Parkinson’s, the second most common form of dementia, is a chronic and progressive degenerative disease of the neurological system.
Parkinson’s is induced when a portion of the brain begins to degenerate and atrophy causing dopamine (a neurotransmitter and hormone) to become deficient. As more and more neurons begin to die, less dopamine is able to be produced leading to a dopamine deficiency. In addition, other neurotransmitters are affected such as adrenaline and noradrenaline.
Some common symptoms include tremors (shaking) while attempting to remain still, difficulty swallowing, stooped posture, wide, uncoordinated steps, constipation, insomnia, muscle atrophy, and stammering speech.
This debilitating disease affects an estimated 1% of the American population over the age of 55. However, Parkinson’s is beginning to be diagnosed at earlier ages.
Studies have repeatedly shown that individuals exposed to and carrying an elevated environmental chemical burden have increased incidences of Parkinson’s disease which induces an inflammatory reaction in the brain. In addition, studies are concomitantly showing elevated inflammatory cytokines in the CSF concluding neuroinflammation (1). Neuroinflammation is the key to controlling neurodegenerative diseases.
Chlorinated pesticides such as DDT, chlordane and lindane are fat-soluble and easily penetrate the blood brain barrier. Chlorinated pesticides, once absorbed, remain in the body for life accumulating with each additional exposure. Research shows that pesticides are extremely toxic to the mitochondria (required for neuron survival) which paralyzes the cell’s ability to make energy or proteins. The mitochondria are adversely affected in PD (3) (4) (5). A 2008 University of Florida study found elevated levels of the pesticides Lindane and Dieldrin concentrated in the brains of PD patients (5). A 2009 study in the Archives of Neurology found that 76% of PD patients actually had the pesticide Hexachlorocyclohexane circulating in their blood (6). A 2007 study found that drinking 3-4 glasses of milk, which is tremendously polluted with contaminants, increased risk of PD by 60%. A 2011 research article in the Journal of Neuroinflammation reported that diesel exhaust particles induced the elevation of proteins associated with neurodegenerative disease. In addtion, their research found that the midbrain (this is where the substantia nigra lies and the neurons which supply dopamine) was the most susceptible part of the brain. Diesel exposure significantly showed neuroinflammation patterns at lower levels of exposure (7). A 2006 study showed that continuously exposing non-toxic levels of heavy metals to neurons resulted in neuroinflammation and the characteristic event (glial cell activation) involved in Parkinson’s and other neurodegenerative diseases (2).
In the presence of environmental chemicals, mitochondria (the portion of the cell involved in energy production and programmed cell death) begin to expire and become impaired. If the mitochondria become impaired or debilitated then the energy system of the cell becomes inadequate. Therefore, the cell, perceiving that it is damaged beyond repair due to insufficient energy sources, undergoes programmed cell death, resulting in a continuous, progressive degeneration of the dopaminergic neurons.
Conventional medicine recognizes that environmental exposure to chemicals can play a significant role in Parkinson’s disease. Unfortunately, they do not address this issue but provide symptomatic improvement which decreases in efficiency as more neurons continue to expire. Medication is usually effective for no more than 10 years.
Our approach is to address the underlying cause of the disease which is environmental induced chemical toxicity to the brain. The brain is in a chronic state of neuroinflammation.
The “accepted” belief is that the disease cannot be halted nor even slowed in its progression yet . Understanding that environmental and mitochondrial toxicity are directly involved in Parkinson’s, treatment is rational and effective.
The ultimate goal of our therapies is to halt the progression of the disease. Intervening at an early stage offers the best possibility for significantly impacting progression since more neurons will still be intact.
Therapies target removal of environmental chemicals, therapeutic levels of nutrients and antioxidants, and complimentary therapies such as major autohemotherapy to increase blood flow, nutrient delivery, and oxygenation to the brain.
1) J Neural Transm Suppl. 2000;(60):277-90.
Changes in cytokines and neurotrophins in Parkinson’s disease.
Nagatsu T, Mogi M, Ichinose H, Togari A.
Institute for Comprehensive Medical Science, Graduate School of Medicine, Fujita Health University Toyoake, Aichi, Japan. firstname.lastname@example.org
2) Rev Environ Health. 2006 Apr-Jun;21(2):105-17.
Involvement of environmental mercury and lead in the etiology of neurodegenerative diseases.
Monnet-Tschudi F, Zurich MG, Boschat C, Corbaz A, Honegger P.
Department of Physiology, University of Lausanne, Switzerland. Florianne.Tschudi-Monnet@unil.ch
3) } Metabolism. 2008 Oct;57 Suppl 2:S50-5.
Parkinson disease: primacy of age as a risk factor for mitochondrial dysfunction.
Division of Endocrinology, Diabetes, and Nutrition, Department of Medicine, St Luke’s-Roosevelt Hospital Center, New York, NY 10025, USA. email@example.com
4) J Cereb Blood Flow Metab. 2006 Feb;26(2):283-90.
Parkinson’s disease and brain mitochondrial dysfunction: a functional phosphorus magnetic resonance spectroscopy study.
Rango M, Bonifati C, Bresolin N.
Department of Neurological Sciences, Parkinson’s Disease Center, Maggiore Policlinico Hospital, IRCCS, University of Milan, Milan, Italy. firstname.lastname@example.org
5) Neuroreport. 2008 Aug 27;19(13):1317-20.
Synergistic microglial reactive oxygen species generation induced by pesticides lindane and dieldrin.
Mao H, Liu B.
Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville, Florida, USA.
6) Arch Neurol. 2009 Jul;66(7):870-5.
Elevated serum pesticide levels and risk of Parkinson disease.
Richardson JR, Shalat SL, Buckley B, Winnik B, O’Suilleabhain P, Diaz-Arrastia R, Reisch J, German DC.
Robert Wood Johnson Medical School, Piscataway, New Jersey, USA. email@example.com
7) J Neuroinflammation. 2011 Aug 24;8(1):105. [Epub ahead of print]Air pollution and the brain: Subchronic diesel exhaust exposure causes neuroinflammation and elevates early markers of neurodegenerative disease.Levesque S, Surace MJ, McDonald J, Block ML.