Bookmark : ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() Natural Support for Parkinson’s DiseaseParkinson's disease is a chronic neurological disorder caused by the death of nerve cells in certain parts of the brain that typically strikes people over the age of fifty-five (55). The symptoms of Parkinson’s disease (referred to as P.D. henceforth) include a "pill rolling" tremor in the hands, so called because it appears that the afflicted person is rolling a small object between thumb and forefinger, difficulty walking along with a shuffling gait, decreased facial expressiveness, and trouble talking. In the latter stages of PD sufferers eventually begin to experience cognitive difficulties and depression too. Although the exact cause of PD is unknown, most experts believe that electrically unstable molecules called free radicals generated in the brain may play a crucial role in killing off nerve cells linked to the disorder. These nerve cells generate a neurotransmitter called dopamine that influences another part of the brain. Most conventional or standard drug treatments for PD work by artificially bolstering brain dopamine levels. Simply taking dopamine orally won't work, however, because this neurotransmitter molecule cannot get through the blood-brain barrier and then enter the brain. Instead, most PD sufferers take a drug called levodopa (L-dopa), which passes into the brain and is then converted into dopamine. Many PD patients take levodopa with carbidopa, a drug that increases the amount of levodopa available to make dopamine. Initially, levodopa dramatically improves PD symptoms. Over time, however, levodopa becomes less effective while the odds of side effects goes up. There are also surgical procedures that can decrease symptoms, such as doing a pallidotomy and implanting a device that delivers deep brain electrical stimulation. Natural Treatments of Merit
Coenzyme Q-10
Coenzyme Q-10 (CoQ10) may slow the progression of PD. In a 16 month double-blind, placebo-controlled study (2002), eighty (80) early stage PD patients were given either CoQ10 (at a dose of 300 mg, 600 mg, or 1,200 mg daily) or a placebo. None were on medication or had need of this. Bottom line: CoQ10, especially at the highest dose level, appeared to have slowed disease progression. A subsequent double-blind, placebo-controlled study involving twenty-eight (28) PD sufferers on medication indicated that 360 mg of CoQ10 daily brought about mild improvement in some symptoms. A larger study failed to duplicate these results. One reason for the lackluster effect of CoQ10 in these studies might lie with the form used. There are some forms of Q10 that are better absorbed and utilized than others. Readers interested in getting premium CoQ10 should check out CARDIUM. S-adenosylmethionine
Depression affects many people with PD, something that is linked to the disease process itself in some instances. The long-term use of levodopa may also contribute to the genesis of “the blues”. There is at least a modicum of research that indicates that levodopa depletes S-adenosylmethionine (SAM-e) in the brain. Given the fact that SAM-e has been shown to be effective in ameliorating depression in a large number of studies, it is logical that depletion may trigger depression or exacerbate existing “blue funk”. To test the impact of SAM-e on PD, scientists a conducted a double-blind study in which twenty-one (21) levadopa taking PD sufferers was given either a combination of oral and injected SAM-e or a placebo daily for 30 days. Bottom line: 72% of the PD patients who took SAM-e felt that their depression was significantly improved after two (2) weeks, while only 30% of those who received a placebo noted any improvement. Given the findings of the aforementioned clinical trial, it would appear that SAM-e might complement levodopa. However, there is a flip side to all this. SAM-e apparently participates in the processing of levadopa in the brain and thus gets used up in the process. As such, it is conceivable that taking extra SAM-e could undermine the effectiveness of levodopa. Needless to say, PD patients who would like try SAM-e should check with a physician knowledgeable concerning its use. One final point: Not all SAM-e products on the market contain active forms of this compound. One that does is SAMePLUS Other CAM Options
There are a great many other promising CAM treatments for PD, but virtually all are supported by very little hard scientific proof of efficacy. Among these are glutathione, which is practically useless unless it is taken in a form that insures it will not be broken down before reaching the brain. Th-Queen has glutathione in patented delivery system that helps reduce this possibility. The amino acid D-Phenylalanine, such as is found in NEPSOL, may also help PD. One of its principle benefits lies in the fact it alleviates depression. And finally, the Ayurvedic herb known as velvet bean or cowhage (Mucuna pruriens) contains L-dopa. In one study it was found that the herb (as a source of L-dopa) worked better in some respects than the pure L-dopa drug. References
1. de Rijk MG, Breteler MB, den Breeijen JH, et al. Dietary antioxidants and Parkinson disease: the Rotterdam study. Arch Neurol. 1997;54:762-765. 2. Liu X, Lamango N, Charlton C. L-dopa depletes S-adenosylmethionine and increases S-adenosyl homocysteine: relationship to the wearing-off effects [abstract]. Abstr Soc Neurosci. 1998;24:1469. 3. Bressa GM. S-adenosyl-l-methionine (SAMe) as antidepressant: meta-analysis of clinical studies. Acta Neurol Scand Suppl. 1994;154:7-14. 4. Carrieri PB, Indaco A, Gentile S, et al. S-adenosylmethionine treatment of depression in patients with Parkinson's disease: a double-blind, crossover study versus placebo. Curr Ther Res. 1990;48:154-160. 5. Liu X, Lamango N, Charlton C. L-dopa depletes S-adenosylmethionine and increases S-adenosyl homocysteine: relationship to the wearing-off effects [abstract]. Abstr Soc Neurosci. 1998;24:1469. 6. Sechi G, Deledda MG, Bua G, et al. Reduced intravenous glutathione in the treatment of early Parkinson's disease. Prog Neuropsychopharmacol Biol Psychiatry. 1996;20:1159-1170. 7. Heller B, Fischer E, Martin R. Therapeutic action of D-phenylalanine in Parkinson's disease. Arzneimittelforschung. 1976;26:577-579. 8. Shults CW, Oakes D, Kieburtz K, et al. Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline. Arch Neurol. 2002;59:1541-1550. 9. Muller T, Buttner T, Gholipour AF, et al. Coenzyme Q10 supplementation provides mild symptomatic benefit in patients with Parkinson's disease. Neurosci Lett. 2003;341:201-204. 10. Storch A, Jost WH, Vieregge P, et al. Randomized, double-blind, placebo-controlled trial on symptomatic effects of coenzyme Q 10 in Parkinson disease. Arch Neurol. 2007 May 14. [Epub ahead of print] 11. Katzenschlager R, Evans A, Manson A, et al. Mucuna pruriens in Parkinson's disease: a double blind clinical and pharmacological study. J Neurol Neurosurg Psychiatry. 2004;75:1672-1677. |