Maternal inflammation as indicated by the presence in maternal blood of early gestational C-reactive protein — an established inflammatory biomarker — appears to be associated with greater risk for schizophrenia in offspring, according to researchers at Columbia University’s Mailman School of Public Health, Columbia University Medical Center, and the New York State Psychiatric Institute. The study, “Elevated Maternal C-Reactive Protein and Increased Risk of Schizophrenia in a National Birth Cohort” is published online in the American Journal of Psychiatry.
Researchers found that increasing maternal C-reactive protein levels were significantly associated with development of schizophrenia in offspring and remained significant after adjusting for potential confounders such as parental history of psychiatric disorders, twin/singleton birth, location of birth, and maternal socioeconomic status. For every 1 mg/L increase in maternal C-reactive protein, the risk of schizophrenia increased by 28 percent.
“This is the first time that this association has been demonstrated, indicating that an infection or increased inflammation during pregnancy could increase the risk of schizophrenia in the offspring,” said Dr. Alan Brown, professor of epidemiology and psychiatry and senior author. “Inflammation has been shown to alter brain development in previous studies, and schizophrenia is a neurodevelopmental disorder. Thus, this study provides an important link between inflammation and schizophrenia and may help us to better understand the biological mechanisms that lead to this disorder. To the extent that the increased inflammation is due to infection, this work may suggest that approaches aimed at preventing infection may have the potential to reduce risk of schizophrenia.” There are many other known causes of inflammation, including tissue injury and autoimmune disease, although the researchers did not examine these specific conditions in this study.
The study was supported by grants R01 MH-082052-05 and K02 MH-065422-09 from NIMH and the State Research Institute and grant T32 MH-16434-31 from NIMH and the Sackler Institute Fellowship.