Abstracts

Vitamin B12 (cobalamin) ranks among the most useful, safe and effective orthomolecules when treating a diverse array of neuropsychiatric conditions. However, most clinicians do not consider vitamnin B12 important unless the serum level is below laboratory reference ranges. Ten research reports, summarized here, indicate metabolic consequences from low-normal (but not deficient) serum B12 levels, and/or clinical improvements following therapy that markedly increased serum B12 levels. My clinical experience, along with the summarized reports, suggests that (1) serum levels of vitamin B12 not "classically" deficient by current laboratory standards are associated with neuropsychiatric signs and symptoms, and (2) clinical improvements results when serum Vitamin B12 levels are optimized or markedly increased following vitamin B12 treatment. Vitamin B12's mechanisms of action are believed to include increased S-adenosylmethionine production, improved methylation, decreased plasma and brain homocysteine, compensation for inborn errors of metabolism, normalized gene expression, correction of long-latency vitamin B12 debt, and anti-inflammatory activity. Clinicians may wish to re-evaluate the importance of lower-than-optimal serum vitamin B12 levels, pursue additional testing such as urinary methylmalonic acid, and consider the potential benefits of vitamin B12 treatment.