A team of investigators led by a BBRF grantee reports that they have gained new insight into circuit-based mechanisms in the human brain that underlie habitual behaviors, specifically those involved in two eating disorders, binge-eating disorder (BED) and bulimia nervosa (BN).
In BN, there are recurring episodes of eating large amounts of food at one sitting with a sense of loss of control, usually coupled with efforts to purge. BED, in contrast, involves similar binge-eating episodes that are not paired with purging.
One of the mysteries posed by eating disorders as well as other disorders including substance-use disorders is why an individual will persist in behaviors that they know will hurt them. The answer is thought to involve, among other things, problems in circuitry underlying the formation of habits. Better understanding such circuitry provides a potential path toward new treatments.
Habits are formed through repeated associations between a rewarding behavior—say, the satisfaction of taking in nourishment—and contextual stimuli experienced or perceived at the time of the behavior—say, a feeling of hunger, or, quite different, the mere sight or thought of food. Eventually the “contextual stimuli” themselves become sufficient to drive the behavior, independent of the reward actually obtained. For this reason, behaviors that are habitual are resistant to changes in what happens as a result of engaging in the behavior. People will continue to smoke or take addictive drugs long after they learn of the likely damage being done to their health. Similarly, people with disorders involving binge eating and/or purging habitually engage in the behavior despite knowing their health is being adversely affected.
Casey H. Halpern, M.D., a 2016 BBRF Young Investigator at the University of Pennsylvania and the VA Medical Center, Philadelphia, and colleagues including Cara Bohon, Ph.D., a 2012 BBRF Young Investigator, began with the hypothesis that people with recurrent binge eating will have altered habit circuitry, compared with healthy controls. They used a combination of functional and structural neuroimaging methods to examine specific parts of the brain in a cohort of eating disorder patients, 21 with BED and 13 with BN. All were female.
The team, reporting in Science Translational Medicine, was inspired by an extensive literature based on experiments with animals—mainly rodents—that point to the brain’s striatum and its complex connectivity with different parts of the cortex as playing a key role in driving and regulating habitual behaviors. The striatum has many functions, prominent among which are processing rewards and bodily movements related to reward-seeking. Much of what happens in the striatum is regulated by dopamine signaling—which has been implicated in the acquisition of habits and the carrying out of habitual behaviors.
Maladaptive behaviors—harmful to the individual—have been central in studies of addiction, and as Drs. Halpern, Bohon and colleagues note, recent evidence has suggested that habitual behavior may also be important in eating disorders. Specifically, “as eating becomes habit-driven, it may be influenced more by external food cues than by the individual’s feeling of satiety [fullness] or actual bodily needs.”
Part of the new study was designed to identify subregions of the human striatum that are most likely to be involved in habitual behavior. This yielded two regions, called the sensorimotor putamen and the associative caudate. Study of the imaging data from eating disorder patients revealed to the team that connectivity of the sensorimotor putamen was altered, both in BED and BN patients, and that the degree of alteration correlated with the severity of the disorder in individual cases.
The observed striatal connectivity alterations were also found to correlate with grey matter microstructure in the affected subregion and with dopamine signaling with the ventral portion of the striatum. The associative caudate subregion of the striatum, though involved in habitual behavior, was not found to exhibit alterations in connectivity in the same patients. “This suggests the sensorimotor putamen may be the key node for promoting habitual behaviors,” not just in BN and BED patients, but generally in human beings, the team said.
Binge eating in response to external cures, such as the sight of food, and “emotional eating,” which is a term for eating that is prompted by depressed mood or other emotional states, have previously been regarded as involving separate processes. The new study, however, provides evidence that both “may be conceptualized as habit-driven behaviors, i.e., related to habit circuitry, and that it is these which may drive the frequency of binge eating episodes.”
The evidence in this study did not indicate that habit circuitry involved in binge eating behaviors was also involved in “restrictive eating” behaviors, for example the restrictive type of anorexia nervosa, involving consistent restriction of food intake.
The team suggested that “future treatments involving modulation of circuitry-based mechanisms may potentially provide a means to treat habitual behaviors that underlie the treatment-resistant nature of many human psychiatric disorders, not limited to eating disorders.”
