Differential associations between early life adversity subtypes and adolescent stress reactivity across neuroendocrine, autonomic, immune, and metabolic systems

Abstract

Early life adversity (ELA) is a heterogeneous construct that can include the consequences of poverty, maltreatment, or serious accidents. This study characterized associations between subtypes of ELA and the physiological responses of multiple systems to acute psychosocial stress. Studies to date have focused on HPA axis reactivity, often neglecting the stress-reactive SNS, HPG axis, metabolic, and innate immune systems. We hypothesized that emotional, physical, and non-intentional ELA would differentially affect stress reactivity in each of these systems. Nine salivary samples, collected serially across the administration of a Trier Social Stress Test for Children (TSST-C), were collected from 92 adolescents [mean age 13.9 (SD = 1.57)] and assayed for cortisol, testosterone, DHEA, uric acid, salivary ɑ-amylase, and interleukin-6 (IL-6). Emotional ELA was associated with a steeper cortisol response to the stressor [b(SE) = 0.007 (0.003), p = .013]. Physical ELA was associated with IL-6 having steeper activation [b(SE) = 0.002 (0.001), p = .047] and recovery slopes [b(SE) = 0.00002 (0.00001), p = .03]. After accounting for age, sex, and body mass index, associations between physical ELA and IL-6 were attenuated. Findings are aligned with the theory of biological salience, which states physiological systems are differentially sensitive to experiences of adversity throughout childhood. Indeed, that different types of ELA are differentially associated with stress reactivity suggests a need for specificity and nuance in studies exploring associations between childhood environment and later biological functioning. Different forms of ELA are likely differentially salient to physiological systems that have distinct and evolutionarily conserved functions which may shape how the individual responds to psychosocial stress later in life. If confirmed with further evidence, biological salience may help to explain previously equivocal associations between ELA and adverse lifespan health outcomes.