Something in the Blood in ME/CFS, Fibromyalgia and Long COVID III: Evidence Builds

[southwestforests]

Hey Y'all; This was in their newsletter yesterday,

And it brings to mind my Dad, who the US Navy and other military doctors in Virginia diagnosed with ME/CFS and Fibromyalgia around 1983 or 4 after his health collapsed in 1982, and a time when in the 80s or 90s his doctors said to him, "There's something wrong with your blood, but we don't know what it is."

Something in the Blood in ME/CFS, Fibromyalgia and Long COVID III: Evidence Builds that Something in the Blood is Causing These Diseases​

by Cort Johnson | Oct 19, 2024

https://www.healthrising.org/blog/2024/10/19/blood-chronic-fatigue-syndrome-fibromyalgia-long-covid/

something in the blood of chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), and long-COVID (LC) patients is causing these diseases is so enticing! Uncover it and bang – you potentially have a trifecta: – an arrow pointing at the cause, a biomarker, and a treatment target.
Recently two more studies suggested that the, or at least an answer for ME/CFS, FM, and long COVID may be hiding in plain sight.
Check out those studies and ones in the past that suggested that something lurking in the blood could tell us much about these diseases.

...

THE GIST​

• The idea something in the blood of ME/CFS, fibromyalgia (FM), and long-COVID (LC) patients is causing these diseases is so enticing! Uncover it and bang – you have an arrow pointing at the cause and a potential treatment target as well.
  
  
• Recently two studies suggested that something in the blood is playing a major role in these diseases. This blog will cover those studies as well as past ones that suggest the same.
  
  
• One study found that exposing muscle tissues to serum from ME/CFS and long-COVID patients for 48 hours produced a “stress-induced hypermetabolic state” resulting in “severe deterioration of muscle function”. The mitochondria were profoundly impacted by the serum.
  
  
• Another study from Akiko Iwasaki’s group at Yale found that giving IgG antibodies from LC patients with neurological symptoms to mice resulted in increased pain sensitivity, pins and needles, burning pain, weakness, and dysautonomia.
  
  
• The authors stated their data “illustrate the pivotal role of autoantibodies as a key driver of neurological disorders in long COVID”.
  
  
• Meanwhile, Andreas Goebel has found “pain sensitizing autoantibodies” in no less than four chronic pain conditions, including fibromyalgia. His most recent fibromyalgia study found that giving IgG antibodies to mice quickly turned them into fibromyalgia mice. Goebel found that the antibodies were attacking a central way station for sensory signals coming from the body called the dorsal root ganglia
  
  
• For his next trick, using tissue cultures Goebel found signs that the same thing was happening in long COVID.
  
  
• When San Diego researchers took serum samples from ME/CFS patients with insomnia and healthy controls and injected them into connective tissue cells called fibroblasts from mice, the fibroblasts showed signs that their circadian rhythms were disrupted – suggesting that something in the serum might be disrupting sleep.
  
  
• When an ME Research UK-funded study added plasma from ME/CFS patients and healthy controls to the endothelial cells found in our blood vessels they found across-the-board reductions in nitric oxide production – even at rest – in people with ME/CFS. The authors proposed that something in the plasma was not only interfering with blood vessel functioning but possibly with mitochondrial functioning as well. That set the stage for…

• 
  
• …Bhupresh Prusty’s study finding that IgG antibodies from ME/CFS patient’s serum caused the mitochondria in the endothelial cells that line the blood vessels to become fragmented.
  
  
• Back to fibromyalgia, UK researchers created a fibromyalgia mouse model and transferred blood and serum from the FM mice into healthy mice. After separating the blood into 4 immune components they found that neutrophils from FM patients were responsible for turning healthy mice into FM mice.
  
  
• The 2016 study form Fluge and Mella that started all this off found that giving ME/CFS patients’ serum to progenitor muscle cells resulted in increased mitochondrial respiration (i.e. a state of hypermetabolism) that appeared to be driven, interestingly enough, by energy depletion. As other studies have found, the muscle cells transitioned from relying on clean-burning fatty acid-derived energy to running mostly on a dirty source of energy – amino acids.
  
  
• If something in the blood is causing or greatly contributing to these diseases some treatment possibilities include IVIG, targeted treatments to remove specific autoantibodies, and blood cleansers like plasmapheresis and immunoadsorption.
  
  
• A recent session of Drs. Ruhoy and Kaufman “Unraveled” podcast discussed plasmapheresis and a blog is coming up on that.
  
  
• Hopefully, enough evidence has accrued that a real hunt for the mystery substance in the blood is underway. Currently, it appears that IgG autoantibodies are the lead candidate – and they are getting some funding. Likewise, the Open Medicine Foundation is funding a study examining the role neutrophils may be playing in ME/CFS.
  
  
• Time will tell. As Ron Davis says sometimes about difficult projects “This is not a trivial problem” )), and finding the X factor in the blood is apparently not an easy task. The payoff, though, (biomarker, potential treatment target) could be enormous.

 

[bad1080]

blood definitely plays a role but blood purification seems to be only temporarily helpful after which it needs to be repeated, so there must be more to it than just that.

 

[Viala]

Back to fibromyalgia, UK researchers created a fibromyalgia mouse model and transferred blood and serum from the FM mice into healthy mice. After separating the blood into 4 immune components they found that neutrophils from FM patients were responsible for turning healthy mice into FM mice.

I wonder how they created fibromyalgia, might be the cause of the disease or at least one of the causes.

One study found that exposing muscle tissues to serum from ME/CFS and long-COVID patients for 48 hours produced a “stress-induced hypermetabolic state” resulting in “severe deterioration of muscle function”. The mitochondria were profoundly impacted by the serum.

This is smart. They could use the blood and alter it's content one by one to figure out which component is responsible for the symptoms. By comparing the samples, if there is a large enough database, it should be also possible to find something in common. Wonder what is the biggest ME/CFS samples database in the world.

 

[southwestforests]

I wonder how they created fibromyalgia,

These might help answer that,

https://pubmed.ncbi.nlm.nih.gov/24314231/

https://www.sciencedirect.com/science/article/abs/pii/S0163725821001613

https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-024-03018-6

 

[Atlas]

Back to fibromyalgia, UK researchers created a fibromyalgia mouse model and transferred blood and serum from the FM mice into healthy mice. After separating the blood into 4 immune components they found that neutrophils from FM patients were responsible for turning healthy mice into FM mice.

This neutrophil finding is interesting as it's possible there may be a connection to the slower neutrophil chemotaxis observed in ME/CFS by Ron Davis's team. (As of yet unconfirmed).

Summary from OMF today:

• Neutrophils are an important part of the immune system that work to clear infections in the body, making them of interest in ME/CFS.

• Ron Davis, PhD and his team at the ME/CFS Collaborative Centre at Stanford University have developed a platform for assessing neutrophils.

• Early results show that neutrophils from ME/CFS patients move slower than healthy controls. If these results are validated, the platform has potential to become a diagnostic tool for ME/CFS.

• Data collection is underway to validate the neutrophil assessment platform, so the study falls in the “Recruitment, Data Collection” stage of the research process.

Neutrophil Assessment Platform

Neutrophils are an important part of the innate immune system, which circulate in the bloodstream trying to identify and clear infections. They are traditionally quite challenging to study as they can’t be frozen and are easily activated during analysis. Neutrophils may provide interesting insight into ME/CFS, so Ron Davis, PhD and his team at the ME/CFS Collaborative Centre at Stanford University have developed a new method for isolating and studying neutrophils.


Through their innovative platform, Dr. Davis’ team is able to isolate neutrophils as they move through a filter matrix towards an attractant. They can then view their movement through the matrix with a microscope and automatically track the neutrophils using code also developed by the team.



An important early discovery through the development of this platform is that ME/CFS patients’ neutrophils move slower than those from healthy controls. The team is currently working on validating that result now that the platform and its tracking code is developed—the completed platform allows them to analyse many more cells at a time with what’s called a high-throughput method. Ultimately, the neutrophil assessment platform has potential to be converted into a diagnostic tool, which is desperately needed in ME/CFS.



Dr. Davis’ study using the neutrophil assessment platform is starting to ramp up on data collection, landing it in the “Recruitment, Data Collection” stage of the research process.