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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.
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This was a plasma cytokine study. I am guessing at some point they will do a spinal fluid cytokine study. That should address the central/peripheral cytokine issue.
Cort Johnson's Blog said:In fact, the authors tantalizingly noted because ME/CFS appears at least in part to be a central nervous disorder cerebral spinal fluid may very well be a better medium to investigate than peripheral blood. That could suggest we’re due some more important findings in a couple of weeks when the Simmaron Research Foundation/Chronic Fatigue Initiative CSF study is published.
I would just like to mention that maybe we need a bit of caution in interpreting cytokines as the cause of our symptoms. Firstly from my own experience (and I realise this is N=1), I have had many cytokines tested and many of them have been raised. By treating with a combination of nexavir and abx, I was able to normalise all cytokines for a period of around 6 months - but none of my symptoms improved.
So I take this study, which shows PWC's feel ill no matter whether their cytokines are raised or lowered, as evidence that cytokines are likely not responsible for our symptoms.
@Jonathan Edwards does it mean that rheumatologists would be a good candidate home for medical specialty? Our field so need and deserve a home soemwhere in medicine. See if I mentioned 'cytokines' to my GP, she would roll her eyes and sigh. Not her ballgame.CRP and ESR only measure inflammation that includes IL-6 production. That is quite a wide range but by no means all sort. CRP does not go up in lupus a lot of the time.
I don't actually think there is likely to be that much 'inflammation' of a traditional sort in ME but it looks as if there may well be cytokine involving immune reactions. There are lots of immune disease where there is no typical inflammation - immune thrombocytopenia, Grave's disease, anti-phispholipid syndrome etc etc. To understand what is going on here I think we have to move beyond simple terms like inflammation and deal with specific cellular interactions. That requires a considerable knowledge of immunology so it isn't much help in general discussion I am afraid!
Well, there certainly seems to be a piece of the puzzle missing. Other diseases involving cytokine abnormalities or microglial activation don't exhibit exertion intolerance/PEM to the degree of ME/SEID.To my mind this study is quite useful in showing that the immune system is the wrong thing to focus on. We can't make energy normally. There is something wrong with the metabolism.
Worth noting that half of the sample came from the NIH/'XMRV' cohort where all cases had a viral-like onset. Let's say half of the remaining cohort (CFI one) also had a viral-like onset and three-quarters of cases, but not all, probably have a viral-like illness. Certainly the NIH cohort means this sample is enriched for patients with a viral onset.
IFN-gamma drives faster tryptophan degradation, causes cognitive problems?
Which is quite dramatic. I wonder if there is a way of testing this?
Yup, one thing I started toying with was that this swathe of cytokine shifts in the early stage might reflect poor HPA control as much as anything. The question then is what is going on later and I cannot work that out.
Well, there certainly seems to be a piece of the puzzle missing. Other diseases involving cytokine abnormalities or microglial activation don't exhibit exertion intolerance/PEM to the degree of ME/SEID.
From what I've read the cytokine issue in major depression is similar to the one in MECFS - there's plenty of evidence things are awry but no clear direction, and results can be inconsistent between labs (as mentioned in this meta analysis).Anyone looking into cytokine studies in Major Depression? We may be side swiped with this by a certain brigade.
Perhaps the results from the gene expression study that Dr Montoya mentioned on the recent conference call might be used to validate, to some extent, the results of the present study (assuming the cohorts are different).
That study looked at the m-RNA from 200 ME/CFS patients and 400 controls. (See this post.)
If the expression of the genes from the Montoya study, corresponding to the cytokines measured in the present study, show the same relative differences between: patients at less than 3 years, more than 3 years, and controls, then the present study might (effectively) be considered at least partially validated in a different set of patients (and likewise Montoya's study similarly cross-validated).
On the other hand, if the gene expression for those same cytokines is different, then that wouldn't necessarily prove things one way or the other, since the levels of the cytokines measured in the present study could be affected after gene expression (i.e., post-transcriptionally).