🧬 Family & Essentiality

🌿 Plain-Language Summary

Molybdenum is required only in tiny amounts but is vital as a cofactor for enzymes that process sulfur amino acids, purines, and aldehydes. Deficiency is extremely rare, and most people meet needs easily with a varied diet.

⚗️ Molecular & Chemical IDs

• Element: Mo (Molybdenum)
• Atomic number: 42
• Key enzymes: sulfite oxidase, xanthine oxidase/dehydrogenase, aldehyde oxidase

⚡ Functions

• Detoxifies sulfite → sulfate (via sulfite oxidase)
• Purine metabolism: xanthine → uric acid (via xanthine oxidase)
• Metabolism of aldehydes and some drugs (via aldehyde oxidase)
• Supports balance of sulfur, nitrogen, and purine metabolism

🍽️ Absorption & Bioavailability

🥗 Food Sources

• Legumes (lentils, beans), whole grains
• Nuts, seeds
• Organ meats (e.g., liver)

🇦🇺 Australian NRVs (NHMRC)

• RDI (Adults): 45 µg/day
• Pregnancy: 50 µg/day
• Lactation: 50 µg/day
• UL (Adults): 2000 µg/day

🚨 Deficiency & Excess

Deficiency (very rare)

Seen in genetic MoCo deficiency → severe neurologic problems. Acquired deficiency has been reported in long-term TPN without molybdenum supplementation.

Excess

High intakes may raise uric acid, causing gout-like symptoms. Very high doses may interact with copper status.

🧪 Testing & Monitoring

• No routine biomarker for clinical use
• Plasma or urinary Mo measured in research or specialised labs

🔄 Interactions

• High molybdenum intake may reduce copper status
• Important to balance overall trace mineral intake (Mo, Cu, Zn)

📊 Evidence Snapshot

• 🔬✅ Well-established: Cofactor for sulfite and purine metabolism enzymes
• ⚠️❌ Unproven/hype: Claims for energy or performance benefits at high intakes are unsupported