It is well established that acute stress produces negative effects on high level cognitive functions. However, these effects could be due to the physiological components of the stress response (among which cortisol secretion is prominent), to its psychological concomitants (the thoughts generated by the stressor) or to any combination of those. Our study shows for the first time that the typical cortisol response to stress is sufficient to impair metacognition, that is the ability to monitor one's own performance in a task. In a pharmacological protocol, we administered either 20 mg hydrocortisone or placebo to 46 male participants, and measured their subjective perception of stress, their performance in a perceptual task, and their metacognitive ability. We found that hydrocortisone selectively impaired metacognitive ability, without affecting task performance or creating a subjective state of stress. In other words, the single physiological response of stress produces a net effect on metacognition. These results inform our basic understanding of the physiological bases of metacognition. they are also relevant for applied or clinical research about situations involving stress, anxiety, depression, or simply cortisol use. The negative impact of stress on human higher-order cognition is now well documented in cognitive neuroscience 1. In particular, acute stress alters executive functions engaging the prefrontal cortex 2 , such as decision-making 3-5 , attention 6 , working memory 7-9 , learning 10,11 or cognitive flexibility 12. However, stress may affect cognition via multiple channels, which remain to be disentangled. At the physiological level, it is now well known that stress leads to a cascade of neuromodulator production, all of which impact brain functions, with a fast release of catecholamines (noradrenaline, dopamine, and then adrenaline) and a slower cortisol response very specific to stress 13,14. These endocrine changes prepare the body to "fight or flight", affecting breathing, heart rate, blood pressure, but also reducing prefrontal control, while enhancing amygdala function 2,13. Another channel must be considered though, by which stress affects cognition via psychological factors, associated with how individuals perceive the situation and how they react to it (e.g., rumination 15). Therefore, to evaluate the net effects of the biological components of stress (e.g. cortisol) on cognition, one should separate them from the psychological effects associated with the stress induction paradigm. In this study, we aim at doing so by using a pharmacological approach. Within higher order cognitive functions, we focus on metacognition. This process refers to the ability to assess one's own mental states 16 , for instance by evaluating the confidence that our own decisions are correct. Literature in this field has mainly focused on the cognitive determinants and neural bases of metacognition 17 , pointing to the key role of prefrontal cortex 18,19. Two recent studies suggest that acute stress would impact met...