1. Langsjoen PH, Langsjoen PH, Folkers K (1985). "Long-term efficacy and safety of coenzyme Q10 for idiopathic dilated cardiomyopathy." Am J Cardiol 65: 521-523, qtd. in Pizzorno: 666-667.
2. Am J Cardiol 2007;99:1409-1412. - May 15th issue of the American Journal of Cardiology.
CoQ10 Reverses Muscle Damage from Statin Cholesterol Drugs
Statin drugs, such as Lipitor and Zocor, lower cholesterol levels, but at the same time they interfere with the making of coenzyme Q10 in the body. Scientists now suspect that CoQ10 deficiency may partly or fully contribute to the development of muscle damage in those on these cholesterol lowering drugs.. Dr. Giuseppe Caso and colleagues from Stony Brook University, Stony Brook, New York gave 100 mg of CoQ10 for one month to 32 patients using statins. Pain intensity decreased by 40% after a month of CoQ10 treatment whereas patients treated with vitamin E (as placebo) experienced no change in pain intensity. Sixteen of 18 coenzyme Q10-treated patients experienced a decrease in pain.
3. Bhagavan, H. N. and R. K. Chopra (2006). "Coenzyme Q10: absorption, tissue uptake, metabolism and pharmacokinetics." Free Radic Res 40(5): 445-53. Available data on the absorption, metabolism and pharmacokinetics of coenzyme Q10 (CoQ10) are reviewed in this paper. CoQ10 has a fundamental role in cellular bioenergetics. CoQ10 is also an important antioxidant. Because of its hydrophobicity and large molecular weight, absorption of dietary CoQ10 is slow and limited. In the case of dietary supplements, solubilized CoQ10 formulations show enhanced bioavailability. The T(max) is around 6 h, with an elimination half-life of about 33 h. The reference intervals for plasma CoQ10 range from 0.40 to 1.91 micromol/l in healthy adults. With CoQ10 supplements there is reasonable correlation between increase in plasma CoQ10 and ingested dose up to a certain point. Animal data show that CoQ10 in large doses is taken up by all tissues including heart and brain mitochondria. This has implications for therapeutic applications in human diseases, and there is evidence for its beneficial effect in cardiovascular and neurodegenerative diseases. CoQ10 has an excellent safety record.
4. Eur Heart J. 2006 Nov;27(22):2675-81. Belardinelli R, et al. Lancisi Heart Institute, Via Conca, 71 Torrette di Ancona, Italy.
Coenzyme Q10 and exercise training in chronic heart failure.
There is evidence that plasma CoQ10 levels decrease in patients with advanced chronic heart failure (CHF). However, it is not known whether oral CoQ10 supplementation may improve cardiocirculatory efficiency and endothelial function in patients with CHF. We studied 23 patients in NYHA class II and III (20 men, three women, mean age 59 years) with stable CHF secondary to ischemic heart disease [ejection fraction 37+/-7%], using a double-blind, placebo-controlled cross-over design. Patients were assigned to each of the following treatments: oral CoQ10 100 mg tid, CoQ10 plus supervised exercise training (ET) (60% of peak VO(2), five times a week), placebo, and placebo plus ET. Each phase lasted 4 weeks. Both peak VO(2) and endothelium-dependent dilation of the brachial artery (EDDBA) improved significantly after CoQ10 and after ET as compared with placebo. CoQ10 main effect was: peak VO(2)+9%, EDDBA +38%, systolic wall thickening score index (SWTI) -12%; ET produced comparable effects. CoQ10 supplementation resulted in a four-fold increase in plasma CoQ10 level, whereas the combination with ET further increased it. No side effects were reported with CoQ10. Oral CoQ10 improves functional capacity, endothelial function, and LV contractility in CHF without any side effects. The combination of CoQ10 and ET resulted in higher plasma CoQ10 levels and more pronounced effects on all the abovementioned parameters.
5. Bonakdar, R. A. and E. Guarneri (2005). "Coenzyme Q10." Am Fam Physician 72(6): 1065-70. Coenzyme Q10 is a vitamin-like substance used in the treatment of a variety of disorders primarily related to suboptimal cellular energy metabolism and oxidative injury. Studies supporting the efficacy of coenzyme Q10 appear most promising for neurodegenerative disorders such as Parkinson's disease and certain encephalomyopathies for which coenzyme Q10 has gained orphan drug status. Results in other areas of research, induding treatment of congestive heart failure and diabetes, appear to be contradictory or need further clarification before proceeding with recommendations. Coenzyme Q10 appears to be a safe supplement with minimal side effects and low drug interaction potential.
6. Exp Neurol. 2004 Aug;188(2):491-4.
“Pilot trial of high dosages of CoQ10 in patients with Parkinson's disease.”
The safety and tolerability of high dosages of coenzyme Q10 were studied in 17 patients with Parkinson's disease (PD) in an open label study. The subjects received an escalating dosage of coQ10 -- 1200, 1800, 2400, and 3000 mg/day with a stable dosage of vitamin E (alpha-tocopherol) 1200 IU/day. The plasma level of coQ10 was measured at each dosage. Thirteen of the subjects achieved the maximal dosage, and adverse events were typically considered to be unrelated to coQ10. The plasma level reached a plateau at the 2400 mg/day dosage and did not increase further at the 3000 mg/day dosage. The data suggest that in future studies of CoQ10 in PD, a dosage of 2400 mg/day (with vitamin E/alpha-tocopherol 1200 IU/day) is an appropriate highest dosage to be studied.
7. Chapidze, G., S. Kapanadze, et al. (2005). "Prevention of coronary atherosclerosis by the use of combination therapy with antioxidant coenzyme Q10 and statins." Georgian Med News(118): 20-5. The goal of the present research was to assess the efficacy of combination treatment with antioxidant coenzyme Q10 and simvastatin as well as coenzyme Q10 without statin therapy in order to prevent coronary atherosclerosis. 42 outpatients were divided into 2 groups: receiving coenzyme Q10 (Hasco-Lek, Poland) 60mg daily and its combination with simvastatin (zocor, vasilip) 10mg daily for an 8-week period. The treatment with coenzyme Q10 demonstrated its potential independent role in positive modification of oxidative stress, antiatherogenic fraction of lipid profile, atherogenic ratio, platelet aggregability. Taking into consideration the obtained results the study supports the use of coenzyme Q10 in combination with statins. Suggested attractive approach may result in complete correction of dislipidemia, reverse of endothelial dysfunction, reduce degree of oxidative stress and platelet aggregability. Consequently such a combination may be beneficial in preventing of further development of atherosclerosis in native coronary arteries as well as in bypass grafts in all coronary heart disease patients with or without myocardial revascularization.
8. Clin Cardiol. 2004 May;27(5):295-9.
“CoQ10 in patients with end-stage heart failure awaiting cardiac transplantation: a randomized, placebo-controlled study.”
The number of patients awaiting heart transplantation is increasing in proportion to the waiting period for a donor. Studies have shown that coenzyme Q10 (CoQ10) has a beneficial effect on patients with heart failure. HYPOTHESIS: The purpose of the present double-blind, placebo-controlled, randomized study was to assess the effect of CoQ10 on patients with end-stage heart failure and to determine if CoQ10 can improve the pharmacological bridge to heart transplantation. METHODS: A prospective double-blind design was used. Thirty-two patients with end-stage heart failure awaiting heart transplantation were randomly allocated to receive either 60 mg U/day of Ultrasome--CoQ10 (special preparation to increase intestinal absorption) or placebo for 3 months. All patients continued their regular medication regimen. Assessments included anamnesis with an extended questionnaire based partially on the Minnesota Living with Heart Failure Questionnaire, 6-min walk test, blood tests for atrial natriuretic factor (ANF) and tumor necrosis factor (TNF), and echocardiography. RESULTS: Twenty-seven patients completed the study. The study group showed significant improvement in the 6-min walk test and a decrease in dyspnea, New York Heart Association (NYHA) classification, nocturia, and fatigue. No significant changes were noted after 3 months of treatment in echocardiography parameters (dimensions and contractility of cardiac chambers) or ANF and TNF blood levels. CONCLUSIONS: The administration of CoQ10 to heart transplant candidates led to a significant improvement in functional status, clinical symptoms, and quality of life. However, there were no objective changes in echo measurements or ANF and TNF blood levels. Coenzyme Q10 may serve as an optional addition to the pharmacologic armamentarium of patients with end-stage heart failure. The apparent discrepancy between significant clinical improvement and unchanged cardiac status requires further investigation.
9. Judy, W. V., W. W. Stogsdill, et al. (1993). "Myocardial preservation by therapy with coenzyme Q10 during heart surgery." Clin Investig 71(8 Suppl): S155-61. Coenzyme Q10 (CoQ10) is a natural and essential cofactor in the heart. It is the primary redox coupler in the respiratory chain, a potent free radical scavenger, and a superoxide inhibitor. In this study the myocardial protective effects of CoQ10 were determined in high-risk (n = 10) patients during heart surgery compared to that found in placebo controls (n = 10). In both groups, there was a blood CoQ10 deficiency (< 0.6 microgram/ml), low cardiac index (CI < 2.4 l/m2 per minute), and low left ventricular ejection fraction (LVEF < 35%) before treatment. CoQ10 (100 mg per day) was given orally for 14 days before and 30 days after surgery. Presurgical CoQ10 treatment significantly (P < 0.01) improved blood and myocardial CoQ10 and myocardial ATP compared to that found in the control group. Cardiac functions (CI and LVEF) were improved but not significantly. After cardiac cooling, rewarming, and reperfusion; blood and tissue CoQ10 and tissue ATP levels were maintained in the normal ranges in the CoQ10 patients. Cardiac pumping (CI) and LVEF were significantly (P < 0.01) improved. The recovery course was short (3-5 days) and uncomplicated. In the control group blood and tissue CoQ10, tissue ATP levels, and cardiac functions were depressed after surgery. The recovery course was long (15-30 days) and complicated. Positive relationships between blood and myocardial CoQ10, myocardial ATP, cardiac function, and the postoperative recovery time and course found in both study groups show the therapeutic benefits of CoQ10 in preserving the myocardium during heart surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
10. Singh RB. Mol Cell Biochem. 2003 Apr;246(1-2):75-82.
“Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction.”
In a randomized, double-blind, controlled trial, the effects of oral treatment with CoQ10, 120 mg/day, a bioenergetic and antioxidant cytoprotective agent, were compared for 1 year, on the risk factors of atherosclerosis, in 73 (CoQ10, group A) and 71 (B vitamin group B) patients after acute myocardial infarction (AMI). After 1 year, total cardiac events (24.6 vs. 45.0%, p < 0.02) including non-fatal infarction and cardiac deaths were significantly lower in the intervention group compared to control group. The extent of cardiac disease, elevation in cardiac enzymes, left ventricular enlargement, previous coronary artery disease and elapsed time from symptom onset to infarction at entry to study showed no significant differences between the two groups. Plasma level of vitamin E and high density lipoprotein cholesterol (1.26 +/- 0.43 vs. 1.12 +/- 0.32 mmol/L) showed significant (p < 0.05) increase whereas thiobarbituric acid reactive substances, malondialdehyde and diene conjugates showed significant reduction respectively in the CoQ10 group compared to control group. Approximately half of the patients in each group (n = 36 vs. 31) were receiving lovastatin (10 mg/day) and both groups had a significant reduction in total and low density lipoprotein cholesterol compared to baseline levels. It is possible that treatment with CoQ10 in patients with recent MI may be beneficial in patients with high risk of atherothrombosis, despite optimal lipid lowering therapy during a follow-up of 1 year. Adverse effect of treatments showed that fatigue (40.8 vs. 6.8%, p < 0.01) was more common in the control group than CoQ10 group.
11. Aejmelaeus, R., T. Metsa-Ketela, et al. (1997). "Ubiquinol-10 and total peroxyl radical trapping capacity of LDL lipoproteins during aging: the effects of Q-10 supplementation." Mol Aspects Med 18 Suppl: S113-20. Evidence is rapidly accumulating that oxidative modification of low density lipoprotein (LDL) may play an important role in the pathogenesis of atherosclerosis. In this study we measured the total peroxyl radical trapping capacity of human plasma LDL phospholipids (TRAPLDL) with a luminescent method. The study was carried out with 70 healthy volunteers, aged 28-77. In males an age-related decrease in TRAPLDL was observed. In the age group under 50 years the mean TRAPLDL was 31.36 +/- 1.45 pmol peroxyl radicals/nmol Pi; among those over 50 years it was significantly lower at 26.67 0.94 pmol/nmol Pi. As regards the components of TRAPLDL, the concentration of LDL-ubiquinol did not change and a non-significant decrease in the LDL-tocopherol concentration was detected with age. In females, the mean TRAPLDL, LDL-ubiquinol-10 and tocopherol concentrations did not differ between the age groups. When 17 of the participants were given coenzyme Q10 (Q10) supplementation, 100 mg/day, a highly significant increase in LDL-ubiquinol concentration was detected. Our results indicate that LDL antioxidant defenses tend to decrease with age in the Finnish male population. The decline is most significant in males under 50 years; in older age groups the values remain stable at a low level. Q10 supplementation doubles the number of ubiquinol-10-containing LDL molecules and may therefore have an inhibitory effect on LDL oxidation.
12. Cephalalgia. 2002 Mar;22(2):137-41.
“Open label trial of coenzyme Q10 as a migraine preventive.”
The objective was to assess the efficacy of CoQ10 as a preventive treatment for migraine headaches. Thirty-two patients (26 women, 6 men) with a history of episodic migraine with or without aura were treated with coenzyme Q10 at a dose of 150 mg per day. Thirty-one of 32 patients completed the study; 61.3% of patients had a greater than 50% reduction in number of days with migraine headache. The average number of days with migraine during the baseline period was 7.34 and this decreased to 2.95 after 3 months of therapy, which was a statistically significant response. Mean reduction in migraine frequency after 1 month of treatment was 13.1% and this increased to 55.3% by the end of 3 months. Mean migraine attack frequency was 4.85 during the baseline period and this decreased to 2.81 attacks by the end of the study period, which was a statistically significant response (P < 0.001). There were no side-effects noted with CoQ10. From this open label investigation CoQ10 appears to be a good migraine preventive. Placebo-controlled trials are now necessary to determine the true efficacy of CoQ10 in migraine prevention
13.. Balercia, G., G. Arnaldi, et al. (2002). "Coenzyme Q10 levels in idiopathic and varicocele-associated asthenozoospermia." Andrologia 34(2): 107-11. Levels of coenzyme Q10 (CoQ10) and of its reduced and oxidized forms (ubiquinol, QH2, and ubiquinone, Qox) have been determined in sperm cells and seminal plasma of idiopathic (IDA) and varicocele-associated (VARA) asthenozoospermic patients and of controls. The results have shown significantly lower levels of coenzyme Q10 and of its reduced form, QH2, in semen samples from patients with asthenospermia; furthermore, the coenzyme Q10 content was mainly associated with spermatozoa. Interestingly, sperm cells from IDA patients exhibited significantly lower levels of CoQ10 and QH2 when compared to VARA ones. The QH2/Qox ratio was significantly lower in sperm cells from IDA patients and in seminal plasma from IDA and VARA patients when compared with the control group. The present data suggest that the QH2/Qox ratio may be an index of oxidative stress and its reduction, a risk factor for semen quality. Therefore, the present data could suggest that sperm cells, characterized by low motility and abnormal morphology, have low levels of coenzyme Q10. As a consequence, they could be less capable in dealing with oxidative stress which could lead to a reduced QH2/Qox ratio. Furthermore, the significantly lower levels of CoQ10 and QH2 levels in sperm cells from IDA patients, when compared to VARA ones, enable us to hypothesize a pathogenetic role of antioxidant impairment, at least as a cofactor, in idiopathic forms of asthenozoospermia.
14. South Med J. 2001 Nov;94(11):1112-7.
“Randomized, double-blind, placebo-controlled trial of coenzyme Q10 in isolated systolic hypertension”
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 (CoQ10), an over-the-counter nutritional supplement, in a cohort of 46 men and 37 women with isolated systolic hypertension. We conducted a 12-week randomized, double-blind, placebo-controlled trial with twice daily administration of 60 mg of oral CoQ10 and determination of plasma CoQ10 levels before and after the 12 weeks of treatment. RESULTS: The mean reduction in systolic blood pressure of the CoQ10-treated group was 17.8 +/- 7.3 mm Hg (mean +/- SEM). None of the patients exhibited orthostatic blood pressure changes. CONCLUSIONS: Our results suggest CoQ10 may be safely offered to hypertensive patients as an alternative treatment option.
15. Balercia, G., F. Mosca, et al. (2004). "Coenzyme Q(10) supplementation in infertile men with idiopathic asthenozoospermia: an open, uncontrolled pilot study." Fertil Steril 81(1): 93-8. OBJECTIVE: To clarify a potential therapeutic role of coenzyme Q(10) (CoQ(10)) in infertile men with idiopathic asthenozoospermia. DESIGN: Open, uncontrolled pilot study. PATIENT(S): Infertile men with idiopathic asthenozoospermia. INTERVENTION(S): CoQ(10) was administered orally; semen samples were collected at baseline and after 6 months of therapy. MAIN OUTCOME MEASURE (S): Semen kinetic parameters, including computer-assisted sperm data and CoQ(10) and phosphatidylcholine levels. RESULT(S): CoQ(10) levels increased significantly in seminal plasma and in sperm cells after treatment. Phosphatidylcholine levels also increased. A significant increase was also found in sperm cell motility as confirmed by computer-assisted analysis. A positive dependence (using the Cramer's index of association) was evident among the relative variations, baseline and after treatment, of seminal plasma or intracellular CoQ(10) content and computer-determined kinetic parameters. CONCLUSION(S): The exogenous administration of CoQ(10) may play a positive role in the treatment of asthenozoospermia. This is probably the result of its role in mitochondrial bioenergetics and its antioxidant properties.
16. Littarru, G. P. and L. Tiano (2005). "Clinical aspects of coenzyme Q10: an update." Curr Opin Clin Nutr Metab Care 8(6): 641-6. PURPOSE OF REVIEW: Coenzyme Q10 is administered for an ever-widening range of disorders, therefore it is timely to illustrate the latest findings with special emphasis on areas in which this therapeutic approach is completely new. These findings also give further insight into the biochemical mechanisms underlying clinical involvement of coenzyme Q10. RECENT FINDINGS: Cardiovascular properties of coenzyme Q10 have been further addressed, namely regarding myocardial protection during cardiac surgery, end-stage heart failure, pediatric cardiomyopathy and in cardiopulmonary resuscitation. The vascular aspects of coenzyme Q10 addressing the important field of endothelial function are briefly examined. The controversial issue of the statin/coenzyme Q10 relationship has been investigated in preliminary studies in which the two substances were administered simultaneously. Work on different neurological diseases, involving mitochondrial dysfunction and oxidative stress, highlights some of the neuroprotective mechanisms of coenzyme Q10. A 4-year follow-up on 10 Friedreich's Ataxia patients treated with coenzyme Q10 and vitamin E showed a substantial improvement in cardiac and skeletal muscle bioenergetics and heart function. Mitochondrial dysfunction likely plays a role in the pathophysiology of migraine as well as age-related macular degeneration and a therapy including coenzyme Q10 produced significant improvement. Finally, the effect of coenzyme Q10 was evaluated in the treatment of asthenozoospermia. SUMMARY: The latest findings highlight the beneficial role of coenzyme Q10 as coadjuvant in the treatment of syndromes, characterized by impaired mitochondrial bioenergetics and increased oxidative stress, which have a high social impact. Besides their clinical significance, these data give further insight into the biochemical mechanisms of coenzyme Q10 activity.
