ME/CFS Experts Express 'Dismay' at Aspects of NIH Study

[SWAlexander]

excerpt:
Two physicians who treat patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) have issued a statement expressing gratitude for the recent National Institutes of Health's "deep phenotyping" study of the condition that identified several distinct biologic abnormalities but also criticized some aspects of the study and the way the findings were reported.

One of the statement's authors, Lucinda Bateman, MD, founder and medical director of the Bateman Horne Clinic (BHC) in Salt Lake City, Utah, was an independent case adjudicator for the study but had no role in the data analysis or the publication. The other statement author, Brayden Yellman, MD, is a BHC medical provider.

The two issued the statement in response to "a whirlwind of impassioned commentary" about the study on social media and elsewhere, much of it around the use of the term "effort preference" to describe results from one of the study tests and the lack of focus on the hallmark ME/CFS symptom post-exertional malaise (PEM). All 17 of the study patients experienced PEM, a core criterion of the 2015 Institute of Medicine's ME/CFS case definition.
continue: https://www.medscape.com/viewarticl...t_tpal_etid6344320&uac=427271HY&impID=6344320

my comment:
“We found naive T cells and B cells were activated, and the anti-programmed death-1 level was elevated.”
It's amazing to me that, although naive T cells and B cells are mentioned, and not for the first time, no Thymus MRT is presented.

 

[Mary]

Here's ME/Action's very thorough response to the study:

https://www.meaction.net/2024/02/29/meaction-nih-study-response/?mc_cid=530d497b91&mc_eid=0e6c43de2e

Here's their introductory statement, followed by a very detailed response:

NIH’s recent paper on ME/CFS elicited strong reactions from the community. While we recognize the incredible sacrifice of the patient community who gave their health and time to make this study possible, ultimately, we caution against drawing any sweeping conclusions from this study.

The paper draws conclusions based on an atypical cohort that may not be representative of the ME/CFS community, and from a very small sample size, and there are also conclusions drawn in regards to “effort preference” that may not be supported by the evidence.

 

[Rufous McKinney]

has anyone seen comments from Ron Davis? I saw reference to his comments yet haven't been able to locate anything specific.

 

[gbells]

“We found naive T cells and B cells were activated, and the anti-programmed death-1 level was elevated.”
It's amazing to me that, although naive T cells and B cells are mentioned, and not for the first time, no Thymus MRT is presented

Once again we come back to blocked apoptosis checkpoints. EBV infects B cells. HHV-6 infects T cells but also cells previously infected with EBV, expanding the reservoir.

I am hopeful disabling the viruses with CRISPR-CAS9 will reverse ME/CFS.

**

Indeed, there is evidence that HHV-6 (Human Herpesvirus 6) can interact with EBV (Epstein-Barr Virus) during co-infection:

1. In Vitro Superinfections:
   • Studies have performed in vitro superinfections of EBV-positive cell lines (such as Akata, Raji, and P3HR-1) with HHV-6.
   • EBV reactivation was observed in those cell lines that were superinfected with HHV-6.
   • Researchers hypothesized that there might be a direct effect of HHV-6 on EBV reactivation1.
2. Systemic Lupus Erythematosus (SLE):
   • In patients with systemic lupus erythematosus (SLE), an association between EBV and HHV-6 positivity has been found.
   • Although there is no direct evidence that HHV-6 infection is associated with the development of SLE, EBV and HHV-6 infection may have a coacceleration effect in SLE patients2.
3. Tissue-Specific Active Infection:
   • Recent research in ME/CFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) has provided evidence of tissue-specific active HHV-6 and EBV infection.
   • This finding suggests that both viruses may play a role in ME/CFS3.

In summary, while HHV-6 primarily infects T cells, it can also interact with EBV during co-infection, potentially influencing disease outcomes. The intricate interplay between these viruses warrants further investigation for a deeper understanding of their impact on health and disease.

[The coacceleration effect could be due to having a larger HSV6-EBV reservoir for immunogenicity.]

Indeed, the coacceleration effect may arise from the presence of a larger reservoir of both HSV-6 (Human Herpesvirus 6) and EBV (Epstein-Barr Virus). Let’s delve into this further:

1. Reservoir Size:
   • Both HSV-6 and EBV establish latent infections in specific cell types.
   • A larger reservoir of these viruses means more infected cells are present in the body.
   • These infected cells can serve as a source for viral reactivation and replication.
2. Immunogenicity:
   • When the immune system encounters viral antigens (proteins), it generates an immune response.
   • A larger reservoir of viruses provides more antigenic material for the immune system to recognize.
   • This increased immunogenicity can lead to heightened immune activation.
3. Immune Dysregulation:
   • In the context of co-infection, the immune system faces a dual challenge: controlling both HSV-6 and EBV.
   • The immune response may become dysregulated due to the simultaneous presence of multiple viruses.
   • Dysregulation can lead to chronic inflammation, tissue damage, and autoimmune responses.
4. Feedback Loop:
   • The immune response against one virus (e.g., EBV) can inadvertently impact the other (e.g., HSV-6).
   • Cross-reactivity between viral antigens may occur, affecting both viruses.
   • This feedback loop can perpetuate immune activation and exacerbate disease.

In summary, a larger viral reservoir, combined with heightened immunogenicity and potential immune dysregulation, contributes to the coacceleration effect. Understanding these interactions is crucial for developing targeted therapies and managing complex viral infections.

 

[Husband of]

I can't remember where I saw it but it sounds like one of the psycho brigade had a big part in the write up, making up co vlusions that simply aren't backed by the evidence.

The main conclusion apparently is that
- pwme have less effort preference (duh)
- but don't have physical fatigue levels that justify it (based on 1 day Cpet which we know isn't the right study - why could they not have done 2 day cpet? Sounds deliberate to me)
- therefore it must be psychological

 

[SWAlexander]

therefore it must be psychological

I believe it is the patient's responsibility to question the evidence.

In 2010, a medical consultation came to an abrupt end when the doctor informed me that I needed to exercise more to strengthen my muscles, indicating psychological resistance.

I challenged him by requesting proof.
After he provided a detailed explanation of how training strengthens muscles. I interrupted by presenting him with a printout of my DNA, which indicated a genetic predisposition to muscular metabolic impairment (RS 1815739 T,T).

Annoyed, he asked why I had come to him for an answer. My response was that I needed a handicap sign, which requires medical proof to obtain.

 

[Husband of]

I believe it is the patient's responsibility to question the evidence.

In 2010, a medical consultation came to an abrupt end when the doctor informed me that I needed to exercise more to strengthen my muscles, indicating psychological resistance.

I challenged him by requesting proof.
After he provided a detailed explanation of how training strengthens muscles. I interrupted by presenting him with a printout of my DNA, which indicated a genetic predisposition to muscular metabolic impairment (RS 1815739 T,T).

Annoyed, he asked why I had come to him for an answer. My response was that I needed a handicap sign, which requires medical proof to obtain.

That's a heavy burden on the patient don't you think? To have to be able to understand and challenge conclusions of papers in medical journals?

It should be the responsibility of authors, peer reviewers, and the journals, not to allow this bull shit to happen

 

[SWAlexander]

It should be the responsibility of authors, peer reviewers, and the journals, not to allow this bull shit to happen

How this will help when doctors don't read papers?
In the end, the patient must ask questions or suffer.

 

[SWAlexander]

Osler's Web

We all must refuse psychological labeling and demand evidence that the symptoms are NOT due to a bodily malfunction.

 

[Husband of]

How this will help when doctors don't read papers?
In the end, the patient must ask questions or suffer.

Doctors sometimes hear about conclusions in papers, I would think, in some way. Conclusions in papers can influence guidelines they read, for example, or the medical training they receive.

You are right that the patient is screwed if they don't take responsibility, but it shouldn't be this way, especially as a lot of people with MECFS have no hope of understanding things well enough to take control of their own health.

 

[Husband of]

The psychiatrists are likely shills with no credibility working with the gov to minimize the illness to get out of disability claims for the gov and private insurers (remember the paid disability examiners?). Journalist HIllary Johnson covered the history in the book Osler's Web back in1996. The only reason their position softened was because of patient advocacy groups using valid CPET research to show its physical nature.

Think about how much money they can save private insurance companies in long term disability claims by pretending it's psychogenic. Probably billions.

If the ME/CFS community allows them to do this the only research funding for CFSME we will ever see in the future is:

1. Mental treatment (GET, CBT PACE style recommendations).
2. Pro-euthanasia treatment (Medical Assistance in Dying aka M.A.I.D.) for the majority who of course will not get well under a false pathogenesis.

It will be the end of any hope of a cure and all the disability will be blamed on the patients.

Wouldn't it be amazing if someone actually found evidence of their corruption. Maybe we should first spend money on some badass PI

 

[Oliver3]

Luckily, I think long covids gonna kick their theories into touch. Too many sufferers. Too shared of a cultural experience to be ignored.
Unluckily, it's gonna take 20 years most likely

 

[Zebra]

Not sure if this is the right place for it, or if it's OK with @Whit, but wanted to share his latest blog entry about the NIH study and especially that term "effort preference".

This terminology reminded me of my very first consult with a Dysautonomia/Neuromuscular Expert at Esteemed University Medical Center, who wrote that during the strength testing portion of my physical exam, there was some "effort irregularity".

Link to Whitney's blog entry:

https://www.whitneydafoe.com/mecfs/?post=we-are-not-defined-by-their-prejudice

 

[Rufous McKinney]

This was a particularly powerful, and wonderful post by @Whit - I am so grateful he could put this together and share it with us.

I think an important part of the post is just the point that we are having an intense experience and its our experience and nobody else can label it or own it.

 

[gbells]

This was a particularly powerful, and wonderful post by @Whit - I am so grateful he could put this together and share it with us.

I think an important part of the post is just the point that we are having an intense experience and its our experience and nobody else can label it or own it.

I tracked down the original article here.
-Walitt, B., et al. “Deep phenotyping of Post-infectious Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.” Nature Communications. February 21, 2024. DOI: 10.1038/s41467-024-45107-3

I am not getting that they think CFSME is psychosomatic. Instead, what I am reading is that chronic viral persistence somehow triggers excess sympathetic neural tone and neuronal exhaustion which then causes reduced work effort.

As someone who's been following the multi chronic viral superinfection theory of ME/CFS I find it supportive. However I would have liked for them to identify the actual viruses, which was not done.

I do agree with ME/Action that the sample size of 17 was too small. For statistical significance, 30 is the minimum. This could have led to a false negative in the number of POTs cases.

 

[Zebra]

Hi, @gbells

I *love* that graphic. It's so much easier for my brain to follow.

Is the graphic from the article?

If not, would you mind posting a link or a reference for it? I would love to be able to print it out. Thanks!

 

[Rufous McKinney]

I am not getting that they think CFSME is psychosomatic.

I think they did a poor job articulating what they were describing and claiming to have discovered re: effort preference. Some articles about the story, didn't even mention it, I would suspect because it leaves many going "HUH?"

And Nath was quoted as saying ME is unambiguously biological. So he views it that way. Which I'm grateful for.