Possible explanations for this are (1) increased levels of structurally analogous steroids, like 17OHP and 21DF, may disrupt or prevent cortisol from binding to CBG or albumin, leading to a higher percentage of free cortisol (15, 21, 22); (2) increased concentrations of adrenal androgens in patients with CAH may decrease 11β-hydroxy steroid dehydrogenase type 2 activity, preventing cortisol conversion to inactive cortisone (36); (3) androgens may lower CBG levels, potentially increasing the free cortisol concentrations (37, 38). Here, ALB is linked to congenital adrenal hyperplasia.