Childhood adversity moderates the influence of proximal episodic stress on the cortisol awakening response and depressive symptoms in adolescents

Abstract

Childhood adversity (CA) is known to predict sensitization to proximal stressors. Researchers have suggested that disruptions in hypothalamus-pituitaryadrenal axis functioning may be a biological mechanism. If so, CA may predict altered associations between proximal life stress and markers of cortisol secretion. We examined whether CA moderates associations between recent episodic stress and (a) the cortisol awakening response (CAR), and (b) depressive symptoms, in 241 adolescents aged 14-17 years (cortisol n ¼ 196). Salivary cortisol was sampled at 0, 30, and 60 min postawakening for 2 days. The CAR was calculated as the area under the curve with respect to increase and waking cortisol. CA and episodic stress were assessed using contextual-threat-method-coded objective interviews. CA significantly interacted with episodic stress to predict both the CAR and depression. Among those with low CA, episodic stress predicted increased CAR but did not predict depression. For adolescents with high CA, episodic stress predicted lower CAR and higher depression. These interactions were found only for independent (uncontrollable, fateful) events, and not for dependent (self-generated) stress. Increased allostatic load resulting from CA exposure may interfere with adolescents' ability to optimally regulate their CAR in relation to recent stress, contributing to increased depression risk.

Interpersonal childhood adversity and stress generation in adolescence: Moderation by HPA axis multilocus genetic variation

“…As a preliminary step, we tested for population stratification effects (i.e., confounding effects that occur when race is correlated with outcomes of interest and specific genotypes). As reported elsewhere (for full details, see Starr et al, 2017), in the current sample, non-Caucasian youth had higher MGPS than did Caucasian youth, t (239) = 2.10, p = .036, and race moderated the association between MGPS and depressive symptoms. Race was also marginally associated with ICA, t (239) = 1.68, p = .094; scores were higher for non-White adolescents.…”

“…Youth were recruited to participate from the community of a mid-sized metropolitan area. Families were recruited using a range of recruitment methods, including online and community advertisements (50.6% of families), a commercial mailing list of families with potentially age-eligible children (40.2%), and ResearchMatch (4.1%), an online clinical research registry (additional recruitment details are included in Starr et al, 2017). Participants were excluded from study participation if they had a major physical, neurological, or pervasive developmental disorder, a prior diagnosis of any bipolar or psychotic disorders, English language difficulties, or previous participation of siblings or any other household member.…”

“…More recent evidence suggests that this effect may be specific to interpersonal stress generation, with Hernandez and colleagues (2016) showing that CA predicted higher levels of interpersonal dependent stress (but not noninterpersonal dependent or independent stress) in young adults. Notably, CA has been linked with greater stress reactivity, with CA predicting a stronger association between proximal stressors and depression (Kim et al, 2014; McLaughlin, Conron, Koenen, & Gilman, 2010; Shapero et al, 2014; Starr et al, 2017; Starr, Hammen, Conway, Raposa, & Brennan, 2014). In addition to depression, changes in stress reactivity following CA may result in other negative outcomes, such as increased stress generation.…”

Interpersonal life stress, inflammation, and depression in adolescence: Testing Social Signal Transduction Theory of Depression

“…In a recent study that carefully dated both the occurrence of different stressful life events and youths' development of depression, for example, interpersonal life events were found to be statistically unique predictors of subsequent onset of MDD across two adolescent samples; in contrast, noninterpersonal events were unrelated to depression (Vrshek-Schallhorn et al, 2015). In a second longitudinal study, exposure to interpersonal life events interacted with a multilocus genetic profile score to prospectively predict increases in depressive symptoms in adolescents but, again, these effects were specific to interpersonal stressors (Feurer et al, 2017; see also Starr et al, 2017;Starr, Dienes, Li, & Shaw, 2019). Finally, a third study found that interpersonal life events involving targeted rejection precipitated onset of depression three times faster than other types of major life events (Slavich, Thornton, Torres, Monroe, & Gotlib, 2009; see also Massing-Schaffer et al, 2019).…”

Greater lifetime stress exposure predicts blunted cortisol but heightened DHEA responses to acute stress

“…One reason for this difference may be that early adversity is often conceptualized as childhood‐ specific stressors, such as childhood maltreatment (e.g., Carpenter et al, ), or all stressors occurring prior to age 13 or 15, whereas the STRAIN considers early adversity as all stressors experienced prior to 18 years of age. Alternatively, it is possible that early adversity may interact with recent stressors to modulate HPA axis function (e.g., Starr et al, ).…”