Stress, Environment and Early Psychosis

Abstract

Existing literature provides extended evidence of the close relationship between stress dysregulation, environmental insults, and psychosis onset. Early stress can sensitize genetically vulnerable individuals to future stress, modifying their risk for developing psychotic phenomena. Neurobiological substrate of the aberrant stress response to hypothalamic-pituitary-adrenal axis dysregulation, disrupted inflammation processes, oxidative stress increase, gut dysbiosis, and altered brain signaling, provides mechanistic links between environmental risk factors and the development of psychotic symptoms. Early-life and later-life exposures may act directly, accumulatively, and repeatedly during critical neurodevelopmental time windows. Environmental hazards, such as pre- and perinatal complications, traumatic experiences, psychosocial stressors, and cannabis use might negatively intervene with brain developmental trajectories and disturb the balance of important stress systems, which act together with recent life events to push the individual over the threshold for the manifestation of psychosis. The current review presents the dynamic and complex relationship between stress, environment, and psychosis onset, attempting to provide an insight into potentially modifiable factors, enhancing resilience and possibly influencing individual psychosis liability.

Keywords: Psychosocial stressors; environment; first-episode psychosis; hypothalamic-pituitary-adrenal; psychosis onset.; stress.

Fig. (1)

Stress-diathesis conceptualization of psychosis development.

Fig. (2)

Possible mechanisms of oxidative disruption and inflammatory alterations resulting in neuroanatomical changes in early psychosis.

Fig. (3)

Schematic of the hypothesized impact of risk vs. protective environmental factors on psychosis risk across developmental stages.