mind enhancing

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Nootropics - reviewing piracetam and analogues

by James South M.A.

Over 30 years have passed since the "Nootropic Revolution" quietly began with the

development of Piracetam in the late medical efficacy with a virtual absence of toxicityand side effects; something rarely seen with more standard medical drugs.

More importantly, they offered promise not only in the realm of fighting disease, but alsoin the virtually unexplored realm of drugs that could not only postpone or even reverse

"normal" brain aging, but could even make "normal" brains work better!

The Piracetam-nootropics have been exhaustively researched; since the first scientificstudies on Piracetam in the late 1960's over 1000 scientific papers on Piracetam,

Oxiracetam, Pramiracetam, and Aniracetam have been published with about two thirds of

them on Piracetam.

The action of the Piracetam-nootropics has been studied in a broad range of animals;

goldfish, mice, rats, guinea pigs, rabbits, cats, dogs, marmosets, monkeys and humans.

The toxicity of Piracetam and its "cousins" is amazingly low- almost non-existent. In

acute toxicity studies, intravenous doses of Piracetam given to rats (8g/ Kg bodyweight)and oral doses given to mice, rats, and dogs (10g/ Kg or more) produced no toxicity.

This would be equivalent to 560-700 grams (1.23 to 1.54 pounds) for a 154 pound

human. Rats given 100-1000mg/ Kg orally for 6 months and dogs given 10,000mg/ Kgorally for one year showed no toxic effect, a teratogenic (birth defect causing) effects

were found, either (Tacconi and Wurtman 1986).

The Piracetam-nootropics are among the toxicologically safest drugs ever developed.

The four main commercially available "racetam" nootropics all share a pyrrolidinenucleus, while Piracetam, Oxiracetam, and Pramiracetam, also share an acetyl group.

The racetams (especially Piracetam and Oxiracetam) are closely related in structure to the

amino acid Pyroglutamic Acid. Pyroglutamic Acid has been shown in some studies to

have weak nootropic activity (Gouliaev and Senning 1994). Pyroglutamic Acid isnaturally present in many human foods, as well as the mammalian brain.

The concept and definition of a "nootropic drug" was first proposed in 1972 by C.E.Giurgea, the principal Piracetam researcher and research coordinator for UCB, the

Belgian company that launched Piracetam. "The main features... defining a nootropic

drug are

(A) the enhancement, at least under some conditions, of learning acquisitions as well as

the resistance of learned behaviors to agents that tend to impair them;


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(B) the facilitation of interhemispheric flow of information;

(C) the partial enhancement of the general resistance of the brain and particularly itsresistance to physical and chemical injuries;

(D) the increase in the efficacy of the tonic cortico-subcortical control mechanisms; and

(E) [absence of the usual negative pharmacologic effects of psychotropic drugs].

" Giurgea,and Salama 1977). Giurgea derived the term "nootropic" from the i words

"noos" (=mind) and "tropein" (=to turn toward).

Schaffler and Klausnitzer (1988) have given an excellent brief overview of some of thechief effects of the Piracetam-nootropics. "From animal biochemistry it is known that

[Piracetam-nootropics] enhance brain metabolism by stimulation of oxidative catabolism,

increase of ATP-turnover and cAMP levels, enhancement of phospholipid-metabolism

and protein biosynthesis. [Piracetam-nootropics have] an impact on the hippocampalrelease of acetylcholine and on the dopaminergic turnover, too. Pharmacologically there

exist protective effects with regard to several noxes [harmful agents] and an impact onthe associative cortical sphere and on hippocampal structures, which are related with

learning and memory, especially when the respective functions are impaired. The

performatory enhancements are related with an increased arousability of hippocampalpyramid cells, facilitated transmission of the thalamic afferences, increased release of

hippocampal acetylcholine and enhanced synaptic transmission.

The clinical biochemistry indicates enhancing functions on the utilization of oxygen andglucose under the conditions of decreased brain metabolism, as well as improvements in

local perfusion. Due to this profile [Piracetam-nootropics] can be expected to be of value

in the treatment of disease which are related to impairments in the above mentionedfeatures, such as several types of senile dementia, (e.g. Primary Degenerative Dementia=

Alzheimers type: Multi Infarct [stroke] Depantia), ischaemic [poor brain blood flow]

insults, hypoxia, anoxia and toxicologically or dietary based deficiencies." (Footnotes inthe original text omitted here).

From the beginning of Piracetam research, the ability of the Piracetam-nootropics to

partly or completely prevent or reverse the toxic action of a broad array of chemicals andconditions has been repeatedly demonstrated. Aniracetam reverses the memory

impairment in rats induced by Clonidine. Piracetam, Oxiracetam, Pramiracetam, and

Aniracetam all antagonize the normally lethal neuromuscular blockade induced byHemicholinium-3 (HC3) in mice. Piracetam, Oxiracetam, and Aniracetam have all

attenuated or reversed the Scopalamine (anticholinergic agent)- induced amnesia in rats

and mice under a broad range of experimental conditions.

Oxiracetam has reversed the typical "spaced out" electroencephalogram of healthy

humans given Valium, restoring a normal vigilance electroencephalogram while


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maintaining Valium's anti-anxiety effects. Piracetam and Aniracetam have ameliorated

the amnesia produced by the protein synthesis inhibitor Cycloheximide.

Piracetam, Oxiracetam, Pramiracetam, and Aniracetam all attenuate or reverse the

amnesia in mice and rats induced by electroconvulsive shock treatment in both passive

and active learning conditions.

When mice were given Oxydipentonium, a short acting curare-like agent which induces

asphyxia, at a dose sufficient to kill 90-100% of the placebo treated controls, the twogroups of Piracetam treated mice had a 90 and 100% survival rate.

When humans, rats, mice and rabbits have been put under diverse hypoxic experimental

conditions, Piracetam, Oxiracetam, and Aniracetam have acted to attenuate or reverse thehypoxia-induced amnesia and learning difficulties. as well as to speed up recovery time

from hypoxia and reduce the time needed to renormalize the electroconvulsive shock

treatment (Gouliaev and Senning Giurgea and Salama 1977).

A classic series of experiments on the protective power of Piracetam against barbiturate

poisoning was reported by Moyersoons and Giurgea in 1974. Rabbits connected toelectroconvulsive shock treatment machines were given either Piracetam or saline

injections before intravenous (I.V.) administration of the fast acting barbiturates-

Secobarbital.

When Piracetam was given I.V. one hour before Secobarbital, 10/10 rabbits survived

versus 3/10 survivors given saline. Electroconvulsive shock treatment records showed

only minimal abnormalities in the Piracetam rabbits, while the saline rabbits showedmassive electroconvulsive shock treatment silence, rapidly followed by death. When

given only one-half hour before Secobarbital, 7/11 Piracetam rabbits survived versus 3/1

1 control rabbits.

Electroconvulsive shock treatment records of the Piracetam rabbits showed somewhat

more abnormalities than those given one hour Piracetam pre-treatment, but still far morenormal appearing than the saline control rabbits' electroconvulsive shock treatment.

Piracetam was also given orally one hour before Secobarbital. 8/9 Piracetam rabbits

survived while only 3/9 controls survived. The electroconvulsive shock treatment records

of both groups were similar to those of the rabbits given Piracetam and saline I.V. onehour before Secobarbital.

The experiments then treated Piracetam against a more slow acting barbiturateAllobarbital, giving the Piracetam I.V. two minutes after the Allobarbital infusion 11/13

Piracetam rabbits survived, while only 2/13 saline control rabbits survived

electroconvulsive shock treatment. Records of the Piracetam rabbits again showedelectrical silences to be almost absent, and if present, to be shorter and appear later than

in the control animals.


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In the Allobarbital experiment, one of the two surviving control rabbits actually presented

a more normal electroconvulsive shock treatment after Allobarbital than did one of the

survivors eleven Piracetam survivors..

Yet an electroconvulsive shock treatment recorded the next morning (about 18 hours

later) showed that the control was still asleep, and it was not aroused by a loud noise.The Piracetam rabbit, however, was well awake, behaved normally, moved around and its

electroconvulsive shock treatment was normal.

Thus, whether given I.V. or orally, and before or after general lethal (to controls)

barbiturate infusion, Piracetam served to protect both life and brain structure and

function, as evidenced by electroconvulsive shock treatment records and post recovery

behavior.

The rabbit experiments just described are hardly unusual. The Piracetam-nootropics

routinely show an ability to stabilize or normalize the electroconvulsive shock treatment's

of humans and animals under a broad range of experimental and medical conditions.

The electroconvulsive shock treatment records the electro-chemical activity of largegroups of cortical neurons, and thus provides a "macro" picture of brain activity. Aging,

dementia, hypoxia and benzodiazepines all promote a similar shift in electroconvulsive

shock treatment frequency patterns.

Low frequency delta waves (0-4 cycles per second) and theta waves (4-8 cps) are

increased, while alpha waves (8-12 cps) and beta waves (beta-1; 12-20 cps, beta 2; 20-32

cps) diminish. The average frequency of the delta and alpha waves also drops, ascompared to healthy normal subjects.

Nootropics - clinical studies

Giaguinto and colleagues (1986) gave 12 healthy humans 5mg Valium orally at 10PM the

night before their experiment. The next morning they were given either I.V. Oxiracetamor saline in a double blind crossover experiment. Oxiracetam strongly decreased the

excessive delta activity while simultaneously strongly increasing alpha activity, and also

induced a modest increase in beta activity. Thus Oxiracetam restored the

electroconvulsive shock treatment to a pattern indicating increased vigilance andalertness, yet without destroying Valium's anti-anxiety effect.

Itil and co-workers (1986) treated four groups of 15 patients suffering mild to moderatedementia with either Oxiracetam or placebo for three months. The double blind study

used Oxiracetam in doses of 800, 1600 and 2400mg daily. Quantitative electroconvulsive

shock treatment data indicated that in patients with dementia, Oxiracetam had a mode ofaction similar to other vigilance enhancing compounds. The majority of patients who had

abnormal slow electroconvulsive shock treatment patterns before treatment showed a

"normalization" of their brain waves- i.e. a decrease in slow (delta and theta) and an

increase in alpha waves. Saletu and colleagues (1985) conducted a four week double


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blind trial of Oxiracetam (2400 mg per day) or placebo in 40 patients (mean age; 80

years) suffering from the "organic brain syndrome of late life." Their results showed a

clear trend towards a decrease in delta and theta wave activity, an increase in alpha andbeta wave activity, as well as an increase in the dominant frequency and the centroid of

alpha activity after Oxiracetam treatment. Their report noted: "The attenuation of the

slow activity and the elevation of the alpha and/or slow wave beta activity after[Oxiracetam - other studies have shown similar results with Piracetam and Aniracetam]

reflect CNS changes that are just oppositional to those seen in normally and

pathologically aging subjects... The increase in delta and theta activities and decrease inalpha activity in normal and pathological aging are due to deficits in the vigilance

regulatory systems which can be counteracted by nootropic drugs."

Nootropics - and the healthy

Piracetam-nootropics have also shown the ability to improve learning and memory in

healthy individuals not suffering from disease or severe age-related degeneration. In

1976 Dimond and Brouwers reported the results of some of a series of seven double blindtrials, involving 16 second and third year college students "in excellent health and good

physical and mental condition."

Subjects received either 4.8 grams a day Piracetam or placebo for 14 days. In three

different measures of verbal learning and memory, the results showed a highly significantdifference in favor of the Piracetam students over the controls, with confidence levels of

P=.01, P=.02 and P=.01. The authors stated "the fact is that Piracetam improves verbal

learning and in this it would appear to be a substance which is.. capable of extending the

intellectual functions of man.. our subjects were not senile, suffering from generalizedbrain disorder, confusional states, or any other pathology of the brain... It is therefore

possible to extend the power which [individuals gifted with high intelligence and good

memory] possess to still higher levels despite the fact that the range of their achievementis a high."

Giurgea and Salama report the confirmation of Dimond/ Brouwer's work by Wedl andSuchenwirth in 1977. Wedl found significant improvement in mental performance in a

group of 17 healthy young volunteers given 3.2 grams per day Piracetam for five days.

Mindus and colleagues (1976) reported the results of a double blind crossover trial with18 healthy middle aged people (median age 56), with no evidence of somatic or mental

disease, based on medical records and administration of several intelligence tests (group

mean IQ; 120 plus or minus 11).

Most of the subjects were in intellectually demanding jobs, but had reported a slight

reduction for some years in their capacity to retain or recall information.

After four weeks of 4.8 grams per day Piracetam, Piracetam subjects were switched to

placebo for four weeks, while the original placebo group then received Piracetam for four

weeks.


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Results of a series of paper and pencil tests, as well as computerized tests to measure

perceptual motor reactions, showed a clear benefit of Piracetam over placebo.

The three different paper and pencil tests showed superior effects on performance

compared to placebo, with confidence levels of P


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The Greek philosophers saw the role of philosophy to be a method of developing and

perfecting nous/ reason. They understood nous/ reason to be the integrative mind, where

logic works complementarily with intuition, and reason and emotion are in harmony.With a developed nous, one could clearly see and understand "the forest and the trees"

simultaneously. From a modern neurological perspective it is obvious that the cerebral

basis for a well-functioning nous would be the effective, complementary, simultaneousintegrated function of cortical hemispheres, with neither hemisphere being automatically

dominant or silent.

This in turn would require the corpus callosum and anterior commisure to optimize

information flow between the two hemispheres. Research has shown the Piracetam-

nootropics to facilitate such intercebral information transfer- indeed, it's part of the

definition of a "nootropic drug."

Giurgea and Moyersoons reported in 1970 that Piracetam increased by 100% the

transcallosal evoked responses elicited in cats by stimulation of one hemisphere and

recorded from a symmetrical region of the hemisphere.

Buresova and Bures (1976) in a complex series of experiments involving monocular(one-eye) learning in rats, demonstrated that "...Piracetam enhances transcommisural

encoding mechanisms... and some forms interhemispheric transfer..."

Dimond (1976, 1979) used a technique called "dichotic listening" to verify the ability of

Piracetam to promote interhemispheric transfer in humans. In a dichotic listening test,

different words are transmitted simultaneously into each ear by headphone. In most

people the speech center is the left cortex, because the nerves from the ears cross over tothe opposite side of the brain, most people will recall more of the words presented right

ear than the left ear. Words received by the right ear directly reach the left cortex speech

center, while words presented to the left ear must reach the left cortex speech centerindirectly, by crossing the corpus callosum. Dimond's experiments with young healthy

volunteers showed that Piracetam significantly improved left ear word recall, indicating

Piracetam increased interhemispheric information transfer.

Okuyama and Aihara (1988) tested the effect of Aniracetam on the transcallosal response

of anaesthetised rats. The transcallosal response was recorded from the surface of the

frontal cortex following stimulation of the corresponding site on the opposite corticalhemisphere. Aniracetam at two different I.V. doses (10 mg and 30mg per Kg)

significantly increased the amplitude of the negative wave compared to its level prior to

drug, P


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NOT to be major agonists or inhibitors of the synaptic action of most neurotransmitters.

Thus, major nootropic researchers Pepeu and Spignoli (1990) state; "the pyrrolidinone

derivatives [Piracetam-nootropics] show little or no affinity for CNS receptors fordopamine, glutamate, serotonin, GABA, or benzodiazepine... So far, little effect of

nootropic drugs has been demonstrated on brain monoamine and amino acid

neurotransmitters' metabolism and release."

They also note however that "... a number of investigations on the electrophysiological

actions of nootropic drugs have been carried out... Taken together, these findings indicatethat the nootropic drugs of the [Piracetam-type] enhance neuronal excitability within

specific neuronal pathways."

Gouliaev and Senning similarly state "... we think that the racetams exert their effect onsome species [of molecule] present in the membrane of all excitable cells, i.e. the ion

carriers or ion channels and that they somehow accomplish an increase in the excitatory

response... It would therefore seem that the racetams act as potentiators of an already

present activity (also causing the increase in glucose utilization observed), rather thanpossessing any activity of their own, in keeping with their very low toxicity and lack of

serious side effects. The result of their action is therefore an increase in general nesensitivity towards stimulation."

Thus the Piracetam-nootropics would NOT be prone to the (often serious effects of drugswhich directly amplify or inhibit neurotransmitter c e.g. MAO inhibitors, Prozac-style

"selective serotonin reuptake inhibitors, tricyclic antidepressants, amphetamines,

benzodiazepines, etc.

The notable absence of biochemical, physiological, neurotogical, psychological side

effects, even with high dose and/ or long term nootropic use, is routinely attested to in the

vast literature on them. Thus in their 1977 review Giurgea and Salama point out:"Piracetam active in previously described situations, is devoid of usual 're pharmacologic

activities even in high doses... In normal subjects.. no side effects or 'doping' effects were

ever observed. Nor did Piracetam induce any sedation, tranquillization. locomotorstimulation or psychodysleptic symptomatology.."

Itil and co-workers reported in 1983 that "This investigation has confirmed that

[Pramiracetam] is a safe and well tolerated compound that can be given in dosages up to1500 mg without significant side effects. In fact side effects were reported more

frequently following both placebo and... phenelzine sulfate [an 'active control' drug] than

following any of the four doses evaluated."

After a major 12 week study with 272 Alzheimer and stroke dementia patients, Maina

and colleagues (1989) reported; "Thirty five minor side effects were recorded in 30patients on [Oxiracetam] and 33 unwanted effects in 26 patients on placebo, but none of

these was withdrawn from the study... As far as tolerability is concerned, clinical

assessments and laboratory evaluations did not reveal any difference between treatment

and placebo]."


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Moglia and co-workers (1986) concluded from a study of 43 organic syndrome patients

that "side effects during [Oxiracetam] treatment headache (3 cases), constipation (1 case),sleep disturbances (1 Side effects during placebo treatment were headache (2 case

constipation (1 case). The side effects spontaneously disappears required neither

medication nor treatment interruption. No significant [adverse] change in neurologicaland laboratory ex( lions, ECG and EEG could be detected at the end of treatment, both in

the [Oxiracetam] and in the placebo groups." When side effects are occasionally reported

in the clinical literature on Piracetam-nootropics. they are usually of a type to suggestslight over-stimulation, mainly headaches, agitation, insomnia and irritability. Yet other

studies find these same symptoms to be improved by Piracetam-nootropics when these

symptoms are pre-existing in the patients. Thus Itil (1986) notes, "...[ Piracetam] showed

more improvement than [Oxiracetam] in factors of paranoid delusion and agitation."Maina (1989) noted that "[Oxiracetam] does not act only by increasing arousal and

alertness. If this were the case, there would probably be a worsening of the IPSC-E

anxiety and tension [scores]. However, in our study there was actually a decrease in

anxiety and tension." Branconnier (1983), reporting on his group's study ofPramiracetam in 32 Alzheimer patients noted that after four weeks' treatment, there was a

significant decrease in anxiety-tension (P=.004) and hostility (P=.03), and a clean trendover placebo (P=.08) for Pramiracetam to improve existing sleep disturbances.

One potentially limiting factor in obtaining clinical benefit from Piracetam-nootropicshas been bought to light through the research of Mondadori (1992) on steroid interactions

with nootropics. Mondadori has shown that either deficient or excessive levels of adrenal

steroids can block the memory benefits of Piracetam-nootropics in animals. High doses

of either corticosterone or aldosterone abolish the memory enhancing benefits ofPiracetam-nootropics, while giving corticosterone or aldosterone to rats with no adrenals

restores the positive memory effects of nootropics. Mandadori also notes that cortisol

levels are frequently elevated in Alzheimer patients, which might explain the inconsistentresults obtained with nootropics in different Alzheimer clinical studies.

Nootropics - Synergy.

Since Piracetam-nootropics act (in part) through subtly amplifying neuronal electrical

excitability, they will tend to increase the activity of other drugs that modify neural

activity taken simultaneously. This in turn may increase both the positive action of theother drug, as well as possibly lead to the occasional nootropic over-stimulation effects.

Thus even caffeine may be sufficiently stimulating to bring on the "nootropic over

stimulation effect," especially in those very sensitive to caffeine. A key normal regulatorof neuronal sensitivity is the essential mineral, Magnesium. Dietary surveys in the

Western world routinely show most people to be at least marginally Mg deficient, with

many getting half or less of the recommended dietary Magnesium intake (Wester 1987).

Thus, the occasional over stimulation seen with Piracetam-nootropics may simply

evidence an undetected synaptic Magnesium deficiency, and Magnesium

supplementation may provide a natural remedy to minimize such over stimulation


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Piracetam-nootropics have been combined in many clinical and experimental situations

with other drugs, almost always with a positive, synergistic effect. Many clinical

experiments have demonstrated Piracetam and Oxiracetam to synergize with anti-epileptic medications, especially carbamazepine (Tegretol). A simultaneous enhancement

of the anti-epileptic drug's anti-seizure activity, combined with improvement or

elimination of the memory, alertness and comprehension cognitive deficits induced 1:anti-epileptic drug, have been found in multiple studies (Chaudhry Piracetam combined

with Pentoxifylline (a caffeine analogue cerebral flow enhancer) increased both "psycho-

intellectual performance measures of cerebral blood flow), significantly more than placeeither drug alone (Parnetti 1985).

Human and animal studies have shown increased benefit from combining Piracetam with

Choline, the raw material for neuronal production of be neurotransmitter Acetylcholine,as well as Phosphatidylcholine, a fluidizing component of cell membranes (Ferris 1982).

When Piracetam was combined with Hydergine in experiments with mice both brain

survival time and learning/ memory deficits induced poxia, it was noted that "The effect

of the combination was greater than the sum of the effects of the individual agents andindicates that synergism had occurred" (Berga 1986). A 1994 report looked at the synergy

between Piracetam and intensive speech therapy given to post-stroke aphasic patients; "Ingeneral, changes under [Piracetam] were 160% of the changes observed in patients

receiving placebo, while getting the same intensive speech therapy" (Di 1994).

Those wishing to get the maximum benefit from Piracetam-nootropics may to include in

their regimen nutrients known to enhance brain structure function in various ways.

The B-complex vitamins (including NADH), Lipoic Acid, CoQ10, Magnesium, andManganese are all essential to brain ATP energy production through the glyolytic and

citric acid cycles and the electron transport side chain.

DMAE is an excellent Choline precursor passes the blood brain barrier better than

Choline or Lecithin. Acetyl L-carnitine enhances the activity of the enzyme (Choline

Acetyl Transferase (CAT) that combines Acetyl groups with Choline to produceAcetylcholine.

Acetyl L-carnitine also renews the structure and energy generating power of aging

neuronal mitochondria. Phosphatidylserine is a natural neuronal membrane componentand stabilizer. Antioxidants, such as vitamins C and E, as well as Pycnogenol or grape

seed extract, may protect polyunsaturated fat-rich neuronal and mitochondrial membranes

from the damage caused by the inevitable release of large numbers of free radicals,generated through brain mitochondrial energy production.

Nootropics - their differences

Individual differences of action between Piracetam, Oxiracetam, Pramiracetam, and

Aniracetam are often subtle, and in many studies they show similar modes of action. One

intriguing benefit I have seen reported only for Pramiracetam, is its ability to increase


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goal directed and purposive behavior (Branconnier 1983). After trying Pramiracetam in

my regimen several years ago. I did notice an increase in my tendency to quickly take

care of routine household, auto and personal maintenance chores I habitually tended toignore, avoid or postpone.

I have taken Piracetam for eight years, Pramiracetam and Aniracetam for the past twoyears and Oxiracetam for about 9 months. During the past year, my lifelong severe

writer's block has gradually disappeared, and my writing output of the past year has

exceeded that of the previous decade. Some studies on dementia comparing Piracetamand Oxiracetam (the two most nearly identical racetams). have suggested that Oxiracetam

may be more effective in restoring the cognitive deficits of dementia (decreased memory,

concentration and alertness), while Piracetam may be more effective at normalizing the

emotional problems of dementia (agitation, tension-anxiety, hostility, insomnia,uncooperativeness).

Quantitatively, Piracetam is the least potent racetam, with clinical doses typically being

2400 mg to 4800 mg per day, occasionally even 6000 mg to I0,000 mg per day.

Oxiracetam is usually given 500 mg to 2400 mg per day. Aniracetam doses are typically750 mg to 1500mg per day, while Pramiracetam has shown benefit even at 150 mg to 500

mg per day, although 600 mg to 1500 mg per day is more typical.

Piracetam and Oxiracetam are highly water soluble (96-98%), while Aniracetam and

Pramiracetam are more fat soluble. Their lipophilicity may allow for less frequent dosing

(once or twice daily) with Aniracetam and Pramiracetam, compared to 3 to 4 doses a day

with Piracetam and Oxiracetam.

Aniracetam is favored by the Japanese, who have contributed much research on it. It is

widely used there as an agent to rapidly promote clarity of thought.

Nootropics - uses and conclusion

During the past 30 years, the Piracetam-nootropics have been used to treat an amazingly

broad range of human ailments and conditions, either or with other drugs, with moderate

to major benefit. Piracetam-nootropics have been used to treat various forms of dementia

and "organic brain syndrome." They have been used successfully to treat dyslexia,epilepsy and age-associated memory impairment. Piracetam-nootropics have successfully

treated post-concussional syndrome, vertigo, alcohol withdrawal, cerebrovascular

insufficiency and hypoxia. They have shown benefit in normalizing blood flow parametercreased platelet aggregation, increased red blood cell (RBC) deformability, decreased

adherence of damaged and sickle cell RBC's dothelium (blood cell lining) and increased

Prostacyclin (PG12) production and activity.

Yet the most exciting potential benefits of the racetams have yet seriously explored in

clinical studies.


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The racetams are cerebral homeostatic normalizers, neuroprotectants, cerebral metabolic

enhancers and brain integrative agents. They enhance brain energy, especially under

deficit condition: hypoxia, chemical toxicity or impaired cerebral microcirculation. Theypreserve, protect and enhance synaptic membrane and receptor structure and plasticity.

They enhance brain integration- horizontally, by increased coupling of the cerebralhemispheres; and vertically by enhancing cerebral connection with and tonic control of

the limbic system, through nootropics effects on the hippocampus- a major link between

cerebrum and system.

This vertical integration increase may help to integrate reason (cerebrum and emotion

(limbic system- sometimes called the "horse brain"). The increased tonic cortico-

subcortical control and regulation may prevent our limbic passions and desires from"running away with us" as in crimes of passion.

In middle aged and older individuals who do not yet suffer any specific neural malady or

major mental impairment, nootropics may not only slow down or postpone entropic brainaging, but they may even reverse mild neural/ mental decline. Thus a person at 50 might

be smarter, have better memory, quicker reflexes and greater vigilance and alertness thanwhen they were 40. The racetams may literally be safe and effective pharmacologic tools

to enhance, protect and optimize truly normal, fully human neuropsychological structures

and function, well into old age.

HOME to order

REFERENCES www.piracetam.com

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