Objective: Cobalamin (vitamin B12) and folic acid play crucial roles in the the production of S-adenosylmethionine (SAM), a unique methyl group-donating molecule for various biochemical reactions. These cofactors are known to be important for the normal functioning of the human central nervous system. Both cobalamin and folic acid deficiency may lead or at least contribute to the pathogenesis of some neuropsychiatric disorders such as mental and memory derangements, cognitive defects, as well as mood and behavioral changes. They might also be related to schizophrenia, a complex psychiatric disease that is caused by multiple genetic and environmental factors. In one study, it was argued that common genetic variants that inşuence folate metabolism might have potential implications for schizophrenia pathogenesis and treatment. Correspondingly, some epidemiologic and genome-wide association study (GWAS) data showed that folate deficiency must be a risk factor for schizophrenia. Several cross-sectional studies have also shown that blood folate levels in patients with schizophrenia were lower than those in the control groups. The aim of our study is to investigate whether there is a relationship between serum folic acid and cobalamine levels and the negative symptoms of schizophrenia in the patients hospitalized and followed-up in a research and training hospital.
Methods: The archival data of the schizophrenic patients, who were hospitalized between the years of 2003-2013 in Psychiatry Clinic, Ankara Oncology Training and Research Hospital, were reviewed according to the diagnostic criteria of schizophrenia based on DSM-IV-TR. Schizophrenia patients without blood cobalamine and folic acid levels as well as Positive and Negative Symptom Scale (PANSS) scores were excluded. On a total of 158 patients, the relationship between serum folic acid and cobalamine versus PANSS subscale scores were explored by Pearson’s Correlation Analysis. We set the alpha level to 0.05 for statistical significance.
Results: We found no statistically significant relationship between serum folic acid or cobalamine versus the PANSS subscales.
Conclusion: It is known that the folic acid and vitamin B12 deficiencies lead broad medical conditions from severe anemia to impaired nerve conduction. There are some studies claiming an implication of these two essential cofactors in the pathogenesis of psychiatric conditions, including schizophrenia. In one of these studies, an inverse correlation between serum folate and cobalamin levels and the severity of the negative symptoms, but not positive ones, in a group of schizophrenic patients was reported. Two small placebo-controlled trials also showed relative improvements by taking dietary supplement of folic acid in the schizophrenic patients with folate deficiency. On the contrary, some studies revealed no significant benefits by taking folic acid and vitamin B12 in the severity of symptoms in schizophrenia. Our data indicate that this issue has not been resolved yet, and more clinical trials are needed to document the relationships, if there are any, between the symptomatology of schizophrenia and these important cofactors.