11.22 Vitamin B12 Deficiency & Toxicity

There are 2 primary symptoms of vitamin B12 deficiency:

Megaloblastic (Macrocytic) Anemia

Neurological Abnormalities

Megaloblastic (Macrocytic) Anemia

This is the same type of anemia that occurs in folate deficiency that is characterized by fewer, enlarged, immature red blood cells. In vitamin B12 deficiency, this can occur because there is not enough cobalamin to convert 5-methyl THF to THF (illustrated in Figure 11.211). Thus, THF is not available for normal DNA synthesis and the red blood cells do not divide correctly.

Neurological Abnormalities

Vitamin B12 deficiency also results in nerve degeneration and abnormalities that can often precede the development of anemia. These include a decline in mental function and burning, tingling, and numbness of legs. These symptoms can continue to worsen and deficiency can be fatal1.

The most common cause of vitamin B12 deficiency is pernicious anemia, a condition of inadequate intrinsic factor production that causes poor vitamin B12 absorption. This condition is common in people over the age of 50 because they have the condition atrophic gastritis2. Atrophic gastritis is a chronic inflammatory condition that leads to the loss of glands in the stomach, as shown in the figure in the following link.

Web Link

Atrophic Gastritis

The loss of glands leads to decreased intrinsic factor production. It is estimated that ~6% of those age 60 and over are vitamin B12 deficient, with 20% having marginal status3. In addition to the elderly, vegans are also at risk for vitamin B12 deficiency because they do not consume animal products. However, the deficiency may take years to develop in adults because of stores and recycling of vitamin B122. Deficiency has the potential to occur much quicker in infants or young children on vegan diets because they do not have stores that adults do4.

Folate/Folic Acid masking vitamin B12 deficiency

As mentioned above, folate and vitamin B12 lead to the same megaloblastic (macrocytic) anemia. If high levels of folate or folic acid (most of the concern is with folic acid since it is fortified in foods and commonly taken in supplements) is given during vitamin B12 deficiency, it can correct this anemia. This is referred to as masking because it does not rectify the deficiency, but it “cures” this symptom. This is problematic because it does not correct the more serious neurological problems that can result from vitamin B12 deficiency. There are some people who are concerned about the fortification of cereals and grains with folic acid because people who are B12 deficient might not develop macrocytic anemia, which makes a vitamin B12 deficiency harder to diagnose2.

No toxicity of vitamin B12 has been reported.

References & Links

1. Byrd-Bredbenner C, Moe G, Beshgetoor D, Berning J. (2009) Wardlaw’s perspectives in nutrition. New York, NY: McGraw-Hill.

2. Whitney E, Rolfes SR. (2008) Understanding nutrition. Belmont, CA: Thomson Wadsworth.

3. Allen L. (2009) How common is vitamin B-12 deficiency? Am J Clin Nutr 89(2): 693S-696S.

4. Gropper SS, Smith JL, Groff JL. (2008) Advanced nutrition and human metabolism. Belmont, CA: Wadsworth Publishing.


Atrophic Gastritis – http://catalog.nucleusinc.com/enlargeexhibit.php?ID=3754