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Concept of central neuroinflammation and Mitochondrial Disorder

Concept of central neuroinflammation

Neuroinflammation is a complex process. It involves both the Peripheral Nervous System and the Central Nervous System. Represents a rich breeding ground for various central nervous system disorders, including depression, anxiety, and pain

 Fibromyalgia and Mitochondrial Disorder*

Mitochondrial dysfunction is thought of as a real possibility in chronic fatigue syndrome, but it is rarely associated with fibromyalgia or pain.  It turns out, however, that multiple studies suggest that mitochondrial dysfunction could indeed play a significant role in fibromyalgia.

Studies suggest the energy factories may be running a bit low in FM. Muscle biopsies have found patterns of mitochondrial dysfunction (abnormal mitochondria, mitochondrial defects and muscle fiber abnormalities) similar to those typically found in mitochondrial disorders. Some skin biopsies have shown patterns of neurogenic inflammation and oxidative stress – two factors that negatively impact the mitochondria.  Peripheral blood cells  have demonstrated CoQ10 deficiency, mitochondrial dysfunction, oxidative stress and mitochondrial degradation.

In 2013 a Spanish group [1] proposed that a mitochondrial dysfunction in FM patients was driving an inflammatory process. Now, in 2015 they have returned with a study looking at mitochondrial dysfunction, oxidative stress and inflammation using skin biopsies from people with FM.

This Spanish study [2] looked at the levels of mitochondrial enzymes, mitochondrial proteins, ATP, CoQ 10 and TNF-a from a small patch of skin in the left shoulder region, as well as in the blood and saliva of 23 people with FM and 20 healthy controls.

Significant reductions in mitochondrial enzyme activity (in complexes I, II, III and IV) were found in the FM patients but not the healthy controls. That in combination with reduced levels of mitochondrial proteins indicated that mitochondrial functioning was indeed significantly reduced. So were CoQ10 and ATP levels and mitochondrial DNA levels [3]. In fact, every aspect of mitochondrial functioning tested was found to have taken a significant hit in the FM patients.

That suggested mitochondrial damage had occurred and that finding set the stage for the next test. Since damaged mitochondrial DNA are known to spark an inflammatory response the researchers asserted they should  also be able to find evidence of inflammation in the skin – and they did.  Double the levels of the pro-inflammatory cytokine TNF-a were found in the skin of the FM patients.

Not only were the increased cytokine levels strongly associated with reduced mtDNA – suggesting that the mitochondrial problems had indeed sparked the inflammation – but they were highly correlated with the pain levels in FM (p<.001) as well. That suggested the mitochondrial problems could be causing or contributing to the pain the FM patients were experiencing.

A threefold increase in TNF-a levels in the saliva and the blood collected from the biopsy area relative to the healthy controls suggested that widespread or systemic inflammation and oxidative stress was present as well. The FM patients looked pretty much like a soup of mitochondrial dysfunction, oxidative stress and inflammation [4].

Whether mitochondrial dysfunction is causing inflammation or inflammation is knocking out the mitochondria is unclear, however.  The fact that anti-inflammatory drugs have not generally been found to be particularly effective in FM argues against an inflammatory origin.

Several studies, on the other hand, suggest that mitochondrial enhancers such as CoQ10 may be helpful in reducing the pain and headache symptoms [5] in FM, and some practitioners have had good results with D-Ribose  in ME/CFS and/or FM.

CoQ10 is a particularly intriguing nutrient given its ability to both boost ATP production and reduce levels of oxidative stress. CoQ10 levels are reportedly low in many neurodegenerative disorders including Parkinson’s disease, diabetes, fibromyalgia and cancer.

A fibromyalgia study by this Spanish research group found a 40% reduction in CoQ10 levels in FM [4]. With dozens of mostly small studies examining mitochondrial dysfunction and CoQ10 levels/supplementation in FM and other disorders under its belt, this Spanish research group has been leading the way in this area.

On the ME/CFS side Maes has been producing review papers and studies on oxidative stress, mitochondrial functioning and inflammation for years. Presentations on the exercise problems in ME/CFS at the IACFS/ME Conference                     [6] also appeared to be pointing an arrow at the mitochondria.

  • Spanish researchers have recently analysed the role of the mitochondria as the origin of inflammation in fibromyalgia.
  • Researchers have shown that there is significant mitochondrial dysfunction.
  • In this way, it is evident that the activation of inflammation in a group of patients is due to oxidative stress caused by an important mitochondrial dysfunction.
  • These levels of inflammation correlated with pain.
  • This implies that the origin is mitochondrial damage, which would probably explain the causes of the symptoms.
  • The study tries to give possible answers to the etiology of the disease and implies that treatments or protectors of the mitochondria would inhibit the activation of inflammation, reducing symptoms.

 

 

* Is Fibromyalgia A Mitochondrial Disorder? by Cort Johnson | Mar 4, 2015 | Energy Production, Fibromyalgia and Pain, https://www.healthrising.org/blog/2015/03/04/is-fibromyalgia-a-mitochondrial-disorder/

1 Oxidative Stress in Fibromyalgia: Pathophysiology and Clinical Implications. Estrés oxidativo en la fibromialgia: fisiopatología e implicaciones clínicas Mario D. Cordero https://www.reumatologiaclinica.org/en-pdf-S2173574311000086

2 Oxidative stress, mitochondrial dysfunction and, inflammation common events in skin of patients with Fibromyalgia. B. Sánchez-Domínguez, P. Bullón, L. Román-Malo, F. Marín-Aguilar, E. Alcocer-Gómez, A.M. Carrión, J. A. Sánchez-Alcazar, M. D. Cordero. Mitochondrion 21 (2015) 69–75 https://pubmed.ncbi.nlm.nih.gov/25662535/

3 Mitochondrial Imbalance as a New Approach to the Study of Fibromyalgia. A. Martínez-Lara, A. M. MorenoFernández, M. Jiménez Guerrero, C. Díaz-López, M. De-Miguel, D. Cotán, J.A. Sánchez-Alcázar https://www.dovepress.com/getfile.php?fileID=60908

4 Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells of fibromyalgia patients: implications in the pathogenesis of the disease. M. D. Cordero, M. De Miguel, Ana M Moreno Fndez, I. M Carmona López, J. Garrido Maraver, D. Cotán, L. Gómez Izquierdo, P. Bonal, F. Campa, P. Bullon, P. Navas & J. A. Sánchez Alcázar. https://arthritis-research.biomedcentral.com/articles/10.1186/ar2918

5 Coenzyme Q10 supplementation for prophylaxis in adult patients with migraine—a meta-analysis. Suhairul Sazali, Salziyan Badrin, […], and Nur Suhaila Idris. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7786797/

6 https://www.iacfsme.org/