Authors
Background
Adolescence is a crucial time for the development of psychopathological (i.e., internalizing and externalizing) symptoms, which can reduce well-being in later life. Parental symptoms are among the most prominent risk factors for adolescent psychopathological symptoms. At the same time, adolescents actively shape their environment, and thus, their symptoms might also predict parental psychopathological symptoms. Whereas theoretical models on how parental psychopathological problems are passed on to children and vice versa concern effects within individual families, empirical support has mainly been derived from between-family or group-level findings. These findings only inform us about how families differ from each other and do not allow conclusions about within-family effects. Therefore, this study examined the longitudinal associations between parental and adolescent internalizing and externalizing symptoms from early to late adolescence from a within-family perspective, to provide innovative and comprehensive insights into the transmission of psychopathology.
Method
The sample consisted of 497 Dutch adolescents (43.1% girls; Mage T1 =13.0 years) and their parents from the general population. Across six years, adolescents and their mothers and fathers reported annually on their internalizing and externalizing symptoms. We used random-intercept cross-lagged panel models (RI-CLPMs) to disentangle how fluctuations in parental psychopathological symptoms are associated with fluctuations in adolescent symptoms (i.e., within-family associations) from how families differ in their average symptoms levels (i.e., between-family associations).
Results
Between families, we found that in families in which mothers reported higher levels of internalizing and externalizing symptoms than in other families, adolescents also reported higher levels of internalizing and externalizing symptoms (βs = .22-32, p < .001). For fathers, only higher levels of externalizing symptoms were associated with higher levels of adolescent externalizing symptoms (β = .13, p = .026). Within families, we found that mothers reported significant increases in internalizing symptoms compared to their own average one year after adolescents reported increases in their own internalizing symptoms (β = .10-.12, ps = .001). For fathers, no significant longitudinal associations were found within families (ps ≥ .153). Sensitivity analyses further indicated bidirectional associations between increases in maternal internalizing symptoms and increases in girls’ internalizing symptoms, but only unidirectional associations from increases in boys’ internalizing symptoms to increases in maternal internalizing symptoms.
Conclusion
Our findings indicate that associations within families differ from associations between families. Across families, increased adolescent symptoms are more likely to occur in families with more maternal, but not paternal symptoms compared to other families. Within families, associations between parental and adolescent internalizing symptoms are mainly driven by adolescent-to-mother effects.
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