Parkinson’s Disease – Complementary Suggestions - Part 2

The Parkinson’s paradox is that it results from low levels of the brain neurotransmitter dopamine, however, when the dopamine level is increased, brain cells die due to dopamine metabolism.  There is a Missing Link between normal dopamine levels and health, and more and more studies suggest that an increased levels of antioxidants may be it.

One in 625 people in the United States develops Parkinson’s Disease (P.D) at the mean age of 55. According to a 2001 study at the Boston University School of Medicine, the use of alternative therapies (AT) in Parkinson’s was widespread.   About 40 percent of all patients reviewed used some form of AT, with vitamins, herbs, massage, and Acupuncture being the most common methods.  Since then, research on Parkinson’s AT possibilities has expanded considerably, especially in Europe and Asia. 

The more they delve into the causes of the disease, the closer scientists seem to get to other brain degenerative conditions such as  Alzheimer’s,  Huntington’s,  amyotrophic lateral sclerosis (ALS) and even schizophrenia.  Although they each involve different parts of the brain and different mechanisms, a common denominator emerges: free radicals.  In reviewing studies on both Parkinson’s and Alzheimer’s, for example,  M.F. Beal, from the Medical College of Cornell University, determined that there is increasing evidence that oxidative damage has a ‘key role’  in both diseases.  Prevention, palliation and even reversing of these conditions, numerous studies reveal, depend on antioxidants.  Even in the rare cases of ‘familial ‘ Parkinson’s,  when gene mutations are involved, NAC, a natural antioxidant substance precursor of glutathione, saved the day, at least in vitro,  preventing cell death.  Many of  the studies on antioxidants mentioned here are performed in vitro or on animals, however, these substances are not only very safe, but are also needed in all metabolic processes. 

Vitamin E – a  Protective Role

A review and meta-analysis of the risk of Parkinson’s in relation of vitamin E intake found that both moderate and high levels have a protective effect against Parkinson’s.  According to this analysis, the eight studies under investigation revealed that vitamin C and beta carotene intake did not reduce the risk of Parkinson’s.

Vitamin E (alpha-tocopherol) Prevents Pesticide-Induced Parkinson’s

A group  of researchers from Emory University, Atlanta, induced Parkinson’s in rodents by treating them with the pesticide rotenone.  The vitamin E protected the rodent’s brain from oxidative damage and blocked the oxidative and processes and immune changes which are believed to lead to Parkinson’s.

Coenzyme Q10 Prevents Neurological Damage

In comparing the blood plasma of Parkinson’s disease patients with healthy patients, a group of Japanese researchers found that the P.D. is characterized by a higher level of oxidized Coenzyme Q10 in the blood plasma, a determination which is a recognized sign of oxidative stress (OS). 

A study by the German Parkinson Society found that clinical trials support the use of Coenzyme Q10 in Parkinson’s disease.

The argument that Parkinson is in effect linked with oxidative stress (OS) disease (leading to cell destruction by free radicals in absence of sufficient antioxidants) is supported also by other studies. Buhmann C. and his team of  researchers from Hamburg, Germany  determined that treatment with single drug Levodopa (LD), which is given to boost the dopamine levels in the blood, leads to increase oxidative stress. The metabolism of dopamine appears to cause neurological damage.  The German team noted that when a drug that counteracts dopamine is given together with Levodopa or alone, the level of antioxidants, such as Vitamin E, in the blood plasma increase. The treatment with Levodopa alone, was particularly found to reduce the amount of  plasma Coenzyme Q10 (Ubiquinone). 

Other studies show that supplementation with Ubiquinone improves the prognosis of Parkinson as it prevents cell-death caused by dopamine metabolism.  Ubiquinone , which is synthesized in the body as part of the energetic metabolic path, is also present in foods such as fatty fish, organ meats and whole grains. According to naturopath Elson M. Haas, it ought to be considered  a vitamin, as low levels of it has been associated with known physiological  dysfunction.

In a study with patients with  Parkinson, encephalitis, multiple sclerosis and amyotropic lateral sclerosis, a team of Canadian researchers also concluded that:  “Patients of all four disorders should display excessive oxidative stress,…and elevated antioxidant supplementation, given with L-Dopa, ought to prolong the ‘honeymoon’ period in which the benefits of the drug outweigh its subsequent disadvantages.”

How much CoQ10?

In a pilot trial by the Department of Neuroscience, University of California, San Diego, the patients received a stable daily doze of 1200 IU Vitamin E  (alpha-tocopherol)  together with  an ‘escalating dosage’ of CoQ10 where the amount in the blood reached a plateau at 2400 mg.  A higher amount of CoQ10 did not result in increased plasma levels.

Tea/" title="Green Tea">Green Tea, Blueberries

A group of researchers in Haifa Israel has also lumped Parkinson, Alzheimer’s, amyotrophic lateral sclerosis and Huntington Diseases under oxidative stress diseases considering what they call “accumulated evidence.” They also note an iron “misregulation” in the brain. They contend that  iron and copper chelating treatment (eliminating the excess of these metals) and flavonoid poliphenold antioxidants such as those found in Tea/" title="Green Tea">Green Tea and blueberries, improve age-related cognitive decline and have neuroprotective capacity in models of Parkinson’s and Alzheimer’s.

Beyond  the Tea/" title="Green Tea">Green Tea Poliphenols

An even more exciting finding by the same Israeli researchers is that the value of Tea/" title="Green Tea">Green Tea in neurodegenerative diseases such as Parkinson’s and Alzheimer’s does not consist in a single radical scavenging action of its  most known poliphenol, but in a “spectrum of cellular mechanisms” which the researchers credit with: “chelation of excess iron, scavenging of free radicals, activation of survival genes and cell signaling pathways, and regulation of mitochondrial function and possibly of the ubiquitin-proteasome system.”

EM-X: An Antioxidant Concoction Drink

An experiment in rats at the Faculty of Medicine, Imperial College in London, determined that a natural undiluted antioxidant drink, EM-X (a ferment of unpolished rice, papaya and seaweeds with microorganisms) has “potential neuroprotective effects.”

NAC, Vitamin C - Offers  ‘Complete’ Protection from Cell Death

Tukov and colleagues from the School of Pharmacy, University of Mississippi, further proved the protective action of antioxidants, specifically glutathione,  in neurological damage.   Researchers induced a  Parkinson’s-like neurodegenerative disorder in horses by using  a compound called repin extracted from the plant Centaurea repens known to cause this disease in horses.  The repin usually causes mitochondrial dysfunction,  oxidative stress, and toxicity due to dopamine metabolism. The study shows that, as it causes the disease, it also  lowers the level of the antioxidant glutathione (GTH) in the blood.  The researchers increased the glutathione levels in the blood of the animals prior to repin exposure by treating them with  N-acetyl-L-Cystein (NAC).  This precursor of GTH  was found to “completely protect the cells from repin-induced mitochondrial and dopaminergic toxicity.

Glutahione (GTH)  and the enzyme derived from it, glutathione peroxidase are  the most important antioxidants in the body without which life cannot exist.  The GTH  protects the organism from lipid oxidation as well as oxidation from metal toxicity and other environmental toxins such as pesticides, plastics, solvents, dyes, car exhaust, and nitrates. (HAAS). A major function of  other antioxidant vitamins is to spare the GTH.

Further in this study, the researchers found that pre-treatment with antioxidants CoQ10 and ascorbic Acid also “completely blocked repin-induced dopaminergic toxicity.

The study lead to the conclusion that oxidative damage due to depletion of GTH  may lead to neuronal cell death such as that in Parkinson’s and Alzheimer’s.

Another study by researchers in Israel also showed that administration of NAC protected cell viability in Parkinson’s even in what they call ‘familial’ Parkinson’s disease, which is associated with a certain genetic mutation.

The benefit of NAC in preventing dopamine cell death resulted from dopamine-induced synthesis/toxicity was also demonstrated by a study in South Korean University of  Ulsan College of Medicine. 

CAPE – A Bee Propolis Derivative

An antioxidant flavonoid from propolis, caffeic Acid phenethyl ester (CAPE) is being recognized as an outstanding protector against oxidative damage.  The CAPE has already proven its worth as an anti-inflammatory, antioxidant, antiviral and Immunity booster as well as a promising agent in ischemia and some neurological conditions due to low potassium.   A study at the Anderson Cancer Center in Texas determined it is also an anti-Cancer compound.   A recent study in Germany has determined its value as a neuroprotective in rodents with dopamine induced cell death.

Resveratrol  -  Much More Than  Antioxidant

According to researcher S. Dore from Johns Hopkins University, School of Medicine, Baltimore,  the value of resveratrol, the polyphenol in red wine, consists in its action of ‘signaling’  genes and proteins, enabling them to express themselves, that is remind them to open up to their cellular environment and do whatever they are supposed to do physiologically.  Dore proposes that such a role makes resveratrol a promising agent in neurological diseases such as strokes, amyotrophic lateral sclerosis, Parkinson’s, Alzheimer’s, and other age-related disorders.

Traditional Chinese Medicine (TCM)

In TCM Parkinson’s is caused by an “insufficiency of liver and kidney and deficiency of qi (vital force) and blood and a simultaneous excess in the Biao, which represent the conditions of  ‘wind, fire, phlegm and stasis.’ According to Q. J. Zhang and his colleagues from the Shanghai University of Traditional Chinese Medicine TCM, treatment with herbs and Acupuncture based on individual differentiation appear to merit further consideration.

Another study by researchers in Beijing found that two extracts from traditional Chinese herbs, schisanhenol (Sal), a compound extracted from kernels of schisandra rubriflora herb, and salvianolic Acid (Sal A - an antioxidant compound from the red-rooted plant, salvia miltiorrhiza radix) together with a third antioxidant of synthetic origin, significantly protected the brain from oxidative stress injury.  The two plants are widely employed in TCM.

Kami-shoyo-san

A combination of ten herbs that is being used in TCM to treat muscular disturbances such as Parkinson’s was examined by Japanese scientists from the Nagoya University.  The researchers found that several of these ten herbs were indeed effective in reducing tremors associated with parkinsonism: Radix Bulpleuri, Radix Paeoniae, Radix Angelicae Sinensis, and Radix Glycyrrhizae.

Ayurvedic Cleansing and Herbs

An Indian group verified the claim of a traditional concoction of herbs and nutrients in the treatment of Parkinson’s.  The  Ayurvedic approach provides for a process of cleansing prior to therapy. The patients in this study were receiving 200 mg. of L-Dopa together with the following: cow’s milk containing powdered Mucuna Pruriens, Hysoscyamus reticulatus seeds, Withania Somnifera, and Sida cordifolia roots. According to researchers, only the patients who underwent a cleansing treatment prior to the herbal treatment benefited with improvement in daily activities with reduced tremors, stiffness and cramps.

References:

Rajendran PR, Thompson RE, Reich SG. The use of alternative therapies by patients with Parkinson's Disease. Boston, MA. Neurology. 2001 Sep 11;57(5):790-4.

Buhmann C, Arlt S, Kontush A, Moller-Bertram T, Sperber S, Oechsner M, Stuerenburg HJ, Beisiegel U. Plasma and CSF markers of oxidative stress are increased in Parkinson's Disease and influenced by antiparkinsonian medication. Hamburg, Germany. Neurobiol Dis. 2004 Feb;15(1):160-70.”Links D monotherapy tended to result in an increase of autooxidation and in a decrease of plasma antioxidants with significance for ubiquinol-10.”

Foster HD, Hoffer A. The two faces of L-DOPA: benefits and adverse side effects in the treatment of Encephalitis lethargica, Parkinson's Disease, multiple sclerosis and amyotrophic lateral sclerosis. Department of Geography, University of Vic. Victoria, BC, Canada.

Mandel S, Weinreb O, Amit T, Youdim MB. Cell signaling pathways in the neuroprotective actions of the Tea/" title="Green Tea">Green Tea polyphenol (-)-epigallocatechin-3-gallate: implications for neurodegenerative diseases. Haifa, Israel. J Neurochem. 2004 Mar;88(6):1555-69 Erratum in: J Neurochem. 2004 Apr;89(2):527.

Datla KP, Bennett RD, Zbarsky V, Ke B, Liang YF, Higa T, Bahorun T, Aruoma OI, Dexter DT. The antioxidant drink effective microorganism-X (EM-X) pre-treatment attenuates the loss of nigrostriatal dopaminergic neurons in 6-hydroxydopamine-lesion rat model of Parkinson's Disease. J Pharm Pharmacol. 2004 May;56(5):649-54.

Mandel S, Youdim MB. Catechin polyphenols: neurodegeneration and neuroprotection in neurodegenerative diseases. Haifa, Israel Free Radic Biol Med. 2004 Aug 1;37(3):304-17.

Shults CW, Flint Beal M, Song D, Fontaine D. Pilot trial of high dosages of coenzyme Q10 in patients with Parkinson's Disease. San Diego, Calif. Exp Neurol. 2004 Aug;188(2):491-4.

Steele PE, Tang PH, DeGrauw AJ, Miles MV. Clinical laboratory monitoring of coenzyme Q10 use in neurological and muscular diseases. Cincinnati, USA. Am J Clin Pathol. 2004 Jun;121 Suppl:S113-20.

Sohmiya M, Tanaka M, Tak NW, Yanagisawa M, Tanino Y, Suzuki Y, Okamoto K, Yamamoto Y.  Redox status of plasma coenzyme Q10 indicates elevated systemic oxidative stress in Parkinson's Disease. Gunma, Japan.  J Neurol Sci. 2004 Aug 30;223(2):161-6

Weinreb O, Mandel S, Amit T, Youdim MB. Neurological mechanisms of Tea/" title="Green Tea">Green Tea polyphenols in Alzheimer's and Parkinson's diseases.  Haifa, Israel. J Nutr Biochem. 2004 Sep;15(9):506-16

Tukov FF, Rimoldi JM, Matthews JC. Characterization of the role of glutathione in repin-induced mitochondrial dysfunction, oxidative stress and dopaminergic neurotoxicity in rat pheochromocytoma (PC12) cells.  Mississippi,  USA. Neurotoxicology. 2004 Dec;25(6):989-99. “The results support the view that GSH depletion, leading to oxidative damage and subsequent mitochondrial dysfunction, may serve as a trigger for neuronal cell death.”

Paracelsus-Elena-Klinik, Kassel. Differential therapy of advanced Parkinson's Disease with special reference to complementary therapeutic approaches. Schweiz Rundsch Med Prax. 2004 Nov 3;93(45):1869-72.

Zheng H, Weiner LM, Bar-Am O, Epsztejn S, Cabantchik ZI, Warshawsky A, Youdim MB, Fridkin M. Design, synthesis, and evaluation of novel bifunctional iron-chelators as potential agents for neuroprotection in Alzheimer's, Parkinson's, and other neurodegenerative diseases. Rehovot, Israel.Bioorg Med Chem. 2005. Feb 1;13(3):773-8.

Elkon H, Melamed E, Offen D. Oxidative stress, induced by 6-hydroxydopamine, reduces proteasome activities in PC12 cells: implications for the pathogenesis of Parkinson's Disease. J Mol Neurosci. 2004;24(3):387-400. “Administration of the antioxidant N-acetylcysteine to 6-OHDA-treated cells prevented the alteration in proteasome functions. Moreover, reduction in cell viability owing to administration of proteasome inhibitor MG132 or lactacystin was partially prevented by the endogenous antioxidant-reduced glutathione.”

Choi HJ, Lee SY, Cho Y, Hwang O. Inhibition of vesicular monoamine transporter enhances vulnerability of dopaminergic cells: relevance to Parkinson's Disease. Seoul, South Korea Neurochem Int. 2005 Mar;46(4):329-35. Epub 2005 Jan 17.  “… the thiol agent N-acetylcysteine and quinone reductase inducer dimethyl fumarate abolish BH4/ketanserin-induced cell death, suggesting that quinone production plays an important role.”

Testa CM, Sherer TB, Greenamyre JT.  Rotenone induces oxidative stress and dopaminergic neuron damage in organotypic substantia nigra cultures. Atlanta, GA. Brain Res Mol Brain Res. 2005 Mar 24;134(1):109-18. Epub 2005 Jan 6.

Noelker C, Bacher M, Gocke P, Wei X, Klockgether T, Du Y, Dodel R. The flavanoide caffeic Acid phenethyl ester blocks 6-hydroxydopamine-induced neurotoxicity Bonn, Germany. Neurosci Lett. 2005 Jul 22-29;383(1-2):39-43.

Etminan M, Gill SS, Samii A. Intake of vitamin E, vitamin C, and carotenoids and the risk of Parkinson's Disease: a meta-analysis. Division of Clinical Epidemiology, Royal Victoria Hospital and McGill University Montreal, Quebec, Canada.

Dore S. Unique properties of polyphenol stilbenes in the brain: more than direct antioxidant actions; gene/protein regulatory activity. Baltimore, MD. Neurosignals. 2005;14(1-2):61-70.

Zhang QJ, Zhang YY, Huang WY. Traditional Chinese Medicine in Parkinson’s Disease. Institute of Cardio-cerebrovascular Disease, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200437, China.

Ishikawa T, Funahashi T, Kudo J. Effectiveness of the Kampo kami-shoyo-san (TJ-24) for tremor of antipsychotic-induced parkinsonism. Psychiatry Clin Neurosci.2000 Oct;54(5):579-82.

Nagashayana N, Sankarankutty P, Nampoothiri MR, Mohan PK, Mohanakumar KP. Association of L-DOPA with recovery following Ayurveda medication in Parkinson's Disease. Thiruvananthapuram, India.

This article written by, Elena Marcus