This fat-soluble substance, which resembles a vitamin, is present in all respiring eukaryotic cells, primarily in the mitochondria. It is a component of the electron transport chain and participates in aerobic cellular respiration, which generates energy in the form of ATP. Ninety-five percent of the human body’s energy is generated this way.Therefore, those organs with the highest energy requirements—such as the heart, liver, and kidney—have the highest CoQ10 concentrations.
There are three redox states of CoQ10: fully oxidized (ubiquinone), semiquinone (ubisemiquinone), and fully reduced(ubiquinol). The capacity of this molecule to act as a two-electron carrier (moving between the quinone and quinol form) and a one-electron carrier (moving between the semiquinone and one of these other forms) is central to its role in the electron transport chain due to the iron–sulfur clusters that can only accept one electron at a time, and as a free-radical–scavenging antioxidant.
There are two major factors that lead to deficiency of CoQ10 in humans: reduced biosynthesis, and increased use by the body. Biosynthesis is the major source of CoQ10. Biosynthesis requires at least 12 genes, and mutations in many of them cause CoQ deficiency. CoQ10 levels also may be affected by other genetic defects (such as mutations of mitochondrial DNA, ETFDH, APTX, FXN, and BRAF, genes that are not directly related to the CoQ10 biosynthetic process). The role of statins in deficiencies is controversial. Some chronic disease conditions (cancer, heart disease, etc.) also are thought to reduce the biosynthesis of and increase the demand for CoQ10 in the body, but there are no definite data to support these claims.
Usually, toxicity is not observed with high doses of CoQ10. A daily dosage up to 3,600 mg was found to be tolerated by healthy as well as unhealthy persons. Some adverse effects, however, largely gastrointestinal, are reported with very high intakes. The observed safe level (OSL) risk assessment method indicated that the evidence of safety is strong at intakes up to 1200 mg/day, and this level is identified as the OSL.
Although CoQ10 may be measured in blood plasma, these measurements reflect dietary intake rather than tissue status. Currently, most clinical centers measure CoQ10levels in cultured skin fibroblasts, muscle biopsies, and blood mononuclear cells. Culture fibroblasts can be used also to evaluate the rate of endogenous CoQ10biosynthesis, by measuring the uptake of 14C-labelled p-hydroxybenzoate.
CoQ10 shares a biosynthetic pathway with cholesterol. The synthesis of an intermediary precursor of CoQ10, mevalonate, is inhibited by some beta blockers, blood pressure-lowering medication, and statins, a class of cholesterol-lowering drugs. Statins can reduce serum levels of CoQ10 by up to 40%.
CoQ10 is not approved by the U.S. Food and Drug Administration (FDA) for the treatment of any medical condition. It is sold as a dietary supplement. In the U.S., supplements are not regulated as drugs, but as foods. How CoQ10 is manufactured is not regulated and different batches and brands may vary significantly.
A 2004 laboratory analysis by ConsumerLab.com of CoQ10 supplements on the market found that some did not contain the quantity identified on the product label. Amounts varied from “no detectable CoQ10“, to 75% of stated dose, and up to a 75% excess.
Generally, CoQ10 is well tolerated. The most common side effects are gastrointestinal symptoms (nausea, vomiting, appetite suppression, and stomachaches), rashes, and headaches.
While there is no established ideal dosage of CoQ10, a typical daily dose is 100–200 milligrams. Note that different supplement brands may have varying ingredients and strengths 
A 2014 prospective study of 420 chronic heart failure patients for two years found a statistically significant 44% reduction in both cardiovascular and all-cause mortality in patients taking 300 mg CoQ10 a day versus placebo, as well as reductions in hospitalizations, cardiovascular events, and NYHA class severity.
A prior 2014 Cochrane Collaboration meta-analysis had found “no convincing evidence to support or refute” the use of CoQ10 for the treatment of heart failure.However, a 2013 meta-analysis showed that “supplementation with CoQ10 resulted in a pooled mean net change of 3.67% (95% CI: 1.60%, 5.75%) in the ejection fraction, and -0.30 (95% CI: -0.66, 0.06) in the New York Heart Association functional class”. Evidence with respect to preventing heart disease in those who are otherwise healthy is poor.
Regarding the efficacy of CoQ10 for hypertension, a 2016 Cochrane review concluded that studies looking at the effects of CoQ10 on blood pressure provided moderate-quality evidence that coenzyme Q10 does not lower blood pressure.
Available evidence suggests that “CoQ10 is likely ineffective in moderately improving” the chorea associated with Huntington’s disease.
While CoQ10 can improve some measurements regarding sperm quality, there is no evidence that CoQ10 increases live births or pregnancy rates.
Supplementation of CoQ10 has been found to have a beneficial effect on the condition of some sufferers of migraine. An explanation for this is the theory that migraines are a mitochondrial disorder, and that mitochondrial dysfunction can be improved with CoQ10. The Canadian Headache Society guideline for migraine prophylaxisrecommends, based on low-quality evidence, that 300 mg of CoQ10 be offered as a choice for prophylaxis.
CoQ10 has been routinely used to treat muscle breakdown associated as a side effect of use of statin medications. A 2015 meta-analysis of randomized controlled trials found that CoQ10 showed a trend to decrease muscle pain in statin myopathy, but this decrease was not statistically significant. A 2018 meta-analysis concluded that there was statistically significant evidence that oral CoQ10 supplementation ameliorated statin-associated muscle symptoms, including muscle pain, muscle weakness, muscle cramps, and muscle tiredness, implying that CoQ10 supplementation might be an efficacious approach to manage statin-induced myopathy.
No large well-designed clinical trials of CoQ10 in cancer treatment have been conducted. The National Cancer Institute identified issues with the few, small studies that have been done stating, “the way the studies were done and the amount of information reported made it unclear if benefits were caused by the CoQ10 or by something else”. The American Cancer Society has concluded, “CoQ10 may reduce the effectiveness of chemo and radiation therapy, so most oncologists would recommend avoiding it during cancer treatment.”
A 1995 review study found that there is no clinical benefit to the use of CoQ10 in the treatment of periodontal disease. Most of the studies suggesting otherwise were outdated, focused on in vitro tests, had too few test subjects and/or erroneous statistical methodology and trial setup, or were sponsored by a manufacturer of the product.
Coenzyme Q10 has potential to inhibit the effects of warfarin (Coumadin), a potent anticoagulant, by reducing the INR, a measure of blood clotting. The structure of coenzyme Q10 is very much similar to the structure of vitamin K, which competes with and counteracts warfarin’s anticoagulation effects. Coenzyme Q10 should be avoided in patients currently taking warfarin due to the increased risk of clotting.
The oxidized structure of CoQ10 is shown on the top-right. The various kinds of Coenzyme Q may be distinguished by the number of isoprenoid subunits in their side-chains. The most common Coenzyme Q in human mitochondria is CoQ10. Q refers to the quinone head and 10 refers to the number of isoprene repeats in the tail. The molecule below has three isoprenoid units and would be called Q3.
Biosynthesis occurs in most human tissue. There are three major steps:
- Creation of the benzoquinone structure (using phenylalanine or tyrosine)
- Creation of the isoprene side chain (using acetyl-CoA)
- The joining or condensation of the above two structures
The initial two reactions occur in mitochondria, the endoplasmic reticulum, and peroxisomes, indicating multiple sites of synthesis in animal cells.
An important enzyme in this pathway is HMG-CoA reductase, usually a target for intervention in cardiovascular complications. The “statin” family of cholesterol-reducing medications inhibits HMG-CoA reductase. One possible side effect of statins is decreased production of CoQ10, which may be connected to the development of myopathyand rhabdomyolysis.
Genes involved include PDSS1, PDSS2, COQ2, and ADCK3 (COQ8, CABC1).
Increasing the endogenous biosynthesis of CoQ10 has gained attention in recent years as a strategy to fight CoQ10 deficiency.
CoQ10 is a crystalline powder insoluble in water. Absorption follows the same process as that of lipids; the uptake mechanism appears to be similar to that of vitamin E, another lipid-soluble nutrient. This process in the human body involves secretion into the small intestine of pancreatic enzymes and bile, which facilitates emulsificationand micelle formation required for absorption of lipophilic substances. Food intake (and the presence of lipids) stimulates bodily biliary excretion of bile acids and greatly enhances absorption of CoQ10. Exogenous CoQ10 is absorbed from the small intestine and is best absorbed if taken with a meal. Serum concentration of CoQ10 in fed condition is higher than in fasting conditions.
Data on the metabolism of CoQ10 in animals and humans are limited. A study with 14C-labeled CoQ10 in rats showed most of the radioactivity in the liver two hours after oral administration when the peak plasma radioactivity was observed, but CoQ9 (with only 9 isoprenyl units) is the predominant form of coenzyme Q in rats. It appears that CoQ10 is metabolised in all tissues, while a major route for its elimination is biliary and fecal excretion. After the withdrawal of CoQ10 supplementation, the levels return to normal within a few days, irrespective of the type of formulation used.
Some reports have been published on the pharmacokinetics of CoQ10. The plasma peak can be observed 2–6 hours after oral administration, depending mainly on the design of the study. In some studies, a second plasma peak also was observed at approximately 24 hours after administration, probably due to both enterohepatic recycling and redistribution from the liver to circulation. Tomono et al. used deuterium-labeled crystalline CoQ10 to investigate pharmacokinetics in humans and determined an elimination half-time of 33 hours.
The importance of how drugs are formulated for bioavailability is well known. In order to find a principle to boost the bioavailability of CoQ10 after oral administration, several new approaches have been taken; different formulations and forms have been developed and tested on animals and humans.
Nanoparticles have been explored as a delivery system for various drugs, such as improving the oral bioavailability of drugs with poor absorption characteristics.However, this protocol has not proved successful with CoQ10, although reports have differed widely. The use of aqueous suspension of finely powdered CoQ10 in pure water also reveals only a minor effect.
A successful approach was to use the emulsion system to facilitate absorption from the gastrointestinal tract and to improve bioavailability. Emulsions of soybean oil (lipid microspheres) could be stabilised very effectively by lecithin and were used in the preparation of soft gelatin capsules. In one of the first such attempts, Ozawa et al.performed a pharmacokinetic study on beagles in which the emulsion of CoQ10 in soybean oil was investigated; about twice the plasma CoQ10 level than that of the control tablet preparation was determined during administration of a lipid microsphere. Although an almost negligible improvement of bioavailability was observed by Kommuru et al. with oil-based softgel capsules in a later study on dogs, the significantly increased bioavailability of CoQ10 was confirmed for several oil-based formulations in most other studies.
Facilitating drug absorption by increasing its solubility in water is a common pharmaceutical strategy and also has been shown to be successful for CoQ10. Various approaches have been developed to achieve this goal, with many of them producing significantly better results over oil-based softgel capsules in spite of the many attempts to optimize their composition. Examples of such approaches are use of the aqueous dispersion of solid CoQ10 with the polymer tyloxapol, formulations based on various solubilising agents, such as hydrogenated lecithin, and complexation with cyclodextrins; among the latter, the complex with β-cyclodextrin has been found to have highly increased bioavailability. and also is used in pharmaceutical and food industries for CoQ10-fortification. Also some other novel carrier systems, such as liposomes, nanoparticles or dendrimers, may be used to increase the bioavailability of CoQ10.
CoQ10 was first discovered by Fredrick L. Crane and colleagues at the University of Wisconsin–Madison Enzyme Institute in 1957. In 1958, its chemical structure was reported by Karl Folkers and coworkers at Merck. In the early 1970s, Gian Paolo Littarru and Karl Folkers observed that a deficiency of CoQ10 was associated with human heart disease. The 1980s witnessed a steep rise in the number of clinical trials due to the availability of large quantities of pure CoQ10 and methods to measure plasma and blood CoQ10 concentrations. The redox functions of CoQ in cellular energy production and antioxidant protection are based on the ability to exchange two electrons in a redox cycle between ubiquinol (reduced CoQ) and ubiquinone (oxidized CoQ). The antioxidant role of the molecule as a free-radicalscavenger was widely studied by Lars Ernster. Numerous scientists around the globe started studies on this molecule since then in relation to various diseases including cardiovascular diseases and cancer.
Detailed reviews on occurrence of CoQ10 and dietary intake were published in 2010. Besides the endogenous synthesis within organisms, CoQ10 also is supplied to the organism by various foods. Despite the scientific community’s great interest in this compound, however, a very limited number of studies have been performed to determine the contents of CoQ10 in dietary components. The first reports on this aspect were published in 1959, but the sensitivity and selectivity of the analytical methods at that time did not allow reliable analyses, especially for products with low concentrations. Since then, developments in analytical chemistry have enabled a more reliable determination of CoQ10 concentrations in various foods:
CoQ10 levels in selected foods Food CoQ10 concentration (mg/kg) Beef heart 113 liver 39–50 muscle 26–40 Pork heart 12–128 liver 23–54 muscle 14–45 Chicken breast 8–17 thigh 24–25 wing 11 Fish sardine 5–64 mackerel: – red flesh 43–67 – white flesh 11–16 salmon 4–8 tuna 5 Oils soybean 54–280 olive 4–160 grapeseed 64–73 sunflower 4–15 canola 64–73 Nuts peanut 27 walnut 19 sesame seed 18–23 pistachio 20 hazelnut 17 almond 5–14 Vegetables parsley 8–26 broccoli 6–9 cauliflower 2–7 spinach up to 10 Chinese cabbage 2–5 Fruit avocado 10 blackcurrant 3 grape 6–7 strawberry 1 orange 1–2 grapefruit 1 apple 1 banana 1
Meat and fish are the richest sources of dietary CoQ10; levels over 50 mg/kg may be found in beef, pork, chicken heart, and chicken liver. Dairy products are much poorer sources of CoQ10 compared to animal tissues. Vegetable oils also are quite rich in CoQ10. Within vegetables, parsley and perilla are the richest CoQ10 sources, but significant differences in their CoQ10 levels may be found in the literature. Broccoli, grapes, and cauliflower are modest sources of CoQ10. Most fruit and berries represent a poor to very poor source of CoQ10, with the exception of avocados, which have a relatively high CoQ10 content. In the developed world, the estimated daily intake of CoQ10 has been determined at 3–6 mg per day, derived primarily from meat. Cooking by frying reduces CoQ10 content by 14–32%.
- Ernster, L.; Dallner, G. (1995). “Biochemical, physiological and medical aspects of ubiquinone function”. Biochimica et Biophysica Acta. 1271 (1): 195–204. doi:10.1016/0925-4439(95)00028-3. PMID 7599208.
- Dutton, P. L.; Ohnishi, T.; Darrouzet, E.; Leonard, M. A.; Sharp, R. E.; Cibney, B. R.; Daldal, F.; Moser, C. C. (2000). “4 Coenzyme Q oxidation reduction reactions in mitochondrial electron transport”. In Kagan, V. E.; Quinn, P. J. Coenzyme Q: Molecular mechanisms in health and disease. Boca Raton: CRC Press. pp. 65–82.
- Okamoto, T.; Matsuya, T.; Fukunaga, Y.; Kishi, T.; Yamagami, T. (1989). “Human serum ubiquinol-10 levels and relationship to serum lipids”. International Journal for Vitamin and Nutrition Research. 59 (3): 288–292. PMID 2599795.
- Aberg, F.; Appelkvist, E. L.; Dallner, G.; Ernster, L. (1992). “Distribution and redox state of ubiquinones in rat and human tissues”. Archives of Biochemistry and Biophysics. 295 (2): 230–234. doi:10.1016/0003-9861(92)90511-T. PMID 1586151.
- Shindo, Y.; Witt, E.; Han, D.; Epstein, W.; Packer, L. (1994). “Enzymic and non-enzymic antioxidants in epidermis and dermis of human skin”. Journal of Investigative Dermatology. 102 (1): 122–124. doi:10.1111/1523-1747.ep12371744. PMID 8288904.
- Trevisson, E.; Dimauro, S.; Navas, P.; Salviati, L. (Oct 2011). “Coenzyme Q deficiency in muscle”. Current Opinion in Neurology. 24 (5): 449–456. doi:10.1097/WCO.0b013e32834ab528. PMID 21844807.
- Hyson, H. C.; Kieburtz, K.; Shoulson, I.; et al. (Sep 2010). “Safety and tolerability of high-dosage coenzyme Q10 in Huntington’s disease and healthy subjects”. Movement Disorders. 25 (12): 1924–1928. doi:10.1002/mds.22408. PMID 20669312.
- Hathcock, J. N.; Shao, A. (Aug 2006). “Risk assessment for coenzyme Q10(Ubiquinone)”. Regulatory Toxicology and Pharmacology. 45 (3): 282–288. doi:10.1016/j.yrtph.2006.05.006. PMID 16814438.
- Montero, R.; Sánchez Alcázar, J. A.; Briones, P.; et al. (Jun 2008). “Analysis of coenzyme Q10 in muscle and fibroblasts for the diagnosis of CoQ10 deficiency syndromes”. Clinical Biochemistry. 41 (9): 697–700. doi:10.1016/j.clinbiochem.2008.03.007. PMID 18387363.
- Kishi, T.; Watanabe, T.; Folkers, K. (1977). “Bioenergetics in clinical medicine XV. Inhibition of coenzyme Q10-enzymes by clinically used adrenergic blockers of beta-receptors”. Research Communications in Chemical Pathology and Pharmacology. 17 (1): 157–164. PMID 17892.
- Mortensen, S. A.; Leth, A.; Agner, E.; Rohde, M. (1997). “Dose-related decrease of serum coenzyme Q10 during treatment with HMG-CoA reductase inhibitors”. Molecular Aspects of Medicine. 18 (Suppl.): S137–S144. doi:10.1016/S0098-2997(97)00014-9. PMID 9266515.
- Ghirlanda, G.; Oradei, A.; Manto, A.; Lippa, S.; Uccioli, L.; Caputo, S.; Greco, A. V.; Littarru, G. P. (1993). “Evidence of plasma CoQ10-lowering effect by HMG-CoA reductase inhibitors: a double-blind, placebo-controlled study”. Journal of Clinical Pharmacology. 33 (3): 226–229. doi:10.1002/j.1552-4604.1993.tb03948.x. PMID 8463436.
- White, J. (14 May 2014). “PDQ® Coenzyme Q10“. National Cancer Institute, National Institutes of Health, U.S. Dept. of Health and Human Services. Retrieved 29 Jun 2014.
- “ConsumerLab.com finds discrepancies in strength of CoQ10 supplements”. Townsend Letter for Doctors and Patients. Aug–Sep 2004. p. 19.
- Wyman, M.; Leonard, M.; Morledge, T. (Jul 2010). “Coenzyme Q10: a therapy for hypertension and statin-induced myalgia?”. Cleveland Clinic Journal of Medicine. 77 (7): 435–442. doi:10.3949/ccjm.77a.09078. PMID 20601617.
- “Benefits of Coenzyme Q10“. Benefits of CoQ10. Retrieved 28 September 2017.
- Mortensen, Svend A.; Rosenfeldt, Franklin; Kumar, Adarsh; Dolliner, Peter; Filipiak, Krzysztof J.; Pella, Daniel; Alehagen, Urban; Steurer, Günter; Littarru, Gian P. (Dec 2014). “The Effect of Coenzyme Q10 on Morbidity and Mortality in Chronic Heart Failure”. Heart Failure. American College of Cardiology Foundation (6): 641–649.
- Madmani, M. E.; Yusuf Solaiman, A.; Tamr Agha, K.; Madmani, Y.; Shahrour, Y.; Essali, A.; Kadro, W. (2 Jun 2014). “Coenzyme Q10 for heart failure”. Heart Group. Cochrane Database of Systematic Reviews. John Wiley & Sons (6): CD008684. doi:10.1002/14651858.CD008684.pub2 – via The Cochrane Library. (Subscription required (help)).
- Fotino, A Domnica; Thompson-Paul, Angela M; Bazzano, Lydia A (2013). “Effect of coenzyme Q10 supplementation on heart failure: a meta-analysis”. The American Journal of Clinical Nutrition. American Society for Nutrition. 97 (2): 268–275. doi:10.3945/ajcn.112.040741. Retrieved 20 March 2018.
- Flowers, N.; Hartley, L.; Todkill, D.; Stranges, S.; Rees, K. (4 Dec 2014). “Co-enzyme Q10 supplementation for the primary prevention of cardiovascular disease”. The Cochrane Database of Systematic Reviews. 12: CD010405. doi:10.1002/14651858.CD010405.pub2. PMID 25474484.
- Ho, M. J.; Li, E. C.; Wright, J. M. (3 Mar 2016). “Blood pressure lowering efficacy of coenzyme Q10 for primary hypertension”. The Cochrane Database of Systematic Reviews (3): CD007435. doi:10.1002/14651858.CD007435.pub3. PMID 26935713.
- Armstrong, M. J.; Miyasaki, J. M. (7 Aug 2012). “Evidence-based guideline: pharmacologic treatment of chorea in Huntington disease: report of the guideline development subcommittee of the American Academy of Neurology”. Neurology. American Academy of Neurology. 79 (6): 597–603. doi:10.1212/wnl.0b013e318263c443. PMC 3413759. PMID 22815556.
- Lafuente, R.; González Comadrán, M.; Solà, I.; López, G.; Brassesco, M.; Carreras, R.; Checa, M. A. (Sep 2013). “Coenzyme Q10 and male infertility: a meta-analysis”. Journal of Assisted Reproduction and Genetics. 30 (9): 1147–1156. doi:10.1007/s10815-013-0047-5. PMC 3800531. PMID 23912751.
- Markley, H. G. (Oct 2012). “CoEnzyme Q10 and riboflavin: the mitochondrial connection”. Headache (Review). 52 (Suppl. 2): 81–87. doi:10.1111/j.1526-4610.2012.02233.x. PMID 23030537.
- Yorns, W. R.; Hardison, H. H. (Sep 2013). “Mitochondrial dysfunction in migraine”. Seminars in Pediatric Neurology. 20 (3): 188–193. doi:10.1016/j.spen.2013.09.002. PMID 24331360.
- Pringsheim, T.; Davenport, W.; Mackie, G.; et al. (Mar 2012). “Canadian Headache Society guideline for migraine prophylaxis”. Canadian Journal of Neurological Science. 39 (2 Suppl. 2): S1–S59. PMID 22683887.
- Banach, M.; Serban, C.; Sahebkar, A.; Ursoniu, S.; Rysz, J.; Muntner, P.; Toth, P. P.; Jones, S. R.; Rizzo, M.; Glasser, S. P.; Lip, G. Y.; Dragan, S; Mikhailidis, D. P. (Jan 2015). “Effects of coenzyme Q10 on statin-induced myopathy: a meta-analysis of randomized controlled trials”. Mayo Clinic Proceedings (Systematic Review and Meta-Analysis). Lipid and Blood Pressure Meta-analysis Collaboration Group. 90(1): 24–34. doi:10.1016/j.mayocp.2014.08.021. PMID 25440725.
- Qu, H., Guo, M., Chai, H., Wang, W.T., Gao, Z.Y. and Shi, D.Z., 2018. Effects of Coenzyme Q10 on Statin‐Induced Myopathy: An Updated Meta‐Analysis of Randomized Controlled Trials. Journal of the American Heart Association, 7(19), p.e009835.
- “Coenzyme Q10“. American Cancer Society. Retrieved 20 Feb 2014.
- Watts, T. L. P. (1995). “Coënzyme Q10 and periodontal treatment: is there any beneficial effect?”. British Dental Journal. Department of Periodontology and Preventive Dentistry, UMDS, Guy’s Hospital London. 178 (6): 209–213. doi:10.1038/sj.bdj.4808715. PMID 7718355.
- Folkers, K.; Hanioka, T.; Xia, L.; McRee, J., Jr; Langsjoen, P. (1991). “Coenzyme Q10 increases T4/T8 ratios of lymphocytes in ordinary subjects and relevance to patients having the aids related complex”. Biochemical and Biophysical Research Communications. 176 (2): 786–791. doi:10.1016/S0006-291X(05)80254-2. PMID 1673841.
- Littarru, G. P.; Nakamura, R.; Ho, L.; Folkers, K.; Kuzell, W. C. (Oct 1971). “Deficiency of Coenzyme Q10 in Gingival Tissue from Patients with Periodontal Disease”. Proceedings of the National Academy of Sciences. 68 (10): 2332–2335. doi:10.1073/pnas.68.10.2332. PMC 389415. PMID 5289867.
- Nakamura, R.; Littarru, G. P.; Folkers, K.; Wilkinson, E. G. (Apr 1974). “Study of CoQ10-Enzymes in Gingiva from Patients with Periodontal Disease and Evidence for a Deficiency of Coenzyme Q10“. Proceedings of the National Academy of Sciences. 71 (4): 1456–1460. doi:10.1073/pnas.71.4.1456. PMC 388248. PMID 4151519.
- McRee, J. T.; Hanioka, T.; Shizukuishi, S.; Folkers, K. (1993). “Therapy with coenzyme Q10 for patients with periodontal disease”. Journal of Dental Health. 43(5): 659–666. doi:10.5834/jdh.43.659.
- Hanioka, T.; Tanaka, M.; Ojima, M.; Shizukuishi, S.; Folkers, K. (1994). “Effect of topical application of coenzyme Q10 on adult periodontitis”. Molecular Aspects of Medicine. 15 (Suppl.): S241–S248. doi:10.1016/0098-2997(94)90034-5. PMID 7752836.
- Wilkinson, E. G.; Arnold, R. M.; Folkers, K. (1976). “Bioenergetics in clinical medicine. VI. adjunctive treatment of periodontal disease with coenzyme Q10“. Research communications in chemical pathology and pharmacology. 14 (4): 715–719. PMID 785563.
- Bentinger, M.; Tekle, M.; Dallner, G. (May 2010). “Coenzyme Q—biosynthesis and functions”. Biochemical and Biophysical Research Communications. 396 (1): 74–79. doi:10.1016/j.bbrc.2010.02.147. PMID 20494114.
- Espinós, Carmen; Felipo, Vicente; Palau, Francesc (2009). Inherited Neuromuscular Diseases: Translation from Pathomechanisms to Therapies. Springer. pp. 122ff. ISBN 978-90-481-2812-9. Retrieved 4 Jan 2011.
- Bhagavan, Hemmi N.; Chopra, Raj K. (2006). “Coenzyme Q10: Absorption, tissue uptake, metabolism and pharmacokinetics”. Free Radical Research. 40 (5): 445–453. doi:10.1080/10715760600617843. PMID 16551570.
- Bogentoft 1991[verification needed]
- Ochiai, A.; Itagaki, S.; Kurokawa, T.; Kobayashi, M.; Hirano, T.; Iseki, K. (Aug 2007). “Improvement in intestinal coenzyme Q10 absorption by food intake”. Yakugaku Zasshi. 127 (8): 1251–1254. doi:10.1248/yakushi.127.1251. PMID 17666877.[verification needed]
- Žmitek; et al. (2008). “Improving the bioavailability of CoQ10“. Agro Food Industry Hi Tech. 19 (4): 9.
- Kishi, H.; Kanamori, N.; Nisii, S.; Hiraoka, E.; Okamoto, T.; Kishi, T. (1964). “Metabolism and Exogenous Coenzyme Q10 in vivo and Bioavailability of Coenzyme Q10 Preparations in Japan”. Biomedical and Clinical Aspects of Coenzyme Q. Amsterdam: Elsevier. pp. 131–142.
- Ozawa, Y.; Mizushima, Y.; Koyama, I.; Akimoto, M.; Yamagata, Y.; Hayashi, H.; Murayama, H. (1986). “Intestinal absorption enhancement of coenzyme Q10with a lipid microsphere”. Arzneimittel-Forschung. 36 (4): 689–690. PMID 3718593.
- Tomono, Y.; Hasegawa, J.; Seki, T.; Motegi, K.; Morishita, N. (1986). “Pharmacokinetic study of deuterium-labelled coenzyme Q10 in man”. International Journal of Clinical Pharmacology, Therapy, and Toxicology. 24 (10): 536–541. PMID 3781673.
- Mathiowitz, Edith; Jacob, Jules S.; Jong, Yong S.; Carino, Gerardo P.; Chickering, Donald E.; Chaturvedi, Pravin; Santos, Camilla A.; Vijayaraghavan, Kavita; Montgomery, Sean; Bassett, Michael; Morrell, Craig (1997). “Biologically erodible microspheres as potential oral drug delivery systems”. Nature. 386 (6623): 410–414. doi:10.1038/386410a0. PMID 9121559.
- Hsu, C. H.; Cui, Z.; Mumper, R. J.; Jay, M. (2003). “Preparation and characterization of novel coenzyme Q10 nanoparticles engineered from microemulsion precursors”. AAPS PharmSciTech. 4 (3): 24–35. doi:10.1208/pt040332. PMC 2750625. PMID 14621964.[verification needed]
- Joshi, S. S.; Sawant, S. V.; Shedge, A.; Halpner, A. D. (Jan 2003). “Comparative bioavailability of two novel coenzyme Q10 preparations in humans”. International Journal of Clinical Pharmacology and Therapeutics. 41 (1): 42–48. doi:10.5414/CPP41042. PMID 12564745.[verification needed]
- Kommuru, T. R.; Ashraf, M.; Khan, M. A.; Reddy, I. K. (1999). “Stability and bioequivalence studies of two marketed formulations of coenzyme Q10 in beagle dogs”. Chemical & Pharmaceutical Bulletin. 47 (7): 1024–1028. doi:10.1248/cpb.47.1024. PMID 10434405.
- Bhagavan, H. N.; Chopra, R. K. (Jun 2007). “Plasma coenzyme Q10 response to oral ingestion of coenzyme Q10 formulations”. Mitochondrion. 7 (Suppl.): S78–S88. doi:10.1016/j.mito.2007.03.003. PMID 17482886.[verification needed]
- US 6197349, Westesen, K. & B. Siekmann, “Particles with modified physicochemical properties, their preparation and uses”, published 2001
- US 4483873, Ohashi, H.; T. Takami & N. Koyama et al., “Aqueous solution containing ubidecarenone”, published 1984
- Žmitek, Janko; Smidovnik, Andrej; Fir, Maja; Prosek, Mirko; Žmitek, Katja; Walczak, Jaroslaw; Pravst, Igor (2008). “Relative Bioavailability of Two Forms of a Novel Water-Soluble Coenzyme Q10“. Annals of Nutrition and Metabolism. 52 (4): 281–287. doi:10.1159/000129661. PMID 18645245.
- Kagan, Daniel; Madhavi, Doddabele (2010). “A Study on the Bioavailability of a Novel Sustained-Release Coenzyme Q10-β-Cyclodextrin Complex”. Integrative Medicine. 9 (1).
- Crane, F.; Hatefi, Y.; Lester, R.; Widmer, C. (1957). “Isolation of a quinone from beef heart mitochondria”. Biochimica et Biophysica Acta. 25 (1): 220–221. doi:10.1016/0006-3002(57)90457-2. PMID 13445756.
- Langsjoen, Peter H. “Introduction of Coezyme Q10“. Archived from the original on 23 December 1999.[self-published source?]
- Folkers, K.; Littarru, G. P.; Ho, L.; Runge, T. M.; Havanonda, S.; Cooley, D. (1970). “Evidence for a deficiency of coenzyme Q10 in human heart disease”. International Journal of Vitamin Research. 40 (3): 380–390. PMID 5450999.
- Littarru, G. P.; Ho, L.; Folkers, K. (1972). “Deficiency of coenzyme Q10 in human heart disease. I.”. International Journal for Vitamin and Nutrition Research. 42 (2): 291–305. PMID 5053855.
- Littarru, G. P.; Ho, L.; Folkers, K. (1972). “Deficiency of coenzyme Q10 in human heart disease. II”. International Journal for Vitamin and Nutrition Research. 42 (3): 413–434. PMID 5086647.
- Mellors, A.; Tappel, A. (1966). “The Inhibition of Mitochondrial Peroxidation by Ubiquinone and Ubiquinol”. Journal of Biological Chemistry. 241 (19): 4353–4356. PMID 5922959.
- Mellors, A.; Tappel, A. (Jul 1966). “Quinones and Quinols as Inhibitors of Lipid Peroxidation”. Lipids. 1 (4): 282–284. doi:10.1007/BF02531617. PMID 17805631.
- Pravst, Igor; Žmitek, Katja; Žmitek, Janko (2010). “Coenzyme Q10Contents in Foods and Fortification Strategies”. Critical Reviews in Food Science and Nutrition. 50 (4): 269–280. doi:10.1080/10408390902773037. PMID 20301015.
- Weber, C.; Bysted, A.; Hølmer, G (1997). “The coenzyme Q10 content of the average Danish diet”. International Journal of Vitamin and Nutrient Research. 67(2): 123–129. PMID 9129255.
Idebenone – synthetic analog with reduced oxidant generating properties MitoQ – mitochondrion-targeted version of CoQ10 with increased bioavailability and efficacy “List of USP Verified CoQ10 Ingredients”. U.S. Pharmacopeial Convention. Archived from the original on 9 February 2009. Bonakdar, Robert Alan; Guarneri, Erminia. “Coenzyme Q10“. American Family Physician.
green leaves have long been used to treat inflammation, so anti-inflammatory properties of chlorophyll and their break-down products after digestion were put to the test. And, indeed, they may represent “valuable and abundantly available anti-inflammatory agents.” Maybe that’s one reason why cruciferous vegetables, like kale and collard greens, are associated with decreased markers of inflammation.
In a petri dish, for example, if you lay down a layer of arterial lining cells, more inflammatory immune cells stick to them after you stimulate them with a toxic substance. We can bring down that inflammation with the anti-inflammatory drug aspirin or, even more so, by just dripping on some chlorophyll. Perhaps that’s one of the reasons kale consumers appear to live longer lives.
As interesting as I found that study to be, this next study blew my mind. The most abundant energy source on this planet is sunlight. However, only plants are able to use it directly—or so we thought. After eating plants, animals have chlorophyll in them, too, so might we also be able to derive energy directly from sunlight? Well, first of all, light can’t get through our skin, right? Wrong. This was demonstrated by century-old science—and every kid who’s ever shined a flashlight through her or his fingers, showing that the red wavelengths do get through. In fact, if you step outside on a sunny day, there’s enough light penetrating your skull and going through to your brain that you could read a book in there. Okay, so our internal organs are bathed in sunlight, and when we eat green leafy vegetables, the absorbed chlorophyll in our body does actually appear to produce cellular energy. But, unless we eat so many greens we turn green ourselves, the energy produced is probably negligible.
However, light-activated chlorophyll inside our body may help regenerate Coenzyme Q10. CoQ10 is an antioxidant our body basically makes from scratch using the same enzyme we use to make cholesterol—that is, the same enzyme that’s blocked by cholesterol-lowering statin drugs. So, if CoQ10 production gets caught in the crossfire, then maybe that explains why statins increase our risk of diabetes—namely, by accidently also reducing CoQ10 levels in a friendly-fire type of event. Maybe that’s why statins can lead to muscle breakdown.
Given that, should statin users take CoQ10 supplements? No, they should sufficiently improve their diets to stop taking drugs that muck with their biochemistry! By doing so—by eating more plant-based chlorophyll-rich diets—you may best maintain your levels of active CoQ10, also known as ubiquinol. “However, when ubiquinol is used as an antioxidant, it is oxidized to ubiquinone. To act as an effective antioxidant, the body must regenerate ubiquinol from ubiquinone,” perhaps by using dietary chlorophyll metabolites and light.
Researchers exposed some ubiquinone and chlorophyll metabolites to the kind of light that makes it into our bloodstream. Poof! CoQ10 was reborn. But, without the chlorophyll or the light, nothing happened. By going outside we get light and, if we’re eating our veggies, chlorophyll, so maybe that’s how we maintain such high levels of CoQ10 in our bloodstream. Perhaps this explains why dark green leafy vegetables are so good for us. We know sun exposure can be good for us and that eating greens can be good for us. “These benefits are commonly attributed to an increase in vitamin D from sunlight exposure and consumption of antioxidants from green vegetables”