• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Association of mitochondrial dysfunction and fatigue: A review of the literature (ME/CFS related)

Bob

Senior Member
Messages
16,455
Location
England (south coast)
Association of mitochondrial dysfunction and fatigue: A review of the literature.
Kristin Filler, Debra Lyon, James Bennett, Nancy McCain, Ronald Elswick, Nada Lukkahatai, Leorey N. Saligan.
BBA Clinical, Available online 13 April 2014

http://www.sciencedirect.com/science/article/pii/S221464741400004X

This is very much a CFS-related paper: The study reviewed 25 papers, 18 of which investigated only patients with chronic fatigue syndrome (CFS), with three more investigating ME, or ME and CFS:

"Eighteen studies investigated only patients with chronic fatigue syndrome (CFS); remaining studies investigated a combination of myalgic encephalomyelitis (ME) and CFS (n = 2), ME (n = 1), multiple sclerosis (n = 1), HIV-related fatigue (HRF) (n = 1), systemic lupus erythematosus (SLE) (n = 1), and cancer-related fatigue (CRF) (n = 1)."

Abstract
Fatigue is often described by patients as a lack of energy, mental or physical tiredness, diminished endurance, and prolonged recovery after physical activity. Etiologic mechanisms underlying fatigue are not well understood; however, fatigue is a hallmark symptom of mitochondrial disease, making mitochondrial dysfunction a putative biological mechanism for fatigue. Therefore, this review examined studies that investigated the association of markers of mitochondrial dysfunction with fatigue and proposes possible research directions to enhance understanding of the role of mitochondrial dysfunction in fatigue. A thorough search using PubMed, Scopus, Web of Science, and Embase databases returned 1220 articles. After the application of inclusion and exclusion criteria, a total of 25 articles meeting eligibility criteria were selected for full review. Dysfunctions in the mitochondrial structure, mitochondrial function (mitochondrial enzymes and oxidative/nitrosative stress), mitochondrial energy metabolism (ATP production and fatty acid metabolism), immune response, and genetics were investigated as potential contributors to fatigue. Carnitine was the most investigated mitochondrial function marker. Dysfunctional levels were reported in all the studies investigating carnitine; however, the specific type of carnitine that was dysfunctional varied. Genetic profiles were the second most studied mitochondrial parameter. Six common pathways were proposed: metabolism, energy production, protein transport, mitochondrial morphology, central nervous system dysfunction and post-viral infection. Coenzyme Q10 was the most commonly investigated mitochondrial enzyme. Low levels of Coenzyme Q10 were consistently associated with fatigue. Potential targets for further investigation were identified as well as gaps in the current literature.
 

A.B.

Senior Member
Messages
3,780
CFS subjects had serum lipid fractions that resembled those commonly found in patients poisoned with ciguatoxin, a marine toxin

From Wikipedia:

Hallmark symptoms of ciguatera in humans include gastrointestinal and neurological effects.[5][6] Gastrointestinal symptoms include nausea, vomiting, and diarrhea, usually followed by neurological symptoms such as headaches, muscle aches, paresthesia, numbness, ataxia, vertigo, and hallucinations.[1][6] Severe cases of ciguatera can also result in cold allodynia, which is a burning sensation on contact with cold.[5] Neurological symptoms can persist and ciguatera poisoning is occasionally misdiagnosed as multiple sclerosis.[7]

Dyspareunia and other ciguatera symptoms have developed in otherwise healthy males and females following sexual intercourse with partners suffering ciguatera poisoning, signifying that the toxin may be sexually transmitted.[8] Diarrhea and facial rashes have been reported in breastfed infants of poisoned mothers, suggesting that ciguatera toxins migrate into breast milk.[9]

The symptoms can last from weeks to years, and in extreme cases as long as 20 years, often leading to long-term disability.[10] Most people do recover slowly over time.[11] Often patients recover, but symptoms then reappear. Such relapses can be triggered by consumption of nuts, seeds, alcohol, fish or fish-containing products, chicken or eggs, or by exposure to fumes such as those of bleach and other chemicals. Exercise is also a possible trigger.[1] Filipino and Chinese people may possibly be more susceptible.

Edit:
Chronic phase lipids in sera of chronic fatigue syndrome (CFS), chronic ciguatera fish poisoning (CCFP), hepatitis B, and cancer with antigenic epitope resembling ciguatoxin, as assessed with MAb-CTX.

http://www.ncf-net.org/pdf/Hokama3.pdf
 
Last edited:

August59

Daughters High School Graduation
Messages
1,617
Location
Upstate SC, USA
I have been following the "United Mitochondrial Disease Foundation" for the lest year or so. I just received a newsletter from them which is highlighting their upcoming symposium set for June 5-7 in Pittsburgh, PA.

I actually found this link on their website which may have already been posted.
http://www.envita.com/lyme-disease/...algia-autoimmune-disease-chronic-lyme-disease

The speakers at the symposium in June has some familiar names, but cannot tie them to specific research or studies.

They are well organized and are very broad in the scope of research they pursue. I think it is definitely a disease and a area of research to follow!!