Intergenerational continuity in high-conflict family environments: Investigating a mediating depressive pathway.

Journal Article (Journal Article)

Emerging evidence suggests that family conflict shows continuity across generations and that intergenerational family conflict can be more intense and deleterious than conflict experienced in a single generation. However, few investigations have identified etiological mechanisms by which family conflict is perpetuated across generations. Addressing this limitation, we sampled 246 families from a multigenerational, high-risk, longitudinal study of parents (G1s) and their children (G2s), followed from adolescence to adulthood as well as the children (G3s) of G2 targets. Specifically, the current study examined whether G2s' depressive symptoms measured at multiple time points across development explained continuity in family conflict from 1 generation (G1-G2) to the next (G2-G3). Results revealed that after controlling for externalizing symptoms, depressive symptoms served as mediators of intergenerational family conflict in both men and women, but in different ways. Specifically, G2 women's young adulthood represented a period of vulnerability in which G2 depressive symptoms were especially likely to mediate intergenerational continuity in family conflict. Additionally, in both men and women, higher G1-G2 family conflict was associated with higher depressive symptoms that persisted from adolescence into young adulthood and then subsequently predicted the development of G2-G3 family conflict. Results did not support the hypothesis that G2 partner depressive symptoms moderated the relation between G2 depressive symptoms and G2-G3 family conflict. Implications of findings regarding the roles that G2 gender and G2 depressive symptoms play in the intergenerational transmission of family conflict are discussed. (PsycINFO Database Record

Full Text

Duke Authors

Cited Authors

  • Rothenberg, WA; Hussong, AM; Chassin, L

Published Date

  • February 2018

Published In

Volume / Issue

  • 54 / 2

Start / End Page

  • 385 - 396

PubMed ID

  • 29058932

Pubmed Central ID

  • PMC5788736

Electronic International Standard Serial Number (EISSN)

  • 1939-0599

International Standard Serial Number (ISSN)

  • 0012-1649

Digital Object Identifier (DOI)

  • 10.1037/dev0000419


  • eng