Cause of EBV Fatigue found + Biomarkers (Mitochondria “Cellular Chronic Fatigue")

[sometexan84]

The Tomas paper seems to conclude that there is no difference between ME/CFS patients and healthy controls when it comes to mitochondrial complexes. So Tomas et al conclude the mitochondrial dysfunction must be upstream of the mitochondrial respiratory chain:

But these ME/CFS energy metabolism papers often contradict each other. An earlier Tomas paper contradicted the Myhill energy metabolism papers. And the Lawson study found higher than normal ATP levels the cells of ME/CFS patients.

Indeed they do contradict each other. This study addresses all of this, including (2) papers by Tomas. Remember, this study was done on EBV infected cells. They mention that they "resolved these inconsistencies by revisiting the issue of mitochondrial function and capacity in immortalized lymphocytes (lymphoblastoid cell lines or lymphoblasts)."

 

[sometexan84]

Just to say, Complex V is NOT a small part of the process, any more than any part of a pipeline is less important. If Complex V (also known as ATP Synthase) doesn't do its function properly, the earlier parts of the chain generate ROS, which either signals the mitochondria to adapt to the new conditions, or it signals the cell to kill itself.

ATP synthase is worth looking up. The head of the molecule spins at 21,000 rpm!

Right. Just trying to simplify things to help others understand who might not have the background info as some of us.

 

[sometexan84]

I cannot seem to find any supplements or drugs which boost complex V.

There are quite a few substances which boost complexes I to IV, detailed in this post.

In this particular study, if you're noting this is all happening via EBV infection, the drug to boost complex V is Valtrex/Valacyclovir.

 

[sometexan84]

From what I can understand, these papers, while both showing a problem in the mitos, show different problems. While I am always excited to see new research, i 'm just not sure what to make of it when results conflict with one another. Does anyone know of good review articles? Is anyone working to reconcile these results?

They go over this in the study. And they reference 69 other studies, many of which are 2018 and 2019. They discuss the inconsistencies and how they decided to address them in this study.

 

[sometexan84]

I looked up inherited mitochondrial diseases affecting ATP synthase, and was surprised at how localized some of them were. One would think that a mito mutation would affect all cells in the body, but some diseases affect just single organs, or parts of the brain, without affecting others. That could explain why my body doesn't show any signs of mitochondrial disease while parts of my brain aren't working right. It could still be mito dysfunction, just highly localized.

Well, if EBV infected cells have mito dysfunction, then EBV would have to be in contact w/ the cells. So, wherever in your body EBV resides, that's the area where there will be mito dysfunction.

Same w/ Prusty's paper on mito dysfunction w/ HHV-6. HHV-6 has to come into contact w/ other cells to cause mito dysfunction or fragmentation in this case I suppose.

 

[Learner1]

True. But there's a 100% chance I can't help if you don't give me more info.

Thanks for the offer. I am doing just fine.

 

[pattismith]

AICAR seems interesting:

One of the effects Methotrexate has is by increasing AICAR
Methotrexate has a toxic effect on folate metabolism so you may take folinic acid 24h00 hours after the methotrexate intake in order to manage it.

I plan to take methotrexate on a low weekly regimen.

https://www.researchgate.net/figure...-of-aminoimidazole-carboxamide_fig2_320984986