Myalgic Encephalomyelitis is clear to see in the blood

[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

Why would you expect me to have a cogent theory for the cause of ME? I don't have a medical science background. Even the world experts in that area don't have a solid, completely detailed theory. If someone did, it would be possible to test it. The existing theories aren't detailed enough to test that way. Is "cell danger response" understood well enough to actually test, or are there still too many unknowns complicating testing?

Not having my own detailed theory doesn't mean I can't point out flaws or weaknesses in other theories. If a theory involves mitochondrial dysfunction but the available data doesn't show the predicted signs at the magnitude required to explain the symptoms, then to me it's a poorly supported theory.

Because you have no ideas abd just criticuse everything with zero ability to do so

 

[Oliver3]

Was this question directed to me?

About three years ago, I felt this hard something on my jaw: that felt odd. I wondered if something was on my bone? While at my GP, he felt it and said Parotid gland, and I should get it checked out. My daughter was around, so I needed to be a grown up, so I went to the ENT across the street. I agreed to get a biopsy.

So this lead to a diagnosis of Low Grade b-cell Non Hodgkins lymphoma. Some weird cells. I got a consult with UCLA oncologist. Did a Pet Scan. I had some "busy" lymph glands etc.

But there is no reason to treat it, unless symptoms arise. The "hard thing" I felt, went away. My GP told me if I just got out of all this stress and into a hammock I'd be well.

So I'm in the hammock now. Tell things to flow and stop acting up.

Yes sorry, good news in its own way

 

[Oliver3]

Why would you expect me to have a cogent theory for the cause of ME? I don't have a medical science background. Even the world experts in that area don't have a solid, completely detailed theory. If someone did, it would be possible to test it. The existing theories aren't detailed enough to test that way. Is "cell danger response" understood well enough to actually test, or are there still too many unknowns complicating testing?

Not having my own detailed theory doesn't mean I can't point out flaws or weaknesses in other theories. If a theory involves mitochondrial dysfunction but the available data doesn't show the predicted signs at the magnitude required to explain the symptoms, then to me it's a poorly supported theory.

Cell danger response has been proved in theory with the use of suramin. Are you aware of the trial. Or read or watched his lectures. The guy is a bonified expert

 

[Oliver3]

The Stanford work is interesting, and I think it can lead to actual treatments, someday. I don't think it will be a simple path to a treatment, since mechanisms such as that are probably used in multiple ways in the body, so a pill that boosts muscle vigor might also boost cancer cell vigor, or harden capillaries, or some other such unexpected side effects.

Pure negative speculation.
Of course there will be side effects. Both good n bad. Mitochondria are implicated in loads of diseases. To not recognise that is just silly.
Restoring mitochondrial integrity is gonna be a key element to treatment m.e, a disease based on energy production

 

[Oliver3]

Why would you expect me to have a cogent theory for the cause of ME? I don't have a medical science background. Even the world experts in that area don't have a solid, completely detailed theory. If someone did, it would be possible to test it. The existing theories aren't detailed enough to test that way. Is "cell danger response" understood well enough to actually test, or are there still too many unknowns complicating testing?

Not having my own detailed theory doesn't mean I can't point out flaws or weaknesses in other theories. If a theory involves mitochondrial dysfunction but the available data doesn't show the predicted signs at the magnitude required to explain the symptoms, then to me it's a poorly supported theory.

https://annals-general-psychiatry.biomedcentral.com/articles/10.1186/s12991-023-00477-8

 

[NameHere]

That’s a great question. While few studies in ME/CFS have used zonulin or lactulose/mannitol testing to assess gut permeability before and after treatment, one longitudinal study stands out for its use of multiple immune biomarkers of bacterial translocation.

Maes & Leunis (2008) evaluated ME/CFS patients with signs of gut-derived immune activation. They measured:

• IgA and IgM antibodies to LPS (lipopolysaccharides from gram-negative bacteria)
• LBP (lipopolysaccharide-binding protein)
• sCD14 (a soluble receptor involved in LPS signaling)

Patients received a comprehensive treatment targeting leaky gut, which included:

• Antioxidants (e.g., glutamine, N-acetylcysteine)
• Anti-inflammatory nutrients and omega-3 fatty acids
• Dietary modifications to reduce gut inflammation
• Probiotic and immunomodulatory support

After this intervention, the study reported:

• Significant decreases in all three biomarkers (IgA/IgM to LPS, LBP, sCD14)
• Marked clinical improvements in fatigue, cognitive function, and overall symptoms
• A strong correlation between biomarker normalization and symptom relief

Maes, M., & Leunis, J.-C. (2008). Normalization of leaky gut in chronic fatigue syndrome is accompanied by a clinical improvement in symptoms. Neuro Endocrinol Lett, 29(6), 902–910.
PMID: 19112401

This is one of the few ME/CFS studies to show objective improvements in gut barrier function alongside symptom reduction, using pre/post immune biomarkers related to bacterial translocation.

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.

 

[Violeta]

You're right that it's important to question methodology — and Van Campen et al. (2020) isn’t perfect. But I’d argue it still offers valuable insight for several reasons:

1. Fukuda vs. stricter criteria: True, Fukuda is broad, but this cohort came from a specialized ME/CFS clinic, with patients averaging ~7 years of illness. While not formally diagnosed with CCC or ICC, these weren’t generic fatigue cases.
2. Objective measurements: The main outcome — ≥13% reduction in cerebral blood flow (CBF) during tilt — was assessed via extracranial Doppler, not questionnaires. This is objective, quantifiable physiology, not self-report.
3. Control group: Yes, healthy controls aren't ideal — lifestyle-matched controls would be better. But even sedentary individuals without ME/CFS typically don’t experience PEM, cognitive dysfunction, or marked orthostatic intolerance. The pattern in ME/CFS appears qualitatively distinct.
4. Key finding:
   • 86% of ME/CFS patients showed a significant drop in CBF during tilt, even without meeting criteria for POTS or orthostatic hypotension.
   • If you include milder cases (≥10% CBF reduction), around 90% showed cerebral hypoperfusion.
   • Importantly, 58% of patients showed no heart rate or blood pressure abnormalities, yet 82% of them still had reduced cerebral blood flow.
5. Striking contrast with controls:
   • Healthy controls had only a 7% average reduction in CBF during tilt.
   • In contrast, ME/CFS patients had a 26% average reduction — a nearly fourfold difference, highlighting a robust and disease-specific physiological abnormality.

So while cerebral hypoperfusion might not be the root cause for everyone, it appears to be a widespread and measurable downstream dysfunction that may contribute significantly to cognitive symptoms, fatigue, and orthostatic intolerance — even in patients who look "normal" on standard tilt test metrics.

https://fatigacronica.es/prueba-mesa-basculante-tilt-test-diagnostico-sfc-em/

Ginkgo biloba for hypoperfusion.

Ginkgo biloba L. extract protects against chronic cerebral hypoperfusion by modulating neuroinflammation and the cholinergic system​

https://pubmed.ncbi.nlm.nih.gov/27765355/​

In the present study, we sought to determine the effects of GBE on CCH-induced neuroinflammation and cholinergic dysfunction in a rat model of bilateral common carotid artery occlusion (BCCAo)

Carotid artery occlusion increased glial proliferation in the hippocampus and white matter, whereas proliferation was significantly attenuated by ginkgo biloba extract treatment. Ginkgo biloba also attenuated the carotid artery occlusion-related increases in the hippocampal expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6), TLR4, myeloid differentiation primary response gene 88, RAGE, Ang-II, and phosphorylated MAPKs (ERK, p38, and JNK). Furthermore, GBE treatment restored the choline acetyltransferase ( expression in the basal forebrain following carotid artery occlusion.

Conclusions: These findings suggest that ginkgo biloba extract has specific neuroprotective effects that may be useful for the treatment of chronic cerebral hypoperfusion. The pharmacological mechanism of GBE partly involves the modulation of inflammatory mediators and the cholinergic system.

 

[Oliver3]

https://www.gov.uk/government/publi...atigue-syndrome-mecfs-the-final-delivery-plan

 

[Oliver3]

Good news that the British medical system I'd starting to take m.e. seriously.
Also good to see that EDS is recognised as an overlapping condition.
( theyree still miles behind on that in my view but the fact they mentioned it at all shocked ne in a good way)

 

[Violeta]

@Gala, is it known what causes cerebral hypoperfusion?

I think I saw in one of your messages that you eat 70% fat, various animal protein, but not a lot. What do you eat besides that? I am having a hard time finding a diet that doesn't cause me problems. I may not be able to eat the eggs, fish, or meat, but I am curious what the other 30% of your diet consists of. Thank you.

 

[pamojja]

I think I saw in one of your messages that you eat 70% fat, various animal protein, but not a lot. What do you eat besides that?

That could also be me, how I initially changed from a 30 years vegetarian low-fat diet. In case it's me, 70% of calories from fat meant as kilocalories. 1g fat has 9 kcal, protein and carbs 4 kcal only. So 70% of calories actually is more like one third of the mass of one's diet.

In my case almost grain free, eat still lots of veggies, fermented too, and daily legumes, some fats come from a handful of nuts daily, ghee and coconut oil. Some fruits daily.

 

[Violeta]

I've been counting on grains as a last resort for calories, but it's not working. And even legumes cause me ammonia issues. I was having difficulty digesting cellulose, so vegetables weren't working, but that seems to have improved a little. I am almost to the point of trying meat again. The main thing holding me back is that I then smell awful and can't get the smell off my body. Too much information, but I am at the end of my rope.

I can eat A2 A2 dairy from a particular farm, but I don't know how much to rely on that.

I will try to work out something with the 70% calories from fat, more veggies, protein from A2A2 dairy, and a little bit of fruit. I will try to add some coconut oil, too.

Thank you for the feedback.

 

[pamojja]

I've been counting on grains as a last resort for calories, but it's not working.

I actually eat Tsampa only. Which is the main stable in Tibet and consists of roasted Barley flour. Traditionally mixed with buttered tea. I use it with vegetables boiling water. Or as cereal.

And even legumes cause me ammonia issues.

Maybe try to experiment with different kinds? There are so many. Same with veggies. There might some be with much less cellulose, and better tolerated.

I can eat A2 A2 dairy from a particular farm,

Not available to me, I usually use goat or sheep yogurt instead. Along with coconut water yogurt mainly.

If meat wouldn't work. As last resort, though terrible tasting, I would try an elemental diet first.

Best wishes.

 

[Wishful]

I was having difficulty digesting cellulose,

We're not supposed to digest cellulose. Ruminants and termites depend on microbes to break the bonds in cellulose, and I'm pretty sure humans don't support those microbes or provide the time required. I don't know whether cellulose has any significant effect on the human microbial environment, aside from how the intestinal contents move and mix.

Intolerance of fermentable dietary fibre is definitely possible. I went through that, and a probiotic capsule fixed it, so I must have somehow lost a critical strain.

 

[Wishful]

I am almost to the point of trying meat again.

FWIW, I stopped eating meat a few days ago (ran out, and can't drive for another 3 weeks), and I've started feeling lethargic again. I'll have to avoid the foods I added instead, to see whether it's something in those (soy sauce?) or the lack of something in meat.

I think it's good to change your diet occasionally, even trying things that caused (non-serious) problems before. My ME sensitivities have changed over time, and some foods have been okay, then a problem, then okay again, then a problem again.

 

[Wishful]

Restoring mitochondrial integrity is gonna be a key element to treatment m.e, a disease based on energy production

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.

 

[Oliver3]

Mitochondriahttps://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2022.945142/full

Mitochondria are part of the disease process in many illnesses.. look at the heart muscle here.
Did you read naviauxs stuff.
Did you look into how anti purigenic therapy restores mitochondrial function?
Smthg tells me no.

 

[Oliver3]

https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2023.1209890/full

Just anothercexample of mitochondria being an essential part of disease progression.
But hey, just ignore tye vast swathes of data eh?

 

[Oliver3]

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.

Hey look...eds abd mitochondrial dysfunction phenotype.

You also ignored the fact the British government is now recognising the crossover between eds abd m.e.
The fact is I could quote the myriad studies about mitochondrial dysfunction in all disease, the FACT that anti purigenic signalling restored mitochondrial function in autistic patients and naviaux says this is directly applicable to m.e.
Let's just ignore all that for your car analogy...at least it's changed from the robot one. Mixing it up a bit

 

[Oliver3]

https://pmc.ncbi.nlm.nih.gov/articles/PMC11854588/