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TABLE 1 Dietary Reference Intakes for Molybdenum by Life Stage Group DRI values (mg /day) EARa RDAb AIc ULd males females males females Life stage group NDe 0 through 6 mo 2 6 through 12 mo 3 ND 1 through 3 y 13 13 17 17 300 4 through 8 y 17 17 22 22 600 9 through 13 y 26 26 34 34 1,100 14 through 18 y 33 33 43 43 1,700 19 through 30 y 34 34 45 45 2,000 31 through 50 y 34 34 45 45 2,000 51 through 70 y 34 34 45 45 2,000 > 70 y 34 34 45 45 2,000 Pregnancy £ 18 y 40 50 1,700 19 through 50 y 40 50 2,000 Lactation £ 18 y 35 50 1,700 19 through 50 y 36 50 2,000 a EAR = Estimated Average Requirement. b RDA = Recommended Dietary Allowance. c AI = Adequate Intake. d UL = Tolerable Upper Intake Level. Unless otherwise specified, the UL represents total intake from food, water, and supplements. e ND = Not determinable. This value is not determinable due to the lack of data of adverse effects in this age group and concern regarding the lack of ability to handle excess amounts. Source of intake should only be from food to prevent high levels of intake.

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PART III: MOLYBDENUM 357 MOLYBDENUM M olybdenum functions as a cofactor for several enzymes, including sulfite oxidase, xanthine oxidase, and aldehyde oxidase. The require- ments for molybdenum are based on controlled balance studies with specific amounts of molybdenum consumed. Adjustments were made for the bioavailability of molybdenum. The Tolerable Upper Intake Level (UL) is based on impaired reproduction and growth in animals. DRI values are listed by life stage group in Table 1. Legumes, grain products, and nuts are the major contributors of dietary molybdenum. Molybdenum deficiency has not been observed in healthy people. Molybdenum compounds appear to have low toxicity in humans. MOLYBDENUM AND THE BODY Function Molybdenum, in a form called molybdopterin, acts as a cofactor for several enzymes, including sulfite oxidase, xanthine oxidase, and aldehyde oxidase. These enzymes are involved in catabolism of sulfur amino acids and heterocylic compounds such as purines and pyrimidines. A clear molybdenum deficiency syndrome that produces physiological signs of molybdenum restriction has not been achieved in animals, despite major reduction in the activity of these molybdoenzymes. Rather, the essential nature of molybdenum is based on a genetic defect that prevents sulfite oxidase synthesis. Because sulfite is not oxi- dized to sulfate, severe neurological damage leading to early death occurs with this inborn error of metabolism. Absorption, Metabolism, Storage, and Excretion The absorption of molybdenum is highly efficient over a wide range of intakes, which suggests that the mechanism of action is a passive (nonmediated) diffusion process. However, the exact mechanism and location within the gas- trointestinal tract of molybdenum absorption have not been studied. Protein- bound molybdenum constitutes 83–97 percent of the total molybdenum in erythrocytes. Potential plasma molybdenum transport proteins include a- macroglobulin.

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 358 Evidence suggests that the kidneys are the primary site of molybdenum homeostatic regulation. Excretion is primarily through the urine and is directly related to dietary intake. When molybdenum intake is low, about 60 percent of ingested molybdenum is excreted in the urine, but when molybdenum intake is high, more than 90 percent is excreted in the urine. Although related to dietary intake, urinary molybdenum alone does not reflect status. DETERMINING DRIS Determining Requirements The requirements for molybdenum are based on controlled balance studies with specific amounts of molybdenum consumed. Adjustments were made for the bioavailability of molybdenum. Information on dietary intake of molybdenum is limited because of lack of a simple and reliable analytical method for deter- mining molybdenum in foods. Criteria for Determining Molybdenum Requirements, by Life Stage Group Life stage group Criterion 0 through 6 mo Average molybdenum intake from human milk 7 through 12 mo Extrapolation from 0 through 6 mo AI 1 through 18 y Extrapolation from adult EAR 19 through 30 y Balance data 31 through > 70 y Extrapolation of balance data from 19 through 30 y Pregnancy £ 18 y Extrapolation of adolescent female EAR based on body weight 19 through 50 y Extrapolation of adult female EAR based on body weight Lactation £ 18 y Adolescent female EAR plus average amount of molybdenum secreted in human milk 19 through 50 y Adult female EAR plus average amount of molybdenum secreted in human milk The UL The Tolerable Upper Intake Level (UL) is the highest level of daily nutrient intake that is likely to pose no risk of adverse effects for almost all people. Members of the general population should not routinely exceed the UL. Inad- equate data exist to identify a causal association between excess molybdenum

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PART III: MOLYBDENUM 359 intake in normal, apparently healthy individuals and any adverse health out- comes. In addition, studies have identified levels of dietary molybdenum in- take that appear to be associated with no harm. Thus, the UL is based on ad- verse reproductive effects in rats fed high levels of molybdenum. The UL applies to all forms of molybdenum from food, water, and supplements. More soluble forms of molybdenum have greater toxicity than insoluble or less soluble forms. National surveys do not provide percentile data on the dietary intake of molybdenum. Data available from the Third National Health and Nutrition Examination Survey (NHANES III, 1988–1994) indicate that the average U.S. intakes from molybdenum supplements at the 95th percentile were 80 mg/day for men and 84 mg/day for women. Because there was no information from national surveys on percentile distribution of molybdenum intakes, the risk of adverse effects could not be characterized. DIETARY SOURCES Foods The molybdenum content of plant-based foods depends on the content of the soil in which the foods were grown. Legumes, grain products, and nuts are the major contributors of dietary molybdenum. Animal products, fruits, and many vegetables are generally low in molybdenum. Dietary Supplements Data from NHANES III indicated that the median intakes of molybdenum from supplements were 23 mg/day for men and 24 mg/day for women. Bioavailability Little is known about the bioavailability of molybdenum, except that it has been demonstrated to be less efficiently absorbed from soy than from other food sources (as is the case with other minerals). It is unlikely that molybde- num in other commonly consumed foods would be less available than the mo- lybdenum in soy. The utilization of absorbed molybdenum appears to be simi- lar regardless of food source. Dietary Interactions This information was not provided at the time the DRI values for this nutrient were set.

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 360 INADEQUATE INTAKE AND DEFICIENCY Molybdenum deficiency has not been observed in healthy people. A rare meta- bolic defect called molybdenum cofactor deficiency results from the deficiency of molybdoenzymes. Few infants with this defect survive the first days of life, and those who do have severe neurological and other abnormalities. EXCESS INTAKE Molybdenum compounds appear to have a low toxicity in humans. Possible reasons for the presumed low toxicity of molybdenum include its rapid excre- tion in the urine, especially at higher intake levels. More soluble forms of mo- lybdenum have greater toxicity than insoluble or less soluble forms. There are limited toxicity data for molybdenum in humans; most of the data apply to animals. In the absence of adequate human studies, it is impos- sible to determine which adverse effects might be considered most relevant to humans. Special Considerations Individuals susceptible to adverse effects: People who are deficient in dietary copper or who have some dysfunction in copper metabolism that makes them copper-deficient could be at increased risk of molybdenum toxicity. However, the effect of molybdenum intake on copper status in humans remains to be clearly established.

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PART III: MOLYBDENUM 361 KEY POINTS FOR MOLYBDENUM Molybdenum functions as a cofactor for certain enzymes, 3 including sulfite oxidase, xanthine oxidase, and aldehyde oxidase. The requirements for molybdenum are based on controlled 3 balance studies with specific amounts of molybdenum consumed. The UL is based on impaired reproduction and growth in animals. Information on dietary intake of molybdenum is limited because 3 of lack of a simple and reliable analytical method for determining molybdenum in food. Usual intake is well above the dietary molybdenum requirement. The molybdenum content of plant-based foods depends on 3 the content of the soil in which the foods were grown. Legumes, grain products, and nuts are the major contributors of dietary molybdenum. Molybdenum deficiency has not been observed in healthy 3 people. A rare and usually fatal metabolic defect called molybdenum cofactor deficiency results from the deficiency of molybdoenzymes. Molybdenum compounds appear to have a low toxicity in 3 humans. There are limited toxicity data for molybdenum in humans; 3 most of the data apply to animals. Possible reasons for the presumed low toxicity of molybdenum 3 include its rapid excretion in the urine, especially at higher intake levels.