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Parkinson's disease: carbidopa, nausea, and dyskinesia

Authors Hinz M, Stein A, Cole T

Received 4 August 2014

Accepted for publication 17 September 2014

Published 14 November 2014 Volume 2014:6 Pages 189—194

DOI https://doi.org/10.2147/CPAA.S72234

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Professor Arthur Frankel


Marty Hinz,1 Alvin Stein,2 Ted Cole3

1Clinical Research, NeuroResearch Clinics, Cape Coral, FL, 2Stein Orthopedic Associates, Plantation, FL, 3Cole Center for Healing, Cincinnati, OH, USA

Abstract: When ʟ-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 ʟ-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 ʟ-dopa. The research into the etiology of these phenomena has identified the causative agent of the irreversible dyskinesias as carbidopa, not ʟ-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 ʟ-dopa and may be perceived as irreversible if proper corrective action is not taken.

Keywords: vitamin B6, PLP, irreversible, pyridoxal 5'-phosphate

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