Re: Re: Emailing: ias-piracetam

[Guest guest]

I believe all the nootropics are protective and healing to neural

structures. As I have stated already, since it is quite non-toxic and

inexpensive, you could start with very small doses to see how he responds.

I don't know of studies for ADD but it is known to help dyslexia and other

learning problems. Jaquelyn

[ ] Re: Emailing: ias-piracetam

Jaquelyn,

Thank you for sharing this article with us, this is very informative.

Our son reacted the one and only time I gave him Idebednone, his

heart raced and he became very agitated. He also could not handle

CoQ10, and is very sensitive to anything derived from soy. Since this

product is also a nootropic, could this also have the same effect on

our child. Just wondering if this is worth a try, he is on the higher

functioning end of the spectrum, with Add tendancies, and though he

reads, the comprehension is not what it should be, and as we have

been chelating he has remembered lots of things prior to being verbal

and has questioned things in the past often in the last year.

Obviously these things are stored in parts of the brain that seem to

turn on at times. It is wonderful to see the changes, and yet we

continue to progess and regress as we go through the process of

chelation. If this product were something to be considered with good

results, is this a product that a child would have to remain on for

ever? And just your thoughts, is this a product that can heal the

areas of the brain, and be discontinued after a certain amount of

time, Thanks Leah

- In @y..., " JMcCandless " <JMcCandless@p...> wrote:

> 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.

>

> HOME to order

>

>

> REFERENCES

www.piracetam.com

>

> 1. Gouliaev, A. & Senning, A, (1994) " Piracetam and

other structurally related nootropics " Brain Res Rev 19, 180-222.

>

> 2. Giurgea, C. (1973) " The 'Nootropic' approach to the

pharmacology of the integrative activity of the brain " Cond Reflex 8,

ID8-115.

>

> 3. Gamzu, E. et al (1989) " Recent developments in 2-

pyrrolidinone -containing nootropics " Drug Dev Res 18, 177-89.

>

> 4. a- Barbosa, M. et al (1991) " The effects of

Piracetam on lipofuscin of the rat cerebellar and hippocampa; neurons

after long-term alcohol treatment and withdrawal " Alcoholism:Clin Exp

Res 15, 834-38.

>

> 5. Skondia, V. & Kabes, J. (1985) " Piracetam in

alcoholic psychoses: a double-blind, crossover, placebo controlled

study " J Int Med Res 13, 185-87.

>

> 6. Stegink, A. (1972) " The clinical use of Piracetam, a

new nootropic drug " Arzneim-Forsch/Drug Res 22, 975-77.

>

> 7. Croisile, B. et al (1993) " Long-term and high dose

treatment of Alzheimer's disease " Neurol 43, 301-05.

>

> 8. DeBerdt, W. (1994) " Interaction between

psychological and pharmacological treatment in cognitive impairment "

Life Sci 55, 2057-66.

>

> 9.Herrschaft, H. (1989) " Effects and therapeutic

efficacy of nootropic drugs in acute and chronic cerebral ischaemia

in man " in Pharmacology of Cerebral Ischemia. J. Kriegelstein, ed.

CRC Press: Boca Raton, FL.

>

> 10. Platt, D. et al (1993) " On the efficacy of

Piracetam in geriatric patients with acute cerebral ischaemia: a

clinically controlled double blind study " Arch Gerontal Geriatr 16,

149-64.

>

> 11. Chouinard, G. et al (1983) " Piracetam in elderly

psychiatric patients with mild diffuse cerebral impairment "

Psychopharmacol 81, 100-06.

>

> 12. Wilsher, C. et al (1987) " Piracetam and dyslexia-

..effects on reading tests " J Clin Psychopharmacol 7, 230-37.

>

> 13. lkllal, P. et al (1986) " Evaluation of the efficacy

of Piracetam in treating information processing, reading and writing

disorders in dyslexic children " Int J Psychophysiol 4, 41-52.

>

> 14. Wilsher, C. (1986) " Effects of Piracetam on

development dyslexia " Int J Psychophysiol 4, 29-39.

>

> 15. Mondadori, C. & Schmutz, M. (1986) " Synergistic

effects of oxiracetam and Piracetam in combination with antiepileptic

drugs " Acta Neurol Scand 74 (suppi 109), 113-116.

>

> 16. Chaudhry, H. et al (1992) " Clinical use of

Piracetam in epileptic patients " Curr Ther Res 52, 355-60.

>

> 17. Mindus, P. et al (1976) " Piracetam-induced

improvement of mental performance " Acta Psychiat Scand 54, 150-60.

>

> 17A. Saletu, B. & Gruenberger, J. (1985) " Memory

dysfunction and vigilance: neurophysiological and

psychopharmacological aspects " Ann NY Acad Sci 444, 406-27.

>

> 18. Hakkrainen, H. & Hakamies, L. (1978) " Piracetam in

the treatment of post-concussional syndrome " Eur Neurol 17, 50-55.

>

> 19. Giurgea, C. & Salama, M. (1977) " Nootropic drugs "

Prog Neuro-Psychopharmac 1, 235-47.

>

> 20. Obeso, J. et al (1986) " Antimyoclonic action of

Piracetam " Clin Neuropharmacol 9, 58-64.

>

> 21. Moriau, M. et al (1993) " Treatment of the Raynaud's

phenomenon with Piracetam " Arzheim Forsch/Drug Res 43, 526-35.

>

> 22. Tacconi, M. & Wurtman, R. (1986) " Piracetam:

physiological disposition and mechanism of action " in Advances in

Neurology, vol. 43 S. Fahn et al, ed. Raven Press: NY.

>

> 23. Pepeu, G. & Spignoli, G. (1990) " Neurochemical

actions of 'nootropic drugs' " in Advances in Neurology vol. 51, R.

Wurtman et al, ed. Raven Press: NY.

>

> 24. s, K. (1993) " Efficacy of cerebroprotective

substances in the management of functional disorders induced by the

cytotoxic brain oedema-producing substance hexachlorophene " Nauyn-

Schiedeberg's Arch Pharmacol 347, 79-83.

>

> 25. Grau, M. et al, (1987) " Effect of Piracetam on

electrocorticogram and local cerebral glucose utilization in the rat "

Gen Pharmac 18, 205-II.

>

> 26. Schaffer, K. & Klausnitzer, W. (1988) " Randomized

placebo-controlled double-blind cross-over study on anti hyporidotic

effect of Piracetam using psychophysiological measures in healthy

volunteers " Arzneim Forsch/Drug Res 38, 288-91.

>

> 27. Mondadori, C. et al (1986) " Effects of oxiracetam

on learning and memory in animals: comparison with Piracetam " Clin

Neuropharmacol, 9, suppi 3, S27-S38.

>

> 28. Pepeu, G. & Spignoli, G. (1989) " Nootropic drugs an

dbrain cholinergic mechanisms " Prog Neuro-Psychopharmacol & Biol

Psychiat 13, S77-S88.

>

> 30. Bartus, R. et al (1981) " Profound effects of

combining choline and Piracetam on memory enhancement and cholinergic

function in aged rates " Neurobiol Aging 2, 105-11.

>

> 31. Platel, A. et al (1984) " Habituation of exploratory

activity in mice: effects of combinations of Piracetam and choline on

memory processes " Pharacol Biochem Behav 21, 209-12.

>

> 33. Ferns, S. et al (1982) " Combination

choline/Piracetam treatment of senile dementia " Psychopharmacol Bull

18, 96-98.

>

> 34. , R. et al (1984) " Comparison of therapeutic

response to long-term treatment with lecithin versus Piracetam plus

lecithin in patients with Alzheimer's disease " Psychopharacol Bull

20, 542-45.

>

> 35. son, M. et al (1987) " Reversal of scopalamine-

induced amnesia and alterations in energy metabolism by the nootropic

Piracetam " Brain Res 424, 1-9.

>

> 37. Pilch, H. & Mueller, W. (1988) " Piracetam elevates

muscarinic cholinergic receptor density in the frontal cortex of aged

by not of young mice " Psychopharmacol 94, 74-78.

>

> 38. Stoll, L. et al (1991) " Age-related deficits of

central muscarinic cholinergic receptor function in the mouse:

partial restoration by chronic Piracetam treatment " Neurobiol Aging

13, 39-44.

>

> 39. Branconnier, R. (1983) " The efficacy of the

cerebral metabolic enhancers in the treatment of senile dementia "

Psychopharmacol Bull 19, 212-19.

>

> 40. Nickolson, V. & Wolthuis, 0. (1976) " Effect of the

acquisition - enhancing drug Piracetam on rat cerebral energy

metabolism " Biochem Pharmacol 25, 2241-44.

>

> 41. Giurgea, C. & Moyersoons, F. (1972) " The

pharmacology of corticol evoked potentials " Arch Int Pharmacodyn Ther

199, 67-78.

>

> 42. Buresova, 0. & Bures, J. (1976) " Piracetam induced

facilitation of interhemispheric transfer of visual information in

rats " Psychopharmacologia 46, 93-102.

>

> 43. Dimond, S. et al (1979) " Some effects of Piracetam

on chronic schizophrenia " Psychopharmacol 64, 341-48.

>

> 44. Okuyama, S. & Aihara, H. (1988) " Actions of

nootropic drugs on transcallosal response of rats " Neuropharmacol 27,

67-72.

>

> 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.

>

> HOME to order

>

> other articles by South

> 1. Centrophenoxine, the brain booster

> 2. DHEA, the next generation

> 3. GHB, the elixir of life

> 4. Growth Hormone, the real fountain of youth

> 5. Idebenone the ultimate anti-aging drug?

> 6. South's personal supplement regime

> 7. Laetrile (B17) the answer to Cancer

> 8. NADH, the body and mind energizer

> 9. Nootropics, reviewing the smart drugs.

> 10. Pregnenolone the role of the " happy " hormone

> 11. Pyritinol, the oldest smart drug?

> 12. Resveratrol anti-heart, anti-cancer

> 13. SAMe for mood, liver, heart, and brain protection

> 14. Silver for internal and topical infections

> 15. Thymus Gland: its vital but overlooked role.

> 16. Tired of being tired?

> 17. Tryptophan, nature's answer to Prozac

> 18. Vinpocetine, superior cerebral enhancer and

protector.

> 19. Weight loss, the anti-aging way

> 20. 5-HTP Prozac's true alternative

>

>

>

>

>

>

>

>

>

>

>

>

>

[Guest guest]

Jacquelyn

Thank you for all your help. I am chelating the kids

this weekend. I plan to start the piracetam after we

finish with chelation this weekend. Should I start

with the choline first even though I bought the

twinlabs one. I have had good luck with twinlabs and

since they are so allergic I am scared to change.

Do you think it is neccessary to start with the

choline first or can I try the piracetam first then

add choline later? I also have the DMAE if I can do

that instead of choline even better since the

allergist has them on DMAE anyways. ( I have not

given it to them yet) Thanks for your advice.

Ana

-- JMcCandless <JMcCandless@...> wrote:

> I believe all the nootropics are protective and

> healing to neural

> structures. As I have stated already, since it is

> quite non-toxic and

> inexpensive, you could start with very small doses

> to see how he responds.

> I don't know of studies for ADD but it is known to

> help dyslexia and other

> learning problems. Jaquelyn

> [ ] Re: Emailing:

> ias-piracetam

>

>

> Jaquelyn,

> Thank you for sharing this article with us, this is

> very informative.

> Our son reacted the one and only time I gave him

> Idebednone, his

> heart raced and he became very agitated. He also

> could not handle

> CoQ10, and is very sensitive to anything derived

> from soy. Since this

> product is also a nootropic, could this also have

> the same effect on

> our child. Just wondering if this is worth a try, he

> is on the higher

> functioning end of the spectrum, with Add

> tendancies, and though he

> reads, the comprehension is not what it should be,

> and as we have

> been chelating he has remembered lots of things

> prior to being verbal

> and has questioned things in the past often in the

> last year.

> Obviously these things are stored in parts of the

> brain that seem to

> turn on at times. It is wonderful to see the

> changes, and yet we

> continue to progess and regress as we go through the

> process of

> chelation. If this product were something to be

> considered with good

> results, is this a product that a child would have

> to remain on for

> ever? And just your thoughts, is this a product that

> can heal the

> areas of the brain, and be discontinued after a

> certain amount of

> time, Thanks Leah

>

>

> - In @y..., " JMcCandless "

> <JMcCandless@p...> wrote:

> > 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)

>

=== message truncated ===

=====

Always

Ana Brushingham

__________________________________________________

[Guest guest]

I would start the DMAE first and make sure how they respond to that before

adding the piracetam. It can be quite activating to some kids, whereas

piracetam has no activating effects, and will not be useful without the

choline or DMAE.

[ ] Re: Emailing:

> > ias-piracetam

> >

> >

> > Jaquelyn,

> > Thank you for sharing this article with us, this is

> > very informative.

> > Our son reacted the one and only time I gave him

> > Idebednone, his

> > heart raced and he became very agitated. He also

> > could not handle

> > CoQ10, and is very sensitive to anything derived

> > from soy. Since this

> > product is also a nootropic, could this also have

> > the same effect on

> > our child. Just wondering if this is worth a try, he

> > is on the higher

> > functioning end of the spectrum, with Add

> > tendancies, and though he

> > reads, the comprehension is not what it should be,

> > and as we have

> > been chelating he has remembered lots of things

> > prior to being verbal

> > and has questioned things in the past often in the

> > last year.

> > Obviously these things are stored in parts of the

> > brain that seem to

> > turn on at times. It is wonderful to see the

> > changes, and yet we

> > continue to progess and regress as we go through the

> > process of

> > chelation. If this product were something to be

> > considered with good

> > results, is this a product that a child would have

> > to remain on for

> > ever? And just your thoughts, is this a product that

> > can heal the

> > areas of the brain, and be discontinued after a

> > certain amount of

> > time, Thanks Leah

> >

> >

> > - In @y..., " JMcCandless "

> > <JMcCandless@p...> wrote:

> > > 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)

> >

> === message truncated ===

>

>

> =====

> Always

>

> Ana Brushingham

>

> __________________________________________________

>