Minerals >> Molybdenum Deficiency

Dietary molybdenum deficiency has never been observed in healthy people. 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. 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. The symptoms disappeared when the administration of amino acid solutions was discontinued. Molybdenum supplementation (160 mcg/day) reversed the amino acid intolerance and improved his clinical condition.

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: 1) isolated sulfite oxidase deficiency, in which only sulfite oxidase activity is affected and 2) molybdenum cofactor deficiency, in which the activity of all three molybdoenzymes is affected. 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.

The Recommended Dietary Allowance (RDA)

The recommended dietary allowance (RDA) for molybdenum was most recently revised in January 2001. It was based on the results of nutritional balance studies conducted in eight healthy young men under controlled laboratory conditions. The RDA values for molybdenum are listed in the table below in micrograms (mcg)/day by age and gender.

See also:

• Molybdenum: Essential trace element for virtually all life forms

• Molybdenum Deficiency

• Molybdenum Deficiency: Gastroesophageal Cancer

• Molybdenum Functions: The biological form of molybdenum present...

• Molybdenum Safety

• Molybdenum Food sources & Supplements

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