Deficiency

Molybdenum

Essential trace mineral that enables sulfite-processing enzymes and is mainly useful for preventing rare deficiency.

Molybdenum

Essential trace mineral that enables sulfite-processing enzymes and is mainly useful for preventing rare deficiency.

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evidence

Safe

risk

Overview

Forms

Safety

Stack

Quick Take

Usually skip it - most adults get enough from beans and grains unless a clinician suspects a rare deficiency.

Molybdenum is an essential trace mineral found mainly in beans, lentils, whole grains, and organ meats, although content varies with soil. It forms the molybdenum cofactor used by sulfite oxidase, xanthine oxidase, aldehyde oxidase, and mARC enzymes. Evidence mainly supports correcting rare deficiency, preventing deficiency during long-term parenteral nutrition, and normalizing sulfite-related metabolism when intake is very low. People with medically confirmed low status benefit most.

Proven Benefits

Corrects confirmed deficiency

Prevents TPN-related deficiency

May normalize sulfite metabolism

May normalize xanthine/urate

May ease methionine intolerance

Protocol

Amount

45 mcg

Frequency

Once daily

When

Any time of day - with or without food; consistency matters more than timing.

Onset Time

Days to weeks in deficiency; little to notice if already sufficient.

Who Should Consider

People on long-term parenteral nutrition

Adults with medically confirmed low molybdenum status

People with severe malabsorption under medical care

Those with unusually low legume and whole-grain intake

Food Sources

Lentils (~100-150 mcg per cooked cup; varies by soil)
Black beans (~120-130 mcg per cooked cup)
Split peas (~120-130 mcg per cooked cup)
Oatmeal (~20-30 mcg per cooked cup)
Whole wheat bread (~20-40 mcg per 2 slices)
Beef liver (~90-110 mcg per 85 g)

How It Works

Molybdenum is incorporated into the molybdenum cofactor, which activates enzymes such as sulfite oxidase and xanthine oxidase. These enzymes help convert sulfite to sulfate and metabolize purines and aldehydes, so deficiency disrupts sulfur amino acid metabolism and can alter uric acid production.

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