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 anxiolytic as well as analgesic effects in response to a wide range of biologic, behavioral, cognitive socio-cultural, and environmental stressors. Several studies are reviewed which demonstrate that the presence of the BE anxiolytic effect is coincident with efficacious outcome in exposure therapy with Phobic patients. It has been hypothesized that in the treatment of phobic avoidance, the controlled stress of imaginal and in vivo exposure activates the stress-induced release of BE into the blood stream. The neuroendocrine literature indicates BE is coreleased with Adrenocorticotrophic Hormone (ACTH) and that the stress-induced anxiolytic effect of BE appears to be momentarily blocked by ACTH at their common receptor sites. The more rapidly decaying ACTH soon disperses, resulting in a delayed BE anxiolytic effect within minutes of the exposure. Of the four studies found in the literature that report both ACTH and BE response to stress in humans, all four demonstrate a differential ACTH and delayed BE response within 15, 7, 5, and 3 minutes of exposure to stress. Although indirect, these results are consistent with and suggest support for an hypothesized bio-behavioral mechanism which 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 cognitive-behavioral treatment of various anxiety disorders suggest future research directions.