Urgent Update on Ubiquinone (Coenzyme Q10)

An article in the June 2000 issue of Journal of Orthomolecular Medicine was written to expand upon the material in this web site. Also, to facilitate study of ubiquinone, the article includes references from Langsjoen's "Introduction to Coenzyme Q10" that list the clinical trials and symposia where most of the progress has been made and reported.

Table of Contents

  1. Ubiquinone (coenzyme Q10): Body Pool and Turnover.
  2. Update on Ubiquinone in Stroke.
  3. Plea for Encouragement of "Grass-Roots" Evaluation of Ubiquinone in Stroke

1. Ubiquinone (coenzyme Q10): Body Pool and Turnover.

Ubiquinone and ascorbic acid (AA) are the two most important essential nutrients. They, along with other essential nutrients, have been rejected as unpatentable and unprofitable by certain "interests", according to expose's by Pauling and others [1,2]. These were possibly the most lethal errors of modern medicine because no cell, organ, function, remedy, etc, can avoid failure unless essential nutrients, especially these two, are optimal. Supplementation of both is mandatory: for ascorbate, lifelong (since humans can't synthesize it); for ubiquinone, it is increasingly necessary with age, stress, or disease.

Naturally, much concerning the pharmacokinetics and clinical use of ubiquinone has been learned since the 1970's in the clinical trials and symposia well described in 1995 by one of the leaders in this work, Peter H. Langsjoen, MD, FACC, in his Introduction to Coenzyme Q10. Possibly the most important details not reported previously on this web site are those related to ubiquinone body pool and turnover rate that mandate human supplementation. Adult human body pool has been found to be approximately 2 grams [3,4] and requires replacement of about 0.5 grams/day based on its average turnover rate of about 4 days in various tissues[5]. This must be supplied either by endogenous synthesis or from exogenous sources. Synthesis decreases progressively in humans above age 21. Furthermore, the average ubiquinone content of the western diet is less than 5 mg/day [6]. Thus, ubiquinone supplementation appears to be the only way for older people, and certainly the ill, to obtain the major proportion of the 0.5 gram/day need. Failure to supplement by the aged, ill or stressed, can have tragic consequences in the form of irreversible damage in the brain, other organs and mitochondria everywhere [7,8]. We have a manuscript in process on the systematics of ubiquinone deficiency in terminal disease.

In addition to production of adenosine triphosphate (ATP, molecules for energy), and maintenance of cellular and mitochondrial membrane fluidity, ubiquinone has a possibly even greater value. This is its free radical quenching ability (50 times greater than vitamin E), that prevents the above mentioned irreversible oxidative damage. In Professor Littarru's authoritative 91 page book, he devotes 65 pages (71%) to ubiquinone's defense against free radical damage [9]. He points out that knowledge of mitochondrial aging in unsupplemented mammals has been published since 1985 [9]. See Littarru's references and those in Ernster et al 1995 [5] for: early findings by Cutler that mammalian aging is accelerated by peroxidation and slowed by defense processes [10]; Linnane et al that aging mutations occur at a very high rate in mitochondria (compared to intranuclear DNA which are stabilized by histones) if ubiquinone, AA, etc are low [11]. In this aging mechanism Littarru and others have also stated that low values of ubiquinone permit oxidative damage to the DNA of mitochondria to accumulate, permanently and progressively impairing their ability to function. If, by supplementation, the ubiquinone level is restored to its proper value, the rate of oxidative damage will be lessened, but the impairment remains.

Because of its free radical dependence (in contrast to glycation), this process gives increased emphasis to the importance of the theory of aging proposed by Denham Harman in the 1960's [12, 13]. Actually, Harman first integrated the theoretical and experimental work (by himself and others) to predict in 1972 that mitochondrial aging is a principal cause of early death [14]. Doesn't it appear that physicians who tell their patients not to take ubiquinone, are saying: "Age more rapidly, have more health problems including cardiopathy, intellectual impairment (especially strokes), etc, and die early"? Isn't this what is happening in America today?

2. Update on Ubiquinone in Stroke.

Since 1972, in studies of stroke in three animal models (dog, rat, gerbil) ubiquinone was the only agent giving complete protection and this was over two times more often than the next best agent (naloxone) of the many tested to date. Some of the animals were pretreated and some post-stroke (less than 12 hrs). At the February 2000 annual winter meeting of the American Stroke Association, failures to produce any beneficial effect on stroke outcome by three new pharmaceuticals in large clinical trials were reported. Drug companies around the world have invested vast amounts of time and money into development of brain-protecting drugs over the past decade. Overall, about 50 potential drugs have been tried in humans; only a few are still being tested. The rest have been abandoned. It seems unlikely that those doing research on these agents could be unfamiliar with the ubiquinone results in the three animal models. If mainstream medicine has any humanistic motivation, why doesn't it use ubiquinone in the interim?

The first human observation using ubiquinone in stroke was in a patient predicted by the very experienced stroke specialists in a large California facility to remain permanently comatose. But, she recovered completely after about 10 days in coma [15]. She had been in treatment for a memory problem with oral ubiquinone 400 mg/day for a month prior to an accidental head trauma with massive hemorrhage. In a second case (unpublished), a woman in her 60's, the mother of Dr. H. H. Fudenberg's former secretary, had a similar stroke with the same prognosis of permanently vegetative; he traveled from South Carolina to Oklahoma, got the patient out of hospital and gave her 400 mg ubiquinone b.i.d. (starting four days post-stroke, which we felt would be too late) and she recovered to much better than her pre-stroke condition (i.e., mental acuity, speech, agility, equal to what she had experienced in her 40's). There has been a third case which we "do not advertise" because it is extremely important to elevate ubiquinone as rapidly as possible to minimize the ischemic reperfusion injury. This is a 70 year old professional dancer in Seattle who was given ubiquinone in similar oral dosing starting on the 11th day and made progress much above predicted; he regained speech and ability to do dance steps but had difficulty with names and his recovery plateaued after a few weeks; his stroke was not comatose and his recovery was not complete to his pre-stroke condition.

3. Plea for Encouragement of "Grass-Roots" Evaluation of Ubiquinone in Stroke.

Can't the medical (and lay) readers of this web site help stimulate a grass-roots evaluation of this simple innocuous treatment? We emphasize that we are not advising people to self-treat. However, everyone must realize that, each year in the U.S. alone, over 650,000 families have a loved one hospitalized for stroke. Only one-fourth of these escape death or permanent disability. The families have a right to know that ubiquinone exists at their health food stores, has the properties described above and appears likely to avert the tragic prognoses. If you pass this information to such families, many, in their desperation, may elect ubiquinone. We request that you suggest: (1) this be done with the best open-minded preventive medicine supervision available (and all such physicians be made aware of this web site); and (2) the supervising physician report by email (apresi@aol.com) the patient identification, date of stroke, treating stroke center, prognosis, time delay before ubiquinone (swallowed or intubation), dosage including other agents, and progress up to 4 weeks post-stroke.

References

  1. Pauling LJ: How to live longer and feel better. New York, Avon Books, 1987; 413.
  2. Ely JTA: Ascorbic Acid and Some Other Modern Analogs of the Germ Theory, J Orthomol Med, 1999; 14: 143-156.
  3. Bliznakov EG, Wilkins DJ: Biochemical and clinical consequences of inhibiting Coenzyme Q10 biosynthesis by lipid-lowering HMG-CoA reductase inhibitors (statins): A critical overview. Advances in Therapy, 1998; 15(4), 218-28.
  4. Kalen A, Appelkvist E-L, Dallner G: Age related changes in the lipid composition of rat and human tissue. Lipids, 1989; 24: 579-584.
  5. Ernster L, Dallner G: Biochemical, physiological and medical aspects of ubiquinone function. Biochim Biophys Acta, 1995; 1271: 195-204.
  6. Weber C, Bysted A, Holmer G: The coenzyme Q10 content of the average Danish diet. Int J Vitam Nutr Res. 1997; 67: 123-129.
  7. Bliznakov E. Aging, mitochondria, and coenzyme Q10: The neglected relationship. Biochimie, 1999; 81:1131-1132.
  8. Linnane AW, Kovalenko S, Gingold EB: The universality of bioenergetic disease: age associated cellular bioenergetic degradation and amelioration therapy. Ann NY Acad Sci, 1998; 854: 202-213.
  9. Littarru GP: Energy and Defense. Roma, Casa Editrice Scientifica Internazionale. 1995; 91. ISBN 88-86062-24-9.
  10. Cutler RG: Peroxide-producing potential of tissues: Inverse correlation with longevity of mammalian species. Proc Natl Acad Sci USA, 1985; 82: 4798-4802.
  11. Linnane AW, Marzuki S, Ozawa T, Tanaka M: Mitochondrial DNA mutations as an important contributor to aging and degenerative diseases. Lancet, 1989; 25: 642-645.
  12. Harman D: Prolongation of life: role of free radical reactions in aging. J Am Geriatr Soc. 1969; Aug; 17(8): 721-35.
  13. Harman D: The aging process. Proc Natl Acad Sci U S A. 1981; Nov. 78(11): 7124-8.
  14. Harman D: The biological clock: The mitochondria? J Am Geriatr Soc, 1972; 20(4):145-47.
  15. Ely JTA, Fudenberg HH, Bliznakov EG, Branch JD: Hemorrhagic Stroke in human pretreated with coenzyme Q10: Exceptional recovery as seen in animal models. J Orthomol Med, 1998; 13(2): 105-109.



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