Molybdenum

What is molybdenum and what does it do in the body?

Molybdenum is an essential trace element. According to the NIH Office of Dietary Supplements, it is a structural component of the molybdopterin cofactor, which the body makes itself, and it is needed for four enzymes to work: sulfite oxidase, xanthine oxidase, aldehyde oxidase, and mitochondrial amidoxime reducing component (mARC). These enzymes metabolize sulfur-containing amino acids and heterocyclic compounds, including purines and pyrimidines; xanthine oxidase, aldehyde oxidase, and mARC also take part in the metabolism of drugs and toxins. ^[1]

Adults absorb 40–100% of the molybdenum in food; infants absorb nearly all of the molybdenum in breast milk or formula. The kidneys mainly regulate and excrete its level in the body; molybdenum in the form of molybdopterin is stored in the liver, kidney, adrenal glands, and bone. ^[1] Because molybdenum deficiency is rare, its status is not assessed clinically; in a small study of 30 healthy people, the serum level was reported as 0.28–1.17 ng/mL (mean 0.58 ng/mL), and urinary molybdenum does not reflect status. ^[1]

That an element takes part in enzymes does not mean that intake above the requirement will make those enzymes work better. In this guide, “role in the body,” “deficiency,” and “effect of supplementation” are treated as separate questions.

How much molybdenum is needed per day?

The U.S. Food and Nutrition Board (FNB), on which NIH relies, derived an estimated average requirement (EAR) for molybdenum based on two carefully controlled balance studies in eight young men and, on that basis, set a recommended dietary allowance (RDA); the values for children and adolescents were extrapolated from adult values. ^[1] EFSA, on the other hand, gave an “adequate intake” (AI) level. TÜBER 2022 also lists the adult value as an AI. ^{[3] [2]}

NIH’s value for ages 14–18 is 43 µg. ^[1] The values are for population-level planning; the difference between institutions arises from the difference in type (RDA and AI) and derivation method and is not an individual dose recommendation.

Which foods contain molybdenum?

According to NIH, legumes are the richest source; whole grains, nuts, and beef liver also contain high levels. The amount in food depends on the molybdenum content of the soil and of the water used for irrigation; because USDA FoodData Central does not list molybdenum values, information about food contents is limited. The main sources in the U.S. are legumes, grains, leafy vegetables, beef liver, and milk; milk and cheese products are the main source for children and adolescents. ^[1]

The table is from NIH’s U.S. servings. The same source reports that mean molybdenum intake from foods in the U.S. was 109 µg in men and 76 µg in women according to the 1984 Total Diet Study, and that the mean amount from supplements in NHANES 1988–1994 was 23 µg for men and 24 µg for women; NIH states that most people in the U.S. appear to get enough molybdenum, but that national surveys no longer collect molybdenum intake data. ^[1]

According to NIH, amounts in supplements are about 50–500 µg; forms such as molybdenum chloride, sodium molybdate, molybdenum glycinate, and amino acid chelate exist, and no study compares the relative bioavailability of these forms. ^[1]

Does molybdenum deficiency occur?

NIH states that no molybdenum deficiency has been reported apart from people carrying the genetic mutation that impairs molybdopterin synthesis. There is no group known to be at risk of deficiency. Acquired deficiency has been reported in a single case: in 1981, a patient receiving molybdenum-free total parenteral nutrition developed tachycardia, tachypnea, headache, night blindness, and coma; the findings resolved when molybdenum was given. ^[1]

What is molybdenum cofactor deficiency?

Molybdenum cofactor deficiency (MoCD) is a very rare metabolic disease caused by mutations in genes that impair molybdopterin biosynthesis; the function of sulfite-metabolizing enzymes is impaired, encephalopathy and seizures develop, and according to NIH the neurological damage is severe, usually resulting in death within days of birth. This is not a condition arising from inadequate molybdenum intake from food. ^[1]

Replacement therapy with cyclic pyranopterin monophosphate (cPMP), the precursor of the cofactor, in type A disease was reported in a 2015 prospective cohort study: of 16 newborns enrolled in a compassionate-use program, 11 had type A and 5 had type B. No serious drug-related adverse events were seen across more than six thousand doses; in type A patients, urinary S-sulfocysteine, xanthine, and urate levels returned to nearly normal within two days and stayed normal during treatment lasting up to five years. In type A, eight patients improved, three patients treated early remained seizure-free and showed near-normal development; no biochemical or clinical response was detected in type B patients. The study is an uncontrolled observational one, and its funding includes, in addition to public sources, a commercial entity that developed the treatment product. ^[8] This treatment is a drug approach specific to a newborn disease; it has nothing to do with molybdenum supplementation.

Does molybdenum supplementation improve health outcomes?

NIH states that molybdenum is not a standard treatment for any disease or disorder; the fact sheet does not report any study showing that molybdenum supplementation improved a clinical outcome. ^[1] Studies examining the physiological response to intake, on the other hand, are small.

In a study of four young men in which each intake level was given for 24 days, molybdenum from food was varied between 22 and 1,490 µg/day and followed with stable isotopes. No adverse effects were observed at any intake level; molybdenum was absorbed at 88–93% at every level, and the amount and proportion excreted in urine increased with intake; the authors attributed this to regulation of molybdenum retention through urinary excretion, conservation at low intake, and rapid urinary elimination of the excess at high intake. ^[5] Kinetic modeling of the same four men showed that as intake increased, absorption and urinary excretion increased and the proportion deposited in tissues decreased; the authors thought that these adaptations may help prevent deficiency and toxicity. ^[6] These studies are physiological studies with a sample size of four; they do not measure the effect of supplementation on a health outcome.

Is excess molybdenum harmful?

According to NIH, acute molybdenum toxicity is rare and can occur with industrial mining and metal-processing exposure; in healthy people, a molybdenum-rich diet generally poses no health risk because molybdenum is rapidly excreted in urine. In a region of Armenia where the soil is very rich in molybdenum, joint pain, gout-like symptoms, and high blood uric acid levels were reported in people consuming 10–15 mg of molybdenum per day. ^[1] NIH bases this finding on a single study conducted in Armenia.

A 1999 review reports that molybdenum compounds appear to have a low degree of toxicity in humans, but that a dose–response relationship cannot be calculated with the available data. According to the same review, oral absorption in humans is 28–77% and urinary excretion is 17–80% of the dose given (different from the 40–100% range NIH gives for adult absorption); because molybdenum toxicity is related to copper intake or depleted copper stores, people with inadequate copper intake or impaired copper metabolism may be at greater risk. Because no human study exists, the derivation rests on animal studies: reproductive and fetal development effects were found as the critical effect in rats and mice, and in one study the no-observed-adverse-effect level (NOAEL) and lowest-observed-adverse-effect level (LOAEL) were 0.9 and 1.6 mg molybdenum/kg/day, respectively. ^[7]

NIH’s tolerable upper intake levels (UL) are also based, in the absence of human data, on levels associated with reproductive and fetal development impairment in rats and mice: 2,000 µg/day for ages 19 and over, including pregnancy and breastfeeding (1,700 µg for ages 14–18). ^[1] In EFSA’s 2025 summary (Scientific Committee on Food, based on 2000), the UL for adults, pregnant women, and breastfeeding women is 0.6 mg/day (600 µg). ^[4] TÜBER Annex 1.5.5 also lists 0.6 mg for ages 19–50. ^[2] That is, the two numbers are the products of different institutions and differ by more than threefold. The UL is an upper limit for habitual daily intake, not a single-serving limit.

NIH states that molybdenum has no known clinically significant drug interaction. ^[1]

How is molybdenum supplementation regulated in Türkiye?

Approval from the Ministry of Agriculture and Forestry is mandatory for every dietary supplement to be marketed in Türkiye. ^[12] According to Article 5 of Communiqué 2013/49 as amended by 2015/44, vitamins and minerals can be used only if listed in Annex-1 and in the forms in Annex-2; daily maximum limits are set in line with Annex-3 through the label declaration, and in products containing vitamins and minerals, the amount stated on the label is at least 15% of the nutrient reference value for ages 11 and over. ^[9] Statements on label, presentation, and advertising claiming to prevent, treat, or cure disease cannot appear. ^[10]

In the main table of the Ministry’s Restricted Substances List (September 21, 2026), there is no separate row containing a daily amount limit for molybdenum; in the table “Sources of Vitamins and Minerals Used Before December 31, 2025,” “chemical synthesis” is shown as the source for “Molybdenum (µg).” Because molybdenum is not botanical, the Plant List does not apply. ^[11]

Evidence table: claim, population, and limits

A personal dose or supplement decision for molybdenum is made by evaluating diet, copper status, and medications used together; this guide does not recommend personal doses.