Volume : VIII, Issue : I, January - 2018

How frequency is vitamin B12 deficiency?

Blagovesta Pencheva

Abstract :

 

Much attention has been given to B–vitamins, in particular to folate and vitamin B12, because of their potential influence on cardiovascular diseases (CVD). The rates of deficiency vary depending on the country, as local laws, the economic situation, cultural trends and the environment can affect supply of vitamins and minerals. Vitamin B–12 deficiency and depletion are common in some  countries, particularly among the elderly, and are most prevalent in poorer populations around the world(1,2,3). Pernicious anemia is a common cause of megaloblastic anemia throughout the world and especially in persons of European . Dietary deficiency of vitamin B12 due to vegetarianism is increasing and causes hyperhomocysteinemia. In large surveys in the United States and the United Kingdom, ≈6% of those aged ≥60 y are vitamin B–12 deficient (plasma vitamin B–12 < 148 pmol/L), with the prevalence of deficiency increasing with age. The deficiency affected ≤3% of those aged 20–39 y, ≈4% of those aged 40–59 y, and ≈6% of persons aged ≥70 y. Deficiency was present in <1% of children and adolescents but was ≤3% in children aged <4 y. Marginal depletion (serum vitamin B–12 148–221 pmol/L) was more common and occurred in ≈14–16% of those aged 20–59 y and >20% of those >60 y. Plasma methylmalonic acid (MMA) concentrations were markedly higher after age 60 y. The term vitamin B12 includes several chemical compounds similar in chemical structure (4,5,6,7). There are 4 known kinds of vitameres of vitamine B12: (a) cyanocobalamin, which is metabolized in the body to an active coenzyme; (b) hydroxocobalamin which is not normally present in the human body; (c) adenosylcobalamin (adoB12), an active cofactor; and (d) methylcobalamin (MeB12), an enzymatically active cofactor (1,3) About 60% of the total amount of B12 in the body is stored in the liver and 30% is stored in the muscles . The body has a special circuit between the digestive tract and the liver. It is then reabsorbed at the end of the small intestine (the ileum) and taken back to the liver where it is used again(figure 1). The body can store vitamin B12 for years in the liver. Vitamin B12 is very stable at high temperature, while in strongly acidic and strongly alkaline conditions it loses its activity. Its levels are negatively affected by alcohol and estrogens. Serum vitamin B12 binds to proteins known as transcobalamins. The majority of the vitamin, approximately 80%, is transported on the inactive TCI (also called haptocorrin). Haptocorrin  is a glycoprotein produced by the salivary glands of the mouth. It primarily serves to protect Vitamin B12 from acid degradation in the stomach by producing a Haptocorrin–Vitamin B12 complex. Once the complex has traveled to the more neutral duodenum, pancreatic proteases degrade haptocorrin, releasing free cobalamin, which now binds to intrinsic factor for absorption by ileal enterocytes(figure 1). The active transport protein for vitamin B12 is transcobalamin II (TCII), which carries about 20% of the vitamin in the circulation (2,7,8). Holo–transcobalamin (holo–TC) is TCII with attached cobalamin, which delivers vitamin B12 to the cells. The low serum vitamin B12 concentration can be associated with a deficiency of TCI. Methylmalonic acid and homocysteine ​​are indicators of the status of vitamin B12 in the body cells. High levels of Methymalonic Acid (MMA) and Homocysteine (HC) have been identified as better indicators of B–12 deficiency than the actual serum B–12 level itself.  Methylmalonic acid is considered to be a specific indicator of cobalamin metabolism (8,9,10). Homocysteine ​​is a derivative of methionine which is supplied through the proteins in the food. The body converts the greater part of homocysteine ​​back to methionine with the help of vitamin B12 (11,12). In case of B12 deficiency, homocysteine ​​levels increase, because this reaction cannot take place. Normal serum levels of homocysteine ​​are from 2.2 to 13.2 μmol / l. Vitamin B12 is not synthesized by multicellular or unicellular eukaryotes (4,8,12). All of the substrate cobalt–corrin molecules, from which B12 is made, are synthesized by bacteria. The human body has the ability to convert any form of B12 to an active form, by means of enzyme action. Animals store vitamin B12 in the liver and muscles. Meat (lamb, veal, beef and turkey), liver, eggs, cheese and milk are sources of vitamin B12. As vegetarian diets generally include high content of folic acid, elevated levels of homocysteine ​​in vegetarians are typically due to the low intake of B12 (4,6,9).

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Article: Download PDF   DOI : 10.36106/ijar  

Cite This Article:

Blagovesta Pencheva, How frequency is vitamin B12 deficiency?, INDIAN JOURNAL OF APPLIED RESEARCH : Volume-8 | Issue-1 | January-2018

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