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MOLYBDENUM
What does it do? Molybdenum is an essential trace mineral. It is needed for the proper function of certain enzyme-dependent processes, including the metabolism of iron. Preliminary evidence indicates that molybdenum, through its involvement in detoxifying sulfites, might reduce the risk of sulfite-reactive asthma attacks.1 However, a physician should be involved in the evaluation and treatment of sulfite sensitivity.
Where is it found? The amount of molybdenum in plant foods varies significantly and is dependent upon the mineral content of the soil. The best sources of this mineral are beans, dark green leafy vegetables, and grains. Hard tap water can also supply molybdenum to the diet. Molybdeum is also available as a supplement.
Molybdenum has been used in connection with the following condition (refer to the individual health concern for complete information):
| Rating | Health Concerns |
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Asthma |
 Reliable
and relatively consistent scientific data showing a substantial health benefit. Contradictory, insufficient, or preliminary studies
suggesting a health benefit or minimal health benefit. An herb is primarily supported by traditional use, or
the herb or supplement has little scientific support and/or minimal health benefit. |
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Who is likely to be deficient? Although molybdenum is an essential mineral, no deficiencies have been reported in humans.
How much is usually taken? No recommended dietary allowance (RDA) has been established for molybdenum. The estimated range recommended by the Food and Nutrition Board as safe and adequate is 75–250 mcg per day for adults.
Are there any side effects or interactions? Molybdenum is needed to convert purine to uric acid, and excessive intake could, in rare cases, increase uric acid levels and potentially trigger gout. Molybdenum interferes with the absorption of copper; long-term supplementation with molybdenum could, in theory, result in copper deficiency. Molybdenum has been reported to cause psychosis in a patient taking 300 to 800 mcg per day for 18 days. This report is as yet unsubstantiated by any other human or animal research.2
References:
1. Johnson JL, Wuebbens MM, Mandell R, et al. Molybdenum cofactor deficiency in a patient previously characterized as deficient in sulfite oxidase. Biochem Med Metabol Biol 1988;40:86–93.
2. Momcilovic B. A case report of acute human molybdenum toxicity from a dietary molybdenum supplement—a new member of the “Lucor metallicum” family. Arh Hig Rada Toksikol 1999;50:289–97.
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