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Poster #18 - Asymmetric Adrenocortical-Parasympathetic Reactivity to Social Stress in Adolescent Girls Endorsing Non-Suicidal Self-Injury

Thu, March 21, 4:00 to 5:15pm, Baltimore Convention Center, Floor: Level 1, Exhibit Hall B

Integrative Statement

Non-suicidal self-injury (NSSI) is trans-diagnostic and has been described as intentional self-directed bodily damage without conscious suicidal intent (Nock & Favazza, 2009). Young adults who self-injure experience heightened negative emotions in their daily interactions and have endorsed affect regulation as a primary motivation for engaging in self-injury (Klonsky, 2009). Our central objective was to characterize multi-system physiological mechanisms underlying altered stress reactivity in adolescent girls who self-injure.

We used an adapted Trier Social Stress Test to evaluate adrenocortical (cortisol) and parasympathetic (respiratory sinus arrhythmia; RSA) responses to acute social evaluative stress in female adolescents (N = 177; M = 14.59 years, SD = 1.39) with (n = 80) and without (n = 97) histories of self-injury. NSSI was assessed with the Self-Injurious Thoughts and Behaviors Interview. While we collected prospective clinical data, we focused the current analyses on concurrent associations. Allostatic frameworks (Miller, Chen, & Zhou, 2007) theorize that chronic exposure to interpersonal stress leads to attenuated reactivity of the HPA axis to minimize neurotoxicity. Based on prior work linking NSSI with emotion dysregulation and family conflict, we hypothesized that adolescent girls with a history of NSSI would show attenuated cortisol reactivity to social evaluation. Based on prior research linking NSSI with greater RSA reactivity during negative mood induction (Crowell et al., 2005), we hypothesized that girls with a history of NSSI would show RSA suppression during social evaluation. Since brain regions implicated in regulation of cortisol and RSA show significant overlap (Ulrich-Lai & Herman, 2009), we evaluated potential multisystem reactivity profiles as a biomarker of having a NSSI history in adolescent girls. We hypothesized that asymmetric or reciprocal HPA-RSA reactivity as expressed in the concomitant attenuated cortisol reactivity and pronounced RSA suppression would be a multi-system biomarker of NSSI history in adolescent girls.

Utilizing multilevel modeling, we found an attenuated cortisol response to acute psychosocial stress in adolescent girls with a history of NSSI relative to those without a history (Table 1), adjusting for age, baseline depressive symptoms, cortisol timing, birth control use, and corticosteroid medication use. Reduced cortisol responses to stress have been shown to decrease sensitivity to punishment and limit the ability of young people to maintain positive social engagement in challenging social contexts. In contrast, we did not find group differences in RSA change associated with NSSI history.

A logistic regression model was conducted to ascertain the effects of age, baseline depressive symptoms, physiological indices capturing baseline and reactivity, and cross system-physiological interactions on the likelihood of having a lifetime history of NSSI assessed at baseline (see Table 2). A significant cross-system physiological interaction effect was observed for cortisol reactivity*RSA change (OR = 1.21 [1.01, 1.46]; p < .05). Specifically, adolescent girls who show asymmetric or reciprocal HPA-RSA reactivity in the context of a social speech stressor were the most likely to have a prior history of NSSI. Broader implications for understanding multisystem alterations in stress regulation and vulnerability for psychopathology will be discussed.

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