Prenatal exposure to influenza, elevated toxoplasma antibody, rubella, genital–reproductive infections, and other infections have been associated with an increased risk of schizophrenia among offspring.
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For many years, researchers have proposed that schizophrenia might have neurodevelopmental etiologies, and hypothesized that several prenatal environmental factors could be potential causal agents. However, we have only recently witnessed the emergence of epidemiologic evidence implicating specific prenatal risk factors in schizophrenia.
Many epidemiologic studies support a potential role for prenatal viral insults in schizophrenia. One of the first major pieces of evidence is the consistent demonstration of a 5 percent to 15 percent excess of births in the winter and early spring among individuals destined to develop schizophrenia (Torrey and Kaufmann).
Our group and others have conducted birth cohort studies to address whether in utero exposure to infectious agents, prospectively documented by biomarker assays of archived maternal sera, and by detailed obstetric records, confer an increased risk of schizophrenia in adult offspring.
In the CHDS birth cohort, we demonstrated that exposure to influenza during early to mid-pregnancy was related to a threefold increased risk of schizophrenia among offspring (Brown et al., 2004a ).