Immune-Enhancing, Nootropic
by James South MA

Pyritinol was patented by Merck in 1961. Most of the research on Pyritinol has been published in British, French, German, Czech, and Swiss journals. Thus the drug is virtually unknown in America, not to mention ignored by the AMA and FDA.

Pyritinol has been used clinically in a wide range of disorders. A 1981 report states: "Pyritinol... is widely used throughout Europe for the treatment of organic psychosyndromes..., cerebral circulatory disorders..., alcoholism..., dyslexic factors..., behavior and intellect disorders in children... and post-cerebral infarction [stroke] states....

In patients suffering from cerebral trauma it has been reported to be of therapeutic benefit in influencing the immediate post-operative recovery state and as an aid in rehabilitation...." (1)

Pyritinol has also shown excellent benefit on the clinical course of victims of traumatic coma (caused by head injury). Pyritinol has both reduced the normal high death rate in such cases, and has rapidly returned coma patients to more or less normal waking consciousness, even when the brain injuries were so severe the patient ultimately died. (2)  Pyritinol has also been used successfully to treat rheumatoid arthritis patients. (3)  Pioneer nootropic researcher I.Hindmarch has also noted that "The clinical properties of Pyritinol have also been demonstrated using experimentally induced hypoxia [low brain oxygen] where a 68% [decrease] on psychometric assessments was reduced to 21% by 600 mg and to 12% by 1000 mg of the drug." (4)

Pyritinol is almost identical to pyridoxine (vitamin B6), yet it has no B6 activity. (4)  Pyritinol is also known as pyrithioxine, and pyridoxine disulfide. In the Pyritinol molecule, two pyridoxine sulfide molecules are linked together by their two sulfur atoms.

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One of the keys to understanding Pyritinol’s wide mode of action was first revealed in 1989.  Two Czech scientists performed sophisticated experiments on 6 nootropic drugs to determine their free radical-quenching power. Pyritinol proved to be far superior to the acknowledged antioxidant nootropics, centrophenoxine (Lucidril) and DMAE, while piracetam and oxiracetam showed no antioxidant effect. Pavlik and Pilar state: "There is growing evidence that free-radical interactions are implicated in the pathogenesis of many diseases including radiation injury, atherosclerosis, arthritis, cancer and aging.... The most dangerous [kind] of oxygen radicals is the hydroxyl radical that can attack proteins, lipids, nucleic acids and, actually, almost any molecule of a living cell. If the production of hydroxyl radical escapes the control mechanisms, then … substantial damage to cell functions [and structure] may occur.... It was found that Pyritinol exerted a pronounced scavenger action against hydroxyl radicals which was confirmed by the electron spin resonance spectroscopic technique in spin trapping experiments". (5)  It is interesting to note that brain proteins were protected from hydroxyl radical damage by Pyritinol in these experiments. As will now be explained, the superior hydroxyl radical antioxidant effect of Pyritinol is what provides much of the immune, arthritis, and neuroprotective benefits of Pyritinol.

Three of the most common ‘free radicals’ that are continuously being produced in human cells are superoxide radical, hydrogen peroxide, and hydroxyl radical.  Superoxide radicals are normally produced through white blood cell germ-killing activities, energy metabolism, and in many disease states. "It is believed that the activity of superoxide is at least partly.... responsible for aging and most if not all degenerative diseases". (6A)

Fortunately the body has two different enzymes - copper-zinc SOD and manganese SOD - to neutralize superoxide radicals.  Unfortunately, SOD production drops with age: "Lowered levels of SOD... have been found in elderly persons.... Decreases in all human tissues examined have found in humans, progressing from ages 1 to 89". (6B)  SOD converts neutralize superoxide radicals into oxygen and hydrogen peroxide.  Hydrogen peroxide is less cell-damaging than neutralize superoxide radicals, but it is still injurious if it accumulates in cells.

Although hydrogen peroxide has some uses in the body (e.g. white blood cells secrete it to kill germs), the body’s need to continuously rid itself of hydrogen peroxide is shown by the fact that our cells possess two completely different enzymes - catalase and glutathione peroxidase - to ensure neutralization of hydrogen peroxide.  Hydrogen peroxide uncontrolled can damage cell membranes and structures, as well as promote inflammation.

The brain is particularly vulnerable to damage by hydrogen peroxide. (6C) Unfortunately, under conditions all too common in our cells, neutralize superoxide radicals and hydrogen peroxide "will react with each other in what is known as the Haber-Weiss reaction. The product of this reaction is a free radical even more damaging than superoxide known as the hydroxyl radical...." (6D). And to make matters worse, human cells have no enzymatic defense against hydroxyl radical. hydroxyl radical is normally quenched primarily by cholesterol, Vitamin C or proanthocyanidins, (6E). (Thus, the elevated cholesterol levels found in most modern humans may actually be a defensive tactic used by the body to quench the excesses of hydroxyl radical induced by our toxic modern diet, environment and lifestyles). hydroxyl radical’s are so injurious to cells that when huge uncontrollable numbers of them are generated in a person exposed to massive levels of X-ray or gamma radiation, the flesh may literally melt from the bones within hours!

As Pavlik and Pilar note: "There are some clinical reports that may be viewed as supporting the opinion that Pyritinol may also have a [hydroxyl] scavenger effect in vivo. Camus [et al] (1978) and Berry (1986) used Pyritinol successfully, instead of the … more toxic scavenger penacillamine, for the treatment of some cases of rheumatoid arthritis. [So did Lemmel et al, reporting in 1993. (3)] The protection of cartilage and synovial protein against free-radical -induced degradation … may be an important factor in the treatment of rheumatoid arthritis. The same line of reasoning may be applied to some cases of stroke or brain trauma ..., where the generation of hydroxyl free-radicals … is abundant … and where Pyritinol was successfully used for treatment .... Finally, the potency of Pyritinol to protect proteins in brain against radical induced polymerization, in conjunction with recent reports that Pyritinol enhanced cholinergic transmission in brain ..., substantiates its use for the treatment of cognitive disorders". (5)

Increased brain cell energy

Another key benefit of Pyritinol has been known since the 1960’s: its ability to enhance or normalize glucose transport through the blood-brain barrier and to increase brain cell energy production from glucose.(7)  In a placebo-controlled, double-blind study, Hoyer and colleagues examined 87 patients suffering from various brain disorders.  Careful measurements of cerebral blood flow, oxygen uptake, glucose uptake, and cerebral metabolic rate were taken. Of the 45 patients receiving Pyritinol, 27 (60%) suffered from disturbed glucose uptake/cerebral energy metabolism. "Cerebral uptake of glucose, … which … was reduced to approximately 50% of the normal value, increased significantly during Pyritinol treatment … and returned to normal.... The clinical disturbances generally also improved to the same extent as did the disturbed glucose metabolism". (7)

Enhanced Glucose Transport

Pyritinol’s ability to enhance glucose transport through the blood-brain barrier when it is low is a highly significant benefit of Pyritinol.  Although the brain is usually less than 2% of total bodyweight, the brain must produce and use about 20% - 500 calories per day - of the body’s total energy production.  And under normal, non-fasting conditions, the brain can only ‘burn’ glucose (sugar) for fuel.  Unlike virtually all other body cells, nerve cells cannot use fat as an energy fuel.  Brain cells also cannot store any significant amount of glucose - they are completely dependent upon a continuous delivery of glucose from the blood, through the blood-brain barrier.  Thus, brain glucose uptake is a major rate-limiting factor for crucial brain energy production.  Low cerebral glucose uptake necessarily translates into low brain carbohydrate energy metabolism.

And brain energy metabolism is so important to optimal, healthy brain function that "... brain carbohydrate metabolism is impaired in a variety of dementias [e.g. Alzheimer’s, stroke, metabolic, or drug toxicity dementias] and … the degree of reduction in brain carbohydrate metabolism is correlated with the severity of the dementias ...." (7)  Pyritinol is good for optimal brain carbohydrate metabolism , and what is good for brain carbohydrate metabolism is good for the brain and the mind!

Effective Immune Enhancer

A surprising effect of Pyritinol was first reported in 1993: Pyritinol may be an effective immune enhancer through its stimulation of neutrophil migration. (9)  Neutrophils are a major type of white blood cell (WBC) - they typically constitute about 60% of the total number of white blood cells in the blood. Wherever there is a wound, cut, sore, abrasion etc., neutrophils are attracted to leave the bloodstream and travel to the site of injury/infection - the process of chemotaxis.  Once at the site of injury, neutrophils proceed to engulf germs - especially bacteria - that may now be growing at the injury site.  Neutrophils then secrete a powerful mix of free radicals and oxidants, such as hydrogen peroxide and hypochlorous acid, which destroy the germs before they can seriously multiply and overwhelm the body. However, neutrophils sooner or later die "in the line of duty" from their own germ-killing free radical barrage.

One neutrophil averages 5 to 20 germ kills before succumbing. The free radicals neutrophils release also typically promote inflammation at the site of injury, a process that all too easily gets out of control and proceeds to excess. Excessive inflammation promotes excessive swelling, tenderness, redness, heat and pain at the injury site. The pus that forms with cuts and wounds is in large part made up of dead neutrophils.

In a study with rabbit neutrophils, Elferink and De Koster found that Pyritinol, at levels likely to be achieved in tissue, through oral doses, strongly promoted neutrophil chemotaxis (migration to injury site), but did not increase free radical levels or inflammation. (9)  Given the earlier discussion on Pyritinol’s antioxidant effects, this differential effect of Pyritinol on neutrophil activity (increases migration, but not free radicals or inflammation) becomes comprehensible.  When large numbers of neutrophils release huge amounts of hydrogen peroxide and hydrogen peroxide, this generates huge quantities of inflammatory, tissue-damaging hydroxyl radicals.  Yet Pyritinol is a powerful quencher of hydroxyl radicals. Thus Pyritinol is able to reduce hydroxyl radical-induced inflammation and tissue damage - the unpleasant side effect that usually accompanies successful germ-killing by neutrophils.

Immune Defense

Neutrophils comprise the body’s first line of white blood cell immune defense - they are normally first to arrive at wound/injury sites.  Yet our modern sugar-rich diet has been shown in multiple studies to significantly impair neutrophil activity.

When human volunteers were given various forms and levels of sugar in drinks, the number of germs a neutrophil could kill before dying from its own free radical release typically dropped 50 - 80%! The effect began within one hour of sugar intake, peaked at two hours, and was still significant five hours after sugar ingestion. (10)  Thus a sugar-rich diet literally enhances neutrophil self-destruction as neutrophils kill germs, yet Pyritinol enhances neutrophil survival through reducing the hydroxyl radical excesses that normally lead to neutrophil death.

Another key property of Pyritinol is its vigilance-enhancing effect.  Pyritinol increases nerve activity in the locus coeruleus. (11)  "In humans, the number of neurons in the locus coeruleus declines with advancing age.  Degeneration appears to advance slightly faster in males than females. The locus coeruleus is a brain area that … is particularly susceptible to neuronal degeneration in Alzheimer’s disease.... [There are many] studies indicating a role of this system in control of attention and … learning and memory". (11)

EEG Power

"Pyritinol has also been shown to produce a vigilance response, both behaviorally and electrophysiologically (EEG recordings) in animals and in healthy human volunteers.  More recently, using topographic brain mapping of EEG, it has been shown that 600 mg Pyritinol resulted in an increase in total (EEG) power and … other changes indicative of improved vigilance.... Specific studies of the effects of Pyritinol on … memory using a battery of seven tests … showed that repeated daily doses of Pyritinol 300mg improved memory performance [which is in part a function of locus coeruleus  - regulated vigilance] over a wide range of measures in volunteers aged from 16 to 66 years". (4)

Who might benefit?

1. Pyritinol may be useful in various forms of dementia, organic brain syndrome, head injury, stroke aftermath, coma, and cerebral circulatory disorders. Vinpocetine, piracetam, oxiracetam, and phosphatidyl serine may be useful synergists with Pyritinol.

2. Pyritinol may be useful as an anti-brain aging nootropic drug.

3. Pyritinol may be useful as an aid to increased focus and concentration, memory, alertness and information processing in both young and old, normal or mildly brain dysfunctional persons.

4. Pyritinol may be useful in Attention Deficit Disorder (ADD), hyperkinetic, or mildly retarded children to increase drive, alertness, concentration and learning ability. (12, 13)

5. Pyritinol may be useful as part of a health-optimizing antioxidant program, along with vitamins C and E, selenium, zinc and lipoic acid.

6. Pyritinol may be useful in the treatment of rheumatoid arthritis. In a large, double blind yearlong trial comparing Pyritinol to a standard anti-rheumatoid drug (Auranofin), the response rate was superior for Pyritinol (78% vs. 59%, at one year).  "Every individual efficacy parameter showed a numerical trend for better results in the Pyritinol group...." (3)

Pyritinol Side-Effects

Most published studies on Pyritinol report few if any side effects, with skin rashes and/or gastric upset occasionally noted. E.g. "In general, the tolerability of the drug was good.  Practically no problems occurred during the trial.... None of the reported symptoms were rated as serious or persisted over a long period of time". (14) "No undesirable side-effects were observed". (13) "With the exception of cutaneous [skin] symptoms ... there were no significant differences in the incidence of adverse reactions in the drug and placebo group.... No significant changes were observed in [clinical laboratory] parameters". (1)

The one major exception to Pyritinol’s low side-effect profile occurred in the large-scale rheumatoid arthritis trial. The authors note that Pyritinol side effects "were mostly nuisance events, which led to stopping therapy [in some cases], but did not constitute a health risk for the patient and were fully and rapidly reversible." (3)  However, they also note a general trend in the Pyritinol-arthritis literature of about 2% potentially serious adverse effects involving blood, kidney or liver, which makes it important for regular monitoring of liver enzymes, urine status and blood cell status when using Pyritinol to treat rheumatoid arthritis. Therefore, Pyritinol should be used in rheumatoid arthritis treatment only with the knowledge and supervision of a physician.

Pyritinol Doses

A wide range of doses have been used in Pyritinol studies.  These have ranged from as low as 100 mg twice daily (12) to 200 mg three time’s daily  (14) or 200 mg four times daily. (15)  For anti-aging, cognition-enhancing or antioxidant purposes, 100 mg Pyritinol two or three times daily is generally safe and adequate.  Higher doses (400 - 1000 mg daily) should probably be used only with physician supervision, just to err on the safe side.  Pyritinol may be taken either on empty stomach or after food, as desired.  Persons only prone to insomnia should probably only take Pyritinol morning and early afternoon.  There may be a mutual enhancement of action between Pyritinol and other nootropic drugs, allowing/requiring lower doses of some or all the drugs in order to avoid an over-excitation effect.



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1. K.Kitamura (1981) "Therapeutic Effect of Pyritinol on Sequelae of Head Injuries" J Int Med Res 9, 215-21.

2. G. Dalle Ore et al (1980) "The Influence of the Administration of Pyritinol on the Clinical Course of Traumatic Coma", J Neuroserg Sci 24, 1-8.

3. E.-M. Lemmel (1993) "Comparison of Pyritinol and Auranofin in the Treatment of Rheumatoid Arthritis" Br J Rheumatol 32, 375-82.

4. I. Hindmarch et al (1990) "Psychpharmacalogical Effects of Pyritinol in Normal Volunteers" Neuropsychobiol 24, 159-64.

5. A. Pavlik & J. Pilar (1989) "Protection of Cell Proteins Against Free-Radical Attack by Nootropic Drugs: Scavenger Effects of Pyritinol Confirmed by Electron Spin Resonance Spectroscopy" Nueropharmacol 28, 557-61.

6. R. Bradford & H. Allen, Oxidology, Chula Vista, CA: R.W. Bradford Foundation, 1997. A:p.65 B:p323 C:p.142 D:p.66 E:p.175.

7. S. Hoyer et al (1977) "Effect of Pyritinol-HCL on Blood Flow and Oxidative Metabolism of the Brain in Patients with Dementia" Arzneim Forsch/Drug Res 27, 671-74.

8. R. Branconnier (1983) "The Efficacy of the Cerebral Metabolic Enhancers in the Treatment of Senile Dementia" Psychopharmacol Bull 1983 Spring;19(2):212-9.

9. J. Elferink & B. de Koster (1993) "Differential Stimulation of Neutrophil Functions by Pyrithioxine" Int J Immunopharmac 15, 641-46.

10. R. Huemer & J. Challem, "The Natural Health Guide to Beating the Supergerms", NY: PocketBooks, 1997. Pp.124-27.

11. H.-R. Olpe et al (1985) "Locus Coeruleus as a Target for Psychogeriatric Agents" Ann NY Acad Sci 444, 394-405.

12. G. Logue et al (1974) "The Effects of Pyrithioxine on the Behavior and Intellectual Functioning of Learning-Disabled Children" S.Afr Med J 48, 2245-46.

13. D. Lane O’Kelly (1975) "Pyritinol in the Treatment of Chronic Alcoholics" J Int Med Res 3, 323-27.

14. K. Fischhof et al (1992) "Therapeutic Efficacy of Pyritinol in Patients with Senile Dementia of the Alzheimer Type (SDAT) and Multi-Infarct Dementia (MID)" Neuropsychobiol 26, 65-70.

15. A. Cooper & R. Magnus (1980) "A Placebo-Controlled Study of Pyritinol in Dementia" Pharmatherapeutica 2, 317-22.