Control Of Feeding Behavior Research Articles

Investigating the Role of CART/GPR160 Signaling in Stress-Induced Anorexia

Stress-induced anorexia represents a conserved adaptive response across diverse species. While this response can be crucial for survival in specific situations, it may become detrimental when prolonged stress exposure leads to unhealthy eating patterns, contributing to eating disorders like anorexia nervosa and bulimia. Feeding behavior is intricately connected to the stress response, as stress levels can influence appetite and energy expenditure. Central to the stress response are corticotropin-releasing hormone (CRH)-producing neurons, which secrete CRH, stimulating the production of ACTH in the pituitary gland and subsequently triggering the release of cortisol, a stress hormone, from the adrenal glands. The presence of CRH in the hypothalamus, a brain region involved in controlling feeding, suggests a complex interplay where stress and metabolic signals converge. One such signal is the peptide cocaine- and amphetamine-regulated transcript (CART) which has been shown to regulate feeding behavior, satiety, and metabolic function by signaling through its receptor GPR160 and downstream glucagon-like peptide (GLP)-1 signaling. In this study, we hypothesize that CART/GPR160 signals within CRH-producing neurons to control feeding behavior and stress responses. To test this hypothesis, we used a multifaceted approach, utilizing both wild type and GPR160-floxed rats in which GPR160 was knocked down specifically in CRH neurons using an AAV-Cre under the control of the CRH promoter injected bilaterally into the paraventricular nucleus. We monitored food and water intake, investigated CRH secretion from hypothalamic explants treated with CART, and assessed physiological changes in GPR160, CART, and other related molecules in various brain regions following acute stress. We also examined the effects of GPR160 knockdown in PVN neurons on plasma cortisol levels in response to restraint stress. While further studies are necessary to fully define the roles of CART and GPR160 in stress responses and feeding behavior control, our preliminary findings indicate that this ligand-receptor pair could serve as a novel therapeutic target for treating psychiatric diseases related to eating disorders. NIH. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Feeding under fire: Relations between parental stress hormones and controlling feeding behaviors

Under stress, parents tend to use more controlling feeding behaviors toward their children (Berge et al., 2017; Doan et al., 2022; Loth et al., 2016). However, the majority of prior work focuses on subjective reports of stress, and there is a dearth of research examining parental physiological stress and its impact on feeding behaviors. In the current study, we examined how parental physiological stress reactivity would influence their feeding behaviors under mild stress in a lab-based setting. Parents (n = 83, 50 % females) and their children (59% female, Mage = 42 months, SD = 4.48) participated. Stress was induced using the Trier Social Stress Test in the laboratory (Kirshbaum et al., 1993). Salivary samples were collected at 4 time points during the visit to index stress reactivity and later assayed for cortisol and DHEA. Parent-child interactions during the anticipatory period of the stress test were observationally coded for parent use of controlling feeding behaviors. To examine whether parent stress physiology predicts their feeding behaviors, we ran a Poisson regression using income, parent ethnicity, parent sex (mom/dad), time of day, and DHEA/cortisol ratio as predictors of controlling feeding behavior. Latinx parents used less controlling feeding behaviors, b = −0.323, p = 0.041 than non-Latinx parents. Parents with a higher DHEA/Cortisol ratio were less likely to use controlling feeding behaviors, b = −0.231, p = 0.008. To our knowledge, this is the first study to show that for both mothers and fathers, DHEA relative to cortisol has a protective role in controlling feeding practices, and lends support to the role of acute stress reactivity in predicting behavioral outcomes.

Activation patterns in male and female forebrain circuitries during food consumption under novelty.

The influence of novelty on feeding behavior is significant and can override both homeostatic and hedonic drives due to the uncertainty of potential danger. Previous work found that novel food hypophagia is enhanced in a novel environment and that males habituate faster than females. The current study's aim was to identify the neural substrates of separate effects of food and context novelty. Adult male and female rats were tested for consumption of a novel or familiar food in either a familiar or in a novel context. Test-induced Fos expression was measured in the amygdalar, thalamic, striatal, and prefrontal cortex regions that are important for appetitive responding, contextual processing, and reward motivation. Food and context novelty induced strikingly different activation patterns. Novel context induced Fos robustly in almost every region analyzed, including the central (CEA) and basolateral complex nuclei of the amygdala, the thalamic paraventricular (PVT) and reuniens nuclei, the nucleus accumbens (ACB), the medial prefrontal cortex prelimbic and infralimbic areas, and the dorsal agranular insular cortex (AI). Novel food induced Fos in a few select regions: the CEA, anterior basomedial nucleus of the amygdala, anterior PVT, and posterior AI. There were also sex differences in activation patterns. The capsular and lateral CEA had greater activation for male groups and the anterior PVT, ACB ventral core and shell had greater activation for female groups. These activation patterns and correlations between regions, suggest that distinct functional circuitries control feeding behavior when food is novel and when eating occurs in a novel environment.

The interplay between leptin, glucocorticoids, and GLP1 regulates food intake and feeding behaviour.

Nutritional, endocrine, and neurological signals converge in multiple brain centres to control feeding behaviour and food intake as part of the allostatic regulation of energy balance. Among the several neuroendocrine systems involved, the leptin, glucocorticoid, and glucagon-like peptide 1 (GLP1) systems have been extensively researched. Leptin is at the top hierarchical level since its complete absence is sufficient to trigger severe hyperphagia. Glucocorticoids are key regulators of the energy balance adaptation to stress and their sustained excess leads to excessive adiposity and metabolic perturbations. GLP1 participates in metabolic adaptation to food intake, regulating insulin secretion and satiety by parallel central and peripheral signalling systems. Herein, we review the brain and peripheral targets of these three hormone systems that integrate to regulate food intake, feeding behaviour, and metabolic homeostasis. We examine the functional relationships between leptin, glucocorticoids, and GLP1 at the central and peripheral levels, including the cross-regulation of their circulating levels and their cooperative or antagonistic actions at different brain centres. The pathophysiological roles of these neuroendocrine systems in dysregulated intake are explored in the two extremes of body adiposity - obesity and lipodystrophy - and eating behaviour disorders.

Parabrachial nucleus neuron circuits that control feeding behavior and energy balance

Parabrachial nucleus neuron circuits that control feeding behavior and energy balance

Mindfulness eating based on spiritual interventions on diet compliance and blood sugar levels in type 2 DM patients

Introduction: Diet is one component of diabetes mellitus (DM) self-management for controlling blood sugar levels. Several obstacles in the implementation of the diet program have the potential for non-compliance, so that blood sugar levels tend to increase. Mindfulness eating based on spiritual intervention is one of the interventions that is expected to form adaptive eating behavior control to achieve dietary compliance and controlled blood sugar levels. The purpose of this study was to analyze the effect of mindfulness eating based on spiritual intervention on dietary compliance and blood sugar levels in patients with type 2 diabetes. Methods: The study's quasi-experimental, untreated control group design included dependent pre- and post-test samples. The population used was all patients with type 2 diabetes. The sample was taken using a simple random sampling technique with determination according to inclusion and exclusion criteria. The independent variables in this study were mindfulness eating based on spiritual intervention, while the dependent variables were dietary compliance and blood sugar levels. A glucometer and the Personal Diabetes Questionnaire (PDQ) were the tools employed in this investigation. The t-test was used as the statistical test. Results: There were a total of 50 samples that were divided between the control group and the intervention group. The results of the statistical test showed that mindfulness eating based on spiritual intervention had a statistically significant effect on dietary compliance (p < 0.001) and blood glucose levels (p < 0.001) compared to the control group. Conclusion: The value of diet adherence is greatly increased by mindfulness eating practices based on spiritual intervention, and mean blood glucose levels are significantly reduced at the conclusion of the study. Exercises in mindfulness eating that are based on spiritual intervention can be popularized as a way to deal with dietary issues and blood sugar regulation.

Glycemic Challenge Is Associated with the Rapid Cellular Activation of the Locus Ceruleus and Nucleus of Solitary Tract: Circumscribed Spatial Analysis of Phosphorylated MAP Kinase Immunoreactivity.

Rodent studies indicate that impaired glucose utilization or hypoglycemia is associated with the cellular activation of neurons in the medulla (Winslow, 1733) (MY), believed to control feeding behavior and glucose counterregulation. However, such activation has been tracked primarily within hours of the challenge, rather than sooner, and has been poorly mapped within standardized brain atlases. Here, we report that, within 15 min of receiving 2-deoxy-d-glucose (2-DG; 250 mg/kg, i.v.), which can trigger glucoprivic feeding behavior, marked elevations were observed in the numbers of rhombic brain (His, 1893) (RB) neuronal cell profiles immunoreactive for the cellular activation marker(s), phosphorylated p44/42 MAP kinases (phospho-ERK1/2), and that some of these profiles were also catecholaminergic. We mapped their distributions within an open-access rat brain atlas and found that 2-DG-treated rats (compared to their saline-treated controls) displayed greater numbers of phospho-ERK1/2+ neurons in the locus ceruleus (Wenzel and Wenzel, 1812) (LC) and the nucleus of solitary tract (>1840) (NTS). Thus, the 2-DG-activation of certain RB neurons is more rapid than perhaps previously realized, engaging neurons that serve multiple functional systems and which are of varying cellular phenotypes. Mapping these populations within standardized brain atlas maps streamlines their targeting and/or comparable mapping in preclinical rodent models of disease.

Gut–vagus–NTS neural pathway in controlling feeding behaviors

Gut–vagus–NTS neural pathway in controlling feeding behaviors

Neonatal oxytocin gives the tempo of social and feeding behaviors.

The nonapeptide oxytocin (OT) is a master regulator of the social brain in early infancy, adolescence, and adult life. Here, we review the postnatal dynamic development of OT-system as well as early-life OT functions that are essential for shaping social behaviors. We specifically address the role of OT in neonates, focusing on its role in modulating/adapting sensory input and feeding behavior; both processes are involved in the establishing mother-infant bond, a crucial event for structuring all future social interactions. In patients and rodent models of Prader-Willi and Schaaf-Yang syndromes, two neurodevelopmental diseases characterized by autism-related features, sensory impairments, and feeding difficulties in early infancy are linked to an alteration of OT-system. Successful preclinical studies in mice and a phase I/II clinical trial in Prader-Willi babies constitute a proof of concept that OT-treatment in early life not only improves suckling deficit but has also a positive long-term effect on learning and social behavior. We propose that in early postnatal life, OT plays a pivotal role in stimulating and coordinating the maturation of neuronal networks controlling feeding behavior and the first social interactions. Consequently, OT therapy might be considered to improve feeding behavior and, all over the life, social cognition, and learning capabilities.

Identification of a GABAergic neuroblast lineage modulating sweet and bitter taste sensitivity

In Drosophila melanogaster, processing of gustatory information and controlling feeding behavior are executed by neural circuits located in the subesophageal zone (SEZ) of the brain.1 Gustatory receptor neurons (GRNs) project their axons in the primary gustatory center (PGC), which is located in the SEZ.1,2,3,4 To address the function of the PGC, we need detailed information about the different classes of gustatory interneurons that frame the PGC. In this work, we screened large collections of driver lines for SEZ interneuron-specific labeling and subsequently used candidate lines to access the SEZ neuroblast lineages. We converted 130 Gal4 lines to LexA drivers and carried out functional screening using calcium imaging. We found one neuroblast lineage, TRdm, whose neurons responded to both sweet and bitter tastants, and formed green fluorescent protein (GFP) reconstitution across synaptic partners (GRASP)-positive synapses with sweet sensory neurons. TRdm neurons express the inhibitory transmitter GABA, and silencing these neurons increases appetitive feeding behavior. These results demonstrate that TRdm generates a class of inhibitory local neurons that control taste sensitivity in Drosophila.

Fibroblast growth factor 21 and dietary macronutrient intake in female mice

Fibroblast growth factor- 21 (FGF21) is a metabolic stress hormone that is released from the liver in response to various nutritional challenges. Because of its notable effects to improve metabolic health, including body fat loss, glucose control, and hepatosteatosis, several pharmaceutical analogs of FGF21 are in development for the treatment of metabolic disease. In addition, a small but developing literature clearly demonstrates that FGF21 also controls feeding behavior. Pharmacological administration of FGF21 reduces the consumption of simple sugars and other sweet tastants, and it increases the consumption of dietary proteins in males, suggesting another potential mechanism by which FGF21-treatment could improve metabolic health— by promoting healthy eating. Despite that sex is a key biological variable influencing feeding behavior and macronutrient selection, the current literature to date primarily on males. In this study, we investigated the effect of FGF21 on sucrose intake and macronutrient selection in female mice. Similar to our previous findings in male mice, we report that FGF21 administration decreases the consumption of sucrose solution by females, and that this is offset by increased chow intake. Also in agreement with our previous findings in males, we report that FGF21 increases the consumption of dietary protein by female mice, and this is offset by either reduced carbohydrate or by reduced fat intake. Lastly, we find that the effect of FGF21 to direct macronutrient intake in females depends on its actions in neurons. Overall, our data support a role for FGF21 to direct macronutrient intake in a similar manner in female and male mice.

Tissue distribution of appetite regulation genes and their expression in the Amazon fish Colossoma macropomum exposed to climate change scenario

Climate change leads to an increase in water acidification and temperature, two environmental factors that can change fish appetite and metabolism, affecting fish population in both wild and aquaculture facilities. Therefore, our study tested if climate change affects gene expression levels of two appetite-regulating peptides – Neuropeptide Y (NPY) and Cholecystokinin (CCK) – in the brain of tambaqui, Colossoma macropomum. Additionally, we show the distribution of these genes throughout the body. Amino acid sequences of CCK and NPY of tambaqui showed high similarity with other Characiformes, with the closely related order Cypriniformes, and even with the more distantly related order Salmoniformes. High apparent levels of both peptides were expressed in all brain areas, while expression levels varied for peripheral tissues. NPY and CCK mRNA were detected in all peripheral tissues but cephalic kidney for CCK. As for the effects of climate change, we found that fish exposed to extreme climate scenario (800 ppm CO2 and 4.5 °C above current climate scenario) had higher expression levels of NPY and lower expression levels of CCK in the telencephalon. The extreme climate scenario also increased food intake, weight gain, and body length. These results suggest that the telencephalon is probably responsible for sensing the metabolic status of the organism and controlling feeding behavior through NPY, likely an orexigenic hormone, and CCK, which may act as an anorexigenic hormone. To our knowledge, this is the first study showing the effects of climate change on the endocrine regulation of appetite in an endemic and economically important fish from the Amazon. Our results can help us predict the impact of climate change on both wild and farmed fish populations, thus contributing to the elaboration of future policies regarding their conservation and sustainable use.

Appetite regulating genes in zebrafish gut; a gene expression study.

The underlying molecular pathophysiology of feeding disorders, particularly in peripheral organs, is still largely unknown. A range of molecular factors encoded by appetite-regulating genes are already described to control feeding behaviour in the brain. However, the important role of the gastrointestinal tract in the regulation of appetite and feeding in connection to the brain has gained more attention in the recent years. An example of such inter-organ connection can be the signals mediated by leptin, a key regulator of body weight, food intake and metabolism, with conserved anorexigenic effects in vertebrates. Leptin signals functions through its receptor (lepr) in multiple organs, including the brain and the gastrointestinal tract. So far, the regulatory connections between leptin signal and other appetite-regulating genes remain unclear, particularly in the gastrointestinal system. In this study, we used a zebrafish mutant with impaired function of leptin receptor to explore gut expression patterns of appetite-regulating genes, under different feeding conditions (normal feeding, 7-day fasting, 2 and 6-hours refeeding). We provide evidence that most appetite-regulating genes are expressed in the zebrafish gut. On one hand, we did not observed significant differences in the expression of orexigenic genes (except for hcrt) after changes in the feeding condition. On the other hand, we found 8 anorexigenic genes in wild-types (cart2, cart3, dbi, oxt, nmu, nucb2a, pacap and pomc), as well as 4 genes in lepr mutants (cart3, kiss1, kiss1r and nucb2a), to be differentially expressed in the zebrafish gut after changes in feeding conditions. Most of these genes also showed significant differences in their expression between wild-type and lepr mutant. Finally, we observed that impaired leptin signalling influences potential regulatory connections between anorexigenic genes in zebrafish gut. Altogether, these transcriptional changes propose a potential role of leptin signal in the regulation of feeding through changes in expression of certain anorexigenic genes in the gastrointestinal tract of zebrafish.

AgRP neurons control feeding behaviour at cortical synapses via peripherally derived lysophospholipids.

Phospholipid levels are influenced by peripheral metabolism. Within the central nervous system, synaptic phospholipids regulate glutamatergic transmission and cortical excitability. Whether changes in peripheral metabolism affect brain lipid levels and cortical excitability remains unknown. Here, we show that levels of lysophosphatidic acid (LPA) species in the blood and cerebrospinal fluid are elevated after overnight fasting and lead to higher cortical excitability. LPA-related cortical excitability increases fasting-induced hyperphagia, and is decreased following inhibition of LPA synthesis. Mice expressing a human mutation (Prg-1R346T) leading to higher synaptic lipid-mediated cortical excitability display increased fasting-induced hyperphagia. Accordingly, human subjects with this mutation have higher body mass index and prevalence of type 2 diabetes. We further show that the effects of LPA following fasting are under the control of hypothalamic agouti-related peptide (AgRP) neurons. Depletion of AgRP-expressing cells in adult mice decreases fasting-induced elevation of circulating LPAs, as well as cortical excitability, while blunting hyperphagia. These findings reveal a direct influence of circulating LPAs under the control of hypothalamic AgRP neurons on cortical excitability, unmasking an alternative non-neuronal route by which the hypothalamus can exert a robust impact on the cortex and thereby affect food intake.

GIPR Agonism Inhibits PYY-Induced Nausea-Like Behavior.

The induction of nausea and emesis is a major barrier to maximizing the weight loss profile of obesity medications, and therefore, identifying mechanisms that improve tolerability could result in added therapeutic benefit. The development of peptide YY (PYY)-based approaches to treat obesity are no exception, as PYY receptor agonism is often accompanied by nausea and vomiting. Here, we sought to determine whether glucose-dependent insulinotropic polypeptide (GIP) receptor (GIPR) agonism reduces PYY-induced nausea-like behavior in mice. We found that central and peripheral administration of a GIPR agonist reduced conditioned taste avoidance (CTA) without affecting hypophagia mediated by a PYY analog. The receptors for GIP and PYY (Gipr and Npy2r) were found to be expressed by the same neurons in the area postrema (AP), a brainstem nucleus involved in detecting aversive stimuli. Peripheral administration of a GIPR agonist induced neuronal activation (cFos) in the AP. Further, whole-brain cFos analyses indicated that PYY-induced CTA was associated with augmented neuronal activity in the parabrachial nucleus (PBN), a brainstem nucleus that relays aversive/emetic signals to brain regions that control feeding behavior. Importantly, GIPR agonism reduced PYY-mediated neuronal activity in the PBN, providing a potential mechanistic explanation for how GIPR agonist treatment reduces PYY-induced nausea-like behavior. Together, the results of our study indicate a novel mechanism by which GIP-based therapeutics may have benefit in improving the tolerability of weight loss agents.

The feed beyond need: mechanisms of the hedonic control of eating

Eating behaviors arise from a combination of several factors namely, physiological, emotional, social and genetic, including the prevailing state of the environment that the individual has been exposed to from the commencement of development. Several factors are known to affect the control of eating behaviors, distinguishable by the synergism of the homeostatic and hedonic control mechanisms, which are complementary. While undeniably homeostasis is under the control of the hormonal interchange between the intestine and the brain, the desire to eat is focused on the brain reward system, which includes acquisition and addictions and binge eating. In today's world, the easy availability of processed foods, high in sugars and fats, which stimulate the reward areas, can flood the brain with neurotransmitters linked to pleasure and happiness. This often results in an uncontrollable desire to eat, technically termed hedonic hunger. A presentation of an integrated perspective of the mechanisms involved in the control of hedonic eating behavior is given. It is crucial to understand these mechanisms, particularly paying attention to the ways the modern food environment induces excessive consumption and its contributions to the present obesity epidemic.

Fibroblast Growth Factor 21 Facilitates the Homeostatic Control of Feeding Behavior.

Fibroblast growth factor 21 (FGF21) is a stress hormone that is released from the liver in response to nutritional and metabolic challenges. In addition to its well-described effects on systemic metabolism, a growing body of literature now supports the notion that FGF21 also acts via the central nervous system to control feeding behavior. Here we review the current understanding of FGF21 as a hormone regulating feeding behavior in rodents, non-human primates, and humans. First, we examine the nutritional contexts that induce FGF21 secretion. Initial reports describing FGF21 as a ‘starvation hormone’ have now been further refined. FGF21 is now better understood as an endocrine mediator of the intracellular stress response to various nutritional manipulations, including excess sugars and alcohol, caloric deficits, a ketogenic diet, and amino acid restriction. We discuss FGF21’s effects on energy intake and macronutrient choice, together with our current understanding of the underlying neural mechanisms. We argue that the behavioral effects of FGF21 function primarily to maintain systemic macronutrient homeostasis, and in particular to maintain an adequate supply of protein and amino acids for use by the cells.

As early as birth, oxytocin plays a key role in both food and social behavior

Oxytocin (OT) is a neurohormone that regulates the so-called "social brain" and is mainly studied in adulthood. During postnatal development, the mechanisms by which the OT system structures various behaviors are little studied. Here we present the dynamic process of postnatal development of the OT system as well as the OT functions in the perinatal period that are essential for shaping social behaviors. Specifically, we discuss the role of OT, in the newborn, in integrating and adapting responses to early sensory stimuli and in stimulating suckling activity. Sensory dialogue and suckling are involved in mother-infant bonds and structure future social interactions. In rodents and humans, neurodevelopmental diseases with autism spectrum disorders (ASD), such as Prader-Willi and Schaaf-Yang syndromes, are associated with sensory, feeding and behavioral deficits in infancy. We propose that in early postnatal life, OT plays a key role in stimulating the maturation of neural networks controlling feeding behavior and early social interactions from birth. Administration of OT at birth improves sensory integration of environmental factors and the relationship with the mother as well as sucking activity as we have shown in mouse models and in babies with Prader-Willi syndrome. Long-term effects have also been observed on social and cognitive behavior. Therefore, early feeding difficulties might be an early predictive marker of ASD, and OT treatment a promising option to improve feeding behavior and, in the longer term, social behavioral problems.

SNPs detection in 5’-UTR region of the MC4R gene in Garut sheep

The melanocortin-4 receptor (MC4R) gene has been linked to controlling feeding behavior and body weight. The objective of this study was to detect the polymorphism within the 5’-UTR region of the MC4R gene in Garut sheep. A total of 36 blood samples were isolated and amplified using primers (forward: 5’-TTCGTTTGGGGCAAGTCAAG-3’ and reverse: 5’-GGAAACGCTCACCAACATGT-3’). Two SNPs, g.396C/T and g.399C/G, were discovered in the 5‘UTR region based on sequence alignment (position number based on Genbank acc no. NC_040274). For both SNPs, only two genotypes were found in the samples. Both SNPs had identical allele and genotype frequencies. The C allele (86%, n=26) was higher than the T (g.396C/T) and G allele (g.399C/G) (14%, n=10). The homozygous CC genotype has a higher frequency (72%) in both SNP g.396C/T and g.399C/G, followed by CT and CG genotype (28%), respectively. The Hardy-Weinberg equilibrium analysis resulted in the sample population did not deviate (χ2<5.59). Further analysis could be suggested to provide an overview of this polymorphism effect in Garut sheep’s growth traits.

Stressed out and fed up: The effect of stress on maternal feeding behaviors and the moderating role of executive function

Stress is associated with a range of unhealthy eating habits, yet few studies have examined how stress may influence the intergenerational transmission of eating habits from parents to their children. Specifically, there is a lack of data regarding the role of stress on feeding practices. Moreover, most work investigating the associations between parental stress and their feeding behaviors has been correlational, limiting our understanding of causality. In the current study, we used an experimental design, induced high and low stress in mothers using a standard laboratory stressor, and observed mother-child interactions during a snack break. We also examined the potential role of maternal executive functioning (EF) for buffering the effects of stress on maternal feeding behaviors. Levels of maternal stress were manipulated with the Trier Social Stress Task (TSST) in a community sample (N = 80 dyads, Child Mage = 41.89 months, female = 43). We measured maternal EF with a series of computerized tasks. Maternal feeding behaviors were coded for controlling behaviors, which included pressuring and restricting behaviors. Results indicate a main effect of stress on controlling feeding behaviors, such that mothers in the high-stress condition exhibited higher levels of controlling behaviors. The effect of stress on controlling feeding behaviors was ameliorated among mothers with higher levels of EF after controlling for child age and income. Results provide causal evidence for the role of stress on feeding behaviors and suggest EF as a factor to be considered in the treatment and prevention of diet-related illnesses.