Meeting Abstract
Because glucocorticoids can be measured in a variety of tissues, as well as feces and urine, using commercially available assays, the measure and manipulation of these hormones has become a widespread tool in field and laboratory studies of stress biology. Unfortunately, with the increased study of cortisol and corticosterone (CORT) there has been an apparent increase in the false equating of CORT with stress. First, many authors refer to CORT as a “stress hormone”. It is not. If anything it is an anti-stress hormone. Glucocorticoids are metabolic hormones with numerous target tissues and effects, and the elevation of CORT in response to a stressor is only one component of a complex stress response. Referring to CORT as a stress hormone diminishes the multifaceted effects of CORT and downplays the other components of the stress response. Second, many authors equate CORT administration with applying a stressor. Activation of the HPA axis and increases in plasma CORT are just a small component of the stress response. For this reason, the stress response and CORT administration are not synonymous and misuse of these terms results in problems in both hypotheses and predictions, and maybe more importantly, interpretation of results. In this presentation we present bibliometric data on this issue, as well as specific examples of how the effects of CORT administration can differ from manipulation of stressors. We recommend an increased distinction between stress and CORT in the literature and during presentations. Rather than a minor point of semantics, this distinction is important both for how we design studies and how we interpret their results.
