secondary mitochondriopathy

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bread.

Senior Member
Messages
499
I believe if you look at all the available evidence out there regarding me/cfs (which will 100% and definitely not be one disease but multiple diseases with a similar pathological endpoint) you have to come to the conclusion that a very significant part of patients with me/cfs (especially the severly affected population) deals with a secondary mitochondriopathy, there are potentially hundreds of routes how you could end up there and absolutely zero (reliable) ways to find out for sure.

I think it is completely horrifying how scientists and doctors are dancing around this very obvious problem. For gods sake, we are not having enough energy for the most part, who on earth could think mitochondria are not the main issue, by the way, I am talking about actual mitochondrial damage here. PBMCs tell me absolutely NOTHING about mitochondria in my muscles or nerve tissue.

If you think otherwise, please tell me why I am wrong, I would be delighted.


@JenB @Jonathan Edwards

why is nobody looking at this you think?
 
A

Archie

Senior Member
Messages
168
Few thoughts on this very big issue.


First , there was this guy in 460-370 BC


Diseases-Begin-in-the-Gut-300x157.png


I doubt he was wrong ...



Then there is talk about CFS/ME being cousing with other disorders :

Could the Gut Cure Neuroinflammation? An MS and ME/CFS/FM Inquiry

http://simmaronresearch.com/2019/01/gut-cure-neuroinflammation-m-s-mecfs-inquiry/



secondary mitochondriopathies occur in context with systemic inflammations:


https://www.imd-berlin.de/en/subjec...-atp-marker-of-mitochondrial-dysfunction.html


"When do reduced levels of intracellular ATP materialise?

Usually, secondary mitochondriopathies occur in context with systemic inflammations. Even though isolated reductions of ATP are possible, they most commonly appear accompanied by laboratory proof of an activation of the immune system (TNF-alpha, IP-10), as well as proof of oxidative or nitrosative stress (MDA-LDL, nitrotyrosine). Consequentially, reductions of ATP have been found in patients with inflammatory diseases, in context with the chronic fatigue syndrome (Myhill, 2009), cellular hypoxia (Bell, 2007), active EBV infections (Vernon, 2006), as well as fibromyalgia and chronic degenerative inflammatory processes. Furthermore, toxic influences may distort leukocytes’ mitochondrial functions. Aluminium for example can reduce the ATP formation in leukocytes through the induction of oxidative stress (Han, 2013). It can be deduced that this indirect effect works for other metals and pollutants as well. Even though most of the time it is hard to tell apart whether an ATP reduction is primary or the result of altered biochemical processes, the parameter itself constitutes a valuable indicator of current mitochondrial functionality."


The GI microbiome and its role in Chronic Fatigue Syndrome: A summary of bacteriotherapy

https://search.informit.com.au/documentSummary;dn=119626231492520;res=IELHEA


So if i tryed to theorize in my so cloudy mind this for a second....The dude who lived 460-370 BC was probably right, something is messing up things in our gut`s, it makes both direct and undirect negative effects that cause inflammation not just in gut but also in brain, and same time prevents self-healing mechanism to proceed becouse the gut is too broken and it must also cause disturbance to gut-brain connection . Many things from unbalanced/wrong type bacterias to poisonous substances, nutrional deficiencys, lack of prebiotics/fiber etc can start causing these issues, many drugs that are not even antibiotics are known to effect negative way to good bacterial populations,some natural antimicrobial do the same.


Our "sophisticated" culture is master of messing up our gut"s health, in Western World at least where Coca-cola & big Mac etc followed by Big Pharma drugs , Monsanto poisoned food , poisoned water etc


So yes, no wonder if Mitochondrias start to think they need more rest . Today this wiew, i am not sure how i see things in future...
 
Learner1

Learner1

Senior Member
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6,326
Location
Pacific Northwest
Good points. Arsenic can hinder ATP production, too.

Oxidative and nitrosative stress (and the formation of peroxynitrites) is a known feature of ME/CFS. I found it interesting st the recent NIH Conference when Ron Tompkins, in his summary, added in "oxidative and nitrosative stress" when none of the presenters discussed it.

Mitochondria have come up in these places:
  • Sarah Myhill and John McLaren Howard have produced papers on mitochondrial issues in ME/CFS, snd developed a test for mitochondrial function which can be ordered through Acumen.
  • Maes and Morris wrote a paper on oxidative and nitrosative stress, the gormation of peroxynitrites and the damage to mitochondrial membranes.
  • Garth Nicolson has done studies with lipid membrane and nutrient replenishment to repair damaged mitochondrial membranes in chronic fatigue.
  • Martin Pall wrote a couple of papers on peroxynitrites and reducing their problems through nutrients.
  • Alan Light has found correlations between patients with various minor mtDNA mutations and the CellTrend antibodies.
  • Mitochondrial complex V was discussed at the recent Emerge Australia Conference.
I was recently at the FDA Voice of the Patient meeting for adult mitochondrial myopathu (it coincided with the NIH Conference, so I went). The symptoms and experiences of many of the patients weren't so different from what I experience and those shared by patients here on PR.

For myself, I have reason to believe my mitos were damaged by some combo of Cipro, carboplatin, paclitaxel, and artesunate. I have a ME/CFS diagnosis, diagnosed by a top expert, get PEM and have all the other symptoms.

But, I have also been able to follow up with the mitochondrial issues by:
  • Doing a MitoSwab test for mitochondrial content and function of Complexes I-IV
  • Doing a HDRI nitrotyrosine test, which is a marker for peroxynitrites
  • Doing a comprehensive nutrient test (Genova Diagnostics NutrEval) to identify deficiencies in nutrients Pall and Nicolson noted as essential to shutting down peroxynitrites and rebuilfing damaged membranes.
  • Doing genetic testing to identify genes which might be exacerbating any problem
I found that, as the researchers have found, I had high peroxynitrites, mitochondria complexes working at 370% of normal genrrating huge amounts of stress, impaired complex I (as peroxynitrites are known to do), and genes that exacerbated the problem.

I embarked on a protocol suggested by my nutrient testing, and suggested by Pall and Nicolson, retested 9 months later and found major improvements, whivh agreed with my symptom improvement.

It may not be everyone's problem, but I suspect a good proportion of payoents may have similar issues - peroxynitrites have been linked to msny chronic snd serious diseases.
 
Pearshaped

Pearshaped

Senior Member
Messages
583
where I live docs dont believe that there's something like secondary mito.disease.

They think if you had mito issuess,this must have been detected already in early childhood.period.

I was told I'd fullfill almost all symptoms of mitochondrial disease but a specialist in this field told my GP that this would be almost impossible,since I am an adult.
We need Research but what we need even more: Docs who are willing to do further education.
 
Hip

Hip

Senior Member
Messages
18,305
bread. said:
I think it is completely horrifying how scientists and doctors are dancing around this very obvious problem.
Click to expand...

There have been quite a few studies examining mitochondrial or glycolysis dysfunction over the years, as a search on PubMed will indicate. Unfortunately not enough research to come to any conclusions about why mitochondria and/or glycolysis appear to be dysfunctional. But that's the usual story with ME/CFS: not enough money or interest in doing basic research.

There have also been some treatments proposed, including dichloroacetate (DCA), which stimulates mitochondrial energy metabolism, improves fatigue, brain fog and pain in just over 1 in 3 ME/CFS patients (those with comorbid autoimmune conditions are less likely to respond). Refs: 1 2

And if you are a Group B ME/CFS patient (according to the Myhill mitochondrial dysfunction test), then D-ribose may help.
 
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B

bread.

Senior Member
Messages
499
Hip said:
There have been quite a few studies examining mitochondrial or glycolysis dysfunction over the years, as a search on PubMed will indicate. Unfortunately not enough research to come to any conclusions about why mitochondria and/or glycolysis appear to be dysfunctional. But that's the usual story with ME/CFS: not enough money or interest in doing basic research.

There have also been some treatments proposed, including dichloroacetate (DCA), which stimulates mitochondrial energy metabolism, improves fatigue, brain fog and pain in just over 1 in 3 ME/CFS patients (those with comorbid autoimmune conditions are less likely to respond). Refs: 1 2

And if you are a Group B ME/CFS patient (according to the Myhill mitochondrial dysfunction test), then D-ribose may help.
Click to expand...


i know from other threads that we have a quite similar story.
 
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