For the third year in a row, Dr. Carmen Scheibenbogen and the Charité Fatigue Center (CFC) at Charité —Universitätsmedizin (a good German tongue twister :)) in Berlin are bringing us an ME/CFS and long-COVID International Conference. The conference, which is being live-streamed from May 12th to 13th, is in English and free, and you can register here. (Videos will be available after the conference).
For the 3rd year in a row, the Charité Fatigue Center is putting on an international conference.
I’ve gone on and on over the remarkable transformation Dr. Scheibenbogen and others have brought to Germany’s ME/CFS space. We’ve gone from having no German ME/CFS research for decades to Germany becoming a hub of ME/CFS research.
Nineteen of the speakers are German. Forget about Germany, for a moment, though — let’s talk about Europe. Nine of the 35 speakers at the ME/CFS International Conference at Charité from May 12th to 13th are from other European countries. Two more are from Japan, one is from Israel, and four are from the U.S. Of the four U.S. speakers, David Putrino at Mount Sinai is co-chairing the conference.
Speakers from Germany, the Netherlands, Austria, and Norway.
After a clinical section (which includes off-purpose drugs used in Germany) comes a cardiovascular section. We’ll see some familiar names (Systrom, Wust) and some less familiar ones including Jürgen Steinacker on muscle mitochondria, Christian Puta on post-exertional malaise and Karl Johan Tronstad on blood metabolites.
All Together Now!
Christian Puta is a nice example of: a) how deeply embedded some German researchers have become in ME/CFS and long COVID; and b) how this field is cohering around some central findings.
Puta’s 2024 tome, co-written by 20 other German researchers, posits that microcirculation and mitochondrial issues are causing problems with oxygen extraction by the cells. The inability of the cells to get enough oxygen during exercise results in exercise intolerance, lactic acid buildup, and immune activation. Note how these different research groups (Germany, Norway, U.S.) are coming to the same conclusions.
Researchers are settling in around a common theme – problems getting oxygen into the cells and being used to produce energy. (Image by Christine Miller – Wikimedia Commons).
“Upon physical activity, affected patients exhibit a reduced systemic oxygen extraction and oxidative phosphorylation capacity. Accumulating evidence suggests that these are mediated by dysfunctions in mitochondrial capacities and microcirculation…”
Tronstadt, a Norwegian researcher who is speaking on metabolism at the conference, came to a similar conclusion in a 2021 metabolic phenotype paper:
“We suggest that elevated energy strain may result from exertion-triggered tissue hypoxia (low oxygen levels) and lead to systemic metabolic adaptation and compensation.”
Check out the latest from David Systrom and company (thanks, Matthias) in the US from a recent conference abstract reporting on a huge comparative study of invasive exercise results in ME/CFS and long COVID.
“ME/CFS and LC share symptomatic, reduced aerobic capacity at peak exercise, which is driven by preload insufficiency and impaired systemic O2 extraction, the latter compatible with peripheral left-to-right shunting and/or limb skeletal muscle dysfunction.”
Something in the Blood…
Antibodies that may be attacking tissues or dysregulating bodily functions are a major focus.
Autoimmune and autoantibody presentations dominate the immune and clinical trials sections. The idea that an autoimmune/autoreactive response to a virus has been driving these diseases gained ground with long COVID.
The latest iteration of the fascinating “something in the blood” (or now the gut!) saga continues as Jeroen den Dunnen will tell us if he’s been able to produce ME/CFS in mice by giving them IgG antibodies from people with ME/CFS.
Christiana Franke will tell us if she found autoantibodies to neuronal antigens in both ME/CFS and long COVID and if they are causing neurological problems in these diseases. Given the frequent EBV reactivation, finding autoantibodies that mimic EBV sequences in ME/CFS and long COVID could be a big deal. Ditto with finding “autoreactive” (but not necessarily autoimmune) B-cells that may be impacting regulatory functions in ME/CFS.
Autoantibodies—antibodies produced by B or T cells that target our tissues – possibly in response to a pathogen—are also all the rage in the first clinical trials section, where efforts to remove bad B-cells and antibodies via blood cleansing (immunoadsorption), B-cell targeting, plus interestingly, a report on a Japanese Rituximab trial fill the agenda.
The second clinical trials section features three attempts to increase energy (Rapamycin, oxaloacetate, hyperbaric oxygen therapy, Mitodicure), targeting the coronavirus in long COVID, the Open Medicine-funded Mestinon/LDN trial.
Klaus Wirth thinks he may know why people with these diseases can get so ill.
Klaus Wirth, who, with Carmen Scheibenbogen and Mathew Lohn, created the longest series of ME/CFS hypotheses papers ever done, will tackle perhaps the knottiest question in all of ME/CFS – why people can get so sick that they are unable to move. He believes he has an answer. (An interview with Dr. Wirth is coming up.)
Once again, the conference, which will be live-streamed from May 12th to 13th, is in English and free. You can register here. (Videos will be available after the conference.)
Thanks, Cort, for the registration link. I’m sure a lot of it will be over my head, but I look forward to hearing as many of the sessions as I can handle.
Looking forward to your reporting and analysis of the conference. Thanks for everything you do.
Thanks!
You are welcome Cort 🙂
As you say, quite a bit of consistency building on the exercise issue, great!
I am now looking forward to researches pinpointing ‘the why’. And ‘the how’ ( to treat)
We are registered at ACSFCEM. Thank you for spreading the word. Dr. Carmen Scheibenbogen and the team at the Charité in Berlin are doing a great job and we look forward to the latest research.
For what it’s Wirth, my money is on the autonomic nervous system causing the exercise issues. As well as the T cell exhaustion
I echo your thoughts Mattias, my 25 daughter did Systrom’s icPET a few years ago and the findings 100% supported their hypothesis and I’m sure is included in their findings! (She also has SFN/dysautonomia/hdEDS). Mestinon & LDN help a lot, but are not a cure, Also, working with another research team, she has complete t-cell exhaustion, and some of the lowest NK cells they had seen. Not a contest you want to win…..AND it showed constant antigen stimulation. We just figured out last year that her underlying cause was a newer (in humans) strain of babesia (odocolie) that was most likely reactivated and caused her to fall ill in her freshman year of college in 2018! However, it has been a beast to get rid of despite 2 rounds of treatment. We suspect that is why she is only showing small improvement in t-cell function than we had hoped (after TPE/TA-1 shots and antimalarials/antibiotics for Babesia). BUT, there are improvements! So we are sort of alternating between strengthening the immune system and treatment for babesia so that maybe(?) we can get her body to put the babesia into remission and then her immune system and t-cells will go back into balance. I suspect many of the research findings re causes can be true at once, it’s not one or the other. She is starting the rapamyacin trial this July after spine surgery in June so hopefully that will help. I hope this isn’t too much to share, but just that my daughter is a living example of so many researchers’ atypical/abnormal findings. I believe they are headed down the right path to this octopus of a disease……and Cort – we would NEVER have found out any of this if it hadn’t been for you and HR. Am ever grateful…..
I’m glad your daughter has some improvement. May I ask where she goes for her treatments?
Thank you
We live in Boston area so saw Mass General Brigham team there 2020-2025. And then saw Dr David Kaufman in Seattle in 2024 who discovered the Babesia odocoli and we did the TPE with him. Many others prescribe the TA-1 shots. They are helpful for some but not all?
Was it worth the trip to MGB? I suffer with severe ME, live in Ma, and pay a high price for travel.
Hi Kathleen,
Drs. Felsenstein (ID) and Systrom (Pul) at MGH were key to helping my daughter initially in 2020-2024 when she was first seen by them to figure out what was wrong (ME/CFS/SFN, etc.) – but they are not taking /and or seeing patients anymore.
We are now coordinating our care between Dr. Joshua Claunch (neuroimmune/ME/CFS specialist) who sees patients at UMASS in the MS clinic one day per week and privately via telehealth (links are below).
We are still working with Dr. Kaufman in Seattle. There may be other drs at UMASS who are specializing in ME/CFS also, I am just not aware of who they are. I hope this helps, I have 2 other friends whose young adult daughters see Dr. Claunch as well and he’s very approachable and very up to date on the research (in our opinion:)
https://www.practicalneuropsychiatry.com/
https://www.umassmed.edu/ms-neuroimmunology/specialty-care/
Betsy, Thank you for the information. May I ask who did tests for the t cell exhaustian tupe tests. And were they covered by insurance.
Hi Sarah,
So t-cell exhaustion tests was done as part of a research study. They are not commercially available yet – so frustrating! (So we didn’t pay for them).
Drs. Sellin & Gil (at UMASS) believe that t-cell exhaustion will become a biomarker for ME/CFS at some point so then they could be available in clinics.
Wish I had better news, but Dr. Claunch at UMASS is very up to speed on ME/CFS and Long Covid research – per our experience and another friend’s daughter with him. My daughter has had ME/CFS for 8 years, our friend’s daughter for 3 years. Both got sick freshman year of college and have been struggling ever since.
I hope this helps.
Thankyou for all the help that you give our community Cort.
You make a huge difference.
Cort will you do a conference summary?
Yes! This is something I would like to since I am sound and motion sensitive and will be unable to listen in on the conference at all.
FYI the hyperlink in the piece for Puta’s “2024 tome” was not working for me, here is another
https://link.springer.com/article/10.1007/s15010-024-02386-8
Thanks for this. It seems that views are really coming together in terms of the cause of PEM. This, Systrom’s major new paper etc.
I often get down about the lack of progress, so it’s wonderful when we see progress like this.
On any given topic there seem to be rashes of papers that come out all around the same time for every topic involved. It’s really encouraging 🙂
Looking at the speakers, I love that Iceland (with a population of around 390.000, i.e half of the city of Frankfurt in Germany) has newly founded a national ME/CFS clinic and is presenting it in the conference! The Akureyri Clinic is named after the town in Northern Iceland where it is located which notoriously experienced an epidemic of ME/CFS 75 years ago, and is also looking to build an ME/CFS case database for research. https://events.mecfs-research.org/en/events/conference_2025/speakers/c4F82NbSRnOx4xYRIY2n8Q
The conference is supported by ME/CFS Research Foundation, a private German ME/CFS research foundation that also came up with nice ideas like the social media Lemon Challenge for ME/CFS.
The link to Puta’s 2024 is not working, maybe you’d like to fix it 🙂
This is a great lineup! I am hoping to watch at least a few of the sessions
Very curious to see what Wirth and company has to say about why some people become very severe.
As for his interview, any idea when that may be published? Anxious to read it!
Shouldn’t take long 🙂
Very interesting, I hope Cort will do a conference summary, would be very appreciated!
Will do!
Cort, it is not Jeroen The Dune but Jeroen den Dunnen 🙂
Just watched Prof Fluge present on a preliminary study the drug Daratumumab. Saw positive results in 6 out of 10 patients. Large clinical trial planned.
Caveats include this may be beneficial for subset of ME/CFS patients with autoimmune traits. I wonder what proportion of patients, roughly, have autoimmune traits?
Daratumumab is a very serious drug. We need to know -objective- which patiënts will benefit from it first. But good to see.
Stellar presenters coming up!
Michael Peluso – Targeting viral persistence in PCS
Systrom – LDN and mestinon trial
Putrino – low dose rapamycin
Wirth – mitochondrial dysfunction
I would also like to point out the excellent research projects on MECFS in Austria, especially in Vienna. The WE&ME Foundation funds these with donations. A list of the research projects can be found at: https://www.weandmecfs.org/de/projects
Nice! How about that! 🙂
To me, Mr. Wirth’s (admittedly very conplicated) hypothesis ist propably the best I have ever read about ME/CFS.
In my understanding, he postulates that there is a kind of “point of no return” that changes Long Covid (but, of course, also other initial dideases or vaccinations, etc.) into ME/CFS.
Once being trapped in this vicious cycle, it does not really matter any longer what the initial problem was. The sickness is self-perpetuating.
This would also explain why studies all over the world fail (e.g. rituximab) on a regular basis, as the selection criteria do never include wheter the person has MECFS like symptoms because of the initial trigger (e.g. autoimmunity or viral persistence) or whether he/she has already entered the vicious circle (where treating the initial trigger would not be sufficient any longer).
In my opinion, this is the “Elephant in the room” and…..unfortunately again…..there has been no discussion about this hypothesis during the live sessions.
If his hypothesis turns out to be true, all the other funds spent to try to cure the disease by treating the initial trigger would keep on failing. Of course, such treatments could improve symptoms as you eliminate a part of the enemy (e.g. AABs) but you’ll never gonna solve the problem.
This is why I think that it would be important to have a broad discussion about the credibility of this hypothesis (and I hope he’s right).
Maybe I am wrong. Maybe he is wrong. But I think that we should find this out. For this reason, I kindly ask you, Cort, to include this topic into your Interview with him (my understanding is that this is an upcoming interview,right?).
He has explained the science behind this several times. I am much more interested in the discussion of why this is still not properly recognized. In particular:
– What could be the weakness of his hypothesis?
– Why is Prof. Scheibenbogen (as a Co-author of his hypothesis) conducting studies for B-Cell depletion if she supports the postulate that this can never be a curative treatment or MECFS?
– Why is it so hard for him to generate funds if this is (still:my personal oponion) propably the best theory about this f…. sickness?
Again, he has explained his theory quite often (although he will never be a marketing guy 😉) and I would really like to understand whether there is real hope here.
I guess that Prof. Scheibenbogen is currently probably focussing on getting medications that can make symptoms better to patients as fast as possible, e.g. by repurposing medications that are already approved by regulators for other diseases – which is probably faster than going through the regulatory approval process for a completely new drug.
Also, in my opinion, ME/CFS is probably a complex cascade dysregulation in the body (a system out of balance), so maybe adressing one element of that dysregulation can lead to some overall improvement (like some people get a bit better but not cured by Low Dose Naltrexone or chang,ing their diet).
Looking forward to watching Wirth’s presentation as soon as it’s online!
Hi Oliver, ME/CFS is not Long Covid, nor is it an outcome of LC. I have had ME/CFS since 1984 and although the symptoms were awful, they were not life threatening. When I got Covid twice in the same year, the symptoms (despite taking Paxlovid) were life-threatening heart problems and high blood pressure followed by unbelievable difficulty with walking and balance.
“People with any type of COVID-19 infection were twice as likely to have a major cardiac event, such as heart attack, stroke or even death, for up to three years after diagnosis.Dec 18, 2024”
Covid also attacked my hearing.
Sensorineural Hearing Loss as a Complication of COVID-19 and the COVID-19 Vaccine
https://pmc.ncbi.nlm.nih.gov/articles/PMC10665765/
I have been reading posts by patients with Long Covid on the Mayo Clinic Connect site. They seem to have a much better understanding of this that these doctors who try to fit things into little boxes they have conceived.
Do I still have symptoms of ME/CFS? Yes, but LC is so much worse. I do think ME/CFS makes you more susceptible to Covid.
Hi Betty, i don’t know if you have been vaccinated with the mRNA vaccine against covid-19. But it is well know that the vaccins can lead to heart problems also.
https://cardiovascular-research-and-innovation.reseaprojournals.com/Articles/myocarditis-after-sars-cov-2-infection-and-covid-19-vaccination-epidemiology-outcomes-and-new-perspectives
Also long covid can be caused by mRNA vaccins. Also high IgG4 can be caused by
mRNA vaccins.
”evidence suggests that the reported increase in IgG4 levels detected after repeated vaccination with the mRNA vaccines may not be a protective mechanism; rather, it constitutes an immune tolerance mechanism to the spike protein that could promote unopposed SARS-CoV2 infection and replication by suppressing natural antiviral responses. Increased IgG4 synthesis due to repeated mRNA vaccination with high antigen concentrations may also cause autoimmune diseases, and promote cancer growth and autoimmune myocarditis in susceptible individuals.”
https://pubmed.ncbi.nlm.nih.gov/37243095/
Yes, but Covid is orders of magnitude more likely to cause these issues than a vaccine. Pretty standard situation with vaccines… a select few will respond poorly. Idk why you insist on posting this on every thread that mentions LC. This is not unknown. This person is speaking of their overt covid infection, not vaccine injury.
First of all, this was directed at Betty to tell her about the heart problems that can occur after mRNA vaccination. Secondly, there is little attention for the damage caused by mRNA vaccinations. Thirdly, I dare to doubt your statement that these are fairly standard and rare side effects. What is even stranger is that it is not allowed to be discussed and independent researchers are not given data to investigate the pros and cons of mRNA vaccines. This also applies to the continuing excess mortality and increase in serious cancer and people who die suddenly. There is clearly a relationship with the mRNA vaccines, although it cannot be determined on the basis of these studies whether it is really the cause. And these independent researchers do not receive the data that is needed for this. There has also never been a double-blind study that demonstrates the effectiveness of mRNA vaccines. Science should be transparent.
That’s an excellent post!
I must say that I found all the talk about autoantibodies and viruses a little bit frustrating. I think a proportion of ME/CFS patients have autoantibodies or active viruses, but I would hazard a guess it might be 30% or less.
As you say, I think it’s far more likely, for the majority of patients, that viruses trigger the illness, but do not have a role, or at least major role, in perpetuating the illness.
I found Dr Wirth’s presentation interesting, yet very complex. I do think it’s a valid theory.
I was a bit disappointed in the lack of brain focus. For me, the brain / CNS and its interaction with the autonomic nervous system (which impacts immunity) is where the most likely explanation exists for the illness. I am especially interested in brain connectivity and neurotransmitter functionality. I think these areas can explain a lot.
Nath et al’s study strongly implicated the brain. Klimas said after the study that the t is central to the illness.
I maintain the view that the immune system
Is a little bit of a distraction
I think Davis’s itaconate shunt theory is another interesting one. Like Wirth’s, it explains the circular perpetuation of the illness, with less concern for the trigger.
Thanks for your compliments on my post 😀
I will dive a bit deeper into Naths / Klimas’ hypotheses.
I have to admit that I have never fully undestood the Itaconate shunt theory (maybe, because my favourite is still the Wirth theory 😀)
But I will dive deeper into them now.
Thabks for these remarks.
Oliver, sprechen Sie deutsch? Anfangs Woche ist in Berlin die ME/CFS-Konferenz über die Bühne gegangen. Die Mehrheit der Forscherinnen und Forscher, die präsentiert haben, forschten schon lange vor der Corona-Pandemie zu ME/CFS.
Bei ME/CFS ist es schon lange Konsens, dass der spezifische Trigger (EBV, Grippe, Covid ect.) nichts mit dem Pathomechanismus zu tun hat. Auch dass es bei ME/CFS einen leichten Verlauf gibt, der oftmals reversibel ist, und eine Art point-of-no-return, wo die Krankheit sich stark verschlimmert und die Prognose sehr viel schlechter ist. Das ist ebenfalls Konsens.
So viel ich weiss, gab es auf der Konferenz keinen einzigen Beitrag, der diese beiden Sichtweisen bestreiten würde.
Klaus Wirths Theorie zum Pathomechanismus hat er hier vorgestellt. Es geht um ein Problem des Sodiumtransports in den Mitochondrien:
“Our working hypothesis is that mitochondrial dysfunction and damage together with malperfusion plays a key role for exercise intolerance, PEM and even systemic symptoms as explained in several publications. Our drug is conceived to treat and prevent ionic disturbances otherwise well known form experimental medicine that cause mitochondrial damage.
The key assumption of this hypothesis, a rise in intracellular sodium in myocytes, has been proven by the demonstration of elevated intracellular sodium in skeletal muscle (23-Na MRI study in ME/CFS patients). This study was performed based on our hypothesis. Several papers published early this year prove skeletal muscle pathology, structural damage to myocytes and mitochondria which is a breakthrough in ME/CFS research.”
From the comments section under that link:
https://www.healthrising.org/blog/2024/02/08/me-cfs-mcas-gynecological-disorders-klaus-wirths-blood-vessel-diseases/
Es gibt zwei ernstzunehmende Hypothesen zum Pathomechanismus: Autoimmunität und Herpesreaktivierungen. Die führenden Forscherinnen zur Autoimmunität forschen in Berlin und München.
Führend bei der Erforschung der Theorie der HHV-6b-Reaktivierungen sind Jacqueline Cliff an der Brunel University in London und weitere Kollegen wie Bhupesh Prusty in Tallinn. Ich bedauere es, dass sie dieses Jahr nicht an der Konferenz waren. Denn sie haben sehr gute Resultate in den letzten Jahren, die zeigen, dass sie wahrscheinlich auf der richtigen Spur sind.
Hi Lina,
sorry for my late reply. Yes, I am German but lets try to discuss this in English language that others can also follow.
In think that there have been some missunderstandings: I have attended the conference and I think that I have a very good overview about all the “players” (you named Mr. Prusty as an example).
You are right: Noone gad any contradiction brought forward against Mr. Wirths hypothesis.
…..at least not directly!
But my problem is that I think that indirectly, noone is really listening to him. Orherwise, there would be a big big discussion about the study design and the selection of patients.
Again: If he is right, we are talking about different diseases here, lets mame them
MECFS and Pre-MECFS
– Based on his theory, MECFS (with its hallmark symptom if PEM) is manifested by the “Sodium-Pump-Problem” as its function is reversed.
– Based on his theory, there are different mechanisms how MECFS is triggered (AABs, Viruses, MCAS, etc. or even a combination). All of them can cause PEM too but are NOT MECFS as the Sodium Pump is still ok.
– He says that real MECFS is independent from AABs, Viruses, etc.
My point/problem is:
If I take a medicine and design a study (lets say BC007) and select 100 patients. All of them have PEM so I assume that all of them have the same desease (MECFS) Now, if the study fails as BC007 cannot beat the placebo effect, we think that it is not effective.
However, if Mr. Wirth is right, all of these studies are designed to fail because, in this case BC007, might have an effect on AABs (and all persons who suffer under PEM from Pre-MECFS) but the effect will be almost zero for (Sodium-Pump)- related “real” MECFS.
So the discussion I am missing is, whether he is right or not. If he is, we will nwvwr be successful with any of our studies. We would first jave to pre-select patiens with “Pre-MECFS” from them with (“Sodium-Pump”) MECFS.
I forgot: I agree about your statement about the pathomechanisms. But understanding the pathomechanisms will not cure the “Sodium-Pump” MECFS persons (if he is right). Dont get me wrong: it is still important to understanding this. But we will never cure MECFS out of any if these hypothesis (if he is right).
Therefore, I think that he needs much more focus until he is proven wrong.
Hi Oliver, thank you for your reply.
I think that I am personally not so much interested into Wirth’s work because it seems to me that he has – if at all – understood something about irreversible mitochondrial damage in ME/CFS. The severely affected. As I explained above. I believe that this is just one small piece of a big puzzle of organ damage / pathological changes in ME/CFS.
I was only a moderate and I am slowly but gradually recovering with pacing. I think that my mitochondria regenerate well. My issue is rather brain damage and flare-ups and relapses.
I am convinced that herpes reactication is a thing in ME/CFS because I responded well to acyclovir during ME/CFS acute episodes.
The most important thing for me is therefore that the HHV-6b theory gets thoroughly researched and confirmed or ruled out as fast as possible.
Since I already have a drug that works for me and have also managed to adapt my lifestyle to illness level Klaus Wirth’s work is totally irrelevant to me personally.
Ok, understood. Thank you very much for clarification. I think our discussion was/is a typical example of all of the discussions:
This disease is soooooo complex and we are not even sure whether it is really one disease or 20…..
I am mild, too. But on the other hand very different. I have no brain issues, no POTS, no Nervous System Issues, but have (mild) PEM. So mitochondria are important for me 🙂
I think that Wirth’s theory is so important because it is so well founded and Ms. Scheibenbogen has published it together with him (so there must be something true in it). And if he would be right, this would change the whole approach, because:
– We could treat PEM effectively
– Everyone would accept that MECFS is real and that it can be healed
– Big pharma would jump on that train
– We could much better separate between people with (curable) PEM and other symptoms. Once we have such a biomarker, we could focus on the other symptoms much better because these would not be biased by the PEM mechanisms any longer.
At the moment, I have the feelibg that PEM is like the hole in the Titanic and we are standing on Deck trying to fix the broken chimneys (no offense meant: I understand that the other symptoms can be debilitating).
In my opinion, his theory is the key, but, of course, he can be wrong (or I just dont understand it coreectly).
This is why I complained about a missing discussion on his theory.
Another question:
So you responded well to acyclovir and this is the drug that works for you, right?
Could you please provide some more inputs?
Why not Valacyclovir?
How did you find out that it was Herpes-Virus -related?
Did you do any specific blood test?
What Herpes viruses were your major problem?
Sorry to be so indiscreet, but I am asking because I might have the same origin (did an LLT and several Herpes Virusesshowed massive amplitudes). However, so far, no doctor has any idea how to treat.
Hi Oliver, my intuition told me that I had viral reactivation. I then convinced a throat-nose-ears doctor to prescribe me acyclovir on speck – and it worked. : ) That was before I knew that there was ME/CFS and that I fulfilled the criteria. I thought – and still do – that I have smoldering herpes virus reactivation that affected the immune system first and jumped over to the brain too when I became moderate.
Valacyclovir and acyclovir are the same.
If you’re only mild I can recommend that you learn to pace yourself perfectly in order to avoid any more flare-ups. Your chance at recovering fully is intact.
When you avoid flare-ups you avoid at the same time that the inflammation process during the acute episodes (what you call PEM) does harm to your immune system and you can thus allow it to fix the damage and to regenerate by itself slowly.
It will take time and if your still young you might think you don’t have it – but actually that is a very promising path of action.
If acyclovir would work for you too to fight the acute flare-ups (PEM) it were still not a cure. And I have read the story of a doctor who self-medicates with acyclovir and continues working full-time. Over time her ME/CFS worsened when at the same time she got problems with the acyclovir side-effects.
If you want to read more and other views on the mitochondria in ME/CFS check out the material that is provided on the website of the British ME association website.
Check out specifically their report on the mitochondria and herpes viruses. But also their guides on pacing and activity management, and flare-ups are worth reading.
Scheibenbogen does indeed do great work. But other researchers are really good as well. And I think especially for patients with a mild course the ME association provides more detailed information and advice.
Oliver, ME/CFS is not difficult to diagnose and it is not a complex illness. It has been understood for a long time what the main characteristics are, and what the typical co-occurring symptoms that arise only in subgroups of patients, like for example POTS.
There are the Canadian consensus criteria to diagnose.
I am glad you got the diagnosis even when you’re only a mild patient. I think that’s rather a problem than understanding the main features of ME.
Take care (and pace!)
HI Gijs, I did not take the MRNA vaccines for two reasons. One, I am very reactive to all kinds of chemicals and medications. And two, when I researched MRNA technology in the beginning of all of this, I could find no evidence that anything had been accomplished over 30 years of experimenting with MRNA technology.
I spent 10 years getting a dangerous drug off the world-wide market so I am much more skeptical than most when it comes to medications and vaccines.
I am not anti-vax. But, I am concerned about the number of vaccines children are now being given especially combination products. I have never been able to figure out how one vaccine could protect you from several things at once. After all, you would never get measles, mumps and rubella at the same time.
Any vaccine can have adverse effects in some people. That is why there is a National Vaccine Injury Compensation Program, a fact that has largely been ignored in the vaccine debates.
Hi Betty, i think we agree. Your increased healthproblems -with your heart- can also be due to covid-19 virus itself, like you write. It is the same with the flu. Many don’t know you can heart problems from that either. Take care! I hope you feel better in time!
Curious… Do you think you’d make the same choice now, knowing how COVID affected you? I suppose it’s impossible to know what the alternative could’ve been if you’d had the vaccine… but I’m wondering how you feel about it now?
Hi Gijs, I forgot to add the link to the National Vaccine Injury Compensation Program https://www.hrsa.gov/vaccine-compensation
The National Vaccine Injury Compensation Program (VICP) provides compensation for injuries or death resulting from covered vaccines.
Here’s a breakdown of potential compensation:
1. Medical Expenses:
The VICP covers past and future medical expenses related to the vaccine injury, including diagnosis, treatment, rehabilitation, and ongoing care.
There is no limit on the amount of compensation for medical expenses.
2. Lost Earnings:
Compensation can be awarded for past and future lost wages due to the inability to work because of the vaccine injury.
There is no limit on compensation for lost earnings.
3. Pain and Suffering:
The VICP provides compensation for pain and suffering, both past and future, related to the injury.
However, compensation for pain and suffering is capped at $250,000.
4. Death Cases:
In the event of a vaccine-related death, a statutory death benefit of $250,000 is awarded.
Compensation for the pain and suffering of the deceased prior to death can also be awarded, with a maximum of $250,000.
Important Considerations:
No-Fault System: The VICP is a “no-fault” system, meaning you don’t have to prove negligence on the part of the vaccine manufacturer or healthcare provider.
Covered Vaccines: Only injuries from specific vaccines listed on the Vaccine Injury Table are covered by the VICP.
Filing a Petition: To receive compensation, you must file a petition with the U.S. Court of Federal Claims.
Legal Representation: While not required, most people hire a lawyer to assist with the complex legal process.
Attorney Fees: The VICP generally pays reasonable attorney fees and costs, regardless of whether compensation for the injury is awarded, if certain requirements are met.
Disclaimer: This information is for general knowledge and should not be considered legal advice. Consult with a qualified attorney for advice specific to your situation.
About The National Vaccine Injury Compensation Program
What Can You Receive Compensation For? Under the Vaccine Injury Compensation Act, you can receive compensation for: * Medical Expenses (Past and Future) * Pain …
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http://www.vaccineinjuryteam.com
National Vaccine Injury Compensation Program – HRSA
May 1, 2025 — COVID-19 claims. For claims associated with the COVID-19 vaccine or other COVID-19 related countermeasures, please file your Request for Benefits with the Count…
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Health Resources and Services Administration | HRSA (.gov)
Hi Cort
We have only just today discovered this great website!
I would like to be able to access the conference online sessions if at all possible.
Having lived with ME/CFS for 19 years I am always keen to read and learn of advances in knowledge about this illness ( when my brain lets me!)
Hi James, to access the conference videos once they come online, go to this website: https://events.mecfs-research.org/en/events/conference_2025
It says: “The International ME/CFS Conference 2025 has concluded. You may still register in order to receive a notification once presentations are available on demand on our website.”
To register, scroll down to “More Information” and click on the green “Registration” tile.
I would not have taken the Covid vaccines for the reasons I mentioned before. That said, there are people who never had Covid but developed Long Covid after the vaccines.
Finally, if having a case of Covid in August 2022 wasn’t enough to protect me from getting Covid again in May 2023, not even a year later, how would a vaccine offer protection.
Covid is a very unusual virus, rapidly mutating all the time. I think it is hard to stay ahead of it with a vaccine.
The vaccines are known to have reduced the likelihood of developing LC. And while in some cases they led to vaccine injuries similar to LC, that was FAR less likely with a vaccine than it was with an infection. I’m not sure why you assume that because you got LC from the virus that you automatically would have gotten it from the vaccine. Those who were vaccinated were far less likely to end up with LC than those who were unvaccinated (except the few unlucky people who reacted to the vaccine the same way). Getting the virus itself causes dramatic damage to the immune system… getting the vaccine is far less likely to do so, so it’s quite likely that someone who developed LC from the virus would not have ever done so from the vaccine.
Your comments are questionable. Many studies use models based on assumptions, which makes them less reliable. Some statements are outdated. The immune system is affected by the mRNA vaccine. The effectiveness disappears within a few months. There has never been a double-blind mRNA vaccine study. Lie 1: if you are vaccinated you can no longer get corona (Biden) lie 2: if you are vaccinated you can no longer infect someone else Lie 3: the mRNA vaccine is safe. The longer term effects have never been studied.
”As the immunity provided by these vaccines rapidly wanes, their ability to prevent hospitalization and severe disease in individuals with comorbidities has recently been questioned, and increasing evidence has shown that, as with many other vaccines, they do not produce sterilizing immunity, allowing people to suffer frequent re-infections. Additionally, recent investigations have found abnormally high levels of IgG4 in people who were administered two or more injections of the mRNA vaccines.”
https://pmc.ncbi.nlm.nih.gov/articles/PMC10222767/
Only received the email on May 15 th.
Dear LH, I do not want to get into a vaccine debate, but I do want to explain my decision so you don’t think I fall into the anti-vaxer camp.
One of the earliest symptoms I had of ME/CFS was severe reactions to drugs, chemicals and foods that had never bothered me before. I also had chronic infections and bad reactions to antibiotics to treat them.
Finally, I decided to see if I had “mast cell” disorder. I went to an allergy clinic where they scratch tested me and found that I was reactive to all kinds of chemicals. Then they decided to do a trial of medication to see if it would help. I was given low doses of two antihistamines, Singular and Tagamet. The next day my vision was so blurry I could hardly see.
I figured it had to be the medications so I stopped them all, but the blurriness continued until the next day when I went to an optometrist. My eye pressure was so high, he sent me immediately to a glaucoma specialist.
This doctor recommended laser surgery which I agreed to because I was afraid I was losing my vision. All went well, until we took a 13 hour plane trip to visit our daughter in Maui. I think there may have been a nick in the artery that was affected by the air pressure in the plane.
When we got to Maui, my left eye turned bright red and drooped and I had the most horrible headache of my life.
We contacted the glaucoma specialist who was very concerned. As it happened, his former partner was practicing on Maui and he was able to give me some drops to help control the pressure until we got back to Orlando.
As soon as we returned, I was diagnosed with a carotid cavernous fistula which is where there has been a rupture in the carotid artery behind the eye and it connects to the vein behind the eye. This can result in blindness or a stroke.
I was rushed into surgery where a specialist threaded instruments up through the carotid artery and vein in my abdomen into the brain where he separated the vein and artery with platinum coils.
The vision in my left eye is getting worse and if anything happens to my right eye, I would be diagnosed as functionally blind.
I still have glaucoma and it is also getting worse. I have a new ophthalmologist and I hope he will have some answers to save my vision.
Now if all of this happened from O-T-C drugs like antihistamines, Tagamet and Singular, why would I risk taking a new type of vaccine?
I’m a bit late to the party here, but what did Wirth end up saying about his theory for why some patients get severely ill? I haven’t been able to find anything on what he said.