Dr Patterson on Long Haul Covid vs ME/CFS

[Martin aka paused||M.E.]

they never even had the intention to build them because funding. Like why lie ?

I didn't recognize it as a lie. I see it as two facts that hindered them from repairing the needle.

I understand your frustration though. We are all in the same boat. I don't want to criticize anyone.

But there was so much bs thrown out in the past as a potential treatment that I'm reserved now and very skeptical about new and fast discoveries.

 

[bensmith]

Are y’all seeing any benefit from antiretrovirals? How was the med at first? Hard to start?I see some benefit with ivm.

@IThinkImTurningJapanese @Martin aka paused||M.E.

 

[Martin aka paused||M.E.]

Are y’all seeing any benefit from antiretrovirals? How was the med at first? Hard to start?I see some benefit with ivm.

@IThinkImTurningJapanese @Martin aka paused||M.E.

I didn’t have any problems starting on Tenofovir… but I heard that some react very badly.

 

[bensmith]

@Martin aka paused||M.E. ty. Any help? How long you been on them?

 

[Martin aka paused||M.E.]

@Martin aka paused||M.E. ty. Any help? How long you been on them?

Can’t judge it yet. I only take it for a week now. And in combination with other things so I have to monitor my AB levels and symptoms to say anything with certainty.

 

[hapl808]

And plenty of people have taken ivermectin (or other anti-parasitic drugs) over the years for CFS.

Here's a discussion on PR with maybe 5-10 people saying they tried it. It's an extremely common drug, especially in certain parts of the world. I personally took albendazole instead of ivermectin but it was really a toss-up on what to try for me. (I found very modest temporary improvement, but not enough to discount placebo effect really.)

 

[Badpack]

And plenty of people have taken ivermectin (or other anti-parasitic drugs) over the years for CFS.

Here's a discussion on PR with maybe 5-10 people saying they tried it. It's an extremely common drug, especially in certain parts of the world. I personally took albendazole instead of ivermectin but it was really a toss-up on what to try for me. (I found very modest temporary improvement, but not enough to discount placebo effect really.)

Yea, the real thing seams to be the Maraviroc+statin combination ? Not sure why they added Ivermectin to begin with tbh. This is his full treatment plan. Not sure if there are any synergistic effects.

He seems to have answer for everything ?

 

[dylemmaz]

Yea, the real thing seams to be the Maraviroc+statin combination ? Not sure why they added Ivermectin to begin with tbh. This is his full treatment plan. Not sure if there are any synergistic effects.

on twitter yesterday patterson said ivermectin doesn’t work the best alone but in combination with other things it works well.

he seems to be good at responding to people on twitter so i’d guess if you have questions for him replying to his posts is probably the best way to get them answered. i see he replied to @Martin aka paused||M.E. there today

 

[Badpack]

on twitter yesterday patterson said ivermectin doesn’t work the best alone but in combination with other things it works well.

he seems to be good at responding to people on twitter so i’d guess if you have questions for him replying to his posts is probably the best way to get them answered. i see he replied to @Martin aka paused||M.E. there today

He answer. But always pretty cryptic and very selective. Not sure about this all, but i mean, what else is out there mh.

 

[Martin aka paused||M.E.]

He answer. But always pretty cryptic and very selective. Not sure about this all, but i mean, what else is out there mh.

I’ve just registered… they will get in touch with me they say. Exactly, what else out there...

 

[Badpack]

I’ve just registered… they will get in touch with me they say. Exactly, what else out there...

They collaborating with a lab in Spain Madrid. And planing for another one in the UK soon. It's a german company. I wrote them today if they could do the testing here in Germany to. Still waiting for a response. I also wrote the IMD Berlin. The best lab we have. They cant do his panel but offered some of it.

Rantes 28€ großer T-helferstatus 102€ interleukin 6 28€ interleukin 8 28€ VEGF 28€ TNF alpha

Some are in the großer T-helferstatus. But some are missing like sCD40L and GM-CSF.

 

[Martin aka paused||M.E.]

They collaborating with a lab in Spain Madrid. And planing for another one in the UK soon. It's a german company. I wrote them today if they could do the testing here in Germany to. Still waiting for a response. I also wrote the IMD Berlin. The best lab we have. They cant do his panel but offered some of it.

Rantes 28€ großer T-helferstatus 102€ interleukin 6 28€ interleukin 8 28€ VEGF 28€ TNF alpha

Some are in the großer T-helferstatus. But some are missing like sCD40L and GM-CSF.

Yes, I've talked to IMD too. I think that's where @mitoMAN also got tested. I did those tests at Lab4More but I'm now very interested in the things they can't test like you already mentioned sCD40L and so on...

 

[Badpack]

https://journal.chestnet.org/article/S0012-3692(21)03635-7/fulltext

No oxygen. The exact same result was shown for Cfs. So strange how ppl still argue that these are 2 different diseases. LongCovid = Cfs. Should Patterson really find a treatment for long covid, it very well should work for us.

Im back checking a lot of twitter accounts that praise him to death. Some are very old Cfs accounts, some are just made days ago. Hard to find a real conclusion. Time will tell, thats for sure.

 

[Jyoti]

THIS THREAD IS BEING CLOSED FOR MODERATION.

 

[Rebeccare]

THIS THREAD HAS BEEN RE-OPENED. PLEASE BE RESPECTFUL OF ONE ANOTHER AND MINDFUL OF THE FORUM RULES.

 

[TinaYesen]

No oxygen. The exact same result was shown for Cfs. So strange how ppl still argue that these are 2 different diseases. LongCovid = Cfs.

Yes, I get the same sense based on data presented in the last Solve ME LC seminar (Session I–Long Covid: What Do We Know So Far? Thursday, July 1, 2021) (image below) That much of LC symptoms are identical to ME symptoms.

Just today my ME doctor was talking as if I had something drastically different from LC, but my other doctors have diagnosed me with suspected LC and confirmed ME, aka potentially one in the same.

I get the sense LC doctors aren't working enough with ME specialists. This is one reason why researchers/physicians keeping ME and LC SO distinct is bad. Just today my doctor openly told me if I go to Dr. Pattetson who has no clinical findings to support his treatments, he will drop me as a patient. The hostility between ME doctors and LC doctors is not helping patients.

BUT (big but) keeping LC and ME separate is really good for us from a research perspective. One reason it may have been difficult to pinpoint pathology for ME is the different ways our ME manifests in each of us. If that is even partly due to the source virus that triggered our ME, researchers are eliminating that variable, which is a hugely good thing.

How I expect (and hope) we'll start talking about these conditions is three different diseases:

1. "Non-ME Long-COVID" - LC that doesn't reach the later chronic state of ME e.g. patient who is ill 6 weeks and recovers fully OR LC that doesn't match the ME ICC/CCC criteria e.g. patient only has one or a few lingering symptoms. E.g. my nana who feels fine except for her 6 months of just brain fog, nothing else, nothing physical.

2. "COVID-induced ME" (or ME Long-COVID) - ICC or CCC criteria ME (6 months or longer with neuroimmune multi-system components) triggered by the COVID virus.

3. "ME" - ICC or CCC-ME where possible specified. Aka, "I have ICC-ME."

Speaking about our 3 conditions in this way would help us all, and would help researchers as well to study the diseases without making messy studies.

 

[sometexan84]

I'm apathetic about the treatment, but I would like to shed some light on the cytokines in ME/CFS.

I think the cytokine profiles for LC and ME/CFS match up a bit better when you take a closer look.

For instance, RANTES (CCL5). I guess they're saying it's increased in COVID and/or LC. And in ME/CFS, this and other cytokine analyses are inconclusive... is what they're saying

Here's CCL5 in ME/CFS from a 2017 and a 2015 study. Notice in BOTH, CCL5 is actually higher than controls, but then lower in "severe" CFS.

This is part of the problem in finding consistency w/ the ME/CFS cytokine profiles vs healthy controls. It can fluctuate based on length and severity of illness.

My take is that if RANTES/CCL5 is indeed the source of the "cytokine storm", then the storm might settle down later in the illness. So after a certain period of time, you'll no longer show super high levels here. Which would make sense why Patterson is finding more consistency here, because no one's had Long Covid for a long enough period of time for their CCL5 to go down. If you'd had ME/CFS for 10+ yrs, CCL5 is likely to no longer be super high.

Also, in the Health Rising article Has Bruce Patterson Cracked Long COVID?, it mentions how there's no consistency in cytokine levels in ME/CFS studies. This is really not true.

First off, that review only used Fukuda criteria, and thus were left w/ only 15 studies. I think Fukuda criteria is flawed, as there was a point where I wouldn't even qualify. I don't think the pain symptoms should be a requirement.

There are actually way more than 15 studies on this, and I'll show this below.

But second, I don't think they interpreted the data correctly.

For instance, here's their "summary" of what Montoya found in his 2017 study, they say out of all those cytokines studied, only TGF-β (increased) and Resistin (decreased) were different from controls...

But if you look at the actual study, there really are things that stick out and in fact seem significant. IL-2 for example, it's another one Patterson says is higher in Long Covid. And if you just believe the 15 study review, then you think IL-2 in ME/CFS is the same as controls.

But here's the actual data from Montoya's study for IL-2

To me, this seems very important. IL-2 (like many others) increases in ME/CFS severity (which I also link to length of illness). When you avg together the mild, moderate, and severe, these IL-2 levels still are higher than controls. And maybe these mild patients brought down the avg enough to where it no longer fell in the "significant" range.

But I think patterns like that are very important, and relevant.

Lastly, if you want to see the most comprehensive info on ME/CFS cytokines, see the mepedia.org's page. You can actually seem some consistency in some, like high IFN-γ, IL-1, IL-2, etc. And there are links to a TON of different studies, not just from the 2000's.

 

[Martin aka paused||M.E.]

I'm apathetic about the treatment, but I would like to shed some light on the cytokines in ME/CFS.

I think the cytokine profiles for LC and ME/CFS match up a bit better when you take a closer look.

For instance, RANTES (CCL5). I guess they're saying it's increased in COVID and/or LC. And in ME/CFS, this and other cytokine analyses are inconclusive... is what they're saying

Here's CCL5 in ME/CFS from a 2017 and a 2015 study. Notice in BOTH, CCL5 is actually higher than controls, but then lower in "severe" CFS.

View attachment 44381
View attachment 44382
View attachment 44383
This is part of the problem in finding consistency w/ the ME/CFS cytokine profiles vs healthy controls. It can fluctuate based on length and severity of illness.

My take is that if RANTES/CCL5 is indeed the source of the "cytokine storm", then the storm might settle down later in the illness. So after a certain period of time, you'll no longer show super high levels here. Which would make sense why Patterson is finding more consistency here, because no one's had Long Covid for a long enough period of time for their CCL5 to go down. If you'd had ME/CFS for 10+ yrs, CCL5 is likely to no longer be super high.

Also, in the Health Rising article Has Bruce Patterson Cracked Long COVID?, it mentions how there's no consistency in cytokine levels in ME/CFS studies. This is really not true.
View attachment 44384

First off, that review only used Fukuda criteria, and thus were left w/ only 15 studies. I think Fukuda criteria is flawed, as there was a point where I wouldn't even qualify. I don't think the pain symptoms should be a requirement.

There are actually way more than 15 studies on this, and I'll show this below.

But second, I don't think they interpreted the data correctly.

For instance, here's their "summary" of what Montoya found in his 2017 study, they say out of all those cytokines studied, only TGF-β (increased) and Resistin (decreased) were different from controls...
View attachment 44385

But if you look at the actual study, there really are things that stick out and in fact seem significant. IL-2 for example, it's another one Patterson says is higher in Long Covid. And if you just believe the 15 study review, then you think IL-2 in ME/CFS is the same as controls.

But here's the actual data from Montoya's study for IL-2
View attachment 44386
To me, this seems very important. IL-2 (like many others) increases in ME/CFS severity (which I also link to length of illness). When you avg together the mild, moderate, and severe, these IL-2 levels still are higher than controls. And maybe these mild patients brought down the avg enough to where it no longer fell in the "significant" range.

But I think patterns like that are very important, and relevant.

Lastly, if you want to see the most comprehensive info on ME/CFS cytokines, see the mepedia.org's page. You can actually seem some consistency in some, like high IFN-γ, IL-1, IL-2, etc. And there are links to a TON of different studies, not just from the 2000's.

View attachment 44387

That makes me think that I have another illness that comes with the exact same symptoms and also reacts to Atovan and Abilify bc I don't fit in what you describe as consistent

 

[Badpack]

I'm apathetic about the treatment, but I would like to shed some light on the cytokines in ME/CFS.

I think the cytokine profiles for LC and ME/CFS match up a bit better when you take a closer look.

For instance, RANTES (CCL5). I guess they're saying it's increased in COVID and/or LC. And in ME/CFS, this and other cytokine analyses are inconclusive... is what they're saying

Here's CCL5 in ME/CFS from a 2017 and a 2015 study. Notice in BOTH, CCL5 is actually higher than controls, but then lower in "severe" CFS.

View attachment 44381
View attachment 44382
View attachment 44383
This is part of the problem in finding consistency w/ the ME/CFS cytokine profiles vs healthy controls. It can fluctuate based on length and severity of illness.

My take is that if RANTES/CCL5 is indeed the source of the "cytokine storm", then the storm might settle down later in the illness. So after a certain period of time, you'll no longer show super high levels here. Which would make sense why Patterson is finding more consistency here, because no one's had Long Covid for a long enough period of time for their CCL5 to go down. If you'd had ME/CFS for 10+ yrs, CCL5 is likely to no longer be super high.

Also, in the Health Rising article Has Bruce Patterson Cracked Long COVID?, it mentions how there's no consistency in cytokine levels in ME/CFS studies. This is really not true.
View attachment 44384

First off, that review only used Fukuda criteria, and thus were left w/ only 15 studies. I think Fukuda criteria is flawed, as there was a point where I wouldn't even qualify. I don't think the pain symptoms should be a requirement.

There are actually way more than 15 studies on this, and I'll show this below.

But second, I don't think they interpreted the data correctly.

For instance, here's their "summary" of what Montoya found in his 2017 study, they say out of all those cytokines studied, only TGF-β (increased) and Resistin (decreased) were different from controls...
View attachment 44385

But if you look at the actual study, there really are things that stick out and in fact seem significant. IL-2 for example, it's another one Patterson says is higher in Long Covid. And if you just believe the 15 study review, then you think IL-2 in ME/CFS is the same as controls.

But here's the actual data from Montoya's study for IL-2
View attachment 44386
To me, this seems very important. IL-2 (like many others) increases in ME/CFS severity (which I also link to length of illness). When you avg together the mild, moderate, and severe, these IL-2 levels still are higher than controls. And maybe these mild patients brought down the avg enough to where it no longer fell in the "significant" range.

But I think patterns like that are very important, and relevant.

Lastly, if you want to see the most comprehensive info on ME/CFS cytokines, see the mepedia.org's page. You can actually seem some consistency in some, like high IFN-γ, IL-1, IL-2, etc. And there are links to a TON of different studies, not just from the 2000's.

View attachment 44387

Seems like moderate blood markers show where the disease is really going. And severe patients either went in an immunological exhaustion after a long illness or the damage is done to the body and nothing much is needed to keep it in this state anymore. Seems just like Long Haulers, you need an early immune intervention to stop it in its tracks before too much damage is done to the vascular system and autonomic nervous system.

 

[Martin aka paused||M.E.]

Seems like moderate blood markers show where the disease is really going. And severe patients either went in an immunological exhaustion after a long illness or the damage is done to the body and nothing much is needed to keep it in this state anymore. Seems just like Long Haulers, you need an early immune intervention to stop it in its tracks before too much damage is done to the vascular system and autonomic nervous system.

Immunological exhaustion is exactly the fitting term for my cellular immune status and cytokines