Article

Markers of inflammation in midlife women with intimate partner violence histories.

Department of Psychological and Brain Sciences, University of Louisville, Kentucky 40292, USA.
Journal of Women's Health (Impact Factor: 1.9). 11/2011; 20(12):1871-80. DOI: 10.1089/jwh.2011.2788
Source: PubMed

ABSTRACT Lifetime occurrence of intimate partner violence (IPV) in women has been associated with increased prevalence of aging-related chronic diseases, including those with a pathophysiology involving inflammation. To begin to identify potential biologic mediators of this relationship, this cross-sectional study examined associations between past IPV and circulating levels of C-reactive protein (CRP) and interleukin-6 (IL-6)-measures linked with emergence of aging-related diseases-along with in vitro IL-6 production by peripheral blood mononuclear cells (PBMC) stimulated with either phytohemagglutinin A (PHA) or lipopolysaccharide (LPS).
Apparently healthy, midlife women with divorce histories were recruited from the community. Histories of intimate partner psychological aggression, physical assault, sexual coercion, and stalking were assessed, along with current depression, posttraumatic stress symptoms, and health-related characteristics. At two visits, blood was drawn for assessment of biologic measures; measures were averaged across visits.
In this sample (n=68), a history of being stalked was significantly positively correlated with CRP levels; in a multiple regression analysis that included body mass index (BMI) and current symptoms, this association was attenuated by adjusting for BMI. Physical assault history was significantly negatively correlated with PHA-stimulated IL-6 production. This was most apparent for severe assault and was not accounted for by BMI or symptoms.
IPV histories remitted for an average of 10 years were associated with biologic mediators of inflammation. The profile was not uniformly proinflammatory, suggesting that in situations of traumatic or chronic stress, different aspects of the inflammatory response are differentially regulated and subjected to diverse compensatory mechanisms.

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