Abstract
The biological embedding model (BEM) suggests that fitness costs of maternal loss arise when early-life experience embeds long-term alterations to hypothalamic-pituitary-adrenal (HPA) axis activity. Alternatively, the adaptive calibration model (ACM) regards physiological changes during ontogeny as short-term adaptations. Both models have been tested in humans but rarely in wild, long-lived animals. We assessed whether, as in humans, maternal loss had short- and long-term impacts on orphan wild chimpanzee urinary cortisol levels and diurnal urinary cortisol slopes, both indicative of HPA axis functioning. Immature chimpanzees recently orphaned and/or orphaned early in life had diurnal cortisol slopes reflecting heightened activation of the HPA axis. However, these effects appeared short-term, with no consistent differences between orphan and non-orphan cortisol profiles in mature males, suggesting stronger support for the ACM than the BEM in wild chimpanzees. Compensatory mechanisms, such as adoption, may buffer against certain physiological effects of maternal loss in this species.
Highlights
In mammals, mothers are essential for the early development of their infants since they provide postnatal care (Maestripieri and Mateo, 2009)
We used a series of Bayesian linear mixed models (LMMs) to test our predictions regarding the effect of maternal loss on overall cortisol levels and diurnal slopes
While we found an effect of maternal loss on diurnal cortisol slopes in immature chimpanzees whose mothers died recently, these effects were neither present in individuals who lost their mothers more than 2 years earlier nor in mature male chimpanzees
Summary
Mothers are essential for the early development of their infants since they provide postnatal care (Maestripieri and Mateo, 2009). Exposure to harsh social conditions during childhood, such as those that can result from maternal loss, may lead to repeated and prolonged activation of the HPA axis early in life. These activations provide an adaptive physiological response by mobilizing energy that helps children to cope with the immediate socioecological challenges but may result in long-term HPA axis dysfunction (i.e., either hypo- or hyper-responsiveness to stressor; Miller et al, 2011; Ehrlich et al, 2016; Berens et al, 2017). Assessing the consequences of traumatic early-life events, such as maternal loss, on the functioning of the HPA axis can provide insight into the mechanisms underlying the documented fitness costs of such events
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