Food-related Reward Research Articles

Examining the roles of reward sensitivity and difficulties in emotion regulation in relation to low-restraint binge eating.

Leading treatments for binge eating target dietary restraint, but up to 35% of the people with binge eating report low restraint. This study examined the roles of reward sensitivity and emotion dysregulation in relation to low-restraint binge eating. Women with binge eating (low-restraint: n = 22; high-restraint: n = 69) and controls (n = 49) completed self-report measures of generalized reward sensitivity and emotion dysregulation and a picture-viewing task assessing craving and pleasure for high-calorie food. As expected, food-related craving and emotion dysregulation were greater in the clinical than in the control group, but no differences emerged between high- and low-restraint binge eating groups. However, correlational analyses found that, within the clinical group, the number of restraint days related to greater anticipatory sensitivity for generalized rewards and lower pleasure ratings of food. Results suggest that emotion dysregulation characterizes both high- and low-restraint binge eating. As self-reported food liking was linked with lower restraint, greater enjoyment of palatable foods may uniquely contribute to low-restraint binge eating. Increasing emphasis on emotion regulation and food-related reward sensitivity may enhance treatment outcomes for individuals with low-restraint binge eating.

Consequences of chronodisruption on body weight regulation and metabolism

The prevalence of overweight and obesity has increased dramatically. At the same time, lack of sleep has become a part of the modern lifestyle, as well as shift and night work. As a result, chronodisruption, i. e. a change in physiological processes that are controlled by the internal clock, becomes commonplace. Epidemiological data show that too short but also too long sleep are associated with an increased risk of obesity, also seen for night shift work. Overweight and obesity are associated with metabolic syndrome and data likewise report an increased risk by both short and long sleep. It has not yet been conclusively clarified how chronodisruption influences the metabolic risks. Clinical experimental studies report on neuroendocrine and circadian mechanisms and it has been shown that lack of sleep increases the hunger-promoting hormone ghrelin as well as subjective feelings of hunger and increases leptin levels. Lack of sleep also increases hedonic hunger and food-related reward signals. Through preventive measures, chronodisruption and thus, the risk of obesity can be counteracted. The extent to which smartwatches and fitness trackers, which according to the manufacturer can measure and analyze sleep, provide an objective picture of sleep has not been sufficiently investigated. However, smartwatches and fitness trackers can - probably - increase awareness of sleep in the modern society.

Associations between maternal pre-pregnancy BMI and infant striatal mean diffusivity

BackgroundIt is well-established that parental obesity is a strong risk factor for offspring obesity. Further, a converging body of evidence now suggests that maternal weight profiles may affect the developing offspring’s brain in a manner that confers future obesity risk. Here, we investigated how pre-pregnancy maternal weight status influences the reward-related striatal areas of the offspring’s brain during in utero development.MethodsWe used diffusion tensor imaging to quantify the microstructure of the striatal brain regions of interest in neonates (N = 116 [66 males, 50 females], mean gestational weeks at birth [39.88], SD = 1.14; at scan [43.56], SD = 1.05). Linear regression was used to test the associations between maternal pre-pregnancy body mass index (BMI) and infant striatal mean diffusivity.ResultsHigh maternal pre-pregnancy BMI was associated with higher mean MD values in the infant’s left caudate nucleus. Results remained unchanged after the adjustment for covariates.ConclusionsIn utero exposure to maternal adiposity might have a growth-impairing impact on the mean diffusivity of the infant’s left caudate nucleus. Considering the involvement of the caudate nucleus in regulating eating behavior and food-related reward processing later in life, this finding calls for further investigations to define the prognostic relevance of early-life caudate nucleus development and weight trajectories of the offspring.

Daily ovarian hormone exposure and loss of control eating in adolescent girls: A registered report.

The daily biobehavioral factors that precipitate loss of control eating (LOCE) in adolescent girls are not well known. Ovarian hormone levels are key biological factors associated with the etiology of eating disorders in adolescent girls. Yet, models on how daily ovarian hormone exposure predicts LOCE in adolescent girls are underdeveloped. The goal of this study is to examine the daily patterns and mechanisms of ovarian hormone levels on LOCE across the menstrual cycle in adolescent girls and the mediating roles of food-related reward anticipation and response inhibition. Ecological momentary assessment (EMA) paired with daily hormonal sampling will be used to examine (1) daily associations between within-person hormones and LOCE, and (2) the mediating role of within-person food-related reward anticipation and response inhibition. Normally cycling adolescent girls who have reached menarche will provide daily saliva samples for hormone analysis and complete EMA for 35 days. During EMA, girls will report LOCE and will complete task-based and self-report measures of food-related response inhibition and reward anticipation. This work has implications for the development of new real-world biobehavioral models of LOCE in adolescent girls, which will guide theory improvements and treatment for LOCE. Results will provide preliminary evidence for treatment targets for novel interventions for adolescent girls-for example, a response inhibition intervention. Adolescent eating disorders are severe mental health conditions, often marked by loss of control eating. Estrogen and progesterone play a role in the development and persistence of loss of control eating. The current study will examine how daily exposure to estrogen and progesterone predicts loss of control eating in adolescent girls and identify possible daily mechanisms linking estrogen and progesterone exposure and loss of control eating.

Altered neural reward processing is associated with reward-related decision-making in adolescents with severe obesity

Obesity is associated with altered food-related reward processing, but its impact on non-food reward remains unclear. This question is both timely due to rising rates of severe obesity and important because adolescence is a period of heightened reward seeking behavior. We used computational modeling and functional magnetic resonance imaging (fMRI) to examine monetary reward processing using classic experimental tasks in 35 adolescents (14-18 years-old, 13 male) with severe obesity (OB; n=18) and without obesity (nonOB; n=17). Participants completed the Balloon Analog Risk Taking Task (BART) to assess reward-related decision-making and the Monetary Incentive Delay (MID) task to assess neural correlates of reward anticipation. BART model-based parameters revealed no differences in reward sensitivity but less adaptive decision-making (response consistency) in OB compared to nonOB. Other metrics (e.g., number of balloons popped, number of pumps, and total points) did not differ between groups. During MID reward anticipation, OB had lower activation than nonOB in ventral tegmental area (VTA) and prefrontal cortex, canonical regions for reward and cognitive control, respectively. Weight status moderated associations between VTA activation and BART metrics such that higher VTA activation was associated with more risky decision-making (more popped balloons) in OB but not nonOB. Functional connectivity of VTA with right inferior frontal gyrus (IFG) and left superior temporal gyrus (STG) was greater higher in OB than nonOB. Associations between value-related VTA-STG connectivity and BART metrics were moderated by weight status such that higher connectivity was associated with greater number of pumps and points for nonOB and less risky decision-making for OB. Therefore, differences in activation and connectivity between groups may suggest differences in decision-making strategies. Together, findings reveal that VTA, prefrontal, and temporal engagement during monetary reward anticipation differs in OB and nonOB adolescents and may contribute to individual differences in reward-related decision-making. Such domain-general alteration of reward processing may have far reaching consequences, not only for food intake but also functions central to motivational behavior such as learning and socialization during adolescence, a sensitive period in development. These findings highlight the importance of considering reward more broadly when designing and tailoring behavioral interventions in adolescent obesity

Food-related reward sensitivity across the spectrum of body weight and impulsive eating: Pilot findings from a multi-method approach

Overweight with and without comorbid binge-eating disorder (BED) has been associated with increased reward sensitivity, though evidence is heterogeneous. To disentangle this heterogeneity and gain insights into mechanisms of impaired reward processing, this study applied multi-method neuro-behavioural techniques.Reward sensitivity was investigated in N = 49 participants allocated to three subgroups: overweight individuals with BED (BED+, n = 17), overweight individuals without BED (BED-, n = 15), and normal-weight controls (NWC, n = 17). Applying a free exploration paradigm (food vs. non-food stimuli), eye tracking and electroencephalographic data were gathered. A valid cue before stimulus onset indicated the position of food, and the end points analysed after the cue and stimulus onset were attentional approach, attention allocation, and conflict processing (e.g., conflict between looking at the potentially rewarding food stimulus or not). The effect of negative mood was tested using mood induction. The study's main hypothesis was that individuals with overweight, particularly under negative mood, would have increased food-related reward sensitivity.All participants showed increased food-specific attentional approach (p < .001). BED + allocated more attention to food stimuli than non-food stimuli compared to the healthy control (p = .045). For individuals with overweight but without BED (BED-), results indicate that conflict processing might be prolonged after the stimulus onset (p = .011). No group-specific effect of negative mood was found.Preliminary results in overweight individuals with and without comorbid BED suggest that food stimuli are generally rewarding stimuli, but even more so for participants with binge eating psychopathology. Prolonged conflict processing during the confrontation with competing food and non-food stimuli was solely found in the BED- sample and might indicate a compensation mechanism. Replication is warranted. The multi-method approach seems to be promising to give indications for the development of psychotherapeutic treatment.

The role of everyday activities on likelihood of dietary lapse: an ecological momentary assessment study.

Developing a more nuanced understanding of factors predicting risk of dietary lapse (i.e., instances of non-adherence to a reduced calorie diet) is important, because dietary lapses contribute to suboptimal weight outcomes. The study investigated, for the first time, how various everyday activities affected likelihood of dietary lapses at two timescales-both in-the-moment, and in the hours after engaging in an activity. Participants (N = 107) with overweight/obesity in a behavioral weight loss program completed ecological momentary assessment surveys on dietary adherence and daily activities for 3 weeks at mid-treatment. Generalized estimating equations revealed that socializing predicted greater concurrent lapse risk, while work/school, doing chores, cooking, or practicing a spiritual activity/prayer/meditation were associated with reduced lapse risk. In terms of subsequent effects, cooking and indoor hobbies were associated with greater lapse risk in the next few hours, whereas spiritual activity/meditation was associated with reduced risk. Certain activities may have affected concurrent and subsequent lapse risk due to: their influence on the presence of tempting food, the compatibility of engaging in the activity and eating simultaneously, and the reward reaped from the activity (potentially reducing desire for food-related reward). Findings speak to the importance of attending to the timescale of relationships between activities and lapses, which has clinical implications for providing nuanced and optimally timed interventions for overweight/obesity.

The effects of lisdexamfetamine dimesylate on eating behaviour and homeostatic, reward and cognitive processes in women with binge-eating symptoms: an experimental medicine study

Lisdexamfetamine dimesylate (LDX) is the only drug currently approved by the FDA for the treatment of Binge-Eating Disorder (BED), but little is known about the behavioural mechanisms that underpin the efficacy of LDX in treating BED. We examined the behavioural and neural effects of an acute dose of LDX (50 mg) in 22 women with binge-eating symptomatology using a randomised, crossover, double-blind, placebo-controlled experimental medicine design. LDX reduced self-reported appetite ratings and intake of both a pasta meal and a palatable cookie snack. LDX also decreased the eating rate of pasta but not of cookies and reduced self-reported liking ratings for pasta at the end of the meal. When viewing food pictures during an fMRI scan, LDX reduced activity bilaterally in the thalamus. LDX enhanced sustained attention and reduced impulsive responding in a continuous performance task but had no effect on emotional bias or working memory. These results suggest the observed effects of LDX on food intake (and by implication the efficacy of LDX in treating BED) may be related to the actions of the drug to enhance satiety, reduce food-related reward responding when full and/or increase cognitive control. Novel pharmacotherapies for BED might be most effective if they have a broad spectrum of effects on appetite, reward and cognition.

Task- and Rest-based Functional Brain Connectivity in Food-related Reward Processes among Healthy Adolescents

It is known that the nucleus accumbens, orbitofrontal cortex and insula play a role in food-related reward processes. Although their interconnectedness would be an ideal topic for understanding food intake mechanisms, it nevertheless remains unclear especially in adolescent. Therefore, this study aims to investigate the effect of hunger on functional connectivity in healthy adolescents using task- and rest-based imaging. Fifteen participants underwent two MRI sessions, pre-lunch (hunger) and post-lunch (satiety), including food cue task and resting-state. During task- and rest-based imaging, functional connectivity was greater when hungry as opposed to satiated between the right posterior insula/nucleus accumbens, suggesting involvement of salient interoceptive stimuli signals. During task-based imaging, an increase was observed in functional connectivity when hungry as opposed to satiated between the medial and lateral orbitofrontal cortex which contributes to the perception of food deprivation as a frustration. A decrease was identified when hungry as opposed to satiated in functional connectivity in the right anterior orbitofrontal/accumbens and posterior insula/medial orbitofrontal cortices reflecting suppression of the affective and sensorial information. Conversely, functional connectivity was increased during aversive stimuli between the right medial orbitofrontal cortex and right posterior insula when hungry as opposed to satiated. This suggests that the value of valence could occur in the shift in connectivity between these two regions. In addition, during rest-based imaging, a left-sided lateralization was reported (accumbens/lateral orbitofrontal and accumbens/posterior insula) when hungry as opposed to satiated which may represent changes in internal state due to focus on the benefit of an upcoming meal.

Reward and psychopathological correlates of eating disorders: The explanatory role of leptin

It has been hypothesized that leptin level alterations in Eating Disorders (EDs) represent a maintaining factor for pathological reward-related ED behaviors, given leptin role in the dopaminergic reward systems. The aim of the present study was to evaluate the role of leptin in EDs as a mediator for the relationship between Body Mass Index (BMI) and several pathological behaviors, such as dietary restraint, compensatory exercise, vomiting, binge eating and emotional eating. Sixty-two patients with EDs and 41 healthy controls (HC) had their blood drawn and completed psychometric tests for the evaluation of general psychopathology, ED psychopathology and emotional eating. Moderated linear regression models showed that, in the presence of high levels of ED psychopathology, leptin levels were negatively associated with dietary restraint and compensatory exercise, and positively with emotional eating and binge eating. Finally, leptin showed an indirect effect on the association between BMI and all these reward-related behaviors. These results suggest that a variation of BMI maintains these pathological ED behaviors through a variation in leptin levels. Considering the role of leptin in reward circuits, the results seem to confirm an aberrant food-related reward mechanism in ED patients.

Ovarian Hormones and Reward Processes in Palatable Food Intake and Binge Eating.

Ovarian hormones are associated with risk for binge eating in women. Recent animal and human studies suggest that food-related reward processing may be one set of neurobiological factors that contribute to these relationships, but additional studies are needed to confirm and extend findings.

History of withdrawal modulates drug- and food-cue reactivity in cocaine dependent participants

While the centrality of withdrawal in the diagnosis of addiction has been decreasing with each successive edition of the Diagnostic and Statistical Manual of Mental Disorders, psychometric and neurobiological evidence provides withdrawal a central role in the development and maintenance of addiction. The current study offers insight into these conflicting positions by using secondary analyses to assess how a history of DSM-assessed withdrawal influences the magnitude of bias in neural reactivity to drug- and/or food-related reward cues. To this end, we separated an existing sample of cocaine-dependent participants (Denomme et al., 2018) into those with (WD) and without (N-WD) a history of withdrawal, and compared food- and drug-cue reactivity between these groups, and to a non-dependent control group (ND). Analyses indicated that biases in neural reactivity towards drug- versus food-related cues only occurred among the WD participants (within: left dorsomedial prefrontal cortex, left anterior cingulate cortex, left orbitofrontal cortex, left caudate nucleus, and right ventrolateral prefrontal cortex). Thus, withdrawal status may be an important factor to consider when interpreting dependence-related biases in neural reactivity following reward-related cues. Interestingly, while N-WD participants did not show these broad biases in neural reactivity, the magnitude of their bias correlated positively with years of lifetime substance use history, particularly when psychopathic traits were low. It may be that for individuals who’s addiction has not yet reached a compulsive state (see Wise and Koob, 2014), the magnitude of their drug > food bias could serve as a valuable biomarker of addiction severity.

S206. Effect of Alcohol on Ad Lib Eating: The Role of Food-Related Reward and Inhibitory Control

Heavy alcohol use is associated with obesity. This may be due to calories in the alcohol beverage itself or to effects of alcohol on food consumption. For example, alcohol may increase food consumption by increasing the value of food rewards, or by decreasing inhibition, which limits food intake.

White matter integrity disparities between normal-weight and overweight/obese adolescents: an automated fiber quantification tractography study.

Obese adults have been shown to have poorer white brain matter integrity relative to normal-weight peers, but few studies have tested whether white matter integrity is compromised in overweight and obese adolescents. Also, it is unclear if age interacts with body mass to affect white matter integrity in adolescents. We used Automated Fiber Quantification, a tractography method, to compare fractional anisotropy between normal-weight and overweight/obese adolescents in the corpus callosum, corticospinal tract, cingulum, inferior fronto-occipital fasciculus, and uncinate fasciculus. Further, we tested whether any differences were moderated by age. Forty-seven normal-weight and forty overweight/obese adolescents were scanned using a diffusion tensor imaging (DTI) scan sequence. Overweight/obese compared to normal-weight adolescents had decreased white matter integrity in the superior frontal corpus callosum, left and right uncinate fasciculi, left inferior fronto-occipital fasciculus, and left corticospinal tract, which may be related to heightened reward processing. Overweight/obese compared to normal-weight adolescents had increased white matter integrity in the orbital and anterior frontal corpus callosum, right inferior fronto-occipital fasciculus, left cingulum, and left corticospinal tract, which may be related to heightened attentional processing. As age increased, six tracts showed poorer white matter integrity as body mass index percentile (BMI%) increased, but three tracts showed greater white matter integrity as BMI% increased. Future research examining associations between white matter integrity and neural indices of food-related reward and attention are needed to clarify the functional significance of white matter integrity discrepancies between normal-weight and overweight/obese adolescents.

Author response: Early weight loss in parkinsonism predicts poor outcomes: Evidence from an incident cohort study.

We thank Dr. Marinelli for the comment on our article,1 and agree that further research into the relationship between protein misfolding and weight loss in Parkinson disease (PD) is needed. Furthermore, several other potential mechanisms for weight loss deserve further study, including other aspects of brain metabolism, whole-body metabolic rate, appetite regulation, and food-related reward mechanisms.

Impact of Dietary Fats on Brain Functions

Background: Adequate dietary intake and nutritional status have important effects on brain functions and on brain health. Energy intake and specific nutrients excess or deficiency from diet differently affect cognitive processes, emotions, behaviour, neuroendocrine functions and synaptic plasticity with possible protective or detrimental effects on neuronal physiology. Lipids, in particular, play structural and functional roles in neurons. Here the importance of dietary fats and the need to understand the brain mechanisms activated by peripheral and central metabolic sensors. Thus, the manipulation of lifestyle factors such as dietary interventions may represent a successful therapeutic approach to maintain and preserve brain health along lifespan.Methods: This review aims at summarizing the impact of dietary fats on brain functions.Results: Starting from fat consumption, nutrient sensing and food-related reward, the impact ofgut-brain communications will be discussed in brain health and disease. A specific focus will be on the impact of fats on the molecular pathways within the hypothalamus involved in the control of reproduction via the expression and the release of Gonadotropin-Releasing Hormone. Lastly, the effects of specific lipid classes such as polyunsaturated fatty acids and of the “fattest” of all diets, commonly known as “ketogenic diets”, on brain functions will also be discussed.Conclusion: Despite the knowledge of the molecular mechanisms is still a work in progress, the clinical relevance of the manipulation of dietary fats is well acknowledged and such manipulations are in fact currently in use for the treatment of brain diseases.

Neural Food Reward Processing in Successful and Unsuccessful Weight Maintenance.

Weight loss maintenance is one of the biggest challenges in behavioral weight loss programs. The present study aimed to examine metabolic influences on the mesolimbic reward system in people with successful and unsuccessful long-term weight loss maintenance. Thirty-three women with obesity at least 6 months after the completion of a diet were recruited: seventeen women were able to maintain their weight loss, whereas sixteen showed weight regain. Using functional magnetic resonance imaging in combination with the assessment of appetite-regulating hormones, neural reward processing during hunger and satiety was investigated. An incentive delay task was employed to investigate the expectation and receipt of both food-related and monetary reward. Only participants with successful weight loss maintenance showed a satiety-induced attenuation of brain activation during the receipt of a food-related reward. Furthermore, in successful weight loss maintenance, the attenuation of active ghrelin levels was related to brain activation in response to food-related reward anticipation during satiety. The findings suggest that an attenuated influence of satiety signaling on the neural processing of food-related reward contributes to unsuccessful weight loss maintenance. Thus, intact satiety signaling to the mesolimbic reward system may serve as a promising target for tackling weight cycling.

Peripheral Endocannabinoid Responses to Hedonic Eating in Binge-Eating Disorder.

Reward mechanisms are likely implicated in the pathophysiology of binge-eating behaviour, which is a key symptom of binge-eating disorder (BED). Since endocannabinoids modulate food-related reward, we aimed to investigate the responses of anandamide (AEA) and 2-arachidonoylglycerol (2-AG) to hedonic eating in patients with BED. Peripheral levels of AEA and 2-AG were measured in 7 obese BED patients before and after eating favorite (hedonic eating) and non-favorite (non-hedonic eating) foods. We found that plasma levels of AEA progressively decreased after eating the non-favorite food and significantly increased after eating the favorite food, whereas plasma levels of 2-AG did not differ significantly between the two test conditions, although they showed a trend toward significantly different time patterns. The changes in peripheral AEA levels were positively correlated to the subjects’ sensations of the urge to eat and the pleasantness while eating the presented food, while changes in peripheral 2-AG levels were positively correlated to the subjects’ sensation of the pleasantness while eating the presented food and to the amount of food they would eat. These results suggest the occurrence of distinctive responses of endocannabinoids to food-related reward in BED. The relevance of such findings to the pathophysiology of BED remains to be elucidated.

Integration of homeostatic signaling and food reward processing in the human brain.

Food intake is guided by homeostatic needs and by the reward value of food, yet the exact relation between the two remains unclear. The aim of this study was to investigate the influence of different metabolic states and hormonal satiety signaling on responses in neural reward networks. Twenty-three healthy participants underwent functional magnetic resonance imaging while performing a task distinguishing between the anticipation and the receipt of either food- or monetary-related reward. Every participant was scanned twice in a counterbalanced fashion, both during a fasted state (after 24 hours fasting) and satiety. A functional connectivity analysis was performed to investigate the influence of satiety signaling on activation in neural reward networks. Blood samples were collected to assess hormonal satiety signaling. Fasting was associated with sensitization of the striatal reward system to the anticipation of food reward irrespective of reward magnitude. Furthermore, during satiety, individual ghrelin levels were associated with increased neural processing during the expectation of food-related reward. Our findings show that physiological hunger stimulates food consumption by specifically increasing neural processing during the expectation (i.e., incentive salience) but not the receipt of food-related reward. In addition, these findings suggest that ghrelin signaling influences hedonic-driven food intake by increasing neural reactivity during the expectation of food-related reward. These results provide insights into the neurobiological underpinnings of motivational processing and hedonic evaluation of food reward. ClinicalTrials.gov NCT03081585. This work was supported by the German Competence Network on Obesity, which is funded by the German Federal Ministry of Education and Research (FKZ 01GI1122E).

Neural Activation to Food Cues and Cognition in Sedentary Obese Endometrial Cancer Survivors Seeking Weight Loss

PURPOSE: Sedentary behavior and obesity increase the risk of endometrial cancer (EC), particularly Type I forms, which are increasing in the U.S. Further, although death rates from most cancers are decreasing, overall mortality rates for EC are increasing; and, obese EC patients have significantly poorer survival rates compared to normal weight EC patients. No prior studies have examined neural activation in response to food cues as well as sedentary behavior and cognition in obese EC survivors. METHODS: Therefore, we evaluated appetitive behavior using a visual food cue functional magnetic resonance imaging (fMRI) task as well as sedentary behavior and cognition using Trails A & B and Symbol Digits Modalities Tests in 42 obese EC survivors seeking weight loss. RESULTS: We found increased activation in response to high-calorie food cues after eating a meal in brain regions associated with food-related reward (dorsolateral prefrontal cortex, amygdala; whole brain cluster corrected, p<0.05) in obese EC survivors. In addition, cognitive tests suggest scores in obese EC patients are lower than normative data for similar age and gender. We are currently evaluating correlations between sedentary behavior, cognitive scores and neural signals in differentially activated brain regions. CONCLUSIONS: To our knowledge, this is the first study to evaluate cognitive and sedentary behavior correlates of neural activation in response to food cues in obese EC survivors and, these data may also help inform future work in other adult obese populations with and without cancer. This work was supported by NIH NCI R01-CA175100.