Both animal experimental and human clinical research have shown Vinpocetine to restore impaired brain carbohydrate/ energy metabolism.

In 1976 Vamosi and colleagues reported their favorable results comparing Vinpocetine with Xanthinol Nicotinate in treating 143 patients with various cerebrovascular diseases. They measured a large number of blood and cerebrospinal fluid variables before and after treatment, such as glucose, lactate, pyruvate, oxygen, pH, electrolyte levels, etc. They concluded from their study "…Though not all the changes are significant statistically, yet connected with each other they prove that Vinpocetine enhances both glycolytic and oxidative reactions of glucose breakdown in eNS [brain]. The changes in the concentration of K [potassium] and Mg [magnesium]. .. may be considered a sign of recovery of the energy metabolism of the nerve cells.…"¹

Vamosi's study also demonstrated a superior clinical efficacy of Vinpocetine over Xanthinol Nicotinate.

In his review on the use of Vinca alkaloids in dementia, Nicholson observed that …"…vincamine increases mitochondrial respiratory rate in mitochondrial suspensions ... , indicating that vinca alkaloids can increase the rate of ATP synthesis ... In addition, elevation of cortical cyclic AMP levels may increase ATP availability ... and this may contribute to the metabolic activity of Vinpocetine...."²

Karpati and Szporny resulted favorable results of Vinpocetine used to treat anaesthetized dogs. Anesthetics reduce brain aerobic metabolism and ATP production-this is a key aspect of their ability to produce unconsciousness. Based on their experiments they note that…"…Increase of cerebral arterial-venous oxygen difference, cerebral metabolic rate for oxygen and cerebral oxygen utilization indicate that RGH-4405 [Vinpocetine] affects cerebral metabolism, with a dose-dependent rise in endogenous respiration of cerebral tissue ... Our results indicate that rate of cerebral [energy production] metabolism is increased by Vinpocetine."

Karpati and Szporny conducted a study with cats that were subjected to repeated episodes of brain hypoxia. They reported that "... transitory and partial interference even with normal cerebral circulation caused an increase of Neurochemical disturbances due to hypoxia ... deficient formation of intermediaries in the Krebs cycle was observed, mainly due to shortage of oxygen. These and cytological studies refer to a selective failure of mitochondrial metabolism ... RGH-4405 [Vinpocetine] had favorable effects on these parameters ... It seems probable that the effect of RGH-4405 [Vinpocetine] is even more pronounced in vascular insufficiency..."³

These are just a few of the many reports indicating the ability of Vinpocetine to safely and effectively restore failing neuronal energy metabolism, even under hypoxic or ischaemic (poor blood flow) conditions.


1. B. Vamosi (1976) “Comparative study of the effect of Ethyl Apovincaminate and Xantinol Nicotinate in cerebrovascular diseases” Arzneim Forsch (drug research) 28,1980-84. Hereafter abbreviated “A.F. (D.R.)”
2. C. Nicholson (1990) “Pharmcology of nootropics and metabolically active compounds in relation to their use in dementia.” Psychopharm 101, 147-59.
3. K. Biro (1976) “Protective activity of Ethyl Apovincaminate on ischemic anoxia of the brain” A.F. (D.R.) 28, 1918-20.