Absorption of vitamin B12 from food requires normal function of the stomach, pancreas, and the digestive tract (‘intestine’).
The most common causes of vitamin B12 deficiency are an autoimmune condition (‘pernicious anemia’) and poor absorption (‘malabsorption’) of food-bound vitamin B12; both causes become more common with increasing age (30, 47).
Pernicious anemia is the end stage of an autoimmune inflammation of the stomach, resulting in destruction of stomach cells needed for vitamin B12 absorption by one's own antibodies. Treatment generally requires injections of vitamin B12 or high-dose oral supplementation (31, 32, 33, 34).
Food-bound vitamin B12 malabsorption is a chronic inflammation of the stomach, resulting in destruction of acid-producing gland cells, required for the release of vitamin B12 from the proteins in food. Individuals with food-bound vitamin B12 malabsorption do not have an increased requirement for vitamin B12; they simply need it in the crystalline form found in fortified foods and dietary supplements.
An infection by the bacteria Heliobacter pylori can induce chronic inflammation of the stomach, which may progress to ‘atrophic gastritis’, resulting in a loss of glands in the stomach, decreased acid production, and vitamin B12 deficiency (30).
Other causes of vitamin B12 deficiency include surgical resection of the stomach or portions of the small intestine.
Since vitamin B12 is found only in foods of animal origin, a strict vegetarian or vegan diet has resulted in cases of vitamin B12 deficiency.
Alcoholics (35) and individuals with acquired immunodeficiency syndrome (AIDS) (2) may experience reduced intestinal absorption of vitamin B12.
Vitamin B12 deficiency results in impairment of the activities of B12-requiring enzymes: diminished activity of methionine synthase traps vitamin B9 (folate) in a form that is not usable by the body, resulting in symptoms of folate deficiency. Thus, in both folate and vitamin B12 deficiencies, folate is unavailable to participate in DNA synthesis, resulting in the production of large, immature, hemoglobin-poor red blood cells (‘megaloblastic anemia’) (2). Megaloblastic anemia should not be treated with folic acid until the underlying cause has been determined (36).
The neurologic symptoms of vitamin B12 deficiency include numbness and tingling of the arms and more commonly the legs, difficulty walking, memory loss, disorientation, and dementia with or without mood changes.
The origins of other symptoms, such as tongue soreness, appetite loss, and constipation, are unclear, but they may be related to the stomach inflammation underlying some cases of B12 deficiency (27).
Authored by Dr Peter Engel in 2010, reviewed and revised by Angelika Friedel on 29.06.2017
