The longitudinal associations between academic competence-building and depression symptoms were investigated among 741 early adolescents in Singapore. Extending from past studies on academic achievement and depression, the current research tested two competing hypotheses – the academic incompetence hypothesis versus the adjustment erosion hypothesis using a 3-wave longitudinal study over an academic year. The former hypothesis suggests that prior deficits in academic competence-building lead to subsequent depression symptoms, whereas the latter posits that previous depression leads to subsequent deficits in competence-building. Longitudinal associations between a higher-order competence-building factor (operationalized using multiple constituent motivational variables) and depression were examined using a random intercept cross-lagged panel model. Results indicated that within-individual decreases in competence-building prospectively predicted subsequent within-individual increases in depression symptoms, but the opposite effect was not observed. Within-individual fluctuations in competence-building also predicted end-of-year grades and teacher-reported adjustment problems. Overall, the current findings were consistent with the academic incompetence hypothesis, suggesting that interventions aimed at sustaining academic competence-building could offer protection against the worsening of depression. These results clarified the within-individual developmental dynamics between academic competence-building and depression symptoms in adolescents over time.

Inhibitory control (IC) deficits have been associated with psychiatric symptoms in all ages. However, longitudinal studies testing the direction of the associations in childhood are scarce. We used a sample of 2,874 children (7 to 9 years old) to test the following three hypotheses: (a) IC deficits are an underlying risk factor with a potentially causal role for psychopathology, (b) IC deficits are a complication of psychopathology, and (c) IC deficits and psychopathology are associated at the trait level but not necessarily causally related. We used the go/no-go task to assess IC, the parent-rated Strengths and Difficulties Questionnaire to evaluate externalizing/internalizing symptoms, and the random intercepts cross-lagged panel model to test the hypotheses. The results showed no support for the underlying risk factor hypothesis, suggesting that IC unlikely has a causal role in this age group's psychopathology. The complication hypothesis received support for externalizing symptoms, suggesting that externalizing symptoms may hamper the normal development of IC. IC deficits and both externalizing and internalizing symptoms were correlated at the trait level, indicating a possible common origin. We suggest that it may be useful to support children with externalizing symptoms to promote and protect their IC development.