Maes Q10 2009

Volgens een recent verschenen studie van Maes en kollega's

zijn de Q10-koncentraties in het (bloed)plasma van ME/CVS-patiënten

beduidend lager dan die in het plasma van gezonde proefpersonen.

een essentiële komponent voor de laatste stap in de produktie van energie/ATP

(de elektronentransport-keten) uit brandstof (glucose, omgezet in pyruvaat) en zuurstof

én een belangrijke antioxidant (voor enkele studies op dit gebied: klik hier, hier en hier).

Tevens is er volgens de onderzoekers een direkte relatie tussen de ernst van de klachten (pijn etc./FibroFatigue-schaal: klik hier, kognitieve problemen en cirkulatieproblemen).

Tot slot merken de auteurs op dat Q10-tekorten een maatstaf zijn voor chronisch hartfalen en dat die tekorten wellicht het vroege overlijden van een deel van de ME/CVS-patiënten (onderzoek van Jason uit 2006: klik hier) mede zouden kunnen verklaren.

Coenzyme Q10 deficiency in

myalgic encephalomyelitis/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.

Neuro Endocrinol Lett. 2009;30(4):470-6.

Maes M, Mihaylova I, Kubera M; Uytterhoeven M, Vrydags N, Bosmans E.

Abstract

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 :g/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 :g/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 should be treated with CoQ10

in order to treat 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.

Keywords:

Coenzyme Q10, chronic fatigue syndrome, inflammation, oxidative stress, mitochondria, cytokines, heart failure, coronary artery disease, mortality, statins