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Allostatic load refers to the toll of chronic demands that a system manages (McEwen & Stellar, 1993); this wear and tear is linked to negative health consequences later in life (McEwen & Seeman, 2006). The chronic stress of early life adversity (ELA) in the form of poverty or orphanage-rearing is linked to indicators of accelerated aging (Elwenspoek et al, 2017; Esposito et al, 2016). One mediating pathway might be early exposure to pathogens, such as latent Herpes viruses which require continuous immune surveillance to remain quiescent. Herpes cytalomeglaovirus (CMV) is more prevalent in poor communities and more likely to spread among children who receive group care. (Dowd et al, 2012). Among older adults, carrying CMV is associated with an accumulation of senescent T-cells reflecting the immune effort involved in containing this virus.
Infancy is an important period for the development of attention and executive function skills. We see the impact of ELA in deficits in attention, for example, in post-institutionalized children, (Gunnar et al, 2007; Wiik et al,2010). This research asks if the price of early adversity in the form of CMV exposure and subsequent chronic immune activation detract from the development of cognitive skills such as attention.
Participants were 50 children (28F) age 13-21yr (median=16) who spent the majority of their pre-adoptive lives in institutional care (6-45mo, median=13). Parents completed the MacArthur Health & Behavior Questionnaire reporting on behavior related to attention and impulsivity (ADHD). Blood was drawn for immunoassay. CMV was assessed by antibody titer, with higher values reflecting greater viral load. Immunophenotyping characterized the CD4 and CD8 T-cells by their stage of development (naïve to terminally differentiated) and whether they were tagged with CD57 protein, an index of experience in fighting pathogens. Previous reports of these data showed that post-institutionalized youth displayed more terminally differentiated cells tagged with CD57 (TEMRA) than non-adopted children, this was particularly true for CD8 cells, and was mediated by CMV titers.
CMV and TEMRA were highly correlated (r=.51, p>.001), indicative of ELA environment. These were standardized and averaged to form a Load variable. Load was correlated with parent report of ADHD (r=.33, p<.05). Because males typically show greater ADHD, a regression explored the interaction of sex and load on ADHD scores. The model was significant, R²=.46, F(3,45)=12.10, p<.001. Load, β=.89, t=2.15, p<.001 and sex β=-.56, t=-4.80, p<.001 predicted ADHD scores, while the interaction was only a trend, β=-.74, t=-1.80, p=.08.
Although in a small sample, these results show that concomitants of ELA environment relate to attention and behavior regulation. Future work will need to determine if this is evidence of a biomarker of ELA, or if there is a mechanism at work. The allostatic load argument is that resources needed to deal with containing the virus simply pull away resources that would otherwise be devoted to development. However, there may be direct mechanisms that impact outcome; for example, Bilbo & Schwartz (2012) posit that there are sensitive periods in early brain development when exposure to pathogens impact neural organization.
Bonny Donzella, University of Minnesota
Presenting Author
Brie M Reid, University of Minnesota, Institute of Child Development
Non-Presenting Author
Melissa L. Engel, University of Minnesota
Non-Presenting Author
Dagna Sheerar, University of Wisconsin
Non-Presenting Author
Christopher L. Coe, University of Wisconsin
Non-Presenting Author
Megan Gunnar, University of Minnesota
Non-Presenting Author