CONCEPT
Glucocorticoid Resistance
The molecular mechanism through which chronic stress breaks the feedback loop that should limit the stress response — cortisol receptors desensitize, cortisol can no longer signal the brain to stop producing the signals that produce cortisol, and the resistance phase sustains itself beyond its adaptive window.
Glucocorticoid resistance is the specific molecular pathology that explains why the resistance phase can sustain itself past the point where adaptation has given way to damage. Under healthy regulation, cortisol binds to glucocorticoid receptors in the hypothalamus and pituitary, signaling the upstream cascade to reduce CRH and ACTH production — a negative feedback loop that limits cortisol elevation to what the current demand requires. Under chronic stress, the receptors desensitize. The feedback signal weakens. Cortisol can no longer effectively tell the brain to stop producing cortisol, producing a runaway system in which elevation sustains itself independent of ongoing demand. This is the molecular basis of the grinding compulsion: the organism cannot de-escalate because the neurochemical mechanism for de-escalation has been broken by the very stress it was supposed to limit.
In The You On AI Field Guide
The phenomenon was characterized through the 1990s and 2000s as researchers sought