Cellular Nitrogen and Energy Metabolism in ME/CFS, 2025, Armstrong et al

John Mac

John Mac

Senior Member (Voting Rights)

STUDY HYPOTHESIS AND DESCRIPTION​

ME/CFS, a condition diagnosed by symptoms like extreme tiredness after exertion (known as post-exertional malaise), ongoing fatigue, and mental cloudiness or “brain fog,” may stem from a basic problem with how energy is made and used in the body.

We hypothesize that in ME/CFS, nitrogen compounds might be mishandled in immune cells because the mitochondria (energy factories of the cell) are using amino acids (building blocks of proteins) to make energy. To explore this idea, scientists will grow immune cells from blood samples and feed them special types of sugar, fats, and amino acids that can be tracked. This will allow them to see how the metabolism of these cells in ME/CFS patients is different from people without the condition.

This study uses innovative methods to deepen our understanding of ME/CFS and possibly uncover the root causes of its symptoms.

Objectives
  1. Observe how amino acids are used by cells from ME/CFS patients compared to healthy controls.
  2. Observe how sugars are used by cells from ME/CFS patients compared to healthy controls.
  3. Observe how fats are used by cells from ME/CFS patients compared to healthy controls.
  4. Observe the usage rate of sugars, fats, and amino acids in ME/CFS and controls.
  5. Test the Nitrogen Hypothesis.
ns1.omf.ngo

Nitrogen Hypothesis - Open Medicine Foundation

This project aims to test the nitrogen hypothesis, which is that damaging, nitrogen-containing by-products of energy metabolism accumulate more readily in the cells of ME/CFS patients.
ns1.omf.ngo ns1.omf.ngo
 
Some more info from the web page.

Updates and Potential​

  • Lymphoblast experiments are completed.
  • We have expanded to look at cells with known genetic anomalies.
  • Both the lymphoblast samples and cells with mutations have been prepared and are currently producing metabolite data for analysis.
  • Expecting both projects to be completed in 2025.
  • There will be 3 publications for this work.
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Utsikt said:
Is there any mention of what the hypothesise that drives this change in metabolism? Or why it might persist outside the very local environment in the body?
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The basis of this hypothesis is that the increased reliance on amino acids for ATP production has consequences that could explain many of the symptoms and that the increased reliance on amino acids could be driven by many factors that may be different between people.
 
Utsikt said:
Are those factors expected to persist for the cells you’re testing in the settings you’re going to test for them?
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That would be the expectation. The increased use of amino acids is meant to happen in a stressed state, it's more Carbon efficient than glucose/fat (which is why we use it during stress, females go to this well faster) but it produce more negative byproducts and removes amino acids from the other roles they play like neurotransmission, nucleotide synthesis, digestive enzyme production, etc.

In addition, the consideration is built around the idea that there are an array of in-born errors of metabolism in the stress metabolism pathway that aren't a problem until someone experiences a long-term stressor like a complicated acute infection event that typically takes longer to recover (weeks/months), that longer term use of the stress pathways uncovers previously existing flaws in the genetics that were never a problem prior and creates a self-perpetuating condition.
 
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