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Early Family Stress, Biobehavioral and Psychosocial Functioning, and Inflammation


Family stress such as conflict, abuse, neglect, or insensitive parenting, experienced in early life during childhood and adolescence increases risk for adverse health outcomes. Heightened inflammation is thought to be a key pathway by which early family stress increases risk for poor health. Studies have established a link between early family adversity and inflammation, and theoretical models posit several mechanisms linking early family stress to inflammation, including disruptions in biological stress systems (i.e., altered hypothalamic-pituitary-adrenal (HPA) axis and heightened sympathetic nervous system responses to stress) and psychosocial functioning (i.e., higher threat appraisals, heightened emotional reactivity to stress, poorer social relationships). Empirical studies also suggest that disrupted sleep may be an important pathway. The current study tests these putative pathways in a single study, which has been relatively uncommon in prior research. Participants were 91 late adolescents from Latino and European-Americans backgrounds. Participants completed the Trier Social Stress Test (TSST), a well-validated, widely used laboratory-based acute social stressor, and completed questionnaires assessing their family environment from childhood through mid-adolescence. They provided blood and saliva samples for the assessment of their inflammatory, hypothalamic-pituitary-adrenal axis, and sympathetic nervous system responses to the TSST. Additionally, they completed questionnaires assessing their sleep, cognitive appraisals of the stress task, their emotional responses to the TSST, and their current social relationships. Results showed that growing up in a stressful family environment was not related to heightened inflammatory responses to the TSST. However, late adolescents who grew up in a stressful family environment exhibited dampened cortisol responses to the TSST, poorer sleep, heightened threat appraisals, lower emotional reactivity, and poorer social relationships. In turn, dampened cortisol responses were associated with greater increases in inflammation across the laboratory session. Heightened threat appraisals, lower emotional reactivity, and more supportive social relationships were related to attenuated cortisol responses. Together, these findings suggest that early family stress impacts HPA-axis responses to stress, sleep, and psychosocial functioning, but that these in turn, may have little impact on inflammatory responses to stress, at least during late adolescence.

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