Some refs about Corti..
1 ) Cortisol regulation abnormalities are noticed in posttraumatic stress disorder (PTSD). The basal cortisol level is often lowered. The reactivity of the hypothalamic-pituitary-adrenal (HPA) tests stimulation is increased. Exposure to a traumatic event may have more effects than PTSD itself on the HPA axis. At molecular level, some cortisol-related genes are more expressed in case of PTSD. In functional brain imaging, administration of glucocorticoids normalizes the abnormal activation of some areas previously modified by PTSD. Molecules targeting glucocorticoids receptors are used experimentally in animals, with encouraging results.
2 ) An imbalance in the secretion of stress hormones precedes so-called civilization diseases, such as diabetes, obesity, cardiovascular disease and even depression. “It is our genetic makeup and the factors in our environment that determine whether or not these diseases develop,” he explains.
3 ) Le diagnostic d’ESPT est défini dans la quatrième édition révisée du Manuel statistique et diagnostique des troubles mentaux de l’American Psychiatric Association (DSM IV-TR) [tableau](1). Chez une personne ayant été exposée à un événement traumatique (avoir été victime ou témoin d’une agression, d’un accident grave, d’une catastrophe, etc., ayant entraîné des morts, une menace vitale, des blessures graves ou une menace de l’intégrité physique; et avoir manifesté immédiatement une intense réaction de peur, d’impuissance ou d’horreur), l’ESPT nécessite la présence de 3 catégories de symptômes cliniques: ✓ les reviviscences: souvenirs pénibles répétitifs, cauchemars, etc. ; ✓ l’évitement de tout ce qui peut évoquer le traumatisme (pensées, lieux, personnes, etc.); ✓ l’hyperéveil : insomnie, état d’hypervigilance, etc. Le diagnostic d’ESPT aigu nécessite une durée d’au moins 4 semaines, et celui d’ESPT chronique d’au moins 3 mois.
4)
In the physiological response to stress, the HPA axis is
mobilized following activation of the adrenergic system in order to cope with the stressor. The kernels
paraventricular cells of the hypothalamus secrete
Corticotropin-Releasing Hormone (CRH), which stimulates
the corticotropic cells of the anterior pituitary, which
in turn secrete adrenocorticotropic hormone (ACTH)
to activate the release of glucocorticoids by the
adrenal cortex, especially cortisol. This cortisol
circulating acts at the peripheral level (motor response)
and at the central level on the prefrontal and limbic regions (memorization). Return to cortisol levels
normal is facilitated by feedback loops
on the HPA axis via cortisol itself and ACTH, but
also via inhibitory efferents emanating from the
prefrontal cortex and hippocampus, which inactivate the
hypothalamic secretion of CRH. If the cortisol level
is increased as a direct result of the trauma,
the commonly held assumption about PTSD
chronic is that of a modification of the mechanisms
control in the direction of adaptation of the axis
HHS to chronic stress, with hyperreactivity of this axis (comparable to hypervigilance), and
low cortisol levels
Cortisol and PTSD
Sampling methods
Classically, the authors study the total cortisol
measured in plasma (which includes the free fraction
active and the fraction linked mainly to Cortisol Binding Globulin [CBG]) or free cortisol assayed in
urine or saliva. The saliva dosage is
increasingly favored because of its ease of use (non-invasive technique, easy handling). In
physiological situation, cortisol is secreted according to a
circadian rhythm, with peak values on waking
So....?
If there's a Cortisol crash. The same traumatic symptoms can be triggered if a person can be sensitive to an additive in their system. If the arimistane progresses against the current it is possible that it acts thus in spite of the expected results of its consumer.
Maybe it can possibly hijack the effects of other products if it's Stacked?
