Commentary on Hinz et al. (2011) on the Non-Validity and Clinical Relevance of Neurotransmitter Testing

Hinz et al. [1] comments that if the author [2] had included papers published by Hinz et al. in regards to renal physiology, the author may have developed a different conclusion regarding the non-validity of neurotransmitter testing. They comment that the author’s understanding of renal physiology is not discussed and is superficial [1]. Instead, this assumption represents a narrow understanding of clinical neurophysiology. The author is familiar with the publications of Hinz et al. and did not include them in the original paper because the conclusions of these papers are speculative and theoretical and offer no science in validating any form of neurotransmitter testing [1-11]. The referenced papers by Hinz et al. limit their focus to renal physiology and precursor amino acid loading. They do not discuss physiological properties of neurotransmitter activity before and after monoamine renal physiology. These mechanisms include modulation of rate-limiting enzyme for synthesis, neurotransmitter transport outside of the kidneys, neurotransmitter homotrophic and heterotrophic modulation, receptor site sensitivity, and post-translational receptor expressions, to name a few. Assessing neurotransmitter clinical validity exclusively by monoamine renal physiology demonstrates a lack of understanding of neurotransmitter dynamics. There is no evidence from any of the papers published or referenced by Hinz et al. that urinary neurotransmitter testing of any type correlates with neurotransmitter activity of the central nervous system.