
Revolutionizing Parkinsons Disease Treatment
For treatment to be effective, treatment must target that cause of the disease. This may seem like an obvious statement, but it is very uncommon in modern medicine to treat the cause of the problem instead just treating the symptoms. Most medications attempt to fix merely the symptoms as long as you continue to take them, usually for the rest of your life or until they stop working. This is certainly the case for most dopamine agonists for treatment of Parkinson’s Disease.
At Sunridge we are not interested in only treating symptoms. Our doctors strive to treating the underlying cause of a patient’s Parkinsons Disease. This is the only way to have long lasting results.
In most cases of Parkinsons Disease we are able to identify the cause of the disease for our patients. However, sometimes it is more difficult.
Understanding Parkinsons Disease
Parkinsons disease is a progressive disease which affects nerve cells in a part of the brain called the basal ganglia. The basal ganglia control movement and balance in the body and produce an inhibitory neurotransmitter called dopamine. In Parkinsons disease, the cells that produce dopamine gradually die off and this alters the processing of information about movement in the brain, which is why patients with Parkinson’s typically have trouble with movement.
People usually start to have symptoms between the ages of 50 and 60, but in some people symptoms start earlier. In time, Parkinsons affects muscles all through your body, so it can lead to problems like trouble swallowing or constipation. In the later stages of the disease, a person with Parkinsons may have a fixed or blank expression, trouble speaking, and other problems. Some people also have a decrease in mental skills and suffer from dementia.
Patients who follow our Parkinsons treatment protocol will typically notice improvements in:
- Fine Motor Control, Balance and Resting Tremor
- Memory, Mood and Sleep
- Mobility, Strength and Independence
Causes of Parkinson’s Disease
There is no single cause or single risk factor for developing Parkinson’s disease yet there is a body of research that has linked Parkinson’s disease to:
- Exposures to environmental toxins including heavy metals and pesticides
- Chronic Infections
- History of Head Trauma
- Preventing Parkinson’s
There is no single cause or single risk factor for developing Parkinson’s disease yet there is a body of research that has linked Parkinsons disease to.
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A key component to the design of our successful integrative treatments is focussing on repairing the malfunctions in your body’s own internal defense mechanism so that it can do the job it was designed to do. With a stronger, healthier immune system, our patients feel better, have more energy and greatly reduce the possibility of recurring disease.
Di Monte, D.A., Chan, P. and Sandy, M.S. (1992), Glutathione in Parkinson’s disease: A link between oxidative stress and mitochondrial damage?. Ann Neurol., 32: S111-S115. https://doi.org/10.1002/ana.410320719. Several links exist between the two mechanisms of neuronal degeneration (i.e., oxygen radical production and mitochondrial damage) proposed to have a role in Parkinson’s disease. Indeed, mitochondria are critical targets for the toxic injury induced by oxygen radicals, and experimental evidence suggests that mitochondrial damage may cause an increased generation of oxygen radicals. A potentially important link between these two mechanisms of neurodegen-eration is glutathione.
Because of the scavenging activity of glutathione against accumulation of oxygen radicals, its decrease in the brains of parkinsonian patients has been interpreted as a sign of oxidative stress; however, this change may also result from or lead to mitochondrial damage. It is conceivable therefore that regardless of whether oxidative stress or mitochondrial damage represents the initial
insult, these toxic mechanisms may both contribute to neuronal degeneration via changes in glutathione levels.
Rybicki, B.A., Johnson, C.C., Uman, J. and Gorell, J.M. (1993), Parkinson’s disease mortality and the industrial use of heavy metals in Michigan. Mov. Disord., 8: 87-92. https://doi.org/10.1002/mds.870080116. Parkinson’s disease (PD) mortality rates in Michigan counties for 1986–1988 were calculated with respect to potential heavey metal exposure (iron, zinc, copper, mercury, magnesium, and manganese) from industry based on recent census data. Individuals were counted as a PD death if the diagnosis was listed as an “underlying” or “related” cause of death on the death certificate.
Counties with an industry in the paper, chemical, iron, or copper related-industrial categories (ICs) had statiscally significantly (p < 0.05) higher PD death rates than counties without these industries. Significant correlations of chemical (rs =0.22;p = 0.05), paper (rs =0.22;p = 0.05) and iron (rs =0.29;p = 0.008) industry densities with PD death rates were also present. Counties were divided into high (>15/100,000 individuals 45 years old and over) and low (< = 15/100.000) PD death rate counties by cluster analysis.
Geographically, counties with high PD mortality were located mainly in the southern half of the lower peninsula and eastern half of the upper peninsula; low PD death rate counties formed two distinct clusters in the western edge of the upper peninsula and the north-central portion of the lower peninsula.
Other possible risk factors that may explain the varied distribution of PD death rates in Michigan were examined. Those significantly correlated with PD mortality included population density (rs =0.31;p= 0.005), farming density (rs= 0.25;p =0.02), and well water use (rs =−0.24;p =0.03). These ecologic findings suggest a geographic association between PD mortality and the industrial use of heavy metals.
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