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What is Coenzyme Q10?

Coenzyme Q10 is often abbreviated to CoQ10 and referred to by chemists as ubiquinone because it belongs to a class of compounds known as quinines and because it is found in nearly every cell of the human body ~ it is ubiquitos.CoQ10 is found naturally in the mitochondria, an energy creating structure within cells. In the mitochondria, CoQ10 is involved in making a substance called ATP which serves as the primary energy source for cells. CoQ10 is also known to be an antioxidant that means it is able to neutralize free radicals throughout the body. Free radicals occur throughout the body and are known to be involved in the aging process as well as in disease processes such as heart disease and cancer.


Coenzyme Q10 is a substance that acts very much like a vitamin in the body. It is a member of the ubiquinone family, which are characterized by solubility in fat, hydrophobicity, and which are involved in electron transport and energy production. Coenzymes are non-proteinaceous substances that combine in the body with apoenzymes, which are proteinaceous, to form active enzyme systems. These enzyme systems are in turn involved in the breakdown of proteins (often into their component amino acids, which feed, fuel, repair and maintain the health of the body). Since vitamins are essential precursors to enzyme systems ("essential" meaning that the must be consumed and are physiologically necessary), and coenzyme Q10 is needed by the body, it is often considered a vitamin, however it is not truly "essential" - your body can produce coenzyme Q10.

Coenzyme Q10 can supply or remove oxygen from biologically active molecules. Every cell in your body contains intercellular components (organelles) called mitochondria, which produce 95% of the total energy of the body. Coenzyme Q10 is an integral part of the membranes of the mitochondria where it is involved in the production of ATP (adenosine triphosphate), the basic energy molecules of the cell. It is important to understand that ATP, produced by your mitochondria IS energy in potentia; that is, when you breath, sit, stand, run, exercise, walk, digest, laugh, whistle or mow the lawn, even think - everything that takes energy, which is everything you do - comes at the cost of your ATP stores. Supplementing coenzyme Q10 aids in the body's cellular respiration and energy production; it's that fundamental and it is fundamentally that important. Our bodies could not survive without coenzyme Q10, as it is necessary in the synthesis of ATP (Pizzorno 1999). If body levels start dropping, so does our general health; scientists have estimated that once body levels of coenzyme Q10 drop below the 25% deficiency levels, many health problems begin to flourish, including cardiovascular problems, immune system depression, periodontal problems, lack of energy, and weight gain, and it may be a contributing factor to the aging process (Pizzorno 1999).

Coenzyme Q10 is a nutrient necessary to the functioning of every cell in our bodies and now you know why. The greater the oxidative stress on a given organ tissue, the greater the need for coenzyme Q10, which may explain its usefulness in heart conditions (Pizzorno 1999). Levels of coenzyme Q10 begin to decline around age 30 and steadily decrease with age, making supplementation increasingly important. Since coenzyme Q10 production occurs in the same metabolic pathway as does cholesterol, it is suspected that the increased cholesterol synthesis that occurs as we age may be responsible for the drop off in coenzyme Q10 levels (Hendler 2001). It may be that as our cholesterol synthesis increases, the body's capacity to produce coenzyme Q10 necessarily decreases (since both share the same metabolic pathway - specifically, coenzyme Q10 production diverts some farnesyl diphosphate away from squalene production which in turn is used to make cholesterol) (Pizzorno 1999). It is also suspected that increasing coenzyme Q10 in the body can help decrease lipid peroxidation (Aejmelaeus 1997).

How do I get CoQ10?

CoQ10 is produced in the body naturally. However, it is sometimes not produced in sufficient quantities throughout the body and the body is not able to redistribute CoQ10 through the blood supply. The body's natural CoQ10 supply can be supplemented with nutritional supplements or through food. Meat and fish are the best sources of CoQ10 although the better sources from these foods are organs such as lungs, heart, liver and kidneys foods many consumers choose not to eat


Specific, Researched Uses of Coenzyme Q10 in Common Ailments


In general, Coenzyme Q10 benefits as an adjuvant therapy in cases where disease etiology is affected by oxidative stress and/or mitochondrial dysfunction, which include Parkinson's Disease, congestive heart failure, hypertension, migraine, macular degeneration, asthenozoospermia (infertility due to poor sperm motility), and Friedrich's ataxia (an inherited nerve-degenerative disease) (Littaru 2005). It is also quite helpful in cases of periodontal disease (Pizzorno 1999). It is very important to understand, however, that in most cases coenzyme Q10 is beneficial when used as an adjuvant therapy (not a primary therapy except where indicated), and nothing on this page is meant to be construed as a recommendation, diagnosis, or an endorsement of coenzyme Q10 as a primary medicinal treatment or cure of any disease.

Parkinson's Disease:


Patients diagnosed with Parkinson's Disease for 5 years were divided into four groups and given varying amounts of CoEnzyme Q10 and Vitamin E. The four groups were as follows: 300mg of coenzyme Q10, 600mg of coenzyme Q10, 1200mg of coenzyme Q10, or placebo; all groups received Vitamin E. The patients' improvement in mental function, motor ability and activities of daily living were dose dependent; those receiving 1200 mg of coenzyme Q10 each day showed the greatest improvement (44% less decline in the above function categories as compared to the placebo group). Patients receiving the smaller amounts of coenzyme Q10 did not fare as well as those in the 1200 mg group, but did better than those not receiving any coenzyme Q10 (Shults 2002).

Since then much research into coenzyme Q10 and Parkinson's Disease has been initiated but has mostly not been completed. However, a recent meta-analysis of coenzyme Q10/Parkinson's Disease studies has indicated that coenzyme Q10 is indeed of some benefit to sufferers of Parkinson's Disease (Weber 2006), but left conclusive value as to its benefit in question for further research.

NOTE regarding statins and PD: though statins reduce the levels of coenzyme Q10 in the body, and coenzyme Q10 is known to benefit in PD, it has not been shown that statins worsen the severity of PD (Lieberman 2005). (More under "Statins", below.)

Cardio-Vascular Disease (CVD):

Perhaps the best researched aspect of coenzyme Q10 is it's use as an adjuvant therapy in cases of heart disease, both in preventative and palliative scenarios. The reason why coenzyme Q10 is so beneficial to the heart is because Coenzyme q10 possesses the ability to protect the heart during periods of aschemia, or oxygen deprivation. When the mitochondria are performing optimally, cellular respiration is at its best, too, and this is quite beneficial to your heart. Additionally, researchers believe that Coenzyme q10 prevents the oxidation of low-density lipoproteins (LDL; i.e., the "bad" cholesterol), making it an important supplement for anyone with high cholesterol (more on this topic under "Statins", below).

Numerous studies have shown that pre-treatment with coenzyme Q10 helps heart patients come through various open heart surgeries in better health and with shorter recovery times than those who have not been so treated (Judy 1993, Rosenfeldt 1999, 2005). In a study performed in 1998, Coenzyme q10 was shown to halve the total number of subsequent cardiovascular incidents in patients who had suffered myocardial infarctions (heart attack), as long as the Coenzyme q10 was begun within three days of the infarction (Singh 1998). That's a really big deal as anyone who has had or knows someone who has had a heart attack can attest. Maybe most exciting are the studies that show that coenzyme Q10 has helped patients with severe cardiomyopathy to live well beyond their usual life expectancies 1 and has helped those with congestive heart failure (Sinatra 1997) as well as those awaiting heart transplant enjoy an improved quality of life (Berman 2004). Also of interest, and a topic that is currently undergoing more rigorous study, is the use of coenzyme Q10 in reducing liver and cardio-toxicity due to cancer chemotherapy (Roffe 2004). (Interesting side note: one study we found indicated that baseline coenzyme Q10 levels were strongly predictive of melanoma metastasis (Rusciani 2006).)

But you certainly do not have to be in such dire health circumstances to benefit from coenzyme Q10. Overall, it has been shown to improve ejection fraction and end diastolic volume of the heart (Weant 2005), and it can be used as part of a lifestyle method of reducing hypertension (Wilburn 2004).


High cholesterol is very common health concern in America today; odds are almost certain that you or someone you know has been instructed by their physician to reduce their cholesterol level. Statin drugs, also known as HMG-CoA Reductase Inhibitors, are extremely popular prescriptions for the reduction of cholesterol (accounting for many of the top sellers for the pharmaceutical companies). But, as discussed above, cholesterol and coenzyme Q10 are produced through the same metabolic pathway and when you block the pathway to effect a reduction in cholesterol, you also effect a reduction in endogenous coenzyme Q10 production. This, as the reader may suspect, is not good. Another problem that occurs with prolonged use of statin drugs is a condition known as rhabdomyolysis. Rhabdomyolysis is why statin users have to have their liver enzymes checked periodically. It is a nasty condition whereby skeletal muscle tissue is destroyed and its contents (many things, but of most concern is potassium) dumped into the blood stream, taxing the liver and causing, in the worst case scenario, acute renal failure if left untreated.

Some good news is on the horizon: coenzyme Q10 has shown to be of promise in combination with statin drugs (Chapidze 2005), AND it may be able to help reverse rhabdomyolysis (Farswan 2005). As is nearly always the case, it looks good, but more study is needed.

Migraine Headache

There is good preliminary evidence that coenzyme Q10 is a safe, natural, and highly effective way to reduce the occurrence of migraine headache (Bianchi 2004, Modi 2006, Sandor 2005). While general consensus must remain guarded, there is one stand-out study that is worth mentioning because it is of the double-blind, randomized, placebo-controlled variety. This study showed that 100mg, 3x/day reduced the 50%-responder-rate of migraine attack by 47.6% as compared to 14.4% for placebo (Sandor 2005).

Asthenozoospermia/Asthenospermia (infertility due to low sperm motility)

We didn't expect to find this when we began our research into coenzyme Q10, but a new avenue of research into this versatile substance has to do with male fertility. The studies we found were universally promising. In men with infertility or low fertility with a diagnosis of idiopathic asthenozoospermia (low sperm motility), coenzyme Q10 has been shown to improve sperm fertilization rates, sperm count, and sperm motility (Alleva 1997, Ballercia 2004, Lewin 1997, Mancini). The reason for this is theorized to be that the coenzyme Q10 concentration in the sperm is directly responsible for reactive oxygen species (ROS) quenching. As we age we are exposed to environmental toxins which accumulate in the body; without proper anti-oxidant defences (e.g. endogenous coenzyme Q10) these toxins take their toll on the body's tissues and cells. Sperm cells are also susceptible to such attacks, so increasing coenzyme Q10 and other anti-oxidants in the diet can help to reverse male infertility when it is due to these oxidative stresses (Sheweita 2005, Sinclair 2000).

For men diagnosed with varicocele, the benefits of coenzyme Q10 are less clear as there seems to be some as yet unarticulated molecular pathology at work in these patients (Balercia 2002, Mancini). 


Usage should be adjusted according to the problem it is being taken to address, but is typically effective in the range of 100-300 mg/day. As coenzyme Q10 is lypophilic it should always be taken with food as this will increase its absorption rate.

Side Effects

There are no contraindications for coenzyme Q10; it is exceedingly safe. According to the PDR for Nutritional Supplements, precautions include only Warfarin users. Coenzyme Q10 may decrease the effectiveness of Warfarin, though this warning is based on only one report. The PDR also indicates that it may reduce the need for certain type II diabetes medicines, so the type II diabetic user should be aware of this. Adverse reactions include mild gastrointestinal symptoms in some persons (Hendler 2001), though we have received no reports of this.



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.

Works Cited

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.

Alleva, R., A. Scararmucci, et al. (1997). "The protective role of ubiquinol-10 against formation of lipid hydroperoxides in human seminal fluid." Mol Aspects Med 18 Suppl: S221-8. Defective sperm function in infertile men has been associated with increased lipid peroxidation and impaired function of antioxidant defenses in spermatozoa. Evidence strongly suggests that CoQ10, a lipid-soluble component of the respiratory chain acts, in its reduced form (ubiquinol), as a potent antioxidant in various biological systems, such as lipoproteins and membranes. In this study we assayed CoQ10 content in both the reduced and oxidized form (ubiquinol/ubiquinone), and hydroperoxide levels in seminal plasma and seminal fluid from 32 subjects with a history of infertility. Our results showed a significant correlation between ubiquinol content and sperm count (r = 0.62; P < 0.05) in seminal plasma. An inverse correlation between ubiquinol content and hydroperoxide levels both in seminal plasma and in seminal fluid (r = -0.56; P = 0.01) was found. Using multiple regression analysis we also found a strong correlation among sperm count, motility and ubiquinol-10 content (P < 0.01) in seminal fluid. An inverse correlation between ubiquinol/ubiquinone ratio and percentage of abnormal morphology was also observed in total fluid. These results suggest that ubiquinol-10 inhibits hydroperoxide formation in seminal fluid and in seminal plasma. Since peroxidation in sperm cells is an important factor affectingmale infertility, ubiquinol could assume a diagnostic and/or a therapeutic role in these patients.

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.

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.

Berman, M., A. Erman, et al. (2004). "Coenzyme Q10 in patients with end-stage heart failure awaiting cardiac transplantation: a randomized, placebo-controlled study." Clin Cardiol 27(5): 295-9. BACKGROUND: 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.

Bhagavan, H. N. and R. K. Chopra (2005). "Potential role of ubiquinone (coenzyme Q10) in pediatric cardiomyopathy." Clin Nutr 24(3): 331-8. Pediatric cardiomyopathy (PCM) represents a group of rare and heterogeneous disorders that often results in death. While there is a large body of literature on adult cardiomyopathy, all of the information is not necessarily relevant to children with PCM. About 40% of children who present with symptomatic cardiomyopathy are reported to receive a heart transplant or die within the first two years of life. In spite of some of the advances in the management of PCM, the data shows that the time to transplantation or death has not improved during the past 35 years. Coenzyme Q10 is a vitamin-like nutrient that has a fundamental role in mitochondrial function, especially as it relates to the production of energy (ATP) and also as an antioxidant. Based upon the biochemical rationale and a large body of data on patients with adult cardiomyopathy, heart failure, and mitochondrial diseases with heart involvement, a role for coenzyme Q10 therapy in PCM patients is indicated, and preliminary results are promising. Additional studies on the potential usefulness of coenzyme Q10 supplementation as an adjunct to conventional therapy in PCM, particularly in children with dilated cardiomyopathy, are therefore warranted.

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.

Bianchi, A., S. Salomone, et al. (2004). "Role of magnesium, coenzyme Q10, riboflavin, and vitamin B12 in migraine prophylaxis." Vitam Horm 69: 297-312. Migraine is a neurovascular syndrome characterized by recurrent headache associated with other symptoms, eventually preceded by aura. This chapter reviews the involvement of some mineral, coenzyme, and vitamin defects in the pathogenesis of migraine headaches and focuses on their potential therapeutic use in the preventive treatment for migraine. The therapeutic potential of magnesium, coenzyme Q(10), riboflavin, and vitamin B(12) can be cautiously inferred from some published open clinical trials; it should, however, be considered that double-blind randomized larger studies are needed to correctly estimate the impact of the placebo effect in these promising therapies.

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.

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.

Farswan, M., S. P. Rathod, et al. (2005). "Protective effect of coenzyme Q10 in simvastatin and gemfibrozil induced rhabdomyolysis in rats." Indian J Exp Biol 43(10): 845-8. Administration of simvastatin (80 mg/kg, po. evening dose) and gemfibrozil (600 mg/kg, po twice) for 30 days produced significant decrease in the level of reduced glutathione, superoxide dismutase, catalase and increase in the level of lipid peroxidation and various serum parameters (creatine phosphokinase, lactate dehydrogenase, serum glutamate oxaloacetate transaminase, creatinine, urea and blood urea nitrogen). This suggested involvement of oxidative stress in rhabdomyolysis. Increase in the level of reduced glutathione, superoxide dismutase, catalase and decrease in the level of lipid peroxidation and serum parameters after administration of antioxidant CoQ10 (10 mg/kg.ip) proved the protective effect of CoQ10 in rhabdomyolysis.

Hendler, Sheldon Saul and Rorvik, David, Eds. 2001. PDR for Nutritional Supplements. 1st ed. Montvale, NJ: Medical Economics Thomson Healthcare.

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)

Levy, H. B. and H. K. Kohlhaas (2006). "Considerations for supplementing with coenzyme Q10 during statin therapy." Ann Pharmacother 40(2): 290-4. OBJECTIVE: To review the literature concerning the effects of statin use on coenzyme (Co) Q10 concentrations and explain the rationale behind considering CoQ10 supplementation. DATA SOURCES: A MEDLINE search was conducted through January 2006. Search terms included ubiquinone, coenzyme Q10, HMG-CoA reductase inhibitors, statins, myotoxicity, and clinical trials. DATA SYNTHESIS: Statin therapy reduces blood CoQ10 concentrations. Studies exploring how this affects the development of myotoxicity have been small and dissimilar, thus limiting the ability to draw strong conclusions. Isolated studies suggested that statins induce mitochondrial dysfunction, but the clinical implications of this effect are limited. Limited data suggest that patients with familial hypercholesterolemia, heart failure, or who are over 65 years of age might represent at-risk populations who would benefit from CoQ10 supplementation. CONCLUSIONS: Routine CoQ10 supplementation for all patients taking statins to prevent myotoxicity is not recommended. However, certain subpopulations might be at risk and warrant further study.

Lewin, A. and H. Lavon (1997). "The effect of coenzyme Q10 on sperm motility and function." Mol Aspects Med 18 Suppl: S213-9. In sperm cells, the majority of coenzyme Q10 (CoQ10) an energy promoting agent and antioxidant, is concentrated in the mitochondria of the midpiece, so that the energy for movement and all other energy-dependent processes in the sperm cell also depend on the availability of CoQ10. The reduced form of CoQ10-ubiquinol also acts as an antioxidant, preventing lipid peroxidation in sperm membranes. The objective of the study was to evaluate the effect of CoQ10 on sperm motility in vitro, after incubation with 38 samples of asthenospermic and normal motility sperm, and to evaluate the effect of CoQ10 administration in vivo in 17 patients with low fertilization rates after in vitro fertilization with intracytoplasmic sperm injection (ICSI) for male factor infertility. All 38 sperm samples from patients registered in our infertility clinic had normal concentrations and morphology. Of these, 16 patients had normal motility (mean 47.5%) and 22 patients were asthenospermic (mean motility 19.1%). Sperm samples were divided into four equal parts and incubated for 24 h in: HAM's medium alone, in HAM's medium with 1% DMSO and HAM's with 5 microM or 50 microM CoQ10. While no significant change in motility after incubation was observed in the samples with initial normal motility, a significant increase in motility was observed in the 50 microM CoQ10 subgroup of sperm from asthenospermic men, with a motility rate of 35.7 +/- 19.5%, as compared to 19.1 +/- 9.3% in the controls (P < 0.05). The 17 patients with low fertilization rates after ICSI were treated with oral CoQ10, 60 mg/day, for a mean of 103 days before the next ICSI treatment. No significant change was noted in most sperm parameters, but a significant improvement was noted in fertilization rates, from a mean of 10.3 +/- 10.5% in their previous cycles, to 26.3 +/- 22.8% after CoQ10 (P < 0.05). In conclusion, the administration of CoQ10 may result in improvement in sperm functions in selective patients. Further investigation into the mechanisms related to these effects is needed.

Lieberman, A., K. Lyons, et al. (2005). "Statins, cholesterol, Co-enzyme Q10, and Parkinson's disease." Parkinsonism Relat Disord 11(2): 81-4. 'Statins', drugs that lower cholesterol are widely used. Statins block cholesterol in the body and brain by inhibiting HMG-Co-A reductase. This pathway is shared by CoQ-10. An unintended consequence of the statins is lowering of CoQ-10. As CoQ-10 may play a role in PD, its possible statins may worsen PD. Such a report has appeared. Statins came into wide use in 1997-1998, 6 years before our study began. Thus 74% of our patients on a statin had a PD duration of 1-6 years versus 56% of our patients not on a statin. A direct comparison of patients on a statin and not on a statin would bias the study in favor of the statins: patients on a statin would have a shorter disease duration and less advanced PD. Therefore we divided the patients into two groups. Group I consisted of 128 patients on a statin, and 252 not on a statin who had PD for 1-6 years. In this group, disease severity (Hoehn & Yahr Stage), levodopa dose, Co-enzyme Q10 use, prevalence of 'wearing off', dyskinesia and dementia were similar. Group II consisted of 45 patients on a statin and 200 patients not on a statin who had PD for 7-22 years. In this group disease severity, levodopa dose, Co-enzyme Q10 use, prevalence of wearing off, dyskinesia and dementia were similar. Statins although they may affect Co-enzyme Q10 levels in the body and the brain, do not worsen PD at least as assessed by stage, and prevalence of wearing-off, dyskinesia, and dementia.

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.

Mancini, A., B. Conte, et al. (1994). "Coenzyme Q10 levels in human seminal fluid: diagnostic and clinical implications." Mol Aspects Med 15 Suppl: s249-55. The levels of Coenzyme Q10 (CoQ10) were determined by HPLC in seminal fluid samples obtained from 77 patients who performed a standard semen analysis for infertility, previous phlogosis or varicocele. CoQ10 was determined in total seminal fluid (n = 60), in seminal plasma (n = 44) and in the cell pellet (n = 37). The molecule, in total fluid, showed a linear correlation with sperm count and motility. In the pellet of spermatozoa, a trend toward an inverse correlation between CoQ10 (expressed as ng/10(6) cells) and semen parameters could be observed. A different pattern was shown in varicocele patients, in whom, in total fluid, the correlation between CoQ10 and sperm count was preserved, but the one between CoQ10 and sperm motility was lacking; moreover, a higher proportion of CoQ10 was present in seminal plasma, and the inverse trend between cellular CoQ10 and sperm count and motility was not observed. These data suggest a pathophysiological role of ubiquinone in human seminal fluid and a molecular defect in the spermatozoa of varicocele patients.

Mancini, A., G. Conte, et al. (1998). "Relationship between sperm cell ubiquinone and seminal parameters in subjects with and without varicocele." Andrologia 30(1): 1-4. In a previous paper it was demonstrated that Coenzyme Q10, a lipidic molecule with important antioxidant properties, is present at remarkable levels in human seminal fluid, and shows a direct correlation with seminal parameters (sperm count and motility). In patients with varicocele, on the contrary, correlation with sperm motility was lacking and a higher proportion of Coenzyme Q10 was found in seminal plasma. In the present study, the levels of Coenzyme Q10 in the cell pellet of spermatozoa, obtained after centrifugation of semen, were evaluated. In nonvaricocele subjects it was observed that a higher concentration of Coenzyme Q10 (expressed as ng of the molecule per million of cells) was present in the spermatozoa of oligospermic and asthenospermic patients (sperm count < 20 x 10(6) spermatozoa ml-1, sperm motility < 40%). This relationship was not observed in varicocele subjects, who also showed slightly lower intracellular absolute values of the conenzyme. Since Coenzyme Q10 is an antioxidant molecule involved in the defence of the cell from free radical damage, higher intracellular concentrations may represent a mechanism of protection of the spermatozoa. In varicocele patients, this mechanism could be deficient, leading to higher sensitivity to oxidative damage.

Mancini, A., L. De Marinis, et al. (1994). "Coenzyme Q10 concentrations in normal and pathological human seminal fluid." J Androl 15(6): 591-4. Coenzyme Q10 (CoQ10) levels were assayed in total seminal fluid or both in seminal fluid and seminal plasma in 77 subjects with normal or pathological findings at standard semen analysis. CoQ10 levels showed a significant correlation with sperm count and with sperm motility. An interesting exception was constituted by patients with varicocele, in whom the correlation with sperm concentration was preserved, whereas the correlation with sperm motility was lacking. Moreover, they showed an increased ratio of plasma CoQ to total seminal CoQ10 in comparison with the other subjects. These data suggest a pathophysiological meaning of CoQ10 in human seminal fluid and a possible molecular defect in varicocele patients. CoQ10 measurement could represent an important examination in infertile patients; moreover, from these results a rationale might arise for a possible treatment with exogenous CoQ10 in dyspermic patients.

Mancini, A., D. Milardi, et al. (2003). "Coenzyme Q10: another biochemical alteration linked to infertility in varicocele patients?" Metabolism 52(4): 402-6. Previously we demonstrated that coenzyme Q10 (CoQ10) is present in human seminal fluid and shows a direct correlation with seminal parameters except in patients with varicocele (VAR). We have now evaluated CoQ10 distribution in VAR, versus control subjects, in order to discover metabolic abnormalities within this condition. We studied 32 patients with VAR (11 with oligoasthenozoospermia, 13 with asthenozoospermia, and 8 with normozoospermia), and, as controls, the following groups of subjects, matched with VAR patients according to seminal parameters: 16 patients with idiopathic oligozoospermia, 11 patients with isolated asthenozoospermia, and 14 normal fertile men. CoQ10 was assayed in total seminal fluid, plasma, or cell pellet by high-performance liquid chromatography (HPLC). We found a significantly higher proportion of CoQ10 in seminal plasma in VAR; cellular CoQ10 showed an inverse correlation with sperm concentration and motility in VAR, at variance with controls. As seminal plasma ubiquinone reflects an interchange between intracellular and extracellular compartments, the different distribution in VAR patients could represent a greater sensitivity to peroxidative damage and could suggest reduced utilization for energy, which in turn could cause a defective motility even in patients with a normal cell count. These data suggest a pathophysiological role of CoQ10 in seminal plasma and a possible molecular defect in VAR.

Mancini, A., D. Milardi, et al. (2005). "Seminal antioxidants in humans: preoperative and postoperative evaluation of coenzyme Q10 in varicocele patients." Horm Metab Res 37(7): 428-32. Coenzyme Q10 in seminal fluid shows a direct correlation with seminal parameters except in patients with varicocele. To evaluate whether surgical treatment of varicocele could revert CoQ10 abnormalities, we have studied CoQ10 distribution in thirty-three VAR patients, before and 6-8 months after varicocelectomy, twenty patients with idiopathic oligozoospermia, eleven with isolated asthenozoospermia and sixteen normal fertile men. CoQ10 was assayed in total seminal fluid, plasma or cell pellet by HPLC. A significantly higher CoQ10 proportion in seminal plasma in VAR vs. controls (mean +/- SEM: 61.68 +/- 2.41 vs. 41.60 +/- 1.99%, respectively) was present; total CoQ10 correlated with sperm motility in controls, but not in VAR; an inverse correlation between cellular CoQ10 and motility was present in VAR, but not in controls. Postoperatively, a partial reversion was observed, since the plasma-to-total CoQ10 ratio decreased, but the correlation between total CoQ10 and motility was not restored. On the contrary, the peculiar correlation between cellular CoQ10 and motility was no more detectable in postoperative VAR patients. A partial postoperative reversal of abnormalities in CoQ10 distribution and correlation with seminal parameters was therefore present.


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