The objectives of this study were to assess whether socioeconomic status (SES) is associated with dysregulation of the cortisol diurnal rhythm and whether this association is independent of race and occurs equally in whites and blacks; and to determine if an association between SES and cortisol can be explained (is mediated) by behavioral, social, and emotional differences across the SES gradient.
Seven hundred eighty-one subjects from a multisite sample representing both whites and blacks provided six saliva cortisol samples over the course of the day: at awakening, 45 minutes, 2.5 hours, 8 hours, and 12 hours after awakening, and at bedtime.
Both lower SES (education and income) and being black were associated with higher evening levels of cortisol. These relationships were independent of one another and SES associations with cortisol were similar across racial categories. The evidence was consistent with poorer health practices (primarily smoking), higher levels of depressive symptoms, poorer social networks and supports, and feelings of helplessness (low mastery) mediating the link between SES and cortisol. However, we found no evidence for psychosocial or behavioral mediation of the association between race and cortisol response.
Lower SES was associated in a graded fashion with flatter diurnal rhythms as a result of less of a decline during the evening. This association occurred independent of race and the data were consistent with mediation by health practices, emotional and social factors. Blacks also showed a flatter rhythm at the end of the day. This association was independent of SES and could not be explained by behavioral, social, or emotional mediators.
CARDIA = Coronary Artery Risk Development in Young Adults Study; SES = socioeconomic status; HPA = hypothalamic–pituitary adrenocortical; BMI = body mass index; AUC = area under the curve; CES-D = Center for Epidemiologic Studies Depression scale; MIDUS = Midlife in the U.S. Survey; PAH = Physical Activities History questionnaire.
From the Department of Psychology (S.C.), Carnegie Mellon University, Pittsburgh, PA; the State University of New York at Stony Brook (J.E.S.), Stony Brook, NY; the University of California at San Francisco (E.E.), San Francisco, CA; the Technical University of Dresden, Dresden, Germany (C.K.); Kaiser Permanente, Oakland, CA (S.S.); and UCLA School of Medicine (T.S.), Los Angeles, CA.
Address correspondence and reprint requests to Sheldon Cohen, PhD, Department of Psychology, Carnegie Mellon University, Pittsburgh, PA 15213. E-mail: firstname.lastname@example.org
Received for publication March 15, 2005; revision received July 19, 2005.
Work on this manuscript was supported (or partially supported) by contracts University of Alabama at Birmingham, Coordinating Center, N01-HC-95095 University of Alabama at Birmingham, Field Center, N01-HC-48047 University of Minnesota, Field Center, N01-HC-48048 Northwestern University, Field Center, N01-HC-48049 Kaiser Foundation Research Institute, N01-HC-48050 University of California, Irvine, Echocardiography Reading Center, N01-HC-45134 Harbor-UCLA Research Education Institute, and Computed Tomography Reading Center, N01-HC-05187 from the National Heart, Lung and Blood Institute and by the MacArthur Research Network on SES and Health through grants from the John D. and Catherine T. MacArthur Foundation. Preparation of the manuscript was also facilitated by the Pittsburgh Mind–Body Center (HL65111 & HL65112).