The cortisol reactivity threshold model: Direction of trait rumination and cortisol reactivity association varies with stressor severity.

Various internalizing risk factors predict, in separate studies, both augmented and reduced cortisol responding to lab-induced stress. Stressor severity appears key: We tested whether heightened trait-like internalizing risk (here, trait rumination) predicts heightened cortisol reactivity under modest objective stress, but conversely predicts reduced reactivity under more robust objective stress. Thus, we hypothesized that trait rumination would interact with a curvilinear (quadratic) function of stress severity to predict cortisol reactivity. Evidence comes from 85 currently non-depressed emerging adults who completed either a non-stressful control protocol (n = 29), an intermediate difficulty Trier Social Stress Test (TSST; n = 26), or a robustly stressful negative evaluative TSST (n = 30). Latent growth curve models evaluated relationships between trait rumination and linear and quadratic effects of stressor severity on the change in cortisol and negative affect over time. Among other findings, a significant Trait Rumination x Quadratic Stress Severity interaction effect for cortisol's Quadratic Trend of Time (i.e., reactivity, B = .125, p = .017) supported the hypothesis. Rumination predicted greater cortisol reactivity to intermediate stress (rp = .400, p = .043), but blunted reactivity to more robust negative evaluative stress (rp = -0.379, p = 0.039). Contrasting hypotheses, negative affective reactivity increased independently of rumination as stressor severity increased (B = .453, p = 0.044). The direction of the relationship between an internalizing risk factor (trait rumination) and cortisol reactivity varies as a function of stressor severity. We propose the Cortisol Reactivity Threshold Model, which may help reconcile several divergent reactivity literatures and has implications for internalizing psychopathology, particularly depression.

Neural predictors of emotional inertia in daily life.

Assessing emotional dynamics in the brain offers insight into the fundamental neural and psychological mechanisms underlying emotion. One such dynamic is emotional inertia-the influence of one's emotional state at one time point on one's emotional state at a subsequent time point. Emotion inertia reflects emotional rigidity and poor emotion regulation as evidenced by its relationship to depression and neuroticism. In this study, we assessed changes in cerebral blood flow (CBF) from before to after an emotional task and used these changes to predict stress, positive and negative emotional inertia in daily life events. Cerebral blood flow changes in the lateral prefrontal cortex (lPFC) predicted decreased non-specific emotional inertia, suggesting that the lPFC may feature a general inhibitory mechanism responsible for limiting the impact that an emotional state from one event has on the emotional state of a subsequent event. CBF changes in the ventromedial prefrontal cortex and lateral occipital cortex were associated with positive emotional inertia and negative/stress inertia, respectively. These data advance the blossoming literature on the temporal dynamics of emotion in the brain and on the use of neural indices to predict mental health-relevant behavior in daily life.

Nonsynonymous HTR2C polymorphism predicts cortisol response to psychosocial stress I: Effects in males and females.

BACKGROUND: Genetic influences on stress reactivity may provide insight into depression risk mechanisms. The C-allele of rs6318, a putatively functional polymorphism located within the HTR2C gene, has been reported to predict greater cortisol and negative affective reactivity to lab-induced stress. However, the potential moderating effect of sex has not been examined despite X-linkage of HTR2C. We hypothesized that sex moderates the effect of rs6318 on cortisol and affective reactivity to lab-induced stress, with males showing stronger effects. METHODS: Non-depressed young adults (N=112; 39 female) screened via clinical interview provided a DNA sample and completed either a negative evaluative Trier Social Stress Test, or a non-evaluative control protocol. Salivary cortisol and self-reported affect were assessed at four timepoints. RESULTS: Contrary to hypotheses, C-carriers showed blunted rather than exaggerated cortisol responses to lab-induced stress in multilevel models (b=0.467, p<0.001), which persisted when covarying subclinical depressive symptoms. This effect was not moderated by sex (b=0.174, p=0.421), and remained significant when examining females (b=0.362, p=0.013) and males (b=0.537, p<0.001) separately. C-carriers also exhibited marginally greater reactivity in negative self-focused affect in response to stress than non-carriers when covarying subclinical depressive symptoms (b=-0.360, p=0.067), and exhibited higher levels of subclinical depressive symptoms than non-carriers (F=6.463, p=0.012). CONCLUSIONS: Results support a role for the rs6318 C-allele in dysregulated stress responding, and suggest that the C-allele may contribute to risk for depression.