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Brain food: vinpocetine – part i by david tolson | mind and muscle articles

StoreAttorneysPractice AreasFaqsContact Us Posted on Sep 3, 2011 in Nootropics, Supplements After piracetam, vinpocetine (ethyl-apovincaminate, 14,-ethoxycarbonyl-(3alpha, 16alpha-ethyl)-14, 15-eburnamine) is perhaps the most well-knownnootropic and is regarded by some as more important [1]. First synthesized about forty years ago,vinpocetine is a derivative of vincamine, which is found in the periwinkle plant (Vinca minor). Othercompounds in the vinca alkaloid family include vinburnine, vintoperol and brovincane [2]. Afterbeing synthesized in Hungary, the neuroprotective and nootropic properties of vinpocetine werediscovered, and appeared under the name Cavinton in 1978. Since that point, it has been used in over40 countries including Japan, Hungary, Germany, Poland and Russia, primarily for the treatment andprevention of stroke and other cerebrovascular diseases [3-4]. This article will discuss theexperimental and clinical research, safety and ideal use of this compound.
In 1955, Vincamine was first extracted in large quantities from the leaves of the periwinkle plant, andin 1959 it was used to treat cerebrovascular disorders. Various active derivatives have beendiscovered and it is thought that the fused, five-membered eburnane ring system is responsible for thepharmacological activity of these compounds [2]. Vinpocetine is a cis (3S, 16S)-derivative ofvincamine, and is the strongest derivative discovered so far. A related compound, vintoperol (thetrans (3S, 16R)-derivative), increases blood flow in the lower extremities (whereas vinpocetineprimarily enhances cerebral blood flow), but produces some toxic side effects [5].
Extensive animal research has been conducted on vinpocetine’s therapeutic effects. It has been foundto have neuroprotective and memory-enhancing effects and other beneficial properties.
Much of the research has focused on vinpocetine’s effects on hypoxia (low oxygen supply) andischemia (low blood supply), both of which are commonly seen during strokes. In a rat model ofcentral ischemia, 77% of hippocampal neurons were damaged, and administration of vinpocetinereduced this damage to 37%. This effect has been replicated, both in rats and other animals, and inother areas of the brain [1, 6]. Vinpocetine’s neuroprotective effect in rats subjected to middlecerebral artery (MCA) occlusion was found to be over twice as effective as other neuroprotectants(nimodipine, MK-801) [7].
Vinpocetine is also neuroprotective in many other situations. It protects against excitotoxicity inducedby glutamate and N-methyl-D-aspartate (NMDA), and is equally as effective as nimodipine [7]. Inrats subjected to radiation, it increases cerebral blood flow and improves central energy metabolism[8]. In cells treated with beta-amyloid, vinpocetine improved mitochondrial function, oxidative stress,and other signs of toxicity [9].
In animal models, vinpocetine also improves learning and memory. In one study, vinpocetineimproved recall on a passive avoidance test [1]. In others, it protected against the deficits caused byscopolamine and hypoxia induced by various means [10].
Vinpocetine may have effects on a wider population than just those that are subjected to braindamage or other injury. To test this, vinpocetine’s effects on astrocytes under normal conditions weremeasured. Vinpocetine significantly increased mitochondrial function and reduced lactatedehydrogenase release while increasing intracellular ATP and phosphocreatine (PCr) concentrationsand cell proliferation [11]. If these effects hold true in in vivo situations, vinpocetine has the potentialto improve brain function in normal individuals.
There is a significant body of evidence indicating that vinpocetine has beneficial effects in humans.
Some of the research is discussed by McDaniel et al. [1]. In three controlled trials involvingindividuals with memory dysfunction of various origins, vinpocetine improved attention,concentration and memory. In two of these studies, vinpocetine caused a 3.1-5.1 improvementrelative to placebo on the Mini-Mental Status Questionnaire (scale of 39), which measures spatial andtemporal orientation skills, mathematical ability, short-term memory and knowledge of synonyms andantonyms. In one study, 87% of patients were rated as improved (11% with placebo), while inanother, 21% were rated as strongly improved (7% with placebo).
These results are similar to those found by other researchers. A meta-analysis of six studies in patientswith “degenerative senile cerebral dysfunction” (total of 731 patients) found that vinpocetine had ahighly significant effect on tests of speech and movement capacity, muscular coordination andstrength, and perceptual ability [6]. However, the research on patients with Alzheimer’s has not beenpromising. A one-year open-label study with 15 patients found no improvement [1, 6]. Given thesmall number of patients, the statistical power of this study was small. Still, it may be that vinpocetineis primarily useful in situations with less cognitive impairment.
Vinpocetine could have multiple benefits for stroke patients. These include increased cerebral blood flow, decreased platelet aggregability, and direct neuroprotective effects [12]. PET studies in chronicstroke patients indicate that vinpocetine increases cerebral glucose uptake and metabolism. In a trialwith 15 chronic ischemic stroke patients, two weeks of vinpocetine treatment significantly increasedcerebral blood flow [6]. Other studies have demonstrated improved cerebral glucose metabolism,oxygenation, and blood flow in stroke patients as well [13]. However, there is not yet enoughresearch to demonstrate improved outcomes in stroke patients given vinpocetine [6].
Vinpocetine has also been examined in the treatment of hearing loss. It is associated with significantimprovement of tinnitus (ear ringing) after acoustic trauma, indicating that it may protect againstnoise-induced hearing loss [6]. It also improved hearing function in patients with tuberculosis [14].
These results are in line with experimental studies, which have found vinpocetine to preventototoxicity.
Little research has examined vinpocetine’s effects in healthy humans. In one study, 20 healthyfemales (age 25-40) were given either 10, 20, or 40 mg of vinpocetine or placebo for a three dayperiods in crossover fashion. On the third day of each period, the subjects underwent a variety ofpsychological tests. On the Sternberg Memory Scanning Test, in which subjects decide whether a digitwas contained in a previously displayed set of 1-3 digits, 40 mg vinpocetine significantly increasedperformance compared to the other groups. No effects were found on other psychological parameters,including performance on a choice reaction time task [1, 15]. It is difficult to draw conclusions fromthis study because of the short treatment periods, but it does suggest that vinpocetine can improvecognition in at least some ways in healthy individuals.
In another study, two weeks of a combined supplement of ginkgo and vinpocetine improved reactiontime and working memory in healthy adults [16]. However, one cannot know whether this effect wasdue to ginkgo, vinpocetine, or the combination.
Like other nootropics, vinpocetine is exceptionally safe. Side effects are not noted with a greaterincidence than placebo in most studies, and no significant side effects have been noted with dosagesup to 360 mg daily [1, 17]. Some studies have reported flushing, rashes, or minor gastrointestinaldiscomfort, but these were not a cause for patient dropouts [6]. The only concern is that vinpocetinedecreases platelet aggregation, so it should not be used—or only used with a high amount ofcaution—with blood thinners [1, 6].
The study in healthy humans gives us a good idea of what vinpocetine’s ideal dosage should be, whichis definitely over 20 mg daily (since 20 mg was not effective, whereas 40 mg was). Similarly, ameta-analysis of Italian and German studies found that 30 mg daily was superior to 15 mg daily [10].
A study in patients with cognitive impairment found that 30 mg daily and 60 mg daily were botheffective [1]. These studies place the probable ideal dosage of vinpocetine at 30-40 mg daily. Indeed,most studies use a dosage of 30 mg daily [6].
Like the other nootropics we have discussed, vinpocetine displays a bell-shaped dose-response curve[1]. For this reason, one should use an effective dose and no more.
Vinpocetine’s absorption in a fasted state is approximately 6.7% [12]. However, if it is taken withfood, this increases to 60-100% [10]. For this reason, it is essential to take vinpocetine with a meal.
The primary metabolites are apovincaminic acid and ethanol (not enough to cause a noticeable effect)[18]. Due to vinpocetine’s low oral bioavailability, transdermal administration has been explored. Adelivery system consisting of 1% vinpocetine, 4% oleic acid, 20% PEG-40 hydrogenated castor oil,10% purified diethylene glycol monoethyl ether, and 65% distilled water (w/w) has been described[19]. However, given that vinpocetine’s desirable dosage can easily be reached at an affordable price,transdermal administration should not be necessary.
After consumption, vinpocetine reaches the bloodstream within a few minutes, crosses theblood-brain barrier, and is present in the brain in 10 minutes [20]. Vinpocetine tends to concentrateitself in the brain, with the concentration about twice the expected level, indicating preferentialuptake [6, 13]. After oral administration to healthy volunteers in one study, maximum CNS levels were seen 100 minutes after administration, and at the 110 minute point a gradual decrease began[13, 21]. According to another article, maximum levels are reached an hour after administration, andthe majority is eliminated by the 8 hour point [10]. The reported half-life ranges from 1-2 to almost 5hours [10, 18]. In any case, it is generally recommended to take vinpocetine three times a day tomaintain adequate levels of the compound.
The present research with vinpocetine is promising, and it makes a worthwhile addition to a nootropicstack. Unlike many other nootropics, research exists indicating that it improves cognition in someways in healthy individuals. The ideal dosage is 10-15 mg three times daily. Part II will explorevinpocetine’s mechanism of action.
For questions or comments regarding this article, email dvdtlsn@bulknutrition.com.
1. Nutrition. 2003 Nov-Dec;19(11-12):957-75. “Brain-specific” nutrients: a memory cure? McDanielMA, Maier SF, Einstein GO.
2. J Chromatogr A. 2003 May 9;996(1-2):195-203. Lipophilicity of vinpocetine and relatedcompounds characterized by reversed-phase thin-layer chromatography. Karoly M, Vamos J, NemesA, Racz A, Noszal B.
3. Altern Med Rev. 2002 Jun;7(3):240-3. Vinpocetine. Monograph. [No authors listed] 4. Acta Neurol Scand. 2002 Dec;106(6):325-32. PET studies on the brain uptake and regionaldistribution of [11C]vinpocetine in human subjects. Gulyas B, Halldin C, Sandell J, Karlsson P,Sovago J, Karpati E, Kiss B, Vas A, Cselenyi Z, Farde L.
5. Acta Pharm Hung. 2002;72(1):25-36. [Investigation of vasoactive agents with indole skeletons atRichter Ltd.] [Article in Hungarian]. Karpati E, Biro K, Kukorelli T.
6. Eur J Pharmacol. 2003 Apr 25;467(1-3):103-9. Pharmacological evidence for a correlationbetween hippocampal CA1 cell damage and hyperlocomotion following global cerebral ischemia ingerbils. Katsuta K, Umemura K, Ueyama N, Matsuoka N.
7. Acta Pharm Hung. 2002;72(2):84-91. [Neuroprotective effects of vinpocetine in vivo and in vitro.
Apovincaminic acid derivatives as potential therapeutic tools in ischemic stroke] [Article inHungarian]. Dezsi L, Kis-Varga I, Nagy J, Komlodi Z, Karpati E.
8. Eksp Klin Farmakol. 2003 Sep-Oct;66(5):14-6. [Effect of vinpocetine on cerebral circulation inrats after exposure to radiation] [Article in Russian]. Vereshchagin VK.
9. Free Radic Res. 2000 Nov;33(5):497-506. Vinpocetine attenuates the metabolic dysfunctioninduced by amyloid beta-peptides in PC12 cells. Pereira C, Agostinho P, Oliveira CR.
10. Brain Res Bull. 2000 Oct;53(3):245-54. Role of sodium channel inhibition in neuroprotection:effect of vinpocetine. Bonoczk P, Gulyas B, Adam-Vizi V, Nemes A, Karpati E, Kiss B, Kapas M,Szantay C, Koncz I, Zelles T, Vas A.
11. Neurotoxicology. 2002 May;23(1):19-31. Piracetam and vinpocetine exert cytoprotective activityand prevent apoptosis of astrocytes in vitro in hypoxia and reoxygenation. Gabryel B, Adamek M,Pudelko A, Malecki A, Trzeciak HI.
12. Chem Pharm Bull (Tokyo). 2003 Aug;51(8):914-22. Investigation and physicochemicalcharacterization of vinpocetine-sulfobutyl ether beta-cyclodextrin binary and ternary complexes.
Ribeiro L, Loftsson T, Ferreira D, Veiga F.
13. J Neurol Sci. 2002 Nov 15;203-204:259-62. Clinical and non-clinical investigations using positronemission tomography, near infrared spectroscopy and transcranial Doppler methods on theneuroprotective drug vinpocetine: a summary of evidences. Vas A, Gulyas B, Szabo Z, Bonoczk P,Csiba L, Kiss B, Karpati E, Panczel G, Nagy Z.
14. Vestn Otorinolaringol. 2003;(3):35-40. [Cavinton prevention of neurosensory hypoacousis inpatients with different forms of tuberculosis] [Article in Russian]. Maliavina US, Ovchinnikov IuM,Fasenko VP, Maliev BM, Kalinina MV, Dadasheva BB.
15. Eur J Clin Pharmacol. 1985;28(5):567-71. Psychopharmacological effects of vinpocetine innormal healthy volunteers. Subhan Z, Hindmarch I.
16. Hum Psychopharmacol. 2001 Jul;16(5):409-416. Cognitive effects of a Ginkgo biloba/vinpocetinecompound in normal adults: systematic assessment of perception, attention and memory. Polich J,Gloria R.
17. World J Urol. 2001 Nov;19(5):344-50. Phosphodiesterase 1 inhibition in the treatment of lowerurinary tract dysfunction: from bench to bedside. Truss MC, Stief CG, Uckert S, Becker AJ, Wefer J,Schultheiss D, Jonas U.
18. Nucl Med Biol. 2002 Oct;29(7):753-9. Cerebral uptake of [ethyl-11C]vinpocetine and1-[11C]ethanol in cynomolgous monkeys: a comparative preclinical PET study. Gulyas B, Vas A,Halldin C, Sovago J, Sandell J, Olsson H, Fredriksson A, Stone-Elander S, Farde L.
19. Pharmazie. 2004 Apr;59(4):274-8. Preparation and evaluation of microemulsion of vinpocetinefor transdermal delivery. Hua L, Weisan P, Jiayu L, Hongfei L.
20. Orv Hetil. 2003 Nov 16;144(46):2271-6. [Human positron emission tomography with oral11C-vinpocetine] [Article in Hungarian]. Vas A, Christer H, Sovago J, Johan S, Cselenyi Z, Kiss B,Karpati E, Lars F, Gulyas B.
21. Eur J Nucl Med Mol Imaging. 2002 Aug;29(8):1031-8. Epub 2002 May 07. Drug distribution inman: a positron emission tomography study after oral administration of the labelled neuroprotectivedrug vinpocetine. Gulyas B, Halldin C, Sovago J, Sandell J, Cselenyi Z, Vas A, Kiss B, Karpati E,Farde L.
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