Piracetam research and benefits

There seems to be a lot of negativity directed towards nootropics including piracetam even on this board. A few negative individualys have claimed there are no benefits from taking this drug. In this thread I will attempt to present some of the research and information on the subject. Feel free to add your own.

http://sulcus.berkel...ripts/_774.html

Piracetam is a psychoactive drug widely used in European and Asian countries for its ability to augment cognitive, learning, and memory abilities, to decrease oxidative and hypoxic stress and to stabilize cells in the blood and CNS (central nervous system). With no known toxicity or addictive properties documented in the past two decades, the drug has been used overseas to address numerous neurological and physical disorders including: myoclonus, Down's syndrome, sickle cell anemia, dyslexia, senile dementia, and others. However, as piracetam is not currently approved by the FDA (Federal Drug Administration) or manufactured by any U.S. pharmaceutical companies, there is very little clinical information and research in the United States. The goal of this paper is to introduce the study of nootropic drugs, summarize current theories on their mechanism of action, and describe relevant applications of piracetam as documented in recent international and domestic research.

Piracetam is among the most popular of the smart drugs due to its reported efficacy in enhancing cognitive ability and alleviating various ailments among normal and disease-afflicted individuals. The exact mechanism of action for piracetam is still undetermined but believed to affect many physiological systems simultaneously.

Recent human research has finally started to shed light on the mechanism(s) and effects of piracetam. Elderly psychiatric patients have been administered piracetam for years to improve memory (8) and treat Alzheimer's disease and multi-farct dementia. The synergistic effect of choline with piracetam was not observed in the elderly (9) but PET (positron emission tomography) experiments have verified improved glucose metabolism in piracetam-using AD patients. (10) These studies and others have collectively led scientists toward a cholinergic mechanism of action and/or influence on ion transport..

Although the exact details of piracetam metabolism haven't been deduced, a recent review of piracetam and other structurally related nootropics indicate piracetam potentiates an increase of sodium/calcium influx or decrease in potassium efflux during neurotransmission. Many common psychoactive pathways such as muscarinic, dopaminergic, GABAergic receptors show no affinity when piracetam is used.



"The piracetam-like nootropics are capable of achieving reversal of amnesia induced by, e.g., scopolamine, electroconvulsive shock and hypoxia. Protection against barbiturate intoxication is observed and some benefit in clinical studies with patients suffering from mild to moderate degrees of dementia has been demonstrated. No affinity for the alpha 1-, alpha 2-, beta-, muscarinic, 5-hydroxytryptamine-, dopamine, adenosine-A1-, mu-opiate, gamma-aminobutyric acid (GABA) (except for nefiracetam (GABAA)), benzodiazepine and glutamate receptors has been found. The racetams possess a very low toxicity and lack serious side effects. Increased turnover of different neurotransmitters has been observed as well as other biochemical findings, e.g., inhibition of enzymes such as prolylendopeptidase. So far, no generally accepted mechanism of action has, however, emerged. We believe that the effect of the racetams is due to a potentiation of already present neurotransmission and that much evidence points in the direction of a modulated ion flux by, e.g., potentiated calcium influx through non-L-type voltage-dependent calcium channels, potentiated sodium influx through alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor gated channels or voltage-dependent channels or decreases in potassium efflux. Effects on carrier mediated ion transport are also possible." (11)

For nearly three decades, piracetam has exhibited extremely low toxicity in research with humans. Although extremely large doses of piracetam have been administered to humans in clinical studies, average daily doses for normal people range between 800-4000 milligrams, which is a rather large amount for a psychoactive substance.



"The classical measure of drug toxicity, the LD-50 (the dose causing death for 500f test animals), is not applicable; standard dosing methods (oral, intravenous injection, intraperitoneal injection) cannot deliver enough piracetam to kill laboratory animals. Doses of greater than 20g/day have been given to people suffering from myoclonic seizure disorders, without serious side effects [Karacostas et al., 1993]. The recommended dose of piracetam for infants with myoclonic seizures is 10-20g/day (approximately 1-2 rounded tablespoons), a phenomenally high dose by normal drug standards." (13)



The documented efficacy and extremely low toxicity of piracetam also make it a lucrative nootropic for private industry, especially the various analogues under development such as vinpocetine, aniracetam, pramiracetam, oxiracetam, and others. These drugs have been under intensive research and development during this past decade. The piracetam analogues also demonstrate the low toxicity associated with nootropics and in some cases, even greater efficacy.

Alarmist opinion regarding the safety of nootropics has quieted over the past few years as piracetam has been acknowledged as the drug of choice for treating myoclonus, a seizure-like condition characterized by uncontrollable muscle twitching or jerking. (14) A nationwide multi-institution study in Japan found:



"Piracetam was effective in myoclonus, especially that of cortical origin, in both monotherapy and polytherapy. Piracetam also had positive benefits on gait ataxia and convulsions but not on dysarthria, and feeding and handwriting improved much more significantly. Psychologically significant improvement was seen in decreased motivation, sleep disturbance, attention deficit, and depression, all of which might be possibly secondary benefits associated with improvement of myoclonus. There was no positive correlation between clinical and electrophysiological improvement. Tolerance was good, and side effects were transient. However, hemtological abnormalities observed in at least two patients in the present study should be kept in mind when relatively large doses of piracetam are administered, especially in combination with other antimyoclonic drugs." (15)



These desirable effects have been associated with alterations in lipid membrane fluidity within the brain. Membrane fluidity is an indicator of permeability, influenced by many factors such as cholesterol content, fatty acid profile, and degree of lipid peroxidation. Higher levels of cholesterol content, fatty acid saturation (hydrogenation) and peroxidation (form of oxidative stress) cause lipid membranes to become rigid and impermeable. Piracetam has already been shown to alleviate oxidative stress caused by excess hydrogen peroxide and increase membrane fluidity in the brain.



"In vitro preincubation of brain membranes of aged mice with piracetam (0.1-1.0 mmol/L) enhanced membrane fluidity, as indicated by decreased anisotropy of the membrane-bound fluorescence probe 1,6-diphenyl-1,3,5-hexatriene (DPH). Piracetam had similar in vitro effects on brain membranes of aged rats and humans, but it did not alter brain membrane fluidity in young mice. Chronic treatment of young and aged rats with piracetam (300 mg/kg once daily) significantly increased membrane fluidity in some brain regions of the aged animals, but had no measurable effect on membrane fluidity in the young rats. The same treatment significantly improved active avoidance learning in the aged rats only. It is suggested that some of the pharmacological properties of piracetam can be explained by its effects on membrane fluidity." (16)



Hypoxia (a condition of low oxygen levels in the tissues caused by hypobaric conditions, decreased oxygen-carrying capacity of the blood, and impaired circulation) has been treated with piracetam because of its protective effects from lipid peroxidation.

Medical applications are being researched in Russia including improvement of metabolic and hormonal indices disturbed by collateral damage from heart disease (17) and treatment of hypoxia-related damage from prostaglandin synthesis (powerful hormones created by oxygen free radicals and polyunsaturated fatty acids). (18) Vast amounts of anecdotal evidence among athletes, academics, elderly people, and parents with children afflicted by DS (developmental delays in closing of heart muscle wall cause de-oxygenated blood to circulate resulting in chronic hypoxia) support piracetam's usefulness in treating hypoxia-related symptoms.

However, the treatment of Down's Syndrome remains the center of controversy regarding the applications of piracetam. A recent presentation at by the Pediatric Academic Societies in San Francisco included a study reporting that piracetam does not enhance cognitive abilities in moderate to high-functioning 7-13 year-old children with DS.



"Piracetam, a drug reported to enhance cognitive performance in many neurobehavioural conditions, has become popular in the treatment of children with Down Syndrome (DS). However, reports of its efficacy in DS have been anecdotal, not from evidence-based studies. Some caregivers have noted no effect of piracetam, while others claim substantial improvement in cognitive functioning. To address the need for objective analysis, we conducted a double-blind placebo-controlled crossover study assessing the cognitive and behavioral effects of piracetam in children with DS... Piracetam did not show significant effects over placebo on any outcome measure (ANCOVA, covariate was age at baseline). All significant interactions (p's < 0.05) with drug order or the covariate were examined further to ensure drug effects were not being masked. That analysis did not alter the results. Piracetam administration was associated with CNS stimulatory effects: aggressiveness (n=4), agitation (n =3), sexual arousal, (including masturbation in public, n=2), irritability (n=1), and poor sleep (n=1). Conclusion. Piracetam has received a great deal of attention in the popular press purporting its efficacy in improving cognitive function in children with Down Syndrome. In this study, we were unable to substantiate these claims, even at doses associated with adverse effects. Neither cognitive nor behavioural measures demonstrated improvement under piracetam. Due to the serious adverse effects, it is unlikely that larger doses can be tolerated."(19)

Fortunately, because nootropics exhibit favorable activity in cognitive enhancement and are relatively safe, piracetam has fared reasonably well within this tumultuous context of science and politics. With orphan drug status as a treatment for myoclonus, and a study of piracetam and Ts65dn mice (an animal model for trisomy 21) currently underway at John Hopkins, U.S. research is finally starting to pick up speed. A new study assessing the feasibility of piracetam and school-aged children has gained attention at Kennedy-Kriger Institute in an effort to raise awareness for the possible application of piracetam and possibly acquire funding for a large-scale study by the FDA. In addition, with adequate media coverage and an American manufacturer, the expected profitability of piracetam may eventually speed the FDA approval process, illuminating the future of piracetam and its users in the United States.

http://www.altonweb....e=piraceab.html

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GVS-111 prevents oxidative damage and apoptosis in normal and Down's syndrome human cortical neurons

Pelsman A, Hoyo-Vadillo C, Gudasheva TA, Seredenin SB, Ostrovskaya RU, Busciglio J
Department of Neuroscience, University of Connecticut Health Center, 263 Farmington Avenue, CT 06030, USA

The neuroprotective activity of a novel N-acylprolyl-containing dipeptide analog of the nootropic 2-oxo-1-pyrrolidine acetamide (Piracetam) designated as GVS-111 (DVD-111/Noopept) was tested in two in vitro models of neuronal degeneration mediated by oxidative stress: normal human cortical neurons treated with H2O2, and Down's syndrome (DS) cortical neurons. Incubation of normal cortical neurons with 50 microM H2O2 for 1h resulted in morphological and structural changes consistent with neuronal apoptosis and in the degeneration of more than 60% of the neurons present in the culture. GVS-111 significantly increased neuronal survival after H2O2-treatment displaying a dose-dependent neuroprotective activity from 10nM to 100 microM, and an IC(50) value of 1.21±0.07 microM. GVS-111 inhibited the accumulation of intracellular free radicals and lipid peroxidation damage in neurons treated with H2O2 or FeSO4, suggesting an antioxidant mechanism of action. GVS-111 exhibited significantly higher neuroprotection compared to the standard cognition enhancer Piracetam, or to the antioxidants Vitamin E, propyl gallate and N-tert-butyl-2-sulpho-phenylnitrone (s-PBN). In DS cortical cultures, chronic treatment with GVS-111 significantly reduced the appearance of degenerative changes and enhanced neuronal survival. The results suggest that the neuroprotective effect of GVS-111 against oxidative damage and its potential nootropic activity may present a valuable therapeutic combination for the treatment of mental retardation and chronic neurodegenerative disorders.

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http://www.antiaging...nootropics.html

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 toxicity and side effects; something rarely seen with more standard medical drugs.

More importantly, they offered promise not only in the realm of fighting disease, but also in 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 scientific studies 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/ Kg orally 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 pyrrolidine nucleus, 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 is naturally 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: he four main commercial

(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;
(B) the facilitation of interhemispheric flow of information;
© the partial enhancement of the general resistance of the brain and particularly its resistance 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 the chief 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 hippocampal release of acetylcholine and on the dopaminergic turnover, too. Pharmacologically there exist protective effects with regard to several noxes [harmful agents] and an impact on the 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 hippocampal pyramid 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 and glucose 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 mentioned features, such as several types of senile dementia, (e.g. Primary Degenerative Dementia= Alzheimer’s type: Multi Infarct [stroke] Dementia), ischaemic [poor brain blood flow] insults, hypoxia, anoxia and toxicologically or dietary based deficiencies." (Footnotes in the 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 and conditions 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 by Hemicholinium-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 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 two groups 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 the hypoxia-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 to electroconvulsive 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 showed massive 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 more normal 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. one hour before Secobarbital.

The experiments then treated Piracetam against a more slow acting barbiturate Allobarbital, 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 showed electrical silences to be almost absent, and if present, to be shorter and appear later than in the control animals.

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 large groups 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, as compared 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. Oxiracetam or 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 and alertness, yet without destroying Valium's anti-anxiety effect.

Itil and co-workers (1986) treated four groups of 15 patients suffering mild to moderate dementia 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 of action 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 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 and beta 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 in alpha 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 blind trials, 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 significant difference 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 generalized brain 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 achievement is a high."

Giurgea and Salama report the confirmation of Dimond/ Brouwer's work by Wedl and Suchenwirth 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 with 18 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.

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<.001, P<.001 and P<.05. In four of the six computerized tests Piracetam showed a significant effect over placebo, with confidence levels of P<.05 for three and P<.029 for the fourth.

A fifth test showed a clear trend in favor of Piracetam, with P<.10. Wilsher and co-workers (1979) related their results with 4.8 grams per day Piracetam in a double blind, crossover trial to study the benefits of Piracetam for dyslexic students.

Interestingly, the 14 healthy student controls, matched for IQ with the dyslexic subjects, demonstrated a significantly better result on a test measuring ability to memorize nonsense syllables while using Piracetam as compared to placebo.

Their improvement from baseline was a 19.5% decrease in the number of trials needed to learn the nonsense syllables while using Piracetam, versus a 10.9% decrease from baseline while using placebo. P<.05. Piracetam-nootropics may increase learning and memory in healthy individuals, where they are not merely attenuating or reversing pathology, through their distinctive power to promote what has been termed "hemispheric super-connection."

Yeah, I noticed the negativity. I try to be conservative with what I supplement with, and I use piracetam. So far, the studies, including in healthy humans, have convinced me it is worth using. If anyone knows of a reason NOT to use it, I would be delighted to hear it.

Yeah, you noticed the negativity? I think the term is better understood "skepticism." Do you notice that the only place one can read of the "marvels" of Piracetam also happen to be the very same places selling it? I could easily portray Piracetam as a miracle drug...however, I would have not include any of the peer reviewed literature on the matter.

Standards to sell a product are often quite different than more scientific standards because of something called "bias."

Definition of Bias

Bias: 1. When a point of view prevents impartial judgment on issues relating to the subject of that point of view. In a clinical trial, bias refers to effects that a conclusion that may be incorrect as, for example, when a researcher or patient knows what treatment is being given. To avoid bias, a blinded study may be done. 2. Deviation of results or inferences from the truth, or processes leading to such systematic deviation. Any trend in the collection, analysis, interpretation, publication, or review of data that can lead to conclusions that are systematically different from the truth.

Do you really think such an avid supporter of selling supplements should be the final word on the efficacy of a medicine? Why does James South, MA among such a small flock of Piracetam supporters? Care to mention any medical practitioners who have such a pro Piracetam stance?

From a site that sells his products:

SOUTH MA, JAMES
An avid supporter of supplementation, James South is a biochemist who for over 25-years has "experimented" on himself with leading edge products. Author of numerous articles and newsletters, including editor-in-chief of the much respected Optimal Health Review, Mr. South is deeply involved with international research and has been responsible for many of the leading nutrient formulations in the United States. He often appears on radio talk shows and many people consider that James South is one of the greatest authorities regarding anti-aging medicine due to his professional knowledge and training and personal experiences.

I've read many people's accounts of positive effects from piracetam on mental-health forums frequented by non-peddling regulars who don't crow about piracetam or hype it or even mention it with regularity. Some people on the boards I've used for advice and research have actually talked about quitting it because of insomnia or overstimulation.

I personally had pretty noticeable effects when briefly using piracetam with Adderall and Red Bull (prob. the taurine & b6, I was pulling desperate all-nighters). I am being treated for a form of bipolar disorder so perhaps the effects were more pronounced for me than for others, as bipolar is believed to involve overactivity of glutamate and the very ion channels discussed above. Piracetam seems to positively modify these channels. This is pure conjecture, but the positive effects of some of the -racetams could be analagous to bipolar hypomania, in which one is elevated in cognition, creativity, focus, and drive and does not experience the deletirious effects of mania. A lot of people long to be perpetually hypomanic because if you're not prone to anger or unreasonable spending or any of that kind of stuff hypomania is generally a very pleasurable and productive state to be in.

I am taking a mood stablizer which seems to work in the opposite manner that piracetam does. It antagonizes glutamate and the aforementioned sodium/calcium channels. I don't know if taking piracetam again with this higher dose of Lamictal would mean the piracetam has no effect or if at the proper dose it would work well while not pushing me into a state of agitation or anger, which is a possibility with my dumb old brain chemistry.

Other studies actually suggest--and have shown some evidence--that piracetam regulates glutamate rather than upping it, and in some ways is a "smart drug" in the sense that it corrects imbalances and maintains equilibrium at the right dose.

Lamictal, the glutamate antagonist, is actually an epilespy drug and piracetam is sometimes prescribed as an adjunct to it! Which would suggest to me that there is little chance of piracetam having adverse effects. Epileptics, naturally, are very sensitive to excitatory neurotransmitters. This stuff is endlessly fascinating.

I've done a lot of layman-like research in the past few days and have found much interesting info, some of it contradictory but all of it nudging me toward giving piracetam another try, and adding hydergine to experiment with its monoanamine effects on depression.

If anyone is interested in the research I can post it. A lot of it relates to glutamate, which might just be interesting to me because of my concerns about glutamate and Lamictal.

This board has been very helpful for finding leads for research. I appreciate that.

Reading Internet forums and assessing effects of a self administered therapy has zero data value. The sample size is too small (n=1) and the results are way too subject to the placebo effect. Which is much more powerful than you might suspect:

Doctors in one study successfully eliminated warts by painting them with a brightly colored, inert dye and promising patients the warts would be gone when the color wore off. In a study of asthmatics, researchers found that they could produce dilation of the airways by simply telling people they were inhaling a bronchiodilator, even when they weren't. Patients suffering pain after wisdom-tooth extraction got just as much relief from a fake application of ultrasound as from a real one, so long as both patient and therapist thought the machine was on. Fifty-two percent of the colitis patients treated with placebo in 11 different trials reported feeling better -- and 50 percent of the inflamed intestines actually looked better when assessed with a sigmoidoscope ("The Placebo Prescription" by Margaret Talbot, New York Times Magazine, January 9, 2000).*

I tried piracetam due to those forum discussions and found it to me the most effective creativity enhancer I've yet tried. I haven't done all that much to date due to the expense, but it was a significant improvement from Adderall alone. I've also been on Provigil in the past.

I was just relating my thoughts about glutamate because as someone who is likely more sensitive to glutamate than the average individual I am probably more sensitive to the glutaminergic effects of piracetam. And I have felt them, though naturally you can't exactly extrapolate that to the larger population. But it's worth research. Perhaps piracetam would push those with severe bipolar disorder (and not also on a mood stabilizer, I would think) into mania.

At any rate I'm very fascinated by these possibilities and by the research. I'm also saddled with ADD and can't say that's not a factor.

EDIT: I also think the use of piracetam in mainstream epilespy treatment is an interesting angle. It's been shown to be effective as an adjunct, though I can't say I've researched that aspect in depth.

I am a pretty negative guy. When I see ads for spark plugs that increase your gas mileage by 50%, I get all negative and say ‘If that’s the case then why don’t cars have them already?”’. When I see books that tell you how to make $5000 a day trading stocks risk-free, I get all negative and say ‘If that’s true then why are they selling books instead of trading stocks?’. When I see machines that electrically stimulate your muscles, giving you a Schwarzenegger-like physique while you watch TV, I get all negative and say ‘If that’s the case why doesn’t everyone have one?’. And when I hear that a pill that 99.9% of the population has never heard of makes you smarter, I get all negative and say ‘If that’s the case then why doesn’t everyone take it?’. So yes, I am pretty negative.

Here are my last comments on piracetam:
1) No reputable scientists or doctors support the intelligence-boosting claims. The only doctor I can find who does is Ward Dean--look him up on QuackWatch.org for an insight into his credibility (Make sure you read the 'Why I don't pay income taxes anymore' link--he might want to take that down)
2) No pharmaceutical companies are investigating piracetam or any of its derivatives as an intelligence-booster. There are companies spending fortunes investigating intelligence boosters (especially ampakines) but no piracetam
3) If a drug that makes people permanently smarter were available, everyone would want it.
4) If a scientists discovered that a drug made people smarter, it would be by far the biggest discovery of their career. Other scientists and drug companies would notice and start their own research. They would develop the drug, get it approved for depression/ADD/etc. and it would be a blockbuster. They would make billions of dollars. Companies like making billions of dollars, so they pay close attention to this kind of thing.

If you choose to accept the wild claims at face value, then you have no right to complain when someone like LifeMirage tells you what you want to hear. And believe me, there will always be someone telling you what you want to hear.

Mr. Negativity, signing off.

P.S. If you ever win the Nobel prize as a result of your piracetam-taking, don't hesitate to say 'I told you so'

I wasn't taking it for intelligence increase, myself. More than anything I was taking it in the hopes that it would help with my depression-stalled creativity, and it did, or some combination of the medicines I was taking did. I just have terrible brain fog and decreased verbal ability, and while taking that combination I was able to polish off a number of stories using very creative word combinations, probably the best writing I've done, and writing is my career.

Just anecdotal, and it doesn't mean much. I just figured the stuff was cheap enough that it won't hurt to try, especially because it's used as an adjunct to the epilepsy med I'm on.

Cheers!

PS I don't doubt that lots of those dudes are quacks!

What is all of this "wild claims at face value", "assessing effects of a self administered therapy has zero data value","the only place one can read of the "marvels" of Piracetam also happen to be the very same places selling it?".

I guess pubmed is a terrible source. Yes, I do have access to more than just the abstracts. As xanadu has said, use the search function here, as much of the research has been pointed out time and time again.

I have plenty of evidence and reasons why to take it, but if anyone knows of a reason NOT to use it, I would be delighted to hear it.

A few comments:

"Reading Internet forums and assessing effects of a self administered therapy has zero data value. The sample size is too small (n=1) and the results are way too subject to the placebo effect.

I agree that scientific research provides the best places to look. However, at the end of the day, I don't care about how well the substance I am taking affects 90% of the population. The only thing that matters to me is how well *I* perform. Remember that even in those studies of hard-core stimulants such as amphetamine which have been documented extensively by the military - not everyone benefited. What works for someone else may not work for you.

I am a pretty negative guy. When I see ads for spark plugs that increase your gas mileage by 50%, I get all negative and say ‘If that’s the case then why don’t cars have them already?”’. When I see books that tell you how to make $5000 a day trading stocks risk-free, I get all negative and say ‘If that’s true then why are they selling books instead of trading stocks?’. When I see machines that electrically stimulate your muscles, giving you a Schwarzenegger-like physique while you watch TV, I get all negative and say ‘If that’s the case why doesn’t everyone have one?’. And when I hear that a pill that 99.9% of the population has never heard of makes you smarter, I get all negative and say ‘If that’s the case then why doesn’t everyone take it?’. So yes, I am pretty negative.

Here are my last comments on piracetam:
1) No reputable scientists or doctors support the intelligence-boosting claims. The only doctor I can find who does is Ward Dean--look him up on QuackWatch.org for an insight into his credibility (Make sure you read the 'Why I don't pay income taxes anymore' link--he might want to take that down)
2) No pharmaceutical companies are investigating piracetam or any of its derivatives as an intelligence-booster. There are companies spending fortunes investigating intelligence boosters (especially ampakines) but no piracetam
3) If a drug that makes people permanently smarter were available, everyone would want it.
4) If a scientists discovered that a drug made people smarter, it would be by far the biggest discovery of their career. Other scientists and drug companies would notice and start their own research. They would develop the drug, get it approved for depression/ADD/etc. and it would be a blockbuster. They would make billions of dollars. Companies like making billions of dollars, so they pay close attention to this kind of thing.

That's a very convincing argument. If piracetam and other nootropics are so good, why isn't everyone using them. Well, why do so many people drink coffee? The benefit of coffee does not seem that noticible to me. I can understand why the majority of people don't use nootropics -- most people care more about how they look than about how they perform. Why don't I use creatine? Well, I don't care about muscle mass that much. You can get a slight increase in the horsepower of your car by upgrading the air intake and installing a less-restrictive exhaust. The cost of these parts translate into marginally better fuel economy and slightly increased horsepower for as long as you drive your car -- no placebo effect, this can be measured on the dyno in a controlled environment. But would most people go through all this trouble for an extra 2 or 4 horsepower? Probably not. My argument is that most people do try to optimize every aspect of their lives. What good is a slight cognitive increase if one spends all day working on the assembly line and comes home to watch TV for three hours? Plus, given the choice between beer and nootropics, I think the common answer to that question is clear. But ask what do competitive students at MIT, Caltech, and U. Illinois use to enhance their academic performance? I would really like to know the answer to this question because most students are on a strict budget and need all the mental performance they can get.

You guys are really lucky I barely have a life right now...and I LOVE destroying pseudoscience -- some might say that I am being insulting; but no, I just say let's stick to the evidence. Quickly, I can copy/past most of this all too familiar pseudo scientific debate...

Cronwood: before you resort to authority status to defend an argument, I advise you check your references. Please do present your reasons to take Piracetam. We are all interested in your elaborate scientific argument. A practical and wise scientist such as yourself wouldn't resort to an anecdote, right?

You reference Pubmed as a source of information, but have yet to reference a single scientific study. Thus far you have claimed that your have "plenty of evidence and reasons to take [Piracetam]." Please support your argument.

Let me present the argument that Piracetam appears to be an ineffective cognition enhancer when compared to the acetylcholinesterase inbitor Aricept (donepezil HCL), Provigil (Modafinil), or Ritalin -- then I will support my arguement using evidence.

There is no data supporting the use of Piracetam as an effective cognitive enhancer in Alzheimer's, dyslexia, or other mixed models of memory loss. There may be a few outlying data that might suggest Piracetam could be useful, but as cognitive enhancer, Piracetam has failed to demonstrate real results compared to the aforementioned compounds; so it was quickly discarded, then Oxiracetam was developed. After Oxiracetam, Aniracetam, Pramiracetam, etc. failed to be effective, other, more potent racetams were developed, such as nefiracetam, which can exhibit catastrophic toxic effects upon the male genitalia. Leviracetam was found to be far more effective than nefiracetam, but once again, toxicity concerns and lack of relevant effect eliminated it from consideration (this might be wrong, feel free to correct any of my data).

As a scientist, when you see mixed or conflicting results, it's usually best to keep your mouth shut until there is some real evidence to support your hypothesis or theory. Otherwise, you might look pretty silly in the future. It's like saying Global Warming is a hoax. The fact there is no scientific data saying Global Warming is not happening strongly suggests that it is. Conversely, demonstrating that that there is no evidence saying Piracetam is effective, or that the results are mixed, leads us to favor compounds without "mixed", terribly weak or indistinguishable or conflicting results; especially if the compound carries a significant cost or it may be low in purity or contaminated.

Back in 1991 (don't forget Piracetam was synthesized in the 1960s, yet still in 1991, the effects were STILL not proven by science...twenty years after the development of piracetam and no evidence!)

Drugs Aging. 1991 Jan;1(1):17-35. 

Piracetam. An overview of its pharmacological properties and a review of its therapeutic use in senile cognitive disorders.

Vernon MW, Sorkin EM.

Adis International Drug Information Services, Auckland, New Zealand.

Piracetam is the first of the so-called 'nootropic' drugs, a unique class of drugs which affect mental function. In animal models and in healthy volunteers, the drug improves the efficiency of the higher telencephalic functions of the brain involved in cognitive processes such as learning and memory. The pharmacology of piracetam is unusual because it protects against various physical and chemical insults applied to the brain. It facilitates learning and memory in healthy animals and in animals whose brain function has been compromised, and it enhances interhemispheric transfer of information via callosal transmission. At the same time, even in relatively high dosages it is devoid of any sedative, analeptic or autonomic activities. How piracetam exerts its effects on memory disorders is still under investigation, although among other proposed mechanisms of action it is thought to facilitate central nervous system efficiency of cholinergic neurotransmission. Results from trials involving elderly patients with senile cognitive disorders have been equivocal, as have the results obtained when piracetam has been combined with acetylcholine precursors. Piracetam seems to be almost completely devoid of adverse effects, and is extremely well tolerated. In conclusion, opinion is divided as to the benefits of piracetam in the treatment of senile cognitive decline. Although double-blind studies in the elderly have produced mixed results, some such trials (particularly those involving larger numbers of patients) have reported favourable findings, thus offering some reason for cautious optimism in a notoriously difficult area of therapeutics. However, further investigations of piracetam alone and in combination therapy are required before any absolute conclusions can be drawn.
Publication Types:

* Review

PMID: 1794001 [PubMed - indexed for MEDLINE]

A recent study: 2005:

Wiad Lek. 2005;58(9-10):528-35. 

Alzheimer's disease therapy--theory and practice

[Article in Polish]

Gabryelewicz T, Barcikowska M, Jarczewska DL.

Z Zakladu Badawczo-Leczniczego Chorob Zwyrodnieniowych GUN IMDiK PAN w Warszawie.

Alzheimer's disease (AD), a progressive degenerative disorder of the brain, affects a significant proportion of elderly population. The pharmacotherapy of AD is evolving rapidly. However, many doctors suggest the treatment which does not provide benefits in patients with the disease. The primary aim of this article was to review avaiable data on the patophysiologic background of AD and thus the most commonly used therapeutic agents, specifically cholinesterase-inhibitors (rivastigmine), Ginkgo biloba, piracetam and selegiline. Relevant double-blind, randomized, placebo-controlled studies were identified through a comprehensive search of Medline, NICE, Embase and CENTRAL databases. CONCLUSIONS: Only inhibitors of acetylcholinesterase are approved in mild and moderate stages of AD treatment. There is no evidence that Ginkgo biloba, selegiline, piracetam provide cognitive or behavioural improvement.

PMID: 16529064 [PubMed - in process]

2004

Int J Neuropsychopharmacol. 2004 Sep;7(3):351-69. Epub 2004 Jul 1.  Related Articles, Links

Evidence-based pharmacotherapy of Alzheimer's disease.

Evans JG, Wilcock G, Birks J.

Cochrane Dementia and Cognitive Improvement Group, University of Oxford, UK.

Dementia is an acquired global impairment of cognitive capacities. Approximately 5% of people aged over 65 yr are affected by dementia, and some 70% of cases are thought to be due primarily to Alzheimer's disease. Descriptions of the clinical manifestations of Alzheimer's disease have been increasingly refined in the last decade but there is no diagnostic test for what remains fundamentally a pathologically defined condition. At the present time interventions for Alzheimer's disease are limited to those that modify the manifestations of the disease, and foremost amongst the candidates available are the cholinesterase inhibitors. The rationale for the use of cholinergic drugs for Alzheimer's disease lies in enhancing the secretion of, or prolonging the half-life of, acetylcholine in the brain. Several potential compounds have been tested, but short half-lives and a high incidence of cholinergic and other adverse effects have eliminated most. Only three are widely licensed for use, donepezil, galantamine and rivastigmine. Their efficacy is relatively modest. These drugs have been tested in 32 randomized, placebo-controlled trials. The trials assess cognitive function primarily, and in addition they may assess global function, activities of daily living, quality of life and behavioural disturbance typically over 3 or 6 months. The performance of each drug is summarized in a Cochrane review, a systematic review carried out according to strict guidelines. There was a significant benefit in favour of treatment compared with placebo for cognition and activities of daily living, but withdrawals due to adverse events were significantly higher for treatment than placebo for all three drugs. There is little evidence from direct comparisons between the three drugs. There are several economic analyses of the cost-effectiveness of these drugs, but the findings cannot be considered robust owing to inadequate data. A range of other pharmacological treatments have been tested, including selegiline, piracetam, vitamin E, Ginkgo biloba, anti-inflammatory drugs and hormone replacement therapy, but, so far, Cochrane reviews have not established the efficacy of these interventions for Alzheimer's disease. A Cochrane review of memantine shows benefits on cognitive and global function of the same order of magnitude as seen for the cholinesterase inhibitors.Memantine has been licensed in Europe for treatment of patients with moderately severe to severe Alzheimer's disease.

Publication Types:

* Review


PMID: 15228642 [PubMed - indexed for MEDLINE]

Neurology. 1993 Feb;43(2):301-5. 

Long-term and high-dose piracetam treatment of Alzheimer's disease.

Croisile B, Trillet M, Fondarai J, Laurent B, Mauguiere F, Billardon M.

Department of Neurology, Hopital Neurologique, Lyon, France.

Preclinical research suggests that piracetam (a nootropic drug) may improve cognitive functions, but previous studies have failed to demonstrate a clear benefit for the treatment of Alzheimer's disease (AD). We report a 1-year, double-blind, placebo-controlled, parallel-group study with a high dose of piracetam (8 g/d per os) in 33 ambulant patients with early probable AD. Thirty subjects completed the 1-year study. No improvement occurred in either group, but our results support the hypothesis that long-term administration of high doses of piracetam might slow the progression of cognitive deterioration in patients with AD. The most significant differences concerned the recall of pictures series and recent incident and remote memory. The drug was well-tolerated.

Publication Types:

* Clinical Trial
* Randomized Controlled Trial


PMID: 8437693 [PubMed - indexed for MEDLINE]

Abstract: Sixty children with dyslexia (41 boys, 19 girls; ages 9 to 13) were enrolled in a 10-week summer tutoring program that emphasized word-building skills. They were randomly and blindly assigned to receive either placebo or piracetam, a purportedly memory-enhancing drug that has been reported to facilitate reading skill acquisition. The children were subtyped as "dysphonetic" or "phonetic" on the basis of scores from tests of phonological sensitivity and phoneme-grapheme correspondence skills. Of the 53 children who completed the program, 37 were classified as dysphonetic and 16 as phonetic. The phonetic group improved significantly more in word-recognition ability than the dysphonetic group. Overall, the children on medication did not improve more than the nonmedicated ones in any aspect of reading.

The phonetic subgroup on piracetam gained more in word recognition than any subgroup but did not improve significantly more than the phonetic subgroup on placebo. Results are discussed in relation to findings from previous studies of piracetam in children with dyslexia.[2]

1.
Abbreviated Journal Title: J Learn Disabil
Date Of Publication: 1991 Nov
Journal Volume: 24
Page Numbers: 542 through 549
Country of Publication: UNITED STATES
Language of Article: Eng
Special Journal List:
Issue/Part/Supplement: 9
ISSN: 0022-2194

Now, we do have results from very well established scientists and medical researchers that (ad hominem here: Not a Ward Dean or James South sales article) that suggest other compounds are really effective at improving cognition.

While there may be some evidence that might suggest (in some studies, but not most of the double blind, randomized trials where a placebo in involved!) that these Piracetan may be effective in elderly or demented subjects, there is zero solid evidence that the conventionally accepted nootropics would affect memory functions of an individual with a perfectly functioning memory -- or one with a damaged memory. It is theoretically possible, but unproven nonetheless.

We do have solid evidence from randomized, double blind, placebo controlled trials in healthy subjects that suggest that prescription-only drugs such as Provigil AKA modafinil, Aricept AKA donezepil HCL, and Ritalin AKA Concerta AKA methylphenidate can improve short and long term memory functions -- once again -- in healthy subjects...

This and this too

http://www.ncbi.nlm....l=pubmed_docsum

First, here is the data suggesting Aricept may be an effective cogitive enhancer in Alzehimer demented subjects.

Cochrane Database Syst Rev. 2006 Jan 25;(1):CD001190.

* Cochrane Database Syst Rev. 2003;(3):CD001190.

Donepezil for dementia due to Alzheimer;s disease.

Birks J, Harvey RJ.

University of Oxford, Department of Clinical Geratology, Radcliffe Infirmary, Woodstock Road, Oxford, UK, OX2 6HE. jacqueline.birks@geratol.ox.ac.uk

BACKGROUND: Alzheimer's disease is the most common cause of dementia in older people. One of the aims of therapy is to inhibit the breakdown of a chemical neurotransmitter, acetylcholine, by blocking the relevant enzyme. This can be done by a group of chemicals known as cholinesterase inhibitors. OBJECTIVES: The objective of this review is to assess whether donepezil improves the well-being of patients with dementia due to Alzheimer's disease. SEARCH STRATEGY: The Cochrane Dementia and Cognitive Improvement Group's Specialized Register was searched using the terms 'donepezil', 'E2020' and 'Aricept' on 12 June 2005. This Register contains up-to-date records of all major health care databases and many ongoing trial databases.Members of the Donepezil Study Group and Eisai Inc were contacted. SELECTION CRITERIA: All unconfounded, double-blind, randomized controlled trials in which treatment with donepezil was compared with placebo for patients with mild, moderate or severe dementia due to Alzheimer's disease. DATA COLLECTION AND ANALYSIS: Data were extracted by one reviewer (JSB), pooled where appropriate and possible, and the pooled treatment effects, or the risks and benefits of treatment estimated. MAIN RESULTS: 23 trials are included, involving 5272 participants. Most trials were of 6 months or less duration in selected patients. Available outcome data cover domains including cognitive function, activities of daily living, behaviour , global clinical state and health care resource costs.For cognition there is a statistically significant improvement for both 5 and 10 mg/day of donepezil at 24 weeks compared with placebo on the ADAS-Cog scale (-2.01 points MD, 95%CI -2.69 to -1.34, p<0.00001); -2.80 points, MD 95% CI -3.74 to -2.10, p<0.00001) and for 10 mg/day donepezil compared with placebo at 52 weeks (1.84 MMSE points, 95% CI, 0.53 to 3.15, p=0.006).The results show some improvement in global clinical state (assessed by a clinician) in people treated with 5 and 10 mg/day of donepezil compared with placebo at 24 weeks for the number of patients showing improvement or no change (OR 2.18, 95% CI 1.53 to 3.11, p=<0.0001, OR 2.38, 95% CI 1.78 to 3.19, p<0.00001). Benefits of treatment were also seen on measures of activities of daily living and behaviour, but not on the quality of life score .There were significantly more withdrawals before the end of treatment from the 10 mg/day (but not the 5 mg/day) donepezil group compared with placebo which may have resulted in some overestimation of beneficial changes at 10 mg/day. Benefits on the 10 mg/day dose were marginally larger than on the 5 mg/day dose. Two studies presented results for health resource use, and the associated costs. There were no significant differences between treatment and placebo for any item, the cost of any item, and for the total costs, and total costs including the informal carer costs. A variety of adverse effects were recorded, with more incidents of nausea, vomiting, diarrhoea, muscle cramps, dizziness, fatigue and anorexia (significant risk associated with treatment) in the 10 mg/day group compared with placebo but very few patients left a trial as a direct result of the intervention. AUTHORS' CONCLUSIONS: People with mild, moderate or severe dementia due to Alzheimer's disease treated for periods of 12, 24 or 52 weeks with donepezil experienced benefits in cognitive function, activities of daily living and behaviour. Study clinicians rated global clinical state more positively in treated patients, and measured less decline in measures of global disease severity. There is some evidence that use of donepezil is neither more nor less expensive compared with placebo when assessing total health care resource costs. Benefits on the 10 mg/day dose were marginally larger than on the 5 mg/day dose. Taking into consideration the better tolerability of the 5 mg/day donepezil compared with the 10 mg/day dose, together with the lower cost, the lower dose may be the better option. The debate on whether donepezil is effective continues despite the evidence of efficacy from the clinical studies because the treatment effects are small and are not always apparent in practice.


Publication Types:
* Meta-Analysis
* Review

PMID: 16437430 [PubMed - indexed for MEDLINE]

We would also have reason to suspect Donzepil might have also such effects in healthy subjects -- first, we have data from a VERY well respected researcher from Standford University, (Jerome Yesavage) and at least three other randomized, placebo controlled trials that seems to confirm these effects in healthy subjects. It is a scientific assumption to assume these four research findings are sufficient evidence to confirm donezepil can significantly improve the memory function in patients with normal working memories in advanced simulator aviation tasks. It's long term safety is still in question.

Ref1:

Neurology. 2002 Jul 9;59(1):123-5. 

Comment in:

* Neurology. 2003 Sep 9;61(5):721; author reply 721.

Donepezil and flight simulator performance: effects on retention of complex skills.

Yesavage JA, Mumenthaler MS, Taylor JL, Friedman L, O'Hara R, Sheikh J, Tinklenberg J, Whitehouse PJ.

Palo Alto Veterans Affairs Health Care System, Stanford University School of Medicine, Stanford, CA 94305-5550, USA. yesavage@stanford.edu
We report a randomized, double-blind, parallel group, placebo-controlled study to test the effects of the acetylcholinesterase inhibitor, donepezil (5 mg/d for 30 days), on aircraft pilot performance in 18 licensed pilots with mean age of 52 years. After 30 days of treatment, the donepezil group showed greater ability to retain the capacity to perform a set of complex simulator tasks than the placebo group, p < 0.05. Donepezil appears to have beneficial effects on retention of training on complex aviation tasks in nondemented older adults.

Publication Types:

* Clinical Trial
* Randomized Controlled Trial

PMID: 12105320 [PubMed - indexed for MEDLINE]

Ref 2:

Neuropsychopharmacology. 2003 Jul;28(7):1366-73. Epub 2003 May 14. 

Psychoactive drugs and pilot performance: a comparison of nicotine, donepezil, and alcohol effects.

Mumenthaler MS, Yesavage JA, Taylor JL, O'Hara R, Friedman L, Lee H, Kraemer HC.

Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA. msm@stanford.edu

The cholinergic system plays a major role in cognitive abilities that are essential to piloting an aircraft: attention, learning, and memory. In previous studies, drugs that enhance the cholinergic system through different pharmacologic mechanisms have shown beneficial effects on cognition; but dissimilar cognitive measures were used and samples were not comparable. A comparison within the same cognitive tasks, within comparable samples appears desirable. Toward this aim, we compared effect sizes (ES) of performance-enhancing doses of nicotine (a nicotinic receptor agonist) and donepezil (an acetylcholinesterase inhibitor) as found in our prior work on pilot performance. We also compared cholinergic ES to those of performance-impairing doses of alcohol. In three randomized, placebo-controlled trials, we assessed the flight performance of aircraft pilots in a Frasca 141 simulator, testing I: the acute effects of nicotine gum 2 mg; II: the effects of administration of 5 mg donepezil/day for 30 days; and III: the acute and 8 h-carryover effects of alcohol after a target peak BAC of 0.10%. We calculated the ES of nicotine, donepezil, and alcohol on a flight summary score and on four flight component scores. Compared to placebo, nicotine and donepezil significantly improved, while alcohol significantly impaired overall flight performance: ES (nicotine)=0.80; ES (donepezil)=1.02; ES (alcohol acute)=-3.66; ES (alcohol 8 h)=-0.82. Both cholinergic drugs showed the largest effects on flight tasks requiring sustained visual attention. Although the two tested cholinergic drugs have different pharmacologic mechanisms, their effects on flight performance were similar in kind and size. The beneficial effects of the cholinergic drugs on overall flight performance were large and the absolute (ie nondirectional) sizes were about one-fourth of the absolute ES of acute alcohol intoxication and roughly the same as the absolute 8 h-carryover ES of alcohol.

Publication Types:

* Clinical Trial
* Randomized Controlled Trial


    PMID: 12784106 [PubMed - indexed for MEDLINE]

Most people I know are looking for acute (noticeable) effect. They want a drug to function specifically to enhance their learning and/or memory for specific tasks (ie school). The military also is investigating drugs to lower possibility of error in advanced tasks.

Please present your evidence (from Pubmed) that might suggest Piraetam is at all effective at increasing learning and memory in a healthy subject. Or at least explain what references from Pubmed you find to be most compelling support to substantiate spending your hard earned money on Piracetam rather than something that actually has some scientific evidence to support its purported use.

Peace out.

Edited by nootropikamil, 17 June 2006 - 06:10 AM.

Xanadu, what do you think of the duration of the studies you refer to? Or the durations of the studies that were the basis for meta analysis?

nootropikamil, if you want to find the benefits with piractam, you should look into the effects on CBF (Cerebral Blood Flow), Language, such as reading, writing, and verbal learning/recall, effects in cerebral glucose utilization, as well as increased intra brain communication.

You seem to be getting a little edgy again, not ment to be an insult or slam.

nootropikamil, if you want to find the benefits with piractam, you should look into the effects on CBF (Cerebral Blood Flow), Language, such as reading, writing, and verbal learning/recall, effects in cerebral glucose utilization, as well as increased intra brain communication.

You seem to be getting a little edgy again, not ment to be an insult or slam.

A little edgy? I think it's called scientific and skeptical. You should try it rather than relying on pseudoscience and anecdotal authority to establish an argument. Not meant to be an insult or slam; just asking you to stop presenting a well established scientific myth as truth.

You still have yet to present a scientific argument or a reference to support your argument. Therefore, I rest my case: Piracetam is ineffective as a cognition enhancer and not worth its cost. The only individuals supporting the use of Piracetam are those selling it or those who are unable to provide any evidence to support their claim. Case closed.

Peace out.

I think one reason that the benefits of piracetam in healthy subjects are hard to quantify is due to the nature of the benefits themselves. It's a really subjective thing. How would you quantify beauty or pleasure? If an artist produced more beautiful work after using piracetam, who could document the change? Who could say with scientific certainty exactly how much more beautiful his work became after ingesting the drug for a certain amount of time? How can you weigh creativity? The benefits of piracetam are very subjective but real. For me, what I get is that ideas come to me more readily than before. When I have a tough problem to solve and the usual methods don't work, instead of getting frustrated I may just step back a little and ponder and then two or three possible approaches come to mind, one of which happens to work. My memory seems better and there have been studies showing many memory enhancing benefits from it. It seems to enhance the effects of other drugs slightly.

I think part of the reason science in general does not want to recognise something like piracetam lies in the way we pursue scientific research. Why does science not recognise ESP and other phenomena? There have been many remarkable demonstrations and most people have had hunches that turned out to be true that could not be explained rationally. Yet science tells us this is all false and bogus. If it can't be weighed, seen or measured in some way, it doesn't exist. Or if it can be measured but the measurements are inconsistant, it doesn't exist. At least according to most scientists.

The benefits of piracetam in the elderly or demented are so pronounced that even many medical researchers have no choice but to recognise them. That does not mean that healthy and non elderly people get no benefits at all. It simply means that not every young person does benefit and the benefits they get are harder to pin down and quantify.

There are lots of other treatment methods and substances that are not recognised by mainstream science even though there are many who have benefited from them. In time, some of these practices have won grudging approval from some doctors and scientists. An example of that is acupuncture. It's one of the things many doctors do not want to talk about let alone believe in but it has been demonstrated so many times that the medical establishment has been forced to conceed it has some uses, primarily in pain control.

I have no need to argue with negative people nor to change their minds. Let them go off and do their thing. Not everyone will benefit from piracetam or in the same way. Likewise, if someone says a sunset is not beautiful, meditation doesn't help and vitamins are a fraud, let them go their own way and don't trouble them further.

Anyone that is looking into using piracetam should not be discouraged by nootropikamil's comments. He likes to insight by over-claiming or other tactics. Instead do a search on this board as well as pubmed. When looking at pubmed the benefits I sited may be a good pointer for you. Not only is it very neuroprotective, but it also has cognitive benefits as well.

Edit: Oh yeah, check out the thread titled
Piracetam
What effect did it have on you?
May 4th 2006

to see what was said just last month

Piracetam is ineffective as a cognition enhancer and not worth its cost.  The only individuals supporting the use of Piracetam are those selling it or those who are unable to provide any evidence to support their claim.  Case closed. 

Peace out.

Ok. Then why do you sell it??? http://www.nootropik...hg?categoryId=3

You just admitted that you are selling what you believe to be a completely worthless product.

On another forum, you present a biased archive presenting and "aggressively highlighting" only pro-Piracetam comments and conclusions which came from Pubmed: http://nootropics.ip...hp?showtopic=14. The conclusions that you highlight there are in conflict with your thesis above. I think this needs to be resolved so that people are not confused.

Also, why do you take these substances if they produce no effect for you? I assume that you are not taking piracatam currently. But I do recall from other threads that you mention supplementation of oxiracetam and maybe aniracetam. Right? But why would you throw synthetic chemicals into your body if they produce no effect for you? You have pointed out on several occasions that these substances often contain impurities such as lead and other heavy metals which can be detrimental to enhancing IQ and hence your academic pursuits. Sure, you can spend several hundred dollars to have this stuff tested by a lab, but you are only testing a sample of the substance. In our phone conversation, you mentioned that these tests are therefore not a 100% guarantee. There is always some risk. So why take a risk given no benefit and some financial cost? No matter how little they cost you, $10 a month or so would be better allocated to www.mprize.com rather than achieving what you claim to be no tangible benefit. Do you agree?

Now, from personal experience, I cannot conclude that piracetam is beneficial. My GRE verbal is still in the 650 - 730 range, I have not seen an increase or decrease in my scores since I started taking it. So do not think that I am supporting piracetam.

You seem to be getting a little edgy again

I'm diggin' it. Universal agreement on subjects is nice, but it's invaluable to hear counter arguments when they're backed by data. Most especially in a subject such as the enhancement of human reasoning and performance. Even the most studied drugs in that area are pretty lacking on studies compared to medications whose sole use lies in treatment of disease. We've all got bias, and when presented with such a derth of data it's imperative to get a second opinion. Well, imperative when the second opinion is also working in a logical manner from the available data as nootropikamil does. I know for myself that it's far, FAR, too tempting at times to fill in gaps left by lack of followup studies with my own hopes, and after time goes by it's an easy process to forget that the seemingly solid result I'm recalling was actually just an undeclared variable.

I sell a lot of stuff I am sure does not have too much of an effect. Why do you think FDA considers Piracetam a dietary supplement and not a drug?

I believe Piracetam can protect the brain from insult, and can have beneficial effects on membrane fluidity. So effects of other drugs/supplements one might be taking might be enhanced by Piracetam. Also: look how cheap Piracetam is. I would recommend taking Piracetam if one can easily afford it. However, I recommend Oxiracetam and Aniracetam as more effective racetams. They are non toxic and free of significant side effects -- if you have a pure source.

Click here to read all of the positive scientific studies conducted on Piracetam -- in MANY colors!!! I need to lower the fonts.

Peace. I need to get going today and won't be typing at the computer all day...

Therefore, I rest my case: Piracetam is ineffective as a cognition enhancer and not worth its cost.  The only individuals supporting the use of Piracetam are those selling it or those who are unable to provide any evidence to support their claim.  Case closed. 

Peace out.

I cant't believe that you are even allowed to post still. Very tolerant moderators/admins here.

Edit: Sorry about this post. I just have a problem with discussing a topic with someone who has already determined the said topic is pseudoscience. Especially if they go on to say, "and I LOVE destroying pseudoscience". Arguing something for entertainment value that may influence someone looking for direction can bring me to disgust at times. Again, I shouldnt have posted it, I was frustrated.

Edited by cnorwood19, 18 June 2006 - 11:57 PM.

Piracetam is ineffective as a cognition enhancer and not worth its cost.  The only individuals supporting the use of Piracetam are those selling it or those who are unable to provide any evidence to support their claim.  Case closed. 

Peace out.

Ok. Then why do you sell it??? http://www.nootropik...hg?categoryId=3

You just admitted that you are selling what you believe to be a completely worthless product.

On another forum, you present a biased archive presenting and "aggressively highlighting" only pro-Piracetam comments and conclusions which came from Pubmed: http://nootropics.ip...hp?showtopic=14. The conclusions that you highlight there are in conflict with your thesis above. I think this needs to be resolved so that people are not confused.

Also, why do you take these substances if they produce no effect for you? I assume that you are not taking piracatam currently. But I do recall from other threads that you mention supplementation of oxiracetam and maybe aniracetam. Right? But why would you throw synthetic chemicals into your body if they produce no effect for you? You have pointed out on several occasions that these substances often contain impurities such as lead and other heavy metals which can be detrimental to enhancing IQ and hence your academic pursuits. Sure, you can spend several hundred dollars to have this stuff tested by a lab, but you are only testing a sample of the substance. In our phone conversation, you mentioned that these tests are therefore not a 100% guarantee. There is always some risk. So why take a risk given no benefit and some financial cost? No matter how little they cost you, $10 a month or so would be better allocated to www.mprize.com rather than achieving what you claim to be no tangible benefit. Do you agree?

Now, from personal experience, I cannot conclude that piracetam is beneficial. My GRE verbal is still in the 650 - 730 range, I have not seen an increase or decrease in my scores since I started taking it. So do not think that I am supporting piracetam.

I think nootropic compounds can help certain individuals whom may have damaged their brains...or perhaps for those whom wish to protect their brains from cognitive decline. The "nootropics" that are the dietary supplements sold on the web may protect the brain.

When measured next to drugs such as Aricept, Provigil, Ritalin, and other various prescription drugs that have demonstrated efficacy in healthy subjects, the clinical effect of the "dietary supplement" type nootropics available in the USA are not significant enough to warrant their use as effective medicines. They may do something...but just not enough. The racetams may have beneficial effects on "receptor plasticity"...(what exactly does that mean?)



Is it ethical to portray these compounds as effective cognition enhancers in healthy subjects when there is no supporting data?

Edit: Update May 9, 2007.

Edited by adam_kamil, 09 May 2007 - 08:59 AM.

You seem to be getting a little edgy again

I'm diggin' it.

Yeah, it's sometimes hard to be the skeptical one in a forum.

But I came to a realization a few months ago...if there is no evidence of something...it's silly to assume it even might be true. And if there is evidence that something actually works, it's best to stick to that; at least until further research is published. If we lie to ourselves and convince each other that a cognition enhancer is effective for healthy subjects based on zero evidence, how can we expect to advance respect to this field? The most successful scientists are the most skeptical, and that's a fact.

Have a great weekend.

The following link is to a statement from a chemist saying that she finds Piracetam helpful for meditation and lucid dreaming:

Statement about Piracetam

Edited by mike, 18 June 2006 - 12:17 PM.

Piracetam In CerebralVascular Disorders


Neurol Neurochir Pol 1981 Jul-Aug;15(4):447-51
Comparative evaluation of psychoactive drugs used in patients with subacute and chronic cerebrovascular disorders

Wasilewski R, Lebiediewa N, Kozlowa E, Wolkow W.

The report is based on 315 patients with subacute and chronic cerebral circulatory disturbances caused mostly by atherosclerosis aged 30 to 82 years, treated for 1-6 months. In 90 cases Piracetam (Nootropil) was given, 107 received Piritinol (Encephabol, Enerbol), 77 Piriditol, 41 Centrophenoxin. The patients were allocated randomly to these groups. In the treated patients improvement was achieved in a considerable proportion of cases (44-82%) treated with different drugs. This improvement manifested itself as regression or decreased intensity of neurotic complaints, labyrinthine-cerebellar signs, pyramidal signs, anxiety and fears, improvement of recent memory, attention, psychomotor activity. The best results were obtained with Nootropil, moderately good with Centrophenoxin, Encephabol, and poor with Piriditol. Drug tolerance was best with Encephabol, while that of other drugs was slightly worse. The only disquieting symptoms were activation of epileptic seizures in several patients treated with Nootropil or Centrophenoxin. The best way of administration was giving the drugs in two doses in the morning hours and at noon. The authors regard as useful the treatment of patients with subacute and chronic cerebral circulatory failure with psychoenergizing drugs.

Hey Xanadu, I didnt really think this thread would end up down this road. Anyway, here are a few IDs to look at. If the studies are hard to understand, the reviews give more of a synopsis. I tend to agree with one of the reviewers that say there are beneficial results to healthy or impaired as well as young or old, but the most noticable effects will be in the old and/or impaired.

All IDs can be referenced at Pubmed.nl

Studies
PMID: 3370078
PMID: 8457235
PMID: 10555876
PMID: 8272204
PMID: 3305591
PMID: 3522509
PMID: 7865703
PMID: 3522510
PMID: 3556550

Reviews
PMID: 16459490
PMID: 16007238
PMID: 12073660
PMID: 10338102
PMID: 1794001

IMMINST Poll
http://www.imminst.o...9&t=6477&hl=&s=

Again, the microcirculation, intrabrain communication, improvements in patients with dyslexia, neuroprotective properties, and the regulation to normality of multiple brain functions make piracetam worth taking, for me that is. I still have not found the reason why NOT to take it. Maybe stress on the adrenals? That may be a stretch though.

Edit: By the way, the studies above do not have the "troubles" that nootropikamil was pointing out, below, with the article.

Edited by cnorwood19, 18 June 2006 - 11:49 PM.

The following link is to a statement from a chemist saying that she finds Piracetam helpful for meditation and lucid dreaming:

Statement about Piracetam

I welcome differences of opinion on matters of science. Especially when there is 30 years of data to cite conflicting, weak, and anecdotal evidence.

I am happy this discussion is still alive and doing quite well. It seems there are a few die hard Piracetam fans left in this world...is it coincidental that those whom support the use of Piracetam cannot support their argument with any real scientific data?

1. Opinions from non blinded subjects that are considered "experts." Check the reference above...

2. Data from in vitro (ie test tube or petri dish) studies (check the first xanadu's first Pubmed reference cited in this thread -- it is not even a reference from a study in a living creature!):

GVS-111 prevents oxidative damage and apoptosis in normal and Down's syndrome human cortical neurons

Pelsman A, Hoyo-Vadillo C, Gudasheva TA, Seredenin SB, Ostrovskaya RU, Busciglio J
Department of Neuroscience, University of Connecticut Health Center, 263 Farmington Avenue, CT 06030, USA

The neuroprotective activity of a novel N-acylprolyl-containing dipeptide analog of the nootropic 2-oxo-1-pyrrolidine acetamide (Piracetam) designated as GVS-111 (DVD-111/Noopept) was tested in two in vitro models of neuronal degeneration mediated by oxidative stress: normal human cortical neurons treated with H2O2, and Down's syndrome (DS) cortical neurons. Incubation of normal cortical neurons with 50 microM H2O2 for 1h resulted in morphological and structural changes consistent with neuronal apoptosis and in the degeneration of more than 60% of the neurons present in the culture. GVS-111 significantly increased neuronal survival after H2O2-treatment displaying a dose-dependent neuroprotective activity from 10nM to 100 microM, and an IC(50) value of 1.21±0.07 microM. GVS-111 inhibited the accumulation of intracellular free radicals and lipid peroxidation damage in neurons treated with H2O2 or FeSO4, suggesting an antioxidant mechanism of action. GVS-111 exhibited significantly higher neuroprotection compared to the standard cognition enhancer Piracetam, or to the antioxidants Vitamin E, propyl gallate and N-tert-butyl-2-sulpho-phenylnitrone (s-PBN). In DS cortical cultures, chronic treatment with GVS-111 significantly reduced the appearance of degenerative changes and enhanced neuronal survival. The results suggest that the neuroprotective effect of GVS-111 against oxidative damage and its potential nootropic activity may present a valuable therapeutic combination for the treatment of mental retardation and chronic neurodegenerative disorders.

3. Studies from 25 years ago that do not include use of a placebo involved are NOT considered valid data for consideration due to (first off) something called bias (the second reference xanadu is not placebo controlled -- or worthless!)

Piracetam In CerebralVascular Disorders

Neurol Neurochir Pol 1981 Jul-Aug;15(4):447-51
Comparative evaluation of psychoactive drugs used in patients with subacute and chronic cerebrovascular disorders

Wasilewski R, Lebiediewa N, Kozlowa E, Wolkow W.

The report is based on 315 patients with subacute and chronic cerebral circulatory disturbances caused mostly by atherosclerosis aged 30 to 82 years, treated for 1-6 months. In 90 cases Piracetam (Nootropil) was given, 107 received Piritinol (Encephabol, Enerbol), 77 Piriditol, 41 Centrophenoxin. The patients were allocated randomly to these groups. In the treated patients improvement was achieved in a considerable proportion of cases (44-82%) treated with different drugs. This improvement manifested itself as regression or decreased intensity of neurotic complaints, labyrinthine-cerebellar signs, pyramidal signs, anxiety and fears, improvement of recent memory, attention, psychomotor activity. The best results were obtained with Nootropil, moderately good with Centrophenoxin, Encephabol, and poor with Piriditol. Drug tolerance was best with Encephabol, while that of other drugs was slightly worse. The only disquieting symptoms were activation of epileptic seizures in several patients treated with Nootropil or Centrophenoxin. The best way of administration was giving the drugs in two doses in the morning hours and at noon. The authors regard as useful the treatment of patients with subacute and chronic cerebral circulatory failure with psychoenergizing drugs.

Geez, aren't you guys aware of the scientific fallacy called Anecdotal evidence?

http://www.cuyamaca....s/anecdotal.asp

Description:

The argument draws a conclusion from cases specifically chosen to support the conclusion (often while ignoring cases that might tend to undermine the conclusion).

Examples:

"Criminals are never given the punishment they deserve. Just look at that guy who tried to kill that little girl. After the plea bargaining, he practically got off scot free!"

"Abortion is morally wrong. In one case a woman had an abortion merely so her pregnancy would not interfere with a trip to Europe that she and her husband were planning."

Discussion:

There is, of course, nothing wrong with presenting representative cases to illustrate an inductive conclusion properly drawn from a fair sample. The representative case serves to put a human face on what would otherwise be just a mass of cold statistics. However, it is the inductive argument as a whole (i.e. all those cold statistics) that justifies the conclusion. The anecdote merely illustrates and humanizes the properly drawn conclusion.

The fallacy of Anecdotal Evidence mimics this legitimate use of illustrative story-telling. It presents us with a case that puts a human face upon a conclusion. The fallacy of Anecdotal Evidence errs, however, in using the single case in place of the properly conducted study. The fallacy implies that the anecdote is illustrating a properly drawn conclusion, when in fact it is attempting to replace the proper inductive argument altogether.

In some ways this fallacy is similar to Uncharacteristic Sample and also to Hasty Generalization. Like Uncharacteristic Sample, the sample is not adequately diverse, and so is unrepresentative of the class it is chosen to represent. Like Hasty Generalization, the sample is (usually) too small to support a general conclusion. However, I treat this as a separate fallacy in the Circularity category. The implication of an anecdote is that it is just one representative instance, and that many other instances could be cited as well. If this presumption is true (and often it isn't), then the reasoning is neither hasty nor uncharacteristic. However, it is still circular, since the anecdote is offered as a "sample" only because it supports the desired conclusion.

Second, have you guys ever heard of the placebo effect?

"The physician's belief in the treatment and the patient's faith in the physician exert a mutually reinforcing effect; the result is a powerful remedy that is almost guaranteed to produce an improvement and sometimes a cure." -- Petr Skrabanek and James McCormick, Follies and Fallacies in Medicine, p. 13.

Forty years ago, a young Seattle cardiologist named Leonard Cobb conducted a unique trial of a procedure then commonly used for angina, in which doctors made small incisions in the chest and tied knots in two arteries to try to increase blood flow to the heart. It was a popular technique -- 90 percent of patients reported that it helped -- but when Cobb compared it with placebo surgery in which he made incisions but did not tie off the arteries, the sham operations proved just as successful. The procedure, known as internal mammary ligation, was soon abandoned ("The Placebo Prescription" by Margaret Talbot, New York Times Magazine, January 9, 2000).*

Doctors in one study successfully eliminated warts by painting them with a brightly colored, inert dye and promising patients the warts would be gone when the color wore off. In a study of asthmatics, researchers found that they could produce dilation of the airways by simply telling people they were inhaling a bronchiodilator, even when they weren't. Patients suffering pain after wisdom-tooth extraction got just as much relief from a fake application of ultrasound as from a real one, so long as both patient and therapist thought the machine was on. Fifty-two percent of the colitis patients treated with placebo in 11 different trials reported feeling better -- and 50 percent of the inflamed intestines actually looked better when assessed with a sigmoidoscope ("The Placebo Prescription" by Margaret Talbot, New York Times Magazine, January 9, 2000).*

Peace.

The following link is to a statement from a chemist saying that she finds Piracetam helpful for meditation and lucid dreaming:

Statement about Piracetam

What is the benefit of lucid dreaming?

Click HERE to rent this advertising spot for BRAIN HEALTH to support LongeCity (this will replace the google ad above).

The following link is to a statement from a chemist saying that she finds Piracetam helpful for meditation and lucid dreaming:

Statement about Piracetam

What is the benefit of lucid dreaming?

It looks like hella fun, regardless of any benefit.