Homocystine is the double-bonded form of homocysteine, but it occurs only transiently before being converted to the harmless cystathionine via a vitamin B6-dependent enzyme. Increasing evidence supports a role for an elevation of homocysteine in schizophrenia. It has been demonstrated that neural tube defects are related to a genetic defect in homocysteine metabolism. Sufficient intake of folic acid is believed to reduce this risk by enhancing methylation of homocysteine and its conversion to methionine, thereby compensating for this genetic defect (homocystinuria). Plasma homocysteine levels are elevated when folate levels are in the lower half of the normal range.