High dose coQ10 safe and well tolerated
A brief communication published in the December 13, 2005 issue of the journal Neurology reported that a high daily dose of orally administered coenzyme (coQ10) Q10 was shown to be safe over an eight month period.
To evaluate the long-term safety of over 600 milligrams per day coenzyme Q10, researchers from Massachusetts General Hospital and their colleagues conducted a trial of 3000 milligrams per day coQ10 among 31 patients with amyotrophic lateral sclerosis (ALS). ALS is a disease involving the death of neurons that may be caused in part by dysfunction of the mitochondria, the cells’ energy plants. CoQ10 is an antioxidant that is a cofactor in the mitochondrial electron transport chain, and has been found to be protective against ALS in animal models of the disease. Trials of coQ10 in Huntington and Parkinson’s disease have indicated that doses higher than 600 milligrams per day may be necessary to help treat these neurological conditions.
The participants in the study had blood samples analyzed for various factors including kidney and liver values before beginning the study. Coenzyme Q10 combined with vitamin E was orally administered in gradually increasing doses starting with 600 milligrams until a 3,000 milligram daily dose was reached after three months. This dose was continued for five months until the study’s conclusion. Plasma levels of the compound were monitored monthly. Adverse events were compared with a placebo group from a previous clinical trial.
The researchers found no changes in vital signs, or laboratory abnormalities over the course of the study. Plasma levels of coQ10 measured after the 2400 milligram per day dose was attained were not statistically different from those measured after 3,000 milligrams per day was reached. Adverse events were similar to those reported in the placebo group. The nine serious adverse events occurring during the trial were rated as unlikely to be related to coQ10.
ALS is a rapidly progressive neuromuscular disease caused by the destruction of nerve cells in the brain and spinal cord. This causes the loss of nervous control of voluntary muscles, resulting in the degeneration and atrophy of the muscles. Eventually the respiratory muscles are affected which leads to death from an inability to breathe.
Mitochondrial dysfunction has been linked to neurodegenerative diseases (Beal 1996; Beal 1999b). Defects in mitochondrial DNA have also been proposed as a causative mechanism in sporadic ALS (Murphy et al. 1999; Beal 2000; Manfredi et al. 2000).
When coQ10 was administered to rats bred to develop ALS, a significant increase in survival time was observed. After only two months of coQ10 supplementation, mitochondrial energy expenditure in the brain increased by 29% compared to the group not getting coQ10. The human equivalent dose of coQ10 to achieve these results was 100-200 mg a day. The conclusion by the scientists was "CoQ10 can exert neuroprotective effects that might be useful in the treatment of neurodegenerative diseases" (Matthews et al. 1998).
Vitamin E is a potent antioxidant. Deficiency is associated with progressive neurologic deterioration. Several studies in the 1940s described improvement in ALS patients when supplemented with alpha-tocopherol (vitamin E) (Wechsler 1940; Rosenberger 1971; Werbach 1996).
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