Elevated blood lactate in resting conditions correlate with post-exertional malaise severity in patients with ME/CFS - Ghali et al Dec 2019

Sly Saint

Sly Saint

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Abstract


Elevated blood lactate after moderate exercise was reported in some of patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). We hypothesised that blood lactate could be also elevated in resting conditions.

We aimed investigating the frequency of elevated lactate at rest in ME/CFS patients, and comparing characteristics of ME/CFS patients with and without elevated lactate. Patients fulfilling international consensus criteria for ME/CFS who attended the internal medicine department of University hospital Angers-France between October 2011 and December 2017 were included retrospectively.

All patients were systematically hospitalised for an aetiological workup and overall assessment. We reviewed their medical records for data related to the assessment: clinical characteristics, comorbidities, fatigue features, post-exertional malaise (PEM) severity, and results of 8 lactate measurements at rest. Patients having ≥1 lactate measurement ≥2 mmol/L defined elevated lactate group.

The study included 123 patients. Elevated (n = 55; 44.7%) and normal (n = 68; 55.3%) lactate groups were comparable except for PEM, which was more severe in the elevated lactate group after adjusting for age at disease onset, sex, and comorbidities (OR 2.47, 95% CI: 1.10–5.55). ME/CFS patients with elevated blood lactate at rest may be at higher risk for more severe PEM. This finding may be of interest in ME/CFS management.
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full paper
https://www.nature.com/articles/s41598-019-55473-4
 
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.
 
mariovitali said:
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.
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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.
 
Mij said:
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.
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Im not sure, it was a part of a bigger blood panel at the hospital
 
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...
 
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.
We reviewed all medical records of patients attending the outpatient clinic of the internal medicine department of Angers University Hospital and diagnosed as having ME/CFS between October 1, 2011 and December 31, 2017. The diagnosis of ME/CFS was established by the same physician after a systematic 3-day hospitalisation during which an aetiological workup and an overall assessment of fatigue features and PEM severity were realised for each patient. We enrolled retrospectively all adult patients aged ≥18 years who met the International Consensus Criteria (ICC) 20114.
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The following biological data were also gathered for each patient: lactate assessment, immunological assay, infectious disease screen for HIV, hepatitis B and C, Lyme disease, enterovirus, Mycoplasma pneumoniae, Chlamydia pneumoniae, serum zinc, 25- hydroxyvitamin D, morning (8 am) and evening (8 pm) plasma cortisol, testosterone, iron studies, plasma vitamin B12 and serum folate, full blood count and differential, erythrocyte sedimentation rate, electrolytes, calcium, phosphate, fasting glucose, C-reactive protein, liver function, serum protein electrophoresis, renal function, thyroid function, and creatine kinase.
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I recall some studies testing lactate in CFS patients after exertion about 20 years ago:

New chronic fatigue evidence emerges

Monday, 17 May 1999

Australian researchers say they have new conclusive evidence about chronic fatigue syndrome.

Previously thought to be a psychological condition, doctors from the Royal Hospital in Adelaide say they have definite biochemical evidence for the condition.

Endocronologist Richard Burnet says patients with chronic fatigue syndrome have specific changes in lactate levels after they exercise.

He says his research shows patients with the condition are unable to metabolize glucose properly in their bodies and that the glucose turns to lactic acid, in effect poisoning their system.

Dr Burnet hopes to do further research into why the process occurs and how to reverse it.
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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.
 
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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 was curious about how PEM was measured. It is described at the end of the paper:

PEM assessment.

The PEM item from the standardised auto-questionnaire of Centres for Disease Control and Prevention Symptom Inventory (CDC SI)36 was used to measure PEM symptoms over the past month.

Perceived frequency of PEM was rated on a 4-point scale (1=a little of the time, 2=some of the time, 3=most of time, 4=all of the time), and its intensity was measured on a 3-point scale (1=mild, 2=moderate, 3=severe).
Te intensity score was converted into equidistant score (0=symptom not reported, 1= mild, 2.5=moderate, 4=severe).

Te frequency and intensity scores were then multiplied to create the PEM severity score ranging from 0–16. In the absence of validated threshold that defnes PEM severity, we used the median PEM score on the CDC SI questionnaire to set the cut-of score ≥12 defning more severe PEM.
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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.
 
butter. said:
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!
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A primary one should have been ruled out now, cf some recent findings which are gathered here:

https://forums.phoenixrising.me/threads/mitochondra-in-me-cfs.78406/

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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