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Parkinson’s: Tracing the Biochemical Sequence
Parkinson’s is an elusive, progressive, and devastating illness, disabling about 6.5 million people in this country.. There are pharmaceutical drugs that can minimize the effects, and for clients who come to us with this diagnosis, we suggest a few natural remedies to add to their routine, along with their medications.
There is a little compartment in the brainstem called the “substantia nigra” which means “black substance” in Latin. This area is where the neurotransmitter, dopamine, is synthesized. Dopamine is severely diminished in people with Parkinson’s, and at the Balancing Center we have found that clients with Parkinson’s are showing that their substantia nigra appears to have been significantly damaged. Although there surely must be other reasons, in the cases we have worked with so far it looked as though the substantia nigra had been eroded by a parasitic microorganism. We identified this intruder as a mycoplasma.
The first thing to do, in that case, is to reveal the sequestered mycoplasma with remedies that will allow the immune system to locate it, identify it, and release it by the body’s own natural process. When the release of this microorganism comes close to completion, we work with supplementation that will rebuild the structure of the substantia nigra. That repair might take three or four weeks.
A few weeks later, we ask the body-consciousness if it is time to think about tracing the steps required to construct accurate dopamine. This starts with the synthesis of tyrosine from phenylalanine. Tyrosine is synthesized by adding a hydroxyl to the phenyl ring of the phenylalanine.
If the body-consciousness indicates that this can’t be done, we have to take a little side-trip to activate the conversion of folic acid to tetrahydrofolic, and to assure the phosphorylation of B6 as both of these are required before that little hydroxyl can be attached to the phenylalanine. Once those issues are handled, tyrosine can be synthesized.
Once tyrosine is established, we ask if another hydroxyl can be added to it. If the second hydroxyl is not being placed in the right position, very likely there is a toxin that is diverting it, so we identify and detoxify the toxin, and find a supplement that will be able to guide the hydroxyl into position. This will create accurate L-dopa.
Now we need to make sure that L-dopa can get through the membrane of the newly reconstructed substantia nigra. Once it gets there, the decarboxylase enzyme has to be available to convert it to dopamine. If not, we ask the body to tell us what it needs to make it available.
Sometimes decarboxylase enzymes are blocked by commonly prescribed pharmaceuticals, and if so, we suggest biotin to help the body circumvent that side-effect, while still maintaining the intended positive effect of the drug. (SSRIs tend to deactivate the decarboxylase enzymes, thus preventing the synthesis of many of the monoamines.) If a heavy metal, or perhaps a mineral or vitamin deficiency is in the way of synthesizing the required decarboxylase, we ask the body-consciousness to tell us what it is, and offer the supplement that it selects from our sample kit.
Next we check to see if the dopamine, having been derived by the decarboxylation of L-dopa, is accurate. If so, this is excellent. We’re getting closer to resolution. But first there are three more very important things we need to ask:
First: Can dopamine be released from the membrane of the substantia nigra? If not, check the membrane permeability of that little structure, possibly the trace mineral rubidium would allow the membrane to relax and let the dopamine find its way out.
Second: There is a flexible protein structure, present in the brainstem and the brain, called α-synuclein. In the case of Parkinson’s, it is being constructed incorrectly, and arranged in such a way that it diverts the various pathways of dopamine, so that dopamine can’t reach its target receptor sites. So far we have found that a combination of CLA and B-5 allows the body to correct the inaccurate form of α-synuclein.
Third: Once the α-synuclein is cleared up, the dopamine has to enter the pyramid tract, to be distributed throughout the brain and body. Full receptivity to the tract might require a vitamin, a mineral, or possibly a detoxifier. The pyramid tract carries information to the cerebellum, so finally dopamine can access the cerebellum, and the sensation of being out of balance, and the fear of falling is no longer a problem.
Any foreign substance, whether it is a pathogen, an agricultural toxin, a petrochemical, or pharmaceutical, can interfere with the completion of a few, or perhaps several of these steps, and contribute to the creating of Parkinson’s. There is not “One Cause” that will yield to “One Cure,” as is usually hoped for in setting up medical research projects, nor does it yield easily to statistical evaluation. This appears to be a very individual process that requires precise and unique remedies for each client.
It is interesting to note that while most illnesses have their basis in some sort of emotional crisis or a series of similar emotional decisions, in most of the cases of Parkinson’s we have seen, this has not been part of the equation. For one man, there was an intense trauma that rewired the α-synuclein, and at the same time he became susceptible to mycoplasma. That combination initiated his Parkinson’s, but for the most part, toxic exposures seem to be the major player in its development.
Another vital question must also be considered: How capable are the kidneys and the liver, in their task of releasing a potentially difficult toxic load? They might need to be attended to, in order to enhance their efficiency, before embarking upon a full program of detoxification.
When so many toxic substances have accumulated, and so few have been detoxified by the body’s normal detoxification routes, this indicates that we need to proceed with caution. Detoxification, once initiated, might need to be spaced out over a period of time, to keep it gradual and comfortable for the client. The body-consciousness can guide those decisions.
A different hazard often accompanies Parkinson’s, apparently unrelated to dopamine. This is the diminished ability to initiate muscular movement. Some people with Parkinson’s experience an intermittent muscular “freeze” from time to time, while others experience significant on-going muscular inhibition.
We have found that this source of neuromuscular inhibition requires better communication between the neurotransmitter glutamate, and the motor transmission within the cortex of the brain. We are speculating that glutamate, or perhaps a metabolite of glutamate, may be what initiates a signal in the primary and pre-motor areas in the cortex, in response to that ephemeral vibration called intention. After being triggered from a spark from the basal ganglia, the motor signals send an impulse down the spinal cord and out to the muscles, when muscular movement is requested.
It is possible that intention, whether conscious or unconscious, is what sparks the transmission of the glutamate (or its metabolite) signal. That seems to happen somewhere within the basal ganglia, possibly in the caudate nucleus. Glutamate shortage, or some sort of intermittent glutamate disengagement, could be what causes the disconcerting moments of intermittent “freeze.” This suggests that a more continuous disruption within the glutamate pathway, due perhaps to the intrusion of a microorganism or a toxin, could be the reason for on-going immobility.
This is an interesting possibility to consider for other immobilizing illnesses as well, like ALS perhaps, or muscular dystrophy, not only Parkinson’s.
The initial transition from glutamine to glutamate can be diminished by a biochemical error that occurs with an oat allergy. In that case, releasing the basis for the oat allergy could free up the glutamate availability. If this hypothesis is right, and if the required metabolite could be coaxed into full functioning, then voluntary muscular action would be initiated once again, and movement would eventually become easy and effortless.
Muscular inhibition may be due not only to this, but it might occur in combination with something else that we have not identified, perhaps involving the sequence of the second messenger system. In that case it would require more creative questions, and could lead to other suggestions for unexpected solutions.
This approach might be an interesting avenue to explore, in understanding the etiology of Parkinson’s, and from there, toward understanding the line of questions that could eventually reveal the answers. At the Balancing Center, the cases we have had are reporting promising results.
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