Molybdenum Effect on Unbound Copper
Excess molybdenum interferes with copper metabolism by increasing fecal copper excretion and altering copper distribution in the body, which can lead to copper deficiency when molybdenum intake is excessive. 1
Mechanism of Copper Interference
Molybdenum affects copper through multiple pathways:
- Decreases copper absorption from the gastrointestinal tract by forming complexes that prevent copper uptake 2
- Increases biliary excretion of absorbed copper, effectively removing copper that has already entered the body 2
- Alters copper distribution in plasma by creating a non-ceruloplasmin copper fraction that does not react with standard copper assays 3
- Forms copper-molybdenum-sulfur compounds (related to thiomolybdates) that sequester copper and make it biologically unavailable 4
Clinical Significance
Toxicity Risk
The interaction between molybdenum and copper is dose-dependent and clinically relevant:
- In animals, molybdenum toxicity manifests primarily through copper depletion, causing anemia, poor growth, diarrhea, and bone deformities 5
- Copper-deficient individuals are at greater risk of molybdenum toxicity because molybdenum further depletes already inadequate copper stores 6
- The effect is bidirectional: both copper deficiency and copper excess reduce molybdenum's ability to interfere with copper metabolism 3
Safe Dosing Parameters
For routine supplementation in parenteral nutrition:
- Low-birth-weight infants: 1 mcg/kg/day 1
- Infants and children: 0.25 mcg/kg/day (maximum 5.0 mcg/day) 1
- General population upper tolerable limit: 2 mg/day 7
For therapeutic use in copper overload (Wilson's disease):
- Tetrathiomolybdate: 120 mg/day divided into 6 doses of 20 mg each 7
- This therapeutic dose is substantially higher than nutritional requirements and requires medical supervision 7
Monitoring Considerations
When molybdenum supplementation is used:
- Monitor plasma copper and ceruloplasmin levels, especially in patients on long-term parenteral nutrition 1
- Measure copper status every 6-12 months in patients receiving chronic molybdenum supplementation 1, 7
- Consider CRP levels simultaneously with copper measurement, as inflammation elevates ceruloplasmin and can mask copper deficiency 1
Critical Pitfall
The primary clinical concern is copper deficiency induced by excessive molybdenum, not molybdenum toxicity per se. In veterinary medicine, molybdenum is deliberately used to treat copper toxicity 1, demonstrating its potent copper-depleting effect. This same mechanism poses risk in humans with marginal copper status who receive molybdenum supplementation without adequate copper intake 6.