90 Vegi-Caps AOR04028
100% Vegetarian
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SUPPLEMENT FACTS:
Serving Size: 1 Capsule %DRI
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Vinpocetine (from Voacanga africana (seed)) ..... 15 mg *
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*Dietary Reference Intake not established.
Other ingredients: microcrystalline cellulose. Capsule: vegetarian (hydroxypropylmethylcellulose).
AOR guarantees that no ingredients not listed on the label have been added to the product. Contains no wheat, gluten, corn, nuts, dairy, soy, eggs, fish, or shellfish.
Suggested Use
Take one to three capsules daily, or as directed by a qualified health consultant.
Main Applications
As reported by literature:
Cognitive enhancement.
ARCD.
Cerebrovascular disorders.
Hearing function.
Kidney function.
Eye health.
Source
Voacanga Africana (seed).
Pregnancy / Nursing No studies have been conducted. Best to avoid.
Cautions
None known.
To function optimally, the brain needs a steady supply of nutrients, including glucose for fuel and oxygen with which to burn it, creating ATP, the cellular energy reserve. Many people rely on Ginkgo biloba to help ensure the delivery of these nutrients, because it enhances cerebral microcirculation - the flow of blood into the tiny capillaries feeding the cells of the brain. But Ginkgo has its limits as a cognitive-enhancing botanical. For one thing, it`s a bit of a one-act pony, having little impact on brain function beyond this one effect (increasing microcirculation). As well, Ginkgo cannot be used by persons taking "blood-thinning" drugs (i.e. anticoagulants, such as warfarin (Coumadin)) because of drug interactions: when combined with warfarin or even aspirin, Ginkgo can dangerously increase bleeding times, putting a person at risk of hemorrhagic stroke.
A phytonutrient found in the periwinkle (Vinca minor) and originally developed by the Hungarian pharmaceutical giant Gedden Richte transcends these limitations. Vinpocetine is a true cerebral metabolic enhancer. While Vinpocetine, like Ginkgo biloba, enhances cerebral microcirculation, Vinpocetine is especially remarkable in this regard, as it does so without reducing blood flow elsewhere in the body, by reducing the resistance of fine blood vessels within the brain. It accomplishes this by reducing excessive activity by a form of the enzyme type 1 phosphodiesterase in the brain - a mechanism similar to Viagra, which acts on another form of the same enzyme in the penis. In effect, Vinpocetine is Viagra for the brain.
But Vinpocetine also supports brain metabolism by mechanisms not related to its effects on microcirculation, and thus in no way shared by Ginkgo. First, by enhancing red blood cells` ability to "flex" their shape so as to more easily cross the blood-brain barrier (the layer of tight cell-to-cell contacts that protects the brain from a potentially-toxic environment), Vinpocetine directly supports the delivery of oxygen to the brain. Additionally, Vinpocetine facilitates the take-up and release of blood sugar across the blood-brain barrier, supporting optimal partitioning of fuel supplies. And studies in red blood cells and damaged neurons show that Vinpocetine directly increases ATP levels in these cells, supporting optimal brain energy levels.
Vinpocetine also demonstrates powerful neuroprotective effects. By subjecting experimental animals to simulated strokes, scientists have been able to show that Vinpocetine provides protection against the brain damage that follows the cutting off of oxygen and glucose delivery, reducing the ravaging cerebral edema that follows the stroke and prolonging survival of both brain cells and the organism as a whole.
These neuroprotective effects can be partly attributed to Vinpocetine`s ability to maintain brain cell metabolism during the ischemic crisis, but also to Vinpocetine`s role as a powerful antioxidant scavenger of hydroxyl radicals. More recently, research has demonstrated Vinpocetine`s power to regulate the flow of ions across neuron membranes, notably voltage-dependent neuronal sodium-ion channels and some of the molecular cascades initiated by the flood of calcium ions into the cell. These ion flows are upset in moments of crisis such as excitotoxicity and during a stroke, and lead to brain cell death. Thus, by regulating sodium channels, and moderating the downstream effects of opened calcium floodgates, Vinpocetine delivers another important mechanism of brain cell protection.
Vinpocetine, like Ginkgo, has a mild anticoagulant effect, which can protect the brain against the formation of killer blood clots, which can cut off circulation in the brain, triggering a stroke. But unlike Ginkgo, Vinpocetine has no clinically significant interactions with "blood-thinning" drugs, making it safe for users of aspirin, warfarin, and other common anticoagulants.
Vinpocetine also has more direct effects on brain function. Most importantly, Vinpocetine increases long-term potentiation (LTP), the increase in the strength of neuroelectrical transmission between neurons, which happens when the same association is made repeatedly, and which helps move information from short-term memory into long-term memory. In other words, Vinpocetine facilitates the more permanent storage of information in the brain by stimulating the central cellular mechanism, which forms the basis of learning and memory.
Many clinical trials have demonstrated Vinpocetine`s ability to support brain function. Most of these trials have been performed in stroke victims, but research also supports Vinpocetine`s positive impact on cognitive function in organic dementias and in normal, healthy adults. A meta-analysis of seven double-blind clinical trials involving a total of 731 people suffering from age-related dementias or cognitive deficits following a stroke found that Vinpocetine improved cognitive and neurological function on a wide variety of measures, including scores tests of memory and mental function like the Sandoz Clinical Assessment-Geriatric (SCAG) and the Mini-Mental Status Questionnaire (MMSQ), neurological symptoms such as coordination and repetitive speaking patters (palilalia), and overall functional status as evaluated using the Clinical Global Impression (CGI) scale. Furthermore, there were no serious side effects related to Vinpocetine use. Overall, the investigators concluded, the results of these trials prove that patient users of Vinpocetine "become more vivid, the cognitive performance improves, and the daily activity is more intense."
Vinpocetine may also have important benefits outside of the brain. Studies in persons who have suffered damage to the nerves of the ears after exposure to high-intensity noise levels have reported that Vinpocetine improves hearing and reduces tinnitus, especially if initiated within the first week after trauma. Vinpocetine also appears to support visual health by improving microcirculation in the eye in the capillaries of the retina itself, the central arteries feeding the retina, and the layer of the eye between the retina and the white outer coat of the eyeball. Studies using closely-related Vinca alkaloids suggests that Vinpocetine may be of specific use in normal-tension glaucoma, and Vinpocetine itself was reported to enhance the effectiveness of drugs that lower intraocular pressure in the treatment of glaucoma in an open study. Finally, Vinpocetine was reported to remove calcification of the kidneys associated with long-term calcification; similar removal of soft-tissue calcifications has been demonstrated in other tissues in animal models.
The standard dose used in clinical trials is 15 to 45 milligrams of Vinpocetine daily.
References
Nagy Z, Vargha P, Kov¡cs L, B¶n¶czk P. Meta-analysis of Cavinton. Praxis. 1988 Sep; 7(9):63-8.
Subhan Z, Hindmarch I. Psychopharmaco-logical effects of vinpocetine in normal healthy volunteers. Eur J Clin Pharmacol. 1985;28(5):567-71.
Balestreri R, Fontana L, Astengo F. A double-blind placebo controlled evaluation of the safety and efficacy of vinpocetine in the treatment of patients with chronic vascular senile cerebral dysfunction. J Am Geriatr Soc. 1987 May;35(5):425-30.
Fischhof PK, Moslinger-Gehmayr R, Herrmann WM, et al. Therapeutic efficacy of vincamine in dementia. Neuropsychobiology. 1996;34(1):29-35.
Molnar P, Gaal L, Horvath C. The impairment of long-term potentiation in rats with medial septal lesion and its restoration by cognition enhancers. Neurobiology (Bp). 1994;2(3):255-66.
Kiss B, Karpati E. Mechanism of action of vinpocetine. Acta Pharm Hung. 1996 Sep;66(5):213-24.
Konopka W, Zalewski P, Olszewski J, et al. Treatment results of acoustic trauma. Otolaryngol Pol. 1997;51 Suppl 25:281-4.
Ueyoshi A, Ota K. Clinical appraisal of vinpocetine for the removal of intractable tumoral calcinosis in haemodialysis patients with renal failure. J Int Med Res. 1992 Sep;20(5):435-43.
Kahan A, Olah M. Use of ethyl apovincaminate in ophthalmological therapy. Arzneimittelforschung. 1976;26(10a):1969-72.
Pliushko DG, Sobko EG. Drug therapy of initial open-angle glaucoma. Oftalmol Zh. 1989;(2):72-4.
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