Editor’s comment: Mitochondria are the energy producers of the cells. The mitochondria supply this energy in the form of adenosine triphosphate (ATP), the molecule upon which all cellular functions in the body depend. Coenzyme Q10 acts as the catalyst that makes it possible for the mitochondria to produce ATP. Previous research has demonstrated that mitochondrial dysfunction is present in both fibromyalgia and ME/CFS (chronic fatigue syndrome). However, this is the first study to suggest that the type of mitochondrial dysfunction may serve as a marker that is able to differentiate FM from ME/CFS. For more information about mitochondrial dysfunction in FM, see “Dr. Myhill on Fibromyalgia and Mitochondrial Dysfunction.”
Could mitochondrial dysfunction be a differentiating marker between Chronic Fatigue Syndrome and Fibromyalgia?
By J. Castro-Marrero, et al.
Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM) are complex and serious illnesses. It is estimated to affects up to 2.5% and 5% of the general population worldwide, respectively. The aetiology is unknown; however, recent studies suggest that mitochondrial dysfunction has been involved in the pathophysiology of both conditions.
We have investigated the possible association between mitochondrial biogenesis and oxidative stress in patients with CFS and FM. We studied 23 CFS patients, 20 FM patients and 15 healthy controls.
Peripheral blood mononuclear cells (PBMC) showed decreased levels of CoQ10 from CFS patients (p<0.001 compared to controls) and FM subjects (p<0.001 compared to controls) and ATP levels for CFS patients (p<0.001 compared to controls) and for FM subjects (p<0.001 compared to controls).
On the contrary, CFS/FM patients had significantly increased levels of lipid peroxidation, respectively (p<0.001 for both CFS and FM patients respect to controls) indicative of oxidative stress-induced damage.
Mitochondrial citrate synthase activity was significantly lower in FM patients (p<0.001) and however, in CFS resulted in similar levels than controls.
Mitochondrial DNA content (mtDNA/gDNA ratio) was normal in CFS and reduced in FM patients vs. healthy controls, respectively (p<0.001).
Expression levels of PGC-1? and TFAM by immunoblotting showed significantly lower in FM patients (p<0.001) and were normal in CFS subjects compared to healthy controls.
These data lead to the hypothesis that mitochondrial dysfunction-dependent events could be a marker of differentiation between CFS and FM indicating the mitochondria as a new potential therapeutic target for these conditions.
Source: Antioxidants & Redox Signaling, April 22, 2013. By J. Castro-Marrero, M.D. Cordero, N. Saez-Francas, C. Jimenez-Gutiérrez, F.J. Aguilar-Montilla, L. Aliste, and J. Alegre-Martin. Vall de Hebron Univ Hospital Research Institute, CFS Unit, BARCELONA, Barcelona, Spain; email@example.com .