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Metabolic Cardiology
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Coenzyme Q10, so named for its ubiquitous nature in cells, is a fat-soluble compound that functions as an antioxidant and coenzyme in the energy-producing pathways. Ubiquinol – known as the reduced form – and ubiquinone – the oxidized form – both coexist in the body and regenerate each other in our cells through sequential redox reactions. As an antioxidant, the reduced form of CoQ10 inhibits lipid peroxidation in both cell membranes and serum low-density lipoprotein, and protects proteins and DNA from oxidative damage. In vitro, CoQ10 inhibits LDL oxidation more than beta-carotene and alpha-tocopherol.64 CoQ10 also has membrane-stabilizing activity. However, its bioenergetic activity and electron transport function for its role in oxidative phosphorylation are probably its most important functions.
Nonalcoholic Fatty Liver Disease
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
Coenzyme Q10 is a fat-soluble vitamin and is an important antioxidant. Levels in the body occur by endogenous synthesis or exogenously through food and supplement. Dietary sources of coenzyme Q10 are relatively understudied compared to supplements, despite the finding that low dose supplement and dietary source from organ meat can lead to similar serum levels (Weber, Bysted, and Hølmer 1997). With regard to cooking methods of animal products rich in coenzyme Q10, conflicting results exist if boiling versus frying can lead to retention. However, one study found no difference between the preparation methods and that coenzyme Q10 from organ meat had higher digestibility than that from muscle meat.
Micronutrient Supplementation and Ergogenesis — Metabolic Intermediates
Published in Luke Bucci, Nutrients as Ergogenic Aids for Sports and Exercise, 2020
Coenzyme Q10 supplementation has consistently shown improved physiological and physical parameters in both trained and untrained subjects, consistent with hypothetical mechanisms of action. Thus, coenzyme Q10 supplementation appears to be a viable option to improve aerobic performance. The long-term safety of coenzyme Q10 supplementation has been thoroughly documented in thousands of subjects.520–523,941,944–946 Likewise, the ability of orally administered coenzyme Q10 to increase blood and tissue levels has also been extensively documented in both animals and humans.520–523,941,944–946 Coenzyme Q10 is available at health food stores, mail order vitamin companies, and sporting goods stores. Attention to bioavailability is found for some products that offer coenzyme Q10 in oil, or emulsified. Thus, coenzyme Q10 is poised to be a nutritional ergogenic aid, providing further research studies confirm that performance in actual sports settings is improved.
The new European guidelines for prevention of cardiovascular disease are misleading
Published in Expert Review of Clinical Pharmacology, 2020
Uffe Ravnskov, Abdullah Alabdulgader, Michel de Lorgeril, David M. Diamond, Rokuro Hama, Tomohito Hamazaki, Björn Hammarskjöld, Zoe Harcombe, Malcolm Kendrick, Peter Langsjoen, Kilmer S. McCully, Harumi Okuyama, Sherif Sultan, Ralf Sundberg
Statins block the production of both cholesterol and coenzyme Q10. Cholesterol is necessary for a steady renewal of all our cells and for the production of many vital substances, and coenzyme Q10 is necessary for almost all cells to generate energy and normal function. Therefore, it is not surprising that many independent researchers have documented that statin treatment may result in unacceptable side effects which in many cases disappear when the treatment is discontinued [1,47–51]. The most frequent side effect is muscle problems, because muscle cells utilize the most energy in the body and are therefore most directly impaired by coenzyme Q10 deficiency. Considering that today, millions of people are treated with statins, such treatment may be one of the causes of the epidemic of heart failure reported in many countries. In accordance, heart failure is associated with statin use and treatment with coenzyme Q10 is able to treat it [51].
Coenzyme Q10 supplementation improves acute outcomes of stroke in rats pretreated with atorvastatin
Published in Nutritional Neuroscience, 2019
Sanaz Nasoohi, Leila Simani, Fariba Khodagholi, Sara Nikseresht, Mehrdad Faizi, Nima Naderi
Based on the existing data, there are a few presumptive mechanisms that may explain the lack of statins’ efficacy. Importantly, it has been shown that statins may directly induce apoptosis in neurons and astrocytes by impairing normal cholesterol biogenesis15,16 and elevate apoptotic gene transcripts in the brain of animals.17 Nevertheless, considering atorvastatin high-molecular weight, its penetration through blood–brain barrier (BBB) is highly limited despite its high lipophilicity.18 Intriguingly, atorvastatin appears not to be protective against Parkinson despite other statins,19 the fact that might be explained by less BBB penetration and overweight its peripheral impact on CoQ10 depletion. On the other side, statins-induced systemic HMG-CoA reductase inhibition has been shown to reduce levels of farnesyl pyrophosphate, the intermediate product of the mevalonate cycle, leading to coenzyme Q10 (CoQ10, ubiquinone) and dilicol depletion.20 CoQ10 is a lipid-soluble endogenous proenzyme with established implication in oxidative phosphorylation and energy metabolism as well as the antioxidant defense system. While CoQ10 supplementation was soon recognized to improve statins-induced myopathy,21 recent investigations suggest that coenzyme Q10 might be also a promising prescription for neurodegenerative disorders like Parkinson’s disease.
Clinical profiles and risk assessment in patients with antiphospholipid antibodies
Published in Expert Review of Clinical Immunology, 2019
Masaru Kato, Ryo Hisada, Tatsuya Atsumi
Coenzyme Q10 is a member of the mitochondrial respiratory chain that plays an important role in preventing mitochondrial disruption and oxidative stress, with some beneficial effects of its supplementation on cardiovascular disease [80]. A randomized, placebo-controlled trial involving 36 patients with APS showed an improvement of endothelial function and a decrease of prothrombotic and proinflammatory mediators in monocytes following the supplementation of coenzyme Q10 [81]. Furthermore, coenzyme Q10 prevented the formation of neutrophil extracellular traps in ex vivo cultured neutrophils of patients with APS [81]. Because of the absence of clinically significant side effects, coenzyme Q10 might act as safe adjunct not only to standard therapies in patients with APS but also to primary thrombosis prophylaxis in asymptomatic aPL carriers.