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The neural mechanisms underlying susceptibility to eating more in response to large portions (i.e., the portion size effect) remain unclear. Thus, the present study examined how neural responses to portion size relate to changes in weight and energy consumed as portions increase. Associations were examined across brain regions traditionally implicated in appetite control (i.e., an appetitive network) as well as the cerebellum, which has recently been implicated in appetite-related processes. Children without obesity (i.e., BMI-for-age-and-sex percentile < 90; N = 63; 55% female) viewed images of larger and smaller portions of food during fMRI and, in separate sessions, ate four meals that varied in portion size. Individual-level linear and quadratic associations between intake (kcal, grams) and portion size (i.e., portion size slopes) were estimated. The response to portion size in cerebellar lobules IV–VI was associated with the quadratic portion size slope estimated from gram intake; a greater response to images depicting smaller compared to larger portions was associated with steeper increases in intake with increasing portion sizes. Within the appetitive network, neural responses were not associated with portion size slopes. A decreased cerebellar response to larger amounts of food may increase children's susceptibility to overeating when excessively large portions are served. [ABSTRACT FROM AUTHOR]

Background The novel liver-gut hormone liver-expressed antimicrobial peptide-2 (LEAP2) is a centrally acting inverse agonist, and competitive antagonist of orexigenic acyl ghrelin (AG), at the GH secretagogue receptor, reducing food intake in rodents. In humans, the effects of LEAP2 on eating behavior and mechanisms behind the postprandial increase in LEAP2 are unclear, though this is reciprocal to the postprandial decrease in plasma AG. Methods Plasma LEAP2 was measured in a secondary analysis of a previous study. Twenty-two adults without obesity attended after an overnight fast, consuming a 730-kcal meal without or with subcutaneous AG administration. Postprandial changes in plasma LEAP2 were correlated with postprandial changes in appetite, high-energy (HE) or low-energy (LE) food cue reactivity using functional magnetic resonance imaging, ad libitum food intake, and plasma/serum AG, glucose, insulin, and triglycerides. Results Postprandial plasma LEAP2 increased by 24.5% to 52.2% at 70 to 150 minutes, but was unchanged by exogenous AG administration. Postprandial increases in LEAP2 correlated positively with postprandial decreases in appetite, and cue reactivity to HE/LE and HE food in anteroposterior cingulate cortex, paracingulate cortex, frontal pole, and middle frontal gyrus, with similar trend for food intake. Postprandial increases in LEAP2 correlated negatively with body mass index, but did not correlate positively with increases in glucose, insulin, or triglycerides, nor decreases in AG. Conclusions These correlational findings are consistent with a role for postprandial increases in plasma LEAP2 in suppressing human eating behavior in adults without obesity. Postprandial increases in plasma LEAP2 are unrelated to changes in plasma AG and the mediator(s) remain uncertain. [ABSTRACT FROM AUTHOR]

Acute exercise suppresses appetite and alters food-cue reactivity, but the extent exercise-induced changes in cerebral blood flow (CBF) influences the blood-oxygenlevel- dependent (BOLD) signal during appetite-related paradigms is not known. This study examined the impact of acute running on visual food-cue reactivity and explored whether such responses are influenced by CBF variability. In a randomised crossover design, 23 men (mean ± SD: 24 ± 4 years, 22.9 ± 2.1 kg/m2) completed fMRI scans before and after 60 min of running (68% ± 3% peak oxygen uptake) or rest (control). Five-minute pseudo-continuous arterial spin labelling fMRI scans were conducted for CBF assessment before and at four consecutive repeat acquisitions after exercise/rest. BOLD-fMRI was acquired during a food-cue reactivity task before and 28 min after exercise/rest. Food-cue reactivity analysis was performed with and without CBF adjustment. Subjective appetite ratings were assessed before, during and after exercise/rest. Exercise CBF was higher in grey matter, the posterior insula and in the region of the amygdala/hippocampus, and lower in the medial orbitofrontal cortex and dorsal striatum than control (main effect trial p ≤ .018). No time-by-trial interactions for CBF were identified (p ≥ .087). Exercise induced moderate-to-large reductions in subjective appetite ratings (Cohen's d = 0.53--0.84; p ≤ .024) and increased food-cue reactivity in the paracingulate gyrus, hippocampus, precuneous cortex, frontal pole and posterior cingulate gyrus. Accounting for CBF variability did not markedly alter detection of exercise-induced BOLD signal changes. Acute running evoked overall changes in CBF that were not time dependent and increased food-cue reactivity in regions implicated in attention, anticipation of reward, and episodic memory independent of CBF. [ABSTRACT FROM AUTHOR]

The neural underpinnings of the integration of internal and external cues that reflect nutritional status are poorly understood in humans. The hypothalamus is a key integrative area involved in short‐ and long‐term energy intake regulation. Hence, we examined the effect of hunger state on the hypothalamus network using functional magnetic resonance imaging. In a multicenter study, participants performed a food cue viewing task either fasted or sated on two separate days. We evaluated hypothalamic functional connectivity (FC) using psychophysiological interactions during high versus low caloric food cue viewing in 107 adults (divided into four groups based on age and body mass index [BMI]; age range 24–76 years; BMI range 19.5–41.5 kg/m2). In the sated compared to the fasted condition, the hypothalamus showed significantly higher FC with the bilateral caudate, the left insula and parts of the left inferior frontal cortex. Interestingly, we observed a significant interaction between hunger state and BMI group in the dorsolateral prefrontal cortex (DLPFC). Participants with normal weight compared to overweight and obesity showed higher FC between the hypothalamus and DLPFC in the fasted condition. The current study showed that task‐based FC of the hypothalamus can be modulated by internal (hunger state) and external cues (i.e., food cues with varying caloric content) with a general enhanced communication in the sated state and obesity‐associated differences in hypothalamus to DLPFC communication. This could potentially promote overeating in persons with obesity. [ABSTRACT FROM AUTHOR]

Children of overweight and obese parents have an increased risk of obesity. Little is known the neural mechanisms underlying this relationship, specifically the brain systems implicated in self-regulation of food intake. The primary goal here is to examine relationships between maternal body mass index (BMI) and brain responses to food cues in children. Seventy-six children (8.62 ± 1.02 years; 28 M,48F) were included in this study. Height and weight were assessed for children and their biological parents. Maternal height and weight before pregnancy were extracted from the Electronic Medical Records (EMR). BMI (kg/m2) or BMIz (age- and sex-specific BMI) were calculated. Children underwent a magnetic resonance imaging session where they viewed food and non-food images before and after glucose ingestion. The dorsolateral prefrontal cortex (dlPFC) and anterior cingulate cortex (ACC) food cue reactivity was the measurement of interest for region-of-interest (ROI) analyses. Whole-brain exploratory analysis was performed as well. Non-parametric methods were used for data analysis. ROI and whole brain analyses showed that maternal current BMI was inversely associated with child's ACC and dlPFC food cue reactivity after glucose ingestion, adjusting for age and sex. No significant relationships were found between paternal BMI and child's food cue reactivity. Child BMIz was negatively associated with the ACC food cue reactivity after glucose ingestion. Our results supported the role of maternal adiposity on child's responses to appetitive food cues in brain self-regulation circuitry, which may influence eating behavior and obesity risk in children. [ABSTRACT FROM AUTHOR]

Objective: Emotion regulation difficulties in anorexia nervosa (AN) and bulimia nervosa (BN) might underlie bingeing and purging in BN, extreme fasting in AN, or combinations of these symptoms in binge‐purge type AN. In this study, we tested for decreased food cue reactivity in response to negative emotions in AN, and the opposite pattern for BN. Furthermore, we explored subgroup differences (restrictive vs. binge‐purging AN; history of AN in BN). Method: Patients with AN (n = 41), BN (n = 39), and matched controls (n = 70) completed an emotional eating questionnaire. In a laboratory experiment, we induced negative emotions and measured food cue reactivity (pleasantness, desire to eat (DTE), and corrugator muscle activity). Results: AN reported emotional undereating, while BN reported emotional overeating. In the laboratory task, BN showed increased DTE and an appetitive corrugator response during negative emotions, selectively towards high‐calorie foods. AN showed generalized reduced cue reactivity to high‐calorie food regardless of emotional state. This pattern appears to be characteristic of restrictive AN, while cue reactivity of both BN subgroups pointed towards emotional overeating. Conclusions: The emotional over‐ versus undereating framework might help to explain bingeing and restricting along the anorectic‐bulimic disorder spectrum, which calls for novel transdiagnostic theories and subgroup‐specific treatments. Highlights: Emotional eating might be an emotion regulation strategy in both bulimia nervosa (BN) and anorexia nervosa (AN).While AN shows decreased reactivity to food pictures in negative mood, BN shows increased reactivity.These reactions might explain restriction and bingeing symptomatology and have the potential to discriminate between eating disorder subtypes. [ABSTRACT FROM AUTHOR]

Neural patterns associated with viewing energy-dense foods can predict changes in eating-related outcomes. However, most research on this topic is limited to one follow-up time point, and single outcome measures. The present study seeks to add to that literature by employing a more refined assessment of food craving and consumption outcomes along with a more detailed neurobiological model of behavior change over several time points. Here, a community sample of 88 individuals (age: M = 39.17, SD = 3.47; baseline BMI: M = 31.5, SD = 3.9, range 24–42) with higher body mass index (BMI) performed a food craving reactivity and regulation task while undergoing functional magnetic resonance imaging. At that time—and 1, 3, and 6 months later—participants reported craving for and consumption of healthy and unhealthy foods via the Food Craving Inventory (FCI) and ASA24 (N at 6 months = 52–55 depending on the measure). A priori hypotheses that brain activity associated with both viewing and regulating personally desired unhealthy, energy-dense foods would be associated with self-reported craving for and consumption of unhealthy foods at baseline were not supported by the data. Instead, regression models controlling for age, sex, and BMI demonstrated that brain activity across several regions measured while individuals were regulating their desires for unhealthy food was associated with the self-reported craving for and consumption of healthy food. The hypothesis that vmPFC activity would predict patterns of healthier eating was also not supported. Instead, linear mixed models controlling for baseline age and sex, as well as changes in BMI, revealed that more regulation-related activity in the dlPFC, dACC, IFG, and vmPFC at baseline predicted decreases in the craving for and consumption of healthy foods over the course of 6 months. [ABSTRACT FROM AUTHOR]

In today's society, obesity rates are rising as food intake is no longer only a response to physiological hunger signals that ensure survival. Eating can represent a reward, a response to boredom, or stress reduction and emotion regulation. While most people decrease food intake in response to stress or negative emotions, some do the opposite. Yet, it is unclear who shows emotional overeating under which circumstances. Emotion regulation theories describe emotional overeating as a learned strategy to down-regulate negative emotions. Cognitive theories, by contrast, attribute emotional overeating to perceived diet breaches in individuals who chronically attempt to diet. After consuming "forbidden foods", they eat more than individuals who do not restrict their food intake. This laboratory study investigated emotional overeating by exposing individuals to a personalized emotion induction while showing images of palatable foods. Outcome variables indexed cue reactivity to food images through picture ratings (valence, desire to eat), facial expressions (electromyography of the corrugator supercilii muscle), and brain reactivity by detecting event-related potentials (ERPs) by means of electroencephalography (EEG). The influence of emotion condition (negative, neutral) and individual differences (self-reported trait emotional and restrained eating) on outcome variables was assessed. Valence ratings and appetitive reactions of the corrugator muscle to food pictures showed a relative increase in the negative condition for individuals with higher emotional eating scores, with the opposite pattern in lower scores. Desire to eat ratings showed a similar pattern in individuals who showed a strong response to the emotion induction manipulation, indicative of a dose-response relationship. Although no differences between conditions were found for ratings or corrugator activity with restrained eating as a predictor, an ERP at P300 showed increased activation when viewing food compared to objects in the negative condition. Findings support emotion regulation theories: Emotional eaters showed an appetitive reaction in rating patterns and corrugator activity. EEG findings (increased P300) suggest a motivated attention toward food in restrained eaters, which supports cognitive theories. However, this did not translate to other variables, which might demonstrate successful restraint. Future studies may follow up on these findings by investigating eating disorders with emotion regulation difficulties. [ABSTRACT FROM AUTHOR]

Emotions can influence our eating behaviors. Facing an acute stressor or being in a positive mood are examples of situations that tend to modify appetite. However, the question of how the brain integrates these emotion-related changes in food processing remains elusive. Here, we designed an emotional priming fMRI task to test if amygdala activity during food pictures differs depending on the emotional context. Fifty-eight female participants completed a novel emotional priming task, in which emotional images of negative, neutral, or positive situations were followed by pictures of either foods or objects. After priming in each trial, participants rated how much they liked the shown foods or objects. We analyzed how brain activity during the contrast "foods > objects" changed according to the emotional context—in the whole brain and in the amygdala. We also examined the potential effect of adiposity (i.e., waist circumference). We observed a higher difference between liking scores for foods and objects after positive priming than after neutral priming. In the left amygdala, activity in the contrast "foods > objects" was higher after neutral priming relative to negative priming. Waist circumference was not significantly related to this emotional priming effect on food processing. Our results suggest that emotional context alters food and nonfood perception, both in terms of liking scores and with regard to engagement of the left amygdala. Moreover, our findings indicate that emotional context has an impact on the salience advantage of food, possibly affecting eating behavior. [ABSTRACT FROM AUTHOR]

The conscious perception of the hedonic sensory properties of caloric foods is commonly believed to guide our dietary choices. Current and traditional models implicate the consciously perceived hedonic qualities of food as driving overeating, whereas subliminal signals arising from the gut would curb our uncontrolled desire for calories. Here we review recent animal and human studies that support a markedly different model for food reward. These findings reveal in particular the existence of subcortical body-to-brain neural pathways linking gastrointestinal nutrient sensors to the brain's reward regions. Unexpectedly, consciously perceptible hedonic qualities appear to play a less relevant, and mostly transient, role in food reinforcement. In this model, gut-brain reward pathways bypass cranial taste and aroma sensory receptors and the cortical networks that give rise to flavor perception. They instead reinforce behaviors independently of the cognitive processes that support overt insights into the nature of our dietary decisions. [ABSTRACT FROM AUTHOR]

Color nutrition information (CNI) based on a traffic light system conveys information about food quality with a glance. The color red typically indicates detrimental food characteristics (e.g., very high sugar content) and aims at inhibiting food shopping and consumption. Red may, however, also elicit cross-modal associations with sweet taste, which is a preferable food characteristic. We conducted two experiments. An eye-tracking study investigated whether CNI has an effect on cue reactivity (dwell time, saccadic latency, wanting/liking) for sweet foods. The participants were presented with images depicting sweets (e.g., cake). Each image was preceded by a colored circle that informed about the sugar content of the food (red = high, green = low, gray = unknown). It was tested whether the red circle would help the participants to direct their gaze away from the 'high sugar' item. A second experiment investigated whether colored prime circles (red, green, gray) without nutrition information would influence the assumed sweetness of a food. In Experiment 1, CNI had the opposite of the intended effect. Dwell time and saccadic latency were higher for food items preceded by a red compared to a green circle. This unintended response was positively associated with participants' liking of sweet foods. CNI did not change the wanting/liking of the displayed foods. In Experiment 2, we found no evidence for color priming on the assumed sweetness of food. Our results question whether CNI is helpful to influence initial cue reactivity toward sweet foods. [ABSTRACT FROM AUTHOR]

Summary: Background/Objectives: Neuroimaging investigations of brain pathways involved in reward and motivation have primarily focused on adults. This study sought to identify brain responses to visual food cues and explore its relationships with adiposity and sex in pre‐pubertal children. Methods: Brain responses to palatable food vs. non‐food cues were measured in 53 children (age: 8.18 ± .66 years; sex: 22 boys, 31 girls) after an overnight fast. Whole‐brain analysis (cluster‐correction Z > 2.3, P < .05) was performed to examine brain food cue reactivity and its relationships with adiposity and sex. Results: Greater brain activity in response to food vs. non‐food cues was observed in regions implicated in reward (orbital frontal cortex, striatum), taste (insula, postcentral gyrus), appetite (hypothalamus), emotion (amygdala), memory (hippocampus), visual processing (occipital cortex) and attention (parietal cortex). A negative association was found between percent body fat and food cue reactivity in the medial prefrontal cortex and lateral orbital frontal cortex adjusting for age and sex. Boys compared with girls had increased food cue reactivity in right hippocampus and visual cortex. Conclusions: These data suggest that body fat and sex are important moderators of brain food cue reactivity in children. [ABSTRACT FROM AUTHOR]