Eating disorders are characterized by irregular eating habits and unhealthy relationships with food. Bulimia Nervosa (BN) is a subtype of eating disorders marked by recurrent episodes of binge eating associated with inappropriate behaviours that compensate for the overeating, such as forced vomiting. Anorexia Nervosa (AN) is also a severe eating disorder, which is differentiated from BN by a persistent restriction of energy intake and significantly decreased body weight (American Psychiatric Association, 2013). Many individuals with eating disorders demonstrate impaired processing of rewarding food stimuli. For example, patients with AN are less sensitive to food reward and experience less pleasure from the anticipation of palatable food, compared to individuals without eating disorders (Jiang, Soussignan, Carrier, & Royet, 2019). Neurobiological research has suggested that the impairment of food reward processing may be associated with dysfunction of the brain reward circuit.
Brain reward system refers to a group of structures that are activated by rewarding stimuli such as food and addictive drugs. The brain shows increased release of the neurotransmitter dopamine in response to a rewarding stimulus. Thus, the structures associated with the reward system are those involved in dopamine use and release. The mesolimbic dopamine system is thought to be a major dopamine pathway in the reward system. It connects the ventral tegmental area (VTA), which releases dopamine in multiple regions of the brain, and the nucleus accumbens, which is strongly associated with motivation and reward. Another core component of the reward system is the ventral palladium (VP), which mediates the perception of pleasure that results from consuming rewarding stimuli (Bear, Connors, & Paradiso, 2016). Previous studies have indicated that impaired processing in the brain reward system have been involved in the pathology of eating disorders. However, it remains unclear whether the behavioural and neural factors related to subjective experiences of food cues are influenced differently in patients with and without eating disorders.
To address this, Jiang et al. (2019) conducted a fMRI study to investigate whether AN patients, BN patients, and healthy individuals are characterized differently by either elevated or reduced sensitivity in the brain reward system in response to food odors. fMRI, or functional magnetic resonance image, is a technique for measuring brain activity by detecting changes associated with blood flow. A total of 39 women participated in this study, including 14 AN patients, 13 BN patients, and 12 healthy individuals. Twenty-eight odorants were used as stimuli for the fMRI scanning session, including 14 food odorants (e.g., bacon, banana, pizza, potato) and 14 non-food odorants (e.g., fresh grass, tar, pine, tobacco) not evoking food. Food odorants are further classified into high-calorie food odors (e.g., bacon, beef) and low-calorie food odors (e.g., apricot, banana).
Two experiment sessions were planned for each participant on two consecutive days; participants were alternatively scanned in hunger and satiety states. In each session, two tasks were performed during which participants reported their “liking” (pleasantness) or “wanting” (the desire to eat) ratings for food odors. After each odorant was delivered, participants’ responses were acquired with a five key-press button box. During the liking task, the participants pressed one of five buttons depending on their liking judgement (very unpleasant, unpleasant, neutral, pleasant, very pleasant). During the wanting task, if the odor evoked food, the participants pressed one of five buttons, depending on their desire to eat the food evoked by the odor (not at all, not desired, just a little, much desired, urge). Researchers used event-related fMRI in participants to record their brain activity while they were performing the tasks. Both participants’ behavioural responses (ratings for food odors) and signals from fMRI scanner were recorded and later analyzed by the researchers.
The behavioural data revealed that AN patients liked high-calorie food odors less than did healthy participants, which means that they displayed clearly less sensory pleasure in response to high-calorie food. Moreover, AN patients reported lower wanting scores, meaning that they had less desire to eat odor-cued food. Similarly, BN participants reported lower wanting scores than healthy participants, but only for odors evoking high-calorie food. Thus, the desire to eat food was influenced by the food nutritional content in both patient groups, although less influences in BN than in AN patients. The lower self-reported reward scores for food odors in AN and BN patients than in healthy participants raised questions among the researchers. They hypothesized that the differences might reflect decreased responsivity in brain reward system in individuals with eating disorders in response to food reward cues.
Indeed, the neuroimaging data revealed that brain activation within the food reward system differentiated the three groups of participants. AN patients exhibited lower VTA activation than BN patients to food odors when rating their desire to eat (during the wanting task), suggesting that AN patients are less likely to be attracted to food odors. Previous research has indicated that the VTA likely responds to the expectation of rewards but not to the anticipation of non-rewarding stimuli. Thus the results suggested that AN patients might not regard food as a rewarding stimulus. Moreover, AN and BN patients smelling high-calorie food odors in the hunger state revealed low activation of the anterior VP during the wanting task, compared to healthy participants. The VP function is considered a major mechanism of reward in the brain; an intact VP is necessary for reward processing and motivation. Therefore, a lack of activation in the VP during the wanting tasks in AN and BN patients suggested a possible dysregulation of this brain area which might impair the processing of motivation signals and the associated experience of desire in these patients.
In conclusion, this study provided evidence for the dysfunction of the reward system in food stimuli processing in patients with eating disorders. AN and BN patients shared similar decreased activation of brain regions underlying reward processes. BN patients exhibited more specified reactivity for odors evoking high-calorie food. These results revealed the complexity of etiology underlying eating disorders, and the difficulty of developing effective treatment. Patients cannot just “pull it together” and change their eating behaviours and their attitudes toward food all of a sudden. It’s not that simple. More research is needed to explore the detailed mechanism of the dysfunction of the brain reward system in these two eating disorders.
References:
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders DSM-5 (5th ed.). Arlington, VA: American Psychiatric Association.
Bear, M., Connors, B., & Paradiso, M. (2016). Neuroscience: Exploring the brain (Fourth ed.). Philadelphia: Wolters Kluwer.
Jiang, T., Soussignan, R., Carrier, E., & Royet, J.-P. (2019). Dysfunction of the mesolimbic circuit to food odors in women with anorexia and bulimia nervosa: A fMRI study. Frontiers in Human Neuroscience, 13. https://doi.org/10.3389/fnhum.2019.00117
