Nutritional Treatment of Heart Disease with

L-carnitine, Coenzyme Q10, Magnesium, and Vitamin E

The use of nutritional supplements in the treatment as well as prevention of disease is clearly the future of medicine. Nutrition is currently going through a renaissance, and the prospects for alleviating suffering and improving the quality of life are very real, and have generated an excitement heretofore unknown. It's not just in the laboratories; clinicians are finding that nutrient and herbal supplements are indeed quite effective if, and only if, the proper combinations at the proper doses are provided to the appropriate sites.

There is a novel nutritional therapy composed of four nutritional factors each one having been shown to be remarkably effective in the treatment (as well as the prevention) of heart disease. This empirical, but effective, formulation aptly illustrates the three fundamental principles of nutritional therapeutics: type, dose, and site.

Cardiac insufficiency (with its plethora of symptoms, including arrhythmias, pulse abnormalities, pressure on the chest, difficulty breathing, and a sense of something being wrong in the area of the heart) is a condition which, if left untreated, will result in heart attack. Although there are many causes of cardiac insufficiency (i.e., atherosclerosis, ischemia, vasospasm), the ultimate biochemical defect is an insufficient supply of cellular energy (i.e., ATP). The combination of L-Carnitine, coenzyme Q10, magnesium, and vitamin E is an extremely effective treatment for cardiac insufficiency, as the nutrients provided cover most of the known mechanisms of cardiac dysfunction.

CCME: L-carnitine, Coenzyme Q10, Magnesium, and Vitamin E
CCME stands for L-Carnitine, Coenzyme Q10, Magnesium, and vitamin E a combination of the most important energy-generating nutrients. This quartet of nutrients regulates the most remarkable process in life, because the process is life, at least multicellular life. Of all the nutritional factors required for life, L-carnitine, coenzyme Q10, magnesium, and vitamin E must be ranked among the most important for optimizing mitochondrial energy production. Other nutrients are essential, to be sure, and the emphasis on CCME should not be interpreted as diminishing the cardiovascular benefits of niacin, riboflavin, pantothenic acid, thiamin, and many other nutrients and food factors.

Carnitine, coenzyme Q10, magnesium, and vitamin E all interact in the mitochondrial generation of energy. Carnitine carries fats across the inner membrane for beta-oxidation. Coenzyme Q10 is the key factor in the electron transport system. Magnesium is an essential cofactor for many of the enzyme systems which support energy production. Moreover, it is required for ATP stability, as ATP is synthesized as the magnesium complex. Vitamin E is in the membrane where it can scavenge the free radicals generated by the electron transport system.

L-carnitine (the rate-determining factor in beta oxidation) increases ATP generation via its effects on beta oxidation, as well as its role in the removal of acetyl units from the mitochondria. The latter process is important because accumulation of acetyl units is known to inhibit various parts of the respiratory process. Other important actions of L-carnitine include vasodilation of the blood vessels and increased ability to sustain cardiac contractions.1 Finally, supplemental L-carnitine has been well-documented to reduce blood and tissue lipids, which is associated with a reduced risk of developing heart disease.6-8

Lipids provide 60-80% of the metabolic energy required by the heart, which explains why such high levels of L-carnitine are stored in cardiac muscle. Moreover, interference with fatty acid oxidation can have dire consequences on myocardial function. Cognizance of L-carnitine's import has led to numerous investigations, the results of which have documented its cardiovascular benefits in both animals2,3 and humans.4-6 Carnitine is perhaps best known for its lipid-lowering activity, specifically, its ability to rapidly and markedly decrease plasma triglycerides7 and increase HDL cholesterol.8

Coenzyme Q10
Coenzyme Q10 is an integral part of the electron transport system, and hence regulates the ATP-generating capabilities. In addition to its well-known role in carrying electrons, recent studies have shown that coenzyme Q10 transports protons for the proton gradient used to drive oxidative phosphorylation. The latter, of course, is required for ATP synthesis. Thus, coenzyme Q10 plays a pivotal role in all energy-generating systems. All organisms with an Electron Transport System have an absolute requirement for coenzyme Q10. Both animal9 and human10,11 studies have unequivocally proven the beneficial effects of supplementary coenzyme Q10 in numerous types of heart disease, as well as hypertension and stroke.12

Magnesium is now recognized as a first-line medicine for the treatment of heart attacks.13-14 A study published in The Lancet, for example, reported the effects of a double-blind, randomized, placebo controlled study in 2,316 patients with suspected myocardial infarction.15 The dose of magnesium was high (about 8.7 grams given intravenously over a 24-hour period), but the results were remarkable: magnesium reduced cardiovascular mortality by 25. The author's conclusion: "Intravenous magnesium sulfate is a simple, safe, and widely applicable treatment. Its efficacy in reducing early mortality of myocardial infarction is comparable to, but independent of, that of thrombolytic or antiplatelet

These findings have been confirmed and reconfirmed in many clinics and laboratories. Teo and colleagues, for example, in an analysis of seven clinical studies, concluded that magnesium (in doses of 5-10 grams by intravenous injection) reduced the odds of death by an astounding 55%.16

Studies of magnesium have revealed it to be Nature's "calcium channel blockerÓ17; unlike its drug counterparts, however, magnesium has no toxic side effects. Another important effect of supplemental magnesium is its ability to mitigate the cardiotoxic effects of catecholamines. Prielipp and associates, for example, published results of a clinical trial in which magnesium (10 mg per kg body weight per hour, or approximately 700 mg per hour for an average adult) attenuated the cardiotoxic effects of epinephrine in 17 bypass patients.18 Interestingly, the drug captopril-an angiotensin-converting enzyme (ACE) inhibitor-has been demonstrated to work by raising intracellular magnesium.19

Vitamin E
The fourth member of this team is vitamin E-the major lipid-soluble antioxidant. A substantial body of evidence has accumulated on vitamin E's therapeutic as well as preventive actions against disease of the heart and blood vessels.20 Supplemental vitamin E, for example, is known to decrease LDL oxidation, which reduces macrophage-mediated (inflammatory) damage to endothelial cells, thereby preventing the production of foam cells and plaque which are characteristic of atherosclerosis.21 By blocking inflammation, vitamin E acts as a primary defense against cardiovascular diseases.

Vitamin E also plays a pivotal role in the inhibition of platelet aggregation.22 Platelets aggregate because arachidonic acid is converted into pro-aggregatory thromboxanes; this conversion is an oxidative process responsive to vitamin E treatment.23 The ability of vitamin E to inhibit platelet aggregation is vitally important, as excessive, uncontrolled platelet aggregation is now acknowledged to be a primary causative factor in myocardial infarction. An ancillary mechanism involves vitamin E's ability to block redox cycling of catecholamine - the net result being a diminution in abnormal sympathetic stimulation of the heart.

Effective, Easy, and Economical
CCME is a combination of four nutrients that individually are documented to be effective in treating heart disease. My recommendations for doses of CCME are listed in Table III. As can be seen, treatment requires higher levels than does prevention of heart disease. CCME is by no means an optimal formulation, as it lacks other cardioprotective nutrients (e.g., vitamin C, B-carotene, taurine, selenium, isoflavonoids, and garlic).

L-carnitine, Coenzyme Q10, Magnesium, and Vitamin E

CCME is, however, therapeutically effective; more importantly, it is practical, hence patient compliance is not a problem. CCME is completely safe, and no toxic side effects have ever been reported (save for the laxative effect of magnesium salts). The icing on the cake is that CCME - in addition to being effective and safe - is very inexpensive as compared with currently prescribed drugs. CCME's cost efficacy is even more impressive when compared to mechanical procedures (e.g., heart transplantation and bypass surgery) that are major contributors to the spiraling cost of health care. CCME is effective, easy, and economical: what more could one possibly expect in clinical medicine?

Reprinted from the Journal of Optimal Nutrition (JON) Vol. 3(3), 1994

1.  Suzuki Y, Kamikawa T, Yamazaki N. Effect of L-carnitine on cardiac hemodynamics. Japanese Heart Journal 22; 219-226, 1981.

2. Challaner D, Mandelbaum L, Elliott W, protective effect of L-carnitine in experimental intoxication with diphtheria toxin. Journal of Laboratory and Clinical Medicine. 77; 616-622, 1971.

3.  McFalls E. Carnitine protection against adriamycin-induced cardiomyopathy in rats. Life Sciences 38; 497-505, 1986.

4.  Kamikawa L, Susuki Y, Kobyashi A, et al. Effects of L-carnitine  on exercise tolerance in patients with stable angina pectoris. Japanese Heart Journal 25; 587-597, 1984.

5. Rebuzzi A, Schiavani G, Amico C, et al. Beneficial effects of L-carnitine  in the reduction of the necrotic area in acute myocardial infarction. Drugs Exptl Clin Res 10; 219-223, 1984.

6. Vacha G, Ginrelli G, Siliprandi M, et al. Favorable effects of L-carnitine  treatment on hypertriglyceridemia in hemodialysis patients: decisive role of low levels of high-density lipoprotein-cholesterol. American Journal of Clinical Nutrition. 38; 532-540, 1983.

7. Pola P, Savi L, Grilli M, et al. Carnitine in the therapy of dyalipidemic patients. Current Therapeutic Research. 27; 208-216, 1980.

8. Ferrari R, Cutchirti F, Visioli G. The metabolic effects of L-carnitine in angina pectoris. International Journal of Cardiology 5; 213-216, 1984.

9. Kishimoto C, Tamaki S, Matsumori A, et al. The protections of coenzyme Q10 against experimental viral myocarditis in mice. Japanese Circulation Journal 48; 1358-1361, 1984.

10. Kamikawa I, Kobayasi A, Yamashita I, et al. Effects of coenzyme Q10 on exercise tolerance in chronic stable angina pectoris. American Journal of Cardiology 56; 247-251, 1985.

11. Judy W, Hall J, Toth P, et al. Long term management of end stage heart failure with coenzyme Q10  in Biomedical and Clinical Aspects of Coenzyme Q10, Vol. 5, K. Folkers and Y Yamamura (editors) Elsevier Science Publishing Company, Inc., New York, 1986, pp. 291-302.

12. Goldenberg I, Cohn J. New inotropic drugs for heart failure. Journal of the American Medical Association 258: 493-496, 1987.

13. Anon. Magnesium for acute myocardial infarction? The Lancet 338: 667-668, 1991.

14. Durlatch J. New trends in international magnesium research. Magnesium Research 5: 23-27, 1992.

15. Woods KL, Fletcher S, Roffe C, et al. Intravenous magnesium sulphate in suspected acute myocardial infarction: results of the second Leicester Intravenous Magnesium Intervention Trial (LIMIT-2). The Lancet 339: 1553-1558, 1992.

16. Teo KK, Yusuf S, collins R, et al. Effects of intravenous magnesium in suspected acute myocardial infarction: overview of randomized trials. British Medical Journal 303: 1499-1503, 1991.

17.  Touyz RM. Magnesium supplementation as an adjuvant to synthetic calcium channel antagonists in the treatment of hypertension. Medical Hypotheses 36: 140-141, 1991.

18. Prielipp KC, Zaloga GP, Butterworth JF, et al. Magnesium inhibits the hypertensive but not the cardiotonic actions of low-dose epinephrine. Anesthesiology, 74:978-979, 1991.

19. O'Keeffe S, Grimes H, Finn J, et al. Effects of captopril therapy on lymphocyte potassium and magnesium concentrations in patients with congestive heart failure. Cardiology 80: 100-105, 1992.

20. Ferrari R, et al. Oxygen free radical-mediated heart injury in animal models and during bypass surgery in humans: effects of alpha-tocopherol. Annals of the New York Academy of Sciences 570: 237-253, 1989.

21. Esterbauer H, et al. The role of vitamin E and carotenoids in preventing oxidation of low density lipoproteins. Annals of the New York Academy of Sciences 570: 254-257, 1989.

22. Jandsk J, et al. Reduction of platelet adhesiveness by vitamin E supplementation in humans. Thrombosis Research 49: 393-404, 1988.

23 Fukusawa K, et al. Vitamin E. Deficiency increases the synthesis of platelet-activating factor (PAF) in rat polymorphonuclear leukocytes. Lipids 24: 236-239, 1989.

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