Parkinson’s Disease Alternatives Complementary Treatments

Parkinson’s Disease
Located in Boulder, CO NatureMed offers a program for people suffering from Parkinson's disease. Patients can take advantage of this program while on prescription medication.

Background: Evidence has accumulated to support the view that Parkinson's disease can originate from long-term, subclinical damage to the nervous system caused by environmental chemicals (Cooper 1991; Farina et al. 1994; Calne et al. 1986, 1987a,b). Initial reports have also linked the development of Parkinsonism to drugs  and to industrial workers who were exposed to chemicals, especially exposure to industrial solvents (Smargiassi et al. 1998; Kim et al. 2000). Pesticides and herbicides used on farms and in households have also been the subject of studies to investigate the possible link to Parkinson's disease (Zuber et al. 1991; Butterfield et al. 1993; Linazasoro et al. 1995; Veldman et al. 1998).

Symptoms due to low-level chronic exposure develop gradually. It has been suggested by researchers that long-term exposure to subtoxic levels of chemicals is much more likely to lead to neurological disorders, such as Parkinsonism, than to physically based diseases. Betarbet (2000) reported in Nature Neuroscience that chronic systemic pesticide exposure reproduced the features of Parkinson's disease.

Persons who use pesticides in their homes are twice as likely to develop Parkinson's disease as people who are not exposed to pesticides (Stephenson 2000). A combination of different pesticides is even more likely to create greater toxicity issues than an individual chemical. This disturbing but not unexpected finding was reported by Thiruchelvam et al. (2000) in Neuroscience. Paraquat (a common herbicide) and Maneb (a common fungicide) did not affect mice that were exposed to either of them. However, when both chemicals were combined, the dopamine neurons started to die at rather low exposure levels--at only a fraction of the levels normally regarded as toxic. Ongoing exposure led to progressive neurotoxicity. There are countless combinations of low-level toxic residues in our food and water. The possible effects to our health produced by these low-level toxic residues are unknown.

Individuals with familial Parkinson's disease have much lower levels of detoxifying enzymes than healthy individuals, possibly only about 30% of normal levels (Ritchie 1980; Meyer et al. 1990; Daly et al. 1993; 1994; Bandmann et al. 1997; 2000; Agundez et al. 1998; Harhangi et al. 1999; Bialecka et al. 2002). As a result, accumulation of toxic chemicals is higher in such individuals than it is in persons with normal liver function. Because toxic chemicals are commonly fat-soluble, they are therefore stored in lipid structures such as those present in the brain.
 
Intravenous Glutathione is Very Effective for Parkinsons
 
Parkinson's disease (PD) is a progressive neurodegenerative disease involving neurodegeneration of dopaminergic neurons of the substantia nigra (SN), a part of the midbrain. Oxidative stress has been implicated to play a major role in the neuronal cell death associated with PD. Importantly; there is a drastic depletion in cellular levels of the thiol tripeptide glutathione within the SN of PD patients. Glutathione (GSH) exhibits several functions in the brain chiefly acting as an antioxidant and a redox regulator. GSH depletion has been shown to affect mitochondrial function probably via selective inhibition of mitochondrial complex I activity.
 
An important biochemical feature of neurodegeneration during PD is the presence of abnormal protein aggregates present as intracytoplasmic inclusions called Lewy bodies. Oxidative damage via GSH depletion might also accelerate the build-up of defective proteins leading to cell death of SN dopaminergic neurons by impairing the ubiquitin-proteasome pathway of protein degradation. Replenishment of normal glutathione levels within the brain may hold an important key to therapeutics for PD. Several reports have suggested that iron accumulation in the SN patients might also contribute to oxidative stress during PD.