I wish to comment on recent work linking non-alcholic fatty liver disease (NAFLD) with a high risk of cardiovascular mortality.1,2 One issue which has not been addressed in these studies is the potential role of coenzyme Q10 (CoQ10) deficiency in the pathogenesis both of NAFLD and subsequent cardiovascular disease.
CoQ10 is a vitamin-like substance that plays a key role in the biochemical process supplying all cells with energy. CoQ10 also has antioxidant and anti-inflammatory action. An adequate supply of CoQ10 is particularly important in tissues with a high energy requirement, such as the heart and liver. Most of the body’s daily requirement for CoQ10 is provided by endogenous synthesis. Although CoQ10 is synthesised throughout the body, because of its size and high metabolic capacity, the liver serves as the major site of CoQ10 synthesis. In NAFLD patients where hepatic metabolic capacity has been compromised, reduction in CoQ10 production is likely to have a deleterious effect on both liver and cardiovascular function. Thus NAFLD is associated with heart failure, arrhythmias, valvular dysfunction and atherosclerosis. Depleted CoQ10 levels may be a particular problem in NAFLD patients prescribed statins, which inhibit both cholesterol and CoQ10 synthesis.
The question arises as to whether supplementation with CoQ10 in NAFLD could reduce the risk of cardiovascular disease, either by direct systemic replacement, or by stimulating the liver to synthesise more CoQ10. Recent controlled clinical trials (Q-SYMBIO and KISEL-103,4) have demonstrated, via direct supplemental replacement of systemic CoQ10, significant benefit in reducing the risk of cardiovascular mortality in patients with, or at risk of, cardiovascular disease.
In addition, Yessilova et al,5 reported depleted blood CoQ10 levels in NAFLD patients, with the decrease in CoQ10 correlating with increased liver inflammation and cirrhosis. Randomised controlled trials6,7 have shown CoQ10 supplementation significantly reduced levels of inflammation and oxidative stress in liver tissue, and improved liver function, and hence the capacity for increased endogenous CoQ10 synthesis.
In conclusion, we therefore suggest that supplementation with CoQ10 (3 x 100 mg Bio-Quinone daily) may reduce the risk of cardiovascular disease in NAFLD, initially by direct replacement, and subsequently by increased endogenous synthesis following improved liver function.
Conflict of interest
Dr Mantle is medical adviser to Pharma Nord (UK) Ltd.
David Mantle (FRSC FRCPath)
Pharma Nord (UK) Ltd
Northumberland NE61 2DB
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