CoQ10- Approved in Japan for treatment of Congestive Heart Failure

[Guest guest]

CoQ10- Approved in Japan for treatment of Congestive Heart Failure What does congestive heart failure, gum disease and obesity have in common? Very often, a deficiency of coenzyme Q10 (CoQ10). A lack of CoQ10 has also been implicated in arrhythmias, strokes, hypertension, heart attacks, atherosclerosis, muscular dystrophy and AIDS and many of these diseases can be prevented and treated successfully with CoQ10. Since its discovery and isolation 40 years ago hundreds of clinical research studies have been done on CoQ10 and it is now abundantly clear that this nutrient is absolutely vital to health. Coenzyme Q10 (ubiquinone/ubiquinol) is a fat-soluble quinone with a structure similar to that of vitamin K. It is a powerful antioxidant both on its own and in combination with vitamin E and is vital in powering the body's energy production (ATP) cycle. CoQ10 is found throughout the body in cell membranes, especially in the mitochondrial membranes and is particularly abundant in the heart, lungs, liver, kidneys, spleen, pancreas and adrenal glands. The total body content of CoQ10 is only about 500-1500 mg and decreases with age. CoQ10 was first isolated from beef heart mitochondria by Dr. Frederick Crane of Wisconsin, U.S.A., in 1957. The same year, Professor Morton of England defined a compound obtained from vitamin A deficient rat liver to be the same as CoQ10. Professor Morton introduced the name ubiquinone, meaning the ubiquitous quinone. In 1958, Professor Karl Folkers and coworkers at Merck, Inc., determined the precise chemical structure of CoQ10: 2,3 dimethoxy-5 methyl-6 decaprenyl benzoquinone, synthesized it, and were the first to produce it by fermentation. In the mid-1960's, Professor Yamamura of Japan became the first in the world to use coenzyme Q7 (a related compound) in the treatment of human disease: congestive heart failure. In 1966, Mellors and Tappel showed that reduced CoQ6 was an effective antioxidant. In 1972 Gian Paolo Littarru of Italy along with Professor Karl Folkers documented a deficiency of CoQ10 in human heart disease. By the mid-1970's, the Japanese perfected the industrial technology to produce pure CoQ10 in quantities sufficient for larger clinical trials. Peter Mitchell received the Nobel Prize in 1978 for his contribution to the understanding of biological energy transfer through the formulation of the chemiosmotic theory, which includes the vital protonmotive role of CoQ10 in energy transfer systems. Coenzyme Q10 has received particular attention in the prevention and treatment of various forms of cardiovascular disease. It is highly effective in preventing the oxidation of low-density lipoprotein cholesterol (LDL) which leads to atherosclerosis. Several studies have shown that patients with congestive heart failure and other cardiovascular diseases have significantly lower levels of CoQ10 in their heart tissue than do healthy people and supplementation with as little as 100 mg/day has been shown to markedly improve their condition. CoQ10 is now approved in Japan for the treatment of congestive heart failure. Nutritional factors play an important role in the development and treatment of cardiovascular disease (CVD). However, health care professionals may overlook, or even disregard, some of these factors for several reasons, including inadequate training and conflicting reports in the biomedical literature. This review provides a synopsis of more than two-dozen nutritional approaches to primary and secondary prevention and therapy of CVD. Favorable cardiovascular effects have been reported with the use of unsaturated fatty acids, vegetarian and semi-vegetarian diets, dietary fiber, plant sterols, alcoholic beverages, vitamins (niacin, E, C, B6, B12, folate), minerals (potassium, calcium, magnesium, selenium), conditionally-essential nutrients (coenzyme Q10, L-carnitine, taurine) and botanical agents (garlic, hawthorn, gugulipid). In contrast, trans-fatty acids, oxysterols, homocysteinemia, carbohydrate intolerance, and excessive sodium chloride and iron have been associated with undesirable cardiovascular effects. A nutritional approach to CVD provides a pivotal adjuvant to traditional pharmaceutical and/or surgical interventions by maximizing the likelihood of success in decreasing CVD morbidity and mortality and minimizing the economic and social costs associated with this disease. Possible undesirable consequences of long term nutritional supplementation with vitamin E and of adverse drug-nutrient interactions between the statins and CoQ10 are also considered. Although additional intervention studies are needed, current scientific evidence generally supports nutritional supplementation with these nutrients as an effective adjunctive strategy for CVD control. Coenzyme Q10 is a redox component in the respiratory chain. CoQ10 is necessary for human life to exist; and a deficiency can be contributory to ill health and disease. A deficiency of CoQ10 in myocardial disease has been found and controlled therapeutic trials have established CoQ10 as a major advance in the therapy of resistant myocardial failure. The cardiotoxicity of adriamycin, used in treatment modalities of cancer, is significantly reduced by CoQ10, apparently because the side-effects of adriamycin include inhibition of mitochondrial CoQ10 enzymes. Models of the immune system including phagocytic rate, circulating antibody level, neoplasia, viral and parasitic infections were used to demonstrate that CoQ10 is an immunomodulating agent. It was concluded that CoQ10, at the mitochondrial level, is essential for the optimal function of the immune system. Heart attacks and strokes produce a burst of free radicals (ischemia-reperfusion) which can result in extensive tissue damage. Patients with high CoQ10 levels suffer less damage from these events and Japanese researchers have found that CoQ10 supplementation prior to and immediately following open heart surgery is highly beneficial in preventing reperfusion injury - a common complication in heart surgery. Supplementation with CoQ10 has also been found beneficial in patients with chronic stable angina, mitral valve prolapse and irregular heart beat (arrhythmias). Several studies also indicate that CoQ10 may be beneficial in the treatment of hypertension (high blood pressure). A study of 109 patients with long-standing, essential hypertension, who were on antihypertensive drugs, concluded that supplementation with an average of 225 mg/day of CoQ10 improved functional status, allowed about half the patients to discontinue most of their blood pressure medications and resulted in an average decrease of systolic blood pressure from 159 to 147 mm Hg and a diastolic pressure decrease from 94 to 85 mm Hg. Smaller, more recent Japanese studies have confirmed these findings. Reports from several research groups--including two small double-blind clinical studies--indicate that supplemental coenzyme Q10 (CoQ) is moderately effective as a treatment for hypertension, in humans and in animals. Its efficacy is associated with a decrease in total peripheral resistance, and appears to reflect a direct impact of CoQ on the vascular wall. A reasonable interpretation of these findings is that CoQ is acting as an antagonist of vascular superoxide-- either scavenging it, or suppressing its synthesis. By improving the efficiency of shuttle mechanisms that transfer high-energy electrons from the cytoplasm to the mitochondrial respiratory chain, CoQ may decrease cytoplasmic NADH levels and thereby diminish the reductive power that drives superoxide synthesis in endothelium and vascular smooth muscle. If CoQ therapy does indeed lower vascular superoxide levels, it can be expected to decrease the atherothrombotic risk associated with hypertension, and may have broader utility in the management of disorders characterized by endotheliopathy. Coenzyme Q10 is a great boost to heart health, but it has many other beneficial effects. Physical exercise *reduces* blood levels of CoQ10 and supplementation with 60 mg/day has been found to improve athletic performance. Administration of CoQ10 alone or in combination with vitamin B6 (pyridoxine) boosts the immune system and may be useful in the treatment of AIDS and other infectious diseases. An adequate level of CoQ10 in the body is essential to proper muscle functioning and several studies have indeed shown that supplementation with 100-150 mg/day of CoQ10 markedly improves the condition of people suffering from muscular dystrophy. Many overweight people have very low levels of CoQ10 and supplementation may enable them to lose weight due to the effect of CoQ10 in speeding up the metabolism of fats. CoQ10 has been used with success in combatting periodontal diseases, especially gingivitis (gum disease). Tissue affected by gingivitis is deficient in CoQ10 and experiments have shown that supplementation with as little as 50 mg/day can decrease inflammation. More recent research has shown that topical application of CoQ10 dissolved in soya oil (85 mg/ml) to affected areas (periodontal pockets) reduces bleeding and the depth of the pocket. Research carried out in Denmark has provided some tantalizing evidence that CoQ10 may also be effective in the fight against certain cancers. A trial involving the treatment of 32 breast cancer patients with megadoses of vitamins, minerals, essential fatty acids and coenzyme Q10 (90 mg/day) in addition to conventional therapy showed a highly beneficial effect of the supplementation. Two of the patients in the trial whose tumours had not regressed had their CoQ10 dosages increased to 390 mg/day and 300 mg/day respectively with the result that their tumours disappeared completely within three months. CoQ10 supplementation is also very important for cancer patients undergoing chemotherapy with heart toxic drugs such as adriamycin and athralines. Recent research has also shown that certain cholesterol-lowering drugs (lovastatin, etc.) block the natural synthesis of CoQ10 so supplementation with 100 mg/day is recommended for patients taking these drugs. Despite considerable worldwide efforts, no single etiology has been identified to explain the development of chronic fatigue syndrome (CFS). It is likely that multiple factors promote its development, sometimes with the same factors both causing and being caused by the syndrome. A detailed review of the literature suggests a number of marginal nutritional deficiencies may have etiologic relevance. These include deficiencies of various B vitamins, vitamin C, magnesium, sodium, zinc, L-tryptophan, L-carnitine, coenzyme Q10, and essential fatty acids. Any of these nutrients could be marginally deficient in CFS patients, a finding that appears to be primarily due to the illness process rather than to inadequate diets. It is likely that marginal deficiencies not only contribute to the clinical manifestations of the syndrome, but also are detrimental to the healing processes. Therefore, when feasible, objective testing should identify them and their resolution should be assured by repeat testing following initiation of treatment. Moreover, because of the rarity of serious adverse reactions, the difficulty in ruling out marginal deficiencies, and because some of the therapeutic benefits of nutritional supplements appear to be due to pharmacologic effects, it seems rational to consider supplementing CFS patients with the nutrients discussed above, along with a general high-potency vitamin/mineral supplement, at least for a trial period. The body can synthesize coenzyme Q10 and it is also found in several dietary sources, notably organ meats. The level of CoQ10 in human organs peaks around the age of 20 years and then declines fairly rapidly. The decrease in CoQ10 concentration in the heart is particularly significant with a 77-year-old person having 57 per cent less CoQ10 in the heart muscle than a 20-year-old. Some experts involved in CoQ10 research believe that many people, especially older people and people engaging in vigorous exercise may be deficient in CoQ10 and may benefit from supplementation. The recommended daily dosage for health maintenance is 30 mg; however, considerably higher amounts are required in the treatment of the various diseases for which supplementation has been found beneficial. CoQ10 should be taken with a meal containing some fat or even better, in combination with extra virgin olive oil which enhances its absorption quite substantially. CoQ10 supplements are readily absorbed by the body and no toxic effects have been reported for daily dosages as high as 300 mg. The safety of CoQ10, however, has not been established in pregnancy and lactation, so caution is advised here until more data becomes available. Hans R. Larsen, MSc ChE. Coenzyme Q10: The Wonder Nutrient. International Journal of Alternative and Complementary Medicine, Vol. 16, No 2, February 1998, pp. 11-12. Littarru, Gian Paolo, et al. Clinical aspects of coenzyme Q: Improvement of cellular bioenergetics or antioxidant protection? In Handbook of Antioxidants, eds. Enrique Cadenas and Lester Packer, NY, Marcel Dekker, Inc., 1996, pp. 203-39 PETER H. LANGSJOEN, M.D., F.A.C.C. INTRODUCTION TO COENZYME Q10 Murray, Michael T. Encyclopedia of Nutritional Supplements, Rocklin, CA, Prima Publishing, 1996, pp. 296-308 Research on coenzyme Q10 in clinical medicine and in immunomodulation. Drugs Exp Clin Res (SWITZERLAND) 1985, 11 ( p539-45 Kendler BS. Recent nutritional approaches to the prevention and therapy of cardiovascular disease. Prog Cardiovasc Nurs 1997 Summer;12(3):3-23 Kendler BS. Nutritional strategies in cardiovascular disease control: an update on vitamins and conditionally essential nutrients. Prog Cardiovasc Nurs 1999 Autumn;14(4):124-9 Greenberg, Steven and Frishman, William H. Co-enzyme Q10: A new drug for cardiovascular disease. Journal of Clinical Pharmacology, Vol. 30, 1990, pp. 596-608 Hanaki, Yoshihiro, et al. Ratio of low-density lipoprotein cholesterol to ubiquinone as a coronary risk factor. New England Journal of Medicine, Vol. 325, September 12, 1991, pp. 814-15 Baggio, E., et al. Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure. Molec. Aspects Med., Vol. 15 (suppl), 1994, pp. S287-94 Oda, T. Coenzyme Q10 therapy on the cardiac dysfunction in patients with mitral valve prolapse. Dose vs effect and dose vs serum level of coenzyme Q10. In Biomedical and Clinical Aspects of Coenzyme Q, Vol. 5, eds. Folkers, K. and Yamamura, Y., Amsterdam, Elsevier, 1986, pp. 269-80 Langsjoen, P., et al. Treatment of essential hypertension with coenzyme Q10. Molec. Aspects Med., Vol. 15 (suppl), 1994, pp. S265-72 McCarty MF. Coenzyme Q versus hypertension: does CoQ decrease endothelial superoxide generation? Med Hypotheses 1999 Oct;53(4):300-4 Vanfraechem, J.H.P. and Folkers, K. Coenzyme Q10 and physical performance. In Biomedical and Clinical Aspects of Coenzyme Q, Vol. 3, eds. Folkers, K. and Yamamura, Y., Amsterdam, Elsevier, 1981, pp. 235- 41 Folkers, K., et al. The activities of coenzyme Q10 and vitamin B6 for immune responses. Biochemical and Biophysical Research Communications, Vol. 193, May 28, 1993, pp. 88-92 Littarru, G.P., et al. Deficiency of coenzyme Q10 in gingival tissue from patients with periodontal disease. Proceedings of the National Academy of Sciences USA, Vol. 68, 1971, p. 2332 Lockwood, K., et al. Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q10. Biochemical and Biophysical Research Communications, Vol. 199, 1994, pp. 1504-08 Werbach MR. Nutritional strategies for treating chronic fatigue syndrome. Altern Med Rev 2000 Apr;5(2):93-108 Mindell, Earl. Earl Mindell's Vitamin Bible, NY, Warner Books, 1991, p. 289 http://www.evitamins.com/ency_description.asp?encyclopedia=46 & x=18 & y=12