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Submitted to: American Chemical Society Symposium Series
Publication Type: Proceedings Publication Acceptance Date: 2/1/1998 Publication Date: N/A Citation: N/A Interpretive Summary: In vitro, pharmacological, and lower life form findings have stimulated speculations about the nutritional importance of vanadium. Between 1971 and 1985 several research groups described possible signs of vanadium deficiency for some animals. However, it was difficult to determine whether the changes caused by vanadium deprivation in these early experiments, which used questionable diets, were true deficiency signs, indirect changes caused by an enhanced need for vanadium in some metabolic function, or manifestations of a pharmacological action of vanadium. Since 1985, studies with goats and rats apparently have found true responses to low intakes of vanadium. Responses of goats fed a vanadium- deficient diet included skeletal deformities and death within 90 days of birth. In rats, vanadium deprivation affected changes in thyroid weight and plasma thyroxine and triiodothyronine concentrations caused by feeding deficient or luxuriant iodine. Vanadium deprivation also depressed the activity of pancreatic amylase, and affected serum lactate dehydrogenase in an opposite manner when dietary iodine was deficient than when it was luxuriant. These findings indicate physiological amounts of vanadium affect thyroid hormone and carbohydrate metabolism, and when combined with the knowledge that homeostatic mechanisms exist for vanadium, and that vanadium has functional roles in lower forms of life, provide circumstantial evidence that vanadium is an essential element for higher forms of life. A daily dietary intake of 10 ug of vanadium probably will meet any postulated vanadium requirements of humans. Technical Abstract: In vitro, pharmacological, and lower life form findings have stimulated speculations about the nutritional importance of vanadium. Between 1971 and 1985 several research groups described possible signs of vanadium deficiency for some animals. However, it was difficult to determine whether the changes caused by vanadium deprivation in these early experiments, which used questionable diets, were true deficiency signs, indirect changes caused by an enhanced need for vanadium in some metabolic function, or manifestations of a pharmacological action of vanadium. Since 1985, studies with goats and rats apparently have found true responses to low intakes of vanadium. Responses of goats fed a vanadium- deficient diet included skeletal deformities and death within 90 days of birth. In rats, vanadium deprivation affected changes in thyroid weight and plasma thyroxine and triiodothyronine concentrations caused by feeding deficient or luxuriant iodine. Vanadium deprivation also depressed the activity of pancreatic amylase, and affected serum lactate dehydrogenase in an opposite manner when dietary iodine was deficient than when it was luxuriant. These findings indicate physiological amounts of vanadium affect thyroid hormone and carbohydrate metabolism, and when combined with the knowledge that homeostatic mechanisms exist for vanadium, and that vanadium has functional roles in lower forms of life, provide circumstantial evidence that vanadium is an essential element for higher forms of life. A daily dietary intake of 10 ug of vanadium probably will meet any postulated vanadium requirements of humans. |
