The biological effects of acute psychosocial stress on delay discounting Kenta Kimura a, * , Shuhei Izawa b , Nagisa Sugaya c , Namiko Ogawa d , Kosuke C. Yamada e , Kentaro Shirotsuki f , Ikuyo Mikami g , Kanako Hirata d , Yuichiro Nagano g , Toshikazu Hasegawa h a Center for Applied Psychological Science (CAPS), Kwansei Gakuin University, Hyogo, Japan b Health Administration and Psychosocial Factor Research Group, National Institute of Occupational Safety and Health, Japan, Kanagawa, Japan c Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan d Graduate School of Human Sciences, Waseda University, Saitama, Japan e National Institute of Advanced Industrial Science and Technology, Tokyo, Japan f Faculty of Human Relations, Tokai Gakuin University, Gifu, Japan g Faculty of Human Studies, Bunkyo Gakuin University, Saitama, Japan h Department of Cognitive and Behavioral Sciences, The University of Tokyo, Tokyo, Japan Received 21 November 2012; received in revised form 25 March 2013; accepted 29 April 2013 Psychoneuroendocrinology (2013) 38, 2300—2308 KEYWORDS Delay discounting; Inter-temporal choice; C-reactive protein; Cortisol; HPA axis; TSST; Impulsivity Summary Organisms prefer to receive rewards sooner rather than later because they exces- sively discount the subjective value of future rewards, a phenomenon called delay discounting. Recent studies have reported an association between cortisol–—which is secreted by the hypo- thalamic—pituitary—adrenal (HPA) axis–—and delay discounting. However, no study has examined whether acutely induced psychosocial stress modulates delay discounting. Thus, the present study examined the effect of acute psychosocial stress and its hormonal and inflammatory correlates on the rate of delay discounting. To accomplish this purpose, we assessed the participants’ discounting rates using the questionnaire version with inter-temporal choice before and after an acute psychosocial stress task (the Trier Social Stress Test; TSST). The results demonstrated that TSST increased rates of delay discounting in only cortisol responders (not in non-responders), indicating the possible influence of the pathway from the HPA axis to the dopaminergic systems under acute stress. Furthermore, the findings of correlation analysis indicated a U-shaped relationship between baseline level of C-reactive protein and delay discounting rate, suggesting a complex relationship between inflammatory markers and delay discounting rate. # 2013 Elsevier Ltd. All rights reserved. * Corresponding author at: Center for Applied Psychological Science, Kwansei Gakuin University, 1-155 Uegahara-1bancho, Nishinomiya, Hyogo, 662-8501, Japan. Tel.: +81 798 54 6925; fax: +81 798 51 0984. E-mail address: kkimura@kwansei.ac.jp (K. Kimura). Available online at www.sciencedirect.com jou rn a l home pag e : ww w. el sev ier. com/ loca te /psyn eu en 0306-4530/$ — see front matter # 2013 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.psyneuen.2013.04.019