Coenzyme Q₁₀
Part 1

An Antioxidant Drug

Previous coenzyme-Q₁₀ studies

In 2002, Ferrante and collegues tested coenzyme- Q10 as a treatment in a mouse model of HD. In this study, there were signs that it could relieve symptoms, but only to a minimal degree. It was thought that coenzyme-Q₁₀ would not make an effective or efficient treatment for HD patients. Nevertheless, studies were conducted in subsequent years to test the effects of coenzyme-Q₁₀ in human patients with neurodegenerative disorders similar to HD, such as Parkinson’s disease and ALS. In those studies, higher doses of coenzyme-Q₁₀ than those used in the Ferrante 2002 study produced good results. The patients had a significantly slower rate of nerve cell death and symptom progression. For more information on other neurodegenerative and related diseases, click here.

The Huntington Study Group (2001) conducted a clinical trial involving 347 early-stage HD patients at 23 sites in the United States and Canada. The trial was done to test the efficacy of coenzyme Q10 and remacemide, an anti-glutamate drug. The participants were monitored between July 1997 and June 1998 and were assigned to four different treatments:

• 25% received remacemide (200 mg thrice a day)
• 25% received CoQ10 (300 mg twice a day)
• 25% received a combination of remacemide and CoQ10
• 25% received a placebo (no medication at all)

The primary measure of the drug’s effectiveness was change in Total Functional Capacity (TFC) of the people with HD. TFC is a standardized scale used to assess capacity to work, handle finances, perform domestic chores and self-care tasks, and live independently. The TFC scale ranges from 13 (normal) to 0 (severe disability). The average TFC score of the participants before the study was 10.2. None of the treatments significantly altered the decline in TFC. However, subjects treated with coenzyme Q10 showed a 13% slower decline in the TFC compared to subjects who were not treated with coenzyme Q10. For comparison, slowing the decline by 15% would translate into about one more year of independence for people with HD. The supplement was well-tolerated by the study participants and showed no adverse effects on the participant’s other capacities. No changes in the decline in TFC relative to the placebo group were seen in the participants treated with remacemide. However, improvements in chorea were observed. (For more information on remacemide, an anti-glutamate drug, click here.

The researchers concluded that although there was a trend toward slowing of the progression of HD with coenzyme Q10 treatment, the effects were not large enough to recommend coenzyme Q10 as a treatment for early HD. In part, this is because the financial costs of coenzyme Q10 are considerable--daily doses of the drug as used in the study would range from $60 to $150 per month. Also, because coenzyme Q10 is a nutritional supplement, it is worth remembering that it is not subjected to the same quality and content regulations as pharmaceutical drugs. Different brands and formulations of coenzyme Q10 may differ chemically or may contain additives, and there is little information about how these different contents might affect a person with HD. Finally, it should be emphasized that the findings of this study are not applicable to people at risk for HD, or for people at the intermediate or advanced stages of HD.

Nevertheless, the results of the study suggest that therapies that affect the energy supply in cells can affect the course of HD. Additional studies are called for to identify dosage effects and to study effectiveness for people in different stages of HD.

Koroshetz, et al. (1997) treated 18 early-stage HD patients with oral coenzyme Q10 for 2 to 8 weeks. The patients were recruited from the Massachusetts General Hospital HD Unit and were all ambulatory, with half of them still working. Brain lactate level was used as the criteria to measure the effectiveness of the supplement. They hypothesized that treatment with CoQ10 could increase the efficiency of the respiratory chain, and consequently, lower lactate levels. (For more on lactate, click {http://www.stanford.edu/group/hopes/treatmts/ebuffer/j1.html|here.)

The researchers discovered that upon treatment with CoQ10, the participants experienced significant decreases in brain lactate levels. Lactate levels reversed back to their original levels following withdrawal of therapy, indicating that the findings were indeed due to CoQ10 treatment. This study supports the theory that CoQ10 could increase the amount of energy available in cells, perhaps by increasing the efficiency of the respiratory chain.

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Last Modified: 04/12/2007

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