NEUROENDOCRINE AND BEHAVIORAL INTERACTION IN EXPOSURE TREATMENT OF PHOBIC AVOIDANCE

A large body of literature on the human stress response provides ample evidence of the involvement of Beta Endorphin (BE), and its anxiolyti c as well as analgesic effects in response to a wide range of biologic , behavioral, cognitive socio-cultural, and environmental stressors. S everal studies are reviewed which demonstrate that the presence of the BE anxiolytic effect is coincident with efficacious outcome in exposu re therapy with Phobic patients. It has been hypothesized that in the treatment of phobic avoidance, the controlled stress of imaginal and i n vivo exposure activates the stress-induced release of BE into the bl ood stream. The neuroendocrine literature indicates BE is coreleased w ith Adrenocorticotrophic Hormone (ACTH) and that the stress-induced an xiolytic effect of BE appears to be momentarily blocked by ACTH at the ir common receptor sites. The more rapidly decaying ACTH soon disperse s, resulting in a delayed BE anxiolytic effect within minutes of the e xposure. Of the four studies found in the literature that report both ACTH and BE response to stress in humans, all four demonstrate a diffe rential ACTH and delayed BE response within 15, 7, 5, and 3 minutes of exposure to stress. Although indirect, these results are consistent w ith and suggest support for an hypothesized bio-behavioral mechanism w hich may help to explain the clinical phenomenon of anxiety reduction in response to exposure. The implications of this model with regard to etiology, differential diagnosis, and pharmacological, as well as cog nitive-behavioral treatment of various anxiety disorders suggest futur e research directions.