Myalgic Encephalomyelitis is clear to see in the blood

[Wishful]

You literally ignore ALL evidence that refutes your narrow-minded, niche, unusual, and unsupported view of how ME/CFS works. You are deliberately ignorant of the research that has been published.

No, however I lack the knowledge level of biology to properly understand many (most?) of those research papers. When I read about something like endothelial permeability, based on some p-value threshold, I cannot judge it properly. When it's a small study and a small effect, I don't place strong value on it. A study might claim evidence of mitochondrial dysfunction in muscles, but even when my ME symptoms were awful (for me), I could still lift heavy things or ride my bike 40 km in hilly terrain, so I consider that strong evidence that my mitochondria were pumping out ATP without problems. I'd expect vascular dysfunction to limit physical capacity too, so a study showing small effects in some people is less convincing to me than my own experience.

As for the brain being a likely cause, that's easy for me to accept, since I can liken humans to computer-driven robots: one transistor failure in the CPU can cause major problems, yet be extremely difficult to locate the failure. I could imagine the robot showing overheating motors, or power supply fluctuations, or other analogs of connective tissue or vascular dysfunction, caused by that single transistor failure. You can claim that it's obviously a motor or wiring dysfunction based on some measurements, but replacing those components wouldn't fix the problem.

 

[Oliver3]

The distribution of mitochondria are not equal throughout the body.
Have you looked at bob naviauxs work?
You have to recognise that your experience of m.e. is pretty unusual.
I'd give anything to be able to cycle 40 km.

Using the analogy of a robot is entirely bogus.
As I've previously stated, alzheimers is likely starting in the kidneys.

Why do people with autism have connective tissue problems?
And why did they respond to suramin?
Perhaps listen to a naviaux lecture on the cell danger response. It's pretty amazing that he was able to show proof of concept and reverse some of the issues involved.

 

[Gala]

No, however I lack the knowledge level of biology to properly understand many (most?) of those research papers. When I read about something like endothelial permeability, based on some p-value threshold, I cannot judge it properly. When it's a small study and a small effect, I don't place strong value on it. A study might claim evidence of mitochondrial dysfunction in muscles, but even when my ME symptoms were awful (for me), I could still lift heavy things or ride my bike 40 km in hilly terrain, so I consider that strong evidence that my mitochondria were pumping out ATP without problems. I'd expect vascular dysfunction to limit physical capacity too, so a study showing small effects in some people is less convincing to me than my own experience.

As for the brain being a likely cause, that's easy for me to accept, since I can liken humans to computer-driven robots: one transistor failure in the CPU can cause major problems, yet be extremely difficult to locate the failure. I could imagine the robot showing overheating motors, or power supply fluctuations, or other analogs of connective tissue or vascular dysfunction, caused by that single transistor failure. You can claim that it's obviously a motor or wiring dysfunction based on some measurements, but replacing those components wouldn't fix the problem.

I believe many of the neurological symptoms in ME/CFS may be secondary to chronic cerebral hypoperfusion. When blood flow to the brain is persistently low, oxygen and nutrient delivery becomes limited, which can damage neurons and trigger neuroinflammation. This might help explain why vascular-targeting drugs like ivabradine, Mestinon, enoxaparin, propranolol, or nattokinase are often effective. Several of these are among the top 21 treatments with the highest reported benefits in ME/CFS, according to new data from TreatME/OMF
Health Rising, 2025

One study that really caught my attention was by Van Campen et al. (2020), involving over 400 ME/CFS patients. They found that 86% showed significant reductions in cerebral blood flow during tilt table testing — even without orthostatic hypotension or tachycardia. This suggests that cerebral hypoperfusion could be a central mechanism in ME/CFS.
https://pmc.ncbi.nlm.nih.gov/articles/PMC7044650/

 

[Oliver3]

Don't forget, this is a spectrum disease. The fact that you can do all these things means you are very high functioning. It's not the normal experience of m.e. for sure but I see you and recognise that's your version of m.e

You're disparaging of research , whilst admitting you don't understand the papers is however, not something you should use as a main source of your argument.

Inflammation in the brain is definitely part of m.e. I think that's what part of your experience is. But why?
And why are there Inflammatory markers in the blood for most of us?

Limiting tgis to just the brain is such a backwards step.
No ines saying the brains not involved. But it's a phenotypical disease.
You're obviously prone to inflammation in the brain, triggering shut down of mitochondria abd putting your brain into the dauer state naviaux talks about.
Did you say you have thyroid issues? I can't remember? If you have any autoimmune disorder that's at base, poor intestinal gut integrity. In your case the inflammation abd mitochondrial shut down only happens in the brain.
You might have a genetically lower level of mitochondria expressed in the brain.

You cannot ,however, say that you have no idea about certain aspects of tgis disease , which Is clear in many research studies, and clearly part of many of our experience, and just dismiss it.

Anti purigenic therapies work in this disease as do dopamine enhancers.
You may lack dopamine like many if us.
I'd say your high functioning physical ability means that your connective tissue is stronger than most of us but part of it, maybe the blood brain barrier, or the gut I'd compromised, coupled with mitochondria that are nit working well in the brain

 

[Oliver3]

Creo que muchos de los síntomas neurológicos en la EM/SFC podrían ser secundarios a una hipoperfusión cerebral crónica. Cuando el flujo sanguíneo al cerebro es persistentemente bajo, el oxígeno y los nutrientes se ven limitados, lo que puede dañar las neuronas y desencadenar neuroinflamación. Esto podría explicar por qué los fármacos vasculares como la ivabradina, el mestinón, la enoxaparina, el propranolol o la natoquinasa suelen ser eficaces. Varios de ellos se encuentran entre los 21 tratamientos con mayores beneficios reportados en la EM/SFC, según los nuevos datos de TreatME/OMF ( Health Rising, 2025 ).

Un estudio que realmente me llamó atención la la fue el de Van Campen et al. (2020), con más de 400 pacientes con EM/SFC. Descubrieron que el 86 % presentó reducciones significativas del flujo sanguíneo cerebral durante la prueba de mesa basculante, incluso sin hipotensión ortostática ni taquicardia. Esto sugiere que la hipoperfusión cerebral podría ser un mecanismo central en el EM/SFC.
https://pmc.ncbi.nlm.nih.gov/articles/PMC7044650/

This also happens in autism

 

[Gala]

Esto también sucede en el autismo.

and ADHD

Oops, the Spanglish is causing me some trouble — sorry about that! Haha

 

[Oliver3]

Heheh

 

[Wishful]

Using the analogy of a robot is entirely bogus.

Why bogus? I didn't post it as proof of any theory, but rather as as an example of how a tiny malfunction in a controller (brain or CPU) can have major effects on what it controls, in ways that would easily--but wrongly--ascribed to what is showing the symptoms. Hot motor? Bad motor! However, it could be hot because the computer is sending "reverse" pulses after each "forward" pulse.

My eye muscles seem to be able to move to the sides normally, so I don't ascribe my double-vision to those. Eye alignment is controlled by brain cells, so a problem there seems more likely.

 

[Wishful]

in that you only get pem through mental / emotional exertion

No, back when I did get PEM, it was from physical exertion too. It was unusual in that the trigger seemed to be muscle damage (straining muscles in ways they weren't accustomed to) rather than exertion*duration levels. That was effectively blocked by cumin, while the cognitive triggering was not blocked. Both triggering types stopped after 2.5 years of taking cumin. I still seem to have worse days after driving to town, but I'm not sure whether that's PEM or some other mechanism (maybe gut changes due to driving for hours?).

 

[Oliver3]

Bogus because an entirely different system. Simplistic versus high complex bidirectional . No comparison

 

[Oliver3]

No, back when I did get PEM, it was from physical exertion too. It was unusual in that the trigger seemed to be muscle damage (straining muscles in ways they weren't accustomed to) rather than exertion*duration levels. That was effectively blocked by cumin, while the cognitive triggering was not blocked. Both triggering types stopped after 2.5 years of taking cumin. I still seem to have worse days after driving to town, but I'm not sure whether that's PEM or some other mechanism (maybe gut changes due to driving for hours?).

Ah anti inflammatory...you have brain inflammation

 

[Wishful]

The distribution of mitochondria are not equal throughout the body.

Certainly. I can't rule out that mitochondrial dysfunction in some small number of brain cells isn't the root cause of ME, but that's hard to verify, and would unlikely show up on blood or CSF tests.

 

[Wishful]

Ah anti inflammatory...you have brain inflammation

That's leaping to a conclusion based on too little evidence. If cumin's effect on me were due to anti-inflammatory properties, then other anti-inflammatories should have had similar effects, but didn't. I simply accept that it was due to an unknown interaction between cuminaldehyde and some cells in my body.

 

[Wishful]

Bogus because an entirely different system. Simplistic versus high complex bidirectional . No comparison

No, I consider it valid. I'm not claiming that every human function can be modeled by a robot, but it doesn't invalidate the observation that very small failures in a central controller can cause major problems that appear to be body problems. It doesn't prove that all problems are due to a central controller, but it does show that body problems can possibly be due to a central control problem. It can also be due to a problem in the bidirectional aspects. The more complex the bidirectional dynamics, the more potential for unexpected behaviour.

 

[Wishful]

I believe many of the neurological symptoms in ME/CFS may be secondary to chronic cerebral hypoperfusion.

I consider that plausible. I think it's unlikely the core dysfunction, since many people don't seem to have significant hypoperfusion.

I skimmed the paper. First flaw: Fukuda criteria. Second flaw: measurements via questionnaires. Third flaw: healthy controls, rather than limited physical activity lifestyle controls. Maybe that hypoperfusion is common in sedentary people? It doesn't convince me that 90% of PWME suffer from significant hypoperfusion or that it's a cause of many symptoms for 90% of PWME. I can accept that it may play a role in severity of some symptoms in some PWME.

 

[Dysfunkion]

I don't think either of you (Oliver and Wishful) are wrong, this is multi systemic and phenotype based. Olivers finding upon looking at the demographics in which this occurs appear to be right on the money. THOUGH I have also noticed through what I've done so far how physically local symptom control can be. No combination of biomarkers so far has led to anything certain that immediately goes "ah this specifically causes the ME to occur", we really only have a bunch of links to clusters of people that often get it. Often this gets more difficult because we also only have our own experiences paired with this research to go off of. So often you'll have one person with experiences that strongly support their hypothesis and then you'll have someone with vastly different one's with a different PEM presentation that runs right up against it. I think it's best to look at the intersections more closely and work from there with individuals based on how they're responding to get more progress. This condition appears to be so individual with common overlaps that the problem is that with getting anywhere with it. Another big issue is the environment which everyone with it has issues with that appears to just get worse and worse as years go by. More pollution, worse food, higher ambient radiation, and much more environmental stress from the general state of the world.

I think what we need to most is more specific phenotype identification, it almost seems like the only way. The walls we'll run into here though is do we even have the technology to find this out and tailor prevention to the individuals life before they get the most severe complications from the condition? Is it something that can be analyzed by just looking at something in the child early on and starting the prevention protocol where if they follow it they'll be able to enjoy a more normal life so as long as they avoid this, that, and something else? Since ME is so comorbid with so many things, this is where it gets really messy. If you prevent the ME, this person is still going to have this or that chronic health issue. But in doing something to prevent the ME you might also prevent that other condition from over taking their lives too. What happens when what must be done also might handicap the persons quality of life greatly anyways while keeping both at bay? I can relate to being in that boat myself. A big part of the problem with controlling ME is also controlling the individuals quality of life too on top of the individual factors that are already the first issue in the way.

 

[Oliver3]

Certainly. I can't rule out that mitochondrial dysfunction in some small number of brain cells isn't the root cause of ME, but that's hard to verify, and would unlikely show up on blood or CSF tests.

There you go...we agree. It's mitochondrial.
Ignoring the huge swathe of data that opposing your ' it's all in the brain ' assertion is just poor form.
It may represent that way in you.
But understand, your experience us such an outlier .
I still haven't heard a cogent theory from you. And I'm OK with leaving it at that. If you come up with smthg truly persuasive, I will of course listen.
I feel like you've provided no ideas but a robot analogy. That's not good enough.
Meanwhile , I abd others have provided you with loads of data.
Have you looked at all at naviauxs work.
Mitochondria ate at the heart of many illnesses. We can go into those if you want. But please bring some substance to your very basic idea otherwise what's the point

 

[Oliver3]

I don't think either of you (Oliver and Wishful) are wrong, this is multi systemic and phenotype based. Olivers finding upon looking at the demographics in which this occurs appear to be right on the money. THOUGH I have also noticed through what I've done so far how physically local symptom control can be. No combination of biomarkers so far has led to anything certain that immediately goes "ah this specifically causes the ME to occur", we really only have a bunch of links to clusters of people that often get it. Often this gets more difficult because we also only have our own experiences paired with this research to go off of. So often you'll have one person with experiences that strongly support their hypothesis and then you'll have someone with vastly different one's with a different PEM presentation that runs right up against it. I think it's best to look at the intersections more closely and work from there with individuals based on how they're responding to get more progress. This condition appears to be so individual with common overlaps that the problem is that with getting anywhere with it. Another big issue is the environment which everyone with it has issues with that appears to just get worse and worse as years go by. More pollution, worse food, higher ambient radiation, and much more environmental stress from the general state of the world.

I think what we need to most is more specific phenotype identification, it almost seems like the only way. The walls we'll run into here though is do we even have the technology to find this out and tailor prevention to the individuals life before they get the most severe complications from the condition? Is it something that can be analyzed by just looking at something in the child early on and starting the prevention protocol where if they follow it they'll be able to enjoy a more normal life so as long as they avoid this, that, and something else? Since ME is so comorbid with so many things, this is where it gets really messy. If you prevent the ME, this person is still going to have this or that chronic health issue. But in doing something to prevent the ME you might also prevent that other condition from over taking their lives too. What happens when what must be done also might handicap the persons quality of life greatly anyways while keeping both at bay? I can relate to being in that boat myself. A big part of the problem with controlling ME is also controlling the individuals quality of life too on top of the individual factors that are already the first issue in the way.

I agree with the general gist of what you say. This is the thing. Say in autism, or heart disease, we see different expressions of illnesses. Breast cancer is the same. I think it's nine distinct illnesses.
But the fact that wishful wants to ignore vast swathes if evidence is plain ignorant

 

[Oliver3]

I consider that plausible. I think it's unlikely the core dysfunction, since many people don't seem to have significant hypoperfusion.

I skimmed the paper. First flaw: Fukuda criteria. Second flaw: measurements via questionnaires. Third flaw: healthy controls, rather than limited physical activity lifestyle controls. Maybe that hypoperfusion is common in sedentary people? It doesn't convince me that 90% of PWME suffer from significant hypoperfusion or that it's a cause of many symptoms for 90% of PWME. I can accept that it may play a role in severity of some symptoms in some PWME.

Hypodusion is common in autism . It's postulated by man as a response to ecogenic factors, I e. Poisons in the environment, coming into contact with a sensitive. I.e. connective tissue disordered invidual. It's likely a response in autism at least to try and prevent inflammation in the brain.
To repeat. It's not solely a brain disease. In the same way most disease is an interplay between several factors.

Have you considered autism wishful. Many of us with m.e have high functioning traits

 

[Oliver3]

That's leaping to a conclusion based on too little evidence. If cumin's effect on me were due to anti-inflammatory properties, then other anti-inflammatories should have had similar effects, but didn't. I simply accept that it was due to an unknown interaction between cuminaldehyde and some cells in my body.

You do a lit if that. See how annoying it is