It is suggested that disruption to pubertal development may contribute to the link between adversity and psychosis risk, but not by altering GM development.
Abstract
Abstract Background Childhood adversity increases psychosis risk, but the biological mechanisms responsible remain elusive. A possible but underexplored pathway involves altered pubertal and grey matter (GM) development. Methods In youth from the Adolescent Brain Cognitive Development study (N = 3462), we investigated the effect of adversity at age 9–11 (indexing threat, socioeconomic deprivation and interpersonal deprivation) on psychotic‐like experiences (PLEs) four years later, and the mediating role of pubertal timing and tempo. We then investigated whether pathways could be further explained by the influence of puberty on longitudinal GM change. Analyses for males and females were conducted separately. Results Associations were found between all adversity types and greater PLEs, of which most were mediated by earlier pubertal timing and/or slower tempo. Mediation effects tended to be stronger in females, and for socioeconomic deprivation pathways. Results did not support the presence of serial mediation pathways from adversity to PLEs via puberty‐related GM variation. Conclusion Findings suggest that disruption to pubertal development may contribute to the link between adversity and psychosis risk, but not by altering GM development. Investigating puberty alongside alternative biological systems may help contextualise our findings.
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BACKGROUND
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BACKGROUND
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INTRODUCTION
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