Vitamin B12 (cobalamin) is a workhorse vitamin. It helps keep nerve and blood cells healthy, make DNA, and prevent megaloblastic anemia. Cobalamin is different from other vitamins because it is not plant-sourced, but is found naturally in a wide variety of animal products such as meat, fish, eggs, and dairy.
The July 2017 issue of Nature Reviews includes a disease primer that discusses the epidemiology, mechanism/pathophysiology, diagnosis/screening, prevention, and management of vitamin B12 deficiency.
B12 status varies through the lifetime, creating a need to consider patient factors when interpreting diagnostic biomarkers of B12 status. Inadequate intake, impaired absorption, chemical inactivation, or inherited B12 transport or metabolism impairment may lead to deficiency. Diagnosis is critical because B12 deficiency can be life-threatening.
Clinical B12 deficiency with hematological and neurological manifestations is relatively uncommon. On the other hand, 2.5-26% of the general population has subclinical deficiency and it’s unclear if these people will progress to deficiency or continue to have low but stable B12 levels.
B12 deficiency’s signs and symptoms are weakness, constipation, numbness and tingling in the hands and feet, confusion, poor memory, and mouth or tongue soreness. Vitamin B12 deficiency can affect individuals at any age, but vegans and elders are at increased risk. It is often difficult to diagnose elderly patients because its typical clinical manifestations are absent or are confused with dementia.
Increased consumption of animal products and fortified foods may prevent B12 deficiency, as will oral or parenteral B12 supplementation. Initially, higher doses are required to replete B12 stores in the body.
Hematologic abnormalities respond to B12 treatment in about 5 days and completely recover in 4 to 6 weeks. Neurological abnormalities are slower to correct. B12 deficiency not due to nutritional deficiency may require lifelong treatment. read more…