In chronic stress response, all body functions have become compromised due to prolonged hormone, immune and metabolic depletion. This can lead to a cascade of chronic degenerative diseases from which the weakened body has a reduced chance to recover. Adrenal exhaustion progresses in three stages.
Adrenal Function Testing
Assessment of adrenal output and function involves evaluating levels of cortisol, DHEA-S, epinephrine(adrenaline), and other supporting hormones such as norepinephrine, and pregnenolone. Evaluation can be accomplished through serum, urine, and salivary testing, although serum testing is most likely to be covered by insurance.
Stage I is distinguished by an increase in output of ACTH by the anterior pituitary gland, increased adrenocortical stimulation, increased cortisol output and an increased probability of pregnenolone steal and decreased DHEA. When in a chronic stress response, pregnenolone, the common precursor to cortisol, DHEA and other hormones is preferentially diverted to cortisol production at the expense of the rest of the steroidal hormones. Generally, in Stage I cortisol increases and DHEA and its metabolites decrease or an imbalance occurs especially between testosterone and estrogen.
Stage II adrenal exhaustion is marked by the transition from increased to decreased cortisol output. This stage is characterized by continuing high levels of ACTH and thus: adrenocortical stimulation, normal total cortisol output, low or borderline low morning, noon or afternoon cortisol levels, normal nighttime cortisol level, and an increased probability of pregnenolone steal and a further decrease in DHEA. This is a transitional phase in which although ACTH stimulation remains high or even increases, the adrenal output of cortisol declines due to the adrenal fatigue associated with continued hyperstimulation.
Stage III adrenal exhaustion is an advanced stage of adrenal exhaustion characterized by decreased total cortisol output. This stage is characterized by continuing high levels of ACTH and thus adrenocortical stimulation, low total cortisol output, and increased probability of a low nighttime cortisol level and pregnenolone steal and even further decrease in DHEA. The adrenal glands are now exhausted to the point that even though there is ongoing hyperstimulation (high ACTH); they continue to lose their capacity and reserve to produce enough cortisol. The eventual result is a crash of the hypothalamic-pituitary-adrenal axis (HPAA) in which essential neuroendocrine feedback loops are unable to return the system to homeostasis.