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VANADIUM: Diabetes Therapy
Source: Dr. Atkins Vita-Nutrient Solution
Author: Robert C. Atkins, M.D.

The case for nutrients to replace pharmaceuticals is powerfully strengthened by the recent explosion of knowledge about a trace mineral that dramatically helps diabetics: vanadium.


Diabetes is on a dramatic upsurge, and we need all the help we can get. Diabetics make up 4 percent of the population, but use 11 percent of our health dollars. Some medical observers estimate that another eighty million Americans also exhibit some of the characteristics of diabetes-insulin resistance, excess insulin release, high triglycerides, high blood pressure. Plus, the majority of the overweight population has problems related to elevated insulin. Vanadium is on its way to being recognized as an essential nutrient for all who suffer from these insulin-related problems. 1

The human studies with vanadium executed so far are impressive: they show that it can greatly reduce the needs for insulin and hypoglycemic medications. Vanadium also lowers blood sugar as well as the need for insulin. 2,3 Vanadyl sulfate has been found to benefit both Type I and Type II diabetes. In humans it appears to have the insulin-mimicking effect that Type I diabetics4 need, as well as the ability to overcome the insulin resistance that is the defining abnormality in Type II diabetes.5


A nutrient has to jump through many hoops before it can be considered essential. Such an examination is now taking place for vanadium. While a handful of studies have suggested that the mineral is essential for animals, its status for humans has yet to be proven. Though we do ingest 10-60 micrograms per day from food, there have not been any studies in humans that examine the effects of a vanadium-free diet. One thing, however, appears clear from animal studies: vanadium is vitally important in the treatment of diabetes. 6

1. Brichard, S., et al., Trends in Pharmacological Sciences, 1995; 16(8): 265-70.
2. Orvig, C., et al., Metabolic Ions In Biological Systems, 1995; 31: 575-94.
3. Boden, G, et al., Metabolism, 1996; 45(9): 1130-35.
4. Yuen, V., et al., Canadian Journal of Physiology and Pharmacology, 1995; 73: 55-64.
5. Cohen, N., et al., Journal of Clinical Investigation, 1995; 95(6): 2501-09.
6. Harland, P., et al., Journal of the American Diabetic Association, 1994; 94(8): 891-94.


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