Evidence-based·Last reviewed May 30, 2026·How we grade evidence

Molybdenum

MineralTrace mineral

Useful mainly for correcting confirmed molybdenum deficiency (rare); cofactor enzyme function in affected individuals.

Quick decision guide

May help most

Correcting confirmed molybdenum deficiency (rare); cofactor enzyme function in affected individuals

Common dosing range

45–50 mcg/day (RDA); supplement doses of 50–250 mcg/day are common in multivitamins

When to expect effects

Weeks

Watch out for

High doses (above UL of 2,000 mcg/day) increase copper excretion and raise uric acid

What is it

Molybdenum is an essential trace mineral that serves as a cofactor for four enzymes: sulfite oxidase, xanthine oxidase, aldehyde oxidase, and mitochondrial amidoxime reducing component. It is found in beans, lentils, grains, and organ meats.

Is it worth it for you?

Use this as a quick fit check, not a diagnosis.

Worth considering if

You have confirmed molybdenum deficiency (extremely rare; usually inborn errors or prolonged parenteral nutrition)
You are taking a comprehensive multivitamin that includes molybdenum at RDA levels

Probably skip if

You are seeking detoxification, sulfite sensitivity relief, or antioxidant effects — no clinical evidence
You have gout — high molybdenum activates xanthine oxidase, worsening uric acid
You take high-dose zinc and are concerned about copper deficiency — high molybdenum adds risk

Evidence at a glance

molybdenum cofactor deficiency (genetic or acquired)

Strong Evidence
Effect
Essential for survival in severe cofactor deficiency; prevents progressive neurological damage
Best fit
Patients with confirmed molybdenum cofactor deficiency or prolonged parenteral nutrition without molybdenum
Time
Days to weeks

Evidence for 1 use

AI-assisted evidence assessment — talk to your doctor before relying on any single supplement.

molybdenum cofactor deficiency (genetic or acquired)

Corrects deficiency
Strong Evidence

Molybdenum is an essential cofactor for sulfite oxidase, xanthine oxidase, aldehyde oxidase, and mitochondrial amidoxime reducing component. Genetic molybdenum cofactor deficiency causes severe neonatal neurological disease. Acquired deficiency can occur with long-term parenteral nutrition. Supplementation is lifesaving in these contexts. Dietary deficiency in otherwise healthy adults is essentially unknown.

Effect size
Essential for survival in severe cofactor deficiency; prevents progressive neurological damage
Time to effect
Days to weeks
Best fit
Patients with confirmed molybdenum cofactor deficiency or prolonged parenteral nutrition without molybdenum

Bottom line: Critical for deficiency states; no benefit demonstrated for healthy adults with adequate intake.

How it works

Molybdenum functions inside the body as the molybdenum cofactor (Moco), a complex molecule built around the metal that fits into the active site of molybdenum-dependent enzymes. The most important is sulfite oxidase, which converts toxic sulfite (a byproduct of sulfur amino acid metabolism) to harmless sulfate. Xanthine oxidase breaks down purines to uric acid, while aldehyde oxidase metabolizes various aldehydes and drugs. Dietary requirements are small because so little molybdenum is needed by these enzymes. Absorption is high (40-100%), and excess molybdenum is excreted in urine. Frank molybdenum deficiency is extraordinarily rare in humans on normal diets.

How to take it

1. Typical dose
45–50 mcg/day (at RDA level in a multivitamin is appropriate)
2. Timing
Any time
3. With food
With or without food
4. How long to try
Ongoing as part of a multivitamin; do not supplement separately unless deficiency confirmed

What to track

Copper status if taking high doses long-term
Uric acid if predisposed to gout and supplementing above RDA

2 commercial forms

Compare the main delivery options and what they’re best suited for.

Sodium molybdate

Common form in multivitamins and standalone supplements. Inexpensive and effective for repletion.

Inorganic salt; well absorbed.

Molybdenum amino acid chelate (glycinate)

Marketed for gentler absorption. Functional difference from molybdate is unclear at the small doses typically used.

Chelated form; similar bioavailability to molybdate.

Safety

Know the common side effects, key cautions, and who should avoid it.

Common side effects

Well-tolerated at doses below the UL of 2,000 mcg/day

Serious risks

Who should avoid it

Pregnancy & breastfeeding

RDA increases to 50 mcg/day during pregnancy; do not exceed the UL of 2,000 mcg/day; standard prenatal multivitamin amounts are safe.

Interactions

copperModerate

High molybdenum increases urinary copper excretion; long-term high-dose supplementation can cause copper deficiency

sulfate supplementsMinor

Sulfate may compete with molybdate for absorption at high doses

Food sources

Black-eyed peas (1 cup, cooked)

Amount
288 mcg
%DV

Lima beans (1 cup, cooked)

Amount
141 mcg
%DV

Lentils (1 cup, cooked)

Amount
148 mcg
%DV

Soybeans (1 cup, cooked)

Amount
132 mcg
%DV

Beef liver (3 oz, cooked)

Amount
33 mcg
%DV

Oats (1 cup, cooked)

Amount
28 mcg
%DV

Brown rice (1 cup, cooked)

Amount
31 mcg
%DV

Eggs (1 large)

Amount
9 mcg
%DV

Choosing a product

What to look for on the label — and what to be skeptical of.

Look for

Dose in mcg clearly stated
Amino acid chelate or glycinate form for absorption
Included in a complete multivitamin rather than standalone supplement

Be skeptical of

'Detoxifies sulfites'
'Antioxidant powerhouse'
'Supports heavy metal detox'
'Boosts sulfur metabolism'

Frequently asked questions

Do I need to supplement molybdenum?

Almost certainly not. A serving of beans or lentils typically exceeds the RDA. Frank molybdenum deficiency from diet alone is essentially unknown.

Can molybdenum cause gout?

High doses can elevate uric acid via xanthine oxidase activation. People with gout or hyperuricemia should avoid high-dose molybdenum supplements.

Does molybdenum help with sulfite intolerance?

It theoretically supports sulfite oxidase, but clinical evidence in humans is limited. If your status is marginal, supplementation might help; for most people, dietary intake is already adequate.

Can molybdenum cause copper deficiency?

Yes, at high doses over time. Molybdenum increases copper excretion. This is rarely a problem at typical multivitamin levels but matters at therapeutic doses.

Is molybdenum in my multivitamin enough?

Yes. Most multivitamins contain 50-100 mcg, which meets or exceeds the RDA.

References by claim

molybdenum cofactor deficiency (genetic or acquired)

Schwahn et al., 2024PubMed (2024) link

Misko et al., 1993PubMed (1993) link

Safety

NIH Office of Dietary Supplements — MolybdenumNIH ODS link

Track Molybdenum with Pilora

Set up dose reminders, check interactions, and join the community in the Pilora iPhone app.

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Evidence-based·Last reviewed May 30, 2026·Evidence current as of May 30, 2026·How we grade evidence

Disclaimer: These statements have not been evaluated by the FDA. This page is educational, not a substitute for personalized medical advice. Evidence grades are AI-assisted assessments — talk to your doctor before starting any new supplement, especially if you’re pregnant, breastfeeding, on medications, or managing a chronic condition.