Emailing: ias-piracetam

December 28, 2001

piracetam (smart drug) article by South

Piracetam - the original nootropic

by South MA to order

Piracetam (technically known as 2-oxo-pyrrolidone) was developed in

the mid-1960's by UCB pharmaceutical company of Belgium. It was originally used

to treat motion sickness. (1) Between 1968 and 1972, however, there was an

explosion of Piracetam research which uncovered its ability to facilitate

learning, prevent amnesia induced by hypoxia and electroshock, and accelerate

electroencephalograph return to normal in hypoxic animals. (1) By 1972 700

papers were published on Piracetam. (1) Yet already by 1972 Piracetam's

pharmacologic uniqueness led C.E. Ciiurgea, UCB's principal Piracetam researcher

and research coordinator, to formulate an entirely new category of drugs to

describe Piracetam: the nootropic drug. (2)

According to Giurgea, nootropic drugs should have the following

characteristics:

1) they should enhance learning and memory.

2) They should enhance the resistance of learned behaviors/memories

to conditions which tend to disrupt them (e.g. electroconvulsive shock,

hypoxia).

3) They should protect the brain against various physical or

chemical injuries (e.g. barbiturates, scopalamine).

5) They should ''increase the efficacy of the tonic

cortical/subcortical control mechanisms. "

6) They should lack the usual pharmacology of other psychotropic

drugs (e.g. sedation, motor stimulation) and possess very few side effects and

extremely low toxicity. (3)

As research into Piracetam and other nootropics (e.g. pyritinol,

centrophenoxine, oxiracetam, idebenone) progressed over the past 30 years,

section 5) of Gilirgea's original definition has been gradually dropped by most

researchers. (3) Nonetheless, the nootropic drugs represent a unique class of

drugs, with their broad cognition enhancing, brain protecting and low toxicity/

side effect profiles. It is an interesting comment on the AMA/FDA stranglehold

on American medicine that as of January 2001, not a single nootropic drug has

ever been given FDA approval for use in the U.S.

Piracetam has been used experimentally or clinically to treat a wide

range of diseases and conditions, primarily in Europe. (Although much of the

research on Piracetam has been published in English, a large amount of Piracetam

research has been published in German, French, Italian, and Russian.)

Piracetam has been used successfully to treat alcoholisrn/ alcohol

withdrawal syndrome in animals and man. (4,5,19) Piracetam has brought

improvement, or slowed deterioration, in " senile involution " dementia and

Alzheimer's disease. (6,7) Piracetam has improved recovery from aphasia (speech

impairment) after stroke. (8) Piracetam has restored various functions (use of

limbs, speech, EEC, slate of consciousness) in people suffering from acute and

chronic cerebral ischemia (decreased brain blood flow). (9,10) Piracetam has

improved alertness, co-operation, socialization, and IQ in elderly psychiatric

patients suffering from " mild diffuse cerebral impairment. " (11)

Piracetam has increased reading comprehension and accuracy in

dyslexic children. (8,12) Piracetam increased memory and verbal learning in

dyslexic children, as well as speed and accuracy of reading, writing and

spelling. (13,14) Piracetam potentiated the anticonvulsant action of various

anti-epileptic drugs in both animals and man, while also eliminating cognitive

deficits induced by anti-epileptic drugs in humans. (15,16) Piracetam has

improved mental performance in " aging, nondeteriorated individuals " suffering

only from " middle-aged forgetfulness. " (17) Elderly outpatients suffering from

" age-associated memory impairment " given Piracetam showed significant

improvement in memory consolidation and recall. (8) Piracetam reversed typical

EEC slowing associated with " normal " and pathological human aging, increasing

alpha and beta (fast) electroencephalograph activity and reducing delta and

theta (slow) electroencephalograph activity, while simultaneously increasing

vigilance, attention and memory. (17A)

Piracetam reduced the severity and occurrence of major symptoms of

" post-concussional syndrome, " such as headache, vertigo, fatigue and decreased

alertness (18), while it also improved the state of consciousness in deeply

comatose hospitalized patients following head injuries. (19) Piracetam has

successfully treated motion sickness and vertigo. (1) Piracetam " is one of the

best available drugs for treating myoclonus [severe muscle spasms] of cortical

origin. " (20) Piracetam has successfully treated Raynaud's syndrome (severe

vasospasm in hands and/or feet), with " a rapid and marked improvement. The

efficacy of Piracetam has been maintained in several patients already followed

for 2-3 years. " (21) Piracetam has been used to inhibit sickle cell anemia,

both clinically and experimentally. (11) Piracetam has improved Parkinson's

disease, and may synergize with standard L-dopa treatment. (1) A key part of

Piracetam's specialness is its amazing lack of toxicity. Piracetam has been

studied in a wide range of animals: goldfish, mice, rats, guinea pigs, rabbits,

cats, clogs, marmosets, monkeys, and humans. (1,19) In acute toxicity studies

that attempted to determine Piracetam's " LD50 " (the lethal dose which kills 50%

of test animals), Piracetam failed to achieve an LD50 when given to rats

intravenously at 8gm/kg bodyweight. (1) Similarly, oral LD50 studies in mice,

rats, and dogs given l0gm Piracetam/kg bodyweight also produced no LD50! (1)

This would he mathematically equivalent to giving a 70 kg (154 pound) person

700gm (1.54 pounds) of Piracetam! As Tacconi and Wurtman note, ''Piracetam

apparently is virtually non-toxic. Rats treated chronically with 100 to 1,000

mg/kg orally for 6 months and dogs treated with as much as l0g/kg orally for 1

year did not show any toxic effect. No teratogenic (birth deformity) effects

were found, nor was behavioral tolerance noted. " (22) Thus, Piracetam must be

considered one of the toxicologically safest drugs ever developed.

From the earliest days of Piracetam research, the ability of

Piracetam to partly or completely prevent or reverse the toxic action of a broad

array of chemicals and conditions has been repeatedly demonstrated.

a-Barbosa and colleagues discovered that long-term (12 month)

alcohol-feeding to rats significantly increased formation of lipofuscin (an

age-related waste pigment) in brain cells. Giving high dose Piracetam to the

alcohol-fed rats reduced their lipofuscin levels significantly below both the

control and alcohol/no Piracetam rats' levels. (4) Piracetam antagonized the

normally lethal neuromuscular blockade (which halts breathing) induced by mice

by intravenous hemicholinium-3 (HC-3) (23), and Piracetam also blocked the

lethal neuromuscular blockade induced in cats by d-tubocurarine. (1) Piracetam

reversed learning and memory deficits in mice caused by the anti-cholinergic

substance, HC-3. (23) When mice were given oxydipentonilim, a short-acting

curare-like agent which halts breathing, at a dose sufficient to kill 90% of one

group and 100% of another group of placebo-treated controls, the two groups of

Piracetam-treated mice had a 90% and 100% survival rate. (19)

Rapid synthesis of new protein in brain cells is required for memory

formation. Piracetam has ameliorated the amnesia induced by rodents by

cycloheximide, a protein synthesis inhibitor. (1)

Hexachlorophene is a toxic chemical that induces edema, membrane

damage, and increased sodium /decreased potassium in brain cells.

(Hexachlorophene was used in shampoos, soaps and other personal care products

until about a decade ago.) Rats were fed hexachlorophene orally for 3 weeks,

then given Piracetam or one of 5 other drugs by injection for 6 days.

Hexachlorophene seriously disrupted the rats' ability to navigate a horizontal

ladder without frequently falling off the rungs. Piracetam reduced the fall

rate 75% compared to saline-injected controls on the first day of treatment.

None of the other drugs came close to that improvement. (24)

Piracetam increases the survival rate of rats subjected to severe

hypoxia. (1,25) When mice, rats and rabbits have been put under diverse

experimental hypoxic (low oxygen) conditions, Piracetam has acted to attenuate

or reverse the hypoxia-induced amnesia and learning difficulties, while speeding

up post-hypoxic recovery time and reducing time to renormalize the EEC}.

(1,2,25) When a single 2400mg dose of Piracetam was given to humans tested

under 10.5% oxygen (equivalent to 5300m./17,000 ft. altitude), eye movement

reflexes were enhanced, while breathing rate and choice reaction time were

reduced by Piracetam. (26)

Electro convulsive shock (electro convulsive shock) is a powerful

disruptor of learning and memory. When a group of rats were taught to avoid a

dark cubicle within their cage there was 100% retention of the learned behavior

24 hours later.

Giving a maximal electro convulsive shock right after learning

caused the learning-retention rate to drop lo 20% 24 hours later in the control

group, while Piracetam-treated electro convulsive shock rats still had a 100%

retention of the avoidance behavior 24 hours later. (2) Other experiments with

mice and rats show Piracetam's ability to attenuate or reverse electro

convulsive shock-induced amnesia. (19.27)

When given the fast acting barbiturate secobarbital, combined with

Piracetam injected 1 hour before the secobarbital, 10 of 10 rabbits survived,

with only minimal abnormalities in their electroencephalograph records. The

electroencephalograph records the electrical activity of large groups of

corticol neurons, and also reflects cerebral oxygen/glucose metabolism and blood

flow. (25)

Only 3 of 10 rabbits given) secobarbital with saline injection

survived, and most of that groups' electroencephalograph records showed rapid

onset of electrical silence, followed quickly by death. When secobarbital was

given to rabbits combined with oral Piracetam, 8 of 9 survived, with only 3 of 9

saline-fed controls surviving. The electroencephalograph records of both

groups were similar to those of the rabbits given i.v. Piracetam and saline.

(28)

By the 1980s neuroscientists had discovered that brain cholinergic

neural networks, especially in the cortex and hippocampus, are intimately

involved in memory and learning. Normal and pathological brain aging, as well

as Alzheimer's-type dementia were also discovered lo involve degeneration of

both the structure and function of cholinergic nerves, with consequent

impairment of memory and learning ability. (29)

During this same period a growing body of evidence began to show

that Piracetam works in part through a multimodal cholinergic activity. Studies

with both aged rats and humans which combined Piracetam with either choline or

lecithin (phosphatidyl choline), found radically enhanced learning abilities in

rats, and produced significant improvement in memory in Alzheimer's patients.

(30-35)

Yet giving choline or lecithin alone (they are precursors for the

neurotransmitter acetylcholine) in these studies provided little or no benefit,

while Piracetam alone provided only modest benefit.

Animal research has also shown that Piracetam increases

high-affinity choline uptake, a process that occurs in cholinergic nerve endings

which facilitates acetylcholine formation. (23,29) " High-affinity choline uptake

rate has been shown to be directly coupled to the impulse flow through the

cholinergic nerve endings and it is a good indicator of acetylcholine

utilization nootropic drugs (including Piracetam) activate brain cholinergic

neurons " (29) HC-3 induces both amnesia and death through blocking high-affinity

choline uptake in the brain an din peripheral nerves that control breathing.

Since Piracetam blocks HC-3 asphyxiation death and amnesia, this is further

evidence of Piracetam's pro-high-affinity choline uptake actions. (23,29)

Scopalamine is a drug that blockades acetylcholine receptors and

disrupts energy metabolism in cholinergic nerves. When rats were given

Scopalamine, it prevented the learning of a passive avoidance task, and reduced

glucose utilization in key cholinergic brain areas. When rats given Scopalamine

were pretreated with 100/kg Piracetam, their learning performance became almost

identical to rats not given Scopalamine. (36) The Piracetam treatment also

reduced the Scopalamine depression of glucose-energy metabolism in the rats'

hippocampus and anterior cingulate cortex, key areas of nerve damage and glucose

metabolism reduction in Alzheimer's disease.(36)

German researchers added to the picture of Piracetam's cholinergic

effects in 1988 and 1991. Treatment for 2 weeks with high dose oral Piracetam

in aged mice elevated the density of frontal cortex acetylcholine receptors

30-40%, restoring the levels to those of healthy young mice. A similar decline

in cortex acetylcholine receptors occurs in " normal " aging in humans. (37) The

same group of researchers then discovered that there is a serious decline in the

functional activity of acetylcholine receptors in aged mice; with many receptors

becoming " desensitized " and inactive. Oral treatment with high dose Piracetam

also partially restored the activity of acetylcholine cortex nerves, as measured

by the release of their " second messenger, " inositol-1-phosphate. (38)

Glutamic acid (glutamate) is the chief excitatory neurotransmitter

in the mammalian brain. Piracetam has little affinity for glutamate (glutamate)

receptors, yet it does have various effects on glutamate neurotransmission. One

subtype of glutamate receptor is the AMPA receptor. Micromolar amounts [levels

which are achieved through oral Piracetam intake] of Piracetam enhance the

efficacy of AMPA-induced calcium influx [which " excites " nerve cells to fire] in

cerebeller [brain] cells. Piracetam also increases the maximal density of [AMPA

glutamate receptors] in synaptic membranes from rat cortex due to the

recruitment of a subset of AMPA receptors which do not normally contribute to

synaptic transmission. " (1) Further support for involvement of the glutamate

system in Piracetam's action is provided by a Chinese study which showed that

the memory improving properties of Piracetam can be inhibited by ketamine, an

NMDA (another major subtype of glutamate receptor) channel blocker. (1)

Furthermore, high dose injected Piracetam decreases mouse brain glutamate

content and the glutamate/GABA ratio, indicating an increase in excitatory nerve

activity (1)

At micrornolar levels, Piracetam potentiates potassium-induced

release of glutamate from rat hippocampal nerves. (1)

Given that acetylcholine and glutamate are two of the most central

" activating " neurotransmitters and the facilatory effects of

acetylcholine/glutamate neural systems on alertness, focus, attention, memory

and learning. Piracetam's effects on acetylcholine/glutamate neurotransmission

must he presumed to play a major role in its demonstrated ability to improve

mental performance and memory. Although Piracetam is generally reported to have

minimal or no side effects, it is interesting to note that Piracetam's

occasionally reported side effects of anxiety, insomnia, agitation, irritability

and tremor (18) are identical to the symptoms of excess acetylcholine/glutamate

neuroactivity.

In spite of the many and diverse neurological/psychological effects

Piracetam has shown in human, animal and cell studies, Piracetam is generally

NOT considered to he a significant agonist (direct activator) or inhibitor of

the synaptic action of most neurotransmitters. Thus, major nootropic

researchers Pepeu and Spignoli report that " the pyrrolidinone derivatives

[Piracetam and other racetams] show little or no affinity for central nervous

system receptors for dopamine, glutamate; serotonin, GABA or benzodiazepine. "

(23) They also note however that " a number of investigations on the

electrophysiological actions of nootropic drugs have been carried out. Taken

together, these findings indicate that the nootropic drugs of the

[Piracetam-type] enhance neuronal excitability [electrical activity] within

specific neuronal pathways. " (23)

Grau and colleagues note that " there exist papers giving data of

bioelectric activity as affected by Piracetam, and suggesting that it acts as a

non-specific activator of the excitability. [i.e. brain electrical activity]

thus optimizing the functional state of the brain. " (25)

Gouliaev and Senning similarly state " we think that the racetams

exert their effect on some species [of molecule] present in the cell membrane of

all excitable cells, i.e. the ion carriers or ion channels and that they somehow

accomplish an increase in the excitatory (electrical) 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

than possessing any [neurotransmitter-like] 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 neuronal sensitivity toward

stimulation. " (1)

Thus Piracetam is NOT prone to the often serious side effects of

drugs which directly amplify or inhibit neurotransmitter action e.g. MAO

inhibitors; Prozac® style " selective serotonin reuptake inhibitors " , tricyclic

antidepressants, amphetamines, Ritalin®, benzodiazepines (Valium), etc.

A key finding on Piracetam in various studies is its ability to

enhance brain energy, especially under deficit conditions. Energy (ATP) is

critical to the brain's very survival; it typically uses 15-20% of the body's

total ATP production, while weighing only 2-3% or so of bodyweight. Brain cells

must produce all their own ATP from glucose (sugar) and oxygen - they cannot

" borrow " ATP from other cells. Branconnier has observed that " evidence from

studies of cerebral blood flow, oxygen uptake and glucose utilization have shown

that brain carbohydrate metabolism is impaired in a variety of dementias and

that the degree of reduction in brain carbohydrate metabolism is correlated with

the severity of the dementia. " (39) In a 1987 study, Grau and co-workers gave

saline or Piracetam i.v. to rats who were also fed i.v. radioactive

deoxygilicose to help measure brain metabolism. Compared to saline controls,

Piracetam rats had a 22% increase in whole brain glucose metabolism, while the

increase in 12 different brain regions ranged from L6 to 28%. (25) This

increase in brain energy metabolism occurred under normal oxygen conditions.

In 1976 Nickolson and Wolthuis discovered that Piracetam increased

the activity of adenylate kinase in rat brain. Adenylate kinase is a key energy

metabolism enzyme that converts ADP into ATP and AMP and vice versa. It comes

into play especially when low brain oxygen begins to reduce mitochondrial ATP

production. As existing ATP is used up, ADP is formed. Under the influence of

adenylate kinase, 2ADP becomes ATP plus AMP. Thus Piracetam-activated adenylate

kinase can slow down the drop in ATP in oxygen-compromised brains. This helps

explain Piracetam's ability to prevent abnormalities in animals subjected to

hypoxia or barbiturates. When oxygen levels return toward normal, adenylate

kinase can convert AMP into ADP, which can then be used in the reactivated

mitochondria to make more ATP. This accounts for the ability of Piracetam to

speed up recovery from hypoxia seen in animal studies. (40)

In their 1987 study with rats, Piercey and colleagues found that

Piracetam could restore scopalamine depressed energy metabolism modestly in many

brain areas, and significantly in the hippocampus and anterior cingulate cortex.

(36)

Piracetam has also been shown to increase synthesis and turnover of

cytochrome b5, a key component of the electron transport chain, wherein most ATP

energy is produced in mitochondria. (22) Piracetam also increases permeability

of mitochondrial membranes for certain intermediaries of the Krebs cycle, a

further plus for brain ATP production. (25) In his 1989 paper on cerebral

ischemia in humans, Herrschaft notes that the Herman Federal Health Office has

conducted controlled studies that indicate a " 'significant positive " effect of

Piracetam (4.8 - 6gm/day) to increase cerebral blood flow, cerebral oxygen usage

metabolic rate and cerebral glucose metabolic rate in chronic impaired human

brain function - i.e. multi-infarct dementia, senile dementia of the Alzheimer

type, and pseudo-dementia. (9)

The cerebral cortex in humans and animals is divided into two

hemispheres, the left and right cortex. In most humans the left hemisphere

(which controls the right side of the body) is the language center, as well as

the dominant hemisphere. The left cortex will tend to be logical, analytical,

linguistic and sequential in its information processing, while the right cortex

will usually be intuitive, holistic, picture-oriented and simultaneous in its

information processing.

Research has shown that most people favor one hemisphere over the

other, with the dominant hemisphere being more electrically active and the

non-dominant hemisphere relatively more electrically silent, when a person is

being tested or asked to solve problems or respond to information. The two

cortical hemispheres are linked by a bundle of nerve fibers: the corpus callosum

and the anterior commisure. In theory these two structures should unite the

function of the two hemispheres. In practice they act more like a wall

separating them.

From a neurological perspective, the cerebral basis for a

well-functioning mind would he the effective, complementary, simultaneous

integrated function of both cortical hemispheres, with neither hemisphere being

automatically or permanently dominant. This in turn would require the corpus

callosum and cerebral commisure to optimize information flow between the two

hemispheres. Research has shown Piracetam to facilitate such inter-cerebral

information transfer-indeed, it's part of the definition of a " nootropic drug. "

Giurgea and Moyersoons reported in 1972 that Piracetam increased by

25 to 100% the transcallosal evoked responses elicited in cats by stimulation of

one hemisphere and recorded from a symmetrical region of the other hemisphere.

(41) Buresova and Bures, in a complex series of experiments involving monocular

(one-eye) learning in rats, demonstrated that " Piracetarn enhances

transcommisural encoding mechanisms and some forms of inter-hemispheric

transfer. " (42)

Dimond and co-workers used a technique called " dichotic listening "

to verily 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 to the opposite

side of the brain, most people will recall more of the words presented to the

right ear than the left ear. This occurs because 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 center indirectly, by crossing the

corpus callosum from the right cortex. Dimond's research with healthy young

volunteers showed that Piracetam significantly improved left ear word recall,

indicating Piracetam increased interhemispheric transfer. (43)

Okuyama and Aihara tested the effect of aniracetam, a Piracetam

analog, 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 cortical hemisphere. The

researchers reported that " the present results indicate that

Piracetam...increased the amplitude of the negative wave, thereby facilitating

inter-hemispheric transfer. Thus, it is considered that the functional increase

in interhemispheric neuro-transmission by nootropic drugs may be related to the

improvement of the cognitive function [that nootropics such as Piracetam and

aniracetam promote]. " (44)

The notable absence of biochemical, physiological, neurological or

psychological side effects, even with high dose and/or long-term Piracetam use,

is routinely attested to in the Piracetam literature. Thus in their 1977 review

Giurgea and Salama point out: " Piracetam is devoid of usual 'routine'

pharmacologic activities [negative side effects] even in high doses. In normal

subjects no side effects or 'doping' effects were ever observed. Nor did

Piracetam induce any sedation, tranquilization, locomotor stimulation or

psychodysleptic symptomatology. " (19) Wilshen and colleagues, in their study

on 225 dyslexic children, note that " Piracetam was well tolerated, with no

serious adverse clinical or laboratory effects reported. " (12) In this

particular study (as in many others), the incidence of (mild) side effects was

higher in the placebo group than in the Piracetam group! In his 1972 8 week

study on 196 patients with " senile involution " dementia, Stegink reported that

" No adverse side effects of Piracetam [2.4gm/day] were reported. " (6) In their

study of 30 patients treated for one year with 8gm Piracetam/day, Croisile and

colleagues observed that " Few side effects occurred during the course of the

study - one case of constipation in the Piracetam group.... Piracetam had no

effect on vital signs, and routine tests of renal, hepatic, and hematological

functions remained normal. No significant changes in weight, heart rate, or

blood pressure occurred.... " (7)

Yet as noted in the section on glutamate, because Piracetam is a

cholinergic/glutamatergic activator, there is the potential for symptoms related

to cholinergic/glutamatergic excess to occur, especially in those unusually

sensitive to Piracetam. Such symptoms - anxiety, insomnia, irritability,

headache, agitation, nervousness, and tremor - are occasionally reported in some

people taking Piracetam. (11,18) Reducing dosage, or taking magnesium

supplements (300-500mg/day), which reduce neural activity, will frequently

alleviate such " overstimulation " effects. Persons consuming large amounts of

MSG (monosodium glutamate) and/or aspartame in their diet should be cautious in

using Piracetam, as should those who are highly sensitive to MSG-laden food (the

" Chinese restaurant syndrome " ). Caffeine also potentiates Piracetam's effects,

as do other nootropics such as deprenyl, idebenone, vinpocetine, and

centrophenoxine, and it may be necessary to use Piracetam in a lower dosage

range if also using any of these drugs regularly. Those wishing to augment

Piracetam's cholinergic effects may wish to combine it with cyprodenate or

centrophenoxine, which are much more powerful acetylcholine enhancers than

choline or lecithin.

B complex vitamins, NADH, lipoic acid, CoQ10, or idebenone, and

magnesium will enhance Piracetam's brain energy effects. In the clinical

literature on Piracetam, dosages have ranged from 2.4 gm/day (6,11) up to

8gm/day (7,21), continued for years (7,21). Piracetam has a relatively short

half-life in the blood, although there is some short-term bioaccumulation in the

brain. (1,22) Piracetam is therefore usually taken 3-4 times daily. 1.6 gm, 3

times daily, or 1.2 gm 3-4 times daily is a fairly typical Piracetam dosage,

although some people report noticeable improvement in memory and cognition from

just 1.2 gm twice daily.

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REFERENCES www.piracetam.com

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The above article is copyrighted and may not be copied without the

written permission of International Antiaging Systems, Les Autelets Suite A,

Sark GY9 0SF, Channel Islands, UK.

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