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Coenzyme Q10 Slows Progression of Parkinsons

Results of a recent study presented at the annual meeting of the American Neurological Association in New York City suggest that the popular food supplement coenzyme Q10 could slow down the progression of Parkinson's disease. Lead researcher Professor Clifford Shults of the University of California in San Diego and his colleagues enrolled 80 Parkinson's patients for the trial.

Results of a recent study presented at the annual meeting of the American Neurological Association in New York City suggest that the popular food supplement coenzyme Q10 could slow down the progression of Parkinson’s disease.

Lead researcher Professor Clifford Shults of the University of California in San Diego and his colleagues enrolled 80 Parkinson’s patients for the trial. All of whom had early-stage Parkinson’s, and did not yet need levodopa. The patients were randomly assigned to a treatment with 300, 600, or 1200 mg/d of coenzyme Q10, or an inactive placebo.
Results after eight months of treatment revealed that patients who had received the highest dose of Q10 were fairing significantly better than those given the placebo. So much so that they exhibited a 44% reduction in disease progression, compared with the placebo group. Even patients treated with the lowest dose the supplement were more able at carrying out simple daily activities, for example dressing and washing, and demonstrated better mental functioning and mood.

The findings suggest that Q10 slows the progression of the neurodegenerative disease; although Shults stresses that his research is not conclusive proof as the study group was relatively small. He also believes that it would be “premature” to recommend the supplement to people with the disease.

Previous research has produced evidence suggesting that the function of mitochondriae – the “power-houses” of cells – is impaired in Parkinson’s patients, and that the mitochondriae appear to be lacking Q10. The authors conclude that their findings: “are supportive of the view that mitochondrial dysfunction does play a role in the pathogenesis of sporadic Parkinson’s disease.”

SOURCE/REFERENCE: Archives of Neurology 2002; 59:1541-1550

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