Life Extension Final Clerance Sale

Life Extension Magazine

LEF Magazine September 1993



Vanadyl Sulfate

A significant problem facing diabetics is a phenomenon known as insulin resistance. Insulin resistance is a failure of cell receptor sites to utilize insulin, thereby causing a dangerous elevation of glucose in the blood. Insulin resistance occurs during aging, and results in impaired glucose metabolism and disposal.

Type I diabetes is caused by the inability of the pancreas to produce insulin. This form of insulin dependent diabetes is also called juvenile diabetes, and sometimes strikes teenagers. In type II, the patient's pancreas produces normal amounts of insulin, but the tissues (muscle, liver, fat) do not respond efficiently to its presence. Current treatments that simply raise insulin levels in the blood can cause severe cardiovascular side effects. In order to prevent these vascular complications, an insulin substitute is needed that will address the underlying problem of insulin resistance.

Historical Use of Vanadium Salts

Undocumented observations from the nineteenth century suggest the use of vanadium to treat diabetes. One documented report in 1899 in France showed that diabetics treated with sodium vanadate excreted less sugar in their urine. Following the discovery of insulin 23 years later, the interest in vanadium salts dissipated.

In 1980, vanadate was demonstrated to mimic the actions of insulin in rats. This was followed by several years of research in which the insulin mimicking effects of vanadate were examined in a large variety of experimental settings. It turns out that vanadate mimics almost all known bioeffects of insulin. This includes the key action of insulin in transporting glucose into muscle and fat cells. One study showed that vanadate could stimulate glucose uptake in cells that had lost 60% of their insulin receptors and were therefore, insulin resistant. These studies provided a basis for studying the potential therapeutic value of vanadium as a therapy for diabetes.

Vanadium Lowers Glucose Levels in Diabetic Animals

A turning point occurred in 1985, when researchers showed that the oral administration of vanadate to type I diabetic rats lowered their blood glucose to normal values. Further studies demonstrated that vanadate therapy can effectively reverse tissue damage caused by chronic elevated glucose levels. In some cases, insulin binding capacity was fully restored, thereby eliminating the problem with insulin resistance.

It should be mentioned that in spite of these findings, insulin therapy is still required for type I diabetic animals, suggesting that vanadate therapy for human type I diabetes will be used a s a supplement, rather than as the primary therapy. In type II diabetic animals, vanadate therapy significantly lowered blood glucose levels and greatly increased the uptake and metabolizing of glucose in all types of muscles. Moreover, vanadate therapy markedly increased overall tissue responsiveness to insulin, thereby dealing with the problem of insulin resistance. For type II diabetics, who produce normal levels of insulin, but whose elevated glucose levels are caused by insulin resistance, vanadate may be an effective therapy.

Vanadyl sulfate is a popular product in the bodybuilding market. Vanadyl sulfate's ability to promote muscle uptake of glucose produces a significant anabolic effect on muscle mass. This anabolic effect is also important for antiaging purposes. Aging causes catabolic wasting of muscle mass. Supplementation with nutrients like arginine, chromium picolinate and vanadyl sulfate can help prevent this condition.

Vanadyl sulfate contains vanadium bound to sulfur. It is considered the most biologically active form of vanadium. Vanadyl sulfate should be taken with meals. The recommended dose is one 7.5 mg tablet per day for life extension purposes. Diabetics may want to adjust their dose to up to four tablets per day. Diabetics should carefully monitor their glucose levels as vanadyl sulfate can cause a significant drop in blood glucose levels causing reactive hypoglycemia.