Depression Reuptake Inhibitor Depletion of Neurotransmitters
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Depression Reuptake Inhibitor Depletion of Neurotransmitters

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Depression Reuptake Inhibitor Depletion of Neurotransmitters

Written by: Marty L. Hinz, MD
President Clinical Research
NeuroResearch Clinics, Inc
Cape Coral, Florida USA Research Office
 

POSTED by J1237 Jan 31, 2009 06:59PM: I have suffered with severe depression and anxiety for about 10 years.  I was very, extremely skeptical about the NeuroResearch formulas after having been on a myriad of antidepressant SSRI's.  I thought it was just a money making scheme and I was scared. Let me just say that I'm glad I did my research and I'm glad I tried it because it has made a WORLD OF DIFFERENCE.

 

  Depression Reuptake Inhibitor Depletion of Neurotransmitters

 The National Institute of Drug Abuse presents a detailed discussion on its website on how reuptake inhibitors deplete neurotransmitters.22 Medicines used to treat depression are not the only drugs that block reuptake; cocaine and amphetamines block reuptake as well.22 Reuptake inhibitors block the uptake of neurotransmitters back into the pre-synaptic neuron.  In doing so, synaptic levels are increased.  As synaptic neurotransmitter levels rise, relief of symptoms is observed.  

  Monoamine Oxidase (MAO) and the Catecholamine O-Methyl Transferase (COMT) enzymes metabolize serotonin, dopamine, norepinephrine, and epinephrine.  The monoamine neurotransmitters are relatively stable and are not metabolize until they come in contact with the MAO and COMT enzymes.  When neurotransmitters are in the vesicles of the pre-synaptic

Depression Reuptake Inhibitor Depletion of Neurotransmitters

neuron, they are not exposed to metabolism by the MAO and COMT enzymes; they are safe and stable.  When neurotransmitters are in the synapse between the pre-synaptic and post-synaptic neuron, they are exposed to enzymatic metabolism, which leads to the depletion of neurotransmitters if proper levels of amino acid precursors are not administered to compensate for this process.24

  In depressed patients, synaptic neurotransmitter levels are not high enough to prevent disease symptoms, as illustrated in figure 2.   Treatment with reuptake inhibitors leads to a decrease in presynaptic neurotransmitter levels (where they are safe from enzymatic metabolism) and an increase in the number of neurotransmitters in the synapse, as illustrated in figure 2.  The blocking of neurotransmitter reuptake increases synaptic levels and the probability that neurotransmitters will experience enzymatic metabolism.

Depression Reuptake Inhibitor Depletion of Neurotransmitters

Depression Reuptake Inhibitor Depletion of Neurotransmitters

Figure 2: Titled: “The effects of reuptake inhibitors on neurotransmitter levels, reuptake inhibition may deplete neurotransmitters.” In the left picture, prior to treatment, neurotransmitter levels are not high enough to prevent symptoms of disease. In the center picture, reuptake is blocked, neurotransmitters move from the vesicles of the pre-synaptic neuron to the synapse. In the right picture, the neurotransmitters are depleted, the increase in synaptic neurotransmitter levels results in an increase in MAO and COMT metabolism. Source of picture: The National Institute of Drug Abuse.

Depression Reuptake Inhibitor Depletion of Neurotransmitters

  With regards to figure 2, the net effect of enzymatic metabolism is the depletion of neurotransmitter levels in the central nervous system.  Neurotransmitters do not cross the blood brain barrier.  Therefore, the only way to increase central nervous system levels or to prevent the overall depletion of neurotransmitters when administering prescription drugs that block reuptake is to provide amino acid precursors, which are then synthesized into neurotransmitters.  Administering L-tyrosine (not phenylalanine or n-acetyl-tyrosine) or L-dopa is the only way to predictably raise dopamine, norepinephrine, and epinephrine.  Administering tryptophan or 5-hydroxytryptophan (5-HTP) is the only way to predictably raise serotonin levels in the central nervous system.  It is noted that 5-HTP, L-dopa and tyrosine are available in the United States without a prescription. The ability of tryptophan to raise serotonin levels is limited because it is a rate-limited reaction.

  The effects of neurotransmitter depletion by drugs may have far ranging implications. It has been found in studies that depletion of serotonin by drugs may also lead to a reduction the number of serotonin synapses in the hippocampus.43

  Its no secret, NeuroResearch Clinics uses the nutrients 5-HTP, tyrosine, levodopa, and cysteine to treat medical patients in order to get these results. Proper use of these simple ingredients in medical treatment is not simple. From time to time a patient will say, "Why do I want to take that, I can go to a health food store and buy it?" People off the street buying in a health food store is like going to an art store and buying a bunch of oil paints then going home and expecting to paint like a mater artist even though there was no previous painting experience. These nutrients have tremendous potential due to their chemical properties. This potential is only fully realized in the hands of the trained professional using neurotransmitter testing. Treatment is not just giving a nutrient pill, it is the whole medical management approach doctors are trained in to insure that that treatment is on track in order to get symptoms under control.

The Peer Reviewed Research of NeuroResearch Clinics

  The neurotransmitter treatment research findings of NeuroResearch Clinics have not been ignored. The University of Minnesota Medical School is writing a series of papers on the neurotransmitter testing research of NeuroResearch Clinics. The first of a series of papers by University of Minnesota Medical School based on the neurotransmitter testing research of NeuroResearch was published in "NeuroPsychiatric Disease and Treatment" May 1, 2009. Ingrid Kohlstadt, MD of Johns Hopkins in her new medical text book released February 7, 2009 included a chapter on depression written by Marty L. Hinz, MD  President Clinical Research NeuroResearch Clinics outlining in depth the proper use of amino acids and neurotransmitter testing in treatment of depression.

University of Minnesota Medical School neurotransmitter testing paper on the research of NeuroResearch Clinics.

 

The medical text book chapter on depression written by Marty L. Hinz, MD-Ingrid Kohlstadt, MD editor-Johns Hopkins released February, 7, 2009

Depression Reuptake Inhibitor Depletion of Neurotransmitters-research

 
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Depression Reuptake Inhibitor Depletion of Neurotransmitters-research  
Depression Reuptake Inhibitor Depletion of Neurotransmitters-research  
Depression Reuptake Inhibitor Depletion of Neurotransmitters-research  
Depression Reuptake Inhibitor Depletion of Neurotransmitters-research  
   
   
   
 
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Depression Reuptake Inhibitor Depletion of Neurotransmitters