Endogenous cortisol predicts decreased loss aversion in young men.

Human and nonhuman animals respond asymmetrically to predicted punishments and rewards (Dayan & Seymour, 2008; Kahneman, 2011). In human decision making, for example, people pay more to avoid losses than to gain equivalent rewards. Because such loss aversion counterproductively diminishes an individual’s expected payoffs, it has become one of the most studied choice biases. It is unclear whether biological markers of punishment or stress exposure—most notably the glucocorticoid stress hormone cortisol of the hypothalamicpituitary-adrenal (HPA) axis—predict this particular form of behavioral punishment sensitivity. Acute glucocorticoid administration desensitizes subjects to threat and punishment, whereas chronic administration sensitizes them, increasing anxiety (Aerni et al., 2004; de Quervain & Margraf, 2008; Schelling et al., 2006; Soravia et al., 2006). This mirrors the mainstream view that acute stress responses are adaptive, whereas chronic exposure is detrimental (Chrousos, 2009). There is evidence that HPA-axis traits specifically undermine decision making. HPA disturbances predict addictive behavior (Koob & Kreek, 2007; Marinelli & Piazza, 2002; Putman, Antypa, Crysovergi, & van der Does, 2010; Sinha, 2008), and the relation between longterm HPA activity and pathological gambling (Wohl, Matheson, Young, & Anisman, 2008) may reflect altered punishment sensitivity. In nonclinical populations, the threat of financial loss (i.e., imminent poverty) chronically elevates cortisol (Haushofer, de Laat, & Chemin, 2012). Yet it is unknown whether chronically elevated cortisol, in turn, alters exposure to new losses by altering decision making. Such a feedback cycle might be adaptive (negative feedback) or maladaptive (positive feedback), depending on whether it limits or exacerbates financial loss. In the present study, we sidestepped the issue of causation and simply assessed whether an individual’s maladaptive loss aversion increased with chronic exposure to endogenous cortisol, which we assayed using hair samples.