• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Immune network analysis of cerebrospinal fluid in ME/CFS with atypical & classical presentations

ljimbo423

Senior Member
Messages
4,705
Location
United States, New Hampshire
I wonder if the smouldering inflammatory process in atypical patients aligns to the group that rarely/never contracts infections, whereas the immune exhaustion in classical patients aligns to the group that seems to regularly contract infections.

When I read that, I had the same question. I fall into the Immune exhaustion/classical category and use to catch every cold and flu around. I found that fairly low doses of colostrum stopped that pattern. Now I get sick 3-4 times a year instead of 6-8.
 

duncan

Senior Member
Messages
2,240
I'd like to see the paper in its entirety.

I'd like to see more concerning which CSF elements were looked at. For instance, were there any signs of pleocytosis or elevated proteins etc? Any bacterial of viral footprints? ME, by definition, on paper might show other signs of inflammation.
 

Gijs

Senior Member
Messages
690
{...}''The patients belong to Dr Peterson's cohort who have catalogued (and frozen) biological samples, and carefully collected data and history about them''.

This is what worries me. It is a specific group of samples after an 'outbrake'' of a mysterious disease. Who said that this group is THE ME group? It could have been a specific infection what was going on in Lake Tahoe. These samples are not representative for ME/CFS patiënts. Only a very minor subgroup.
 

Cheesus

Senior Member
Messages
1,292
Location
UK
{...}''The patients belong to Dr Peterson's cohort who have catalogued (and frozen) biological samples, and carefully collected data and history about them''.

This is what worries me. It is a specific group of samples after an 'outbrake'' of a mysterious disease. Who said that this group is THE ME group? It could have been a specific infection what was going on in Lake Tahoe. These samples are not representative for ME/CFS patiënts. Only a very minor subgroup.

That could be the case, but I think the purpose of this paper is not really to draw conclusions, but to persuade funding bodies to cough up the dough for larger studies. So hopefully that kind of cohort bias would be caught by subsequent studies.
 

TreePerson

Senior Member
Messages
292
Location
U.K.
This is the opposite for me. Classical presentation, haven't had a cold in over 8 years of illness.

Yes I'm the same. I have had maybe three colds in 24 years but so far no seizures or demyelinisation or cancer. Fingers crossed. Kind of hoping I'm in the classical group despite lack of infections. Has there been a survey on here re the frequency have infections?
 

Tally

Senior Member
Messages
367
And what about acute classic onset,atypical presentation
Paper says "All cases (both classical and atypical) met either the 1994 CDC criteria and/or the 2003 Canadian consensus criteria." So if you don't satisfy the criteria they didn't include people like that in their study.

I'd like to see the paper in its entirety.
@AndyPR included it in the original post of this thread but here it is again http://www.nature.com/tp/journal/v7/n4/full/tp201744a.html
 

Marky90

Science breeds knowledge, opinion breeds ignorance
Messages
1,253
Happy to see another paper from them, even though it seems to create more questions than potential answers. I`m starting to wonder whether a lot of ME/CFS-cases in actuality are stem cell disorders. Disposing us to getting a immune system going awry. Although that would be somewhat bleak, there is the fact that a case of sickle cell disease just recently was cured completely by genetical engineering.

We might have to look closer on the earlier phases of immune cells for answers. Compare those cells to controls etc. This has hardly been done as far as i know, yet. When u start the research way down the mechanism-line, the hypothesizes quickly stack up, and the way forth becomes foggy. Clouded with researcher bias and non replicated studies as the fundament for further research.

Baffled about their choice of journal. That`s just.. Yeah.
 

Marky90

Science breeds knowledge, opinion breeds ignorance
Messages
1,253
Why? Atypical ME would seem to be a better candidate for rtx response than classical.

Well, it`s possible. But then one is presuming that the overactive immune system (based on cytokines) is more likely to have pathological b-cells than the other. I don`t think it`s that simple, mostly based on JE pointing out that such wordings don`t really make any immunological sense . It`s prone to oversimplification, a bit like the the "sustained stress response" theory. You can`t with good reason apply findings to theories that lack findings.

There is also the possibility, as i touched on above, that the cause is way down the line. Ritux and cyclo might just hit dysregulation, not cause. But that`s another issue to the one u brought up obviously.
 

Cheesus

Senior Member
Messages
1,292
Location
UK
Yes I'm the same. I have had maybe three colds in 24 years but so far no seizures or demyelinisation or cancer. Fingers crossed. Kind of hoping I'm in the classical group despite lack of infections. Has there been a survey on here re the frequency have infections?

What was your onset like?
 

Kati

Patient in training
Messages
5,497
Happy to see another paper from them, even though it seems to create more questions than potential answers. I`m starting to wonder whether a lot of ME/CFS-cases in actuality are stem cell disorders. Disposing us to getting a immune system going awry. Although that would be somewhat bleak, there is the fact that a case of sickle cell disease just recently was cured completely by genetical engineering.

We might have to look closer on the earlier phases of immune cells for answers. Compare those cells to controls etc. This has hardly been done as far as i know, yet. When u start the research way down the mechanism-line, the hypothesizes quickly stack up, and the way forth becomes foggy. Clouded with researcher bias and non replicated studies as the fundament for further research.

Baffled about their choice of journal. That`s just.. Yeah.

Regarding the choice of journal, Dr Hornig seem to publish a lot in these. There may be many reasons to this: 1) other journals do not accept, and this seems to be a problem with our disease. 2) Dr Hornig has connections (or already built relationships from past research) with tthis journal 3) a desire to publish in psychiatric journals to counteract the CBT/GET work from the british psychs. 4) a mix and match of all of the above.

I do not personally think this is a stem cell problem partly because more of us would get sick early in life. There may be immune signalling issues, auto-immunity issues expressed differently amongst us, metabolic issues, or blood flow issues. Or a mix and match of all of the above. :D
 
Last edited:

TreePerson

Senior Member
Messages
292
Location
U.K.
What was your onset like?
Mixed. Following three years of intense sustained stress I came down with a mild flu like virus which felt as though it didn't go away. I kept feeling ill and my temperature control had gone weird. Following that I had very mild PEM after long walks decorating etc muscle twitching. My hair went thin. Over the course of a year with every subsequent stressful event or infection this deteriorated to full blown ME. So possibly staged I am never sure.
 

Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
I've just scanned this paper but a few preliminary thoughts :

Obviously I welcome more quality research;

But I share concerns about using a single practitioner's cohort - they could be self-selecting;

While ME/CFS should be heterogenous (being a symptom based diagnosis) there does appear to be a binary split in terms of constant fatigue/wired and tired; no alcohol tolerance/alcohol improves symptoms; no colds flus in years/frequent infections;

The ambiguous language around the conclusions about the atypical group (non immune factors) 'suggests' to me a stress/psychological onset (maybe I'm wrong but that possibility doesn't personally concern me).
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
but atypical cases either had prior histories of viral encephalitis,

I am a measles encephalitis survivor. I wonder if this means I fit atypical ME?

As for the Rituximab response, or even cyclophosphamide, this paper generates ideas for tests that might be important in determining responders and non-responders. Rather than fitting this case, its something that can be tested for.

This kind of study needs to be replicated on other cohorts from other locations, and in greater numbers. It is however a great start down that road, and is supportive of the intuition many of us have that even ME might be two or more diseases, though CFS is probably even more than two.
 

Marky90

Science breeds knowledge, opinion breeds ignorance
Messages
1,253
Regarding the choice of journal, Dr Hornig seem to publish a lot in these. There may be many reasons to this: 1) other journals do not accept, and this seems to be a problem with our disease. 2) Dr Hornig has connections (or already built relationships from past research) with tthis journal 3) a desire to publish in psychiatric journals to counteract the CBT/GET work from the british psychs. 4) a mix and match of all of the above.

I do not personally think this is a stem cell problem partly because more of us would get sick early in life. There may be immune signalling issues, auto-immunity issues expressed differently amongst us, metabolic issues, or blood flow issues. Or a mix and match of all of the above. :D

Gotccha, I was thinking the same.

With regards to your second paragraph: Many stem cell diseases appear late in life,so I dont think thats really an argument against imo. Besides, all of the areas you listed are possible in different stem cell diseases too..
 

duncan

Senior Member
Messages
2,240
"This cytokine panel was developed as an assay for investigating acute phase (sickness) responses and neuroimmune dysregulation in neuropsychiatric disorders..."

Two questions I'm grappling with:

First, why is this panel being applied to ME/CFS sufferers? There is very little "acute" about the disease, and although technically cognitive declines could fall under a neuropsychiatric umbrella, I think that it could be a bit of overreach to default to a neuro psychiatric disorder - by this logic, anybody with cognitive deficits caused by a brain tumor also would by extension fall under a neuropsychiatric disorder, and that just isn't the case.

Second, how do the two subcategory ME/CFS results they put forth in this paper compare with how the panel profiles neuropsychiatric disorders?
 
Last edited: