Cobalt is part of the vitamin B12 molecule as cobalamin, and there is little evidence of other roles of cobalt in human nutrition.
The cobalt atom in B12 is surrounded and attached to a methyl group, a deoxyadenosyl group and a hydroxyl group or a cyano group.
The human requirement for cobalt is not the ionic form of the metal, but for a preformed metallovitamin that cannot be synthesized from dietary metal. Therefore, it is the vitamin B12 content of foods in the diet that is of importance in human nutrition.
In the past, cobalt was recommended for treating anemia, nephritis and infection in addition to the usual hemopoietic agents. Reports of goiter, myxedema and congestive heart failure have been found in five patients.
Industrial exposure to high amounts of cobalt and consumption of beer contaminated with excessive amounts of cobalt produce cardiomyopathy with a high mortality risk.4
Dietary sources of cobalt are the same as vitamin B12, such as foods of animal origin or fermented foods where the bacteria produce the vitamin. Organ meats are the best source of vitamin B12 (liver, kidney, heart, and pancreas), followed by clams, oysters, extra-lean beef, seafood, eggs, milk and yogurt, chicken, cheese, and miso (a fermented soybean product).
Since the primary sources of vitamin B12 in the diet are animal products, vegetarians have a high risk of developing B12 deficiency. Therefore, it is recommended to supplement in order to prevent the vitamin B12 deficiency.
Other conditions that may be associated with an increased risk for cobalt deficiency include:
Caution with pregnancy or nursing, consult physician before using.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship.
Vitamin B12 deficiency and Hyperhomo-cysteinemia: It has been suggested that vitamin B12 deficiency and hyperhomocysteinemia impact the metabolism of some trace elements, particularly cobalt and nickel. A study found that vitamin B12-deficient pigs fed an oral supplement of cobalt (1 mg/kg), had 47% lower serum homocysteine concentrations than B12-deficient pigs fed a lower dose of cobalt (0.13 mg/kg). However, B12 status of both groups was not affected. Nickel supplementation also improved B12 status in the liver and serum, and decreased the concentration of serum homocysteine. The results suggested that cobalt and nickel influenced response of the pig to vitamin B12 deficiency. In addition, the accumulation of homocysteine in the serum, a symptom of B12 deficiency, can be attenuated by cobalt and nickel even though the mode of action of these elements seems to differ. 8
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