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Because this subtle modification leads to increased brain uptake and alpha-2 receptor affinity, it is preferred over the natural alkaloid both for distribution and activity. Vinpocetine is quickly metabolized and excreted as vincamine, the natural product. It has a plasma half-life of only about two hours. Of course, this means that it's best taken about three times per day, a minor inconvenience considering its substantial effects on memory. Memory enhancement is in fact a property of alpha-2 adrenergic agents in general: Yohimbine, guanfacine, and clonidine are all alpha-2 agents. They’ve been shown to positively affect memory in humans and other primates. And, perhaps counterintuitively, both agonists and antagonists of the alpha-2 receptor can enhance memory at certain doses: The alpha-2 antagonists do it in smaller concentrations by blocking presynaptic alpha-2 receptors, the “inhibitory feedback” ones… They increase brain adrenaline by making the body think it's low. On the other hand, agonists of the alpha-2 receptor inhibit memory at smaller concentrations and then enhance it at larger ones… This occurs when their effect at postsynaptic receptors overrides those at presynaptic ones. In this manner, adrenergic drugs can demonstrate opposing effects on memory that depend on dose. Agonists display a U-shaped curve and antagonists the inverted form. The effect of vinpocetine on memory is consistent with it being a weak alpha-2 antagonist, stimulating adrenaline formation by blocking inhibitory alpha-2 receptors. And since vinpocetine it is so rapidly metabolized and doesn't build up, there is very little opportunity for the reverse effect to occur. With doses ranging from 0 to 40 mg per day, vinpocetine goes from having no effect towards having progressively beneficial effects. The relatively low potency and short half-life of vinpocetine makes it safe. These two built-in safety measures ensure consistent pro-memory results in human trials… And there have been enough of those to confidently ascertain the proper dose range. In addition, there is also evidence that vinpocetine exerts its effects primarily through brain alpha-2 receptors: This study involved twelve healthy females aged 25 to 40 years. The researchers gave them either 10, 20, or 40 mg of vinpocetine per day. Although the subjects were few in number, it was a crossover designed study. That means that each subject served as their own control. Since each subject participates in both placebo and vinpocetine trial arms, studies of this type eliminate the chance of unequal allocation between groups. The researchers used four different kinds of tests: - Reaction time - General arousal - Memory - And a self-rating scale There were no changes in arousal, reaction time, or self-rating... yet, in a bizarre fashion, vinpocetine selectively improved memory This was a dose-dependent effect, with the 40 mg per day group exhibiting the greatest improvements: The selectivity shown by vinpocetine on memory is unique to adrenergic drugs. Although it did not improve the “choice reaction time” or “flicker fusion” tests, this matters little because there are other drugs for those issues. In other words, the parameters that are not improved by vinpocetine are the very same ones enhanced by cholinergic drugs, or those that increase acetylcholine and/or act on its receptors… Nicotine, galantamine, huperzine, and uridine monophosphate are all natural ways to increase general attention and state of arousal. In fact, no single drug can be expected to do everything; there is no single brain structure or neurotransmitter responsible for all activity. Yet it does seem apparent that the brain alpha-2 adrenergic system has peculiar effects on memory – and vinpocetine could be worth taking for that reason alone. Besides the more well-known cholinergic deficit, Alzheimer's disease is also characterized by reduced adrenergic neurons in the brain. The locus coeruleus is the epicenter of brain adrenergic activity, sending out projections to other regions it decides to modulate. This locus coeruleus has been shown to focus blood flow to areas that need it the most… This effect could be responsible for the retrieval of stored information. “These effects are consistent with the idea that LC-NE (locus coeruleus/norepinephrine) enhances coupling of blood distribution changes with local oxygen demands and improves the ability to quickly redistribute blood to subsequently active brain regions.” Incidentally, the ability to increase cerebral blood flow is the classic effect of vinpocetine. More research has been conducted on vinpocetine's ability to help people recover from stroke than anything. Even though the majority of vinpocetine-memory studies focus on Alzheimer's disease, this supplement is actually used as much in vascular dementia than any other type. Vascular dementia is simply that induced by impaired blood flow to the brain. “Early experiments with vinpocetine indicated five main pharmacological and biochemical actions: (1) selective enhancement of the brain circulation and oxygen utilization without significant alteration in parameters of systemic circulation…” Vinpocetine doesn't affect peripheral blood flow much because of its rapid brain uptake and high elimination rate through the kidneys. Even the highest doses (about 17 mg) will only lead to plasma concentrations of 100 ng/ml, a concentration too low to do much of anything in the bloodstream... This dose corresponds to a concentration of only .288 μM, and the only reason vinpocetine is active at all is because of its high brain uptake.  It has been shown using radioactive vinpocetine that 3.7% of the dose ends up in the brain… And that’s high, considering the brain only accounts for 1.8% of total body mass. Using the same 16.9 mg dose as in the pharmacokinetic study, and a 1.4 liter brain volume, this would imply that vinpocetine levels are four to five times higher in the brain than in the plasma (1.28 μM vs .288 μM). And this 1.28 μM brain concentration would translate to a approximately 16% displacement of rauwolscine from the alpha-2 receptor… That is significant when considering that it is one of the strongest ligands known. Even adrenaline itself has trouble displacing rauwolscine, an effect explained by the two occupying slightly different binding sites on the receptor. Vinpocetine also has mild activity on the dopamine receptor (usually a good thing)...  And its metabolite vincamine interacts with the beta-1 receptor.  But there's much more indication that vinpocetine works primarily on alpha-2 adrenergic receptors, such as this study below: This study used intravenous vinpocetine in living rats.  The researchers removed a small portion of their skulls to facilitate access to the locus coeruleus – the brain region that sends out projections of adrenergic neurons to activate other areas. Then they administered graded doses of vinpocetine to the rats – all the while measuring the firing rate of the isolated neurons. Vinpocetine clearly caused an increase in firing rate (of neurons): And the doses used weren't all that high. The upper limit of 1 mg/kg (for mice) corresponds to 80 mg in average-sized humans. Considering that about 40 mg of vinpocetine per day is the effective dose, you'd be forced to conclude this effect would occur at clinical concentrations. The author of the study is under the impression that vinpocetine's effects can be ascribed to adrenergic activity alone… And that viewpoint is perfectly in accordance with all the data I've seen. “The effective dose range was in very good agreement with the dose range corresponding to the memory-enhancing effects of the compound. Our results supplied direct electrophysiological evidence that vinpocetine increases the activity of ascending noradrenergic pathways. This effect can be related to the cognitive-enhancing characteristics of the compound.” Yet, despite the overwhelming evidence pointing towards vinpocetine being an alpha-2 antagonist, no mention is made of this in mechanistic sections of review articles. The more common explanations of vinpocetine's effect involve sodium channels, NMDA receptors, and the enzyme phosphodiesterase. Yet the concentrations needed to inhibit these targets are all highly unrealistic… The phosphodiesterase activity is the only one of those (besides alpha-1/alpha-2 receptors) worth considering. “Vinpocetine produced a dose-dependent increase in the firing rate of locus coeruleus neurons in a dose range which was in very good agreement with the doses corresponding to the memory-enhancing effects of the compound.” The NMDA receptor is a glutamate ion channel that acts to increase intracellular calcium. Although vinpocetine inhibits this receptor in vitro, the high levels required preclude this mechanism from consideration. Moreover, this NMDA antagonist activity would have effects uncharacteristic of vinpocetine – should concentrations even get that high. Piracetam is a nootropic drug that also increases cerebral blood flow – but it does so by activating the NMDA receptor, inhibiting it. And since there are two other forms of glutamate receptors (the AMPK and kainate subtypes), a weak and selective NMDA inhibitor would do little by way of total glutamate inhibition. The idea that vinpocetine exerts its effects through sodium channels should be embarrassing to whoever first proposed it… But its inhibitory effects on phosphodiesterase are certainly interesting and relevant. The inhibition of phosphodiesterase can actually explain the reliable increase in guanosine triphosphate (GTP) induced by vinpocetine. However, increased cyclic guanosine monophosphate (cGMP) coincidentally is also the classic effect of alpha-2 receptors. (cGMP is a cyclic nucleotide derived from GTP.) “This effect is not in agreement with the report by Greengard (1979) who subdivided the neurotransmitters into two classes: neurotransmitters associated with the cGMP system (alpha-adrenoceptors) and neurotransmitters associated with cAMP system (beta-adrenoceptors).” It is peculiar there are two rational ways to explain the classic cGMP rise that occurs with vinpocetine – receptor antagonism and enzyme inhibition. But its Ki (measure of bond tightness between an enzyme and a corresponding enzyme inhibitor) on phosphodiesterase is consistently measured at 14 to 15 μM… So I think it's safe to exclude that from occurring in vivo. And if vinpocetine indiscriminately increased cGMP everywhere, as implied by inhibiting phosphodiesterase (a ubiquitous enzyme), it would probably just have the ultimate effect of a metabolic stimulant… ...and not that of a powerful nootropic. Yet vinpocetine is more complex and has been shown to have specific effects on the locus coeruleus, cerebral brain flow, and memory. For these reasons, and a few more, vinpocetine is probably best viewed as an alpha-2 antagonist – somewhat similar to yohimbine. “The above effect of vinpocetine is consistent with the finding of Olpe...that cognitive enhancers activate the noradrenergic neurons in the locus coeruleus.” Vinpocetine is a man-made chemical similar to a substance found in Vinca minor (periwinkle) plant. It’s not approved for therapeutic use in the U.S., but is widely available in dietary supplements, often marketed as nootropics. It’s banned for sale as a supplement in Australia, Canada, and New Zealand. ----Important Message---- Use this oxygen-promoting secret to double penile blood flow in 45 seconds The key to getting impressively rigid and engorged “down there” anytime you want? Great blood flow. Because the more oxygen-rich blood you have flowing into your penile chambers, the bigger and thicker you will be “down there.” As blood rushes into every nook and cranny of your member, you will swell up with power and last for 30 minutes or more.  [And this oxygen-promoting secret actually doubles penile blood flow in just 45 seconds.](  ---------- Daily Medical Discoveries is dedicated to uncovering secret, buried or censored studies that can help men live great lives to 120 and beyond. You are subscribed because you joined one of our lists by opting in. We never rent or share your email address. Daily Medical Discoveries is published by Calworth Glenford LLC which also publishes other affiliated companies. By giving us your email address, you consent for Daily Medical Discoveries and its affiliated companies to delivering you a healthy daily portion of email issues and advertisements. 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