Linking specific biological signatures to different childhood adversities: findings from the HERO project.

BACKGROUND: Although investigations have begun to differentiate biological and neurobiological responses to a variety of adversities, studies considering both endocrine and immune function in the same datasets are limited. METHODS: Associations between proximal (family functioning, caregiver depression, and anxiety) and distal (SES-D; socioeconomic disadvantage) early-life adversities with salivary inflammatory biomarkers (IL-1ß, IL-6, IL-8, and TNF-α) and hair HPA markers (cortisol, cortisone, and dehydroepiandrosterone) were examined in two samples of young U.S. children (N = 142; N = 145). RESULTS: Children exposed to higher SES-D had higher levels of TNF-α (B = 0.13, p = 0.011), IL-1ß (B = 0.10, p = 0.033), and DHEA (B = 0.16, p = 0.011). Higher family dysfunction was associated with higher cortisol (B = 0.08, p = 0.033) and cortisone (B = 0.05, p = 0.003). An interaction between SES-D and family dysfunction was observed for cortisol levels (p = 0.020) whereby children exposed to lower/average levels of SES-D exhibited a positive association between family dysfunction and cortisol levels, whereas children exposed to high levels of SES-D did not. These findings were partially replicated in the second sample. CONCLUSIONS: Our results indicate that these biological response systems may react differently to different forms of early-life adversity. IMPACT: Different forms of early-life adversity have varied stress signatures, and investigations of early-life adversities with inflammation and HPA markers are lacking. Children with higher socioeconomic disadvantage had higher TNF-α, IL-1ß, and DHEA. Higher family dysfunction was associated with higher hair cortisol and cortisone levels, and the association between family dysfunction and cortisol was moderated by socioeconomic disadvantage. Biological response systems (immune and endocrine) were differentially associated with distinct forms of early-life adversities.

Attachment security buffers the HPA axis of toddlers growing up in poverty or near poverty: Assessment during pediatric well-child exams with inoculations.

Poverty is associated with poor physical and emotional development. Activation of the hypothalamic-pituitary-adrenocortical (HPA) axis is argued to be one of the pathways through which poverty acts on these outcomes. While studies of school-aged children have found some evidence for this, there is little evidence for this hypothesis early in development. This may be, in part, because for very young children, the security of their attachment relationships with parents moderates the impact of poverty on HPA axis functioning. The current study investigated the relations between family income as a percentage of the federal poverty limit (FPL), salivary cortisol and attachment (Attachment Q-sort) during well-child checkups with inoculations in 177 toddlers between 12- and 22-months of age. Approximately half of the toddlers were in families living below 150% FPL, with 47% of these classified as securely attached, compared to 72% of toddlers in families living above 150% FPL. Cortisol levels increased in response to the inoculation and this did not differ by poverty or attachment security. Overall, however, beginning at clinic arrival toddlers in families living below 150% FPL who had an insecure attachment had significantly higher cortisol compared to toddlers living in poverty or near poverty with secure attachments. This finding held when we removed toddlers with high levels of negative life events in their families and primary caregivers who exceeded the screening cutoff for depressive symptoms. Thus, attachment was a significant moderator of the association between poverty and HPA axis activity, with significant implications for screening and referral of caregiving dyads at risk.