Project description:BackgroundConditioned eating in response to external food cues may contribute to obesity risk in young children.ObjectivesTo develop a brief, parent-reported scale to measure external food cue responsiveness for preschool-age children.MethodsFocus groups with parents of preschool-age children were conducted to create an initial pool of items reflecting children's behavioral responses to external food cues. Items were included in a nationally-distributed online survey of parents of preschool-age children (n = 456). Factor analysis was used to reduce the initial item pool, the scale's psychometric properties were assessed, and scores were correlated with reported snacking behaviors.ResultsNine items met inclusion criteria in the final scale, which had high internal consistency (alpha = 0.86). Final scores were the mean across the nine items. External food cue responsiveness was greater among children with, versus without, usual TV advertisement exposure. Furthermore, greater external food cue responsiveness mediated the relationship between children's usual TV advertisement exposure and snacking during TV viewing. Findings remained statistically significant when adjusted for food responsiveness as measured with the Child Eating Behavior Questionnaire.ConclusionsFindings provide preliminary evidence that external food cue responsiveness is measurable by parental report in preschool-age children.
Project description:Physiological needs bias perception and attention to relevant sensory cues. This process is 'hijacked' by drug addiction, causing cue-induced cravings and relapse. Similarly, its dysregulation contributes to failed diets, obesity, and eating disorders. Neuroimaging studies in humans have implicated insular cortex in these phenomena. However, it remains unclear how 'cognitive' cortical representations of motivationally relevant cues are biased by subcortical circuits that drive specific motivational states. Here we develop a microprism-based cellular imaging approach to monitor visual cue responses in the insular cortex of behaving mice across hunger states. Insular cortex neurons demonstrate food-cue-biased responses that are abolished during satiety. Unexpectedly, while multiple satiety-related visceral signals converge in insular cortex, chemogenetic activation of hypothalamic 'hunger neurons' (expressing agouti-related peptide (AgRP)) bypasses these signals to restore hunger-like response patterns in insular cortex. Circuit mapping and pathway-specific manipulations uncover a pathway from AgRP neurons to insular cortex via the paraventricular thalamus and basolateral amygdala. These results reveal a neural basis for state-specific biased processing of motivationally relevant cues.
Project description:BackgroundWhile neuroimaging studies have revealed that reward dysfunction may similarly contribute to obesity and addiction, no prior studies have examined neural responses in individuals who meet the "clinical" food addiction phenotype.MethodsWomen (n = 44) with overweight and obesity, nearly half of whom (n = 20) met criteria for moderate-to-severe Yale Food Addiction Scale 2.0 (YFAS 2.0) food addiction, participated in a functional magnetic resonance imaging cue reactivity task. Participants viewed images of highly processed foods, minimally processed foods, and household objects while thinking about how much they wanted each item. Differences in neural responses by YFAS 2.0 food addiction to highly processed and minimally processed food cues were investigated.ResultsThere was a significant interaction between participant group and neural response in the right superior frontal gyrus to highly versus minimally processed food cues (r = 0.57). Individuals with YFAS 2.0 food addiction exhibited modest, elevated responses in the superior frontal gyrus for highly processed food images and more robust, decreased activations for minimally processed food cues, whereas participants in the control group showed the opposite responses in this region. Across all participants, the household items elicited greater activation than the food cues in regions associated with interoceptive awareness and visuospatial attention (e.g., insula, inferior frontal gyrus, inferior parietal lobe).ConclusionsWomen with overweight or obesity and YFAS 2.0 food addiction, compared to those with only overweight or obesity, exhibited differential responses to highly and minimally processed food cues in a region previously associated with cue-induced craving in persons with a substance-use disorder. Overall, the present work provides further support for the utility of the food addiction phenotype within overweight and obesity.
Project description:There is increasing evidence that brain-derived neurotrophic factor (BDNF) impacts on the development of obesity. We are the first to test the hypothesis that BDNF levels might be associated with neural reactivity to food cues in patients suffering from obesity and healthy controls. We assessed visual food cue-induced neural response in 19 obese patients and 20 matched controls using functional magnetic resonance imaging and analyzed the associations between BDNF levels, food cue-reactivity and food craving. Whole-brain analysis in both groups revealed that food cues elicited higher neural activation in clusters of mesolimbic brain areas including the insula (food > neutral). Patients suffering from obesity showed a significant positive correlation between plasma BDNF levels and visual food cue-reactivity in the bilateral insulae. In addition, patients suffering from obesity with positive food cue-induced insula activation also reported significantly higher food craving than those with low cue-reactivity-an effect that was absent in normal weight participants. The present findings implicate that BDNF levels in patients suffering from obesity might be involved in food craving and obesity in humans. This highlights the importance to consider BDNF pathways when investigating obesity and obesity treatment.
Project description:Obesity and smoking constitute two of the main causes of preventable deaths in the developed countries today. Many smokers motivate consumption as a means to control their body weight because smoking cessation increases the risk to gain weight. Although it is well established that nicotine reduces feeding in animals and that smoking is associated with reduced body weight in quasi-experimental studies of humans, acute nicotine effects are mixed and little is known about the brain networks supporting these effects. Thus, we investigated 26 normal-weighted never-smokers who received either nicotine (2?mg) or placebo gums following a double-blinded randomized cross-over design. We used functional magnetic resonance imaging (fMRI) to investigate reactivity to palatable food cues after both overnight fasting and following a standardized caloric intake (75?g oral glucose tolerance test (OGTT)). Participants viewed food or low-level control pictures in a block design and rated their current appetite after each block. Nicotine had a small- to medium-sized effect on subjective appetite and significantly altered food-cue reactivity in a region sensitive to caloric intake that extended from the right hypothalamus to the basal ganglia. During placebo sessions, the OGTT reduced functional coupling of this region with a 'salience network' (ie, amygdala, ventromedial prefrontal cortex) in processing of food pictures. Furthermore, nicotine reduced coupling with the nucleus accumbens and the OGTT reduced coupling with an 'interoceptive network' (ie, insula, operculum) instead. We conclude that locally restricted acute effects of nicotine in the hypothalamic area have profound effects on food-processing networks.
Project description:Food cue-reactivity tasks are used to induce and evaluate food cravings. Extant research has implicated the role of tasting foods in heightening cue-elicited food craving. The present study was the first to evaluate a taste manipulation during a food cue-reactivity task to optimize cue-elicited craving and predict food intake. Participants with overweight/obesity (N = 35; M age = 33.46 years [SD = 13.27]; M BMI = 32.91 kg/m2 [SD = 5.34]) engaged in one laboratory session and were randomized to a 'No Taste' or 'Taste' condition. All participants reported baseline food craving and observed two types of high-calorie food cues during a cue-reactivity task: photographic and real foods. The Taste group tasted real food cues and the No Taste group did not. Cue-elicited craving was assessed after the presentation of each food cue. Calorie intake of palatable foods was subsequently measured during a bogus taste test. Results indicated that cue-elicited craving to high-calorie foods was greater for the No Taste relative to the Taste group and that calorie intake was greater for the Taste relative to the No Taste group; both effects were nonsignificant, but of medium-size. Cue-elicited craving was significantly greater following exposure to high-calorie real food cues compared to photographic food cues. Results provide initial evidence that presenting high-calorie real (vs. photographic) food cues and forgoing taste manipulation during a food cue-reactivity task may optimize cue-elicited craving, and that taste manipulation could increase subsequent food intake. Future research should be conducted to replicate findings in larger samples with greater power to detect significant effects.
Project description:ObjectiveFood-cue-reactivity entails neural and experiential responses to the sight and smell of attractive foods. Negative emotions can modulate such cue-reactivity and this might be central to the balance between restrictive versus bulimic symptomatology in Anorexia Nervosa (AN) and Bulimia Nervosa (BN).MethodPleasantness ratings and electrocortical responses to food images were measured in patients with AN (n = 35), BN (n = 32) and matched healthy controls (HC, n = 35) in a neutral state and after idiosyncratic negative emotion induction while electroencephalography (EEG) was recorded. The EEG data were analyzed using a mass testing approach.ResultsIndividuals with AN showed reduced pleasantness for foods compared to objects alongside elevated widespread occipito-central food-object discrimination between 170 and 535 ms, indicative of strong neural cue-reactivity. Food-object discrimination was further increased in the negative emotional condition between 690 and 1200 ms over centroparietal regions. Neither of these effects was seen in individuals with BN.DiscussionEmotion modulated food-cue-reactivity in AN might reflect a decreased appetitive response in negative mood. Such specific (emotion-)regulatory strategies require more theoretical work and clinical attention. The absence of any marked effects in BN suggests that emotional cue-reactivity might be less prominent in this group or quite specific to certain emotional contexts or food types.Public significanceNegative affectivity is a risk factor for the development of eating disorders and individuals with eating disorders experience problems with emotion regulation. To better understand the effects of negative emotions, the present study investigated how they affected neural correlates of food perception in anorexia nervosa and bulimia nervosa.
Project description:ObjectiveTheories on emotional eating are central to our understanding of etiology, maintenance, and treatment of binge eating. Yet, findings on eating changes under induced negative emotions in binge-eating disorder (BED) are equivocal. Thus, we studied whether food-cue reactivity is potentiated under negative emotions in BED, which would point toward a causal role of emotional eating in this disorder.MethodsPatients with BED (n = 24) and a control group without eating disorders (CG; n = 69) completed a food picture reactivity task after induction of negative versus neutral emotions. Food-cue reactivity (self-reported food pleasantness, desire to eat [DTE], and corrugator supercilii muscle response, electromyogram [EMG]) was measured for low- and high-caloric food pictures.ResultsPatients with BED showed emotion-potentiated food-cue reactivity compared to controls: Pleasantness and DTE ratings and EMG response were increased in BED during negative emotions. This was independent of caloric content of the images.ConclusionsFood-cue reactivity in BED was consistent with emotional eating theories and points to a heightened response to all foods regardless of calorie content. The discrepancy of appetitive ratings with the aversive corrugator response points to ambivalent food responses under negative emotions in individuals with BED.