Discussion in 'Latest ME/CFS Research' started by GreyOwl, Jul 7, 2016.
Thanks very much for posting, looks to me as if it is fitting in with what Ron Davies is finding.
Maladaptive cellular respiration? I had no idea such a thing was possible. Very, very interesting. Can't wait to see what Dr. Naviaux's research turned up.
As Always we probably never hear anything about this 'exiting' research again. Everytime they may have found a new possible marker.
Does this explain why frequent small meals rich in protein are often rated as helpful by patients?
I disagree. I think there is a commonality coming out of current research internationally which makes me hopeful that the mechanisms in this complicated illness will soon be understood. I think that it has taken a long time to get to here because of the bizarre concerted efforts to prevent research, but I really am hopeful that what I am seeing now will turn out to be a watershed moment in this history.
Everything they found in ME (CCC) patiënts is the result of oxygen deficiency in the cells (problem microbloodflow and red blood cell shapes).
Thanks for posting @GreyOwl. Good find. Hadn't seen this. Taking an in depth look now.
This study was discussed on this thread last year.
One of the authors, @ChrisArmstrong has spent some time with us on PR.
@Never Give Up quoted one of the studies on which the study in the OP was based. The study in the OP is new.
ETA: no, I am wrong. The study in the OP was the same study @Never Give Up quoted, and the same study discussed here in another thread. As you were.
Lol. I read this back at the time but had forgotten it completely. I just saw a metabolic study in Australia that I assumed was recent and thus I had missed. Damn fog
This was what stuck out for me back then:
"Mitochondrial dysfunction has been suggested as a po- tential cause of depleted ATP and fatigue-like symptoms (Filler et al. 2014). However, in our study the quantitation of blood glycolytic metabolites revealed that glycolysis inhibition is occurring implying a lower level of acetyl- CoA production."
I also thought it was unusual that it was female only. Not necessarily bad, just unusual (I realise the reasons for this).
I can be wrong but this study is maybe related to why someone here has had a huge lift of PEM by taking amino acids. I think it was @Mary
Its a smart move. Since this is only a pilot study they decided to decrease diversity as much as possible. Age and gender were restricted. To go to a larger study they will need to diversify the patient type though.
Please note, something that was important in their 90s research, that some of the findings were only found early morning, such as allantoin. I think the timing might be important. The chemistry may not be the same at different times of the day, which might create additional confounds.
Yea it was a smart move. We just dont see that kind of 'drilling down' very often, thats all, certainly not in M.E research. Its usually very vague. Suprised me. It just cant be applied to other groups though, as it is so specific, which is fine, providing they follow up.
Interesting - I'm sure you're referring to this statement in the article:
FWIW, it wasn't amino acids per se which cut my PEM in half (from 2 days to 1), but branched chain amino acids. I still take them, afraid to stop!
Although I think the mechanism by which BCAAs help with PEM is different than cited above. Here are the articles which got me started on BCAAs:
Anyways, I'm really glad to see this study!
And I really like your how you said this @GreyOwl - there is no sane explanation for how we have been ignored, sidelined, marginalized ad infinitum:
There is one thing puzzling to me about the study - it says that blood lactate was reduced. Isn't blood lactate what tends to be elevated in ME/CFS?
Interesting, thanks Mary. I will read those links in a minute.
If not too much of a personal question (feel free not to answer), are you underweight at all since M.E/CFS?
It can be both, or normal. Its part of the hetrogeniety of the disease and the different metabolomics for each of us. Davis recently pointed these issues out at the London conference where one patient had an issue with trytophan metabolism, another with biotin. There were differences between patients. The underlying take away is that our TCA and other metabolic pathways are not working properly, and they are fundamental for life.
Not at all, I'm afraid! The opposite actually. I gained weight and then lost most of it excruciatingly slowly because of course my activity is so limited. I know some people with ME/CFS do lose weight or can't keep it on, but I don't have any such problem .....
Thank you for this info. FWIW, at least one of the articles I linked above talks about a high tryptophan ratio to something else, I forget what, but tryptophan was involved.
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