Yeah you are right about the Methionine. He shouldn't be taking it without the other amino acids as it will induce depletion and over the long term exasperate his condition. Seen here:
Neurotransmitter depletion | AMA Certified Category 1 CME Relative Nutritional Deficiency Conference. Whenever you have that initial consult with Dr. Chad make sure to give all the details about the issues with the Cysteine and you will also probably want to ask which supplement brand you should get for the Methionine because it is absolutely essential to make sure that what you are getting is actually what it claims to be. Some supplement companies will put fillers in there products which will make a claim of lets say 500 mg of Methionine per capsule into actually being 200 or something. So you could take 11 of the 500 mg pills thinking you are getting the 5500 mg of Methionine needed but you are actually only getting 2200 which would mess everything up.
With the phases I think the best way to describe them is by pasting an excerpt from their dual-gate lumen model of renal monamine transport paper that describes what each phase status represents.
"To determine the phase of serotonin and dopamine with certainty requires two urinary monoamine neurotransmitter assays to be performed with the subject simultaneously taking a different amino acid dosing of dopamine and/or serotonin amino acid precursors on each test and comparing the results.1,2
In phase 1, monoamine neurotransmitters synthesized by the kidneys are excreted into the urine instead of being secreted into the system via the renal vein where they are needed (Figures 1 and and2).2). Increasing the amino acid dose in phase 1 will correct the problem of urinary monoamine excretion into the urine at the expense of secretion into the system. 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 subjects) to 540 mg of L-dopa per day in the subjects not under treatment for Parkinsonism or Restless Leg Syndrome.1,2
By increasing the amino acid dosing of serotonin and dopamine precursors above the dosing of phase 1, the phase 2 response is observed (Figures 1 and and2).2). In phase 2, urinary monoamine levels are low (<475 micrograms dopamine per gram of creatinine or <80 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, serotonin and/or dopamine is being primarily secreted into the system and not excreted 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 systemic levels are not increasing appropriately.”1,2
As serotonin and dopamine amino acid precursors are increased above the phase 1 and the phase 2 levels, all subjects enter the phase 3 response (Figures 1 and and2).2). 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."
Source:
The dual-gate lumen model of renal monoamine transport
Also the ranges of the 5-htp and L-dopa for non-parkinsonism have expanded beyond the 3000 mg 5-htp and 540 mg l-dopa range since this paper was written.
So with your husband on the last test that he did being in both phase 3 for serotonin and dopamine is a very good sign for him being able to quickly get relief of symptoms. To explain why, think about what the description of the phases talks about. When you are in phase 3 any increase in amino acid administration will just increase the # value in phase 3. For instance he had a 2449 serotonin in phase 3 which means that the 5-htp administration is too high. The dopamine is a 701 phase 3 which actually means it is in the therapeutic range for phase 3. So with knowing this it now makes sense as to why they were decreasing the 5-htp administration because they were trying to get that 2449 phase 3 serotonin to drop back down to the 80-240 phase 3 range. My guess is that when he starts this back up he will probably start on that last recommended dosage and do a test on it to see what it does to the serotonin value. It could drop the serotonin too far back into phase 2 or phase 1 so they might then have to increase it back to 8 NR and 2 RE a day or something like that. It could also push the dopamine into a high phase 3 because with decreased 5-htp intake means increased L-dopa synthesis (they function in competitive inhibition in synthesis, transport, and metabolism. Source:
APRESS: apical regulatory super system, serotonin, and dopamine interaction) which could cause the dopamine to get to high.
With the Norepinephrine and Epinephrine they have no involvement in the initial stabilization of most monamine conditions as they are primarily serotonin and dopamine caused. They also hold no value in the initial determination of administration of the nutrients. They come into play after the serotonin and dopamine have been optimized in the phase 3 therapeutic range and the patient has taken the supplements continuously for 6 months. My memory on this is not perfect so I many be wrong on specifics but I believe they determined for the Norepinephrine it takes 1-3 months for it to stabilize and for the Epinephrine it takes 3-6 months. Norepinephrine controls the Hypothalamic Pituitary Axis which includes the Adrenal cortex, sex hormones, cortisol, and many other things. Norepinephrine and Epinephrine don't get talked about that much in the videos I have seen of his or the papers I have read so to get a full explanation of their full involvement you would likely need to get Dr. Hinz or Dr. Chad to fully explain it. The main thing to note is that the main things that regulate function are serotonin and dopamine. You can see how all of these things function together in this chart though:
https://web.archive.org/web/20161015...atary-axis.jpg
If none of that really made sense to you don't sweat it either haha. It took me quite a while to really grasp all of this information, and it works whether or not you understand it all! And sorry if this was a bit of a lengthy post to read, its hard to explain all of this without doing so.
Edit: One thing I want to add with the phases is that the excerpt that I pasted was only describing the phase description in the kidneys. The OCT-2 transporter is identical and homologous in both the kidneys and brain (and other organs), so when you determine the status of the OCT-2 as being phase 1 in the kidneys for example it is then known that it is also phase 1 in the brain. Phase 1 in the brain means the transporter is preventing reuptake into the presynaptic neuron because it is trying to increase post-synaptic firing. Phase 2 indicates that their is adequate amounts of neurotransmitters in the synapse which is allowing for adequate post-synaptic firing, but their is inadequate amounts of neurotransmitters in the pre-synaptic vesicles so that is why you see the number decrease because the neurotransmitters are being reuptaked back into the pre-synaptic neuron. This is represented by phase 2 in the kidneys the neurotransmitters are reuptaked back into the blood rather than into the urine. With phase 3 you now have both adequate amounts of neurotransmitters in the synapse and adequate amounts in the pre-synaptic vesicles which is represented by a now increase in urinary values.