Elucidating the link between parent and adolescent psychopathology: a test of transmission specificity and genetic and environmental liabilities
The tendency for psychopathology to aggregate within families is well-documented, though little is known regarding the level of specificity at which familial transmission of symptomology occurs. The current study first tested competing higher-order structures of psychopathology in adolescence, indexing general and more specific latent factors. Second, parent-offspring transmission was tested for broadband domain specificity versus transmission of a general liability for psychopathology. Lastly, genetic and environmental mechanisms underlying the familial aggregation of psychopathology were examined using nuclear twin-family models. The sample was comprised of five hundred adolescent twin pairs (mean age 13.24 years) and their parents drawn from the Wisconsin Twin Project. Twins and parents completed independent diagnostic interviews. For aim 1, correlated factors, bifactor, and general-factor models were tested using adolescent symptom count data. For aim 2, structural equation modeling was used to determine whether broadband domain-specific transmission effects were necessary to capture parent-offspring resemblance in psychopathology above and beyond a general transmission effect indexed by the latent correlation between a parental internalizing factor and offspring P-factor. For aim 3, general factor models were fitted in both generations, and factor scores were subsequently extracted and used in nuclear twin-family model testing. Results indicated that the bifactor model exhibited the best fit to the adolescent data. Familial aggregation of psychopathology was sufficiently accounted for by the transmission of a general liability. Lastly, the best fitting reduced nuclear twin-family model indicated that additive genetic, sibling-specific shared environmental, and nonshared environmental influences contributed to general psychopathology. Parent-offspring transmission was accounted for by shared genetics only, whereas co-twin aggregation was additionally explained by sibling-specific shared environmental factors. Results provide novel insight into the specificity and etiology of the familial aggregation of psychopathology.