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Association of Social Support with Hippocampal Volume Depends on Maltreatment Subtype and Exposure Level

Sat, March 25, 1:30 to 3:00pm, Salt Palace Convention Center, Floor: 1, Meeting Room 151 G

Abstract

Although maltreatment poses a substantial threat to the development of children and adolescents, the mechanisms by which maltreatment affects the developing brain remain contentious. Recent theory proposes a neurocognitive social transactional model, suggesting that neurocognitive alterations in the wake of child maltreatment influence quality and quantity of social relationships, which, in turn, moderate the risk for psychiatric disorders (McCrory, Foulkes, & Viding, 2022). Accordingly, research on this moderating function of social support demonstrated that it merely relates to higher hippocampal volume at low, but not high levels of adversity across development (Luby, Tillman, & Barch, 2019). Likewise, social support coincided with hippocampal volume increases among non-maltreated, but decreases among maltreated adults, with emotional and physical neglect appearing to drive these effects (Foerster et al., 2021). This study aimed to examine whether the association of social support and hippocampal volume depends on type and extent of maltreatment exposure in adolescents with and without a maltreatment history.
To this end, we obtained T1-weighted MRI scans from 98 adolescents aged 12-17 (M=14.68, SD=1.95; 51% girls) comparing participants with low (n=29) and high (n=29) maltreatment exposure to a carefully matched nonmaltreated control group (n=40). Pre-processing and hippocampal volume extraction was conducted in Freesurfer. We assessed maltreatment with the Maltreatment Classification System (Barnett, Manly, & Cicchetti, 1993), based on caregiver interviews and child protection services records (if available). The number of social supports were measured with the Arizona Social Support Interview Schedule (Barrera, 1980; Kaufman, 1991). First, we assessed the individual effects of maltreatment exposure as well as social support on hippocampal volume across the full sample. Second, we tested the effect of social support on hippocampal volume within subgroups of maltreatment exposure level and subtypes.
Hippocampal volume did not differ between maltreatment exposure groups or subtypes. In addition, an association between social support and hippocampal volume emerged neither across the full sample nor within nonmaltreated, low and high maltreatment-exposed adolescents. However, when investigating this relationship within the exposure subtype groups, the quantity of social support was positively associated with hippocampal volume within the group of participants exposed to low levels of neglect (n=25; r=.53, p=.007; see Figure 1). This association survived controlling for ICV, age, gender, and socioeconomic status (β=.43, p=.008), and also differed significantly from the correlations within the nonmaltreated participants (n=40; r=.11, p=.487; Fisher z=1.78, p=.037) as well as the participants with high levels of neglect exposure (n=22; r=.01, p=.963; Fisher z=1.85, p=.032). Within the subgroups of abuse-exposed participants, we did not find any effect of social support.
Extending previous evidence, we could show that the impact of social support on hippocampal volume in adolescence depends on the degree and type of maltreatment exposure. In keeping with the neurocognitive social transactional model, our findings highlight the importance of examining intermediary social outcomes in the wake of maltreatment.

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