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The Cortene Way and CFS/M.E.

Research into CFS/M.E. is very complex, there are multiple possible starting points and these can branch into a multitude of subsets. There is clear definition of the immune/neurological and endocrine pathways and the question is what came first. It is known that the immune system will trip the neurological pathways and vice versa. Stress is very harmful and is known to trigger a number of pathways.

The  HPA (hypothalamus/pitituary/adrenal) pathways are known to be defective and the following study looks at the possibilites. Here is an excerpt:

Stress

“Stress” is an unfortunate term. Usually we think of stress as emotional; in biology, though, stress means any threat that disrupts the balance (or homeostasis) of the body. The stress response or HPA axis, prepares the body to respond to the threat. Any threat then, whether infectious, emotional, physical, chemical, etc, will initiate the stress response.
Once triggered, the stress response suppresses non-critical functions such as growth and metabolism (i.e., hypothyroidism, long linked to ME/CFS) and reproduction (i.e., hypogonadism, also connected with ME/CFS). It also releases cortisol to make sure the brain, heart and muscles have sufficient glucose (at the expense of less critical functions like digestion). Cortisol also primes the immune system for action (and has a delayed proinflammatory effect).
As noted in Part 1, studies indicate that chronic stress causes a progression from high to low cortisol and can result in the development of cortisol sensitivity – a situation in which the body becomes more responsive to cortisol. (When cortisol sensitivity occurs low cortisol can have the same or greater effects than high cortisol does in healthy individuals.) This increased cortisol sensitivity cannot be measured by cortisol/synacthen tests (which measure level not effect) but it does results from epigenetic changes that can be shown.
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Cortene’s new hypothesis for ME/CFS will shortly be tested in a small exploratory drug trial
Studies indicate that ME/CFS patients show the same alterations in cortisol levels and cortisol sensitivity seen in chronic stress. These findings help to explain the overlap of immune and metabolic symptoms found in ME/CFS and chronic stress but they do not explain the neurological issues found in ME/CFS.
The stress response also involves brain neurotransmitters such as serotonin, norepinephrine, dopamine and GABA (gamma-aminobutyric acid), which focus on and deal with the stress in a stressor-specificway. These neurotransmitters – which may have been under-appreciated in ME/CFS research – are at the core of Pereira’s hypothesis.
Animal studies indicate that short, medium and long term responses to stress are governed by two factors, CRF (corticotropin-releasing factor) and UCN1, that affect the release of serotonin (and norepinephrine) in the brain and cortisol (and epinephrine) from the adrenal glands.

Read more>> https://www.healthrising.org/blog/2018/02/17/cortene-chronic-fatigue-syndrome-hypothesis/

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