|Use of Niacin to Modulate LSD and Psilocybin Trips|
Psychedelic Abstracts Online
MILLER A I,WILLIAMS H L, MURPHREE H B
Niacin, niacinamide, or atropine versus LSD-25 model psychoses in human volunteers.
J.Pharmacol.& Exper.Therap., 119:169 (1957)
Studies in 16 volunteers using the double blind method showed that atropine (1 mg orally), niacin (up to 600 mg orally), and niacinamide (up to 600 mg orally) did not alter the pattern of response to LSD when they were given in combination with LSD (75 mcg orally). Niacin seemed to produce a release from the anxiety associated with the LSD-induced illusions without lessening or eliminating the illusions.
AGNEW N, HOFFER A
Nicotinic acid modified lysergic acid diethylamide psychosis.
J.Ment.Sc. London 101:12 (1955)
200 mg nicotinic acid given i.v. to 5 normal subjects at the height of the LSD experience (100 mg orally) strikingly reduced the LSD-induced disturbances in all subjects except one. 3 Gm. nicotinic acid given by mouth daily for 3 days prior to 100 mcg. LSD orally in 5 normal cases reduced the LSD-induced disturbances in concentration and vision, but in some instances produced a psychosis more closely resembling schizophrenia than that observed after LSD alone.
Studies with niacin and LSD.
Lysergic Acid Diethylamide and Mescaline in Experimental Psychiatry, Grune & Stratton Inc. 1956, p 44
200 mg nicotinic acid given i.v. at the height of the effects of LSD (100 mcg) caused almost all the LSD phenomena to disappear with 2-5 minutes. 3 Gm. nicotinic acid given daily for 3 days prior to 100 mcg LSD caused the LSD phenomena to appear after about 1 hour instead of after 15-30 minutes and seemed to prevent most of the perceptual phenomena, the main changes noted being feelings of unreality and depersonalization.
LUCHINS, D; BAN, THOMAS A; LEHMANN, H E
A review of nicotinic acid, N-methylated indoleamines and schizophrenia.
International Pharmacopsychiatry; 1978 Vol 13(1) 16-33
Reviews published literature to investigate the hypothesis that endogenously formed, N-methylated metabolites of indoleamines may play a role in the pathogenesis of schizophrenia. Although N-methylated indoleamines can be produced in vivo and have significant psychotomimetic effects, little evidence exists concerning a specific increase in the methylation of indoleamines in schizophrenic patients. It is noted that even if the relationship between schizophrenia and N-methylated indoleamines had existed, nicotinic acid would not be an appropriate therapeutic agent.
The biochemistry of the schizophrenias.
Journal of Orthomolecular Psychiatry; 1978 Vol 7(1) 6-16
Analyzes studies that have found chronic schizophrenia to be the result of an underlying metabolic block on the dominant tryptophan niacin pathway, i.e., an inherited defect or insufficient activity of enzyme 3-hydroxyanthranilate-oxygenase. Findings are summarized on niacin, MAO enzyme, coenzymes nicotinamide-adenine dinucleotide (NAD) and NAD phosphate (NADP), and tryptophan metabolism, including deficiencies that induce psychotomimetic effects in humans. It is recommended that the treatment of schizophrenia focus on (a) replacement of the missing enzyme through niacin or niacinamide supplementation and by increasing NADP hydrogenase (NADPH), a reduced form of NADF; (b) reduction of substrate by dietary restriction of tryptophan, methionine, betaine, cysteine, homocysteine, and choline; by preventing transmethylation with phenothiazine and penicillamine drugs; by degradation of psychotomimetic compounds with (c) niacin supplements, (d) supplementation with vitamins C, B1, B2, and B6; and (e) special procedures required after testing for other metabolic problems.
ABRAMSON H A, JARVIK M E, LEVINE A, KAUFMAN M R, HIRSH M W
Lysergic acid diethylamide (LSD-25): XV. The effects produced by substitution of a tap water placebo.
J.Psychol. 40:367 (1955)
Studies in 33 normal subjects revealed that tap water is capable of eliciting certain responses from certain subjects who believe they have received LSD.