Written by Anthony Hardie, 91outcomes
(91outcomes.blogspot.com) -- Researchers have found evidence of cellular dysfunction – including decreased levels of CoQ10 – in people suffering from a debilitating chronic pain condition.
Published this month in Arthritis Research & Therapy (January 28, 2010), the study by Mario Cordero et al found reduced levels of coenzyme Q10 (CoQ10) and several other measures of cellular dysfunction, including cellular suicide (oxidative stress) and cellular self-cannibalization of dysfunctional mitochondria – microorganisms that live within cells and are responsible for nearly all of the body’s energy production – in study subjects with the chronic pain condition currently known as fibromylagia.
Fibromyalgia is one of three ill-defined conditions that are presumptive conditions for VA service-connection. In other words, if a veteran had qualifying service in the Persian Gulf, and he or she has been diagnosed with fibromyalgia, it is presumed by law that the condition was caused by the Gulf War service and no further proof of a “nexus” linking the Gulf War service to the condition is required as it is all non-presumptive conditions.
The studies findings also may provide support for the theory that oxidative stress (essentially cellular suicide) and mitophagy (self-cannibalism by the cell of the dysfunctioning mitochondria microorganisms in the cells) play a role in the pathophysiology (changes from normal functions) of fibromyalgia.
These findings may have profound impact on treatment, including supplementation with Coenzyme Q-10 (CoQ10) and other supplements (ATP and others) that impact on cellular energy and health.
The study’s abstract (summary) is as follows:
Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells of fibromyalgia patients: implication in the pathogenesis of the disease
Introduction: Fibromyalgia is a chronic pain syndrome with unknown etiology. Recent studies have shown some evidence demonstrating that oxidative stress may have a role in the pathophysiology of fibromyalgia.
However, it is still not clear whether oxidative stress is the cause or the effect of the abnormalities documented in fibromyalgia. Furthermore, the role of mitochondria in the redox imbalance reported in fibromyalgia is also controversial.
We undertook this study to investigate the role of mitochondrial dysfunction, oxidative stress and mitophagy in fibromyalgia.
Methods: We studied 20 patients (2 males and 18 females) recruited from the database of the Sevillian Fibromyalgia Association and 10 healthy controls. We evaluated mitochondrial function in blood mononuclear cells from fibromyalgia patients measuring coenzyme Q10 levels by high performance liquid chromatography (HPLC), and mitochondrial membrane potential by flow cytometry.
Oxidative stress was determined by measuring mitochondrial superoxide production by MitoSOXTM, and lipid peroxidationin blood mononuclear cells and plasma from fibromyalgia patients. Autophagy activation was evaluated by quantifying the fluorescence intensity of LysoTrackerTM Red staining of blood mononuclear cells.
Mitophagy was confirmed by measuring citrate synthase activity and electron microscopy examination of blood mononuclear cells.
Results: We found reduced levels of coenzyme Q10, decreased mitochondrial membrane potential, increased level of mitochondrial superoxide in blood mononuclear cells, and increased levels of lipid peroxidation in both blood mononuclear cells and plasma from fibromyalgia patients. Mitochondrial dysfunction was also associated with increased expression of autophagic genes and the elimination of dysfunctional mitochondria by mitophagy.
Conclusions: These findings may support the role of oxidative stress (essentially cellular suicide) and mitophagy (self-cannibalism of the mitochondria in the cells) in the pathophysiology (changes from normal functions) of fibromyalgia.
Author: Mario CorderoManuel De MiguelAna Moreno FernandezInes Carmona LopezJuan Garrido MaraverDavid CotanLourdes Gomez IzquierdoPablo BonalFrancisco CampaPedro BullonPlacido NavasJose Sanchez Alcazar
Credits/Source: Arthritis Research &Therapy 2010, 1