Pyritinol by Ray Sahelian, M.D.

Pyritinol is also known as pyrithioxine, and pyridoxine disulfate. In the Pyritinol molecule, two pyridoxine sulfate molecules are linked together by their two sulfur atoms. Much research with Pyritinol was conducted in the 1970s and 1980s. I prefer a combination of several herbal mind boosting supplements that I have formulated called Mind-Power-Rx.

Pyritinol and the brain
Pyritinol facilitates the recovery of cortical cholinergic deficits caused by nucleus basalis lesions.
J Neural Transm Park Dis Dement Sect. 1994;7(3):195-209. Instituto CAJAL, C.S.I.C., Madrid, Spain.
The effect of a nootropic, Pyritinol, on the recovery of cortical cholinergic deficits induced by injury of the nucleus basalis has been tested on two groups of unilateral quisqualic acid nbM-lesioned rats. The first group had a 30 nmol lesion producing a cortical cholinergic impairment at 21 days, with a spontaneous recovery at 45 days. The second group had a 50 nmol lesion that produced a deeper cholinergic deficit, which did not recover at 45 days. Pyritinol enhanced the recovery in the 30 nmol group of animals on the 21st day after surgery. The recovery was measured as an increase in the activities of acetylcholinesterase (AChE), choline acetyltransferase (ChAT) and the high affinity choline uptake system, and the histochemical densities of the cortical AChE network and the M2 receptor. Histochemical analysis of the nbM enabled cortical recovery to be related to the number of surviving neurons and also to their hypertrophy and AChE-ChAT hyperactivity. Pyritinol enhanced recovery in 30 nmol lesioned animals but in the other group, with a lower number of surviving neurons and a lower ability of the cells to become hypertrophic, the drug was unable to promote cortical recovery.

Effects of subchronic administration of pyritinol on receptor deficits and phosphatidylinositol metabolism in the brain of the aged mouse.
Neuropharmacology. 1993 Feb;32(2):119-25. Department of Psychopharmacology, Central Institute of Mental Health, Mannheim, Germany.
The effect of pyritinol, a commonly used nootropic drug, on receptor properties and function was investigated in different neuronal systems, possibly associated with age-related decline in brain function. Chronic treatment (15 days) of aged (22 months) female NMRI mice with pyritinol (200 mg/kg) restored the reduced density of N-methyl-D-aspartate receptors in the aged mouse brain. Changes caused by pyritinol may be due to beneficial effects on age-related alterations of the properties of the neuronal membrane.

Therapeutic efficacy of pyritinol in patients with senile dementia of the Alzheimer type (SDAT) and multi-infarct dementia.
Neuropsychobiology. 1992;26(1-2):65-70. Psychiatric Hospital Baumgartner Hohe, Vienna, Austria.
This trial was performed to investigate the efficacy of pyritinol in the treatment of senile dementia. Initially, a total of 183 inpatients were screened for eligibility. Of 164 patients who met the inclusion criteria, 156 completed the trial. Allocation of the patients to the Senile Dementia of the Alzheimer Type group or the Multi-Infarct Dementia group was based on the Hachinski Ischemic Score, computed tomography scans and electroencephalographic (EEG) findings. In a 12-week double-blind treatment phase either 200 mg pyritinol dihydrochloride -monohydrate or placebo was given 3 times daily. The EEG mapping demonstrated significant differences between placebo and pyritinol, with the latter decreasing slow and increasing fast alpha and beta activity, which reflects improvement of vigilance. Based on the results of this trial, it can be accepted that the therapeutic effect of pyritinol is superior to placebo in patients with mild to moderate dementia of both degenerative and vascular etiology.

Psychopharmacological effects of pyritinol in normal volunteers.
Neuropsychobiology. 1990-1991;24(3):159-64. HPRU, Robens Institute, University of Surrey, Guildford, UK.
Twelve healthy male volunteers received pyritinol 600 or 1,200 mg or placebo for 3 days according to a randomised, double-blind crossover design. On the 1st and 3rd days of each of the three treatment periods subjects completed a battery of psychological tests including Critical Flicker Fusion (CFFT), Choice Reaction Time (CRT), tests of memory and subjective drug effects at 1, 2, 4 and 6 h after dosing. Significant improvements in CFFT and CRT were found after pyritinol. There were no significant differences on the other tests, however, the observed enhancement in performance could be attributed to the effect of the drug.

Pyritinol treatment of SDAT patients: evaluation by psychiatric and neurological examination, psychometric testing and rCBF measurements.
Int Clin Psychopharmacol. 1989 Jan;4(1):25-38. Department of Neurology, University Hospital Centre, Zagreb, Yugoslavia.
A group of 26 patients with the diagnosis of Senile Dementia of Alzheimer type (SDAT) was included by random assignment in a double-blind, cross-over trial of pyritinol versus placebo. The patients had a mild to moderate degree of dementia. Psychiatric and neurological examination, psychometric testing, and measurement of the regional cerebral blood flow (rCBF) at rest and during mental activation were used to assess treatment effects. The results of the study showed that pyritinol was associated with a significant improvement in cognitive performance. RCBF data showed that treatment with pyritinol normalized the pattern of blood flow increase during activation and improved the score on the test used for activation.

Pyritinol side effects
Acute pancreatitis due to pyritinol: an immune-mediated phenomenon.
Gastroenterology. 1998 Aug;115(2):452-4.Department of Medicine, Kantonsspital, Olten, Switzerland.
A 23-year-old man experiencing three episodes of acute pancreatitis of undetermined etiology is described. Repeated questioning revealed that all three events had occurred after intake of the drug pyritinol. Controlled rechallenge with a single dose of the drug led to a fourth episode of acute pancreatitis. Skin testing was negative, but lymphocyte stimulation tests and double fluorescence analysis detected pyritinol-activated CD4 and CD8 lymphocytes. Together with the clinical observation that the intervals between drug intake and start of symptoms of acute pancreatitis became shorter with repeated exposure, the data are consistent with an immune-mediated origin of the pancreatitis. Pyritinol has to be added to the list of drugs capable of inducing acute pancreatitis.

Erythema multiforme-like eruption in association with severe headache following pyritinol.
Dermatology. 1993;187(1):42-6. Department of Dermatology, University of Munich, FRG.
A 46-year-old woman presented with an unusual erythema multiforme-like eruption and severe headache 10 days after treatment with pyritinol for cerebral concussion. Histopathologic findings were consistent with erythema multiforme. Skin lesions and headache cleared after withdrawal of the drug. According to neurological examination and magnetic resonance imaging of the brain, the headache may have resulted from a slight, pyritinol -induced vasculitis. Previous reports on severe pyritinol -induced side effects and possible pathogenetic mechanisms are reviewed. Since pyritinol cannot be considered as an essential drug for cerebral concussion, adverse effects as described here raise doubts as to its general use in the given indication.

Pyritinol has been promoted as a smart pill.