Social anxiety disorder (SAD) is a pervasive problem associated with debilitating impairments in social settings. This research explored the affective and physiological reactions to social evaluation and examined the efficacy of an arousal reappraisal intervention in altering cardiovascular reactivity and affective responses. Across two studies, socially anxious participants exhibited a disjunction between subjective ratings and physiological responses. Whereas anxious individuals reported more anxiety and negative affect during a stressful public speaking task relative to nonanxious controls, no differences emerged in physiological reactivity as a function of anxiety. In the second experiment socially anxious and nonanxious participants instructed to reframe stress arousal as a positive coping tool exhibited reduced attentional bias and improvements in physiological functioning: decreased vasoconstriction and increased cardiac efficiency. This research suggests that outcomes in SAD may be improved by reappraising stress arousal. © The Author(s) 2013.

Contrary to lay beliefs, physiological changes that co-occur with stress are not necessarily bad. Much can be done during stressful experiences to promote adaptive responses. In this article, we review recent research on one method for improving acute stress responses: reappraising arousal. A growing body of research suggests that cognitive appraisals are powerful tools that help shift negative stress states to more positive ones. Arousal reappraisal instructs individuals to think of stress arousal as a tool that helps maximize performance. By reframing the meaning of the physiological signals that accompany stress, arousal reappraisal breaks the link between negative affective experiences and malignant physiological responses. We demonstrate how this approach can benefit physiological reactivity, attention, and performance and explore its potential applications. © The Author(s) 2013.

Prior research has revealed racial disparities in health outcomes and health-compromising behaviors, such as smoking and drug abuse. It has been suggested that discrimination contributes to such disparities, but the mechanisms through which this might occur are not well understood. In the research reported here, we examined whether the experience of discrimination affects acute physiological stress responses and increases risk-taking behavior. Black and White participants each received rejecting feedback from partners who were either of their own race (in-group rejection) or of a different race (out-group rejection, which could be interpreted as discrimination). Physiological (cardiovascular and neuroendocrine) changes, cognition (memory and attentional bias), affect, and risk-taking behavior were assessed. Significant participant race × partner race interactions were observed. Cross-race rejection, compared with same-race rejection, was associated with lower levels of cortisol, increased cardiac output, decreased vascular resistance, greater anger, increased attentional bias, and more risk-taking behavior. These data suggest that perceived discrimination is associated with distinct profiles of physiological reactivity, affect, cognitive processing, and risk taking, implicating direct and indirect pathways to health disparities.

Background

Depression rates increase markedly for girls across the adolescent transition, but the social-environmental and biological processes underlying this phenomenon remain unclear. To address this issue, we tested a key hypothesis from Social Signal Transduction Theory of Depression, which posits that individuals who mount stronger inflammatory responses to social stress should exhibit greater increases in depressive symptoms following interpersonal life stress exposure than those who mount weaker inflammatory responses to such stress.

Method

Participants were 116 adolescent girls (M_age  = 14.71) at risk for psychopathology, defined as having a history of mental health concerns (e.g., psychiatric treatment, significant symptoms) over the past 2 years. At baseline, we characterized their inflammatory reactivity to social stress by quantifying their salivary proinflammatory cytokine responses to a laboratory-based social stressor. Then, 9 months later, we assessed the interpersonal and noninterpersonal stressful life events that they experienced over the prior 9 months using an interview-based measure of life stress.

Results

As hypothesized, greater interpersonal life stress exposure was associated with significant increases in depression over time, but only for girls exhibiting stronger salivary tumor necrosis factor-α and interleukin-1β reactivity to social stress. In contrast, noninterpersonal stress exposure was unrelated to changes in depression longitudinally, both alone and when combined with youths' cytokine reactivity scores.

Discussion

These results are consistent with Social Signal Transduction Theory of Depression and suggest that heightened inflammatory reactivity to social stress may increase adolescents' risk for depression. Consequently, it may be possible to reduce depression risk by modifying inflammatory responses to social stress.

Background

During adolescence, peer victimization is a potent type of social stressor that can confer enduring risk for poor mental and physical health. Given recent research implicating inflammation in promoting a variety of serious mental and physical health problems, this study examined the role that peer victimization and cognitive vulnerability (i.e. negative cognitive styles and hopelessness) play in shaping adolescents' pro-inflammatory cytokine responses to an acute social stressor.

Methods

Adolescent girls at risk for psychopathology (n = 157; M_age  = 14.73 years; SD = 1.38) were exposed to a laboratory-based social stressor before and after which we assessed salivary levels of three key pro-inflammatory cytokines - interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α).

Results

As hypothesized, adolescents with greater peer victimization exposure exhibited greater increases in IL-6 and IL1-β in response to the laboratory-based social stressor. Moreover, for all three cytokines individually, as well as for a combined latent factor of inflammation, peer victimization predicted enhanced inflammatory responding most strongly for adolescents with high levels of hopelessness.

Conclusions

The findings reveal a biological pathway by which peer victimization may interact with cognitive vulnerability to influence health in adolescence.

Poor physiological self-regulation has been proposed as a potential biological vulnerability for adolescent suicidality. This study tested this hypothesis by examining the effect of parasympathetic stress responses on future suicide ideation. In addition, drawing from multilevel developmental psychopathology theories, the interplay between parasympathetic regulation and friendship support, conceptualized as an external source of regulation, was examined. At baseline, 132 adolescent females (M age = 14.59, SD = 1.39) with a history of mental health concerns participated in an in vivo interpersonal stressor (a laboratory speech task) and completed self-report measures of depressive symptoms and perceived support within a close same-age female friendship. Respiratory sinus arrhythmia (RSA) was measured before and during the speech task. Suicide ideation was assessed at baseline and at 3, 6, and 9 months follow-up. The results revealed that females with greater relative RSA decreases to the laboratory stressor were at higher risk for reporting suicide ideation over the subsequent 9 months. Moreover, parasympathetic responses moderated the effect of friendship support on suicide ideation; among females with mild changes or higher relative increases in RSA, but not more pronounced RSA decreases, friendship support reduced risk for future suicide ideation. Findings highlight the crucial role of physiological and external regulation sources as protective factors for youth suicidality.

Objective

This study tests a novel, within-person model that reexamines depression and stress as risk factors for suicidal ideation and behavior among adolescent girls with and without sexual/physical abuse histories.

Method

This longitudinal study includes data from 220 adolescent girls between 12 and 16 years of age (M = 14.69 years, SD = 1.37; 61% White). At baseline, adolescents reported the presence or absence of prior abuse as part of a clinical interview. At baseline and every 3 months for 18 months, adolescents completed measures of suicidal ideation and behavior, depressive symptoms, and stress.

Results

Multilevel models examined within-person mean, deviations from within-person mean, depression, and stress and their interactions with abuse as predictors of suicidal ideation and behavior. In addition to within-person mean depression, higher-than-usual depression (odds ratio [OR] = 1.99) and higher-than-usual stress (OR = 1.53) predicted greater risk of suicidal ideation at each follow-up assessment. Periods of higher-than-usual stress (1 SD increase) and periods of higher-than-usual depression (1 SD increase) were associated with an 82% and 57% increase in the odds of suicidal behavior, respectively, but only among those with abuse histories.

Conclusion

Depression, stress, and abuse are well-known risk factors for suicidal ideation and behavior; however, it has been unclear for whom, and when, these factors have their greatest impact. These results show that depression and stress are potent risk factors among those with a history of abuse and that within-person elevations in these risk factors signal increased short-term risk of suicidal ideation and behavior. (PsycINFO Database Record

In recent decades, stress response models of adolescent depression have gained attention, but it remains unclear why only certain adolescents are vulnerable to the depressogenic effects of stress while others are not. Building on evidence that affective and physiological responses to stress moderate the impact of stress exposure on depression, the current study examined whether the interaction between severity of interpersonal stress, subjective affective reactivity, and hypothalamic-pituitary-adrenal (HPA) axis reactivity to an acute, in-vivo psychosocial stressor prospectively predicted depressive symptoms nine months later. Hypotheses were examined with a clinically-oversampled group of 182 adolescent girls (aged 12-16) to ensure an examination of the widest possible range of risk. Self-report measures of affect and salivary cortisol samples were collected before and after an in-vivo stress task to assess affective reactivity and HPA axis reactivity, respectively. Severity of interpersonal stress between baseline and nine months was assessed using a semi-structured interview and was objectively coded for severity and content theme (i.e., interpersonal vs. non-interpersonal). Results indicate that experiences of severe interpersonally-themed stress predict elevated levels of depressive symptoms longitudinally only for adolescent girls with elevated affective reactivity to stress, and suggest that these deleterious effects of stress are most exacerbated for girls with elevated physiological responses to stress. Findings suggest that it may be critical to examine both affective and physiological stress responses when assessing risk for depression in adolescents.

Prior studies suggest that hypothalamic-pituitary-adrenal (HPA) axis stress response is a relatively stable risk factor for suicidal behavior in adults, and also that fluctuations in developmentally salient social stress (i.e., peer stress) predict acute suicidal ideation and behavior in adolescent females. Here, we test the hypothesis that periods of high peer stress are prospectively associated with concurrent episodes of suicidal ideation and behavior, but that abnormal cortisol responses to stress at baseline act as a diathesis that strengthens this stressor-suicidality link, using a longitudinal, multi-wave study design. We measured cortisol responses to an adolescent modification of the Trier Social Stress Test in 220 adolescent females recruited for mental health concerns, and measured stress (peer, academic, and mother-child) and suicidal ideation and behaviors repeatedly across 18 months. Logistic multilevel models revealed the predicted interaction between altered cortisol response and elevated periods of peer stress in predicting suicidal behavior, but not ideation. Higher-than-usual peer stress predicted suicidal ideation regardless of HPA function, but predicted suicide attempt only among those with blunted cortisol responses. Results suggest that peer stress serves to trigger suicidal ideation among female youth, but only triggers suicidal behavior among those with blunted cortisol reactivity.

Adopting a multi-level approach, this study examined risk factors for adolescent suicidal ideation, with specific attention to (a) hypothalamic-pituitary-adrenal (HPA) axis stress responses and (b) the interplay between HPA-axis and other risk factors from multiple domains (i.e., psychological, interpersonal and biological). Participants were 138 adolescent females (M(age) = 14.13 years, SD = 1.40) at risk for suicidal behaviors. At baseline, lifetime suicidal ideation and a number of risk factors were assessed (i.e., depressive symptoms, impulsiveness, pubertal status and peer stress). Participants were exposed to a psychosocial stress task and HPA-axis responses were assessed by measuring cortisol levels pre- and post-stressor. At 3 months post-baseline, suicidal ideation again was assessed. Using group-based trajectory modeling, three groups of cortisol stress-response patterns were identified (i.e., hyporesponsive, normative, and hyperresponsive). As compared to females in the normative and hyporesponsive group, females in the hyperresponsive group were more likely to report a lifetime history of suicidal ideation at baseline, above and beyond the effects of the other predictors. Moreover, as compared to females in the normative group, females in the hyperresponsive group were at increased risk for reporting suicidal ideation 3 months later, after controlling for prior ideation. No interactions between cortisol group and the other risk factors were significant, with the exception of a non-significant trend between impulsiveness and cortisol group on lifetime suicidal ideation. Findings highlight the importance of HPA-axis responses to acute stressors as a risk factor for suicidal ideation among adolescents.