Introduction: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a medical illness characterized by disorders in inflammatory and oxidative and nitrosative (IO&NS) pathways.

Methods: 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.

Results: 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.

Discussion: 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.

Download full-text PDF

Source

Publication Analysis

Top Keywords

plasma coq10
12
normal controls
12
coenzyme q10
8
myalgic encephalomyelitis/chronic
8
encephalomyelitis/chronic fatigue
8
fatigue syndrome
8
me/cfs
8
syndrome me/cfs
8
fatigue autonomic
8
patients me/cfs
8

Similar Publications

Introduction: Coenzyme Q10 (CoQ10) is a fat-soluble vitamin-like quinone. The plasma levels of CoQ10 are reduced in patients with chronic kidney disease (CKD). CoQ10 supplementation can improve mitochondrial function and decrease oxidative stress in these patients.

View Article and Find Full Text PDF

Coenzyme Q10 (CoQ10) plays a crucial role in facilitating electron transport during oxidative phosphorylation, thus contributing to cellular energy production. Statin treatment causes a decrease in CoQ10 levels in muscle tissue as well as in serum, which may contribute to the musculoskeletal side effects. Therefore, we aimed to assess the effect of newly initiated statin treatment on serum CoQ10 levels after acute ST-elevation myocardial infarction (STEMI) and the correlation of CoQ10 levels with key biomarkers of subclinical or clinically overt myopathy.

View Article and Find Full Text PDF

The prolonged consumption of D-galactose (Gal) has been associated with severe damage in the liver and brain via exacerbation of oxidative stress, non-enzymatic glycation, and the aging process. The current study was initiated for a comparative assessment of beeswax alcohol (BWA, final 0.5% and 1.

View Article and Find Full Text PDF

Important metabolic variables that lead to the development of many diseases, including "mitochondrial diseases," include increased oxidative stress and mitochondrial malfunction. Given that the clinical picture and metabolic alterations in individuals suspected of having mitochondrial illnesses lack distinct characteristics, the development of sensitive and specific diagnostic techniques to detect alterations in mitochondrial bioenergetics is imperative. High-resolution respirometry (HRR), is a minimally invasive technique that enables the analysis of mitochondrial function in platelets taken from peripheral blood.

View Article and Find Full Text PDF
Article Synopsis
  • Lipoprotein(a) [Lp(a)] is recognized as a key independent risk factor for atherosclerotic cardiovascular disease (ASCVD), prompting research into various lipid-lowering drugs that might reduce its levels.
  • A systematic review of 29 studies showed that traditional lipid-lowering agents like statins and fibrates generally do not significantly affect Lp(a) concentrations, whereas Lp(a) apheresis and PCSK-9 inhibitors were effective.
  • Emerging RNA-targeting therapies, such as anti-sense oligonucleotides, demonstrated promise in lowering Lp(a) levels, but it's still unclear if these reductions will lead to fewer cardiovascular events in patients.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!