Molybdenum and Copper Excretion
Yes, molybdenum can help with copper excretion, specifically in the form of tetrathiomolybdate for treating copper overload in Wilson's disease. 1
Mechanism and Clinical Application
Molybdenum as tetrathiomolybdate is used to treat copper overload in Wilson's disease at a dose of 120 mg/day divided into 6 doses of 20 mg each. 1 This represents a formal guideline recommendation from ESPEN (European Society for Clinical Nutrition and Metabolism) published in Clinical Nutrition in 2022. 1
How Molybdenum Affects Copper
The interaction between molybdenum and copper works through several pathways:
Molybdenum increases fecal copper excretion by forming complexes that prevent copper absorption and enhance biliary excretion of absorbed copper. 2, 3 This is the primary route of copper elimination when using molybdenum therapy.
High concentrations of molybdenum can induce copper deficiency in animals through competitive mechanisms, demonstrating its potency in reducing copper bioavailability. 1
Tetrathiomolybdate specifically binds to hepatic copper in proportion to liver copper content, with the copper-molybdenum complexes then being excreted predominantly through feces rather than urine. 4
Important Clinical Distinctions
Wilson's Disease vs. General Copper Toxicity
For Wilson's disease specifically:
- D-penicillamine (250-500 mg/day initially) remains the first-line chelation therapy according to the American Association for the Study of Liver Diseases. 5, 6
- Tetrathiomolybdate serves as an alternative copper-reducing agent when standard chelation is not suitable. 1
For acute copper poisoning:
- Standard chelation with D-penicillamine is preferred as it induces cupruresis (urinary copper excretion), allowing for more precise individual monitoring. 3
Route of Excretion Matters
Molybdenum supplementation does NOT increase urinary copper excretion - it works exclusively by increasing fecal copper elimination. 2, 3 In contrast, penicillamine induces cupruresis, making it more suitable when individual monitoring of copper elimination is needed. 3
Safety Considerations
The upper tolerable limit for molybdenum is 2 mg/day for general supplementation, with toxicity reported at 300-800 mg/day causing hallucinations and seizures. 1 However, therapeutic doses of tetrathiomolybdate (120 mg/day) for Wilson's disease have been used safely under medical supervision. 1
Key Caveats
Individuals with copper deficiency or inadequate dietary copper are at greater risk of molybdenum toxicity since molybdenum can further deplete copper stores. 7
Molybdenum absorption is highly efficient (approximately 90%), but most absorbed molybdenum is eliminated through urine, not feces. 1, 2 This contrasts with the copper-molybdenum complexes, which are excreted in feces.
Regular monitoring of both copper and liver function is essential when using molybdenum therapy for copper overload. 5
Practical Algorithm
For copper overload management:
Confirm diagnosis with serum copper, ceruloplasmin, 24-hour urinary copper, and slit-lamp examination for Kayser-Fleischer rings. 5, 6
For Wilson's disease: Initiate D-penicillamine as first-line; consider tetrathiomolybdate (120 mg/day in divided doses) as alternative. 1, 6
For acute copper poisoning: Use D-penicillamine for better monitoring capability through urinary copper measurement. 3
Monitor response through serial copper levels and liver function tests every 6-12 months. 5