Myalgic Encephalomyelitis is clear to see in the blood

[Dysfunkion]

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

So if I read that right what you're saying is you think there is nine different core illnesses at the heart of various conditions and that the conditions overlaying them can overlap and this is part of what creates the phenotypes? I hope I understood that all correctly.

 

[NameHere]

• Specific probiotics (e.g., Lactobacillus plantarum, Bifidobacterium longum, Akkermansia)
• Sodium butyrate or tributyrin to restore SCFA production
• Glutamine, zinc carnosine, quercetin, vitamin D to repair mucosal barriers
• Antimicrobial herbal therapy (when specific pathogens are detected)
• Personalized elimination diets (low-FODMAP, gluten-free, histamine-free…)
• Antifungal treatments (if Candida spp. overgrowth is present)

I talk about this topic in more detail in this article:
https://fatigacronica.es/alteraciones-digestivas-sfc-em/

Excellent article. I would be interested to know if there have been any studies showing before/after zonulin, or before/after lactulose-mannitol test, proving that these things increase intestinal barrier function. So far, I haven't found anything in my pubmed searches.

 

[Oliver3]

So if I read that right what you're saying is you think there is nine different core illnesses at the heart of various conditions and that the conditions overlaying them can overlap and this is part of what creates the phenotypes? I hope I understood that all correctly.

https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2023.1305972/full

I'm not saying it's 9 different illnesses. That's specific to breast cancer I believe but yes the same idea applies. The phenotypes in m.e. seem remarkably similar to conditions such as fibro., comorbid with autisn etc..like you say, depending how genes and epigenetics are expressed, these genes are expressed in certain ways to fit into certain phenotypes.

The rcccx theory covers this idea and I think it's correct. Ibs, migraine, intercranial hypertension. Brain profusion.. ut depends what and how these genes that are expressed that creates the phenotype such as tge or I posted I'm the study

 

[Oliver3]

I am NOT trying to be a Negative Nelly, but this was my takeaway from the original linked reference:



Am I missing something? (Please be gentle in your response, thank you.)

It's a very generic biomarker but it points to a system understress

 

[Oliver3]

https://news.stanford.edu/stories/2...to common diseases,, and cancer, among others

 

[Oliver3]

The above is very encouraging. More evidence that mitochondria plays a key role in many diseases. The fact they can be repaired gives me hope

 

[Oliver3]

https://www.mdpi.com/1467-3045/47/2/134

Link between connective tissue type and mitochondria.
Also to point out to wishful, not all tissue has to be eds. As its a spectrum disease, it may only say show up as ibs or mitral valve prolapse, or somewhere in the brain.
But that tissue type is prone to mitochondrial dysfunction

 

[Strawberry]

Did you get vasopressin level tested?

I’ll just chime in here. Dr Kaufman tested my vasopressin years ago and he said it was non existent. It seems that and NK cell function are good markers. I’m sure there are more.

I need to read more of this thread. Unsure what it means.

Editing to add after reading, hyper mobile…. So possible EDS.

 

[Oliver3]

I’ll just chime in here. Dr Kaufman tested my vasopressin years ago and he said it was non existent. It seems that and NK cell function are good markers. I’m sure there are more.

I need to read more of this thread. Unsure what it means.

Editing to add after reading, hyper mobile…. So possible EDS.

It's obviously extremely complex.
Heds especially is just determined through yhe beighton score primarily which is I think close to useless when you have borderline traits or atypical.
The connective tissue study I posted on intercranial hyoertension is so reminiscent of Jen breas experience. It's a new phenotype that wouldn't have fitted previous less sensitive anakysis
My feeling is. No eds traits. No m.e. .
In a way I hope I'm wrong because it is so complex but there's a hell of a loyof recent evidence I'm yhe last couple of years adding up to this.
That mitochondrial stand ford patent makes me hopeful .

 

[Rufous McKinney]

The above is very encouraging. More evidence that mitochondria plays a key role in many diseases. The fact they can be repaired gives me hope

Dr Prusty was looking at the fragmented mitochondria in us. I have heard very little from him in the last year, wonder what he is now doing?

I'm still trialing the Plasmalogens, which may be helping cell membranes generally. Which would help the mitochondria as well. The main noticeable effect is on my lymphatic system. But if that system is still dumping stored up toxins, then no wonder I still mostly feel lousy. But I can "see" directly, that swollen lymph nodes have improved.

 

[Oliver3]

I was wondering about him recently too funnily enough.
That's greatcyoure getting some results.
Thecstandford paper saying they've realised how to restore mitochondrial integrity is hopeful.
Seems like a lot of science is moving in that direction

 

[Rufous McKinney]

That's greatcyoure getting some results.

I was given two bottles of Blue Scorpion venom, from Cuba, by a family friend. It's a cancer cure.

But my NH Lymphoma diagnosis, is a Watch and Wait situation and I have no symptoms to track. So I won't be trying the venom. A friend poisoned the well, by making me afraid to try it, generally. Maybe it cures ME CFS?

 

[Oliver3]

Sheesh I have no idea about that.
So are you in remission so to speak?

 

[Gala]

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.

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/

 

[Gala]

Excellent article. I would be interested to know if there have been any studies showing before/after zonulin, or before/after lactulose-mannitol test, proving that these things increase intestinal barrier function. So far, I haven't found anything in my pubmed searches.

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.

 

[Wishful]

I still haven't heard a cogent theory from you.

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.

 

[Wishful]

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.

 

[Gala]

¿Por qué esperarías que tuviera una teoría convincente sobre la causa de la EM? No tengo formación en ciencias médicas. Ni siquiera los expertos mundiales en ese campo tienen una teoría sólida y completamente detallada. Si alguien la tuviera, sería posible comprobarla. Las teorías existentes no son lo suficientemente detalladas como para comprobarlo de esa manera. ¿Se comprende la "respuesta celular al peligro" lo suficientemente bien como para realmente comprobarla, o aún hay demasiadas incógnitas que complican las pruebas?

No tener una teoría detallada propia no significa que no pueda señalar las fallas o debilidades de otras teorías. Si una teoría implica disfunción mitocondrial, pero los datos disponibles no muestran los signos previstos con la magnitud necesaria para explicar los síntomas, entonces, para mí, es una teoría con poco fundamento.

Justo hoy publiqué una teoría unificadora sobre la EM/SFC, la COVID persistente y las enfermedades de fatiga postinfecciosa a lo largo de la historia. Como dije desde el principio, me parece mucho más simple y sensato que buscar nuevos virus o causas ocultas. La clave ahora es el orden en que se tratan los síntomas, y creo que empezar por restaurar la barrera intestinal y el endotelio es el mejor enfoque. Pero tendremos que seguir experimentando e investigando.


https://fatigacronica.es/sindrome-inmunovascular-progresivo-sip-em-sfc/

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Resumen de la teoría: “Síndrome inmunológico progresivo (SIP)”

Una nueva propuesta busca renombrar la Encefalomielitis Miálgica/Síndrome de Fatiga Crónica (EM/SFC) como "Síndrome Inmunológico Progresivo" (SIP). Define la enfermedad como una disfunción inmunitaria crónica y progresiva, desencadenada por una infección y caracterizada por activación inmunitaria persistente, reactivaciones virales y complicaciones vasculares y neurológicas.


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Evaluación de las principales reivindicaciones


Cambio de nombre de EM/SFC a PIS: no reconocido oficialmente; no utilizado en las guías clínicas (p. ej., NICE 2021)
Curso progresivo: EM/SFC puede empeorar en algunos casos, pero en otros se estabiliza o mejora; "progresivo" no es universalmente aplicable.
Disfunción inmunitaria (p. ej., adoquinas, desequilibrio Th1/Th2): cierta evidencia (p. ej., Hornig et al. 2015), pero los resultados son inconsistentes entre los estudios.
Disminución de la función de las células NK: moderadamente compatible; se observa en metanálisis, pero no es específico de EM/SFC
Reactivación viral (VEB, VHH-6): observada en algunos pacientes; no está vinculada de manera consistente como mecanismo causal.
Predisposiciones genéticas (p. ej., MTHFR, GST, PIEZO1): la mayoría de las asociaciones son especulativas o débiles; los GWAS grandes no encontraron genes fuertes de EM/SFC
Microcoágulos, hiperviscosidad sanguínea: hipótesis emergente (especialmente de la investigación sobre COVID prolongada); aún controvertida y no validada en EM/SFC
Pruebas de diagnóstico exhaustivas (citocinas, PCR viral, microbioma): no recomendadas por las pautas clínicas actuales; pueden generar pruebas excesivas y confusión.
Implicaciones terapéuticas (antivirales, inmunomoduladores, anticoagulantes)Experimental; la mayoría no validados por ensayos de alta calidad



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Resumen final

Algunos hallazgos (como la disminución de la actividad de las células NK o las firmas inmunes tempranas) están moderadamente respaldados.

Muchas otras afirmaciones (genética, microcoágulos, paneles de diagnóstico) no están probadas o son preliminares.

La teoría generaliza excesivamente al sugerir una progresión universal y la necesidad de cambiar el nombre de la enfermedad.

Utilice este marco como hipótesis de trabajo, pero compárelo siempre con el consenso científico y las pautas clínicas antes de sacar conclusiones o realizar pruebas costosas.

 

[Rufous McKinney]

So are you in remission so to speak?

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.

 

[Rufous McKinney]

So this lead to a diagnosis of Low Grade b-cell Non Hodgkins lymphoma.

To clarify, the test results indicated I did NOT HAVE some type of lymphoma related to EBV. I"m not really sure what all that means, frankly. I always figured the chronic EBV would get me somehow.