Literature DB >> 22986624

Child maltreatment, dating perpetration of physical assault, and cortisol reactivity among disadvantaged female adolescents.

L Oriana Linares1, Patrick E Shrout, Anne Nucci-Sack, Angela Diaz.   

Abstract

OBJECTIVE: Few studies have examined hypothalamic-pituitary-adrenal axis stress reactivity and its relationship to histories of child maltreatment and physical aggression. We examined the relation of a history of childhood sexual abuse (CSA) and perpetration of dating violence to patterns of cortisol change before (resting) and after (reactivity) exposure to a laboratory stressor.
METHODS: In a sample of 40 disadvantaged sexually active female adolescent patients (ages 14-17 years), we collected self-reports of lifetime child maltreatment (5 types) and past-year female perpetration of physical assault (PA) acts toward a romantic partner. We assessed changes in salivary cortisol trajectories during resting and reactivity phases following the viewing of a teen dating violence vignette.
RESULTS: Reports of CSA (CSA+ group) were associated with reports of perpetration of severe dating PA (PA+ group), but the relation of these reports to laboratory-assessed patterns of cortisol changes following the stressor was opposite. As compared with subjects without victimization or perpetration histories (referent group), the CSA+ group showed the most pronounced positive slope (reactivity), whereas the PA+ group showed the least positive slope following the laboratory stressor after the overlap between these groups was statistically adjusted. While showing less reactivity to the laboratory stressor, the PA+ group had higher levels of resting cortisol, which stayed high during reactivity as compared to the referent group.
CONCLUSION: The laboratory paradigm to elicit neuroendocrine stress-related cortisol reactivity appears to be a promising tool for identifying altered cortisol physiology among female adolescents with mixed histories of CSA and perpetration of dating PA.
Copyright © 2012 S. Karger AG, Basel.

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Year:  2012        PMID: 22986624     DOI: 10.1159/000342958

Source DB:  PubMed          Journal:  Neuroendocrinology        ISSN: 0028-3835            Impact factor:   4.914


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