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

Abstract

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.

Keywords: Childhood trauma; Cognition; Obstetric complications; Psychosis.

Fig. 1

Proposed developmental trajectory for the onset of cognitive difficulties from pre-, perinatal, and early childhood environmental risk factors in individuals with psychotic disorders. OCs confer changes on the brain beginning in-utero, which can persist into the postnatal period. These changes are evidenced in cognitive changes apparent as early as infancy that may extend through adulthood. While many women experience OCs over the course of their pregnancy, most offspring do not go on to develop neurodevelopmental disorders like schizophrenia; therefore, understanding the additional risk factors that combine with OCs to portend risk for schizophrenia is needed (Ellman et al. 2018). For example, there is evidence OCs can impact one another. PNMS has been associated with greater risk of infection, increased engagement in adverse health behaviors, and increased risk for gestational complications (Lipner et al. 2019). Individuals with a history of OCs are also more likely to experience stressful events during childhood, such as peer victimization, which may subsequently increase the risk for psychotic experiences in adulthood (Liu et al. 2020). Poorer cognitive functioning also likely impacts the way that individuals are treated within their childhood environment by parents, peers, and teachers (McIntosh et al. 1993; Haager and Vaughn 1995). As we strive to understand early environmental and genetic risk factors for cognitive impairments, we must consider transactional ways in which early “hits” or “primers” can work synergistically or additively with postnatal environmental factors (Estes and McAllister 2016). Sequelae resulting from perinatal adversities may be compounded by environmental risk factors in the postnatal period, including chronic stress and trauma during childhood. Figure adapted from Lipner et al. (2019)

Fig. 2

Methodological considerations for future studies examining early life environmental risk factors and cognitive outcomes in individuals on the psychosis spectrum