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De voordelen van Co-enzym Q10*
Uit verschillende studies blijken de voordelen van co-enzym Q10.

Zo blijkt uit een Spaanse studie dat een mediterraan dieet aangevuld met Q10 tot duidelijk minder schade aan het DNA en duidelijk minder chronische ontstekingen van de bloedvaten te leiden. In de studie onder vijfenzestigplussers kregen de deelnemers vier weken lang of een westersdieet, een mediterraandieet of en mediterraandieet aangevuld met dagelijks 200 mg Q10.

Uit een Chinese studie onder mensen met en zonder hartproblemen blijkt dat co-enzym Q10 leidt tot veel betere functies van de endotheelcellen in de bloedvaten. Endotheelcellen bevinden zich aan de binnenkant van bloedvaten en het hart en zijn betrokken bij aderverkalking, het stollen van het bloed, de aanmaak van nieuwe bloedvaten, ontstekingen en het regelen van de bloeddruk door het verwijden van de bloedvaten. 12 weken aanvulling met 300 mg co-enzym Q10 bleek tot de voordelen te leiden.

Uit een Duitse studie blijkt dat de gereduceerde vorm van Q10 te weten ubiquinol veel beter opgenomen wordt in het lichaam en tot wel bijna vijf keer hogere Q10 waarden geeft en bovendien ook nog eens zorgt voor lagere waarden slecht cholesterol (LDL) en voor een betere aanmaak van rode bloedcellen.

Mediterranean diet supplemented with coenzyme Q10 induces postprandial changes in p53 in response to oxidative DNA damage in elderly subjects.
Gutierrez-Mariscal FM, Perez-Martinez P, Delgado-Lista J, Yubero-Serrano EM, Camargo A, Delgado-Casado N, Cruz-Teno C, Santos-Gonzalez M, Rodriguez-Cantalejo F, Castańo JP, Villalba-Montoro JM, Fuentes F, Perez-Jimenez F, Lopez-Miranda J.
Lipid and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital/University of Cordoba, Spain.
Coenzyme Q10 (CoQ) is a powerful antioxidant that reduces oxidative stress. We explored whether the quality of dietary fat alters postprandial oxidative DNA damage and whether supplementation with CoQ improves antioxidant capacity by modifying the activation/stabilization of p53 in elderly subjects. In this crossover study, 20 subjects were randomly assigned to receive three isocaloric diets during 4 weeks each: (1) Mediterranean diet (Med diet), (2) Mediterranean diet supplemented with CoQ (Med+CoQ diet), and (3) saturated fatty acid-rich diet (SFA diet). Levels of mRNAs were determined for p53, p21, p53R2, and mdm2. Protein levels of p53, phosphorylated p53 (Ser20), and monoubiquitinated p53 were also measured, both in cytoplasm and nucleus. The extent of DNA damage was measured as plasma 8-OHdG. SFA diet displayed higher postprandial 8-OHdG concentrations, p53 mRNA and monoubiquitinated p53, and lower postprandial Mdm2 mRNA levels compared with Med and Med+CoQ diets (p < 0.05). Moreover, Med+CoQ diet induced a postprandial decrease of cytoplasmatic p53, nuclear p-p53 (Ser20), and nuclear and cytoplasmatic monoubiquitinated p53 protein (p < 0.05). In conclusion, Med+CoQ diet improves oxidative DNA damage in elderly subjects and reduces processes of cellular oxidation. Our results suggest a starting point for the prevention of oxidative processes associated with aging.
PMID: 21404051 [PubMed - in process] PMCID: PMC3312623

Effects of coenzyme Q10 on vascular endothelial function in humans: a meta-analysis of randomized controlled trials.
Gao L, Mao Q, Cao J, Wang Y, Zhou X, Fan L.
Department of Geriatric Cardiology, General Hospital of Chinese People's Liberation Army, Beijing 100853, China.
The purpose of this study was to quantify the effect of coenzyme Q10 on arterial endothelial function in patients with and without established cardiovascular disease.
Endothelial dysfunction has been implicated in the pathogenesis of atherosclerosis.
The search included MEDLINE, Cochrane Library, Scopus, and EMBASE to identify studies up to 1 July 2011. Eligible studies were randomized controlled trials on the effects of coenzyme Q10 compared with placebo on endothelial function. Two reviewers extracted data on study characteristics, methods, and outcomes. Five eligible trials enrolled a total of 194 patients. Meta-analysis using random-effects model showed treatment with coenzyme Q10 significantly improvement in endothelial function assessed peripherally by flow-mediated dilatation (SMD 1.70, 95% CI: 1.00-2.4, p<0.0001). However, the endothelial function assessed peripherally by nitrate-mediated arterial dilatation was not significantly improved by using fix-effects model (SMD -0.19, 95% CI: -1.75 to 1.38, p = 0.81).
Coenzyme Q10 supplementation is associated with significant improvement in endothelial function. The current study supports a role for CoQ10 supplementation in patients with endothelial dysfunction.
Copyright © Elsevier Ireland Ltd. All rights reserved.


Ubiquinol-induced gene expression signatures are translated into altered parameters of erythropoiesis and reduced low density lipoprotein cholesterol levels in humans.
Schmelzer C, Niklowitz P, Okun JG, Haas D, Menke T, Döring F.
Department of Molecular Prevention, Institute of Human Nutrition and Food Science, Christian-Albrechts-University of Kiel, Heinrich-Hecht-Platz 10, Kiel, Germany. sek@molprev.uni-kiel.de
Studies in vitro and in mice indicate a role for Coenzyme Q(10) (CoQ(10) ) in gene expression. To determine this function in relationship to physiological readouts, a 2-week supplementation study with the reduced form of CoQ(10) (ubiquinol, Q(10) H(2) , 150 mg/d) was performed in 53 healthy males. Mean CoQ(10) plasma levels increased 4.8-fold after supplementation. Transcriptomic and bioinformatic approaches identified a gene-gene interaction network in CD14-positive monocytes, which functions in inflammation, cell differentiation, and peroxisome proliferator-activated receptor-signaling. These Q(10) H(2) -induced gene expression signatures were also described previously in liver tissues of SAMP1 mice. Biochemical and NMR-based analyses showed a reduction of low density lipoprotein (LDL) cholesterol plasma levels after Q(10) H(2) supplementation. This effect was especially pronounced in atherogenic small dense LDL particles (19-21 nm, 1.045 g/L). In agreement with gene expression signatures, Q(10) H(2) reduces the number of erythrocytes but increases the concentration of reticulocytes. In conclusion, Q(10) H(2) induces characteristic gene expression patterns, which are translated into reduced LDL cholesterol levels and altered parameters of erythropoiesis in humans.
Copyright © Wiley Periodicals, Inc.
 (Mei 2012)