SUMMARY OF A RECENT PUBMED SEARCH AND OTHER MATERIALS

Table of Contents

• PREFACE
• Caution regarding Candida.
• PubMed Abstracts
• An Introduction to Coenzyme Q10
• Urgent Update on Coenzyme Q10
• Clinicians' Electronic Questionaire

NOTICE: The purpose of this site is to inform the public (noninteractively) and its physicians regarding 40 years of progress on Q10 and the implicit mandate in indexed literature to determine if these striking results are reproducible in all clinical specialties. For this to occur at the University of Washington Medical Center, we would need to robot (automate) the complex 14 step HPLC assay sufficiently to make it inexpensive to run and affordable. To determine if the demand for the test justifies this considerable effort, we ask that physicians accomplish the extremely brief electronic questionnaire linked to this page. None of the authors listed here is available for consultation by patients.

Preface (by an Experimenter)

Among both patients and clinicians, many may be surprised to learn that lack of readily available over-the-counter molecules appears to cause more morbidity and mortality than any other factor in populations on the "western" diet. Our manuscript "On the Science of Essential Nutrients" expands upon this concept. Two of these essential molecules, pyridoxine (vitamin B6) and Q10 (Coenzyme Q10 or ubiquinone) have something else in common: Their structures and many of their clinical and biochemical characteristics were determined by Karl Folkers and his coworkers. We won't discuss B6 (and its cofactors Mg and other B vitamins) here except to suggest that the national vascular disease epidemic due to its tragic underuse* has resulted from misconceptions regarding easily avoidable neuropathy not observed when taken properly in large studies (JM Ellis,KS McCully. Res Commun Mol Path Pharm 89(2): 208-220, 1995 and its 20 refs).

*J. Orthomolecular Med. 11(2): 95-99, 1996
(reprints available from the Editor's office 416-733-2117)

All informed medical scientists in my acquaintance agree: (1) the common occurrence of Q10 "deficiency states" and their tragic consequences in numerous disorders are not widely recognized today; although (2) it has been textbook knowledge for decades that Q10 is a molecule that has great importance in bioenergetics in the mitochondria of all human cells; and more recently it has been identified as a vital component of all cell membranes and a most powerful antioxidant. It is synthesized in all tissues (from tyrosine using a complex and easily imperiled process requiring a number of vitamins and trace elements). After age 20, our synthesis of Q10 declines and brain levels are known to fall markedly after age 50. Foods contain very inadequate levels (less than 20 ppm; 15 pounds of peanut butter contain 100 mg, a reasonable daily supplement). In addition, it is reported that certain pharmaceuticals designed to lower cholesterol (unnecessary in most cases, it has also been reported for years, if vitamin E is adequate) block mevalonic acid, a precursor of both cholesterol and Q10! Even a high metabolic rate or strenuous physical work or endurance exercise accelerate Q10 turnover lowering levels unless the increased demands are met. Thus there are a number of common ways blood and tissue levels of Q10 can be low resulting in an unending variety of disorders in the heart, brain, lymphoid tissue and etc throughout the body. Striking results have been reported in many patients with advanced CVD, cancer and infectious diseases simply by oral supplementation of Q10.

Karl Folkers (to whom I first talked prior to my design in the 1980's of an experiment to study the effect of Q10 on thymic involution in young and old mice) and a cardiologist named Peter Langsjoen have been leaders in research and clinical trials on Q10. I list the following abstracts mostly from PubMed to show the flavor of some of their work in cardiology and cancer primarily (and the incredible potential that may exist). Because of a paper we published on possible Q10 protection in human stroke (Ely et al 1996, abstract 15 below), I added two abstracts on the animal work. Unfortunately, there appears to be no convenient economical Q10 blood assay available to facilitate large scale studies. If one were, it would be possible for our cardiologists, oncologists, neurologists, psychiatrists, gerontologists, internists, allergists, immunologists, etc, and patients themselves to determine whether or not symptoms abate with rising blood Q10 (on oral Q10).

Thus, widespread elective supplementation driven by public interest and guided by physician monitoring could provide a basis for controlled trials in many other disorders if justified. This appears possible if there is enough demand for UW Medical Center and Laboratory Medicine to provide the HPLC method as a semi-automated low cost assay of blood Q10. To estimate the test demand, as suggested by ranking experts here in clinical chemistry, I have included a short questionnaire for clinicians on this web site. The quality of care may markedly improve and its cost may be greatly decreased by this simple step. Peter Langsjoen, MD, is a biochemist as well as a cardiologist. A paper is included here that he had written in 1995 for the clinical science community on Q10 (8pp incl 65 refs). Emile G. Bliznakov,MD, has written (with G.L. Hunt) an outstanding comprehensive 240 page text for scientists and lay readers including descriptions of his own extremely important pioneering work that demonstrated the ability of Q10 to restore immune defense against cancer and viral diseases in extremely old animals. Available in paperback from Bantam Books it currently sells for ~$7 at the University Book Store. Also see our Urgent Update on other recent findings including mitrochondrial aging.

CAUTION RE CANDIDA. In some people, absorption of supplemental Q10 from the gut may be very low (see FAQ in Langsjoen's "Introduction..."). We recently conducted a study supporting an Ely hypothesis (see Abstracts 17 and 19 below) that overgrowth of Candida albicans in the gut may explain this problem. Although no side effects have been found for Q10 itself, certain classes of people who have Candida colonizing the region of gut just beyond the stomach (duodenum and proximal jejunum) are likely to encounter two problems. The orally supplemented Q10 may, all or in large part, be consumed by the Candida preventing the human host from elevating Q10 blood levels and gaining the expected benefits. Of possibly much greater concern is this colonization which, from our recent study of the literature, we fear: (1) can result in high mortality unless corrected promptly; (2) has been recognized since the early 1980's and identified as a cause of multiple organ failure and other lethal syndromes (Joshi et al 1981; Roy and McCallum, 1984; Marshall et al, 1988);* (3) has gone unread because of both the time pressures on physicians today and the shear size of the 40 million pp/decade of indexed medical science research literature received at our library (it isn't possible to even turn 40 million pp in a decade); and (4) finally colonization occurs when Candida from the mouth are able to pass thru the stomach because its acid is reduced by any of numerous procedures still common today including over-the-counter proton pump inhibitors and even habitual use of antacid tablets.

*Joshi SN, Garvin PJ, Sunwoo YC. Candidiasis of the duodenum and jejunum. Gastroenterology 1981; 80: 829-33.
Roy A, McCallum RW. Candidiasis of the duodenum: the role of continuous cimetidine therapy. Gastrointestinal Endoscopy 1984; 30: 47-8.
Marshall JC, Christou NV, Horn R, Meakins JL. The microbiology of multiple organ failure. The proximal gastrointestinal tract as an occult reservoir of pathogens. Arch Surg 1988; 123: 309-315.

Selected PubMed Abstracts

Abstract 1

Accession No.: 89095659.

Author: Langsjoen-P-H. Folkers-K. Lyson-K. Muratsu-K. Lyson- T. Langsjoen-P.

Title: Effective and safe therapy with coenzyme Q10 for cardiomyopathy.

Source: Klin-Wochenschr. 1988 Jul 1. 66(13). P 583-90.

Journal Title: KLINISCHE WOCHENSCHRIFT.

Abstract: Coenzyme Q10 (CoQ10) is indispensable in mitochondrial bioenergetics and for human life to exist. 88/115 patients completed a trial of therapy with CoQ10 for cardiomyopathy. Patients were selected on the basis of clinical criteria, X- rays, electrocardiograms, echocardiography, and coronary angiography. Responses were monitored by ejection fractions, cardiac output, and improvements in functional classifications (NYHA). Of the 88 patients 75%-85% showed statistically significant increases in two monitored cardiac parameters. Patients with the lowest ejection fractions (approx. 10%-30%) showed the highest increases (115 delta %-210 delta %) and those with higher ejection fractions (50%-80%) showed increases of approx. 10 delta %-25 delta % on therapy. By functional classification, 17/21 in class IV, 52/62 in class III, and 4/5 in class II improved to lower classes. Clinical responses appeared over variable times, and are presumably based on mechanisms of DNA-RNA-protein synthesis of apoenzymes which restore levels of CoQ10 enzymes in a deficiency state. 10/21 (48%) of patients in class IV, 26/62 (42%) in class III, and 2/5 (40%) in class II had exceptionally low control blood levels of CoQ10. Clinical responses on therapy with CoQ10 appear maximal with blood levels of approx. 2.5 micrograms CoQ10/ml and higher during therapy.

Abstract 2

Accession No.: 85216668.

Author: Langsjoen-P-H. Vadhanavikit-S. Folkers-K.

Title: Response of patients in classes III and IV of cardiomyopathy to therapy in a blind and crossover trial with coenzyme Q10.

Source: Proc-Natl-Acad-Sci-U-S-A. 1985 Jun. 82(12). P 4240-4.

Journal Title: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA.

Abstract: Coenzyme Q10 (CoQ10), a biochemically established redox component of respiration including the coupled mechanisms of electron transfer and oxidative phosphorylation, is naturally present in the human myocardium. A double-blind and double- crossover trial has been conducted by administering CoQ10 and a matching placebo orally to two groups of patients having class III or IV cardiomyopathy (classification according to criteria of the New York Heart Association). Group A received CoQ10 and then placebo; group B received placebo and then CoQ10. Blood levels of CoQ10 and cardiac function were determined at 0 and 4 weeks (control stabilization period) and at 16 and 28 weeks (after the 12-week CoQ/placebo-treatment periods). For group A, significant increases in CoQ10 blood levels and cardiac function occurred during CoQ10 treatment and then decreased during crossover to placebo. For group B, there was no change in CoQ10 blood levels and cardiac function during placebo treatment, but increases in both parameters occurred in crossover to CoQ10. These patients, steadily worsening and expected to die within 2 years under conventional therapy, generally showed an extraordinary clinical improvement, indicating that CoQ10 therapy might extend the lives of such patients. This improvement could be due to correction of a myocardial deficiency of CoQ10 and to enhanced synthesis of CoQ10-requiring enzymes.

Abstract 3

Accession No.: 86274037.

Author: Langsjoen-P-H. Vadhanavikit-S. Folkers-K.

Title: Effective treatment with coenzyme Q10 of patients with chronic myocardial disease.

Source: Drugs-Exp-Clin-Res. 1985. 11(8). P 577-9.

Journal Title: DRUGS UNDER EXPERIMENTAL AND CLINICAL RESEARCH.

Abstract: Nineteen patients with chronic myocardial disease (NYHA Classes III and IV) were given Coenzyme Q10 in a controlled double- blind cross-over study. All had either low or borderline levels of CoQ10 in their blood, and showed a significant change into the normal range with oral CoQ10 replacement. Eighteen patients reported improvement in activity tolerance with replacement therapy. Combined clinical observations, stroke volume measured by impedance cardiography, and ejection fractions calculated from systolic time intervals, all showed significant improvement in parallel with CoQ10 administration. This application of the principles of bioenergetics introduces a promising new dimension to the study and treatment of the complex problem of myocardial failure.

Abstract 4

Accession No.: 92118020.

Author: Folkers-K. Langsjoen-P. Langsjoen-P-H.

Title: Therapy with coenzyme Q10 of patients in heart failure who are eligible or ineligible for a transplant.

Source: Biochem-Biophys-Res-Commun. 1992 Jan 15. 182(1). P 247-53.

Journal Title: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS.

Abstract: Twenty years of international open and seven double blind trials established the efficacy and safety of coenzyme Q10 (CoQ10) to treat patients in heart failure. In the U.S., ca. 20,000 patients under 65 years are eligible for transplants, but donors are less than 1/10th of those eligible, and there are many more such patients over 65, both eligible and ineligible. We treated eleven exemplary transplant candidates with CoQ10; all improved; three improved from Class IV to Class I; four improved from Classes III-IV to Class II; and two improved from Class III to Class I or II. After CoQ10, some patients required no conventional drugs and had no limitation in lifestyle. The marked improvement is based upon correcting myocardial deficiencies of CoQ10 which improve mitochondrial bioenergetics and cardiac performance. These case histories, and very substantial background proof of efficacy and safety, justify treating with CoQ10 patients in failure awaiting transplantation.

Abstract 5

Accession No.: 91115532.

Author: Langsjoen-P-H. Langsjoen-P-H. Folkers-K.

Title: A six-year clinical study of therapy of cardiomyopathy with coenzyme Q10. Source: Int-J-Tissue-React. 1990. 12(3). P 169-71.

Journal Title: INTERNATIONAL JOURNAL OF TISSUE REACTIONS.

Abstract: One hundred and forty-three cases of chronic, stable, non- secondary, non-hypertrophic cardiomyopathy, 98% of whom were in NYHA Classes III and IV, were given 100 mg of coenzyme Q10** orally in addition to their conventional medical programme in an open-label long-term study. Blood CoQ10 levels, clinical status, myocardial function and survival have been recorded now for almost 6 years. Mean control/CoQ10 levels of 0.85 micrograms/ml rose to 2 micrograms/ml in 3 months and remained stable at that level. Mean ejection fraction of 44% measured by systolic time interval analysis rose to 60% within 6 months and stabilized at that level with 84% of patients showing statistically significant improvement. Eighty-five percent of patients improved by one or two NYHA Classes. Survival figures were encouraging with an 11.1% mortality in 12 months and 17.8% mortality in 24 months, comparing favourably with several reports in the literature. There was no positive evidence of toxicity or intolerance in a total of 368.9 patient-years of exposure. Coenzyme Q10 is safe and effective long-term therapy for chronic cardiomyopathy. (**Ely estimate: $1/day retail!)

Abstract 6

Accession No.: 91115531.

Author: Langsjoen-P-H. Folkers-K. Lyson-K. Muratsu-K. Lyson- T. Langsjoen-P.

Title: Pronounced increase of survival of patients with cardiomyopathy when treated with coenzyme Q10 and conventional therapy.

Source: Int-J-Tissue-React. 1990. 12(3). P 163-8.

Journal Title: INTERNATIONAL JOURNAL OF TISSUE REACTIONS.

Abstract: During 1982-86, 43/137 patients with cardiomyopathy, Classes II, III and IV, had ejection fractions (EF) below 40%, and a mean EF of 25.1 +/- 10.3%. During treatment of these 43 patients with coenzyme Q10 (CoQ10), EF increased to 41.6 +/- 14.3% (p less than 0.001) over a mean period of 3 months (range, 2-4 months). At four subsequent periods up to 36 months. EF ranged from 43.1 +/- 13.3 to 49.7 +/- 6.4% (each period, p less than 0.001). The mean CoQ10 control blood level was 0.85 +/- 0.26 micrograms/ml which increased on treatment to 1.7 to 2.3 micrograms/ml for five periods up to 36 months (each period, p less than 0.001). The survival rates for all 137 patients treated with CoQ10 and for the 43 patients with EF below 40% were both about 75%/46 months. These two survival rates were comparable between 24 and 46 months, which is of extraordinary significance and importance when compared to** survival of about 25%/36 months for 182 patients with EF below 46% on conventional therapy without CoQ10. The improved cardiac function and pronounced increase of survival show that therapy with CoQ10 is remarkably beneficial due to correction of CoQ10 deficiency in mechanisms of bioenergetics.(**Ely: Survival 3:1 !)

Abstract 7

Accession No.: 90164427.

Author: Langsjoen-P-H. Langsjoen-P-H. Folkers-K.

Title: Long-term efficacy and safety of coenzyme Q10 therapy for idiopathic dilated cardiomyopathy.

Source: Am-J-Cardiol. 1990 Feb 15. 65(7). P 521-3.

Journal Title: AMERICAN JOURNAL OF CARDIOLOGY.

Abstract: (Ely:no Abstract in Medline)

Abstract 8

Author: Lockwood-K. Moesgaard-S. Yamamoto-T. Folkers-K.

Title: Progress on therapy of breast cancer with vitamin Q10 and the regression of metastases.

Source: Biochem-Biophys-Res-Commun. 1995 Jul 6. 212(1). P 172-7.

Journal Title: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS.

Abstract: Over 35 years, data and knowledge have internationally evolved from biochemical, biomedical and clinical research on vitamin Q10 (coenzyme Q10; CoQ10) and cancer, which led in 1993 to overt complete regression of the tumors in two cases of breast cancer. Continuing this research, three additional breast cancer patients also underwent a conventional protocol of therapy which included a daily oral dosage of 390 mg of vitamin Q10 (Bio-Quinone of Pharma Nord) during the complete trials over 3-5 years. The numerous metastases in the liver of a 44-year-old patient "disappeared," and no signs of metastases were found elsewhere. A 49-year-old patient, on a dosage of 390 mg of vitamin Q10, revealed no signs of tumor in the pleural cavity after six months, and her condition was excellent. A 75-year-old patient with carcinoma in one breast, after lumpectomy and 390 mg of CoQ10, showed no cancer in the tumor bed or metastases. Control blood levels of CoQ10 of 0.83-0.97 and of 0.62 micrograms/ml increased to 3.34-3.64 and to 3.77 micrograms/ml, respectively, on therapy with CoQ10 for patients A-MRH and EEL.

Abstract 9

Accession No.: 95272328.

Author: Lockwood-K. Moesgaard-S. Hanioka-T. Folkers-K.

Title: Apparent partial remission of breast cancer in 'high risk' patients supplemented with nutritional antioxidants, essential fatty acids and coenzyme Q10.

Source: Mol-Aspects-Med. 1994. 15 Suppl. P s231-40.

Journal Title: MOLECULAR ASPECTS OF MEDICINE.

Abstract: Thirty-two typical patients with breast cancer, aged 32- 81 years and classified 'high risk' because of tumor spread to the lymph nodes in the axilla, were studied for 18 months following an Adjuvant Nutritional Intervention in Cancer protocol (ANICA protocol). The nutritional protocol was added to the surgical and therapeutic treatment of breast cancer, as required by regulations in Denmark. The added treatment was a combination of nutritional antioxidants (Vitamin C: 2850 mg, Vitamin E: 2500 iu, beta-carotene 32.5 iu, selenium 387 micrograms plus secondary vitamins and minerals), essential fatty acids (1.2 g gamma linolenic acid and 3.5 g n-3 fatty acids) and Coenzyme Q10 (90 mg per day). The ANICA protocol is based on the concept of testing the synergistic effect of those categories of nutritional supplements, including vitamin Q10, previously having shown deficiency and/or therapeutic value as single elements in diverse forms of cancer, as cancer may be synergistically related to diverse biochemical dysfunctions and vitamin deficiencies. Biochemical markers, clinical condition, tumor spread, quality of life parameters and survival were followed during the trial. Compliance was excellent. The main observations were: (1) none of the patients died during the study period. (the expected number was four.) (2) none of the patients showed signs of further distant metastases. (3) quality of life was improved (no weight loss, reduced use of pain killers). (4) six patients showed apparent partial remission.

Abstract 10

Accession No.: 94197748.

Author: Lockwood-K. Moesgaard-S. Folkers-K.

Title: Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q10.

Source: Biochem-Biophys-Res-Commun. 1994 Mar 30. 199(3). P 1504-8.

Journal Title: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS.

Abstract: Relationships of nutrition and vitamins to the genesis and prevention of cancer are increasingly evident. In a clinical protocol, 32 patients having -"high-risk"- breast cancer were treated with antioxidants, fatty acids, and 90 mg. of CoQ10. Six of the 32 patients showed partial tumor regression. In one of these 6 cases, the dosage of CoQ10 was increased to 390 mg. In one month, the tumor was no longer palpable and in another month, mammography confirmed the absence of tumor. Encouraged, another case having a verified breast tumor, after non-radical surgery and with verified residual tumor in the tumor bed was then treated with 300 mg. CoQ10. After 3 months, the patient was in excellent clinical condition and there was no residual tumor tissue. The bioenergetic activity of CoQ10, expressed as hematological or immunological activity, may be the dominant but not the sole molecular mechanism causing the regression of breast cancer.

Abstract 11

Accession No.: 93277598.

Author: Folkers-K. Morita-M. McRee-J-Jr.

Title: The activities of coenzyme Q10 and vitamin B6 for immune responses.

Source: Biochem-Biophys-Res-Commun. 1993 May 28. 193(1). P 88-92.

Journal Title: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS.

Abstract: Coenzyme Q10 (CoQ10) and vitamin B6 (pyridoxine) have been administered together and separately to three groups of human subjects. The blood levels of CoQ10 increased (p less than 0.001) when CoQ10 and pyridoxine were administered together and when CoQ10 was given alone. The blood levels of IgG increased when CoQ10 and pyridoxine were administered together (p less than 0.01) and when CoQ10 was administered alone (p less than 0.05). The blood levels of T4-lymphocytes increased when CoQ10 and pyridoxine were administered together (p less than 0.01) and separately (p kess than 0.001). The ratio of T4/T8 lymphocytes increased when CoQ10 and pyridoxine were administered together (p less than 0.001) and separately (p less than 0.05). These increases in IgG and T4- lymphocytes with CoQ10 and vitamin B6 are clinically important for trials on AIDS, other infectious diseases, and on cancer.

Abstract 12

Accession No.: 93236579.

Author: Folkers-K. Brown-R. Judy-W-V. Morita-M.

Title: Survival of cancer patients on therapy with coenzyme Q10.

Source: Biochem-Biophys-Res-Commun. 1993 Apr 15. 192(1). P 241-5.

Journal Title: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS.

Abstract: Over ca. 25 years, assays in animal models established the hematopoietic activities of coenzyme Q's in rhesus monkeys, rabbits, poultry, and children having kwashiorkor. Surprisingly, a virus was found to cause a deficiency of CoQ9. Patients with AIDS showed a-"striking"-clinical response to therapy with CoQ10. The macrophage potentiating activity of CoQ10 was recorded by the carbon clearance method. CoQ10 significantly increased the levels of IgG in patients. Eight new case histories of cancer patients plus two reported cases support the statement that therapy of cancer patients with CoQ10, which has no significant side effect, has allowed survival on an exploratory basis for periods of 5-15 years. These results now justify systematic protocols.

Abstract 13

Accession No.: 86149560.

Author: Ogawa-N. Tsukamoto-S. Hirose-Y. Kuroda-H.

Title: Survival effect of coenzyme Q10 and naloxone on experimental stroke gerbils.

Source: Pharmacol-Biochem-Behav. 1986 Feb. 24(2). P 315-7.

Journal Title: PHARMACOLOGY, BIOCHEMISTRY AND BEHAVIOR.

Abstract: Coenzyme Q10 (CoQ10) and the opiate antagonist naloxone were compared as to their effect on the survival of mongolian gerbils with unilateral carotid ligation-induced stroke. Without medication all of the stroke gerbils died within 28 hours, but with a subcutaneous implantation of a 10 mg pellet of naloxone, 20% of the gerbils lived for 4 weeks. When a 250 mg pellet of CoQ10 was implanted subcutaneously, a definite effect on survival was observed, with 45% of the stroke gerbils living for 4 weeks. ...Ely comments: This experiment was terminated at 4 weeks; none of the surviving gerbils had died after the 4th day. As well as in this post-stroke treatment of gerbils, remarkable results have been obtained in other animal models using coenzyme Q10 including pretreatment of dogs and rats (Cahn 1981, below).

Abstract 14

Author: Cahn J, Borzeix MG, Angignard J, Akimjak JP, Dupont JM.

Title: Possible use of coenzyme Q10 in acute cerebral disease.

In: Folkers K, Yamamura Y, eds. Biomedical and Clinical Aspects of Coenzyme Q. Vol 3. Amsterdam: Elsevier;1981:385-395.

Abstract: The primary injury to nervous tissue in stroke or TIA is a blood brain barrier breakdown, immediately followed by a vasogenic edema. The changes in the permeability of the blood brain barrier to proteins as well as the astrocytic edema could be related to peroxidation of the membranes or to redox potential changes. The purpose of this study is to show that some hemodynamic, cerebral metabolic changes and neurological symptoms occurring during an experimental cerebral infarct in the dog or during a TIA in the rat can be diminished or abolished by a previous administration of Coenzyme Q10.

Abstract 15

Author: Ely J.T.A., Fudenberg H.H., Bliznakov E.G., Branch J.D.

Title: Hemorrhagic Stroke in Human Pretreated with Coenzyme Q10: Exceptional Recovery as Seen in Animal Models.

Source: Journal of Orthomolecular Medicine. 1998 13(2), P 105-109.

Journal Title: JOURNAL OF ORTHOMOLECULAR MEDICINE.

Abstract: Minimizing neurologic injury from stroke is still the elusive goal of large scale controlled clinical trials of new synthetic agents whose efficacy is dependent upon prompt post-insult administration. In 26 years of animal model stroke studies, one substance that afforded a markedly higher degree of protection than all others tested was a normal endogenous molecule, coenzyme Q10 (Q10). Because of increasing worldwide use of Q10, we are able serendipidously to report on possibly the first observation of a human recovering almost completely from unexpected and severe stroke following four weeks of pretreatment with Q10 at a pharmacologic dose commonly employed for a wide variety of disorders. Clearly, clinical studies are needed to confirm the significance of our observed result. These would be facilitated by the safety and efficacy of Q10 already proven in nine large scale international trials in cardiomyopathy, etc., and its apparent benefits in numerous disorders, including AIDS and possibly aging itself. However, the confirmation should be done in trials specifically designed for stroke because of detection difficulty arising from the anticipated protection. If confirmed, this result does not diminish the urgent need for development of synthetic stroke agents, but may facilitate their realization by decreasing the protective functions needed from the agents.

Abstract 16

Author: Langsjoen PH, Langsjoen AM.

Title: Overview of the use of CoQ10 in cardiovascular disease.

Source: BioFactors 1999 9:273-84. http://wwwcsi.unian.it/coenzymeQ/overview.html .

Journal Title: BioFactors.

Abstract: The clinical experience in cardiology with CoQ10 includes studies on congestive heart failure, ischemic heart disease, hypertensive heart disease, diastolic dysfunction of the left ventricle, and reperfusion injury as it relates to coronary artery bypass graft surgery. The CoQ10-lowering effect of HMG-CoA reductase inhibitors and the potential adverse consequences are of growing concern. Supplemental CoQ10 alters the natural history of cardiovascular illnesses and has the potential for prevention of cardiovascular disease through the inhibition of LDL cholesterol oxidation and by the maintenance of optimal cellular and mitochondrial function throughout the ravages of time and internal and external stresses. The attainment of higher blood levels of CoQ10 (>3.5microg/ml) with the use of higher doses of CoQ10 appears to enhance both the magnitude and rate of clinical improvement. In this communication, 34 controlled trials and several open-label and long-term studies on the clinical effects of CoQ10 in cardiovascular diseases are reviewed.

Abstract 17

Author: Ely JTA, Fudenberg HH, Krone CA, Thoreson J

Title:Lethal Candidiasis: An Interpretive Review with Emphasis on Neglected, Safe, Effective, Inexpensive Therapies

Source: Italian Review of Medical and Surgical Research. VII (2/4): 57-63, 1999. .

Journal Title: Italian Review of Medical and Surgical Research.

Abstract:
1. Supplemental coenzyme Q10 (Q10) has been documented to be an effective biological response modifier in most human diseases and in animal models of aging and stroke.
2. Since the advent of antibiotics and other factors, candidiasis has become possibly the commonest, most involved, and most often lethal, infectious complication dominating M&M and care cost in numerous diseases.
3. In many diseases including AIDS, burns, cancer, drug addiction, dyspepsia, multiple organ failure, surgical sepsis, Chronic Fatigue Immune Dysregulation Syndrome, autism and other cognitive function disorders, Candida is a causative or coexistent factor and growing evidence suggests it, especially when colonizing the duodenum and proximal jejunum (CanDPJ), may be a more common cause of death than the primary condition. In patients with CanDPJ symptoms, a large intake of Q10 may cause negligible rise in blood level and no clinical improvement. The case reported herein is consistent with Q10 loss to the fungus.
4. Large scale studies of Can-TF, if successful in developing DH and a strong cytotoxic T-cell response against Candida species, can provide a basis for a safe, effective and inexpensive modality for the high M&M groups cited above.

Abstract 18

Author:Ely JTA, Krone CA.

Title:A brief update on ubiquinone (Coenzyme Q10).

Source: J Orthomolecular Medicine 2000; 15(2):63-68..

Journal Title: J Orthomolecular Medicine.

Abstract 19

Author:Krone CA, Elmer GW, Ely JT, Fudenberg HH, Thoreson J.

Title:Does gastrointestinal Candida albicans prevent ubiquinone absorption?

Source: Med Hypotheses 2001 Nov;57(5):570-2 .

Journal Title: Medical Hypotheses.

Abstract:
Ubiquinones (coenzyme Qs, (CoQ)) are essential for oxidative phosphorylation in yeasts and humans, although the isomers present in each are different. The human coenzyme Q, CoQ10, is administered orally for the treatment of heart disease and other disorders. Some patients, however, require much higher doses than others to attain a therapeutic CoQ10 blood level. We propose that one possible explanation for this variability is Candida colonization of the GI tract. Many common medical treatments including antibiotics and anti-hyperchlorhydric agents increase the risk of GI tract Candida colonization. Subsequent uptake and utilization of supplemental CoQ10 by the yeast could diminish availability for the human subject. Data from a patient and an in vitro pilot study using two pathogenic strains of C. albicans support this hypothesis. If C. albicans in the GI tract can hinder availability and interfere with therapeutic effects of CoQ10, it could be of clinical significance for large numbers of patients.