10. TRACKING DEPRESSION, EATING DISORDER AND SLEEP DISTURBANCE SYMPTOMS FROM ADOLESCENCE TO YOUNG ADULTHOOD: A CROSS-LAGGED TWIN STUDY

Background Adolescence and early adulthood are critical developmental periods during which psychiatric symptoms commonly emerge and co-occur. Eating disorder symptoms are of particular concern due to the rising prevalence and substantial morbidity among young people. Depressive symptoms and sleep disturbances frequently co-occur with eating disorder symptoms, yet it remains unclear whether these associations reflect shared genetic liability or prospective developmental relationships across time. Methods Data were analysed from 13,396 participants in the Twins Early Development Study with self-reported measures of depressive symptoms, eating disorder symptoms, and sleep disturbances at ages 16, 21, and 26. Univariate and multivariate ACE twin models were used to estimate additive genetic (A), shared environmental (C), and non-shared environmental (E) influences on each domain and their within-time associations. We apply a genetically informed cross-lagged twin model to decompose prospective associations into genetic and environmental components, enabling us to test whether longitudinal relationships persist beyond within-time genetic overlap. Results Eating disorder symptoms showed the highest heritability (49–54%), compared to depressive symptoms (28–30%) and sleep disturbances (28–36%), with minimal shared environmental effects across domains. Within-time associations were moderate (r≈0.23–0.40) and partly attributable to shared genetic influences, particularly between depressive symptoms and both eating disorder symptoms and sleep disturbances. Longitudinal analyses revealed moderate stability across domains, with the strongest for eating disorder symptoms. Bidirectional cross-lagged associations emerged between eating disorder symptoms and sleep disturbances, with each prospectively predicting the other across development (β≈0.20). Smaller reciprocal associations were observed between depressive symptoms and sleep disturbances (β≈0.10–0.12), whereas depressive symptoms showed stronger prospective prediction of later eating disorder symptoms than the reverse. Discussion These findings suggest that the co-occurrence of depressive symptoms, eating disorder symptoms, and sleep disturbances is partly driven by shared genetic liability, alongside individual-specific environmental influences. Longitudinal analyses indicate that some associations persist over time beyond this shared genetic overlap, particularly the reciprocal relationship between eating disorder symptoms and sleep problems. This suggests that sleep may play an important role in the developmental course of psychopathology and could represent a potential target for early intervention. Distinguishing shared genetic risk from prospective symptom relationships may help clarify developmental mechanisms and inform prevention strategies in adolescent mental health.