Na activity cause the abnormal levels seen in that study? Just a thought.

The PKM2 paper didn't impress me. It seems to be based on a mouse model of ME. Does a mouse swimming less vigorously mean clear proof of (complex theory about ME), or did whatever the mouse was subjected to just give it a "fuck you researcher!" attitude?

Hey, I can't do analogies about detailed biological mechanisms. I don't have a proper feel for Na/Ca transport or fatty acid bindings. Car engines and computers I have a better feel for.

That's why I saud your analogies were far too crude to be used in such a complex system as the human body with poly directional loops.
I mean it's good to question things but at least try and understand there are vast swathes of literature in mitochondria being a major part of most disease processes including ageing.
I included the ' psychiatric ' illnesses because your fixated with the brain being a central computer. How can someone with say schizophrenia have mito issues in the brain but still function.
It depends on the quality and distribution in organs in the body abd how they talk to genes etc.
I'm an auto didact myself....but I've read a fair bit of literature and you're just thinking of this in a way that's too simplistic.
There's so much literature on mitochondria and also how it controls metabolic features that don't you think it's a bit ignorant to just ignore that stuff.
Don't you think naviaux using anti purigenic therapies to restore mitochondrial dysfunction and improve symptoms is amazing?
Chris Armstrong mentioned purines in his recent short presentation about where he's at.
I followed a guy from Bristol uni who was working on anti purigenic therapies to alter blood pressure sensors in the neck and cure high bp. Can't remember the name off the top of my head.
Chris Armstrong is gonna drop information about causes n potential treatments later tgis year I believe.
The hopeful thing is, I think the whole field is moving in the right direction.
But just thinking a few cells in the brain are abberant doesn't take into account huge complexity and so many studies saying connective tissue and mitochondria are involved here

 

[Gala]

This is the strongest evidence I've seen for a given protocol's potential to decrease intestinal permeability. But this study does have limitations as follows:

1. LPS is not exclusively a biomarker for intestinal permeability; it can also be raised by infections in the body, and LPS can also enter via the oral route. Thus, the lactulose-mannitol test would be a better biomarker of intestinal permeability
2. 24 of 41 participants experienced lowered LPS IgA and IgM antibodies; this is 58%
3. The study (it seems?) has not been repeated by others

The protocol was not the same in all the participants, but all of them did receive the following:

1. The leaky gut diet, which is "a milk and gluten-free and low-carb diet"
2. Glutamine, zinc and NAC
3. Other NAIOSs, "which were given according to the immune and biochemical status of the patients, i.e. L-carnitine, coenzyme Q10, taurine and lipoic acid (in case of carnitine and/or coenzyme Q10 shortage); or curcumine and quercitine (in case of systemic or intracellular inflammation)."

I didn't see anywhere where they were taking probiotics. I also did not see LBP or sCD14 being measured in this study.

You're right, and I apologize for mixing several studies together. I've now updated the website to include this and other specific studies conducted in ME/CFS patients. These are very small studies and should be examined more thoroughly:

Clinical Evidence for Digestive Treatments in ME/CFS and Long COVID

1. Probiotics in ME/CFS

• Lactobacillus casei Shirota (LcS): A pilot double-blind controlled study (Nakamura et al., 2009) in 39 ME/CFS patients. They received 24 billion CFU over 8 weeks. Results: increased Lactobacillus and Bifidobacterium levels, with improvements in anxiety. (Rao et al., 2019).
• Bifidobacterium infantis 35624: In a randomized clinical trial, 48 participants took this strain for 8 weeks. Significant reductions were observed in TNF-α, IL-6 and CRP levels. (Groeger et al., 2013).
• Lactobacillus + Bifidobacterium (mixed strains): In a small study with 15 participants, emotional symptoms improved, though changes in fatigue were not measured. (Wallis et al., 2018).

2. Synbiotics in Long COVID

• An RCT (Castelli et al., 2024) with 26 Post-COVID Fatigue patients administered synbiotics containing L. rhamnosus, L. plantarum, B. lactis, B. longum, FOS, and zinc for 3 months. Results: improvements in fatigue, post-exertional malaise, and cerebral metabolites. (Ranisavljev et al., 2024).

3. Fermented Diet in Long COVID

• Ongoing trial NCT06560554 (UCSF, 2024) is testing a fermented-food-rich diet aimed at modulating the microbiota and reducing neuroinflammatory symptoms. Results pending. (Karnatovskaia et al., 2025).

4. Antimicrobials (natural and pharmacological)

• Observational studies using neomycin in ME/CFS patients with SIBO have shown improvements in pain, cognitive function, and digestion. (Pimentel, 2000).

5. Intestinal Permeability Repair

• Corbitt et al. (2018): Limited evidence on probiotics in ME/CFS, though some studies show improvement in inflammatory markers and emotional well-being.
• Stallmach et al. (2024): Highlighted that microbiota-targeted interventions may modulate neuroinflammation and gut permeability, though more controlled trials are needed.
• In a longitudinal observational study (Maes, 2008), ME/CFS patients with elevated IgA/IgM against bacterial LPS received gut-targeted treatment (nutrients, diet, anti-inflammatories). Clinical improvements were observed alongside immune normalization.

See more on this in our article


I’m also working on another article exploring treatments tested in populations other than ME/CFS. Fortunately, there are many more studies with larger sample sizes in that context. I plan to publish it in the coming days.

Microbiome Findings in ME/CFS and Long COVID​

It does seem that similar microbial features appear in our case profiles:

• Reduced bacterial diversity, especially in Firmicutes
• Significant drop in microbial metabolites, such as acetate, butyrate, isobutyrate, and certain amino acids (alanine, serine, and hypoxanthine)
  (Giloteaux et al., 2016; Wang et al., 2024)

However, rebuilding a stable gut microbiome seems difficult to achieve through supplements alone. A more effective approach might involve nourishing and protecting the gut with:

• High-dose glutamine (4–6 g/day)
• Butyrate
• Prebiotics (inulin, FOS, GOS, resistant starch, pectins, psyllium)
• Unpasteurized fermented foods (sauerkraut, kimchi, kefir, live yogurt, kombucha)

Meanwhile, we could explore more direct options such as targeted enemas with specific bacterial strains (though studies on this are scarce and anecdotal) or fecal microbiota transplantation (FMT) — ideally using only a limited, preselected set of strains to avoid triggering new imbalances.

There’s still much to discover and develop in this field, which affects a large portion of the population. In the meantime, probiotic supplementation is unlikely to cause harm and may be beneficial, though the evidence suggests its effects are modest and likely require long-term, sustained treatment.

 

[Violeta]

The PKM2 paper didn't impress me. It seems to be based on a mouse model of ME. Does a mouse swimming less vigorously mean clear proof of (complex theory about ME), or did whatever the mouse was subjected to just give it a "fuck you researcher!" attitude?

I can't believe I am replying to such a ridiculous comment. The person who posted certainly must have overlooked this part of the paper.

Studies have found increased glycolytic activity and reduced efficiency of mitochondrial oxidative phosphorylation in CFS patients, leading to energy deficiency and the accumulation of metabolic waste, such as lactate3.

PKM2 plays a crucial role in this process. PKM2 is a key enzyme in the glycolytic pathway, catalyzing the conversion of phosphoenolpyruvate to pyruvate, generating ATP. However, PKM2 is not solely involved in energy metabolism; it also regulates various functions such as cell proliferation, signal transduction, and gene expression4. Particularly under pathological conditions, PKM2 can influence cellular metabolism and signaling by altering its oligomerization state. When PKM2 exists in a dimeric form, its glycolytic activity is low, but when it switches to a tetrameric form, glycolytic efficiency increases significantly5.

Research suggests that abnormal activation of PKM2 in hippocampal cells may enhance glycolysis and lactate accumulation, leading to mitochondrial dysfunction and accelerating the progression of CFS6. Furthermore, the activation of PKM2 not only promotes glycolysis but also regulates lactate accumulation, which further alters the acidic environment within cells. This metabolic disorder is considered a crucial mechanism underlying energy production deficits in CFS patients.

At the same time, excessive activation of PKM2 is closely related to mitochondrial dysfunction. PKM2 enhances glycolysis, increases lactate production, and leads to the accumulation of acidic metabolic byproducts, weakening the mitochondria’s ability to generate energy9. Additionally, lactate accumulation may further induce neuroinflammation through the regulation of epigenetic modifications (such as H4K12la) and the activation of the NF-κB signaling pathway, aggravating the pathological progression of CFS10. Neuroinflammation is considered a major contributor to cognitive dysfunction and emotional problems in CFS. Inflammatory responses not only impair the normal function of the central nervous system but may also cause neuronal damage and reduced synaptic plasticity through long-term neuroinflammation11. In CFS patients, elevated levels of various pro-inflammatory cytokines, particularly tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), have been found, which are closely associated with neuroinflammation12.

6 https://www.mdpi.com/1422-0067/23/2/691

7 https://www.sciencedirect.com/science/article/pii/S1567724913002390?via=ihub

9 https://pmc.ncbi.nlm.nih.gov/articles/PMC5161229/

10 https://pmc.ncbi.nlm.nih.gov/articles/PMC6818755/

 

[Oliver3]

I can't believe I am replying to such a ridiculous comment. The person who posted certainly must have overlooked this part of the paper.

Studies have found increased glycolytic activity and reduced efficiency of mitochondrial oxidative phosphorylation in CFS patients, leading to energy deficiency and the accumulation of metabolic waste, such as lactate3.

PKM2 plays a crucial role in this process. PKM2 is a key enzyme in the glycolytic pathway, catalyzing the conversion of phosphoenolpyruvate to pyruvate, generating ATP. However, PKM2 is not solely involved in energy metabolism; it also regulates various functions such as cell proliferation, signal transduction, and gene expression4. Particularly under pathological conditions, PKM2 can influence cellular metabolism and signaling by altering its oligomerization state. When PKM2 exists in a dimeric form, its glycolytic activity is low, but when it switches to a tetrameric form, glycolytic efficiency increases significantly5.

Research suggests that abnormal activation of PKM2 in hippocampal cells may enhance glycolysis and lactate accumulation, leading to mitochondrial dysfunction and accelerating the progression of CFS6. Furthermore, the activation of PKM2 not only promotes glycolysis but also regulates lactate accumulation, which further alters the acidic environment within cells. This metabolic disorder is considered a crucial mechanism underlying energy production deficits in CFS patients.

At the same time, excessive activation of PKM2 is closely related to mitochondrial dysfunction. PKM2 enhances glycolysis, increases lactate production, and leads to the accumulation of acidic metabolic byproducts, weakening the mitochondria’s ability to generate energy9. Additionally, lactate accumulation may further induce neuroinflammation through the regulation of epigenetic modifications (such as H4K12la) and the activation of the NF-κB signaling pathway, aggravating the pathological progression of CFS10. Neuroinflammation is considered a major contributor to cognitive dysfunction and emotional problems in CFS. Inflammatory responses not only impair the normal function of the central nervous system but may also cause neuronal damage and reduced synaptic plasticity through long-term neuroinflammation11. In CFS patients, elevated levels of various pro-inflammatory cytokines, particularly tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), have been found, which are closely associated with neuroinflammation12.

6 https://www.mdpi.com/1422-0067/23/2/691

7 https://www.sciencedirect.com/science/article/pii/S1567724913002390?via=ihub

9 https://pmc.ncbi.nlm.nih.gov/articles/PMC5161229/

10 https://pmc.ncbi.nlm.nih.gov/articles/PMC6818755/

Great post.
It gives me hope so much Is known.

 

[Wishful]

The person who posted certainly must have overlooked this part of the paper.

No, I recall reading that. However, when I paper says that something may have this or that effect, without providing evidence that this or that effect is actually occurring at a level to cause significant symptoms, I don't take it as a major discovery. I put it in the "wait for actual confirmation" pile. Someone can publish a really complex theory based on "may"s, based on a mouse's swimming pattern, but that doesn't mean that it's a supported theory.

 

[Oliver3]

No, I recall reading that. However, when I paper says that something may have this or that effect, without providing evidence that this or that effect is actually occurring at a level to cause significant symptoms, I don't take it as a major discovery. I put it in the "wait for actual confirmation" pile. Someone can publish a really complex theory based on "may"s, based on a mouse's swimming pattern, but that doesn't mean that it's a supported theory.

I knew you'd say that.
What about the suramin trial.
What about the other thousand studies on mitochondria and disease.
It's just pure ignorance.
Your ' theory' is some cells in a car, motor cause m.e.
I don't put that in a file. I put it in the bin

 

[Wishful]

A more effective approach might involve nourishing and protecting the gut with:

A nice theory, and maybe it will work for some people with specific gut issues, but various prebiotics, probiotics, fermented foods and butyrate (butter), had no noticeable benefit in general. One time a probiotic capsule did fix a problem, but has no noticeable benefits in general. A good flushing out from food poisoning has worked wonders twice so far (fixed existing food intolerances), but so did a single meal with squash, which I've never seen listed as a gut restorative.

Microbiome management has great potential, but I think we're still in the equivalent of applying leeches or soaking in "healing waters". I can imagine sometime in the not too distant future where we swallow a sensor capsule and an AI reads our gut environment and prescribes diet and supplements to adjust our guts with a reasonable chance of success.

 

[Wishful]

What about the suramin trial.

It's about autism in mice. I'm not claiming that mitochondrial dysfunction has no effect on the body. I am saying that the link in ME is unproven. I can accept that some PWME have mitochondrial dysfunction in their muscles as part of their ME, but that doesn't mean that it's the root cause for all PWME. Likewise with vascular dysfunction, or gut dysbiosis or connective tissue problems; they could be caused by ME or could make ME worse, but aren't necessarily a factor in other PWME.

If a human trial of suramin fixes ME, that will prove the theory (or at least strongly support it, since there's always a possibility that it has benefits via a completely unrelated mechanism). If the trial shows no significant improvement for PWME, will you insist that the cell danger response theory of ME is still valid? Science is about testing theories and accepting the outcomes. It's not about worshiping a theory because it sounds good.

Your ' theory' is some cells in a car, motor cause m.e.

No. I do think that it's likely to involve a relatively small number of brain cells involved in an abnormal feedback loop. That loop might involve multiple organs, and the signals involved in that probably aren't drastically abnormal, but the ratios cause positive feedback. One thing I liked in the paper on muscle cells was that the study of metabolites focused on abnormal ratios rather than absolute levels of each one. In a complex feedback loop, having a number of factors only a few percent high or low could still add up to a large overall response.

Now that I think about it, it can be even more complex if timing of signals is involved. If a specific signal is delayed or sped up, it can cause a serious and unexpected response, but if you're just looking at signals at random times, or long after the event, you won't find anything suspicious.

I suggest that ME research groups (and medical research in general) should involved a systems engineer, to get a different perspective on how the body works. I doubt that medical schools teach much in the way of feedback theory. Our body's subsystems can be modeled by mathematical equations, including feedback signals and including time. Add engineers!

 

[Oliver3]

Did you go onto see the suramin trial IN HUMANS. You are talking from a place of utter ignorance.
The suramin trials proved naviauxs theory ...so you understand???? Einstein
There's no point talking to you.
You have NO IDEA of what you're talking about.
Zero knowledge of anything but a laughably simple idea of a few cells, with ZERO evidence to back it up.
Yet we provide evidence and common knowledge that mitochondria are involved and are in fatiguing illnesses, in fact all illness.
Get a grip. Educate yourself. At least bring some idea. For someone who doesn't like the idea of ' may' that's all your worthless idea depends on

 

[Oliver3]

It's about autism in mice. I'm not claiming that mitochondrial dysfunction has no effect on the body. I am saying that the link in ME is unproven. I can accept that some PWME have mitochondrial dysfunction in their muscles as part of their ME, but that doesn't mean that it's the root cause for all PWME. Likewise with vascular dysfunction, or gut dysbiosis or connective tissue problems; they could be caused by ME or could make ME worse, but aren't necessarily a factor in other PWME.

If a human trial of suramin fixes ME, that will prove the theory (or at least strongly support it, since there's always a possibility that it has benefits via a completely unrelated mechanism). If the trial shows no significant improvement for PWME, will you insist that the cell danger response theory of ME is still valid? Science is about testing theories and accepting the outcomes. It's not about worshiping a theory because it sounds good.

No. I do think that it's likely to involve a relatively small number of brain cells involved in an abnormal feedback loop. That loop might involve multiple organs, and the signals involved in that probably aren't drastically abnormal, but the ratios cause positive feedback. One thing I liked in the paper on muscle cells was that the study of metabolites focused on abnormal ratios rather than absolute levels of each one. In a complex feedback loop, having a number of factors only a few percent high or low could still add up to a large overall response.

Now that I think about it, it can be even more complex if timing of signals is involved. If a specific signal is delayed or sped up, it can cause a serious and unexpected response, but if you're just looking at signals at random times, or long after the event, you won't find anything suspicious.

I suggest that ME research groups (and medical research in general) should involved a systems engineer, to get a different perspective on how the body works. I doubt that medical schools teach much in the way of feedback theory. Our body's subsystems can be modeled by mathematical equations, including feedback signals and including time. Add engineers!

Anti purigenic therapy to improve mitochondrial health

 

[Oliver3]

Open medicine foundations recent work om metabolism being at the root of m.e.
The stress state causes a switch which naviaux emphasises and what he calls the ' dauer' state. Which is German for hibernation. Armstrong talks about how this stress state switches patients to use amino acids as fuel which of course effects the organism, lowers energy production and has many downstream effects.

 

[Oliver3]

https://naviauxlab.ucsd.edu/science-item/mitochondrial-disease-research/

 

[Rufous McKinney]

Anti purigenic therapy to improve mitochondrial health

That the cells "harden" their boundaries, and stop relating to other cells- is fascinating.


Wish I could try some of this stuff, my brain is NOT a developing child.

 

[Rufous McKinney]

Which is German for hibernation.

there has to be something adaptive about this mechanism's existence in bodies, enabling it to be triggered.

 

[Oliver3]

there has to be something adaptive about this mechanism's existence in bodies, enabling it to be triggered.

I think you're right. It's why I think naviaux et al are cautious about anti purinegic therapies because the organism is trying to protect itself.
Naviaux calls autism ( and by proxy m.e. which he thinks is directly applicable ( an ecogenic illness. By that he means poisons in the environment are triggering tgis shut down.
He stresses since 1980 smthg like 5,000 new chemicals, untested, ( and counting)have entered the environment. Also stressors in society are contributing, blue light, radiation, electricity itself ( I added that one from studying jack kruse ) to triggering the cell danger response. If you reopen the organism to the insults of modern life, then what happens ?
I saw Ron Davies saying he thinks the adaptive response us a sickness response in origin, designed to take away ill people from the tribe. I'm not sure ge still thinks that or uf its correct.

But Chris Armstrong is reinforcing these ideas with his research saying that whatever the stressor initially it's plunging us into this metabolic switch. If the stressor keeps being there then you become stuck.

I think connective tissue is the thing that makes is special..usually intelligent, hyoerintuitive etc
But it predisposed us to this metabolic switch.

I did read an article on multiple sclerosis genes initially being an adaptation to certain viruses as ancient herders travelled west about 5,000 years ago. What worked then might not be good now.

I'm sure neandathal genes are strong in us too, though that's my silly speculation.

That's why I think we need to find ways to strengthen the organism through regenerative meds.

These are just my extrapolation from seeing eds people being so similar to us.

But sometimes maybe it's a case of bad luck. Like someone born blind. There doesn't seem. To be an adaptive mechanism at play three.
However, there are many of us so it likely is ab adaptation.

 

[Oliver3]

That the cells "harden" their boundaries, and stop relating to other cells- is fascinating.


Wish I could try some of this stuff, my brain is NOT a developing child.

Naviaux was given the recipe by Bayer and built his own factory. Then the pandemic hit. So I don't know what he's up to.
The standfordstudy on strengthening mitochondria that they've patented is good. I wish I could get it

Have you heard of that German naturopath, I think it's klinghardt but dont quote me on that. He did a lot of work with finding ways to open up the vascularity in the necks of autistic kids.
He wanted to get his hands on suramin.

As I've said before, there's researchers looking into anti purigenic therapies to target the bp sensors in the neck.
I wonder if these therapies create a loss of profit because its a road down which curative therapies may appear. Which socks.

If only there was a drive to fund this stuff