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Coenzyme Q10 (CoQ10), also known as ubiquinone and ubidecarenone, is often described as a vitamin or at least a vitamin-like substance. However, it is not strictly a vitamin, as it can be synthesised in the liver. CoQ10 is synthesised from the amino acid tyrosine (this synthesis in turn requires other vitamins and minerals) but is also absorbed from a wide variety of foods.
There has been a proliferation of research results showing possible causes of deficiency. It is possible to evaluate these to try to identify indications for supplementation in health and disease. Evidence of benefit from supplementation is harder to find.
As with other vitamins and dietary supplements the strongest case for use can be made in conditions where deficiency is associated with disease and where supplementation corrects or prevents the disease. It is more difficult to establish benefit in health maintenance and disease prevention. In common with other naturally occurring antioxidant compounds, many claims are made for benefit through antioxidant activity.
In common with other coenzymes, it is a cofactor upon which other enzymes depend for their function. It appears to be a coenzyme for a number of cell enzymes, including enzymes within the mitochondrial oxidative phosphorylation pathway which produces adenosine triphosphate (ATP). This is fundamental to energy production within cells. It may also have a role as an antioxidant and it undoubtedly has antioxidant activity. It was discovered in the USA and England in 1957 and by the 1970s, could be produced in large enough quantities to allow more research to be done.
Since the 1980s it has been possible to measure normal blood and tissue levels of CoQ10, although the latter procedure is not always easily reproducible. It has thus been possible to define deficiency of CoQ10 and possible associated disease. Deficiency can arise through:
- Reduced biosynthesis.
- Increased utilisation.
- Reduced dietary intake.
- A combination of these factors (probably most often the cause).
There are a number of interesting therapeutic possibilities but there is no clear evidence of benefit in any of these to date.
Some examples of possible indications and interesting research findings include the following.
Use with statins
Administration of HMG-CoA reductase inhibitors ('statins') has been associated with a reduction in CoQ10 levels (due to inhibition of mevalonate synthesis). There has been speculation that this reduction may be associated with statin-induced myopathy. However, the reduction may just reflect reduction in the lipoprotein carriers of CoQ10 and may not be statin-specific.
There are mixed reports on the benefits of CoQ10 in helping statin-associated myalgia but routine CoQ10 supplementation is not currently recommended. There is a lack of evidence to support routine CoQ10 supplementation and even though there are few safety concerns more research is needed to support such a recommendation. The National Institute for Health and Care Excellence (NICE) does not recommend prescribing it to increase statin adherence.
There is evidence that impairment of mitochondrial function and oxidative damage contribute to the pathophysiology of Parkinson's disease (PD). Changes in levels of CoQ10 in the cerebrospinal fluid of patients with PD have been found but the clinical significance is unclear.
There are good theoretical reasons for expecting benefit from CoQ10 supplementation in heart disease. There is concern that therapies (such as statins) that may lower CoQ10 levels may also precipitate worsening of heart failure. There are currently limited data to support the role of CoQ10 supplementation - research is ongoing[6, 7].
The role and benefits of CoQ10 have been investigated in a number of conditions but thus far there have been no recommendations for the supplementation. This includes the following conditions:
- Thyroid disease
- Chronic fatigue syndrome
- Mitochondrial disorders
The British National Formulary for Children (BNFC) does list the unlicensed used of CoQ10 for mitochondrial disorders.
CoQ10 is widely available and patients may initiate therapy themselves. CoQ10 supplementation appears safe without major adverse effects. It has not been tested in pregnancy. A possible interaction with coumarin anticoagulants has been reported at high doses.
Further reading and references
Quinzii CM, Emmanuele V, Hirano M; Clinical presentations of coenzyme q10 deficiency syndrome. Mol Syndromol. 2014 Jul5(3-4):141-6. doi: 10.1159/000360490.
Liu HT, Huang YC, Cheng SB, et al; Effects of coenzyme Q10 supplementation on antioxidant capacity and inflammation in hepatocellular carcinoma patients after surgery: a randomized, placebo-controlled trial. Nutr J. 2016 Oct 615(1):85. doi: 10.1186/s12937-016-0205-6.
Taylor BA, Lorson L, White CM, et al; A randomized trial of coenzyme Q10 in patients with confirmed statin myopathy. Atherosclerosis. 2015 Feb238(2):329-35. doi: 10.1016/j.atherosclerosis.2014.12.016. Epub 2014 Dec 17.
Lipid modification - cardiovascular risk assessment and the modification of blood lipids for the prevention of primary and secondary cardiovascular disease; NICE Clinical Guideline, July 2014 (updated September 2016)
Mischley LK, Allen J, Bradley R; Coenzyme Q10 deficiency in patients with Parkinson's disease. J Neurol Sci. 2012 Jul 15318(1-2):72-5. doi: 10.1016/j.jns.2012.03.023. Epub 2012 Apr 27.
Lei L, Liu Y; Efficacy of coenzyme Q10 in patients with cardiac failure: a meta-analysis of clinical trials. BMC Cardiovasc Disord. 2017 Jul 2417(1):196. doi: 10.1186/s12872-017-0628-9.
Pierce JD, Mahoney DE, Hiebert JB, et al; Study protocol, randomized controlled trial: reducing symptom burden in patients with heart failure with preserved ejection fraction using ubiquinol and/or D-ribose. BMC Cardiovasc Disord. 2018 Apr 218(1):57. doi: 10.1186/s12872-018-0796-2.