Vanadium is an essential mineral required in humans for the correct function of the insulin system. In particular, vanadium in the diet may be required to maintain the sensitivity of the cells to insulin. Controversy exists as to the amount of vanadium required in the diet, and it is not fully understood how vanadium is able to cause its insulin sensitising effect. Research suggests that vanadium containing compounds have insulinomimetic effect in humans and animals. Vanadium compounds have been shown to increase glucose uptake by cells, increase glucose oxidation and increase glycogen synthesis. The ability of vanadium compounds to decrease blood glucose levels has been known for many decades. Therefore vanadium compounds may be particularly useful for those with poor insulin sensitivity, and those with severe insulin resistance, such as patients with type 2 diabetes. A number of studies have investigated the ability of the vanadium compound vanadyl sulphate to improve glucose disposal in diabetic patients.
Vanadium is available in some multivitamins. Here is is usually present as vanadyl sulphate. However, generally to take advantages of vanadium compounds, a supplement of vanadyl sulphate must be taken, as the amount of vanadium in multivitamins are very low. Vanadium salts can cause some toxicity if taken in very high amounts for long periods of time, but the safety record of vanadyl sulphate is very good. Vanadyl sulphate is an effective insulin sensitising agent and would be a useful supplement for those who wish to reverse the insulin resistance they may have developed from consuming the Western diet. Athletes can also use vanadyl sulphate as an effective glucose disposal agent. In athletes the increased synthesis of glycogen resulting from vanadyl sulphate supplementation may hold advantages in energy storage in muscle cells.
For example, researchers administered a placebo for 2 weeks, followed by 100 mg per day of vanadyl sulphate for 3 weeks, followed by a placebo for 2 weeks, to patients with type 2 diabetes. These patients were already being treated with sulphonylurea drugs and diet. The insulin resistance in the patients was tested before and after treatment. As expected the glycaemic control at baseline was poor, but improved significantly following treatment with vanadyl sulphate. The improved insulin sensitivity came about through a combination of increased glucose disposal and a decrease in hepatic glucose production. There was also an improved glycogen synthesis following treatment. The improvements caused by the vanadyl sulphate were maintained following the second placebo group when vanadyl sulphate supplementation has ceased. This suggests that vanadyl sulphate is causing beneficial changes to cellular mechanisms of glucose disposal and metabolism, perhaps by repleting the subject of vanadium.
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