Coenzyme Q:The Ubiquitous Quinone
Part III

This article first appeared in the
November, 1993
issues of VRP's newsletter

Coenzyme Q: The Ubiquitous Quinone Part I

Coenzyme Q: The Ubiquitous Quinone Part II

Coenzyme Q: The Ubiquitous Quinone Part III


by A.S. Gissen
In part 2 of our review of Coenzyme Q10 (CoQ10), we examined the broad spectrum of research into CoQ's role in varied conditions such as cancer, muscular dystrophies, physical performance and athletics, diabetes, and periodontal disease. In the third and final part of our look at CoQ, we will explore the role that CoQ10 plays in immune function, antioxidant protection, and brain function.

CoQ and Immune Function
Vitamin and nutritional deficiencies are well known to be common causes of immunodeficiencies. Persons having nutritional and vitamin deficiencies have impaired cell-mediated immunity, as well as decreased microbicidal activity of immune cells and increased susceptibility to infections. Being vitally important to the generation of cellular energy, it is not surprising that deficiencies of CoQ result in suppression of the immune system. However, the result of supplemental CoQ10 is quite provocative, as it produces a significant enhancement of the immune system in both normal and immuno-depressed animals.

In 1970, it was first reported that CoQ6 and CoQ10, when administered to rats, significantly enhanced the activity of immune cells' ability to kill bacteria, as well as elevating their antibody response.(44) By 1982, more than half a dozen studies had documented significant immunological enhancement following the administration of CoQ10. These results included decreasing the number of tumors, and increasing the number of survivors, following exposure to carcinogens;(45) increasing the number of survivors following exposure of rats to a leukemia-inducing virus, which interestingly caused a CoQ deficiency after infection;(46) and reversing an age-related decrease in CoQ levels in the thymus of aging animals.(47) The immune potentiating activity of CoQ was paralleled by a protection of immune-suppressed animals against otherwise lethal infections.(48) When compared to other antioxidants like vitamin E, it was found that these immune-enhancing properties were specific to CoQ, as the antioxidants did not stimulate the immune system to an equal degree.(49) A similar activity of CoQ10 was also found in human patients with conditions such as diabetes, cancer, and cardiovascular disease, with CoQ10 administration resulting in significantly enhanced levels of immunoglobulins (IgG).(50)

At a 1981 conference on Coenzyme Q, several reviews were presented that documented the significant role that CoQ has on immune function.(51) The conclusions of these researchers were that:

1. In extensive studies, using many experimental models which evaluated various parameters of immune function (phagocytic rate, antibody level, cancer, viral, and parasitic infections), a role of CoQ as an immuno-modulating agent was established.

2. During some infections and aging, an organism develops a Coenzyme Q- enzyme deficiency.

3. Results indicate that CoQ is an important component, probably at the mitochondrial level, for the optimal function of the immune system.

4. The lack of toxicity, as demonstrated in clinical and experimental tests, indicates that CoQ10 is an appropriate candidate for clinical application in disease states where the immune system is not functioning at an optimal level.

5. Research indicates that tumors, infections, and some of the immunity-related "diseases of aging" should be included in a new entity, "diseases of bioenergetics."

CoQ and AIDS
While the above results are certainly provocative, the most exciting immune-related research on CoQ10 has been in the area of Acquired Immune Deficiency Syndrome (AIDS). In the early 1990's, a series of reports were published showing that CoQ10 deficiency could play a role in the development of AIDS. These investigations were begun after the observation that, among other things, many AIDS patients have significant heart-function failure, similar to persons with CoQ10-deficiency related heart-failure.(52) Subsequent measurements of blood CoQ10 levels revealed that Human Immunodeficiency Virus (HIV) positive patients that were asymptomatic had normal levels of CoQ10, Aids Related Complex (ARC) patients had significantly lower levels, and full- blown AIDS patients had the lowest levels. Thus, AIDS was associated with CoQ10 levels that were severely and significantly depressed, while HIV-positive persons without symptoms had normal levels that declined as they progressed to ARC, and further declined as they developed AIDS. Based on these investigations, a small pilot-study was begun to investigate the effects of CoQ10 supplementation on patients with ARC and AIDS. The results of this study showed that ARC patients on CoQ10 therapy remained free of opportunistic infections and didn't progress to AIDS over a period of more than 4 years. The authors concluded that this excellent clinical response was possibly because, "... the delicate equilibrium between host and virus has been tipped in favor of the host in this disease state through the use of oral CoQ10."(52)

CoQ and Peroxidation
Free-radical mediated lipid-peroxidation appears to be of critical importance in various degenerative diseases, including atherosclerosis. Studies have suggested that the oxidative modification of low-density lipoprotein (LDL) is central to the induction of atherosclerotic changes in blood vessels. In research comparing the relative effectiveness of various antioxidants in preventing free-radical induced peroxidation of LDL, CoQ10 was found to be more effective than either lycopene (a carotenoid), beta- carotene, or vitamin E.(53) This effect was specific to the reduced form of CoQ10 (ubiquinol), and not oxidized CoQ10 (ubiquinone). Although oxidized CoQ10 (ubiquinone) is the only supplemental form of CoQ10, other studies have shown that dietary supplementation with CoQ10 results in increased levels of reduced CoQ10 (ubiquinol) within circulating lipoproteins, as well as increased resistance of LDL to the initiation of lipid peroxidation.(54) It appears that after oral supplementation, CoQ10 appears mainly in its reduced, antioxidant form in the body. Not surprisingly, research has shown that the ratio LDL to CoQ10 is an important indicator of the risk of developing atherosclerosis, being even more important than the often cited ratio of HDL to total cholesterol.(55) Indeed, while CoQ10 has been repeatedly shown to be a physiologically important lipid-soluble antioxidant, it may be the most important lipid-soluble antioxidant.

CoQ and Brain Function
It is well established that deficiencies of myocardial CoQ10 results in derangements of cardiac energy production, eventually leading to cardiac cell death. This is the biochemical basis for the success in using CoQ10 in cardiomyopathy. Recent evidence now shows that a similar mechanism may be involved in degenerative brain disorders. In the case of Parkinson's disease, research has shown that deficiencies in CoQ10-dependant enzymes may play a part in the development of the cell death that results in Parkinson's disease.(56) In Alzheimer's disease, as well, deficiencies of CoQ10-dependent enzymes have been found.(57) Attempts to improve the mental functions in Alzheimer's patients have been very encouraging, with reversals of mental deterioration being documented in several studies, including those using genetically-confirmed Alzheimer's patients.(58) Although these preliminary studies await confirmation, it is not surprising that CoQ10 deficiencies, leading to cellular energy deficiencies, would result in the cell death that is a hallmark of both Parkinson's and Alzheimer's disease In fact, the use of supplemental CoQ10 to prevent brain deterioration has been an indicated use of CoQ10 for many years in Japan.(59)

Using Coenzyme Q10
With the vast amount of positive results that have been published about CoQ10 in the last three decades, it is not surprising that CoQ10 has become one of the best- selling supplements in the United States. Few dietary supplements are as well proven, or hold as much potential for improving health, as does CoQ10. However, as with any biologically-active dietary supplement, how CoQ10 is used is important in order to attain maximum benefit from supplementation.

CoQ10 is fat-soluble, and like most other fat-soluble compounds, is poorly absorbed from the gastrointestinal tract, especially when taken on an empty stomach. For this reason it is important to take CoQ10 with meals to ensure maximum absorption. The dosage of CoQ10 is also a very important consideration. Although small dosages of CoQ10 will ensure a good dietary amount of CoQ, and prevent the decrease in blood levels seen when purified diets free of CoQ are consumed, they will not significantly raise blood levels in persons with depressed CoQ10 levels due to disease or aging. Human research has found that doses of at least 30 milligrams are needed to significantly raise blood levels of CoQ10.(60) Due to the vast amount of research that has been conducted on CoQ10 supplementation, dosages have varied over a wide range. In most of these studies CoQ10 was administered in two or three divided doses, with meals, throughout the day. The usual dosages used to correct CoQ10 deficiency in disease states has been from 60 to 200 milligrams a day. Also, the increase in blood levels seen after supplementation is not uniform, as some people seem to absorb CoQ10 poorly and require larger doses to attain maximum benefit. One important consideration to keep in mind when determining the appropriate dosage is that despite rarely occurring nausea or gastrointestinal upset, toxicity and side-effects have not been encountered in several decades of clinical use at doses up to several hundred milligrams a day. Younger persons, as well as persons with no CoQ10-related deficiency disease, may wish to supplement with CoQ10 in doses of 10-30 milligrams in one daily dose, or even consider taking 30 milligrams with one meal every other day. CoQ10 is fat-soluble, and has a half-life in the body of several days, so healthy persons can benefit from less frequent supplementation than those who have CoQ10-related diseases, and should take CoQ10 in several doses throughout the day.

When purchasing CoQ10, the purity of the material should be carefully considered. Very few companies in the world manufacture CoQ10, and the pharmaceutical- grade product in its pure state is a bright yellow to orange color. CoQ10 has a very long shelf-life when protected from light and excessive heat, with little deterioration occurring over periods of up to several years at room temperature. When exposed to light, however, CoQ10 will degrade quite rapidly. If a CoQ10 product is being sold at a price that seems to good to be true, it probably is. Production of CoQ10 can barely meet the world-wide demand. Prices are relatively uniform between the different primary manufacturers, and should be among the different retailers.

The following book offers a good general review of CoQ research for the layperson:

E. Bliznakov, Coenzyme Q: The Miracle Nutrient. Bantam Books, NY. 1986.

The following six volume set offers a good review of CoQ research for the scientist:

K. Folkers, et al.(eds): Biomedical and Clinical Aspects of Coenzyme Q, Vol. 1-6, Elsevier Science Publishers, Amsterdam. 1976 - 1991.

References: Part 3
44) E.G. Bliznakov, A.C. Casey, E. Premuzic, Experentia 1970; 26: 953-954. 45) E.G. Bliznakov, Proc Nat Acad Sci USA 1973; 70: 390-394.
46) E.G. Bliznakov, A.C. Casey, T. Kishi, et al, Internat J Vitam Nutr Res 1975; 45: 388-395.
47) E.G. Bliznakov, T. Watanabe, S. Saji, et al, J Med 1978; 9: 337-346.
48) G. Hogenauer, P. Mayer, J. Drews, In: K. Folkers and Y. Yamamura (eds.), Biochemical and Clinical Aspects of Coenzyme Q, Vol. 3. Elsevier / North Holland Biomedical Press, Amsterdam. 1981, p. 325-334.
49) A.C. Casey, E.G. Bliznakov, Chem-Biol Interactions 1972; 5: 1-12.
50) K. Folkers, S. Shizukuishi, K. Takemura, et al, Res Commun Chem Path Pharm 1982; 38: 335-338.
51) E.G. Bliznakov, In: K. Folkers and Y. Yamamura (eds.), Biochemical and Clinical Aspects of Coenzyme Q, Vol. 3. Elsevier / North Holland Biomedical Press, Amsterdam. 1981, p. 311-323.
52) P.H. Langsjoen, P.H. Langsjoen, K. Folkers, In: K. Folkers, G.P. Littarru, and T. Yamagami (eds.), Biochemical and Clinical Aspects of Coenzyme Q, Vol. 6 Elsevier Science Publishers, Amsterdam. 1991, p. 409-415.
53) R. Stocker, V.W. Bowry, B. Frei, Proc Natl Acad Sci USA 1991; 88:1646-1650.
54) D. Mohr, V.W. Bowry, R. Stocker, Biochem Biophys Acta 1992; 1126: 247-253.
55) Y. Hanaki, et al, N Engl J Med 1991; 325: 814-815.
56) T. Matsubara, T. Azuma, S. Yoshida, et al, In: K. Folkers, G.P Littarru, and T. Yamagami (eds.), Biochemical and Clinical Aspects of Coenzyme Q, Vol. 6. Elsevier Science Publishers, Amsterdam. 1991, p. 159-166.
57) C. Edlund, M. Soderberg, K. Kristensson, et al, Biochem Cell Biol 1992; 70: 422-428.
58) M. Imagawa, et al, Lancet 1992; 340: 671.
59) K. Anderson: Orphan Drugs. New York: The Linden Press / Simon & Schuster, 1983, p. 238-239.
60) T. Kishi, T. Okamoto, N. Kanamori, et al, In: K. Folkers and Y. Yamamura (eds.), Biochemical and Clinical Aspects of Coenzyme Q, Vol. 3. Elsevier / North Holland Biomedical Press, Amsterdam. 1981, p. 67-70.

 

 

 

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