Towards an Evolutionary Theory of Stress Responses

Extensive experimental and comparative studies provide a solid understanding of the physiological basis stress response system its variation across within species. However, lagging behind this is formal theoretical framework to help unify wealth existing verbal hypotheses linking mechanisms fitness, explain how such has evolved. We propose an evo-mecho approach, combining optimality models evolutionary simulations with empirical evidence about underlying physiology, show mechanistic constraints predictability environmental risks shape response. A deeper evolution will require mechanistically informed models, phylogenetically controlled analyses, studies. All organisms have cope threats, yet precise form varies hugely individuals, populations, While are increasingly understood, responses evolved remains elusive. Here, we that important insights can be gained from incorporate analysis (the ‘evo-mecho’ approach). Our approach reveals as key factors shaping evolution, generating testable predictions species contexts. call for integrated research programme theory, advance scientific core evolutionary–developmental model explaining development individual differences in responsiveness life stages, through plastic adjustments particular environments. extension CORT-fitness hypothesis including reproduction challenge. stating baseline GC levels reflect exposure challenges and, therefore, individuals or populations high GCs lower fitness than those GCs. stress-induced hormone mediate life-history tradeoff between protective damaging effects GCs, higher positively correlated survival but negatively reproduction. produced by rodents, birds, reptiles, amphibians. most mammals (except rodents) fish. integrates knowledge psychological, physiological, molecular mechanisms. computer program simulating population specified genetic traits change generations due predefined processes mutation selection. explore dynamics adapt new conditions natural steroid hormones vertebrates, cortisol corticosterone, secreted naturally adrenal gland (see ‘HPA axis’) interrenal ‘HPI axis’); generally regulation glucose metabolism energy balance. endocrine axis comprising sequential involvement hypothalamic corticotropin-releasing (CRH), pituitary adrenocorticotropic (ACTH), released mammals, reptiles. fish amphibians homologous mammalian/avian HPA system, which excreted structures kidneys (interrenal). artificially selects trait, typically observe changes other, genetically traits. numerical optimisation technique used find best (i.e., fitness-maximising) decision strategy iterative calculation runs backwards sequence points, evaluating available options (e.g., possible levels) each state time interval since last predatory attack) terms expected future reproductive success at next point. process whereby organism reacts stressors, detection stressor circulating elevated external (such presence predator); also termed ‘stress-induced hormone’ ‘stress-associated [62.MacDougall-Shackleton S.A. et al.Glucocorticoids “stress” not synonymous.Integr. Org. Biol. 2019; 1: 1-8Google Scholar]. other products genes mediating responses. activation coordinated neurophysiological brain periphery demands stressors. three features characterise response: level molecules before appears; peak (maximum) reached period after detected; decay phase, when molecule return baseline. stimulus feature environment creates demanding threatening situation organism. part autonomic nervous responsible fast, unconscious stressors elicit fight-flight-or-freeze reactions. association some parameter, stressor. Positive temporal autocorrelation (our focus here) implies stressful events occur clusters overdispersed), rather randomly spaced intervals.