Aging alters the body's ability to absorb and utilize nutrients, some more than others. One nutrient that frequently feels the effect of aging is vitamin B12. An estimated 12% to 14% of seniors have a vitamin B12 deficiency. This number rises to approximately 25% among seniors who are institutionalized. A recent review by Tufts University researchers published in Nutrition in Clinical Care provides guidance for identifying, evaluating, and treating this deficiency.

Physiology of absorption

Vitamin B12 is bound to protein in food. During the early stages of digestion, acid and pepsin in the stomach cleave the vitamin off the protein. The vitamin molecule then adheres to a protein secreted by the stomach for transport to the proximal small intestine. There it separates from the protein, combines with intrinsic factor, and travels to the terminal ileum for absorption.

Etiology of deficiency

B12 deficiency can result from inadequate intake, atrophic gastritis, and pernicious anemia (a megaloblastic anemia). These are all common conditions among seniors. B12 is found in foods of animal origin (eggs, dairy, meat) and in some fortified cereals. Seniors with marginal intakes of these foods are at risk for deficiency.

Type B atrophic gastritis (related to Helicobacter pylori infection) results in a reduction of stomach acid production and subsequent impaired B12 absorption. In the case of pernicious anemia, B12 is not absorbed because there is an absence of intrinsic factor.

Hematological signs

A red flag for a potential B12 deficiency is an increased mean corpuscular volume (MCV) indicating macrocytic red blood cells. This can indicate either a B12 or a folate deficiency. Treating megaloblastic anemia with folate, if it is in fact a B12 deficiency, masks hematological indicators and can lead to irreversible neurologic damage. To differentiate between folate and B12 deficiency, one option is to measure serum levels of B12. However, because there is no consensus as to what level of B12 indicates a deficiency, serum methylmalonic acid level is a better indicator of B12 status. If a patient is B12 deficient, a Schilling test should be done to determine if the deficiency is due to malabsorption.

CNS and mental changes

Patients showing impaired cognitive function should be evaluated for a B12 deficiency. Hematological indicators can be masked by high levels of folate in the diet, leaving neurologic indicators as the only sign of a problem. Neurologic symptoms may include gait abnormalities, personality changes, dementia, psychosis, and depression. These abnormalities may be irreversible if treatment is delayed.

Treatment

The U.S. RDA for B12 is 2.4 µg per day. However, this amount may not be sufficient for patients with a B12 deficiency caused by atrophic gastritis. In this case, supplemental doses may be needed.

Patients who are poor eaters should be prompted to choose more foods that are good sources of B12, including eggs, milk, cheese, and meat. If they are unable to consume enough of these foods, they should be prescribed a multivitamin that contains the RDA of B12.

Pernicious anemia is treated with large oral doses or intramuscular injections of B12. An alternate treatment option is an intranasal gel.

Physicians who work with seniors must be aware of the biochemical and neurological signs of B12 deficiency. Prompt treatment is essential because, left untreated, it can result in permanent neurologic damage.