Molybdenum

Your intake

What each level of molybdenum does

Approximate dose-response bands. Individual response varies — these are starting points, not prescriptions.

1. Severely lowYOU ARE HERE

   0 mcg – 14.85 mcg

   Well below target. Risk of deficiency symptoms tied to sulfite oxidase.

2. Insufficient

   14.85 mcg – 45 mcg

   Below the recommended daily target. Long-term adequacy not assured.

3. Adequate

   45 mcg – 67.5 mcg

   Daily target met. Standard nutritional support for sulfite oxidase.

4. Therapeutic

   67.5 mcg – 90 mcg

   Common for specific health goals. Check the evidence for your situation before sustaining this level.

5. High

   90 mcg – 2000 mcg

   Approaching the tolerable upper limit. Monitor and consider clinical guidance.

6. Over upper limit

   2000 mcg – +

   Above the tolerable upper limit. Risk of adverse effects — back off or consult a clinician.

Overview

Trace mineral cofactor for four human enzymes (sulfite oxidase, xanthine oxidase, aldehyde oxidase, mitochondrial amidoxime-reducing component). Deficiency is essentially unknown in unrestricted diets; rare congenital co-factor deficiency is severe and presents in infancy.

Functions

• ●Cofactor for sulfite oxidase (sulfite → sulfate)
• ●Cofactor for xanthine oxidase (purine catabolism → uric acid)
• ●Cofactor for aldehyde oxidase (drug and dietary aldehyde metabolism)
• ●Cofactor for mARC (xenobiotic detoxification)

Mechanism

Molybdopterin cofactor is built and inserted into Mo-enzymes that perform oxygen-atom-transfer reactions. Sulfite oxidase is the most clinically critical — its deficiency lets sulfite accumulate and damage neurological tissue, often fatal in infancy.

Benefits

• ●Adequacy supports normal sulfur amino acid and purine metabolism
• ●Used medically (tetrathiomolybdate) to treat Wilson disease
• ●No supplementation benefit established in non-deficient adults

Deficiency

Spontaneous deficiency essentially never reported in unrestricted diets. Inherited cofactor deficiency presents within days of birth with intractable seizures, often fatal without rapid diagnosis.

Excess

Very high intakes (10–15 mg/day) cause gout-like syndromes (xanthine oxidase elevates uric acid) and possible copper deficiency. Far above typical food intake.

Forms

• Sodium molybdate
  Standard supplement form; well-absorbed
• Molybdenum glycinate / citrate
  Chelated multivitamin forms
• Tetrathiomolybdate
  Pharmacologic; copper chelation in Wilson disease

Food sources

• Black-eyed peas (cooked) · 1 cup550 mcg
• Lima beans (cooked) · 1 cup140 mcg
• Lentils (cooked) · 1 cup75 mcg
• Oats (cooked) · 1 cup20 mcg
• Eggs (whole) · 1 large5 mcg
• Plain yogurt · 1 cup10 mcg

Supplement forms

Most multivitamins include 45–75 mcg, which covers the RDA. Standalone molybdenum supplementation has no documented benefit in non-deficient adults.

Bioavailability

~50–90% of dietary molybdenum is absorbed; absorption efficiency is high across forms. Tungsten and excess copper compete for absorption.

Longevity relevance

Adequacy is essential but easily achieved through diet. No supplementation signal for healthspan extension.

Relationships

References

• NIH ODS — Molybdenumguideline
• Linus Pauling Institute — Molybdenumreview

About Molybdenum

Cofactor for sulfite oxidase, xanthine oxidase, aldehyde oxidase.

Role

Sulfite oxidase

Daily target

45 mcg (DV)

Upper limit

2000 mcg

Also called

molybdenum, sodium molybdate, molybdenum glycinate