To determine if inducing self-blame would lead to increases in shame and guilt as well as increases in proinflammatory cytokine activity and cortisol. Based on previous research and theory, it was hypothesized that induced shame would be specifically associated with elevations in proinflammatory cytokine activity.
Healthy participants were randomly assigned to write about traumatic experiences in which they blamed themselves (N = 31) or neutral experiences (N = 18) during three 20-minute experimental laboratory sessions over 1 week. Tumor necrosis factor-α receptor levels (sTNFαRII), an indicator of proinflammatory cytokine activity, β2-microglobulin, cortisol (all obtained from oral fluids), and emotion were assessed prewriting and postwriting.
Participants in the self-blame condition showed an increase in shame and guilt as well as an increase in sTNFαRII activity when compared with those in the control condition. Cortisol and β2-microglobulin levels were unaffected by the procedures. Those individuals in the self-blame condition reporting the greatest increases in shame in response to the task showed the greatest elevations in proinflammatory cytokine activity, while levels of guilt and general negative emotion were unrelated to cytokine changes.
These data suggest that inducing self-related emotions can cause changes in inflammatory products, and that shame may have specific immunological correlates.
Department of Psychology (S.S.D., M.E.K., K.H.K.), Cousins Center for Psychoneuroimmunology (S.S.D., M.E.K. J.L.F.), Department of Psychiatry and Biobehavioral Sciences (M.E.K.), Center for Interdisciplinary Research in Immunology and Disease (N.A., J.L.F.), and Department of Microbiology and Immunology (J.L.F.), University of California, Los Angeles, CA. M.E.K. is now at the Department of Psychiatry/Health Psychology program, University of California, San Francisco. K.H.K. is now at the Department of Psychology in Education, University of Pittsburgh.
Address correspondence and reprint requests to Sally S. Dickerson, MA, Department of Psychology, University of California, Los Angeles, CA 90095. E-mail: firstname.lastname@example.org or email@example.com
Received for publication August 19, 2002; revision received May 12, 2003.
Preparation of this article was supported in part by a National Science Foundation Graduate Fellowship (S.S.D), a NIMH Health Psychology Training Grant Fellowship (S.S.D), a Research Scientist Development Award MH00820 (M.E.K.), the Cousins Center for Psychoneuroimmunology at the University of California, Los Angeles and the UCLA Psychology Department 251 Fund. We thank Mette Fryland, Mena Gorre, and Pablo Villanueza for their laboratory assistance, and Tara Gruenewald, James Pennebaker, and Shelley Taylor for their helpful comments on a previous draft of this article.