wigglethemouse
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According to LabCorp explanation It seems like it is involved in gastrointestinal inflammation.....
Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, Paper Pub. 4/1/20 - Dr. Prusty
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stefanosstef
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I will try to do this ECP testing.I've already sent an email in a lab in my country to ask for prices.
Needless to say that my former psychiatrist, a top expert and with huge knowledge and experience in brain and psychopharmacology, called Prusty's paper a classic scientific junk
.More info about this psychiatrist can be found in my journal.
I disagree with him in many things.It's unfortunate that a scientist with such expertise has ego issues and is so closed minded.
What was that test that showed hypometabolism by mitochondria?
Needless to say that my former psychiatrist, a top expert and with huge knowledge and experience in brain and psychopharmacology, called Prusty's paper a classic scientific junk
.More info about this psychiatrist can be found in my journal.I disagree with him in many things.It's unfortunate that a scientist with such expertise has ego issues and is so closed minded.
What was that test that showed hypometabolism by mitochondria?
@stefanosstef well thats quite normal as i learned now from another forum. Doctors calling work from others junk and later admitting they didn't even read it. I mean if 100 doctor make a hypothesis about a disease, 99 will be wrong. So if you just call everything scientific junk you will be right 99% of the time and look like a genius without contributing anything of worth. No one knows whats right or wrong but Prusty is at least trying with his whole heart.
stefanosstef
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I very much agree.That was what I had in mind exactly but I hadn't realized it.But I have a strong instinct that this hypothesis will be proven correct.I hope so, I have taken this personally.
Hoosierfans
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I will try to do this ECP testing.I've already sent an email in a lab in my country to ask for prices.
Needless to say that my former psychiatrist, a top expert and with huge knowledge and experience in brain and psychopharmacology, called Prusty's paper a classic scientific junk
I disagree with him in many things.It's unfortunate that a scientist with such expertise has ego issues and is so closed minded.
What was that test that showed hypometabolism by mitochondria?
It is the GENIE test, created by Richie Shoemaker (CIRS expert) and his cohorts. It looks at certain genes and whether they are upregulated or downregulated. For me it showed that my cells cannot use glucose very well — it is sitting on the outside of my cells and causing a form of insulin resistence and it is then affecting my mitos since they dont have fuel to run on. And, the infections are blocking my electron transport chain.
https://www.survivingmold.com/treat...pression-inflammation-explained-now-available
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It's not really fair to call it junk. I mean after all, we know what kind of junk psychiatrists have produced especially in the field of ME/CFS.
I'm not sure what to make of that test and Shoemakers work. He says that he has "targeted therapies based on our published, peer-reviewed work." But I don't see how any of his treatments, like Cholestyramine, are going to have an effect on gene expression. Do you mind showing us the results of your test with all the private info blacked out?
@MonkeyMan Thanks for this link
Eosinophil cationic protein serum levels and allergy in chronic fatigue syndrome
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1398-9995.1996.tb04570.x
Abstract
Chronic fatigue syndrome (CFS) is a syndrome of uncertain etiopathogenesis characterized by disabling fatigue associated with a variable number of somatic and/or neuropsychologic symptoms. In patients with CFS, several immunologic abnormalities can be detected, including a higher prevalence of allergy. The aim of this study was to determine whether CFS patients, well studied for their allergy profile, show signs of eosinophil activation, as detectable by the measurement in serum of eosinophil cationic protein (ECP) levels. In 35 consecutive CFS outpatients (diagnosis based on the Centers for Disease Control case definition), ECP was measured in serum by a competitive enzyme immunoassay (ECP‐FEIA kit, Kabi Pharmacia Diagnostics, Uppsala, Sweden). Fourteen disease‐free subjects with no history of CFS or allergy were selected as controls. ECP serum levels were significantly higher in CFS patients than in controls (18.0 ±11.3 μg/l vs 7.3 ± 2.1 pg/1; P<0.01). In the CFS population, the prevalence of RAST positivity to one or more allergens was 77%, while no control showed positive RAST. Twelve of the 14 CFS patients with increased ECP serum levels were RAST‐positive. However, CFS RAST‐positive patients had no significantly higher ECP serum levels than CFS RAST‐negative patients (19.3 ± 12.4 μg/l vs 13.6 ± 3.7 μg,/1; P = 0.4). This is the first report of increased serum levels of ECP in CFS. On the basis of the available data, it is discussed whether eosinophil activation has a pathogenetic role in CFS or is linked to the frequently associated allergic condition, or, finally, whether a common immunologic background may exist for both atopy and CFS.
Eosinophil cationic protein serum levels and allergy in chronic fatigue syndrome
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1398-9995.1996.tb04570.x
Abstract
Chronic fatigue syndrome (CFS) is a syndrome of uncertain etiopathogenesis characterized by disabling fatigue associated with a variable number of somatic and/or neuropsychologic symptoms. In patients with CFS, several immunologic abnormalities can be detected, including a higher prevalence of allergy. The aim of this study was to determine whether CFS patients, well studied for their allergy profile, show signs of eosinophil activation, as detectable by the measurement in serum of eosinophil cationic protein (ECP) levels. In 35 consecutive CFS outpatients (diagnosis based on the Centers for Disease Control case definition), ECP was measured in serum by a competitive enzyme immunoassay (ECP‐FEIA kit, Kabi Pharmacia Diagnostics, Uppsala, Sweden). Fourteen disease‐free subjects with no history of CFS or allergy were selected as controls. ECP serum levels were significantly higher in CFS patients than in controls (18.0 ±11.3 μg/l vs 7.3 ± 2.1 pg/1; P<0.01). In the CFS population, the prevalence of RAST positivity to one or more allergens was 77%, while no control showed positive RAST. Twelve of the 14 CFS patients with increased ECP serum levels were RAST‐positive. However, CFS RAST‐positive patients had no significantly higher ECP serum levels than CFS RAST‐negative patients (19.3 ± 12.4 μg/l vs 13.6 ± 3.7 μg,/1; P = 0.4). This is the first report of increased serum levels of ECP in CFS. On the basis of the available data, it is discussed whether eosinophil activation has a pathogenetic role in CFS or is linked to the frequently associated allergic condition, or, finally, whether a common immunologic background may exist for both atopy and CFS.
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stefanosstef
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If I'm reading this correctly it means that 14 out of 35 CFS patients had elevated ECP?If that is the case, individual testing wouldn't give any answers, meaning that this can't be considered a biomarker.
mariovitali
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I posted a a finding to Bhupesh. The software i use identified a connection of NLRP3 (Inflammasome) with eosinophils but also with Mitochondrial fusion / fission, mitochondrial ROS and many more concepts possibly related to ME. He replied as "very interesting" so let's hope he may get some further ideas out of this.
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I looked at the paper you mentioned in the tweet and it mentions that extracellular ATP triggers and maintains allergic inflammation. That's interesting since that connects Naviaux's theory about purinergic signaling to ECP. If it's true that some patients might have elevated ECP then maybe Suramin might help since it inhibits P2 receptor signaling... Maybe this is of note to Prusty since he's working with Naviaux.
After a long thought, I would like to define ME/CFS like this.
ME/CFS is a state of infection-mediated immune dysfunction that begins as a very simple malfunction of the innate immune system which starts safeguarding the body way too much than what it should be doing.
If this initial phase is not handled carefully and wisely, the body starts accumulating other molecular and biochemical dysfunctions leading to varying amounts of secondary physical defects including neurological damages. Innate immune sensing of mitochondria and subsequent metabolic changes play a key role during the accumulation of secondary molecular dysfunctions.
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Thank you Bhupesh. Does this indicate that any cure after a number of years untreated is improbable, probably impossible? It has become irreversible?
No, it's actually opposite. There should be a cure.
No, it's actually opposite. There should be a cure.
Learner1
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Brilliant! Can someone ask him to put in a font that's readable by ME/CFS patients?
This is interesting to me, as my ME/CFS was triggered by my cancer treatment, a significant car accident, and the tragic death spiral of my sibling. The viruses and bacterial infections I had came years before, but rose up again when my body wasn't able to fight.
So, it seems there's more than one route into this disease.
As for the cure, the devil is in the details. It would depend upon which secondary defects and metabolic changes occur. From my experience, these seem to have a cascading effect, where one change/defect leads to others, which, in turn, lead to still others. And so on.
Even if one fixes the problem with the innate immune system, unrolling all of the multiplied changes/defects might not be straightforward. There are no doctors with expertise in mitochondria and metabolism for acquired mitochondrial or metabolic pathologies - I've looked. There are endocrinologists but they are extremely limited in scope. And all of the major mito specialists, who are very few, deal mainly with children with genetic mito diseases and are impossible to get into if one doesn't have a lot of data, preferably genetic and a muscle biopsy.
Functional medicine, looking at the body as a system of interrelated systems, offers the most hope, but resources there are pretty rare in most areas.
This is interesting to me, as my ME/CFS was triggered by my cancer treatment, a significant car accident, and the tragic death spiral of my sibling. The viruses and bacterial infections I had came years before, but rose up again when my body wasn't able to fight.
So, it seems there's more than one route into this disease.
As for the cure, the devil is in the details. It would depend upon which secondary defects and metabolic changes occur. From my experience, these seem to have a cascading effect, where one change/defect leads to others, which, in turn, lead to still others. And so on.
Even if one fixes the problem with the innate immune system, unrolling all of the multiplied changes/defects might not be straightforward. There are no doctors with expertise in mitochondria and metabolism for acquired mitochondrial or metabolic pathologies - I've looked. There are endocrinologists but they are extremely limited in scope. And all of the major mito specialists, who are very few, deal mainly with children with genetic mito diseases and are impossible to get into if one doesn't have a lot of data, preferably genetic and a muscle biopsy.
Functional medicine, looking at the body as a system of interrelated systems, offers the most hope, but resources there are pretty rare in most areas.
wigglethemouse
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Same virus but different pathophysiology: If active HHV-6 infection reaches brain and cause acute localized damage, it might cause neurological problems overnight. But when it reactivates slowly (chronically) it might cause Alzheimer's, dementia, mood disorders, even CFS.
Same HHV-6 if reactivates in heart muscles can cause cardiomyopathy. If it reactivates in liver, it causes liver failure. Under some other reactivation conditions, it can even be lethal. Same HHV-6 if reactivates in immune cells can cause immune dysfunction.
This is just one example. Damage to neuronal cells will have a different clinical presentation in comparison to muscle cells or immune cells. Hypometabolic damage and mitochondrial damage will remain the same under both the conditions.
Murph
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tbh I'm not in love with people defining a disease before the research is finished. Making hypotheses is great, but definitions? They seem a bit definitive and that's dangerous if it closes you off to thinking about other options.
knackers323
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When are we expecting the next bit of news regarding Prustys research?
same action in covid-19, maybe it gets a lot of founding now.
godlovesatrier
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So covid not only persists in some patients but wreaks mitochondrial havoc. Brilliant. As you say could be a good thing if they defined a mito link and those of us who are in that ME subset who are not misdiagnosed with ME might get some relief. It seems to evade the immune system so well. No wonder it can cause such long term damage. You would need a naturally strong immune system to keep covid in check I think.
Treeman
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Saw a video on youtube of Prusty saying their looking at drugs that they know repair mitochondria. Anyone know these drugs?