[Webinar] Thursday, June 17th 7PM ET - Frontline COVID-19 Critical Care doctors unveiling I-RECOVER Protocol for Long Haul COVID Syndrome (LHCS)

junkcrap50

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Frontline COVID-19 Critical Care (FLCCC) Alliance will be giving a webinar tomorrow evening announcing their management protocol for Long-haul COVID Syndrome (LHCS). They will be sharing their experience, which they claim has returned many patients back to health.

Tomorrow, Thursday, June 17th, at 7PM EST.

https://zoom.us/webinar/register/WN_2CY5VGh7Rk6NeDPZOpzKyQ
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It appears they have published today a PDF of the I-RECOVER protocol on their website. Tomorrow will be the presentation and discussion.
https://covid19criticalcare.com/covid-19-protocols/i-recover-protocol/

Long Haul Covid patients here on Phoenix Rising would be interested to tune in.
ME/CFS patients may also be interested to see if there is anything learned that can apply to pre- or non-covid ME/CFS.
 

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I only saw reference to Fluvoxamine-
they had SSRIs listed below all that under a second option. Maybe they can help somebody, but did not help me.

If this cures long covid folks: well great for them. I. wish them the best. I hope they get better soon.

We're more or less told we can 't have ivermectin.

I've taken prednisone during acute Eppstein barr round IV: and all my symptoms returned when the pills stopped. And so much for sleeping while on prednisone.
 

seamyb

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As a long hauler, I can safely say this is a multilevel hype protocol for kool kids with a good dose of look at the shiny shiny at each stage. Wouldn't cure a salmon.

Most of these things have been widely discussed on reddit and slack with over a year's consensus saying they don't work. But still you get multiple brand new accounts on reddit reporting that ivermectin is the rad new thing for longhaulers.
 

junkcrap50

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Are there any statistics to support their claims @junkcrap50 or is based on their observations?
No idea. They just said that in their announcement.
As a long hauler, I can safely say this is a multilevel hype protocol for kool kids with a good dose of look at the shiny shiny at each stage. Wouldn't cure a salmon.

Most of these things have been widely discussed on reddit and slack with over a year's consensus saying they don't work. But still you get multiple brand new accounts on reddit reporting that ivermectin is the rad new thing for longhaulers.
Yeah. I looked at it and didn't see anything really new. But wanted to share it in case anyone didn't know this stuff, missed it, or was interested.
 

Learner1

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This was posted elsewhere by @Judee , I believe. I'm not familiar with the group, but the advice looks fairly decent. However, there are a lot more things that one could add to that list of things to take that might further the benefit.
 

Rvanson

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I only saw reference to Fluvoxamine-
Fluvoxamine can be kind of hard on the liver, compared to most of the newer antidepressants.

500 mg twice a day of vitamin C is nothing. I've been using it since I was 12. I prefer 3000 mg per day in divided doses, or the new liposomal version, which I combine with the regular version of Vitamin C.
 

nerd

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I have some objections to it. Most and foremost the recommendation of Fluvoxamine. I'd be cautious with taking it until research has excluded the possibility that this syndrome isn't CFS/ME in disguise with tryptophan-mediated pathology.

The motivation for taking SSRIs is that COVID-19 is a serotonin intoxication syndrome. Taking it during the early phase (i.e. during the infection) reduces the serotonin toxicity of a potential subsequent disease (i.e. COVID-19). During COVID-19, Fluvoxamine isn't indicated anymore because it's too late to reduce serotonin levels this way. From there on, serotonin antagonists are indicated, e.g. cyproheptadine.

The Post-COVID/Long hauler syndrome is something quite different though. It's not associated with antibodies. It's not associated with an acute disease. So it can not be an acute serotonin syndrome. It has nothing to do with the condition that occurs in hospitals except for its causality. If it was the same disease, the platelets would (keep) getting destroyed like in COVID-19 and this would show up in blood tests. Fluvoxamine doesn't treat the causality. It's not a virostatic. It prevents the serotonin-mediated disease that happens after the infection.

Corticosteroids are another issue. They are anti-inflammatories, so they might help symptomatically. They are also helpful for acute COVID-19. But, due to immune suppression, they will be counterproductive in case there is residual viral activity. Other anti-inflammatories might be preferable choices for low-level inflammation.

I would only take concentrated EPA, no DHA since recent evidence suggests that the DHA of Omega 3 fatty acids are counterproductive to EPA's heart-protective function, just as Omega 6 fatty acids are counterproductive.

I would use L-Carnitine instead of Atorvastatin unless blood cholesterol levels are elevated.

There is no need to combine various generations of antihistamines. If you can get prescribed Rupatadine (i.e. a third-generation antihistamine), this is the best choice because it also inhibits cytokine release. But this doesn't make it a mast cell stabilizer. It's more like a mast cell silencer. Ketotifen is a mast cell stabilizer. These two could be combined. For effective mast cell stabilization, ketotifen would have to be taken twice daily (12h-12h). There is no need for other antihistamines because they have more side effects for a smaller effectivity spectrum.

Histamine isn't the primary problem of MCAS. It's just the waste you don't want to see accumulate. A low histamine diet can increase the buffer of this waste you can take.

They also list H2 antihistamines. I think this depends on whether gastric issues occur. These gastric issues might resolve just by taking mast cell stabilizers. If not, only then do H2 antihistamines make sense. Insufficient gastric acid can be as troublesome as too much of it, after all.

Interesting that they also list LDN.

I'd also be very cautious with Diazepam, and other SSRIs (not just Fluvoxamine).
Montelukast might help if there is residual inflammation in the lungs or against bronchospasms. But it also comes with risks for neuropsychiatric conditions.
 
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junkcrap50

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They seemed to start out on the right foot but seem to have defaulted back to the same old, same old, unfortunately.
Well, they are establishment / mainstream medicine doctors or at least starting from that point of view. They have been forced to confront Long COVID due to the pandemic and it's widespread effects. Had the pandemic been different in being more limited, less lethal, or not as taken as seriously, then Long COVID wouldn't be taken seriously and wouldn't even be a thing. There are still many doctors and scientists who don't taken Long COVID seriously now or believe it's a real thing.

I think it's pretty remarkable they are taking MCAS as a real thing and seriously. MCAS is and has been pretty fringe among mainstream medicine.

Montelukast might help if there is residual inflammation in the lungs or against bronchospasms. But it also comes with risks for neuropsychiatric conditions.
Nonetheless, it is commonly used to treat MCAS.

Histamine isn't the primary problem of MCAS.
What is the problem? All the cytokines, inflammatory molecules that mast cells release along with histamine?

While I agree and that you may be right, significant symptom relief is seen when controlling for only histamine. It does have many downstream effects. So, to many of those patients, that's all they need. So, what is all the other inflammatory molecules and cytokines causing and doing?

If you can get prescribed Rupatadine (i.e. a third-generation antihistamine), this is the best choice because it also inhibits cytokine release.
I hadn't heard of Rupatadine used for MCAS, but quickly searching it has been studied for that. But I see it's not approved for use in the USA, which must be why it's not more widely seen or mentioned with MCAS.
 

Judee

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Well, they are establishment / mainstream medicine doctors or at least starting from that point of view. They have been forced to confront Long COVID due to the pandemic and it's widespread effects. Had the pandemic been different in being more limited, less lethal, or not as taken as seriously, then Long COVID wouldn't be taken seriously and wouldn't even be a thing. There are still many doctors and scientists who don't taken Long COVID seriously now or believe it's a real thing.

I think it's pretty remarkable they are taking MCAS as a real thing and seriously. MCAS is and has been pretty fringe among mainstream medicine.
I was hopeful though because when I listened to a portion of one of their podcast videos a while back, the one doctor seemed very sympathetic to the plight and frustrations of long haulers and others with "unexplained long term illnesses like Chronic Fatigue Syndrome and Lyme" is the way I think I remember him saying it.
 

hapl808

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I think the justifications (and significant data) on taking fluvoxamine for Covid-19 is very different than for Long Covid. My understanding is there was a significant result in a double blind RCT for fluvoxamine in reducing hospitalization and severe Covid-19. There may be hypotheses for why this worked (although I don't believe they thought the effects on serotonin were related), but the data seem to support it. I don't believe equivalent data exist for treating Long Covid with it, just theories as far as I know.
 

nerd

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Meanwhile, I also saw their webinar. They recommend Fluvoxamine for the same reason SSRIs sometimes are recommended for CFS/ME, namely for its anti-inflammatory purposes. They link it with acute COVID-19, not realizing that COVID-19 is a serotonin syndrome and not just organizing pneumonia. I assume this is the reason why they have so much faith in Fluvoxamine. If you assume its anti-inflammatory mechanism is the only mechanism that helps against COVID-19, it should also work later on. Because, obviously, it works against COVID-19. Why shouldn't it work against LHS then? Dr. Mobeen knows the role of serotonin by the way.

What is the problem? All the cytokines, inflammatory molecules that mast cells release along with histamine?
At least, there is more than histamine signaling. It's unclear what cytokines or possibly viral mediators are released once a trigger occurs.

While I agree and that you may be right, significant symptom relief is seen when controlling for only histamine. It does have many downstream effects. So, to many of those patients, that's all they need. So, what is all the other inflammatory molecules and cytokines causing and doing?
My concern isn't really that they address histamine as a solution, but that they imply that MCAS is kind of the causality. I think it plays a predisposing role that affects the manifestation of symptoms. If it was the causality, why doesn't mast cell stabilization cure CFS/ME? Why does it only help with the symptoms? Why does it occur after an infection and never disappear again? There must be some signaling towards the mast cells as well. I'm not satisfied with the explanation of the FLCCC that it's all about rogue macrophages. I think what they will observe is that the repolarization therapy will have to maintain for related symptoms not to reoccur.

I hadn't heard of Rupatadine used for MCAS, but quickly searching it has been studied for that. But I see it's not approved for use in the USA, which must be why it's not more widely seen or mentioned with MCAS.
I wasn't aware of that. I used it against my allergies before. It didn't really do much to MCAS issues. For example, when I still was on a low-histamine diet, I tried to break protocol with Rupatadin. It still triggered severe headache and all the other typical symptoms.

@nerd, I wish you could contact the FLCCC doctors and tell them all this.

They seemed to start out on the right foot but seem to have defaulted back to the same old, same old, unfortunately.
I don't think they would listen since it comes from someone with conflicts of interest. My conflict is that I hope LHS and CFS/ME is finally recognized as the same disease.

They have been asked many many times to come up with a guideline for long haulers, despite the lack of data. And this is the best that was available if you only look at long haulers, leaving out CFS/ME as a whole. There is so much to learn from CFS/ME.

I don't believe equivalent data exist for treating Long Covid with it, just theories as far as I know.
When the serotonin syndrome hypothesis was still in its early shoes and the data on SSRIs' supportive function already existed, their first theory was the sigma-1 receptor. This theory seems to have sustained.

Actually it’s associated with antibodies:
What I meant were SARS-CoV-2 antibodies, indicating that the same viral pathology triggers LHS just as it triggers COVID-19. In this case, it seems to be different. Some of the antibodies that this study determined are quite familiar to the CFS/ME world.
 

pamojja

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I would only take concentrated EPA, no DHA since recent evidence suggests that the DHA of Omega 3 fatty acids are counterproductive to EPA's heart-protective function, just as Omega 6 fatty acids are counterproductive.
Did you take a closer look at that study? Discussed for example here: https://www.longecity.org/forum/top...h-epa-alone-is-best-omega-3-carboxylic-acids/ or here: https://www.longecity.org/forum/top...to-heart-rhythm-disorder-atrial-fibrillation/

Honestly, this really slightest bad-effect in a patient population not representing me doesn't concerns me at all. And then the too obvious agenda to propagate an pantentable EPA product.. Too many already replicated studies showing benificial effects.

Additionally have been taken 2.3g (+0.3 from diet) of EPA, and 1.6g (+0.6 from diet) DHA daily during the last 13 years. Therefore in total 4.8 g/d EPA+DHA for 13 years. Only experienced remission from disabilties (PAD, COPD, PEMs..), but no adverse effect at all.