Children's Long-Term Exposure to Intimate Partner Violence and Internalizing Outcomes: A Latent Profile Analysis

Background and Purpose: Exposure to intimate partner violence (IPV) has been shown to impede child well-being across various dimensions. However, the majority of existing studies focus on postnatal exposure to IPV, with limited attention given to prenatal exposure. Furthermore, prior work in this field often falls short of capturing the complex nature of IPV exposure, such as developmental timing and chronicity. According to the developmental psychopathology perspective, child developmental outcomes are consistently impacted by the changing external environment, including parental relationships. This study explores the longitudinal profiles of children’s exposure to IPV from prenatal to school-age stages and examines the relations between these profiles and internalizing symptoms in adolescence. We hypothesize that children will display distinct profiles of long-term IPV exposure, and children who were exposed to IPV at multiple stages will exhibit worse internalizing symptoms.

Methods: The sample comprised 1,495 adolescents from the Future of Families and Child Wellbeing Study. IPV exposure at each developmental stage was measured by maternal reports on the frequency of IPV victimization in the past year, including physical, psychological, sexual, and economic IPV. This study included four distal outcomes: adolescent-reported depressive symptoms and anxious symptoms measured by the Center for Epidemiologic Studies Depression Scale (CES-D) (α = 0.76) and the Brief Symptom Inventory 18 (α = 0.76), respectively; and anxious/depressive symptoms (α = 0.78) and internalizing symptoms (α = 0.75) measured by the Child Behavior Checklist. We employed repeated measures latent profile analysis (RMLPA) to identify profiles of IPV exposure from the prenatal stage to age 9. Then, we compared the pairwise means for each outcome among latent profiles to investigate the relations between identified profiles and adolescents’ internalizing symptoms at age 15.

Results: RMLPA identified three profiles of IPV exposure: stable low IPV exposure (Profile 1), comprising the majority of the sample (89.8%); chronic early IPV exposure and toddlerhood peak (Profile 2; 6.2%); and school-age peak IPV exposure (Profile 3; 4.0%). Adolescents in the chronic early IPV exposure and toddlerhood peak profile consistently reported worse internalizing symptoms than those in the stable low IPV exposure profile. Adolescents in the school-age peak IPV exposure profile exhibited more pronounced depressive symptoms, measured by CES-D, than those in the stable low IPV exposure profile.

Conclusions and Implications: To the best of our knowledge, this study is one of few studies that perform RMLPA on IPV exposure across developmental stages including the prenatal period. This approach provides an integrated investigation of the developmental timing and chronicity of IPV exposure, casting light on how unique combinations of timing and chronicity of IPV exposure contribute to adolescents’ internalizing symptoms differently. Frequent IPV exposure during infancy, toddlerhood, and preschool age emerges as a salient risk factor for internalizing symptoms in adolescence. Conversely, youth may be more resilient against internalizing symptoms even when exposed to IPV during the school-age stage. Research should continue to investigate the heterogeneity in children’s experiences of IPV exposure to guide future intervention and prevention programs.