Serum Coenzyme Q10 Research Articles

Serum Coenzyme Q10 Levels and Oxidative Status in Patients with Fibromyalgia Syndrome

Objectives: The aim of this study was to determine the relationship between serum coenzyme Q10 [CoQ10] levels and symptoms of fatigue associated with fibromyalgia syndrome [FMS].Methods: Patients diagnosed with primary FMS and domographically matching healthy normal controls [HNCs] were sought to participate in the study. The total antioxidant status, total oxidative status, and CoQ10 levels were measured in blood samples from the patients and the controls.Results: A total of 40 patients with FMS and 30 HNCs were recruited. There were no statistically significant differences between the two groups in regard to C-reactive protein, mean erythrocyte sedimentation rate, mean age, and mean body mass index [p > 0.05]. The mean time from symptom onset to diagnosis for the FMS patients was 2.88 years, and the average number of tender points was 14. The serum CoQ10 levels were significantly lower in the FMS patients compared with the HNC group [p = 0.000]. The serum total oxidative status and oxidative stress index levels were higher, and the serum total antioxidant status levels were lower in the FMS patients compared with those of the HNC group [p < 0.05]. The visual analog scale [VAS] pain scores and the VAS fatigue scores were significantly higher in the FMS group than in the HNC group [p = 0.000]. The serum CoQ10 levels were negatively correlated with the mean Modified Fatigue Impact Scale scores [p = 0.02, r = 0.30], VAS pain scores [p = 0.00, r = 0.38], and VAS fatigue scores [p = 0.03, r = 0.28].Conclusions: The CoQ10 deficiency may contribute to the etiopathogenesis of FMS fatigue.

Effects of lifestyle factors on urinary oxidative stress and serum antioxidant markers in pregnant Japanese women: A cohort study.

Oxidative stress plays a major pathological role in pregnancy-related complications. Although oxidative stress is induced by exogenous toxins in association with a poor lifestyle in normal subjects, there is little information on the factors altering oxidative stress and antioxidant levels during pregnancy. The purpose of this study was to determine the relationship between lifestyle factors and oxidative stress/antioxidant levels during each trimester and 1-month postpartum. This prospective cohort study followed 54 healthy women through pregnancy; first, second, and third trimester and 1-month postpartum. Participants were administered a questionnaire on characteristics and lifestyle factors. Morning blood and urine samples were obtained to measure urinary biopyrrins and serum coenzyme Q10 (CoQ10) levels. The levels of urinary biopyrrins and serum CoQ10 increased significantly throughout pregnancy, with peak values registered during the third trimester. Higher biopyrrin levels were significantly associated with non-consumption of morning meal during the first trimester, smoking during the third trimester and 1-month postpartum, alcohol consumption during the third trimester, high food-based polyunsaturated fatty acid intake during the third trimester, and poor mental health scores during the first and third trimesters. Higher CoQ10 levels were significantly associated with no smoking during pregnancy and at 1-month postpartum, and with a high frequency of exercise during the third trimester and 1-month postpartum. Thus, pregnancy represents a state of oxidative stress, which can be counterbalanced by increased levels of antioxidants, such as CoQ10. We speculate that certain lifestyle choices such as avoiding smoking can reduce oxidative stress and increase antioxidant levels during pregnancy.

Plasma Coenzyme Q10 and Tocopherols in Thoroughbred Race Horses: Effect of Coenzyme Q10 Supplementation and Exercise

The fundamental role of coenzyme Q10 (CoQ10) in cellular bioenergetics is well established in humans and several other species, yet there is no information about its role in horses. In continuation of our study of serum CoQ10 in Thoroughbred race horses, we examined the effect of CoQ10 supplementation and exercise on changes in plasma CoQ10 and α- and γ-tocopherol concentrations. Two groups of horses, five per group, were used. One group received 1.9 g of CoQ10 daily and the second group 3.4 g as a dietary supplement. Both groups were subjected to graduated training sessions that involved low-intensity exercise (gallop) followed by high-intensity exercise (breeze). CoQ10 supplementation resulted in a significant increase in plasma CoQ10 during low-intensity exercise, whereas the increase following high-intensity exercise was markedly attenuated in both groups (P < .05). There were no changes in plasma α- and γ-tocopherol concentrations following the two exercise sessions. γ-Tocopherol constituted approximately 5% of α-tocopherol; this is the first report of plasma γ-tocopherol in horses. The attenuated response of plasma CoQ10 in horses receiving CoQ10 supplementation following high-intensity exercise may be attributed to its consumption during severe oxidative stress. This finding indicates that in horses not receiving any CoQ10 supplementation, high-intensity exercise would result in a marked depletion of endogenous CoQ10 in plasma, which could compromise their health and physical performance. This documents the importance of CoQ10 in horses. The study also establishes the safety and tolerability of high-dose CoQ10 in Thoroughbred race horses.

AB0660 Serum coenzyme-q10 activity and oxidative status in patients with fibromyalgia

ObjectivesIn this study, we aimed to show the relationship between CoQ10 and fatigue symptoms of Fibromyalgia (FM).MethodsA total of 40 patients diagnosed as primary FM according to the ACR criteria...

Serum levels of coenzyme Q10, tocopherols, and C‐reactive protein in adolescent girls and premenopausal women

ObjectiveGiven the importance of anti‐oxidant dietary compounds for chronic disease prevention, we examined the differences in serum levels of Coenzyme Q10 (CoQ10), α‐tocopherol (α‐Toc), γ‐tocopherol (γ‐Toc), and C‐reactive protein (CRP) between adolescent girls and premenopausal women.MethodsBaseline body mass index (BMI) and serum levels of CoQ10, α‐Toc, γ‐Toc, and CRP from 207 adolescent girls (13 to 19 yr) were compared with those from 183 premenopausal women (34 to 47 yr) by t‐test. Associations of age and BMI with serum biomarkers were assessed using multiple regression.ResultsAdolescent girls had significantly lower mean BMI and serum CoQ10, α‐Toc, γ‐Toc, and CRP levels than premenopausal women (BMI: 22.1 vs. 26.1 kg/m2, P &lt;0.0001; CoQ10: 376 vs. 544 ng/mL, P&lt;0.0001; α‐Toc: 6.9 vs. 13.5 μg/mL, P&lt;0.0001; γ‐Toc: 1.28 vs. 1.69 μg/mL, P&lt;0.0001; CRP: 1.29 vs. 2.13 mg/L, P&lt;0.0001). The differences in CoQ10, α‐Toc, and γ‐Toc remained after adjusting for BMI. CRP and γ‐Toc were significantly and positively associated with BMI in both age groups.ConclusionsLower serum CoQ10, α‐Toc, γ‐Toc, and CRP levels observed in the adolescent girls relative to premenopausal women suggest that adolescent girls may have reduced need for circulating antioxidants as a consequence of their lower inflammation status as indicated by the lower CRP values.This research was supported by Department of Defense Grant BC032028 and National Institutes of Health grants R03CA130061 and S10RR020890.

Serum coenzyme Q10 levels are associated with coronary flow reserve in hemodialysis patients

Accelerated atherosclerosis is the major cause of mortality in patients on chronic hemodialysis (HD). The aim of this study was to evaluate the relation between coenzyme Q10 (CoQ10) levels and coronary flow reserve (CFR) in HD patients as an indicator of atherosclerosis. Seventy-one chronic HD patients and 65 age- and sex-matched healthy individuals were included in the study. Plasma CoQ10 levels were performed by high-performance liquid chromatography measurements. CFR was assessed by transthoracic Doppler echocardiography. Serum CoQ10 levels (1.36 ± 0.43 vs. 2.53 ± 0.55, P < 0.001) and CFR values (1.73 ± 0.11 vs. 2.32 ± 0.28, P < 0.001) were significantly lower in HD patients compared with controls. There was a significant positive correlation between CFR and serum levels of CoQ10 (r = 0.669, P < 0.001). A linear regression analysis showed that serum levels of CoQ10 were still significantly and positively correlated with CFR (regression coefficient = 0.235, P < 0.001). Our data have demonstrated that HD patients exhibit decreased plasma CoQ10 levels and CFR values. The study also showed for the first time that serum CoQ10 levels independently predict CFR in HD patients.

Coenzyme Q10 in Equine Serum: Response to Supplementation

Although the importance of coenzyme Q10 (CoQ10) in health and disease and its critical role in cellular bioenergetics have been well established in various species, there is a total lack of information on the role of CoQ10 in horses. Therefore, the present study was undertaken first to ascertain the occurrence of CoQ10 and/or possibly other homologs of coenzyme Q (CoQ) in horse serum, and then to examine the response to CoQ10 supplementation on serum CoQ10 concentration. The study was carried out with 2-year-old Thoroughbred horses. Total CoQ (reduced and oxidized forms) in serum was assayed by high-performance liquid chromatography. The data show that horse serum contains CoQ as CoQ10, at a much lower concentration as compared with that of humans and several other species. There is no evidence for the presence of coenzyme Q9 or other homologs of CoQ. On supplementation with CoQ10 at 800 mg a day (1.47 mg/kg body weight), there was a significant increase in serum CoQ10 concentration, approximately 2.7-fold at 60 days. CoQ10 supplementation at this dosage was found to be safe and well tolerated. Additional studies are needed to examine whether maintaining higher serum CoQ10 concentrations is of potential health benefit to the horses, as assessed by selected biochemical markers and also in terms of performance.

Mitochondria function and structure in brown adipose tissue is influenced by maternal low salt intake during the perinatal period

ObjectiveTo evaluate brown adipose tissue (BAT) structure and function in female offspring of dams fed low salt diet during the perinatal period.MethodsFemale Wistar rats were fed low (LS: 0.15%) or normal (NS: 1.3% NaCl) salt diet since 8 weeks of age. At 12 weeks of age they were mated. After weaning, all offspring, were fed standard chow. Body temperature (T) was measured during 24 hours in adult female offspring (oLS or oNS) exposed to a cold (C) or room temperature (RT) environment. Gene expression (GE) of uncoupling protein‐1 (UCP1). PPARγ (PP), PGC1α (PG) and FOX C2 (FO) and mitochondria surface area (MIT) by electron microscopy were analyzed in BAT. Serum coenzyme Q10 was measured by HPLC.Results(p&lt;0.05, n=5/group): Compared to RT, during day time, T was lower in both offspring groups exposed to C. During night time, T was lower only in oNS exposed to C. Compared to oNS, GE of UCP1, PP and FO were lower (20%, 19%, and 57%, respectively) in oLS exposed to RT but not to C. GE of UCP1 and PG were higher (24% and 43%, respectively) in oLS exposed to C than in oLS exposed to RT. MIT was higher (76%) in oNS exposed to C than oNS exposed to RT. Compared to RT, Q10 was higher (110%) in oNS and lower (53%) in oLS exposed to C.ConclusionsLow salt intake during the perinatal period is associated with alterations in the response to cold exposure and of gene expression of factors related to energy metabolism in the offspring.Supported by FAPESP.

Serum fetuin-A, coenzyme Q10 and plasma fatty acid levels in obese and healthy subjects

Aim: The aim of this study was to investigate serum fetuin-A, coenzyme Q10 and plasma fatty acids profiles in obese and healthy subjects. Subjects & Methods: The study was performed on a total of 105 obese subjects (22 male and 83 female) aged 38.3 ± 12.9 years and 80 healthy subjects (20 male and 60 female) aged 36.3 ŷ 11.3 years. Plasma fatty acid composition was measured by gas chromatography-mass spectrometry, serum coenzyme Q10 level was measured by high-performance liquid chromatography and serum fetuin-A level was measured by ELISA methods. Results: Plasma myristic acid, palmitic acid, palmitoleic acid, 10c-heptadecanoic acid, linoleic acid, heneikosanoic acid, saturated fatty acids levels and D9-desaturase activity of the obese subjects were significantly higher (p ü 0.05), whereas behenic acid levels and elongase activity were significantly lower (p ü 0.05) than the same parameters in the controls. There were no significant differences between plasma monounsaturated fatty acids, polyunsaturated fatty acids, serum coenzyme Q10 and fetuin-A levels in either of the groups. Discussion: Our results demonstrate that plasma saturated fatty acid levels of obese subjects were significantly increased. Also, the plasma levels of some fatty acids and enzyme activities of both groups were significantly different from each other. The role of these findings in the development of obesity needs to be investigated further. In addition, our results, demonstrating that fetuin-A levels were not associated with BMI or waist circumference, suggest that fetuin-A may not play a critical role in the development of obesity.

Coenzyme Q10 and its Relation with Oxidant and Antioxidant System Markers in Patients with End-Stage Renal Disease

Rationale and objectives: Oxidative stress is increased in chronic kidney disease (CKD) patients and end-stage renal disease (ESRD) patients undergoing dialysis treatment. Coenzyme Q10 (CoQ10) is a ubiquitous and strong antioxidant. Role of CoQ10 is not fully evaluated in renal patients. We aimed to investigate the relationship of CoQ10 with oxidant and antioxidant system markers in patients with renal disease. Material and methods: Forty patients with CKD (stages 3–5) who were managed conservatively without dialysis treatment, 40 hemodialysis, and 60 chronic ambulatory peritoneal dialysis (CAPD) patients were included in the study. Biochemical and whole blood analyses were done using hospital auto-analyzers from stored samples. Serum CoQ10, malondialdehyde (MDA), superoxide dismutase (SOD), and antioxidant activity (AOA) levels were determined. Main findings: There was no difference among the groups in terms of serum CoQ10 levels. However, other components of antioxidant system, namely, SOD and AOA were significantly higher in CAPD patients when compared to CKD patients. MDA levels were not significantly different among the groups. Principal conclusion(s): The results of this study showed no difference among CKD, CAPD, and hemodialysis patients in terms of serum CoQ10 levels.

Coenzyme Q10 and cognition in atorvastatin treated dogs

Statins have been suggested to protect against Alzheimer's disease (AD). Recently, however, we reported that aged dogs that underwent chronic statin treatment exhibited cognitive deficits compared with age matched controls. In human studies, blood levels of Coenzyme Q10 (CoQ10) decrease with statin use. CoQ10 is important for proper mitochondrial function and is a powerful antioxidant, two important factors for cognitive health in aging. Thus, the current study tested the hypothesis that CoQ10 levels in the serum and/or parietal cortex are decreased in statin treated dogs and are associated with poorer cognition. Six aged beagles (>8 years) were administered 80mg/day of atorvastatin for 14.5 months and compared with placebo-treated animals. As predicted, serum CoQ10 was significantly lower in statin-treated dogs. Parietal cortex CoQ10 was not different between the two groups. However, poorer cognition was correlated with lower parietal cortex CoQ10. This study in dogs suggests that serum CoQ10 is reduced with atorvastatin treatment. CoQ10 levels in brain may BE linked to impaired cognition in response to atorvastatin, in agreement with previous reports that statins may have a negative impact on cognition in the elderly.

Coenzyme Q10, Rosuvastatin, and Clinical Outcomes in Heart Failure: A Pre-Specified Substudy of CORONA (Controlled Rosuvastatin Multinational Study in Heart Failure)

The purpose of this study was to determine whether coenzyme Q₁₀ is an independent predictor of prognosis in heart failure. Blood and tissue concentrations of the essential cofactor coenzyme Q₁₀ are decreased by statins, and this could be harmful in patients with heart failure. We measured serum coenzyme Q₁₀ in 1,191 patients with ischemic systolic heart failure enrolled in CORONA (Controlled Rosuvastatin Multinational Study in Heart Failure) and related this to clinical outcomes. Patients with lower coenzyme Q₁₀ concentrations were older and had more advanced heart failure. Mortality was significantly higher among patients in the lowest compared to the highest coenzyme Q₁₀ tertile in a univariate analysis (hazard ratio: 1.50, 95% confidence interval: 1.04 to 2.6, p = 0.03) but not in a multivariable analysis. Coenzyme Q₁₀ was not an independent predictor of any other clinical outcome. Rosuvastatin reduced coenzyme Q₁₀ but there was no interaction between coenzyme Q₁₀ and the effect of rosuvastatin. Coenzyme Q₁₀ is not an independent prognostic variable in heart failure. Rosuvastatin reduced coenzyme Q₁₀, but even in patients with a low baseline coenzyme Q₁₀, rosuvastatin treatment was not associated with a significantly worse outcome. (Controlled Rosuvastatin Multinational Study in Heart Failure [CORONA]; NCT00206310).

Positive correlation between maternal serum coenzyme Q10 levels and infant birth weight

The purpose of this study was to examine the relationship between the level of maternal serum coenzyme Q10 (CoQ10), which is a lipid-soluble antioxidant, maternal body weight gain, fat mass gain, and infant birth weight. A longitudinal observational study was conducted with 50 healthy pregnant women (average age: 31.1 years, average body mass index (BMI): 21.3 kg/m(2) at prepregnancy) at each trimester. CoQ10 levels were measured by high performance liquid chromatography. Maternal weight and body composition were measured by a bioelectrical impedance analysis. The CoQ10 levels significantly increased throughout pregnancy from the first trimester to the third trimester (P < 0.001), and correlated with not only the serum cholesterol levels (P < 0.01) but also with the serum acetoacetic acid levels (P < 0.05) in the third trimester. The CoQ10 levels correlated with the maternal weight gain (P < 0.05) and fat mass gain (P < 0.05) from the second to the third trimester, after adjusting for lipid markers, age, and smoking habits. The level of CoQ10 during the third trimester was also significantly associated with the infant birth weight (P < 0.05) after adjusting for gestational age, maternal prepregnancy BMI, and smoking habits. Therefore, it is concluded that the level of maternal CoQ10 is positively associated with fetal growth, balancing rapid metabolic changes in the last half of a normal pregnancy.

COENZYME Q10 LONG-TERM SUPPLEMENTATION MAY RESULT IN WITHDRAWAL EFFECT IN MYOCARDIUM: PP.13.492

Objective: Coenzyme Q10 (CoQ10) is used as cardioprotector. CoQ10 is endogenous substance and long-term administration of exogenous CoQ10 can influence on its tissue biosynthesis. The aim of the study was to examine the possibility of replenishment of coenzymes Q myocardial level by long-term supplementation with solubilized CoQ10 and to estimate myocardial CoQ content after discontinuation of supplementation. Design and Methods: Male conscious Wistar rats (n = 30) were supplemented with solubilized CoQ10 (10 mg/kg/day per os; Kudesan solution, “Akvion”, Russia). Serum and myocardial levels of CoQ9, CoQ10 were measured after 3 weeks (n = 6), 6 weeks (n = 8) of administration and 2 weeks (n = 8), 6 weeks (n = 8) after discontinuation. Tissue samples were collected 3–4 h after the last administration. Age-matched rats served as control. Myocardial levels of CoQ were estimated in supernatants of homogenates. Assay carried out using HPLC with electrochemical detection after liquid extraction with ethanol-hexane mixture. Statistical analysis was performed with two-tailed t-test. Results: Serum CoQ10 level after 3 and 6 weeks of supplementation was 10 time higher than in control rats. 2 weeks after discontinuation serum CoQ10 level was 3 time higher than in control group and 6 weeks after discontinuation CoQ10 level was not different from control values. CoQ9 serum concentration did not differ between groups. Myocardial content of CoQ10 increased by 40% and 60%, CoQ9 – by 75% and 50% after 3 and 6 weeks of treatment, correspondently. Discontinuation of CoQ10 supplementation evoked the fall of CoQ9 (by 50%) and CoQ10 (by 60%) levels below the control values in 2 weeks; recovery to the control levels was detected in 6 weeks. Conclusion: Results demonstrate CoQ10 withdrawal effect in rat myocardium. These data have to take account of long-term treatment the patients with cardiovascular diseases.

A randomized double-blind placebo-controlled study of oral coenzyme Q10 to relieve self-reported cancer-treatment-related fatigue in newly diagnosed breast cancer patients.

9006 Background: Coenzyme Q10 (CoQ) is an antioxidant supplement with known cardioprotective effects and potential anticancer benefits. We performed a randomized, double-blind, placebo-controlled study of oral CoQ in female breast cancer patients to determine CoQ's effects on self-reported fatigue, depression and quality of life (QOL). Methods: Eligible women with newly diagnosed breast cancer and planned adjuvant chemotherapy were randomized to oral supplements of 300 mg CoQ or placebo, each combined with 300 IU Vitamin E, divided into three daily doses. Treatment was continued for 24 weeks. Participants were stratified by anthracycline (yes/no) and radiation therapy (yes/no). Blood tests, QOL measures, and serum CoQ and Vitamin E levels were obtained at baseline, 8, 16 and 24 weeks. Mixed effects models were used to assess treatment differences in outcomes over time. Results: Between 8/2004 and 3/2009, 236 women were enrolled. Treatment arms were well balanced with respect to age (range 28-85), PS (0, 1, 2) (91%, 8%, 4%), ethnicity (87% White/11%Black/2%Hispanic) and planned therapy (84% anthracycline; 61% RT). No serious adverse events were noted. At 24 weeks, there were no significant differences between the CoQ and placebo arms on the POMS-Fatigue (LS means 5.88 vs. 7.24, p = .27); FACIT-Fatigue (40.2 vs. 39.7, p = .77); FACT-B subscale (25.6 vs. 25.7, p = 0.92); or CES-D (10.1 vs. 10.5, p = 0.82). In the 86 pts with complete CoQ serum samples, baseline and 24 week CoQ levels in the CoQ and placebo arms were 0.72/1.98 and 0.77/0.82 μ g/mL, respectively. In this subset, higher CoQ levels were modestly associated with less fatigue. Conclusions: Supplementation with conventional doses of CoQ led to sustained increases in serum CoQ levels, but did not result in improved self-reported fatigue or QOL after 24 weeks of treatment in women with breast cancer receiving adjuvant therapy. The modest association between higher CoQ levels and less fatigue in patients with complete assays suggests that further exploration of the relationship between CoQ dose and self-reported fatigue may be warranted. Supported by NIH/NCI/DCP grant 3 U10 CA081851. No significant financial relationships to disclose.

Is there is Need for Ubiquinone (CoQ10) Supplementation in Statin- Associated Myopathy?

Statins are currently the most effective drugs in reducing low-density lipoprotein cholesterol (LDL-C). With their mechanism of action, by inhibiting 3-hydroxy-3 methylglutharyl coenzyme A reductase, statins decrease cholesterol production. The same biosynthetic pathway is shared by ubiquinone or coenzyme Q10. Statins block production of dekaprenyl-4-benzoate, a precursor of coenzyme Q10 (CoQ10), which is an essential component in mitochondrial transport system. Ubiquinone deficiency may affect oxidative phosphorylation and adenosine triphosphate production, which can subsequently result in impairing of muscle energy metabolism and contribute to development of myopathy. Statin therapy also decreases antioxidant status in the body, resulting in to increase in free radical damage to cells in various parts of body; liver, nerves, muscles. Statins can decrease natural antioxidant protection present in our body and predispose toxicity. Statin-associated myopathy is the most common side effect of statin treatment often lead to statin dose reduction, or therapy cessation, which can negatively affect cardiovascular risk management. The spectrum of statin-related myopathy ranges from common but clinically benign myalgia to rare but life-threatening rhabdomyolysis. Observational studies suggest that myalgia can occur in up to 10% of persons prescribed statins, whereas rhabdomyolysis continues to be rare. Statins lower circulating levels of CoQ10 up to 54%, whereas several studies did not confirmed a lowering of CoQ10 levels in muscles during statin therapy and the evidence was given also on low dose of statin therapy, which did not appear to reduce intramuscular levels of CoQ10 in symptomatic patients with statin myopathy. The conflicting results have been published on the impaired mitochondrial function, which was found during the analysis of the myocyte cells in patients treated with statins. The supplementation of CoQ10 results in increasing of serum CoQ10, but it is not clear if it relieves myopatic symptoms in statin treated patients. Yet available intervention studies reported contrasting results and just two of them proved benefit of CoQ10 supplementation. Hence coenzyme Q10 supplementation is not currently recommended for routine use in the prophylaxis of statin toxicity.

Blood CoQ10 levels and safety profile after singe‐dose or chronic administration of PureSorb‐Q™40: Animal and human studies

Coenzyme Q10 (CoQ10) is known to be highly hydrophobic and, as such, insoluble in water: this leads to serious inconvenience when trying to incorporate it in food products. Its absorption is also known to be very limited. PureSorb-Q40 (P40) (Water-soluble type CoQ10 powder, CoQ10 content 40 w/w % was developed in order to improve its use with food products and to enhance its absorption. In the present study the absorption of this novel formulation was compared to a conventional lipid soluble CoQ10 by administering both products to rats and humans. Acute, single-administration studies in rats showed that P40 has a higher absorption, compared to lipid soluble CoQ10, both in prandial and fasting states. Similarly, single administration in humans revealed a higher absorption level for P40, taken in the fasting state or together with meals. In the rat study, no adverse effects were observed with P40 at doses up to 2,000 mg/kg in both sexes. In a double-blind, placebo controlled, comparative study conducted on 46 healthy volunteers and randomly divided into two groups, in the group receiving 900~mg of CoQ10 per day, for 4 consecutive weeks, the average level at two weeks was 8.79 +/- 3.34 microg/mL, similar to the corresponding level after 4 weeks (8.33 +/- 4.04 microg/mL). After 2 weeks of washout, serum CoQ10 level decreased to 1.30 +/- 0.49 microg/mL. P40 intake did not cause any significant changes in symptoms and clinical laboratory tests as assessed by physical, hematological, blood biochemical or urinalysis. Clinical examinations also did not reveal any abnormalities. The above blood (serum) CoQ10 level at 2 weeks after start of intake was compared with other reported values. The same dose of CoQ10 (900mg/day), when administered by softgel capsules yielded a plasma CoQ10 concentration of 3.6 microg/mL, while P40 levels were 8.79 +/- 3.34 microg/mL. These levels are remarkably high for instance when compared to the corresponding levels obtained, in patients affected by Parkinson's disease, with CoQ10 doses up to 2,400mg/day. A clinical study was conducted using doses of 300 mg/day and 600 mg/day, in patients affected by cardiovascular disease. Also in this case there was linearity in the response with the levels obtained by administering P40 at a dose of 100 and 900 mg/day.

Safety Assessment of PureSorb-QTM40 in Healthy Subjects and Serum Coenzyme Q10 Level in Excessive Dosing

PureSorb-Q40 (water-soluble type CoQ10 powder, CoQ10 content is 40 w/w%; hereinafter referred to as P40) is reported in the single-dose human and rat studies to have a greater absorption rate and absorbed volume of CoQ10 even taken postprandially, than those of regular CoQ10, which is lipid-soluble and generally taken in the form of soft-gel capsules. Thus, it was anticipated that the serum CoQ10 level might be higher with P40 tablets than with soft-gel capsules, even for the same dose of CoQ10. In the present study, in order to confirm the safety and measure the serum CoQ10 level for the case of an excessive dose of P40, a double-blinded Placebo controlled comparative study was conducted on 46 healthy volunteers and they were randomly divided into two groups. The P40 tablets or placebo were repeatedly taken by the volunteers. As the result of the study, for the group of taking 2250 mg/d of P40 (that is, 900 mg/d of CoQ10) for 4 consecutive wk, the serum CoQ10 level peaked at 2 wk after the start of intake at 8.79 +/- 3.34 microg/mL, and at 4 wk, it was at the level of 8.33 +/- 4.04 microg/mL. At 2 wk from withdrawal of intake, the serum CoQ10 level decreased to 1.30 +/- 0.49 microg/mL. The serum CoQ10 levels at these three points were significantly higher than those of the first day of intake and the Placebo group, which had no significant change throughout the study. Furthermore, P40 intake did not cause any significant changes in symptoms or clinical laboratory results as assessed by physical, hematological, blood biochemical or urinalysis tests. Physician examinations also did not reveal any abnormalities. These results confirm that P40 is an extremely safe material and it can produce better absorption of CoQ10.

Coenzyme Q10 and Adverse Effects of Statins

Background: Current evidence has established that statins are potent and effective agents with several pleiotropic effects in the treatment of coronary artery disease (CAD). Statins may have toxic effects, if given in higher doses and in combination. Design: Literature review. Methods: An Internet search and discussions with colleagues. Results: The 1990s have been called the ‘statin decennial’ and the Nobel laureates suggested ‘CAD: eliminated with statins’. Statins were also proclaimed as wonder drugs, influencing a wide range of physiological, biochemical and biological functions. The list appears to be long and includes hypolipidaemic, vasodilative, antithrombotic, antioxidant, anti-inflammatory, antiproliferative, anticoagulant, angiogenic and bone formation inducing functions. In January 2002, the television network CNN announced in a dispatch from London that deaths resulting from the treatment of hypercholesterolaemia with cerivastatin (Baycol) have now exceeded 100. Concerned Americans discussed this issue in May 2002, and published advice with the intention of summarizing for professionals current knowledge about statin use, focusing on myopathy. The criteria for the diagnosis of myopathy are not concerned with the symptoms of patients in the absence of raised muscle enzymes. Coenzyme Q10 is not considered in prophylaxis because one study showed no decrease in coenzyme Q10 in muscles in the presence of toxicity, although some studies indicated a reduction in serum levels. Conclusion: Several studies have reported a significant reduction in serum coenzyme Q10 in patients taking statins. Such concern was also expressed by the International College of Cardiology at their meeting in April 2002; it was proposed that coenzyme Q10 should be considered in the prevention as well as the treatment of statin intoxication.

Coenzyme Q10, exercise lactate and CTG trinucleotide expansion in myotonic dystrophy

Steinert’s myotonic dystrophy (DM) is a genetic autosomal dominant disease and the most frequent muscular dystrophy in adulthood. Although causative mutation is recognized as a CTG trinucleotide expansion on 19q13.3, pathogenic mechanisms of multisystem involvement of DM are still under debate. It has been suggested that mitochondrial abnormalities can occur in this disease and deficiency of coenzyme Q 10 (CoQ10) has been considered one possible cause for this. The aim of this investigation was to evaluate, in 35 DM patients, CoQ10 blood levels and relate them to the degree of CTG expansion as well as to the amount of lactate production in exercising muscle as indicator of mitochondrial dysfunction. CoQ10 concentrations appeared significantly reduced with respect to normal controls: 0.85 ± 0.25 vs. 1.58 ± 0.28 μg/ml (p < 0.05). Mean values of blood lactate were significantly higher in DM patients than controls (p < 0.05) both in resting conditions (2.9 ± 0.55 vs. 1.44 ± 1.11 mmol/L) and at the exercise peak (6.77 ± 1.79 vs. 4.90 ± 0.59 mmol/L), while exercise lactate threshold was anticipated (30–50% vs. 60–70% of the predicted normal maximal power output, p < 0.05). Statistical analysis showed that serum CoQ10 levels were significantly (p < 0.05) inversely correlated with both CTG expansion degree and lactate values at exercise lactate threshold level. Our data indicates the occurrence of reduced CoQ10 levels in DM, possibly related to disease pathogenic mechanisms associated with abnormal CTG trinucleotide amplification.