Mineral

Molybdenum

Molybdenum (Mo, element 42)

Evidence TierAWADA NOT PROHIBITED

tuneTypical Dose

45–75

watchEffect Window

N/A, requirement-based nutrient status.

check_circleCompliance

WADA NOT PROHIBITED

Overview

Clinical Summary

Molybdenum is a trace mineral cofactor for enzymes such as sulfite oxidase and xanthine oxidase. It is used mainly in rare deficiency or specialized clinical nutrition contexts.

True molybdenum deficiency is rare, but correction prevents neurologic and metabolic complications in severe malnutrition or long-term parenteral nutrition. Its key role supports sulfite detoxification and amino acid metabolism. Minority claims involve detox support, but direct outcome evidence is limited. For typical diets, additional molybdenum provides little clear benefit and excessive intake may be harmful.

Functions as a molybdopterin cofactor for sulfite oxidase, xanthine oxidase, aldehyde oxidase, and mARC enzymes.

Outcomes

What This Is Expected To Influence

Primary Outcomes

Essential cofactor for sulfite oxidase, xanthine oxidase, and aldehyde oxidase

Secondary Outcomes

Sulfite detoxification
Purine metabolism

Safety

Contraindications and Interactions

Contraindications

Copper deficiency
Severe kidney impairment without supervision

Side effects

Gout-like symptoms at very high doses
Copper depletion at >10 mg/day

Interactions

No significant known interactions

Avoid if

Gout-prone populations at high doses
Renal impairment without supervision

Evidence

Study-level References

molybdenum-SRC-001Review

Sourceopen_in_new

Sardesai VM. Molybdenum: an essential trace element. Nutr Clin Pract. 1993;8(6). doi:10.1177/0115426593008006277. PMID:8302261.

Population: Review of human and animal literature on molybdenum as an essential trace element

Dose protocol: Not an efficacy dosing trial. Review of deficiency pathology and cofactor biochemistry.

Key findings: Molybdenum is a required cofactor for sulfite oxidase, xanthine oxidase, and aldehyde oxidase. Acquired deficiency during prolonged TPN and inborn cofactor errors cause fatal neurological damage from sulfite accumulation, establishing biological necessity.

Notes: Evidence strongly supports essentiality and deficiency harm. It does not support routine nootropic enhancement beyond adequacy.

Paper content

This review covers molybdenum as an essential trace element, focusing on its role as part of molybdenum cofactor required for xanthine oxidase, aldehyde oxidase, and sulfite oxidase. Deficiency is rare in free-living humans but has been reported in prolonged parenteral nutrition, and inborn errors of the cofactor cause severe neurological disease.

molybdenum-SRC-002Retrospective and prospective open-label studies with natural history comparison

Sourceopen_in_new

Schwarz G, Basel DG, Schwahn BC, et al. Increased Survival in Patients With Molybdenum Cofactor Deficiency Type A Treated With Cyclic Pyranopterin Monophosphate. J Inherit Metab Dis. 2025;48(2). doi:10.1002/jimd.70000. PMID:40132614.

Population: Patients with molybdenum cofactor deficiency Type A, treated (N=14) vs untreated (N=37)

Dose protocol: Open-label prospective and retrospective cohort studies of fosdenopterin (synthetic cPMP) replacement in MoCD Type A patients (N=14 treated vs N=37 untreated natural history).

Key findings: Treated patients had significantly reduced risk of premature death compared with untreated patients (Cox hazard ratio 5.1, 95% CI 1.32-19.36, p=0.01). Urinary S-sulfocysteine and xanthine normalized in treated patients but remained abnormal in untreated patients. Treated patients showed improved cognitive and motor milestones on Bayley subscales.

Notes: Confirms that restoring molybdenum cofactor function via cPMP replacement prevents the lethal neurological consequences of MoCD Type A. Reinforces essentiality evidence. Does not support supplementation beyond adequacy in healthy populations.