Cobalt is one of many essential mineral needed by our body in very small amounts to enhance productions of red blood cell and the formation of myelin nerve coverings It also is vital as a necessary cofactor for making the thyroid hormone thyroxine and stored in the red blood cells, the plasma, liver, kidney, spleen, pancreas, etc.
1. Dietary cobalt and Cobalt whole blood concentrations in healthy adult male
Recently, there has been an increase in the marketing and sales of dietary supplements, energy drinks, and other consumer products that may contain relatively high concentrations of essential elements. According to the study of assessement of Co whole blood concentrations in four healthy adult male volunteers who ingested a commercially available Co supplement (0.4mg Co/day) for 15 or 16days by ChemRisk, LLC, indicated that the mean whole blood Co concentration in the volunteers after 15 or 16days of dosing was 3.6μg Co/L and ranged from 1.8 to 5.1μg Co/L. The mean observed concentration in the study group was approximately 9-36 times greater than background concentrations. Further studies of Co whole blood concentrations following supplementation over longer time periods with additional monitoring of physiological parameters may provide useful information for evaluating the health of persons who take various doses of Co(1).
2. Cobalamin absorption: Mammalian physiology and acquired and inherited disorders
Vitamin B12 (cobalamin) is a cobalt-containing compound synthesized by bacteria and an essential nutrient in mammals, which take it up from diet. mIn the review to summarize the causes leading to vitamin B12 deficiency including decreased intake, impaired absorption and increased requirements, found that under physiological conditions, vitamin B12 bound to the gastric intrinsic factor is internalized in the ileum by a highly specific receptor complex composed by Cubilin (Cubn) and Amnionless (Amn). Following exit of vitamin B12 from the ileum, general cellular uptake from the circulation requires the transcobalamin receptor CD320 whereas kidney reabsorption of cobalamin depends on Megalin (Lrp2). Whereas malabsorption of vitamin B12 is most commonly seen in the elderly, selective pediatric, nondietary-induced B12 deficiency is generally due to inherited disorders including the Imerslund-Gräsbeck syndrome and the much rarer intrinsic factor deficiency. Biochemical, clinical and genetic research on these disorders considerably improved our knowledge of vitamin B12 absorption. This review describes basic and recent findings on the intestinal handling of vitamin B12 and its importance in health and disease(2).
3. Cobalamin deficiency and spina bifida and other neural tube defects
Cobalamin deficiency in the newborn usually results from cobalamin deficiency in the mother. Megaloblastic anaemia, pancytopenia and failure to thrive can be present, accompanied by neurological deficits if the diagnosis is delayed. According to the study by the the McGill University-Montreal Montreal Children's Hospital Research Institute of the McGill University Health Center, most cases of spina bifida and other neural tube defects result from maternal folate and/or cobalamin insufficiency in the periconceptual period. Polymorphisms in a number of genes involved in folate and cobalamin metabolism exacerbate the risk. Inborn errors of cobalamin metabolism affect its absorption, (intrinsic factor deficiency, Imerslund-Gräsbeck syndrome) and transport (transcobalamin deficiency) as well as its intracellular metabolism affecting adenosylcobalamin synthesis (cblA and cblB), methionine synthase function (cblE and cblG) or both (cblC, cblD and cblF). Inborn errors of folate metabolism include congenital folate malabsorption, severe methylenetetrahydrofolate reductase deficiency and formiminotransferase deficiency(3).
4. Inherited cobalamin malabsorption and Gene involved
Inherited malabsorption of cobalamin (Cbl) causes hematological and neurological abnormalities that can be fatal. According to the study by the Ohio State University, in the revealed population-specific mutations, mutational hotspots, and functionally distinct regions in the three causal genes. We identified mutations in 126/154 unrelated cases (82%). Fifty-three of 126 cases (42%) were mutated in CUBN, 45/126 (36%) were mutated in AMN, and 28/126 (22%) had mutations in GIF. We found 26 undescribed mutations in CUBN, 19 in AMN, and 7 in GIF for a total of 52 novel defects described herein. We excluded six other candidate genes as culprits and concluded that additional genes might be involved(4).
5. Cobalamin) deficiency and complications
Vitamin B12 (or cobalamin) deficiency is well known in geriatric patients, but not in those with spinal cord injury (SCI). According to the study by the Veterans Affairs Puget Sound Health Care System, Cobalamin deficiet SCI patients presented with depression and fatigue, 2 had worsening pain, 2 had worsening upper limb weakness, and 2 had memory decline. Of the 12 patients with subnormal serum vitamin B12 levels, 6 were asymptomatic. Classic laboratory findings of low serum vitamin B12, macrocytic red blood cell indices, and megaloblastic anemia were not always present. Anemia was identified in 7 of the 16 patients and macrocytic red blood cells were found in 3 of the 16 patients. Only 1 of the 16 SCI patients had a clear pathophysiologic mechanism to explain the vitamin B12 deficiency (ie, partial gastrectomy); none of the patients were vegetarian. Twelve of the SCI patients appeared to experience clinical benefits from cyanocobalamin replacement (some patients experienced more than 1 benefit), including reversal of anemia (5 patients), improved gait (4 patients), improved mood (3 patients), improved memory (2 patients), reduced pain (2 patients), strength gain (1 patient), and reduced numbness (1 patient)(5).
6. Psychiatric manifestations of vitamin B12 deficiency
There is a report of a case of a patient with vitamin B12 deficiency, who has presented severe depression with delusion and Capgras' syndrome, delusion with lability of mood and hypomania successively, during a period of two Months. Case report - Mme V., a 64-Year-old woman, was admitted to the hospital because of confusion. She had no history of psychiatric problems. She had history of diabetes, hypertension and femoral prosthesis. The red blood count revealed a normocytosis with anemia (hemoglobin=11,4 g/dl). At admission she was uncooperative, disoriented in time and presented memory and attention impairment and sleep disorders. She seemed sad and older than her real age. Facial expression and spontaneous movements were reduced, her speech and movements were very slow. She had depressed mood, guilt complex, incurability and devaluation impressions. She had a Capgras' syndrome and delusion of persecution. Her neurologic examination, cerebral scanner and EEG were postponed because of uncooperation. Further investigations confirmed anemia (hemoglobin=11,4 g/dl) and revealed vitamin B12 deficiency (52 pmol/l) and normal folate level. Antibodies to parietal cells were positive in the serum and antibodies to intrinsic factor were negative. An iron deficiency was associated (serum iron=7 micromol/l; serum ferritin concentration=24 mg/l; serum transferrin concentration=3,16 g/l). This association explained normocytocis anemia(6).
7. Effect of dietary organic supplementation on milk production, follicular growth, embryo quality, and tissue mineral concentrations in dairy cows
In the study to evaluate the potential effects of organic trace mineral supplementation on reproductive measures in lactating dairy cows, Cows were blocked by breed and randomly assigned at dry-off to receive inorganic trace mineral supplementation (control; n = 32) or to have a portion of supplemental inorganic Zn, Cu, Mn, and Co replaced with an equivalent amount of the organic forms of these minerals (treatment; n = 31), found that replacing a portion of inorganic supplemental trace minerals with an equivalent amount of these organic trace minerals (Zn, Mn, Cu, and Co) increased milk production in mid-lactation, but did not affect postpartum follicular dynamics, embryo quality, or liver and luteal trace mineral concentrations(7).
8. zinc-nickel-cobalt solution (ZnNiCo) and inflammation in adipose tissue
In the study to test the effect of a zinc-nickel-cobalt solution (ZnNiCo) on adipocyte function and to identify potential health effects of this solution in the context of obesity and associated disorders, indicated that the trace elements present in ZnNiCo are able to modulate the expression level of several inflammation related transcripts in adipocytes. These studies suggest that ZnNiCo could play a role in the prevention of inflammation in adipose tissue in obesity(8).
9. Cobalt-containing supplements
Cobalt-containing supplements are readily available in the U.S. and have been marketed to consumers as energy enhancers. However, little information is available regarding cobalt (Co) body burden and steady-state blood concentrations following the intake of Co dietary supplements. According to the study by the ChemRisk, LLC, 4840 Pearl East Circle, Boulder, CO 80301, United States, Pre-supplementation blood Co concentrations were less than the reporting limit of 0.5μg/L, consistent with background concentrations reported to range between 0.1 and 0.4μg/L. The mean whole blood Co concentration in the volunteers after 15 or 16days of dosing was 3.6μg Co/L and ranged from 1.8 to 5.1μg Co/L. The mean observed concentration in the study group was approximately 9-36 times greater than background concentrations. Further studies of Co whole blood concentrations following supplementation over longer time periods with additional monitoring of physiological parameters may provide useful information for evaluating the health of persons who take various doses of Co(9).
10. Vitamin B12 malabsorption: Mammalian physiology and acquired and inherited disorders
Vitamin B12 (cobalamin) is a cobalt-containing compound synthesized by bacteria and an essential nutrient in mammals. According to the study by the Hospitalier National d'Ophtalmologie des Quinze-Vingts, malabsorption of vitamin B12 is most commonly seen in the elderly, selective pediatric, nondietary-induced B12 deficiency is generally due to inherited disorders including the Imerslund-Gräsbeck syndrome and the much rarer intrinsic factor deficiency. Biochemical, clinical and genetic research on these disorders considerably improved our knowledge of vitamin B12 absorption(10).
11. The effects of Co on FA composition in blood
In the study to examine the amount of Co needed to obtain this effect. High-yielding dairy cows (n 4), equipped with ruminal cannulas, used in a 4 × 4 Latin square design, found that there was a linear effect of increasing the level of Co on milk FA composition. The effects of Co on FA composition in blood were insignificant compared with the effects on milk. In milk fat, the concentration of cis-9-18 : 1 was reduced by as much as 38 % on T4 compared with T1. Feed intake and milk yield were negatively affected by increasing the Co level(11).
12. For more information of Cobalamin (Vitamin B12), please visit Vitamin B12 in vitamins and minerals section
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