Corroborative evidence for an association between initial hypothalamic-pituitary-adrenocortical axis reactivity and subsequent habituation in humans

Background: The extant literature predicts that initial hypothalamic-pituitary-adrenocortical (HPA) axis response magnitude and subsequent habituation are associated with health, such that both heightened stress reactivity and non-habituation to repeated stressors are associated with disease. Yet, despite evidence for an association between initial HPA axis reactivity and subsequent habituation, the extant literature often considers health implications of these stress response patterns independently or make interpretations based on an initial response alone. This may be because past tests of the association between reactivity and habituation were subject to statistical bias (e.g., regression to the mean), and no prior work has examined the association between initial cortisol reactivity and subsequent habituation using analytic strategies capable of estimating the unbiased relationship between initial value (i.e., reactivity) and subsequent change (i.e., habituation). Accordingly, the present investigation drew from two previously published studies to test the association between initial HPA axis reactivity and subsequent habituation using analytic strategies capable of estimating the relationship between initial reactivity and subsequent habituation with minimal bias. Methods: We examined salivary cortisol and plasma ACTH responses to three repeated social-evaluative stressors (Study 1) and salivary cortisol responses to two repeated social-evaluative stressors (Study 2). Results: As predicted, results indicated a negative relationship (Pearson's r ranging from -0.27 to -0.91) where initial HPA axis reactivity was associated with subsequent habituation across both studies, even when using estimation procedures capable of producing an unbiased estimate of this relationship. Conclusions: Results support the claim that initial HPA axis reactivity to acute stress is associated with subsequent habituation, such that initially high reactors are likely to habituate, whereas initially blunted reactors are likely to sensitize. In view of these results, hypothesized long-term health implications of acute cortisol reactivity and habituation patterns should be considered in tandem

Moderators of inflammation-related depression: a prospective study of breast cancer survivors.

Inflammation has been shown to predict depression, but sensitivity to inflammation varies across individuals. Experimental studies administering potent pro-inflammatory agents have begun to characterize this sensitivity. However, risk factors for inflammation-associated depression in naturalistic contexts have not been determined. The present study examined key psychological and behavioral risk factors (state anxiety, perceived stress, negative affect, disturbed sleep, and childhood adversity) as potential moderators of the relationship between inflammation and depressive symptoms in a prospective longitudinal study of breast cancer survivors. Women with early stage breast cancer were recruited after completing primary cancer treatment (nfinal = 161). Depressive symptoms, inflammatory markers (CRP, IL-6, and sTNF-RII), and key risk factors were assessed post treatment (T1), at 6 and 12-month follow-ups (T2 and T3), and during a final follow-up (TF) 3-6 years after T1; childhood adversity was measured only at T3. Inflammatory markers were combined into a single inflammatory index prior to analyses. Women who reported higher levels of state anxiety, perceived stress, negative affect, and/or sleep disturbance at T1 (post-treatment) exhibited higher depressive symptoms at times when inflammation was higher than typical (interaction βs ranged from .06 to .08; all ps < .014). Results demonstrate the relevance of these risk factors for understanding inflammation-associated depression in a clinical context and could inform targeted strategies for prevention and treatment among at-risk populations

Vulnerability to inflammation-related depressive symptoms: Moderation by stress in women with breast cancer

BackgroundStress precipitates depression and may do so in part by increasing susceptibility to inflammation-induced depressive symptoms. However, this has not been examined among individuals facing a major life stressor. Accordingly, the present study tested the moderating role of stress on the longitudinal association between inflammation and depressive symptoms among women with breast cancer.MethodsWomen recently diagnosed with early-stage breast cancer (N = 187) were enrolled before starting adjuvant/neoadjuvant treatment. Blood draws and self-reported depressive symptoms were collected pre-treatment, post-treatment, and at 6, 12, and 18-month post-treatment follow ups. C-reactive protein (CRP) was used to index inflammation. Measures of psychological stress, including cancer-related stress, general stress perceptions, and childhood stress, were administered pre-treatment.ResultsStress moderated the association between CRP and depressive symptoms, such that higher levels of CRP were associated with elevated depressive symptoms only among women who reported high cancer-related stress (β = 0.080, p = .002) and perceived stress (β = 0.053, p = .044); childhood stress effects were non-significant. Moreover, elevated CRP was associated with increased odds of exhibiting clinically significant depressive symptoms (OR = 1.64, p < .001) among women who reported high cancer-related stress. Results were independent of age, BMI, race and cancer-related covariates.ConclusionsStress was found to heighten sensitivity to inflammation-associated depressive symptoms over a 2-year period, with notably stronger effects for subjective stress responses to a concurrent life event. Individuals who are most distressed following a major life event may exhibit the greatest risk for inflammation-induced depression

Psychosocial Resilience to Inflammation-Associated Depression: A Prospective Study of Breast-Cancer Survivors

Stress can lead to depression, in part because of activation of inflammatory mechanisms. It is therefore critical to identify resilience factors that can buffer against these effects, but no research to date has evaluated whether psychosocial resilience mitigates the effects of stress on inflammation-associated depressive symptoms. We therefore examined psychosocial resources known to buffer against stress in a longitudinal study of women with breast cancer (N = 187). Depressive symptoms and inflammation were measured over a 2-year period extending from after diagnosis into survivorship. Cancer-related stress and psychosocial resources-social support, optimism, positive affect, mastery, self-esteem, and mindfulness-were measured after diagnosis. As hypothesized, women who reported having more psychosocial resources showed weaker associations between stress and depressive symptoms and weaker associations between stress and inflammation-related depressive symptoms. Results highlight the importance of psychosocial resilience by demonstrating a relationship between psychosocial resources and sensitivity to inflammation-associated depressive symptoms

Trait Rumination Predicts Elevated Evening Cortisol in Sexual and Gender Minority Young Adults

Stress may contribute to illness through the impaired recovery or sustained activity of stress-responsive biological systems. Rumination, or mental rehearsal of past stressors, may alter the body’s stress-responsive systems by amplifying and prolonging exposure to physiological mediators, such as cortisol. The primary aim of the current investigation was to test the extent to which the tendency to ruminate on stress predicts diminished diurnal cortisol recovery (i.e., elevated evening cortisol) in a sample of sexual and gender minority young adults. Participants included 58 lesbian, gay, bisexual, and transgender young adults (Mage = 25.0, SD = 4.1) who completed an initial online survey that assessed trait rumination and current depressed mood. Participants completed daily evening questionnaires and provided salivary cortisol samples at wake, 45 min post-wake, 12 h post-wake, and at bedtime over seven consecutive days. Trait rumination predicted significantly higher cortisol concentrations at bedtime, but was unrelated to other cortisol indices (e.g., morning cortisol, diurnal slope, total output). The association with trait rumination was not accounted for by daily negative affect, and was largely independent of depressed mood. These results have implications for identifying and treating those who may be at risk for impaired diurnal cortisol recovery and associated negative health outcomes