Coenzyme Q10 deficiency in Myalgic ncephalomyelitis/ chronic fatigue syndrome (ME/CFS) is related to fatigue, autonomic and neurocognitive symptoms and is another risk factor explaining the early mortality in ME/CFS due to cardiovascular disorder.
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a medical illness characterized by disorders in inflammatory and oxidative and nitrosative (IO&NS) pathways.
This paper examines the role of Coenzyme Q10 (CoQ10), a mitochondrial nutrient which acts as an essential cofactor for the production of ATP in mitochondria and which displays significant antioxidant activities. Plasma CoQ10 has been assayed in 58 patients with ME/CFS and in 22 normal controls; the relationships between CoQ10 and the severity of ME/CFS as measured by means of the FibroFatigue (FF) scale were measured.
Plasma CoQ10 was significantly (p=0.00001) lower in ME/CFS patients than in normal controls. Up to 44.8% of patients with ME/CFS had values beneath the lowest plasma CoQ10 value detected in the normal controls, i.e. 490 microg/L. In ME/CFS, there were significant and inverse relationships between CoQ10 and the total score on the FF scale, fatigue and autonomic symptoms. Patients with very low CoQ10 (<390 microg/L) suffered significantly more from concentration and memory disturbances.
The results show that lowered levels of CoQ10 play a role in the pathophysiology of ME/CFS and that symptoms, such as fatigue, and autonomic and neurocognitive symptoms may be caused by CoQ10 depletion. Our results suggest that patients with ME/CFS would benefit from CoQ10 supplementation in order to normalize the low CoQ10 syndrome and the IO&NS disorders. The findings that lower CoQ10 is an independent predictor of chronic heart failure (CHF) and mortality due to CHF may explain previous reports that the mean age of ME/CFS patients dying from CHF is 25 years younger than the age of those dying from CHF in the general population. Since statins significantly decrease plasma CoQ10, ME/CFS should be regarded as a relative contraindication for treatment with statins without CoQ10 supplementation.
"Plasma CoQ10 was also observed to be significantly lower in ME/CFS and depressed patients with CFS compared to controls  . Significant, inverse relationships were observed with plasma CoQ10 levels and severity of illness scores of ME/CFS patients, specifically, greater fatigue and autonomic symptoms were associated with lower levels of CoQ10 . However, in patients with depression there was no correlation observed with severity of illness total or individual scores and plasma CoQ10 levels . "
[Show abstract][Hide abstract] 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 1,220 articles. After 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.
Biochimica et Biophysica Acta - Clinical 06/2014; 1:12–23. DOI:10.1016/j.bbacli.2014.04.001
"Fatigue is another typical symptom found in FM patients. Low levels of CoQ 10 in plasma in patients with chronic fatigue syndrome have been reported , and it has been suggested that patients with this syndrome would benefit from CoQ 10 supplementation in order to normalize the low CoQ 10 levels . Furthermore, fatigue or lack of energy has been frequently reported in patients taking statins . "
[Show abstract][Hide abstract] ABSTRACT: Recently, Coenzyme Q10 (CoQ10) deficiency has been implicated in the pathophysiology of fibromyalgia (FM). It is our objective to present the findings of the FM evaluation before and after oral CoQ10 treatment using the American College of Rheumatology (ACR) Diagnostic Criteria of 1990 and 2010, and Symptom Checklist-Revised (Scl-90-R). Four patients with FM were examined using the trigger points, the Fibromyalgia Impact Questionnaire, visual analog scale (pain, fatigue, and sleep), Widespread Pain Index, symptom severity scale, and Scl-90-R. Previously, CoQ10 contents from patients were analyzed by high-performance liquid chromatography. All patients showed CoQ10 deficiency. All patients meet the ACR 1990 and 2010 criteria. After treatment, all patients showed an important improvement in clinical symptoms in all evaluation methods. According to our results, and evaluated by three methods, patients with FM are candidates for treatment with CoQ10. However, more controlled clinical trials and investigations are needed to clarify the precise mechanism(s) by which CoQ10 may contribute in pathological and therapeutic processes of FM and to provide data on its effectiveness in FM.
"Lowered levels of coenzyme Q10, zinc and glutathione have been reported in ME/CFS [126,127,131] with amelioration of oxidative stress occurring during remission . As well as decreased coenzyme Q10 , decreased vitamin C and E will impact mitochondrial function, increasing lipid peroxidation. "
[Show abstract][Hide abstract] ABSTRACT: It is of importance whether myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a variant of sickness behavior. The latter is induced by acute infections/injury being principally mediated through proinflammatory cytokines. Sickness is a beneficial behavioral response that serves to enhance recovery, conserves energy and plays a role in the resolution of inflammation. There are behavioral/symptomatic similarities (for example, fatigue, malaise, hyperalgesia) and dissimilarities (gastrointestinal symptoms, anorexia and weight loss) between sickness and ME/CFS. While sickness is an adaptive response induced by proinflammatory cytokines, ME/CFS is a chronic, disabling disorder, where the pathophysiology is related to activation of immunoinflammatory and oxidative pathways and autoimmune responses. While sickness behavior is a state of energy conservation, which plays a role in combating pathogens, ME/CFS is a chronic disease underpinned by a state of energy depletion. While sickness is an acute response to infection/injury, the trigger factors in ME/CFS are less well defined and encompass acute and chronic infections, as well as inflammatory or autoimmune diseases. It is concluded that sickness behavior and ME/CFS are two different conditions.
BMC Medicine 03/2013; 11(1):64. DOI:10.1186/1741-7015-11-64 · 7.25 Impact Factor
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