Coenzyme Q10 in Early Parkinson Disease

I read with great interest the study of the effects of coenzyme Q₁₀ (CoQ₁₀) in early Parkinson disease by Shults et al and the Parkinson Study Group.¹ Commendably, Shults and colleagues examined 3 levels of dosing and recorded changes in the blood (plasma) CoQ₁₀ level. The level of plasma CoQ₁₀increased significantly in the groups receiving CoQ₁₀; however, the increases observed do not appear particularly large considering the doses received. The plasma CoQ₁₀level increased from approximately 0.5 mg/L to about 1.8, 2.2, and 4.0 mg/L, respectively, with 300, 600, and 1200 mg/d of CoQ_10. One explanation may be that CoQ₁₀pharmacokinetics is affected by Parkinson disease, although serum CoQ₁₀ levels were not found to differ significantly in 33 patients with Parkinson disease and 31 matched controls.² Another possibility may be the antagonism of CoQ₁₀ uptake by the high dose (1200 IU) of vitamin E received by the subjects in the study of Shults and colleagues. In a study with patients who had mild hypercholesterolemia,³ 200 mg of CoQ₁₀ (100 mg twice daily) increased the plasma CoQ₁₀ level from 0.72 to 4.66 mg/L; however, when 700 mg (350 mg twice a day) of vitamin E (as d-α-tocopherol) was also given, the plasma CoQ₁₀level increased only from 0.84 to 2.71 mg/L. A study with rats found vitamin E to enhance or suppress the accumulation of CoQ₁₀in various tissues in a dose-dependent manner, although no significant differences in brain or serum levels were observed.⁴ Thus, investigation of possible pharmacokinetic interactions between CoQ₁₀ and vitamin E in humans appears warranted if vitamin E is to be included in future studies of CoQ₁₀in Parkinson disease and other conditions.

According to Shults et al,¹ the results of several clinical studies indicate that the dosage of CoQ₁₀ may be crucial. Although this conclusion is logical, it might be more appropriate to consider the levels of CoQ₁₀ in the organs or blood achieved in particular patient groups. The heart failure study⁵ referred to by these authors provides a good example. In that study, 200 mg of CoQ₁₀raised the serum CoQ₁₀ level from 0.95 to 2.2 mg/L, but no significant therapeutic effects were observed. In a second group of patients with heart failure,⁶ the same preparation and dose (this time at 100 mg twice a day) increased the serum CoQ₁₀level from 1.09 to 3.25 mg/L, and significant improvements in cardiac function were observed. Could dose-response studies designed to evaluate the benefit of various blood levels of CoQ₁₀in Parkinson or Huntington disease be the next step?

Dr Hunter is employed by Pharma Nord ApS (Vejle), a company that manufactures nutritional supplements including CoQ_10.