Molybdenum

Molybdenum is a cofactor for four human enzymes: sulfite oxidase (metabolises sulphur amino acids), xanthine oxidase (catabolises purines to uric acid), aldehyde oxidase, and mitochondrial amidoxime-reducing component. Isolated dietary deficiency has essentially never been documented in humans on normal diets.

Daily requirements

The Abumrad case — how we know molybdenum is essential

In 1981, Abumrad et al. reported a patient on long-term TPN who developed intolerance to sulphur amino acids, tachycardia, headache, night blindness, and coma. Molybdenum supplementation reversed everything within days. This is the case that established molybdenum as a human essential trace mineral. Real-world dietary deficiency in free-living adults has not been reported.

Molybdenum cofactor deficiency (genetic)

A rare autosomal recessive disorder causing loss of sulfite oxidase, xanthine oxidase, and aldehyde oxidase activity. Presents in the neonatal period with intractable seizures, developmental regression, and death in infancy unless treated with cyclic pyranopterin monophosphate (cPMP, fosdenopterin, approved 2021). Not a "dietary molybdenum" issue — the biosynthetic pathway is broken.

Toxicity

High dietary intake (10–15 mg/day, ~200–300× the RDA) has been reported to cause gout-like syndrome via xanthine oxidase induction and elevated uric acid. Environmental cases in high-molybdenum soil regions (parts of Armenia) documented this in the 1960s. Not a real-world concern from supplements or normal diets in most of the world.

Food sources

Any diet containing legumes covers molybdenum many times over. Isolated supplementation is essentially unnecessary in normal circumstances.

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Not medical advice. Neonatal seizures with unusual biochemistry warrant urgent metabolic workup — this is where the rare molybdenum-cofactor deficiency is diagnosed.

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