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African Americans are disproportionately exposed to adversity across the lifespan, which includes both stressful and traumatic events. Adversity, in turn, is associated with alterations in pain responsiveness. Racial differences in pain responsiveness among healthy adults are well established. However, the extent to which adversity type and timing are associated with alterations in pain responsiveness among healthy African-American adults is not well understood. The present study included 160 healthy African-American adults (98 women), ages 18 to 45. Outcome measures included pain tolerance and temporal summation of pain to evoked thermal pain. Composite scores were created for early-life adversity (childhood trauma, family adversity) and recent adversity (perceived stress, chronic stress burden). A measure of lifetime racial discrimination was also included. Higher levels of recent adversity were associated with higher temporal summation of pain, controlling for gender, age, and education. Neither early-life adversity nor lifetime racial discrimination were associated with temporal summation of pain. The present findings suggest that heightened temporal summation of pain among healthy African-American adults is associated with exposure to recent adversity events. Improved understanding of how recent adversity contributes to heightened temporal summation of pain in African Americans could help to mitigate racial disparities in pain experiences by identifying at-risk individuals who could benefit from early interventions. [ABSTRACT FROM AUTHOR]

Background: Dysfunction in major stress response systems during the acute aftermath of trauma may contribute to risk for developing posttraumatic stress disorder (PTSD). The current study investigated how PTSD diagnosis and symptom severity, depressive symptoms, and childhood trauma uniquely relate to diurnal neuroendocrine secretion (cortisol and alpha-amylase rhythms) in women who recently experienced interpersonal trauma compared to non-traumatized controls (NTCs). Method: Using a longitudinal design, we examined diurnal cortisol and alpha-amylase rhythms in 98 young women (n = 57 exposed to recent interpersonal trauma, n = 41 NTCs). Participants provided saliva samples and completed symptom measures at baseline and 1-, 3-, and 6-month follow-up. Results: Multilevel models (MLMs) revealed lower waking cortisol predicted the development of PTSD in trauma survivors and distinguished at-risk women from NTCs. Women with greater childhood trauma exposure exhibited flatter diurnal cortisol slopes. Among trauma-exposed individuals, lower waking cortisol levels were associated with higher concurrent PTSD symptom severity. Regarding alpha-amylase, MLMs revealed women with greater childhood trauma exposure exhibited higher waking alpha-amylase and slower diurnal alpha-amylase increase. Conclusions: Results suggest lower waking cortisol in the acute aftermath of trauma may be implicated in PTSD onset and maintenance. Findings also suggest childhood trauma may predict a different pattern of dysfunction in stress response systems following subsequent trauma exposure than the stress system dynamics associated with PTSD risk; childhood trauma appears to be associated with flattened diurnal cortisol and alpha-amylase slopes, as well as higher waking alpha-amylase. [ABSTRACT FROM AUTHOR]

Childhood trauma (CT) is associated with long-lasting alterations of the hypothalamic–pituitary–adrenal (HPA) axis and elevated risk for stress exposure in adulthood. Although HPA alterations are present in the early aftermath of trauma, it remains unclear how initial HPA activity is associated with subsequent stress exposure and whether CT exposure influences the strength and direction of this association. The present study examined prospective associations between hair cortisol content (HCC) and stress exposure from baseline to 3-month follow-up in young adult women with recent (i.e. past 3 months) exposure to interpersonal violence (IPV; i.e. physical or sexual assault) and non-traumatized controls. History of significant CT abuse or neglect was determined based on clinical cutoffs for a self-report CT measure: 12 women had abuse or neglect and recent IPV exposure (CT + IPV); 7 women had abuse or neglect but no IPV exposure (CT); 15 women had no history of trauma (NTC). HCC was computed for 3 cm sections reflecting cortisol secretion during the 3 months preceding the baseline assessment. The interaction of cumulative trauma and HCC predicted stress exposure over 3-month follow-up, controlling for baseline stress exposure and depressive symptoms. Simple slopes analyses revealed that lower baseline HCC predicted greater stress exposure in the CT + IPV group compared to the CT group; HCC was not associated with stress exposure in the NTC group. The present findings highlight the potential utility of HCC as a predictor of stress exposure for women with a history of childhood abuse or neglect, particularly in the context of recent IPV. Lay summary Adults with a history of CT show long-lasting alterations in major stress response systems, including the HPA axis. They are also more likely to experience stressful life events in adulthood. However, it is not clear how altered HPA activity influences risk for stress exposure and whether CT affects their relationship. The results from this study show that lower HPA activity (measured with hair cortisol) predicted greater stress exposure in women with CT – particularly for women who also experienced recent incidents involving physical or sexual assault. [ABSTRACT FROM AUTHOR]

Background: Altered hypothalamic-pituitary-adrenal (HPA) function is common in youth with major depressive disorder (MDD) but variability in the strength and direction of HPA alterations has prompted a search for symptom-based subtypes with unique neuroendocrine signatures. This study investigated the extent to which depressive symptom composites were differentially associated with cortisol responses to psychosocial stress.Methods: This study examined salivary cortisol responses to the Trier Social Stress Test (TSST) in 145 adolescents who varied in their risk for MDD: 38 had current MDD; 35 were healthy but at high risk for MDD based on having one or both parents with unipolar MDD; and 72 were healthy youth with no personal or family history of a psychiatric disorder. Multilevel models examined within-person change in cortisol levels during a 2-h resting phase prior to the TSST and both linear and quadratic changes in cortisol levels following the TSST.Results: Anticipatory cortisol reactivity was lower in MDD youth compared to low-risk youth, and in youth with higher compared to lower depressive symptom severity. Whereas affective symptoms were associated with increased anticipatory cortisol reactivity and more rapid recovery to the TSST, neurovegetative symptoms were associated with decreased anticipatory cortisol reactivity and slower recovery.Limitations: The cross-sectional design does not permit inferences regarding temporal relations between cortisol responses and depressive symptom composites.Conclusions: The present findings suggest that heterogeneity among studies examining HPA reactivity in depressed youth may be driven, in part, by differences in depressive symptom composites across samples. [ABSTRACT FROM AUTHOR]

Background: Childhood maltreatment can trigger enduring changes in major stress response systems, particularly in the context of major depressive disorder (MDD). However, the relative impact of maltreatment versus MDD on hypothalamic-pituitary-adrenal axis and sympathetic-adrenal-medullary system stress reactivity is not well understood.Method: This study examined salivary cortisol and alpha-amylase responses to the Trier Social Stress Test (TSST) in 26 maltreated (15 with current MDD) and 26 non-maltreated (17 with current MDD) women.Results: Maltreated women showed greater anticipatory cortisol reactivity during the TSST protocol compared to non-maltreated women. Maltreated women also showed rapid deceleration in cortisol levels. Whereas non-maltreated women showed initial declines in alpha-amylase levels but rapidly increasing alpha-amylase levels during the TSST protocol, maltreated women did not exhibit changes in alpha-amylase levels during the TSST protocol. Contrary to expectation, MDD did not impact cortisol or alpha-amylase responses.Limitations: The present study is limited by retrospective report of childhood maltreatment, cross-sectional design, and modest sample sizes.Conclusions: These findings suggest that childhood maltreatment plays a greater role driving alterations in cortisol and alpha-amylase stress reactivity than MDD. Understanding the biological embedding of maltreatment is critical for elucidating mechanisms linking these experiences to risk for negative mental and physical health outcomes. [ABSTRACT FROM AUTHOR]

Background: Although stress plays a critical role in vulnerability to nicotine use and dependence, the stress response factors that contribute to smoking behaviors remain poorly elucidated. To minimize the confounding effects of chronic nicotine use, assessing individuals with relatively short smoking histories is critical for characterizing the neurobiological substrates associated with nicotine dependence early in the course of illness.Objectives: This pilot study examined sympathetic nervous system (alpha-amylase) and hypothalamic-pituitary-adrenal axis (cortisol, dehydroepiandrosterone) responses to the Trier Social Stress Test (TSST) in young adult smokers. Associations among objective indices of recent smoking (salivary cotinine, carbon monoxide in the breath [CO]), behavioral measures of nicotine dependence and withdrawal, and salivary biomarkers in response to the TSST were investigated.Methods: Smokers (N = 64; 28 males, 36 females) provided saliva samples at 30 min intervals for 2 h prior to the TSST and every 10 min for 1 h following the TSST.Results: Alpha-amylase responses to the TSST were positively associated with salivary cotinine levels but negatively associated with CO levels. Individuals with a lower level of nicotine dependence had increased cortisol responses to the stressor, whereas those with a higher level of nicotine dependence did not show any cortisol changes in response to the stressor.Conclusions: These findings indicate that different mechanisms may be involved at different levels of nicotine dependence severity. Recent nicotine use and lower dependence severity may be associated with increased activation of the stress response systems. In contrast, more severe levels of dependence may downregulate stress response systems. [ABSTRACT FROM AUTHOR]

The stress generation hypothesis was tested in two different longitudinal studies examining relations between weekly depression symptom ratings and stress levels in adolescents and emerging adults at varied risk for depression. The participants in Study 1 included 240 adolescents who differed with regard to their mothers' history of depressive disorders. Youth were assessed annually across 6 years (Grades 6–12). Consistent with the depression autonomy model, higher numbers of prior major depressive episodes (MDEs) were associated with weaker stress generation effects, such that higher levels of depressive symptoms predicted increases in levels of dependent stressors for adolescents with two or more prior MDEs, but depressive symptoms were not significantly related to dependent stress levels for youth with three or more prior MDEs. In Study 2, the participants were 32 remitted-depressed and 36 never-depressed young adults who completed a psychosocial stress task to determine cortisol reactivity and were reassessed for depression and stress approximately 8 months later. Stress generation effects were moderated by cortisol responses to a laboratory psychosocial stressor, such that individuals with higher cortisol responses exhibited a pattern consistent with the depression autonomy model, whereas individuals with lower cortisol responses showed a pattern more consistent with the depression sensitization model. Finally, comparing across the two samples, stress generation effects were weaker for older participants and for those with more prior MDEs. The complex, multifactorial relation between stress and depression is discussed. [ABSTRACT FROM PUBLISHER]

Objectives This prospective study investigated whether within-individual relations between depression vulnerability factors (childhood trauma, dysfunctional attitudes, maladaptive coping) and depressive symptom trajectories varied as a function of the number of prior major depressive episodes (MDEs) experienced in their lifetime. Design Participants were 68 young adults who varied with regard to their history of depression; 32 were remitted depressed and 36 were never depressed. Methods Depressive symptoms and disorders were assessed using semi-structured psychiatric interviews conducted twice over a 6-month period; interviews yielded weekly ratings of depressive symptoms during the follow-up interval. Childhood trauma, dysfunctional attitudes and coping were assessed with self-report measures. Data analyses were conducted using time-lagged multilevel models. Results Individuals with more previous MDEs who reported greater childhood trauma exposure, more dysfunctional attitudes, or greater use of maladaptive coping strategies experienced more rapid increases in depressive symptoms during the follow-up period. A significant interaction of coping, number of previous MDEs, and time was found indicating that among individuals with less adaptive coping (i.e., lower primary or lower secondary control coping scores), depressive symptoms rating ( DSR) increased significantly in relation to number of prior depressive episodes; no change in DSR was observed for never-depressed individuals. Among individuals with higher primary control coping scores, significant increases in DSR scores were observed for individuals with ≥3 prior MDEs only. Conclusions Findings highlight the need for treatment and prevention programmes that target stress reactivity and coping strategies early in the course of depression. Practitioner points Findings highlight the need to conduct multi-dimensional assessments of depression vulnerability that examine the interplay among risk factors over time., Relations between vulnerability factors (childhood trauma, dysfunctional attitudes, maladaptive coping) and depressive symptoms were stronger for individuals with more prior major depressive episodes (MDEs)., Interventions for recurrent depression should focus on secondary control coping strategies that emphasize accommodation to stressful life events., Future studies should assess high-risk individuals before their first MDE to determine whether vulnerability factors linked with recurrence are pre-existing and relatively stable, or if they reflect 'scars' from MDEs. [ABSTRACT FROM AUTHOR]

This study examined cortisol and affective reactivity to a psychosocial stress task in 102 young adults who varied in risk for depression (56 remitted depressed, 46 never depressed). Participants were randomly assigned to either a stress (i.e., social-evaluative threat) or control (i.e., no social-evaluative threat) condition. For never-depressed individuals, cortisol responses were significantly greater in the stress compared to the control condition. Moreover, cortisol responses were significantly greater for never-depressed than remitted-depressed individuals in the stress condition. For individuals with a history of depression, cortisol responses did not differ significantly between the stress and control conditions. Negative affective reactivity also was higher for never depressed, but not remitted depressed, individuals in the stress compared to the control condition. Moreover, cortisol responses were inversely related to negative affect during the recovery phase in both stress and control conditions. Findings indicate the lack of a robust cortisol response to social evaluation stress among remitted-depressed individuals as compared to that of never-depressed controls. Future studies should investigate unique and interactive links between these hypothalamic-pituitary-adrenal and affective reactivity alterations and risk for subsequent depressive episodes. [ABSTRACT FROM AUTHOR]

Abstract: Background: Alterations of hypothalamic-pituitary-adrenal (HPA) function are well-established in adults with current depression. HPA alterations may persist into remission and confer increased risk for recurrence. Methods: A modified version of the Trier Social Stress Test (TSST) was administered at baseline to 32 young adults with remitted major depressive disorder and 36 never-depressed controls. Participants were randomly assigned to either a ‘high-stress’ condition involving social evaluation or a ‘low-stress’ control condition. Cortisol concentrations were measured in saliva samples throughout the TSST. Participants were assessed again after 6 months for the occurrence of stressful life events and depressive symptoms/disorders during the follow-up period. Results: Participants who exhibited enhanced cortisol reactivity in the low-stress condition showed increases in depressive symptoms over follow-up, after controlling for stressful life events during the follow-up period. Anticipatory stress cortisol and cortisol reactivity each interacted with history of depressive episodes to predict depression trajectories. Limitations: The single TSST administration limits conclusions about whether alterations of cortisol reactivity represent trait-like vulnerability factors or consequences (“scars’) of past depression. Conclusions: These results extend previous findings on stress sensitivity in depression and suggest that altered HPA function during remission could reflect an endophenotype for vulnerability to depression recurrence. Findings support interactive models of risk for depression recurrence implicating HPA function, depression history, and sensitivity to minor stressors. Results may have implications for interventions that match treatment approaches to profiles of HPA function. [Copyright &y& Elsevier]

This longitudinal study investigated the stress autonomy, stress sensitization, and depression vulnerability hypotheses in adolescents across 6 years (i.e., Grades 6 through 12). Participants were 240 children (Time 1 mean age = 11.86, SD = 0.57) who varied in risk for depression on the basis of their mother's history of mood disorders. All analyses were conducted as multilevel models to account for nesting in the data. Results were consistent with the stress sensitization hypothesis. The within-subject relation of stress levels to depressive symptoms strengthened with increasing numbers of prior depressive episodes. In addition, evidence consistent with the vulnerability hypothesis was found. The relation of stress levels to depressive symptoms was stronger for adolescents who were at risk for depression on the basis of maternal depression history and for those who had experienced more depressive episodes through Grade 12. These findings suggest that onsets of depression in adolescents may be predicted by both relatively stable and dynamic transactions between stressful life events and vulnerabilities such as maternal depression and youths' own history of depressive episodes. [ABSTRACT FROM AUTHOR]