Hello Ian,

Part of the answer is that Cortisol fries neurons, particularly those that measure serum cortisol levels, and thus the feedback loop for this glucocorticoid becomes damaged:

http://psycnet.apa.org/record/2001-11162-007

here is a possible Tx:

Low-dose cortisol for symptoms of posttraumatic stress disorder

A Aerni, R Traber, C Hock… - American Journal of …, 2004 - Am Psychiatric Assoc

And lastly, Adrenal Fatigue has been connected to PTSD. From the seminal work of Hans Selye, organs shut down in respinse to chronic stress. Link:

https://www.synapse.koreamed.org/search.php?where=aview&id=10.5124/jkma.2011.54.1.81&code=0119JKMA&vmode=FULL

Even if there is a lack of scientific dimostration of these words of Sigmund Freud, they seems to me very intriguing , thinking about your question:

"It will be seen, then, that preparedness for anxiety and the hypercathexis of the reception systems constitute the last line of defence of the shield against stimuli. In the case of quite a number of traumas, the difference between systems that are unprepared and systems that are well prepared through beyond hypercathected may be a decisive factor in determining the outcome..." ( Ref. Freud, S. (1920) : Beyond the Pleasure Principle. The Standard Edition Vol. XVIII ( 1920-1922) pp 31-32.

It would seem, in some sense, that anxiety response, with her biological correlates would prepare the mind to the stress impact. The chronic stress would impair the adrenal function as Allen Christopher Ernst reminds us, imparings the neurons that mesure cortisol levels and the feedback control of a typical biological correlate of the anxiety response, and a correlation between PTSD and chronic stress has been found. A similar meaning can have the connection between "adrenal fatigue" and PTSD of the Hans Selye work.

The occurence of PTSD in the case the mind is not prepared, even about not by anxiety, is would be more frequent, as a experiment, cited by Boris Cyrulnik would suggest: it has been told to a group of soldiers before a combat to choose to write a letter to someone meaningful for them, i.e. the girlfriend, a parent, or a friend etc. or not to write it. It has been found that the soldiers who wrote the letter had a minor occurrence of PTSD symptoms. I recognize the possible bias of the experiment but in any case I find it very suggestive regarding both freudian vision both more modern vision of the function of mentalization in the trauma ( Fonagy). In the work cited, ( p. 32) Freud says that "trauma dreams" dont have an allucinatory accomplishment of a wish purpose, but they have the function of repeting the trauma( with his anxiety response ) and, in a modern vision, to elaborate it.

Allen Christopher Ernst I'm familiar with the negative feedback regulation of the HPA axis, but this feedback mechanism, at least on its surface, seems to be incompatible with findings of elevated cortisol levels in depressed patients (Vreeman et al., 2009), given the well-established link between stress and depression (Tafet & Nemeroff, 2015)Article Major Depressive Disorder and Hypothalamic-Pituitary-Adrenal...

Article The Links Between Stress and Depression: Psychoneuroendocrin...

Also, "adrenal fatigue" does not exist, as recently reviewed by Cadegiani & Kater (2016) Article Adrenal fatigue does not exist: A systematic review

There are many finding about cortisol levels and stress and cortisol levels have been regarded even as a possibile bio marker of "endogenous depression". The elevation of cortisol levels under stress is observed in many situations and can give other metabolic problems.The interest of the question is about the PTSD. We can add that cortisonic treat can give different psychiatric symptomatology: depression, mania and psychosis. So the question is very puzzling

This question still perplexes me. I've provided an excerpt (see below) from an Annual Research Review from the Journal of Child Psychology and Psychiatry that touches on this topic.

"However, prolonged or repeated cortisol elevations can have damaging impacts on the body. Thus, mechanisms have evolved to downregulate the HPA axis under conditions of chronic activation (Fries, Hesse, Hellhammer, & Hellhammer, 2005). This is likely why individuals experiencing chronic stressors initially exhibit frequent, prolonged elevations in cortisol, but then often have suppressed levels and blunted reactivity.

Finally, a meta-analysis supports prenatal programming of the axis, primarily on baseline cortisol measures and, disconcertingly, equivalent effect sizes for hyper and hyposecretion (Pearson, Tarabulsy, & Bussieres, 2015). Mounting evidence is emerging for prenatal development as a time during which programming of the axis may occur; however, whether this means elevations or suppressions is not completely clear."

Article Annual Research Review: Early adversity, the hypothalamic-pi...

Can anyone proffer a plausible biological mechanism that could explain how chronic exposure to stress, and consequently GCs, lead to both hypo- and hyper-activity of the HPA axis?