Treatment Options for Parkinsons
In Parkinson's disease high doses of vitamin B6, iron, and manganese should be avoided. High doses of vitamin B6 may decrease the effectiveness of of L-dopa therapy, and high doses of iron and manganese can aggravate the disease. Parkinson disease, and low body stores of these B vit
Ericson et al . 63 have studied the relation of GABA and cranial nerve disease (such as Parkinson's disease) . GABA and GAD concentrations were reduced in Parkinson's disease patients' brains and plasma After gene therapy (to plant into GAD65 or GAD67), the GAD activation and GABA release were increased . In addition, nitric oxide (NO) is an intra- or interneuronal messenger that modulates neurotransmitter release in the mammalian brain . Nitric oxide synthase (NOS), including neuronal isoform (nNOS) and endothelial isoform (eNOS), was related with neurotransmitters (glutamate and GABA) .64-66 It caused neuron depolarization and calcium ion flow into cell acceptors and excited the chain reaction of toxic free radicals 67 Furthermore, it enlarged nerve damaging and cell death and resulted in inducing neurodegenerative diseases 68 Parkinson's disease patients should keep a stable supply of GABA so that their athletic control system can properly be improved.
One of the most-discussed environmental connections to disease is the relationship between aluminum exposure and Alzheimer's disease. In truth, the connection applies to most neurodegenerative disorders, including Parkinson's and ALS. While no absolute proof of causation currently exists, there is a lot of compelling circumstantial evidence, as well as laboratory evidence, for such a connection.
All of the comments 1 have made concerning Alzheimer's disease also apply to Parkinson's disease. Like Alzheimer's and ALS, Parkinson's disease is associated with free-radical and lipid-peroxidation damage to a very restricted part of the brain called the substantia nigra and its connections. Like the others, excitotoxicity appears to play a central role in the disease process itself. There is strong evidence that iron toxicity is also critical in this disease. Some feel that the free-radical generation caused by mercury is related to the fact that it causes free iron to be released from its binding protein, ferritin. On top of all this, those destined to get Parkinson's disease seem to possess an inherited weakness in their ability to detoxify toxins, both those formed within the body during metabolism and those ingested or inhaled. A recent study, in which one hundred Parkinson's patients were compared to two hundred matched controls, found that Parkinson's patients had a genetic...
Parkinson's disease is a chronic and progressive brain disorder that affects 1-2 of people older than 60 years. It results from the degeneration of nerve cells in the center of the brain that normally produce dopamine, an important neurotransmitter. Inadequate dopamine signalling in the brain results from loss of these cells. The disease typically begins as trembling in the arms and hands, but as it progresses muscle rigidity develops, trembling worsens, and simple movements become difficult. L-dopa, an amino acid that can be converted into dopamine in the brain, is often used in the medical treatment of Parkinson disease.
A low-protein diet can be beneficial in Parkinson's disease.1 L-dopa is one of several amino acids that compete for uptake into the brain from the bloodstream. During L-dopa therapy, restricting dietary protein reduces competition from other amino acids and allows more L-dopa to enter the brain. One limitation of L-dopa therapy is that its beneficial effects unpredictably wax and wane through the day. Protein restriction can reduce these daily fluctuations and make L-dopa therapy more effective, particularly if most of the daily protein is eaten with the evening meal.1 Free-radical damage (see pp. 115) appears to play a role in Parkinson's disease. Diets high in natural antioxidants (such as vitamins E and C and carote-noids) may reduce risk of Parkinson's disease or slow down its progression.2,3
GABA is found in a number of biological species, including (1) bacteria, such as Escherichia coli, Streptococcus pneumoniae, Neurospora crassa, and Lactobacillus brevis (2) insects, such as cockroach, grasshopper, moth, honeybee, and fly (3) plants, such as GABA tea, tomato, soybean, mulberry leaf, germinated brown rice, and petunia and (4) animals, such as human, rat, rabbit, cat, and dog, among others,8 and is widely distributed in living cells of the cerebral cortex and hypothalamus 9 It is decomposed from glutamate by glutamate decarboxylase (GAD) in the substantia nigra, pallidum, and striatum of the basal ganglia. 2,10 more chloride channels in the tract of the cell membrane on the neuron axon, and increase the chloride penetration of the neuron membrane . Low GABA in plasma is reasonably specific to Parkinson's disease, epilepsy, alcoholism, depression, and menopause. 14 Therefore, GABA is an important inhibitory neurotransmitter in the brain and CNS15 for being able to...
In Excitotoxins, The Taste That Kills, I made it clear that there was no evidence that the excitotoxins found in foods are themselves the primary cause of neurodegenerative disorders such as Parkinson's and Alzheimer's disease, but one frightening possibility is that there may be a link between the widespread excitotoxic contamination of our food supply and the heretofore-unexplained dramatic increase in neurodegenerative diseases which have also begun to occur on average at an earlier age. While these diseases existed long before the introduction of excitotoxic food additives, this does not mean that certain food additives High consumption of excitotoxin-containing foods would increase your risk not only of developing one of these diseases, but could also augment the risk of early onset and severity of the disease.264 1 am shocked when I see patients with Alzheimer's or Parkinson's disease consuming foods high in these brain-toxic additives. Hospitals can be the world's worst in this...
Live viruses used in vaccines are also suspected to be associated with other disorders as well, such as multiple sclerosis, ALS, and autism. Particularly startling is the recent report of two cases of parkinsonism reported in young children who had been recently vaccinated with the MMR vaccine. It is important to remember that parkinsonism is extremely rare in
When aluminum combines with glutamate, it forms a compound that can pass through the blood-brain barrier easily, where it is distributed to several areas of the brain. In one study, this complex was found to increase levels of aluminum in the parts of the brain associated with Parkinson's disease (striatum) and Alzheimer's disease (hippocampus).204 The connection to Parkinson's disease was strengthened by a study that found aluminum enhanced lipid peroxidation in the presence of melanin.205 This is an important finding because the part of the brain damaged by Parkinson's disease contains large amounts of melanin. When iron combines with melanin, large numbers of free radicals are produced, which can lead to lipid peroxidation and cell destruction. As the disease advances, the melanin-containing brain cells die off. Now we find that aluminum also promotes this destructive process in the same area of the brain. Autopsy studies of Parkinson's patients, using a microprobe analysis,...
There have been reports of increased aluminum in the bulk of brain tissue in Alzheimer's patients and more recently associations of aluminum with neurofibrillary tangles and neuritic plaques. Aluminum has also been associated with neurofibrillary degeneration in patients with amyotrophic lateral sclerosis and Parkinsonism type dementia.
In the brain, adenosine acts as a neurotransmitter. It is synthesized in glial cells and neurons, and its release into extracellular space is enhanced during states of fatigue and sleep (Adrien, 2001). The adenosine A2A receptors act, in part, by inhibiting the N-methyl-D-aspartate (NMDA) component of excitatory synaptic currents (Gerevich et al., 2002), and the neural distribution of these receptors suggests some probable sites of action of caffeine in the brain. Included are the striatum and medulla, as well as portions of the basal forebrain, the mesopontine area, and the sleep-regulating preoptic nucleus of the hypthothalamus (Boros et al., 2002). The nucleus acubens (Solinas et al., 2002) and the lateral amygdala (Svenningsson et al., 1999) may also be involved. Caffeine probably produces its stimulatory effect, in part, by blocking the A2A receptors that activate the GABAergic neurons populating the inhibitory tracts to the striatal dopaminergic reward system (Daly and Fredholm,...
Despite the expectation of exquisite specificity fostered by the various discrete combinations of RAR and RXR isoforms, these receptors exhibit a great deal of apparent functional redundancy and or ability to compensate for loss of another. In gene knockout experiments, more than one receptor can perform the same function in vivo, although this may represent an artifact of the knockouts and demonstrate what can happen, not necessarily what does occur.11 Nevertheless, receptor ablation has provided enormous insight into receptor function. Deletion of the RARa gene results in postnatal lethality within 24 h RARa-null mice represent only 3 of the population by 1 to 2 months of age. Of these, 60 have webbed digits on both fore and hind limbs. A few mice survive 4 to 5 months, but no males are fertile, and all have severe degeneration of the testis germinal epithelium. RARP-null mice have locomotor defects, reminiscent of Parkinson's disease, but are fertile with normal longevity....
Earlier, I said that excessive quantities of glutamate and other excitotoxins in the brain can result in neuron death that is associated with everything from Alzheimer's dementia, Parkinson's disease and Lou Gehrig's disease (ALS), to strokes and brain injury. This destructive process depends on calcium entry into the neuron triggered by the excitotoxins. Cadmium, in tissue culture, blocks this toxicity. At first, this might seem to be a good thing, but cadmium, even in low concentrations, has been shown to reduce cell survival. It appears that calcium blockage is so efficient that the cell cannot survive.
Abnormalities in the acetylcholine system in the brain may produce motor disturbances. Therefore, choline and lecithin supplements may benefit people with Parkinson disease, Huntington disease, and other nervous disorders characterized by abnormal movements.7 Choline and lecithin may also be beneficial in reducing tardive dyskinesia associated with antipsychotic drug use.1
For example, cocaine and methamphetamine stimulate the release of excess glutamate in the same part of the brain responsible for Parkinson's and Huntington's disease. Both drugs are also capable of producing serious long-term injury to the brain. After repeated use, millions of brain cells and synaptic connections are destroyed. Recall that accumulated attrition of brain cells and their connections accounts for brain aging and degenerative diseases. What this means for chronic users of powerful drugs is an elevated risk for developing Parkinson's or Alzheimer's at forty or even thirty, rather than sixty. Not surprisingly, this is exactly what we are seeing today. The age at which people are developing degenerative diseases of the brain has been sliding steadily toward a younger age group. Also, there has been a dramatic rise in the total incidence of these brain diseases over the last several decades.
Magnesium supplementation is associated with a fall in the rate of ventricular arrhythmias in patients with chronic heart failure,26,27 atrial fibrillation,28-30 and digoxin toxicity.30 It may also be useful in the management of atrial fibrillation in patients with Wolff-Parkinson-White syndrome.32 Torsades de pointes also often responds to magnesium,33-35 even if there is no overt biochemical deficiency. Two randomised studies have demonstrated no benefit of intravenous magnesium in acute myocardial infarction in humans.36,37
Wolfgang Klein and co-workers demonstrated that cells exposed to 1 ppm fluoride exhibit a 50 percent reduction in DNA-repair-enzyme activity.125 Not only does this increase cancer risk, it also encourages aggravation of degenerative diseases of the nervous system, such as Alzheimer's disease, Parkinson's disease, and Lou Gehrig's disease (ALS), as well as other degenerative diseases of aging. When unrepaired DNA damage occurs in reproductive cells, the damage is passed on to children as well.
Adenosine A1 receptors are found all over the brain and spinal cord (Fastbom et al., 1986 Jarvis et al., 1987 Weaver, 1996 Svenningsson et al., 1997a Dunwiddie and Masino, 2001). In the adult rodent and human brain, levels are particularly high in the hippocampus, cortex, and cerebellum. By contrast, A2A receptors have a much more restricted distribution, being present in high amounts only in the dopamine-rich regions of the brain, including the nucleus caudatus, putamen, nucleus accumbens, and tuberculum olfactorium (Jarvis et al., 1989 Parkinson and Fredholm, 1990 Svenningsson et al., 1997b, 1998, 1999a Rosin et al., 1998). They are virtually restricted to the GABAergic output neurons that compose the so-called indirect pathway and that also are characterized by expressing enkephalin and dopamine D2 receptors. There is, indeed, very strong evidence for a close functional relationship between A2A and D2 receptors (Svenningsson et al., 1999a). Parkinson, F.E. and Fredholm, B.B. (1990)...
Additionally, Parkinson patients also benefit from the low-leucine vegan diet because the low-leucine intake decreases the competition with their oral DOPA intake, so they can use lower amounts of DOPA medication to suppress their Parkinson disease symptoms without undesirable side effects from the higher DOPA intake.35
One telling fact is that, of cancer cases, especially lymphomas and leukemias, the highest incidence in the population occurs in people who work on farms. The same is true for Parkinson's disease. Lured into believing these powerful chemicals were safe, farmers drenched everything in pesticides, herbicides, and fungicides including themselves and their families.
Of the complications listed in the 1927 edition of Sajous's Analytic Cyclopedia of Practical Medicine under mercury poisoning is paralysis agitans, also known as Parkinson's disease. A more recent study of nine exposed workers from a thermometer plant found symptoms of Parkinson's disease in four, which eventually cleared in all but one. They also experienced loss of muscle power, tremors, and atrophy of muscle mass, all symptoms associated with motor neuron injury, as in ALS. We know that there is a tremendous overlap in these diseases, with about 30 percent of Parkinson's patients showing signs of dementia and a smaller number having features of ALS this is consistent with the effects of an environmental toxin.
A Because coffee is so widely consumed, it has been extensively researched. On the positive side, coffee drinkers might actually have a lower risk of diabetes and Parkinson's disease. To date, there is no obvious negative connection between caffeine and heart disease, cancer, or blood pressure. Hence, the general answer, according to leading medical and scientific experts, is normal coffee consumption produces no adverse health effects.
This is important because there is a strong link between brain aluminum levels and neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Histological examinations of test animals' brains indicated that damage was concentrated in the left hemisphere of the brain, with a significant reduction in neuron density. This loss of brain cells was greater in animals drinking aluminum fluoride water than in those given sodium fluoride or distilled water. The damaged neurons exhibited clumping, enhanced protein staining, and destructive chromosomal changes. Similar damage was seen in the blood vessels supplying this part of the brain as well, a consistent finding in Alzheimer's disease. An early change that has been observed in the brains of those developing Parkinson's disease is a significant reduction in the energy molecule, CoQIO. Animal experiments have indicated that chronic fluoride exposure at levels equal to accumulated concentrations high
This means that the cell has less energy to carry out its many functions and, as a result, will produce even more free radicals. Soon cells begin to die and obvious illness develops. In Parkinson's disease, we know that this process begins very early and is localized mainly to special neurons in the brain responsible for motor movement. As we shall see later, neurons with deficient energy supplies are up to one hundred times more susceptible to excitotoxic injury and death, ultimately caused by free radicals. We know that some diseases associated with severe muscle weakness and brain malfunction (encephalopathy), and a large number of strokes are caused by inherited mitochondrial malfunction. This inheritance is unusual in that it passes only from the mother, since sperm contribute no mitochondria to conception. Parkinson's disease is also suspected to have a maternal, mitochondrial lineage, so that if your mother had Parkinson's disease your chances for developing the disease are...
Populations at risk of vitamin-B6 deficiency include alcoholics and elderly persons who consume an inadequate diet. Individuals taking medication to treat Parkinson's disease or tuberculosis may take extra vitamin B6 with physician supervision. Carpal tunnel syndrome, a nerve disorder of the wrist, has also been treated with large daily doses of B6. However, data on its effectiveness are conflicting.
A plethora of recent studies suggest Creatine may have therapeutic applications in aging populations, muscle atrophy, fatigue, gyrate atrophy, Parkinson's disease, Huntington's disease and other mitochondrial cytopathies, neuropathic disorders, dystrophies, myopathies and brain pathologies.
Data supporting the efficacy of metoclopramide are contradictory, and positive results are limited to observations with intravenous administra-tion.104 Application in infants is limited because of severe adverse events that occur quite frequently (in more than 20 of patients) including central nervous system effects and interactions with the endocrine system.104 The adverse effects regarding the central nervous system are mainly related to its dopamine-receptor blocking properties in the substantia nigra, and include extrapyramidal effects (dystonic reactions, irritability) and drowsiness, but also asthenia and sleepiness. Isolated cases of metoclopramide-induced methemoglo-binemia and sulfhemoglobinemia have been reported.104,105 Neuroendocrine side-effects such as galactorrhea do occur.106 Also, metoclopramide has been reported to induce torsade de pointes.107
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