Nonsuicidal self-injury (NSSI) is a common but poorly understood phenomenon in adolescents. This study examined the Sustained Threat domain in female adolescents with a continuum of NSSI severity (N = 142). Across NSSI lifetime frequency and NSSI severity groups (No + Mild NSSI, Moderate NSSI, Severe NSSI), we examined physiological, self-reported and observed stress during the Trier Social Stress Test; amygdala volume; amygdala responses to threat stimuli; and resting-state functional connectivity (RSFC) between amygdala and medial prefrontal cortex (mPFC). Severe NSSI showed a blunted pattern of cortisol response, despite elevated reported and observed stress during TSST. Severe NSSI showed lower amygdala–mPFC RSFC; follow-up analyses suggested that this was more pronounced in those with a history of suicide attempt for both moderate and severe NSSI. Moderate NSSI showed elevated right amygdala activation to threat; multiple regressions showed that, when considered together with low amygdala–mPFC RSFC, higher right but lower left amygdala activation predicted NSSI severity. Patterns of interrelationships among Sustained Threat measures varied substantially across NSSI severity groups, and further by suicide attempt history. Study limitations include the cross-sectional design, missing data, and sampling biases. Our findings highlight the value of multilevel approaches in understanding the complexity of neurobiological mechanisms in adolescent NSSI.

Social and economic inequality are chronic stressors that continually erode the mental and physical health of marginalized groups, undermining overall societal resilience. In this comprehensive review, we synthesize evidence of greater increases in mental health symptoms during the COVID-19 pandemic among socially or economically marginalized groups in the United States, including (a) people who are low income or experiencing homelessness, (b) racial and ethnic minorities, (c) women and lesbian, gay, bisexual, transgender, queer, and questioning (LGBTQ+) communities, (d) immigrants and migrants, (e) children and people with a history of childhood adversity, and (f) the socially isolated and lonely. Based on this evidence, we propose that reducing social and economic inequality would promote population mental health and societal resilience to future crises. Specifically, we propose concrete, actionable recommendations for policy, intervention, and practice that would bolster five “pillars” of societal resilience: (1) economic safety and equity, (2) accessible healthcare, including mental health services, (3) combating racial injustice and promoting respect for diversity, equity, and inclusion, (4) child and family protection services, and (5) social cohesion. Although the recent pandemic exposed and accentuated steep inequalities within our society, efforts to rebuild offer the opportunity to re-envision societal resilience and policy to reduce multiple forms of inequality for our collective benefit.

Theoretical perspectives and empirical evidence suggest that the parasympathetic nervous system engages in active monitoring and moderating of inflammatory processes. A clearer understanding of the bidirectional communication between the parasympathetic nervous system and the immune system could lead to novel clinical interventions for inflammatory illnesses. The current study used a large ( N ​= ​836) nationally representative sample of adults in the United States to investigate the associations between resting parasympathetic modulation of the heart, indexed through both high frequency heart rate variability (HF-HRV) and low frequency heart rate variability (LF-HRV), and six circulating markers of inflammation. Statistical analyses revealed robust inverse associations of HF-HRV with interleukin-6 (IL6), C-reactive protein (CRP), and fibrinogen, with or without covariate adjustment. Similar inverse associations were observed between LF-HRV and IL6 and CRP. No significant associations were observed between HRV and either inflammatory adhesion molecules (E-selectin, intracellular adhesion molecule-1) or soluble IL6 receptor. Results are consistent with the cholinergic anti-inflammatory pathway and suggest that parasympathetic modulation of inflammation through the vagus nerve may act on specific inflammatory molecules more than others.

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Parents serve important functions in regulating children's responses to stress and challenge. However, the parental characteristics that modulate the effectiveness of parents as stress buffers remain to be fully characterized. To address this gap, this study examined parental characteristics and behaviors that may explain variation in parents’ ability to buffer cortisol responses to acute stress of 180 children (ages 9–11 years old, M = 9.9 years, SD = .58). Children were randomly assigned to either participate in a public speaking task, the Trier Social Stress Test – modified for children (TSST-M) or a control condition. Children in the TSST-M condition were randomly assigned to prepare for the public speaking task either with their parent (N = 59) or alone (N = 60), whereas 61 children were assigned to the control condition (no TSST-M). We found that parental education moderated the effect of condition on children's responses to acute stress. Children whose parents had lower levels of education exhibited reduced cortisol responses in the parent condition compared to the alone condition, showing a buffered pattern of reactivity. In contrast, children of parents with high levels of education displayed higher cortisol reactivity in the parent condition compared to the alone and control conditions. Parental education was also positively associated with higher levels of state anxiety within the parent condition. These results suggest that highly educated parents may emphasize performance over comfort, amplifying their children's state anxiety and cortisol responses to a public performance.