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Meyer Magarici MD
Venezuelan Systemic Medicine Society
(VSMS) President
Publication date:04/04/06
 


The increase in the number of patients who suffer cardiac insufficiency is alarming, and at the same time it warrants the investigation as to why every day more cases appear.

One of the possible causes is the increase in the popularity of cholesterol reducing medicines (statins), one of which - atorvastatin- is one of the world's greatest selling drugs.

 

These chemical substances act inhibiting an enzyme (HMG-CoA reductase), which blocks cholesterol production; however they also block the production of Co-enzyme (CoQ-10 or Ubiquinone). (Figure 1).

Excessive prescription and the arrival of new more powerful statins, have contributed to the increase in the prevalence and severity of CoQ10 deficiency induced by statins, which has been well documented by clinical studies in humans. (1, 6-9)
 

The Co-enzyme Q-10 is an essential substance in the production of energy derived from carbohydrates, since it acts as a necessary electron transporter for the of oxidative phosphorylation process which occurs in the cellular mitochondria, a process that turns ADP in ATP (the energy containing molecule).

This process generator occurs in all corporal cells, but it acquires greater importance in the myocardial cells, which turns the CoQ10 in a nutrient of critical importance for a normal cardiac function. For that reason, it is reasonable to assume that statins are partly guilty of myocardiopathy and cardiac insufficiency cases increase.

On the other hand, the normal metabolism of our organism continuously produces free oxygen radicals, that also appear when inflammation occurs and as an answer to the physical (ionizing radiations, ultraviolet rays, excess exercise), chemical (environmental contamination, cigarettes) aggressor agents or when there is obstruction of blood flow. The free radicals produce cellular membranes' oxidative damage and also the lipid peroxidation of fats, such as LDL ('bad' cholesterol).

CoQ10 is an important intracellular antioxidant, because he is a great free oxygen radicals scavenger, therefore, it protects the cellular membranes and to the LDL of the oxidative damage that these radicals can cause. CoQ10 induced deficiency by the indiscriminate prescription of statins, but also by the aging process, results in the reduction of antioxidant protection, which leads to oxidative stress and cellular deterioration.

The reduction of the CoQ10 synthesis could also explain the frequently reported adverse effects caused by statins, such as muscular destruction. (2)

On the basis of studies in animals and human beings, several authors have verified that statins CoQ10 induced deficiency can be prevented administering CoQ10, without this affecting statins' capacity to reduce cholesterol. In addition, CoQ10 supplements can contribute to improve cardiac (3) function and resist the adverse effects of the statins. (4,5)

Although millions of people manage to effectively reduce blood cholesterol levels using statins, there are few of those who have noticed that these drugs are dangerous. The potential secondary effects mentioned in the package labels of these products, are: hepatic dysfunction, muscular damage (heart is a muscle) and renal failure.

Additionally, though the consequences of CoQ10 deficiency provoked by statins have been known for many years they have never been sufficiently publicized, especially by the laboratories that produce them. These companies, knowing the obvious importance of CoQ10, patented the combined use of statins+CoQ10. However, the high production costs made them uncompetitive, reason why they preferred not to manufacture these combinations, and not to warn either the doctors and/or patients on the potential risks of the use of statins without CoQ10.

Although the pharmaceutical industry knows how to educate the patients and doctors whenever it launches a new product, this education is very expensive and can only be envisaged when these benefits are protected by patents. CoQ10 is not patentable because it is a natural substance. This explains why many of the doctors who prescribe statins ignore the damage that this be causing to their patients.

Under the optic of systemic medicine, the coenzyme Q10 is an energy adaptogen because it favors ATP synthesis and due to its antioxidant capabilities, it is also an organizational adaptogen which improves organs' structure and function without causing secondary effects. These action mechanisms induce a reduction in cellular chaos (entropy) and provide an endogen auto-healing tendency.

In brief, the daily administration of 100 to 200 mg of CoQ10 improves the energy, structure and cardiac and muscular function, while at the same time reducing the damage caused by statins. Used in combination with another adaptogens it improves the healing potential of myocardiopathy patients.
 

References:

1) Langsjoen PH. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications. Biofactors. 2003;18(1-4):101-11.
2) Rundek T, Naini A, Sacco R, Atorvastatin decreases the coenzyme Q10 level in the blood of patients at risk for cardiovascular disease and stroke. Arch Neurol. 2004 Jun;61(6):889-92.
3) Baggio E., Gandini R., Plancher A.C. Italian multicenter study on safety and efficacy of coenzyme Q10 adjunctive therapy in heart failure. In: Eighth International Symposium on Biomedical and Clinical Aspects of Coenzyme Q (1994) Littarru G.P., Battino M., Folkers K.(Eds) The Molecular Aspects of Medicine, Vol. 15 (Supplement), pp S287-S294.
4) Passi S, Stancato A, Aleo E. Statins lower plasma and lymphocyte ubiquinol/ubiquinone without affecting other antioxidants and PUFA. Biofactors. 2003;18(1-4):113-24.
5) Bargossi AM. Exogenous CoQ10 preserves plasma ubiquinone levels in patients treated with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Int J Clin Lab Res. 1994;24(3):171-6.
6) Strey CH, Young JM, Molyneux SL. Endothelium-ameliorating effects of statin therapy and coenzyme Q10 reductions in chronic heart failure. Atherosclerosis. 2005 Mar;179(1):201-6.
7) Miyake Y, Shouzu A. Effect of treatment with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on serum coenzyme Q10 in diabetic patients. Arzneimittelforschung. 1999 Apr;49(4):324-9.
8) Colquhoun DM, Jackson R, Walters M. Effects of simvastatin on blood lipids, vitamin E, coenzyme Q10 levels and left ventricular function in humans. Eur J Clin Invest. 2005 Apr;35(4):251-8.
9) Mortensen SA, Leth A, Agner E. Dose-related decrease of serum coenzyme Q10 during treatment with HMG-CoA reductase inhibitors. Mol Aspects Med. 1997;18 Suppl:S137-44.

 
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