Parkinson’s: Tracing the Biochemical Sequence
At the Balancing Center we have found that our clients who have been diagnosed with Parkinson’s are showing that the substantia nigra, the “black substance” in the midbrain that connects to the striatum of the basal ganglia, appears to have been eroded, and is significantly diminished. Although there surely must be many other reasons, what we have found in our clients diagnosed with Parkinson’s, is that the substantia nigra has been etched away by an elusive parasitic microorganism. We have 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 the microorganism comes close to completion, we work with supplementation that will rebuild the substantia nigra. The 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.
|| plus OH makes
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.
||plus another OH makes
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.
||LDopa decarboxylase makes
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 close to resolution, but we need to ask if dopamine can be released from the membrane of the substantia nigra. If it can’t be released, we check the membrane permeability of that little structure. Possibly the trace mineral rubidium would allow the membrane to relax and let the dopamine access its required targets.
When that can happen, then the dopamine has to enter the pyramid tract, and be received at the receptor sites that will distribute it throughout the brain and the body. If the receptor sites are not able to receive the dopamine, we ask the body-consciousness to tell us why not---very likely this is yet another toxin---and we make the proper corrections. The pyramid tract receives input from the cerebellum as well as the basal ganglia, and the cerebellum can be a participant in any difficulty with balance and proprioception, so this would need to be explored if the pyramid tract is not functioning as expected.
Any foreign substance, whether agricultural, petrochemical, or pharmaceutical, may interfere with the completion of these steps, so collectively they contribute to the creating of Parkinson’s. It doesn’t have “One Cause” and it won’t yield to “One Cure,” as is usually hoped for in setting up medical research protocols, nor could it yield easily to statistical evaluation, as 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 the cases of Parkinson’s we have seen, this has not been part of the equation. Toxic exposures seem to be the major player in the development of this devastating disability. Each person has his own unique array of toxins and nutrient deficiencies, depending upon what his body has experienced.
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 that often accompanies Parkinson’s, apparently unrelated to dopamine but still involving the basal ganglia in some way, is the diminished ability to initiate muscular movement. Some people experience an intermittent muscular “freeze” from time to time, while others experience significant muscular inhibition.
We have found that this source of neuromuscular inhibition requires better communication between the neurotransmitter glutamate, and the motor neurotransmission within the cortex of the brain. We are speculating that glutamate, or perhaps a metabolite of glutamate, may be what initiates muscular movement by engaging 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.
Actually this might be an interesting possibility to consider for other immobilizing illnesses as well, like ALS perhaps, 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 glutamate availability. If this hypothesis is right, and if the possible required metabolite were also functioning, then voluntary muscular action could be initiated once again, and movement would eventually become easy and effortless, unless there were other factors in the way.
Muscular inhibition may be due not only to this, but it might occur only in combination with something else that we have not identified. In that case it would require more creative questions, and lead to suggestions for unexpected solutions on the part of the practitioner.
This approach might be an interesting avenue to explore, toward resolving the etiology of Parkinson’s. At the Balancing Center, the cases we have had are reporting promising results.