use of  glutathione for treatment of  Parkinson's  disease?
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Glutathione is one of the most powerful antioxidants in the body.  It is also a critical molecule used to detoxify many toxins/poisons.  It also plays a central role in 'recycling' vitamins C and E.\n\nParkinson's disease is recognized as being related to both excessive oxidation and chemical/environmental toxicities.  Glutathione can help with moderating both issues.\n\nGlutathione will be most effective if given intravenously.  It is also available in oral supplemental form.  NAC (N-acetylcysteine) is a precursor for glutathione's synthesis in the body and supplementation of NAC has been shown to increase Glutathione levels.\n\nIf the diagnosis of Parkinson's has already been made, you definitely want to get regular intravenous injections of glutathione (along with lots of other critical nutrients).\n\nPlease note: once Parkinson's has been diagnosed, a large percentage of brain cells in the substantia nigra part of the brain have been destroyed.  No treatment (yet) can reverse this.  So, treatment such as glutathione and other antioxidants and detoxification nutrients may only help to slow the progression of the condition (although I have heard of cases where there is some immediate improvement in symptoms after an IV).\n\nBest wishes and good luck!
959339
aspartame is a poison.  it certainly effects brain chemistry.  has been linked to the same systems as Parkinson's.
699813
Prosavin is a treatment, not a cure.  There is currently no cure for Parkinson's disease.  And even as a treatment, it doesn't always work for everyone.
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Free radicals, during our process of intake and metaboism some of the oxygen are emerge in our body. These are the main free radical which is highly potensive to destroy our body. \n\nAs you can see, oxygen radicals are very powerful and that is the same one which leads for the corrosion of iron.\n\nIn the same way accumulation of free radicals are very much danger to the body. Almost all diseases in our body are due to the act of this highly reactive free radicals.\n\nThe anti-oxidants are the only one to fight against the free radicals. We can get all nececessary anit oxidants from the colored fruits. \n\nThe another method to come out of these free radicals is detoxify our body.\n\nHave a great day.
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Monosodium Glutamate (MSG) is the common or usual name assigned by the FDA to the ingredient that contains approximately 78 percent free glutamic acid, 22 percent sodium, and a maximum of 1 percent contaminant.2               \n\n \n\n The origin of MSG comes from a very nutritious sea vegetable called “kombu” that Japanese had used, as a taste enhancer for thousands of years.  In 1908, Dr. Kikunae Ikeda succeeded to isolate the taste-enhancing chemical from “kombu”.  That chemical was "glutamate."  After that Dr. Ikeda and his friend, Dr. Saburosuke Suzuki formed a company called Ajinomoto and began to market this "taste enhancer" in the form of monosodium glutamate (MSG).\n\nHealth problems caused by using MSG                  \n\nThe isolated "flavor enhancer" chemical MSG has no nutritional value and is not a preservative. It does nothing to food, but it does affect the person using it. \n\nIt is a neurotoxin, which is a poisonous protein complex that acts on the brain and the nervous system.  Neurons are over stimulated to the point of exhaustion and cell death. MSG goes to the brain through membranes in the mouth and throat, and it also enters the blood stream as MSG laden foods are digested. It tricks the brain into thinking that it's getting something tasty. Very little use of MSG takes to create widely diverse and dramatic effects on the human body. Since separate parts of the brain govern different body functions. The body function that is affected will depend on the part of the brain that is attacked by the neurotoxin. If a person has a genetic weakness in a specific part of the brain or had an injury or a stroke, the damaged area will be the part that is easily affected and vulnerable to toxins.
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What are you measuring?\n\nIn our GC experiments, we noticed that cysteine tended to oxidize in the air. Not sure if that helps any.
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Green tea is mainly used for its anti oxidant qualities. And there are plenty of anti oxidants out there including strawberries-yum!\n\nThe other claims are very suspect especially the weight loss claim.\nSorry there is no magic bullet out there.\nLifestyle change is your answer including an excellent diet and loads of healthy exercise
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Why not raise your glutathione level ( Safely and Naturally )\nGlutathione must be manufactured within your cells.\nIf you are interested to know some more... write me.\nTake care
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No need to break it down to "molecular" other wise, try this: Sodium thiosulphate. Dont just use it coz they all vary in their Ph U know the basisity or acidity they concentrate.
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The research community is currently answering that.  They suspect that antioxidants may help, and there is some hopeful evidence of that, but nothing concrete yet.  There are a couple of studies that show that Coenzyme Q10 (aka CoQ10) helps people living with Parkinson's disease.  The most well-known study appeared in the Archives of Neurology in 2002.  It was compelling enough to get the National Institues of Health to fund research that is still going on about CoQ10.  \n\nThe current dose that people are speculating is beneficial is 1200 mgs per day - a pretty large dose.  It can also get a little pricey, because it is popular right now thanks to its benefits to the heart too.\n\nExercise also appears to have some very positive effects, if you call that natural.  \n\nOther than that, there are not a lot of other good natural options - that we know about yet.  I hope that we learn something miraculous soon.
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Phenylalanine\n\n\nhttp://www.wellfx.com/InfoBase/cond_Parkinson.doc_.html\nhttp://www.wellfx.com/InfoBase/vitamin_phenylalanine_.htm
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HEY U CAN USE SOME PROTEIN SUPLLIMENT AND AYURVEDIC DRUG
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The bodies natural ability to heal and repair itself is aided with glconutrient supplementation.\n\nI will tell you what to take. It is safe and natural.
310495
tea - tannins and anti-oxidants (green tea)
52109
There is a study that says that caffeine helps with Parkinson's.  Look at the link for more information.
490223
Parkinson's disease (paralysis agitans or PD) is a movement disorder often characterized by muscle rigidity, tremor, a slowing of physical movement (bradykinesia), and in extreme cases, a loss of physical movement (akinesia). The primary symptoms are due to excessive muscle contraction, normally caused by the insufficient formation and action of dopamine, which is produced in the dopaminergic neurons of the brain. Parkinson's disease was first formally recognised and its symptoms documented in 1817 in An Essay on the Shaking Palsy by the British physician Dr James Parkinson; the associated biochemical changes in the brain of patients were identified in the 1960s.\n\n\n\n\nContents [hide]\n1 Symptoms \n1.1 Motor symptoms \n1.2 Non-Motor Symptoms \n2 Incidence \n3 Related diseases \n3.1 Parkinson-Plus diseases \n4 Pathology \n5 Pathophysiology \n5.1 Genetic \n5.2 Toxins \n5.3 Head trauma \n6 Treatments \n6.1 Levodopa \n6.2 Dopamine Agonists \n6.3 MAO-B Inhibitors \n6.4 Surgical Interventions \n6.5 Nutrients \n6.6 Physical exercise \n7 Prognosis \n8 References \n9 External links \n \n\n\n[edit]\nSymptoms\nParkinson disease affects movement (motor symptoms). Typical other symptoms include disorders of mood, behavior, thinking, and sensation (non-motor symptoms). Individual patients' symptoms may be quite dissimilar; progression is also distinctly individual. There are four major dopamine pathways in the brain; the nigrostriatal pathway, referred to above, mediates movement and is the most conspicuously affected in early Parkinson's disease. The other pathways are the mesocortical, the mesolimbic, and the tuberoinfundibular. These pathways are associated with, respectively: volition and emotional responsiveness; desire, initiative, and reward; and sensory processes and maternal behavior. Reduction in dopamine along the non-striatal pathways is the likely explanation for much of the neuropsychiatric pathology associated with Parkinson's disease.\n\n[edit]\nMotor symptoms\nThe cardinal symptoms are:\n\ntremor: 4-7Hz tremor, maximal when the limb is at rest, and decreased with voluntary movement. It is typically unilateral at onset. This is the most apparent and well-known symptom. However, an estimated 30% of patients have little perceptible tremor; these are classified as akinetic-rigid. \nrigidity: stiffness; increased muscle tone. In combination with a resting tremor, this produces a ratchety, "cogwheel" rigidity when the limb is passively moved. \nbradykinesia/akinesia: respectively, slowness or absence of movement. Rapid, repetitive movements produce a dysrhythmic and decremental loss of amplitude. \npostural instability: failure of postural reflexes, which leads to impaired balance and falls. \n(The mnemonic TRAP (Tremor; Rigidity; Akinesia/bradykinesia; Postural instability) can be used to remember these symptoms.)\n\nOther motor symptoms include:\n\nGait and Posture Disturbances: \nShuffling: gait is characterized by short steps, with feet barely leaving the ground, producing an audible shuffling noise. Small obstacles tend to trip the patient \nDecreased arm swing: a form of bradykinesia \nTurning "en bloc": rather than the usual twisting of the neck and trunk and pivoting on the toes, PD patients keep their neck and trunk rigid, requiring multiple small steps to accomplish a turn. \nStooped, forward-flexed posture. In severe forms, the head and upper shoulders may be bent at a right angle relative to the trunk (camptocormia). \nFestination: a combination of stooped posture, imbalance, and short steps. It leads to a gait that gets progressively faster and faster, often ending in a fall. \nGait freezing: "Freezing" is another word for akinesia, the inability to move. Gait freezing is characterized by inability to move the feet, especially in tight, cluttered spaces or when initiating gait. \nDystonia: abnormal, sustained, painful twisting muscle contractions, usually affecting
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"The nutritive composition of a hot aqueous extract of wild Ganoderma fruit bodies was determined. This extract was assessed for cytotoxicity and in vivo genotoxicity by both acute and subchronic exposure of mice (given by mouth at a dose equivalent to extract of 220g fresh Ganoderma fruit body/kg body weight). To test any alleged protection against mutagens by Ganoderma treatments, the mice were injected intraperitoneally with the radiomimetic mutagen ethyl methanesulfonate (EMS), and after 24hr of treatment their lymphocytes were examined using the comet assay. Ganoderma extract consisted of Folin-positive material (68.9% of dry weight), but protein comprised only 7.3% of dry weight. Glucose accounted for 11. 1% and metals 10.2% of dry weight (K, Mg and Ca being the major components with Ge (often touted as being of value in sales literature for Ganoderma preparations) having the fifth highest metal concentration at 489 microg/g). In comparison to rodent chow, Ganoderma extract was a modest dietary supplement. No evidence was found for genotoxic chromosomal breakage nor cytotoxic effects by Ganoderma extract in the mouse, nor did it protect against the effects of ethyl methanesulfonate. We found no support in this study for the extract having any value in protecting against the test mutagen.\nPMID: 10717357, UI: 20183650" (1)\n\nSince the fungus has been used for 2100 years to treat both liver disease and diabetes, and the most effective treatments of both have been discovered only in about the last 50 years, I'd wait until more studies were done, and any healing components of the fungus described, extracted and purified before I'd count on it. Really, they didn't cure hepatitis or diabetes very well 1000 years ago!