By Michael J. Hollis BSc ND
BWell Clinic
50 thousand new cases of Parkinson disease are being discovered every year. The cause is unknown, but science is getting closer than it has ever been to finding out what that cause is. Parkinson disease is a degenerative disease affecting a very specific type of nerve. It appears the cells that normally protect these special nerves are no longer being protected in old age as they were in youth. Scientists are trying to explain how this is happening, and what weaknesses have been found in dopamine-producing nerves that might be contributing to the disease.
The nerves at issue here produce a special chemical, called dopamine. In patients suffering from Parkinson disease, a specific group of dopamine-producing nerves are affected, located in a tiny region of the brain called the substatia nigra. The slow degradation of dopamine nerve function in this area causes resting tremors, slowness of voluntary movement, and problems with posture that characterize the disease. We suspect that the surrounding tissues that protect these nerves are causing the breakdown in nerve function to occur. These protective tissues are made of glial cells – a potent source of nutrition and a detoxifier of nerve cells in the brain.
When glial cells are not working properly, they get inflamed and produce damaging free radicals that seep through and irritate sensitive nerves in the substantia nigra.1,2 Under a microscope, this irritation can be seen as clumps (or aggregates, called Lewy bodies) within the nerves of Parkinson patients. These clumps have been dissected and have been shown to contain metabolic trash such as iron, ubiquitin, and alpha-synuclein.3 In normal individuals, glutathione in the nerves protects against free radical damage and these clumps are not visible.
When analyzed, the brains of deceased Parkinson disease patients have been shown to have lower levels of glutathione than non-Parkinson disease subjects.4-6 They also show extensive free radical damage in the DNA, lipids, and proteins in the brain. This damage may come directly from free radical damage or from free radical damage due to dopamine – likely a combination of both.7 Damaged dopamine is turned into a metabolite (known as Dopaminochrome, or DACHR) that fuses within the nerve and corrupts the normal energy cycle in the nerve cell – in turn, giving birth to more and more free radicals destroying the nerve from within. Treatment with L-dopa medications, while they improve dopamine function temporarily, may only feed more ‘kindling’ to the fire created by free radicals coming from dysfunctional glial cells – thus accelerating and intensifying the symptoms of Parkinson disease.8
It still remains to be determined whether the glutathione deficiency found in Parkinson disease is due to an overload of free radicals, or due to an underproduction of glutathione. Nonetheless, glutathione precursors and antioxidant therapy appears to be an effective treatment for glial inflammation.
Studies on Parkinson disease patients treated with twice daily I.V. glutathione showed significant improvement after 6 months. The therapeutic effects persisted long after treatment was discontinued (2-4 months after cessation).9 Adjunctive treatment with n-acetyl cysteine may be of further benefit, as it an essential building block for new glutathione in both the brain and the rest of the body.10,11 Patients must be tested to determine glutathione status and other possible deficiency states prior to treatment. This precaution helps the physician to construct an individualized program that suits the patient’s unique biochemical needs. In addition, liver and organic acids tests help to identify areas of breakdown in metabolism throughout the body. Modified Columbia University Rating Scale (CURS),12 Purdue Pegboard, and Webster Step-Second Test (WSST)13 are standardized tools to measure the severity of Parkinson disease.14 Each of the tests conducted not only help us understand the degree to which the body is affected by nerve damage, but how the chemistry of the body leads to the manifestation of the disease process. They are also used to measure progress and show benefit from treatment.
In a more detailed view of the toxic effect of DACHR (a metabolite of damaged dopamine), researchers have evidence to show how DACHR disrupts the energy cycles in nerve cells – and how this metabolite can form Lewy bodies.15 Scientists speculate DACHR’s toxic effects may be related to higher-than-normal levels of calcium inside the dopamine nerve cells. This calcium problem intensifies DACHR’s effects – increasing the rate of production of free radicals15 – and may be the cause of Parkinson disease unusual susceptibility to DACHR.
To correct this imbalance, vitamin E and coenzyme Q10 has been used therapeutically to rebalance cell energy cycles – with promising results.16-18 To correct calcium levels inside nerve cells, vitamin D has also been used. Studies have detected a prevalence of vitamin D deficiency (and associated osteoporosis) in Parkinson’s patients.19,20 Vitamin D is known to affect calcium absorption and metabolism. Parkinson disease patients exhibit lower body weight than normal subjects. This low body mass index (BMI) in Parkinson disease is due to low bone mineral density – more evidence in support of vitamin D deficeincy.21
In one case study, the addition of Vitamin D therapy in a patient with Parkinson disease and vitamin D deficiency showed progressive improvement in symptoms, including decreased rigidity, absence of tremor, and decreased akinesia – leading to a reduction in prescribed L-dopa medication.22
In summary, new and effective treatments are being discovered to not only treat the symptoms of Parkinson’s, but also to reduce or remove possible causes of the symptoms. The importance of testing and appropriate treatment planning is an essential component of symptom management in Parkinson disease. Clinics that specialize in individualized wellness programs can screen for deficiencies that lead to early detection of disease states. Parkinson disease if caught early in its pathological progress, can be treated and the symptoms minimized.
References
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