The novel approach described in this writing requires the administration of serotonin and dopamine amino acid precursors with cofactors to reach the Phase III therapeutic ranges (herein referred to as the target ranges) as guided by the use of urinary serotonin and urinary dopamine organic cation transporter (OCT) functional status determination (herein referred to as ‘OCT assay interpretation’).2–5
The basis for the OCT assay interpretation model requires two or more serial urinary serotonin and dopamine assays while taking varied amino acid precursor daily dosing values. Results of two or more assays are then compared in order to determine the change in urinary serotonin and dopamine levels in response to the change in dosing. A urinary serotonin or dopamine value <80 or 475 μg of monoamine per gram of creatinine, respectively, indicates Phase II responses. A urinary serotonin or dopamine value >80 or 475 μg of monoamine per gram of creatinine, respectively, is interpreted as being in Phase I or Phase III. Differentiation of Phase I from phase III is a follows. If a direct correlation is found between amino acid dosing and urinary assay response, it is referred to as a Phase III response. An inverse correlation is referred to as a Phase I response. The Phase III therapeutic range for urinary serotonin is defined as 80–240 μg of serotonin per gram of creatinine. The Phase III therapeutic range for urinary dopamine is defined as 475–1100 μg of dopamine per gram of creatinine.2–5
Peer-reviewed scientific publications discussing urinary serotonin and urinary dopamine phase analysis under the OCT model were published in 20092,4 and 2010.3,5 These publications outlined the mechanisms of the ‘three-phase model’ in connection with urinary serotonin and urinary dopamine under a novel renal transporter model. This transporter model potentially describes the etiology of the ‘three-phase response’ in monoamine assays during the administration of varied amino acid precursor daily dosing values.3 Urinary serotonin and dopamine levels are primarily dependent upon the interaction of the basolateral monoamine transporters with the apical monoamine transporters of the proximal convoluted renal tubule cells of the kidneys.3
