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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.[1, 2] It was discovered in the United States of America 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:
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 in CoQ10 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.[4, 5]
- A review of the literature did not recommend routine CoQ10 supplementation but suggested that certain sub-populations might benefit - eg, familial hypercholesterolaemia, heart failure and patients aged over 65 years.
- Other reviews highlight the lack of evidence to support routine CoQ10 supplementation even though there are few safety concerns with such supplementation. More research is needed to support such a recommendation.
- There is evidence that impairment of mitochondrial function and oxidative damage contribute to the pathophysiology of Parkinson's disease (PD) and changes in levels of CoQ10 in the cerebrospinal fluid of patients with PD have been found, but the clinical significance is unclear.
- Based on the current evidence, supplementation with CoQ10 is not recommended.
- 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 but, to date, there is no support from data for the role of CoQ10 supplementation.
The role and benefits of CoQ10 have been researched 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
Singh RB, Niaz MA, Kumar A, et al; Effect on absorption and oxidative stress of different oral Coenzyme Q10 dosages and intake strategy in healthy men. Biofactors. 2005
Quiles JL, Ochoa JJ, Battino M, et al; Life-long supplementation with a low dosage of coenzyme Q10 in the rat: effects on antioxidant status and DNA damage. Biofactors. 2005
Berthold HK, Naini A, Di Mauro S, et al; Effect of Ezetimibe and/or Simvastatin on Coenzyme Q10 Levels in Plasma : A Randomised Trial. Drug Saf. 2006
Young JM, Florkowski CM, Molyneux SL, et al; Effect of coenzyme Q(10) supplementation on simvastatin-induced myalgia. Am J Cardiol. 2007 Nov 1100(9):1400-3. Epub 2007 Aug 16.
Siddiqi SA, Thompson PD; How do you treat patients with myalgia who take statins? Curr Atheroscler Rep. 2009 Jan11(1):9-14.
Levy HB, Kohlhaas HK; Considerations for supplementing with coenzyme Q10 during statin therapy. Ann Pharmacother. 2006 Feb
Isobe C, Murata T, Sato C, et al; Increase of oxidized/total coenzyme Q-10 ratio in cerebrospinal fluid in patients with Parkinson's disease. J Clin Neurosci. 2006 Apr 27
Parkinson's disease in over 20s: diagnosis and management; NICE Clinical Guideline (June 2006)
Hargreaves IP, Duncan AJ, Heales SJ, et al; The effect of HMG-CoA reductase inhibitors on coenzyme Q10: possible biochemical/clinical implications. Drug Saf. 2005
Chronic heart failure: Management of chronic heart failure in adults in primary and secondary care; NICE Clinical Guideline (August 2010)
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