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Molybdenum is an essential trace element for virtually all life forms. It functions as a cofactor for a number of enzymes that catalyze important chemical transformations in the global carbon, nitrogen, and sulfur cycles (1). Thus, molybdenum-dependent enzymes are not only required for human health, but also for the health of our ecosystem.
The biological form of molybdenum, present in almost all molybdenum-containing enzymes (molybdoenzymes), is an organic molecule known as the molybdenum cofactor (2). In humans, molybdenum is known to function as a cofactor for three enzymes:
Of these three enzymes, only sulfite oxidase is known to be crucial for human health (4).
Excess dietary molybdenum has been found to result in copper deficiency in grazing animals (ruminants). In ruminants, the formation of compounds containing sulfur and molybdenum, known as thiomolybdates, appears to prevent the absorption of copper. This interaction between thiomolybdates and copper does not occur to a significant degree in humans. One early study reported that molybdenum intakes of 500 mcg/day and 1,500 mcg/day from sorghum increased urinary copper excretion (2). However, the results of a more recent, well-controlled study indicated that very high dietary molybdenum intakes (up to 1,500 mcg/day) did not adversely affect copper nutritional status in eight, healthy young men (5).
Dietary molybdenum deficiency has never been observed in healthy people (2). The only documented case of acquired molybdenum deficiency occurred in a patient with Crohn's disease on long-term total parenteral nutrition (TPN) without molybdenum added to the TPN solution (6). The patient developed rapid heart and respiratory rates, headache, night blindness, and ultimately became comatose. He also demonstrated biochemical signs of molybdenum deficiency, including low plasma uric acid levels, decreased urinary excretion of uric acid and sulfate, and increased urinary excretion of sulfite. Thus, the patient was diagnosed with defects in uric acid production and sulfur amino acid metabolism. The patient's clinical condition improved and the amino acid intolerance disappeared when the TPN solution was discontinued and instead supplemented with molybdenum (160 mcg/day) (6).
Current understanding of the essentiality of molybdenum in humans is based largely on the study of individuals with very rare inborn errors of metabolism that result in a deficiency of the molybdoenzyme, sulfite oxidase. Two forms of sulfite oxidase deficiency have been identified:
Because molybdenum functions only in the form of the molybdenum cofactor in humans, any disturbance of molybdenum cofactor metabolism can disrupt the function of all molybdoenzymes. Together, molybdenum cofactor deficiency and isolated sulfite oxidase deficiency have been diagnosed in more than 100 individuals worldwide. Both disorders result from recessive traits, meaning that only individuals who inherit two copies of the abnormal gene (one from each parent) develop the disease. Individuals who inherit only one copy of the abnormal gene are known as carriers of the trait but do not exhibit any symptoms. The symptoms of isolated sulfite oxidase deficiency and molybdenum cofactor deficiency are identical and usually include severe brain damage, which appears to be due to the loss of sulfite oxidase activity. At present, it is not clear whether the neurologic effects are a result of the accumulation of a toxic metabolite, such as sulfite, or inadequate sulfate production. Isolated sulfite oxidase deficiency and molybdenum cofactor deficiency can be diagnosed relatively early in pregnancy (10-14 weeks' of gestation) through chorionic villus sampling, and in some cases, carriers of molybdenum cofactor deficiency can be identified through genetic testing. No cure is presently available for either disorder, although anti-seizure medications and dietary restriction of sulfur-containing amino acids may be beneficial in some cases (7).
The recommended dietary allowance (RDA) for molybdenum was most recently revised in January 2001 (2). It was based on the results of nutritional balance studies conducted in eight, healthy young men under controlled laboratory conditions (8, 9). The RDA values for molybdenum are listed in the table below in micrograms (mcg)/day by age and gender. Adequate intake (AI) levels were set for infants based on mean molybdenum intake from human milk, exclusively.
|Recommended Dietary Allowance (RDA) for Molybdenum|
|Life Stage||Age||Males (mcg/day)||Females (mcg/day)|
|Infants||0-6 months||2 (AI)||2 (AI)|
|Infants||7-12 months||3 (AI)||3 (AI)|
|Adults||19 years and older||45||45|
Linxian is a small region in northern China where the incidence of cancer of the esophagus and stomach is very high (ten times higher than the average in China and 100 times higher than the average in the U.S.). The soil in this region is low in molybdenum and other mineral elements; therefore, dietary molybdenum intake is also low. Increased intake of nitrosamines, which are known carcinogens, may be one of a number of dietary and environmental factors that contributes to the development of gastroesophageal cancer in this population. Plants require molybdenum to synthesize nitrate reductase, a molybdoenzyme necessary for converting nitrates from the soil to amino acids. Thus, when molybdenum content in the soil is low, plants preferentially convert nitrates to nitrosamines instead of using nitrate to synthesize amino acids. This results in increased nitrosamine exposure for those who consume the plants. Adding molybdenum to the soil in the form of ammonium molybdenate may help decrease the risk of gastroesophageal cancer by limiting nitrosamine exposure. It is not clear whether dietary molybdenum supplementation is beneficial in decreasing the risk of gastroesophageal cancer. In a large intervention trial, dietary supplementation of molybdenum (30 mcg/day) and vitamin C (120 mg/day) did not decrease the incidence of gastroesophageal cancer or other cancers in residents of Linxian over a five-year period (10).
The Total Diet Study, an annual survey of the mineral content in the typical American diet, indicates that the dietary intake of molybdenum averages 76 mcg/day for women and 109 mcg/day for men. Thus, usual molybdenum intakes are well above the RDA for molybdenum. Legumes, such as beans, lentils, and peas, are the richest sources of molybdenum. Grain products and nuts are considered good sources, while animal products, fruits, and many vegetables are generally low in molybdenum (2). Because the molybdenum content of plants depends on the soil molybdenum content and other environmental conditions, the molybdenum content of foods can vary considerably (11).
Molybdenum in nutritional supplements is generally in the form of sodium molybdate or ammonium molybdate (12).
The toxicity of molybdenum compounds appears to be relatively low in humans. Increased serum levels of uric acid and ceruloplasmin (an iron-oxidizing enzyme) have been reported in occupationally exposed workers in a molybdenite roasting plant (13). Gout-like symptoms have also been reported in an Armenian population consuming 10 to 15 milligrams (mg) of molybdenum from food daily (14). In other studies, blood and urinary uric acid levels were not elevated by molybdenum intakes up to 1.5 mg/day (2). There has been only one report of acute toxicity related to molybdenum from a dietary supplement: an adult male reportedly consumed a total of 13.5 mg of molybdenum over a period of 18 days (300-800 mcg/day) and developed acute psychosis with hallucinations, seizures, and other neurologic symptoms (12). However, a controlled study in four, healthy young men found that molybdenum intakes, ranging from 22 mcg/day to 1,490 mcg/day (almost 1.5 mg/day), elicited no serious adverse effects when molybdenum was given for 24 days (9).
The Food and Nutrition Board (FNB) of the Institute of Medicine found little evidence that molybdenum excess was associated with adverse health outcomes in generally healthy people. To determine the tolerable upper level of intake, the FNB selected adverse reproductive effects in rats as the most sensitive index of toxicity and applied a large uncertainty factor because animal data were used (2). Tolerable upper intake levels (UL) for molybdenum are listed by age group in the table below.
|Tolerable Upper Intake Level (UL) for Molybdenum|
|Infants 0-12 months||Not possible to establish*|
|Children 1-3 years||300|
|Children 4-8 years||600|
|Children 9-13 years||1,100 (1.1 mg/day)|
|Adolescents 14-18 years||1,700 (1.7 mg/day)|
|Adults 19 years and older||2,000 (2.0 mg/day)|
*Source of intake should be from food and formula only.
High doses of molybdenum have been found to inhibit the metabolism of acetaminophen in rats (15); however, it is not known whether this occurs at clinically relevant doses in humans.
The RDA for molybdenum (45 mcg/day for adults) is sufficient to prevent deficiency. Although the intake of molybdenum most likely to promote optimum health is not known, there is presently no evidence that intakes higher than the RDA are beneficial. Most people in the U.S. consume more than sufficient molybdenum in their diets, making supplementation unnecessary. Following the Linus Pauling Institute's general recommendation to take a multivitamin-mineral supplement that contains 100% of the daily values (DV) for most nutrients is likely to provide 75 mcg/day of molybdenum because the DV for molybdenum has not been revised to reflect the most recent RDA. Although the amount of molybdenum presently found in most multivitamin-mineral supplements is higher than the RDA, it is well below the tolerable upper intake level (UL) of 2,000 mcg/day and should be safe for adults.
Adults over the age of 50
Because aging has not been associated with significant changes in the requirement for molybdenum (2), our recommendation for older adults is the same as that for adults 50 and younger.
Written in July 2001 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University
Updated in April 2007 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University
Reviewed in April 2007 by:
Judith R. Turnlund, Ph.D., R.D.
Research Nutrition Scientist and Professor of Nutrition
Western Human Nutrition Research Center
University of California, Davis
Copyright 2001-2013 Linus Pauling Institute
The Linus Pauling Institute Micronutrient Information Center provides scientific information on the health aspects of dietary factors and supplements, foods, and beverages for the general public. The information is made available with the understanding that the author and publisher are not providing medical, psychological, or nutritional counseling services on this site. The information should not be used in place of a consultation with a competent health care or nutrition professional.
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