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  1. Article: Parkinson's disease-associated melanin steal.

    Hinz, Marty / Stein, Alvin / Cole, Ted

    publication RETRACTED

    Neuropsychiatric disease and treatment

    2014  Volume 10, Page(s) 2331–2337

    Abstract: Urinary dopamine fluctuations in the competitive inhibition state were first documented in 2009. At that time, it was noted that progressively higher daily dosing values of L-tyrosine decreased the magnitude of these fluctuations. While extensive ... ...

    Abstract Urinary dopamine fluctuations in the competitive inhibition state were first documented in 2009. At that time, it was noted that progressively higher daily dosing values of L-tyrosine decreased the magnitude of these fluctuations. While extensive statistical analysis has been performed by the authors since 2004, it was not until 2012 that a plausible explanation was formulated. In the process, correlations with L-tyrosine administration and the on/off effect of Parkinson's disease were defined. This paper documents the current knowledge with regard to the management of retrograde phase 1 dopamine fluctuations and investigates the hypothesis that they are caused by a melanin steal phenomenon.
    Language English
    Publishing date 2014-12-10
    Publishing country New Zealand
    Document type Journal Article ; Retracted Publication
    ZDB-ID 2186503-6
    ISSN 1178-2021 ; 1176-6328
    ISSN (online) 1178-2021
    ISSN 1176-6328
    DOI 10.2147/NDT.S74952
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Parkinson's disease: carbidopa, nausea, and dyskinesia.

    Hinz, Marty / Stein, Alvin / Cole, Ted

    publication RETRACTED

    Clinical pharmacology : advances and applications

    2014  Volume 6, Page(s) 189–194

    Abstract: When l-dopa use began in the early 1960s for the treatment of Parkinson's disease, nausea and reversible dyskinesias were experienced as continuing side effects. Carbidopa or benserazide was added to l-dopa in 1975 solely to control nausea. Subsequent to ...

    Abstract When l-dopa use began in the early 1960s for the treatment of Parkinson's disease, nausea and reversible dyskinesias were experienced as continuing side effects. Carbidopa or benserazide was added to l-dopa in 1975 solely to control nausea. Subsequent to the increasing use of carbidopa has been the recognition of irreversible dyskinesias, which have automatically been attributed to l-dopa. The research into the etiology of these phenomena has identified the causative agent of the irreversible dyskinesias as carbidopa, not l-dopa. The mechanism of action of the carbidopa and benserazide causes irreversible binding and inactivation of vitamin B6 throughout the body. The consequences of this action are enormous, interfering with over 300 enzyme and protein functions. This has the ability to induce previously undocumented profound antihistamine dyskinesias, which have been wrongly attributed to l-dopa and may be perceived as irreversible if proper corrective action is not taken.
    Language English
    Publishing date 2014-11-14
    Publishing country New Zealand
    Document type Journal Article ; Retracted Publication
    ZDB-ID 2520726-X
    ISSN 1179-1438
    ISSN 1179-1438
    DOI 10.2147/CPAA.S72234
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: The Parkinson's disease death rate: carbidopa and vitamin B6.

    Hinz, Marty / Stein, Alvin / Cole, Ted

    publication RETRACTED

    Clinical pharmacology : advances and applications

    2014  Volume 6, Page(s) 161–169

    Abstract: The only indication for carbidopa and benserazide is the management of L-3,4-dihydroxyphenylalanine (L-dopa)-induced nausea. Both drugs irreversibly bind to and permanently deactivate pyridoxal 5'-phosphate (PLP), the active form of vitamin B6, and PLP- ... ...

    Abstract The only indication for carbidopa and benserazide is the management of L-3,4-dihydroxyphenylalanine (L-dopa)-induced nausea. Both drugs irreversibly bind to and permanently deactivate pyridoxal 5'-phosphate (PLP), the active form of vitamin B6, and PLP-dependent enzymes. PLP is required for the function of over 300 enzymes and proteins. Virtually every major system in the body is impacted directly or indirectly by PLP. The administration of carbidopa and benserazide potentially induces a nutritional catastrophe. During the first 15 years of prescribing L-dopa, a decreasing Parkinson's disease death rate was observed. Then, in 1976, 1 year after US Food and Drug Administration approved the original L-dopa/carbidopa combination drug, the Parkinson's disease death rate started increasing. This trend has continued to the present, for 38 years and counting. The previous literature documents this increasing death rate, but no hypothesis has been offered concerning this trend. Carbidopa is postulated to contribute to the increasing Parkinson's disease death rate and to the classification of Parkinson's as a progressive neurodegenerative disease. It may contribute to L-dopa tachyphylaxis.
    Language English
    Publishing date 2014-10-21
    Publishing country New Zealand
    Document type Journal Article ; Retracted Publication
    ZDB-ID 2520726-X
    ISSN 1179-1438
    ISSN 1179-1438
    DOI 10.2147/CPAA.S70707
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Administration of supplemental L-tyrosine with phenelzine: a clinical literature review.

    Hinz, Marty / Stein, Alvin / Cole, Ted / Ryan, Patricia

    publication RETRACTED

    Clinical pharmacology : advances and applications

    2014  Volume 6, Page(s) 107–110

    Abstract: The subject of this literature review is the alleged relationship between L-tyrosine, phenelzine, and hypertensive crisis. Phenelzine (Nardil(®)) prescribing information notes: "The potentiation of sympathomimetic substances and related compounds by MAO ... ...

    Abstract The subject of this literature review is the alleged relationship between L-tyrosine, phenelzine, and hypertensive crisis. Phenelzine (Nardil(®)) prescribing information notes: "The potentiation of sympathomimetic substances and related compounds by MAO inhibitors may result in hypertensive crises (see WARNINGS). Therefore, patients being treated with NARDIL should not take […] L-tyrosine […]". Interest in the scientific foundation of this claim was generated during routine patient care. A comprehensive literature search of Google Scholar and PubMed revealed no reported cases of hypertensive crisis associated with concomitant administration of L-tyrosine and phenelzine. Review of current US Food and Drug Administration nutritional guidelines relating to ongoing phenelzine studies reveals no mention and requires no consideration of L-tyrosine ingestion in combination with phenelzine. This paper is intended to provide an objective review of the science to then allow the reader to formulate the final opinion.
    Language English
    Publishing date 2014-07-22
    Publishing country New Zealand
    Document type Journal Article ; Review ; Retracted Publication
    ZDB-ID 2520726-X
    ISSN 1179-1438
    ISSN 1179-1438
    DOI 10.2147/CPAA.S67271
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Management of L-dopa overdose in the competitive inhibition state.

    Hinz, Marty / Stein, Alvin / Cole, Ted

    publication RETRACTED

    Drug, healthcare and patient safety

    2014  Volume 6, Page(s) 93–99

    Abstract: 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 ... ...

    Abstract 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.
    Language English
    Publishing date 2014-07-22
    Publishing country New Zealand
    Document type Journal Article ; Retracted Publication
    ZDB-ID 2520700-3
    ISSN 1179-1365
    ISSN 1179-1365
    DOI 10.2147/DHPS.S67328
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: 5-HTP efficacy and contraindications.

    Hinz, Marty / Stein, Alvin / Uncini, Thomas

    publication RETRACTED

    Neuropsychiatric disease and treatment

    2012  Volume 8, Page(s) 323–328

    Abstract: L-5-hydroxytryptophan (5-HTP) is the immediate precursor of serotonin. It is readily synthesized into serotonin without biochemical feedback. This nutrient has a large and strong following who advocate exaggerated and inaccurate claims relating to its ... ...

    Abstract L-5-hydroxytryptophan (5-HTP) is the immediate precursor of serotonin. It is readily synthesized into serotonin without biochemical feedback. This nutrient has a large and strong following who advocate exaggerated and inaccurate claims relating to its effectiveness in the treatment of depression and a number of other serotonin-related diseases. These assertions are not supported by the science. Under close examination, 5-HTP may be contraindicated for depression in some of the very patients for whom promoters of 5-HTP advocate its use.
    Language English
    Publishing date 2012-07-19
    Publishing country New Zealand
    Document type Journal Article ; Retracted Publication
    ZDB-ID 2186503-6
    ISSN 1178-2021 ; 1176-6328
    ISSN (online) 1178-2021
    ISSN 1176-6328
    DOI 10.2147/NDT.S33259
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Parkinson's disease managing reversible neurodegeneration.

    Hinz, Marty / Stein, Alvin / Cole, Ted / McDougall, Beth / Westaway, Mark

    publication RETRACTED

    Neuropsychiatric disease and treatment

    2016  Volume 12, Page(s) 763–775

    Abstract: Traditionally, the Parkinson's disease (PD) symptom course has been classified as an irreversible progressive neurodegenerative disease. This paper documents 29 PD and treatment-induced systemic depletion etiologies which cause and/or exacerbate the ... ...

    Abstract Traditionally, the Parkinson's disease (PD) symptom course has been classified as an irreversible progressive neurodegenerative disease. This paper documents 29 PD and treatment-induced systemic depletion etiologies which cause and/or exacerbate the seven novel primary relative nutritional deficiencies associated with PD. These reversible relative nutritional deficiencies (RNDs) may facilitate and accelerate irreversible progressive neurodegeneration, while other reversible RNDs may induce previously undocumented reversible pseudo-neurodegeneration that is hiding in plain sight since the symptoms are identical to the symptoms being experienced by the PD patient. Documented herein is a novel nutritional approach for reversible processes management which may slow or halt irreversible progressive neurodegenerative disease and correct reversible RNDs whose symptoms are identical to the patient's PD symptoms.
    Language English
    Publishing date 2016-04-05
    Publishing country New Zealand
    Document type Journal Article ; Retracted Publication
    ZDB-ID 2186503-6
    ISSN 1178-2021 ; 1176-6328
    ISSN (online) 1178-2021
    ISSN 1176-6328
    DOI 10.2147/NDT.S98367
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Relative nutritional deficiencies associated with centrally acting monoamines.

    Hinz, Marty / Stein, Alvin / Uncini, Thomas

    publication RETRACTED

    International journal of general medicine

    2012  Volume 5, Page(s) 413–430

    Abstract: Background: Two 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 ... ...

    Abstract Background: Two 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 methods: Monoamine 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.
    Results: Four 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.
    Conclusion: Humans 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.
    Language English
    Publishing date 2012-05-08
    Publishing country New Zealand
    Document type Journal Article ; Retracted Publication
    ZDB-ID 2452220-X
    ISSN 1178-7074 ; 1178-7074
    ISSN (online) 1178-7074
    ISSN 1178-7074
    DOI 10.2147/IJGM.S31179
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The discrediting of the monoamine hypothesis.

    Hinz, Marty / Stein, Alvin / Uncini, Thomas

    publication RETRACTED

    International journal of general medicine

    2012  Volume 5, Page(s) 135–142

    Abstract: Background: The 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 ... ...

    Abstract Background: The 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).
    Methods: Organic 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.
    Results: Results 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.
    Conclusion: It 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.
    Language English
    Publishing date 2012-02-14
    Publishing country New Zealand
    Document type Journal Article ; Retracted Publication
    ZDB-ID 2452220-X
    ISSN 1178-7074 ; 1178-7074
    ISSN (online) 1178-7074
    ISSN 1178-7074
    DOI 10.2147/IJGM.S27824
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Microperforation prolotherapy: a novel method for successful nonsurgical treatment of atraumatic spontaneous anterior sternoclavicular subluxation, with an illustrative case.

    Stein, Alvin / McAleer, Scott / Hinz, Marty

    Open access journal of sports medicine

    2011  Volume 2, Page(s) 47–52

    Abstract: Background: Surgical repair of an atraumatic spontaneous anterior subluxation of the sternoclavicular joint (herein referred to as the "SCJ") is often associated with poor outcome expectations. With traditional treatment, successful conservative therapy ...

    Abstract Background: Surgical repair of an atraumatic spontaneous anterior subluxation of the sternoclavicular joint (herein referred to as the "SCJ") is often associated with poor outcome expectations. With traditional treatment, successful conservative therapy usually incorporates major lifestyle alterations. This manuscript discusses a novel approach known as "microperforation prolotherapy". To illustrate the technique, the care of a patient who benefitted from this treatment is reviewed.
    Purpose: To present a novel form of treatment with an illustrative case that demonstrates the potential efficacy of microperforation prolotherapy of the SCJ.
    Patient and methods: A novel approach to treatment of bilateral subluxation of the sternoclavicular joint with microperforation prolotherapy is discussed. The clinical course of a 21-year-old male with bilateral subluxation of the SCJ, which seriously hampered the patient's athletic and daily living activities, is used as a backdrop to the discussion.
    Results: Following microperforation prolotherapy, the instability of the SCJ was replaced by full stability, complete range of motion, and the opportunity to engage in all of the athletic endeavors previously pursued. There is no scar or other cosmetic defect resulting from the treatment received.
    Conclusion: Anterior sternoclavicular joint subluxation has a poor record of complete recovery with surgical procedures or conservative measures with regard to providing restoration of full lifestyle function. This manuscript documents a novel microperforation prolotherapy treatment that induced healing and restored full stability to the ligament structures responsible for the condition in a completely safe and effective fashion, allowing the patient to resume full lifestyle activities without restriction. The exceptional response to treatment noted here is encouragement for further studies.
    Language English
    Publishing date 2011-06-07
    Publishing country New Zealand
    Document type Case Reports
    ZDB-ID 2586658-8
    ISSN 1179-1543
    ISSN 1179-1543
    DOI 10.2147/OAJSM.S20579
    Database MEDical Literature Analysis and Retrieval System OnLINE

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