hey there, i went looking for stuff on coQ10 (which is what i am assuming you mean) and at this stage i have seen it both recommended for and advised against for ms patients. i have taken it in the past but didn't stick with it.
it's an antioxidant. one of your body's own powerful antioxidants is uric acid, which is known to be low in ms (avg 194) and does fluctuate, getting lower in relapse (avg 160s) and higher in remission (avg 230s). healthy controls sit in the 290-300 neighbourhood. uric acid status is correlated with zinc status. when i boosted my zinc (healthy controls avg 18.2), the uric acid level came up with it. last check, zinc 16.1, uric acid 278.
also ran across this by chance:
Quote:
Serum levels of coenzyme Q10 in patients with multiple sclerosis. de Bustos F, Jimenez-Jimenez FJ, Molina JA, et al. Acta Neurol Scand 2000;101:209-211.
To elucidate whether serum coenzyme Q10 levels are related with the risk for multiple sclerosis (MS) or are a marker for the activity of the disease, we compared serum levels of coenzyme Q10 and the coenzyme Q10/cholesterol ratio, in 31 patients with MS (during exacerbations) and 19 matched controls using a high performance liquid chromatography technique. The mean serum coenzyme Q10 levels and the coenzyme Q10/cholesterol ratio did not differ significantly between the 2 study groups. The values did not correlate with age, age at onset, and duration of the disease. These results suggest that serum coenzyme Q10 concentrations are unrelated with the risk for MS and are not a useful marker of activity of the disease.
and this, not by chance:
Quote:
Am J Med Sci. 1986 Nov;292(5):289-92.Oral zinc therapy normalizes serum uric acid level in Wilson's disease patients.
Umeki S, Ohga R, Konishi Y, Yasuda T, Morimoto K, Terao A.
The authors investigated changes in the serum uric acid (s-UrA) level seen in a Wilson's disease patient who had to undergo oral zinc therapy because of the occurrence of D-penicillamine-induced acute sensitivity reactions, including neutrophilic agranulocytosis, thrombocytopenia, and skin eruptions. Although s-UrA levels were low before oral zinc therapy (mean +/- SD, 1.60 +/- 0.20), they increased (mean +/- SD, 2.63 +/- 0.32) to within normal range (2.8-8.0 mg/dl) after therapy. There were no significant changes in the renal tubular reabsorption of UrA during oral zinc therapy. This therapy also produced an improvement of the decreased cholinesterase (ChE) values usually seen in Wilson's disease. These results suggest that oral zinc therapy can normalize UrA metabolism in Wilson's disease by improving liver dysfunction and increasing UrA synthesis
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