Insights from Invasive Cardiopulmonary Exercise Testing of Patients with ME/CFS (Joseph et al., 2021)

ChookityPop

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Autoantibodies that attack either peripheral or central nervous system. Seems like the peripheral nervous system autoimmunity has a lot less documentation. They know very little about this. These complex carbohydrate antibodies that can potentially damage nerve cells are just now being looked into. I believe they are still trying to confirm whether or not they're actually pathogenic. Which means they are very far away from determining their origin.
If thats the case would the answer be to eliminate carbs?
 

livinglighter

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Is PEM happening as a result of having some form of exertion/exercise intolerance?

I've revisited my medical records and can see what basically reads as exertion intolerance related to a hyperimmune response recorded during wider communications with health professionals about the condition. The comments are made by the immunology team where I met the CFS/ME diagnosis. I wasn't told this in person though, PEM was the only part explained directly to me, so I'm currently connecting the dots.

I was told to monitor my heart rate and stay within my energy evelope as well to avoid triggering PEM.
 

Pyrrhus

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If thats the case would the answer be to eliminate carbs?
No, there may be good reasons for limiting dietary carbohydrates, but this isn't one of them.

Is PEM happening as a result of having some form of exertion/exercise intolerance?
Great question. This study only looks at how dysautonomia results in exercise intolerance, and possibly SFN, but it does not address PEM. PEM may be an entirely separate phenomenon, or it may be related.
 

sometexan84

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If thats the case would the answer be to eliminate carbs?
It's a good question. I'm not going to pretend I know the answer.

I think calling them carbohydrate antibodies is oversimplifying a little. It's more like these saccharides, made up of sugars and sometimes acids, joining together via glycosylation. The end-product seems to usually involve glucose, fucose, galactose, etc.

From what I understand, you could cut carbs, but your body would still produce glucose, and other elements needed to join together and form these types of complex glycan-based antibodies.

You could check out this COVID study on self-carbohydrate antibodies for some specific auto-antibody examples.

Looks like in COVID patients, some of these glycan/carb auto-antibodies include IgG and IgM to....
  • Gangliosides
  • N-linked glycans like GlcNAcβ1-2(GlcNAcβ1-6)Manα1-6[GlcNAcβ1-2(GlcNAcβ1-4)Manα1-3]Manβ1-4GlcNAcβ
  • LacNAc-containing glycans like Galβ1-4GlcNAcβ1-3Galβ1-4GlcNAcβ1-3Galβ1-4GlcNAcβ1-3Gal
  • Blood group H
  • Sialyl Lewis X [Neu5Acα2-3Galβ1-4[Fucα1-3)GlcNAc]
  • BG-H1 (Fucα1-2Galβ1-3GlcNAcβ)
 

Pyrrhus

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As some other studies have found, the ME patients could not reach the same level of oxygen consumption during exercise that healthy people could. (lower peak VO2) Whereas most other studies that showed this difference did not achieve statistical significance for the finding, this study found the difference clearly statistically significant.
Why does this study clearly achieve statistical significance for the observation of a lower peak oxygen consumption (VO2), while other studies could not demonstrate statistical significance?

I don't know the answer to this question, but it is worth pointing out that other studies generally compare weight-adjusted values of peak VO2, but this study compared age-weight-and-gender-adjusted values of peak VO2.

Specifically, this study reported peak VO2 as a percentage of the predicted peak VO2 for a healthy person of their age, weight, and gender, using the following equation for predicted peak VO2:

1627704869818.png




...And note that other exercise studies use a 2-day CPET because the data collected on day 1 is usually insufficient to detect a significantly lower peak oxygen consumption. Therefore, they focus on demonstrating the difference between performance on day 1 and performance on day 2. This fact was notably documented in this classic paper from 2007:

Diminished Cardiopulmonary Capacity During Post-Exertional Malaise (VanNess, Snell, & Stevens. 2007)
https://forums.phoenixrising.me/thr...monary-capacity-during-post-exertional.10414/
(only accessible to Phoenix Rising members with more than 100 posts)
Excerpt:
Purpose:
To compare results from repeated exercise tests as indicators of post-exertional malaise in CFS.

Results:
Multivariate analysis showed no significant differences between control and CFS, respectively, for test 1.
[...]
However, for test 2 the CFS patients achieved significantly lower values for both [peak oxygen consumption] and [anaerobic threshold].
 
Last edited:

roller

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with the muscles, it is million times better since im taking VASTAREL
also much improvement on breathing, dizziness, pains and more.. huge change!
endurance-wise.

e.g. long stairs
before: at the half of it, a break, gasping for air. when up there, very heavy/loud breathing, exhausted totally
after: i walk up the stairs and further.
gross... :)
 

lenora

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A new publication by the team of Phillip Joseph, Anne Oaklander, and David Systrom, which I personally find exciting.

Insights from Invasive Cardiopulmonary Exercise Testing of Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (Joseph et al., 2021)
https://journal.chestnet.org/article/S0012-3692(21)00256-7/fulltext

Main points:
  • 160 ME patients were subjected to both an exercise test (iCPET) and a skin biopsy of the lower leg.
  • Results were compared to 36 healthy people.
  • As many other studies have shown, the ME patients could not reach the same level of oxygen consumption during exercise that healthy people could. (lower peak VO2)
  • During exercise, ME patients had lower blood pressure in the veins transporting blood from the legs to the heart. (lower right atrial pressure)
  • 31% of ME patients showed Small Fiber Neuropathy (SFN) in the lower leg.
  • The authors interpret the findings as possible clinical evidence for dysautonomia of the small nerves that control constriction of the small veins in the legs, which means that:
    1. The small veins in the legs remain abnormally dilated while standing,
    2. which means insufficient blood pressure to return the blood from the legs to the heart,
    3. which means the muscles in the legs have impaired circulation (blood pooling) and possibly insufficient oxygen,
    4. which may mean that the insufficient oxygen in the legs leads to death of the small nerve fibers in the legs. (Small Fiber Neuropathy)
    5. ...Which is exactly what many people have suspected for a while, and is the same mechanism behind dysautonomic orthostatic intolerance!
Excerpt:

Earth to Pyrrhus: Once again thanks for looking up all of the research that you and so many others have done. It's most appreciated.

Also, did you notice that some alien changed your photo? Nice to actually meet you. Yours, Lenora.