Taking high doses of co-enzyme Q10 in the early stages of Huntington’s disease does not delay its progression, according to a clinical trial.
The study, “A Randomized, Double-Blind, Placebo-Controlled Trial Of Coenzyme Q10 In Huntington Disease,” was published in the journal Neurology.
Huntington’s disease is a neurodegenerative disorder stemming from mutations in the huntingtin (HTT) protein. It causes mitochondria, the cell’s powerhouse, to produce less energy than it should.
Vitamin Q10, or CoQ, is an enzyme that helps mitochondria generate energy to maintain cells’ activity and growth. It also works as an antioxidant, protecting cells from harmful molecules.
A previous clinical trial (CARE-HD) showed no improvement in the symptoms of Huntington’s patients who took 300 milligrams of Q10 twice a day. But the study suggested that Q10 delayed the progression of the disease during the 2 1/2 years of the trial period.
“It was unclear if these observations represented actual clinical efficacy,” however, the authors wrote. “After establishing a maximal tolerable dose based on preclinical studies, we sought to address these issues by evaluating the effect of a higher dosage of Q10 in a large group over a 5-year follow-up period.”
The new trial (2CARE, NCT00608881) covered 609 patients with early Huntington’s disease at 48 locations in the US, Canada and Australia. Patients were randomly assigned to receive 2,400-milligram doses of Q10 or a placebo. All were followed over 60 months.
A key focus of the study was whether patients who took Q10 improved their Total Functional Capacity score, a measurement of independence based on ability to perform daily functions.
Another record that researchers kept was the time of death of patients who died.
Q10 was well-tolerated and safe, researchers found. But it failed to delay progressive loss of functional capacity in those taking it.
“In this study, no beneficial effect of CoQ was detected on the primary outcome variable,” the authors wrote. “As such, the trial provides no evidence that CoQ slows the progression of functional decline in HD, and these data do not justify a recommendation for CoQ as a treatment in [patients with Huntington’s disease].”
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