SAFETYLIT WEEKLY UPDATE

We compile citations and summaries of about 400 new articles every week.
RSS Feed

HELP: Tutorials | FAQ
CONTACT US: Contact info

Search Results

Journal Article

Citation

Fanning JR, Lee R, Gozal D, Coussons-Read M, Coccaro EF. Biol. Psychol. 2015; 112: 56-65.

Affiliation

Clinical Neuroscience Research Unit, Department of Psychiatry and Behavioral Neuroscience, Pritzker School of Medicine, University of Chicago, Chicago, IL, USA. Electronic address: ecoccaro@bsd.uchicago.edu.

Copyright

(Copyright © 2015, Elsevier Publishing)

DOI

10.1016/j.biopsycho.2015.09.003

PMID

26423894

Abstract

Recent studies suggest that early life trauma is associated with elevations in circulating markers of inflammation in human subjects. History of aggression as a behavior, or aggression as a personality trait, is also associated with elevations of these inflammatory markers. Since early life trauma is associated with the development and maintenance of aggression in later life we examined the relationship of early life adversity, plasma inflammation markers (IL-6 and CRP) and oxidative stress markers (8-OH-DG and 8-ISO), and aggression in adult subjects with (n=79) and without (n=55) personality disorder. We used a series of mediated and moderated path models to test whether the effects of early adversity on later aggression may be mediated through markers of inflammation. Childhood abuse and parental control were associated with basal IL-6 and CRP concentrations. Path modeling suggested that childhood abuse was associated with aggression indirectly through CRP while parental control influenced aggression indirectly through IL-6 and CRP. Furthermore, these effects were independent of the effect of current depression. The results suggest that disruption of inflammatory processes represent one pathway by which early adversity influences aggression.


Language: en

NEW SEARCH


All SafetyLit records are available for automatic download to Zotero & Mendeley
Print