Optimal hormonal regulation when stressor cues are imperfect

The endocrine system uses information about the environment and the individual's state to regulate circulating concentrations of hormones, and then those hormones, through receptor binding, cause changes in the phenotype. How quickly individuals can up- and down-regulate their hormones can affect baseline and elevated hormone levels and presumably affects how successfully individuals can cope with a varying environment. To respond to environmental change, individuals first need to perceive and process cues about the state of the environment. Individuals may receive imperfect cues about the environment due to perceptual errors, variation in cues, or inexperience with novel stressors. In this paper we use a mathematical model to ask how these imperfect cues should affect how individuals regulate their glucocorticoid concentrations. We find imperfect cues can lead to changes in hormone regulation with individuals generally having higher baseline and lower elevated hormone levels as environmental cues become less reliable. Informational constraints and physiological constraints appear to have generally additive effects, with informational constraints having less of an impact as physiological constraints increase. Our results highlight the different means by which imperfect information can affect hormone regulation. We find that mistakes caused by imperfect cues are commonly responsible for changes in average hormone levels, but imperfect cues also cause individuals to be slower and less certain in their updated estimates of the environmental state, which affects hormone regulation. We also demonstrate the separate effects of false positive and false negative cues and how these are shaped by the relative fitness consequences of baseline and stress-induced hormone levels. Our model shows how given our assumptions imperfect stressor cues should affect endocrine flexibility and regulation, and we hope provides a piece for future conversations and models of endocrine regulation.