A systematic review of mitochondrial abnormalities in ME/CFS/SEID (Holden et al., 2020)

[Pyrrhus]

I thought this 2020 meta-analysis from Staines and Marshall-Gradisnik had already been posted, but I must have missed it...

A systematic review of mitochondrial abnormalities in ME/CFS/SEID (Holden et al., 2020)
https://dx.doi.org/10.1186/s12967-020-02452-3

Excerpt:

Background
Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) or Systemic Exertion Intolerance Disease (SEID) present with a constellation of symptoms including debilitating fatigue that is unrelieved by rest. The pathomechanisms underlying this illness are not fully understood and the search for a biomarker continues, mitochondrial aberrations have been suggested as a possible candidate. The aim of this systematic review is to collate and appraise current literature on mitochondrial changes in ME/CFS/SEID patients compared to healthy controls.

Methods
Embase, PubMed, Scopus and Medline (EBSCO host) were systematically searched for articles assessing mitochondrial changes in ME/CFS/SEID patients compared to healthy controls published between January 1995 and February 2020. The list of articles was further refined using specific inclusion and exclusion criteria. Quality and bias were measured using the Joanna Briggs Institute Critical Appraisal Checklist for Case Control Studies.

Results
Nineteen studies were included in this review. The included studies investigated mitochondrial structural and functional differences in ME/CFS/SEID patients compared with healthy controls. Outcomes addressed by the papers include changes in mitochondrial structure, deoxyribonucleic acid/ribonucleic acid, respiratory function, metabolites, and coenzymes.

Conclusion
Based on the included articles in the review it is difficult to establish the role of mitochondria in the pathomechanisms of ME/CFS/SEID due to inconsistencies across the studies. Future well-designed studies using the same ME/CFS/SEID diagnostic criteria and analysis methods are required to determine possible mitochondrial involvement in the pathomechanisms of ME/CFS/SEID.

 

[Pyrrhus]

From another thread:

A systematic review of mitochondrial abnormalities in myalgic encephalomyelitis/chronic fatigue syndrome/systemic exertion intolerance disease

Authors: Holden S, Maksoud R, Eaton-Fitch N, Cabanas H, Staines D, Marshall-Gradisnik S.
Link: https://pubmed.ncbi.nlm.nih.gov/32727475/"

"Nonetheless, the results suggest that ME/CFS is not a primary mitochondrial disorder, due to the absence of disease-causing genetic variants. Changes in mitochondrial structure, DNA, RNA, respiratory function, metabolites and coenzymes were found, and the authors suggest that these might be due to secondary effects of other disrupted pathways. However, they also note the significant methodological inconsistencies and small sample sizes in these studies, and recommend that these findings be interpreted with caution."

 

[Wishful]

It's good to have a reasonably clear "No, this doesn't seem to be the cause of ME" finding. Funding can go to more promising areas.

 

[wabi-sabi]

I'm not sure this study says mitos aren't the cause versus the quality of the research is so bad we can't make head or tail of it.

 

[bread.]

It's doubtful that mitochondrial dysfunction has no role in this disease(s).

The notion that a disease is not a mitochondrial disease because it's not a mitochondrial genetic disease is semantics at best.

Many auto inflammatory and so-called autoimmune diseases have a common underbelly which is mitochondrial dysfunction. ME is one of them much more likely than not.

 

[Wishful]

It's doubtful that mitochondrial dysfunction has no role in this disease(s).

While abnormal mitochondrial function might play a role in some of the symptoms, the research seems to be saying that there's no evidence that there's anything abnormal about the mitochondria themselves. There don't seem to be genetic differences specific to ME. You can't pull out one mitochondrion and identify it as being from an ME victim. I think that if we do have mitochondria functioning abnormally, it's due to ME changing the environment that the mitochondria are in, and the mitochondria are functioning correctly for those abnormal circumstances.

 

[bread.]

While abnormal mitochondrial function might play a role in some of the symptoms, the research seems to be saying that there's no evidence that there's anything abnormal about the mitochondria themselves. There don't seem to be genetic differences specific to ME. You can't pull out one mitochondrion and identify it as being from an ME victim. I think that if we do have mitochondria functioning abnormally, it's due to ME changing the environment that the mitochondria are in, and the mitochondria are functioning correctly for those abnormal circumstances.

No, that is not what the research is saying. The research says "we don't know" at best.

 

[Wishful]

No, that is not what the research is saying. The research says "we don't know" at best.

Okay, how about "So far we haven't found any obvious signs of mitochondrial abnormalities."? The lack of evidence doesn't prove anything, but it doesn't support theories about it being a mitochondrial disease either.

 

[Rufous McKinney]

what is all the mitochondrial fragmentation observed by researchers like Dr. Prusty? I think that isn't genetic, its induced by the ME conditions, or the viruses hiding out.

You want red blood cells to deform? Find some ATP.

You want your endothelium to contract to send blood to the brain and heart? Find some ATP.

-I have innumerable spinal birth defects. Are these "genetic"? Spinal birth defects are involved clearly in my case. My adult daughter has a milder version of my spinal birth defects. My granddaughter is much better off, but still I am worried about her spine betraying us.