What is Vincamine?
Unlike the racetams, or the somewhat related compound vinpocetine, vincamine is a naturally derived product. More specifically, it is an indole alkaloid that is purified from the leaves of the periwinkle plant (Vinca minor or Vinca roseus). Periwinkle leaves and seeds have been used in teas and tinctures to treat various ailments in European, Chinese, and Indian culture for hundreds of years. Both Galen and Pliny used it in ancient Rome. Vincamine was not identified as the primary active component until 1953. It was first purified on an industrial scale in 1955. Since that time, it has been used primarily for its vasoactive properties on the circulatory system. It is sold under the names Oxycebral SR, Oxygeron, and many others in Europe, where it is prescribed to treat primary degenerative and vascular dementia. It is sold as a “nootropic” dietary supplement in the U.S., along with its structural derivative vinpocetine.
How does it work?
Vincamine has been called and “oxygenator”, and the names that it is sold under imply its effect. The compound dilates blood vessels, which increases the amount of oxygen (and glucose) that is delivered to tissues. The effect also occurs in the brain and is believed to be due to properties of vincamine’s indole skeleton.
It may also decrease levels of metals (e.g., copper and iron) in the central nervous system (CNS). Although trace levels are are necessary for proper function, excessively high levels are thought to contribute to the formation of reactive oxygen species, especially in Alzheimer’s and Parkinson’s diseases.
Studies suggest that any benefits on cognition are not due to the facilitation of hippocampal activity. This part of the brain is responsible for encoding and accessing memories, and vincamine actually inhibited hippocampal neuronal firing.
Vincamine is touted as a compound that can improve memory, cognition, focus, and attention span. Some users report increased visual acuity, which may be attributable to increased blood flow.
Clinical evidence indicates that it may be useful in elderly patients with neurological complaints, including memory dysfunction, transient ischemic attacks (mini-strokes), and headache.
Vincamine has also been used to treat tinnitus (ringing ears) and hypertension. It lowers blood pressure and increase heart rate in animals.
Limited data from older animal studies suggest that it may have an effect on neurotransmitter levels. Specifically, it decreased acetylcholine esterase in the occipital region of the brain. This would have the net effect of increasing acetylcholine levels/transmission in the visual center of the brain.
Vincamine Side Effects
Vincamine is quite safe, particularly when recommended doses are used. Repeated-dose toxicity studies in the rat (oral doses of 30 or 100 mg/kg/day for 6 weeks) did not show any adverse effects. Moreover, it did not induce genetic mutation in bacteria or mouse lymphoma cells. There are no available studies regarding its potential as a carcinogen (cancer-causing agent). However, most plant-derived products are not carcinogenic.
Most side effects have been reported in studies that used intravenous administration. Minor side effects associate with recommended oral dosing include stomach irritation and headache. Some individuals with pre-existing heart conditions (e.g., long QT syndrome) may develop “torsade de pointe”, a life-threatening arrhythmia, with chronic use of vincamine. However, vinpocetine (a structural derivative of vincamine) does not have this effect. People with blood-related disorders or those on blood thinners should consider consulting their physician before taking vincamine or any other supplement that affects blood pressure.
The recommended dose is 40-80 mg/day and should be maintained for at least 20-40 days. A regimen of 30 mg/day for 12 weeks has been used in clinical trials for dementia. Studies suggest that a plasma (blood) concentration of approximately 0.2 μg/ml is necessary to achieve a pharmacological effect. A relatively high level makes it across the blood-brain barrier into the CNS.
The compound has a short elimination half-life (1.7 hours), so sustained release forms or a twice-daily dose is recommended. A pharmacokinetics study in 8 healthy volunteers suggested that vincamine should be taken with food to maximize absorption into circulation; bioavailability was 60-100% greater when the tablet was taken under non-fasting conditions.
Fayed, A.-H. A. “Brain Trace Element Concentration of Rats Treated with the Plant Alkaloid, Vincamine.” Biol. Trace Elem. Res. 136.3 (2010): 314-19. Print
Fischhof, P.K., R. Möslinger-Gehmayr, W.M. Herrmann, A. Friedmann, and D.L. Russmann. “Therapeutic Efficacy of Vincamine in Dementia.”Neuropsychobiology 34.1 (1996): 29-35. Print.
Lohmann, A., E. Dingler, W. Sommer, K. Schaffler, W. Wober, and W. Schmidt. “Bioavailability of Vinpocetine and Interference of the Time of Application with Food Intake.” Arzneimittelforschung 42.7 (1992): 914-17. Print.
Mitchell, John, and Arthur Rook. Botanical Dermatology: Plants and Plant Products Injurious to the Skin. Vancouver: Greengrass, 1979. Print.
Olpe, Hans-Rudolf, German Barrioneuvo, and Gary Lynch. “Vincamine: A Psychogeriatric Agent Blocking Synaptic Potentiation in Hippocampus.” Life Sciences 31.18 (1982): 1947-953. Print.
Perry, Elaine, and Melanie-Jayne R. Howes. “Medicinal Plants and Dementia Therapy: Herbal Hopes for Brain Aging?” CNS Neuroscience & Therapeutics 17.6 (2011): 683-98. Print.
“SUMMARY OF DATA FOR CHEMICAL SELECTION Vincamine.”http://ntp.niehs.nih.gov/ntp/htdocs/chem_background/exsumpdf/vincamine.pdf. Prepared for NCI by Technical Resources International., Inc., Mar. 2004. Web. 2 Jan. 2012.
Vereczkey, L. “Pharmacokinetics and Metabolism of Vincamine and Related Compounds.” European Journal of Drug Metabolism and Pharmacokinetics 10.2 (1985): 89-103. Print.