I'm curious whether there's a consensus as to whether chronic stress can damage the hypothalamic-pituitary-adrenal axis, diminishing the efficacy of negative feedback and leading to further damage, including hippocampal atrophy. This position was argued by Robert Sapolsky: Is there convincing evidence that it is correct? Thanks!
Hi,
Interesting question!
To follow up on Petra's answer, I think that neuron dendritic atrophy is reversible. For example in rodents, hippocampal neurons can grow back within a few days only after chronic exposure to stress has stopped (would need to look a bit deeper into my files for the actual references, let me know if you need them).
As a field evolutionary ecologist, I have seen some studies in animals (excluding mice) that may relate to the concept of chronic stress. However, the particular component of the HPA axis affected by the 'chronic stress' differs from one system to the next.
- work on the so called 'Dasyrurid syndrome' by various authors
- Rudy Boonstra's work on the adaptive stress reactivity in sciurids.
- Norbert Sachser's work in guinea pigs
- Micheal Sheriff's work on how intense and sustained predation stress can lead to population decline through an increase in cortisol profile.
Laboratory studies can indeed induce pathology, but I am not aware of any study in free ranging animals where Sapolski's hypothesis (chronic stress leads to pathological symptoms and 'castrates' subordinate individuals) has been verified. A related issue is perhaps that chronic stress as a concept, is not so useful when one is primarily interested in free ranging/wild animals. My opinion is that stress reactivity should be analysed from a life history perspective even in humans and mice. For example a lot of the stress reactivity profile of an individual is programmed through maternal effects and there is evidence that such a programmation is increasing the 'fit' between an organism's stress reactivity and the predictability of the environment. This could lead us to see pathologies as a mismatch between such a programming and the environment experienced.
I hope it helps, if it is too far from your interests I apologize!
Best.
Here are few articles related to the topic, although they relate primarily to child maltreatment/abuse. You may be interested in the review, as it discusses varying outcomes re: hippocampal atrophy...but I think his assertion is accepted overall.
Compas, B. (2006). Psychobiological processes of stress and coping: Implications for resilience in children and adolescents--comments on the papers of Romeo & McEwen and Fisher et al. Annals of the New York Academy of Sciences, 1094, 226-234.
McCrory, E., DeBrito, S., & Viding, E. (2010). Research review: The neurobiology and genetics of maltreatment and adversity. Journal of Child Psychology and Psychiatry, 51(10), 1079-1095.
Shea, A., Walsh, C., MacMillan, H., & Steiner. (2004). Child maltreatment and HPA axis dysregulation: The relationship to major depressive disorder and post traumatic stress disorder in females. Psychoneuroendocrinology, 30, 162-178.
My question was motivated by an interest in child abuse and child adversity, so these are quite appropriate. Thanks!
Hi,
Interesting question!
To follow up on Petra's answer, I think that neuron dendritic atrophy is reversible. For example in rodents, hippocampal neurons can grow back within a few days only after chronic exposure to stress has stopped (would need to look a bit deeper into my files for the actual references, let me know if you need them).
As a field evolutionary ecologist, I have seen some studies in animals (excluding mice) that may relate to the concept of chronic stress. However, the particular component of the HPA axis affected by the 'chronic stress' differs from one system to the next.
- work on the so called 'Dasyrurid syndrome' by various authors
- Rudy Boonstra's work on the adaptive stress reactivity in sciurids.
- Norbert Sachser's work in guinea pigs
- Micheal Sheriff's work on how intense and sustained predation stress can lead to population decline through an increase in cortisol profile.
Laboratory studies can indeed induce pathology, but I am not aware of any study in free ranging animals where Sapolski's hypothesis (chronic stress leads to pathological symptoms and 'castrates' subordinate individuals) has been verified. A related issue is perhaps that chronic stress as a concept, is not so useful when one is primarily interested in free ranging/wild animals. My opinion is that stress reactivity should be analysed from a life history perspective even in humans and mice. For example a lot of the stress reactivity profile of an individual is programmed through maternal effects and there is evidence that such a programmation is increasing the 'fit' between an organism's stress reactivity and the predictability of the environment. This could lead us to see pathologies as a mismatch between such a programming and the environment experienced.
I hope it helps, if it is too far from your interests I apologize!
Best.
Bradley, I'm glad the articles I included were relevant to your interest! Further exploring the literature, I've found articles that discuss the reversal mentioned by Pierre-Olivier...but only in adults. Apparently, children who are exposed to chronic stress (and definitions vary) do not show the same pathological reversal that is seen in adults.
If you are interested in additional articles/citations, please let me know...
CJ, I would be interested. My review article on the neurobiological effects of child abuse has been submitted to a journal, but I'm sure it'll have to be revised! Thanks!
Hi Bradley,
Interesting, and relevant, indeed.
We have just completed an extensive review on the "Neuropathology of Stress" for Acta Neuropathologica in which we, together with several experts from different disciplines, update this older hypothesis.
In short; there is very little evidence for actual (neuropathological) damage after stress at adult ages, although functional deficits and subtle structural alterations, e.g. at spine or dendritic level are there for sure, some of which may be long lasting, but many are reversible after appropriate recovery periods or after blockers of the stress system.
When exposed to stress at an early or adolescent ages, these effects are often much more pronounced and longer lasting, and depend on the genetic background. See our other papers on this topic in CurDrugTarget, AmJPathol, Neuropharm, etc. I can send you pdfs if you need and the Acta NP paper when it becomes available later this year.
kind regards,
Paul
Paul, the Acta paper would be great, and if you could send a recent published review too, that'd be great. I've submitted a paper already, but I suspect it will need revision. THANK YOU.
I would have thought there was sufficient evidence of extreme stress leading to damage (alteration) of the HPA axis, to be able to assume a consensus. It is after all the core biology of posttraumatic stress disorder. The problem is that with the other associated neurochemicals involved in the response to stress the widespread involvement of bodily systems is in sufficiently considered.
In free range/wild animals for instance chronic stress is much less common than extreme acute stress. Here, as with humans, an intensely shocking experience (Chase or capture with animals and birds) can lead to sudden cardiac death resulting from an overdose of catecholamines, thus closely associated with an altered HPA. For references see’ Scared to death’ (Zoobiquity by Natterson- Horowitz and Bowers, Published by Alfred A. Knoff. 2012).
As Pierre-Olivier Montigilo and Paul Lucassens’ letters suggest. sctual damage, hippocampal atrophy, as a result of stress may still be in doubt.
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