Molybdenum is a trace mineral the human body requires in very small quantities to function properly. It plays a role in activating specific enzymes that are involved in various metabolic processes throughout the body. These enzymes are responsible for breaking down certain proteins, alcohol, drugs, and toxins.
The mineral is an integral component of a complex called molybdenum cofactor, which is necessary for enzymes such as sulfite oxidase, xanthine oxidase, and aldehyde oxidase. These enzymes help convert harmful sulfites into less toxic sulfates, metabolize purines into uric acid, and process other compounds. Molybdenum deficiency is uncommon in the general population because the body needs only a small amount, and it is present in many common foods.
Symptoms of Molybdenum Deficiency
Symptoms linked to molybdenum deficiency can vary depending on whether the deficiency is inherited or acquired. The severe, inherited form, known as molybdenum cofactor deficiency (MoCD), appears in newborns and can lead to serious neurological issues. Infants with MoCD may seem normal at birth but often develop seizures within a week that are difficult to control. They might also display abnormal muscle tone, feeding difficulties, and an exaggerated startle reaction.
As the condition progresses, brain abnormalities can develop, leading to severe developmental delays where affected individuals might not learn to sit or speak. Other physical signs can include a small head size, distinct facial features, and dislocated eye lenses. These symptoms arise from the body’s inability to synthesize the molybdenum cofactor, impairing enzyme function and leading to a toxic buildup of sulfites, particularly harmful to the brain.
Acquired molybdenum deficiency is much rarer and has been reported in specific circumstances, such as in patients receiving long-term total parenteral nutrition (IV feeding) without molybdenum supplementation. Symptoms in these cases can include a rapid heart rate, headache, and neurological changes, including mental disturbances and coma.
Causes and Risk Factors
Molybdenum deficiency primarily stems from two distinct origins: genetic predisposition or acquired circumstances. The most common cause of a severe deficiency is an inherited metabolic disorder known as molybdenum cofactor deficiency (MoCD).
This genetic condition results from mutations in specific genes (MOCS1, MOCS2, or GPHN), which prevent the body from synthesizing the molybdenum cofactor. This renders molybdenum-dependent enzymes non-functional.
Acquired molybdenum deficiency is exceptionally rare and has been observed in very specific scenarios. The most documented instance involves individuals receiving long-term total parenteral nutrition (TPN) that lacks molybdenum. In such cases, without the mineral supplied intravenously, the body’s stores can become depleted, leading to functional impairment of molybdenum-dependent enzymes. While not typically leading to clinical deficiency in humans, living in geographical areas with molybdenum-poor soil might result in lower dietary intake of the mineral. However, the human body requires such small amounts of molybdenum that dietary intake from a varied diet is usually sufficient, even in areas with lower soil content. The kidneys also regulate molybdenum levels, excreting excess amounts to prevent accumulation.
Diagnosis and Medical Intervention
Diagnosing molybdenum deficiency involves a combination of clinical assessment and laboratory testing. For suspected molybdenum cofactor deficiency (MoCD), doctors look for characteristic signs in newborns and conduct specific biochemical tests.
These tests measure levels of certain metabolites in blood and urine, such as elevated sulfite, S-sulfocysteine, xanthine, and hypoxanthine, alongside low levels of uric acid. Brain imaging, like MRI, can also show specific patterns of brain injury that support a diagnosis. Genetic testing can confirm MoCD by identifying mutations in the MOCS1, MOCS2, or GPHN genes.
Treatment approaches differ significantly for the genetic versus acquired forms. For acquired molybdenum deficiency, which is often linked to prolonged total parenteral nutrition without supplementation, treatment involves adding molybdenum to the nutritional support. This intervention can lead to a rapid resolution of symptoms as the body regains the ability to process sulfites and other compounds.
The genetic form, MoCD, presents a more complex challenge. For MoCD type A, a specific medication called fosdenopterin (Nulibry), which is a cyclic pyranopterin monophosphate (cPMP) replacement, has been approved by the U.S. Food and Drug Administration (FDA). This therapy helps to bypass the metabolic block and can improve survival and reduce symptoms, especially if initiated early in life. For other types of MoCD, treatment primarily focuses on managing symptoms, such as controlling seizures and addressing developmental delays, as there are currently no specific therapies that reverse the neurological damage.
Dietary Sources of Molybdenum
Molybdenum is widely distributed in various foods, making dietary deficiency uncommon for most individuals.
Some dietary sources of molybdenum include:
Legumes, generally considered among the richest sources, include black-eyed peas, lima beans, kidney beans, lentils, and green peas.
Whole grains, including oats, shredded wheat cereal, and whole-wheat bread.
Nuts, such as almonds and peanuts.
Dairy products, including milk and plain yogurt (primary sources for children and teenagers).
Leafy green vegetables (e.g., spinach) and other vegetables (e.g., baked potatoes).
Beef liver and other organ meats.
The amount of molybdenum in plant-based foods can vary depending on the mineral content of the soil where they were grown.