Dr. Ron Davis of Stanford - Research Update - Drug Screening. Video from Emerge Symposium March 2019, Australia

@mariovitali
A member on phoenix rising didnt report a negative outcome.
copaxone didnt change anything in 4-6 weeks. then it was stopped.
thats what i understand.

copaxone may be able to repair the myelin damage.
even if its hepatoxic, this may be the lesser problem.
 
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seems odd that nobody here has been treated with copaxone so far ?
who tried copaxone ?

with all this osmose stress, im wondering how IVs are being compensated...
should be generally a bad thing ?
 
roller* said:
@mariovitali
A member on phoenix rising didnt report a negative outcome.
copaxone didnt change anything in 4-6 weeks. then it was stopped.
thats what i understand.

copaxone may be able to repair the myelin damage.
even if its hepatoxic, this may be the lesser problem.
Click to expand...

From what i read from someone at Phoenix Rising he is severely fatigued, being able to eat only through the use of a tube. They cannot attribute this deterioration to Copaxone.

However, i find it alarming that someone got ME through the use of Fluoroquinolones which are also hepatotoxic :


https://livertox.nlm.nih.gov/Fluoroquinolones.htm

Here is the post mentioning that someone got ME/CFS from Fluoroquinolones also mentioning that the "guys at stanford are also interested at their situation because of the use of fluoroquinolones" :

https://forums.phoenixrising.me/threads/still-very-severe.61317/page-9#post-2196487


Let's hope that one of the "guys" mentioned is Dr. Fereshteh Jahaniani at Stanford who has a PhD in pharmacology
 
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someone on healthrising also tried it for a couple of weeks, and gave up without finding a noticeable effect from copaxone.

by now, we dont know what the "physical" effects are of the signal problem found with the nano needle.

it may be a downstream thing or it may be an important defense mechanism to prevent worse things happening.

but actually, i believe naviaux & co have some more brain in their suggestions.
 
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mariovitali said:
From what i read from someone at Phoenix Rising he is severely fatigued, being able to eat only through the use of a tube. They cannot attribute this deterioration to Copaxone.

However, i find it alarming that someone got ME through the use of Fluoroquinolones which are also hepatotoxic :


https://livertox.nlm.nih.gov/Fluoroquinolones.htm

Here is the post mentioning that someone got ME/CFS from Fluoroquinolones also mentioning that the "guys at stanford are also interested at their situation because of the use of fluoroquinolones" :

https://forums.phoenixrising.me/threads/still-very-severe.61317/page-9#post-2196487


Let's hope that one of the "guys" mentioned is Dr. Fereshteh Jahaniani at Stanford who has a PhD in pharmacology
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Our family member was given fluoroquinolones for cdifficile.She was never again ‘ normal,’
But the question is: can one prove this antibiotic destroyes the health of so many young people?
 
Perrier said:
Our family member was given fluoroquinolones for cdifficile.She was never again ‘ normal,’
But the question is: can one prove this antibiotic destroyes the health of so many young people?
Click to expand...

I am not an expert but the following is very concerning :


https://www.ema.europa.eu/en/news/d...ension-restrictions-quinolone-fluoroquinolone


https://journals.lww.com/em-news/Fu...Fluoroquinolone_Side_Effects_Just_Got.12.aspx


https://www.forbes.com/sites/davidk...inolone-antibiotic-side-effects/#15ecc4c91d45


and also :


Case 2 :

More than 5 years after FQ use, this previously physically robust man remains affected with atrophy, profound muscle weakness, fatigue (recently evolving into a chronic fatigue-like condition), chronic gastrointestinal problems, mood disturbance, recurring muscle pain and tendinopathy, and painful peripheral neuropathy. Formerly vigorous, his problems necessitated limiting work in his physically demanding profession, and ultimately led to his early retirement. Notably, a brother had previously received an FQ for a prostate problem, which was followed by chronic fatigue syndrome that persisted for 5 years and then gradually abated.
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Case 4

New symptoms emerged within a month of treatment and persisted, including diarrhoea, designated as irritable bowel syndrome, new food intolerances resulting in gastrointestinal pain, unilateral migraines, chronic fatigue and new development of frequent upper respiratory and sinus infections. Despite persistence of symptoms, she continued to work as an engineer. Following 7 years with symptoms, she was prescribed moxifloxacin 400 mg daily for 5 days for sore throat with fever. New symptoms during this FQ course included convulsions, gastroenterological (severe acid reflux, nausea, vomiting, abdominal pain, appetite loss, presumed gastroparesis), autonomic (tachycardia episodes with heart rates into the 140s lasting for hours, orthostatic intolerance, hypotension, mydriasis, dry eyes, mouth and sinuses), muscle (extreme weakness, fasciculations), debilitating fatigue, sleep (insomnia), cognitive and somatic sensory symptoms (burning, stabbing, tingling, numbness, vibrating), difficulty breathing and urinary urgency.
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Link : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4600819/
 
mariovitali said:

I am not an expert but the following is very concerning :


https://www.ema.europa.eu/en/news/d...ension-restrictions-quinolone-fluoroquinolone


https://journals.lww.com/em-news/Fu...Fluoroquinolone_Side_Effects_Just_Got.12.aspx


https://www.forbes.com/sites/davidk...inolone-antibiotic-side-effects/#15ecc4c91d45


and also :


Case 2 :



Case 4




Link : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4600819/
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Thank you for posting all this; thank you. And now what? Permanent damage? What do we do? A class action suit? It would be very interesting to know how many people with ME took Cipro and its relatives. This illness has decimated a large swath of young people.
 
I was put on a course of fluoroquinolones a decade ago for an infection and it improved my ME/CFS symptoms somewhat. Back then my symptoms were mild so I didn't think about it twice, but there was an improvement in symptoms after around a week. I would probably try another course if I had access, but it seems difficult to get them prescribed these days. Regarding copaxone, the paper about liver toxicity concludes:
In conclusion, physicians should keep in mind the possibility that GA may induce severe hepatotoxicity. This adverse event is extremely rare.
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In any case, copaxone appears a much safer drug than rituximab for instance and there is always a risk versus benefit analysis to be made with any drug.
 
These case studies are very tragic for the people concerned, but unless they have the cardinal symptom of their illness flaring after exercise in an unusual manner - physical exercise giving mental fatigue and vice versa, an increase in inflammatory symptoms such as swollen lymph nodes, a delay up to days before the symptoms flare and a prolonged recovery - then they can't be said to have ME.

More and more the idea that chronic fatigue is equal to ME is becoming widespread just when we need it distinguished the most and it is to their detriment and ours. Most likely they have some damage caused by the medication but that list of symptoms doesn't equate with ME even if some of them are shared.

There are many diseases but a smaller range of symptoms which is why we need to look for the cardinal ones that distinguish diseases. The current fad for MUS is caused by an ideology of mixing everything together.
 
lansbergen said:
Not enough ATP production?
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I have a vague memory of ATP being recycled through ATP to ADP to AMP. The most efficient place to recycle from is ADP ?
Plus that if it gets to AMP stage then AMP can be excreted and so the time taken to build more ATP takes even longer.
However I am sure somebody has been onto this in the past.
Does anybody else know if this is possibly true?
 
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There were experiments done on muscle cells in vitro where AMP was produced. ATP and ADP cycle from one to the other easily. AMP gains phosphate bonds by a different process that is much more difficult.
 
roller* said:
we may produce endogenous Ouabain in the Hypothalamus

if this is caused by such a process of endogenous production, then an antagonist could be Rostafuroxin (german wiki again only) ?

.. am just wondering, since so much has been tried already... perhaps this one too ?
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I agree with roller. The results could be explained by the patients having high levels of endogenous ouabain (EO), which inhibits the Na+-K+ ATPase. Adding 2-5 nM ouabain to normal plasma + normal leukocytes should reproduce the results seen with the patients' blood. If confirmed, patients plasma should be tested for EO... then an antagonist could be Rostafuroxin.

In addition to the hypothalamus, EO is produced by the adrenal glands, where most of the blood EO comes from.

An intriguing observation is also that (exogenous) ouabain or digitoxin intoxication (these are drugs used as heart tonics) produce fatigue.

For a recent review on EO see https://www.sciencedirect.com/science/article/pii/S0143416020300014?via=ihub

For rostafuroxin papers, see https://www.ncbi.nlm.nih.gov/pubmed/?term=rostafuroxin
 
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