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Developmental biology - Stress Hormones|
Maternal stress creates high stress in baby
Remarkably, the effects of prenatal stress hormones on offspring were consistent across species, regardless of brain or body size. There were also no differences considering sex of offspring, age at time of assessment, timing of stress exposure prenatally, or stress severity.
An animal's stress response tends to be activated by external factors, such as when its see a predator, or whether food is or isn't availabile. One of the studies included in the meta-analysis looked at how maternal stress hormones in pregnant snow hares changed in response to the abundance of their natural predators — lynxes, over a 10-year cycle. The team found that in years where there were more lynxes, snow hare offspring had more stress hormones and anti-predator behaviors.
Higher stress hormone levels among offspring may help extend survival, but also come at a cost that can affect other systems, such as sexual reproduction. In humans, the mere anticipation of stress or just thinking about prior experiences of discrimination, or trauma, can activate a stress response. Overactive stress hormones can lead to chronic health problems in humans, including anxiety, depression and cardiovascular disease.
"Our stress response is meant to be adaptive to acute stress, such as being chased by predators. However, humans' stress response is often triggered by social evaluation threats and is not serving the adaptive purpose for which it was designed."
Prenatal exposure to maternal stress is commonly associated with variation in Hypothalamic Pituitary Adrenal (HPA)-axis functioning in offspring. However, the strength or consistency of this response has never been empirically evaluated across vertebrate species. Here we meta-analyzed 114 results from 39 studies across 14 vertebrate species using Bayesian phylogenetic mixed-effects models. We found a positive overall effect of prenatal stress on offspring glucocorticoids (d’ = 0.43) though the 95% Highest Posterior Density Interval overlapped with 0 (-0.16–0.95). Metaregressions of potential moderators highlighted that phylogeny and life history variables predicted relatively little variation in effect size. Experimental studies (d’ = 0.64) produced stronger effects than observational ones (d’ = -0.01), while prenatal stress affected glucocorticoid recovery following offspring stress exposure more strongly (d’ = 0.75) than baseline levels (d’ = 0.48) or glucocorticoid peak response (d’ = 0.36). These findings are consistent with the argument that HPA-axis sensitivity to prenatal stress is evolutionarily ancient and occurs regardless of a species’ overall life history strategy. These effects may therefore be especially important for mediating intra-specific life-history variation. In addition, these findings suggest that animal models of prenatal HPA-axis programming may be appropriate for studying similar effects in humans.
Authors: Zaneta M. Thayer, Meredith A. Wilson, Andrew W. Kim and Adrian V. Jaeggi
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This graph represents the HPA-axis hormone system that mobilizes animal stress responses.
High maternal stress was found to produce high stress levels after birth in each species.
Image credit: Adrian V. Jaeggi