Treatments for obesity, which commonly focus on diet and exercise, have yielded mixed results, and are typically implemented in specialty care settings, limiting generalizability of study findings. Novel intervention strategies for obesity are urgently needed, and the addiction treatment literature may offer some of the most relevant potential models to inform their development. The current paper is a follow-up to our previous publication in this journal , in which we conceptualized eating addiction as having sensory (e.g., taste, texture) and motor (e.g., crunchy, chewy) components, with a specific treatment for each component. In the current paper, conceptualization of eating addiction is further evolved as displacement behavior, with a suggested treatment.
Leaders in addiction science concur that addiction and obesity both reflect the consequences of ingestive behavior gone awry. The core similarities between these conditions can be summarized as follows. First, in terms of clinical diagnostic features, both addiction and obesity result from repetitive foraging and ingestion behaviors that intensify and persist despite negative and (at times) devastating health and other life consequences. Likewise, despite often repeated attempts to reduce or quit using addictive substances, relapse is common in the addiction recovery process, just as those with obesity who attempt to regulate their food intake through dieting frequently relapse and return to their elevated body weight. Second, only a subset of individuals who are exposed to substances with addictive potential develop addictive behaviors, just as not all people who are exposed to foods and diet patterns that pose difficulties with weight control become obese. Nevertheless, a central barrier to the success of treatment for obesity that is distinct from drug addiction is the fact that food consumption is essential for survival; thus, abstinence is not a feasible or appropriate treatment goal. Accordingly, understanding and targeting the behavioral and psychological precursors to compulsive eating behaviors is essential as a means of facilitating control over food intake to mitigate obesity.
Stress is a precursor that is common both to compulsive eating behavior and alcohol/drug use. Stress in childhood has been shown to predict weight problems during early adolescence and young adulthood , with parallel findings in the addiction literature . One putative explanation for the association of stress and associated life problems with addictive behaviors is offered by displacement theory.
Displacement behavior is an innate, biobehavioral mechanism in the brains of all animals, from fruit flies  to humans . It functions as a response to situations that cannot readily be faced, yet cannot be avoided—situations involving uncertainty, confusion, conflict, or a feeling of being trapped, threatened, or frustrated—herein defined as “stressful situations.” Displacement behavior is a normal behavior or drive (such as licking or grooming) that occurs out of context (e.g., when threatened). Although it is adaptive, if displacement behavior is excessively practiced, it may become destructive; for example, socially isolated, stressed dogs may lick their paws raw . Eating can function as a displacement activity and also potentially lead to maladaptive outcomes. For instance, sheep threatened by a predator will graze despite the danger . Similarly, both male turkeys and cocks, when fighting, will suddenly stop and eat, if food is available, even though they are not hungry, and subsequently resume fighting .
Displacement behavior bears a striking resemblance to addictive behavior. Like addictive behavior, displacement behavior is 1) irrepressible or out of control, and 2) out of context (i.e., not an appropriate response in the various sets of conditions in which it occurs), e.g., an animal that sleeps or feeds when threatened by a predator or an individual who drinks to intoxication or binge eats after encountering a stressor in the workplace. Thus, we hypothesize that an underlying mechanism in the genesis and maintenance of addictive behavior is the brain’s displacement behavior mechanism going rogue and developing a life of its own.
The displacement mechanism is triggered by sensory cues . Initially, a specific sensory cue (e.g., food) suggests to the brain that the behavior or drive (e.g., feeding) associated with the cue might be used as a displacement behavior to deal with problems/stressors/thwarting. The brain then appears to lock onto the respective drive (e.g., feeding drive), and henceforth similar cues trigger the displacement mechanism to activate that drive in stressful situations. Over time, triggering of that drive by the sensory cues may be self-reinforcing when problems/stressors/thwarting are present, to a point that the displacement behavior may become excessive and destructive (e.g., overeating/obesity).
Displacement behavior is thought to result from the rechanneling of overflow brain energy to another drive (e.g., feeding drive) when two drives, e.g., fight vs. escape, equally oppose each other . Moving such opposing drives out of equilibrium, by (1) helping the individual to identify the problem(s) or stressor(s) that form the basis of the opposing drives, thereby fueling overflow brain energy (i.e., displacement sources) and (2) assisting the person in forming strategies to either avoid or effectively resolve these problems/stressors, could form a behavioral intervention approach for targeting the displacement mechanism believed to be underlying addictive behaviors, including eating addiction and obesity. In the present study, as a pilot investigation of the feasibility and acceptability of therapeutic techniques based on the displacement theory, we added a displacement intervention component to an mHealth intervention that was part of a larger ongoing randomized clinical trial.