Validity of urinary monoamine assay sales under the &amp;ldquo;spot baseline urinary neurotransmitter testing marketing model&amp;rdquo;

Hinz, Marty; Stein, Alvin; Uncini, Thomas

doi:10.2147/ijnrd.s22783

Cited by 11 publications

(45 citation statements)

References 120 publications

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“…This did not work because it did not take into account the effects of transporters. This high/low approach to assay interpretation, as a guide to amino acid dosing values, was no more effective than simply giving amino acid precursors randomly 5,7,11…”

Section: Organic Cation Transportersmentioning

confidence: 99%

Relative nutritional deficiencies associated with centrally acting monoamines

Hinz¹,

Stein²,

Uncini³

2012

IJGM

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BackgroundTwo primary categories of nutritional deficiency exist. An absolute nutritional deficiency occurs when nutrient intake is not sufficient to meet the normal needs of the system, and a relative nutritional deficiency exists when nutrient intake and systemic levels of nutrients are normal, while a change occurs in the system that induces a nutrient intake requirement that cannot be supplied from diet alone. The purpose of this paper is to demonstrate that the primary component of chronic centrally acting monoamine (serotonin, dopamine, norepinephrine, and epinephrine) disease is a relative nutritional deficiency induced by postsynaptic neuron damage.Materials and methodsMonoamine transporter optimization results were investigated, reevaluated, and correlated with previous publications by the authors under the relative nutritional deficiency hypothesis. Most of those previous publications did not discuss the concept of a relative nutritional deficiency. It is the purpose of this paper to redefine the etiology expressed in these previous writings into the realm of relative nutritional deficiency, as demonstrated by monoamine transporter optimization. The novel and broad range of amino acid precursor dosing values required to address centrally acting monoamine relative nutritional deficiency properly is also discussed.ResultsFour primary etiologies are described for postsynaptic neuron damage leading to a centrally acting monoamine relative nutritional deficiency, all of which require monoamine transporter optimization to define the proper amino acid dosing values of serotonin and dopamine precursors.ConclusionHumans suffering from chronic centrally acting monoamine-related disease are not suffering from a drug deficiency; they are suffering from a relative nutritional deficiency involving serotonin and dopamine amino acid precursors. Whenever low or inadequate levels of monoamine neurotransmitters exist, a relative nutritional deficiency is present. These precursors must be administered simultaneously under the guidance of monoamine transporter optimization in order to achieve optimal relative nutritional deficiency management. Improper administration of these precursors can exacerbate and/or facilitate new onset of centrally acting monoamine-related relative nutritional deficiencies.

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Section: Organic Cation Transportersmentioning

confidence: 99%

Relative nutritional deficiencies associated with centrally acting monoamines

Hinz¹,

Stein²,

Uncini³

2012

IJGM

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“…Proper OCT assay requires that initially the serotonin and dopamine systems are placed in the competitive inhibition state simultaneously, while administering adequate amounts of serotonin and dopamine amino acid precursors. The assay results are then compared in order to determine the change in urinary serotonin and dopamine concentrations associated with changes in amino acid precursor dosing values 2,3,5,6,11…”

Section: Methodsmentioning

confidence: 99%

“…Previously published literature by the authors provides proof that in the endogenous state transporter-dependent monoamine concentrations are indistinguishable in subjects with and without monoamine-related disease and/or regulatory dysfunction. These findings are an integral part of the challenge to the validity of the monoamine hypothesis 4,6,10…”

Section: Introductionmentioning

confidence: 96%

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The discrediting of the monoamine hypothesis

Hinz¹,

Stein²,

Uncini³

2012

IJGM

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BackgroundThe monoamine hypothesis has been recognized for over half a century as a reference point to understanding electrical dysfunction associated with disease states, and/or regulatory dysfunction related to synaptic, centrally acting monoamine concentrations (serotonin, dopamine, norepinephrine, and epinephrine).MethodsOrganic cation transporters (OCT) are a primary force controlling intracellular and extracellular (including synaptic) concentrations of centrally acting monoamines and their amino acid precursors. A new type of research was analyzed in this paper (previously published by the authors) relating to determining the functional status of the nutritionally driven organic cation transporters. It was correlated with the claims of the monoamine hypothesis.ResultsResults of laboratory assays from subjects not suffering from a hyperexcreting tumor show that centrally acting monoamine concentrations are indistinguishable in subjects with and without disease symptoms and/or regulatory dysfunction. Analysis of centrally acting monoamine concentrations in the endogenous state reveals a significant difference in day-to-day assays performed on the same subject with and without monoamine-related disease symptoms and/or regulatory dysfunction. The day-to-day difference renders baseline testing in the endogenous state non-reproducible in the same subject.ConclusionIt is asserted that the monoamine hypothesis, which claims that low synaptic levels of monoamines are a primary etiology of disease, is not a valid primary reference point for understanding chronic electrical dysfunction related to the centrally acting monoamines. Furthermore, the “bundle damage theory” is a more accurate primary model for understanding chronic dysfunction. The “bundle damage theory” advocates that synaptic monoamine levels are normal but not adequate in states associated with chronic electrical dysfunction and that levels need to be increased to compensate for the chronic postsynaptic electrical dysfunction due to existing damage. The monoamine hypothesis, in failing to accurately explain the etiology of chronic neuronal electrical flow dysfunction in the endogenous state, is reduced to no more than a historical footnote.

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“…L-3,4-dihydroxyphenylalanine (L-dopa) is a metabolite of L-tyrosine and the immediate precursor of dopamine. Dopamine does not cross the blood–brain barrier 1. L-dopa freely crosses the blood–brain barrier, then is synthesized into dopamine without biochemical feedback inhibition 2.…”

Section: Introductionmentioning

confidence: 99%

Management of L-dopa overdose in the competitive inhibition state

Hinz¹,

Stein²,

Cole³

2014

DHPS

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The amino acid L-3,4-dihydroxyphenylalanine (L-dopa) is prescribed for conditions where increased central and/or peripheral dopamine synthesis is desired. Its administration can establish dopamine concentrations higher than can be achieved from an optimal diet. Specific indications include Parkinson’s disease and restless leg syndrome. The interaction between serotonin and dopamine exists in one of two distinctly different physiologic states: the endogenous state or the competitive inhibition state. Management with L-dopa in the competitive inhibition state is the focus of this paper. In the past, control of the competitive inhibition state was thought to be so difficult and complex that it was described in the literature as functionally “meaningless”. When administering L-dopa without simultaneous administration of serotonin precursors, the patient is in the endogenous state. Experience gained with patient outcomes during endogenous L-dopa administration does not allow predictability of L-dopa outcomes in the competitive inhibition state. The endogenous approach typically increases the daily L-dopa dosing value in a linear fashion until symptoms of Parkinson’s disease are under control. It is the novel observations made during treatment with the competitive inhibition state approach that L-dopa dosing values above or below the optimal therapeutic range are generally associated with the presence of the exact same Parkinson’s disease symptoms with identical intensity. This recognition requires a novel approach to optimization of daily L-dopa dosing values from that used in the endogenous state. This paper outlines that novel approach through utilization of a pill stop. This approach enhances patient safety through its ability to prevent L-dopa overdose, while assisting in the establishment of the optimal therapeutic L-dopa daily dosing value.

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Validity of urinary monoamine assay sales under the “spot baseline urinary neurotransmitter testing marketing model”

Cited by 11 publications

References 120 publications

Relative nutritional deficiencies associated with centrally acting monoamines

Relative nutritional deficiencies associated with centrally acting monoamines

The discrediting of the monoamine hypothesis

Management of L-dopa overdose in the competitive inhibition state

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