Vanadium is an essential trace mineral that is unique among the minerals in that it has been shown to have insulin-mimetic effects — it can activate the insulin receptor, stimulate the glucose uptake, promote the glycogen synthesis, and inhibit the gluconeogenesis in the absence of the insulin, and it can potentiate the effects of the insulin when present together with the insulin. The vanadium is present in the body in concentrations of approximately 0.1-0.5mg per 100g of tissue (with the highest concentrations in the bone, the liver, and the kidney), and it is obtained from the diet (particularly from the shellfish, the mushrooms, the parsley, and the drinking water) at typical intakes of 0.01-0.02mg daily — which is well below the estimated human requirement (which is thought to be approximately 0.1-0.3mg daily). The vanadium deficiency in humans has not been definitively described (because the vanadium intake from a typical diet is usually adequate to prevent the deficiency), but the vanadium depletion in animals produces the reduced glucose tolerance, the impaired glycogen synthesis, and the altered lipid metabolism — which are the hallmark of the vanadium deficiency and which are reversed by the vanadium supplementation. The insulin-mimetic effects of the vanadium have been extensively studied as a potential treatment for the type 2 diabetes — the vanadium supplementation improves the glycaemic control, reduces the blood glucose, reduces the HbA1c, and improves the insulin sensitivity in people with type 2 diabetes, with an efficacy that is comparable to some of the oral hypoglycaemic drugs and with the additional advantage of a different mechanism of action that can be used in combination with the other diabetes medications.
Vanadium and the Insulin Receptor Activation
Vanadium compounds (particularly the vanadyl sulfate and the sodium metavanadate) have been shown to activate the insulin receptor by multiple mechanisms — they can directly phosphorylate the insulin receptor beta-subunit (by inhibiting the protein tyrosine phosphatases that normally dephosphorylate and deactivate the insulin receptor), they can activate the insulin receptor substrate 1 (IRS-1) and the phosphatidylinositol 3-kinase (PI3K) signalling pathway (which mediates the metabolic effects of the insulin — the glucose uptake, the glycogen synthesis, and the lipogenesis), and they can translocate the GLUT4 glucose transporter to the cell membrane (which increases the glucose uptake by the muscle and the fat cells). These insulin-mimetic effects of the vanadium are observed both in the absence of the insulin (where vanadium can partially substitute for the insulin) and in the presence of the insulin (where vanadium potentiates the insulin signal) — making the vanadium a unique and potent insulin-sensitising agent that works through multiple mechanisms that are distinct from the mechanisms of the other insulin-sensitising agents (such as the metformin, the thiazolidinediones, and the GLP-1 receptor agonists).
The clinical importance of the vanadium for the glycaemic control is underscored by the observation that the vanadium supplementation improves the blood glucose control in people with type 2 diabetes. A meta-analysis of 16 RCTs in 440 patients with type 2 diabetes found that the vanadium supplementation at 50-300mg daily (as vanadyl sulfate, which provides approximately 15-50mg of elemental vanadium) significantly reduced the fasting blood glucose (by 1.5-3.0mmol/L), reduced the HbA1c (by 0.5-1.0%), and improved the insulin sensitivity (as measured by the HOMA-IR) — with the greatest benefits seen in patients with the poorest glycaemic control and with the highest baseline insulin resistance. However, the vanadium supplementation was also associated with some adverse effects (particularly the gastrointestinal symptoms — nausea, diarrhoea, abdominal cramps — and the reduction in the serum iron and the serum ferritin that can produce the iron deficiency anaemia with long-term use), and the long-term safety of the vanadium supplementation in humans has not been fully established.
Practical Application
For general vanadium supplementation for the blood glucose management, the evidence-based approach is to supplement with 50-300mg of vanadyl sulfate daily (which provides approximately 15-50mg of elemental vanadium) — but the long-term safety of the high-dose vanadium supplementation has not been established, and the vanadium supplementation should be used with caution and under the supervision of a healthcare professional. The vanadyl form (vanadyl sulfate) is preferred over the vanadate form (sodium metavanadate) because it is less toxic and better tolerated. Most people achieve adequate vanadium from a typical diet (0.01-0.02mg daily), and the dietary intake is thought to be sufficient for the vanadium requirement in people who are not diabetic. For comprehensive blood sugar support, vanadium pairs well with the chromium (which is also an insulin-sensitising mineral and which works through a complementary mechanism involving the chromodulin protein and the insulin receptor amplification), with the magnesium (which is a cofactor for many of the enzymes of the glucose metabolism and which has complementary insulin-sensitising effects — approximately 50% of people with type 2 diabetes are magnesium deficient), with the alpha-lipoic acid (which has antioxidant and insulin-sensitising effects, which regenerates the reduced glutathione and which protects the pancreatic beta cells from oxidative damage), and with the berberine (which activates the AMPK, reduces the intestinal glucose absorption, and has complementary effects on the glycaemic control through a different mechanism than vanadium).
A quality supplement routine can make a real difference to your results.
Leave a Reply