Why do depression, conduct, and hyperactivity symptoms co-occur across adolescence? The role of stable and dynamic genetic and environmental influences.
Monika A WaszczukHelena M S ZavosThalia C EleyPublished in: European child & adolescent psychiatry (2020)
Depression, conduct, and hyperactivity symptoms are chronic and frequently co-occur in adolescence. Common genetic and environmental vulnerability to these conditions have previously been demonstrated, however, the manner in which common versus disorder-specific etiological influences operate across development and maintain symptom co-occurrence is unclear. Thus, the current study investigated the role of common genetic and environmental influences in the comorbidity of depression, conduct, and hyperactivity across adolescence. Over 10,000 twins and their parents reported adolescents' symptoms at mean ages 11 and 16 years. Biometric independent pathway models were fitted to estimate genetic and environmental contributions to the continuity of symptom co-occurrence over time, as well as time- and symptom-specific influences. Results found that a common stable genetic factor accounted for the concurrent and longitudinal co-occurrence of depression, conduct, and hyperactivity symptoms. New genetic influences common to these three symptom scales emerged at 16 years, and further contributed to symptom co-occurrence. Conversely, environmental influences largely contributed to the time-specific associations. The findings were generally consistent for self- and parent-reported symptoms. Overall, the results suggest that stable, overlapping genetic influences contribute to the co-occurrence of depression, conduct, and hyperactivity symptoms across adolescence. The results are in line with hierarchical causal models of psychopathology, which posit that much of the developmental co-occurrence between different symptoms is due to common liability. Specifically, current findings indicate that only genetic influences constitute common liability over time. Future studies should identify genetically influenced transdiagnostic risk and maintenance factors to inform prevention and treatment of comorbid internalizing and externalizing symptoms in adolescence.