Discussion in 'Latest ME/CFS Research' started by Dolphin, Apr 11, 2017.
Until biomarkers are identified and put into practice, trying to wade through diagnostic criteria is fraught with contradiction, uncertainty, and confusion.
Kind of feels like cart before horse to me. My personal opinion is that accurate case definitions will follow accurate biomarkers, not the other way around.
But presumably a biomarker is something measurable that is different in people with ME. How do you define people with ME in order to look for a biomarker?
and that is example why CFS needs to be split into subgroups (be it if a person wants to call internationally defined ME a subgroup or whatever) and those groups studied separately. They just cant go looking at a huge range of CFS people lumped as one and easily find a biomarker there.
In other words, the definition is critical and should be analysed carefully, which is what this paper seems to be attempting.
So there are studies where 75% didn't have PEM?! This is a major problem seeing as this is the main defining feature of ME that differentiates it from the many potential reasons for ongoing fatigue.
Are these studies named? Or were different samples collected for this study? Not sure I quite understand what they did.
Right but if the biomarkers are following transient symptoms they will have the same problem. The root cause, or more likely, more likely root causes May turn out to be processes that are difficult or not currently currently possible to measure without scooping out some brain tissue or somesuch thing.
We are accustomed to thinking of easy diseases with one cause. Perhaps most of those have been discovered and what's left Are difficult melodies with multiple root malfunctions, and the roots may be overlapping but not identical for all.
Symptom and probably marker variability is something I've wanted to get a hold of researcher to tell them for years, but how the heck do you reach/talk to interested parties?
You really get nowhere chasing leaves until you're able to see branches and follow them down to roots.
Pem seems to be the most distinctive feature, but in the pre-waterfall stages for me even that wasn't present, just inexplicable episodes of fog and pervasive weariness, with the scattering of other shifting oddities, each of them unremarkable by themselves. Even Pam isn't defined correctly it's not about paddling on the stationary bike, though it is possible to set it off that way....this is an hours long topic by itself. It takes more patience and perseverance than most people have to sort out this kind of thing.
I think you're over complicating things. We are dealing with a disease of the immune system first and foremost, even if the origin of the disease originates out the nervous system, there will still me a measurable immune signature.
We have groups who have identified that the cellular metabolic dysfunction can be replicated in healthy control cells using serum from ME/CFS patients. There must be a factor, or factors in the blood of CFS patients which trigger hypometabolism. Hypometabolism itself appears to be a fairly consistent bio-marker, not tied to transient symptoms.
In the case of Diabetes, it would be very difficult to distinguish subgroups without a biomarker, I would suggest the same is true of ME/CFS.
I hope you are correct.
Do we actually know that the primary locus of this disease is the immune system, or is that merely the conventional wisdom? If asked, I say that it probably stems from the immune system, but I don't know that for a fact. AIDS turned out to be one very clever, adaptable pathogen, but I don't think we'll be that lucky.
I did not know that one specific cellular metabolic dysfunction has been identified as the key....but perhaps I misunderstood your post. which would be no surprise....brain often skips over the meaning of things now, like a flat stone.
There is overwhelming evidence to support the notion of ME/CFS having a major immunological component. From cytokine profiling, to B-cell depletion therapy, to nk-cell dysfunction, to microglial activation in the CNS. It's more than likely that the down-regulation of metabolism stems from the immune system.
You're right, it hasn't. It's one of several metabolic pathways which has been implicated. The point I was trying to make is that some of the metabolic features of ME/CFS can be reproduced in vitro in healthy cells, by taking serum from patients. That implies that there is something in the blood of patients which stimulates cells into that state. That's a very promising discovery, and in my opinion provides more evidence of an immune regulated state.
Thx, I would like to catch up on the developments you've mentioned - many hours reading it sounds like- but not now, time for zzzzz, if that function will work.
You can also try a Google Site Search
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