Exploring joint HPA–inflammatory stress response profiles in adolescent girls: Implications for developmental models of neuroendocrine dysregulation

Prior research has struggled to differentiate cortisol stress response patterns reflective of well‐regulated versus dysregulated hypothalamic–pituitary–adrenal (HPA) axis function among adolescents. Here, we show how exploring profiles of joint HPA–inflammatory stress responsivity, and linking those profiles to pubertal development and peer stress exposure may aid such distinction. Adolescent girls (N = 157, Mage = 14.72 years, SD = 1.38) at risk for psychopathology completed assessments of salivary cortisol and pro‐inflammatory cytokines (i.e., tumor necrosis factor‐α, interleukin‐1β, and interleukin‐6) prior to and following the Trier Social Stress Test. Adolescents, a close friend, and a caregiver completed questionnaire measures of peer stress and pubertal status. Multitrajectory modeling of adolescents’ cortisol and cytokine levels revealed three profiles: low cortisol response–stably low cytokine (n = 75), high cortisol response–stably moderate cytokine (n = 47), and low cortisol response–stably high cytokine (n = 35). Relative to low cortisol response–stably low cytokine, adolescents exhibiting the high cortisol response–stably moderate cytokine profile were more advanced in their pubertal development, but presented with similarly low levels of peer stress exposure. Despite showing cortisol responses that were indistinguishable from low cortisol response–stably low cytokine, adolescents exhibiting the low cortisol response–stably high cytokine profile were more pubertally advanced, but also more likely to have experienced chronic peer strain (self‐report) and relational peer victimization (close friend‐report). These findings thus illustrate the potential value of taking a multisystem approach to studying adolescent stress responsivity and underscore the importance of considering developmental and social factors when interpreting cortisol stress response patterns. Ultimately, such work may help inform developmental models of neuroendocrine dysregulation and related risk for psychopathology.