Martin aka Paused and H.E.L.P treatment

[kjetilv]

Hope you’re ok @Martin aka paused||M.E. , and that it went well. I’m also looking forward to read your update

 

[kjetilv]

Best of luck Martin

PS. What is H.E.L.P. treatment?

There’s a thread on it on the forum: https://forums.phoenixrising.me/threads/is-apheresis-an-effective-treatment-for-long-covid-and-me.85939/page-26#post-2377348
or you could check this Youtube-video

 

[hb8847]

Very interesting, thanks @kjetilv

 

[Rufous McKinney]

Rooting for you @Martin aka paused||M.E. .....

 

[lenora]

Martin, my every good wish for a good recovery accompanies this addition to the Forum. WHEN you feel up to it, please inform us of how you're doing. Better help, young man!

 

[Martin aka paused||M.E.]

Ladies and gentlemen,

first of all: a million thanks to your posts, especially @YippeeKi YOW !! you know the thing with the fan is both sided!

Now the update:
It was an incredibly stressful day but I'm grateful for the people I met and hope to see again. Dr Jaeger and the stuff is great and I saw my friend Asad for the first time.

The Apheresis: I had a blood oxygen of 70% at the beginning and after that it was 74%. All other values were normal, but K dropped after the treatment. The was little fibrinogen at the bottom but the stuff told me a healthy person would have that too. I'm sceptical. But professor Pretorius looked at my blood smear and I don't have the result yet and Dr Jaeger waits for the BIG amount of blood tests. She wants to communicate with my doc about it and with me what makes sense for me. I told her that I think it's not a problem of ME after what I've seen and she said she is no expert but has one. Then came the most interesting part.

I had an hour-long conversation with Dr William Weir (everyone said he's a Nobel Laureate, I couldn't find anything?!?!). He is a very and calm man who really understands what he is talking about. We discussed the immune system and metabolic parts. Came out he is an expert on immunological things where I couldn't really follow but he was patient and explained it for dummies. Regarding the metabolic issues, he acknowledged that I am well educated and know more about the chemistry behind it (atm the moment I study chemistry). It was one of the best conversations I had so far about ME. No blabla. No assumptions. Just about facts. So we weren't not of the same opinion in every aspect but we both found the theories of us very interesting. Then Dr Jaeger joined and we were interviewed by the Apheresis team from the UK. Or to be more precise: I was interviewed. I told my life story in short and everyone, especially the camera man had to fight with tears. It was a very emotional, intimate moment. Then my transport team who had waited for over eight hours got very nervous bc they already had qutting time and we had 156 km to drive. So I left (was the first time I shouk hands with people since Covid). So, unfortunately I couldn't talk to Dr Jaeger long enough.

BUT: She acknowledged that maybe ME/CFS has no Fibrinogen problem. We thought about why the one ME patient went from severe to mild after 13 rounds. I had the idea that it also washes away cytokines and she said that was possible bc it does.

Then we came into a big traffic jam. The poor guys of the ambulance. I can only say that they were great. They never accused me that it took so long and well understood that I wanted to talk to everybody. They were both moved by my experience.

At home I was very tired (it was a 12 hrs day!) but not wrecked. This Apheresis doesn't cause harm.

All in all it was a very exciting experience. But we will see how we proceed.

Off-topic: I'm in the process of founding a NGO for research into ME and when it's done I hope this board, you all will support us because we need every penny.

Thank you for being on this board and fill it with life.

Martin

 

[junkcrap50]

Thank you very much for the report and undergoing the treatment to find out more info for the community.

Were you on any anticoagulation drugs as pre-treatment before starting the apheresis? If so, how long were you on them? (EDIT: Martin answered me on discord saying, no. He did not take any drugs as pretreatment.)

One thought on why ME/CFS patients may not collect much fibrin in the help apheresis filter, at least initially. ME/CFS patients may have more of the fibrin laid down along the blood vessel walls instead of freely floating microclots, due to the length of their illness and/or clearance of the microclot instigator, ie, virus. (I forgot and am unclear on the triggering mechanism proposed for the microclots). Eventually, would the microclots not find a place to stick to or would they float and circulate perpetually? If this is the case, a long pre-treatment with fibrinolytics or other anticoagluation for ME/CFS patients may be needed prior to apheresis.

 

[Martin aka paused||M.E.]

fibrin laid down along the blood vessel walls

No I wasn't. I think your theory of fibrinogen lying in the epithelial cells is unlikely because I wouldn't know how they could possibly enter them (not by osmosis, they'd need an active transport and I don't know of any that carries fibrinogen) and then fibrinogen sticks to LDL which is in the vessels.

 

[GlassCannonLife]

Thank you very much for the report and undergoing the treatment to find out more info for the community.

Were you on any anticoagulation drugs as pre-treatment before starting the apheresis? If so, how long were you on them?

One thought on why ME/CFS patients may not collect much fibrin in the help apheresis filter, at least initially. ME/CFS patients may have more of the fibrin laid down along the blood vessel walls instead of freely floating microclots, due to the length of their illness and/or clearance of the microclot instigator, ie, virus. (I forgot and am unclear on the triggering mechanism proposed for the microclots). Eventually, would the microclots not find a place to stick to or would they float and circulate perpetually? If this is the case, a long pre-treatment with fibrinolytics or other anticoagluation for ME/CFS patients may be needed prior to apheresis.

If this was significant, I wonder if we would be able to capture it with imaging? I'm not sure if anyone has looked for anything like this or what resolution would be required.

 

[SNT Gatchaman]

BUT: She acknowledged that maybe ME/CFS has no Fibrinogen problem. We thought about why the one ME patient went from severe to mild after 13 rounds. I had the idea that it also washes away cytokines and she said that was possible bc it does.

Thank you very much for documenting your experiences and thoughts Martin.

To me, the possibilities would seem to be:

1. LC is not ME (but has symptom overlap)
2. LC is ME but not all ME has the same pathogenesis as LC
3. LC is ME in its early phase, but established ME progresses over time to a different maintenance pathophysiology

I'm of the opinion that there is a progression in ME between initiation -> early-phase -> late-phase. It's possible that micro-clots form at the start due to immune disturbance, and cause progressive compensations, but aren't required for long-term disease maintenance.

If the fundamental problem is platelet hyperactivation, leading to endothelial dysfunction, red cell dysfunction and micro-clots; the micro-clots may only be necessary to get into the persistent pathological state, but might clear over months, while the other factors maintain the problem (via hyperactivated platelets).

Another good thought was voiced by @junkcrap50, that micro-clots may still be present, but be more organised at the margin of capillaries in long-term (or just some) ME. They may be less available to clearance by apheresis if less of the load reaches the venous blood. In that case anti-coagulation may be more useful than apheresis.

Even if apheresis is not then able to treat many by removing micro-clots (because they are no longer present), the demonstration of a biological model that causes the symptoms of ME must represent a huge leap forward. It would be the final nail for BPS for a start.

 

[GlassCannonLife]

I'm of the opinion that there is a progression in ME between initiation -> early-phase -> late-phase.

Why do you believe that to be the case? I see this said quite often but nobody details their reasoning.

 

[SNT Gatchaman]

Why do you believe that to be the case? I see this said quite often but nobody details their reasoning.

Well, at the moment I'm trying to work out a model based around the micro-clot finding (assuming this finding is valid and valid for ME). The pandemic has given us the opportunity to identify micro-clots, which haven't been previously recognised — either technical, or never thought to look, or they just aren't there in ME. But, in the past we also haven't easily researched such large numbers of early-onset ME patients. They often take years to be given a diagnosis, if they even get one at all. Remember the micro-clots were found serendipitously.

If I were to show my working, it's currently six pages, plus references, so is almost a proper scientific paper. Except there are almost certainly big holes and misconceptions, because I am very much out of my field of expertise and reading/learning as I go. So I am reluctant to post it in this form currently.

But the short answer as to why I personally believe this is: the observation that many people have the initial symptoms that last a few weeks or months but then resolve; some have say 2-5 years of ME that may be pretty severe, but still recover; some progress almost inevitably and spontaneous recovery seems to become less likely the longer it goes on. But, it could easily just be a continuum of the same fundamental metabolic/immune etc processes.

 

[SWAlexander]

Is there a connection between ME, LC, Fibrinogen and Cystic Fibrosis? Would apheresis be helpful in case of Cystic Fibrosis?

 

[YippeeKi YOW !!]

I'm of the opinion that there is a progression in ME between initiation -> early-phase -> late-phase. It's possible that micro-clots form at the start due to immune disturbance, and cause progressive compensations, but aren't required for long-term disease maintenance.

While I dont have the deep science-y background to support or validate my opinions, I agree with you @SNT Gatchaman .... it helps explain the outrageous variations in this miserable little snarky shapeshifter of an illness, and why all of us have slightly, or sometimes very, different symptomatologies, and why the protocols or substances (either Rx or OTC) that help one or a few of us do absolutely nothing for the rest, or actually cause setbacks.

I also think that ME cycles back and forth thru initiation -->early phase-->intermediate phase-->late phase, and what worked in one phase won't in another because of the difference in etiologies, which explains why something that helped for anywhere from 3 days to 3 or more months suddenly just stops working. It's bcause the illness has switched into another phase, for which that particular assist is useless.

It's head-bangingly frustrating, and Ive got the forehead bruises to prove it .....

Why do you believe that to be the case? I see this said quite often but nobody details their reasoning.

My reasoning is stated above, but lacks the benefit of strong scientific back-up. Its just conjecture on my part, but conjecture based on what feels like about three centuries of experience, but actually is only just short of a decade ....

EDIT .... for a typo that wasnt my fault ... really ... sticky key on my cranky superannuated laptop .... no, honest ...

 

[YippeeKi YOW !!]

a million thanks to your posts, especially @YippeeKi YOW !! you know the thing with the fan is both sided!

I cant tell you how much that means to me @Martin aka paused||M.E. .... "requited like" is one of life's happier highs, and when it comes from someone you admire as much as I do you, it's beyond sweet ....

 

[GlassCannonLife]

Well, at the moment I'm trying to work out a model based around the micro-clot finding (assuming this finding is valid and valid for ME). The pandemic has given us the opportunity to identify micro-clots, which haven't been previously recognised — either technical, or never thought to look, or they just aren't there in ME. But, in the past we also haven't easily researched such large numbers of early-onset ME patients. They often take years to be given a diagnosis, if they even get one at all. Remember the micro-clots were found serendipitously.

If I were to show my working, it's currently six pages, plus references, so is almost a proper scientific paper. Except there are almost certainly big holes and misconceptions, because I am very much out of my field of expertise and reading/learning as I go. So I am reluctant to post it in this form currently.

But the short answer as to why I personally believe this is: the observation that many people have the initial symptoms that last a few weeks or months but then resolve; some have say 2-5 years of ME that may be pretty severe, but still recover; some progress almost inevitably and spontaneous recovery seems to become less likely the longer it goes on. But, it could easily just be a continuum of the same fundamental metabolic/immune etc processes.

That's interesting, it will be great to read what you've compiled once it's ready.

What I always find confusing about the sentiment that some people recover early and others "pass a threshold" and stay ill, is that is seems to conflate a population based statistic and individual illness. More specifically, those that remain ill for a long time may have been in the position where they were always going to remain ill for long. In those people, there wouldn't be something that changes at a critical point. However, anyone that is slowly improving (perhaps for some time in an undetectable way, before they notice symptom relief) will be more likely for this to manifest in them getting better in a shorter time frame. The people that remain ill then feel that they crossed some type of threshold, when in reality they only crossed a threshold of statistical representation rather than a change in physiology.

I wonder actually, if we had some definitive metric for ME that could be rapidly and easily deployed on any "post viral fatigue" case, how many people get over it in what period of time. Ie, what shape would the graph make (with duration on the x and number of people on the y axes)? Would it be a normal distribution with the majority being resolved in 6 months.? 12 months.? Or would the majority occur in the shortest term (assuming the test is accurate enough to capture this dysfunction at such a small magnitude/short time frame), and it would simply tail off?

Anyway, this is all just me wondering out loud about this.!

We may never know, or there may in fact be some fundamental change that solidifies or establishes the condition into a very chronic state. In either case, treatments/cures should still be pursued and will probably still be very hard to achieve for the full patient population, considering the seeming heterogeneity of the disease overall.

 

[GlassCannonLife]

While I dont have the deep science-y background to support or validate my opinions, I agree with you @SNT Gatchaman .... it helps explain the outrageous variations in this miserable little snarky shapeshifter of an illness, and why all of us have slightly, or sometimes very, different symptomatologies, and why the protocols or substances (either Rx or OTC) that help one or a few of us do absolutely nothing for the rest, or actually cause setbacks.

I also think that ME cycles back and forth thru initiation -->early phase-->intermediate phase-->late phase, and what worked in one phase won't in another because of the difference in etiologies, which explains why something that helped for anywhere from 3 days to 3 or more months suddenly just stops working. It's bcause the illness has switched into another phase, for which that particular assist is useless.

It's head-bangingly frustrating, and Ive got the forhead bruises to prove it .....

My reasoning is stated above, but lacks the benefit of strong scientific back-up. Its just conjecture on my part, but conjecture based on what feels like about three centuries of experience, but actually is only just short of a decade ....

Your post did remind me of what Asad (was it him.?) said about it - where triggering PEM/a crash "re-initiates" a lot of the cascade of problems and perpetuates the illness.

All very interesting in any case!

 

[SNT Gatchaman]

Your post did remind me of what Asad (was it him.?) said about it - where triggering PEM/a crash "re-initiates" a lot of the cascade of problems and perpetuates the illness.

That might have been Prof Ron Davis in a recent talk.

 

[BrightCandle]

@Martin aka paused||M.E. I am sorry this didn't really work for you.

 

[YippeeKi YOW !!]

@Martin aka paused||M.E. I am sorry this didn't really work for you.

You're jumping the gun. It's too soon to tell how much or how little HELP will work for @Martin aka paused||M.E. .... he's very positive about the whole experience, and there's more to come.