B12 and Folic Acid

Abstract

Vitamin B12 deficiency is common in older adults, because of the complex absorption pathway and several factors predisposing to deficiency, including inadequate diet, food-cobalamin malabsorption, a host of gastric and small intestinal disorders, and certain medications. The presentations of B12 deficiency range from the asymptomatic to hematological, neuropsychiatric and other manifestations. Screening may be directed to those at risk and with suggestive clinical features. Diagnosis of obvious B12 deficiency can be suspected on clinical grounds. Correction of deficiency is easily accomplished by B12 replacement and is inexpensive. Diagnosis of subclinical B12 deficiency or metabolic B12 deficiency can be achieved only through use of reference laboratories. Ideally, assessment of status is through measurement of serum or plasma B12 level; the additional verification of methylmalonic acid, holo-transcobalamin and homocysteine levels is utilized in certain situations, when clinical features are similar to B12 deficiency but the B12 levels are normal. Methylmalonic acid levels may be a more reliable indicator of deficiency while homocysteine levels have poor specificity. While hematological manifestations are reversible, neurological complications have a short window of opportunity for correction, emphasizing the importance of early diagnosis. Folate deficiency is also common in older adults and predisposed by dietary preferences or restrictions, malabsorption, losses or increased requirements. Folate deficiency causes reversible hematological features similar to B12 deficiency, but without the neurological manifestations. Folate deficiency has been linked to cognitive impairment and depression. Fortification of food has helped significantly in preventing deficiency. Monitoring folate levels following supplementation is the preferred approach, rather than use of homocysteine levels.