Co – Cobalt is found in igneous rocks at about 25 ppm; shales at 19 ppm; sand- stones at 0.3 ppm; limestone at 0.1 ppm; fresh water at 0.0009 ppm; sea water at 0.00027 ppm; soils at 8 ppm (higher in soils derived from basalt or serpentine. Vast areas of the Earth are known to be absolutely devoid of cobalt.
Marine plants contain cobalt at 0.7 ppm; land plants at 0.5 ppm (accumulator plants include Nyssa sylvatica and Clethra barbinrvis).
Marine animals contain cobalt at 0.5 to5.0 ppm; land animals 0.03 ppm with greatest concentrations in the bone and liver.
Essential for blue green algae, some bacteria and fungi, some plants, insects, birds, reptiles, amphibians and mammals including man. Cobalt functions as a cofactor and activator for enzymes, fixes nitrogen during amino acid production; a single cobalt atom is the central metal component of vitamin B12 which itself is a co-factor and activator (cobamide coenzymes) for several essential enzymes.
B12/Cobalt is chelated in a large terapyrrole ring similar to the phorphyrin ring found in hemoglobin and chlorophyll. The original B12 molecule isolated in the laboratory contained a cyanide group, thus the name cyanocobalamin; there are several different cobalamine compounds that have vitamin B12, activity, with cyanocobalamin and hydroxycobalamin the most active.
Vitamin B12 is a red crystalline substance that is water-soluble; the red color is due to the cobalt in the molecule. Vitamin B12 is slowly deactivated by acid, alkali, light and oxidizing or reducing substances; about 30 percent of B12 activity is lost during cooking (electric, gas or microwave).
In 1948, B12 was isolated from liver extract and demonstrated anti pernicious anemia activity.
The essentiality of cobalt is unusual in that the requirement is for a cobalt complex known as cyanocobalamin or vitamin B12. A pure cobalt requirement is only found in some bacteria and algae and the need for B12/cobalt is thought by some to represent a symbiotic relationship between microbes which generate and manufacture B12 from elemental cobalt and vertebrates that require B12.
Ruminants (i.e.-cows, sheep, goats, deer, antelopes, giraffe, etc.) can use elemental cobalt, however, the microbes fermenting and digesting plant material in their first stomach (rumen) convert elemental cobalt into vitamin B12 which the animal can use.
Carnivores can get their B12 from the ruminant by consuming stomach contents, liver, bone and muscle from their kills.
Poultry, lagomorphs (rabbits and hares), and rodents actively eat feces during the night (coprophagy) and in the process obtain B12 manufactured by intestinal microorganisms.
Metallic cobalt is absorbed at the rate of 20 to 26.2 percent in mice and humans if intrinsic factor is present in the stomach and the stomach pH is 2.0 or less. Intrinsic factor is a mucoprotein enzyme known as Castle’s intrinsic factor and is part of normal stomach secretions.
If a person has hypochlorhydria (low stomach acid – usually a NaCl deficiency) the intrinsic factor will not work and B12/cobalt is not absorbed – this is why doctors frequently give B12 shots to older people on salt restricted diets. Sublingual (under the tongue) and oral spray B12 is available; plant derived cobalt is very bioavailable, however, because of low salt diets and cobalt depleted soils, vegetarians frequently have B12 deficiencies.
The B12 intrinsic factor complex is primarily absorbed in the terminal small intestine or ileum; calcium is required for the B12 to cross from the intestine into the bloodstream as well as an active participation by intestinal cells. Simple diffusion can account for one to three percent of the vitamin’s absorption.
There is an enterohepatic (Intestine direct to the liver) circulation of B12 that recycles B12 from bile and other intestinal secretions which explains why B12 deficiency in vegans may not appear for five to ten years.
The maximum storage level of B12 is 2 mg, which is slowly released to the bone marrow as needed. Excess intake of B12 is shed in the urine i.e. contributing the notion of “expensive urine”.
Vitamin B12/Cobalt joins with folic acid, choline and the amino acid methionine to transfer single carbon groups (methyl groups) in the synthesis of the raw materials to make RNA and the synthesis of DNA from RNA (directly involved in gene function – remember preconception nutrition to prevent birth defects!). Growth, myelin formation (converts cholesterol to the insulating material myelin found around nerves in the brain and large nerve trunks) and RBC synthesis are dependant on B12.
The discovery of the essentiality of cobalt came from observing a fatal disease (“bush sickness”) in cattle and sheep from Australia and New Zealand; it was observed that “bush sickness” could be successfully treated and prevented by cobalt supplements.
Bush sickness was characterized by emaciation (unsupplemented vegans), dull stare, listless, starved look, pale mucus membranes, anorexia (loss of appetite), anemia microcytic/hypochromic) and general unthriftiness.
In humans, a failure to absorb B12/Cobalt results in deficiency disease. This can result from a surgical removal of parts of the stomach (eliminates areas of intrinsic factor production), or surgical removal of the ileum portion of the small bowel, small intestinal diverticula, parasites (tapeworm), celiac disease (allergies to wheat gluten and cows milk albumen) and other malabsorption diseases. Pernicious anemia and demyelination of the spinal cord and large nerve trunks are classic for B12/Cobalt deficiency.
Less than 0.07 ppm cobalt in the soil results in cobalt deficiency in animals and people who eat crops grown from those soils; 0.11 ppm cobalt in the soil prevents and cures Cobalt deficiency.
The RDA for B12/Cobalt is 3 to 4 mcg per day. We prefer expensive urine and like 250 to 400 mcg per day, especially while preparing for pregnancy and nursing (remember a baby being nursed by a deficient mother has their deficiency extended over a long period of time and may result in serious permanent nerve damage).
Cobalt excess in man (20 to 30 mg/day) may create erythropoiesis (increase in RBC production) with increased production of the hormone erythropoieten from the kidney. Cobalt is also a necessary co-factor for the production of thyroid hormone.
Cobalt is a trace mineral nutrient for bacteria. Its only established role in animals is as a component of vitamin B12. Animals like ruminants (cows) that depend on bacteria for vitamin B12 require inorganic cobalt as a nutrient. Only microorganisms are capable of incorporating cobalt into vitamin B12.
The body cannot use unattached cobalt and cobalt supplements are therefore ineffective. Though cobalt has a low order of toxicity, overdosing with cobalt could lead to goiter and over-production of red blood cells in susceptible individuals.
Low concentrations of cobalt salts were once added to beer as an antifoaming agent. However, cobalt was incriminated in several epidemics of cardiac failure among beer drinkers. The typical American diet provides low levels of cobalt. Green leafy vegetables are the richest source, while dairy products and refined grain products are among the lowest. For example, spinach provides 0.4 to 0.6 mcg per gram, and white flour contains 0.003 mcg per gram. The oral intake of cobalt necessary to produce toxicity is many times greater than can be obtained by normal consumption of foods and beverages.
Cobalt Physiology
The only known function of Co is its participation in metabolism as a component of vitamin B12; thus the signs of Co deficiency are in reality signs of a shortage of the vitamin. Vitamin B12 is an essential part of several enzyme systems that perform very basic metabolic functions. Most of the cobalamins occur as two coenzymatically active forms, adenosylcobalarnin and methylcobalamin. Cyanocobalamin is converted within cells to methylcobalamin, a coenzyme for methyltransferase, or adenosylcobalamin, the coenzyme for mutase.
Most reactions of vitamin B12 enzymes involve transfer or synthesis of one-carbon units, for instance, methyl groups. Though the most important tasks of vitamin B12 concern metabolism of nucleic acids and proteins, it also functions in (1) purine and pyrimidine synthesis; (2) transfer of methyl groups; (3) formation of proteins from amino acids; and (4) carbohydrate and fat metabolism (McDowell, 1989). Vitamin B12 promotes red blood cell synthesis and maintains nervous system integrity, which are functions noticeably affected in a deficiency.
Vitamin B12 is metabolically related to other essential nutrients, such as choline, methionine, and folacin, and functions in transmethylation and biosynthesis of labile methyl groups (McDowell, 1989). The purine bases (adenine and guanine) as well as thymine are constituents of nucleic acids; with a folacin deficiency, there is a reduction in biosynthesis of nucleic acids essential for cell formation and function. Deficiency of B12 induces a folacin deficiency by blocking utilization of folacin derivatives. A vitamin B12-containing enzyme removes the methyl group from methylfolate, thereby regenerating tetrahydrofolate (THF), from which is made the 5,20-methylene THF required for thymidylate synthesis.
Metabolism of labile methyl groups plays a significant part in biosynthesis of methionine from homocysteine. A vitamin B12-requiring enzyme, 5-methyltetrahydrofolate-homocysteine methyltransferase, catalyses reformation of methionine from homocysteine. Activity of this enzyme is depressed in liver of vitamin B12-deficient sheep (MacPherson, 1982). This defect could lead to a deficiency of available methionine, which may account for impairment of nitrogen metabolism in vitamin B12-deficient sheep.
Overall synthesis of protein is impaired in vitamin B12-deficient animals. Wagle et al. (1958) demonstrated that rats and baby pigs deprived of vitamin B12 were less able to incorporate serine, methionine, phenylalanine, and glucose into liver proteins. Impairment of protein synthesis may be the principal reason for the growth depression frequently observed in these animals (Friesecke, 1980).
In animal metabolism, propionate of dietary or metabolic origin is converted into succinate, which then enters the tricarboxylic acid (Krebs) cycle. Propionate is a three-carbon, and succinate, a four-carbon compound; therefore, this process requires the introduction of a one-carbon unit. Methylmalonyl CoA isomerase (mutase) is a vitamin B12-requiring enzyme (5′ deoxyadenosyl cobalamin), which catalyzes the conversion of methylmalonyl-CoA to succinyl-CoA.
Metabolism of propionic acid is of special interest in ruminant nutrition because of the large quantities produced during carbohydrate fermentation in the rumen. The main source of energy to ruminants is not glucose but primarily acetic and propionic acids. In Co or vitamin B<SUB12-deficiency, the rate of propionate clearance from blood is depressed, and methylmalonyl-CoA accumulates. This results in an increased urinary excretion of methylmalonic acid and also loss of appetite because impaired propionate metabolism leads to higher blood propionate levels inversely correlated to voluntary feed intake (MacPherson, 1982).Cobalt in Human Nutrition
The average uptake of cobalt by humans is 0.03-0.3 mg per day, and a positive balance has been reported with a daily diet of 0.03 mg of cobalt.
Vitamin B12 is a red crystalline solid, fairly soluble in water and lower alcohols, but not in most other organic solvents. Its empirical formula is C63H88016N14PCO, giving it a cobalt content of 4.35%. The central cobalt atom is in the trivalent state, but is easily reduced to the divalent condition. Vitamin B12 contains four pyrrole rings, as does heme, but these rings are partially reduced whereas heme rings are fully conjugated. Also, in heme the groups binding the pyrrole rings together are all alike, but in vitamin B12 one bridging-CH-group is missing, so there is a five-membered ring in place of a six-membered one. There is also a direct cobalt-carbon bond. Vitamin B12 brings about molecular rearrangements, moving an organic group from one carbon atom in the substrate to another.
Vitamin B12 is the first vitamin found to contain a metal, the only cobalt-containing compound in the human body, and the most complex nonpolymer yet found in nature. It is also one of the most physiologically potent compounds; only about 1 ug per day is required in human nutrition. It is essential, in conjunction with an enzyme, in at least 10 reactions, although only one of these is present in man, where it affects growth and red blood cell formation.
Vitamin B12Most agricultural scientists now believe that cobalt deficiency in ruminants is essentially a deficiency of vitamin B12. The pathological consequences of vitamin B12 deficiency form a syndrome, notable features of which are neurological and muscular lesions, in which the metabolic consequences of hepatic damage may play a significant role (Fell, 1981). The following daily additions have been shown to raise the level of vitamin B12 to satisfactory ranges and overcome cobalt deficiencies: for sheep, 2-5 mg cobalt chloride, and for cows, 20-30 mg cobalt chloride.