You are kidding!! Vanadyl Sulphate?! I have never met one person who has benefited from this supplement, not one!
Not flaming anybody who thinks they have, but are you sure?? I'd say leave it out your arsenal as all the studies I've seen show it to be beneficial only in diabetic rats! But feel free to prove me wrong.
Effect of acute and short-term administration of vanadyl sulphate on insulin sensitivity in healthy active humans.
Jentjens RL, Jeukendrup AE.
Human Performance Laboratory, School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, B15 2TT Birmingham, UK.
Vanadium compounds have been shown to have insulin-like properties in rats and non-insulin-dependent diabetic humans. The purpose of the present study was to examine whether the effects of acute and short-term administration of vanadyl sulfate (VA) on insulin sensitivity also exist in healthy active individuals. Five male and two female participants (age: 24.9 +/- 1.5 years; height: 176.1 +/- 2.9 cm; body mass: 70.1 +/- 2.9 kg) underwent 3 oral glucose tolerance tests (OGTT). The first OGTT was performed to obtain a baseline index of insulin sensitivity (ISI). On the night preceding the second OGTT, participants ingested 100 mg of VS, and the acute effects of VS on ISI were examined. For the next 6 days, participants were instructed to ingest 50 mg of VS twice daily, and a final OGTT was performed on day 7 to determine the short-term effects of VS on ISI. No differences were found in fasting plasma glucose and insulin concentrations after VS administration. Furthermore, ISI after 1 day and 7 days of VS administration was not different compared with baseline ISI (4.8 +/- 0.1 vs. 4.7 +/- 0.1 vs. 4.7 +/- 0.1, respectively). These results demonstrate that there are no acute and short-term effects of VS administration on insulin sensitivity in healthy humans.
Oral vanadyl sulphate does not affect blood cells, viscosity or biochemistry in humans.
Fawcett JP, Farquhar SJ, Thou T, Shand BI.
School of Pharmacy, University of Otago, Dunedin, New Zealand.
Vanadyl sulphate (VOSO4) is used to improve performance in weight training athletes. Concerns about its safety have arisen because vanadium compounds may cause anaemia and changes in the leukocyte system. In this study, the effects of oral VOSO4 (0.5 mg/kg/day) on haematological indices (red and white cell and platelet counts, red cell mean cell volume and haemoglobin level), blood viscosity (haematocrit, plasma viscosity and blood viscosity at 10s-1 and 100s-1 shear rates) and biochemistry (lipids and indices of liver and kidney function) were investigated in a twelve week, double blind, placebo controlled trial in 31 weight training athletes. Blood viscosity was evaluated at 0, 2, 4, 8 and 12 weeks and haematological indices and biochemistry were measured before and at the end of treatment. Both the treatment group and placebo group showed increases in haematocrit (3.3-3.6%) and blood viscosity (9-11% at 100s-1 shear; 35-38% at 10s-1 shear) but there were no significant effects of treatment. Similarly there were no treatment effects on haematological indices and biochemistry. Concerns about the adverse effects of oral vanadyl sulphate on blood are not supported by the results of this trial.
Vanadyl sulfate inhibits NO production via threonine phosphorylation of eNOS.
Li Z, Carter JD, Dailey LA, Huang YC.
Center for Environmental Medicine, Asthma and Lung Biology, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
Exposure to excessive vanadium occurs in some occupations and with consumption of some dietary regimens for weight reduction and body building. Because vanadium is vasoactive, individuals exposed to excessive vanadium may develop adverse vascular effects. We have previously shown that vanadyl sulfate causes acute pulmonary vasoconstriction, which could be attributed in part to inhibition of nitric oxide production. In the present study we investigated whether NO inhibition was related to phosphorylation of endothelial nitric oxide synthase (eNOS). VOSO4 produced dose-dependent constriction of pulmonary arteries in isolated perfused lungs and pulmonary arterial rings and a right shift of the acetylcholine-dependent vasorelaxation curve. VOSO4 inhibited constitutive as well as A23187-stimulated NO production. Constitutive NO inhibition was accompanied by increased Thr495 (threonine at codon 495) phosphorylation of eNOS, which would inhibit eNOS activity. Thr495 phosphorylation of eNOS and inhibition of NO were partially reversed by pretreatment with calphostin C, a protein kinase C (PKC) inhibitor. There were no changes in Ser1177 (serine at codon 1177) or tyrosine phosphorylation of eNOS. These results indicate that VOSO4 induced acute pulmonary vasoconstriction that was mediated in part by the inhibition of endothelial NO production via PKC-dependent phosphorylation of Thr495 of eNOS. Exposure to excessive vanadium may contribute to pulmonary vascular diseases.