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

Authors Hinz M, Stein A, Cole T

Received 7 July 2014

Accepted for publication 22 July 2014

Published 21 October 2014 Volume 2014:6 Pages 161—169

DOI https://doi.org/10.2147/CPAA.S70707

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Marty Hinz,1 Alvin Stein,2 Ted Cole3

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

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.

Keywords: L-dopa, levodopa, vitamin B6, pyridoxal 5'-phosphate

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