Vitamin B12 deficiency (Hypocobalaminemia) Treatments

About Vitamin B12 deficiency (Hypocobalaminemia)

Cyanocobalamin, courtesy of kupirijo.

Vitamin B12 deficiency or hypocobalaminemia is a low blood level of vitamin B12. It can cause permanent damage to nervous tissue if left untreated long enough. Vitamin B12 itself was discovered through investigation of pernicious anemia, which is an autoimmune disease that destroys parietal cells in the stomach that secrete intrinsic factor. Pernicious anemia, untreated, is usually fatal within three years. Once identified, however, it can be treated successfully and with relative ease, although it cannot be cured and continued treatment is required. Intrinsic factor is critical for the normal absorption of B12 in amounts that occur in foods, and thus a lack of intrinsic factor, as occurs in pernicious anemia, causes a vitamin B12 deficiency. Many other subtler kinds of vitamin B12 deficiency and their biochemical effects have since been elucidated.

The results of the Framingham Offspring Study indicate that B12 deficiency may be more common than was previously believed. Deficiency is most significantly linked to improper absorption rather than low consumption, as many who consume high amounts of B12 may still experience deficiency.

The total amount of vitamin B12 stored in the body is between 2–5 mg in adults. Around 50% is stored in the liver, but approximately 0.1% is lost each day by secretions into the gut, as not all the vitamin in the gut is reabsorbed. While bile is the main vehicle for B12 excretion, most of the B12 secreted in bile is recycled via the enterohepatic circulation. Due to the extreme efficiency of this mechanism, the liver can store several years worth of vitamin B12 under normal conditions and functioning.[citation needed] How quickly B12 levels may change when dietary intake is low, however, depends on the balance between how much B12 is obtained from the diet, how much is secreted, and how much is absorbed. B12 deficiency may arise in the span of a year if initial stores are low and genetic factors are unfavorable. In contrast, deficiency may not appear for decades. In infants and children, B12 deficiency appears much more quickly when a vitamin poor diet is consumed.

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Meat or Aleo Vera?

B12 deficiency is a serious problem that can cause bad results so that we should eat meat (liver) , fish , egg, cheese and drink milk to get enough b12 vitamin our bodies need. some sources say aleo vera is the only plant contains b12 vitamin. If it's true great news for vegans and vegetarians.

In some dangerious conditions b12 shots and pills are necassary. Doctors inform you on this.

Healthy days for everyone!

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B12 can be supplemented in healthy subjects by oral pill; sublingual pill, liquid, or strip; intranasal spray; transdermal patch or by injection. B12 is available singly or in combination with other supplements. B12 supplements are available in forms including cyanocobalamin, hydroxocobalamin, methylcobalamin, and adenosylcobalamin (sometimes called "cobamamide" or "dibencozide"). Oral treatments involve giving 250 µg to 1 mg of B12 daily.

Vitamin B12 can be given as intramuscular or subcutaneous injections of hydroxycobalamin, methylcobalamin, or cyanocobalamin. Body stores (in the liver) are partly repleted with half a dozen injections in the first couple of weeks (full repletion of liver stores requires about 20 injections) and then maintenance with monthly injections throughout the life of the patient. Vitamin B12 can also be easily self-administered by injection by the patient, using the same fine-gauge needles and syringes used for self-administration of insulin.
B12 has traditionally been given parenterally (by injection) to ensure absorption. However, oral replacement is now an accepted route, as it has become increasingly appreciated that sufficient quantities of B12 are absorbed when large doses are given. This absorption does not rely on the presence of intrinsic factor or an intact ileum. Generally 1 to 2 mg daily is required as a large dose. By contrast, the typical Western diet contains 5–7 µg of B12 (Food and Drug Administration (FDA) Daily Value ). It has been appreciated since the 1960s that B12 deficiency in adults resulting from malabsorption (including loss of intrinsic factor) can be treated with oral B12 supplements when given in sufficient doses. When given in oral doses ranging from 0.1–2 mg daily, B12 can be absorbed in a pathway that does not require an intact ileum or intrinsic factor. In two studies, oral treatment with 2 mg per day was as effective as monthly 1 mg injections.

Hypokalemia, an excessively low potassium level in the blood, is anecdotally reported as a complication of vitamin B12 repletion after deficiency. Excessive quantities of potassium are used by newly growing and dividing hematopoeitic cells, depleting circulating stores of the mineral.

Research has established the effectiveness of other routes of B12 administration, primarily intranasal and sublingual dosing, but neither has been proven to be superior to oral dosing; recommendations are based on a consumers individual circumstances. The sublingual route, in which B12 is absorbed under the tongue, is manufactured in a variety of forms, such as lozenges, pills, and lollipops. A 2003 study found no significant difference in absorption for serum levels from oral vs. sublingual delivery of 500 µg (micrograms) of cobalamin, although the study measured only serum levels as opposed to tissue levels, which is more reflective of B12 levels. Sublingual methods of replacement may be effective only because of the typically high doses (500 micrograms), which are swallowed, not because of placement of the tablet. As noted below, such very high doses of oral B12 may be effective as treatments, even if gastro-intestinal tract absorption is impaired by gastric atrophy (pernicious anemia).

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