The effect of personal relative deprivation on food choice: An experimental approach

Growing evidence suggests that relative disadvantage is more relevant than absolute socioeconomic factors in explaining disparities in healthfulness of diet. In a series of pre-registered experiments, we tested whether personal relative deprivation (PRD), i.e. the sense that one is unfairly deprived of a deserved outcome relative to others, results in choosing more palatable, rewarding foods. Study 1 (N = 102) demonstrated the feasibility and effectiveness of a game for inducing real-time experiences of PRD. Study 2 (N = 287) showed no main effect of PRD condition on hypothetical food choices, but an interaction between chronic PRD and condition revealed that those in the PRD condition chose more rewarding foods when feeling chronically deprived. In Study 3 (N = 260) the hypothesized main effect was found on real, non-hypothetical food choices: those in the PRD condition chose more rewarding foods, controlling for sensitivity to palatable food. Our results provide preliminary indications that the experience of being relatively deprived, rather than the objective amount or resources, may result in a higher preference for high-caloric and palatable foods. It may be suggested that efforts to reduce societal disparities in healthfulness of diet may need to focus on perceptions of injustice beyond objective inequalities.

Metabolic sensing in AgRP neurons integrates homeostatic state with dopamine signalling in the striatum

Agouti-related peptide (AgRP) neurons increase motivation for food, however whether metabolic sensing of homeostatic state in AgRP neurons potentiates motivation by interacting with dopamine reward systems is unexplored. As a model of impaired metabolic-sensing, we used the AgRP-specific deletion of carnitine acetyltransferase (Crat) in mice. We hypothesized that metabolic sensing in AgRP neurons is required to increase motivation for food reward by modulating accumbal or striatal dopamine release. Studies confirmed that Crat deletion in AgRP neurons (KO) impaired ex vivo glucose-sensing, as well as in vivo responses to peripheral glucose injection or repeated palatable food presentation and consumption. Impaired metabolic-sensing in AgPP neurons reduced acute dopamine release (seconds) to palatable food consumption and during operant responding, as assessed by GRAB-DA photometry in the nucleus accumbens, but not the dorsal striatum. Impaired metabolic-sensing in AgRP neurons suppressed radiolabelled 18F-fDOPA accumulation after ~30 minutes in the dorsal striatum but not the nucleus accumbens. Impaired metabolic sensing in AgRP neurons suppressed motivated operant responding for sucrose rewards during fasting. Thus, metabolic-sensing in AgRP neurons is required for the appropriate temporal integration and transmission of homeostatic hunger-sensing to dopamine signalling in the striatum.

The relationship between reward context and inhibitory control, does it depend on BMI, maladaptive eating, and negative affect?

Background Recent studies suggest that higher Body Mass Index (BMI) is associated with reduced inhibitory control in contexts of palatable food. However, due to limitations of previous studies, it remained the question whether this reduction is specific to food contexts, and whether it generalizes to other contexts of reward, such as money. This main question was addressed in the current study. In addition, we explored the effect of maladaptive eating and stress regarding inhibitory control across the contexts that differed in terms of reward. Methods In total, 46 participants between 19 and 50 years old (39% males and 61% females) with an average BMI of 23.5 (SD = 3.9) participated. Participants filled out questionnaires and performed a go/no-go task (indexing inhibitory control) with three conditions (neutral, food, and money condition). Results Relatively high (above median) BMI was associated with challenged inhibitory control in the food relative to the neutral context, but not in the money relative to neutral context. Explorative analyses suggested that maladaptive eating and stress were associated with reduced inhibitory control in the food context. Only rumination was associated with reduced inhibitory control in the money context. Conclusions The effects of BMI, maladaptive eating behavior, and stress on inhibitory control were specific to the food context, and did not generalize to a non-intrinsic reward condition, operationalized with money pictures. Our results imply that (research on) interventions directed at improving inhibitory control in relation to overweight and obesity, should consider food-reward context.

Corticostriatal dynamics underlying components of binge-like eating in mice

Binge eating (BE) is a maladaptive repetitive feeding behavior present across nearly all eating disorder diagnoses. BE is associated with poor psychosocial outcomes (e.g., suicidal ideation) and increased risk for obesity. Despite the substantial negative impact of BE, its underlying neural mechanisms are largely unknown. Many other repetitive behavior disorders (e.g., obsessive compulsive disorder) show dysfunction within corticostriatal circuitry. Additionally, previous pre clinical and clinical work has highlighted an imbalance between goal directed and habitual responding in BE. The aim of the current study was to longitudinally examine in vivo neural activity within corticostriatal regions associated with habitual behavior, the infralimbic cortex (IL) and dorsolateral striatum (DLS), using a robust pre clinical model for BE. Female C57BL/6 mice (N = 32) were randomized to receive: 1) intermittent (daily, 2-hour) binge-like access to palatable food (BE mice), or 2) continuous, non-intermittent (24-hour) access to palatable food (non-BE mice). In vivo calcium imaging was performed via fiber photometry at the baseline timepoint and after 4 weeks (chronic timepoint) of engagement in the model for BE. Feeding behaviors (feeding bout onset, offset) during the recordings were captured using contact lickometers which generated TTL outputs for precise alignment of BE behavior to neural data. Results in the IL showed no specific changes in neural activity related to BE. However, BE animals showed decreased DLS activity from the baseline to chronic timepoint at feeding onset and offset. Additionally, BE mice had significantly lower DLS activity at feeding onset and offset during the chronic time point compared to non-BE mice. These results point to a role for DLS hypofunction in chronic BE, highlighting a potential target for future treatment intervention.

Orbitofrontal cortex and dorsal striatum functional connectivity predicts incubation of opioid craving after voluntary abstinence

We recently introduced a rat model of incubation of opioid craving after voluntary abstinence induced by negative consequences of drug seeking. Here, we used resting-state functional MRI to determine whether longitudinal functional connectivity changes in orbitofrontal cortex (OFC) circuits predict incubation of opioid craving after voluntary abstinence. We trained rats to self-administer for 14 d either intravenous oxycodone or palatable food. After 3 d, we introduced an electric barrier for 12 d that caused cessation of reward self-administration. We tested the rats for oxycodone or food seeking under extinction conditions immediately after self-administration training (early abstinence) and after electric barrier exposure (late abstinence). We imaged their brains before self-administration and during early and late abstinence. We analyzed changes in OFC functional connectivity induced by reward self-administration and electric barrier–induced abstinence. Oxycodone seeking was greater during late than early abstinence (incubation of oxycodone craving). Oxycodone self-administration experience increased OFC functional connectivity with dorsal striatum and related circuits that was positively correlated with incubated oxycodone seeking. In contrast, electric barrier–induced abstinence decreased OFC functional connectivity with dorsal striatum and related circuits that was negatively correlated with incubated oxycodone seeking. Food seeking was greater during early than late abstinence (abatement of food craving). Food self-administration experience and electric barrier–induced abstinence decreased or maintained functional connectivity in these circuits that were not correlated with abated food seeking. Opposing functional connectivity changes in OFC with dorsal striatum and related circuits induced by opioid self-administration versus voluntary abstinence predicted individual differences in incubation of opioid craving.

The Orexigenic Force of Olfactory Palatable Food Cues in Rats

Environmental cues recalling palatable foods motivate eating beyond metabolic need, yet the timing of this response and whether it can develop towards a less palatable but readily available food remain elusive. Increasing evidence indicates that external stimuli in the olfactory modality communicate with the major hub in the feeding neurocircuitry, namely the hypothalamic arcuate nucleus (Arc), but the neural substrates involved have been only partially uncovered. By means of a home-cage hidden palatable food paradigm, aiming to mimic ubiquitous exposure to olfactory food cues in Western societies, we investigated whether the latter could drive the overeating of plain chow in non-food-deprived male rats and explored the neural mechanisms involved, including the possible engagement of the orexigenic ghrelin system. The olfactory detection of a familiar, palatable food impacted upon meal patterns, by increasing meal frequency, to cause the persistent overconsumption of chow. In line with the orexigenic response observed, sensing the palatable food in the environment stimulated food-seeking and risk-taking behavior, which are intrinsic components of food acquisition, and caused active ghrelin release. Our results suggest that olfactory food cues recruited intermingled populations of cells embedded within the feeding circuitry within the Arc, including, notably, those containing the ghrelin receptor. These data demonstrate the leverage of ubiquitous food cues, not only for palatable food searching, but also to powerfully drive food consumption in ways that resonate with heightened hunger, for which the orexigenic ghrelin system is implicated.

Cerebral μ-opioid and CB1 receptor systems have distinct roles in human feeding behavior

Eating behavior varies greatly between individuals, but the neurobiological basis of these trait-like differences in feeding remains poorly understood. Central μ-opioid receptors (MOR) and cannabinoid CB1 receptors (CB1R) regulate energy balance via multiple neural pathways, promoting food intake and reward. Because obesity and eating disorders have been associated with alterations in the brain’s opioid and endocannabinoid signaling, the variation in MOR and CB1R system function could potentially underlie distinct eating behavior phenotypes. In this retrospective positron emission tomography (PET) study, we analyzed [11C]carfentanil PET scans of MORs from 92 healthy subjects (70 males and 22 females), and [18F]FMPEP-d2 scans of CB1Rs from 35 subjects (all males, all also included in the [11C]carfentanil sample). Eating styles were measured with the Dutch Eating Behavior Questionnaire (DEBQ). We found that lower cerebral MOR availability was associated with increased external eating—individuals with low MORs reported being more likely to eat in response to environment’s palatable food cues. CB1R availability was associated with multiple eating behavior traits. We conclude that although MORs and CB1Rs overlap anatomically in brain regions regulating food reward, they have distinct roles in mediating individual feeding patterns. Central MOR system might provide a pharmacological target for reducing individual’s excessive cue-reactive eating behavior.