Bulimia nervosa is associated with psychiatric distress, functional impairment, medical complications, and increased risk for future obesity, depression, suicide attempts, substance abuse, and health problems (1
). As well, individuals with subthreshold bulimia nervosa, such as those who report a frequency of binge eating and compensatory behavior below diagnostic thresholds, evidence psychiatric distress, functional impairment, medical complications, and seek treatment (3
). Thus, numerous studies have investigated biological correlates of bulimic pathology, with the hope of elucidating the etiological processes that give rise to this pernicious disorder.
Theorists have hypothesized that people who show elevated reward from food intake may be at risk for bulimic pathology (6
). Specifically, it may be that individuals who show a particularly strong activation in mesolimbic reward circuitry in response to food intake are at increased risk for binge eating. In support of the hyper-responsivity theory, women with bulimia nervosa show greater sensitivity to financial reward than healthy controls when measured by behavioral performance in some (8
), but not all studies (10
). Bulimic symptoms also correlate positively with self-reported reward sensitivity (11
). Further, women with versus without bulimia nervosa prefer sweeter and higher-fat foods than healthy controls (12
In contrast to the results reviewed above, a few brain imaging studies have produced findings that suggest that individuals with bulimia nervosa may show reduced responsivity of brain reward circuitry. Specifically, positron emission tomography (PET) studies found that women who had recovered from bulimia nervosa showed less activation of the right anterior cingulate cortex and left cuneus in the occipital cortex in response to receipt of glucose versus artificial saliva and lower baseline medial OFC serotonin 2A receptor binding, even after a glucose preload (14
). Another PET study found less μ-opioid binding in the temporinsular cortex at rest among women with bulimia nervosa compared to controls (16
). Because these frontal and mesolimbic brain regions appear to encode reward from food intake (17
), these results imply that individuals with bulimic pathology might show a blunted responsivity of reward circuitry to food. These results appear to accord with the evidence that obese relative to lean individuals show reduced activation of the dorsal striatum to consumption of a palatable food versus a tasteless solution (19
Thus, self-report and behavioral data seem to imply that individuals with bulimic pathology may show hyper-responsivity of reward circuitry, whereas the brain imaging studies imply that these individuals potentially show hypo-responsivity of reward circuitry. One explanation for this pattern of findings is that brain imaging studies yield different findings because it is more objective than self-report or behavioral data, which are both sensitive to self-presentation biases. In addition, this literature review revealed a key gap in the literature: no brain imaging studies have examined activation of reward circuitry in response to food receipt among individuals with and without current bulimic pathology.
Theorists have also hypothesized that elevated anticipated
reward from food intake increases risk for binge eating (21
). Incentive salience theory posits that over repeated presentations of a rewarding substance (e.g., food), individuals learn to associate cues with the reward and that consummatory reward decreases while anticipatory reward increases (22
). Cues such as sight and smell of food may eventually lead to physiological responses that trigger food craving and increase risk for binge eating (23
). Naïve monkeys initially showed firing of mesotelencephalic dopamine neurons only in response to food taste, but this firing began to precede food delivery after conditioning, with maximal firing eventually elicited by the conditioned stimuli that predict subsequent food delivery rather than the actual food receipt (24
). Blackburn, Phillips, Jakubovic, and Fibiger (26
) found that dopaminergic firing was greater in the nucleus accumbens of rats after presentation of a conditioned stimulus that usually signaled food receipt than after delivery of an unexpected meal. Thus, reward activation in response to anticipation of food may be more important than response to consumption of food in predicting whether someone initiates an eating episode.
Some evidence suggests that different neural regions are involved in consummatory and anticipatory food reward. Anticipated receipt of a palatable food, versus anticipated receipt of unpalatable food or a tasteless food, results in greater activation in the OFC, amygdala, cingulate gyrus, striatum (caudate nucleus and putamen), ventral tegmental area, midbrain, parahippocampal gyrus, and fusiform gyrus (17
). Anticipation of a pleasant taste, versus actual taste, resulted in greater activation in the dopaminergic midbrain, nucleus accumbens, and the posterior right amygdala (17
). Small and associates (28
) found that anticipation of a pleasant drink resulted in greater activation in the amygdala and mediodorsal thalamus, whereas the receipt of the drink resulted in greater activation in the left insula/operculum. These results suggest that the amygdala, midbrain, nucleus accumbens, and mediodorsal thalamus are more responsive to anticipated consumption versus actual consumption of food, whereas the frontal operculum/insula is more responsive to consumption versus anticipated consumption of food.
Individuals with bulimia nervosa or recurrent binge eating rate pictures of food as more interesting and arousing and report a greater desire to eat than healthy controls (29
). Food craving is cited by 70% of patients with bulimia nervosa as a reason for binge eating (31
). These data suggest that individuals with bulimia nervosa may experience greater anticipatory reward from eating than healthy controls, which is congruent with findings that they report greater urges to binge and less confidence in their ability to control their food intake after exposure to the sight, smell, and taste of food (32
Salivary response, a key component of the cephalic phase response, correlates positively with self-reported hunger and desire to binge eat, suggesting it may serve as a useful proxy for food craving and is related to anticipatory reward (34
). However, findings have been mixed; some studies find that women with bulimia nervosa show more (34
), less (29
), or similar (33
) salivary response to food cues compared to healthy controls. These studies suggest that there are no reliable differences between individuals with and without bulimia nervosa in salivary response to food, although it could be that the measures themselves are unreliable or that these studies had small sample sizes that led to inconsistent results. It is also possible that individuals with bulimia nervosa have an approach-avoidance response to food cues, evidenced by a drive to consume food coupled with negative feelings toward food due to guilt and shame from prior binge eating or high levels of thin-ideal internalization. These positive and negative responses to food cues could lead to inconsistent physiological responses. Indeed, individuals with bulimia nervosa often report more negative feelings while looking at, smelling, or touching food (30
One brain imaging study found that individuals with bulimia nervosa using whole brain analysis showed greater activation in the medial OFC and anterior cingulate cortex (ACC) in response to presentations of pictured food versus non-food images relative to healthy controls (36
). Schienle and colleagues (37
) found that individuals with bulimia nervosa showed greater insula and ACC activation than healthy controls and individuals with binge eating disorder in response to pictures of food versus household items. Interestingly, fMRI studies indicate that obese versus lean individuals show greater activation in reward areas, including the insula, frontal operculum, orbitofrontal cortex, amygdala, and striatum in response to pictures of palatable foods (38
) and anticipated receipt of palatable food (20
). These data suggest that individuals with bulimic pathology show greater anticipatory reward than healthy controls.