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Mitochondrial and Energy Metabolism Dysfunction in ME/CFS — Myhill, Booth and McLaren-Howard Papers

HowToEscape?

Senior Member
Messages
626
"I thought it was coffee that induced mouth ulcers."

If coffee induced mouth ulcers, then masses of people who work night shifts, software developers and airline pilots would be eating through straws.
"Believe none of what you read..." was a sharp observation 150 years ago. On thuh innernet, change that to "believe less than none".
 

Tammy

Senior Member
Messages
2,181
Location
New Mexico
Would you have any articles that you can post?
I don't have any particular posts in mind there are so many. google viruses effect on mitochondria. I happen to believe that viruses mainly the herpetic viruses are root cause of CFS/ME so it makes sense to me.
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
Would you have any articles that you can post?

It's not a virus, but this is about chlamydia pneumoniae and gives a pretty detailed explanation about how it saps the ATP from mitochondria. You don't have to buy the article, you can just Google the title:

http://www.sciencedirect.com/science/article/pii/S1069417X00800199

The 4th paragraph here discussed impacts of cytomegalovirus on mitochondria:

http://mbio.asm.org/content/7/2/e00029-16.full

And then there's this on HHV6:

http://solvecfs.org/hhv-6-mediated-mitochondrial-modulation-and-its-possible-association-to-mecfs/
 
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kangaSue

Senior Member
Messages
1,851
Location
Brisbane, Australia
From this reference;
[Our preliminary work shows that HHV-6 targets the cell’s energy reserve, the mitochondria, during
both active infection and activation from latency leading to mitochondrial dysfunction, a condition that
is also frequently associated with ME/CFS. Using a unique latent and chromosomally integrated
HHV-6 cell culture model, we have observed down regulation of a small non-coding human microRNA
in response to viral infection that induces expression of tumor suppressor protein p53 and
subsequently that of Drp1 leading to mitochondrial fragmentation. Because of these events,
mitochondria from the infected cells tend to have lower ATP generation capacity and reduced
efficiency for maintaining calcium homeostasis.]
(my bolding)

So, there is a growing body of evidence reported elsewhere of a disruption to calcium ion transport in the muscle of ME/CFS patients and we see here that mitochondria from virus infected cells tend to have lower ATP generation capacity and reduced efficiency for maintaining calcium homeostasis, is it too simplistic putting 2 and 2 together to conclude that viruses can cause ME/CFS due to calcium disruption?
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
...is it too simplistic putting 2 and 2 together to conclude that viruses can cause ME/CFS due to calcium disruption?

That is just one mechanism. Unfortunately, there's a long list of things that can go wrong, and the different infectious agents interact differently with the mitochondria to create different types of mitochondrial dysfunction.

Beating the bugs back and systematically encouraging repair and recycling of mitochondria and their proper function should definitely be factors in curing CFS.
 

Hip

Senior Member
Messages
17,824
It's not a virus, but this is about chlamydia pneumoniae and gives a pretty detailed explanation about how it saps the ATP from mitochondria. You don't have to buy the article, you can just Google the title:

Thanks very much for the links, but I don't think they will be able to explain the mitochondrial dysfunction that may exist in ME/CFS.

In chronic infections, viruses like cytomegalovirus and HHV-6 only infect a very tiny subset of cells, thus even if they are able to inhibit mitochondrial function in those cells they infect, this would not affect the vast majority of cells in the body, which will not be infected.

Thus the papers you posted above wouldn't provide any mechanism or any explanation for a global, body-wide mitochondrial and energy metabolism dysfunction in the cells of ME/CFS patients, which increasing evidence suggests may exist.

The only way I can see that an infection could cause a global body-wide mitochondrial and energy metabolism dysfunction is if that infection precipitated some kind of autoimmune attack on the mitochondria, or autoimmune attack on some other aspects of energy metabolism.



The only virus I am aware of which can trigger an autoimmune attack on the mitochondria, and which has been shown to impede mitochondrial energy production, is coxsackievirus B, when it infects the cells of the heart muscles. I provided details of this in the first post of this thread, and suggested that a mitochondrial autoimmune attack in the skeletal muscles, precipitated by coxsackievirus B infection, might be the cause of ME/CFS.

The coxsackievirus B-triggered autoimmune attack on mitochondria I also talk about in this post.
 
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Kenny Banya

Senior Member
Messages
356
Location
Australia
It's not a virus, but this is about chlamydia pneumoniae and gives a pretty detailed explanation about how it saps the ATP from mitochondria. You don't have to buy the article, you can just Google the title:

http://www.sciencedirect.com/science/article/pii/S1069417X00800199

The 4th paragraph here discussed impacts of cytomegalovirus on mitochondria:

http://mbio.asm.org/content/7/2/e00029-16.full

And then there's this on HHV6:

http://solvecfs.org/hhv-6-mediated-mitochondrial-modulation-and-its-possible-association-to-mecfs/
Shit! I tested positive for this exact bacteria!
I was on an 8 day course of antibiotics for it September/October. No improvement though
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
Shit! I tested positive for this exact bacteria!
I was on an 8 day course of antibiotics for it September/October. No improvement though
Shit! I did, too! I've been working on killing it for a year, and it is extremely persistent.

C.pneumoniae is an extremely nasty bug, and one short course of antibiotics won't kill it. It has 3 different life cycle phases, and takes different strategies to deal with them.

Jose Montoya at Stanford and Dr. Stratton at Vanderbilt seem to be the authorities, and they recommend various antibiotic protocols over time. The cpnhelp website has a lot of info, too.

My doctor has had me on rifampin, azithromycin, probiotics, botanicals, and oxidative therapies (high dose IVC and ozone, HBOT, etc.) and it's a real battle. I have a suppressed immune system, unhappy mitochondria, and problems with heme synthesis, as well as 4 other chronic infections, so perhaps you'll be luckier than I.
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
In chronic infections, viruses like cytomegalovirus and HHV-6 only infect a very tiny subset of cells, thus even if they are able to inhibit mitochondrial function in those cells they infect, this would not affect the vast majority of cells in the body, which will not be infected.

Thus the papers you posted above wouldn't provide any mechanism or any explanation for a global, body-wide mitochondrial and energy metabolism dysfunction in the cells of ME/CFS patients, which increasing evidence suggests may exist.

The only way I can see that an infection could cause a global body-wide mitochondrial and energy metabolism dysfunction is if that infection precipitated some kind of autoimmune attack on the mitochondria, or autoimmune attack on some other aspects of energy metabolism.



The only virus I am aware of which can trigger an autoimmune attack on the mitochondria, and which has been shown to impede mitochondrial energy production, is coxsackievirus B, when it infects the cells of the heart muscles. I provided details of this in the first post of this thread, and suggested that a mitochondrial autoimmune attack in the skeletal muscles, precipitated by coxsackievirus B infection, might be the cause of ME/CFS.

Hmm... how do you know it's a problem with every mitochondria in the body? Or that it has to be an autoimmune reaction?

I'm not sure either is the case.

But, these bugs do disrupt a lot of processes and create chemicals and ROS that can go far beyond just the cells that are infected.
 

Kenny Banya

Senior Member
Messages
356
Location
Australia
Shit! I did, too! I've been working on killing it for a year, and it is extremely persistent.

C.pneumoniae is an extremely nasty bug, and one short course of antibiotics won't kill it. It has 3 different life cycle phases, and takes different strategies to deal with them.

Jose Montoya at Stanford and Dr. Stratton at Vanderbilt seem to be the authorities, and they recommend various antibiotic protocols over time. The cpnhelp website has a lot of info, too.

My doctor has had me on rifampin, azithromycin, probiotics, botanicals, and oxidative therapies (high dose IVC and ozone, HBOT, etc.) and it's a real battle. I have a suppressed immune system, unhappy mitochondria, and problems with heme synthesis, as well as 4 other chronic infections, so perhaps you'll be luckier than I.
Thank you for the heads up. So kind of your detailed reply.
I guess my specialist should know about its persistence, but I will raise it when I see her next week.
Much appreciated
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
Thank you for the heads up. So kind of your detailed reply.
I guess my specialist should know about its persistence, but I will raise it when I see her next week.
Much appreciated
You are quite welcome. The cpnhelp website is a good place to get educated and reading Stratton's papers and Jose Montoya's papers are helpful.

Rifampin seems to be best to start, along with pulsed azithromycin or doxycycline. And lots of probiotics.

Get educated and then go give your specialist a kick in the butt, OK? You need a hard core approach... this is not something to fiddle around with...
 

Hip

Senior Member
Messages
17,824
Hmm... how do you know it's a problem with every mitochondria in the body?

This is not known for sure at present, because not enough research has been performed on different cell types. Myhill, Booth and McLaren-Howard found mitochondrial dysfunction in the neutrophil cells in the blood. Fluge and Mella found that healthy muscle cells when exposed to the blood serum of ME/CFS patients developed altered mitochondrial functioning. I am not sure what other cell types may have been tested in other studies.

But if we assume energy metabolism dysfunction is the cause, or a major component, of ME/CFS, then logic dictates that important cells like muscle cells and brain cells must be afflicted with this energy metabolism dysfunction, otherwise how do we explain the physical and cognitive symptoms of ME/CFS? It may not be every cell in the body that is affected by the energy metabolism dysfunction, but certainly you would expect all the skeletal muscle cells and the brain cells to be affected.

We know something must be badly wrong with the energy metabolism of muscle cells in ME/CFS because of the excess lactic acid they produce during exercise: in very severe patients, a 6 yard walk from bed to bathroom can produce more lactic acid release than even a healthy marathon runner produces during a race! See Dr Mark Vink's lactic acid study.



Or that it has to be an autoimmune reaction?

An autoantibody targeting the mitochondria or energy metabolism seems a likely explanation, because we know rituximab can completely cure around a third of ME/CFS patients treated with this drug, and improves another third of patients, so it appears that autoimmunity is causing the energy metabolism dysfunction.

And the study I talk about in the first post shows how coxsackievirus B infection can trigger mitochondrial autoantibodies, and energy metabolism dysfunction in the heart muscles. Coxsackievirus B has a long history of association with ME/CFS, with numerous studies finding coxsackievirus B infections in the skeletal muscles of ME/CFS patients (via muscle biopsy testing).

But there might be some other mechanism. If you can come up with any other ideas about how a viral infection could cause global energy metabolism dysfunction in all the muscle cells and brain cells via an autoimmune mechanism, I'd certainly be interested in hearing them.
 
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Messages
1,478
Just thought I would put my twopeneth in. Mitochondrial disruption is likely only part of a chain reaction of events that are metabolic in origin not microbiological. Myhill suggests this is a chain reaction due to oxidative stress and it is likely that dysfunctional methylation is involved. My own personal experience suggests that I experienced mitochondrial dysfunction after poor methylation due to b12 and folate depletion. I did have a bug infection that triggered my illness, but I believe this only depleted my b12 beyond a tipping point whereby a further chain reaction occurred that affected my mitochondria due to oxidative stress. The bug itself didn't attack the mitochondria, my imbalanced metabolism did. Just my own conclusions but thought I would post my current thinking.
 

Hip

Senior Member
Messages
17,824
My own personal experience suggests that I experienced mitochondrial dysfunction after poor methylation due to b12 and folate depletion. I did have a bug infection that triggered my illness, but I believe this only depleted my b12 beyond a tipping point whereby a further chain reaction occurred that affected my mitochondria due to oxidative stress.

To try to equate ME/CFS with vitamin B12 deficiency is just nonsense.