Nicotinic Acid in the Treatment of Scizophrenias

Thomas A. Ban: Nicotinic Acid in the Treatment of Schizophrenias. Canadian Mental Health Association Collaborative Study. Introduction

Toronto: Canadian Mental Health Association; 1971 (17 pages)

Reviewed by Thomas A. Ban

CONTENT: This booklet opens with a quote from Abram Hoffer that reads: “….For too long has the society of physicians and non-physicians been unable to treat schizophrenia because of lack of knowledge. Today this is no longer the case. But too many schizophrenics are being deprived from their chance of recovery because the use of nicotinic acid has not expanded very rapidly….” (Nicotinic Acid and/or Nicotinamide for Treating Schizophrenia: A Compilation of Saskatchewan Research Information.  Regina: White Cross Publications; 1964))

To examine the value of nicotinic acid in the treatment of schizophrenias, the Canadian Mental Health Association (CMHA) Collaborative Study was conducted in the late 1960s to test in 12 clinical trials the following four “general hypotheses”: (1) Nicotinic acid has a beneficial effect over and above the effect of standard treatment (four trials); (2)  The therapeutic efficacy of nicotinic acid in schizophrenia can  be increased by the administration of pyridoxine, ascorbic acid and/or penicillamine (three trials); (3) Patients who test positive for “mauve factor”, “pink spot” or ”bufotenin-like substance” in their urine respond more favorably to nicotinic acid  (three trials); (4) Nicotinic acid administration can prevent and counteract the exacerbation psychopathology in schizophrenia induced by the combined administration of a monoamine oxidase inhibitor (tranylcypromine), and a methyl donor (methionine) (two trials).

 Description of the design of the 12 clinical trials is followed by a review of the “Theoretical background of the study”. Special attention is given to hypotheses which postulate that the culprit in schizophrenia is the formation of endogenous psychotoxic methylation products of catecholamines and/or indoleamines, such as adrenochrome (methylation product of epinephrine), 3,4-dimethoxyphenylehylamine (DMPEA) (methylation product of dopamine), N,N-dimethyltryptamine (methylation product of serotonin). For the CMHA Collaborative Study, the adrenochrome hypothesis was of particular importance because Hoffer suggested the administration of high doses of nicotinic order to reduce the formation of excessive amounts of epinephrine under stress. His rationale for this treatment was that nicotinic acid converts to nicotinamide, a substance that competes with norepinephrine for available methyl groups.

The booklet includes details (in tables) on the 12 clinical trials and schematic presentations (in figures) of tryptophan metabolism and the formation of DMPEA from dopamine, adrenochrome from epinephrine, and N-methylnicotinamide from nicotinamide. It also includes a list of references.

AUTHOR’S COMMENT: The CMHA Collaborative Study was designed and coordinated by Thomas A. Ban in consultation with Heinz E. Lehmann. It was conducted during the second part of the 1960s amid strong controversy about the treatment. This is the first of three booklets, published by the Canadian Mental Health Association, in which information on the study is presented. 


Thomas A. Ban

January 8, 2015