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Noah Robinson
Noah Robinson

Buy Piracetam Online



Hello, I'm new to the nootropics scene and am a student at uni in England and tried Ritalin which I was really impressed with. A friend is also sending me some Modafinil which could be pretty good, but these are just temporary concentration enhancers really. After doing some research I think I'd like to try piracetam, I read it improves your general cognition and also social ability which I really want to try out.




buy piracetam online



Reputable UK-based nootropic sites don't sell piracetam because it is prescription-only in the UK. However, they do sell aniracetam, oxiracetam, noopept, nefiracetam, pramiracetam, sunifiram, phenylpiracetam and even coluracetam. IMHO these are better than plain piracetam for the simple reason that you need to take a lot less of them for very similar effect. If you want it for study with a slight stimulant effect, I'd suggest oxiracetam, but take it with citicoline. Two reputable sites are: nootropics.co.uk (which sells most of its -racetams in pill form, rather than capsules) and mindnutrition.com which sells powders as well as capsules (don't bother with their premixed formulas, though -- they mix in too many things). One that does sell piracetam (but they call it nootrocetam) is nootropics.eu . They used to be UK based, but seem to be taking their payments now via a Spanish payment processing system. I think it's so that they can sell piracetam. As for intellimeds.co.uk -- I have to say I've used them without any problem (most recently for coluracetam, but previously for noopept powder, oxiracetam and others). Again, they don't sell piracetam, but they do sell almost everything else. If you want the real deal, manufactured as a prescription medicine, then Doc Simon's piracetam / geratam (same thing) is the way to go, and pay the high postage costs (but cheap product). I preferred geratam because it is pure white and doesn't have the sunset-yellow colouring that the other brand they sell has in it.


I ordered some piracetam from New Star Nootropics last year, and I had no issues. It declared on the packaging what it was, and as it's not illegal to import without a prescription, there were no issues.


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Piracetam has been shown to improve the function of the neurotransmitteracetylcholinewhich is vital for cognitive function and memoryprocesses. Furthermore, piracetam may have an effect on NMDA glutamatereceptors, which are involved with higher learningand memoryprocesses. Some research suggest that piracetam can also be used to treat depression and anxiety. Piracetam must be taken with a choline supplement to prevent choline deficiencies.


Originally marketed by UCB Pharma in 1971, piracetam was the first nootropic drug to modulate cognitive function without causing sedation or stimulation 1. It is not approved for any medical or dietary use by the FDA. In the UK, piracetam is prescribed mainly for myoclonus, but is used off-label for other conditions such as learning difficulties in children, memory loss or other cognitive defects in the elderly, and sickle-cell vaso-occlusive crises 4. Evidence to support its use for many conditions is unclear.


Piracetam modulates the cholinergic, serotonergic, noradrenergic, and glutamatergic neurotransmission although the drug does not display high affinity to any of the associated receptors (Ki >10μM). Instead, piracetam increases the density of postsynaptic receptors and/or restore the function of these receptors through stabilizing the membrane fluidity 1. In the forebrain of aging mice, the density of NMDA receptors was increased by approximately 20% following 14 days of piracetam treatment. Based on the findings of various animal and human studies, the cognitive processses including learning, memory, attention and consciousness were enhanced from piracetam therapy without inducing sedation and psychostimulant effects 5. Piracetam mediate neuroprotective effects against hypoxia-induced damage, intoxication, and electroconvulsive therapy 5.


In two studies involving alcohol-treated rats with evidences of withdrawal-related neuronal loss, piracetam was shown to reduce the extent of neuronal loss and increase the numbers of synapses in the hippocampus by up to 20% relative to alcohol-treated or alcohol-withdrawn rats 1. This suggests that piracetam is capable in promoting neuroplasticity when recoverable neural circuits are present 1. Although the mechanism of action is not fully understood, administration of piracetam prior to a convulsant stimulus reduces the seizure severity and enhances the anticonvulsant effectiveness of conventional antiepileptics such as carbamazepine and diazepam 3.


Piracetam interacts with the polar heads in the phospholipids membrane and the resulting mobile drug-lipid complexes are thought to reorganize the lipids and influence membrane function and fluidity 1. Such interaction has been reported in a study that investigated the effects of neuronal outgrowth induced by beta amyloid peptides; while amyloid peptides cause lipid disorganization within the cell membranes leading to neuronal death, piracetam demonstrated to decrease the destabilizing effects of amyloid peptide 2. The authors suggest that piracetam induces a positive curvature of the membrane by occupying the polar groups in the phospholipids to counteract the negative curvature induced by amyloid peptides , which in turn would decrease the likelihood of membrane fusion 1. This mechanism of action is thought to improve membrane stability, allowing the membrane and transmembrane proteins to maintain and recover the three-dimensional structure or folding for normal function 4 such as membrane transport, chemical secretion, and receptor binding and stimulation 1.


Through restored membrane fluidity, piracetam promotes restored neurotransmission such as glutamatergic and cholinergic systems, enhances neuroplasticity and mediates neuroprotective and anticonvulsant effects at the neuronal level 1. It is also demonstrated that piracetam also improves the fluidity of platelet membranes. At the vascular level, piracetam decreases adhesion of erythrocytes to cell wall and reduces vasospasm which in turn improves microcirculation including cerebral and renal blood flow 1.


Piracetam displays a linear and time-dependent pharmacokinetic properties with low intersubject variability over a large range of doses. Piracetam is rapidly and extensively absorbed following oral administration with the peak plasma concentration is reached within 1 hour after dosing in fasted subjects. Following a single oral dose of 3.2 g piracetam, the peak plasma concentration (Cmax) was 84 µg/mL. Intake of food may decrease the Cmax by 17% and increase the time to reach Cmax (Tmax) from 1 to 1.5 hours. Tmax in the cerebrospinal fluid is achieved approximately 5 hours post-administration 4.


Piracetam is predominantly excreted via renal elimination, where about 80-100% of the total dose is recovered in the urine. Approximately 90% of the dose of piracetam is excreted in the urine as unchanged drug 4.


The cases of overdose with piracetam is rare. The highest reported overdose with piracetam was oral intake of 75g which was associated with diarrhea and abdominal pain; the signs were most likely related to the extreme high dose of sorbitol contained in the used formulation. In cases of acute, significant overdosage, stomach emptying by gastric lavage or induced emesis is recommended as there are no known antidotes for piracetam 4. Management for an overdose will most likely be symptomatic treatment and may include hemodialysis, where the extraction efficacy of the dialyser is 50 to 60% for the drug 4.


INTRODUCTION: previous studies have suggested that smoking, living alone and having a high body mass index may increase risk of developing dementia whereas a normal body mass index, having received education and moderate alcohol consumption may decrease risk. Dementia risk also increases with age and is thought to be higher in hypertensives. METHOD: we used data collected in the Hypertension in the Very Elderly Trial (HYVET), and cognitive function was assessed using the Mini-Mental State Examination (MMSE) at baseline and annually. Participants with a fall in MMSE to 30 (HR 1.84, 95% CI 1.24-2.72), increased risk of incident dementia as did piracetam use (HR 2.72, 95% CI 1.60-4.63). Receiving formal education was associated with a reduced risk (HR 0.59, 95% CI 0.45-0.78). There was no association with smoking, alcohol and gender. Similar results were found when examining mean annual change in the MMSE score. DISCUSSION: our results for BMI and education agree with those from other studies. The increased risk associated with piracetam may reflect awareness of memory problems before any diagnosis of dementia has been made. Trial participants may be healthier than the general population and further studies in the general population are required. 041b061a72


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