Fight Parkinson's and Huntington's with Vitamins and Antioxidants by Kedar N. Prasad
Author:Kedar N. Prasad
Language: eng
Format: epub
Tags: Health/Nutrition
Publisher: Inner Traditions/Bear & Company
Published: 2016-03-02T00:00:00+00:00
PROPOSED MICRONUTRIENT SUPPLEMENT AND LOW-DOSES OF NS AID IN COMBINATION WITH STANDARD THERAPY IN PARKINSONâS PATIENTS
Levodopa therapy is considered the gold standard for the treatment of Parkinsonâs disease; however, in vitro studies suggest that treatment of neuronal cells in culture with L-dopa is very toxic, thus treatment in humans is discontinued after about five years. This toxic effect is no doubt due to the fact that L-dopa generates excessive amounts of free radicals during auto-oxidation as well as during the oxidative metabolism of its product, DA.
It should also be noted, however, that in animal studies it appears that there is no evidence of similar effects of L-dopa in vivo (Melamed et al. 1998). In a randomized, double-blind, placebo-controlled trial involving 361 patients with early-stage Parkinsonâs, the effects of various doses of levodopa for a period of forty weeks were investigated (Fahn et al. 2004). The results showed that the patients receiving the highest dose of levodopa had significantly more dyskinesia, hypertonia, infection, headache, and nausea than those receiving placebo. The clinical data showed that levodopa treatment either slowed the progression or improved the symptoms of the disease. However, neuroimaging data suggested that levodopa treatment increased the rate of loss of nigrostriatal DA nerve terminals, or it reduced the levels of DA transporter more than was produced by placebo treatment.
A further investigation of this issue revealed that the dose amount of levodopa is a factor in producing motor complications of dyskinesia, and these can develop as early as five to six months at high levodopa doses (Fahn 2005). Given that levodopa has the potential to cause increased oxidative damage both in the brain and outside the brain, it appears rational to propose that reducing oxidative stress and chronic inflammation in combination with standard therapy may be one of the rational choices for reducing the progression and improving management. Such a strategy may improve the effectiveness of levodopa therapy by reducing the side effects that occur as a result of increased oxidative damage. This would then allow levodopa treatment to be effective for a longer period than is utilized at present and may even allow for a reduction of the dosage of levodopa without sacrificing its efficacy.
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