Learner1
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I'm taking 200mg a day as a part of this product by Paul Stamets, the world's foremost authority on mushrooms.
Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, Paper Pub. 4/1/20 - Dr. Prusty
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godlovesatrier
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Don't forget, reishi, shitakki, maitakki are all extremely high in amino acids. I take the following when I need to PEM buffer, usually 2 capsules 3x a day.
https://www.naturisimo.com/products...Pa19Zftm1HtpJ6Gc6WR5f9mSlRvtLkORoCVHoQAvD_BwE
I've been taking this for 2 years now. Most of these mushrooms do not increase testosterone, which is perfect for me as lot of adaptogens do increase T - which ultimately makes me angry.
But I notice that all adaptogens including mushroom complexes will cause anxiety, insomnia, restlesslness, increased hunger, etc.
https://www.naturisimo.com/products...Pa19Zftm1HtpJ6Gc6WR5f9mSlRvtLkORoCVHoQAvD_BwE
I've been taking this for 2 years now. Most of these mushrooms do not increase testosterone, which is perfect for me as lot of adaptogens do increase T - which ultimately makes me angry.
But I notice that all adaptogens including mushroom complexes will cause anxiety, insomnia, restlesslness, increased hunger, etc.
Learner1
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ME/CFS patients tend to be depleted in certain amino acids. I am female and take testosterone, which has greatly helped. Adaptogens have caused me no issues as you describe.
This speaks to working with a knowledgeable doctor and having lab testing that identifies ones individual needs, rather than following someone else's formula.
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godlovesatrier
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On the contrary many Phoenix rising members will tell you how bad adaptogens were for them. Too many people have told me as much. I would say for 60% they don't help. But for me they've been pretty instrumental when I'm in a bar way.
It just goes to the heart of the research in this thread. What are we identifying? One type of ME? If so which one and how do we diagnose it? It's frustrating to have a disease made up of so many damn misdiagnoses and potential subsets.
It just goes to the heart of the research in this thread. What are we identifying? One type of ME? If so which one and how do we diagnose it? It's frustrating to have a disease made up of so many damn misdiagnoses and potential subsets.
Learner1
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Exactly. That's why we need individualized diagnostics and treatment vs a one size fits all cure. It is possible to do an awfully lot with the tools that exist today, rather than waiting for the "Holy Grail."
Learner1
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Just a thought here. I've been seeing journal articles implicating ceramides, sphingolipids etc. in cellular communication, mitochondrial function, and in interaction with the microbiome.
Seems like they should be considered in looking at all of this...
From the conclusions of Naviaux's metabolomics study:
"Pathway abnormalities included sphingolipid, phospholipid, purine, cholesterol, microbiome, pyrroline-5-carboxylate, riboflavin, branch chain amino acid, peroxisomal, and mitochondrial metabolism."
https://www.hindawi.com/journals/mi/2016/9890141/
"However, there is a great need to investigate the role of sphingolipids as intermediates in the crosstalk between intestinal immunity and microorganisms. This review focuses on recent investigations that describe some mechanisms involved in the regulation of cytokine profiles by sphingolipids."
https://phys.org/news/2020-05-lysosome-mitochondria-longevity.html
"Unexpectedly, the scientists discovered that NFYB-1 steers the activity of mitochondria through another part of the cell called the lysosome, a place where basic molecules are broken down and recycled as nutrients. "We think the lysosome talks with the mitochondria through special fats called cardiolipins and ceramides, which are essential to mitochondrial activity," says Max Planck Director, Adam Antebi, whose laboratory spearheaded the study. Remarkably, simply feeding the NFYB-1 mutant worms cardiolipin restored mitochondrial function and worm health in these strains.
Because cardiolipins and ceramides are also essential for human mitochondria, this may mean human health and aging can be improved by understanding on how such molecules facilitate communication between different parts of the cell."
https://link.springer.com/article/10.1007/s00018-007-7076-0
"We end with a discussion of sphingolipids and glycosphingolipids in the etiology and pathology of a number of diseases, such as cancer, immunity, cystic fibrosis, emphysema, diabetes, and sepsis, areas in which sphingolipids are beginning to take a central position, even though many of the details remain to be elucidated."
Seems like they should be considered in looking at all of this...
From the conclusions of Naviaux's metabolomics study:
"Pathway abnormalities included sphingolipid, phospholipid, purine, cholesterol, microbiome, pyrroline-5-carboxylate, riboflavin, branch chain amino acid, peroxisomal, and mitochondrial metabolism."
https://www.hindawi.com/journals/mi/2016/9890141/
"However, there is a great need to investigate the role of sphingolipids as intermediates in the crosstalk between intestinal immunity and microorganisms. This review focuses on recent investigations that describe some mechanisms involved in the regulation of cytokine profiles by sphingolipids."
https://phys.org/news/2020-05-lysosome-mitochondria-longevity.html
"Unexpectedly, the scientists discovered that NFYB-1 steers the activity of mitochondria through another part of the cell called the lysosome, a place where basic molecules are broken down and recycled as nutrients. "We think the lysosome talks with the mitochondria through special fats called cardiolipins and ceramides, which are essential to mitochondrial activity," says Max Planck Director, Adam Antebi, whose laboratory spearheaded the study. Remarkably, simply feeding the NFYB-1 mutant worms cardiolipin restored mitochondrial function and worm health in these strains.
Because cardiolipins and ceramides are also essential for human mitochondria, this may mean human health and aging can be improved by understanding on how such molecules facilitate communication between different parts of the cell."
https://link.springer.com/article/10.1007/s00018-007-7076-0
"We end with a discussion of sphingolipids and glycosphingolipids in the etiology and pathology of a number of diseases, such as cancer, immunity, cystic fibrosis, emphysema, diabetes, and sepsis, areas in which sphingolipids are beginning to take a central position, even though many of the details remain to be elucidated."
Metabolomic results from our virus reactivation assays are helping us now to tailor design a few drugs & to try them. Trying to conceptualize an RNA-based therapy. Trying to make the diagnostics cost- and time-effective and to cover a few unsolved questions.
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I looked into what RNA-based therapies are and it's a class of drugs that includes "inhibitors of mRNA translation (antisense)," and also RNAi gene therapy which silences mRNAs. So, basically I think the "something in the blood," if it exists, is an mRNA or a group of mRNAs that are secreted by HHV6 and other viruses.
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If I'm not mistaken, there are MANY mRNAs for HHV-6 alone. I think it's at least from U1-U100.
Here is a list
https://hhv-6foundation.org/research/genes-proteins
It will be interesting to know what are the common mRNAs between HHV-6, EBV and other herpes viruses.
https://hhv-6foundation.org/research/genes-proteins
It will be interesting to know what are the common mRNAs between HHV-6, EBV and other herpes viruses.
No new drugs will take a lot of time. We are focusing on drugs which are already available and are either FDA approved or are under different stages of clinical trial for other purposes.
In fact we are actually testing some new metabolites as drugs also.
Hoosierfans
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@raghav do you know what meds they are looking at? My doc is super interested as we just did some testing and it is show a hypometabolism issue w my mitos caused by a (yet to be determined) infection.
@Hoosierfans I too would love to know what he is testing, but he has not revealed it to me.
I have a question for all ME/CFS patients. Have you ever tested Eosinophil cationic protein (ECP) levels in your blood? If yes, can you share the values in this format. Severity of the disease:ECP values. Please also mention selection criteria for ME/CFS. Also can be sent by DM.
I do not know if this is a biomarker or not. I have certain hypothesis and I would like your help in justifying it or rejecting it.
yes, like hemoglobin counts, platelet counts, blood sedimentation rate, CRP values.
Please share this with other patients who are not in Twitter
Dissemination of knowledge is crucial. But I am wondering how to communicate key research findings to the patient community without damaging the scientific career which is already at a stake
From Google
What does high eosinophil cationic protein mean?
BACKGROUND: Eosinophil cationic protein (ECP) is a potent cytotoxic secretory protein with bactericidal and antiviral properties. ECP is released by activated eosinophils and regarded as a marker of eosinophilic inflammation. High levels of ECP have been reported in cases of active asthma and other allergic diseases.
PROINFLAMMATORY ROLE OF EOSINOPHILS IN EGID
The eosinophil cationic proteins major basic protein (MBP), eosinophil peroxidase (EPO), and eosinophil cationic protein (ECP) are cytotoxic to epithelium at concentrations similar to those found in biological fluids from patients with eosinophilia.
What does high eosinophil cationic protein mean?
BACKGROUND: Eosinophil cationic protein (ECP) is a potent cytotoxic secretory protein with bactericidal and antiviral properties. ECP is released by activated eosinophils and regarded as a marker of eosinophilic inflammation. High levels of ECP have been reported in cases of active asthma and other allergic diseases.
PROINFLAMMATORY ROLE OF EOSINOPHILS IN EGID
The eosinophil cationic proteins major basic protein (MBP), eosinophil peroxidase (EPO), and eosinophil cationic protein (ECP) are cytotoxic to epithelium at concentrations similar to those found in biological fluids from patients with eosinophilia.
https://www.labcorp.com/tests/004180/eosinophil-cationic-protein-ecp
Eosinophils are effector cells that play a role in allergic and nonallergic inflammation.1,2 The most prominent feature of these cells is large cytoplasmic granules, each containing four basic proteins, the most plentiful of which is eosinophil cationic protein (ECP).3 ECP is a protein with ribonuclease activity that is released during eosinophil activation. While the full physiologic role of ECP has not been completely defined, this protein has been attributed with cytotoxic, neurotoxic, fibrosis-promoting, and immune-regulatory functions.1,3,4 Studies suggest that ECP may play a role in regulating mucosal and immune cells and may directly fight parasitic, bacterial, and viral infections.3
ECP is often elevated in diseases in which an eosinophil-mediated tissue inflammation plays a role.1,3,5 Measuring ECP levels has been used to evaluate eosinophil-mediated allergic inflammation, asthma, and rhinitis.1 Levels can be increased during both seasonal and perennial rhinitis1,6 and may reflect current allergen exposure.1,6 In atopic dermatitis, ECP has been shown to correlate with the symptoms and total clinical score.7
Eosinophilic inflammation is a relatively common feature of asthma.4,6,8-10 Although not diagnostic for asthma, elevated ECP levels are thought to reflect the degree of asthma-related bronchial eosinophilic inflammation.6,11 Increased ECP levels correspond to symptom onset and can precede bronchial hyper-reactivity.1,4 ECP has been used to assess asthma severity and support the management of anti-inflammatory therapy.5,11,12 It should be noted, however, that ECP is better correlated to symptom score than to lung function parameters, especially in children with mild and moderate asthma.6
ECP levels can be increased in a number of gastrointestinal disorders, including eosinophil intestinal diseases (esophagitis, gastroenteritis, and colitis), gastrointestinal food allergy, and intestinal parasitoses.1 ECP levels can also be increased in non−IgE-mediated conditions, including nonallergic asthma with aspirin intolerance, respiratory infections, sinonasal polyposis, and idiopathic hypereosinophilia (HES) syndrome.1,3 ECP has also been used as a disease activity marker in Churg-Strauss syndrome (CSS), a condition that is also known as allergic granulomatosis or allergic angiitis.13 CSS is a disorder marked by blood vessel inflammation that can restrict blood flow to vital organs and tissues, sometimes permanently damaging them.1,12 In a recent study, Niccoli and coworkers showed that ECP levels independently predicted the severity of coronary artery disease in patients with angina.14
Eosinophils are effector cells that play a role in allergic and nonallergic inflammation.1,2 The most prominent feature of these cells is large cytoplasmic granules, each containing four basic proteins, the most plentiful of which is eosinophil cationic protein (ECP).3 ECP is a protein with ribonuclease activity that is released during eosinophil activation. While the full physiologic role of ECP has not been completely defined, this protein has been attributed with cytotoxic, neurotoxic, fibrosis-promoting, and immune-regulatory functions.1,3,4 Studies suggest that ECP may play a role in regulating mucosal and immune cells and may directly fight parasitic, bacterial, and viral infections.3
ECP is often elevated in diseases in which an eosinophil-mediated tissue inflammation plays a role.1,3,5 Measuring ECP levels has been used to evaluate eosinophil-mediated allergic inflammation, asthma, and rhinitis.1 Levels can be increased during both seasonal and perennial rhinitis1,6 and may reflect current allergen exposure.1,6 In atopic dermatitis, ECP has been shown to correlate with the symptoms and total clinical score.7
Eosinophilic inflammation is a relatively common feature of asthma.4,6,8-10 Although not diagnostic for asthma, elevated ECP levels are thought to reflect the degree of asthma-related bronchial eosinophilic inflammation.6,11 Increased ECP levels correspond to symptom onset and can precede bronchial hyper-reactivity.1,4 ECP has been used to assess asthma severity and support the management of anti-inflammatory therapy.5,11,12 It should be noted, however, that ECP is better correlated to symptom score than to lung function parameters, especially in children with mild and moderate asthma.6
ECP levels can be increased in a number of gastrointestinal disorders, including eosinophil intestinal diseases (esophagitis, gastroenteritis, and colitis), gastrointestinal food allergy, and intestinal parasitoses.1 ECP levels can also be increased in non−IgE-mediated conditions, including nonallergic asthma with aspirin intolerance, respiratory infections, sinonasal polyposis, and idiopathic hypereosinophilia (HES) syndrome.1,3 ECP has also been used as a disease activity marker in Churg-Strauss syndrome (CSS), a condition that is also known as allergic granulomatosis or allergic angiitis.13 CSS is a disorder marked by blood vessel inflammation that can restrict blood flow to vital organs and tissues, sometimes permanently damaging them.1,12 In a recent study, Niccoli and coworkers showed that ECP levels independently predicted the severity of coronary artery disease in patients with angina.14
Learner1
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Says it's experimental. Any way insurance would cover this? What ICD10 code myst we have to justify running it? Or, how much is the cash price?
Learner1
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After bring surprised by high list prices if insurance bounces a LabCorp test, I've learned the hard way this is an important question to know the answer to...
