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That's a VERY important point, I think there are ways to circumvent this issue, granted so far no org has found good structures/means yet.

That's exactly the point: no amount of criticizing bad research will stop it from happening. It happens for ALL diseases but in relatively lower numbers. The (more realistic) goal is to get more funding for better research for that you and people on this forum will be heard, in terms of...

I agree with basically everthing you say, but, if capacity and resources are a rare good, one should be as conscious as possible/aware of the utility of ones actions and be aware of tradeoffs one is making and be honest about potential shortcomings in terms of setting and reaching concrete...

All good, but that is a complete misrepresentation of what I am saying. I am not saying it has no value, but that relatively speaking, too much energy goes into discussing 'old & bad science' with little to show for it. For an ME patient who is (the right kind of) scientist it could make sense...

Yes, I disagree, telling laymen to invest their little energy in highly complex matters that they will not solve is not optimal to put it mildly. Patients will neither find the structural abnormalities from their beds nor will they crack the complex pathways. There is a difference between...

I understand what you are saying, but in most cases, 'criticizing bad research' on a patient forum or a blog will not improve it—not even the next iteration of it. That's not really happening, that’s what should happen, maybe, but it doesn’t in the vast majority of cases. The reason why PD has...

This thread has been split from Speculations about the genetics of ME/CFS and DecodeME Yes, not easy, but it's the way forward. We will not reach a tipping point for ME/CFS unless there is significantly more investment and engagement by patients and more importantly their loved ones...

Could measures/chances to secure further funding be improved by (crowd)funding to hire people for writing grant applications, do political lobbying work and so forth? As I am quite sure the answer is yes: Are there currently existing organizational structures that could make use of such funds to...

How expensive (for a large-very large WGS)? Is anyone currently trying to get funding for it and could it happen in parallel to the GWAS? Thank you.

That's a very interesting idea. I am not sure though, that ME/CFS cells (we haven't looked at too many celltypes?) behave normally or work as in healthy controls? I guess that is not a neceassary ingredient for your idea to have merit, though. Are there research methods and technology that...

This is more or less the model that many of the "ME/CFS = EV infection" proponents use. I think it's somewhat plausible. What is important to add is that there are celltypes not only long lived but that don't differentiate and/or are not getting replaced, at least not in sufficient numbers?

Very interesting study, I thought I would mention that measures to increase volume (saline, desmo,fludro,..) worked well for me in the earlier phase of my illness but stopped working after a while. Recently I started a retrial of desmopressin and was quite surprised when it made me feel MUCH...

I have measured all of them and GFAP in my own samples (very severe ME), all negative, but again, I did not expect them to be elevated, as I think we deal with something more akin to past 'acute injury' as opposed to 'neurodegeneration'. I think 'time of sampling' is paramount. PS: If LC mouse...

Thank you, I have read this study! I think it's highly underrated how significant these findings could be, we need much larger samples though. If replicated in big cohorts this would largely destroy neurology's resistance to take the issue seriously. Timing and cohort size are the main issues.

I find it likely that it is a property of LC and also ME/CFS, but very unlikely that GFAP remains elevated for such a long period without reinfection or re-injury, also, potentially there is a 'sub-acute neurodegenerative' subgroup. There is a similar phenomenon in mild TBI.

The main issue at hand, in terms of commonly used biomarkers to determine CNS damage (such as GFAP), is that LC patients were not controlled for illness duration or onset (in relation to GFAP). There is a kinetic time dynamic to these biomarkers; in classical neurodegenerative disorders...

What's pretty insane about this, apart from the study population size, is that GDF15 is fully expected to be higher in an older population.

I doubt that GDF15 will be a good predictor/biomarker for LC and ME/CFS, but the study design (not in terms of how many patients were used!) is what we need much more of, we need to get a better grip of acute vs sub-acute vs chronic disease vs recovery (the PVFS subgroup,in case it really...

Could someone with more spoons summarise Dr. Edwards' and Dr. Armstrong's points in a few paragraphs? I will then use this this info and run it through two more experts for mice modelling, ask for improvements and then send it to the authors of the study.

I would love to hear a fair critique of the methodology used in this paper by you, with this valuable information the methodology might actually end up being improved for the upcoming MECFS research this group plans to do. Exchanging information/knowledge to improve outcomes for pwME!