Monamine Transporter Optimization

For everything and anything else not covered in the other RLS/WED sections.
ViewsAskew
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Monamine Transporter Optimization

Postby ViewsAskew » Tue Nov 12, 2013 3:35 am

I have NOT read all this, nor have I researched it. Just posting to offer other ideas to people. Please do your research if you decide to try this.

http://www.neurosupport.com/Restless_Leg_Syndrome.htm

COPIED from their site:
Most patients with Restless Leg Syndrome have three or more neurotransmitter related diseases active at initiation of treatment. If on the patient’s problem list is listed Restless Leg Syndrome it needs to be the disease that dominates and is the focus of treatment. While getting the Restless Leg Syndrome symptoms under control the rest of the neurotransmitter related disease symptoms will come under. The protocol used at initiation of treatment for Restless Leg Syndrome is identical for Parkinson disease.

Discussion
In Parkinson’s disease damage to the post-synaptic dopamine neurons of the substantia nigra in the brain leads to decreased flow of the electricity regulating fine motor function. Increasing dopamine levels in the central nervous system and substantia nigra with L-dopa increases the flow of electricity in the remaining viable neurons leading to restoration of fine motor control and relief of symptoms.

Based on clinical experience it appears that damage to post-synaptic dopamine neurons is also the etiology of Restless Leg Syndrome. The same amino acid approach that leads the relief of symptoms in Parkinson’s disease leads to relief of symptoms in Restless Leg Syndrome. The exception is that patient’s with Restless Leg Syndrome need approximately one fourth to one half of the L-dopa dosing values that Parkinson patients need to achieve relief of symptoms.

Traditional treatment of Restless Leg Syndrome includes the prescription drugs Requip and Mirapex, both of which are “dopamine agonists”. In general a dopamine agonist binds the receptors of the post-synaptic neurons and mimics the effects of dopamine. It would seem a more reasonable approach to simply increase dopamine levels properly.

L-dopa depletes
L-dopa freely crosses the blood brain barrier then is synthesized into dopamine without biochemical feed back regulation. The more L-dopa that is administered the more dopamine is found in the system. Prescribing only L-dopa depletes L-tyrosine, serotonin and sulfur amino acids inducing symptoms associated with depletion of these amino acids if properly balanced amino acids of these systems are not simultaneously administered.

Etiology
Having been in medicine for 38 years it is apparent that Restless Leg Syndrome was a very rare disorder 30 years ago and is now a significant problem seen in clinics today. It is hypothesized that the increased prevalence of neurotoxins in the environment have contributed greatly to this increased in a disease that was rare 30 years ago. Just as with Parkinson’s disease damage to the post-synaptic neurons, Restless Leg Syndrome appears to be due to neuron damage caused a defect in electrical flow that regulates motor control of the legs. Increasing dopamine levels causes increased flow of electricity leading to resolution of symptoms.
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