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Friday, September 16, 2016

Dietary Minerals Cobalamin deficiency and spina bifida and other neural tube defects

Kyle J. Norton(Scholar, Master of Nutrients), all right reserved.
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
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Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.

                                 Dietary Minerals 

Dietary Minerals are the group of minerals which is essential for our body to sustain normal functions and physical health.

                                        Cobalt

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.

                 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).


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