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Introduction: Much attention has been devoted to testing the possibility that early life adversity leads to systematic differences in health later in life. While the basic tenant of this "early root of health disparities" hypothesis enjoys strong empirical support, it remains unclear which mechanisms underlie the higher odds of mental health problems following adversity, uphold them for decades, and for whom or under which circumstances the impact of these early experiences are enhanced (or buffered). The hypothalamic-pituitary-adrenal (HPA) axis, and its end product cortisol, is one of the neurophysiological mechanisms that has been researched most extensively. Still, the exact role of cortisol in these associations remains to be clarified.
Aims/Hypotheses: This study examined whether children who grew up in low socioeconomic status (SES) families or have endured chronic peer victimization had distinct levels of hair cortisol secretion (HCC) at the end of adolescence. Because previous findings have reported both higher and lower cortisol secretion in the context of these adverse environments, we explored the possibility that non-linear, rather than linear, models best depict these complex associations.
Study Population and Methods: A total of 579 17-year-olds provided hair for cortisol measurement. Multiple indicators of SES (e.g., household income, parents’ education) and parental practices (e.g., coercion, affection) were collected on more than 10 occasions, between 5 months and 15 years of age, and were aggregated using confirmatory factor analyses. Information about peer victimization was collected on seven occasions between the ages of 6 and 15 years and summarized into three trajectories of consistently lower, moderate, and higher peer victimization from childhood to adolescence.
Results: The associations of hair cortisol with both SES and peer victimization were best described using non-linear functions. Specifically, girls who grew up in lower SES families secreted higher cortisol levels than those who grew up in moderate SES families, as did girls living in higher SES families. The same patterns of findings were noted for peer victimization, while statistically controlling for familial SES, in addition to various cortisol confounders. Specifically, youth who belonged to either the lower or higher trajectories of peer victimization had higher hair cortisol concentrations, especially when these experiences occurred during childhood (versus adolescence, see Figure 1). Interestingly, parenting practices and the use of proactive strategies to cope with peer victimization moderated these associations. Specifically, the adverse environments were associated with an even greater deviation from the sample’s mean HCC for youth who were also exposed to the most negative parental practices or infrequently used proactive strategies in the face of peer victimization (see Figure 2).
Conclusion: Our findings provide further support for persistent dysregulation of cortisol secretion following early adversity, with expression potentially varying according to the severity of experiences and the children’s environments or individual characteristics.