Summary of Molybdenum
Primary Information, Benefits, Effects, and Important Facts
Molybdenum is an essential mineral. The human body requires very low quantities of molybdenum to support three groups of enzymes.
Molybdenum deficiencies are extremely rare, since molybdenum is easily available through the diet, as it is found in grains and water. The body easily retains molybdenum, and only needs a few micrograms.
Molybdenum functions as a cofactor for three groups of enzymes, meaning it is needed for the enzymes to do their job. It is incorporated into a molecule called molybdopterin, which forms the actual cofactor. A molybdenum deficiency would impair the functions of these enzymes, which would prevent the body from processing amino acids that contain sulfur. Molybdenum deficiencies are characterized by symptoms similar to sulfur toxicity.
Molybdenum supplementation is unnecessary. Due to the lack of evidence and very low risk of deficiency, molybdenum may not even need to be added to multivitamin formulas.
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How to Take Molybdenum
Recommended dosage, active amounts, other details
Molybdenum supplementation is not recommended because there is no evidence to support any benefits from supplementation, deficiencies are extremely rare, and molybdenum is easily obtained through the diet.
More research is needed to determine if long-term supplementation is safe. For this reason, molybdenum doses should not exceed 50µg (0.05mg).
Research Breakdown on Molybdenum
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Molybdenum tends to vary significantly between food sources due to the soil it was grown in (similar in concept to selenium) although the best food sources have been stated to be certain seeds, legumes, cereal grains, and leafy green vegetables. Grains are one of the main sources of dietary molybdenum for American citizens according to one survey.
Foods that have had their molybdenum content estimated include:
Black rice at 4.7µg/100g with lower levels in glutinous rice (3.7µg/100g) and milled rice (2.7µg/100g)
Rice cereals (category) at around 2.7µg/100g
Legumes (category) averaging 2.3µg/100g, although the highest levels can be found in black soybeans (Seoritae; 32.7µg/100g while sprouts have 6.48µg/100g) and mungbeans (26.7µg/100g, only 2.16µg/100g in the sprout); processed soybean products seem to have low molybdenum content
Parlsey at 2.98µg/100g
Crown daisy at 2.00µg/100g
Chinese chive at 2.18µg/100g
Laver (seaweed) at 2.89-6.29µg/100g
Oyster at 1.55µg/100g
Egg yolk of eggs from chickens at 0.91µg/100g
Cow's milk at 0.37µg/100g, with lower contents for low fat
As a general statement most meats, vegetables, and fruits tend to have low levels of molybdenum (0.50µg/100g or less). Drinking water can also be considered a source of molybdenum. Ground and well water can have varying concentrations depending on the soil that the water runs through, and it seems that intake of molybdenum from drinking water (US study) generally does not exceed 20µg each day. This provides about half of the molybdenum's recommended daily allowance.
Molybdenum is found in significant concentrations in certain grain and legume products including breads and beans, with a high level in peanuts as well. Molybdenum is naturally low in many vegetables, and most fruits and animal products. It is present in the water supply at a satisfactory concentration, generally providing almost half of the RDI by water alone since requirements for the mineral are low.
Molybdenum is a trace essential mineral that is a component of a few enzymes including xanthine oxidase (XO), xanthine dehydrogenase (XDH), sulfite oxidase (SOX), and aldehyde oxidase (AO), It is essential in the catabolism of sulfur-containing amino acids, xanthines, purines, and pyrimidines. Molybdenum was first discovered because of its role in maintaining intestinal XO activity of the rat, initially being called liver residue factor and XO factor before being identified as a molybdenum Subsequent studies revealed that it is also associated with the enzymes SOX and AO.
While molybdenum was initially given the status of essential mineral due to being a component of all the above enzymes, it seems that its role in SOX appears to be most relevant; Although lack of XO does not appear to cause any major clinical abnormalities despite altered serum biomarkers, impaired SOX activity causes neurological impairments leading to mental retardation shortly after birth due to an alteration in sulfate/sulfite kinetics and reduced brain mass.
Molybdenum is used by the above enzymes in a form bound to an organic ligand known as molybdopterin. Together, molybdenum and molybdopterin form the complex known as the molybdenum cofactor, which plays a critical role in the active site of these enzymes by by catalyzing the transfer of an oxygen in a two-electron reaction.
Molybdenum is an essential mineral that binds to the organic ligand molybdopterin. Together, molybdenum and molybdopterin form the molybdenum cofactor, which is critical for the function of several enzymes involved in the metabolism of purines, pyrimidines, and xanthines as well as sulfite metabolism.
Molybdenum's criteria for dietary intake is currently based on maintaining a molybdenum balance to support its role in as an enzymatic cofactor. Currently the recommended daily allowance (RDA) values are:
Infants: 2µg (0-6 months) up to 3µg (7-12 months)
Children: 17µg (1-3 years) up to 22µg (4-8 years)
Adults: 34µg (9-13 years), 43µg (ages 14-18), and 45µg for all other age groups with no differences between sexes
The requirement is increased to 50µg for women who are pregnant or lactating irrespective of age while the tolerable upper intake (TUL) is currently set at 2,000µg (2mg) a day for adults over the age of 19 due to potential reproductive side effects of excess molybdenum intake.
The requirements for molybdenum are based on how much molybdenum intake is required each day to make sure there is no long term bodily losses of this mineral. This recommended daily intake is readily achieved, and the human diet (plus water intake) tend to provide more than enough molybdenum even with the lowest estimates.
It has been reported that, currently, there are no known cases of molybdenum deficiency in free living subjects. Intentionally removing all molybdenum from the diet of rats does not impair health in any noticeably way aside from reducing the activity of one of the molybdenum-dependent enzymes (xanthine oxidase) by 10%. The one way to induce molybdenum deficiency in research animals appears to be through administration of an antagonist like tungsten.
Molybdenum deficiency, however, has been noted in hospital setting in a patient on total parental nutrition (TPN) devoid of molybdenum over the course of six months; major symptoms appeared to be a high L-methionine level in serum with low L-cystiene and taurine, with a general impairment of sulfur elimination. The patient was normalized when molybdenum (as ammonium molybdate) was added to TPN.
The mammalian body appears to be very resilient to deficiencies of molybdenum and there are no known cases of free living (ie. non-hospitalized) subjects developing a deficiency. When a deficiency does occur, it appears to result in impaired sulfur metabolism.
Whole blood tends to contain on average 5ng/mL molybdenum with serum containing 0.58ng/mL, usually in the form of molybdate. Serum levels have been noted to range between 0.28-1.17ng/mL in healthy humans and can fluctuate depending on dietary intake. Type II diabetics exhibit higher (0.84µg/L or 0.84ng/mL) serum molybdenum levels on average which seems to correlate with the severity of disease complications. Patients on hemodialysis have also been noted to have elevated serum molbdenum (5.79ng/g compared to 0.81ng/g for healthy individuals).
Consuming 50% of the recommended daily intake in otherwise healthy adult men (22µg a day) has either been associated with a significant reduction in molybdenum serum levels after 14 days or resulted in a reduced molybdenum balance in otherwise healthy male subjects. Although the typical diet provides more than enough molybdenum to avoid a deficiency, these studies demonstrate that serum levels can decrease within a couple weeks in response to reduced intake.
Following absorption, molybdenum is transported to the liver and excess is excreted in the bile, forming an enterohepatic excretion/reabsorption cycle with the intestines. It seems to preferentially accumulate in the liver, kidneys, adrenal glands, and intestines while excess intakes of molybdenum seem to cause alterations in these organs (kidneys and adrenals mostly) in rat studies.
Molybdenum is eliminated in both urine and feces in a dose-dependent manner. Low doses (22µg) have been noted to have a relative increase in fecal elimination (from 10% up to 40%), possibly secondary to a reduction in overall elimination.
The lower end of this dosage range (24-122µg a day) seems to maintain molybdenum balance in serum quite well, while daily doses of 466-1468µg that are associated with a relative increase of fecal elimination put the body into a positive molybdenum balance where retention exceeds elimination.
Molybdenum is eliminated primarily via the urine at standard doses. At higher doses (450µg+ daily) there is a shift to fecal elimination while the body also becomes unable to fully eliminate all excess molybdenum. This results in an overall retention of molybdenum.
In type II diabetic patients, the serum molybdenum concentrations correlated with severity of diabetes with 25% of subjects with slight-to-moderate complications from diabetes and 58% of subjects with severe complications exhibiting a serum concentration higher than the upper limit of reference values (1.2µg/L). It also seemed that urinary molybdenum was lower in diabetics with severe complications compared to those with slight-to-moderate complications. In instances of kidney damage, molybdenum also seems to be higher in serum prior to hemodialysis.
Serum molybdenum appears to be higher in subjects with type II diabetes, which may be secondary to impaired kidney function causing a retention of molybdenum (which is primarily eliminated by the kidneys).
A study in females rats given additional molybdenum in their drinking water (5-100mg/L in addition to 0.025mg/kg in the diet) noted that concentrations of 10mg/L or above appeared to prolong the estrus cycle. A later study, however, failed to find this effect when using much higher doses of 5, 17, or 60mg/kg over 90 days.
There is mixed evidence on how molybdenum interacts with estrogen in rats. Further evidence is needed.
In men who were sampled at an infertility clinic, it was noted that higher blood concentrations of molybdenum were associated with lower testosterone concentrations in serum.
One observational study found an inverse relationship between molybdenum and testosterone, but it is currently uncertain whether molybdenum has a causative role or if it is merely a biomarker of infertility.
It seems that the greatest currently known need for dietary molybdenum is during the early stages of embryonic development, in part due to the need of the rapidly-developing brain to have access to sulfated molecules produced by sulfite oxidase. However, excess molybdenum (10-100mg/L, but not 5mg/L) in the female rat's drinking water appears to reduce litter size and average weight of the pups; fetal resorption increased while conception rate was unaffected. The alterations in estrus noted in this study failed to be replicated elsewhere with higher doses (up to 60mg/kg) in the rat, but fertility was not tested in the latter study.
Animal studies indicate that very high molybdenum intake may lead to fetal toxicity.
In rats, administration of varying doses of molybdenum (as sodium molybdate dihydrate) over 90 days does not appear to cause mortality nor was it associated with decreased fertility. The lowest observed adverse effect level (LOAEL) was determined to be 60mg/kg per day in the rat due to some alterations in organ structure (kidney and adrenal) relative to control while the no observed adverse effect level (NOAEL) was established at 17mg/kg per day. The minor changes in the kidneys seen at 60mg/kg may precede damage as another study noted signs of nephrotoxicity at 80mg/kg (but not 40mg/kg).
An increase in renal copper concentrations has been noted with molybdenum intake (three-fold increase at 60mg/kg) despite no changes in dietary copper. Due to copper's toxic effects on the kidneys, this may play a role in molybdenum's nephrotoxic effects.
A study in rats on molybdenum toxicity reported a no observed adverse effect level (NOAEL) of 17mg/kg, with a lowest observed adverse effect level (LOAEL) of 60mg/kg. This may be due to increased renal copper concentrations, a known cause of renal toxicity.
One case report in a male patient in his late 30s exists where ingestion of 300-800µg molybdenum for 18 days (in part due to a high-molybdenum supplement) resulted in neurological symptoms including psychosis and hallucinations resulting in a grand mal seizure and cortical brain damage. The patient was treated with chelation therapy with success, but reintroduction of the supplement to demonstrate causation was not attempted.
At least one case report suggests high molybdenum intake from dietary supplements promotes the development of psychosis and seizures.
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