Molybdenum gout

by Nathan Wei, MD, FACP, FACR

Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.

Click here: Second Opinion Arthritis Treatment Kit

One very interesting topic is the relationship of trace minerals to the development of different forms of arthritis. One such relationship is that of molybdenum to gout.

Molybdenum is a trace mineral that is required for enzymes that are involved in catabolism, including the catabolism of purines and other amino acids. Molybdenum is a transition metal with atomic number 42 and an atomic weight of 95.94 daltons. Its symbol is Mo. Organic forms of molybdenum are found in living matter ranging from bacteria to animals, including humans.

In spite of its low abundance in general, molybdenum deficiency in humans is rare but it has been described. A patient on long-term total parenteral nutrition (TPN) developed a syndrome characterized by hypouricemia, hypermethioninemia, low urinary sulfate excretion, tachycardia, tachypnea and mental and visual disturbances. The syndrome worsened with the administration of

L-methionine and the patient eventually became comatose. The patient improved when molybdenum, in the form of ammonium molybdate, was added to the TPN.

Both tungsten and copper are molybdenum antagonists. Conditions where tungsten and copper are deficient can lead to molybdenum excess.

Molybdenum is required for the effective performance of the xanthine oxidase enzyme for the breakdown of uric acid.

Gout (inflammation of the joints due to accumulation of uric acid) can be triggered by excessive amounts of molybdenum. It can occur when molybdenum intakes exceed 10 to 15 mg daily.

Gout is caused by molybdenum because it leads to decreased uric acid excretion by the kidneys. Those with hyperuricemia and/or gout should exercise caution in the use of supplementation with doses of molybdenum greater than U.S. RDA amounts.

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