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CoQ10 Research and Clinical Studies

Various studies have been conducted on CoQ10 to determine its benefits. While CoQ10’s health benefits as a cardio-protective have long been established, in the past four years, new discoveries have been made showing CoQ10’s benefits in fighting cancer and in combating age related diseases. CoQ10 has been shown to help in protecting the brain after cardiac arrest, in slowing early macular degeneration, preventing migrane, slowing neurodegenerative diseases such as Parkinson’s and Alzheimer’s.

You can read more on the health benefits of Coq10

We summarize here some of the major research and studies on CoQ10

CoQ10 for heart health

A randomized double-blind, placebo-controlled study showed that 73 patients who were administered CoQ10 for one year after a first heart attack suffered 25% attacks as opposed to 45% for patients who did not receive CoQ10. Moroever only 13.7% patients receiving CoQ10 had only non-fatal heart attacks as compared to 25.3% who were not given CoQ10. It has also been shown that statin drugs taken to lower cholesterol, deplete the heart of CoQ10. Supplementing CoQ10 helps to prevent damage to heart muscle tissue and cardio myopathy. In a study conducted on mice, it was shown that CoQ10 inhibits acute viral myocarditis which can be a fatal infection of the heart walls. It also reduces oxidative stress and DNA damage in the heart wall lining.

Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction.

Singh RB. Mol Cell Biochem. 2003 Apr;246(1-2):75-82.

In a randomized, double-blind, controlled trial, the effects of oral treatment with CoQ10, 120 mg/day, a bioenergetic and antioxidant cytoprotective agent, were compared for 1 year, on the risk factors of atherosclerosis, in 73 (CoQ10, group A) and 71 (B vitamin group B) patients after acute myocardial infarction (AMI). After 1 year, total cardiac events (24.6 vs. 45.0%, p < 0.02) including non-fatal infarction and cardiac deaths were significantly lower in the intervention group compared to control group. The extent of cardiac disease, elevation in cardiac enzymes, left ventricular enlargement, previous coronary artery disease and elapsed time from symptom onset to infarction at entry to study showed no significant differences between the two groups. Plasma level of vitamin E and high density lipoprotein cholesterol (1.26 +/- 0.43 vs. 1.12 +/- 0.32 mmol/L) showed significant (p < 0.05) increase whereas thiobarbituric acid reactive substances, malondialdehyde and diene conjugates showed significant reduction respectively in the CoQ10 group compared to control group. Approximately half of the patients in each group (n = 36 vs. 31) were receiving lovastatin (10 mg/day) and both groups had a significant reduction in total and low density lipoprotein cholesterol compared to baseline levels. It is possible that treatment with CoQ10 in patients with recent MI may be beneficial in patients with high risk of atherothrombosis, despite optimal lipid lowering therapy during a follow-up of 1 year. Adverse effect of treatments showed that fatigue (40.8 vs. 6.8%, p < 0.01) was more common in the control group than CoQ10 group.

Randomized, double-blind, placebo-controlled trial of coenzyme Q10 in isolated systolic hypertension.

South Med J. 2001 Nov;94(11):1112-7.
Increasing numbers of the adult population are using alternative or complementary health resources in the treatment of chronic medical conditions. Systemic hypertension affects more than 50 million adults and is one of the most common risk factors for cardiovascular morbidity and mortality. This study evaluates the antihypertensive effectiveness of oral coenzyme Q10 (CoQ10), an over-the-counter nutritional supplement, in a cohort of 46 men and 37 women with isolated systolic hypertension. We conducted a 12-week randomized, double-blind, placebo-controlled trial with twice daily administration of 60 mg of oral CoQ10 and determination of plasma CoQ10 levels before and after the 12 weeks of treatment. RESULTS: The mean reduction in systolic blood pressure of the CoQ10-treated group was 17.8 +/- 7.3 mm Hg (mean +/- SEM). None of the patients exhibited orthostatic blood pressure changes. CONCLUSIONS: Our results suggest CoQ10 may be safely offered to hypertensive patients as an alternative treatment option.

Protection of the brain after a heart attack

Owing to oxygen disruption to the brain, heart attacks often lead to irreversible brain damage. Mild hypothermia (reduction of body temperature) is a technique used to reduce neuronal damage. A study was conducted to see if adding CoQ10 to hypothermia would improve the treatment. 49 patients were selected and were administered hypothermia. Some patients were given hypothermia along with CoQ10 while others were given a placebo. It was shown that three-month survival in the CoQ10 group was 68%, compared to only 29% in the placebo group thus reducing the death rate by a remarkable 57%

CoQ10 in fighting cancer

Scientists are finding that using CoQ10 in conjunction with conventional cancer therapy improve results in patients. CoQ10 is Anthracyclines used in cancer chemotherapy cause toxic side effects and damage mitochondria in the heart. In the Journal of Clinical Oncology, studies showed that when CoQ10 was combined along with chemotherapy with anthracyclines, patients showed improved heart rhythm and also that CoQ10 did not interfere with the chemotherapy. It was also indicated that CoQ10 can reduce cardiotoxicity caused by chemotherapy.

The mitochondrial cocktail: Rationale for combined nutraceutical therapy in mitochondrial cytopathies.

Tarnopolsky MA. Department of Pediatrics and Medicine, McMaster University, 1200 Main St. W., HSC-2H26, Hamilton, Ontario, Canada L8N 3Z5.
Mitochondrial cytopathies ultimately lead to a reduction in aerobic energy transduction, depletion of alternative energy stores, increased oxidative stress, apoptosis and necrosis. Specific combinations of nutraceutical compounds can target many of the aforementioned biochemical pathways. Antioxidants combined with cofactors that can bypass specific electron transport chain defects and the provision of alternative energy sources represents a specific targeted strategy. To date, there has been only one randomized double-blind clinical trial using a combination nutraceutial therapy and it showed that the combination of creatine monohydrate, coenzyme Q10, and alpha-lipoic acid reduced lactate and markers of oxidative stress in patients with mitochondrial cytopathies. Future studies need to use larger numbers of patients with well defined clinical and surrogate marker outcomes to clarify the potential role for combination nutraceuticals ("mitochondrial cocktail") as a therapy for mitochondrial cytopathies

Evaluation of coenzyme Q as an antioxidant strategy for Alzheimer's disease.

Wadsworth TL, Bishop JA, Pappu AS, Woltjer RL, Quinn JF. Department of Neurology, Oregon Health & Science University, Portland, OR 97239-3098, USA.

Increasing evidence suggests that Alzheimer's disease (AD) is associated with oxidative damage that is caused in part by mitochondrial dysfunction. Here we investigated the feasibility of modifying Alzheimer pathology with the mitochondrial antioxidant coenzyme Q (CoQ). Exogenous CoQ protected MC65 neuroblastoma cells from amyloid-beta protein precursor C-terminal fragment (APP CTF)-induced neurotoxicity in a concentration dependent manner, with concentrations of 6.25 microM and higher providing near complete protection. Dietary supplementation with CoQ at a dose of 10 g/kg diet to C65/Bl6 mice for one month significantly suppressed brain protein carbonyl levels, which are markers of oxidative damage. Treatment for one month with 2 g lovastatin/kg diet, which interferes with CoQ synthesis, resulted in a significant lowering of brain CoQ10 levels. Mitochondrial energetics (brain ATP levels and mitochondrial membrane potential) were unaffected by either CoQ or lovastatin treatment. Our results suggest that oral CoQ may be a viable antioxidant strategy for neurodegenerative disease. Our data supports a trial of CoQ in an animal model of AD in order to determine whether a clinical trial is warranted.

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