Discussion in 'ME/CFS research' started by Sly Saint, Dec 11, 2019.
This seems like an important paper? I also have heightened lactate at rest
Did you have your blood samples immediately tested or put on ice? If not, it can be increased.
They did not give me proper instructions when my lactate was measured. Mine was in normal range 2 days after 50 minutes of running.
If more than half (55%) have elevated lactate, why isnt this used as a diagnostic tool?
The paper discusses many times the fact that we come across elevated lactate levels in mitochondrial diseases. Interestingly, the agent with which we see a normalisation of impedance on the nanoneedle test in ME/CFS patients is SS31, which is used for mitochondrial disease.
Mitochrondrial diseases prohibit endurance training so what you could be showing is that sedentary individuals have poorer lactate disposition due to insulin resistance.
They never, ever, acknowledge it in the discussion sedentary behavior because it's cheaper and faster to acquire improperly matched controls.
Here, they just show reduced endurance training is detrimental to lactate disposition in a dose-dependent manner, and slapped CFS on it.
If the finding is solid it would be a very interesting lead. The thing that worries me is that the correlation showed up after all sorts of compensations for factors that I would have thought did not need compensating for. The worry is that the numbers have been squeezed around until they show something up.
Im not sure, it was a part of a bigger blood panel at the hospital
More from France then. Wondering if there are more teams across Europe doing research that isn’t on the English speaking radar.
I associate lactate with Jarred Younger - brain MRI work; based on his recent talk in Scandinavia, I think he's due to publish something soon.
Would a link to "low levels of carnitine" in ME show up in a genome-wide association study [Chris Pointing's project]?
I think lactate is always interesting as an intermediary because it is so ubiquitous, it can shift pretty quickly both in location and amount, it has signaling and feedback properties and there are lots of reasons and ways why and how it could remain elevated. It may also be a bother to pin down correctly since we might be dealing with a moving target in more ways than one...
A patient & doctor with severe ME, Mark Vink, previously tested the effects of minor exertion on lactate levels:
"The Aerobic Energy Production & the Lactic Acid Excretion are both Impeded in #MyalgicEncephalomyelitis/#ChronicFatigueSyndrome"
Interesting, though I'm not sure they tested what they think they tested. They say they tested patients at rest. Which is true in the sense that they didn't just come off a CPET or similar. However, the simple effort of getting to the hospital would likely have put some of the patients into PEM. Then add the general unrestfulness of a hospital environment and you may or may not have influenced lactate levels.But it does seem worth trying to replicate.
Lactate also discussed here: https://www.s4me.info/threads/abnor...rcise-testing-in-me-cfs-2019-lien-et-al.9826/
Also interesting is the very thorough work up patients were getting. Is that normal in France? Or just something they do at that one university hospital? At any rate it seems like a good data set that could be useful for developing hypotheses or for some relatively cheap initial road-testing of ideas to see if they're worth taking through to bigger trials.
I recall some studies testing lactate in CFS patients after exertion about 20 years ago:
More info here from another researcher involved (on the local ME/CFS Society site): http://sacfs.asn.au/medical/adelaide_uni_research_1.htm
I seem to recall (but I could be wrong) that a follow-up study didn't replicate the first lot of results and the whole thing quietly died.
This is so damn stupid. People with PhDs.
It is because me is NOT one disease, but a significant part of the me population has a mitochondrial disorder, be it primary or secondary!
You have to take me patients with increased lactate and put them into ONE STUDY GROUP!
I find it a bit weird that there wasn't any significant difference in symptoms between the high and normal lactate group, except for PEM. If it was important to the illness, wouldn't we see more difference between those two groups?
I was curious about how PEM was measured. It is described at the end of the paper:
That seems to me problematic. If someone is pacing really well, they may not have had PEM in the last month, so may score zero on frequency, and therefore zero for PEM.
And the severity is a self reported scale. Does anyone have a copy of the CDC SI questionnaire?
Also the say if anyone scored 2 or more lactate level at any of the 8 time points, they were put in the high lactate group. The graph seems to show only a single time point out of the 8 were lactate was that high for anyone.
A primary one should have been ruled out now, cf some recent findings which are gathered here:
I don´t know if it is right to say "secondary mt-disorder" when mitochondria are affected downstream from something, but only this seems to be the case. In fact one or two findings are saying that mt themselves are even in a better shape in ME!
Only symptom-wise there are associations with mt, so nothing which would explain the illness and its onset (two findings differ in their assessment of some predisposition, as one doesn´t want to rule this out).
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