Environmental Risk Factors and Cognitive Outcomes in Psychosis: Pre-, Perinatal, and Early Life Adversity

Risk for psychosis begins to accumulate as early as the fetal period through exposure to obstetric complications like fetal hypoxia, maternal stress, and prenatal infection. Stressors in the postnatal period, such as childhood trauma, peer victimization, and neighborhood-level adversity, further increase susceptibility for psychosis. Cognitive difficulties are among the first symptoms to emerge in individuals who go on to develop a psychotic disorder. We review the relationship between pre-, perinatal, and early childhood adversities and cognitive outcomes in individuals with psychosis. Current evidence shows that the aforementioned environmental risk factors may be linked to lower overall intelligence and executive dysfunction, beginning in the premorbid period and persisting into adulthood in individuals with psychosis. It is likely that early life stress contributes to cognitive difficulties in psychosis through dysregulation of the body's response to stress, causing changes such as increased cortisol levels and chronic immune activation, which can negatively impact neurodevelopment. Intersectional aspects of identity (e.g., sex/gender, race/ethnicity), as well as gene-environment interactions, likely inform the developmental cascade to cognitive difficulties throughout the course of psychotic disorders and are reviewed below. Prospective studies of birth cohorts will serve to further clarify the relationship between early-life environmental risk factors and cognitive outcomes in the developmental course of psychotic disorders. Specific methodological recommendations are provided for future research.