Vanadium

Vanadium (V) is a transition metal that occurs naturally as a trace element in the human diet. In nutritional supplements, it is most often provided as vanadyl sulfate or sodium metavanadate, with the primary aim of supporting metabolic pathways that resemble insulin signaling and, consequently, glucose and lipid homeostasis.

• Insulin‑mimetic activity: Clinical trials in people with impaired glucose tolerance show that 50–100 µg of vanadium daily can modestly lower fasting glucose and improve insulin sensitivity (e.g., Hurlbut et al., 2003).
• Lipid metabolism: Small‑scale studies report reductions in total cholesterol and triglycerides after 12 weeks of supplementation (Kwon et al., 2014).
• Bone health: Vanadium stimulates osteoblast proliferation in vitro and modestly increases bone mineral density in post‑menopausal women when combined with calcium (Gao et al., 2019).
• Antioxidant capacity: Vanadate can scavenge reactive oxygen species and up‑regulate super‑oxide dismutase activity in animal models (Miller & Ghosh, 2020).
• Cognitive/neurological: Limited animal data suggest neuroprotective effects against oxidative stress, but human data are insufficient to claim a definitive benefit.

• Cellular Entry: Vanadium enters cells mainly as the vanadyl (V⁴⁺) or vanadate (V⁵⁺) ion.
• Biological Activity: Inside the cytoplasm, it is reduced to the biologically active vanadyl form, which then binds to phosphate‑binding sites of enzymes such as protein‑tyrosine phosphatases (PTPs).
• Insulin Signaling Amplification: By inhibiting PTPs, vanadium prolongs the phosphorylated state of insulin‑receptor substrates, thereby amplifying insulin‑receptor signaling downstream (PI3K‑Akt pathway). This results in enhanced glucose uptake via GLUT4 translocation and increased glycogen synthesis.
• AMPK Activation: Vanadium also activates the AMPK pathway, promoting fatty‑acid oxidation and reducing hepatic gluconeogenesis.
• Bone Cell Stimulation: In bone cells, vanadium stimulates the MAPK/ERK cascade, leading to increased osteoblast differentiation.
• Antioxidant Effects: Its redox activity enables modest antioxidant effects through direct scavenging of peroxyl radicals and up‑regulation of endogenous antioxidant enzymes.

• Elemental symbol: V, atomic number 23.
• Common supplement form: Vanadyl sulfate (VOSO₄·xH₂O), molecular weight ≈ 162 g mol⁻¹ (anhydrous). IUPAC name: vanadium(IV) sulfate (for VOSO₄).
• Oxidation states: +2, +3, +4, +5; the biologically active species is the vanadyl (V⁴⁺) ion.
• Key structural features: Vanadyl ion is a d¹ configuration (V⁴⁺) with a short V=O double bond (≈ 1.58 Å) in a distorted octahedral coordination sphere. In aqueous solution, vanadate (VO₄³⁻) adopts tetrahedral geometry. Vanadium exhibits high redox flexibility, enabling it to cycle between V⁴⁺ and V⁵⁺ under physiological conditions, which underlies its insulin‑mimetic and antioxidant actions.

• Natural sources: Vanadium is abundant in fossil‑fuel‑derived crude oil, coal ash, and certain mineral ores such as vanadinite (Pb₅(VO₄)₃Cl) and carnotite (K₂(UO₂)₂(VO₄)₂·3H₂O). It also occurs in trace amounts in whole‑grain cereals, mushrooms, and seafood.
• Extraction/synthesis: Commercial vanadium is primarily obtained from the processing of petroleum residues (e.g., vanadium‑rich crude) using solvent-extraction and precipitation as vanadium pentoxide (V₂O₅). V₂O₅ is then reduced and combined with sulfuric acid to produce vanadyl sulfate, the most common supplement form.
• Quality considerations: Good Manufacturing Practice (GMP)‑certified supplements should specify the vanadium species (e.g., vanadyl sulfate) and provide elemental analysis (µg V per capsule). Purity > 99 % and absence of heavy‑metal contaminants (lead, arsenic) are essential for safety. Testing for residual sulfates and moisture content (especially for hydrate forms) helps ensure dose consistency.