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Stress and Body Shape: Stress-Induced Cortisol Secretion Is Consistently Greater Among Women With Central Fat

Epel, Elissa S. PhD; McEwen, Bruce PhD; Seeman, Teresa PhD; Matthews, Karen PhD; Castellazzo, Grace RN, BSN; Brownell, Kelly D. PhD; Bell, Jennifer BA; Ickovics, Jeannette R. PhD

Original Articles

Objective Excessive central fat puts one at greater risk of disease. In animal studies, stress-induced cortisol secretion has been shown to increase central fat. The objective of this study was to assess whether women with central fat distribution (as indicated by a high waist-to-hip ratio [WHR]), across a range of body mass indexes, display consistently heightened cortisol reactivity to repeated laboratory stressors.

Methods Fifty nine healthy premenopausal women, 30 with a high WHR and 29 with a low WHR, were exposed to consecutive laboratory sessions over 4 days (three stress sessions and one rest session). During these sessions, cortisol and psychological responses were assessed.

Results Women with a high WHR evaluated the laboratory challenges as more threatening, performed more poorly on them, and reported more chronic stress. These women secreted significantly more cortisol during the first stress session than women with a low WHR. Furthermore, lean women with a high WHR lacked habituation to stress in that they continued to secrete significantly more cortisol in response to now familiar challenges (days 2 and 3) than lean women with a low WHR.

Conclusions Central fat distribution is related to greater psychological vulnerability to stress and cortisol reactivity. This may be especially true among lean women, who did not habituate to repeated stress. The current cross-sectional findings support the hypothesis that stress-induced cortisol secretion may contribute to central fat and demonstrate a link between psychological stress and risk for disease.

From the Health Psychology Program, University of California, San Francisco (E.S.E.), San Francisco, CA; Rockefeller University (B.M.), New York, NY; University of California, Los Angeles (T.S.), Los Angeles, CA; University of Pittsburgh (K.M.), Pittsburgh, PA; and Yale University (G.C., K.D.B., J.B., J.R.I.), New Haven, CT.

Received for publication August 13, 1999;

revision received February 15, 2000.

Address reprint requests to: Elissa Epel, PhD, Health Psychology Program, University of California, San Francisco, 3333 California St., Suite 465, San Francisco, CA 94143-0848.

Copyright © 2000 by American Psychosomatic Society
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