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Coenzyme Q10

Summaries of the latest research concerning coenzyme Q10


Statins + coenzyme Q10 may benefit heart failure patients
WUHAN CITY, CHINA. There is now growing evidence that oxidative stress and inflammation are involved in chronic heart failure. Statin drugs such as atorvastatin, simvastatin and pravastatin have recently been shown to posses anti-inflammatory properties and coenzyme Q10 is a powerful antioxidant and essential for cardiac mitochondrial energy production. Unfortunately, statin drugs reduce the level of coenzyme Q10, sometimes to the point of fostering muscle-related problems (myopathies) like rhabdomyolysis.

A team of Chinese researchers at Wuhan University has now come up with the idea of combining the statin drug atorvastatin (Lipitor) with coenzyme Q10 in the treatment of patients with congestive heart failure. They conducted a clinical trial in which heart failure patients on standard treatment were randomized into receiving atorvastatin, coenzyme Q10, atorvastatin + Q10, or a placebo. At the end of the 6-month treatment period the following changes were observed:

  • The level of the inflammatory marker C-reactive protein (CRP) had dropped from 5.5 mg/L (0.55 mg/dL) to 2.0 mg/L in the atorvastatin + coenzyme Q10 group. Levels of the inflammatory marker tumor necrotic factor alpha and the oxidative stress marker malondialdehyde also dropped significantly in the atorvastatin + Q10 group.

  • Left ventricular ejection fraction had increased from 30% to 43% in the atorvastatin + Q10 group.

  • No significant changes were observed in the control group.

The Chinese researchers conclude that atorvastatin and coenzyme Q10 act synergistically to improve heart failure symptoms. They emphasize that the addition of Q10 serves to increase Q10 levels depleted by the illness as well as to counter the negative influence of statin drugs on Q10 levels. Other researchers have found that coenzyme Q10, on its own, is highly beneficial in that it improves cardiac systolic function by enhancing the production of ATP (adenosine triphosphate) and reducing oxidative stress.
Okello, E, et al. Combined statin/coenzyme Q10 as adjunctive treatment of chronic heart failure. Medical Hypotheses, 2009 [Epub ahead of print]

Editor's comment: Combining a statin drug with coenzyme Q10 for the treatment of heart failure is clearly beneficial. However, there are many more effective and far less dangerous natural anti-inflammatories. Thus, a combination of turmeric and Q10 might well prove to be a very effective therapy for chronic heart failure.

Coenzyme Q10 and chronic heart failure
Chronic heart failure (CHF) is on the rise. The connection between CHF, coenzyme Q-10 (CoQ- 10) and statins is discussed frequently outside of mainstream medicine since statins inhibit the synthetic pathway for the endogenous synthesis of this enzyme. A study has just been reported in the Journal of the American College of Cardiology which investigated the relationship between CoQ-10 and survival in patients with CHF. It was found that plasma CoQ-10 was an independent predictor of mortality in a group of 236 patients admitted to hospital with CHF. When a cut-point of 0.73 micromol/L was used, the group above this plasma level had approximately a 65% 5-year survival whereas for those below this level, it was 40%. The authors comment that there had been previously reported an independent inverse association between plasma cholesterol and total mortality and that the myocardium in patients with heart failure is deficient in CoQ-10. The authors cite 12 clinical studies which suggest benefits from CoQ-10 supplementation. In a meta-analysis of 8 studies, it was found that CoQ-10 supplementation significantly improved stroke volume, ejection fraction, cardiac output, and two other indices of cardiac function. Another meta-analysis found improvements in ejection fraction and cardiac output. Some of these studies may underestimate the benefits of CoQ-10 supplementation in that there are considerable differences in bioavailability among various formulations of this enzyme. The authors also comment that a multicenter intervention trial of CoQ-10 as an adjunctive treatment for CHF is underway which is randomized and double blind. However, examination of the description of the trial fails to reveal the nature of the enzyme preparation, only the dose which is 300 mg. Since bioavailability can vary by a factor of 2 or 3, this may be an issue when it comes to interpreting the results, i.e. was the dose high enough?
Molyneux SL, et al. Coenzyme Q10: An independent predictor of mortality in chronic heart failure. Journal of the American College of Cardiology, Vol. 52, No. 18, October 28, 2008, pp. 1435-41

Cystic fibrosis patients deficient in coenzyme Q10
DENVER, COLORADO. Cystic fibrosis (CF) is a serious, inherited childhood disease. The main symptoms are abnormally thick mucus that clogs the lungs and results in breathing difficulties, failure to gain weight, repeat lung infections, and persistent cough and wheezing. It is estimated that about one in 2500 infants are born with the disease. The unusually thick mucus is a potent breeding ground for bacteria, in particular Pseudomonas aeruginosa. Most CF patients also suffer from pancreatic insufficiency (an inability to produce enough pancreatic enzymes to ensure proper digestion) and an inability to absorb fat-soluble vitamins. Standard treatment for CF therefore involves supplementation with pancreatic enzymes and fat-soluble vitamins (vitamin A, beta-carotene, vitamin D, and vitamin E).

Researchers at the University of Colorado School of Medicine now report that coenzyme Q10 deficiency is common among CF patients and that this deficiency may be associated with an increased incidence of P. aeruginosa colonization in very young patients. Their study involved 381 CF patients between the ages of 6 months and 23 years. All underwent thorough medical examinations and repeat blood tests over a 6-year period. The researchers observed that 49% of the study participants were deficient in coenzyme Q10 (measured in blood serum) when initially tested. Not unexpectedly, they also found that 91% had pancreatic insufficiency and in this group 55% exhibited Q10 deficiency. In contrast, only 3% of patients without pancreatic insufficiency were deficient in Q10, perhaps indicating that the pancreatic insufficiency is behind the malabsorption of Q10.

Although there was no overall correlation between Q10 levels and P. aeruginosa colonization, the researchers did observe that infants (less than 2 years old) who had a positive culture for P. aeruginosa had significantly lower Q10 levels in the year preceding diagnosis compared with infants who had negative cultures. They also noted a positive correlation between Q10 levels and levels of beta-carotene, vitamin A and vitamin E, again suggesting that malabsorption of dietary Q10 plays a role in the low serum levels. The researchers conclude that most patients with CF and pancreatic insufficiency have low coenzyme Q10 levels and that the possible beneficial effects of Q10 supplementation should be studied.
Laguna, TA, et al. Decreased total serum coenzyme-Q10 concentrations: a longitudinal study in children with cystic fibrosis. Journal of Pediatrics, Vol. 153, September 2008, pp. 402-07

Editor's comment: There is evidence that fish oil supplementation may help dampen the airway inflammation accompanying CF, so a combination of fish oil and coenzyme Q10 may be a useful supplement for CF patients.

Coenzyme Q10 combats fatigue
OSAKA, JAPAN. Fatigue is a very common affliction and can be defined as difficulty in initiating or sustaining voluntary activity whether mental or physical. There is growing evidence that reactive oxygen species (free radicals) are responsible for exercise-induced protein oxidation and contribute to physical fatigue. Thus, it would seem plausible that coenzyme Q10, a powerful antioxidant and an essential factor in mitrochondrial energy (ATP) production would be a good candidate as an anti-fatigue agent.

Japanese scientists associated with the Osaka City University Graduate School of Medicine now report on a trial aimed at determining whether supplementation with coenzyme Q10 can indeed reduce physical fatigue. Their three double-blind, randomized, placebo-controlled, crossover trials involved 17 healthy volunteers (9 women and 8 men) with an average age of 38 years. The participants were randomized to receive a placebo, 50 mg of coQ10 twice a day, or 150 mg twice a day for one week prior to performing a fatigue-inducing task (2 x 2 hours on a bicycle ergometer with fixed workloads to reach 80% of maximum heart rate).

Just prior to starting the workouts participants also received either a placebo, or 100 mg or 300 mg of coQ10 depending on what group they were assigned to. During the workout subjects were asked to perform non-workload trials with maximum velocity for 10 seconds (30 minutes into the trial and again 30 minutes before the end).

Analysis of blood samples taken at baseline and after the workouts showed no differences except, as expected, a substantially higher plasma level of coQ10 in the supplemented groups. Total coQ10 level was about 4 times higher than placebo in the 100-mg/day group and about 6 times higher in the 300-mg/day group. Study participants were asked to rate their fatigue level on a visual scale (with 0 being no fatigue and 100 being total exhaustion) before and after the workouts. Results were as follows:

Fatigue Rating

Component
Baseline
After Workouts
Placebo
42
79
100 mg/day Q10
38
77
300 mg/day Q10
32
60

As another measure of fatigue, the researchers compared the difference in speed between the first and second 10-second, no-load trials. While placebo takers experienced a 5 RPM drop in velocity, Q10 supplementers only experienced a 1 RPM drop. The researchers conclude that supplementation with 300 mg/day of coenzyme Q10 for one week improves physical performance during fatigue-inducing workload trials, while 100 mg/day does not produce a statistically significant improvement.
Mizuno, K, et al. Antifatigue effects of coenzyme Q10 during physical fatigue. Nutrition, Vol. 24, 2008, pp. 293-99

Coenzyme Q10 relieves muscle pain in statin-treated patients
STONY BROOK, NEW YORK. The enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) is involved in the endogenous production of both cholesterol and coenzyme Q10. Statin drugs inhibit the action of HMG-CoA so, along with cholesterol-reduction, goes a reduction in Q10 levels. Since coenzyme Q10 is essential in the production of energy-providing ATP (adenosine triphosphate), it is perhaps not surprising that patients taking statin drugs often report the development of muscle weakness and pain which, in severe cases, can develop into full-blown rhabdomyolysis, an often fatal muscle disease.

It would seem logical that supplementing with Q10 when taking statin drugs would be a good idea. Now researchers at Stony Brook University report that this is indeed the case. Their clinical trial involved 15 women and 17 men who were being treated with statin drugs for abnormally high cholesterol levels. All had complained of muscle pain and, in some cases, muscle weakness and fatigue as well. The study participants were randomized into 2 groups. One group supplemented with 100 mg/day of Q10 (Q-Sorb softgel), while another group supplemented with 400 IU/day of vitamin E for the 30-day trial period.

All participants completed the Brief Pain Inventory questionnaire at enrolment and at the end of the trial. This questionnaire contains questions about pain location, pain intensity, and pain interference with daily life. The participants also gave blood samples for analysis of lipid (cholesterol) profile and plasma creatine kinase (CK), an indicator of muscle damage at enrolment and at then end of the trial. After 30 days of Q10 intervention pain intensity declined by 40% and the score for interference of pain with daily activities by 38%, while no changes were seen in the vitamin E supplemented group. No changes were observed in CK level or lipid profile in either of the groups. The researchers conclude that coenzyme Q10 may be beneficial for patients on statins by ameliorating myopathic symptoms and improving their well-being and functionality in daily life. They also point out that CK level may not be an appropriate indicator for statin-related muscle pain.
Caso, G, et al. Effect of coenzyme Q10 on myopathic symptoms in patients treated with statins. American Journal of Cardiology, Vol. 99, 2007, pp. 1409-12

New supplement helps prevent congestive heart failure
TORONTO, CANADA. A dysfunction of the left ventricle (ejection fraction less than or equal to 40 per cent) often leads to congestive heart failure, which now affects about 1.5 per cent of all Canadians. Research has shown that the heart muscle cells (myocytes) of people with left ventricular dysfunction are depleted of carnitine, coenzyme Q10, and taurine and the extent of depletion correlates directly with the severity of the heart failure. It is also known that patients with left ventricular dysfunction (LVD) have a poorer prognosis of surviving bypass surgery than do patients without this problem.

Cardiologists at St. Michael's Hospital and the University of Toronto reasoned that supplementation with carnitine, coenzyme Q10, and taurine might increase ejection fraction and reduce the extent of LVD. They enrolled 41 patients scheduled for bypass surgery in their clinical trial. Half the patients received a placebo for 30 days before their surgery while the other half supplemented with 250 ml of a nutritional drink MyoVive. The MyoVive drink contained 3000 mg of l-carnitine, 150 mg of coenzyme Q10, and 3000 mg of taurine; it also contained other micronutrients including potassium (750 mg), vitamin-C (250 mg), and vitamin-E (538 mg). Biopsy samples of the heart muscle were obtained during the bypass surgery and analyzed for carnitine, coenzyme Q10, and taurine.

The researchers found that the myocyte level of coenzyme Q10, carnitine, and taurine was 144 per cent, 40 per cent, and 66 per cent respectively higher in the supplement group than in the placebo group providing clear proof that the supplements actually found their way to the heart cells. They also noted that while the left ventricular end-diastolic volume (LVEDV) fell by 7.5 ml in the supplement group it increased by 10.0 ml in the placebo group. A lower LVEDV indicates a better prognosis for the outcome of bypass surgery. The researchers conclude that supplementation with MyoVive may be useful in the management of left ventricular dysfunction and may improve the outcome of bypass surgery.
Jeejeebhoy, Farida, et al. Nutritional supplementation with MyoVive repletes essential cardiac myocyte nutrients and reduces left ventricular size in patients with left ventricular dysfunction. American Heart Journal, Vol. 143, June 2002, pp. 1092-1100

Coenzyme Q10 prevents migraines
CLEVELAND, OHIO. A team of researchers from the Cleveland Clinic and Thomas Jefferson University in Philadelphia reports that coenzyme Q10 is effective in preventing migraines. There is increasing evidence that migraine may be caused by some sort of mitochondrial impairment. Coenzyme Q10 has been used successfully in the treatment of mitrochondrial disorders so the researchers reasoned that it might be beneficial in the treatment of migraines. Their clinical trial involved 31 patients who, after a one-month baseline evaluation, were given 150 mg of coenzyme Q10 at breakfast for a three-month period. At the end of the period 61.3 per cent of the patients had a greater than 50 per cent reduction in the number of days they spent with migraine. The frequency of attacks declined from an average of 7.34/month before treatment to 2.95 at the end of the three-month treatment period. The average number of days spent with migraine decreased from 4.85 to 2.81 per month. No adverse treatment effects were observed in any of the patients. The researchers conclude that coenzyme Q10 effectively prevents episodic migraine headaches (with or without aura).

They call for randomized, placebo-controlled trials to confirm their findings and suggest that dosages above 150 mg/day may prove to be even more effective. They also point out that coenzyme Q10 has been found effective in the treatment of congestive heart failure and chronic muscular dystrophy and that no side effects have been observed at daily dosages as high as 3000 mg/day. The effect of oral supplementation takes about a month to be felt and may take as long as three months to reach its full potential. A daily intake of 100-150 mg will increase normal blood levels by a factor of two.
Rozen, T.D., et al. Open label trial of coenzyme Q10 as a migraine preventive. Cephalalgia, Vol. 22, 2002, pp. 137-41

Many health benefits of coenzyme Q10
SEATTLE, WASHINGTON. Dr. John Ely of the University of Washington and Dr. Cheryl Krone of the Applied Research Institute in Palmerston North, New Zealand have cooperated to produce a fascinating report summarizing the latest research about coenzyme Q10 (ubiquinone). It is now known that the tissues and blood of an adult human contain a total of about 2000 mg of coenzyme Q10 and that 500 mg/day is required to maintain this body pool. The average diet provides only about 5 mg/day so the remainder must be synthesized internally. The ability to synthesize coenzyme Q10 declines sharply with age and a deficiency can lead to irreversible damage in the brain and other organs. Besides its essential role in the production of adenosine triphosphate (the body's "energy" molecules), coenzyme Q10 is also a powerful quencher of free radicals (50 times more effective than vitamin E). It has been found to be entirely safe in daily intakes as high as 800 mg.

Animal experiments and at least three cases involving humans have found coenzyme Q10 to be highly effective in reversing the effects of a stroke (400-800 mg/day as soon as possible after the event) and have also been found beneficial in the treatment of congestive heart failure when combined with vitamin-E and vitamin-C. Some fairly recent research has established that statins (cholesterol-lowering agents) depress the synthesis of coenzyme Q10 and has concluded that patients on statins need to supplement with at least 200 mg/day in order to avoid serious deterioration in heart function. [48 references]
Ely, John T.A. and Krone, Cheryl A. A brief update on ubiquinone (coenzyme Q10). Journal of Orthomolecular Medicine, Vol. 15, No. 2, Second Quarter 2000, pp. 63- 68

Successful treatment of chronic fatigue syndrome
TORONTO, CANADA. Doctors at the Canadian College of Naturopathic Medicine report the case of a 31-year-old man who was successfully treated for chronic fatigue syndrome (CFS) with supplements. The patient had developed CFS six years prior to the treatment in the aftermath of a viral infection. His symptoms, apart from excessive fatigue, included low grade fever, swollen lymph nodes, gastrointestinal upsets, muscle pain, and unrefreshing sleep. Research has shown that CFS patients have low blood levels of acylcarnitine, free carnitine, and total carnitine. There is also some evidence that supplementation with the reduced form of nicotinamide adenine dinucleotide (NADH) can be beneficial in the treatment of CFS. The naturopaths therefore decided to put the patient on a supplement regimen including L-carnitine (500 mg twice a day with meals), NADH (2.5 mg three times a day before meals) and coenzyme Q10 (100 mg twice a day). After six weeks following this protocol the patient was re-examined. He reported a marked reduction in muscle aches and post-exertional fatigue and also said that his mental concentration was improved. He reported no adverse effects and plans to continue with the supplement program.

The two naturopathic physicians involved in the trial point out that while the supplement regimen appears to have been successful in this particular case there is still much to be learned about the treatment of CFS.
Ross, Cory and Logan, Alan C. Mitrochondrial support in the treatment of chronic fatigue syndrome: a case report. Journal of Orthomolecular Medicine, Vol. 15, No. 1, First Quarter 2000, pp. 15-17

Coenzyme Q10 prevents stroke damage
SEATTLE, WASHINGTON. Extensive research has shown coenzyme Q10 to be useful in the prevention and treatment of various forms of heart disease and numerous other disorders including AIDS. There is also substantial evidence from animal experiments that supplementation with CoQ10 may retard aging. CoQ10 is essential in providing energy and stability to the cells' mitochondria and is a strong antioxidant which protects LDL (low-density lipoprotein) against oxidation. Unfortunately, dietary intake and internal synthesis of CoQ10 is often low and low levels in the blood have been associated with an increased risk of heart disease, cancer, and other disorders. Human brain concentrations of Q10 decline with age and at age 80 years are only half the value as at age 40 years. Animal experiments (using gerbils) have shown that coenzyme Q10 markedly improves survival after artificially-induced ischemic stroke.

Now researchers at the University of Washington report a case where a 69-year-old woman suffered a severe stroke (cerebral hemorrhage) due to a fall on pavement. The researchers were astounded at the quick and complete recovery of the patient. They ascribe it to the fact that she had been taking 400 mg/day of coenzyme Q10 for about four weeks prior to her fall to help alleviate unrelated disorders. The Q10 was taken with five grams of fat (peanut butter) to improve absorption. The researchers point out that the neuroprotective effect of Q10 given both before and after a stroke has been well established in animal experiments. They conclude that Q10 supplementation may protect against neurological damage from stroke in humans if taken as a regular supplement (100 mg/day or more) or if given within six hours of the occurrence of the stroke. They urge large scale clinical trials to validate their hypothesis and point out that numerous clinical trials have shown Q10 to be entirely safe.
Ely, John T.A., et al. Hemorrhagic stroke in human pretreated with coenzyme Q10: exceptional recovery as seen in animal models. Journal of Orthomolecular Medicine, Vol. 13, No. 2, Second Quarter 1998, pp. 105-09



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