The dietary supplement Coenzyme (CoQ10), an antioxidant sold as a dietary supplement, has garnered attention as a potential means to protect individuals from diseases such as Huntington’s disease and Parkinson’s disease.
New research discovers that although small doses of the antioxidant coenzyme Q10 appear to increase blood levels of this naturally occurring compound in patients with Parkinson’s disease, it does not improve Parkinson’s disease symptoms.
The research is found online and will appear in the July 2007 print issue of Archives of Neurology.
Parkinson’s disease is a neurodegenerative disorder characterized by tremors and difficulty with walking or other movements. The biological mechanisms underlying the condition are not fully understood, but researchers suspect a malfunction of the mitochondria, parts of the cells that help convert food to energy, according to background information in the article.
Coenzyme (CoQ10), an antioxidant sold as a dietary supplement, is also involved in mitochondrial processes.
“Because of these functions, CoQ10 has attracted attention concerning neuroprotective actions in neurodegenerative disorders linked to mitochondrial defects or oxidative [oxygen-related] stress, such as Huntington’s disease and Parkinson’s disease,” the authors write.
Previous studies indicate that high doses of CoQ10 (1,200 milligrams) may slow the deterioration associated with Parkinson’s disease.
Researchers conducted a randomized clinical trial of a 300-milligram dose of CoQ10 in 131 patients with Parkinson’s disease who did not have changes in motor functions and were on stable treatment for their condition.
Those assigned to the treatment group took 100 milligrams of CoQ10 three times daily for three months, followed by a two-month “washout” period. The researchers assessed Parkinson’s disease symptoms before treatment began, each month during treatment and again after the washout period.
Blood tests were performed at the beginning of the study, after three months of treatment and after the washout period.
A total of 106 patients completed the full three months of the study—55 in the CoQ10 group and 51 in the placebo group. The compound was well tolerated overall, and the percentage of patients who experienced adverse effects—including viral infection, diarrhea and hearing loss—did not differ between the two groups.
Blood levels of CoQ10 increased in the treatment group from an average of 0.99 milligrams per liter to an average of 4.46 milligrams per liter after three months.
“Although we demonstrated a significant increase in plasma levels of CoQ10 toward levels observed with high doses of standard CoQ10 formulations in Parkinson’s disease and other disorders, our study failed to show improvement of Parkinson’s disease symptoms and did not meet its primary or secondary end points,” which were changes on scales that measured Parkinson’s disease symptoms and their effects on physical and mental functioning, the authors write.
“Our study further demonstrated that 300 milligrams per day of nanoparticular CoQ10 is safe and well tolerated in patients with Parkinson’s disease already taking various antiparkinsonian medications.”
“Since we did not find symptomatic effects of CoQ10 in Parkinson’s disease, our study does not support the hypothesis that restoring the impaired energy metabolism of the diseased dopaminergic neurons leads to symptomatic benefits in Parkinson’s disease,” the authors conclude.
“Future studies will need to explore the protective effects of CoQ10 at the highest effective dose (equivalent to about 2,400 milligrams per day of a standard formulation) over a long treatment period and in a large cohort of patients both sufficient to clearly define the protective potential of this compound in Parkinson’s disease.”
Source: JAMA/Archives of Neurology