Or are you saying (higher up) that even that would be deadly, in more than half of our cells? I imagine various cell types are more resistant to such signals (immune privileged, or just too important to slow down as much)... But at the extreme end, maybe that's what the most severe ME involves...?
From what I heard, if over half your cells gave bad mitos, you're pretty well screwed. Cancer is a condition of abnormal mitos, with different types of abnormal across the spectrum of cancer types. Neurodegenerative diseases and diabetes are conditions of abnormal mitochondria. And Naviaux's list of cell dangers can damage mitos.
Any can lead to a pitiful death.
Yes, mitochondria are continuously splitting and merging to share their mtDNA, hopefully selecting for less damaged copies. Usually recycling/renewing entirely on an order of days. One of my first posts, here, 4 years back was on a
Naviaux's metabolic features study thread, about this:
It seems to vary, but we agree that they recycle over a relatively short period of time rather than living for a long time. Do, the recycling and repair mechanisms offer a chance to improve ones crop of mitos in a reasonable but not immediate timeframe.
I'm not sure how much the HHV-6 hypometabolic state gets in the way of this mito maintenance...? I think the mitos still merge into smaller bodies, but just don't form the big super-efficient networks. I think no obvious mtDNA damage (or common SNPs) were found in past studies of ME/CFS patient mitochondria...?
I think that may vary for each of us, depending on how many other cell dangers we have fallen prey to. For instance, arsenic, can fill up the mitos and actually stop of slow ATP production. It's a fairly common toxin and carcinogen. Other people have other toxins, EMF exposure, infections, iron overload causing Fenton reactions and hydroxyl radicals, peroxynitrites, etc that can impact mitos and widely varying nutrient statuses which affect the ability to repair and operate mitochondria. It's ridiculous to think only one thing is going in here. Or maybe it is in your mitos, but I am positive there have been multiple environmental factors affecting mine. .
Simpler to cut off the problem futher upstream, whatever the bistability (trapping) mechanism is, then I'd hope the rest will largely fall into place....
Well, that would be nice. But you'd have to cut off ALL the above factors upstean, before resources were depleted and too much damage was done.
Well, anyway, anti-oxidants are already a major part of many ME/CFS supplement regimes, combatting oxidative stress from reduced SOD2. (Although it's arguable how much we want to combat this, as per Naviaux's "Oxidative Shielding", if a cell's ROS are still protecting it from chemical or pathogen damage.)
Well, I can re you, having delved pretty deeply into this that simply taking a few antioxidants is not fixing it. Having measured oxidative stress through regular testing throughout my illness and recovery, I have been able, finally, to reduce DNA damage (8OHdG is the marker, but still have incredible oxidative stress causing high lipid peroxides. I have some ideas of why this is happening, but I've beaten back 7 viral and bacterial infections, including EBV abd HHV6, that I didn't feel sick from, only fatigue, and gave find a lot of work on my mitos, and this oxidative stress did not go away.
All of this while I have almost normal energy these days... I think some of my activity is causing even more oxidative stress... I e also found, inadvertently, that increasing my antioxidants in a balanced way across the board, that my energy dramatically increased. So shutting down all the cell dangers and replenishing us important.
Odd that methylation is *up*, when methylation cycle support is a very common intervention (one that seemed to boost me, to an extent, in part). Maybe its ramped up function is aimed at making more methyl groups to add to and silence DNA from being expressed...?
Or maybe it's related to overproduction of peroxynitrites and huge oxidative stress needing more glutathione which can't vbr recycled fast enough.
Certainly the other virus transactivation changes seem to focus on making DNA not RNA. Blocking other viruses (?) but also reducing the cell's ability to make proteins or RNA messengers, or... What else? Repairing cellular machinery, replicating, of course...?
and fixing whatever damage had occurreed anywhere...
