Reward Sensitivity And Inhibitory Control As Influences On Binge Eating: Behavior And Neuroimaging Evidence

Binge eating(BE) is characterized by the consumption of unusually large amounts of food during brief periods of time, often with accompanying distress about bingeing and a perceived loss of control. Binge Eating Disorder(BED) involves at least one BE episode per week for three months but affected individuals do not engage in subsequent inappropriate compensatory behaviors(e.g., excessive dieting or exercise, purging) to prevent weight gain in contrast to Bulimia Nervosa(BN). According to recent studies, many factors contribute to problems with BE including stressors, negative affect, an impulsive personality style, body dissatisfaction, dietary restraint, interpersonal problems, and instrumental feeding from parents.Impulsivity is key personality influence hypothesized to contribute to the onset and maintenance of BE and BED. Impulsivity comprises two factors: reward sensitivity and rash-spontaneous impulsiveness. Whereas reward sensitivity is a motivational approach tendency towards appetitive or rewarding stimuli(e.g., food cues), impulsiveness refers to disinhibited behavior without regard for consequences. These factors have been incorporated within dual process models of BE including incentive-sensitization theory. From this perspective, repeated exposure to rewarding stimuli such as high calorie foods or cues for such foods produces an exacerbated reward response in susceptible individuals. That is, exposure to these stimuli activates the reward system, lead to physiological arousal, cravings, finally resulting in BE episodes, particularly when late stage inhibitory control fails.To date, research linking increased reward sensitivity and inhibition deficits to BE has several limitations. Studies of reward sensitivity have yet to determine whether BE is related to increased responsiveness to specific types of food cues(i.e., high- versus low-calorie foods). Furthermore, researchers have focused almost exclusively on binge-eating groups that are obese or overweight even though a substantial proportion of binge-eaters is of average weight, especially those in Asian countries where much of the world’s population is concentrated. Depending on research paradigm used, studies of inhibitory control deficits related to BE have produced inconsistent results; some studies have found these deficits are general, some have linked them specifically to food cues, and still others have found no such deficits.Finally, neural mechanisms underlying BE have only recently been the focus of investigation and the relative importance of reward versus inhibitory neural responses on responses to food cues in BE groups is unknown. For example, researchers have yet to employ amplitude of low frequency fluctuations(ALFF) to assess whether BED groups and matched controls differ in baseline brain activity in reward and inhibitory control regions. In addition, although stressors and increases in negative affect often precipitate BE episodes in BE groups compared to controls, it is not clear whether increased food consumption under these conditions is due to increased reward responsiveness or reduced inhibitory control to external food cues. Towards addressing these issues, this dissertation comprises six studies designed to evaluate the roles of reward sensitivity and reward sensitivity and inhibitory control as influences on in(1) behavior and(2) neural responses of average-weight BE groups and weight-matched controls.Studies 1 and 2 were designed to evaluate behavior responses related to BE using two different laboratory paradigms. In Study 1, biases in attention disengagement were examined among average-weight women with binge-eating(n = 33) and non-eating disordered controls(n = 31). Participants engaged in a spatial cueing paradigm task wherein they first observed high-calorie food, low-calorie food, or neutral images and then had to quickly locate targets in either the same or a different location. Within both groups, reaction times(RTs) were longer to valid-cued trials(i.e., trials in which targets appeared in locations of preceding cues) than to invalid-cued trials(i.e., trials in which targets appeared in a location different from initial location), reflecting a general inhibition of return(IOR) effect. However, RT findings also indicated women with BE had significantly more difficulty disengaging from high-calorie food images than did controls, even though neither group had disengagement problems related to other image types. Selective attention disengagement difficulties related to high-calorie food images suggested increased reward sensitivity to high- but not low-calorie or non-food cues is related to binge eating risk.In Study 2, normal-weight women with elevations in BE(n = 31) and weight-matched controls without BE(n = 31) engaged in an overnight fast before engaging in a food-related visual Go/No-Go task consisting of high-calorie food, low-calorie food, and neutral household pictures. After the task, participants completed a self-report battery in an environment with readily available snacks that they could eat if they chose. The BE group reported more trait impulsivity, and its members were significantly more likely to snack than controls were during the post-task questionnaire completion. Although groups did not differ in overall false alarm rates(i.e., pressing the space bar when “No-Go” stimuli were presented), BE group responded faster to high-calorie food cues than did controls, and were more accurate in “Go” trials(i.e., pressing the space bar when “Go” stimuli were presented) involving high-calorie food images than low-calorie images compared to controls. Furthermore, faster RTs on “Go” trials and higher false alarm rates were significantly related to more food consumed during post-task questionnaire completion. Results failed to confirm average weight women who BE have inhibitory control deficits in response to food cues but they show increased reward sensitivity to high-calorie food.In Study 3, we assessed associations of BED symptomatology, reward sensitivity and inhibitory control and brain activation responses to food images with food consumption among average weight young adults with elevated BED symptomatology and weight-matched non-disordered controls. During a functional neuroimaging scan, participants who endorsed all DSM-V BED criteria(17 women, 2 men) and non-BED controls(27 women) passively viewed images of high-calorie foods, low-calorie foods and neutral images(cars). Subsequently, participants completed self-report measures of binge-eating, food craving, general reward sensitivity and behavioral inhibition, and emotional distress in the presence of tempting snacks(i.e., specify). Compared to controls, BED group members reported more bingeing behavior, uncontrolled eating, and food cravings as well as marginally higher general reward sensitivity and behavior inhibition scores. BED group participants also showed comparatively more activation in the inferior frontal gyrus(IFG), middle frontal gyrus, and middle temporal gyrus in addition to reduced precuneus and cingulate gyrus responsiveness while viewing food images. In addition to these self-report and neural activation differences, the BED group consumed significantly more chocolate following their scans than controls did. Finally, chocolate consumption negatively correlated with medial frontal gyrus and precuneus in the high- vs. low-calorie food image contrast. In sum, results implicated specific brain regions underlying impulse control(i.e., IFG, middle frontal gyrus, and middle temporal gyrus) as key neural correlates of responsiveness to external food cues and food consumption among individuals with evidence of significant BED symptomatology.Study 4 investigated neural correlates of response inhibition during performance of a Go/No-Go task in which “No-Go” signals or tests of inhibitory control comprised images of high-calorie foods. Participants were 17 women who met all DSM-V criteria for BED based on a structured diagnostic interview and 17 weight-matched controls who did not fulfill criteria for an eating disorder based on the same interview. All participants engaged in the Go/No-Go task during an f MRI scan and then completed a battery of self-report scales. On the questionnaire measures, the BED group reported higher levels of impulsivity, uncontrolled eating, more concerns with eating, weight, shape and food restraint, and more general emotional distress than controls did. On the Go/No-Go task, the BED group made more false alarms(i.e., pressing the key when “No-Go” stimuli were presented) than controls did, reflecting more inhibitory control deficits in the former group. The BED group displayed more activity in the left insula during exposure to high-calorie food cues during “No-Go” trials relative to controls. The insula comprises the primary taste cortex and is involved in the anticipation and consumption of foods. Further, BED group showed significantly greater activity in the precentral gyrus and postcentral gyrus relative to controls during No-Go trials. These regions are implicated in taste perception and their activations were observed in relation to food cues exposure. These results suggested that the BED may have experienced increased control efforts to withhold a response due to poorer inhibitory control from enhanced reward sensitivity to food cues on the high-calorie food image “No-Go” trials.In study 5, resting state functional MRI was used to investigate amplitudes of low frequency fluctuations(ALFF) in spontaneous brain signals with the sample from Study 4. Participants with BED showed a significantly higher resting state activity in the precuneus, middle frontal/superior frontal gyrus and lower resting state activity in the middle temporal gyrus as compared to controls. We further found a significant positive correlation between orbitofrontal cortex(OFC) activation and BMI, while DLPFC activity was positively correlated with trait impulsiveness in the BED subgroup and was unrelated to impulsiveness among controls. The functional connectivity between the OFC and DLPFC was higher in BED group than controls. Findings suggested that increased functional connectivity in reward related regions and inhibition regions might play an important role in the pathophysiology of BED.In Study 6, we examined the impact of acute stressors on neural activation to food images and subsequent food consumption within BED and non-eating disordered control groups. Nineteen participants meeting DSM-IV BED criteria and 27 non-eating disordered controls were randomly assigned to unpleasant(painful cold pressor test followed by negative performance feedback) or neutral lower(non-painful sensory discrimination task followed by positive performance feedback) stressor conditions. Subsequently, they were scanned with f MRI while viewing food and neutral images. After the scans, participants completed a self-report battery in an environment conducive to snacking. During exposure to food images, BED participants in the unpleasant stressor condition reported more liking of high calorie food images and showed less activation in the hippocampus, compared to controls in this condition. BED participants exposed to unpleasant stressors also consumed significantly more chocolate than any other group following the f MRI scan. Crucially, reduced hippocampal activation to high calorie food images predicted more chocolate consumption following f MRI scans in the entire sample. This experiment provides initial evidence suggesting unpleasant acute stressors contribute to reduced inhibitory region responsiveness in relation to external food cues and later food consumption among persons with BED.In conclusion, the present thesis has several novel findings: Women with binge eating show increased reward sensitivity in response to high-calorie food cues and higher level of inhibitory control deficits related to more food consumed; Specific brain regions underlying reward sensitivity and impulse control as key neural correlates of responsiveness to external food cues and food consumption among individuals with BED. The functional connectivity between the OFC and DLPFC might be related to BED. Unpleasant acute stressors contribute to reduced inhibitory region responsiveness in relation to external food cues and later food consumption among persons with BED. Findings in this thesis provided evidences for the incentive-sensitization theory of BED.