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The discrediting of the monoamine hypothesis

Authors Hinz M, Stein A, Uncini T

Received 1 November 2011

Accepted for publication 23 November 2011

Published 14 February 2012 Volume 2012:5 Pages 135—142


Review by Single anonymous peer review

Peer reviewer comments 3

This paper has been retracted.

Marty Hinz 1, Alvin Stein 2, Thomas Uncini 3

1Clinical Research, NeuroResearch Clinics, Inc, Cape Coral, FL, 2Stein Orthopedic Associates, Plantation, FL, 3Fairview University Medical Center, Hibbing, MN, USA

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.

Keywords: monoamine hypothesis, monoamine theory, serotonin, dopamine, neuronal dysfunction, bundle damage theory

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