Impact of parental depression or cancer on offspring's cortisol levels

Vertebrates respond to the perception of potentially noxious stimuli by activating the adrenocortical response to stress, which results in increased levels of circulating glucocorticoid (GC) “stress hormones.” In birds, elevated blood corticosterone (the predominant avian GC) promotes adaptive physiological and behavioral changes aimed at coping with stress, redirecting the individual into a survival mode while suppressing nonessential activities. However, high and prolonged elevations like those occurring during chronic adverse conditions exert deleterious effects on critical body systems, while low levels of blood corticosterone are fundamental for basic physiological processes regardless of exposure to stressors. The fact that the same hormone exerts opposing (“good and bad”) actions depending on its level, its major role in the regulation of body energy balance, and the ambiguity of the term “stress” has promoted the recent development of novel conceptual frameworks such as the Allostasis Model and the Reactive Scope Model. These are aimed at integrating the energy requirements of birds across their lifecycles with the adrenocortical responses, and also at explaining the role of corticosterone in “allostasis” (a term proposed to replace the word “stress”): the maintenance of homeostasis through change. These models will be explained in a first section of this chapter, providing an updated review of the nomenclature describing corticosterone levels and actions. Avian behavioral and neuroendocrine responses are dramatically different when facing predictable versus unpredictable environmental change (also called perturbations or “stressors”). Why, when, and how environmental conditions promote an activation of the hypothalamus–pituitary–adrenal axis will be addressed in a second section, with a classification of the types of perturbations and the resulting effects of corticosterone levels on the normal progression of individuals' lifecycles. Short-term elevations of corticosterone levels activate a facultative “emergency life history stage,” but longer-term exposure disrupt lifecycles, potentially leading to individuals death and population extinction. The avian adrenocortical response shows all the features of a trait subjected to natural selection (high individual variation, repeatability, and a genetic basis), but individuals also display a strong phenotypic plasticity. Several examples of the adaptive variability in the adrenocortical response will be provided in a third section. For example, avian developmental modes range across a spectrum of altricial and precocial species, and the adrenocortical response at hatching and during growth increases across this gradient. This pattern has likely evolved to balance the costs and benefits of corticosterone actions with the ability of young birds to cope with perturbations without parental support. Corticosterone can be also transferred from mothers to offspring (“maternal effects”), potentially translating ecological and environmental conditions into permanent offspring responses, and resulting in phenotypes better adapted to cope with perturbations through “maternal programming.” Adult birds of many avian species have been shown to modulate their adrenocortical response during reproduction and according to the value of their brood. Such findings suggest that modulation of corticosterone secretion allows to trade-off of energy and resources between current reproductive investment and survival, providing a proximate (corticosterone-mediated) mechanism for life history evolution. Many of these findings and hypotheses result from field research conducted on wild avian species, which imposes important challenges compared to laboratory studies that will be addressed in the last section. This section concludes with a description of common methodological tools for assessing adrenocortical function in wild birds, including examples of information that such tools can produce.