Abstract Background: Social skills develop along with metacognitive abilities from early childhood through young adulthood. Impairment in metacognitive and other social cognitive abilities may contribute to poorer social function in clinical high risk for psychosis (CHR) adolescents. However, it is unclear whether social cognitive impairment represents developmental delay in skill acquisition or, rather, a consequence of emerging symptoms. Furthermore, it is unknown how early pharmacotherapy could influence this developmental trajectory. This study examined the hypotheses that (1) age-related trajectories of social cognition differ between CHR and normally developing youth and (2) age-related trajectories are partially explained by history of symptoms and psychotropic medication. Methods: Emotion perception, social perception, and theory of mind abilities were assessed in 675 CHR and 264 age-matched healthy comparison (HC) participants aged 12–35 (average = 19.0 ± 4.5 years). Linear and nonlinear curves were fit to relationships between social cognitive variables and age. Differences in age effects between CHR and HC were modeled as interaction terms. Duration of a prodromal syndrome prior to baseline and medication history were tested for interactions with age effects. Results: Emotion perception and social perception age trajectories did not differ by group. Theory of mind age trajectory, particularly for sarcasm items, had a lower slope for CHR than HC. CHR diverged from HC from mid-adolescence onward (starting to differ between approximately ages 15 and 17.5), with a minimum observation window of 4 years required to detect correlations with age. Age trajectory for theory of mind was unrelated to the presence or duration of a prior prodromal syndrome but did interact with medication history, wherein participants with an antipsychotic or antidepressant medication history did not differ from HCs. Only antipsychotic- and antidepressant-naive CHR participants showed a smaller slope for theory of mind, with differences from HC increasing with advanced age. Conclusion: In the current study, all social cognitive abilities increased during adolescence, but development of theory of mind appeared blunted for CHR participants starting in mid-adolescence. This difference, however, was only true for participants without an antipsychotic or antidepressant medication history, which could suggest benefits of early treatment or subgroups within CHR for whom social cognition is affected differently. These cross-sectional results require longitudinal replication and further inquiry into the relationships between treatment history and social cognitive development. Current results suggest that factors related to risk for psychosis may moderate adolescent social development, and that interventions targeting social cognition may be particularly helpful at this stage
