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

 

[Lolinda]

I like a lot the idea of creating a polarizing list!
But I hope it's a welcome contribution, that the first item is not correct:

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

The paper by Dr Chia does not report any noteworthy difference between CFS and non-CFS, but a big difference between functional dyspepsia and no functional dyspepsia. @Hip

In detail: in the study there are three groups:

• patients suffering from functional dyspepsia + CFS. 82% of them has positive VP1 staining (enteroviral antigen) in stomach biopsies
• patients suffering from functional dyspepsia but having no CFS. 83% of them has positive VP1 staining
• various people who have neither functional dyspepsia nor CFS. 19% of them has positive VP1 staining

Here are the paragraphs of the paper that say these:

Immunoperoxidase staining demonstrated enterovirus VP1 in 343/416 (82%) and 53/66 (83%) of the stomach biopsies from FD patients with and without ME/CFS, respectively, and dsRNA in 268/ 416 (64%) and 41/65 (63%) in the two patient cohorts, respectively (Figure 1). 9/47 (19%) and 5/46 (11%) of the controls stained positive for VP1 and dsRNA, respectively (p < 0.01, χ2 test with Yates correction).

Between 2006 and 2012, 416 patients (85% female, 15% male; 75% Caucasian, 13% Hispanic, 10% Asian; age 44 ± 16) fulfilling the necessary criteria for ME/CFS as established by the international working group on ME/CFS [14] had EGD and biopsies of stomach, as described [10] . Patients with diagnosis of functional dyspepsia presenting with symptoms of epigastric pain, burning, nausea and post-prandial bloating for more than 6 months, without a diagnosis of ME/CFS, underwent the same procedures (n = 42, 74% female, 26% male, age 38 ± 10). The control subjects included asymptomatic volunteers (n = 12; 9 female, 3 males; age 35 ± 8), patient with unexplained anemia (n = 7), NSAID-induced gastritis (n = 3).


I still find this paper very useful, because I do have functional dyspepsia unless I supplement with betaine HCL.
Convincingly, the enterovirus is reported by this paper to be located in the parietal cells. That's the cells that produce betaine HCL! I don't think that parietal cells full of viruses will be very functional and produce those huge amounts of stomach acid that they should.
-> if you wish to test for your stomach's ability to produce stomach acid, here I describe you how you can do that cheaply and safely at home. it's a scientifically validated test that measures the ability of your stomach to produce that big push of stomach acid that is needed to digest food.

Please post your results! I would be curious if you have the same as me, that there is no pH difference, meaning that there is no meal induced push of stomach acid.

 

[Forummember9922]

I like a lot the idea of creating a polarizing list!
But I hope it's a welcome contribution, that the first item is not correct:


The paper by Dr Chia does not report any noteworthy difference between CFS and non-CFS, but a big difference between functional dyspepsia and no functional dyspepsia. @Hip

In detail: in the study there are three groups:

• patients suffering from functional dyspepsia + CFS. 82% of them has positive VP1 staining (enteroviral antigen) in stomach biopsies
• patients suffering from functional dyspepsia but having no CFS. 83% of them has positive VP1 staining
• various people who have neither functional dyspepsia nor CFS. 19% of them has positive VP1 staining

Here are the paragraphs of the paper that say these:

Immunoperoxidase staining demonstrated enterovirus VP1 in 343/416 (82%) and 53/66 (83%) of the stomach biopsies from FD patients with and without ME/CFS, respectively, and dsRNA in 268/ 416 (64%) and 41/65 (63%) in the two patient cohorts, respectively (Figure 1). 9/47 (19%) and 5/46 (11%) of the controls stained positive for VP1 and dsRNA, respectively (p < 0.01, χ2 test with Yates correction).

Between 2006 and 2012, 416 patients (85% female, 15% male; 75% Caucasian, 13% Hispanic, 10% Asian; age 44 ± 16) fulfilling the necessary criteria for ME/CFS as established by the international working group on ME/CFS [14] had EGD and biopsies of stomach, as described [10] . Patients with diagnosis of functional dyspepsia presenting with symptoms of epigastric pain, burning, nausea and post-prandial bloating for more than 6 months, without a diagnosis of ME/CFS, underwent the same procedures (n = 42, 74% female, 26% male, age 38 ± 10). The control subjects included asymptomatic volunteers (n = 12; 9 female, 3 males; age 35 ± 8), patient with unexplained anemia (n = 7), NSAID-induced gastritis (n = 3).


I still find this paper very useful, because I do have functional dyspepsia unless I supplement with betaine HCL.
Convincingly, the enterovirus is reported by this paper to be located in the parietal cells. That's the cells that produce betaine HCL! I don't think that parietal cells full of viruses will be very functional and produce those huge amounts of stomach acid that they should.
-> if you wish to test for your stomach's ability to produce stomach acid, here I describe you how you can do that cheaply and safely at home. it's a scientifically validated test that measures the ability of your stomach to produce that big push of stomach acid that is needed to digest food.

Please post your results! I would be curious if you have the same as me, that there is no pH difference, meaning that there is no meal induced push of stomach acid.

Thanks for the addition to my silly thread.

FWIW just a personal experience, I have had notably less stomach acid since CFS (but tons of other weird GI stuff, frequent diarrhea etc). But I remember getting acid reflux once in the last couple years and thinking woah that hasn't happened in a long time. I had higher EBV numbers and no markers for Enterovirus based on the (probably insufficient) tests I had

 

[Lolinda]

But I remember getting acid reflux once in the last couple years and thinking woah that hasn't happened in a long time

that doesn't mean that you have too much or too little stomach acid, nor that it is just right. it just means as little as that on this day, your lower esophageal sphincter didn't close. If you have just enough, too much or too little stomach acid but it gets out of the stomach where it should stay, then it will burn. A little is enough to burn. I should be able to find a reference for this I think. (The reason why PPIs work in spite of this is that they very very much decrease stomach acid. so if nothing or almost nothing remains, then of course it doesn't burn)

more useful:
EBV can survive in the gastric epithelium and get latent there. they mentioned this by the way somewhere in the following paper:
Dysbiotic infection in the stomach (2015)
so, this is my other candidate to why I don't have that stomach acid push after meals. this candidate is particularly likely and me because I have largely lost stomach acid production 2 weeks into my EBV.

if you have a lot of weird GI stuff, then I think stomach acid is a good idea to research: it could cause SIBO; non-digested food because stomach acid triggers the pancreas; malabsorption a lot of acid dependent things, ....

-> it could be a good idea to do that simple stomach acid test at home that I linked above.


I am just in the process of finding out how to treat the causes of low stomach acid instead of using the band-aid betaine HCL. interestingly, IL1beta inhibits stomach acid 100x so strongly as the PPI omeprazole. mamma mia. And my IL-1beta is elevated.

I don't think your thread is silly!