What are the most polarizing statistics of CFS patients vs controls?

[Forummember9922]

Anyone know of data with the largest gaps between CFS patients and healthy controls?

Enterovirus - Dr. Chia found 135 out of 165 (82%) of CFS/ME patients had stomach biopsy samples that stain positive for enteroviral antigens compared with 7 out of 34 (20%) of the controls

Clots - 'Area Amyloid data' controls (0.10 ± 0.54) ME/CFS (1.37 ± 3.05)

Intestinal Permeability - IgA and IgM against LPS in peripheral blood of ME/CFS patients (67% and 40% of ME/CFS patients showed increased IgA levels and IgM levels, respectively, compared to 0% in controls)

Serum Fibronectin & IGM Fibronectin - Differentiating severe PWME vs controls; 80% confidence (85% with covid induced)

Butyrate Producing Bacteria?

Gut-CFS Prediction (From HealthRising) - Patients with irritable bowel at baseline, and severe gastrointestinal symptoms when they contracted mononucleosis, as well as low levels of IL-13 and/or IL-5 at baseline had nearly an 80% chance of developing severe ME/CFS.

Asking for additions if anyone can think of any? There may have been a wide statistical gap regarding butyrate producing gut bacteria, but i cant seem to locate that percentage.

 

[Wishful]

Keep in mind that those study statistics may be biased by cohort selection. If they define "ME patient" as someone who was triggered by an infection or frequently gets viral infections, that would bias for people with weak immune response. Likewise for other factors. How many of those "clear differences" are only from one study, with no independent replication?

Also, if there are definite differences between ME and controls, it may be a sensitivity to downstream effects. If your intestinal wall is less robust than average, it might take only some subtle variations in some hormones or immune response to have a major effect. Now I wonder how many people might have ME's core dysfunction, but aren't aware of it because they lack those common downstream effects.

 

[Rufous McKinney]

I wonder how many people might have ME's core dysfunction

then what is dysfunctional?

I'd sign up for ME that I am not aware of........

 

[Forummember9922]

Keep in mind that those study statistics may be biased by cohort selection. If they define "ME patient" as someone who was triggered by an infection or frequently gets viral infections, that would bias for people with weak immune response. Likewise for other factors. How many of those "clear differences" are only from one study, with no independent replication?

Also, if there are definite differences between ME and controls, it may be a sensitivity to downstream effects. If your intestinal wall is less robust than average, it might take only some subtle variations in some hormones or immune response to have a major effect. Now I wonder how many people might have ME's core dysfunction, but aren't aware of it because they lack those common downstream effects.

I agree. Do we have the luxury of many replicated, blind as possible, guaranteed unbiased studies?

Also- certainly not trying to paint a picture of what’s root cause. I agree that most of what’s discussed is downstream (of another downstream).

As an example of why I think a higher gap is valuable: Prustys recent studies showing 30-50% increases in herpesviruses- that too me is *not* polarizing enough. Whereas once you cross the 80% threshold you are talking about a clearer disease identifier.

Just wanted to brainstorm/make a convenient list that could serve a purpose of creating a birds eye view to ask, Which observations are of the highest confidence? I will update this list if I come across anything else, and try to actually provide source links for whatever it might be worth🍻 Feel free to advise if a more well-vetted list exists, I would be surprised if one did not

 

[Wishful]

then what is dysfunctional?

There could be effects that are assumed to be normal variations of personality or physical limits. What if one person's ME (core dysfunction) led to dysfunction of memory of names. Some people do have terrible memory for names (me!), so how would that person jump to the conclusion that it's due to ME? They might even have PEM, but it shows itself as even worse ability to remember names. Maybe their ME shows up as some other symptoms, appearing as lower back pain, poor balance, and trouble digesting fatty foods: all symptoms that are fairly common in non-ME people.

I'm just playing with the idea. It seems not impossible. It wouldn't fit the ICC, but that criteria is based on what is considered "normal ME".

 

[Rufous McKinney]

Some people do have terrible memory for names (me!),

I actually made a conscious decision to Work On the Name Thing.

When you use somebody's name, it commands their immediate attention. Its powerful.

Since I am strongly visual (I take in a new person visually, and then blow the name introduction. ) So I decided to just allow myself to admit it, and I often get their name: a second time. "I'm sorry, what was your name again?"

I got way better at it.n By asking that second time, it seems to nail name recall (plus your embarrassed your asking again, but I ask, regardless)

- I worked alot and met alot of people, and I was often surprised at how bad they are at recognizing faces and remember names.

Sometimes, I'd say: Oh yes, Mr. So and So and So, we met at X Meeting in X town in 1968....(this makes the other person look very insecure and often flummoxed). My husband is pretty bad at faces and recalling them, especially : actresses. ("Thats Meryl Streep").

I have one of those types of memories that I'll remember the waitress from seven years ago. If she walks by.

Well, I did have....in the past (now, I"d miss that somebody walked by)

 

[Forummember9922]

Study RE: Neutrophil Apoptosis in CFS
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770396/)

Most polarizing data

TNFRI expression on neutrophils (%)
CFS 12.5 Controls 3.9

TNFRI expression on monocytes (%)
CFS 8.02 Controls 3.1

TNFRI expression on all white blood cells (%)
CFS 7.1 Controls 2.6