Coenzyme Q10
Hemmi N. Bhagavan, Ph.D., F.A.C.N.
Coenzyme Q10 (CoQ10), a naturally occurring compound and antioxidant, is critical to humans for the production of energy. It belongs to the homologous series of compounds called coenzyme Q that share the same basic ring structure but differ in the length of the "isoprenoid" side chain. Because of their wide and ubiquitous distribution in nature, these compounds are also called ubiquinones. CoQ10 stands for CoQ with 10 isoprene units and it is the form present in humans and several other species. CoQ compounds play an essential role in the production of cellular energy in most aerobic organisms, from humans to plants and bacteria (Bliznakov, 1987).
Although CoQ10 is sometimes referred to as a vitamin, by strict definition it does not meet one criteria necessary for this distinction. CoQ10 is a naturally occurring compound that is synthesized in our body. Vitamins, on the other hand, are essential nutrients that are not produced in the body and must be supplied by exogenous sources. CoQ10 could be called a conditionally "essential nutrient" since its production in the body may not meet the needs under certain conditions. Data show that CoQ10 production in the body is reduced as we age. There are other pathologic conditions where CoQ10 status is compromised. Those tissues and organs with high energy requirements such as the heart, liver, skeletal muscle are ones readily affected when CoQ10 supply becomes limiting.
Research conducted during 1960s and 1970s clearly established the role of CoQ10 as a key component of the mitochondrial electron transport system (also known as the respiratory chain) where biological energy in the form of ATP (adenosine triphosphate) is produced. CoQ10 serves as the critical cofactor for at least three mitochondrial enzymes enabling the transfer of electrons between the donors and recipients. Thus, CoQ10 plays an essential role in the synthesis of ATP, the energy that drives all cellular activities and without which cells cease to function (Crane, 2001).
In addition to this role, CoQ10 also functions as an important fat-soluble antioxidant that can regenerate other antioxidants and a membrane stabilizer (Ernster and Dallner, 1995; Crane 2001).
CoQ10 deficiency has been observed in various disease processes such as congestive heart failure (CHF), cardiomyopathy, chronic obstructive pulmonary disease (COPD), acquired immunodeficiency syndrome (AIDS), cancer, hypertension and periodontal disease. The heart has the highest concentration of CoQ10 and it is therefore not surprising that the early clinical trials on the therapeutic potential of CoQ10 focused on heart disease as the target. Dr. Yuichi Yamamura in Japan was the first to demonstrate the clinical efficacy of CoQ in heart failure as far back as in 1967 (Yamamura et al, 1967). Dr. Karl Folkers followed this up and in 1985, he along with Dr. Svend Mortensen and his colleagues demonstrated a strong correlation between CHF and the tissue levels of CoQ10 (Mortensen et al, 1985). The original Japanese findings on the clinical efficacy of CoQ10 in CHF have now been confirmed in numerous clinical trials carried out in several other countries (Langsjoen and Langsjoen, 1998; 1999). In addition to CHF, there are other cardiovascular diseases that have been successfully treated with CoQ10 supplementation. Among these are diastolic dysfunction, angina pectoris, hypertension, ventricular arrhythmias, mitral valve prolapse and also drug induced cardiotoxicities (Sinatra, 1998). In most of these studies, CoQ10 treatment was employed as an adjunct to standard medical therapy.
Among the other conditions where the therapeutic value of CoQ10 has been demonstrated are diseases involving mitochondrial dysfunction such as mitochondrial cytopathies, neurodegenerative diseases such as Parkinson's and Huntington's and immune system disorders (Fuke et al, 2000; Shults et al., 2002).
The advent of the new generation of cholesterol lowering drugs called HMG-CoA reductase inhibitors (also known as "statins") has brought forth a unique and an unexpected interaction with CoQ10. Statins have become very popular and are being widely prescribed to lower cholesterol and thus reduce the risk for heart disease. These drugs block cholesterol production in the body by inhibiting the enzyme called HMG-CoA reductase in the early steps of its synthesis in the mevalonate pathway. However, the same biosynthetic pathway is also shared by CoQ10. Therefore, one unfortunate consequence of statins is the unintentional inhibition of CoQ10 synthesis eventually resulting in CoQ10 deficiency and associated health problems.
Thus, in the long run, statin drugs could predispose the patients to heart disease by lowering their CoQ10 status, the very condition that these drugs are intended to prevent. Dr. Emile Bliznakov, an authority on CoQ10, recently published a scholarly review on the interaction between statins and CoQ10 (Bliznakov, 2002, Bliznakov and Wilkins, 1998). In addition to statins, there are other classes of drugs that inhibit endogenous CoQ10 synthesis. Among these are beta blockers and hypoglycemic agents. An antagonism between warfarin and CoQ10 has been reported (Fuke et al, 2000).
Disclaimer. This material has been provided for information purposes only and should not be construed as recommendations. Please consult your health care provider first if you have any health problems.