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Poster #19 - The Role of Inflammation During the COVID-19 Pandemic: Dimensions of Early Maltreatment and Depression Symptoms

Fri, March 24, 9:30 to 10:15am, Salt Palace Convention Center, Floor: 1, Hall A-B

Abstract

Childhood adversity is associated with increased risk for depression during adolescence and young adulthood (Pagliaccio & Barch, 2016). Early adversity may be associated with biological risk for psychopathology through changes in immune functioning (Reid & Danese, 2020). Depression has been consistently linked to heightened inflammation in adults (Howren et al., 2009) and, more recently, to depression in adolescents (Jones et al., 2020). Research suggests that bi-directional associations may exist in youth with depression (Colasanto et al., 2020); however, little is known about these longitudinal associations during the transition from adolescence to young adulthood in a community sample. Using a dimensional approach to studying effects of adversity (McLaughlin et al., 2016), this study examined 1.) how inflammatory biomarkers may mediate experiences of threat or deprivation on depression symptoms one year later, and 2.) how depression symptoms may mediate experiences of threat and deprivation on inflammation levels one year later. Identifying mechanisms of adversity that increase risk for depression and heightened inflammation may inform intervention efforts and prevent negative health outcomes. This is particularly important in the context of the COVID-19 pandemic, when social, personal, and financial stress were heightened.
The current study included data collected as part of a larger longitudinal project. Participants included 78 adolescents and young adults (53% male; 18 years old at Time 1) and were assessed annually for two years during the COVID-19 pandemic. The Maltreatment and Abuse Chronology of Exposure assessed maltreatment during ages 1-18 (Teicher & Parigger, 2015). Neglect and abuse subscales represented deprivation and threat dimensions, respectively. Depression symptoms were assessed using the Adult Self-Report, internalizing subscale (Achenbach & Rescorla, 2003). Salivary cytokine levels were used to assess inflammatory biomarkers, Interleukin (IL)-6 and C-Reactive Protein (CRP). BMI was included as a covariate for analyses and sex differences were explored.
Structural Equation Modeling (SEM) in Mplus (Muthén & Muthén, 1998-2021), was used to examine direct and indirect effects in hypothesized models (see Figure 1 for conceptual models). All model fits were acceptable. There was a significant direct effect from CRP to depression symptoms (β = .314; p = .001) and from experiences of threat to depression (β = .295; p = .010) during the pandemic; however, there were no significant indirect effects from threat and deprivation on depression through inflammation levels. Additionally, there were significant direct effects from experiences of threat to depression symptoms before the pandemic (β = .452; p = .000) and from depression to heightened CRP levels during the pandemic (β = .222; p = .026). Indirect effects were significant, such that threat predicted higher CRP levels via higher depression symptoms (95% CI: .00026 to .01387). All significant paths remained significant when adding sex as a covariate, except for the indirect effect from threat to CRP levels which became weaker and non-significant (95% CI: -.00032 to .01321).
These findings suggest experiences of threat, not deprivation, during childhood may increase risk for development of depression symptoms. The current study elucidates pathways connecting early adversity, depression, and inflammation during the transition into young adulthood.

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