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Antifatigue effects of coenzyme Q10 during physical fatigue.
Nutrition. 2008 Apr;24(4):293-299.
Mizuno K, Tanaka M, Nozaki S, Mizuma H, Ataka S, Tahara T, Sugino T, Shirai T, Kajimoto Y, Kuratsune H, Kajimoto O, Watanabe Y.
OBJECTIVE: This study examined the effects of coenzyme Q10 administration on physical fatigue.
METHODS: In a double-blinded, placebo-controlled, three crossover design, 17 healthy volunteers were randomized to oral coenzyme Q10 (100 or 300 mg/d) or placebo administration for 8 d. As a fatigue-inducing physical task, subjects performed workload trials on a bicycle ergometer at fixed workloads twice for 2 h and then rested for 4 h. During the physical tasks, subjects performed non-workload trials with maximum velocity for 10 s at 30 min (30-min trial) after the start of physical tasks and 30 min before the end of the tasks (210-min trial).
RESULTS: The change in maximum velocity from the 30- to the 210-min trial in the 300-mg coenzyme Q10-administered group was higher than that in the placebo group. In addition, subjective fatigue sensation measured on a visual analog scale in the 300-mg coenzyme Q10-administered group after the fatigue-inducing physical task and recovery period was alleviated when compared with that in the placebo group.
CONCLUSION: Oral administration of coenzyme Q10 improved subjective fatigue sensation and physical performance during fatigue-inducing workload trials and might prevent unfavorable conditions as a result of physical fatigue.
Reducing exercise-induced muscular injury in kendo athletes with supplementation of coenzyme Q10.
Br J Nutr. 2008 Feb 20;:1-7 [Epub ahead of print].
Kon M, Tanabe K, Akimoto T, Kimura F, Tanimura Y, Shimizu K, Okamoto T, Kono I.
Intensive physical exercise may cause muscular injury and increase oxidative stress. The purpose of this study was to examine the effect of an antioxidant, coenzyme Q10 (CoQ10), on muscular injury and oxidative stress during exercise training. Eighteen male students, all elite Japanese kendo athletes, were randomly assigned to either a CoQ10 group (n 10) or a placebo group (n 8) in a double-blind manner. Subjects in the CoQ10 group took 300 mg CoQ10 per d for 20 d, while subjects in the placebo group took the same dosage of a placebo. All subjects practised kendo 5.5 h per d for 6 d during the experimental period. Blood samples were taken 2 weeks before, during (1 d, 3 d, 5 d) and 1 week after the training. Serum creatine kinase (CK) activity and myoglobin (Mb) concentration significantly increased in both groups (at 3 d and 5 d). Serum CK (at 3 d), Mb (at 3 d) and lipid peroxide (at 3 d and 5 d) of the CoQ10 group were lower than those of the placebo group. The leucocyte counts in the placebo group significantly increased (at 3 d) and neutrophils significantly increased in both groups (at 3 d and 5 d). Serum scavenging activity against superoxide anion did not change in either group. These results indicate that CoQ10 supplementation reduced exercise-induced muscular injury in athletes.
Coenzyme Q10 protects the aging heart against stress: studies in rats, human tissues, and patients.
Ann N Y Acad Sci 2002 Apr; 959:355-9; discussion 463-5.
Rosenfeldt FL, Pepe S, Linnane A, Nagley P, Rowland M, Ou R, Marasco S, Lyon W, Esmore D.
With aging of the population, increasing numbers of elderly patients are presenting for cardiac surgery. However, the results in the elderly are inferior to those in the young. A likely contributing factor is an age-related reduction in cellular energy production in the myocardium during surgery, which is known to induce aerobic and ischemic stress. The lipophilic antioxidant and mitochondrial respiratory chain redox coupler, coenzyme Q10 (CoQ10), has the potential to improve energy production in mitochondria by bypassing defective components in the respiratory chain as well as by reducing the effects of oxidative stress. We hypothesized that CoQ10 pretreatment prior to stress could improve the recovery of the myocardium after stress.
Randomized, double-blind placebo-controlled trial of coenzyme Q10 in patients with acute myocardial infarction.
Cardiovasc Drugs Ther 1998 Sep; 12(4): 347-53.
Singh RB, Wander GS, Rastogi A, Shukla PK, Mittal A, Sharma JP, Mehrotra SK, Kapoor R, Chopra RK.
The effects of oral treatment with coenzyme Q10 (120 mg/d) were compared for 28 days in 73 (intervention group A) and 71 (placebo group B) patients with acute myocardial infarction (AMI). After treatment, angina pectoris (9.5 vs. 28.1), total arrhythmias (9.5% vs. 25.3%), and poor left ventricular function (8.2% vs. 22.5%) were significantly (P < 0.05) reduced in the coenzyme Q group than placebo group. Total cardiac events, including cardiac deaths and nonfatal infarction, were also significantly reduced in the coenzyme Q10 group compared with the placebo group (15.0% vs. 30.9%, P < 0.02). The extent of cardiac disease, elevation in cardiac enzymes, and oxidative stress at entry to the study were comparable between the two groups. Lipid peroxides, diene conjugates, and malondialdehyde, which are indicators of oxidative stress, showed a greater reduction in the treatment group than in the placebo group. The antioxidants vitamin A, E, and C and beta-carotene, which were lower initially after AMI, increased more in the coenzyme Q10 group than in the placebo group. These findings suggest that coenzyme Q10 can provide rapid protective effects in patients with AMI if administered within 3 days of the onset of symptoms. More studies in a larger number of patients and long-term follow-up are needed to confirm our results.
Apparent partial remission of breast cancer in 'high risk' patients supplemented with nutritional antioxidants, essential fatty acids and coenzyme Q10.
Mol Aspects Med 1994; 15 Suppl: s231-40.
Lockwood K, Moesgaard S, Hanioka T, Folkers K.
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.
Protective effect of coenzyme Q10 in cardiotoxicity induced by adriamycin
Gan To Kagaku Ryoho 1984 Mar; 11(3): 502-8.
Okuma K, Furuta I, Ota K.
Cardiotoxicity induced by adriamycin and protective effect by coenzyme Q10 were studied in 80 closely-followed patients receiving chemotherapy with adriamycin. Serial electrocardiograms were recorded immediately before and after the administration of adriamycin each times. The electrocardiographic parameters (heart rate, P-Q duration, QRS-duration, QRS voltage and QTc-duration) were analyzed. In patients treated with adriamycin alone, QTc-duration was prolonged significantly. On the other hand, in patients treated with adriamycin plus coenzyme Q10, QTc-duration was not significantly prolonged. This Suggests that coenzyme Q10 may reduce negative inotropic action induced by adriamycin. Further, the QRS voltage was also significantly decreased in patients treated with adriamycin alone, but was not decreased in patients treated with adriamycin plus coenzyme Q10. These findings suggest that some electrocardiographic changes due to adriamycin may be prevented by coenzyme Q10.
Randomized, double-blind, placebo-controlled trial of coenzyme Q10 in isolated systolic hypertension.
South Med J 2001 Nov; 94(11): 1112-7.
Burke BE, Neuenschwander R, Olson RD.
BACKGROUND: Increasing numbers of the adult population are using alternative or complementary health resources in the treatment of chronic medical conditions. Systemic hypertension affects more than 50 million adults and is one of the most common risk factors for cardiovascular morbidity and mortality. This study evaluates the antihypertensive effectiveness of oral coenzyme Q10 (CoQ), an over-the-counter nutritional supplement, in a cohort of 46 men and 37 women with isolated systolic hypertension.
METHODS: We conducted a 12-week randomized, double-blind, placebo-controlled trial with twice daily administration of 60 mg of oral CoQ and determination of plasma CoQ levels before and after the 12 weeks of treatment.
RESULTS: The mean reduction in systolic blood pressure of the CoQ-treated group was 17.8 +/- 7.3 mm Hg (mean +/- SEM). None of the patients exhibited orthostatic blood pressure changes.
CONCLUSIONS: Our results suggest CoQ may be safely offered to hypertensive patients as an alternative treatment option.
The clinical and hemodynamic effects of coenzyme Q10 in congestive cardiomyopathy.
Am J Ther 1997 Feb-Mar; 4(2-3): 66-72.
Sacher HL, Sacher ML, Landau SW, Kersten R, Dooley F, Sacher A, Sacher M, Dietrick K, Ichkhan K.
Despite major advances in treatment congestive heart failure (CHF) is still one of the major causes of morbidity and mortality. Coenzyme Q(10) is a naturally occurring substance that has antioxidant and membrane stabilizing properties. Administration of coenzyme Q(10) in conjunction with standard medical therapy has been reported to augment myocardial kinetics, increase cardiac output, elevate the ischemic threshold, and enhance functional capacity in patients with congestive heart failure. The aim of this study was to investigate some of these claims. Seventeen patients (mean New York Heart Association functional class 3.0 +/- 0.4) were enrolled in an open-label study. After 4 months of coenzyme Q ( 10 ) therapy, functional class improved 20% (3.0 +/- 0.4 to 2.4 +/- 0.6, p < 0.001) and there was a 27% improvement in mean CHF score (2.8 +/- 0.4 to 2.2 +/- 0.4, p < 0.001). Percent change in the resting variables included the following: left ventricular ejection fraction (LVEF), +34.8%; cardiac output, +15.7%; stroke volume index, +18.9%; end-diastolic volume area, -8.4%; systolic blood pressure (SBP), -4. 4%; and E (max), (SBP / end-systolic volume index [ESVI]) +11.7%. MVo ( 2 ) decreased by 5.3% (31.9 +/- 2.6 to 30.2 +/- 2.4, p = NS). Therapy with coenzyme Q(10) was associated with a mean 25.4% increase in exercise duration and a 14.3% increase in workload. Percent changes after therapy include the following: exercise LVEF, +24.6%; cardiac output, +19.1%; stroke volume index, +13.2%; heart rate, +6.5%; SBP, -4.3%; SBP / ESVI, +18.6%; end-diastolic volume (EDV) area, -6.0%; MVo (2), -7.0%; and ventricular compliance (%Delta SV / EDV) improved >100%. In summary, coenzyme Q(10) therapy is associated with significant functional, clinical, and hemodynamic improvements within the context of an extremely favorable benefit-to-risk ratio. Coenzyme Q(10) enhances cardiac output by exerting a positive inotropic effect upon the myocardium as well as mild vasodilatation.
Effects of Coenzyme Q10 in Early Parkinson Disease: Evidence of Slowing of the Functional Decline
Arch Neurol. 2002 Oct; 59(10): 1541-50.
Shults CW, Oakes D, KieburtzK, Beal MF, Haas R, Plumb S, Juncos JL, Nutt J, Shoulson I, Carter J, Kompoliti K, Perlmutter JS, Reich S, Stern M, Watts RL, Kurlan R, Molho E, Harrison M, Lew M.
Background: Parkinson disease (PD) is a degenerative neurological disorder for which no treatment has been shown to slow the progression.
Objective: To determine whether a range of dosages of coenzyme Q10 is safe and well tolerated and could slow the functional decline in PD.
Design: Multicenter, randomized, parallel-group, placebo-controlled, double-blind, dosage-ranging trial. Setting: Academic movement disorders clinics.
Patients: Eighty subjects with early PD who did not require treatment for their disability.
Interventions: Random assignment to placebo or coenzyme Q10 at dosages of 300, 600, or 1200 mg/d.
Main Outcome Measure: The subjects underwent evaluation with the Unified Parkinson Disease Rating Scale (UPDRS) at the screening, baseline, and 1-, 4-, 8-, 12-, and 16-month visits. They were followed up for 16 months or until disability requiring treatment with levodopa had developed. The primary response variable was the change in the total score on the UPDRS from baseline to the last visit.
Results: The adjusted mean total UPDRS changes were +11.99 for the placebo group, +8.81 for the 300-mg/d group, +10.82 for the 600-mg/d group, and +6.69 for the 1200-mg/d group. The P value for the primary analysis, a test for a linear trend between the dosage and the mean change in the total UPDRS score, was .09, which met our prespecified criteria for a positive trend for the trial. A prespecified, secondary analysis was the comparison of each treatment group with the placebo group, and the difference between the 1200-mg/d and placebo groups was significant (P = .04).
Conclusions: Coenzyme Q10 was safe and well tolerated at dosages of up to 1200 mg/d. Less disability developed in subjects assigned to coenzyme Q10 than in those assigned to placebo, and the benefit was greatest in subjects receiving the highest dosage. Coenzyme Q10 appears to slow the progressive deterioration of function in PD, but these results need to be confirmed in a larger study.
Improved outcomes in coronary artery bypass graft surgery with preoperative coenzyme Q10: a randomized, double-blind, placebo controlled trial. (In: "Coenzyme Q10 protects the aging heart against stress: studies in rats, human tissues, and patients.").
Ann N Y Acad Sci 2002 Apr; 959: 355-9; discussion 463-5.
Rosenfeldt FL, Pepe S, Linnane A, Nagley P, Rowland M, Ou R, Marasco S, Lyon W, Esmore D.
Introduction: On the basis of our previous studies we believed that CoQ10 should have a beneficial effect in patients undergoing cardiac surgery, especially those aged 70 years and over. We therefore set out to test in cardiac surgical patients whether oral CoQ10 therapy (1) increases CoQ10 content in atrial trabeculae and mitochondria, (2) improves mitochondrial respiration, (3) protects the myocardium against posthypoxic contractile dysfunction, and (4) attenuates operative myocardial injury and improves postoperative recovery.
Methods: Patients were randomized to receive orally either CoQ10 (300 mg/day) or placebo for seven days prior to elective cardiac surgery. Trabeculae were excised and mitochondria were isolated from discarded right atrial appendages. Biochemical and clinical parameters were measured postoperatively.
Results: Compared to placebo, therapy increased CoQ10 content of trabeculae (21 ± 4 to 40 ± 5 µg/g w.w., P < 0.001) and isolated mitochondria (5.7 ± 0.8 to 11.2 ± 0.9 µg CoQ10/mg protein, P < 0.0001). Mitochondrial respiration was more efficient after CoQ10 pretreatment (ADP:O, CoQ10 vs. placebo: 4.2 ± 0.2 vs. 2.9 ± 0.4, P < 0.05). After 30 min hypoxia, CoQ10-treated trabeculae exhibited a greater recovery of developed force compared to placebo (64.0 ± 18% vs. 46.2 ± 28%, P < 0.01). CoQ10 patients had a lower release of TnI than placebo patients (39.4 ± 8.5 vs. 64.5 ± 4.1 µg/L, P < 0.001) and a shorter length of hospital stay (6.8 ± 0.7 vs. 8.7 ± 2.1 days, P < 0.05).
Conclusions: Preoperative oral CoQ10 therapy (1) increases CoQ10 content in atrial trabeculae and cardiac mitochondria, (2) improves efficiency of mitochondrial energy production, (3) improves posthypoxic myocardial contractile function, and (4) reduces myocardial damage and shortens the hospital stay.
Protective effects of coenzyme Q10 on the adverse reactions of anthracycline antibiotics: using double blind method--with special reference to hair loss
Gan To Kagaku Ryoho 1983 Oct; 10(10): 2125-9.
Akihama T, Nakamoto Y, Shindo T, Nakayama Y, Miura A.
It was clinically evaluated by double blind method whether co-enzyme Q10 has protective effects on hair loss caused by anthracycline antibiotics. Six cases of acute leukemia, 2 blastic crisis of CML and 11 malignant lymphoma were entered to this study. DCMP regimen for acute leukemia for VEPA for lymphoma were performed. Coenzyme Q10 (or placebo) of 120 mg/day was orally administered. The grade of hair loss was classified into five groups. Five cases were only given to DM and 3 cases receiving DM and CoQ10. ADM was 6 cases and 5 were combined with CoQ10. No significant diffehence in effect of CoQ10 administration rence was recognized between two groups statistically. Elevations of GOT and GPT were less frequent in the group receiving CoQ10.
Coenzyme Q10 in cancer chemotherapy - experimental studies on augmentation of the effects of masked compounds, especially in the combined chemotherapy with immunopotentiators
Gan To Kagaku Ryoho 1983 Mar; 10(3): 768-74.
Kokawa T, Shiota K, Oda K, Okubo S, Okamoto Y, Okubo H.
Immunopotentiators may mitigate the depression of immunological function caused by the cancer itself or by chemotherapeutics. However, it has been found that these immunopotentiators reduce the metabolic activity of the host against drugs, including "masked" chemotherapeutics, which might be activated by metabolization in the body. Reported here is the result of serial experiments carried out on the activation of cyclophosphamide (CPM) in tumor-bearing animals, pretreated with phenobarbital, a drug-metabolizing enzyme inducer, and coenzyme Q10, a physiological activator of the electron transfer system in mitochondrias, in combination with immunopotentiators. Female Donryu rats (120 g body weight) implanted with Yoshida Sarcoma cells (YS) (2.5 X 10(6) i.p.) were treated with CPM (160 mg/kg X 1 i.p.), 84 hrs after implantation; the levels of the normustard-like substances (active metabolites of CPM) were serially measured. Some of the animals were also treated with PSK (125 mg/kg X 5 i.p.), a proteinpolysaccharide immunopotentiator obtained from mycelia of the Coriolus vesicolor, or with OK-432 (10 KE/kg X 5 i.m.), a streptococcal immunopotentiator. The results obtained were as follows: The blood levels of the normustard-like substances were lowered, i.e. the CPM activation was depressed in the YS-bearing rats and the depression was markedly intensified by PSK or OK-432 administration. Phenobarbital (40 mg/kg X 3 i.p.) or coenzyme Q10 (5 mg/rat X 5 i.p.) administration could mitigate the depression of the blood levels caused by the immunopotentiators, and the combination of phenobarbital with coenzyme Q10 could recover the blood levels up to those of the YS-bearing control rats, or even higher. YS-implanted (i.p.) rats treated with CPM+ immunopotentiators+coenzyme Q10 survived longer than those treated with CPM+immunopotentiators. These findings suggest the usefulness of coenzyme Q10 for the enhancement of cancer immunochemotherapy using masked compounds combined with immunopotentiators; all the more so, because coenzyme Q10 has also an immuno-stimulating effect, moreover, it presents almost no side effects in clinical application.
Coenzyme Q10 treatment in serious heart failure.
Biofactors 1999; 9(2-4): 285-9.
Munkholm H, Hansen HH, Rasmussen K.
Several noninvasive studies have shown the effect on heart failure of treatment with coenzyme Q10. In order to confirm this by invasive methods we studied 22 patients with mean left ventricular (LV) ejection fraction 26%, mean LV internal diameter 71 mm and in NYHA class 2-3. The patients received coenzyme Q10 100 mg twice daily or placebo for 12 weeks in a randomized double-blinded placebo controlled investigation. Before and after the treatment period, a right heart catheterisation was done including a 3 minute exercise test. The stroke index at rest and work improved significantly, the pulmonary artery pressure at rest and work decreased (significantly at rest), and the pulmonary capillary wedge pressure at rest and work decreased (significantly at 1 min work). These results suggest improvement in LV performance. Patients with congestive heart failure may thus benefit from adjunctive treatment with coenzyme Q10.
Effect of treatment with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on serum coenzyme Q10 in diabetic patients.
Arzneimittelforschung 1999 Apr; 49(4): 324-9.
Miyake Y, Shouzu A, Nishikawa M, Yonemoto T, Shimizu H, Omoto S, Hayakawa T, Inada M.
Serum coenzyme Q10 (CoQ10: 2- (3,7,11,15,19,23,27,31,35,39- decamethyl- 2,6, 10,14,18, 22,26,30,34 ,38 -tetracontadecaenyl)- 5,6- dimethoxy-3- methyl- 1,4-benzoquinone, CAS 303-98-0) and cholesterol levels were measured to assess the effect of cholesterol-lowering therapy in patients with non-insulin-dependent diabetes mellitus (NIDDM). Twenty healthy volunteers, 97 NIDDM patients and 2 patients with familial hypercholesterolemia were studied. None had overt heart failure or any other heart disease. Mean serum CoQ10 concentrations were significantly (p < 0.01) lower in diabetic patients with normal serum cholesterol concentrations, either with or without administration of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (HMG-CoA RIs) including simvastatin (normal: 0.91 +/- 0.26 (mean +/- SD) mumol 1(-1); diabetic with HMG-CoA RI: 0.63 +/- 0.19; diabetic without HMG-CoA RI: 0.66 +/- 0.21). CoQ10 concentrations were higher (1.37 +/- 0.48, p < 0.001) in diabetic patients with hypercholesterolemia. Simvastatin or low density lipoprotein apheresis decreased serum CoQ10 concentrations along with decreasing serum cholesterol. Oral CoQ10 supplementation in diabetic patients receiving HMG-CoA RI significantly (p < 0.001) increased serum CoQ10 from 0.81 +/- 0.24 to 1.47 +/- 0.44 mumol 1(-1), without affecting cholesterol levels. It significantly (p < 0.03) decreased cardiothoracic ratios from 51.4 +/- 5.1 to 49.2 +/- 4.7%. In conclusion, serum CoQ10 levels in NIDDM patients are decreased and may be associated with subclinical diabetic cardiomyopathy reversible by CoQ10 supplementation.
Phase I study of lovastatin, an inhibitor of the mevalonate pathway, in patients with cancer.
Clin Cancer Res 1996 Mar; 2(3): 483-91.
Thibault A, Samid D, Tompkins AC, Figg WD, Cooper MR, Hohl RJ, Trepel J, Liang B, Patronas N, Venzon DJ, Reed E, Myers CE.
Lovastatin, an inhibitor of the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase (the major regulatory enzyme of the mevalonate pathway of cholesterol synthesis), displays antitumor activity in experimental models. We therefore conducted a Phase I trial to characterize the tolerability of lovastatin administered at progressively higher doses to cancer patients. From January 1992 to July 1994, 88 patients with solid tumors (median age, 57 +/- 14 years) were treated p.o. with 7-day courses of lovastatin given monthly at doses ranging from 2 to 45 mg/kg/day. The inhibitory effects of lovastatin were monitored through serum concentrations of cholesterol and ubiquinone, two end products of the mevalonate pathway. Concentrations of lovastatin and its active metabolites were also determined, by bioassay, in the serum of selected patients. Cyclical treatment with lovastatin markedly inhibited the mevalonate pathway, evidenced by reductions in both cholesterol and ubiquinone concentrations, by up to 43 and 49% of pretreatment values, respectively. The effect was transient, however, and its magnitude appeared to be dose independent. Drug concentrations reached up to 3.9 micrometer and were in the range associated with antiproliferative activity in vitro. Myopathy was the dose-limiting toxicity. Other toxicities included nausea, diarrhea, and fatigue. Treatment with ubiquinone was associated with reversal of lovastatin-induced myopathy, and its prophylactic administration prevented the development of this toxicity in a cohort of 56 patients. One minor response was documented in a patient with recurrent high-grade glioma. Lovastatin given p.o. at a dose of 25 mg/kg daily for 7 consecutive days is well tolerated. The occurrence of myopathy, the dose-limiting toxicity, can be prevented by ubiquinone supplementation. To improve on the transient inhibitory activity of this dosing regimen on the mevalonate pathway, alternative schedules based on uninterrupted administration of lovastatin should also be studied.
Two successful double-blind trials with coenzyme Q10 (vitamin Q10) on muscular dystrophies and neurogenic atrophies.
Biochim Biophys Acta 1995 May 24; 1271(1): 281-6.
Folkers K, Simonsen R.
Coenzyme Q10 (vitamin Q10) is biosynthesized in the human body and is functional in bioenergetics, anti-oxidation reactions, and in growth control, etc. It is indispensable to health and survival. The first double-blind trial was with twelve patients, ranging from 7-69 years of age, having diseases including the Duchenne, Becker, and the limb-girdle dystrophies, myotonic dystrophy. Charcot-Marie-Tooth disease, and the Welander disease. The control coenzyme Q10 (CoQ10) blood level was low and ranged from 0.5-0.84 microgram/ml. They were treated for three months with 100 mg daily of CoQ10 and a matching placebo. The second double-blind trial was similar with fifteen patients having the same categories of disease. Since cardiac disease is established to be associated with these muscle diseases, cardiac function was blindly monitored, and not one mistake was made in assigning CoQ10 and placebo to the patients in both trials. Definitely improved physical performance was recorded. In retrospect, a dosage of 100 mg was too low although effective and safe. Patients suffering from these muscle dystrophies and the like, should be treated with vitamin Q10 indefinitely.
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