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I suppose in that case an obvious research design presents itself. Take a group of ME/CFS patients and match them according to activity levels (number of daily steps) and body mass index to controls and see whether they differ.
I like it. Simple and effective.
Hello @ChrisArmstrong,
So grateful you are here.
Reading about the starvation. I was adopted from Sri Lanka. And there was definitely starvation happening my first year until I moved to Europe.
ME might be h genetic but this could have started my problems at a young age. In hindsight I always had issues with metabolism.
Lactose, sugars, always gut problems, being overactive as a kid and as an athlete.
And although my onset was viral with Cytomegalie. The issues always started with the gut.
And how does this all relate to Post Exertional Malaise?
Regards,
Grigor
Well the starvation is a model for the metabolite pathways we see, it may be starvation at a cellular level but it may be something else that presents similarly. Certainly gut problems seem to be a common thread, there has been some interesting work from our group on this but also Maureen Hanson's group and Hornig's group is studying this area too.
PEM is something I will be studying more, we have some thoughts on it but they are a little more complex and personally I don't like to get behind something until it's line of reasoning is relatively simple (Occam's razor). However the thoughts are in the realm of pH, purine signalling, oxidative stress and glycolysis.
@ChrisArmstrong
In the as yet unpublished paper on the gut microbiome and metabolites in feces do you look into propionate production. I know that reading the Venket Rao et al paper on a the impact of probiotic (yakult) on anxiety in CFS https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2664325/ they suggested that one possible reason for the impact they saw may come from the L Casei Shirota crowding out propionate producing bacteria.
(I have not really delved into the propionate research, just glanced at some papers, but it seems like it may have a U shaped response, reducing inflammation in the gut in small doses and increasing inflammation in the brain in large doses.)
I was interested in this study because A I have issues with anxiety (like Hip and quite a few others here) and B the measure they used was the Beck Anxiety Inventory and it has a has a lot of symptoms (dizzy, lightheaded, hands shaking, heart pounding etc) that seem very CFS/ME very POTS http://www.brandeis.edu/roybal/docs/BAI_website_PDF.pdf
Which makes sense to me I have issues with POTS and a large chunk of my anxiety seems to be POTS related. Indeed when my POTS has been really bad panic is the best term.
P.S.
Oh and I should add that since reading the paper a week or so ago I have been wondering if all the fibre I pride myself in eating is actually being turned into injurious byproducts. If this is another intervention as daft as GET. Another case of applying what works for normal people to a body that is clearly no longer aquainted with normal.
Ah yes I too have anxiety issues so I know what you are talking about there. I think fibre is great and definitely stick with it. i actually helped myself a lot with fibre during bad periods of anxiety. The negative byproducts is a theory and it only happens from the breakdown of proteins into SCFA (not fibre).
Another anecdote here too. On a good day I can shift a ton of firewood as long as I take it steadily but if I tried to saw one of the logs and started to get breathless then everything collapses in a heap.
Incidentally I know we're talking primarily about the immune system here but might the Warburg effect also apply more generally to other cell types?
There is some evidence in ME/CFS of a switch to fast twitch Type II (glycolytic) muscle fibres as discussed in threads such as this :
http://forums.phoenixrising.me/inde...res-from-patients-with-cfs.11860/#post-496278
Yes very interesting information and that thread and research is interesting too. I think I've read similar things on here before, it's the quick increase in oxygen-based energy metabolism that effects people negatively. Glycolysis allows you to create energy without oxygen, we think glycolysis is being used in the muscles. This is why like the model of starvation because that too shows an increase in glucose in blood and a decrease in just about everything else, the reason for it is that the body globally uses amino acids and lipids for fuel except for the brain and muscles which rely on glycolysis.
@ChrisArmstrong I produce lactic acid much quicker since ME/CFS; my anaerobic threshold is much lower; is this in conflict with your results of low lactate?
No not at all, we studied people at rest. As in the answer just above the starvation model suggests that muscles are likely to increase a reliance on glycolysis when activated. Our metabolite findings reflect the global body metabolism at rest (mostly organised by the liver).
@ChrisArmstrong If it is true that ME patients are nutritionally depleted by an ongoing low grade sepsis from immune activation. Why do all our regular blood tests not show up this malnutrition (most of the time)? Is this a reflection of how non-useful these tests are in assessing nutritional status?
Because it's at a very low level that can vary though out the day. We can only tease out these significant pathways by looking at large cohorts not relevant to the individual profile. Not yet anyway.
Thanks for your time here, so does this mean an individual metabolite analysis/report might be worthless? Additionally would this suggest metabolites are not useful as potential biomarkers?
It will tell you what is happening in your blood at that one point in time, which would be altered if you ate or if you exercised or if you had an infection or if it was late in the day or if you were sleepy. So on its own I would take it with a grain of salt and personally I think it is useless. However, well organised longitudinal metabolite profiles I think will be very useful for the individual. We are running a project on this and I think Ron Davis is too.
So far I see no potential biomarkers from metabolites but that's because no one has tested whether you can differentiate someone with ME/CFS from other illnesses by using metabolites. Someone has to show me this first.
Excellent job by Chris Armstrong yesterday at the SMCI webinar... these are very sense concepts and the work is very promising and important. Keep pushing forward,Chris, and hello everybody.
Z
Thank you very much for your support Zaher and the brilliant work you do at Solve ME/CFS.
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