Geoff’s Narration
The Blog
Ron Davis brings researchers together every year to probe deeper into ME/CFS. Among the attendees this year: Akiko Iwasaki, David Systrom, Carmen Scheibenbogen, Jarred Younger, Liisa Selin, Chris Ponting, Andrew Grimson, Paul Hwang, Chris Armstrong, Rob Wust, Kenny DeMeirleir, Bob Naviaux, Bhupresh Prusty.
Have you ever tried to drink out of a firehose?
Me neither. Until last week.
That’s when I attended Ron Davis’s annual Working Group meeting. That’s where a roaring firehose of ME/CFS (myalgic encephalomyelitis/chronic fatigue syndrome) science, research results, data and charts and graphs and concepts and theories and researcher’s names — along with their many titles and university affiliations — came rushing at me.
For four solid days (September 3-6, 2024), from 11 am to 4 pm ET, I tried to drink from this fire hose, intellectually speaking.
Maybe I took in 10% of it…? Okay, more like 5.
I spent most of those four days in bed, where you’ll often find me. I watched the invite-only Zoom meeting on my laptop, usually cloaked (camera off). Yet I asked questions and was an active participant in the meeting’s chat. I typed about how my (or others’) experiences as a patient related to the research of 100 or so speakers. With so many attending, the chat was ever-bubbling, ever-popping with new posts. Blink, and you could miss ten attendees asking probing questions of the speaker or offering comments on the scientific findings displayed on their slides.
I’m no scientist; I’m an advocate. So it’s not surprising I did not grasp much of what was relayed by this pantheon of powerhouse PhDs. My advocacy work over the decades has focused on supporting patients, writing, organizing panels, working with elected officials and more. Since the pandemic, I’ve also been dedicated to Long COVID (LC) and the newly-coined broader community of “infection-associated chronic conditions and illnesses” (IACCIs).
That said, I do work with two Massachusetts research labs as a patient rep. In our meetings, I listen with delight to their delight about just-analyzed blood samples. Then I ask, “Can you please re-state that in layman’s terms?” I mean, I can tell from their excitement that it’s all good. But really, who can understand that impossible-to-understand scientific lingo?
Well, impossible-to-understand scientific lingo reigned at Ron Davis’s meeting. Every half hour or so, some new person presented data on ME/CFS and LC in what (to me) sounded like ancient Greek. Plus, it was all filtered through my cognitive dysfunction. As a result, even if I were allowed to share details about the meeting (I’m not), could I now summarize for you the presentations? Relay groundbreaking news? Tell you about promising treatments? Nope. No. Still no.
So why did I even attend this gathering? And why write this debrief for you?
I’m here to offer hope. I want you to know what I now know only because I was able to attend this closed-door meeting: There are dozens of PhDs who want to help us, who are actively working to help us. That’s their job. And they take their jobs seriously.
At the start of every day, Ashley Haugan, Ron Davis’s daughter, and the nimble meeting organizer, opened with a welcome and any housekeeping items. At the end of every whirlwind day, because this affair is a family affair, Janet Dafoe, Ron Davis’s wife, and a noted patient advocate, shared patients’ feedback that she’d gotten on her Twitter/X account. The feedback was full of gratitude for the researchers.
A slide from the meeting posted by Janet Dafoe
The two meeting moderators were upbeat and super smart. They were able to synthesize what each speaker had just said in their presentation and relate it to the larger context of the meeting. They also deftly read aloud and framed for the room the questions that had come in via the chat for each speaker.
Though I could never summarize for you all that I’d heard, still the four-day firehose experience was amazing. Most remarkable was the last half day. Ron, frustrated by not getting the freewheeling, deep-probing, pulling-it-all-together discussion he was hoping for, forced a new module onto the group. Ron asked the Zoom room to discuss (paraphrasing): What will it take to figure out this disease? How can we integrate our theories, which are now siloed, and instead work together? How do we decide which theories can best explain ME/CFS symptoms, especially PEM?
Ron put deep thinker Rob Phair in charge of this group conversation focused on the big “what’s, why’s and how’s.” To direct us, Rob asked the room:
- Is ME/CFS viral, reactivation viral, or truly post-viral?
- Is ME/CFS primarily an inflammatory disease?
- What is the nature of immune dysfunction in ME? (Exhaustion? Subversion by pathogen? Autoantibodies?)
- What is the source of ME/CFS chronicity?
- Is mitochondrial dysfunction the final common pathway of ME? (Or is mitochondrial dysfunction primary?)
- What is the mechanism of PEM?
This Rob Phair facilitated freewheeling, big picture brainstorm session was focused and limited, because only the presenters of the last four days were given the floor. It was also incredibly stimulating. Some researchers shared their overall theories about what is going on with this disease, i.e. why we are all languishing in our beds.
It may have been like drinking out of firehose but for Rivka the outcome was clear: committed researchers working hard to solve ME/CFS.
An additional exercise was added on near the end of the meeting: Any researcher who spoke was then asked to name another researcher from the conference with whom they’d like to talk or collaborate. That generated some enthusiastic “Let’s connect; here’s my email address” type of interactions. It was great to witness this knocking down of silos. In fact, the Massachusetts researchers I personally work with made valuable connections with two other researchers that, if the relationships build, could clearly advance the field.
In closing: I spent last week hanging out with a bunch of smart-cookie researchers whose careers are focused on explaining, and ending, our suffering. Take heart, friends, we are not alone. I have hope — and I want to share some of that with you.
Check out Jarred Younger’s Update from the Working Group Meeting.
BIO: Rivka Solomon (Twitter/X: RivkaTweets) is an ME/LC/IACCI advocate based in Massachusetts, and a member of MassME. She is also a patient representative working with two collaborating labs: the Selin Lab, at UMass Chan Medical School, Worcester, MA, with Liisa Selin, MD, PhD, and Anna Gil, PhD, and HiFiBiO Therapeutics, Cambridge, MA, with Roshan Kumar, PhD. Funded in part by the Patient-Led Research Fund, these labs are investigating ME/LC immune dysregulation and profiling the immune repertoires of T cells at a single-cell level. The Selin Lab is also working towards a potential biomarker for ME/LC.
Thank you for sacrificing your valuable spoons and attending last week, Rivka! Grateful for relaying this back to the community and offering this insight. We are indebted for your services! Many thanks to all who contributed with making this meeting happen, and for the injecting more hope towards brighter days ahead.
Hopeful that this will event will only continue positive progress.
Thx! It’s difficult that science moves so slowly when our need is for desperately fast urgency. I can tell you that everybody who attended this meeting has a passion to make it move faster.
Cort, even if you can’t share specifics, is there any progress on the itaconate shunt and metabolic trap hypotheses?
Well said, William. And I am so thankful for all these people who keep hanging in there with us. And always a huge thank you to Cort. What a great advocate!!
You’re the perfect person to report on this meeting, Rivka. A person with ME and a talented writer. This was definitely a meeting of the super minds and I’m excited to see what comes of it.
Thank you, Andrea, for your support. It means a lot!
Thank you Rivka for advocating for us!
Much appreciated!
And of course, to Cort.
( we share the same bday coming up!)
Same back to you, Loryn. And I’m also so appreciative of Cort for posting my guest blog. 🙂
Thank you Rivka!! I can imagine how draining that must have been for you. You’ve given us hope and brightened my day!
(comment removed – antagonistic)
Dr Rob Phair took me up on my challenge to come back to Truckee High School, location of the original cluster that cause Drs. Cheney-Peterson to call the CDC for help and which served as the ultimate basis for the confusion of CDC epidemiologists Kaplan and Holmes.
“How Mystery Disease Hit Three Teachers” North Lake Tahoe Bonanza Oct 12 1985.
Dr Phair told me “What you describe is impossible” yet the original CFS cluster is very well documented. The toxic mold sensitizing effect has been reproduced thousands of times. We know it is VERY possible.
By abandoning what CFS was really coined for and substituting some kind of “umbrella CFS construct” these researchers have made an illegitimate data-switch that is not allowed in science.
While I’m sure these “top researchers” have many interesting ideas, they are not related to Holmes 1988 Chronic Fatigue Syndrome.
-Erik Johnson
Incline Village survivor – graduate of Truckee High School.
Original prototype for Holmes 1988 CFS
As always, I expect nothing but hostility and antagonism from the “ME/CFS community” who have fought against the original CFS evidence for four decades now, and counting.
Erik you’ve put your ideas out there – they are accepted by some and rejected by others – there’s nothing new about that in science. Many people are thankful that you introduced mold so you have clearly not gotten “nothing but hostility” from the ME/CFS community. I don’t think anyone rejects the idea that mold can cause ME/CFS: what they reject is the idea that it’s the sole cause.
This comment was removed “As always, the proposition that anyone is trying to “Solve CFS” is utterly false.” as being unnecessarily antagonistic”
Cort. No one proposed that mold is the sole cause.
I am an HBLV “original” and post about that constantly, as I did when you and the CFS research group fought against this same evidence back in 2003.
Your only manner of “response since that time is the pretense of all-knowingness which removes the duty to respond.
When obviously none of you do, for the entire ME/CFS community failed to identify “Mold at Ground Zero for CFS” and continue that battle to this very day.
The ME/CFS community has no right to criticize the CDC/NIH.
For this community has done more to create hopeless confusion than the CDC/NIH ever did.
I’m confused. If mold at ground zero for ME/CFS is what almost you believe everyone missed – and as you know I do believe that the researchers have missed the boat on mold and ME/CFS – then why do you not believe mold is the sole cause? Do you believe its the sole initiating trigger or ???
Dr Stephen Straus of the NIH set up a “potential for conflation” by his deliberate choice of a confusing name. For he knew this is how most people think of the target is “chronic fatigue”
When of course, this opens up the debate to anything that causes fatigue.
Making the syndrome “evaporate” in confusion, as Straus expressed would happen in his letter to Keiji Fukuda. Congratulating him on his 1994 “CFS redefinition”
Which was really to remove Holmes 1988 which was based on real people with real evidence.
This should not have fooled a single scientist, since it is “basic science 101” to Start-at-the-beginning & look at what Cheney-Peterson, Kaplan and Holmes were summoned to investigate, and what it was they were confused about.
Which happened to be a cluster of teachers at Truckee High School who mysteriously got sick at the same time, in the same room, with the aberrant EBV profile that fit the CDC’s new CEBV-Syndrome definition.
If you think like a scientist and regard the CFS syndrome as the actual reason for its creation, it is very simple.
You look at what was in the room and find out what infections those teachers had in common.
As you know, the unknown agents were toxic mold and the newly discovered HBLV.
Making toxic mold and HBLV the actual targets of Holmes 1988 CFS.
What I “believe” is that researchers should employ scientific reasoning rather than regard CFS as a useless label for all-things-fatigue.
And then ask why Dr Stephen Straus set up CFS to fail.
In the ’90’s, my upstairs neighbor let his bathtub run wild. My walls were soaked and a severe mold took over. I had to move out.
Not too long after that I developed chronic fatigue.
I don’t know if it’s the CAUSE or even the MAIN CAUSE.
But it’s worth INVESTIGATING.
Eric… do you think CFS all started in Lk Tahoe?
Yes. The Holmes CFS definition did not exist until the Lake Tahoe outbreak, and was based on this very incident.
Prior to that people called their illness many different (and very confusing) names.
Especially adult mono and EBV syndrome.
There was no syndrome called “CFS”
So yes, “CFS all started at Lake Tahoe”
Only the name CFS. Not the illness. I got pericarditis in 1978 and was never well again.,
CFS is not just a random meaningless name. A new syndrome conceptual framework and associated evidence to which the CFS term was applied by the Holmes committee.
Both the Royal Free disease “ME” and the Lake Tahoe Mystery Illness “CFS” were distinct outbreaks associated with a notable “flu” that devastated the Royal Free Hospital and my little village.
Without the scare factor embodied in the contagious aspect of these incidents there would be no “ME” and no “CFS”
Had ME/CFS since 2015 and first 5 years were very typical symptoms like the orthostatic intolerance, only had mold sensitivity occasionally when I could see the black mold on peoples windows, cleaning it off stopped the reaction simply, but in 2018 after it rained a lot I began to not tolerate my summer house and had to abandon it, nothing I tried fixed it and I figured out mold was probably the cause.
Fast forward a few years and I became intolerant to 2 bedrooms and I developed extreme chemical hypersensitivity, could smell peoples washing line from 50ft away, soon couldn’t go into my bathroom or kitchen anymore due to sensing the mold. There’s something to this mold to CFS connection in my experience, but it could just be that CFS is or causes a low amount of antioxidants to exist in the body, so any toxin becomes an issue.
I started to get SIBO and food intolerances, felt rough all the time so I went to live in a tent in the back garden, after about 4 months I started to get better, took a lot of herbs and things to treat SIBO then I started on high dose thiamine. My reactions improved. Was able to live indoors again in a low mold room with air purifiers, no carpet, removed or washed old fabrics, minimalistic. In the past year i’ve not experienced much PEM and im still living indoors in the same room. I have some issues with periodic air pollution events and I had to put up shielding when a house 25 metres away got a ‘smart meter’, but apart from that i’m doing ok despite my rare hypersensitivities that normal people often don’t believe.
I avoid mold as much as I can now but I am still unconvinced that mold causes CFS, I just cant the logic of it with my personal history. That said i’m also skeptical whether viruses really exist or not, so I don’t know if I would blame ‘magic’ invisible viruses either. Poisoning by toxins seems to be the simplest explanation for CFS, toxins that never leave the body and are hard to detect, but this doesn’t explain everything either, why does it seem to start suddenly with subtle warnings in the run-up, why do some people improve but are never cured ? Despite having minimal symptoms and PEM I still have low physical stamina and if I try to exercise I will feel ill just like years ago. Its possible that the body works totally differently than scientists are allowed to know, which would explain why CFS hasn’t been unravelled.
Consider this.
If one thinks of CFS as everything that doctors applied the name to, of COURSE “CFS is anything and everything”
Doctors and researchers aren’t supposed to conduct “science” that way. What they should have done is ask what Dr Cheney called the CDC to come investigate, specifically.
Which was a particular cluster of sick teachers in a Sick Building who all had EBV reactivation.
It’s kind of obvious NOW, but no doctors in the world could figure it out THEN.
It was Stachybotrys Atra, later renamed Stachybotrys Chartarum (To confuse people, I guess)
“All CFS” is a concept that derives from doctors failing to look at what Dr Gary Holmes was baffled by and proceeding to throw the diagnosis at anyone with fatigue.
It’s not even worthy going the route of “Solving all CFS” under that impossibly confusing perspective.
If any of them remembered basic science, “Start at the beginning” they could at least solve the core basis of the creation of Holmes 1988 Chronic Fatigue Syndrome in just a few minutes.
It is mind boggling how many were deprived of getting help with toxic mold because doctors are utterly bereft of any basic understanding of science methodology.
Doctors and researchers are not bereft of a basic understanding of science methodology.The outbreaks occurred in a wide variety of areas and were probabluy sparked by a wide variety of triggers. Everyone knows that ME/CFS is heterogenous and can be triggered by a wide variety of pathogens – that has been shown in paper after paper. Toxic mold has not been studied well but it is clearly a trigger. The scientific way is take in all the data and analyzying it. By sticking to only one data point, Eric, I don’t think you’re using it.
Applying that methodology to anything that was ever discovered would have prevented it from discovery.
On the basis that it must not be investigated because others don’t already know it.
Hi Erik,
ME/CFS began on the West Coast (San Francisco). See “Osler’s Web”, too bad that it is not in Audible so those who have trouble reading can’t hear this carefully documented history of CFS.
I saw Dr. Paul Cheney for 20 years and he never said that mold was the primary cause of ME/CFS. He did believe that HHV6A was and if you think the HHV6 viruses have nothing to with this, please visit http://www.hhv6-foundation.org which has been studying the effects of the HHV6 viruses since ME/CFS became a national issue. Why, if this is not a crucial factor?
I am endlessly tired of the “more study is needed” industry studying this and that symptom of ME/CFS, but no real effort is put into defining a cause. Good for funding their labs, but not for us.
When I have heard that all ME/CFS patients (and this may be difficult because many non-cases have been swept into the ME/CFS basket) have been tested for HHV6A, I will feel satisfied that I am either right or wrong. And if I am mistaken, I will humbly admit it.
You can’t get this test at Quest. You have to pay a premium at Coppe Labs affiliated with the HHV6 Foundation. Both my daughter and I are positive.
Hi Betty.
ME was coined for the 1955 Royal Free Hospital outbreak.
CFS was a new syndrome created by the CDC in 1988 for the Lake Tahoe outbreak.
“ME/CFS” is a meaningless construct because people don’t think of “ME/CFS” as having anything to do with ME or CFS.
The “EBV syndrome” on the West coast AND Dr Komaroff on the East Coast got no traction because it wasn’t scary like the outbreaks were.
IF you have read Osler’s Web then you know HBLV (HHV6a) was the virus which scared the CDC into action.
Dr Cheney refused to listen to the original CFS cohort about the mold.
He was a nice guy but dropped the ball on this one. In later years, he did tell his own patients about Dr Ritchie Shoemakers work “Mold Warriors. Chapt 23. Mold at Ground Zero for CFS”
But this information didn’t penetrate the “ME/CFS” community who feel no need to look back at the origin of either ME or CFS.
I was Dr Cheney’s first mystery illness patient and I told him about the mold immediately, so I do have direct personal experience with this matter.
I hear you, Betty. What you say about so much research going nowhere is spot on. I think it’s because the researchers are not able to read up on the state of the research and to formulate a question that they can answer and is a desiderate at the same time.
I am also convinced that ME/CFS equals HHV-6 reactivation because I had the chance to be treated with acyclovir during an inflammatory episode and it worked and it has good activity against HHV-1, 2, and 6 by the textbooks.
Why do you think that HHV-6a is involved, though? Have you learned that two researchers from London, Cliff and Lacerda, have found HHV-6b in saliva of ME/CFS patients with viral loads following symptom severity?
https://www.brunel.ac.uk/research/projects/reactivation-of-herpesviruses-in-chronic-fatigue-syndrome
Hi Lina,
This is from the CDC’s web page on HHV-6 A & B.
CFS
CFS is an illness characterized by memory and attention impairment, muscle and multijoint pain, and unrefreshing sleep and weakness lasting longer than 6 months. The etiology of the disease is unknown, and many viruses have been investigated as possible causing agents. The overall scenario is in a way similar to that of multiple sclerosis. Serologic analysis on the presence of antibody to HHV-6 provided inconclusive data. An increase in IgG and IgM titer in the sera of a large number of CFS patients (119 of 154) was found relative to that in the control population (77% vs. 12%) (100). However, this was not specific, as an increase in antibodies to other viruses was also detected, reflecting probably an immunologic dysfunction. Molecular analysis showed a higher prevalence of HHV-6A but not HHV-6B or HHV-7 in CFS patients (64,101,102), and HHV-6A could also be isolated from these patients (103). Whether this reflects an association or the consequence of an immune dysregulation remains to be determined.
Hi Betty
thanky for replying. I am afraid these informations are somewhat outdated.
Are you aware that there are several research teams now investigating the herpes hypothesis more deeply?
Under the link that I sent you above you can learn about a clinical study that is ongoing where the two lead researchers Cliff and Lacerda want to find out whether HHV-6b viral loads (DNA!!!) in saliva go up before or after PEM sets in. In this way they want to determine whether HHV-6b reactivation is the pathomechanism that can explain ME/CFS or wether the causing process is going before HHV-6b reactivation and just triggers an HHV-6b flare-up.
Have you updated yourself over the last couple of years about the herpes research in ME/CFS? It seems to me that you missed the publication of many papers over the last years who are successfully digging deeper into the herpes reactivation hypothesis in ME.
Check out what Jacqueline Cliff and Eliana Lacerda are doing in GB. I am sure you will be very satisfied!
https://www.brunel.ac.uk/research/projects/reactivation-of-herpesviruses-in-chronic-fatigue-syndrome
Eric… the name CFS started with LK Tahoe , but you were not ground zero. I got pericarditis six weeks after my baby was born when I was 26 years old in 1978 and was never well again. I have been diagnosed with CFS by the best drs and researchers in the country.
The name, the evidence that CFS was coined for, the Holmes investigation which caused the CDC to convene the Holmes committee and the Truckee cluster that baffled Dr Holmes all started with my school, my outbreak and my immune markers.
I was the first “patient prototype” selected by Dr Paul Cheney to represent the new CFS syndrome.
One cannot possibly get closer to “Ground Zero for CFS” than that.
“Best doctors and researchers” is a questionable proposition.
They can’t be “best” at anything when they neglected to look into what the CFS syndrome was created to solve.
That’s not even “good” or “competent”
In science that is “Total failure”
I don’t expect Cort will let this post go through. It will be a shock if he does.
Please stop playing the victim Erik – it is getting tiring. As I’ve said MANY times – you can post on HR as much as you want so long as you don’t trash other people.
I disagree, though, with your idea of what constitutes “failure” in science. When you have a similar disease cropping up all over the country it would be unscientific to focus on one outbreak. In order to get a representative sample you are going to focus on as many outbreaks as you can.
Even if it made sense to concentrate on one small group of people out of millions, it’s now fruitless – that was 40 years ago! You couldn’t find most of them if you wanted to, most have had it for 40 years, many now surely have confounding factors, and you can’t study the original environment anymore.
If the same factors that produced ME/CFS in them are producing it in other people you now have MILLIONS of people to potentially study.
Thank you, Cort. I am unable to answer Erik as intelligently and coherently as you do. I wish Erik would be able to understand the amazing work of communicating to this community the research that has been ongoing for decades in ways we can understand. You have sacrificed your time and spent untold hours in putting together this blog. Where would we go to get the information you provide since you are one of the few people who have the ability to gain access to these researchers. All I can say is a big Thank you !
Cort writes:
Even if it made sense to concentrate on one small group of people out of millions, it’s now fruitless – that was 40 years ago! You couldn’t find most of them if you wanted to, most have had it for 40 years, many now surely have confounding factors, and you can’t study the original environment anymore.
If the same factors that produced ME/CFS in them are producing it in other people you now have MILLIONS of people to potentially study.
———–
That same argument was made back in 1985 and in all the years since.
By asserting that no clusters should ever be investigated, none of them were.
“Throw everything into the CFS trashbucket and move on”
Since this same logic prevails today, I expect the Longcovid people will be dealt with in the same exact way.
No research into anything specific.
Ever!
(This is why Stephen Straus created a sacrificial syndrome which he knew was going to be destroyed by, of all people, “CFS advocates”.
Somehow, some way, he knew this is how people are)
Erik, my reply to you is in the comment to Cort’s comment to yours.
Perhaps your CFS diagnosis obscured what you really have.
As Dr Byron Hyde says, the failure to look deeper deprived many of proper diagnosis and treatment.
Erik.. you are too funny.
You are dead set on being ground zero. You must think this makes you special.
This wasn’t my invention. It is common to use “Ground Zero” to describe the first sighting of a phenomenon.
Whether you like it or not, this does make me special.
It means my observations are firsthand eyewitness descriptions rather than hearsay and rumor from people who weren’t there and haven’t got a clue.
——————–
Cable News Network CNN
Oct. 24 1990
Program “Sick and Tired”
Announcer: Fifteen years ago, a mysterious illness swept through the Alpine resorts and towns near Lake Tahoe. Incline Village, Nevada was Ground Zero.
Yes. Holmes 1988 CFS started with the Holmes investigation to Lake Tahoe.
The CFS syndrome definitely “all started in Lake Tahoe”
Just as Myalgic Encephalomyelitis started with the Royal Free Hospital.
These names are for a new dataset that is not previously entered into the medical literature.
No one doubts the Lake Tahoe cluster/epidemic happened. And, of course, there have been many other epidemics of ME/CFS – often with different names. I learned a lot on Erik’s Mold Tour, and certainly molds are among the possible triggers. What all the triggers have in common, though, is activation of the innate immune system. If anyone reading this has a potential explanation for the dearth of ME clusters in recent decades, please post it.
@Robert phair, being an ex-professor in molecular and metabolic physiology and CSO of Streasure4health, i do have an umbrella scientifically-based explanation for the longcovid and mecvs. Stronger: it is our mission to develop a diagnosis not only empowering clinicians to discriminate whether patients will develop pem following exercise, but also providing the tool for clinicians to recognize and prescribe patient-specific effective therapy. We are looking for funding to realize these steps with the academia and for academic collaboration. If you (and others) feel you can help us helping you and the entire community, please contact me, e.g, through our website. In fact, Robert, i think i have seen your presentation at the Cambridge mecfs meeting in 2023, right?
Thanks for putting in the hours robert
Hi Robert I sympathize with your fight but this is the legacy from the 1985 CDC CFS concept that ignored the ME history based on an unidentified pathogen and classified by WHO (1969).
My quote from Beyond the Birdcage: Inconvenient Truths about Myalgic Encephalomyelitis the ME history (1934-2005) . Over time, with the various diverse attachments, many countries developed their own interpretations of its CFS meaning, a real miracle story considering the fatal criticisms and discontent that remained a constant. Without effort or evidence, and instead of generating some intrinsic worth, it subsumed all the credibility ME attracted and reinterpreted the past in terms of itself, a strategy that laid claim to a heritage it didn’t rightly own. ME was enslaved because the next innovation could not coexist with a different explanation of reality – especially one that made more sense. The possible pathogen remains covered up from 1934 Los Angles County General Hospital outbreak A. G. Gilliam MD a study that centered on two particular health events of that period, it was either polio or a certain bacteria thought to be a virus until 1966 that changed the medical world – it is listed in the Allergy and Emerging Infectious Diseases within the CDC with anthrax – Dr A Fauci knows all about it! I was diagnosed with this bacteria 1969 after keeping pet birds. People do not have to remain sick but medicine (molecular biology) with their genetic studies for biomarkers etc will not provide the answers. I chose a different path with very astute medical people in tropical medicine and a professor from a University in Australia with good results. Hope this will open up some dialogue about the ME history. Jennifer
Jennifer.
If any “CFS researcher” had been interested in what this syndrome was coined for, they could have simply asked the members of the original CFS cohort.
Doctors and researchers conspicuously did not do so.
I was amazed at this “oversight” until I made the effort to explain CFS history to them, and found their behavior is very deliberate.
I see them now as nothing but con artists and hijackers.
Jennifer, it sounds as if you are telling us that you got well.
If in fact you did get well, please tell us how.
I myself am one of the folks that fell ill to a pathogen in the fall of 1981 like ,I’m learning, so many others did.
Robert Phair, I am a patient since 1989. I do have a notion about why no clusters are identified now. There are almost no clinicians who will admit to knowing anything about M.E. Who would risk their medical reputation doing what Drs Cheney and Peterson, and the doctor in rural New York, or Dr Ramsey, did years ago?
The same large hospital in Chicago whose doctors gave me a diagnosis in the early 1990s, it has no doctors now who will admit to knowing anything about M.E., even the essential advice, no exercise programs. It strikes me like a high school clique that will reject you for a wrong thought.
I have new things going wrong with me in my eighth decade. I have to explain that I cannot do exercises to deal with those issues, explain it to a cardiologist. It is disheartening. I prefer when the doctor knows more about my health situation than I do.
Dear Eric,
First, I would like to address the mold issue. My husband was a development director for a large chain of hospitals in Florida. The staff offices were in an old Spanish-style building. Five of 19 staff developed pericarditis while working in this building. When the walls were ripped open, there was black mold everywhere. No one developed ME/CFS, but pericarditis can be very serious. My husband recovered after a hospital stay.
Because I work in the field of environmental toxins, Dr. Cheney and I would have a debate every time I had my annual visit. I thought that my exposure to Dursban (a dangerous pesticide that is now off the market for indoor use) was the primary cause and the viral reactivation came as a result of immune suppression by Dursban.
Dr. Cheney said the virus (HHV-6 A) came first and the toxic exposure just made everything worse. I think this is true of mold. We have also heard that there was a toluene spill in Lake Tahoe.
I began to understand Dr. Cheney’s thinking when our organization was working with Gulf War veterans, a third of whom had Gulf War Syndrome which is very similar to ME/CFS.
We were collecting data on the 31 categories of reproductive toxicants that soldiers may have been exposed to during the Gulf War. Dursban was high on the list since it was used everywhere, on blankets, tent parameters, etc. The nerve gas agents were also a concern, but they are just the grandparents of pesticides so the effects are essentially the same if the nerve gas exposures are minimal. A large exposure will kill you.
Since my illness mirrored Gulf War Syndrome, I called the head of epidemiology at the University of Texas, Dallas and told him that I thought GWS was caused by exposure to Dursban and the newly discovered HHV-6 A.
Dursban is no longer on the approved list of pesticides for use by the military and although many veterans exposed to burn pits are ill, they don’t appear to have GW Syndrome.
Mold, pesticides, heavy metals, dioxins and other toxins could interact with a herpes virus(es) to cause chronic illness.
Yet, I have not seen a single study by ME/CFS researchers exploring this hypothesis.
Betty. You are the first person to ever bring up the solvent spill.
I mention it occasionally as an example of one of the Incline Village clues that no one ever looked into. But the actual reason Dr Cheney called the CDC for help was Truckee High School. The first cluster that was reported in real time to have evidence of person to person transmission of the Tahoe flu.
So I focus on that first.
If any doctor had ever responded, I would have told them about the solvent spill and all the other clues. But none ever did.
We never found out of it was toluene or trichloroethylene.
Dr Phair. If you and your organization wish to understand “Chronic Fatigue Syndrome” then I highly recommend that you reconsider your rejection of the evidence that Holmes 1988 CFS was coined for.
I realize this is confusing to researchers but it actually does make sense.
But you need to be willing to talk about it.
I hate to have to insist. I really shouldn’t have to.
But as I made clear to the Open Medicine Foundation
“A CFS researcher MUST respond to the evidence that the Holmes 1988 CFS syndrome was coined to solve”
This is absolutely mandatory.
If they refuse, they are not a CFS researcher.
Not mandatory, not smart, not scientific. Whatever mistakes may have been made were made. Meanwhile would you study someone who’s had diabetes or multiple sclerosis or rheumatoid arthritis for 40 years to understand how the disease started? Of course not – you study people as they are coming down with the disease to do that. That’s what researchers are doing now.
Considering that what you are calling ME/CFS has little or nothing in common with Royal Free ME or Lake Tahoe CFS, there is little likelihood that your “ME/CFS researchers” are even studying the right animal.
Notice that not a single “ME/CFS advocate” is part of an outbreak.
They’ve never even seen one. They do not act like “outbreaks” which ME and CFS were based on – even exist.
It’s like trying to study a zebra by bringing in every other animal in the zoo.
Excluding the actual zebra. That one is not allowed.
CFS will go down in history as the most outrageous act of nonscience ever conducted.
Please answer my question.
I did answer your question.
It is the height of illogic to study something by looking at anything BUT the something one claims they want to study.
Lyme disease is increasing. You might be looking at that and wind up calling it ME/CFS, in spite of the fact that Lyme disease cannot cause “outbreaks”
Which is integral to both ME and CFS.
Your answer is that only your brand of ME/CFS counts. Unfortunately, ME/CFS has shown up in so many different places and in so many ways that no one brand counts: they all count and if you focused only on one you would be missing so much.
My answer is that YOUR brand of “ME/CFS” doesn’t count. The worst regression in medical history.
In your view, what you call ME/CFS is not Royal Free disease “ME.
Nor is it Lake Tahoe Mystery Disease “CFS”
The ME/CFS community has divorced itself from ME and CFS but use this chimera term as if it represents both. “ME/CFS” extracts all history and epidemiological evidence from TWO famous outbreaks, leaving behind only a vague description of post exertion malaise.
Even a cursory examination of the Royal Free and Tahoe outbreaks reveals that the current use of ME/CFS pales by comparison.
Barely even par with how people regard neurasthenia.
You have gone so far backwards that it is impossible for any legitimate scientist to utilize your terminology.
When millions of people now fit the criteria for ME/CFS they are the ones to study, Eric – not some group that got it 40 years. Once again, I ask, how would it benefit us now to try to find them and analyze them?
I live in England. My auntie who is 87 has CFS. I have CFS.
It ran down her family line.
I’m open to any ideas but it. Seems to have been round forever
Oh, Oliver. I’m so so sorry. I’m that is a tuff one. I have a few friends who have family members who are also sick with ME. My heart goes out to you and your auntie.
There would be no benefit to any of you.
(rest of comment removed: derogatory)
Hi Erik, I do believe you’re on the right track with environmental triggers. I’m a classic MECFS patient who was blessed to have been a patient early on in my illness of Dr Andrew Heyman (colleague of Dr Shoemaker).
They treated me for “mold” and I did improve from being 90% bedbound over 2 years to being 0% bedbound ever since. Other improvements were cognitive functioning, energy, elimination of internal tremors/vibrations, significant reduction in nerve and muscle pain, improved immune function and much more. What remains is fatigue and PEM and some brain fog.
They presented their research to congress this year on the effects of mold on veterans. The research must be compelling since they agreed to procure funding that swiftly. The latest meeting was in June if anyone is curious to Google it.
All I can say is had I not followed their treatment protocol I don’t know where I would be today. I’ve tried every treatment and therapy but this was by far what gave me my quality of life back. Not fully and definitely not cured but improved.
If you think about it, this is sort of a neuroimmune illness. Other diseases that fall under that category such as Parkinson’s and MS are environmental related as well. And I believe those patients also improve with reducing environmental exposures. I don’t have time to look up the studies.
Thank you.
Thank you again, Cort.. This is the first day of encouragement that I have felt in many, many yeas. At 89+ years, your messsage means a lot. Thank you for all you do t make our days hopeful . Janet
Oh, Janet. I hear you. It makes me happy to hear that you are feeling some encouragement and hope! That is exactly what I felt too, and wanted to share with others.
A wonderfully energetic and hopeful article … I’m so glad these Ron Davis meetings happen every year. Thank you for reporting back.
I’m glad that Ron Davis holds these meetings annually too. They are a remarkable thing.
Great article! Thanks for taking the time to write this piece, Rivka!
Thank you, Kellyann. Great to be in this advocacy fight with you!
Thanks Rivka. It’s really encouraging seeing experts agree about the explosion of ME/CFS research.
Yes, Alex, so encouraging!
Thanks, Dr. Younger, for the summary. Re: subsets. One possibility is that for each individual the specific originating infectious cause + the viruses that can be reactivated + the epigenetic uniqueness of an individual + the complement of co-morbid disorders in that person may all contribute to the “subgroup.” Therefore, it may required deep lab investigation plus trial-and-error (to some degree) to find the combination of substances that address the unique complement of factors keeping an individual “sick.” The separate and maybe longer-term solution is how to flip the switch back to “health” (as Ron Davis has suggested is the magic bullet).
Yup, that switch is what I want! Thanks, Anita.
Is it realistic from what you’ve heard
Oliver, I am not a scientist, so really have no idea. But I have seen Rob Phair’s itaconate shunt videos, and have heard him postulate that if that itaconate issue is addressed, a switch could flick and a person could get better. I have also heard Ron Davis’s video where he suggests we can get better. (That video was in the last year or so, I think…?) So I think there is hope. Or at least I hope there is hope. (More on the itaconate shunt theory found here: https://www.healthrising.org/blog/2023/12/23/itaconate-shunt-hypothesis-chronic-fatigue-syndrome-fatigue/)
And a separate thanks to Rivka for dedicating so much valuable energy to listening and participating in the chat.
xxoo great to connect this past week.
Rivka, you are a legend for doing this and writing this. Thank you!
Thank you for reading and offering me your support. I so appreciate it.
This is great, Rivka. Thanks so much for pushing through those days, and keeping us up to date! Gives us hope!
Tamesin: It was a privilege to be able to attend. So in turn it was my responsibility to share w the community the hope that I got from being there.
Rivka! magnificent and Thank you. Dr Younger’s update answer the question I was going to ask: time lines. From his update it looks like in 2 or 3 years there will be more important findings. Furthermore, clinic doing clinical trials need to be set up. This looks to me then as though there will not be serious help for patients before 10 years, at least. Severe patients cannot withstand and will not withstand their illness that long. I would like to emphasise this. The severely ill (and in many the illness is progressive) cannot endure the severity of the symptoms. Every week there are suicides announced. This somehow never seems to be addressed in these conferences, or acknowledged. If someone out there wants to refute my impressions, oh please do. I need serious optimism and his update did not offer it to me. Best to all.
Hi Helene. I totally hear you. I have lost many friends to this illness. And I know others who are so sick they can’t communicate at all. This is a tragedy and it often feels like a war, and we advocates often feel war torn. But we keep fighting, because things ARE progressing. I think you are right that it will likely still take years to set up a clinical trial network the way Jarred Younger envisions (and I have heard other researchers call for the same thing, including Nancy Klimas and others). But we are getting closer and closer all the time. There will certainly be more clinical trials in the near future that will include ME/CFS, if the stellar Long COVID advocates get their way. (And I hope they do, and I’m hear to help them!) In terms of if the researchers acknowledge the deaths in our community: That was specifically mentioned at last week’s conference. And I could tell that all who were present all felt it deeply. Thank you again for your words and for your tenacity. I thank ALL of us for our tenacity!
Thank you for sharing this.It really helps.
I am not sure how a session on suicides among ME patients would improve our scientific meetings, but I promise you that every researcher is excruciatingly aware of this unconscionable death toll. All of us – patients, caregivers, advocates, clinicians, and researchers – are war-torn. This disease, especially if we account for the disdain showered upon all of us by ignorant outsiders, is horrifying. Optimism is not something researchers can give to patients. Optimism – and hope too – arise inside oneself. All the severely ill patients see the same research landscape. Some of the severely ill are optimistic; some are pessimistic. The same is true of researchers. I side with Whitney Dafoe who reminds us the world is always changing. I wake up every morning thinking this could be the day we or another research team identifies the core problem causing ME/CFS. I choose optimism because it drives my search for a cure.
I am convinced that i know the core problem of mecfs and long COVID and we can develop the diagnostic tools for clinicians to recognize and provide patient-specific effective therapy. For this, streasure4health is looking for funding/socially-oriented investors and collaboration with clinics seeing patients. Contact me through our website if you can help us help you/the mecfs/lc/pais community
Thankyou Robert. I have printed these words and will remind myself of them daily. As the mother of a severe daughter who has given up hope I need to carry hope for the both of us. Just hearing that you, as an expert researcher in the field, you still have hope empowers me to keeping that belief too. Thankyou for all the researchers positivity and for you in expressing it clearly.
Thanks also to Rivka and Cort for keeping us updated.
Michelle: Caregivers of severe patients have a tuff row to hoe. I am so grateful to you for doing what you do. Do you know about the MEAction Caregivers’ Group? See here: https://www.meaction.net/event/me-partner-caregivers-support-group/all/ And see here: https://www.meaction.net/learn/caregivers/
Thank you Dr. Phair for taking the time to read my comment and respond. Never have I suggested that one needs a session on suicide. It just is rarely mentioned by researchers. Is it because they see less sick people? I don’t know. As for optimism or pessimism: well, it is easier to be philosophical when one is not in horrific agony. ME is a monster: toxic sensations, severe weakness, pain, malaise, inability to eat, sleep, walk, etc etc. Loss of everything normal people have. Plus complete isolation. No medical help at all. Eventually people decide to end it. Whitney’s suffering makes me cry, truth be told. The only thing he has, which many others don’t have, is medical attention. And after years of abandonment and the most hellish suffering many many patients end their life. Every single week there are suicides. Thank you for your dedication and hard work Dr. Phair.
Whitney is my absolute hero.I thank him ,his devoted Parents and all working towards brighter days,for your courage.
The darkest hour is before the dawn.
I interpreted his 2-3 year reference differently. I interpreted him as saying within 2-3 years we might have effectively nailed the molecular basis of ME/CFS.
I’d have to watch again to tell. Or maybe you can ask him on his Youtube page, where folks are asking questions of him.
Thank you Rivka!
It sounds like a really energetic meeting. I feel so sorry for pwME, who have been ill for decades, whilst funding levels have been miniscule and talented researchers have lacked support 🙁
I know I’m relatively new to all this but it does seem as though momentum is building and new researchers are becoming interested in the complexities of ME and Long Covid.
Yes, Tracey, that is VERY true. I have attended this meeting over the last few years, and this year (as Jarred Younger said in his video found above) there were more researchers, more knowledge and more energy.
I’m a Jarred Younger fan and I watched his video earlier.
Wouldn’t it be just great if, at some point in the not too distant future, pwME were actually helped by real *treatments* depending on their possible subgroup?! :0
I love seeing Prof Younger preparing for the pitfalls of large scale, granular, concurrent clinical trials. That is the sort of problem you want to have for ME/CFS research.
Lono: Dr. Younger is such a gift to our community. His wisdom is so welcome.
Thanks you, Rivka.
I left a message on Youtube: “WHY is the automatic transcript function turned OFF? I can’t possibly watch and parse this – I have ME/CFS of 35 year’s standing and my brain doesn’t do audio or videos. Can you turn it on? Thank you.”
I can’t be the only one incapable of extracting anything from such a long video.
Did I miss it somehow? Don’t they trust the automatic transcript? They often have laughable mistakes, but are usually better than nothing.
I’ve been sick a long time too. So I feel your pain and struggle. Unfortunately, I’m not the right person to try to answer these science and medical questions.
Hi, Rivka. I’m confused – I didn’t ask any science or medical question, just about turning the automatic transcript function back on at Youtube. I wouldn’t think that would be YOUR job – but the job of whoever posted the video.
And I was just mentioning that request on this comment thread, not asking for anything to be done here at Health Rising.
But thanks for replying.
Ah. I see now what you were saying. Sorry for the confusion on my part. Ha! Too much going on in my poor little brain.
Hi Rivkq- you didn’t answer the question. Could you address the question and let us know if it has been resolved or if the question should be directed to someone else? I agree it is critical to use tools like that to make this material accessible to ME/CFS patients.
Hi Alicia, I can relate with you as I, too, am in my 3rd decade with ME/CFS. For transcribing YouTube videos, I use the “YouTube Summary with ChatGPT & Claude” chrome extension. Although not in the name, it does write complete transcripts.
Thanks – but way too much effort for me, when the automatic transcript just requires that they NOT TURN THE FEATURE OFF!
Or something else I don’t know, but not up to me.
Thank you Rivka! Your dogged determination to et the latest knowledge & share it with everyone in layman terms is so much appreciated. Daunting task to listen to such an educated group of scientists, researchers and medical professionals. So glad you could share real time patient experience to keep them grounded. Thank you again.
Hi Peg, great to see your name on the screen. Great to have worked with you last year!
To what extent (if at all) were the gut microbiome and FMT (fecal microbiota transplants) discussed?
Hi Michael. There was some discussion about both. And yet, if you wanted to hear details, I wouldn’t be able to share because I just couldn’t take in the details. But both were discussed!
That’s good to hear, thank you! I wrote to Jarred Younger about it recently and I didn’t get a response. If you can recall the people at the meeting who discussed FMT and the gut microbiome I’d like to write to them too.
Do you recall if stool donor quality was mentioned? Anything you’re able to remember would be great, thanks!
Thank you Cort and Rivka ! Sounds like ME/CFS just got a long needed infusion of interest and enthusiasm!!! Collaboration and clinical trials is just what has been lacking… It all sounds hopeful but realistically it will take lots of time . It is however a VERY positive outcome !!!
I want to know why mold toxicity is not a major topic of research within the ME/CFS community when it is clearly a well-documented and often defining issue for countless of us? While much of the research done by these scientists has been inspiring and of great value, without toxic mold being addressed, I don’t see much hope for my life.
Blair on September 9, 2024 at 7:02 pm
I want to know why mold toxicity is not a major topic of research within the ME/CFS community when it is clearly a well-documented and often defining issue for countless of us? While much of the research done by these scientists has been inspiring and of great value, without toxic mold being addressed, I don’t see much hope for my life.
——————
Hi Blair. I can answer that.
It is because all doctors, researchers, the CDC/NIH and yes, the “ME/CFS community” fought to make this unknown.
They were informed that toxic mold was the very clue that started this syndrome.
They don’t want YOU to know about it.
I’m sorry but I don’t recall who mentioned gut microbiome stuff, or FMT stuff, or even if it was the same person. But I’m pretty sure the FMT talk was not extensive. I honestly do not recall. And I don’t recall any mention of stool donor quality. Sorry.
Rivka and Cort, thank you as always for your excellent reporting. My issue isn’t with you. Here’s my issue: Isn’t it time to be tougher on these researchers? Personally, we no longer donate because we’ve been hearing these exact same questions for decades – literally for decades- with no translational answers. Lives of patients leak away day by day. Tragically, many have run out of time before they ran out of hope. Let’s demand more from these great brains. Please let me know when there are actual translational results. And by the way, “invitation only” when this research affects and impacts so many lives so significantly? That exclusivity does not sit well with me, either. We deserve transparency and we deserve results. I do not want to sit and wonder and wait for scraps. None of us should have to be in that position. I was a loyal fan of these researchers for a very, very long time. Not anymore.
Researchers are a step removed from treatments and have to deal with their own currency for maintaining their jobs which is publication of research papers. There are different types of meetings with different functions. This meeting was likely closed to allow a highly technical free exchange of information, without over interpretation of preliminary results. A larger meeting with more stakeholders would mean more sidebars with smaller numbers of people and that is where the good stuff happens, so the goal here is to make the whole thing a side bar. I do think the gatekeeping is really annoying to be on the other side of so I understand your pain. I think the researchers are doing the best they can. The fact that Ron was annoyed with the final discussion means they need some bigger brains on this work- and that is more funding. Would be great to know if we as a group should be petitioning the NIH Director or what we can do. But demanding more isn’t going to work. They are doing basic research which has to have room for experiments that with the best of intentions go nowhere.
Tamara, I most certainly share your view. Thank you. Urgency is required. There are not enough brilliant minds on this. I don’t know how this can be changed. Thank you Cort and Rivka and I thank the researchers too. But there just aren’t enough people on this horror.
The Stanford meetings are held in a informal and confidential setting for the reason that this allows researchers to discuss also their unpublished results (according to Janet Dafoe’s explanation). Therefore, in this case the confidentiality is there to remove limits on discussions.
I think that where ME/CFS research stands now is that they have already uncovered many pieces of the puzzle of what’s wrong in the body with ME/CFS, many more than just a few years ago which is why I personally am hopeful. But what science has not found yet is where the “main switch” of this complex systemic dysregulations in the body lies. It’s why integrative theories (unified theories) are important and there was a step in that direction in the end of the meeting.
I think that there should be a workshop format that focusses specifically on integrating findings.
And I think there should also be an point of contact for the Stanford meeting for patients to nominate researchers who they think should be invited, and to communicate topics they think research should focus on more.
Another point of hope is that research technology is advancing, like Maureen Hanson’s analysis of urine metabolome would not have been possible a few years ago, and Prusty’s team have specifically developed new lab methods for looking at herpes virus reactivation in ME/CFS.
Isn’t Dr Younger amazing? A real blessing for the ME/CFS community.
He seems quite excited by some of the findings that will likely be published in the next 6 months. It gives hope.
I assume long covid researchers were also there.
I’ve heard this so many times. I wouldn’t bet on it.
Fair comment
Good to see so many experts at work. But after all these years or decades it is still: hope? It makes me sad. We as patients deserve to know what has ruined our lives. This is not an indictment of these experts. But disappointment at how slowly science is developing in the field of ME/CFS/POTS/FM
Yes there is hope. This is from a former scientist (not in this field). We don’t deserve to know what causes our disease- remember that for thousands of years people had diseases with nowhere the level of understanding that we have now of so many diseases. Cynically the widespread issue of Long COVID will likely drive the funding that will speed the understanding of ME/CFS. Remember Edison and his 10,000 ways he found that a lightbulb didn’t work? There is more known about this disease now than 5 years ago and long COVID maybe the tipping point to accelerate research (again funding is critical).
Many thanks to Cort and Rivka for your continued commitment to helping those of us with ME/CFS stay connected to current information and a community of professionals looking for solutions!!
Your analogy is not entirely correct by comparing it with 1000 years ago and now. Over the past 100 years and today, medical science has become much more modern. There are plenty of scientists who want to investigate the cause of ME/CFS but are denied funding. While with more resources the cause or perhaps a breakthrough will come a lot closer. So it can be done much faster. If the willingness is there for it. And it’s terrible not to know what you’re suffering from. For everyone at any time.
Thanks to Cort’s reporting on the findings of researchers, I have a greater understanding of what might be going wrong in my body than even a few years ago. Robert Phair’s and Ron Davis’ belief that the problem lies with the Innate Immune System makes a lot of sense in explaining symptoms. I think it also links to ANS dysfunction and the vagus nerve. It seems researchers might have enough information now to start joining up the dots and that’s why I felt hopeful reading about the last half day when Ron Davis asked participants to step back and try to form a bigger picture.
In the meantime, there have been helpful things that have come out of research. For instance, Jarred Younger suggested certain botanicals which help some time ago. Also, I decided to try LOLA recommended by the researchers in Cort’s blog on “Rescuing the Metabolic Problems in ME/CFS & LC – The LOLA Possibility”. I’m happy to say that it has definitely helped me. I can do more before experiencing PEM and the PEM has been clearing quicker when I do.
Another encouraging development was the finding of the master immune switch in the brain! It makes me wonder whether there might be a way to re-set a faulty switch without needing to wait for years of clinical trials. Dan Neuffer and others using his kind of approach have reported on the recovery of too many people to write it off. I don’t think we help ourselves if we expect the answers to come in a certain way.
Of course we all want to find what the underlying cause is and the time it takes is frustrating. I’ve had ME/CFS for 26 years and I find it too painful to think about how my life might have been without the illness. I refuse to give up hope because there are breakthroughs being made and, in any case, when I don’t feel optimistic I can feel overwhelmed sometimes. Every loss of life due to ME/CFS is tragic but they’re not the fault of the researchers, they are the fault of the disease. So I’m extremely grateful to everyone who made the decision to choose this illness to research, despite the stigma attached to it. Thank you, thank you, thank you! And thank you to Cort for reporting on their findings in a way that I can (mostly!) understand😊.
You can replace the 26 by nearly 35 and this is exactly how I feel…
”I’ve had ME/CFS for 26 years and I find it too painful to think about how my life might have been without the illness. I refuse to give up hope because there are breakthroughs being made and, in any case, when I don’t feel optimistic I can feel overwhelmed sometimes.”
THANK YOU THANK YOU THANK YOU
Cort…… for your continued advocacy.
Thank you for your dedication to this debilitating disease. I am 74 year old 13 year sufferer of CF. I finally contacted covid two years ago for which I took Paxlovid. The day after my last pill I woke up feeling better than I had in years. I had my old energy back, my mind could focus and I enthusiastically went to a nursery and bought five rosebushes and six russian sage bushes to plant. This amazing “cure” lasted two days and then I was back to my fatigued self. As a retired RN I feel this is very significant and at least in my case I am convinced the cause of my CF is RNA viral. I had coxsackie virus as a child and covid as an adult. Those are the only two RNA viruses that I am aware of contacting.
Thank you again for your dedication to this horrible condition. I hope and pray a cure or treatment will be discovered in my lifetime.
Thank you, it’s wonderful to hear the enthusiasm. We wait in darkness with a glimmer of hope
Thank you very much. And the words of Dr. Younger pretty much corroborates what we’ve been thinking from patient associations and those of us with these diseases: that research has accelerated and that there are probably subgroups of people with ME/CFS
This is a great description of what it feels like to try and absorb the volume and variation of theories about ME/CFS coming from the medical science community.
We get excited because a sharp-witted reporter who came up with an intriguing headline draws us in. Then we read through the article and end with a sigh–so there’s *Hope*, that lovely H word.
And we return to our bodies, our homes within our houses, deluged by the flood of facts and feelings…and our fears–will this always be all that there is?
It’s why we can applaud the medical & scientific warriors, but also remember that wherever possible, we cannot wait in Hope with a capital H to live.
We have to find the courage to live while we hope.
Thirty plus years have gone by since I became chronically ill post Epstein Barr infection. I’ve been through the journeys of mild to severe, then severe to mild, and just when I thought I’d finally beaten ME/CFS–a glorious 2 months of tears, joy and gardening–severe & terrified all over again.
Now, on my milder days, I remind myself that this is a grace note called remission. I read novels, poetry, non-fiction; I peek at the science; review the latest literature; order a few more snow crocus bulbs & every so often Hope & new facts lead me to a supplement that helps just enough for me to extend my gratitude and profound appreciation for these researchers with passion, patience and a practice of careful, methodical investigation and professional collaboration.
I devote (on average) at least one *spoon* of energy each day to keeping up with the research & making waves in the arena of advocacy.
But the H that keeps me here is the one that hopes as I live–my Humanity. I am a writer, artist, teacher, humorist, gardener, devoted friend, music lover, earring wearer, flower snipper, and all around goofball. And I might come at you with a real firehouse on s truly mild day if I had the equipment.
Thank you, Rivka, for sharing with us the passionate commitment of the people behind the science that we entrust with the faith that their commitment will lead to a cure or conscientious treatment. The 5% you absorbed is more than enough to remind us that we are not alone; we have not been abandoned.
My hope *is* renewed. And so is my determination to continue to create a virtual & practical Home for those of us who live in the wilds of chronically ill bodies. Determined to live while we hope.
Cort, You’re a true hero. I am so grateful for you and all the hope you bring. Your perseverance is remarkable and unmatched. You never give up and it keeps me going. To still participate in this from bed is truly heroic. You are loved by all of us and I pray good things come your way for all you do.
I worry that the field is missing the forest for the trees.
I’m a PhD in microbiology with 30+ years experience in basic and applied research, so I well understand the nature of the folks here wanting to understand and dissect all the details and getting into the nitty gritty. It’s what we are trained and funded to do. But it’s a lot harder sometimes for folks to see the big overall picture.
The literature has clearly been showing that Long Covid is a chronic, systemic low-grade COVID infection. The only treatments that have really moved the needle in case reports are months-long treatments with IVIG or anti-S-monoclonal antibodies (which are no longer FDA approved)…why….because they eliminate the underlying infection. It’s not just a paper here or a paper there – a *vast* body of literature has been accumulating over the last three years that has shown directly or (mostly) indirectly that Long Covid is a chronic infection that is persistently stimulating the immune system (and also complement activation and many other problems).
I saw a great article (Deng et al 2024) that showed that chronic circulating Spike bound tightly to beta1 and beta2 adrenergic receptors triggering signal transduction amplifying what epinephrine normally does (and that this can be partially remediated using metoprolol – which many of us are on – because metoprolol prevents binding of Spike to the beta1 receptors…sounds like a good future blog subject??). I’ve always wondered why metoprolol only partly works….and why I can’t slowly wean myself off of it…and now we know why!
But instead of treating us with beta1 and beta2 blockers to alleviate immediate symptoms….shouldn’t be best approach be to treat the underlying cause – the chronic infection first – and then see what symptoms remain and treat those???
I read an interesting article in the lay press about Feline Infectious Peritonitis (caused by a deadly systemic coronavirus infection in cats). The only treatment that works is remdesivir (and that remdesivir has not been approved in the US for FIP but people have been buying it for their animals from companies in China). But it has to be administered by injection for three months and then still might return because the virus is hidden away in viral reservoirs so a second round of treatment is sometimes needed. I believe the same approach is going to be needed for Long Covid. We are going to need prolonged treatment with antivirals (in combination?) – and this is why the short-term Paxlovid trials have not been successful.
I worry that the research community is drowning in all the minute details of multitudinous studies while simultaneously losing the main overall focus – this is all a low-grade systemic chronic infection. Many of the autonomic symptoms, complement activation, coagulation, chronic immune stimulation, chronic fatigue, chronic systemic inflammation, neuroinflammation (etc)….all could be caused by the low grade chronic infection.
We need to tackle the chronic infection first. The science and the details can come later. We clearly need to understand the disease mechanisms and then use this knowledge to apply to other chronic infections that can trigger chronic fatigue, fibromyalgia, autoimmunity, and it’s associated syndromes.
(P.S. I really enjoy reading your blog! It has been very insightful and recognize all too well how hard it is to keep up on all the details while not being trained in the field and also being – hopefully temporarily – incapacitated.)
Signed
– Long Covid since April 2020.
Hi Carrine, there is a subgroup of Long Covid who have ongoing Covid infection. I have read that the problem of these patients is a defective immune system and these patients often die from Covid in the end.
However, Rivka’s blog doesn’t talk of these patients but of something totally different. It’s about ME/CFS and that patient group of Long Covid who has ME/CFS. This is an illness that has existed long before the Covid pandemic. Thus it’s cause can’t be a Covid infection.
I am writing because I think you are on the right track anyway. ME/CFS is chronic viral reinflammation. There is a whole group of researchers who thinks so too and they are mainly looking into herpes viruses. They hypothesize that the symptoms of ME/CFS can be explained by smoldering HHV-6b reactivation.
https://www.brunel.ac.uk/research/projects/reactivation-of-herpesviruses-in-chronic-fatigue-syndrome
Thank you, Rivka. I am so glad that a group of experts get together every year to get on the same (or similar) pages. This is much needed for many areas of science, and it does give me hope to know this is happening, even if I don’t have a chance (and I do have a science degree) of understanding it. <3
Thank you Rivka! I appreciate all that you do!
I don’t know how I was linked but I want to thank you. I have worked in the medical field and am in bad shape myself. I just wanted to say thank you again. I can handle those long discussions on pathology, radiology and listen even with my worst times. Sometimes I prefer a “get to the point approach” and just say it but I understand that not everyone is used to medical acronyms. At times when my eyes aren’t as affected I rather read through the studies because they show or should show how each field works. It is appreciated very very much.
I deeply respect Dr Jarred Younger for recognizing that ME/CF can and does have multiple causes. Inflammation of the brain is inflammation caused by many factors and sometimes genetic factors added on by hard hitting viruses or bacterial infections that leave our brain in this altered state are similar but far more complex than an overheating vehicle. As the body’s defenses become debilitated the worse and more complex a patient’s condition becomes. In layman’s terms my own body’s system override button is on and my heart is in failure. Self advocacy is so important. DPA and reliable friend who will push for one’s advocacy in this crazy environment called the medical system.
Hi Lina,
Thank you for sending the link to the HHV6 studies being conducted in Great Britain.
New studies, however, do not negate the findings of older studies.
In 1986, two researchers in Gallo’s AIDS lab discovered a new virus. It was so lytic, they had trouble keeping the virus alive to study it. When they did, the researchers discovered it was killing B cells so they name it HBLV.
Then they found that it was killing T cells as well so they renamed it HHV6. After that, for unknown reasons, they subdivided the virus further into HHV6 A and B.
HHV-6 B is a common cause of childhood roseola and is ubiquitous in the population infecting approximately 90%.
HHV-A is an different matter. There are researchers who believe this is an entirely different virus and not just a variant of HHV-6.
This is also from the CDC website:
“A key question is whether the two variants (HHV-6 and HHV-6A) fulfill the criteria defined by the International Committee on Taxonomy of Viruses for classification as different species (13). In our opinion, the information summarized above indicates that the two variant groups may be different species; therefore, the issue of nomenclature should be reconsidered.”
Since there is not a commonly available test for HHV-A, we have no idea of the prevalence in the population. So I stand by the information that I published earlier.
Just wanted to share this compilation of full and free research on Long-Covid and ME/CFS. This is a huge long list of available articles;
https://cyclic-son-34f.notion.site/ab1793499aa34fea8bbc6d9d8be4e846?v=576220a795e24267a8df8f5a94e709b3
Hope people find useful things here!
I submit that Dr Gary Holmes is unfairly maligned.
The Holmes 1987 “Tahoe Study” was the last rational, reasonable, fair and objective assessment of the Lake Tahoe Mystery Disease.
This document was presented in the April 1987 Holmes Committee which was deliberating what to do about the newly discovered HBLV, found in this very group because Cheney-Peterson sent blood to the Gallo lab. Where Dr Stephen Straus, whose EBV theory had been cast into doubt famously went ballistic, screaming and almost attacking Dr Byron Hyde.
Dr Holmes obliquely but honestly referred to this shift in focus by his working name of “Chronic Mononucleosis-Like Syndrome” as opposed to BEING mononucleosis.
At this point the Holmes committee should have used Dr Holmes CMLS name or called the new conceptual medical framework “HBLV syndrome”
Making it clear that EBV “immortalizes” B cells causing the increase that shows up on testing, while HBLV has a cytopathic effect that depletes B cells.
Giving a negative result on EBV serology testing for what APPEARS to doctors to be the much-publicized Chronic Epstein-Barr Virus Syndrome.
At the beleaguered Straus’s behest and by using his power as NIH grant fund reviewer to throw his weight around by the implied threat of never having any of their grant funding approved, the Holmes committee acquiesced to the trivializing CFS name, and completely omitting the discovery of HBLV.
Without which the Holmes committee and creation of a new syndrome would not have happened.
While doctors can be forgiven for their initial confusion “EBV or not EBV” upon learning about CFS for the first time, once they saw the newspaper articles about the discovery of HBLV, their failure to respond like basic medical detectives and ASK what relevance this has to the creation of a new syndrome is gross malfeasance.
Once it is explained to a doctor or researcher that this is why CFS started out so confusing and they continue to behave confused, exhibiting no effort at all to clarify their perspective, “simple ignorance and malfeasance” escalates to medical negligence which, if done in pursuance of promoting their own theory for profit, can safely be called “medical fraud”
I have watched otherwise intelligent doctors and researchers remain invulnerable to all explanations of how the Holmes 1988 CFS syndrome does have evidence that is documented for a span of nearly four decades, with zero signs that they ever had ANY intention of “solving CFS” or clearing up what they KNOW to be a confusing syndrome.
Since Dr Gary Holmes was the very last doctor-researcher to publish an honest and unbiased paper which objectively assessed the information in his possession, I regard Dr Holmes as “The last honest researcher”
Before the CFS chaos from opportunists and charlatans kicked in.
I corresponded with Dr Holmes and offered to try and clear his name, but he is so disgusted by the whole thing that he declined. He just wants to retire and forget the entire sordid episode and spend his time in the mountains.
Given the madness and chronic bickering of the ME/CFS world, possibly the most sensible thing a rational person could to.
I must be crazy to think that anyone gives a damn about the truth. I see no signs of it at all.
-Erik Johnson
Incline Village survivor, original prototype for Holmes 1988 Chronic Fatigue Syndrome
——
A Cluster of Patients With
a Chronic Mononucleosis-like Syndrome
Is Epstein-Barr Virus the Cause?
Gary P. Holmes, MD; Jonathan E. Kaplan, MD; John A. Stewart, MD; Barbara Hunt, RN;
Paul F. Pinsky, MPH; Lawrence B. Schonberger, MD
A cluster of 134 patients who had undergone Epstein-Barr virus (EBV) serological testing because of suspected chronic EBV syndrome was investigated in Nevada. Fifteen case-patients were identified who had severe, persistent fatigue of undetermined etiology for more than two months. When compared with the remaining 119 patients who had less severe illnesses and with 30 age-,
sex-, and race-matched control-persons, these 15 patients had significantly higher antibody titers against various components of EBV and against cytomegalovirus and herpes simplex and measles viruses. Epstein-Barr virus serology could not reliably differentiate individual case-patients from the others, and the
reproducibility of the tests within and among laboratories was poor. As a group, the case-patients appear to have had a syndrome that is characterized by chronic fatigue, fever, sore throat, and lymphadenopathy. The relationship of this
fatigue syndrome to EBV is unclear; further studies are needed to determine its
etiology.
(JAMA 1987;257:2297-2302
Loved reading this post, Rivka! And, love your firehose analogy! Felt like I was right there with you in bed listening along.
I think Jarred and the researchers are spot on pertaining to ME consisting of several subgroups. In fact, I actually think fibromyalgia and long covid are two of several ME-subgroups.
Take also the fase III retuximab-study: 30 % of the retuximab-treated patients improved signifantly, but the remaining 70% did not, so the this result cannot justify a general treatment of the entire group due to the price and the risc profile of this drug.
But if it was feasible to select those patients who actually could improve by means of rituximab, that would be a giant leap ahead scientifically.
Thanks a lot Rivka. May I share this in the upcoming issue of the ME Global Chronicle (https://meglobalchronicle.wordpress.com/home/), to be published at the end of September?
Hope your PEM is mild this time
Best wishes,
Rob Wijbenga from Holland
Hi Rob Wijbenga: YES, please do. I also sent you a note via Twitter/X. — Rivka
How did “CFS” EVER come to be linked with ME?
Simple. Three ME-literate physicians Byron Hyde, Gordon Parish, Alexis Shelokov assessed the Lake Tahoe outbreak under investigation by CDC epidemiologist Dr Gary Holmes. Pronounced the Tahoe outbreak ALONE “possesses all the primary determinants of Ramsay ME”
Tahoe ALONE since no other clusters were investigated and they could not be sure.
The CDC actually agreed this was the case, and called Lake Tahoe “similar to the Royal Free disease, ME”
In essence, as a prototype for Holmes 1988 CFS I had been diagnosed with ME prior to serving as a matrix for the new CFS syndrome.
In science,
However, in science “similar does not mean same”
We had evidence such as the newly discovered HBLV that was not known in ME.
Dr Carlos Lopez of the CDC explained the new CFS syndrome was to COMPARE Lake Tahoe Mystery Illness to ME in order to determine if it was the same or not.
This was never done.
ME was never “renamed” CFS.
Unless and UNTIL due process of comparison is carried out, any assertions that ME was renamed CFS are illegitimate steps of bypassing medical and scientific procedures.
Which disqualifies all such assertions.
Erik – this is the equivalent of historical navel gazing. As much as you’d like to it is impossible to revisit the Incline Village cohort – it’s 40 years later, they are scattered, and they have been confounded by the inevitability of time. You can’t go to them to figure out how ME/CFS got started – all you can find out is what happens to people over time.
ME/CFS is everywhere now – and that’s how it should be studied/
I normally don’t take credit for things but I believe I was very influential in getting Dr Paul Cheney and Dr Jacob Teitelbaum in recognizing mold as a viable cause of CFS . I had been working or speaking with both in earlier years of 2006, 2007 , 2008 and 2009.
As you may or may not remember Dr Teitelbaum’s doctor blew up my heart when treating me giving me a lethal dose of T3 therapy far beyond what I should have had for my age . I was given 100 mcgs when it should have not been above 60 mcgs for my age . I was also given hydrocortisone by his doctor when Dr Shoemaker said you never give it to a mold patient . When I tried to convey to the F&F doctor my concerns about hydrocortisone making me sick he brushed me off . However he only lowered the t3 to 89.6 mcgs still way above the allowed level for me at my age .
He ended up blowing up my LAD and nearly killing me . Dr Cheney was furious because he had warned Dr Teitelbaum that our body was shutting down as a reaction to the cell danger response theory What a horrific outcome for me because researchers could not work together and come to the conclusion there could be more than one causative factor in CFS . They totally ignored Dr Shoemaker and his theories and disabled me after just turning 52 . However , some good came out of this because I never went back to the workplace that ended up
giving me 46 symptoms before the heart attack . The mold was hidden in the walls . How do I know ??? Peeling paint and the next specialist was rushed to that hospital from that room during the work day . Once she arrived at the hospital and stayed overnight she was fine . She never returned to that room and had no future issues .
I then got diagnosed by Dr Cheney in March of 2009 with CFS. He did not believe my cause of CFS was from mold until I convinced him with a reaction to an ice dam leak in my sky light in March of 2010. He then said to me privately “ Yes , mold is the trigger for you . “ I had to convince him through scientific reactions to the leak in my
Home causing a tiny spot of black mold . He finally acknowledged my source of CFS was indeed mold .
I also decided to take it one step further and get diagnosed by Dr Shoemaker in August 2011. I thought I was going in incognito giving him no Cheney information to level the tables. However , upon arriving he stated implicitly “ You have an illness but you don’t have my illness “ He must have known the CFS diagnosis somehow before I arrived . I was shocked and stunned !!! He did not know I already had some testing done by my MD brother that proved I was a CIRS patient too .
Long story short … three weeks later the testing results from Dr Shoemaker came back . Yes , I had CIRS !!!!!! He said I could not get well without him and we parted ways . I knew I could never do his strict and unbending protocol , despite his diagnosis of CIRS .
However good came out of these two diagnoses for the same illness !!! After that Dr Shoemaker and Dr Cheney started exchanging patients according to one of Dr Cheney’s videos . So
I believe I was instrumental in achieving a working relationship between the two different camps
Of thinking about CFS
I also convinced Dr Teitelbaum to put Erik Johnson in his fourth edition of FROM FATIGUED TO FANTASTIC . He knew his doctor was the one who nearly killed me through bad practice and probably felt he owed me . He had helped to get me ‘my money back , from the F&F center , made the doctor apologize to me along with corporate headquarters and helped to get me disability . While Dr Cheney wanted me to sue I did not
BOTTOM LINE .. CFS researchers don’t listen to one another …nor do they take into account variable causes for the illness . With all the chemicals and toxins in the food , water , air and even household furniture and structures and each body being very unique …. It’s not a one size fits all.
I helped three researchers come together and finally accept one another’s views because of a horrific tragedy to me . It’s about time the rest do the same . Oh by the way Dr Cheney said I would be dead by 2019. I am not dead and a few years ago laid down 6 tons of landscaping stone in my yard to
Celebrate . I went from totally non functional with 46 symptoms and then a heart attack to creating huge shade and flower gardens . I have just completed three videos on mold and will be doing two more in October through two Christian pastors . I am not dead and I am very functional . How did I do it ??? I researched every day and created my own protocol. I did not leave my area and remained here .
Just thought I would pop in after seeing the Ron Davis article by rivka , Cort . I was hoping to learn something new but she wasn’t able to share .. that’s ok .I just wanted to give everyone an update on me and plead that everyone work together and stop being so selfish in believing there is only one cause to
this horrific illness .
Hey Cort, could you write a blog post about the Hypothesis of Klaus Wirth from Mitodicure? He already developed a drug called MDC002 of which he thinks could break the pathomechanism of ME/CFS. He developed the drug together with Prof. Scheibenbogen. https://mitodicure.com/science/