As an example, a therapist practicing ET to treat a dog phobia might write out a treatment plan that either gradually or dramatically exposes a person to the anxiety-inducing triggers associated with dogs (videos of dogs, the sound of barking, dog odors, an actual dog). As the person confronts the anxiety activated by those triggers, he or she develops distress tolerance. That is, the person becomes less sensitive (i.e., desensitized) to the triggers and the anxiety that they activate. Through the exposure, the person learns that he or she can survive the physiological surge that is anxiety, while debunking the thoughts that predicted a crisis (e.g., a dog attack). Once the triggers are neutralized, the person can relax more around canines, his or her phobia now easier to control.

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As noted in PLASTICITY, addictive behaviors prime the mesolimbic system much like phobic conditions, as it becomes increasingly sensitive to cues associated with a substances of choice. Not only will the brain fire off more forcefully in the presence of those cues to use, but it associates more & more cues to using over time. That’s what researcher label as sensitization. I use the basics of ET to help the brain desensitize from - to unlearn - the most prominent of cues, those high risk situations, people, or internal states that trigger cravings to use. Fundamentally, ET works by resetting the mesolimbic system, so that it is less reactive, less sensitive to triggers. The key to this behavioral method is context (Torregrossa, MM & Taylor, JR, 2012).

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Over the last 20 years, practitioners have used an intervention known as Cue Exposure Therapy (CET) to treat addictions, with mixed results. The limited effect of CET is due, more times than not, to the lack of context-specific planning. Often, CET is used in offices, in outpatient clinics, in rehabs or on hospital floors. How often, though, do people use or drink in those environments? Hopefully never.

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Learning – and therefore unlearning – is context-dependent. CET rarely demonstrates a sizeable effect because it’s not practiced in the real world, context-specific situations that those with addictive disorders routinely drink or use in (Berridge, K, 2001; Conklin CA, & Tiffany ST, 2002). My application of ET in the treatment of addictive behaviors might be described as mobile, as I plan interventions in a client’s real world – his or her home, favorite bar, or other so-called high risk situations.

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​A traditional approach to relapse prevention planning encourages those in early recovery to avoid high risk situations. A safe plan, no doubt. Such passive coping, however, prevents extinction learning. Consequently, cravings are apt to survive longer and crop up more regularly compared to those who practice more proactive forms of coping with cues to use. As in the treatment of panic disorders, triggers must be confronted if their collective effect is to subside.

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Some neuroscientists argue that dysregulation in the brain’s stress system is what drives addiction (Rajita, 2007; Koob, 2009), as it does panic disorders. Panic & cravings can each be conceptualized as an acute stress response, each linked to intense activation in the basal forebrain – the terminal point of the meso-limbic system. (Koob 2009, 2010, 2013; Martin-Fardon, Zorrilla, Ciccocioppo, & Weiss 2010). Also, panic & cravings share a similar ignition switch, with both experiences tied to the amygdala - the trigger point in the meso-limbic system (Feldstein-Ewing, S, et al., 2011; Rajita, 2007; Potenza, M, et al., 2011). Simply consider the shared symptoms that cravings and panic attacks manifest:

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•Sweating •Rapid pulse •Agitation •Racing thoughts 

•Restless legs & pacing •Obsessiveness •Erratic breathing

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​Those in the throes of a craving usually present as agitated, distressed, fidgety, if not panicky in their intense need to use. The striking similarity in symptomology between panic and cravings highlights neurobiological overlap. Hence, the intuitve use of ET to treat addictions. 

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ET stabilizes the brain's stress system, which runs amok in both anxiety disorders and addictions. In both conditions, the brain becomes hyper-sensitive to stress, resulting in more frequent and intense stress reactions that require a longer recovery time. Basically, ET is thought to normalize activity in the white-hot mesolimbic system, enabling more recruitment from the advanced areas in the forebrain (Marissen, et al., 2007; Vollstadt-Klein, et al., 2011). Increased access to the forebrain promotes greater impulse control, enhanced judgment & forethought, and improved social IQ - the stuff of relationships. It's relationships, finally, that ultimately sustain recovery. My treatment strives in the short-term to manage the biological force - cravings - that perpetuate addiction and relapse, so that someone can begin the longer work of repairing relationships.