Abstract

Previous research has demonstrated that prenatal infections with bacterial or viral agents during pregnancy are associated with an increased risk of schizophrenia in the offspring during adulthood. Furthermore, there has been evidence linking obstetric complications to schizophrenia. In parallel, there is a separate body of evidence relating subclinical chronic inflammation and schizophrenia in individuals, usually in their adulthood, who have already developed schizophrenia. On the other hand, unequivocal experimental, epidemiological and clinical evidence has emerged during the past decade linking inflammation to the development of insulin resistance and metabolic disturbances, which are common in the schizophrenic population. Inflammation might be an important common pathophysiological process related to both schizophrenia psychopathology and metabolic disturbances seen in patients with schizophrenia. Future studies targeting proinflammatory cytokines and their molecular signaling pathways may lead to novel pharmacological intervention strategies treating both psychopathology and medical comorbidity in patients with this devastating mental illness.