PARKINSON'S DISEASE - THE SCIENCE
Parkinson's Disease is a degenerative condition of the central nervous system. It is the second most common neuro-degenerative disease world-wide, after Alzheimer's Disease. Initially the nerves in the substantia nigra, a part of the brain used to control movement, are damaged by a large number of possible causes. This leads to movement difficulties such as a tremor, stiffness and slowing of movement. Symptoms include little or no facial expression, loss of arm swing when walking, soft, slurred or stuttering speech, smaller less well-formed handwriting, a shuffling gait and difficulty initiating walking and turning. Symptoms often begin on one side of the body. As the number and location of damaged nerves in the brain spreads, other functions are lost, leading to depression, anxiety, reduction of memory, attention and cognition and sleep difficulties. Eventually, a diagnosis of brain failure (dementia) may be made.
The initial damage is to nerves in the substantia nigra that use dopamine (dopaminergic neurons) to communicate with adjacent nerves. A protein called alpha-synuclein accumulates into Lewy Bodies within the nerves, and is a marker of the damage being done. It is similar to the beta amyloid plaques that accumulate from the damage done that leads to Alzheimer's Disease.
Parkinson's Disease usually is diagnosed in middle or late life when the damage has progressed to the point of causing visible signs (seen) or noticable symptoms (felt). However the damage to the nerves has started years to decades earlier, and is usually caused by too many neurotoxic factors (pesticides, herbicides, industrial chemicals, heavy metals, physical and mental stress, traumatic brain injury, chronic infections, man-made electromagnetic radiation, excess blue light, poor digestion/absorption etc) and inadequate neurotrophic factors (growth factors, hormones, vitamins, minerals, exercise, sleep etc). These environmental and lifestyle factors are combined with inherited, genetic variations that all together, predispose the individual to the nerve damage that manifests as the Parkinson's Disease constellation of symptoms.
One theory is that the neuro-trophic / neuro-toxic imbalance damages the mitochondria (the energy producing part of cells), leading to increased free radical production (free radicals are a normal result of mitochondrial function, but at excess levels cause cell damage). These free radicals further damage the mitochondria and the rest of the cell, eventually leading to cell dysfunction, and then cell death.
As our lifestyle and environment becomes more toxic, the incidence of Parkinson's Disease is increasing, and more people are experiencing the symptoms at an earlier age.
Conventional, allopathic medicine treats Parkinson's Disease by using medications to increase or replace the dopamine levels in the brain, so as to reduce the distressing signs and symptoms of the condition. This done by:
orally taking a drug that mimics dopamine's effect in the brain (dopamine agonist)
orally taking a drug that blocks the enzymes that breakdown dopamine (COMT or MAO inhibitors)
orally taking the precursor to dopamine (L-dopa), to allow damaged nerves to increase their dopamine production
surgery to implant micro-electrodes that electrically stimulate the damaged brain region to reduce the symptoms.
These approaches can temporarily reduce the symptoms of Parkinson's Disease, but the underlying disorder progresses, and eventually these treatments lose their effectiveness.
Unfortunately these approaches can also affect amino acid neurotransmitter precursors, dopamine, serotonin and other neuro-transmitter levels in other, undamaged regions of the brain and the body, leading to side effects such as nausea, depression, extreme daytime drowsiness, involuntary jerky movements (dyskinesias), insomnia, dizziness, and hallucinations. L-dopa is often given with an enzyme inhibitor (dopa decarboxylase inhibitor ie Carbidopa or Benserazide) to reduce the nausea, but it can lead to vitamin B6, neurotransmitter and thiol (protective sulphur-based amino acid system) depletion and nutritional collapse.
Long term use of L-dopa can lead to fluctuations in its effectiveness (On-Off Phenomenon) and the further development of involuntary movements (dyskinesias) - read the paper.
Parkinson Disease death rates decreased during the first 15 years of use of L-dopa (without Carbidopa or Benserazide). In 1976, one year after the FDA approved the L-dopa/Carbidopa combination drug, the Parkinson's Disease death rate started increasing, and continues to do so - read the paper and watch the video. By 2016 (the latest data available), the death rate had increased by 390%. This may be due to Carbidopa irreversibly binding to and permanently inactivating the active form of vitamin B6 throughout the body, leading to severe vitamin B6 deficiency and dysfunction of over 300 enzymes and proteins (low vitamin B6 is associated with increased coronary artery disease, colorectal cancer, stroke, heart failure and atherosclerosis - read the paper). Vitamin B6 supplementation doesn't counter this effect while the Carbidopa is being taken. There are other management options. Click here
More information about the science behind this protocol can be found here.