Molybdenum

Molybdenum is a trace element that is considered a micronutrient, meaning a nutrient needed in very small amounts. It is required by almost all living organisms and works as a cofactor for enzymes that carry out important chemical transformations in the global carbon, nitrogen, and sulfur cycles. Thus, molybdenum-dependent enzymes are not only required for the health of people, but also for the health of ecosystems.

Molybdenum is an essential trace mineral considered essential in human nutrition. This is because, as tiny as the required amounts are, the consequences of their absence (deficiency) are severe. The active biological form of molybdenum is known as the molybdenum cofactor. It is found in several tissues of the human body and is required for the activity of enzymes that are involved in eliminating toxic substances, including the catabolism of purines, which produces uric acid, formed primarily in the liver and excreted by the kidney into the urine. In addition to being a cofactor of enzymes involved in purine and pyrimidine detoxification, molybdenum also has therapeutic uses, being used in the treatment of:

Molybdenum

SOURCE: Institute of Medicine (US) Panel on Micronutrients. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington DC: U.S. National Academies Press, 2001. https://www.ncbi.nlm.nih.gov/books/NBK222310 (accessed April 2, 2018).

Recent research findings suggest that molybdenum may also have a role in stabilizing the unoccupied glucocorticoid receptor. Glucocorticoids are naturally produced steroid hormones, that inhibit the process of inflammation. Their shape permits them to move across the membrane that surrounds cells in the body, and to be recognized by molecules inside the cell called glucocorticoid receptors.

The body absorbs molybdenum quickly in the stomach and in the small intestine. The mechanism of absorption is uncertain. Following absorption, molybdenum is transported by the blood to the liver and to other tissues of the body. In the molybdate form, it is carried in the blood bound to alpha-macroglobulin and by adsorption to red blood cells. The liver and kidney store the highest amounts of molybdenum. The molybdenum cofactor is made in cells and consists of a molybdenum atom bound to tricyclic pyranopterin molecules, the simplest of which is known as molybdopterin. The cofactor is a component of four main enzymes:

Aldehyde oxidase and xanthine oxidase catalyze hydroxylation reactions involving a number of different molecules with similar structures. Xanthine oxidase and aldehyde oxidase also play a role in the metabolism of drugs and toxins. However, according to the Micronutrient Information Center of the Linus Pauling Institute of Oregon State University, only sulfite oxidase is known to be crucial for human health.

Sources of dietary molybdenum include milk, dried beans, peas, nuts and seeds, eggs, liver tomatoes, carrots and meats. The molybdenum contents are per cup:

The recommended dietary allowances (RDA) for molybdenum are:

Molybdenum in nutritional supplements is available in the form of sodium molybdate or ammonium molybdate. Molybdenum in food is principally in the form of the organic molybdenum cofactors. The efficiency of absorption of nutritional molybdenum in supplements ranges from 88%–93%, and the efficiency of absorption of molybdenum from foods ranges from 57%–88%.

Pregnant women and nursing mothers should be careful not to use supplemental molybdenum in amounts greater than RDA amounts. Those with excess build-up of uric acid in the blood (hyperuricemia) or gout should also exercise caution in the use of supplements. Overall, it is believed that the toxicity of molybdenum compounds appears to be relatively low in humans. The Food and Nutrition Board (FNB) of the Institute of Medicine found little evidence that molybdenum excess was associated with adverse health effects in healthy people. Hyperuricemia and gout-like symptoms have only been reported in occupationally exposed workers in a copper-molybdenum plant and in an Armenian population consuming 10–15 mg of molybdenum from food daily. Other studies report that blood and urinary uric acid levels were not elevated by molybdenum intakes of up to 1.5 mg/day.

Dietary molybdenum deficiency has never been observed in healthy people. Molybdenum cofactor deficiency and isolated sulfite oxidase deficiency are the only two disorders associated with this trace element. Molybdenum cofactor deficiency disorder is severe and usually results in premature death in early childhood since all of the molybdenum cofactor-dependent enzymes are affected. Isolated sulfite oxidase deficiency only affects sulfite oxidase activity. Together, molybdenum cofactor deficiency and isolated sulfite oxidase deficiency have been diagnosed in more than 100 individuals worldwide. They are, however, both inherited disorders and there are no documented cases of their ever occurring as a result of dietary molybdenum deficiency.

Studies have shown that high doses of molybdate inhibit the metabolism of acetaminophen in rats. However, it is not known whether this occurs at clinically relevant doses in humans. High doses of molybdate may also lower the absorption of copper. Likewise, high doses of copper may lower the absorption of molybdenum and decrease overall molybdenum levels.

There is only one report of acute poisoning resulting from intake of a dietary molybdenum supplement. The person consumed a total dose of 13.5 mg of molybdenum over a period of 18 days, at an intake rate of 300–800 μg daily, resulting in visual and auditory hallucinations, several petit mal seizures and one grand mal seizure. The subject was treated with chelation therapy to remove the molybdenum from his body and his symptoms disappeared after several hours.

With molybdenum deficiency being extremely unlikely, molybdenum-related complications are only possible with molybdenum toxicity that may result in gout. High molybdenum levels in people with low copper levels may cause copper deficiency symptoms, but are easily treated with diet readjustments.

The RDA for molybdenum (17–22 μg for children) is sufficient to prevent deficiency. Although the precise amount of molybdenum required to most likely promote optimum health is not known, there is presently no evidence that intakes higher than the RDA are beneficial. Most people in the United States consume more than sufficient molybdenum in their diets, making supplementation unnecessary. If required, it should be noted that the amount of molybdenum presently found in most multivitamin/mineral supplements is higher than the RDA. It is however well below the tolerable upper intake level of 2,000 μg/day and is generally considered safe.

Monique Laberge, PhD