Here’s the brain booster everybody’s talking about

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[Here’s how to become energy efficient and truly be free.]( ---------- Here’s the brain booster everybody’s talking about Should the general public of the United States, Europe, and Russia be polled with the question: “What is the most notorious smart pill?” ...the answer would likely be “piracetam.” It would, almost certainly, be listed as one of the top three. Similarly, if all neurologists were polled, you'd probably get the very same answer… Such is the reputation piracetam has for increasing cognition. Yet, despite its notoriety as the prototypical “smart pill” and hundreds of studies centered on it, most people seem totally confused as to how it works. It is almost as if the bulk of piracetam research serves as a distraction, obscuring what it does with dozens of red herrings. “The modes of action of piracetam and most of its derivatives remain an enigma.” (Malykh, 2010, taken from his massive 27-page review article on piracetam) Yet three separate teams of researchers working in three areas of the globe – US, England, and Italy – all arrived at the same mechanism independently, which reveals just how piracetam works. Although we had to wait until the turn of the century for the details, the mechanism of piracetam was foreshadowed as early as 1971. Piracetam was shown to protect against hypoxia only a decade after its synthesis, years before the term “nootropic” had even been coined (Sara, 1971). Shortly afterwards came reports of piracetam increasing cerebral blood flow in cats (Vlahov, 1980) and dogs (Nicolova, 1979). Yet these findings remained as obscure as the foreign journals they were printed in. Yet the increased cerebral blood flow caused by piracetam was confirmed in humans two decades later (Kessler, 2000), around the time its molecular pathway was elucidated. Piracetam appears to work primarily by increasing cerebral blood flow… Specifically by activating the NMDA (neuron-to-astrocyte) glutamate receptor subtype in astrocytes: [Can't see this image? Click on 'load images' or 'always allow images for this sender'] (Astrocytes are part of the nervous system.) The Italians were the first to demonstrate this effect in 2002, using slices of rat brain and various techniques. They used a variety of drugs while viewing under a confocal microscope, visualizing individual calcium ions (Ca2+) using a chelator-fluorophore called Indo-1. After Indo-1 binds calcium, its fluorescence emission shifts from green light (485 nm) towards dark blue (405 nm). Below is a false-color image depicting the 405/485 ratio (blue to green), a value that can be taken as representative of Ca2+ concentration. [Can't see this image? Click on 'load images' or 'always allow images for this sender'] A progressively “hotter” color is synonymous with more calcium. They found that astrocyte calcium preceded increases in arteriole diameter. (Arterioles are medium-sized microvessels forming a union between smaller capillaries and larger arteries.) This effect was consistent – it worked no matter how the elevated calcium was introduced into the cell. [Can't see this image? Click on 'load images' or 'always allow images for this sender'] This may seem counterintuitive because calcium is known to cause the constriction of muscles, never a relaxation (Ebashi, 1968). Yet, once it's realized that astrocytes don't express muscle proteins, such as actomyosin, the apparent paradox is revealed as such and deftly resolved. Astrocytes are actually a bit removed from the microvascular, a bit too far away to physically interact with them for effect – were it not for elongated processes. Incidentally, living astrocytes aren't actually star-shaped as sometimes assumed. The cells are actually roundish. But they assume a spiny appearance after they've been dehydrated with alcohol and fixed. [Can't see this image? Click on 'load images' or 'always allow images for this sender'] And of all the drugs they used, they found that the ones that interact with NMDA receptors have the most effect. The NMDA-agonist drug ACPD induced a calcium increase and a marked dilation, while two other drugs, MPEP and LY367385, induced vasoconstriction. This is important, as the NMDA-type glutamate receptor is the only type that piracetam is known to directly activate. Ketamine, an NMDA antagonist, has been shown to completely abrogate the positive effects of piracetam. Ketamine is also an amnesic agent, a function opposed to the memory-facilitative effects of piracetam. In fact, glutamate receptors are the only ones piracetam has significant affinity for: “Even at concentrations of 20 mM of piracetam, no or only marginal inhibition was observed for the dopamine- and muscarinic cholinergic receptors and for the peripheral benzodiazepine binding site...while for the benzodiazepine receptor, the GABA receptor, the opiate receptor, and the serotonin receptor, half-maximal inhibitory concentrations between 20 and 50 mM could be determined.” “In contrast to these effects seen only at relatively high piracetam concentrations, piracetam is considerably more active at the L-glutamate receptor with a half-maximal inhibitory concentration of about 1 mM. This relatively specific effect of piracetam at the L-glutamate receptor could also take place under therapeutic conditions in vivo, since brain levels of piracetam in man may range between 0.1 and 1 m.” “It is concluded that effects within the glutaminergic system of the brain could contribute to the therapeutical effects of piracetam in man.” (Bering, 1985) While piracetam has been shown to upregulate acetylcholine receptors at high doses after some time (Stoll, 1992), it does not bind them directly. And that could be a compensatory mechanism for the increased blood flow. Piracetam also upregulates the NMDA receptor (Cohen, 1993). And moreover, the increase in muscarinic acetylcholine receptors induced by piracetam has been shown to occur only in old rats, not young rats (Pilch, 1988). Muscarinic acetylcholine receptors are expressed in pericytes, a type of contractile cell that surrounds fine capillaries. (These are downstream of arterioles.) They can induce tone and may partially offset the increased blood flow caused by piracetam. After all, we cannot have so much blood flow as to induce excessive capillary leakage. It could be necessary to have more muscarinic receptors at times of increased blood flow, such as during piracetam treatment, to achieve the same amount of vascular control you had before. “Traditionally, it was thought that active neurons generate a metabolic signal (a fall in oxygen or glucose concentration, or a rise in carbon dioxide concentration), which triggers an increase in blood flow.” “This idea has recently been superseded, following the discovery that neurotransmitter-mediated signaling, particularly by glutamate, has a major role in regulating cerebral blood flow, and that much of this control is mediated by astrocytes.” (Attwell) Yet, despite the slight compensation of capillary tone following increased muscarinic receptors, all in vivo studies invariably suggest the net effect of piracetam is to increase cerebral blood flow. [Can't see this image? Click on 'load images' or 'always allow images for this sender'] The likelihood of this being the mechanism is strengthened by subsequent studies… [Can't see this image? Click on 'load images' or 'always allow images for this sender'] Especially considering the fact that they were conducted by different study groups, on separate continents, and using different techniques. Not to be outdone, researchers from New York replicated this effect in vivo. They removed a section of skull bone of living rats and delivered rhodamine-2 – a calcium chelator-fluorophore similar to the one used in the Italian study – into their brains. Yet, unlike the Italians' choice, the fluorophore used by the Americans can be photolysed by light. So, after preloading rhodamine-2 with calcium (Ca2+) and delivering this into the rats, they liberated the rhodamine-bound Ca2+ with light while measuring blood flow. They confirmed the calcium-dependent increase previously reported… But unfortunately this group didn’t test any glutaminergic drugs. But confirmation of the primacy of glutamate signaling had come in 2016… A team of Londoners showed that arterioles and capillaries were under different control mechanisms (Mishra, 2016). “However, again unlike the capillary dilation, arteriole dilation was strongly inhibited by blocking NMDA receptors or NO synthase.” (Mishra) This should be no surprise really, as capillaries are small enough to be surrounded by one cell. Pericytes engulf capillaries with claw-like projections somewhat like a giant squid. And each one is spaced apart by a few microns. The contractile proteins of pericytes provide the physical force needed to physically modulate microvessel diameter. And the larger arterioles and much larger arteries and controlled by other mechanisms. While piracetam looks nothing like glutamate, it is nearly identical to its cyclic pyroglutamate form. Glutamate and glutamine can be transformed into cyclic pyroglutamate… Pyroglutamate got its name due its formation through heat, or pyrolysis. But it's also known to occur enzymatically within the body. [Can't see this image? Click on 'load images' or 'always allow images for this sender'] Piracetam is almost an isomer of pyroglutamine, and quite similar to pyroglutamate besides. Also never mentioned is the fact that, like all dicarboxylic acids, glutamate is a strong calcium chelator. Oxalic acid is the smallest dicarboxylic acid, and known to induce kidney stones in large amounts. The presence of oxalic acid in spinach is often cited as the explanation for the unusually low calcium bioavailability of that particular leaf. [Can't see this image? Click on 'load images' or 'always allow images for this sender'] It has been shown that aldosterone is necessary for piracetam to work. (Aldosterone is a steroid hormone produced in the adrenal gland. Among other things, it is involved in regulating blood pressure.) After the offhand discovery that adrenalectomy prevents piracetam action, three subsequent studies confirmed that various animals need aldosterone (Mondadori, 1989). This would make little sense unless viewed under a paradigm involving blood pressure as a central tenet. “...the renin aldosterone system simultaneously co-regulates three functions: sodium balance, potassium balance, and arterial blood pressure.” (Flier, 1985) This seems like a convincing mechanism. And knowing how a drug works provides confidence when using it – and also provides a benchmark to determine timing. Taking certain drugs with piracetam may be redundant, making their combination perhaps trivial. Other cerebral vasodilators such as magnesium and nicotine may blunt piracetam's response. Conversely, certain things could be thought to synergize with piracetam. Nutrients such as choline and glucose would be all the more effective with enhanced cerebral blood flow. And we may achieve enhanced delivery of certain B vitamins needed by the brain (e.g. thiamine, folate, cobalamin) in such conditions. “If blood flow in capillaries obeys Poiseuille’s law of fluid dynamics, with flow proportional to the fourth power of the vessel diameter, then these values lead to the conclusion that a 2.1-fold capillary dilation produced by superfused glutamate in the presence of noradrenaline could, in principle, increase blood flow 1.18 to 2.98-fold, and thus contribute significantly to functional hyperemia.” (Attwell) ----Important Message---- Restore long-lasting “rockiness” with the power of your pointer finger [Can't see this image? 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