Martin aka paused||M.E.
Senior Member
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Amy Proal, PhD, was one of the most exciting speakers at IACFS/ME 2021. Here is a summary of the key aspects of her talk:
- ME/CFS is mostly triggered by an infectious agent (virus, bacteria like lyme, environmental exposure (toxins, mold) — but it may also be a result of injuries leading to structural issues (CCI, AAI, TCS)
- The different causes of disease onset/triggers seem to be responsible for different etiologies of ME/CFS
- In most cases the immune system can not fully clear the infection --> chronic low-level inflammation --> even when the infection is over, there is a pathogen reservoir remaining mostly in the tissues --> evidence for persistent infection with EV and HHV and Covid-19 --> hard to find these viruses; simple blood tests are often not going to identify them, because pathogens can clear from the fluids (where the immune system is more active) and hide in tissues and infect nerves (HHV and some EV are neurotropic) --> the gut is an important reservoir --> EV can directly infect brainstem via cranial nerves like vagus nerve
- The chronic inflammation is picked up by the vagus nerve (which can sense infection/inflammation in any organ) which sends it as a signal to the dorsal brain stem --> activation of microglia
- The vagus nerve senses persistent infections/inflammation and activates the”sickness circuitry” responsible for the flu-like feeling
- Persistent pathogens can produce proteins that can directly interfere with gene expression (transcription and translation), they can dysregulate the immune response
- Most pathogens directly influence the metabolism of the cell they infect --> viruses must pool materials for replication purposes from glycolysis from mitochondria (TCA cycle). -->Metabolic output of the infected cell is changed
- The root cause of autoantibody generation is due to molecular mimicry -->proteins expressed by pathogens which are similar to human proteins
Then she kind of sums up:
All those different triggers (pathogens, stress and injuries) cause glial activation, mast cell activation and stimulation of that brainstem circuitry (this sickness circuitry) --> different “hits” stimulate the same circuitry and simultaneously slow down the immune response --> each exposure makes it easier for the next exposure to cause problems --> immune system is knocked out after ongoing “hits” of different stressors (pathogens, stress, injuries)
- All these “hits” collectively cause microglia priming and the next “hit” amplifies the signal that arrives at the brain
All in all she says that no two people will have the same mix of “hits” that contributes to ME/CFS
She says we need to treat the underlying root causes driving the microglia priming that is causing the neuroinflammation.
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For me that all makes so much sense that I decided to share it. It's an explanation for what I often said here that we don't have the same pathogenesis and as a consequence, we don't have the same blood results and symptoms differ and ergo the treatment that works for you doesn't necessarily work for me.
- ME/CFS is mostly triggered by an infectious agent (virus, bacteria like lyme, environmental exposure (toxins, mold) — but it may also be a result of injuries leading to structural issues (CCI, AAI, TCS)
- The different causes of disease onset/triggers seem to be responsible for different etiologies of ME/CFS
- In most cases the immune system can not fully clear the infection --> chronic low-level inflammation --> even when the infection is over, there is a pathogen reservoir remaining mostly in the tissues --> evidence for persistent infection with EV and HHV and Covid-19 --> hard to find these viruses; simple blood tests are often not going to identify them, because pathogens can clear from the fluids (where the immune system is more active) and hide in tissues and infect nerves (HHV and some EV are neurotropic) --> the gut is an important reservoir --> EV can directly infect brainstem via cranial nerves like vagus nerve
- The chronic inflammation is picked up by the vagus nerve (which can sense infection/inflammation in any organ) which sends it as a signal to the dorsal brain stem --> activation of microglia
- The vagus nerve senses persistent infections/inflammation and activates the”sickness circuitry” responsible for the flu-like feeling
- Persistent pathogens can produce proteins that can directly interfere with gene expression (transcription and translation), they can dysregulate the immune response
- Most pathogens directly influence the metabolism of the cell they infect --> viruses must pool materials for replication purposes from glycolysis from mitochondria (TCA cycle). -->Metabolic output of the infected cell is changed
- The root cause of autoantibody generation is due to molecular mimicry -->proteins expressed by pathogens which are similar to human proteins
Then she kind of sums up:
All those different triggers (pathogens, stress and injuries) cause glial activation, mast cell activation and stimulation of that brainstem circuitry (this sickness circuitry) --> different “hits” stimulate the same circuitry and simultaneously slow down the immune response --> each exposure makes it easier for the next exposure to cause problems --> immune system is knocked out after ongoing “hits” of different stressors (pathogens, stress, injuries)
- All these “hits” collectively cause microglia priming and the next “hit” amplifies the signal that arrives at the brain
All in all she says that no two people will have the same mix of “hits” that contributes to ME/CFS
She says we need to treat the underlying root causes driving the microglia priming that is causing the neuroinflammation.
-----------------
For me that all makes so much sense that I decided to share it. It's an explanation for what I often said here that we don't have the same pathogenesis and as a consequence, we don't have the same blood results and symptoms differ and ergo the treatment that works for you doesn't necessarily work for me.
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