Cook–Medley Hostility Scale

ted whether greater hostility contributes to greater inflammation by promoting higher Th1 activity, lower and Th2 cytokine production in vitro. Participants were 193 healthy men and women (mean age 37.3; 44 % non-white). Hostility was assessed with a 20-item version of the Cook–Medley Hostility Scale disease risk. Examples include poor health behaviors (Everson-Rose et al., 2006), excessive cardiovascular activity in response to stress (Suls and Wan, 1993), and dysregulated beta-adrenergic receptor function (Hughes et al., 2003). While each presents a pathway by which psychological factors might be translated into physiologic effects, these processes in and of themselves may not be sufficient to link hostility with some pathologic outcomes. ing hostility and disease. However, the extant literature does not inform as to which components of the immune system hostility influences to promote a persistent proinflammatory state. Immune-mediated inflammation is dependent upon the coun-ter-regulatory activities of two subpopulations of helper T lympho-cytes, Th1 and Th2. Whether T lymphocytes are categorized as belonging to one subpopulation or the other is determined by which cytokines are released subsequent to activation (Elenkov and Chrousos, 1999). Th1 cytokines are those that express proin-flammatory properties, whereas Th2 cytokines are those expressing anti-inflammatory properties. A disproportionate amount of eithe