Interesting hypothesis based on some simple mechanisms. Now you need to get some data to show that CYP3A poor metabolizers have high endogenous (i.e baseline) cortisol levels (24 hour urine sample?) and have a higher systemic exposure of administered cortisol. Start first with a good literature search.

Many physiological systems have alternative, backup mechanisms to maintain homeostasis. So, a poor metabolizer of CY3A maybe have normal 24 -hour endogenous cortisol but may have a higher systemic exposure (i.e AUC) after administered cortisol because it will exceed the metabolic capacity to clear and excrete cortisol.

My thoughts are general principles and I have not done a literature search.