The HPA and SAM axis mediate the impairment of creativity under stress.

With the ever-changing social environment, individual creativity is facing a severe challenge induced by stress. However, little is known regarding the underlying mechanisms by which acute stress affects creative cognitive processing. The current research explored the impacts of the neuroendocrine response on creativity under stress and its underlying cognitive flexibility mechanisms. The enzyme-linked immuno sorbent assay was employed to assess salivary cortisol, which acted as a marker of stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis. Eye blink rate (EBR) and pupil diameter were measured as respective indicators of dopamine and noradrenaline released by the activation of the sympathetic-adrenal-medullary (SAM) axis. The Wisconsin card task (WCST) measured cognitive flexibility, while the alternative uses task (AUT) and the remote association task (RAT) measured separately divergent and convergent thinking in creativity. Results showed higher cortisol increments following acute stress induction in the stress group than control group. Ocular results showed that the stress manipulation significantly increased EBR and pupil diameter compared to controls, reflecting increased SAM activity. Further analysis revealed that stress-released cortisol impaired the originality component of the AUT, reducing cognitive flexibility as measured by perseverative errors on the WCST task. Serial mediation analyses showed that both EBR and pupil diameter were also associated with increased perseverative errors leading to poor originality on the AUT. These findings confirm that physiological arousal under stress can impair divergent thinking through the regulation of different neuroendocrine pathways, in which the deterioration of flexible switching plays an important mediating role.