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serotonin and dopamine amino
acid precursors, three phases of urinary
neurotransmitter response have been
identified on laboratory assay of the
urine, see figures 6 and 7. The three
phases of response apply to both
serotonin and dopamine. In all the life
forms tested that have kidneys along
with serotonin and catecholamine
systems, the three phases of urinary
neurotransmitter response exist.40
In reviewing the literature it would
appear that the 3 phase of urinary
response to neurotransmitters were
present in previous writings but were
not identified as such. For example, a
1999 article notes that administration
of L-dopa can increase urinary dopamine
levels (phase 3) and decrease urinary
serotonin levels (phase 1).42
Depression neurotransmitter testing: The
3 Phase Response
Figure 6: “The
three phases of urinary neurotransmitter
excretion in response to amino acid
dosing.” The horizontal axis is not
labeled with specific amounts; it
reflects the general trend seen in the
population. Amino acid dosing needs are
highly individualized. The dosing level
needed to inflect into the next level
varies greatly through out the general
population. For example, some patients
inflect into phase 3 on 37.5 mg of 5-HTP
per day, while others need as high as
3,000 mg per day (source: DBS Labs
database).
Depression neurotransmitter testing: The
3 Phases of Response
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Figure 7:
The three
phases of urinary response to amino acid
dosing (Two urinary neurotransmitter
tests are required to determine the
phase with certainty). PHASE 1:
In phase 1, as the amino acid dosing
increases or decreases the urinary
serotonin or dopamine decreases or
increases respectively. In phase 1,
there is inappropriate excretion of
neurotransmitters into the urine instead
of the system where they are needed.
PHASE 2: In phase 2, as the amino acid
dosing increases or decreases the
urinary serotonin or dopamine is low
(< 800 μgr/gr creatinine for serotonin
or < 300 μgr/gr creatinine for
dopamine). In phase 2, there is no
inappropriate excretion of
neurotransmitters into the urine. The
neurotransmitters are being excreted
appropriately into the system and the
urine. PHASE 3: In phase 3, as the
amino acid dosing increases or decreases
the urinary serotonin or dopamine
increases or decreases respectively.
In phase 3, there are adequate systemic
serotonin and dopamine levels. The
excess serotonin and dopamine are
appropriately excreted into the urine.
Depression neurotransmitter testing: The Goal of Treatment
The
goal of treatment is to establish
both urinary serotonin and dopamine
levels in the phase 3 therapeutic range.
To determine the phase of serotonin and
dopamine with certainty requires two
urinary neurotransmitter tests to be
performed with the patient
simultaneously taking a different amino
acid dosing of dopamine and serotonin
amino acid precursors on each test and
comparing the results. Not all patients
will need to have the urinary serotonin
and dopamine levels in the phase 3
therapeutic range for relief of
symptoms. In many cases, adjusting the
amino acids so that the patient moves
closer to the phase 3 therapeutic range
of urinary serotonin and dopamine
induces relief of symptoms. Then, no
further amino acid adjustments or
testing are needed unless disease
symptoms return. If the patient misses
one or more amino acid doses in the week
prior to testing, wait until one week
has passed with the patient properly
taking all of their amino acids
properly.
In
phase 1, neurotransmitters synthesized
by the kidneys are inappropriately
excreted into the urine instead of being
secreted into the system via the renal
vein where they are needed, see figures
6 and 7. Increasing the amino acid dose
in phase 1 will correct the problem of
inappropriate neurotransmitter
excretion. The amino acid precursor
dosing of serotonin and dopamine, where
the individual patient is in phase 1
varies widely in the population. The
level at which the urinary serotonin is
no longer in phase 1 ranges from 37.5 mg
of 5-HTP per day to 3,000 mg of 5-HTP
per day. The level at which the urinary
dopamine is no longer in phase 1 ranges
from no L-dopa ( with the use of
L-tyrosine only in some patients) to 540
mg of L-dopa per day in the patients not
under treatment for Parkinsonism or
Restless Leg Syndrome.
Administration of proper levels of
tyrosine with L-dopa is known as a
“tyrosine base”. Proper use of the
tyrosine base greatly reduces wild
fluctuations in dopamine levels found
with administration of L-dopa alone and
greatly decreases the need for L-dopa.
It is postulated that the tyrosine
hydroxylase enzyme is not completely
shut down with the administration of
levodopa, leading to fluctuations in the
L-dopa produced from tyrosine
synthesized to L-dopa then dopamine,
which ultimately causes fluctuations of
dopamine. By providing ample tyrosine
with administration of levodopa, these
fluctuations of dopamine cease and the
overall dosing needs of L-dopa decrease.
By
increasing the amino acid dosing of
serotonin and dopamine precursors above
the dosing of Phase 1, the Phase 2
response is observed, see figures 6 and
7. In Phase 2, urinary neurotransmitter
levels are low (< 300 micrograms
dopamine per gram of creatinine or < 800
micrograms serotonin per gram of
creatinine, the
neurotransmitter-creatinine ratio
compensates for dilution of the urine)
and the inappropriate excretion of
neurotransmitters into the urine has
ceased. When in Phase 2,
neurotransmitters are being
appropriately secreted into the system
and not into the urine. The model used
to explain phase 2 is, “inappropriate
excretion of neurotransmitters has now
ceased as the amino acid precursor
dosing is increased and the system is
now filing up appropriately.”
As
serotonin and dopamine amino acid
precursors are increased above the Phase
1 and the Phase 2 levels, all patients
enter the Phase 3 response, see figures
6 and 7. Further increases in the amino
acid dosing lead to increases in urinary
dopamine and serotonin neurotransmitter
levels if they are in phase 3. Phase 3
represents appropriate secretion into
the system and appropriate excretion of
excess neurotransmitters synthesized by
the kidneys into the urine.
In
the case of chronic depression, research
has shown neurotransmitter levels need
to be established at levels that are in
phase 3 and higher than the reference
range reported by the laboratory in
order to achieve optimal relief of group
symptoms.40 In the case of
serotonin, the reference range reported
by the research lab is 48.9-194.9
micrograms of serotonin per gram of
creatinine. Whereas, the therapeutic
range of urinary serotonin for the
treatment of chronic depression is
defined as 800 to 2,400 micrograms of
serotonin per gram of creatinine in
phase 3. The reference range reported
by the research lab of urinary dopamine
reported by the laboratory is 40-390
micrograms of dopamine per gram of
creatinine. The therapeutic range of
urinary dopamine for the treatment of
chronic depression is defined as 300 to
600 micrograms of dopamine per gram of
creatinine in phase 3.
It
would appear that in depression, the
same mechanism of action may be at work
as is found in Parkinson’s disease.
There is damage to dopamine and/or
serotonin neuron bundles controlling
affect, which can be compensated for by
increasing serotonin and dopamine
neurotransmitter levels higher than is
normally found in the system. Just as
with Parkinson’s disease, the bundle
damage in chronic depression is
permanent. In most patients simply
returning neurotransmitter levels to
normal or the reference range reported
by the lab, as suggested by the
monoamine theory, will not lead to
relief of symptoms. As with
Parkinsonism, in treatment of depression
may require long-term use of amino acids
to control symptoms. Once symptoms
associated with monoamine
neurotransmitter diseases are controlled
with the proper administration of amino
acid precursors, the need for ongoing
amino acid therapy may permanent if
symptoms have not been addresses fully
under the monoamine theory.
Urinary monoamine neurotransmitter testing is used only when the patient
has not responded to the levels 1
through 3 of the dosing protocol. Over
80% of patients will achieve relief of
depression symptoms without laboratory
testing.
depression neurotransmitter testing-research
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