Abstract
Prenatal infection is associated with brain structural and functional abnormalities and may increase the risk for psychosis through a direct effect on neurodevelopment. Various infections may exert their effect through a proinflammatory immune response but studies of prenatal maternal inflammatory markers and offspring neurodevelopment are scarce. Using the longitudinal Northern Finland Birth Cohort 1986 study, we examined the associations of maternal prenatal C-reactive protein (CRP) levels with psychosis risk factors in adolescent offspring. CRP was measured in maternal sera collected in pregnancy. In offspring, school performance was measured at age 7 years, while school performance, psychotic experiences, and cannabis use were measured at age 16 years. We tested associations of CRP with offspring measures using regression analysis controlling for offspring sex, maternal education level, and prenatal maternal body mass index, smoking and alcohol use in pregnancy, place of birth, maternal psychiatric admission, paternal psychiatric admission, mothers age at birth, and gestational week of CRP sample. We also tested if adolescent cannabis use mediated the associations between maternal CRP and offspring outcomes. Controlling for covariates, maternal CRP was associated with academic performance at age 16 years (beta = .062, 95% CI = 0.036–0.088), but not with possible psychotic experiences at 16 years (odds ratio [OR] = 1.09, 95% CI = 0.96–1.24). Maternal CRP was also associated with adolescent cannabis use (OR = 1.24, 95% CI = 1.07–1.43). These findings suggest that prenatal inflammation may influence later mental illness risk by affecting neurodevelopment and also indirectly by increasing the risk of exposure to cannabis.
Highlights
Evidence from epidemiological birth cohort and other longitudinal studies has linked prenatal infection and risk for psychotic disorders in offspring
This study aims to examine whether maternal immune activation in pregnancy, measured by circulating C-reactive protein (CRP) (CRP) levels, an archetypal inflammatory marker, is associated with neurodevelopmental and environmental risk factors for psychosis in offspring in adolescence, psychotic experiences, poorer academic performance, and substance use
In multivariate analysis, the observed association did not persist after controlling for sex, maternal education level, maternal body mass index (BMI) during pregnancy, smoking during pregnancy, alcohol use during pregnancy, place of birth, maternal psychiatric admission, paternal psychiatric admission, mothers age at birth, and gestational week of CRP sample
Summary
Evidence from epidemiological birth cohort and other longitudinal studies has linked prenatal infection and risk for psychotic disorders in offspring. Further ecological evidence for an association with prenatal infection links the season of birth with schizophrenia.[3] Importantly, given the methodological shortcomings of ecological studies, epidemiological studies with confirmed prenatal exposure to a range of specific infections during pregnancy have provided support for an association between prenatal infection and offspring schizophrenia.[4,5] This has included exposure to second-trimester respiratory infections[6] and to specific infectious agents, such as influenza,[7] Toxoplasma gondii,[8] and herpes simplex virus type 2.9 Recent population-based studies from Sweden and Denmark have suggested that the relationship between prenatal infection and offspring psychosis may interact with other factors, including family history[10,11] and peripubertal trauma.[12]. One possible mechanism is maternal immune activation.[13,14] elevated prenatal inflammatory markers, including C-reactive protein (CRP),[15] and elevated prenatal cytokines have been associated with offspring schizophrenia.[16,17]
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