Next Podcast: Amy Proal, Anna Brooks, Fereshteh Jahaniani

Martin aka paused||M.E.

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2,291
Hey folks,

my next podcast “millions with ME/CFS” will be with Amy Proal, Anna Brooks and Fereshteh Jahaniani.

I would like to collect questions you want us to discuss.
You can name a certain researcher you would like to ask.

For those who don’t know them here are the links to their profiles:

Dr Anna Brooks: https://unidirectory.auckland.ac.nz/profile/a-brooks

Dr Fereshteh Jahaniani
https://www.linkedin.com/in/fereshteh-jahanbani-jahaniani-58455a5b (Sorry the Stanford page is BS)

Amy Proal, PhD
https://polybio.org/team/amy-proal/

This is the first podcast with Fereshteh
https://open.spotify.com/show/123KPwngeYJ8Y8vAcUa10E?si=xPkCF-yiQJ2rgYvizosqaw

Thank you!
 

sometexan84

Senior Member
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1,241
To Amy Proal:

"You recently had an interview w/ Dr John Chia about enterovirus. In the interview, you had actually mentioned Enterovirus hiding in the tissue and the gut lining, which Dr. Chia completely agreed with.

Do you have any thoughts on how dysbiosis and the gut microbiome might influence the innate immune system in the intestinal epithelium, and how this might help perpetuate and perhaps even exacerbate an enterovirus infection in the gut lining?

Similarly, what are your thoughts on enterovirus in the gut lining potentially causing intestinal barrier dysfunction, intestinal permeability ("leaky gut"), and even bacterial translocation from the gut into the bloodstream? Do you believe this sort of bacterial translocation could contribute to Post Exertional Malaise (PEM)?"
 

sometexan84

Senior Member
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1,241
To Anna Brooks:

"Autoimmunity is something we see time and time again in ME/CFS. So many common comorbid autoimmune conditions in ME/CFS such as Hashimoto's, arthritis, psoriasis, fibromyalgia, etc. Some have less common autoimmune conditions, it's actually quite diverse, but autoimmunity appears to be a common denominator.

Some believe ME/CFS might be caused by a persistent Enterovirus in the mucosal barriers, such as the gut lining. As a cellular immunologist, what are your thoughts on the potential loss or dysfunction of a Th17 and/or Treg (FOXP3+ regulatory T cells ) cell population at this site due to infected immune and/or epithelial cells?

What would that mean for autoimmunity and self-tolerance, and could this perhaps influence chronic inflammation and bacterial translocation from the gut to the bloodstream?"
 

sometexan84

Senior Member
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1,241
To Amy Proal:

"You work closely with Dr. Michael VanElzakker. There have been presentations and studies where you guys mention the connections found w/ Long Covid and ME/CFS patients having HPA axis dysregulation, vagus nerve abnormalities, and neuroinflammation.

Is it possible that disturbances to the enteric nervous system in the GI tract could lead to some or all of this via the gut-brain axis, etc?

For example, persistent Coxsackievirus B (which has been implicated in ME/CFS) has been found in neurons and glial cells of the myenteric plexus in Ileocecal CD (ICD), Crohn’s Disease patients. Would something like this be capable of causing the abnormal parasympathetic activity seen in ME/CFS? Could this affect HPA axis, vagus nerve, or lead to neuroinflammation?"
 

sometexan84

Senior Member
Messages
1,241
To Fereshteh Jahaniani:

Many have pointed to MCAS (Mast Cell Activation Syndrome) as the main problem or cause in ME/CFS and even Long Covid. Is there a connection between mast cell activation and platelets (platelet-activating factor, PAF)?

It seems many studies have covered how Platelet-activating factor (PAF) can influence the enteric nervous system and lead to neuroregulatory function alterations. Is there any reason to believe that damage to the enteric nervous system can influence platelets, and PAF?

Does gut bacteria play a role in platelet activation? And if so, are there any recommended probiotics which might alleviate some of this?"
 

sometexan84

Senior Member
Messages
1,241
To Fereshteh Jahaniani:

"In the 1st podcast, you mentioned elevated antiphospholipid antibodies in Long Covid (and ME/CFS) w/ endothelial dysfunction. So, to clarify, the autoantibodies in these cases are likely a good thing, where our bodies are attempting to clear out excess phospholipids?

Is it possible that having elevated anti-phosphatidylserine or other antiphospholipid antibodies could perhaps be due to the molecular mimicry form of autoimmunity?

For example, there are studies demonstrating how a persistent SARS-CoV-2 or Enterovirus can spread via extracellular vesicles formed of phospholipids. Is this something that our immune system might be able to detect and with compromised self-tolerance, perhaps lead to this type of molecular mimicry, where our bodies mistakenly attack phospholipids in other sites?

If so, would would be the implications of something like this?"
 

sometexan84

Senior Member
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1,241
To Anna Brooks:

"Since the 1980's there have been dozens of studies looking at cellular immune abnormalities in ME/CFS looking for common denominators. Very few findings are consistent.

However, there are a few outliers that stand out and are perhaps significant. Is there anything you can tell us about these cell sub-sets?

Consistent results in multiple ME/CFS studies...

Increased CD5, CD19, CD20, CD21 B cells

Increased CD26 expression

Decreased CD56 cells
 

sometexan84

Senior Member
Messages
1,241
@Martin aka paused||M.E. Oh man, so I am actually listening to that entire podcast you did w/ Dr Fereshteh Jahaniani .... and I was not expecting much, but I actually agree w/ a lot of what she's saying.

There are docs that I do not give enough credit to. Which, is honestly kind of eye-opening for me, lol, so thanks!

There are some specific things she mentioned that I agree w/... but more importantly, I like how she mentions the broadness of the disease, and just the unassuming nature of her... honestly, I'd never heard of her before.

That's the sort of ME/CFS scientist I gravitate towards.... because no one knows. That's why Amy Proal's colleague, Dr. VanElzakker is a fave of mine. Like, I have noted that he's not overly presumptuous but very smart, and will literally say "I don't know". And that's someone I can trust.
 
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Martin aka paused||M.E.

Senior Member
Messages
2,291
@Martin aka paused||M.E. Oh man, so I am actually listening to that entire podcast you did w/ Dr Fereshteh Jahaniani .... and I was not expecting much, but I actually agree w/ a lot of what she's saying.

There are docs that I do not give enough credit to. Which, is honestly kind of eye-opening for me, lol, so thanks!

There are some specific things she mentioned that I agree w/... but more importantly, I like how she mentions the broadness of the disease, and just the unassuming nature of her... honestly, I'd never heard of her before.

That's the sort of ME/CFS scientist I gravitate towards.... because no one knows. That's why Amy Proal's colleague, Dr. VanElzakker is a fave of mine. Like, I have noted that he's not overly presumptuous but very smart, and will literally say "I don't know". And that's someone I can trust.
I know her for many years and she is a brilliant researcher. She just has no funding. That’s the big problem.
 

jaybee00

Senior Member
Messages
606
Not sure why AP is being highlighted as some type of expert researcher. She has no academic affiliation and has no lab. She writes speculative review papers that are poorly received.
 

sometexan84

Senior Member
Messages
1,241
Not sure why AP is being highlighted as some type of expert researcher. She has no academic affiliation and has no lab. She writes speculative review papers that are poorly received.
I get what you're saying. But she is a microbiologist, and is well connected to tons of researchers. And she's part of the PolyBio Research Foundation - https://polybio.org/#section-team

It's a team of experts in different but complementary fields collaborating in an effort to find the root cause of ME/CFS and PASC/LC.

Even if she doesn't have all the answers to questions like these, I think it's a good idea to ask, who knows what it might lead to.
 
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