Active Component:

• Organic Vanadium IV Nicotinate

• Calcium Citrate

• Phytosterols

• Riboflavin

 

Form:
Org-V comes as a brilliant green powder to be added at 60mg to 150mg per serve of finished product. This performance ingredient is certified and guaranteed in purity using Fourier Transform (Infra-Red) Raman Spectroscopy. It imparts a metallic taste profile.

 

Recommended Application:

• 60mg - 150mg per serve of finished product (do not exceed recommendations)

  • Endurance training 

  • Weightloss

  • Energy enhancement

 

Research Highlights:

• Potent increase in muscle metabolism and energy availability

• Insulin-like activity in muscle

• Weightloss effect

• Reduced oxidative stress

• Reduced ‘bad’ (HDL) cholesterol

 

Permissible Label and Advertising Claims Under FSANZ:

• Contributes to the protection of cells from oxidative stress

• Contributes to the reduction of tiredness and fatigue

• Contributes to normal energy metabolism

• Reduces blood cholesterol

 

Research Details:

The primary wealth of research regarding vanadium’s effects on humans has been concerned with its capability to significantly increase muscle glucose utilisation along with increasing insulin sensitivity and inhibiting many of the negative effects associated with diabetes. Vanadium is present in small quantities in most foodstuffs, and although it is currently unclear exactly what vanadium’s role is as a trace nutrient, there is some evidence to suggest that it serves as a regulator for phosphate-dependent proteins and is important for healthy cell development (Pessoa, Garribba, Santos, & Santos-Silva, 2015). Consumption of vanadium has been linked to a variety of health outcomes beyond its metabolic benefits, including inhibition of tumor growth (Crans, Yang, Haase, & Yang, 2018), as well as action against various pathogens/diseases such as trypanosomiasis, leishmaniasis, amoebiasis, tuberculosis, pneumonia, HIV, and exhibition of cardioprotective and neuroprotective properties (Rehder, 2016).

 

Vanadium is most metabolically useful and bioavailable in the form of a +IV oxidised organic vanadyl chelate, which is important to maximise the health benefits attainable from this mineral. This class of structure has been demonstrated to increase GLUT4 expression in skeletal muscle, enhancing glucose uptake for up to 72 hours following a very large oral dose of 0.6 mmol/kg or about 190mg/kg in rats (Mohammad, Sharma, & McNeill, 2002). With lower, more human-realistic doses, this effect may last 24 hours (Li, Zhang, Yang, & Gou, 1991). These organic vanadium compounds also increase protein phosphatase 1 activity in skeletal muscle, potentially enhancing conversion of glucose to glycogen for storage and thus maintaining muscle energy availability and increasing glucose utilisation/metabolism, although the effect on glycogen is debated (Semiz, & McNeill, 2002; Goldfine, Patti, Zuberi, Goldstein, LeBlanc, Landaker, & Kahn, 2000; Foot, Bliss, Fernandes, Da Costa, & Leighton, 1992; Semiz, Orvig, & McNeill, 2002). Vanadium ions have been described to ‘exert true insulin-like action on isolated muscle glucose metabolism’ in this regard, particularly compared with related minerals which do not confer this benefit to nearly the same degree (Fürnsinn, Englisch, Ebner, Nowotny, Vogl, & Waldhäusl, 1996). Vanadium chelates have even been explored as potential insulin replacements in the treatment of diabetes (Shechter, Goldwaser, Mironchik, Fridkin, & Gefel, 2003). This is likely due to their ability to enhance muscle cell response to insulin via increased insulin receptor sensitivity, although there may be other enhancing mechanisms also (Cusi, Cukier, DeFronzo, Torres, Puchulu, & Redondo, 2001; Mohammad, Bhanot, & McNeill, 2001; Mohammad, Wang, & McNeill, 2002). Vanadium compounds improve the activity of at least 40 genes downstream of insulin in models of diabetes where their expression is adversely affected or dysregulated (Wei, Li, & Ding, 2007; Willsky, Chi, Liang, Gaile, Hu, & Crans, 2006). 

 

Importantly, while vanadium use decreases blood-sugar it does not result in hypoglycemia, unlike insulin, and thus works to normalise blood-sugar levels (Willsky, Chi, Liang, Gaile, Hu, & Crans, 2006; Hei, Chen, Pelech, Diamond, & McNeill, 1995).

 

Vanadium has also been demonstrated to assist with weightloss in diabetes models, reducing the resultant oxidative stress markers in muscle tissue (Kurt, Ozden, Ozsoy, Tunali, Can, Akev, & Yanardag, 2011). There is evidence to suggest that this weight loss benefit, along with decreased appetite, can be seen within 9 days of ongoing use (Venkatesan, Avidan, & Davidson, 1991). Further, its use is associated with decreased total cholesterol and HDL levels (Goldstein et al., 2000). There is also evidence for vanadium-induced protection against diabetic damage to kidney and liver tissue, particularly beta cells (Mongold, Cros, Vian, Tep, Ramanadham, Siou, & Serrano, 1990).

 

References:

Crans, D. C., Yang, L., Haase, A., & Yang, X. (2018). Health benefits of vanadium and its potential as an anticancer agent. Met. Ions Life Sci, 18, 251-279.

 

Cusi, K., Cukier, S., DeFronzo, R. A., Torres, M., Puchulu, F. M., & Redondo, J. P. (2001). Vanadyl sulfate improves hepatic and muscle insulin sensitivity in type 2 diabetes. The Journal of Clinical Endocrinology & Metabolism, 86(3), 1410-1417.

 

Foot, E., Bliss, T., Fernandes, L. C., Da Costa, C., & Leighton, B. (1992). The effects of orthovanadate, vanadyl and peroxides of vanadate on glucose metabolism in skeletal muscle preparations in vitro. Molecular and cellular biochemistry, 109(2), 157-162.

 

Fürnsinn, C., Englisch, R., Ebner, K., Nowotny, P., Vogl, C., & Waldhäusl, W. (1996). Insulin-like vs. non-insulin-like stimulation of glucose metabolism by vanadium, tungsten, and selenium compounds in rat muscle. Life sciences, 59(23), 1989-2000.

 

Goldfine, A. B., Patti, M. E., Zuberi, L., Goldstein, B. J., LeBlanc, R., Landaker, E. J., & Kahn, C. R. (2000). Metabolic effects of vanadyl sulfate in humans with non—insulin-dependent diabetes mellitus: in vivo and in vitro studies. Metabolism, 49(3), 400-410.

Hei, Y. J., Chen, X., Pelech, S. L., Diamond, J., & McNeill, J. H. (1995). Skeletal muscle mitogen-activated protein kinases and ribosomal S6 kinases: suppression in chronic diabetic rats and reversal by vanadium. Diabetes, 44(10), 1147-1155.

 

Kurt, O., Ozden, T. Y., Ozsoy, N., Tunali, S., Can, A., Akev, N., & Yanardag, R. (2011). Influence of vanadium supplementation on oxidative stress factors in the muscle of STZ-diabetic rats. Biometals, 24(5), 943.

 

Li, S., Zhang, T., Yang, Z., & Gou, X. (1991). Distribution of vanadium in tissues of nonpregnant and pregnant Wistar rats. Hua xi yi ke da xue xue bao= Journal of West China University of Medical Sciences= Huaxi yike daxue xuebao, 22(2), 196.

 

Mohammad, A., Bhanot, S., & McNeill, J. H. (2001). In vivo effects of vanadium in diabetic rats are independent of changes in PI‐3 kinase activity in skeletal muscle. Molecular and cellular biochemistry, 223(1-2), 103-108.

 

Mohammad, A., Sharma, V., & McNeill, J. H. (2002). Vanadium increases GLUT4 in diabetic rat skeletal muscle. Molecular and Cellular Biochemistry, 233(1-2), 139-143.

 

Mohammad, A., Wang, J., & McNeill, J. H. (2002). Bis (maltolato) oxovanadium (IV) inhibits the activity of PTP1B in Zucker rat skeletal muscle in vivo. Molecular and cellular biochemistry, 229(1-2), 125-128.

 

Mongold, J. J., Cros, G. H., Vian, L., Tep, A., Ramanadham, S., Siou, G., & Serrano, J. J. (1990). Toxicological aspects of vanadyl sulphate on diabetic rats: Effects on vanadium levels and pancreatic B‐cell morphology. Pharmacology & toxicology, 67(3), 192-198.

 

Pessoa, J. C., Garribba, E., Santos, M. F., & Santos-Silva, T. (2015). Vanadium and proteins: uptake, transport, structure, activity and function. Coordination chemistry reviews, 301, 49-86.

 

Rehder, D. (2016). Perspectives for vanadium in health issues. Future Medicinal Chemistry, 8(3), 325-338.

 

Semiz, S., & McNeill, J. H. (2002). Oral treatment with vanadium of Zucker fatty rats activates muscle glycogen synthesis and insulin-stimulated protein phosphatase-1 activity. Molecular and cellular biochemistry, 236(1-2), 123-131.

 

Semiz, S., Orvig, C., & McNeill, J. H. (2002). Effects of diabetes, vanadium, and insulin on glycogen synthase activation in Wistar rats. Molecular and cellular biochemistry, 231(1-2), 23-35.

 

Shechter, Y., Goldwaser, I., Mironchik, M., Fridkin, M., & Gefel, D. (2003). Historic perspective and recent developments on the insulin-like actions of vanadium; toward developing vanadium-based drugs for diabetes. Coordination Chemistry Reviews, 237(1-2), 3-11.

 

Venkatesan, N., Avidan, A., & Davidson, M. B. (1991). Antidiabetic action of vanadyl in rats independent of in vivo insulin-receptor kinase activity. Diabetes, 40(4), 492-498.

 

Wei, D., Li, M., & Ding, W. (2007). Effect of vanadate on gene expression of the insulin signaling pathway in skeletal muscle of streptozotocin-induced diabetic rats. JBIC Journal of Biological Inorganic Chemistry, 12(8), 1265-1273.

 

Willsky, G. R., Chi, L. H., Liang, Y., Gaile, D. P., Hu, Z., & Crans, D. C. (2006). Diabetes-altered gene expression in rat skeletal muscle corrected by oral administration of vanadyl sulfate. Physiological genomics, 26(3), 192-201.