Young children's traumatic stress reactions to the COVID-19 pandemic: The long reach of mothers' adverse childhood experiences.

BACKGROUND: The COVID-19 pandemic has negatively impacted parental and child mental health; however, it is critical to examine this impact in the context of parental histories of adversity. We hypothesized that maternal adverse childhood experiences (ACEs) and pandemic-related negative life events would predict child traumatic stress symptoms (TSS) and tested potential mediating pathways through maternal pandemic-related TSS and/or poorer maternal sensitivity during the pandemic. METHODS: Data were collected from a longitudinal sample of low-income, racially/ethnically diverse mothers and their children. Between May and November 2020, mothers (n = 111) of young children (M age = 7.42 years, SD = 0.45) completed questionnaires to assess their own and their child's pandemic-related TSS, exposure to pandemic-related negative events, and parent-child relationship quality. Maternal ACEs, maternal depression, parent-child relationship quality, and child internalizing symptoms had been assessed approximately 1-3 years prior. RESULTS: Structural equation analyses revealed that pandemic negative life events were indirectly associated with child TSS via greater maternal TSS. For mothers, recent pandemic-related negative events were associated with their own TSS, whereas maternal ACEs were not. Maternal ACEs directly predicted greater child TSS, with no evidence of mediation by either maternal TSS or maternal sensitivity. LIMITATIONS: All measures were parent report, and pandemic-related measures were collected at the same time point. CONCLUSIONS: Findings underscore the long reach of mothers' own adverse childhood experiences, highlighting the negative consequences of these prior traumatic exposures alongside current pandemic-related maternal trauma symptoms for children's adjustment during the pandemic.

Adversity in early life and pregnancy are immunologically distinct from total life adversity: macrophage-associated phenotypes in women exposed to interpersonal violence.

Early childhood and pregnancy are two sensitive periods of heightened immune plasticity, when exposure to adversity may disproportionately increase health risks. However, we need deeper phenotyping to disentangle the impact of adversity during sensitive periods from that across the total lifespan. This study examined whether retrospective reports of adversity during childhood or pregnancy were associated with inflammatory imbalance, in an ethnically diverse cohort of 53 low-income women seeking family-based trauma treatment following exposure to interpersonal violence. Structured interviews assessed early life adversity (trauma exposure ≤ age 5), pregnancy adversity, and total lifetime adversity. Blood serum was assayed for pro-inflammatory (TNF-a, IL-1ß, IL-6, and CRP) and anti-inflammatory (IL-1RA, IL-4, and IL-10) cytokines. CD14+ monocytes were isolated in a subsample (n = 42) and gene expression assayed by RNA sequencing (Illumina HiSeq 4000; TruSeq cDNA library). The primary outcome was a macrophage-associated M1/M2 gene expression phenotype. To evaluate sensitivity and specificity, we contrasted M1/M2 gene expression with a second, clinically-validated macrophage-associated immunosuppressive phenotype (endotoxin tolerance) and with pro-inflammatory and anti-inflammatory cytokine levels. Adjusting for demographics, socioeconomic status, and psychopathology, higher adversity in early life (ß = .337, p = 0.029) and pregnancy (ß = .332, p = 0.032) were each associated with higher M1/M2 gene expression, whereas higher lifetime adversity (ß = -.341, p = 0.031) was associated with lower immunosuppressive gene expression. Adversity during sensitive periods was uniquely associated with M1/M2 imbalance, among low-income women with interpersonal violence exposure. Given that M1/M2 imbalance is found in sepsis, severe COVID-19 and myriad chronic diseases, these findings implicate novel immune mechanisms underlying the impact of adversity on health.